I like this book, it’s quite good. Some more quotes:
“Perhaps one of the most useful contributions of understanding the patterns of regional brain activity that characterize personality traits and clinical syndromes is the potential insight it provides into individual differences in cognitive capabilities and styles. Numerous studies have shown that activity in regions of the cortex specialized for particular modes of information processing predicts performance on tasks that benefit from that type of computation. In the vast majority of studies […] increased activity is associated with better performance, whereas deficient activity is associated with decrements in performance. […] Both anxious apprehension and anxious arousal types of anxiety, as well as depression, are characterized by specific cognitive biases and impairments […] Anxiety in general has been strongly associated with an attentional bias to threatening stimuli […] We have argued that these attentional biases toward threat-related stimuli dovetail with specializations of the right posterior region for visual and spatial attention, vigilance, and autonomic arousal, reflecting the activity of an emotional surveillance system (Nitschke et al., 2000). Our recent fMRI research suggests that this area may include temporal, parietal, and occipital regions of the right hemisphere (Compton et al., 2001; Miller, 2000). […] In depression, deficits have been described for explicit memory, executive functions, and visuospatial skills […] We have argued that decreased activity in prefrontal brain regions can account for many of the cognitive impairments in depression, including memory for material on tasks that require or benefit from information-organizing strategies, the ability to access errors accurately, problem solving, and cognitive flexibility. Depression has also been consistently associated with impairments on tasks associated with right posterior regions of the brain (e.g., Deldin, Keller, Gergen, & Miller, 2000; Keller et al., 2000; for review of earlier studies, see Heller & Nitschke, 1997). These findings are consistent with evidence that there is decreased activity in these brain regions (Banich et al., 1992; Liotti & Tucker, 1992; Otto, Yeo, & Dougher, 1987).” (from chapter 4)
“Schmidt (1999) reported that left and right anterior brain activity is differentially associated with sociability and shyness, respectively. From an incentive–threat perspective, sociability reflects an incentive-oriented view of other individuals (often major sources of reward), whereas shyness reflects a threat-oriented view of others (often, also, major sources of punishment). […] Henriques and Davidson (1990, 1991) have shown that currently or previously depressed individuals (i.e., those who present a significant lack of incentive motivation) exhibit relatively less resting left frontal activity. In summary, there is a substantial set of studies demonstrating links between left- and right-sided anterior cortical activity with incentive and threat motivation sensitivity, respectively. […] Given that one component of motivation is the detection, selection, and orientation toward incentives and threats, it appears likely that individual differences in the strength of these two systems would influence information processing in a way that is consistent with the stronger of the two systems under circumstances in which other factors are controlled for. [This hypothesis has been tested and it holds, at least to some extent. Such biological differences may be used to explain part of the inter-individual variation in e.g. risk preferences – US.]” (from chapter 5)
“In the models of development as they are related to personality, we use a combination of approaches. Here I consider three models of the development of personality: a trait or status model, a contextual or environmental model, and an interactional model. […] The trait or status model is characterized by its simplicity. It holds to the view that a trait, or the status of the child at one point in time, is likely to predict a trait or status at a later point in time. A trait model is not interactive and does not provide for the effects of the environment. In fact, in the most extreme form, the environment is thought to play no role either in effecting its display or in transforming its characteristics. A particular trait may interact with the environment, but the trait is not changed by that interaction. […] The prototypic environmental model holds that exogenous factors influence development. Two of the many problems in using this model are (1) our difficulty in defining what environments are and (2) the failure to consider the impact of environments throughout the lifespan. In fact, the strongest form of the developmental environmental or contextual model argues for the proposition that adaptation to current environment throughout the life course has a major influence on our behavior and on our personalities. Moreover, such a model is familiar to students of personality because it represents the idea that context, to a large degree, determines behavior. As environments change, so too does the individual (Lewis, 1997). This dynamic and changing view of environments and adaptation is in strong contrast to the earlier models of environments as forces that act on the individual and that act on the individual only in the early