Econstudentlog

A few papers

i. To Conform or to Maintain Self-Consistency? Hikikomori Risk in Japan and the Deviation From Seeking Harmony.

A couple of data points and observations from the paper:

“There is an increasing number of youth in Japan who are dropping out of society and isolating themselves in their bedrooms from years to decades at a time. According to Japan’s Ministry of Health, Labor and Welfare’s first official 2003 guidelines on this culture-bound syndrome, hikikomori (social isolation syndrome) has the following specific diagnostic criteria: (1) no motivation to participate in school or work; (2) no signs of schizophrenia or any other known psychopathologies; and (3) persistence of social withdrawal for at least six months.”

“One obvious dilemma in studying hikikomori is that most of those suffering from hikikomori, by definition, do not seek treatment. More importantly, social isolation itself is not even a symptom of any of the DSM diagnosis often assigned to an individual afflicted with hikikomori […] The motivation for isolating oneself among a hikikomori is simply to avoid possible social interactions with others who might know or judge them (Zielenziger, 2006).”

“Saito’s (2010) and Sakai and colleagues’ (2011) data suggest that 10% to 15% of the hikikomori population suffer from an autism spectrum disorder. […] in the first epidemiological study conducted on hikikomori that was as close to a nation-wide random sample as possible, Koyama and colleagues (2010) conducted a face-to-face household survey, including a structured diagnostic interview, by randomly picking households and interviewing 4,134 individuals. They confirmed a hikikomori lifetime prevalence rate of 1.2% in their nationwide sample. Among these hikikomori individuals, the researchers found that only half suffered from a DSM-IV diagnosis. However, and more importantly, there was no particular diagnosis that was systematically associated with hikikomori. […] the researchers concluded that any DSM diagnosis was an epiphenomenon to hikikomori at best and that hikikomori is rather a “psychopathology characterized by impaired motivation” p. 72).”

ii. Does the ‘hikikomori’ syndrome of social withdrawal exist outside Japan?: A preliminary international investigation.

Purpose

To explore whether the ‘hikikomori’ syndrome (social withdrawal) described in Japan exists in other countries, and if so, how patients with the syndrome are diagnosed and treated.

Methods

Two hikikomori case vignettes were sent to psychiatrists in Australia, Bangladesh, India, Iran, Japan, Korea, Taiwan, Thailand and the USA. Participants rated the syndrome’s prevalence in their country, etiology, diagnosis, suicide risk, and treatment.

Results

Out of 247 responses to the questionnaire (123 from Japan and 124 from other countries), 239 were enrolled in the analysis. Respondents’ felt the hikikomori syndrome is seen in all countries examined and especially in urban areas. Biopsychosocial, cultural, and environmental factors were all listed as probable causes of hikikomori, and differences among countries were not significant. Japanese psychiatrists suggested treatment in outpatient wards and some did not think that psychiatric treatment is necessary. Psychiatrists in other countries opted for more active treatment such as hospitalization.

Conclusions

Patients with the hikikomori syndrome are perceived as occurring across a variety of cultures by psychiatrists in multiple countries. Our results provide a rational basis for study of the existence and epidemiology of hikikomori in clinical or community populations in international settings.”

“Our results extend rather than clarify the debate over diagnosis of hikikomori. In our survey, a variety of diagnoses, such as psychosis, depression anxiety and personality disorders, were proffered. Opinions as to whether hikikomori cases can be diagnosed using ICD-10/DSV-IV criteria differed depending on the participants’ countries and the cases’ age of onset. […] a recent epidemiological survey in Japan reported approximately a fifty-fifty split between hikikomori who had experienced a psychiatric disorder and had not [14]. These data and other studies that have not been able to diagnose all cases of hikikomori may suggest the existence of ‘primary hikikomori’ that is not an expression of any other psychiatric disorder [28,8,9,5,29]. In order to clarify differences between ‘primary hikikomori’ (social withdrawal not associated with any underlying psychiatric disorder) and ‘secondary hikikomori’ (social withdrawal caused by an established psychiatric disorder), further epidemiological and psychopathological studies are needed. […] Even if all hikikomori cases prove to be within some kind of psychiatric disorders, it is valuable to continue to focus on the hikikomori phenomenon because of its associated morbidity, similar to how suicidality is examined in various fields of psychiatry [30]. Reducing the burden of hikikomori symptoms, regardless of what psychiatric disorders patients may have, may provide a worthwhile improvement in their quality of life, and this suggests another direction of future hikikomori research.”

“Our case vignette survey indicates that the hikikomori syndrome, previously thought to exist only in Japan, is perceived by psychiatrists to exist in many other countries. It is particularly perceived as occurring in urban areas and might be associated with rapid global sociocultural changes. There is no consensus among psychiatrists within or across countries about the causes, diagnosis and therapeutic interventions for hikikomori yet.”

iii. Hikikomori: clinical and psychopathological issues (review). A poor paper, but it did have a little bit of data of interest:

“The prevalence of hikikomori is difficult to assess […]. In Japan, more than one million cases have been estimated by experts, but there is no population-based study to confirm these data (9). […] In 2008, Kiyota et al. summarized 3 population-based studies involving 12 cities and 3951 subjects, highlighting that a percentage comprised between 0.9% and 3.8% of the sample had an hikikomori history in anamnesis (11). The typical hikikomori patient is male (4:1 male-to-female ratio) […] females constitute a minor fraction of the reported cases, and usually their period of social isolation is limited.”

iv. Interpreting results of ethanol analysis in postmortem specimens: A review of the literature.

A few observations from the paper:

“A person’s blood-alcohol concentration (BAC) and state of inebriation at the time of death is not always easy to establish owing to various postmortem artifacts. The possibility of alcohol being produced in the body after death, e.g. via microbial contamination and fermentation is a recurring issue in routine casework. If ethanol remains unabsorbed in the stomach at the time of death, this raises the possibility of continued local diffusion into surrounding tissues and central blood after death. Skull trauma often renders a person unconscious for several hours before death, during which time the BAC continues to decrease owing to metabolism in the liver. Under these circumstances blood from an intracerebral or subdural clot is a useful specimen for determination of ethanol. Bodies recovered from water are particular problematic to deal with owing to possible dilution of body fluids, decomposition, and enhanced risk of microbial synthesis of ethanol. […] Alcoholics often die at home with zero or low BAC and nothing more remarkable at autopsy than a fatty liver. Increasing evidence suggests that such deaths might be caused by a pronounced ketoacidosis.”

“The concentrations of ethanol measured in blood drawn from different sampling sites tend to vary much more than expected from inherent variations in the analytical methods used [49]. Studies have shown that concentrations of ethanol and other drugs determined in heart blood are generally higher than in blood from a peripheral vein although in any individual case there are likely to be considerable variations [50–53].”

“The BAC necessary to cause death is often an open question and much depends on the person’s age, drinking experience and degree of tolerance development [78]. The speed of drinking plays a role in alcohol toxicity as does the kind of beverage consumed […] Drunkenness and hypothermia represent a dangerous combination and deaths tend to occur at a lower BAC when people are exposed to cold, such as, when an alcoholic sleeps outdoors in the winter months [78]. Drinking large amounts of alcohol to produce stupor and unconsciousness combined with positional asphyxia or inhalation of vomit are common causes of death in intoxicated individuals who die of suffocation [81–83]. The toxicity of ethanol is often considerably enhanced by the concomitant use of other drugs with their site of action in the brain, especially opiates, propoxyphene, antidepressants and some sedative hypnotics [84]. […] It seems reasonable to assume that the BAC at autopsy will almost always be lower than the maximum BAC reached during a drinking binge, owing to metabolism of ethanol taking place up until the moment of death [85–87]. During the time after discontinuation of drinking until death, the BAC might decrease appreciably depending on the speed of alcohol elimination from blood, which in heavy drinkers could exceed 20 or 30 mg/100 mL per h (0.02 or 0.03 g% per h) [88].”

“When the supply of oxygen to the body ends, the integrity of cell membranes and tissue compartments gradually disintegrate through the action of various digestive enzymes. This reflects the process of autolysis (self digestion) resulting in a softening and liquefaction of the tissue (freezing the body prevents autolysis). During this process, bacteria from the bowel invade the surrounding tissue and vascular system and the rate of infiltration depends on many factors including the ambient temperature, position of the body and whether death was caused by bacterial infection. Glucose concentrations increase in blood after death and this sugar is probably the simplest substrate for microbial synthesis of ethanol [20,68]. […] Extensive trauma to a body […] increases the potential for spread of bacteria and heightens the risk of ethanol production after death [217]. Blood-ethanol concentrations as high as 190 mg/100 mL have been reported in postmortem blood after particularly traumatic events such as explosions and when no evidence existed to support ingestion of ethanol before the disaster [218].”

v. Interventions based on the Theory of Mind cognitive model for autism spectrum disorder (ASD) (Cochrane review).

“The ‘Theory of Mind’ (ToM) model suggests that people with autism spectrum disorder (ASD) have a profound difficulty understanding the minds of other people – their emotions, feelings, beliefs, and thoughts. As an explanation for some of the characteristic social and communication behaviours of people with ASD, this model has had a significant influence on research and practice. It implies that successful interventions to teach ToM could, in turn, have far-reaching effects on behaviours and outcome.”

“Twenty-two randomised trials were included in the review (N = 695). Studies were highly variable in their country of origin, sample size, participant age, intervention delivery type, and outcome measures. Risk of bias was variable across categories. There were very few studies for which there was adequate blinding of participants and personnel, and some were also judged at high risk of bias in blinding of outcome assessors. There was also evidence of some bias in sequence generation and allocation concealment.”

“Studies were grouped into four main categories according to intervention target/primary outcome measure. These were: emotion recognition studies, joint attention and social communication studies, imitation studies, and studies teaching ToM itself. […] There was very low quality evidence of a positive effect on measures of communication based on individual results from three studies. There was low quality evidence from 11 studies reporting mixed results of interventions on measures of social interaction, very low quality evidence from four studies reporting mixed results on measures of general communication, and very low quality evidence from four studies reporting mixed results on measures of ToM ability. […] While there is some evidence that ToM, or a precursor skill, can be taught to people with ASD, there is little evidence of maintenance of that skill, generalisation to other settings, or developmental effects on related skills. Furthermore, inconsistency in findings and measurement means that evidence has been graded of ‘very low’ or ‘low’ quality and we cannot be confident that suggestions of positive effects will be sustained as high-quality evidence accumulates. Further longitudinal designs and larger samples are needed to help elucidate both the efficacy of ToM-linked interventions and the explanatory value of the ToM model itself.”

vi. Risk of Psychiatric and Neurodevelopmental Disorders Among Siblings of Probands With Autism Spectrum Disorders.

“The Finnish Prenatal Study of Autism and Autism Spectrum Disorders used a population-based cohort that included children born from January 1, 1987, to December 31, 2005, who received a diagnosis of ASD by December 31, 2007. Each case was individually matched to 4 control participants by sex and date and place of birth. […] Among the 3578 cases with ASD (2841 boys [79.4%]) and 11 775 controls (9345 boys [79.4%]), 1319 cases (36.9%) and 2052 controls (17.4%) had at least 1 sibling diagnosed with any psychiatric or neurodevelopmental disorder (adjusted RR, 2.5; 95% CI, 2.3-2.6).”

Conclusions and Relevance Psychiatric and neurodevelopmental disorders cluster among siblings of probands with ASD. For etiologic research, these findings provide further evidence that several psychiatric and neurodevelopmental disorders have common risk factors.”

vii. Treatment for epilepsy in pregnancy: neurodevelopmental outcomes in the child (Cochrane review).

“Accumulating evidence suggests an association between prenatal exposure to antiepileptic drugs (AEDs) and increased risk of both physical anomalies and neurodevelopmental impairment. Neurodevelopmental impairment is characterised by either a specific deficit or a constellation of deficits across cognitive, motor and social skills and can be transient or continuous into adulthood. It is of paramount importance that these potential risks are identified, minimised and communicated clearly to women with epilepsy.”

“Twenty-two prospective cohort studies were included and six registry based studies. Study quality varied. […] the IQ of children exposed to VPA [sodium valproate] (n = 112) was significantly lower than for those exposed to CBZ [carbamazepine] (n = 191) (MD [mean difference] 8.69, 95% CI 5.51 to 11.87, P < 0.00001). […] IQ was significantly lower for children exposed to VPA (n = 74) versus LTG [lamotrigine] (n = 84) (MD -10.80, 95% CI -14.42 to -7.17, P < 0.00001). DQ [developmental quotient] was higher in children exposed to PHT (n = 80) versus VPA (n = 108) (MD 7.04, 95% CI 0.44 to 13.65, P = 0.04). Similarly IQ was higher in children exposed to PHT (n = 45) versus VPA (n = 61) (MD 9.25, 95% CI 4.78 to 13.72, P < 0.0001). A dose effect for VPA was reported in six studies, with higher doses (800 to 1000 mg daily or above) associated with a poorer cognitive outcome in the child. We identified no convincing evidence of a dose effect for CBZ, PHT or LTG. Studies not included in the meta-analysis were reported narratively, the majority of which supported the findings of the meta-analyses.”

“The most important finding is the reduction in IQ in the VPA exposed group, which are sufficient to affect education and occupational outcomes in later life. However, for some women VPA is the most effective drug at controlling seizures. Informed treatment decisions require detailed counselling about these risks at treatment initiation and at pre-conceptual counselling. We have insufficient data about newer AEDs, some of which are commonly prescribed, and further research is required. Most women with epilepsy should continue their medication during pregnancy as uncontrolled seizures also carries a maternal risk.”

Do take note of the effect sizes reported here. To take an example, the difference between being treated with valproate and lamotrigine might equal 10 IQ points in the child – these are huge effects.

June 11, 2017 Posted by | Medicine, Neurology, Pharmacology, Psychiatry, Psychology, Studies | Leave a comment

A few papers

i. Quality of life of adolescents with autism spectrum disorders: comparison to adolescents with diabetes.

“The goals of our study were to clarify the consequences of autistic disorder without mental retardation on […] adolescents’ daily lives, and to consider them in comparison with the impact of a chronic somatic disease (diabetes) […] Scores for adolescents with ASD were significantly lower than those of the control and the diabetic adolescents, especially for friendships, leisure time, and affective and sexual relationships. On the other hand, better scores were obtained for the relationships with parents and teachers and for self-image. […] For subjects with autistic spectrum disorders and without mental retardation, impairment of quality of life is significant in adolescence and young adulthood. Such adolescents are dissatisfied with their relationships, although they often have real motivation to succeed with them.”

As someone who has both conditions, that paper was quite interesting. A follow-up question of some personal interest to me would of course be this: How do the scores/outcomes of these two groups compare to the scores of the people who have both conditions simultaneously? This question is likely almost impossible to answer in any confident manner, certainly if the conditions are not strongly dependent (unlikely), considering the power issues; global prevalence of autism is around 0.6% (link), and although type 1 prevalence is highly variable across countries, the variation just means that in some countries almost nobody gets it whereas in other countries it’s just rare; prevalence varies from 0.5 per 100.000 to 60 per 100.000 children aged 0-15 years. Assuming independence, if you look at combinations of the sort of conditions which affect one in a hundred people with those affecting one in a thousand, you’ll need on average in the order of 100.000 people to pick up just one individual with both of the conditions of interest. It’s bothersome to even try to find people like that, and good luck doing any sort of sensible statistics on that kind of sample. Of course type 1 diabetes prevalence increases with age in a way that autism does not because people continue to be diagnosed with it into late adulthood, whereas most autistics are diagnosed as children, so this makes the rarity of the condition less of a problem in adult samples, but if you’re looking at outcomes it’s arguable whether it makes sense to not differentiate between someone diagnosed with type 1 diabetes as a 35 year old and someone diagnosed as a 5 year old (are these really comparable diseases, and which outcomes are you interested in?). At least that is the case for developed societies where people with type 1 diabetes have high life expectancies; in less developed societies there may be stronger linkage between incidence and prevalence because of high mortality in the patient group (because people who get type 1 diabetes in such countries may not live very long because of inadequate medical care, which means there’s a smaller disconnect between how many new people get the disease during each time period and how many people in total have the disease than is the case for places where the mortality rates are lower). You always need to be careful about distinguishing between incidence and prevalence when dealing with conditions like T1DM with potential high mortality rates in settings where people have limited access to medical care because differential cross-country mortality patterns may be important.

ii. Exercise for depression (Cochrane review).

Background

Depression is a common and important cause of morbidity and mortality worldwide. Depression is commonly treated with antidepressants and/or psychological therapy, but some people may prefer alternative approaches such as exercise. There are a number of theoretical reasons why exercise may improve depression. This is an update of an earlier review first published in 2009.

Objectives

To determine the effectiveness of exercise in the treatment of depression in adults compared with no treatment or a comparator intervention. […]

Selection criteria 

Randomised controlled trials in which exercise (defined according to American College of Sports Medicine criteria) was compared to standard treatment, no treatment or a placebo treatment, pharmacological treatment, psychological treatment or other active treatment in adults (aged 18 and over) with depression, as defined by trial authors. We included cluster trials and those that randomised individuals. We excluded trials of postnatal depression.

Thirty-nine trials (2326 participants) fulfilled our inclusion criteria, of which 37 provided data for meta-analyses. There were multiple sources of bias in many of the trials; randomisation was adequately concealed in 14 studies, 15 used intention-to-treat analyses and 12 used blinded outcome assessors.For the 35 trials (1356 participants) comparing exercise with no treatment or a control intervention, the pooled SMD for the primary outcome of depression at the end of treatment was -0.62 (95% confidence interval (CI) -0.81 to -0.42), indicating a moderate clinical effect. There was moderate heterogeneity (I² = 63%).

When we included only the six trials (464 participants) with adequate allocation concealment, intention-to-treat analysis and blinded outcome assessment, the pooled SMD for this outcome was not statistically significant (-0.18, 95% CI -0.47 to 0.11). Pooled data from the eight trials (377 participants) providing long-term follow-up data on mood found a small effect in favour of exercise (SMD -0.33, 95% CI -0.63 to -0.03). […]

Authors’ conclusions

Exercise is moderately more effective than a control intervention for reducing symptoms of depression, but analysis of methodologically robust trials only shows a smaller effect in favour of exercise. When compared to psychological or pharmacological therapies, exercise appears to be no more effective, though this conclusion is based on a few small trials.”

iii. Risk factors for suicide in individuals with depression: A systematic review.

“The search strategy identified 3374 papers for potential inclusion. Of these, 155 were retrieved for a detailed evaluation. Thirty-two articles fulfilled the detailed eligibility criteria. […] Nineteen studies (28 publications) were included. Factors significantly associated with suicide were: male gender (OR = 1.76, 95% CI = 1.08–2.86), family history of psychiatric disorder (OR = 1.41, 95% CI= 1.00–1.97), previous attempted suicide (OR = 4.84, 95% CI = 3.26–7.20), more severe depression (OR = 2.20, 95% CI = 1.05–4.60), hopelessness (OR = 2.20, 95% CI = 1.49–3.23) and comorbid disorders, including anxiety (OR = 1.59, 95% CI = 1.03–2.45) and misuse of alcohol and drugs (OR = 2.17, 95% CI = 1.77–2.66).
Limitations: There were fewer studies than suspected. Interdependence between risk factors could not be examined.”

iv. Cognitive behaviour therapy for social anxiety in autism spectrum disorder: a systematic review.

“Individuals who have autism spectrum disorders (ASD) commonly experience anxiety about social interaction and social situations. Cognitive behaviour therapy (CBT) is a recommended treatment for social anxiety (SA) in the non-ASD population. Therapy typically comprises cognitive interventions, imagery-based work and for some individuals, behavioural interventions. Whether these are useful for the ASD population is unclear. Therefore, we undertook a systematic review to summarise research about CBT for SA in ASD.”

I mostly include this review here to highlight how reviews aren’t everything – I like them, but you can’t do reviews when a field hasn’t been studied. This is definitely the case here. The review was sort of funny, but also depressing. So much work for so little insight. Here’s the gist of it:

“Using a priori criteria, we searched for English-language peer-reviewed empirical studies in five databases. The search yielded 1364 results. Titles, abstracts and relevant publications were independently screened by two reviewers. Findings: Four single case studies met the review inclusion criteria; data were synthesised narratively. Participants (three adults and one child) were diagnosed with ASD and social anxiety disorder.”

You search the scientific literature systematically, you find more than a thousand results, and you carefully evaluate which ones of them should be included in this kind of study …and what you end up with is 4 individual case studies…

(I won’t go into the results of the study as they’re pretty much worthless.)

v. Immigrant Labor Market Integration across Admission Classes.

“We examine patterns of labor market integration across immigrant groups. The study draws on Norwegian longitudinal administrative data covering labor earnings and social insurance claims over a 25‐year period and presents a comprehensive picture of immigrant‐native employment and social insurance differentials by admission class and by years since entry.”

Some quotes from the paper:

“A recent study using 2011 administrative data from Sweden finds an average employment gap to natives of 30 percentage points for humanitarian migrants (refugees) and 26 percentage point for family immigrants (Luik et al., 2016).”

“A considerable fraction of the immigrants leaves the country after just a few years. […] this is particularly the case for immigrants from the old EU and for students and work-related immigrants from developing countries. For these groups, fewer than 50 percent remain in the country 5 years after entry. For refugees and family migrants, the picture is very different, and around 80 percent appear to have settled permanently in the country. Immigrants from the new EU have a settlement pattern somewhere in between, with approximately 70 percent settled on a permanent basis. An implication of such differential outmigration patterns is that the long-term labor market performance of refugees and family immigrants is of particular economic and fiscal importance. […] the varying rates of immigrant inflows and outflows by admission class, along with other demographic trends, have changed the composition of the adult (25‐66) population between 1990 and 2015. In this population segment, the overall immigrant share increased from 4.9 percent in 1990 to 18.7 percent in 2015 — an increase by a factor of 3.8 over 25 years. […] Following the 2004 EU enlargement, the fraction of immigrants in Norway has increased by a steady rate of approximately one percentage point per year.”

“The trends in population and employment shares varies considerably across admission classes, with employment shares of refugees and family immigrants lagging their growth in population shares. […] In 2014, refugees and family immigrants accounted for 12.8 percent of social insurance claims, compared to 5.7 percent of employment (and 7.7 percent of the adult population). In contrast, the two EU groups made up 9.3 percent of employment (and 8.8 percent of the adult population) but only 3.6 percent of social insurance claimants. Although these patterns do illuminate the immediate (short‐term) fiscal impacts of immigration at each particular point in time, they are heavily influenced by each year’s immigrant composition – in terms of age, years since migration, and admission classes – and therefore provide little information about long‐term consequences and impacts of fiscal sustainability. To assess the latter, we need to focus on longer‐term integration in the Norwegian labor market.”

Which they then proceed to do in the paper. From the results of those analyses:

“For immigrant men, the sample average share in employment (i.e., whose main source of income is work) ranges from 58 percent for refugees to 89 percent for EU immigrants, with family migrants somewhere between (around 80 percent). The average shares with social insurance as the main source of income ranges from only four percent for EU immigrants to as much as 38 percent for refugees. The corresponding shares for native men are 87 percent in employment and 12 percent with social insurance as their main income source. For women, the average shares in employment vary from 46 percent for refugees to 85 percent for new EU immigrants, whereas the average shares in social insurance vary from five percent for new EU immigrants to 42 percent for refugees. The corresponding rates for native women are 80 percent in employment and 17 percent with social insurance as their main source of income.”

“The profiles estimated for refugees are particularly striking. For men, we find that the native‐immigrant employment gap reaches its minimum value at 20 percentage points after five to six years of residence. The gap then starts to increase quite sharply again, and reaches 30 percentage points after 15 years. This development is mirrored by a corresponding increase in social insurance dependency. For female refugees, the employment differential reaches its minimum of 30 percentage points after 5‐9 years of residence. The subsequent decline is less dramatic than what we observe for men, but the differential stands at 35 percentage points 15 years after admission. […] The employment difference between refugees from Bosnia and Somalia is fully 22.2 percentage points for men and 37.7 points for women. […] For immigrants from the old EU, the employment differential is slightly in favor of immigrants regardless of years since migration, and the social insurance differentials remain consistently negative. In other words, employment of old EU immigrants is almost indistinguishable from that of natives, and they are less likely to claim social insurance benefits.”

vi. Glucose Peaks and the Risk of Dementia and 20-Year Cognitive Decline.

“Hemoglobin A1c (HbA1c), a measure of average blood glucose level, is associated with the risk of dementia and cognitive impairment. However, the role of glycemic variability or glucose excursions in this association is unclear. We examined the association of glucose peaks in midlife, as determined by the measurement of 1,5-anhydroglucitol (1,5-AG) level, with the risk of dementia and 20-year cognitive decline.”

“Nearly 13,000 participants from the Atherosclerosis Risk in Communities (ARIC) study were examined. […] Over a median time of 21 years, dementia developed in 1,105 participants. Among persons with diabetes, each 5 μg/mL decrease in 1,5-AG increased the estimated risk of dementia by 16% (hazard ratio 1.16, P = 0.032). For cognitive decline among participants with diabetes and HbA1c <7% (53 mmol/mol), those with glucose peaks had a 0.19 greater z score decline over 20 years (P = 0.162) compared with those without peaks. Among participants with diabetes and HbA1c ≥7% (53 mmol/mol), those with glucose peaks had a 0.38 greater z score decline compared with persons without glucose peaks (P < 0.001). We found no significant associations in persons without diabetes.

CONCLUSIONS Among participants with diabetes, glucose peaks are a risk factor for cognitive decline and dementia. Targeting glucose peaks, in addition to average glycemia, may be an important avenue for prevention.”

vii. Gaze direction detection in autism spectrum disorder.

“Detecting where our partners direct their gaze is an important aspect of social interaction. An atypical gaze processing has been reported in autism. However, it remains controversial whether children and adults with autism spectrum disorder interpret indirect gaze direction with typical accuracy. This study investigated whether the detection of gaze direction toward an object is less accurate in autism spectrum disorder. Individuals with autism spectrum disorder (n = 33) and intelligence quotients–matched and age-matched controls (n = 38) were asked to watch a series of synthetic faces looking at objects, and decide which of two objects was looked at. The angle formed by the two possible targets and the face varied following an adaptive procedure, in order to determine individual thresholds. We found that gaze direction detection was less accurate in autism spectrum disorder than in control participants. Our results suggest that the precision of gaze following may be one of the altered processes underlying social interaction difficulties in autism spectrum disorder.”

“Where people look at informs us about what they know, want, or attend to. Atypical or altered detection of gaze direction might thus lead to impoverished acquisition of social information and social interaction. Alternatively, it has been suggested that abnormal monitoring of inner states […], or the lack of social motivation […], would explain the reduced tendency to follow conspecific gaze in individuals with ASD. Either way, a lower tendency to look at the eyes and to follow the gaze would provide fewer opportunities to practice GDD [gaze direction detection – US] ability. Thus, impaired GDD might either play a causal role in atypical social interaction, or conversely be a consequence of it. Exploring GDD earlier in development might help disentangle this issue.”

June 1, 2017 Posted by | Diabetes, Economics, Epidemiology, Medicine, Neurology, Psychiatry, Psychology, Studies | Leave a comment

A few diabetes papers of interest

i. Cost-Effectiveness of Prevention and Treatment of the Diabetic Foot.

“A risk-based Markov model was developed to simulate the onset and progression of diabetic foot disease in patients with newly diagnosed type 2 diabetes managed with care according to guidelines for their lifetime. Mean survival time, quality of life, foot complications, and costs were the outcome measures assessed. Current care was the reference comparison. Data from Dutch studies on the epidemiology of diabetic foot disease, health care use, and costs, complemented with information from international studies, were used to feed the model.

RESULTS—Compared with current care, guideline-based care resulted in improved life expectancy, gain of quality-adjusted life-years (QALYs), and reduced incidence of foot complications. The lifetime costs of management of the diabetic foot following guideline-based care resulted in a cost per QALY gained of <$25,000, even for levels of preventive foot care as low as 10%. The cost-effectiveness varied sharply, depending on the level of foot ulcer reduction attained.