years of life. […] in the study of personality development, even though we recognize that environments can cause both normal and abnormal behavior, we prefer to treat the person—to increase coping skills or to alter specific behaviors—rather than to change the environment (Lewis, 1997). Yet we can imagine the difficulties that are raised when we attempt to alter specific maladaptive behaviors in environments in which such behaviors are adaptive […] The general environmental model that I have suggested (Lewis, 1997) holds that children’s behavior always is a function of the environment in which the behavior occurs, because the task of the individual is to adapt to its current environment.1 As long as the environment appears consistent, the child’s behavior will be consistent; if the environment changes, so, too, will the child’s behavior. It is the case that maladaptive environments produce both normal and abnormal behavior. From a developmental point of view, I would hold that maladaptive behavior is caused by maladaptive environments; if we change those environments, we may be able to alter the behavior. […]
Although the trait model is most often used in research, the interactional model is usually held to be the one which, from a theoretical point of view, is most likely to account for the development and change in personality. This mismatch between theory and research has serious implications for the growth of our knowledge about human development. Interactional models vary; some researchers prefer to call them “interactional” and others “transactional” (Lewis, 1972; Sameroff & Chandler, 1975). All these models have in common the role of both child and environment in determining the course of development. In these models, the nature of the environment and the characteristics or traits of the child are needed to explain concurrent, as well as subsequent, behavior and adjustment. Such models usually require an active child and an active environment; however, they need not do so. What they do require is the notion that behavior is shaped by its adaptive ability and that this ability is related to environments. Maladaptive behavior may be misnamed because the behavior may be adaptive to a maladaptive environment. […] Although there is some evidence in the developmental literature for an interactional approach, the data are not that strong (Lewis, 1999c). Moreover, without a consideration of the environment over time, it is still relatively unproven whether any interactional model accounts for more of the variance than does an environmental model alone. As is discussed subsequently, without the proper environmental measurement, any serious test of the various developmental models is not possible. […]
earlier traits or characteristics have little relation to later personality characteristics and […] the concurrent environment is most predictive of these characteristics. These results, in general, hold across most longitudinal studies. It has been labeled a simplex pattern, as prediction grows weak as the two age points increase in time. […] I have approached the topic of continuity and discontinuity of personality characteristics by looking at the data in the early period of the lifespan. How do the data for the earlier part of the lifespan, the first two dozen years, agree with the data obtained across the whole lifespan? There appears to be general agreement that the correlations (or stability) of personality characteristics are quite low for the first 30–40 years of life but become stronger at later ages (Caspi & Roberts, 2001). This is explained in such terms as crystallization (Caspi & Roberts, 2001) […] As a field, we have argued for a very powerful hypothesis. We have argued that personality characteristics of individuals are enduring across time and context. In this chapter, I have raised the question of whether or not the data from the past 75 years of development and study supports this powerful hypothesis. It is not supported in the first third of life, and the correlations are, overall, rather weak for the rest of the lifespan.” (from chapter 6)
“From biological perspectives, phenotypic (and thereby genotypic) variability is the raw material on which natural selection operates. Selection in general is seen as a homogenizing force that culls less optimal variants in favor of those that foster survival and reproduction (Willams, 1966). Members of any population differ from one another in what is seen as largely inconsequential ways; individual differences are noise in the evolutionary process that results from nonselective mechanisms such as mutation, recombination, and drift. Studies in evolutionary psychology accordingly focus on topics such as mate selection, with little consideration for individual-difference variables […] This species-general approach to evolutionary psychology confronts long-held beliefs in other fields of psychology that individual differences are anything but inconsequential. Personality theorists, for example, have long shown how individual differences are related to adaptation across the lifespan. Only more recently has it been suggested that these differences are themselves related to reproductive success […] Work in behavioral genetics has shown that a good portion of this variation in personal characteristics is heritable Heritability is often considered to support evolutionary arguments, as “adaptations” must have a genetic component. Paradoxically, however, the more the variability in a population on a certain trait is due to genetic differences (i.e., heritability), the less likely it is that the trait is an “adaptation.” Naturally selected adaptations tend to have by definition very low heritabilities because there is little variation across individuals (e.g., a four-chambered heart). In other words, “heritable diversity is inversely proportional to adaptive importance” (Tooby & Cosmides, 1990, p. 49). [This is not news to me, but this is an important point perhaps not all readers are familiar with – US] […]