CONCLUSIONS—Management of the diabetic foot according to guideline-based care improves survival, reduces diabetic foot complications, and is cost-effective and even cost saving compared with standard care.”

I won’t go too deeply into the model setup and the results but some of the data they used to feed the model were actually somewhat interesting in their own right, and I have added some of these data below, along with some of the model results.

“It is estimated that 80% of LEAs [lower extremity amputations] are preceded by foot ulcers. Accordingly, it has been demonstrated that preventing the development of foot ulcers in patients with diabetes reduces the frequency of LEAs by 49–85% (6).”

“An annual ulcer incidence rate of 2.1% and an amputation incidence rate of 0.6% were among the reference country-specific parameters derived from this study and adopted in the model.”

“The health outcomes results of the cohort following standard care were comparable to figures reported for diabetic patients in the Netherlands. […] In the 10,000 patients followed until death, a total of 1,780 ulcer episodes occurred, corresponding to a cumulative ulcer incidence of 17.8% and an annual ulcer incidence of 2.2% (mean annual ulcer incidence for the Netherlands is 2.1%) (17). The number of amputations observed was 362 (250 major and 112 minor), corresponding to a cumulative incidence of 3.6% and an annual incidence of 0.4% (mean annual amputation incidence reported for the Netherlands is 0.6%) (17).”

“Cornerstones of guidelines-based care are intensive glycemic control (IGC) and optimal foot care (OFC). Although health benefits and economic efficiency of intensive blood glucose control (8) and foot care programs (914) have been individually reported, the health and economic outcomes and the cost-effectiveness of both interventions have not been determined. […] OFC according to guidelines includes professional protective foot care, education of patients and staff, regular inspection of the feet, identification of the high-risk patient, treatment of nonulcerative lesions, and a multidisciplinary approach to established foot ulcers. […] All cohorts of patients simulated for the different scenarios of guidelines care resulted in improved life expectancy, QALYs gained, and reduced incidence of foot ulcers and LEA compared with standard care. The largest effects on these outcomes were obtained when patients received IGC + OFC. When comparing the independent health effects of the two guidelines strategies, OFC resulted in a greater reduction in ulcer and amputation rates than IGC. Moreover, patients who received IGC + OFC showed approximately the same LEA incidence as patients who received OFC alone. The LEA decrease obtained was proportional to the level of foot ulcer reduction attained.”

“The mean total lifetime costs of a patient under either of the three guidelines care scenarios ranged from $4,088 to $4,386. For patients receiving IGC + OFC, these costs resulted in <$25,000 per QALY gained (relative to standard care). For patients receiving IGC alone, the ICER [here’s a relevant link – US] obtained was $32,057 per QALY gained, and for those receiving OFC alone, this ICER ranged from $12,169 to $220,100 per QALY gained, depending on the level of ulcer reduction attained. […] Increasing the effectiveness of preventive foot care in patients under OFC and IGC + OFC resulted in more QALYs gained, lower costs, and a more favorable ICER. The results of the simulations for the combined scenario (IGC + OFC) were rather insensitive to changes in utility weights and costing parameters. Similar results were obtained for parameter variations in the other two scenarios (IGC and OFC separately).”

“The results of this study suggest that IGC + OFC reduces foot ulcers and amputations and leads to an improvement in life expectancy. Greater health benefits are obtained with higher levels of foot ulcer prevention. Although care according to guidelines increases health costs, the cost per QALY gained is <$25,000, even for levels of preventive foot care as low as 10%. ICERs of this order are cost-effective according to the stratification of interventions for diabetes recently proposed (32). […] IGC falls into the category of a possibly cost-effective intervention in the management of the diabetic foot. Although it does not produce significant reduction in foot ulcers and LEA, its effectiveness resides in the slowing of neuropathy progression rates.

Extrapolating our results to a practical situation, if IGC + OFC was to be given to all diabetic patients in the Netherlands, with the aim of reducing LEA by 50% (St. Vincent’s declaration), the cost per QALY gained would be $12,165 and the cost for managing diabetic ulcers and amputations would decrease by 53 and 58%, respectively. From a policy perspective, this is clearly cost-effective and cost saving compared with current care.”

ii. Early Glycemic Control, Age at Onset, and Development of Microvascular Complications in Childhood-Onset Type 1 Diabetes.

“The aim of this work was to study the impact of glycemic control (HbA1c) early in disease and age at onset on the occurrence of incipient diabetic nephropathy (MA) and background retinopathy (RP) in childhood-onset type 1 diabetes.

RESEARCH DESIGN AND METHODS—All children, diagnosed at 0–14 years in a geographically defined area in northern Sweden between 1981 and 1992, were identified using the Swedish Childhood Diabetes Registry. From 1981, a nationwide childhood diabetes care program was implemented recommending intensified insulin treatment. HbA1c and urinary albumin excretion were analyzed, and fundus photography was performed regularly. Retrospective data on all 94 patients were retrieved from medical records and laboratory reports.

RESULTS—During the follow-up period, with a mean duration of 12 ± 4 years (range 5–19), 17 patients (18%) developed MA, 45 patients (48%) developed RP, and 52% had either or both complications. A Cox proportional hazard regression, modeling duration to occurrence of MA or RP, showed that glycemic control (reflected by mean HbA1c) during the follow-up was significantly associated with both MA and RP when adjusted for sex, birth weight, age at onset, and tobacco use as potential confounders. Mean HbA1c during the first 5 years of diabetes was a near-significant determinant for development of MA (hazard ratio 1.41, P = 0.083) and a significant determinant of RP (1.32, P = 0.036). The age at onset of diabetes significantly influenced the risk of developing RP (1.11, P = 0.021). Thus, in a Kaplan-Meier analysis, onset of diabetes before the age of 5 years, compared with the age-groups 5–11 and >11 years, showed a longer time to occurrence of RP (P = 0.015), but no clear tendency was seen for MA, perhaps due to lower statistical power.

CONCLUSIONS—Despite modern insulin treatment, >50% of patients with childhood-onset type 1 diabetes developed detectable diabetes complications after ∼12 years of diabetes. Inadequate glycemic control, also during the first 5 years of diabetes, seems to accelerate time to occurrence, whereas a young age at onset of diabetes seems to prolong the time to development of microvascular complications. […] The present study and other studies (15,54) indicate that children with an onset of diabetes before the age of 5 years may have a prolonged time to development of microvascular complications. Thus, the youngest age-groups, who are most sensitive to hypoglycemia with regard to risk of persistent brain damage, may have a relative protection during childhood or a longer time to development of complications.”

It’s important to note that although some people reading the study may think this is all ancient history (people diagnosed in the 80es?), to a lot of people it really isn’t. The study is of great personal interest to me, as I was diagnosed in ’87; if it had been a Danish study rather than a Swedish one I might well have been included in the analysis.

Another note to add in the context of the above coverage is that unlike what the authors of the paper seem to think/imply, hypoglycemia may not be the only relevant variable of interest in the context of the effect of childhood diabetes on brain development, where early diagnosis has been observed to tend to lead to less favourable outcomes – other variables which may be important include DKA episodes and perhaps also chronic hyperglycemia during early childhood. See this post for more stuff on these topics.

Some more stuff from the paper:

“The annual incidence of type 1 diabetes in northern Sweden in children 0–14 years of age is now ∼31/100,000. During the time period 1981–1992, there has been an increase in the annual incidence from 19 to 31/100,000 in northern Sweden. This is similar to the rest of Sweden […]. Seventeen (18%) of the 94 patients fulfilled the criteria for MA during the follow-up period. None of the patients developed overt nephropathy, elevated serum creatinine, or had signs of any other kidney disorder, e.g., hematuria, during the follow-up period. […] The mean time to diagnosis of MA was 9 ± 3 years (range 4–15) from diabetes onset. Forty-five (48%) of the 94 patients fulfilled the criteria for RP during the follow-up period. None of the patients developed proliferative retinopathy or were treated with photocoagulation. The mean time to diagnosis of RP was 11 ± 4 years (range 4–19) from onset of diabetes. Of the 45 patients with RP, 13 (29%) had concomitant MA, and thus 13 (76.5%) of the 17 patients with MA had concomitant RP. […] Altogether, among the 94 patients, 32 (34%) had isolated RP, 4 (4%) had isolated MA, and 13 (14%) had combined RP and MA. Thus, 49 (52%) patients had either one or both complications and, hence, 45 (48%) had neither of these complications.”

“When modeling MA as a function of glycemic level up to the onset of MA or during the entire follow-up period, adjusting for sex, birth weight, age at onset of diabetes, and tobacco use, only glycemic control had a significant effect. An increase in hazard ratio (HR) of 83% per one percentage unit increase in mean HbA1c was seen. […] The increase in HR of developing RP for each percentage unit rise in HbA1c during the entire follow-up period was 43% and in the early period 32%. […] Age at onset of diabetes was a weak but significant independent determinant for the development of RP in all regression models (P = 0.015, P = 0.018, and P = 0.010, respectively). […] Despite that this study was relatively small and had a retrospective design, we were able to show that the glycemic level already during the first 5 years may be an important predictor of later development of both MA and RP. This is in accordance with previous prospective follow-up studies (16,30).”

“Previously, male sex, smoking, and low birth weight have been shown to be risk factors for the development of nephropathy and retinopathy (6,4549). However, in this rather small retrospective study with a limited follow-up time, we could not confirm these associations”. This may just be because of lack of power, it’s a relatively small study. Again, this is/was of personal interest to me; two of those three risk factors apply to me, and neither of those risk factors are modifiable.

iii. Eighteen Years of Fair Glycemic Control Preserves Cardiac Autonomic Function in Type 1 Diabetes.

“Reduced cardiovascular autonomic function is associated with increased mortality in both type 1 and type 2 diabetes (14). Poor glycemic control plays an important role in the development and progression of diabetic cardiac autonomic dysfunction (57). […] Diabetic cardiovascular autonomic neuropathy (CAN) can be defined as impaired function of the peripheral autonomic nervous system. Exercise intolerance, resting tachycardia, and silent myocardial ischemia may be early signs of cardiac autonomic dysfunction (9).The most frequent finding in subclinical and symptomatic CAN is reduced heart rate variability (HRV) (10). […] No other studies have followed type 1 diabetic patients on intensive insulin treatment during ≥14-year periods and documented cardiac autonomic dysfunction. We evaluated the association between 18 years’ mean HbA1c and cardiac autonomic function in a group of type 1 diabetic patients with 30 years of disease duration.”

“A total of 39 patients with type 1 diabetes were followed during 18 years, and HbA1c was measured yearly. At 18 years follow-up heart rate variability (HRV) measurements were used to assess cardiac autonomic function. Standard cardiac autonomic tests during normal breathing, deep breathing, the Valsalva maneuver, and the tilt test were performed. Maximal heart rate increase during exercise electrocardiogram and minimal heart rate during sleep were also used to describe cardiac autonomic function.

RESULTS—We present the results for patients with mean HbA1c <8.4% (two lowest HbA1c tertiles) compared with those with HbA1c ≥8.4% (highest HbA1c tertile). All of the cardiac autonomic tests were significantly different in the high- and the low-HbA1c groups, and the most favorable scores for all tests were seen in the low-HbA1c group. In the low-HbA1c group, the HRV was 40% during deep breathing, and in the high-HbA1c group, the HRV was 19.9% (P = 0.005). Minimal heart rate at night was significantly lower in the low-HbA1c groups than in the high-HbA1c group (P = 0.039). With maximal exercise, the increase in heart rate was significantly higher in the low-HbA1c group compared with the high-HbA1c group (P = 0.001).

CONCLUSIONS—Mean HbA1c during 18 years was associated with cardiac autonomic function. Cardiac autonomic function was preserved with HbA1c <8.4%, whereas cardiac autonomic dysfunction was impaired in the group with HbA1c ≥8.4%. […] The study underlines the importance of good glycemic control and demonstrates that good long-term glycemic control is associated with preserved cardiac autonomic function, whereas a lack of good glycemic control is associated with cardiac autonomic dysfunction.”

These results are from Norway (Oslo), and again they seem relevant to me personally (‘from a statistical point of view’) – I’ve had diabetes for about as long as the people they included in the study.

iv. The Mental Health Comorbidities of Diabetes.

“Individuals living with type 1 or type 2 diabetes are at increased risk for depression, anxiety, and eating disorder diagnoses. Mental health comorbidities of diabetes compromise adherence to treatment and thus increase the risk for serious short- and long-term complications […] Young adults with type 1 diabetes are especially at risk for poor physical and mental health outcomes and premature mortality. […] we summarize the prevalence and consequences of mental health problems for patients with type 1 or type 2 diabetes and suggest strategies for identifying and treating patients with diabetes and mental health comorbidities.”

“Major advances in the past 2 decades have improved understanding of the biological basis for the relationship between depression and diabetes.2 A bidirectional relationship might exist between type 2 diabetes and depression: just as type 2 diabetes increases the risk for onset of major depression, a major depressive disorder signals increased risk for on set of type 2 diabetes.2 Moreover, diabetes distress is now recognized as an entity separate from major depressive disorder.2 Diabetes distress occurs because virtually all of diabetes care involves self-management behavior—requiring balance of a complex set of behavioral tasks by the person and family, 24 hours a day, without “vacation” days. […] Living with diabetes is associated with a broad range of diabetes-related distresses, such as feeling over-whelmed with the diabetes regimen; being concerned about the future and the possibility of serious complications; and feeling guilty when management is going poorly. This disease burden and emotional distress in individuals with type 1 or type 2 diabetes, even at levels of severity below the threshold for a psychiatric diagnosis of depression or anxiety, are associated with poor adherence to treatment, poor glycemic control, higher rates of diabetes complications, and impaired quality of life. […] Depression in the context of diabetes is […] associated with poor self-care with respect to diabetes treatment […] Depression among individuals with diabetes is also associated with increased health care use and expenditures, irrespective of age, sex, race/ethnicity, and health insurance status.3

“Women with type 1 diabetes have a 2-fold increased risk for developing an eating disorder and a 1.9-fold increased risk for developing subthreshold eating disorders than women without diabetes.6 Less is known about eating disorders in boys and men with diabetes. Disturbed eating behaviors in women with type 1 diabetes include binge eating and caloric purging through insulin restriction, with rates of these disturbed eating behaviors reported to occur in 31% to 40% of women with type 1 diabetes aged between 15 and 30 years.6 […] disordered eating behaviors persist and worsen over time. Women with type 1 diabetes and eating disorders have poorer glycemic control, with higher rates of hospitalizations and retinopathy, neuropathy, and premature death compared with similarly aged women with type 1 diabetes without eating disorders.6 […] few diabetes clinics provide mental health screening or integrate mental/behavioral health services in diabetes clinical care.4 It is neither practical nor affordable to use standardized psychiatric diagnostic interviews to diagnose mental health comorbidities in individuals with diabetes. Brief paper-and-pencil self-report measures such as the Beck Depression Inventory […] that screen for depressive symptoms are practical in diabetes clinical settings, but their use remains rare.”

The paper does not mention this, but it is important to note that there are multiple plausible biological pathways which might help to explain bidirectional linkage between depression and type 2 diabetes. Physiological ‘stress’ (think: inflammation) is likely to be an important factor, and so are the typical physiological responses to some of the pharmacological treatments used to treat depression (…as well as other mental health conditions); multiple drugs used in psychiatry, including tricyclic antidepressants, cause weight gain and have proven diabetogenic effects – I’ve covered these topics before here on the blog. I’ve incidentally also covered other topics touched briefly upon in the paper – here’s for example a more comprehensive post about screening for depression in the diabetes context, and here’s a post with some information about how one might go about screening for eating disorders; skin signs are important. I was a bit annoyed that the author of the above paper did not mention this, as observing whether or not Russell’s sign – which is a very reliable indicator of eating disorder – is present or not is easier/cheaper/faster than performing any kind of even semi-valid depression screen.

v. Diabetes, Depression, and Quality of Life. This last one covers topics related to the topics covered in the paper above.

“The study consisted of a representative population sample of individuals aged ≥15 years living in South Australia comprising 3,010 personal interviews conducted by trained health interviewers. The prevalence of depression in those suffering doctor-diagnosed diabetes and comparative effects of diabetic status and depression on quality-of-life dimensions were measured.

RESULTS—The prevalence of depression in the diabetic population was 24% compared with 17% in the nondiabetic population. Those with diabetes and depression experienced an impact with a large effect size on every dimension of the Short Form Health-Related Quality-of-Life Questionnaire (SF-36) as compared with those who suffered diabetes and who were not depressed. A supplementary analysis comparing both depressed diabetic and depressed nondiabetic groups showed there were statistically significant differences in the quality-of-life effects between the two depressed populations in the physical and mental component summaries of the SF-36.

CONCLUSIONS—Depression for those with diabetes is an important comorbidity that requires careful management because of its severe impact on quality of life.”

I felt slightly curious about the setup after having read this, because representative population samples of individuals should not in my opinion yield depression rates of either 17% nor 24%. Rates that high suggest to me that the depression criteria used in the paper are a bit ‘laxer’/more inclusive than what you see in some other contexts when reading this sort of literature – to give an example of what I mean, the depression screening post I link to above noted that clinical or major depression occurred in 11.4% of people with diabetes, compared to a non-diabetic prevalence of 5%. There’s a long way from 11% to 24% and from 5% to 17%. Another potential explanation for such a high depression rate could of course also be some sort of selection bias at the data acquisition stage, but that’s obviously not the case here. However 3000 interviews is a lot of interviews, so let’s read on…

“Several studies have assessed the impact of depression in diabetes in terms of the individual’s functional ability or quality of life (3,4,13). Brown et al. (13) examined preference-based time tradeoff utility values associated with diabetes and showed that those with diabetes were willing to trade a significant proportion of their remaining life in return for a diabetes-free health state.”

“Depression was assessed using the mood module of the Primary Care Evaluation of Mental Disorders questionnaire. This has been validated to provide estimates of mental disorder comparable with those found using structured and longer diagnostic interview schedules (16). The mental disorders examined in the questionnaire included major depressive disorder, dysthymia, minor depressive disorder, and bipolar disorder. [So yes, the depression criteria used in this study are definitely more inclusive than depression criteria including only people with MDD] […] The Short Form Health-Related Quality-of-Life Questionnaire (SF-36) was also included to assess the quality of life of the different population groups with and without diabetes. […] Five groups were examined: the overall population without diabetes and without depression; the overall diabetic population; the depression-only population; the diabetic population without depression; and the diabetic population with depression.”

“Of the population sample, 205 (6.8%) were classified as having major depression, 130 (4.3%) had minor depression, 105 (3.5%) had partial remission of major depression, 79 (2.6%) had dysthymia, and 5 (0.2%) had bipolar disorder (depressed phase). No depressive syndrome was detected in 2,486 (82.6%) respondents. The population point prevalence of doctor-diagnosed diabetes in this survey was 5.2% (95% CI 4.6–6.0). The prevalence of depression in the diabetic population was 23.6% (22.1–25.1) compared with 17.1% (15.8–18.4) in the nondiabetic population. This difference approached statistical significance (P = 0.06). […] There [was] a clear difference in the quality-of-life scores for the diabetic and depression group when compared with the diabetic group without depression […] Overall, the highest quality-of-life scores are experienced by those without diabetes and depression and the lowest by those with diabetes and depression. […] the standard scores of those with no diabetes have quality-of-life status comparable with the population mean or slightly better. At the other extreme those with diabetes and depression experience the most severe comparative impact on quality-of-life for every dimension. Between these two extremes, diabetes overall and the diabetes without depression groups have a moderate-to-severe impact on the physical functioning, role limitations (physical), and general health scales […] The results of the two-factor ANOVA showed that the interaction term was significant only for the PCS [Physical Component Score – US] scale, indicating a greater than additive effect of diabetes and depression on the physical health dimension.”

“[T]here was a significant interaction between diabetes and depression on the PCS but not on the MCS [Mental Component Score. Do note in this context that the no-interaction result is far from certain, because as they observe: “it may simply be sample size that has not allowed us to observe a greater than additive effect in the MCS scale. Although there was no significant interaction between diabetes and depression and the MCS scale, we did observe increases on the effect size for the mental health dimensions”]. One explanation for this finding might be that depression can influence physical outcomes, such as recovery from myocardial infarction, survival with malignancy, and propensity to infection. Various mechanisms have been proposed for this, including changes to the immune system (24). Other possibilities are that depression in diabetes may affect the capacity to maintain medication vigilance, maintain a good diet, and maintain other lifestyle factors, such as smoking and exercise, all of which are likely possible pathways for a greater than additive effect. Whatever the mechanism involved, these data indicate that the addition of depression to diabetes has a severe impact on quality of life, and this needs to be managed in clinical practice.”

May 25, 2017 Posted by | Cardiology, Diabetes, Medicine, Nephrology, Neurology, Papers, Personal, Pharmacology, Psychiatry, Psychology | Leave a comment

A few diabetes papers of interest

A couple of weeks ago I decided to cover some of the diabetes articles I’d looked at and bookmarked in the past, but there were a lot of articles and I did not get very far. This post will cover some more of these articles I had failed to cover here despite intending to do so at some point. Considering that I these days relatively regularly peruse e.g. the Diabetes Care archives I am thinking of making this sort of post a semi-regular feature of the blog.

i. Association Between Diabetes and Hippocampal Atrophy in Elderly Japanese: The Hisayama Study.

“A total of 1,238 community-dwelling Japanese subjects aged ≥65 years underwent brain MRI scans and a comprehensive health examination in 2012. Total brain volume (TBV), intracranial volume (ICV), and hippocampal volume (HV) were measured using MRI scans for each subject. We examined the associations between diabetes-related parameters and the ratios of TBV to ICV (an indicator of global brain atrophy), HV to ICV (an indicator of hippocampal atrophy), and HV to TBV (an indicator of hippocampal atrophy beyond global brain atrophy) after adjustment for other potential confounders.”

“The multivariable-adjusted mean values of the TBV-to-ICV, HV-to-ICV, and HV-to-TBV ratios were significantly lower in the subjects with diabetes compared with those without diabetes (77.6% vs. 78.2% for the TBV-to-ICV ratio, 0.513% vs. 0.529% for the HV-to-ICV ratio, and 0.660% vs. 0.676% for the HV-to-TBV ratio; all P < 0.01). These three ratios decreased significantly with elevated 2-h postload glucose (PG) levels […] Longer duration of diabetes was significantly associated with lower TBV-to-ICV, HV-to-ICV, and HV-to-TBV ratios. […] Our data suggest that a longer duration of diabetes and elevated 2-h PG levels, a marker of postprandial hyperglycemia, are risk factors for brain atrophy, particularly hippocampal atrophy.”

“Intriguingly, our findings showed that the subjects with diabetes had significantly lower mean HV-to-TBV ratio values, indicating […] that the hippocampus is predominantly affected by diabetes. In addition, in our subjects a longer duration and a midlife onset of diabetes were significantly associated with a lower HV, possibly suggesting that a long exposure of diabetes particularly worsens hippocampal atrophy.”

The reason why hippocampal atrophy is a variable of interest to these researchers is that hippocampal atrophy is a feature of Alzheimer’s Disease, and diabetics have an elevated risk of AD. This is incidentally far from the first study providing some evidence for the existence of potential causal linkage between impaired glucose homeostasis and AD (see e.g. also this paper, which I’ve previously covered here on the blog).

ii. A Population-Based Study of All-Cause Mortality and Cardiovascular Disease in Association With Prior History of Hypoglycemia Among Patients With Type 1 Diabetes.

“Although patients with T1DM may suffer more frequently from hypoglycemia than those with T2DM (8), very few studies have investigated whether hypoglycemia may also increase the risk of CVD (6,9,10) or death (1,6,7) in patients with T1DM; moreover, the results of these studies have been inconclusive (6,9,10) because of the dissimilarities in their methodological aspects, including their enrollment of populations with T1DM with different levels of glycemic control, application of different data collection methods, and adoption of different lengths of observational periods.”

“Only a few population-based studies have examined the potential cumulative effect of repeated severe hypoglycemia on all-cause mortality or CVD incidence in T1DM (9). The Action to Control Cardiovascular Risk in Diabetes (ACCORD) study of T2DM found a weakly inverse association between the annualized number of hypoglycemic episodes and the risk of death (11,12). By contrast, some studies find that repeated hypoglycemia may be an aggravating factor to atherosclerosis in T1DM (13,14). Studies on the compromised sympathetic-adrenal reaction in patients with repeated hypoglycemia have been inconclusive regarding whether such a reaction may further damage intravascular coagulation and thrombosis (15) or decrease the vulnerability of these patients to adverse health outcomes (12).

Apart from the lack of information on the potential dose–gradient effect associated with severe hypoglycemic events in T1DM from population-based studies, the risks of all-cause mortality/CVD incidence associated with severe hypoglycemia occurring at different periods before all-cause mortality/CVD incidence have never been examined. In this study, we used the population-based medical claims of a cohort of patients with T1DM to examine whether the risks of all-cause mortality/CVD incidence are associated with previous episodes of severe hypoglycemia in different periods and whether severe hypoglycemia may pose a dose–gradient effect on the risks of all-cause mortality/CVD incidence.”

“Two nested case-control studies with age- and sex-matched control subjects and using the time-density sampling method were performed separately within a cohort of 10,411 patients with T1DM in Taiwan. The study enrolled 564 nonsurvivors and 1,615 control subjects as well as 743 CVD case subjects and 1,439 control subjects between 1997 and 2011. History of severe hypoglycemia was identified during 1 year, 1–3 years, and 3–5 years before the occurrence of the study outcomes.”

“Prior severe hypoglycemic events within 1 year were associated with higher risks of all-cause mortality and CVD (adjusted OR 2.74 [95% CI 1.96–3.85] and 2.02 [1.35–3.01], respectively). Events occurring within 1–3 years and 3–5 years before death were also associated with adjusted ORs of 1.94 (95% CI 1.39–2.71) and 1.68 (1.15–2.44), respectively. Significant dose–gradient effects of severe hypoglycemia frequency on mortality and CVD were observed within 5 years. […] we found that a greater frequency of severe hypoglycemia occurring 1 year before death was significantly associated with a higher OR of all-cause mortality (1 vs. 0: 2.45 [95% CI 1.65–3.63]; ≥2 vs. 0: 3.49 [2.01–6.08], P < 0.001 for trend). Although the strength of the association was attenuated, a significant dose–gradient effect still existed for severe hypoglycemia occurring in 1–3 years (P < 0.001 for trend) and 3–5 years (P < 0.015 for trend) before death. […] Exposure to repeated severe hypoglycemic events can lead to higher risks of mortality and CVD.”

“Our findings are supported by two previous studies that investigated atherosclerosis risk in T1DM (13,14). The DCCT/EDIC project reported that the prevalence of coronary artery calcification, an established atherosclerosis marker, was linearly correlated with the incidence rate of hypoglycemia on the DCCT stage (14). Giménez et al. (13) also demonstrated that repeated episodes of hypoglycemia were an aggravating factor for preclinical atherosclerosis in T1DM. […] The mechanism of hypoglycemia that predisposes to all-cause mortality/CVD incidence remains unclear.”

iii. Global Estimates on the Number of People Blind or Visually Impaired by Diabetic Retinopathy: A Meta-analysis From 1990 to 2010.

“On the basis of previous large-scale population-based studies and meta-analyses, diabetic retinopathy (DR) has been recognized as one of the most common and important causes for visual impairment and blindness (1–19). These studies in general showed that DR was the leading cause of blindness globally among working-aged adults and therefore has a significant socioeconomic impact (20–22).”

“A previous meta-analysis (21) summarizing 35 studies with more than 20,000 patients with diabetes estimated a prevalence of any DR of 34.6%, of diabetic macular edema of 6.8%, and of vision-threating DR of 10.2% within the diabetes population. […] Yau et al. (21) estimated that ∼93 million people had some DR and 28 million people had sight-threatening stages of DR. However, this meta-analysis did not address the prevalence of visual impairment and blindness due to DR and thus the impact of DR on the general population. […] We therefore conducted the present meta-analysis of all available population-based studies performed worldwide within the last two decades as part of the Global Burden of Disease Study 2010 (GBD) to estimate the number of people affected by blindness and visual impairment.”

“DR [Diabetic Retinopathy] ranks as the fifth most common cause of global blindness and of global MSVI [moderate and severe vision impairment] (25). […] this analysis estimates that, in 2010, 1 out of every 39 blind people had blindness due to DR and 1 out of every 52 people had visual impairment due to DR. […] Globally in 2010, out of overall 32.4 million blind and 191 million visually impaired people, 0.8 million were blind and 3.7 million were visually impaired because of DR, with an alarming increase of 27% and 64%, respectively, spanning the two decades from 1990 to 2010. DR accounted for 2.6% of all blindness in 2010 and 1.9% of all MSVI worldwide, increasing from 2.1% and 1.3%, respectively, in 1990. […] The number of persons with visual impairment due to DR worldwide is rising and represents an increasing proportion of all blindness/MSVI causes. Age-standardized prevalence of DR-related blindness/MSVI was higher in sub-Saharan Africa and South Asia.”

“Our data suggest that the percentage of blindness and MSVI attributable to DR was lower in low-income regions with younger populations than in high-income regions with older populations. There are several reasons that may explain this observation. First, low-income societies may have a higher percentage of unoperated cataract or undercorrected refractive error–related blindness and MSVI (25), which is probably related to access to visual and ocular health services. Therefore, the proportional increase in blindness and MSVI attributable to DR may be rising because of the decreasing proportion attributable to cataract (25) as a result of the increasing availability of cataract surgery in many parts of the world (29) during the past decade. Improved visualization of the fundus afforded by cataract surgery should also improve the detection of DR. The increase in the percentage of global blindness caused by DR within the last two decades took place in all world regions except Western Europe and high-income North America where there was a slight decrease. This decrease may reflect the effect of intensified prevention and treatment of DR possibly in part due to the introduction of intravitreal injections of steroids and anti-VEGF (vascular endothelial growth factor) drugs (30,31).

Second, in regions with poor medical infrastructure, patients with diabetes may not live long enough to experience DR (32). This reduces the number of patients with diabetes, and, furthermore, it reduces the number of patients with DR-related vision loss. Studies in the literature have reported that the prevalence of severe DR decreased from 1990 to 2010 (21) while the prevalence of diabetes simultaneously increased (27), which implies a reduction in the prevalence of severe DR per person with diabetes. […] Third, […] younger populations may have a lower prevalence of diabetes (33). […] Therefore, considering further economic development in rural regions, improvements in medical infrastructure, the general global demographic transition to elderly populations, and the association between increasing economic development and obesity, we project the increase in the proportion of DR-related blindness and MSVI to continue to rise in the future.”

iv. Do Patient Characteristics Impact Decisions by Clinicians on Hemoglobin A1c Targets?

“In setting hemoglobin A1c (HbA1c) targets, physicians must consider individualized risks and benefits of tight glycemic control (1,2) by recognizing that the risk-benefit ratio may become unfavorable in certain patients, including the elderly and/or those with multiple comorbidities (3,4). Customization of treatment goals based on patient characteristics is poorly understood, partly due to insufficient data on physicians’ decisions in setting targets. We used the National Health and Nutrition Examination Survey (NHANES) to analyze patient-reported HbA1c targets set by physicians and to test whether targets are correlated with patient characteristics.”

“we did not find any evidence that U.S. physicians systematically consider important patient-specific information when selecting the intensity of glycemic control. […] the lack of variation with patient characteristics suggests overreliance on a general approach, without consideration of individual variation in the risks and benefits (or patient preference) of tight control.”

v. Cardiovascular Autonomic Neuropathy, Sexual Dysfunction, and Urinary Incontinence in Women With Type 1 Diabetes.

“This study evaluated associations among cardiovascular autonomic neuropathy (CAN), female sexual dysfunction (FSD), and urinary incontinence (UI) in women with type I diabetes mellitus (T1DM). […] We studied 580 women with T1DM in the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Study (DCCT/EDIC).”

“At EDIC year 17, FSD was observed in 41% of women and UI in 30%. […] We found that CAN was significantly more prevalent among women with FSD and/or UI, because 41% of women with FSD and 44% with UI had positive measures of CAN compared with 30% without FSD and 38% without UI at EDIC year 16/17. We also observed bivariate associations between FSD and several measures of CAN […] In long-standing T1DM, CAN may predict development of FSD and may be a useful surrogate for generalized diabetic autonomic neuropathy.”

“Although autonomic dysfunction has been considered an important factor in the etiology of many diabetic complications, including constipation, exercise intolerance, bladder dysfunction, erectile dysfunction, orthostatic hypotension, and impaired neurovascular function, our study is among the first to systematically demonstrate a link between CAN and FSD in a large cohort of well-characterized patients with T1DM (14).”

vi. Correlates of Medication Adherence in the TODAY Cohort of Youth With Type 2 Diabetes.

“A total of 699 youth 10–17 years old with recent-onset type 2 diabetes and ≥80% adherence to metformin therapy for ≥8 weeks during a run-in period were randomized to receive one of three treatments. Participants took two study pills twice daily. Adherence was calculated by pill count from blister packs returned at visits. High adherence was defined as taking ≥80% of medication; low adherence was defined as taking <80% of medication.”

“In this low socioeconomic cohort, high and low adherence did not differ by sex, age, family income, parental education, or treatment group. Adherence declined over time (72% high adherence at 2 months, 56% adherence at 48 months, P < 0.0001). A greater percentage of participants with low adherence had clinically significant depressive symptoms at baseline (18% vs. 12%, P = 0.0415). No adherence threshold predicted the loss of glycemic control. […] Most pediatric type 1 diabetes studies (5–7) consistently document a correlation between adherence and race, ethnicity, and socioeconomic status, and studies of adults with type 2 diabetes (8,9) have documented that depressed patients are less adherent to their diabetes regimen. There is a dearth of information in the literature regarding adherence to medication in pediatric patients with type 2 diabetes.”

“In the cohort, the presence of baseline clinically significant depressive symptoms was associated with subsequent lower adherence. […] The TODAY cohort demonstrated deterioration in study medication adherence over time, irrespective of treatment group assignment. […] Contrary to expectation, demographic factors (sex, race-ethnicity, household income, and parental educational level) did not predict medication adherence. The lack of correlation with these factors in the TODAY trial may be explained by the limited income and educational range of the families in the TODAY trial. Nearly half of the families in the TODAY trial had an annual income of <$25,000, and, for over half of the families, the highest level of parental education was a high school degree or lower. In addition, our run-in criteria selected for more adherent subjects. All subjects had to have >80% adherence to M therapy for ≥8 weeks before they could be randomized. This may have limited variability in medication adherence postrandomization. It is also possible that selecting for more adherent subjects in the run-in period also selected for subjects with a lower frequency of depressive symptoms.”

“In the TODAY trial, baseline clinically significant depressive symptoms were more prevalent in the lower-adherence group, suggesting that regular screening for depressive symptoms should be undertaken to identify youth who were at high risk for poor medication adherence. […] Studies in adults with type 2 diabetes (2328) consistently report that depressed patients are less adherent to their diabetes regimen and experience more physical complications of diabetes. Identifying youth who are at risk for poor medication adherence early in the course of disease would make it possible to provide support and, if needed, specific treatment. Although we were not able to determine whether the treatment of depressive symptoms changed adherence over time, our findings support the current guidelines for psychosocial screening in youth with diabetes (29,30).”

vii. Increased Risk of Incident Chronic Kidney Disease, Cardiovascular Disease, and Mortality in Patients With Diabetes With Comorbid Depression.

Another depression-related paper, telling another part of the story. If depressed diabetics are less compliant/adherent, which seems – as per the above study – to be the case both in the context of the adult and pediatric patient population, then you might also expect this reduced compliance/adherence to ‘translate’ into this group having poorer metabolic control, and thus be at higher risk of developing microvascular complications such as nephropathy. This seems to be what we observe, at least according to the findings of this study:

“It is not known if patients with diabetes with depression have an increased risk of chronic kidney disease (CKD). We examined the association between depression and incident CKD, mortality, and incident cardiovascular events in U.S. veterans with diabetes.”

“Among a nationally representative prospective cohort of >3 million U.S. veterans with baseline estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2, we identified 933,211 patients with diabetes. Diabetes was ascertained by an ICD-9-CM code for diabetes, an HbA1c >6.4%, or receiving antidiabetes medication during the inclusion period. Depression was defined by an ICD-9-CM code for depression or by antidepressant use during the inclusion period. Incident CKD was defined as two eGFR levels 2 separated by ≥90 days and a >25% decline in baseline eGFR.”

“Depression was associated with 20% higher risk of incident CKD (adjusted hazard ratio [aHR] and 95% CI: 1.20 [1.19–1.21]). Similarly, depression was associated with increased all-cause mortality (aHR and 95% CI: 1.25 [1.24–1.26]). […] The presence of depression in patients with diabetes is associated with higher risk of developing CKD compared with nondepressed patients.”

It’s important to remember that the higher reported eGFRs in the depressed patient group may not be important/significant, and they should not be taken as an indication of relatively better kidney function in this patient population – especially in the type 2 context, the relationship between eGFR and kidney function is complicated. I refer to Bakris et al.‘s text on these topics for details (blog coverage here).

May 6, 2017 Posted by | Cardiology, Diabetes, Medicine, Nephrology, Neurology, Psychology, Studies | Leave a comment

A few diabetes papers of interest

1. Cognitive Dysfunction in Older Adults With Diabetes: What a Clinician Needs to Know. I’ve talked about these topics before here on the blog (see e.g. these posts on related topics), but this is a good summary article. I have added some observations from the paper below:

“Although cognitive dysfunction is associated with both type 1 and type 2 diabetes, there are several distinct differences observed in the domains of cognition affected in patients with these two types. Patients with type 1 diabetes are more likely to have diminished mental flexibility and slowing of mental speed, whereas learning and memory are largely not affected (8). Patients with type 2 diabetes show decline in executive function, memory, learning, attention, and psychomotor efficiency (9,10).”

“So far, it seems that the risk of cognitive dysfunction in type 2 diabetes may be influenced by glycemic control, hypoglycemia, inflammation, depression, and macro- and microvascular pathology (14). The cumulative impact of these conditions on the vascular etiology may further decrease the threshold at which cognition is affected by other neurological conditions in the aging brain. In patients with type 1 diabetes, it seems as though diabetes has a lesser impact on cognitive dysfunction than those patients with type 2 diabetes. […] Thus, the cognitive decline in patients with type 1 diabetes may be mild and may not interfere with their functionality until later years, when other aging-related factors become important. […] However, recent studies have shown a higher prevalence of cognitive dysfunction in older patients (>60 years of age) with type 1 diabetes (5).”

“Unlike other chronic diseases, diabetes self-care involves many behaviors that require various degrees of cognitive pliability and insight to perform proper self-care coordination and planning. Glucose monitoring, medications and/or insulin injections, pattern management, and diet and exercise timing require participation from different domains of cognitive function. In addition, the recognition, treatment, and prevention of hypoglycemia, which are critical for the older population, also depend in large part on having intact cognition.

The reason a clinician needs to recognize different domains of cognition affected in patients with diabetes is to understand which self-care behavior will be affected in that individual. […] For example, a patient with memory problems may forget to take insulin doses, forget to take medications/insulin on time, or forget to eat on time. […] Cognitively impaired patients using insulin are more likely to not know what to do in the event of low blood glucose or how to manage medication on sick days (34). Patients with diminished mental flexibility and processing speed may do well with a simple regimen but may fail if the regimen is too complex. In general, older patients with diabetes with cognitive dysfunction are less likely to be involved in diabetes self-care and glucose monitoring compared with age-matched control subjects (35). […] Other comorbidities associated with aging and diabetes also add to the burden of cognitive impairment and its impact on self-care abilities. For example, depression is associated with a greater decline in cognitive function in patients with type 2 diabetes (36). Depression also can independently negatively impact the motivation to practice self-care.”

“Recently, there is an increasing discomfort with the use of A1C as a sole parameter to define glycemic goals in the older population. Studies have shown that A1C values in the older population may not reflect the same estimated mean glucose as in the younger population. Possible reasons for this discrepancy are the commonly present comorbidities that impact red cell life span (e.g., anemia, uremia, renal dysfunction, blood transfusion, erythropoietin therapy) (45,46). In addition, A1C level does not reflect glucose excursions and variability. […] Thus, it is prudent to avoid A1C as the sole measure of glycemic goal in this population. […] In patients who need insulin therapy, simplification, also known as de-intensification of the regimen, is generally recommended in all frail patients, especially if they have cognitive dysfunction (37,49). However, the practice has not caught up with the recommendations as shown by large observational studies showing unnecessary intensive control in patients with diabetes and dementia (50–52).”

“With advances in the past few decades, we now see a larger number of patients with type 1 diabetes who are aging successfully and facing the new challenges that aging brings. […] Patients with type 1 diabetes are typically proactive in their disease management and highly disciplined. Cognitive dysfunction in these patients creates significant distress for the first time in their lives; they suddenly feel a “lack of control” over the disease they have managed for many decades. The addition of autonomic dysfunction, gastropathy, or neuropathy may result in wider glucose excursions. These patients are usually more afraid of hyperglycemia than hypoglycemia — both of which they have managed for many years. However, cognitive dysfunction in older adults with type 1 diabetes has been found to be associated with hypoglycemic unawareness and glucose variability (5), which in turn increases the risk of severe hypoglycemia (54). The need for goal changes to avoid hypoglycemia and accept some hyperglycemia can be very difficult for many of these patients.”

2. Trends in Drug Utilization, Glycemic Control, and Rates of Severe Hypoglycemia, 2006–2013.

“From 2006 to 2013, use increased for metformin (from 47.6 to 53.5%), dipeptidyl peptidase 4 inhibitors (0.5 to 14.9%), and insulin (17.1 to 23.0%) but declined for sulfonylureas (38.8 to 30.8%) and thiazolidinediones (28.5 to 5.6%; all P < 0.001). […] The overall rate of severe hypoglycemia remained the same (1.3 per 100 person-years; P = 0.72), declined modestly among the oldest patients (from 2.9 to 2.3; P < 0.001), and remained high among those with two or more comorbidities (3.2 to 3.5; P = 0.36). […] During the recent 8-year period, the use of glucose-lowering drugs has changed dramatically among patients with T2DM. […] The use of older classes of medications, such as sulfonylureas and thiazolidinediones, declined. During this time, glycemic control of T2DM did not improve in the overall population and remained poor among nearly a quarter of the youngest patients. Rates of severe hypoglycemia remained largely unchanged, with the oldest patients and those with multiple comorbidities at highest risk. These findings raise questions about the value of the observed shifts in drug utilization toward newer and costlier medications.”

“Our findings are consistent with a prior study of drug prescribing in U.S. ambulatory practice conducted from 1997 to 2012 (2). In that study, similar increases in DPP-4 inhibitor and insulin analog prescribing were observed; these changes were accompanied by a 61% increase in drug expenditures (2). Our study extends these findings to drug utilization and demonstrates that these increases occurred in all age and comorbidity subgroups. […] In contrast, metformin use increased only modestly between 2006 and 2013 and remained relatively low among older patients and those with two or more comorbidities. Although metformin is recommended as first-line therapy (26), it may be underutilized as the initial agent for the treatment of T2DM (27). Its use may be additionally limited by coexisting contraindications, such as chronic kidney disease (28).”

“The proportion of patients with a diagnosis of diabetes who did not fill any glucose-lowering medications declined slightly (25.7 to 24.1%; P < 0.001).”

That is, one in four people who had a diagnosis of type 2 diabetes were not taking any prescription drugs for their health condition. I wonder how many of those people have read wikipedia articles like this one

“When considering treatment complexity, the use of oral monotherapy increased slightly (from 24.3 to 26.4%) and the use of multiple (two or more) oral agents declined (from 33.0 to 26.5%), whereas the use of insulin alone and in combination with oral agents increased (from 6.0 to 8.5% and from 11.1 to 14.6%, respectively; all P values <0.001).”

“Between 1987 and 2011, per person medical spending attributable to diabetes doubled (4). More than half of the increase was due to prescription drug spending (4). Despite these spending increases and greater utilization of newly developed medications, we showed no concurrent improvements in overall glycemic control or the rates of severe hypoglycemia in our study. Although the use of newer and more expensive agents may have other important benefits (44), further studies are needed to define the value and cost-effectiveness of current treatment options.”

iii. Among Low-Income Respondents With Diabetes, High-Deductible Versus No-Deductible Insurance Sharply Reduces Medical Service Use.

“Using the 2011–2013 Medical Expenditure Panel Survey, bivariate and regression analyses were conducted to compare demographic characteristics, medical service use, diabetes care, and health status among privately insured adult respondents with diabetes, aged 18–64 years (N = 1,461) by lower (<200% of the federal poverty level) and higher (≥200% of the federal poverty level) income and deductible vs. no deductible (ND), low deductible ($1,000/$2,400) (LD), and high deductible (>$1,000/$2,400) (HD). The National Health Interview Survey 2012–2014 was used to analyze differences in medical debt and delayed/avoided needed care among adult respondents with diabetes (n = 4,058) by income. […] Compared with privately insured respondents with diabetes with ND, privately insured lower-income respondents with diabetes with an LD report significant decreases in service use for primary care, checkups, and specialty visits (27%, 39%, and 77% lower, respectively), and respondents with an HD decrease use by 42%, 65%, and 86%, respectively. Higher-income respondents with an LD report significant decreases in specialty (28%) and emergency department (37%) visits.”

“The reduction in ambulatory visits made by lower-income respondents with ND compared with lower-income respondents with an LD or HD is far greater than for higher-income patients. […] The substantial reduction in checkup (preventive) and specialty visits by those with a lower income who have an HDHP [high-deductible health plan, US] implies a very different pattern of service use compared with lower-income respondents who have ND and with higher-income respondents. Though preventive visits require no out-of-pocket costs, reduced preventive service use with HDHPs is well established and might be the result of patients being unaware of this benefit or their concern about findings that could lead to additional expenses (31). Such sharply reduced service use by low-income respondents with diabetes may not be desirable. Patients with diabetes benefit from assessment of diabetes control, encouragement and reinforcement of behavior change and medication use, and early detection and treatment of diabetes complications or concomitant disease.”

iv. Long-term Mortality and End-Stage Renal Disease in a Type 1 Diabetes Population Diagnosed at Age 15–29 Years in Norway.

OBJECTIVE To study long-term mortality, causes of death, and end-stage renal disease (ESRD) in people diagnosed with type 1 diabetes at age 15–29 years.

RESEARCH DESIGN AND METHODS This nationwide, population-based cohort with type 1 diabetes diagnosed during 1978–1982 (n = 719) was followed from diagnosis until death, emigration, or September 2013. Linkages to the Norwegian Cause of Death Registry and the Norwegian Renal Registry provided information on causes of death and whether ESRD was present.

RESULTS During 30 years’ follow-up, 4.6% of participants developed ESRD and 20.6% (n = 148; 106 men and 42 women) died. Cumulative mortality by years since diagnosis was 6.0% (95% CI 4.5–8.0) at 10 years, 12.2% (10.0–14.8) at 20 years, and 18.4% (15.8–21.5) at 30 years. The SMR [standardized mortality ratio] was 4.4 (95% CI 3.7–5.1). Mean time from diagnosis of diabetes to ESRD was 23.6 years (range 14.2–33.5). Death was caused by chronic complications (32.2%), acute complications (20.5%), violent death (19.9%), or any other cause (27.4%). Death was related to alcohol in 15% of cases. SMR for alcohol-related death was 6.8 (95% CI 4.5–10.3), for cardiovascular death was 7.3 (5.4–10.0), and for violent death was 3.6 (2.3–5.3).

CONCLUSIONS The cumulative incidence of ESRD was low in this cohort with type 1 diabetes followed for 30 years. Mortality was 4.4 times that of the general population, and more than 50% of all deaths were caused by acute or chronic complications. A relatively high proportion of deaths were related to alcohol.”

Some additional observations from the paper:

“Studies assessing causes of death in type 1 diabetes are most frequently conducted in individuals diagnosed during childhood (17) or without evaluating the effect of age at diagnosis (8,9). Reports on causes of death in cohorts of patients diagnosed during late adolescence or young adulthood, with long-term follow-up, are less frequent (10). […] Adherence to treatment during this age is poor and the risk of acute diabetic complications is high (1316). Mortality may differ between those with diabetes diagnosed during this period of life and those diagnosed during childhood.”

“Mortality was between four and five times higher than in the general population […]. The excess mortality was similar for men […] and women […]. SMR was higher in the lower age bands — 6.7 (95% CI 3.9–11.5) at 15–24 years and 7.3 (95% CI 5.2–10.1) at 25–34 years — compared with the higher age bands: 3.7 (95% CI 2.7–4.9) at 45–54 years and 3.9 (95% CI 2.6–5.8) at 55–65 years […]. The Cox regression model showed that the risk of death increased significantly by age at diagnosis (HR 1.1; 95% CI 1.1–1.2; P < 0.001) and was eight to nine times higher if ESRD was present (HR 8.7; 95% CI 4.8–15.5; P < 0.0001). […] the underlying cause of death was diabetes in 57 individuals (39.0%), circulatory in 22 (15.1%), cancer in 18 (12.3%), accidents or intoxications in 20 (13.7%), suicide in 8 (5.5%), and any other cause in 21 (14.4%) […] In addition, diabetes contributed to death in 29.5% (n = 43) and CVD contributed to death in 10.9% (n = 29) of the 146 cases. Diabetes was mentioned on the death certificate for 68.2% of the cohort but for only 30.0% of the violent deaths. […] In 60% (88/146) of the cases the review committee considered death to be related to diabetes, whereas in 40% (58/146) the cause was unrelated to diabetes or had an unknown relation to diabetes. According to the clinical committee, acute complications caused death in 20.5% (30/146) of the cases; 20 individuals died as a result of DKA and 10 from hypoglycemia. […] Chronic complications caused the largest proportion of deaths (47/146; 32.2%) and increased with increasing duration of diabetes […]. Among individuals dying as a result of chronic complications (n = 47), CVD caused death in 94% (n = 44) and renal failure in 6% (n = 3). ESRD contributed to death in 22.7% (10/44) of those dying from CVD. Cardiovascular death occurred at mortality rates seven times higher than those in the general population […]. ESRD caused or contributed to death in 13 of 14 cases, when present.”

“Violence (intoxications, accidents, and suicides) was the leading cause of death before 10 years’ duration of diabetes; thereafter it was only a minor cause […] Insulin was used in two of seven suicides. […] According to the available medical records and autopsy reports, about 20% (29/146) of the deceased misused alcohol. In 15% (22/146) alcohol-related ICD-10 codes were listed on the death certificate (18% [19/106] of men and 8% [3/40] of women). In 10 cases the cause of death was uncertain but considered to be related to alcohol or diabetes […] The SMR for alcohol-related death was high when considering the underlying cause of death (5.0; 95% CI 2.5–10.0), and even higher when considering all alcohol-related ICD-10 codes listed on the death certificate (6.8; 95% CI 4.5–10.3). The cause of death was associated with alcohol in 21.8% (19/87) of those who died with less than 20 years’ diabetes duration. Drug abuse was noted on the death certificate in only two cases.”

“During follow-up, 33 individuals (4.6%; 22 men and 11 women) developed ESRD as a result of diabetic nephropathy. Mean time from diagnosis of diabetes to ESRD was 23.6 years (range 14.2–33.5 years). Cumulative incidence of ESRD by years since diagnosis of diabetes was 1.4% (95% CI 0.7–2.7) at 20 years and 4.8% (95% CI 3.4–6.9) at 30 years.”

“This study highlights three important findings. First, among individuals who were diagnosed with type 1 diabetes in late adolescence and early adulthood and had good access to health care, and who were followed for 30 years, mortality was four to five times that of the general population. Second, 15% of all deaths were associated with alcohol, and the SMR for alcohol-related deaths was 6.8. Third, there was a relatively low cumulative incidence of ESRD (4.8%) 30 years after the diagnosis of diabetes.

We report mortality higher than those from a large, population-based study from Finland that found cumulative mortality around 6% at 20 years’ and 15% at 30 years’ duration of diabetes among a population with age at onset and year of diagnosis similar to those in our cohort (10). The corresponding numbers in our cohort were 12% and 18%, respectively; the discrepancy was particularly high at 20 years. The SMR in the Finnish cohort was lower than that in our cohort (2.6–3.0 vs. 3.7–5.1), and those authors reported the SMR to be lower in late-onset diabetes (at age 15–29 years) compared with early-onset diabetes (at age 23). The differences between the Norwegian and Finnish data are difficult to explain since both reports are from countries with good access to health care and a high incidence of type 1 diabetes.”

However the reason for the somewhat different SMRs in these two reasonably similar countries may actually be quite simple – the important variable may be alcohol:

“Finland and Norway are appropriate to compare because they share important population and welfare characteristics. There are, however, significant differences in drinking levels and alcohol-related mortality: the Finnish population consumes more alcohol and the Norwegian population consumes less. The mortality rates for deaths related to alcohol are about three to four times higher in Finland than in Norway (30). […] The markedly higher SMR in our cohort can probably be explained by the lower mortality rates for alcohol-related mortality in the general population. […] In conclusion, the high mortality reported in this cohort with an onset of diabetes in late adolescence and young adulthood draws attention to people diagnosed during a vulnerable period of life. Both acute and chronic complications cause substantial premature mortality […] Our study suggests that increased awareness of alcohol-related death should be encouraged in clinics providing health care to this group of patients.”

April 23, 2017 Posted by | Diabetes, Economics, Epidemiology, Medicine, Nephrology, Neurology, Papers, Pharmacology, Psychology | Leave a comment

A few autism papers

i. The anterior insula in autism: Under-connected and under-examined.

“While the past decade has witnessed a proliferation of neuroimaging studies of autism, theoretical approaches for understanding systems-level brain abnormalities remain poorly developed. We propose a novel anterior insula-based systems-level model for investigating the neural basis of autism, synthesizing recent advances in brain network functional connectivity with converging evidence from neuroimaging studies in autism. The anterior insula is involved in interoceptive, affective and empathic processes, and emerging evidence suggests it is part of a “salience network” integrating external sensory stimuli with internal states. Network analysis indicates that the anterior insula is uniquely positioned as a hub mediating interactions between large-scale networks involved in externally- and internally-oriented cognitive processing. A recent meta-analysis identifies the anterior insula as a consistent locus of hypoactivity in autism. We suggest that dysfunctional anterior insula connectivity plays an important role in autism. […]

Increasing evidence for abnormal brain connectivity in autism comes from studies using functional connectivity measures […] These findings support the hypothesis that under-connectivity between specific brain regions is a characteristic feature of ASD. To date, however, few studies have examined functional connectivity within and between key large-scale canonical brain networks in autism […] The majority of published studies to date have examined connectivity of specific individual brain regions, without a broader theoretically driven systems-level approach.

We propose that a systems-level approach is critical for understanding the neurobiology of autism, and that the anterior insula is a key node in coordinating brain network interactions, due to its unique anatomy, location, function, and connectivity.”

ii. Romantic Relationships and Relationship Satisfaction Among Adults With Asperger Syndrome and High‐Functioning Autism.

“Participants, 31 recruited via an outpatient clinic and 198 via an online survey, were asked to answer a number of self-report questionnaires. The total sample comprised 229 high-functioning adults with ASD (40% males, average age: 35 years). […] Of the total sample, 73% indicated romantic relationship experience and only 7% had no desire to be in a romantic relationship. ASD individuals whose partner was also on the autism spectrum were significantly more satisfied with their relationship than those with neurotypical partners. Severity of autism, schizoid symptoms, empathy skills, and need for social support were not correlated with relationship status. […] Our findings indicate that the vast majority of high-functioning adults with ASD are interested in romantic relationships.”