Similar to several personality theories, theories of motivation […] and models of social competence […] resource control theory has the balancing of self and other goals at its core. This theoretical perspective is based on the assumption that humans, like other social species, should optimally behave in ways that facilitate personal resource acquisition while at the same time maintaining friendly bonds with other group members. The necessity of meeting one’s needs and simultaneously being a good group member underlies the evolution of much of human behavior and psychological organization: It implies that individuals must balance being egoistic and other-oriented […] the presence of others intensifies intragroup competition for the very resources that the group acquires. In other words, “cooperative” relationships are inevitably contaminated by competition. […]
McGuire and associates […] have demonstrated that hierarchy ascendance is associated with serum serotonin elevations (Brammer, Raleigh, & McGuire, 1994; McGuire, Raleigh, & Brammer, 1984). In the presence of others, top-ranked male vervets had higher than average serotonin levels. When removed from the group, they returned to normal levels (i.e., dominance requires the presence of others). In the absence of the reigning alpha, a new male rose in the hierarchy and, accordingly, enjoyed elevated serotonin until the reigning male returned. The authors concluded that elevated serotonin was both a cause and effect of successful ascendance. The effects of serotonin on mood and behavior are well known: Low levels of serotonin are associated with low self-esteem, anxiety, and depression. Pharmacologically enhanced serotonin (e.g., serotonin reuptake inhibition) decreases anxiety and increases sociability and assertiveness […] In a similar vein, social subordinance in nonhuman primates has been linked with hypercortisolism, an exaggerated stress response (Sapolsky, Alberts, & Altmann, 1997). […]
Shahar, Grob, and Little (2001) examined the relationship between depression and the reported attainment of the goal of achieving an intimate relationship. In young adulthood (ages 18–39), there were no differences on depression—males and females who either had or had not achieved intimate-relationship status were similar in their low levels of depressive symptomology. In mid-age, on the other hand, substantial gaps appeared to emerge; in fact, all four groups differed. Males who had not attained intimate-relationship status showed the highest levels of depression, followed by females who had not, then males who had, and then females who had. By old age, the gender differences disappeared, but the effect of either having attained or not having attained an intimate relationship was pronounced. Those persons who had not established an intimate relationship reported greater depressive symptoms than those who had achieved intimacy with another person.” (from chapter 7)
“Most studies assume that genetics and individual family environment represent the only two influences on personality traits. […] [Many] authors seem to assume that the environment stops at the door of the family home. As many theorists and researchers have argued, the larger sociocultural environment can have a substantial effect on personality and development […] Examining “nonshared” environment (Plomin & Daniels, 1987) does not solve this problem, because twins (identical or fraternal) are necessarily the same birth cohort; thus the larger sociocultural environment is still “shared” environment (but “shared” environment outside of the family). Thus birth cohort might be a nongenetic explanation for the similarity between identical twins raised apart. […] The fact that twins share a birth cohort also means that these studies have likely overestimated the heritability estimates for personality traits. Almost all of the studies examining genetic and environmental effects on personality have included samples of only one birth cohort (or samples very close in birth cohort). If more cohorts were included, then the variance in personality would likely increase. […]