Those results are very different from other results in the field – for example: “[a] meta-analysis of follow-up studies examining outcomes of ASD individuals revealed that, [o]n average only 14% of the individuals included in the reviewed studies were married or ha[d] a long-term, intimate relationship (Howlin, 2012)” – and one major reason is that they only include high-functioning autistics. I feel sort of iffy about the validity of the selection method used for procuring the online sample, this may also be a major factor (almost one third of them had a university degree so this is definitely not a random sample of high-functioning autistics; ‘high-functioning’ autistics are not that high-functioning in the general setting. Also, the sex ratio is very skewed as 60% of the participants in the study were female. A sex ratio like that may not sound like a big problem, but it is a major problem because a substantial majority of individuals with mild autism are males. Whereas the sex ratio is almost equal in the context of syndromic ASD, non-syndromic ASD is much more prevalent in males, with sex ratios approaching 1:7 in milder cases (link). These people are definitely looking at the milder cases, which means that a sample which skews female will not be remotely similar to most random samples of such individuals taken in the community setting. And this matters because females do better than males. A discussion can be had about to which extent women are under-diagnosed, but I have not seen data convincing me this is a major problem. It’s important to keep in mind in that context that the autism diagnosis is not based on phenotype alone, but on a phenotype-environment interaction; if you have what might be termed ‘an autistic phenotype’ but you are not suffering any significant ill effects as a result of this because you’re able to compensate relatively well (i.e. you are able to handle ‘the environment’ reasonably well despite the neurological makeup you’ve ended up with), you should not get an autism diagnosis – a diagnostic requirement is ‘clinically significant impairment in functioning’.

Anyway some more related data from the publication:

“Studies that analyze outcomes exclusively for ASD adults without intellectual impairment are rare. […] Engström, Ekström, and Emilsson (2003) recruited previous patients with an ASD diagnosis from four psychiatric clinics in Sweden. They reported that 5 (31%) of 16 adults with ASD had ”some form of relation with a partner.” Hofvander et al. (2009) analyzed data from 122 participants who had been referred to outpatient clinics for autism diagnosis. They found that 19 (16%) of all participants had lived in a long-term relationship.
Renty and Roeyers (2006) […] reported that at the time of the[ir] study 19% of 58 ASD adults had a romantic relationship and 8.6% were married or living with a partner. Cederlund, Hagberg, Billstedt, Gillberg, and Gillberg (2008) conducted a follow-up study of male individuals (aged 16–36 years) who had been diagnosed with Asperger syndrome at least 5 years before. […] at the time of the study, three (4%) [out of 76 male ASD individuals] of them were living in a long-term romantic relationship and 10 (13%) had had romantic relationships in the past.”

A few more data and observations from the study:

“A total of 166 (73%) of the 229 participants endorsed currently being in a romantic relationship or having a history of being in a relationship; 100 (44%) reported current involvement in a romantic relationship; 66 (29%) endorsed that they were currently single but have a history of involvement in a romantic relationship; and 63 (27%) participants did not have any experience with romantic relationships. […] Participants without any romantic relationship experience were significantly more likely to be male […] According to participants’ self-report, one fifth (20%) of the 100 participants who were currently involved in a romantic relationship were with an ASD partner. […] Of the participants who were currently single, 65% said that contact with another person was too exhausting for them, 61% were afraid that they would not be able to fulfil the expectations of a romantic partner, and 57% said that they did not know how they could find and get involved with a partner; and 50% stated that they did not know how a romantic relationship works or how they would be expected to behave in a romantic relationship”

“[P]revious studies that exclusively examined adults with ASD without intellectual impairment reported lower levels of romantic relationship experience than the current study, with numbers varying between 16% and 31% […] The results of our study can be best compared with the results of Hofvander et al. (2009) and Renty and Roeyers (2006): They selected their samples […] using methods that are comparable to ours. Hofvander et al. (2009) found that 16% of their participants have had romantic relationship experience in the past, compared to 29% in our sample; and Renty and Roeyers (2006) report that 28% of their participants were either married or engaged in a romantic relationship at the time of their study, compared to 44% in our study. […] Compared to typically developed individuals the percentage of ASD individuals with a romantic relationship partner is relatively low (Weimann, 2010). In the group aged 27–59 years, 68% of German males live together with a partner, 27% are single, and 5% still live with their parents. In the same age group, 73% of all females live with a partner, 26% live on their own, and 2% still live with their parents.”

“As our results show, it is not the case that male ASD individuals do not feel a need for romantic relationships. In fact, the contrary is true. Single males had a greater desire to be in a romantic relationship than single females, and males were more distressed than females about not being in a romantic relationship.” (…maybe in part because the females who were single were more likely than the males who were single to be single by choice?)

“Our findings showed that being with a partner who also has an ASD diagnosis makes a romantic relationship more satisfying for ASD individuals. None of the participants, who had been with a partner in the past but then separated, had been together with an ASD partner. This might indicate that once a person with ASD has found a partner who is also on the spectrum, a relationship might be very stable and long lasting.”

Reward Processing in Autism.

“The social motivation hypothesis of autism posits that infants with autism do not experience social stimuli as rewarding, thereby leading to a cascade of potentially negative consequences for later development. […] Here we use functional magnetic resonance imaging to examine social and monetary rewarded implicit learning in children with and without autism spectrum disorders (ASD). Sixteen males with ASD and sixteen age- and IQ-matched typically developing (TD) males were scanned while performing two versions of a rewarded implicit learning task. In addition to examining responses to reward, we investigated the neural circuitry supporting rewarded learning and the relationship between these factors and social development. We found diminished neural responses to both social and monetary rewards in ASD, with a pronounced reduction in response to social rewards (SR). […] Moreover, we show a relationship between ventral striatum activity and social reciprocity in TD children. Together, these data support the hypothesis that children with ASD have diminished neural responses to SR, and that this deficit relates to social learning impairments. […] When we examined the general neural response to monetary and social reward events, we discovered that only TD children showed VS [ventral striatum] activity for both reward types, whereas ASD children did not demonstrate a significant response to either monetary or SR. However, significant between-group differences were shown only for SR, suggesting that children with ASD may be specifically impaired on processing SR.”

I’m not quite sure I buy that the methodology captures what it is supposed to capture (“The SR feedback consisted of a picture of a smiling woman with the words “That’s Right!” in green text for correct trials and a picture of the same woman with a sad face along with the words “That’s Wrong” in red text for incorrect trials”) (this is supposed to be the ‘social reward feedback’), but on the other hand: “The chosen reward stimuli, faces and coins, are consistent with those used in previous studies of reward processing” (so either multiple studies are of dubious quality, or this kind of method actually ‘works’ – but I don’t know enough about the field to tell which of the two conclusions apply).

iv. The Social Motivation Theory of Autism.

“The idea that social motivation deficits play a central role in Autism Spectrum Disorders (ASD) has recently gained increased interest. This constitutes a shift in autism research, which has traditionally focused more intensely on cognitive impairments, such as Theory of Mind deficits or executive dysfunction, while granting comparatively less attention to motivational factors. This review delineates the concept of social motivation and capitalizes on recent findings in several research areas to provide an integrated picture of social motivation at the behavioral, biological and evolutionary levels. We conclude that ASD can be construed as an extreme case of diminished social motivation and, as such, provides a powerful model to understand humans’ intrinsic drive to seek acceptance and avoid rejection.”

v. Stalking, and Social and Romantic Functioning Among Adolescents and Adults with Autism Spectrum Disorder.

“We examine the nature and predictors of social and romantic functioning in adolescents and adults with ASD. Parental reports were obtained for 25 ASD adolescents and adults (13-36 years), and 38 typical adolescents and adults (13-30 years). The ASD group relied less upon peers and friends for social (OR = 52.16, p < .01) and romantic learning (OR = 38.25, p < .01). Individuals with ASD were more likely to engage in inappropriate courting behaviours (χ2 df = 19 = 3168.74, p < .001) and were more likely to focus their attention upon celebrities, strangers, colleagues, and ex-partners (χ2 df = 5 =2335.40, p < .001), and to pursue their target longer than controls (t = -2.23, df = 18.79, p < .05).”

“Examination of relationships the individuals were reported to have had with the target of their social or romantic interest, indicated that ASD adolescents and adults sought to initiate fewer social and romantic relationships but across a wider variety of people, such as strangers, colleagues, acquaintances, friends, ex-partners, and celebrities. […] typically developing peers […] were more likely to target colleagues, acquaintances, friends, and ex-partners in their relationship attempts, whilst the ASD group targeted these less frequently than expected, and attempted to initiate relationships significantly more frequently than is typical, with strangers and celebrities. […] In attempting to pursue and initiate social and romantic relationships, the ASD group were reported to display a much wider variety of courtship behaviours than the typical group. […] ASD adolescents and adults were more likely to touch the person of interest inappropriately, believe that the target must reciprocate their feelings, show obsessional interest, make inappropriate comments, monitor the person’s activities, follow them, pursue them in a threatening manner, make threats against the person, and threaten self-harm. ASD individuals displayed the majority of the behaviours indiscriminately across all types of targets. […] ASD adolescents and adults were also found […] to persist in their relationship pursuits for significantly longer periods of time than typical adolescents and adults when they received a negative or no response from the person or their family.”

April 4, 2017 Posted by | autism, Neurology, Papers, Psychology | Leave a comment

Random stuff

It’s been a long time since I last posted one of these posts, so a great number of links of interest has accumulated in my bookmarks. I intended to include a large number of these in this post and this of course means that I surely won’t cover each specific link included in this post in anywhere near the amount of detail it deserves, but that can’t be helped.

i. Autism Spectrum Disorder Grown Up: A Chart Review of Adult Functioning.

“For those diagnosed with ASD in childhood, most will become adults with a significant degree of disability […] Seltzer et al […] concluded that, despite considerable heterogeneity in social outcomes, “few adults with autism live independently, marry, go to college, work in competitive jobs or develop a large network of friends”. However, the trend within individuals is for some functional improvement over time, as well as a decrease in autistic symptoms […]. Some authors suggest that a sub-group of 15–30% of adults with autism will show more positive outcomes […]. Howlin et al. (2004), and Cederlund et al. (2008) assigned global ratings of social functioning based on achieving independence, friendships/a steady relationship, and education and/or a job. These two papers described respectively 22% and 27% of groups of higher functioning (IQ above 70) ASD adults as attaining “Very Good” or “Good” outcomes.”

“[W]e evaluated the adult outcomes for 45 individuals diagnosed with ASD prior to age 18, and compared this with the functioning of 35 patients whose ASD was identified after 18 years. Concurrent mental illnesses were noted for both groups. […] Comparison of adult outcome within the group of subjects diagnosed with ASD prior to 18 years of age showed significantly poorer functioning for those with co-morbid Intellectual Disability, except in the domain of establishing intimate relationships [my emphasis. To make this point completely clear, one way to look at these results is that apparently in the domain of partner-search autistics diagnosed during childhood are doing so badly in general that being intellectually disabled on top of being autistic is apparently conferring no additional disadvantage]. Even in the normal IQ group, the mean total score, i.e. the sum of the 5 domains, was relatively low at 12.1 out of a possible 25. […] Those diagnosed as adults had achieved significantly more in the domains of education and independence […] Some authors have described a subgroup of 15–27% of adult ASD patients who attained more positive outcomes […]. Defining an arbitrary adaptive score of 20/25 as “Good” for our normal IQ patients, 8 of thirty four (25%) of those diagnosed as adults achieved this level. Only 5 of the thirty three (15%) diagnosed in childhood made the cutoff. (The cut off was consistent with a well, but not superlatively, functioning member of society […]). None of the Intellectually Disabled ASD subjects scored above 10. […] All three groups had a high rate of co-morbid psychiatric illnesses. Depression was particularly frequent in those diagnosed as adults, consistent with other reports […]. Anxiety disorders were also prevalent in the higher functioning participants, 25–27%. […] Most of the higher functioning ASD individuals, whether diagnosed before or after 18 years of age, were functioning well below the potential implied by their normal range intellect.”

Related papers: Social Outcomes in Mid- to Later Adulthood Among Individuals Diagnosed With Autism and Average Nonverbal IQ as Children, Adults With Autism Spectrum Disorders.

ii. Premature mortality in autism spectrum disorder. This is a Swedish matched case cohort study. Some observations from the paper:

“The aim of the current study was to analyse all-cause and cause-specific mortality in ASD using nationwide Swedish population-based registers. A further aim was to address the role of intellectual disability and gender as possible moderators of mortality and causes of death in ASD. […] Odds ratios (ORs) were calculated for a population-based cohort of ASD probands (n = 27 122, diagnosed between 1987 and 2009) compared with gender-, age- and county of residence-matched controls (n = 2 672 185). […] During the observed period, 24 358 (0.91%) individuals in the general population died, whereas the corresponding figure for individuals with ASD was 706 (2.60%; OR = 2.56; 95% CI 2.38–2.76). Cause-specific analyses showed elevated mortality in ASD for almost all analysed diagnostic categories. Mortality and patterns for cause-specific mortality were partly moderated by gender and general intellectual ability. […] Premature mortality was markedly increased in ASD owing to a multitude of medical conditions. […] Mortality was significantly elevated in both genders relative to the general population (males: OR = 2.87; females OR = 2.24)”.

“Individuals in the control group died at a mean age of 70.20 years (s.d. = 24.16, median = 80), whereas the corresponding figure for the entire ASD group was 53.87 years (s.d. = 24.78, median = 55), for low-functioning ASD 39.50 years (s.d. = 21.55, median = 40) and high-functioning ASD 58.39 years (s.d. = 24.01, median = 63) respectively. […] Significantly elevated mortality was noted among individuals with ASD in all analysed categories of specific causes of death except for infections […] ORs were highest in cases of mortality because of diseases of the nervous system (OR = 7.49) and because of suicide (OR = 7.55), in comparison with matched general population controls.”

iii. Adhesive capsulitis of shoulder. This one is related to a health scare I had a few months ago. A few quotes:

Adhesive capsulitis (also known as frozen shoulder) is a painful and disabling disorder of unclear cause in which the shoulder capsule, the connective tissue surrounding the glenohumeral joint of the shoulder, becomes inflamed and stiff, greatly restricting motion and causing chronic pain. Pain is usually constant, worse at night, and with cold weather. Certain movements or bumps can provoke episodes of tremendous pain and cramping. […] People who suffer from adhesive capsulitis usually experience severe pain and sleep deprivation for prolonged periods due to pain that gets worse when lying still and restricted movement/positions. The condition can lead to depression, problems in the neck and back, and severe weight loss due to long-term lack of deep sleep. People who suffer from adhesive capsulitis may have extreme difficulty concentrating, working, or performing daily life activities for extended periods of time.”

Some other related links below:

The prevalence of a diabetic condition and adhesive capsulitis of the shoulder.
“Adhesive capsulitis is characterized by a progressive and painful loss of shoulder motion of unknown etiology. Previous studies have found the prevalence of adhesive capsulitis to be slightly greater than 2% in the general population. However, the relationship between adhesive capsulitis and diabetes mellitus (DM) is well documented, with the incidence of adhesive capsulitis being two to four times higher in diabetics than in the general population. It affects about 20% of people with diabetes and has been described as the most disabling of the common musculoskeletal manifestations of diabetes.”

Adhesive Capsulitis (review article).
“Patients with type I diabetes have a 40% chance of developing a frozen shoulder in their lifetimes […] Dominant arm involvement has been shown to have a good prognosis; associated intrinsic pathology or insulin-dependent diabetes of more than 10 years are poor prognostic indicators.15 Three stages of adhesive capsulitis have been described, with each phase lasting for about 6 months. The first stage is the freezing stage in which there is an insidious onset of pain. At the end of this period, shoulder ROM [range of motion] becomes limited. The second stage is the frozen stage, in which there might be a reduction in pain; however, there is still restricted ROM. The third stage is the thawing stage, in which ROM improves, but can take between 12 and 42 months to do so. Most patients regain a full ROM; however, 10% to 15% of patients suffer from continued pain and limited ROM.”

Musculoskeletal Complications in Type 1 Diabetes.
“The development of periarticular thickening of skin on the hands and limited joint mobility (cheiroarthropathy) is associated with diabetes and can lead to significant disability. The objective of this study was to describe the prevalence of cheiroarthropathy in the well-characterized Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) cohort and examine associated risk factors […] This cross-sectional analysis was performed in 1,217 participants (95% of the active cohort) in EDIC years 18/19 after an average of 24 years of follow-up. Cheiroarthropathy — defined as the presence of any one of the following: adhesive capsulitis, carpal tunnel syndrome, flexor tenosynovitis, Dupuytren’s contracture, or a positive prayer sign [related link] — was assessed using a targeted medical history and standardized physical examination. […] Cheiroarthropathy was present in 66% of subjects […] Cheiroarthropathy is common in people with type 1 diabetes of long duration (∼30 years) and is related to longer duration and higher levels of glycemia. Clinicians should include cheiroarthropathy in their routine history and physical examination of patients with type 1 diabetes because it causes clinically significant functional disability.”

Musculoskeletal disorders in diabetes mellitus: an update.
“Diabetes mellitus (DM) is associated with several musculoskeletal disorders. […] The exact pathophysiology of most of these musculoskeletal disorders remains obscure. Connective tissue disorders, neuropathy, vasculopathy or combinations of these problems, may underlie the increased incidence of musculoskeletal disorders in DM. The development of musculoskeletal disorders is dependent on age and on the duration of DM; however, it has been difficult to show a direct correlation with the metabolic control of DM.”

Rheumatic Manifestations of Diabetes Mellitus.

Prevalence of symptoms and signs of shoulder problems in people with diabetes mellitus.

Musculoskeletal Disorders of the Hand and Shoulder in Patients with Diabetes.
“In addition to micro- and macroangiopathic complications, diabetes mellitus is also associated with several musculoskeletal disorders of the hand and shoulder that can be debilitating (1,2). Limited joint mobility, also termed diabetic hand syndrome or cheiropathy (3), is characterized by skin thickening over the dorsum of the hands and restricted mobility of multiple joints. While this syndrome is painless and usually not disabling (2,4), other musculoskeletal problems occur with increased frequency in diabetic patients, including Dupuytren’s disease [“Dupuytren’s disease […] may be observed in up to 42% of adults with diabetes mellitus, typically in patients with long-standing T1D” – link], carpal tunnel syndrome [“The prevalence of [carpal tunnel syndrome, CTS] in patients with diabetes has been estimated at 11–30 % […], and is dependent on the duration of diabetes. […] Type I DM patients have a high prevalence of CTS with increasing duration of disease, up to 85 % after 54 years of DM” – link], palmar flexor tenosynovitis or trigger finger [“The incidence of trigger finger [/stenosing tenosynovitis] is 7–20 % of patients with diabetes comparing to only about 1–2 % in nondiabetic patients” – link], and adhesive capsulitis of the shoulder (5–10). The association of adhesive capsulitis with pain, swelling, dystrophic skin, and vasomotor instability of the hand constitutes the “shoulder-hand syndrome,” a rare but potentially disabling manifestation of diabetes (1,2).”

“The prevalence of musculoskeletal disorders was greater in diabetic patients than in control patients (36% vs. 9%, P < 0.01). Adhesive capsulitis was present in 12% of the diabetic patients and none of the control patients (P < 0.01), Dupuytren’s disease in 16% of diabetic and 3% of control patients (P < 0.01), and flexor tenosynovitis in 12% of diabetic and 2% of control patients (P < 0.04), while carpal tunnel syndrome occurred in 12% of diabetic patients and 8% of control patients (P = 0.29). Musculoskeletal disorders were more common in patients with type 1 diabetes than in those with type 2 diabetes […]. Forty-three patients [out of 100] with type 1 diabetes had either hand or shoulder disorders (37 with hand disorders, 6 with adhesive capsulitis of the shoulder, and 10 with both syndromes), compared with 28 patients [again out of 100] with type 2 diabetes (24 with hand disorders, 4 with adhesive capsulitis of the shoulder, and 3 with both syndromes, P = 0.03).”

Association of Diabetes Mellitus With the Risk of Developing Adhesive Capsulitis of the Shoulder: A Longitudinal Population-Based Followup Study.
“A total of 78,827 subjects with at least 2 ambulatory care visits with a principal diagnosis of DM in 2001 were recruited for the DM group. The non-DM group comprised 236,481 age- and sex-matched randomly sampled subjects without DM. […] During a 3-year followup period, 946 subjects (1.20%) in the DM group and 2,254 subjects (0.95%) in the non-DM group developed ACS. The crude HR of developing ACS for the DM group compared to the non-DM group was 1.333 […] the association between DM and ACS may be explained at least in part by a DM-related chronic inflammatory process with increased growth factor expression, which in turn leads to joint synovitis and subsequent capsular fibrosis.”

It is important to note when interpreting the results of the above paper that these results are based on Taiwanese population-level data, and type 1 diabetes – which is obviously the high-risk diabetes subgroup in this particular context – is rare in East Asian populations (as observed in Sperling et al., “A child in Helsinki, Finland is almost 400 times more likely to develop diabetes than a child in Sichuan, China”. Taiwanese incidence of type 1 DM in children is estimated at ~5 in 100.000).

iv. Parents who let diabetic son starve to death found guilty of first-degree murder. It’s been a while since I last saw one of these ‘boost-your-faith-in-humanity’-cases, but they in my impression do pop up every now and then. I should probably keep at hand one of these articles in case my parents ever express worry to me that they weren’t good parents; they could have done a lot worse…

v. Freedom of medicine. One quote from the conclusion of Cochran’s post:

“[I]t is surely possible to materially improve the efficacy of drug development, of medical research as a whole. We’re doing better than we did 500 years ago – although probably worse than we did 50 years ago. But I would approach it by learning as much as possible about medical history, demographics, epidemiology, evolutionary medicine, theory of senescence, genetics, etc. Read Koch, not Hayek. There is no royal road to medical progress.”

I agree, and I was considering including some related comments and observations about health economics in this post – however I ultimately decided against doing that in part because the post was growing unwieldy; I might include those observations in another post later on. Here’s another somewhat older Westhunt post I at some point decided to bookmark – I in particular like the following neat quote from the comments, which expresses a view I have of course expressed myself in the past here on this blog:

“When you think about it, falsehoods, stupid crap, make the best group identifiers, because anyone might agree with you when you’re obviously right. Signing up to clear nonsense is a better test of group loyalty. A true friend is with you when you’re wrong. Ideally, not just wrong, but barking mad, rolling around in your own vomit wrong.”

vi. Economic Costs of Diabetes in the U.S. in 2012.

“Approximately 59% of all health care expenditures attributed to diabetes are for health resources used by the population aged 65 years and older, much of which is borne by the Medicare program […]. The population 45–64 years of age incurs 33% of diabetes-attributed costs, with the remaining 8% incurred by the population under 45 years of age. The annual attributed health care cost per person with diabetes […] increases with age, primarily as a result of increased use of hospital inpatient and nursing facility resources, physician office visits, and prescription medications. Dividing the total attributed health care expenditures by the number of people with diabetes, we estimate the average annual excess expenditures for the population aged under 45 years, 45–64 years, and 65 years and above, respectively, at $4,394, $5,611, and $11,825.”

“Our logistic regression analysis with NHIS data suggests that diabetes is associated with a 2.4 percentage point increase in the likelihood of leaving the workforce for disability. This equates to approximately 541,000 working-age adults leaving the workforce prematurely and 130 million lost workdays in 2012. For the population that leaves the workforce early because of diabetes-associated disability, we estimate that their average daily earnings would have been $166 per person (with the amount varying by demographic). Presenteeism accounted for 30% of the indirect cost of diabetes. The estimate of a 6.6% annual decline in productivity attributed to diabetes (in excess of the estimated decline in the absence of diabetes) equates to 113 million lost workdays per year.”

vii. Total red meat intake of ≥0.5 servings/d does not negatively influence cardiovascular disease risk factors: a systemically searched meta-analysis of randomized controlled trials.

viii. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. Did I blog this paper at some point in the past? I could not find any coverage of it on the blog when I searched for it so I decided to include it here, even if I have a nagging suspicion I may have talked about these findings before. What did they find? The short version is this:

“A modest reduction in salt intake for four or more weeks causes significant and, from a population viewpoint, important falls in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. Salt reduction is associated with a small physiological increase in plasma renin activity, aldosterone, and noradrenaline and no significant change in lipid concentrations. These results support a reduction in population salt intake, which will lower population blood pressure and thereby reduce cardiovascular disease.”

ix. Some wikipedia links:

Heroic Age of Antarctic Exploration (featured).

Wien’s displacement law.

Kuiper belt (featured).

Treason (one quote worth including here: “Currently, the consensus among major Islamic schools is that apostasy (leaving Islam) is considered treason and that the penalty is death; this is supported not in the Quran but in the Hadith.[42][43][44][45][46][47]“).

Lymphatic filariasis.

File:World map of countries by number of cigarettes smoked per adult per year.

Australian gold rushes.

Savant syndrome (“It is estimated that 10% of those with autism have some form of savant abilities”). A small sidenote of interest to Danish readers: The Danish Broadcasting Corporation recently featured a series about autistics with ‘special abilities’ – the show was called ‘The hidden talents’ (De skjulte talenter), and after multiple people had nagged me to watch it I ended up deciding to do so. Most of the people in that show presumably had some degree of ‘savantism’ combined with autism at the milder end of the spectrum, i.e. Asperger’s. I was somewhat conflicted about what to think about the show and did consider blogging it in detail (in Danish?), but I decided against it. However I do want to add here to Danish readers reading along who’ve seen the show that they would do well to repeatedly keep in mind that a) the great majority of autistics do not have abilities like these, b) many autistics with abilities like these presumably do quite poorly, and c) that many autistics have even greater social impairments than do people like e.g. (the very likeable, I have to add…) Louise Wille from the show).

Quark–gluon plasma.

Simo Häyhä.

Chernobyl liquidators.

Black Death (“Over 60% of Norway’s population died in 1348–1350”).

Renault FT (“among the most revolutionary and influential tank designs in history”).

Weierstrass function (“an example of a pathological real-valued function on the real line. The function has the property of being continuous everywhere but differentiable nowhere”).

W Ursae Majoris variable.

Void coefficient. (“a number that can be used to estimate how much the reactivity of a nuclear reactor changes as voids (typically steam bubbles) form in the reactor moderator or coolant. […] Reactivity is directly related to the tendency of the reactor core to change power level: if reactivity is positive, the core power tends to increase; if it is negative, the core power tends to decrease; if it is zero, the core power tends to remain stable. […] A positive void coefficient means that the reactivity increases as the void content inside the reactor increases due to increased boiling or loss of coolant; for example, if the coolant acts as a neutron absorber. If the void coefficient is large enough and control systems do not respond quickly enough, this can form a positive feedback loop which can quickly boil all the coolant in the reactor. This happened in the RBMK reactor that was destroyed in the Chernobyl disaster.”).

Gregor MacGregor (featured) (“a Scottish soldier, adventurer, and confidence trickster […] MacGregor’s Poyais scheme has been called one of the most brazen confidence tricks in history.”).

Stimming.

Irish Civil War.

March 10, 2017 Posted by | Astronomy, autism, Cardiology, Diabetes, Economics, Epidemiology, History, Infectious disease, Mathematics, Medicine, Papers, Physics, Psychology, Random stuff, Wikipedia | Leave a comment

Diabetes and the Brain (III)

Some quotes from the book below.

Tests that are used in clinical neuropsychology in most cases examine one or more aspects of cognitive domains, which are theoretical constructs in which a multitude of cognitive processes are involved. […] By definition, a subdivision in cognitive domains is arbitrary, and many different classifications exist. […] for a test to be recommended, several criteria must be met. First, a test must have adequate reliability: the test must yield similar outcomes when applied over multiple test sessions, i.e., have good test–retest reliability. […] Furthermore, the interobserver reliability is important, in that the test must have a standardized assessment procedure and is scored in the same manner by different examiners. Second, the test must have adequate validity. Here, different forms of validity are important. Content validity is established by expert raters with respect to item formulation, item selection, etc. Construct validity refers to the underlying theoretical construct that the test is assumed to measure. To assess construct validity, both convergent and divergent validities are important. Convergent validity refers to the amount of agreement between a given test and other tests that measure the same function. In turn, a test with a good divergent validity correlates minimally with tests that measure other cognitive functions. Moreover, predictive validity (or criterion validity) is related to the degree of correlation between the test score and an external criterion, for example, the correlation between a cognitive test and functional status. […] it should be stressed that cognitive tests alone cannot be used as ultimate proof for organic brain damage, but should be used in combination with more direct measures of cerebral abnormalities, such as neuroimaging.”

“Intelligence is a theoretically ill-defined construct. In general, it refers to the ability to think in an abstract manner and solve new problems. Typically, two forms of intelligence are distinguished, crystallized intelligence (academic skills and knowledge that one has acquired during schooling) and fluid intelligence (the ability to solve new problems). Crystallized intelligence is better preserved in patients with brain disease than fluid intelligence (3). […] From a neuropsychological viewpoint, the concept of intelligence as a unitary construct (often referred to as g-factor) does not provide valuable information, since deficits in specific cognitive functions may be averaged out in the total IQ score. Thus, in most neuropsychological studies, intelligence tests are included because of specific subtests that are assumed to measure specific cognitive functions, and the performance profile is analyzed rather than considering the IQ measure as a compound score in isolation.”

“Attention is a concept that in general relates to the selection of relevant information from our environment and the suppression of irrelevant information (selective or “focused” attention), the ability to shift attention between tasks (divided attention), and to maintain a state of alertness to incoming stimuli over longer periods of time (concentration and vigilance). Many different structures in the human brain are involved in attentional processing and, consequently, disorders in attention occur frequently after brain disease or damage (21). […] Speed of information processing is not a localized cognitive function, but depends greatly on the integrity of the cerebral network as a whole, the subcortical white matter and the interhemispheric and intrahemispheric connections. It is one of the cognitive functions that clearly declines with age and it is highly susceptible to brain disease or dysfunction of any kind.”

“The MiniMental State Examination (MMSE) is a screening instrument that has been developed to determine whether older adults have cognitive impairments […] numerous studies have shown that the MMSE has poor sensitivity and specificity, as well as a low-test–retest reliability […] the MMSE has been developed to determine cognitive decline that is typical for Alzheimer’s dementia, but has been found less useful in determining cognitive decline in nondemented patients (44) or in patients with other forms of dementia. This is important since odds ratios for both vascular dementia and Alzheimer’s dementia are increased in diabetes (45). Notwithstanding this increased risk, most patients with diabetes have subtle cognitive deficits (46, 47) that may easily go undetected using gross screening instruments such as the MMSE. For research in diabetes a high sensitivity is thus especially important. […] ceiling effects in test performance often result in a lack of sensitivity. Subtle impairments are easily missed, resulting in a high proportion of false-negative cases […] In general, tests should be cognitively demanding to avoid ceiling effects in patients with mild cognitive dysfunction.[…] sensitive domains such as speed of information processing, (working) memory, attention, and executive function should be examined thoroughly in diabetes patients, whereas other domains such as language, motor function, and perception are less likely to be affected. Intelligence should always be taken into account, and confounding factors such as mood, emotional distress, and coping are crucial for the interpretation of the neuropsychological test results.”

“The life-time risk of any dementia has been estimated to be more than 1 in 5 for women and 1 in 6 for men (2). Worldwide, about 24 million people have dementia, with 4.6 million new cases of dementia every year (3). […] Dementia can be caused by various underlying diseases, the most common of which is Alzheimer’s disease (AD) accounting for roughly 70% of cases in the elderly. The second most common cause of dementia is vascular dementia (VaD), accounting for 16% of cases. Other, less common, causes include dementia with Lewy bodies (DLB) and frontotemporal lobar degeneration (FTLD). […] It is estimated that both the incidence and the prevalence [of AD] double with every 5-year increase in age. Other risk factors for AD include female sex and vascular risk factors, such as diabetes, hypercholesterolaemia and hypertension […] In contrast with AD, progression of cognitive deficits [in VaD] is mostly stepwise and with an acute or subacute onset. […] it is clear that cerebrovascular disease is one of the major causes of cognitive decline. Vascular risk factors such as diabetes mellitus and hypertension have been recognized as risk factors for VaD […] Although pure vascular dementia is rare, cerebrovascular pathology is frequently observed on MRI and in pathological studies of patients clinically diagnosed with AD […] Evidence exists that AD and cerebrovascular pathology act synergistically (60).”

“In type 1 diabetes the annual prevalence of severe hypoglycemia (requiring help for recovery) is 30–40% while the annual incidence varies depending on the duration of diabetes. In insulin-treated type 2 diabetes, the frequency is lower but increases with duration of insulin therapy. […] In normal health, blood glucose is maintained within a very narrow range […] The functioning of the brain is optimal within this range; cognitive function rapidly becomes impaired when the blood glucose falls below 3.0 mmol/l (54 mg/dl) (3). Similarly, but much less dramatically, cognitive function deteriorates when the brain is exposed to high glucose concentrations” (I did not know the latter for certain, but I certainly have had my suspicions for a long time).

“When exogenous insulin is injected into a non-diabetic adult human, peripheral tissues such as skeletal muscle and adipose tissue rapidly take up glucose, while hepatic glucose output is suppressed. This causes blood glucose to fall and triggers a series of counterregulatory events to counteract the actions of insulin; this prevents a progressive decline in blood glucose and subsequently reverses the hypoglycemia. In people with insulin-treated diabetes, many of the homeostatic mechanisms that regulate blood glucose are either absent or deficient. [If you’re looking for more details on these topics, it should perhaps be noted here that Philip Cryer’s book on these topics is very nice and informative]. […] The initial endocrine response to a fall in blood glucose in non-diabetic humans is the suppression of endogenous insulin secretion. This is followed by the secretion of the principal counterregulatory hormones, glucagon and epinephrine (adrenaline) (5). Cortisol and growth hormone also contribute, but have greater importance in promoting recovery during exposure to prolonged hypoglycemia […] Activation of the peripheral sympathetic nervous system and the adrenal glands provokes the release of a copious quantity of catecholamines, epinephrine, and norepinephrine […] Glucagon is secreted from the alpha cells of the pancreatic islets, apparently in response to localized neuroglycopenia and independent of central neural control. […] The large amounts of catecholamines that are secreted in response to hypoglycemia exert other powerful physiological effects that are unrelated to counterregulation. These include major hemodynamic actions with direct effects on the heart and blood pressure. […] regional blood flow changes occur during hypoglycemia that encourages the transport of substrates to the liver for gluconeogenesis and simultaneously of glucose to the brain. Organs that have no role in the response to acute stress, such as the spleen and kidneys, are temporarily under-perfused. The mobilisation and activation of white blood cells are accompanied by hemorheological effects, promoting increased viscosity, coagulation, and fibrinolysis and may influence endothelial function (6). In normal health these acute physiological changes probably exert no harmful effects, but may acquire pathological significance in people with diabetes of long duration.”

“The more complex and attention-demanding cognitive tasks, and those that require speeded responses are more affected by hypoglycemia than simple tasks or those that do not require any time restraint (3). The overall speed of response of the brain in making decisions is slowed, yet for many tasks, accuracy is preserved at the expense of speed (8, 9). Many aspects of mental performance become impaired when blood glucose falls below 3.0 mmol/l […] Recovery of cognitive function does not occur immediately after the blood glucose returns to normal, but in some cognitive domains may be delayed for 60 min or more (3), which is of practical importance to the performance of tasks that require complex cognitive functions, such as driving. […] [the] major changes that occur during hypoglycemia – counterregulatory hormone secretion, symptom generation, and cognitive dysfunction – occur as components of a hierarchy of responses, each being triggered as the blood glucose falls to its glycemic threshold. […] In nondiabetic individuals, the glycemic thresholds are fixed and reproducible (10), but in people with diabetes, these thresholds are dynamic and plastic, and can be modified by external factors such as glycemic control or exposure to preceding (antecedent) hypoglycemia (11). Changes in the glycemic thresholds for the responses to hypoglycemia underlie the effects of the acquired hypoglycemia syndromes that can develop in people with insulin-treated diabetes […] the incidence of severe hypoglycemia in people with insulin-treated type 2 diabetes increases steadily with duration of insulin therapy […], as pancreatic beta-cell failure develops. The under-recognized risk of severe hypoglycemia in insulin-treated type 2 diabetes is of great practical importance as this group is numerically much larger than people with type 1 diabetes and encompasses many older, and some very elderly, people who may be exposed to much greater danger because they often have co-morbidities such as macrovascular disease, osteoporosis, and general frailty.”

“Hypoglycemia occurs when a mismatch develops between the plasma concentrations of glucose and insulin, particularly when the latter is inappropriately high, which is common during the night. Hypoglycemia can result when too much insulin is injected relative to oral intake of carbohydrate or when a meal is missed or delayed after insulin has been administered. Strenuous exercise can precipitate hypoglycemia through accelerated absorption of insulin and depletion of muscle glycogen stores. Alcohol enhances the risk of prolonged hypoglycemia by inhibiting hepatic gluconeogenesis, but the hypoglycemia may be delayed for several hours. Errors of dosage or timing of insulin administration are common, and there are few conditions where the efficacy of the treatment can be influenced by so many extraneous factors. The time–action profiles of different insulins can be modified by factors such as the ambient temperature or the site and depth of injection and the person with diabetes has to constantly try to balance insulin requirement with diet and exercise. It is therefore not surprising that hypoglycemia occurs so frequently. […] The lower the median blood glucose during the day, the greater the frequency
of symptomatic and biochemical hypoglycemia […] Strict glycemic control can […] induce the acquired hypoglycemia syndromes, impaired awareness of hypoglycemia (a major risk factor for severe hypoglycemia), and counterregulatory hormonal deficiencies (which interfere with blood glucose recovery). […] Severe hypoglycemia is more common at the extremes of age – in very young children and in elderly people.
[…] In type 1 diabetes the frequency of severe hypoglycemia increases with duration of diabetes (12), while in type 2 diabetes it is associated with increasing duration of insulin treatment (18). […] Around one quarter of all episodes of severe hypoglycemia result in coma […] In 10% of episodes of severe hypoglycemia affecting people with type 1 diabetes and around 30% of those in people with insulin-treated type 2 diabetes, the assistance of the emergency medical services is required (23). However, most episodes (both mild and severe) are treated in the community, and few people require admission to hospital.”

“Severe hypoglycemia is potentially dangerous and has a significant mortality and morbidity, particularly in older people with insulin-treated diabetes who often have premature macrovascular disease. The hemodynamic effects of autonomic stimulation may provoke acute vascular events such as myocardial ischemia and infarction, cardiac failure, cerebral ischemia, and stroke (6). In clinical practice the cardiovascular and cerebrovascular consequences of hypoglycemia are frequently overlooked because the role of hypoglycemia in precipitating the vascular event is missed. […] The profuse secretion of catecholamines in response to hypoglycemia provokes a fall in plasma potassium and causes electrocardiographic (ECG) changes, which in some individuals may provoke a cardiac arrhythmia […]. A possible mechanism that has been observed with ECG recordings during hypoglycemia is prolongation of the QT interval […]. Hypoglycemia-induced arrhythmias during sleep have been implicated as the cause of the “dead in bed” syndrome that is recognized in young people with type 1 diabetes (40). […] Total cerebral blood flow is increased during acute hypoglycemia while regional blood flow within the brain is altered acutely. Blood flow increases in the frontal cortex, presumably as a protective compensatory mechanism to enhance the supply of available glucose to the most vulnerable part of the brain. These regional vascular changes become permanent in people who are exposed to recurrent severe hypoglycemia and in those with impaired awareness of hypoglycemia, and are then present during normoglycemia (41). This probably represents an adaptive response of the brain to recurrent exposure to neuroglycopenia. However, these permanent hypoglycemia-induced changes in regional cerebral blood flow may encourage localized neuronal ischemia, particularly if the cerebral circulation is already compromised by the development of cerebrovascular disease associated with diabetes. […] Hypoglycemia-induced EEG changes can persist for days or become permanent, particularly after recurrent severe hypoglycemia”.

“In the large British Diabetic Association Cohort Study of people who had developed type 1 diabetes before the age of 30, acute metabolic complications of diabetes were the greatest single cause of excess death under the age of 30; hypoglycemia was the cause of death in 18% of males and 6% of females in the 20–49 age group (47).”

“[The] syndromes of counterregulatory hormonal deficiencies and impaired awareness of hypoglycemia (IAH) develop over a period of years and ultimately affect a substantial proportion of people with type 1 diabetes and a lesser number with insulin-treated type 2 diabetes. They are considered to be components of hypoglycemia-associated autonomic failure (HAAF), through down-regulation of the central mechanisms within the brain that would normally activate glucoregulatory responses to hypoglycemia, including the release of counterregulatory hormones and the generation of warning symptoms (48). […] The glucagon secretory response to hypoglycemia becomes diminished or absent within a few years of the onset of insulin-deficient diabetes. With glucagon deficiency alone, blood glucose recovery from hypoglycemia is not noticeably affected because the secretion of epinephrine maintains counterregulation. However, almost half of those who have type 1 diabetes of 20 years duration have evidence of impairment of both glucagon and epinephrine in response to hypoglycemia (49); this seriously delays blood glucose recovery and allows progression to more severe and prolonged hypoglycemia when exposed to low blood glucose. People with type 1 diabetes who have these combined counterregulatory hormonal deficiencies have a 25-fold higher risk of experiencing severe hypoglycemia if they are subjected to intensive insulin therapy compared with those who have lost their glucagon response but have retained epinephrine secretion […] Impaired awareness is not an “all or none” phenomenon. “Partial” impairment of awareness may develop, with the individual being aware of some episodes of hypoglycemia but not others (53). Alternatively, the intensity or number of symptoms may be reduced, and neuroglycopenic symptoms predominate. […] total absence of any symptoms, albeit subtle, is very uncommon […] IAH affects 20–25% of patients with type 1 diabetes (11, 55) and less than 10% with type 2 diabetes (24), becomes more prevalent with increasing duration of diabetes (12) […], and predisposes the patient to a sixfold higher risk of severe hypoglycemia than people who retain normal awareness (56). When IAH is associated with strict glycemic control during intensive insulin therapy or has followed episodes of recurrent severe hypoglycemia, it may be reversible by relaxing glycemic control or by avoiding further hypoglycemia (11), but in many patients with type 1 diabetes of long duration, it appears to be a permanent defect. […] The modern management of diabetes strives to achieve strict glycemic control using intensive therapy to avoid or minimize the long-term complications of diabetes; this strategy tends to increase the risk of hypoglycemia and promotes development of the acquired hypoglycemia syndromes.”

February 5, 2017 Posted by | Books, Cardiology, Diabetes, Epidemiology, Medicine, Neurology, Psychology | Leave a comment

Random stuff

i. Fire works a little differently than people imagine. A great ask-science comment. See also AugustusFink-nottle’s comment in the same thread.

ii.

iii. I was very conflicted about whether to link to this because I haven’t actually spent any time looking at it myself so I don’t know if it’s any good, but according to somebody (?) who linked to it on SSC the people behind this stuff have academic backgrounds in evolutionary biology, which is something at least (whether you think this is a good thing or not will probably depend greatly on your opinion of evolutionary biologists, but I’ve definitely learned a lot more about human mating patterns, partner interaction patterns, etc. from evolutionary biologists than I have from personal experience, so I’m probably in the ‘they-sometimes-have-interesting-ideas-about-these-topics-and-those-ideas-may-not-be-terrible’-camp). I figure these guys are much more application-oriented than were some of the previous sources I’ve read on related topics, such as e.g. Kappeler et al. I add the link mostly so that if I in five years time have a stroke that obliterates most of my decision-making skills, causing me to decide that entering the dating market might be a good idea, I’ll have some idea where it might make sense to start.

iv. Stereotype (In)Accuracy in Perceptions of Groups and Individuals.

“Are stereotypes accurate or inaccurate? We summarize evidence that stereotype accuracy is one of the largest and most replicable findings in social psychology. We address controversies in this literature, including the long-standing  and continuing but unjustified emphasis on stereotype inaccuracy, how to define and assess stereotype accuracy, and whether stereotypic (vs. individuating) information can be used rationally in person perception. We conclude with suggestions for building theory and for future directions of stereotype (in)accuracy research.”

A few quotes from the paper:

Demographic stereotypes are accurate. Research has consistently shown moderate to high levels of correspondence accuracy for demographic (e.g., race/ethnicity, gender) stereotypes […]. Nearly all accuracy correlations for consensual stereotypes about race/ethnicity and  gender exceed .50 (compared to only 5% of social psychological findings; Richard, Bond, & Stokes-Zoota, 2003).[…] Rather than being based in cultural myths, the shared component of stereotypes is often highly accurate. This pattern cannot be easily explained by motivational or social-constructionist theories of stereotypes and probably reflects a “wisdom of crowds” effect […] personal stereotypes are also quite accurate, with correspondence accuracy for roughly half exceeding r =.50.”

“We found 34 published studies of racial-, ethnic-, and gender-stereotype accuracy. Although not every study examined discrepancy scores, when they did, a plurality or majority of all consensual stereotype judgments were accurate. […] In these 34 studies, when stereotypes were inaccurate, there was more evidence of underestimating than overestimating actual demographic group differences […] Research assessing the accuracy of  miscellaneous other stereotypes (e.g., about occupations, college majors, sororities, etc.) has generally found accuracy levels comparable to those for demographic stereotypes”

“A common claim […] is that even though many stereotypes accurately capture group means, they are still not accurate because group means cannot describe every individual group member. […] If people were rational, they would use stereotypes to judge individual targets when they lack information about targets’ unique personal characteristics (i.e., individuating information), when the stereotype itself is highly diagnostic (i.e., highly informative regarding the judgment), and when available individuating information is ambiguous or incompletely useful. People’s judgments robustly conform to rational predictions. In the rare situations in which a stereotype is highly diagnostic, people rely on it (e.g., Crawford, Jussim, Madon, Cain, & Stevens, 2011). When highly diagnostic individuating information is available, people overwhelmingly rely on it (Kunda & Thagard, 1996; effect size averaging r = .70). Stereotype biases average no higher than r = .10 ( Jussim, 2012) but reach r = .25 in the absence of individuating information (Kunda & Thagard, 1996). The more diagnostic individuating information  people have, the less they stereotype (Crawford et al., 2011; Krueger & Rothbart, 1988). Thus, people do not indiscriminately apply their stereotypes to all individual  members of stereotyped groups.” (Funder incidentally talked about this stuff as well in his book Personality Judgment).

One thing worth mentioning in the context of stereotypes is that if you look at stuff like crime data – which sadly not many people do – and you stratify based on stuff like country of origin, then the sub-group differences you observe tend to be very large. Some of the differences you observe between subgroups are not in the order of something like 10%, which is probably the sort of difference which could easily be ignored without major consequences; some subgroup differences can easily be in the order of one or two orders of magnitude. The differences are in some contexts so large as to basically make it downright idiotic to assume there are no differences – it doesn’t make sense, it’s frankly a stupid thing to do. To give an example, in Germany the probability that a random person, about whom you know nothing, has been a suspect in a thievery case is 22% if that random person happens to be of Algerian extraction, whereas it’s only 0,27% if you’re dealing with an immigrant from China. Roughly one in 13 of those Algerians have also been involved in a case of ‘body (bodily?) harm’, which is the case for less than one in 400 of the Chinese immigrants.

v. Assessing Immigrant Integration in Sweden after the May 2013 Riots. Some data from the article:

“Today, about one-fifth of Sweden’s population has an immigrant background, defined as those who were either born abroad or born in Sweden to two immigrant parents. The foreign born comprised 15.4 percent of the Swedish population in 2012, up from 11.3 percent in 2000 and 9.2 percent in 1990 […] Of the estimated 331,975 asylum applicants registered in EU countries in 2012, 43,865 (or 13 percent) were in Sweden. […] More than half of these applications were from Syrians, Somalis, Afghanis, Serbians, and Eritreans. […] One town of about 80,000 people, Södertälje, since the mid-2000s has taken in more Iraqi refugees than the United States and Canada combined.”

“Coupled with […] macroeconomic changes, the largely humanitarian nature of immigrant arrivals since the 1970s has posed challenges of labor market integration for Sweden, as refugees often arrive with low levels of education and transferable skills […] high unemployment rates have disproportionately affected immigrant communities in Sweden. In 2009-10, Sweden had the highest gap between native and immigrant employment rates among OECD countries. Approximately 63 percent of immigrants were employed compared to 76 percent of the native-born population. This 13 percentage-point gap is significantly greater than the OECD average […] Explanations for the gap include less work experience and domestic formal qualifications such as language skills among immigrants […] Among recent immigrants, defined as those who have been in the country for less than five years, the employment rate differed from that of the native born by more than 27 percentage points. In 2011, the Swedish newspaper Dagens Nyheter reported that 35 percent of the unemployed registered at the Swedish Public Employment Service were foreign born, up from 22 percent in 2005.”

“As immigrant populations have grown, Sweden has experienced a persistent level of segregation — among the highest in Western Europe. In 2008, 60 percent of native Swedes lived in areas where the majority of the population was also Swedish, and 20 percent lived in areas that were virtually 100 percent Swedish. In contrast, 20 percent of Sweden’s foreign born lived in areas where more than 40 percent of the population was also foreign born.”

vi. Book recommendations. Or rather, author recommendations. A while back I asked ‘the people of SSC’ if they knew of any fiction authors I hadn’t read yet which were both funny and easy to read. I got a lot of good suggestions, and the roughly 20 Dick Francis novels I’ve read during the fall I’ve read as a consequence of that thread.

vii. On the genetic structure of Denmark.

viii. Religious Fundamentalism and Hostility against Out-groups: A Comparison of Muslims and Christians in Western Europe.

“On the basis of an original survey among native Christians and Muslims of Turkish and Moroccan origin in Germany, France, the Netherlands, Belgium, Austria and Sweden, this paper investigates four research questions comparing native Christians to Muslim immigrants: (1) the extent of religious fundamentalism; (2) its socio-economic determinants; (3) whether it can be distinguished from other indicators of religiosity; and (4) its relationship to hostility towards out-groups (homosexuals, Jews, the West, and Muslims). The results indicate that religious fundamentalist attitudes are much more widespread among Sunnite Muslims than among native Christians, even after controlling for the different demographic and socio-economic compositions of these groups. […] Fundamentalist believers […] show very high levels of out-group hostility, especially among Muslims.”

ix. Portal: Dinosaurs. It would have been so incredibly awesome to have had access to this kind of stuff back when I was a child. The portal includes links to articles with names like ‘Bone Wars‘ – what’s not to like? Again, awesome!

x. “you can’t determine if something is truly random from observations alone. You can only determine if something is not truly random.” (link) An important insight well expressed.

xi. Chessprogramming. If you’re interested in having a look at how chess programs work, this is a neat resource. The wiki contains lots of links with information on specific sub-topics of interest. Also chess-related: The World Championship match between Carlsen and Karjakin has started. To the extent that I’ll be following the live coverage, I’ll be following Svidler et al.’s coverage on chess24. Robin van Kampen and Eric Hansen – both 2600+ elo GMs – did quite well yesterday, in my opinion.

xii. Justified by More Than Logos Alone (Razib Khan).

“Very few are Roman Catholic because they have read Aquinas’ Five Ways. Rather, they are Roman Catholic, in order of necessity, because God aligns with their deep intuitions, basic cognitive needs in terms of cosmological coherency, and because the church serves as an avenue for socialization and repetitive ritual which binds individuals to the greater whole. People do not believe in Catholicism as often as they are born Catholics, and the Catholic religion is rather well fitted to a range of predispositions to the typical human.”

November 12, 2016 Posted by | Books, Chemistry, Chess, Data, dating, Demographics, Genetics, Geography, immigration, Paleontology, Papers, Physics, Psychology, Random stuff, Religion | Leave a comment

Random stuff

i. A very long but entertaining chess stream by Peter Svidler was recently uploaded on the Chess24 youtube account – go watch it here, if you like that kind of stuff. The fact that it’s five hours long is a reason to rejoice, not a reason to think that it’s ‘too long to be watchable’ – watch it in segments…

People interested in chess might also be interested to know that Magnus Carlsen has made an account on the ICC on which he has played, which was a result of his recent participation in the ICC Open 2016 (link). A requirement for participation in the tournament was that people had to know whom they were playing against (so there would be no ultra-strong GMs playing using anonymous accounts in the finals – they could use accounts with strange names, but people had to know whom they were playing), so now we know that Magnus Carlsen has played under the nick ‘stoptryharding’ on the ICC. Carlsen did not win the tournament as he lost to Grischuk in the semi-finals. Some very strong players were incidentally kicked out in the qualifiers, including Nepomniachtchi, the current #5 in the world on the FIDE live blitz ratings.

ii. A lecture:

iii. Below I have added some new words I’ve encountered, most of them in books I’ve read (I have not spent much time on vocabulary.com recently). I’m sure if I were to look all of them up on vocabulary.com some (many?) of them would not be ‘new’ to me, but that’s not going to stop me from including them here (I included the word ‘inculcate’ below for a reason…). Do take note of the spelling of some of these words – some of them are tricky ones included in Bryson’s Dictionary of Troublesome Words: A Writer’s Guide to Getting It Right, which people often get wrong for one reason or another:

Conurbation, epizootic, equable, circumvallation, contravallation, exiguous, forbear, louche, vituperative, thitherto, congeries, inculcate, obtrude, palter, idiolect, hortatory, enthalpy (see also wiki, or Khan Academy), trove, composograph, indite, mugginess, apodosis, protasis, invidious, inveigle, inflorescence, kith, anatopism, laudation, luxuriant, maleficence, misogamy (I did not know this was a word, and I’ll definitely try to remember it/that it is…), obsolescent, delible, overweening, parlay (this word probably does not mean what you think it means…), perspicacity, perspicuity, temblor, precipitous, quinquennial, razzmatazz, turpitude, vicissitude, vitriform.

iv. Some quotes from this excellent book review, by Razib Khan:

“relatively old-fashioned anti-religious sentiments […] are socially acceptable among American Left-liberals so long as their targets are white Christians (“punching up”) but more “problematic” and perhaps even “Islamophobic” when the invective is hurled at Muslim “people of color” (all Muslims here being tacitly racialized as nonwhite). […] Muslims, as marginalized people, are now considered part of a broader coalition on the progressive Left. […] most Left-liberals who might fall back on the term Islamophobia, don’t actually take Islam, or religion generally, seriously. This explains the rapid and strident recourse toward a racial analogy for Islamic identity, as that is a framework that modern Left-liberals and progressives have internalized and mastered. The problem with this is that Islam is not a racial or ethnic identity, it is a set of beliefs and practices. Being a Muslim is not about being who you are in a passive sense, but it is a proactive expression of a set of ideas about the world and your behavior within the world. This category error renders much of Left-liberal and progressive analysis of Islam superficial, and likely wrong.”

“To get a genuine understanding of a topic as broad and boundless as Islam one needs to both set aside emotional considerations, as Ben Affleck can not, and dig deeply into the richer and more complex empirical texture, which Sam Harris has not.”

“One of the most obnoxious memes in my opinion during the Obama era has been the popularization of the maxim that “The arc of the moral universe is long, but it bends towards justice.” It is smug and self-assured in its presentation. […] too often it becomes an excuse for lazy thinking and shallow prognostication. […] Modern Western liberals have a particular idea of what a religion is, and so naturally know that Islam is in many ways just like United Methodism, except with a hijab and iconoclasm. But a Western liberalism that does not take cultural and religious difference seriously is not serious, and yet all too often it is what we have on offer. […] On both the American Left and Right there is a tendency to not even attempt to understand Islam. Rather, stylized models are preferred which lead to conclusions which are already arrived at.”