Working with my colleague Keith Campbell, I performed a metaanalysis on college students’ scores on the Rosenberg Self-Esteem Scale (RSE) between 1968 and 1994. We found that college students’ self-esteem scores increased about two thirds of a standard deviation over this 26-year period (Twenge & Campbell, 2001). Thus 1990s college undergraduates scored considerably higher in self-esteem than had their late-1960s counterparts. It is possible that today’s undergraduates actually do feel better about themselves compared with the college students of the 1960s. It could also be that college students now speak the language of self-esteem and understand that one is supposed to possess copious amounts of this supposedly precious substance. […] In sum, the societal trend has been toward meeting new people more often and toward more fluid and changeable relationships. In this world, being extraverted is no longer a quirk of genetics; it is a virtual requirement (e.g., Whyte, 1956). When you are expected to leave your birth family at a young age and create an entirely new support system of your own, being outgoing becomes essential. Extraversion, in its classic form, is not simply about liking to be with people; it is about liking to be with many people (such as at a party) and being comfortable meeting new people. In modern society, both family and career depend, at least in part, on being extraverted. The available evidence suggests that extraversion began to increase in American college students beginning in the late 1960s. In a recent paper (Twenge, 2001a), I found that American undergraduates scored 0.79 to 0.97 standard deviations higher on extraversion scales in 1993 than in 1966 (the measures were the Extraversion scales of the Eysenck Personality Inventory and the Eysenck Personality Questionnaire). […] During the most recent time period included in [Twenge, 2001b], sex differences in assertiveness decreased from a male advantage of 0.40 standard deviations in 1968 to no difference (d = –.07) in 1993. Thus assertiveness, once a solid sex difference favoring men, is now a personality trait with no discernible differences between men and women.” (from chapter 8)
Here’s the link to the article. I’d missed this one, even if it’s a few years old (from December 2008). It is a great article and it covers a lot of stuff – I’ve decided to quote extensively from it below:
“Glycemic control, a worthwhile goal for people with diabetes, is limited by the barrier of iatrogenic hypoglycemia (1). Iatrogenic hypoglycemia 1) causes recurrent morbidity in most people with type 1 diabetes and many with advanced type 2 diabetes and is sometimes fatal, 2) compromises physiological and behavioral defenses against subsequent falling plasma glucose concentrations and thus causes a vicious cycle of recurrent hypoglycemia, and 3) precludes maintenance of euglycemia over a lifetime of diabetes and therefore full realization of the vascular benefits of glycemic control. […] Unfortunately, maintenance of euglycemia over a lifetime of diabetes cannot be accomplished safely with currently available treatment methods because of the barrier of hypoglycemia (1). […]
Hypoglycemia is a fact of life for most people with type 1 diabetes (1). The average patient has untold numbers of episodes of asymptomatic hypoglycemia and suffers two episodes of symptomatic hypoglycemia per week (thousands of such episodes over a lifetime of diabetes). He or she suffers one or more episodes of severe, temporarily disabling hypoglycemia, often with seizure or coma, per year. There is no evidence that this problem has abated over the decade and a half since it was highlighted by the report of the DCCT (2) in 1993. For example, in 2007 the U.K. Hypoglycemia Study Group (9) reported an incidence of severe hypoglycemia of 110 episodes per 100 patient-years (nearly twice that in the DCCT) in patients with type 1 diabetes, who were necessarily treated with insulin, for <5 years and an incidence of 320 episodes per 100 patient-years in those with type 1 diabetes for >15 years. […]
Although they represent only a small fraction of the total hypoglycemia experience, estimates of the frequency of severe hypoglycemia, particularly if determined in prospective, population-based studies, are the most reliable because they are dramatic events that are more likely to be reported (by the patient or an associate) (1). The prospective, population-based data of Donnelly et al. (10) indicate that the overall incidence of hypoglycemia in insulin-treated type 2 diabetes is approximately one-third of that in type 1 diabetes. The incidence of any and of severe hypoglycemia was ∼4,300 and 115 episodes per 100 patient-years, respectively, in type 1 diabetes and ∼1,600 and 35 episodes per 100 patient-years, respectively, in insulin-treated type 2 diabetes. In addition, in population-based studies the incidence of severe hypoglycemia requiring emergency treatment in insulin-treated type 2 diabetes was ∼40% (11) and ∼100% (12) of that in type 1 diabetes. Since the prevalence of type 2 diabetes is ∼20-fold greater than that of type 1 diabetes, and most people with type 2 diabetes ultimately require treatment with insulin, these data suggest that most episodes of iatrogenic hypoglycemia, including severe hypoglycemia, occur in people with type 2 diabetes. […]
Iatrogenic hypoglycemia causes recurrent physical and psychological morbidity and some mortality, impairs defenses against subsequent hypoglycemia, and precludes maintenance of euglycemia over a lifetime of diabetes (1). Hypoglycemia causes brain fuel deprivation that, if unchecked, results in functional brain failure that is typically corrected after the plasma glucose concentration is raised (13). Rarely, it causes sudden, presumably cardiac arrhythmic death or, if it is profound and prolonged, brain death (13). To the extent that there is a macrovascular benefit of glycemic control (6), the barrier of hypoglycemia also contributes to cardiovascular morbidity and mortality.
The physical morbidity of an episode of hypoglycemia ranges from unpleasant symptoms to seizure and coma (1). Hypoglycemia can impair judgment, behavior, and performance of physical tasks. Permanent neurological damage is rare. While there is concern that recurrent hypoglycemia might cause chronic cognitive impairment, long-term follow-up of the DCCT patients is largely reassuring in that regard (14). […]
Three early reports indicated that 2–4% of people with diabetes die from hypoglycemia (1). More recent reports indicated that 6% (14), 7% (15), and 10% (16) of deaths of people with type 1 diabetes were the result of hypoglycemia. Up to 10% of episodes of severe sulfonylurea-induced hypoglycemia in type 2 diabetes may be fatal (17). [my emphasis, US]
In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, 10,251 patients with type 2 diabetes at high cardiovascular risk (but with no history of frequent or recent serious hypoglycemic events) were randomized to either intensive glycemic therapy with an A1C goal of <6.0% or to standard glycemic therapy (7). After a median follow-up of 3.4 years, with stable median A1C levels of 6.4 and 7.5%, respectively, intensive glycemic therapy was discontinued because 5.0% of the patients in the intensive therapy group, compared with 4.0% of those in the standard therapy group, had died. […] the most plausible cause of excess mortality during intensive therapy in the ACCORD study is iatrogenic hypoglycemia […]
Glucose is an obligate oxidative fuel for the brain under physiological conditions (1). The brain accounts for >50% of whole-body glucose utilization. The brain can oxidize alternative fuels, such as ketones, if their circulating levels rise high enough to enter the brain in quantity, but that is seldom the case. Because it cannot synthesize glucose, utilize physiological levels of circulating nonglucose fuels effectively, or store more than a few minutes supply of glucose as glycogen, the brain requires a virtually continuous supply of glucose from circulation. Since facilitated blood-to-brain glucose transport is a direct function of the arterial plasma glucose concentration, that supply requires maintenance of plasma glucose concentration. At some level of hypoglycemia (perhaps ∼50–55 mg/dl [2.8–3.1 mmol/l] since symptoms normally occur at that level [19–21]), blood-to-brain glucose transport becomes limiting to brain glucose metabolism and, therefore, function. […]
Early in the course of type 2 diabetes, by far the most common type of diabetes, hyperglycemia may respond to lifestyle changes, specifically weight loss, or to plasma glucose–lowering drugs that should not, and probably do not, cause hypoglycemia. In theory, when such drugs are effective in the absence of side effects, there is no reason not to accelerate their dosing until euglycemia is achieved. Over time, however, as people with type 2 diabetes become progressively more insulin deficient, these drugs, even in combination, fail to maintain glycemic control. Insulin secretagogues are also effective early in type 2 diabetes, but they can cause hyperinsulinemia and therefore introduce the risk of hypoglycemia. Euglycemia is not an appropriate goal during therapy with an insulin secretagogue or with insulin in people with type 2 diabetes. Nonetheless, as discussed earlier, the frequency of hypoglycemia is relatively low (at least with current glycemic goals that are above the euglycemic range) during treatment with an insulin secretagogue, or even with insulin, early in type 2 diabetes (9) when defenses against hypoglycemia are intact. Thus, over much of the course of the most common type of diabetes it is possible to achieve a meaningful degree of glycemic control with no risk or relatively low risk of hypoglycemia. The challenge is greater in people with advanced type 2 diabetes or type 1 diabetes because of compromised defenses against hypoglycemia. In such patients, therapy with insulin is demonstrably effective, but it is not demonstrably safe. Nonetheless, concerns about hypoglycemia should not be used as an excuse for poor glycemic control by patients or their caregivers. Both should strive to achieve and maintain the greatest degree of glycemic control that can be accomplished safely in a given person with diabetes at a given stage of the progression of his or her diabetes.”
For diabetics, especially type 1 diabetics, there’s a very real risk that the (life-saving and non-optional) treatment may kill the patient. All this stuff above may sound very theoretical, but it’s not. It’s quite simple, really: For me personally, pretty much every time I eat a meal I have a decision to make. I have to take some insulin to enable my body to process the carbohydrates in the meal, and I need to estimate how big of a dosis is optimal. ‘The barrier of hypoglycemia’ is the reason why even though ‘my problem’ is that I don’t produce insulin I can’t just take a ‘big enough’ dosis of insulin when that stuff is needed and solve the problem that way without having to worry – the point is that if the dosis I take is ‘too big’, I’ll get hypoglycemia. And if it’s not ‘big enough’ I may not necessarily get symptoms, but I’ll still harm my body and increase the risk of complications later on (and if I consistently take too little on a day to day basis, the long-term risk will go up a lot). It’s simply impossible to ‘get it just right every time’, it’s very easy to get it wrong among other things because the insulin’s therapeutic index is quite low, and the consequences of getting it wrong may be very severe – and the tradeoff is always there, every day, every meal. I know I’ve written about it before but a lot of people, even relatively well-informed people, I’ve talked to about my disease don’t know this, and this tradeoff really is at the very heart of what living with diabetes is all about.