“It’s fine to be embarrassed by reality. But you still need to face up to reality. Where Hamid, Harris, and I all start is the fact that the vast majority of the world’s Muslims do not hold views on social issues that are aligned with the Muslim friends of Hollywood actors. […] Before the Green Revolution I told people to expect there to be a Islamic revival, as 86 percent of Egyptians polled agree with the killing of apostates. This is not a comfortable fact for me, as I am technically an apostate.* But it is a fact. Progressives who exhibit a hopefulness about human nature, and confuse majoritarian democracy with liberalism and individual rights, often don’t want to confront these facts. […] Their polar opposites are convinced anti-Muslims who don’t need any survey data, because they know that Muslims have particular views a priori by virtue of them being Muslims. […] There is a glass half-full/half-empty aspect to the Turkish data. 95 percent of Turks do not believe apostates should be killed. This is not surprising, I know many Turkish atheists personally. But, 5 percent is not a reassuring fraction as someone who is personally an apostate. The ideal, and frankly only acceptable, proportion is basically 0 percent.”

“Harris would give a simple explanation for why Islam sanctions the death penalty for apostates. To be reductive and hyperbolic, his perspective seems to be that Islam is a totalitarian cult, and its views are quite explicit in the Quran and the Hadith. Harris is correct here, and the views of the majority of Muslims in Egypt (and many other Muslim nations) has support in Islamic law. The consensus historical tradition is that apostates are subject to the death penalty. […] the very idea of accepting atheists is taboo in most Arab countries”.

“Christianity which Christians hold to be fundamental and constitutive of their religion would have seemed exotic and alien even to St. Paul. Similarly, there is a much smaller body of work which makes the same case for Islam.

A précis of this line of thinking is that non-Muslim sources do not make it clear that there was in fact a coherent new religion which burst forth out of south-central Arabia in the 7th century. Rather, many aspects of Islam’s 7th century were myths which developed over time, initially during the Umayyad period, but which eventually crystallized and matured into orthodoxy under the Abbasids, over a century after the death of Muhammad. This model holds that the Arab conquests were actually Arab conquests, not Muslim ones, and that a predominantly nominally Syrian Christian group of Arab tribes eventually developed a new religion to justify their status within the empire which they built, and to maintain their roles within it. The mawali (convert) revolution under the Abbasids in the latter half of the 8th century transformed a fundamentally Arab ethnic sect, into a universal religion. […] The debate about the historical Jesus only emerged when the public space was secularized enough so that such discussions would not elicit violent hostility from the populace or sanction form the authorities. [T]he fact is that the debate about the historical Muhammad is positively dangerous and thankless. That is not necessarily because there is that much more known about Muhammad than Jesus, it is because post-Christian society allows for an interrogation of Christian beliefs which Islamic society does not allow for in relation to Islam’s founding narratives.”

“When it comes to understanding religion you need to start with psychology. In particular, cognitive psychology. This feeds into the field of evolutionary anthropology in relation to the study of religion. Probably the best introduction to this field is Scott Atran’s dense In Gods We Trust: The Evolutionary Landscape of Religion. Another representative work is Theological Incorrectness: Why Religious People Believe What They Shouldn’t. This area of scholarship purports to explain why religion is ubiquitous, and, why as a phenomenon it tends to exhibit a particular distribution of characteristics.

What cognitive psychology suggests is that there is a strong disjunction between the verbal scripts that people give in terms of what they say they believe, and the internal Gestalt mental models which seem to actually be operative in terms of informing how they truly conceptualize the world. […] Muslims may aver that their god is omniscient and omnipresent, but their narrative stories in response to life circumstances seem to imply that their believe god may not see or know all things at all moments.

The deep problem here is understood [by] religious professionals: they’ve made their religion too complex for common people to understand without their intermediation. In fact, I would argue that theologians themselves don’t really understand what they’re talking about. To some extent this is a feature, not a bug. If the God of Abraham is transformed into an almost incomprehensible being, then religious professionals will have perpetual work as interpreters. […] even today most Muslims can not read the Quran. Most Muslims do not speak Arabic. […] The point isn’t to understand, the point is that they are the Word of God, in the abstract. […] The power of the Quran is that the Word of God is presumably potent. Comprehension is secondary to the command.”

“the majority of the book […] is focused on political and social facts in the Islamic world today. […] That is the best thing about Islamic Exceptionalism, it will put more facts in front of people who are fact-starved, and theory rich. That’s good.”

“the term ‘fundamentalist’ in the context of islam isn’t very informative.” (from the comments).

Below I have added some (very) superficially related links of my own, most of them ‘data-related’ (in general I’d say that I usually find ‘raw data’ more interesting than ‘big ideas’):

*My short review of Theological Correctness, one of the books Razib mentions.

*Of almost 163,000 people who applied for asylum in Sweden last year, less than 500 landed a job (news article).

*An analysis of Danish data conducted by the Rockwool Foundation found that for family-reunificated spouses/relatives etc. to fugitives, 22 % were employed after having lived in Denmark for five years (the family-reunificated individuals, that is, not the fugitives themselves). Only one in three of the family-reunificated individuals had managed to find a job after having stayed here for fifteen years. The employment rate of family-reunificated to immigrants is 49 % for people who have been in the country for 5 years, and the number is below 60 % after 15 years. In Denmark, the employment rate of immigrants from non-Western countries was 47,7 % in November 2013, compared to 73,8 % for people of (…’supposedly’, see also my comments and observations here) Danish origin, according to numbers from Statistics Denmark (link). When you look at the economic performance of the people with fugitive status themselves, 34 % are employed after 5 years, but that number is almost unchanged a decade later – only 37 % are employed after they’ve stayed in Denmark for 15 years.
Things of course sometimes look even worse at the local level than these numbers reflect, because those averages are, well, averages; for example of the 244 fugitives and family-reunificated who had arrived in the Danish Elsinore Municipality within the last three years, exactly 5 of them were in full-time employment.

*Rotherham child sexual exploitation scandal (“The report estimated that 1,400 children had been sexually abused in the town between 1997 and 2013, predominantly by gangs of British-Pakistani Muslim men […] Because most of the perpetrators were of Pakistani heritage, several council staff described themselves as being nervous about identifying the ethnic origins of perpetrators for fear of being thought racist […] It was reported in June 2015 that about 300 suspects had been identified.”)

*A memorial service for the terrorist and murderer Omar El-Hussein who went on a shooting rampage in Copenhagen last year (link) gathered 1500 people, and 600-700 people also participated at the funeral (Danish link).

*Pew asked muslims in various large countries whether they thought ‘Suicide Bombing of Civilian Targets to Defend Islam [can] be Justified?’ More than a third of French muslims think that it can, either ‘often/sometimes’ (16 %) or ‘rarely’ (19 %). Roughly a fourth of British muslims think so as well (15 % often/sometimes, 9 % rarely). Of course in countries like Jordan, Nigeria, and Egypt the proportion of people who do not reply ‘never’ is above 50 %. In such contexts people often like to focus on what the majorities think, but I found it interesting to note that in only 2 of 11 countries (Germany – 7 %, & the US – 8 %) queried was it less than 10 % of muslims who thought suicide bombings were not either ‘often’ or ‘sometimes’ justified. Those numbers are some years old. Newer numbers (from non-Western countries only, unfortunately) tell us that e.g. fewer than two out of five Egyptians (38%) and fewer than three out of five (58%) Turks would answer ‘never’ when asked this question just a couple of years ago, in 2014.

*A few non-data related observations here towards the end. I do think Razib is right that cognitive psychology is a good starting point if you want to ‘understand religion’, but a more general point I would make is that there are many different analytical approaches to these sorts of topics which one might employ, and I think it’s important that one does not privilege any single analytical framework over the others (just to be clear, I’m not saying that Razib’s doing this); different approaches may yield different insights, perhaps at different analytical levels, and combining different approaches is likely to be very useful in order to get ‘the bigger picture’, or at least to not overlook important details. ‘History’, broadly defined, may provide one part of the explanatory model, cognitive psychology another part, mathematical anthropology (e.g. stuff like this) probably also has a role to play, etc., etc.. Survey data, economic figures, scientific literatures on a wide variety of topics like trust, norms, migration analysis, and conflict studies, e.g. those dealing with civil wars, may all help elucidate important questions of interest, if not by adding relevant data then by providing additional methodological approaches/scaffoldings which might be fruitfully employed to make sense of the data that is available.

v. Statistical Portrait of Hispanics in the United States.

vi. The Level and Nature of Autistic Intelligence. Autistics may be smarter than people have been led to believe:

“Autistics are presumed to be characterized by cognitive impairment, and their cognitive strengths (e.g., in Block Design performance) are frequently interpreted as low-level by-products of high-level deficits, not as direct manifestations of intelligence. Recent attempts to identify the neuroanatomical and neurofunctional signature of autism have been positioned on this universal, but untested, assumption. We therefore assessed a broad sample of 38 autistic children on the preeminent test of fluid intelligence, Raven’s Progressive Matrices. Their scores were, on average, 30 percentile points, and in some cases more than 70 percentile points, higher than their scores on the Wechsler scales of intelligence. Typically developing control children showed no such discrepancy, and a similar contrast was observed when a sample of autistic adults was compared with a sample of nonautistic adults. We conclude that intelligence has been underestimated in autistics.”

I recall that back when I was diagnosed I was subjected to a battery of different cognitive tests of various kinds, and a few of those tests I recall thinking were very difficult, compared to how difficult they somehow ‘ought to be’ – it was like ‘this should be an easy task for someone who has the mental hardware to solve this type of problem, but I don’t seem to have that piece of hardware; I have no idea how to manipulate these objects in my head so that I might answer that question’. This was an at least somewhat unfamiliar feeling to me in a testing context, and I definitely did not have this experience when doing the Mensa admissions test later on, which was based on Raven’s matrices. Despite the fact that all IQ tests are supposed to measure pretty much the same thing I do not find it hard to believe that there are some details here which may complicate matters a bit in specific contexts, e.g. for people whose brains may not be structured quite the same way ‘ordinary brains’ are (to put it very bluntly). But of course this is just one study and a few personal impressions – more research is needed, etc. (Even though the effect size is huge.)

Slightly related to the above is also this link – I must admit that I find the title question quite interesting. I find it very difficult to picture characters featuring in books I’m reading in my mind, and so usually when I read books I don’t form any sort of coherent mental image of what the character looks like. It doesn’t matter to me, I don’t care. I have no idea if this is how other people read (fiction) books, or if they actually imagine what the characters look like more or less continuously while those characters are described doing the things they might be doing; to me it would be just incredibly taxing to keep even a simplified mental model of the physical attributes of a character in my mind for even a minute. I can recall specific traits like left-handedness and similar without much difficulty if I think the trait might have relevance to the plot, which has helped me while reading e.g. Agatha Christie novels before, but actively imagining what people look like in my mind I just find very difficult. I find it weird to think that some people might do something like that almost automatically, without thinking about it.

vii. Computer Science Resources. I recently shared the link with a friend, but of course she was already aware of the existence of this resource. Some people reading along here may not be, so I’ll include the link here. It has a lot of stuff.

June 8, 2016 Posted by | autism, Books, Chess, Computer science, Data, Demographics, Psychology, Random stuff, Religion | Leave a comment

Nonverbal Communication

“The purpose of the book is to bring together a number of nonverbal behavior researchers to discuss current themes and research. The book is meant for senior undergraduates, graduates, academics and nonverbal communication researchers, as well as for everyone else who wants to interpret and understand better nonverbal behavior and the states of their interlocutors. The texts in this book show the results of contemporary research and theorization of the nature, functions, and modalities of nonverbal behavior in different areas of life.”

From the introduction of the book. The book has two parts; a theoretical part and an applied part. The first half of the book covers theoretical research and as I also noted in my goodreads review I found this part of the book quite weak, but a few of the chapters in the second half of the book, dealing with applied research into these topics, had some interesting stuff (‘If you decide to have a go at this book I’d probably be tempted to recommend only reading the first four chapters of part 2’ – from my goodreads review). My coverage of the book in this post will skip a lot of chapters; I’ll focus on the stuff I found interesting and just ignore the rest. The four chapters mentioned above cover ‘Nonverbal Firsts: When Nonverbal Cues Are the Impetus of Relational and Personal Change in Romantic Relationships’ (chapter 7), ‘Beyond Facial Expression: Spatial Distance as a Factor in the Communication of Discrete Emotions’ (chapter 8), Theoretical Foundation for Emotion-Based Strategies in Political Campaigns (chapter 9), and ‘The Impact of Nonverbal Behavior in the Job Interview’ (chapter 10).

I would note that I actually emailed a few quotes from the last of these chapters to a good friend of mine who recently had a job interview coming up, which is perhaps a good illustration of how potentially useful I consider some of the content covered here to be – this is worth keeping in mind when interpreting the two star (and ‘much closer to one star than three’) goodreads rating. It should however also be recalled that the authors of chapter 8, which is incidentally far from the worst chapter in the book, claim/think the so-called McClintock effect is real, based on outdated research. They write in the chapter that: “Martha McClintock and colleagues reported evidence that the menstrual cycles of co-habiting women can become synchronized, a phenomenon termed the McClintock effect (McClintock, 1971; Hummer & McClintock, 2009). Although controversial, the reality of the phenomenon is now generally accepted (Wysocki & Preti, 2004).” Compare with wikipedia: “A 2013 review of menstrual synchrony concluded that menstrual synchrony is an erroneous theory. […] Harris and Vitzthum concluded, “In light of the lack of empirical evidence for MS [menstrual synchrony] sensu stricto, it seems there should be more widespread doubt than acceptance of this hypothesis””.

Below I have added some quotes from the book, as well as a few observations of my own. I would note that I have read and written about stuff related to the content covered in this post before here on the blog, so if you’re curious to learn more after having read this post, you might consider following some of those links.

“[N]onverbal behaviors have the potential to be transformative. That is, they may act as triggers for a change in a relationship, perception, behavior, or affect. In particular, […] when a nonverbal behavior occurs or is noticed for the first time, these behavioral “firsts” can have big implications, positive or negative, for people in relationships. […] the authors find that touch, eye behavior, and personal space are the cues reported most commonly as triggers for change and which help bring about the start of a romantic relationship, perception of how much or little another cares, relational problems, instant break-ups, and indicators of another’s untrustworthiness.”

“Baxter and Bullis (1986) found that the first time their participants kissed or had sex with a partner altered the degree of commitment that they had to the relationship. In this way, the first appearance of certain nonverbal cues or acts may be important triggers of change within a relationship. […] In our respondents’ reports, we read many accounts of how a single behavior, used for what the respondent recalled was the first time, instantly changed the relationship or the perception of the relationship between the two individuals. There was some variety in the behaviors, but most typically they were handholding, prolonged gaze, kisses, closer proximity, and “changes” in touch behavior. In most of the situations described by our participants, the behavior was received positively and started a romantic relationship. In a few instances, however, it indicated to the respondent that they or another person had romantic feelings that were unreciprocated. These latter situations reportedly resulted in either the termination of the existing relationship or awkwardness in the relationship. […] the same actions – kisses, close personal distance – may have very different outcomes, depending on the reciprocity of the behaviors and feelings. […] a rather common claim about touch is that it “is a signal in the communication process that, above all other communication channels, most directly and immediately escalates the balance of intimacy” […]. Perhaps above all other nonverbal cues, touch has been shown to facilitate dramatic “surge[s] in affective involvement” […] nonverbal cues, although sometimes subtle and easy to miss, may actually be “big” actions in relational change.”

“[P]articipants often commented on the lack of a behavior (e.g., no eye contact, ignoring behavior [which presumably was determined by lack of gaze, not responding, and the like], and not talking [silence]). The themes were consistent whether they were discussing their own or their partner’s behaviors. […] Avoidance of eye contact, silence, and “ignoring,” rather than immediate, engaged, intimate, behavior was common in this group of entries and marked the beginning (or the first signal) of the relationship’s decline.”

The research they presented in the chapter was disappointing to me in a way, due to the methodology applied. Basically they asked people (…well, psychology undergrads…) which non-verbal behaviours ‘stood out’ to them, and then they interpreted the behaviours based on these accounts. Recall biases are a potentially serious problem, and if you ask people to explain relationship changes as a function of nonverbal behaviours then you’ll probably get answers indicating that nonverbal behaviours are important, regardless of whether they really are or not. But on a related note it seems hard to do ‘naturalistic/observational’ research into these topics (‘follow people around with video cameras and try to spot which nonverbal behaviours on display might be associated with relationship formation?’), and even if the self-reports are not wholly reliable they may provide some information. A big problem in the context of research into these things is of course that you can’t really directly observe relationships and relationship formation; these things are to a very large extent nothing but mental constructs in the minds of the people involved, meaning that you probably to some extent sort of have to rely on things like self-report variables. This makes everything quite a bit more ‘fuzzy’ than it otherwise would be. Note that the fact that ‘relationships are mental constructs existing only in the minds of the people involved’ does not to me seem to necessarily indicate that asking people what they think caused a relationship to change will yield reliable answers; people may not know why they feel the way they do about a given individual or why their feelings changed at some point, and/but if you give them a specific reason/variable to consider they’ll be likely to overestimate the importance of said variable. If they’d asked the same people if specific verbal exchanges (‘first time he said ‘I love you’?’) had changed how they felt about that individual, they might have got different answers.

When you consider how ‘squishy’ this stuff is, I think other approaches besides the ones considered by the authors might also be useful to consider if you want to get at the extent to which nonverbal behaviour is important; for example I feel tempted to conclude that the poor relationship outcomes of autistics (“In terms of outcome studies to date, very few adults with ASD have been reported to have successful, long-term romantic relationships […] Between 10 and 30 % of adults in recent studies […] had experience in a romantic relationship.” – link), a population including people who often have great difficulties interpreting nonverbal behaviours and cues, might provide stronger evidence in favour of the importance of nonverbal behaviours in relationship contexts than the study in question provides. Although I’d certainly agree that important confounders are present in this context (…as well), making it very difficult to take the poor relationship outcomes of this group as solely a consequence of nonverbal behavioural aspects.

“[In political contexts,] candidates and issues that emphasize freedom (e.g., fewer restrictions and external constraints on behavior and opportunities, less limitation on social and economic mobility) are more likely to appeal to men than to women. […] political messages or tactics that repeatedly produce anxious feelings (e.g., bewilderment, distress, pain, insecurity, fear) in voters are likely to magnify the influence of voter emotions on voter political judgments. Additional related effects are expected to include greater polarization of competing groups and simplification of decision rules and belief systems (e.g., increased single-issue voting, greater reliance on candidates’ physical features and communication styles than on candidates’ ideological positions).”

“Research shows that there is a positive relation between [job] applicant positive nonverbal behavior and recruiter evaluation. Positive nonverbal behavior can be defined as immediacy behavior which elicits proximity and liking in the interaction partner as for example a high level of eye contact, smiling, confirmative nodding, hand gestures, and variation in pitch and speaking rate […]. Applicants who used more immediacy behavior (i.e., eye contact, smiling, body orientation toward interviewer, less personal distance) were perceived as being more suitable for the job, more competent, more motivated, and more successful than applicants using less immediacy behavior […] Forbes and Jackson (1980) showed that selected applicants maintained more direct eye contact, smiled more, and nodded more during the job interview than applicants who were not selected for the job. Moreover, applicants who maintained a high amount of eye contact with the recruiter, who showed a high energy level, were affective, modulated their voice, and spoke fluently during the job interview were more likely to be invited for a second job interview than applicants revealing less of those nonverbal behaviors”.

“In terms of applicant characteristics, applicants high in communication apprehension who used more nonverbal avoidance behavior (i.e., less talking, less eye contact, less fluent talking) were less effective in mock job interviews and were perceived as less suitable for the job than applicants with low levels of communication apprehension […] Overall, there are only few studies that did not show an effect between applicant nonverbal immediacy behavior and a favorable hiring decision […] and meta-analyses reveal a clear net effect showing that the more the applicant uses nonverbal immediacy behavior, the better the interview outcome for the applicant (i.e., better chances of getting hired or of being evaluated positively) […] Applicant nonverbal behavior seems to have a remarkable impact on the job interview outcome. The more immediacy (or positive) nonverbal behavior the applicant shows during the job interview, the more positive recruiter evaluations of the applicant are.”

“the question can be asked how accurate recruiters are when inferring applicant characteristics. For many personality characteristics, they seem to use the “wrong,” meaning non-diagnostic, cues. […] many more nonverbal cues are used to infer applicant’s personality traits than are cues actually revealing these traits. […] recruiters seem to use the nonverbal cues that are not diagnostic to assess applicants – in a sense they use the wrong cues – and [yet] are still accurate in assessing applicants’ personality. It remains therefore largely unknown how the recruiters make those correct inferences.”

How accurate the inferences are is to some extent an open question (though it’s probably safe to say that interviews provide less relevant information than many people think – including the authors of that chapter: “[interviews] provide very little unique information about a candidate and show little incremental validity over established psychometric tests (of ability and personality) in the prediction of future job performance […] All sorts of extraneous factors like the perfume a person wears at interview have been shown to influence ratings.” – link). A related observation is that assessment accuracy definitely depends upon the dimension of the variable of interest; some personality characteristics are much easier to observe/deduce than are others, as noted e.g. in Funder’s (‘some behaviors are more dependent on the situation than are others’) book (‘traits like extraversion and agreeableness are the ones most likely to become visible in overt social behavior’).

February 17, 2016 Posted by | autism, Books, Psychology | Leave a comment

Eating disorders… (I)

“Dermatologists have an important role in the early diagnosis of eating disorders since skin signs are, at times, the only easily detectable symptoms of hidden anorexia and bulimia nervosa. Forty cutaneous signs have been recognized”

The full title of the book is Eating Disorders and the Skin, but there’s a lot of stuff about eating disorders in general in this book as well, and I figured I’d mostly focus on the ‘general stuff’ in this post. Here’s my goodreads review of the book, which I gave 3 stars.

Here are the DSM-IV-TR diagnostic criteria for anorexia nervosa:

“1. Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g., weight loss leading to maintenance of body weight less than 85% of that expected, or failure to make expected weight gain during period of growth, leading to body weight less than 85% of that expected).

2. Intense fear of gaining weight or becoming fat even though underweight.

3. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight.

4.4. In postmenarcheal females, amenorrhea, i.e., the absence of at least three consecutive menstrual cycles.”

Interestingly, aside from anorexia [-AN] and bulimia [-BN] (diagnostic criteria here), there’s also a big category called ED-NOS – Eating Disorder Not Otherwise Specified. That’s for cases that don’t really fit into the standard criteria for specific eating disorders; they note than an example of this type could be a female fitting all diagnostic criteria for AN except that she has regular menses. It is perhaps worth mentioning here that surprisingly enough (…to me), menstrual irregularities are not limited to cases of AN, thus: “In almost 50% of bulimic patients, menstrual irregularities, such as oligomenorrhea or amenorrhea, take place”. They note in the book that there’s been some concern about the validity of the ED-NOS category, which makes up almost 60% of patients with an eating disorder. Eating disorders are much more common in females than in males (“Males are generally reported to account for 5–10% of anorectics and 10–15% of bulimics identified in the general population”), and particular subgroups mentioned to be at high risk are athletes, models and dancers. It’s noted in the book that most epidemiological studies are conducted in high-risk settings, whereas epidemiological studies assessing risk in the general population are somewhat rarer. One problem complicating matters a little in terms of estimating risk is that an eating disorder cannot be diagnosed through a self-report questionnaire; you need a structured or semi-structured interview to make a diagnosis, which makes things more expensive. As in other contexts one way to get around this issue, at least to some extent, is to employ multi-step screening protocols – in this case a two-step procedure in which individuals at high risk are identified at the first step through inexpensive means, and these individuals are then later assessed more carefully in the second step, employing more accurate (and expensive) methods.

They note that in Western countries, point prevalence of AN in female adolescent (the highest risk sub-group) is estimated at 0.2-1% of the population, whereas the prevalence studies on bulimia nervosa indicates that this eating disorder is somewhat more common, with the majority of studies finding prevalences of 1.5-5%; do recall again that most studies as already mentioned look at high-risk subgroups, so total population prevalence is likely to be lower than this. They observe in the book that general-practice studies find that the incidence of anorexia nervosa is less than one in ten-thousand per year (8 per 100,000 per year); so full-blown AN certainly is likely quite rare in low-risk populations.

On lifetime risk, the book notes that:

“Most of the epidemiological studies on ED [eating disorders] have evaluated the prevalence of full syndromes of both AN [anorexia nervosa] and BN [bulimia nervosa]. The few studies that have evaluated partial or subclinical manifestations of EDs in young females, however, found lifetime prevalence rates of 5–12% for atypical AN and 1–4.8% for atypical BN and up to 14.6% in adolescent samples”.

A review of epidemiological studies concluded that there’s no evidence of either a secular increase in AN or BN over time; to the extent that the number of people with diagnosed BN has increased over time, changes in diagnostic and referral practices likely account for this. On a related topic it is noted in the book that “It is a common idea among clinicians that early-onset cases of anorexia nervosa (AN) are increasing, but few data in the literature are available to demonstrate this trend.”

AN most commonly present among females at the age of 15-19, whereas BN presents a little later, most commonly at the age of 20-24. But eating disorders are not limited to teenagers and young adults: “Even if anorexia nervosa and bulimia nervosa occur characteristically in females during adolescence and young adulthood, there have been case reports of illness beginning after the age of 25 and even after the menopause, and some authors suggest that the rates of eating disorders in older patients may be increasing [2]. Clinical impression suggests that the late-onset cases present with more depressive features than the adolescent counterpart. […] dieting is considered one of the most salient precipitating factors.”

Self-report metrics can only help you so much when you’re trying to assess risk; a major problem in this context is that denial of illness is a very common feature in these patient populations (so you certainly can’t just ask people if their relationship with food/exercise etc. might be unhealthy…): “typically, [the] course [of an eating disorder] is characterized by a high fluidity between the diagnostic classes; furthermore, the patient often denies even to himself the psychiatric nature of the disease” (recall also that “denial of the seriousness of the current low body weight” is included in the diagnostic criteria). The book covers a lot of symptoms which relate to low body weight – like cold intolerance, bradycardia (slow heart rate), acrocyanosis (bluish discoloration of the hands and feet, caused by slow circulation), systemic hypotension (low blood pressure), lots of skin signs (I haven’t decided yet how much detail I’ll go into, so let’s leave it at that now) – or e.g. to purging behaviours (throat and tooth pain due to vomiting and enamel erosion), but it would go much too far to discuss all these in detail here. One to me interesting aspect of the coverage was that whereas BMI is a useful sign, it’s not itself a diagnostic criterion; the authors note that a BMI below 18.5 is considered pathological, but when listing main signs of anorexia nervosa the most important diagnostic sign (or at least the first one listed) is a BMI below 17.5; I assume part of the discussion surrounding the validity of the ED-NOS category probably relate to individuals who’re in this ‘border area’; they likely have some symptoms due to low body mass (like e.g. cold intolerance), but they don’t have full-blown AN (there are a lot of things that can go wrong when you have low body mass – there are a lot of symptoms described in this book!). It’s also important to note that very different symptom patterns can be present at similar levels of BMI, as the severity of symptoms also relate to how fast body mass decreases – the body is actually capable of adjusting quite well to lower energy intake states (in the short run at least), and so “if weight loss is gradual, it is possible to maintain, even for a long time, an apparent metabolic equilibrium.”

Anorexics have high mortality rates: “From a meta-analysis of 119 studies involving 5,590 patients, Steinhausen reported a crude mortality rate of 5% which exceeded 9% in a followup of 10 years.” Remember when thinking about those estimates that most of the people in these studies were likely young women – these numbers are high, and the authors note that anorexia nervosa “represents the major cause of death of young women in the age between 12 and 25 years.”

Most deaths are due to ventricular arrhythmia; the book goes into some detail about how anorexia affects the cardiovascular system, but I won’t discuss this in detail. An important observation is that: “Cardiac findings tend to disappear with weight recovery.” I assume this comment relates mostly to findings like QTc prolongation, QTc dispersion, and mitral valve prolapse, all of which are found in anorexics, whereas I’d be surprised if cardiac abnormalities related to direct damage to the heart muscle resolve themselves after weight gain, but the book does not go into details on this topic, except in the sense that it is noted that heart failure is uncommon in anorexics. Among those who survive their illness, osteoporosis is a major irreversible long-term problem. People with higher body mass tend to have a higher bone mineral density and thus a lower risk of osteoporosis (unless they get type 2 diabetes, in which case the situation is, well, complicated), so perhaps it’s not really surprising that women with AN and very low body mass index tend to develop osteoporosis. They certainly do:

“Osteopenia and osteoporosis represent one of the most relevant and potentially not reversible complications of eating disorders. This complication is particularly severe when eating disorders have an early onset […] Bone loss is an early effect of the disease, already present after 6–12 months […] In untreated patients, bone loss ranges from 4% up to 10% per year […]. In case of recovery, the progressive loss of BMD [bone mineral density] stops, but in most cases, a normal bone mass is not restored [64].”

It’s noted that bone loss is due to both hormonal and metabolic factors; estrogen plays a role, and “BMD loss in AN is more rapid and severe than in other hypoestrogenic conditions”. Despite this observation weight gain is considered the primary treatment modality of osteoporosis in this context (i.e., not estrogen therapy), and research using estrogen therapy to try to boost bone mineral density in anorexics who did not also gain weight has not been successful.

A to me interesting aspect of the coverage which I could not help but discuss here is how eating disorders relate to diabetes; the book has a few remarks on this topic:

“The concurrence of an eating disorder with insulin-dependent diabetes has been outlined by several researchers: especially bulimia nervosa and disorder not otherwise specified (EDNOS) are reported to be significantly higher in females with type 1 diabetes […] In case of comorbidity, ED onset followed the diagnosis of IDDM in 70% of the patients [10]. Specific aspects of diabetes and its management could, in fact, potentially increase a particular susceptibility to the development of an eating disorder: weight gain, associated with initiation of insulin treatment and dietary restraint, might, in fact, trigger body dissatisfaction and the drive for thinness with consequent weight control behaviors ranging from healthy to very unhealthy behaviors […] insulin omission [is] a common weight loss behavior in girls with IDDM and eating disorder […] APA Guidelines 2006 suggest that insulin omission should be considered a specific type of purging behavior in the next DSM revision”.

I don’t know if this suggested change has been implemented at this point, but it would make a lot of sense. To people who don’t know what this ‘insulin omission’ they talk about is all about, the short version is that if you’re a type 1 diabetic in need of regular insulin injections, if you don’t take enough insulin you lose weight and you can eat pretty much whatever you like without gaining weight; which is of course an unfortunate though likely very attractive option for young women to have. The downside of engaging in systematic insulin omission behaviour of that kind is that you’ll likely go blind from your diabetes and/or die of kidney failure or DKA if you do that for an extended period of time.

January 2, 2016 Posted by | Books, Diabetes, Epidemiology, Medicine, Psychology | 4 Comments

Trust

“A commonplace argument in contemporary writing on trust is that we would all be better off if we were all more trusting, and therefore we should all trust more […] Current writings commonly focus on trust as somehow the relevant variable in explaining differences across cases of successful cooperation. Typically, however, the crucial variable is the trustworthiness of those who are to be trusted or relied upon. […] It is not trust per se, but trusting the right people that makes for successful relationships and happiness.”

“If we wish to understand the role of trust in society […], we must get beyond the flaccid – and often wrong – assumption that trust is simply good. This supposition must be heavily qualified, because trusting the malevolent or the radically incompetent can be foolish and often even grossly harmful. […] trust only make[s] sense in dealings with those who are or who could be induced to be trustworthy. To trust the untrustworthy can be disastrous.”

That it’s stupid to trust people who cannot be trusted should in my opinion be blatantly obvious, yet somehow to a lot of people it doesn’t seem to be at all obvious; in light of this problem (…I maintain that this is indeed a problem) the above observations are probably among the most important ones included in Hardin’s book. The book includes some strong criticism of much of the current/extant literature on trust. The two most common fields of study within this area of research are game-theoretic ‘trust games’, which according to the author are ill-named as they don’t really seem to be dealing much, if at all, with the topic of trust, and (poor) survey research which asks people questions which are hard to answer and tend to yield answers which are even harder to interpret. I have included below a few concluding remarks from the chapter on these topics:

“Both of the current empirical research programs on trust are largely misguided. The T-games [‘trust-games’], as played […] do not elicit or measure anything resembling ordinary trust relations; and their findings are basically irrelevant to the modeling and assessment of trust and trustworthiness. The only thing that relates the so-called trust game […] to trust is its name, which is wrong and misleading. Survey questions currently in wide use are radically unconstrained. They therefore force subjects to assume the relevant degrees of constraint, such as how costly the risk of failed cooperation would be. […] In sum, therefore, there is relatively little to learn about trust from these two massive research programs. Without returning their protocols to address standard conceptions of trust, they cannot contribute much to understanding trust as we generally know it, and they cannot play a very constructive role in explaining social behavior, institutions, or social and political change. These are distressing conclusions because both these enterprises have been enormous, and in many ways they have been carried out with admirable care.”

There is ‘relatively little to learn about trust from these two massive research programs’, but one to me potentially important observation, hidden away in the notes at the end of the book, is perhaps worth mentioning here: “There is a commonplace claim that trust will beget trustworthiness […] Schotter [as an aside this guy was incidentally the author of the Micro textbook we used in introductory Microeconomics] and Sopher (2006) do not find this to be true in game experiments that they run, while they do find that trustworthiness (cooperativeness in the play of games) does beget trust (or cooperation).”

There were a few parts of the coverage which confused me somewhat until it occurred to me that the author might not have read Boyd and Richerson, or other people who might have familiarized him with their line of thinking and research (once again, you should read Boyd and Richerson).

Moving on, a few remarks on social capital:

“Like other forms of capital and human capital, social capital is not completely fungible but may be specific to certain activities. A given form of social capital that is valuable in facilitating certain actions may be useless or even harmful for others. […] [A] mistake is the tendency to speak of social capital as though it were a particular kind of thing that has generalized value, as money very nearly does […] it[‘s value] must vary in the sense that what is functional in one context may not be in another.”

It is important to keep in mind that trust which leads to increased cooperation can end up leading to both good outcomes and bad:

“Widespread customs and even very local practices of personal networks can impose destructive norms on people, norms that have all of the structural qualities of interpersonal capital. […] in general, social capital has no normative valence […] It is generally about means for doing things, and the things can be hideously bad as well as good, although the literature on social capital focuses almost exclusively on the good things it can enable and it often lauds social capital as itself a wonderful thing to develop […] Community and social capital are not per se good. It is a grand normative fiction of our time to suppose that they are.”

The book has a chapter specifically about trust on the internet which related to the coverage included in Barak et al.‘s book, a publication which I have unfortunately neglected to blog (this book of course goes into a lot more detail). A key point in that chapter is that the internet is not really all that special in terms of these things, in the sense that to the extent that it facilitates coordination etc., it can be used to accomplish beneficial things as well as harmful things – i.e. it’s also neutrally valenced. Barak et al.‘s book has a lot more stuff about how this medium impacts communication and optimal communication strategies etc., which links in quite a bit with trust aspects, but I won’t go into this stuff here and I’m pretty sure I’ve covered related topics before here on the blog, e.g. back when I covered Hargie.

The chapter about terrorism and distrust had some interesting observations. A few quotes:

“We know from varied contexts that people can have a more positive view of individuals from a group than they have of the group.”

“Mere statistical doubt in the likely trustworthiness of the members of some identifiable group can be sufficient to induce distrust of all members of the group with whom one has no personal relationship on which to have established trust. […] This statistical doubt can trump relational considerations and can block the initial risk-taking that might allow for a test of another individual’s trustworthiness by stereotyping that individual as primarily a member of some group. If there are many people with whom one can have a particular beneficial interaction, narrowing the set by excluding certain stereotypes is efficient […] Unfortunately, however, excluding very systematically on the basis of ethnicity or race becomes pervasively destructive of community relations.”

One thing to keep in mind here is that people’s stereotypes are often quite accurate. When groups don’t trust each other it’s always a lot of fun to argue about who’s to blame for that state of affairs, but it’s important here to keep in mind that both groups will always have mental models of both the in-group and the out-group (see also the coverage below). Also it should be kept in mind that to the extent that people’s stereotypes are accurate, blaming stereotyping behaviours for the problems of the people who get stereotyped is conceptually equivalent to blaming people for discriminating against untrustworthy people by not trusting people who are not trustworthy. You always come back to the problem that what’s at the heart of the matter is never just trust, but rather trustworthiness. To the extent that the two are related, trust follows trustworthiness, not the other way around.

“There’s a fairly extensive literature on so-called generalized trust, which is trust in the anonymous or general other person, including strangers, whom we might encounter, perhaps with some restrictions on what isues would come under that trust. […] [Generalized trust] is an implausible notion. In any real-world context, I trust some more than others and I trust any given person more about some things than about others and more in some contexts than in others. […] Whereas generalized trust or group-generalized trust makes little or no sense (other than as a claim of optimism), group-generalized distrust in many contexts makes very good sense. If you were Jewish, Gypsy, or gay, you had good reason to distrust all officers of the Nazi state and probably most citizens in Nazi Germany as well. American Indians of the western plains had very good reason to distrust whites. During Milosevic’s wars and pogroms, Serbs, Croatians, and Muslims in then Yugoslavia had increasingly good reasons to distrust most members of the other groups, especially while the latter were acting as groups. […] In all of these cases, distrust is defined by the belief that members of the other groups and their representatives are hostile to one’s interests. Trust relationships between members of these various groups are the unusual cases that require explanation; the relatively group-generalized distrust is easy to understand and justify.”

“In the current circumstances of mostly Arab and Islamic terrorism against israel and the West and much of the rest of the world, it is surely a very tiny fraction of all Arabs and Islamists who are genuinely a threat, but the scale of their threat may make many Israelis and westerners wary of virtually all Arabs and Islamists […] many who are not prospects for taking terrorist action evidently sympathize with and even support these actions”

“When cooperation is organized by communal norms, it can become highly exclusionary, so that only members of the community can have cooperative relations with those in the community. In such a case, the norms of cooperativeness are norms of exclusion […] For many fundamentalist groups, continued loyalty to the group and its beliefs is secured by isolating the group and its members from many other influences so that relations within the community are governed by extensive norms of exclusion. When this happens, it is not only trust relations but also basic beliefs that are constrained. If we encounter no one with contrary beliefs our own beliefs will tend to prevail by inertia and lack of questioning and they will be reinforced by our secluded, exclusionary community. There are many strong, extreme beliefs about religious issues as well as about many other things. […] The two matters for which such staunch loyalty to unquestioned beliefs are politically most important are probably religious and nationalist commitments […] Such beliefs are often maintained by blocking our alternative views and by sanctioning those within the group who stray. […] Narrowing one’s associations to others in an isolated extremist group cripples one’s epistemology by blocking out general questioning of the group’s beliefs […] To an outsider those beliefs might be utterly crazy. Indeed, virtually all strong religious beliefs sound crazy or silly to those who do not share them. […] In some ways, the internet allows individuals and small groups to be quite isolated while nevertheless maintaining substantial contact with others of like mind. Islamic terrorists in the West can be almost completely isolated individually while maintaining nearly instant, frequent contact with other and with groups in the Middle East, Pakistan, or Afghanistan, as well as with groups of other potential terrorists in target nations.”

December 7, 2015 Posted by | Anthropology, Books, culture, disagreement, Economics, Game theory, Psychology, Religion | Leave a comment

Couple Resilience: Emerging Perspectives

I didn’t finish this book and I didn’t have a lot of nice things to say about it in my review on goodreads, but as I did read roughly half of it and it seemed easy to blog, I figured I might as well cover it here.

I have added some observations from the book and a few comments below:

“While we know that every marriage brings not only promise but substantial risk, to date we know more about the harmful processes in relationships than we do about what makes them work”

“expressions of positivity, especially gratitude, promote relationship maintenance in intimate bonds”

“Baxter and Montgomery (1996) maintain that the closeness of a relationship may be determined by the extent to which the ‘self becomes’ or changes through participation in that relationship, suggesting that boundaries between ‘self’ and ‘other’ are more permeable and fluid in a close, intimate relationship. […] Not surprisingly, this collective sense of an ‘us’ appears to grow stronger with time and age with older couples demonstrating greater levels of we-ness than couples at middle-age”

“It has been demonstrated […] that affirmation by one’s partner that is in keeping with one’s own self-ideal, is associated with better relationship adjustment and stability […]. Moreover, if a spouse’s positive view of his or her mate is more favorable than the mate’s own view, and if the spouse tries to stabilize such positive impressions then, over time, the person’s negative self-view could begin to change for the better […] Perceiving one’s partner as responsive to one’s needs, goals, values and so forth has generally been associated with greater relationship satisfaction and personal well-being […]. The concomitant experience of feeling validated, understood and cared for […] would arguably be that much more imperative when one partner is in distress. Such responsiveness entails the ability “to discern non-verbal cues, and to ‘read between the lines’ about motivations, emotions, and experiences,” […] Being attuned and responsive to non-verbal and para-verbal cues, in turn, is conducive to couple coping because it enables well spouses to be appropriately supportive without having to be explicitly directed or asked.” (I recall thinking that the topic of ‘hidden support’ along these lines was a very important topic to keep in mind in the future when I first read about it. It’s covered in much more detail in one of the previous books I’ve read on related topics, though I can’t recall at the moment if it was in Vangelisti & Perlman, Hargie, or Regan).

“Sexual resilience […] is a term used to describe individuals or couples who are able to withstand, adapt, and find solutions to events and experiences that challenge their sexual relationship.[…] the most common challenges to sexuality include the birth of the first child […]; the onset of a physical or mental illness […]; an emotional blow to the relationship, such as betrayal or hurt; lack of relational intimacy, such as becoming absorbed by other priorities such as career; and changes associated with aging, such as vaginal dryness or erectile dysfunction. […] People who place a relatively low value on sex for physical pleasure and a relatively high value on sex for relational intimacy […] are motivated to engage in sexual activity primarily to feel emotionally close to their partner. […] these individuals may respond to sexual challenges with less distress than those who place a high value on sex for physical pleasure. On an individual level, they are not overly concerned about specific sexual dysfunctions, but are motivated to find alternative ways of continuing to be sexually intimate with their partner, which may or may not include intercourse. […] Facing sexual difficulties with a high value placed on sex for relational intimacy, with strong dyadic adjustment, and with effective and open communication skills primes a couple to respond well to sexual challenges. […] Acceptance, flexibility, and persistence are characteristics most commonly associated with couples who successfully negotiated the challenges to their sexual relationship. […] When the physical pleasure aspect of sex is viewed as an enjoyed, but not essential, component of sex, couples no longer need to rely on perfect sexual functioning to engage in satisfying sex. Physical pleasure can come to be seen as “icing on the cake”, while relational intimacy is the cake itself.”

“Overall findings from neuroimaging studies of resilience suggest that the brains of resilient people are better equipped to tamp down negative emotion. […] In studies of rodents […] and primates […], early stress has consistently been associated with impaired brain development. Specifically, chronic stress has been found to damage neurons and inhibit neurogenesis in the hippocampus and medial prefrontal cortex […]. Stress has the opposite effect on the amygdala, causing dendritic growth accompanied by increased anxiety and aggression […]. Human studies yield results that are consistent with animal studies.”

I won’t cover the human studies in detail, but for example people have found when looking at the brains of children raised under bad conditions in orphanages in Eastern Europe and Asia that children who were adopted early in life (i.e., got away from the terrible conditions early on) had smaller amygdalae than children who were adopted later. They also note that smaller orbitofrontal volumes have been observed in physically abused children, with arguably(?) (I’m not sure about the validity of the instrument applied) a dose-response relationship between severity of abuse and the level of brain differences/changes observed, and smaller hippocampal volumes have been noted in depressed women with a history of childhood maltreatment (their brains were compared with the brains of depressed women without a history of childhood maltreatment).

“The positive associations between social support and physical health may be due in large part to the effect of positive relationships on cortisol levels […]. The presence of close, supportive relationships have been associated with lower cortisol levels in adolescents […], middle class mothers of 2-year old children […], elderly widowed adults […], men and women aged 47–59 […], healthy men […], college students […], 18–36 year olds from the UCLA community […], parents expecting their first child […], and relationship partners […] Overall, studies on relationship quality and cortisol levels suggest that close supportive relationships play an important role in boosting resilience.”

“Sharpe (2000) offered an insightful, developmental approach to understanding mutuality in romantic relationships. She described mutuality as a result of “merging” that consists of several steps, which occur and often overlap in the lifetime of a relationship. With the progression of the relationship, the partners start to recognize differences that exist between them and try to incorporate them into their existing concept of relationship. Additionally, both partners search for “his or her own comfort level and balance between time together and time apart” […]. As merging progresses, partners are able to cultivate their existing commonalities and differences, as well as develop multiple ways of staying connected. In truly mutual couples, both partners respect and validate each other’s views, work together to accomplish common goals, and resolve their differences through compromise. Moreover, a critical achievement of mutuality is the internalization of the loving relationship.”

November 14, 2015 Posted by | Books, Psychology | Leave a comment

Effects of Antidepressants

I gave the book two stars on goodreads. The contributors to this volume are from Brazil, Spain, Mexico, Japan, Turkey, Denmark, and the Czech Republic; the editor is from Taiwan. In most chapters you can tell that the first language of these authors is not English; the language is occasionally quite bad, although you can usually tell what the authors are trying to say.

The book is open access and you can read it here. I have included some quotes from the book below:

“It is estimated that men and women with depression are 20.9 and 27 times, respectively, more likely to commit suicide than those without depression (Briley & Lépine, 2011).” [Well, that’s one way to communicate risk… See also this comment].

“depression is on average twice as common in women as in men (Bromet et al., 2011). […] sex differences have been observed in the prevalence of mental disorders as well as in responses to treatment […] When this [sexual] dimorphism is present [in rats, a common animal model], the drug effect is generally stronger in males than in females.”

“Several reports indicate that follicular stimulating and luteinizing hormones and estradiol oscillations are correlated with the onset or worsening of depression symptoms during early perimenopause […], when major depressive disorder incidence is 3-5 times higher than the male matched population of the same [age] […]. Several longitudinal studies that followed women across the menopausal transition indicate that the risk for significant depressive symptoms increases during the menopausal transition and then decreases in […] early postmenopause […] the impact of hormone oscillations during perimenopause transition may affect the serotonergic system function and increase vulnerability to develop depression.”

“The use of antidepressant drugs for treating patients with depression began in the late 1950s. Since then, many drugs with potential antidepressants have been made available and significant advances have been made in understanding their possible mechanisms of action […]. Only two classes of antidepressants were known until the 80’s: tricyclic antidepressants and monoamine oxidase inhibitors. Both, although effective, were nonspecific and caused numerous side effects […]. Over the past 20 years, new classes of antidepressants have been discovered: selective serotonin reuptake inhibitors, selective serotonin/norepinephrine reuptake inhibitors, serotonin reuptake inhibitors and alpha-2 antagonists, serotonin reuptake stimulants, selective norepinephrine reuptake inhibitors, selective dopamine reuptake inhibitors and alpha-2 adrenoceptor antagonists […] Neither the biological basis of depression […] nor the precise mechanism of antidepressant efficacy are completely understood […]. Indeed, antidepressants are widely prescribed for anxiety and disorders other than depression.”

“Taken together the TCAs and the MAO-Is can be considered to be non-selective or multidimensional drugs, comparable to a more or less rational polypharmacy at the receptor level. This is even when used as monotherapy in the acute therapy of major depression. The new generation of selective antidepressants (the selective serotonin reuptake inhibitors (SSRIs)), or the selective noradrenaline and serotonin reuptake inhibitors (SNRIs) have a selective mechanism of action, thus avoiding polypharmacy. However, the new generation antidepressants such as the SSRIs or SNRIs are less effective than the TCAs. […] The most selective second generation antidepressants have not proved in monotherapy to be more effective on the core symptoms of depression than the first generation TCAs or MAOIs. It is by their safety profiles, either in overdose or in terms of long term side effects, that the second generation antidepressants have outperformed the first generation.”

“Suicide is a serious global public health problem. Nearly 1 million individuals commit suicide every year. […] Suicide […] ranks among the top 10 causes of death in every country, and is one of the three leading causes of death in 15 to 35-year olds.”

“Considering patients that commit suicide, about half of them, at some point, had contact with psychiatric services, yet only a quarter had current or recent contact (Andersen et al., 2000; Lee et al., 2008). A study conducted by Gunnell & Frankel (1994) revealed that 20-25% of those committing suicide had contact with a health care professional in the week before death and 40% had such contact one month before death” (I’m assuming ‘things have changed’ during the last couple of decades, but it would be interesting to know how much they’ve changed).

“In cases of suicide by drug overdose, TCAs have the highest fatal toxicity, followed by serotonin and noradrenalin reuptake inhibitors (SNRIs), specific serotonergic antidepressants (NaSSA) and SSRIs […] SSRIs are considered to be less toxic than TCAs and MAOIs because they have an extended therapeutic window. The ingestion of up to 30 times its recommended daily dose produces little or no symptoms. The intake of 50 to 70 times the recommended daily dose can cause vomiting, mild depression of the CNS or tremors. Death rarely occurs, even at very high doses […] When we talk about suicide and suicide attempt with antidepressants overdose, we are referring mainly to women in their twenties – thirties who are suicide repeaters.”

“Physical pain is one of the most common somatic symptoms in patients that suffer depression and conversely, patients suffering from chronic pain of diverse origins are often depressed. […] While […] data strongly suggest that depression is linked to altered pain perception, pain management has received little attention to date in the field of psychiatric research […] The monoaminergic system influences both mood and pain […], and since many antidepressants modify properties of monoamines, these compounds may be effective in managing chronic pain of diverse origins in non-depressed patients and to alleviate pain in depressed patients. There are abundant evidences in support of the analgesic properties of tricyclic antidepressants (TCAs), particularly amitriptyline, and another TCA, duloxetine, has been approved as an analgesic for diabetic neuropathic pain. By contrast, there is only limited data regarding the analgesic properties of selective serotonin reuptake inhibitors (SSRIs) […]. In general, compounds with noradrenergic and serotonergic modes of action are more effective analgesics […], although the underlying mechanisms of action remain poorly understood […] While the utility of many antidepressant drugs in pain treatment is well established, it remains unclear whether antidepressants alleviate pain by acting on mood (emotional pain) or nociceptive transmission (sensorial pain). Indeed, in many cases, no correlation exists between the level of pain experienced by the patient and the effect of antidepressants on mood. […] Currently, TCAs (amitriptyline, nortriptiline, imipramine and clomipramine) are the most common antidepressants used in the treatment of neuropathic pain processes associated with diabetes, cancer, viral infections and nerve compression. […] TCAs appear to provide effective pain relief at lower doses than those required for their antidepressant effects, while medium to high doses of SNRIs are necessary to produce analgesia”. Do keep in mind here that in a neuropathy setting one should not expect to get anywhere near complete pain relief with these drugs – see also this post.

“Prevalence of a more or less severe depression is approximately double in patients with diabetes compared to a general population [for more on related topics, see incidentally this previous post of mine]. […] Diabetes as a primary disease is typically superimposed by depression as a reactive state. Depression is usually a result of exposure to psycho-social factors that are related to hardship caused by chronic disease. […] Several studies concerning comorbidity of type 1 diabetes and depression identified risk factors of depression development; chronic somatic comorbidity and polypharmacy, female gender, higher age, solitary life, lower than secondary education, lower financial status, cigarette smoking, obesity, diabetes complications and a higher glycosylated hemoglobin [Engum, 2005; Bell, 2005; Hermanns, 2005; Katon, 2004]”

November 11, 2015 Posted by | Books, Diabetes, Epidemiology, Medicine, Pharmacology, Psychiatry, Psychology | Leave a comment

Understanding Other-Oriented Hope

“This monograph introduces, defines, exemplifies, and characterizes hope that is directed toward others rather than toward the self. […] Because vicarious hope remains a relatively neglected topic within hope theory and research, the current work aims to provide, for the first time, a robust conceptualization of other-oriented hope, and to review and critically examine existing literature on other-oriented hope.”

I really should be blogging more interesting books here instead, such as e.g. Gigerenzer’s book, but this one is easy to blog.

I’ll make this post short, but I do want to make sure no-one misses this crucial point, which is the most important observation in the context of this book: The book is a terrible book. Given that I’ve already shared (some of) my negative views about the book on goodreads I won’t go into all the many reasons why you probably shouldn’t read it here as well; instead I’ll share below a few observations from the book which might be of interest to some of the people reading along.

“Whereas other-interest encapsulates a broad and generalized orientation toward valuing, recognizing, facilitating, promoting, and celebrating positive outcomes for others that have occurred in the past or present, or that may occur in the future, other-oriented hope cleaves that portion of other-interest specific to the harbouring of future-oriented hope for others and (where possible) attendant strivings toward meeting those ends. […] Other-oriented hope is viewed as a specific form of other-interest, one in which we reveal our interest in the welfare of others by apportioning some of our future-oriented mental imaginings to others’ welfare in addition to our own, more self-focused, hope. […] we define other-oriented hope as future-oriented belief, desire, and mental imagining surrounding a valued outcome of another person that is uncertain but possible. […] The dimensions emphasized by Novotny (1989) within an illness context are that hope: is future-oriented; involves active engagement; is an inner resource; reflects possibility; is relational; and concerns issues of importance.”

“Schrank et al. (2010) factor analyzed 60-items taken from three existing hope scales. Four dimensions of hope arose, labelled trust and confidence (e.g., goal striving, positive past experience), positive future orientation (e.g., looking forward, making plans), social relations and personal value (e.g., feeling loved and needed), and lack of perspective (e.g., feeling trapped, becoming uninvolved). […] In the most influential psychological perspective on hope, […] Snyder and colleagues posit that hope is “a positive motivational state that is based on an interactively derived sense of successful (a) agency (goal-directed energy), and (b) pathways (planning to meet goals)” […]. According to this view, hope-agency beliefs provide motivation to pursue valued goals, and hope-pathways beliefs provide plausible routes to meet those goals. […] hope is most often construed as an emotion or as an emotion-based coping process.”

“Lapierre et al. (1993) report that wishes for others is a more frequent category among relatively younger elderly participants and among non-impaired relative to impaired participants. The authors suggest that less healthy individuals (i.e., relatively older and impaired) are more self-focused in their aspirations, emphasizing such fundamental goals as preserving their health. […] Herth identified changes [in hope patterns] as a function of age and impairment level of respondents, with those older than 80 and experiencing mild to moderate impairment being more likely to harbour hope focused on others compared to those who were higher functioning. Moreover, those living in long-term care facilities with moderate to severe impairment directed their hope almost entirely toward others. […] [research] strongly points to the element of vulnerability in another person as a situational influence on other-oriented hope. Learning about others’ vulnerability likely triggers compassion or empathy which, in turn, elicits other-oriented hope. […] In addition to other-oriented hope occurring in response to another’s vulnerability, vicarious hope appears also to be triggered by one’s own vulnerability. […] In related work, Hollis et al. (2007) discuss borrowed hope; for those with no hope, others who have hope for them can be impactful, because hope can be viewed as ‘contagious’.”