I’m currently reading this book. A quote from the beginning of the first chapter which made me question if I should even keep on reading:
“we urge sensitivity to the potential limitations of some traditional scientific methods. The most distinguishing feature of persons is that they construct meaning by reflecting on themselves, the past, and the future. Many writers have questioned the assumptions that meaning construction can be adequately captured by the traditional methods of natural science or that persons can be construed as a collection of quantifiable personality variables that index essential qualities of the individual (Geertz, 1973, 2000; Polkinghorne, 1988; Shweder, 2000; Shweder & Sullivan, 1990; Taylor, 1989). They discourage the positing of abstract global tendencies, urging instead that personal qualities be studied within the specific physical, social, and cultural contexts that comprise the individual’s life (Kagan, 1998)—a theme that has been sounded by a variety of scholars throughout the history of the field (Shweder, 1999). These concerns are as much a part of personality science as are investigations that happily make these assumptions.”
I post this quote here to make clear that if they ‘go too much in that direction’ I’ll just stop reading (related to Miao’s recent comment). I’m not interested in crap, I’m interested in the science. But on another note, if that quote had made me stop reading I’d have missed out on some good stuff – so far it’s mostly been about the science. They haven’t gone too far in the other direction yet – actually chapter 2 was quite technical – and I’ve read about a third of the book at this point. Chapter 2 was interesting, but if I had to quote from that one (In Search of the Genetic Engram of Personality) I’d have to include a lot of quotes like: “studies have generated mixed results” and “studies […] have produced negative results”, “The results of these studies have been mixed” etc. – not a lot of convincing and ‘obviously true’ findings have surfaced yet; as the authors put it: “So what can be said to summarize the discussion in this chapter? In short, the story is complex.” I found chapter 3, on Individual Differences in Childhood Shyness to be quite interesting too, and I’ll quote a bit from that below – it’s interesting also because stuff like this seems far more relevant to me (and perhaps also a few of the readers?) than does stuff on, say, the genetics of bipolar disorder or -schizophrenia (slightly related link).
So, what about that shyness stuff?
“Shyness reflects a preoccupation of the self in response to, or anticipation of, novel social encounters. Although shyness is a ubiquitous phenomenon that a large percentage of adults have reported experiencing at some point in their lives (Zimbardo, 1977), a smaller percentage of adults and children (around 10–15%) are consistently anxious, quiet, and behaviorally inhibited during social situations, particularly unfamiliar social situations (see Cheek & Buss, 1981; Kagan, 1994). […] many of these shy children exhibit a distinct pattern of behavioral and physiological responses during baseline conditions and in response to social challenge in infancy and through the early school-age years […]
Current thinking suggests that the origins of shy behavior may be linked to the dysregulation of some components of the fear system (LeDoux, 1996; Nader & LeDoux, 1999). Fear is a highly conserved emotion that is seen across mammals. It is the study of fear that has produced the most reliable evidence to date concerning the neuroanatomical circuitry of emotion. There is a rich and growing literature from studies of conditioned fear in animals that suggests that the frontal cortex and forebrain limbic areas are important components of the fear system. The frontal cortex is known to play a key role in the regulation of fear and other emotions. This region is involved in the motor facilitation of emotion expression, the organization and integration of cognitive processes that underlie emotion, and the ability to regulate emotions (see Fox, 1991, 1994). The frontal region also appears to regulate forebrain sites involved in the expression of emotion. The amygdala (and central nucleus) is one such forebrain/limbic site. There are demonstrated functional anatomical connections between the amygdala and the frontal region. […] The amygdala (particularly the central nucleus) is known to play a significant role in the autonomic and behavioral aspects of conditioned fear (LeDoux, Iwata, Cicchetti, & Reis, 1988). […]
“infants who exhibit a high degree of motor activity and distress in response to the presentation of novel auditory and visual stimuli during the first 4 months of life exhibit a high degree of behavioral inhibition and shyness during the preschool and early school-age years. There is, in addition, evidence to suggest that there may be a genetic etiology to inhibited behavior. […]