“Similar to recognized drawbacks or risks of self-oriented hope, other-oriented hope may be associated with a failure to accept things the way they are, frustration upon hope being dashed, risk taking, or the failure to limit losses […] There is also an opportunity-cost to other-oriented hope: Time spent hoping for another is time not spent generating, contemplating, or acting toward either one’s own hope or to yet other people’s hope. […] There may be costs to the recipient of other-oriented hope in the form of feeling coerced or controlled by others whose vicarious hope is not shared by the recipient. Therefore, some forms of other-oriented hope may reveal only the desired outcomes of the hoping agent as opposed to the person to whom the hope applies. In the classic example, a parent’s hope for a child may not be hope that is held by the child him- or herself, and therefore may be experienced as a significant source of undue pressure and stress by the child. Such coercive hope is, in turn, likely to be harmful to the relationship between the person harbouring the other-oriented hope and the target of that hope. […] In an extreme form, other-oriented hope bears resemblance to other-oriented perfectionism. Hewitt and Flett (2004) argue that perfectionism can be directed toward the self or others. In the former case, perfectionism involves expectations placed upon oneself for unreasonably high performance, whereas in the latter case, perfectionism involves expecting others to uphold an unreasonably high standard and expressing criticism when others fail to meet this expectation. It is possible that other-oriented hope occasionally takes the form of other-oriented expectations for perfection. For example, a parent may hope that a child performs well in school, but this could take the form of an overly demanding standard of achievement that is difficult or impossible for the child to attain, creating distress in the child’s life and conflict within the parent-child relationship.”

“McGeer (2004) argues for responsive hope being an optimal point between wishful hope, on the one hand (i.e., desire but too little agency, as in wishful thinking) and willful hope, on the other hand (desire but too much agency, as in an incautious or unrealistic pursuit of one’s dreams). To expand on McGeer’s views, responsive other-oriented hope would fall between wishful other-oriented hope, on the one hand (i.e., desires aimed at others but divorced from an action-orientation toward the fulfillment of such desires), and willful other-oriented hope, on the other hand (i.e., desire for, and overzealous facilitation of, others’ future outcomes, ignoring whether such actions are in the other’s best interest or are endorsed by the other). […] Like self-oriented hope, other-oriented hope can be contested and, in extreme instances, such hope may impede coping, such as by encouraging ongoing denial among family members of the objective circumstances faced by their loved one. Hoping against hope for others may, at times, be more costly than beneficial.”

“Acceptance toward others may be exhibited through not judging others, being tolerant of others who are perceived as different than oneself, being willing to engage with others, and not avoiding others who might be predicted to displease us or upset us. It would appear, therefore, that acceptance, like hope, can be directed toward the self or toward others. Interestingly, acceptance of the self and acceptance of others are included, respectively, in measures of psychological well-being and social well-being (Keyes 2005), suggesting that both self-acceptance and other-acceptance are considered key aspects of psychological health.”

“Davis and Asliturk (2011) review research showing that a realistic orientation toward future outcomes, in which one considers both positive and negative possibilities, is associated with coping more effectively with adversity.”

“Weis and Speridakos (2011) conducted a meta-analysis on 27 studies that employed strategies to enhance hope among both mental health clients and community members. They reported modest effects of such psychotherapy on measures of hope and life satisfaction, but not on measures of psychological distress. The authors caution that effects were relatively small in comparison to other psychoeducational or psychotherapeutic interventions.”

October 8, 2015 Posted by | Books, Psychology | Leave a comment

Cognitive Psychology (I)

I could theoretically write a lot of posts about this handbook, but I’m probably not going to do that. As I’ve mentioned before I own a physical copy of this book, and blogging physical books is a pain in the neck compared to blogging e-books – this is one of the main reasons why I’m only now starting to blog the book, despite having finished it some time ago.

The book is a 600+ pages long handbook (752 pages if you include glossary, index etc.), and it has 16 chapters on various topics. Though I’m far from sure, I’d estimate that I spent something like 50 hours on the book altogether so far – 3 hours per chapter on average – and that’s just for ‘reading the pages’, so to speak; if I do decide to blog this book in any amount of detail, the amount of time spent on the material in there will go up quite a bit.

So what’s the book about – what is ‘cognitive psychology’? Here are a few remarks on these topics from the preface and the first chapter:

“the leading contemporary approach to human cognition involves studying the brain as well as behaviour. We have used the term “cognitive psychology” in the title of this book to refer to this approach, which forms the basis for our coverage of human cognition. Note, however, that the term “cognitive neuroscience” is often used to describe this approach. […] Note that the distinction between cognitive psychology and cognitive neuroscience is often blurred – the term ‘cognitive psychology” can be used in a broader sense to include cognitive neuroscience. Indeed, it is in that broader sense that it is used in the title of this book.”

The first chapter – about ‘approaches to human cognition’ – is a bit dense, but I decided to talk a little about it anyway because it seemed like a good way to give you some idea about what the book is about and which sort of content you’ll encounter in it. In the chapter the authors outline four different approaches to human cognition and talk about each of these in a bit of detail. Experimental cognitive psychology is an approach which basically limits itself to behavioural evidence. What they term cognitive neuroscience is an approach using evidence from both behaviour and the brain (that can be accomplished by having people do stuff while their brain activity is being monitored). Cognitive neuropsychology is an approach where you try to use data from brain-damaged individuals to help understand how normal cognition works. The last approach, computational cognitive science, I recently dealt with in the Science of Reading handbook – this approach involves constructing computational models to understand/simulate specific aspects of human cognition. All four approaches are used throughout the book to obtain a greater understanding of the topics covered.

The introductory chapter also gives the reader some information about what the brain looks like and how it’s structured, adds some comments about distinctions between various forms of processing, such as bottom-up processing and top-down processing and serial processing and parallel processing, and adds information about common techniques used to study brain activity in neuroscience (single-unit recording, event-related potentials, positron emission tomography, fMRI, efMRI, magnetoencephalography, and transcranial magnetic stimulation). I don’t want to go too much into the specifics of all those topics here, but I should note that I was unaware of the existence of TMS (transcranial magnetic stimulation) research methodologies and that it sounds like an interesting approach; basically what people do when they use this approach is to use magnetic pulses to try to (briefly, for a short amount of time) disrupt the functioning of some area of the brain and then evaluate performance on cognitive tasks performed while the brain area in question is disrupted – if people perform more poorly on a given task when the brain area in question is disrupted by the magnetic field, it might indicate that the brain area is involved in that task. For various reasons it’s not unproblematic to interpret the results of TMS research and there are various limitations to the application of this method, but this is experimental manipulation of a kind I’d basically assumed did not exist in this field before I started out reading the book.

It’s noted in the first chapter that: “much research in cognitive psychology suffers from a relative lack of ecological validity […] and paradigm specificity (findings do not generalise from one paradigm to others). The same limitations apply to cognitive neuroscience since cognitive neuroscientists generally use tasks previously developed by cognitive psychologists. Indeed, the problem of ecological validity may be greater in cognitive neuroscience.” In the context of cognitive neuropsychology, there are also various problems which I’m reasonably sure I’ve talked about here before – for example brain damage is rarely conveniently localized to just one brain area the researcher happens to be interested in, and the use of compensatory strategies by individuals with brain damage may cause problems with interpretation. Small sample sizes and large patient heterogeneities within these samples also do not help. As for the last approach, computational cognitive science, the problems mentioned are probably mostly the ones you’d expect; the models developed are rarely used to make new predictions because they’re often too general to really make them at all easy to evaluate one way or the other (lots of free parameters you can fit however you like), and despite their complexity they tend to ignore a lot of presumably highly relevant details.

The above was an outline of some stuff covered in the first chapter. The book as mentioned has 16 chapters. ‘Part 1’ deals with visual perception and attention – there’s a lot of stuff about that kind of thing in the book, almost 200 pages – and includes chapters about ‘basic processes in visual perception’, ‘object and face recognition’, ‘perception, motion, and action’, and ‘attention and performance’. Part 2 deals with memory, including chapters about ‘learning, memory, and forgetting’, ‘long-term memory systems’ and ‘everyday memory’. That part I found interesting and I hope I’ll manage to find the time to cover some of that stuff here later on. Part 3 deals with language and includes chapters about ‘reading and speech perception’, ‘language comprehension’, and ‘language production’. I recall wondering a long time ago on this blog if people doing research on those kinds of topics distinguished between language production and language comprehension; it’s pretty obvious that they do.. Part 5 deals with ‘thinking and reasoning’ and includes chapters about ‘problem solving and expertise’, ‘judgment and decision making’, and ‘inductive and deductive reasoning’. Interestingly the first of these chapters talks quite a bit about chess, because chess expertise is one of the research areas people have looked at when looking at the topic of expertise. I may decide to talk about these things later on, but I’m not sure I’ll cover the stuff in part 5 in much detail because Gigerenzer (whose research the authors discuss in chapter 13) covers some related topics in his book Simply Rational, which I’m currently reading, and I frankly like his coverage better (I should perhaps clarify in light of the previous remarks that Gigerenzer does not cover chess, but rather talks about other topics also covered in that section – the coverage overlap relates to Gigerenzer’s work on heuristics). The last part of the book has a chapter on cognition and emotion and a chapter about consciousness.

As you read the chapters, the authors start out by outlining some key features/distinctions of interest. They talk about what the specific theory/hypothesis/etc. is about, then they talk about the research results, and then they give their own evaluation of the research and conclude the coverage with outlining some limitations of the available research. Multiple topics are covered this way – presentation, research, evaluation, limitations – in each chapter, and when multiple competing hypotheses/approaches have been presented the evaluations will highlight strengths and weaknesses of each approach. Along the way you’ll encounter boxes at the bottom of the pages with bolded ‘key terms’ and definitions of those terms, as well as figures and tables with research results and illustrations of brain areas involved; key terms are also bolded in the text, so even if you don’t completely destroy the book by painting all over the pages with highlighters of different colours the way I do, it should be reasonably easy to navigate the content on a second reading. Usually the research on a given topic will be divided into sections if multiple approaches have been used to elucidate problems of interest; so there’ll be one section dealing with cognitive neuropsychology research, and another section about the cognitive neuroscience results. All chapters end with a brief outline of key terms/models/approaches encountered in the chapter and some of the main results discussed. The book is well structured. Coverage is in my opinion a bit superficial, which is one of the main reasons why I only gave the book three stars, and the authors are not always as skeptical as I’d have liked them to be – I did not always agree with the conclusions they drew from the research they discussed in the chapters, and occasionally I think they miss alternative explanations or misinterpret what the data is telling us. Some of the theoretical approaches they discuss in the text I frankly considered (/next to) worthless and a waste of time. It’s been a while since I finished the book and of course I don’t recall details as well as I’d like, but from what I remember and what I’ve gathered from a brief skim again while writing the post it’s far from a terrible book and on a general note it covers some interesting stuff – we’ll see how much of it I’ll manage to talk about here on the blog in the time to come. Regardless of how much more time I’ll be able to devote to the book here on the blog, this post should at least have given you some idea about which topics are covered in the book and how they’re covered.

September 24, 2015 Posted by | Books, Neurology, Psychology | Leave a comment

Loneliness (III)

The last part of the book was disappointing, as the coverage was generally weak and chapter 13 even basically devolved into a self-help chapter; I dislike self-help books immensely. I gave the book 2 stars on goodreads, but ended up significantly closer to one star than three. The truth of the matter is that if the book had been covering a different topic in which I had only had a more fleeting interest, there’s no way I’d have read it to the end.

A few observations from the last part of the book below.

“In 2006 we set out to test the impact of loneliness on responses to inequitable treatment. Our strategy involved a game in which the researcher designates one player as “proposer” and the other as “decider” and gives the proposer ten dollars. The proposer must split the money with the decider—along whatever lines he can get the decider to accept. If the decider rejects the proposal, neither player gets any money. […] It will probably come as no surprise that most people are sensitive to whether or not another person is dealing with them fairly, and that they agree to accept more fair offers than unfair ones. They do this even when, as in our experiment, rejecting an offer leaves them with no reward but their pride and their sense of right and wrong. Lonely players generally followed this pattern, and lonely and non-lonely participants in our game accepted comparable numbers of fair offers. However, lonely players accepted more unfair offers than did nonlonely players. They went along more often when their partner treated them unfairly, even though both lonely and nonlonely players rated the offers as equally and profoundly unfair.

This willingness to endure exploitation even when we have a clear sense that the other person is treating us unfairly does not bode well for our chances of achieving satisfying social connections in the long run, and it can place lonely individuals at greater risk of being scammed, or at least disappointed. Over time, the bad experiences that follow can contribute to the lonely person’s impression that, when you come right down to it, betrayal or rejection is lurking around every corner—a perception that plays into fear, hostility, learned helplessness, and passive coping. […] With an impaired ability to discriminate, persevere, and self-regulate, the lonely, both as children and as adults, often engage in extremes. Sometimes, in an effort to belong, they allow themselves to be pushed around, as in our “proposer/decider” game, when a lonely adult feels resentment, but goes ahead and accepts unfair offers. […] At other times, fear might lead […] to almost paranoid levels of self-protection […] whether driven by loneliness or by other factors, it is usually maladaptive to allow yourself to be taken advantage of. […] the most adaptive strategy is to maintain both the ability to detect cheating or betrayal and the ability to carefully modulate one’s response. The dysregulation caused by loneliness consigns us to the extremes of either suffering passively (responding too little) or being “difficult” (responding too intensely).”

“Among bonobos, if a low-ranking female commits some offense against a dominant female’s child, or grabs a piece of food that an older female had her eye on, or fails to surrender ground when a matriarch moves in to groom a male, the higher-ranking female may refuse to share food with or to accept grooming from her subordinate. This kind of rebuke can throw the younger animal into a tantrum right in front of the cold and rejecting elder. The affront is so stressful that it makes the subordinate physically sick, often causing her to vomit at the feet of her nemesis. It appears that apes do not enjoy social rejection any more than humans do.”

“The solution to loneliness is not quantity but quality of relationships. Human connections have to be meaningful and satisfying for each of the people involved, and not according to some external measure. Moreover, relationships are necessarily mutual and require fairly similar levels of intimacy and intensity on both sides. Even casual chitchat […] needs to proceed at a pace that is comfortable for everyone. Coming on too strong, oblivious to the other person’s response, is the quickest way to push someone away. So part of selection is sensing which prospective relationships are promising, and which would be climbing the wrong tree. Loneliness makes us very attentive to social signals. The trick is to be sufficiently calm and “in the moment” to interpret those signals accurately.”

“The kinds of connections — pets, computers — we substitute for human contact are called “parasocial relationships.” You can form a parasocial relationship with television characters, with people you “meet” online, or with your Yorkshire terrier. Is this an effective way to fill the void when connection with other humans, face to face, is thwarted?

The Greeks […] used the term “anthropomorphism” […] to describe the projection of specifically human attributes onto nonhuman entities. Increasing the strength of anthropomorphic beliefs appears to be a useful tactic for coping with loneliness, divorce, widowhood, or merely being single.16 Pet owners project all sorts of human attributes onto their animal companions, and elderly people who have pets appear to be buffered somewhat from the negative impact of stressful life events. They visit their doctors less often than do their petless age-mates. Individuals diagnosed with AIDS are less likely to become depressed if they own a pet. […] whether it’s a god, a devil, an animal, a machine […], a landmark, or a piece of cast-off sports equipment, the anthropomorphized being becomes a social surrogate, and the same neural systems that are activated when we make judgments about other humans are activated when we assess these parasocial relationships.21 […] Our parasocial relationships follow certain patterns based on aspects of our human relationships. People with insecure, anxious attachment styles are more likely than those with secure attachment styles to form perceived social bonds with television characters. They are also more likely than those with secure attachment styles to report an intensification of religious belief over a given time period, including sudden religious conversions later in life. […] Many proponents of technology tell us that computer-mediated social encounters will fill the void left by the decline of community in the real world. […] Studies have shown that the richer the medium […] the more it fosters social cohesion. This may be why, for those who do choose to connect electronically, multiplayer sites […] are becoming popular meeting places. […] forming connections with pets or online friends or even God is a noble attempt by an obligatorily gregarious creature to satisfy a compelling need. But surrogates can never make up completely for the absence of the real thing.”

August 31, 2015 Posted by | Books, Psychology | Leave a comment

Loneliness (II)

Here’s my first post about the book. I’d probably have liked the book better if I hadn’t read the Cognitive Psychology text before this one, as knowledge from that book has made me think a few times in specific contexts that ‘that’s a bit more complicated than you’re making it out to be’ – as I also mentioned in the first post, the book is a bit too popular science-y for my taste. I have been reading other books in the last few days – for example I started reading Darwin a couple of days ago – and so I haven’t really spent much time on this one since my first post; however I have read the first 10 chapters (out of 14) by now, and below I’ve added a few observations from the chapters in the middle.

“In 1958, in a now-legendary, perhaps infamous experiment, the psychologist Harry Harlow of the University of Wisconsin removed newborn rhesus monkeys from their mothers. He presented these newborns instead with two surrogates, one made of wire and one made of cloth […]. Either stand-in could be rigged with a milk bottle, but regardless of which “mother” provided food, infant monkeys spent most of their time clinging to the one made of cloth, running to it immediately when startled or upset. They visited the wire mother only when that surrogate provided food, and then, only for as long as it took to feed.2

Harlow found that monkeys deprived of tactile comfort showed significant delays in their progress, both mentally and emotionally. Those deprived of tactile comfort and also raised in isolation from other monkeys developed additional behavioral aberrations, often severe, from which they never recovered. Even after they had rejoined the troop, these deprived monkeys would sit alone and rock back and forth. They were overly aggressive with their playmates, and later in life they remained unable to form normal attachments. They were, in fact, socially inept — a deficiency that extended down into the most basic biological behaviors. If a socially deprived female was approached by a normal male during the time when hormones made her sexually receptive, she would squat on the floor rather than present her hindquarters. When a previously isolated male approached a receptive female, he would clasp her head instead of her hindquarters, then engage in pelvic thrusts. […] Females raised in isolation became either incompetent or abusive mothers. Even monkeys raised in cages where they could see, smell, and hear — but not touch — other monkeys developed what the neuroscientist Mary Carlson has called an “autistic-like syndrome,” with excessive grooming, self-clasping, social withdrawal, and rocking. As Carlson told a reporter, “You were not really a monkey unless you were raised in an interactive monkey environment.””

In the authors’ coverage of oxytocin’s various roles in human- and animal social interaction they’re laying it on a bit thick in my opinion, and the less than skeptical coverage there leads me to also be somewhat skeptical of their coverage of the topic of mirror neurons, also on account of stuff like this. However I decided to add a little of the coverage of this topic anyway:

“In the 1980s the neurophysiologist Giacomo Rizzolatti began experimenting with macaque monkeys, running electrodes directly into their brains and giving them various objects to handle. The wiring was so precise that it allowed Rizzolatti and his colleagues to identify the specific monkey neurons that were activated at any moment.

When the monkeys carried out an action, such as reaching for a peanut, an area in the premotor cortex called F5 would fire […]. But then the scientists noticed something quite unexpected. When one of the researchers picked up a peanut to hand it to the monkey, those same motor neurons in the monkey’s brain fired. It was as if the animal itself had picked up the peanut. Likewise, the same neurons that fired when the monkey put a peanut in its mouth would fire when the monkey watched a researcher put a peanut in his mouth. […] Rizzolatti gave these structures the name “mirror neurons.” They fire even when the critical point of the action—the person’s hand grasping the peanut, for instance — is hidden from view behind some object, provided that the monkey knows there is a peanut back there. Even simply hearing the action — a peanut shell being cracked — can trigger the response. In all these instances, it is the goal rather than the observed action itself that is being mirrored in the monkey’s neural response. […] Rizzolatti and his colleagues confirmed the role of goals […] by performing brain scans while people watched humans, monkeys, and dogs opening and closing their jaws as if biting. Then they repeated the scans while the study subjects watched humans speak, monkeys smack their lips, and dogs bark.9 When the participants watched any of the three species carrying out the biting motion, the same areas of their brains were activated that activate when humans themselves bite. That is, observing actions that could reasonably be performed by humans, even when the performers were monkeys or dogs, activated the appropriate portion of the mirror neuron system in the human brain. […] the mirror neuron system isn’t simply “monkey see, monkey do,” or even “human see, human do.” It functions to give the observing individual knowledge of the observed action from a “personal” perspective. This “personal” understanding of others’ actions, it appears, promotes our understanding of and resonance with others.”

“In a study of how people monitor social cues, when researchers gave participants facts related to interpersonal or collective social ties presented in a diary format, those who were lonely remembered a greater proportion of this information than did those who were not lonely. Feeling lonely increases a person’s attentiveness to social cues just as being hungry increases a person’s attentiveness to food cues.28 […] They [later] presented images of twenty-four male and female faces depicting four emotions — anger, fear, happiness, and sadness — in two modes, high intensity and low intensity. The faces appeared individually for only one second, during which participants had to judge the emotional timbre. The higher the participants’ level of loneliness, the less accurate their interpretation of the facial expressions.”

“As we try to determine the meaning of events around us, we humans are not particularly good at knowing the causes of our own feelings or behavior. We overestimate our own strengths and underestimate our faults. We overestimate the importance of our contribution to group activities, the pervasiveness of our beliefs within the wider population, and the likelihood that an event we desire will occur.3 A At the same time we underestimate the contribution of others, as well as the likelihood that risks in the world apply to us. Events that unfold unexpectedly are not reasoned about as much as they are rationalized, and the act of remembering itself […] is far more of a biased reconstruction than an accurate recollection of events. […] Amid all the standard distortions we engage in, […] loneliness also sets us apart by making us more fragile, negative, and self-critical. […] One of the distinguishing characteristics of people who have become chronically lonely is the perception that they are doomed to social failure, with little if any control over external circumstances. Awash in pessimism, and feeling the need to protect themselves at every turn, they tend to withdraw, or to rely on the passive forms of coping under stress […] The social strategy that loneliness induces — high in social avoidance, low in social approach — also predicts future loneliness. The cynical worldview induced by loneliness, which consists of alienation and little faith in others, in turn, has been shown to contribute to actual social rejection. This is how feeling lonely creates self-fulfilling prophesies. If you maintain a subjective sense of rejection long enough, over time you are far more likely to confront the actual social rejection that you dread.8 […] In an effort to protect themselves against disappointment and the pain of rejection, the lonely can come up with endless numbers of reasons why a particular effort to reach out will be pointless, or why a particular relationship will never work. This may help explain why, when we’re feeling lonely, we undermine ourselves by assuming that we lack social skills that in fact, we do have available.”

“Because the emotional system that governs human self-preservation was built for a primitive environment and simple, direct dangers, it can be extremely naïve. It is impressionable and prefers shallow, social, and anecdotal information to abstract data. […] A sense of isolation can make [humans] feel unsafe. When we feel unsafe, we do the same thing a hunter-gatherer on the plains of Africa would do — we scan the horizon for threats. And just like a hunter-gatherer hearing an ominous sound in the brush, the lonely person too often assumes the worst, tightens up, and goes into the psychological equivalent of a protective crouch.”

“One might expect that a lonely person, hungry to fulfill unmet social needs, would be very accepting of a new acquaintance, just as a famished person might take pleasure in food that was not perfectly prepared or her favorite item on the menu. However, when people feel lonely they are actually far less accepting of potential new friends than when they feel socially contented.17 Studies show that lonely undergraduates hold more negative perceptions of their roommates than do their nonlonely peers.”

August 30, 2015 Posted by | Biology, Books, Psychology, Zoology | Leave a comment

Random Stuff / Open Thread

This is not a very ‘meaty’ post, but it’s been a long time since I had one of these and I figured it was time for another one. As always links and comments are welcome.

i. The unbearable accuracy of stereotypes. I made a mental note of reading this paper later a long time ago, but I’ve been busy with other things. Today I skimmed it and decided that it looks interesting enough to give it a detailed read later. Some remarks from the summary towards the end of the paper:

“The scientific evidence provides more evidence of accuracy than of inaccuracy in social stereotypes. The most appropriate generalization based on the evidence is that people’s beliefs about groups are usually moderately to highly accurate, and are occasionally highly inaccurate. […] This pattern of empirical support for moderate to high stereotype accuracy is not unique to any particular target or perceiver group. Accuracy has been found with racial and ethnic groups, gender, occupations, and college groups. […] The pattern of moderate to high stereotype accuracy is not unique to any particular research team or methodology. […] This pattern of moderate to high stereotype accuracy is not unique to the substance of the stereotype belief. It occurs for stereotypes regarding personality traits, demographic characteristics, achievement, attitudes, and behavior. […] The strong form of the exaggeration hypothesis – either defining stereotypes as exaggerations or as claiming that stereotypes usually lead to exaggeration – is not supported by data. Exaggeration does sometimes occur, but it does not appear to occur much more frequently than does accuracy or underestimation, and may even occur less frequently.”

I should perhaps note that this research is closely linked to Funder’s research on personality judgment, which I’ve previously covered on the blog here and here.

ii. I’ve spent approximately 150 hours on vocabulary.com altogether at this point (having ‘mastered’ ~10.200 words in the process). A few words I’ve recently encountered on the site: Nescience (note to self: if someone calls you ‘nescient’ during a conversation, in many contexts that’ll be an insult, not a compliment) (Related note to self: I should find myself some smarter enemies, who use words like ‘nescient’…), eristic, carrel, oleaginous, decal, gable, epigone, armoire, chalet, cashmere, arrogate, ovine.

iii. why p = .048 should be rare (and why this feels counterintuitive).

iv. A while back I posted a few comments on SSC and I figured I might as well link to them here (at least it’ll make it easier for me to find them later on). Here is where I posted a few comments on a recent study dealing with Ramadan-related IQ effects, a topic which I’ve covered here on the blog before, and here I discuss some of the benefits of not having low self-esteem.

On a completely unrelated note, today I left a comment in a reddit thread about ‘Books That Challenged You / Made You See the World Differently’ which may also be of interest to readers of this blog. I realized while writing the comment that this question is probably getting more and more difficult for me to answer as time goes by. It really all depends upon what part of the world you want to see in a different light; which aspects you’re most interested in. For people wondering about where the books about mathematics and statistics were in that comment (I do like to think these fields play some role in terms of ‘how I see the world‘), I wasn’t really sure which book to include on such topics, if any; I can’t think of any single math or stats textbook that’s dramatically changed the way I thought about the world – to the extent that my knowledge about these topics has changed how I think about the world, it’s been a long drawn-out process.

v. Chess…

People who care the least bit about such things probably already know that a really strong tournament is currently being played in St. Louis, the so-called Sinquefield Cup, so I’m not going to talk about that here (for resources and relevant links, go here).

I talked about the strong rating pools on ICC not too long ago, but one thing I did not mention when discussing this topic back then was that yes, I also occasionally win against some of those grandmasters the rating pool throws at me – at least I’ve won a few times against GMs by now in bullet. I’m aware that for many ‘serious chess players’ bullet ‘doesn’t really count’ because the time dimension is much more important than it is in other chess settings, but to people who think skill doesn’t matter much in bullet I’d say they should have a match with Hikaru Nakamura and see how well they do against him (if you’re interested in how that might turn out, see e.g. this video – and keep in mind that at the beginning of the video Nakamura had already won 8 games in a row, out of 8, against his opponent in the first games, who incidentally is not exactly a beginner). The skill-sets required do not overlap perfectly between bullet and classical time control games, but when I started playing bullet online I quickly realized that good players really require very little time to completely outplay people who just play random moves (fast). Below I have posted a screencap I took while kibitzing a game of one of my former opponents, an anonymous GM from Germany, against whom I currently have a 2.5/6 score, with two wins, one draw, and three losses (see the ‘My score vs CPE’ box).

Kibitzing GMs(click to view full size).

I like to think of a score like this as at least some kind of accomplishment, though admittedly perhaps not a very big one.

Also in chess-related news, I’m currently reading Jesús de la Villa’s 100 Endgames book, which Christof Sielecki has said some very nice things about. A lot of the stuff I’ve encountered so far is stuff I’ve seen before, positions I’ve already encountered and worked on, endgame principles I’m familiar with, etc., but not all of it is known stuff and I really like the structure of the book. There are a lot of pages left, and as it is I’m planning to read this book from cover to cover, which is something I usually do not do when I read chess books (few people do, judging from various comments I’ve seen people make in all kinds of different contexts).

Lastly, a lecture:

August 25, 2015 Posted by | Biology, Books, Chess, language, Lectures, Personal, Psychology, Statistics | 2 Comments