In a series of studies with adults, Davidson and his colleagues have noted a relationship between the pattern of resting frontal EEG activity and affective style. Adults who exhibit a pattern of greater relative resting right frontal EEG activity are known to rate affective film clips more negatively […] and are likely to be more depressed […] than adults who exhibit greater relative resting left frontal EEG activity. […] The startle response is a brain-stem- and forebrain-mediated behavioral response that occurs to the presentation of a sudden and intense stimulus, and its neural circuitry is well mapped (Davis, Hitchcock, & Rosen, 1987). Although the startle paradigm has been used extensively in studies of conditioned fear in animals, this measure has been adapted for studies concerning the etiology of anxiety in humans. […] individual differences in the startle response are linked to affective style. For example, adults who score high on trait measures of anxiety (Grillon, Ameli, Foot, & Davis, 1993) and children who are behaviorally inhibited (Snidman & Kagan, 1994) are known to exhibit a heightened baseline startle response. […]
These data [too many findings to quote here] suggest that children who are classified as temperamentally shy during the preschool and early school-age years exhibit a distinct pattern of frontal brain activity, heart rate, and salivary cortisol levels during baseline conditions and in response to stress. […]
One of the goals of our research program on shyness has been to examine the developmental course and outcomes of temperamental shyness beyond the early childhood years, given that temperamental shyness appears to remain stable and predictive of developmental outcomes (Caspi et al., 1988). Overall, the behavioral and physiological correlates and outcomes associated with temperamentally shy children are comparable with those seen in adults who score high on trait measures of shyness. For example, adults who report a high degree of trait shyness are likely to report concurrent feelings of negative self-worth and problems with depression in both elderly (Bell et al., 1993) and young (Schmidt & Fox, 1995) adult populations and to display a distinct pattern of central and autonomic activity during resting conditions and in response to social stressors (see Schmidt & Fox, 1999, for a review). […]
Not all temperamentally shy adults or children are alike. Our research suggests that different etiologies, correlates, and developmental outcomes are associated with individual differences in temperamental shyness […] Cheek and Buss (1981) described at least two types of shyness in undergraduates: individuals who are shy and low in sociability and individuals who are shy and high in sociability. […]
Buss(1986) presented a theory in which he argued that there may be at least two types of shyness: an early-developing fearful shyness that is linked to stranger fear and wariness (perhaps analogous to the behaviorally inhibited children described by Kagan, 1994) and a later-developing self-conscious shyness that is linked to concerns with self-presentation. Little empirical research, however, has been done to substantiate Buss’s theoretical model. Two studies that do exist in the literature have found support for Buss’s claim in young adults. […] Schmidt and Robinson (1992) found differences in self-esteem between the two shyness subtypes; the fearfully shy group reported significantly lower self-esteem than the self-consciously shy and nonshy groups. […]
Cheek and Buss argued that people avoid social situations for different reasons. Some people avoid social situations because they experience fear and anxiety in such situations (i.e., they are shy); others avoid social situations because they prefer to be alone rather than with others (i.e., they are introverted). Cheek and Buss (1981) then noted that if shyness is nothing more than low sociability, then the two traits should be highly related such that being high on one trait means being low on the other. The extent to which they might be orthogonal was an empirical question. Cheek and Buss (1981) noted that the two traits were only modestly related, and they were able to distinguish them on a behavioral level. High shy–high social undergraduates exhibited significantly more behavioral anxiety than did undergraduates who reported other combinations of shyness and sociability.
We (Schmidt, 1999; Schmidt & Fox, 1994) examined the extent to which shyness and sociability were distinguishable on electrocortical and autonomic measures. Using a design identical to that reported by Cheek and Buss (1981), we attempted to distinguish shyness and sociability on regional EEG, heart rate, and heart rate variability measures collected during baseline and during a social stressor. We found that high shy–high social (i.e., the conflicted subtype) undergraduates exhibited a significantly faster and more stable heart rate than high shy–low social (i.e., the avoidant subtype) participants in response to an anticipated unfamiliar social situation (Schmidt & Fox, 1994). […] the two subtypes were distinguishable based on the pattern of activity in the left, but not the right, frontal area. High shy–high social (the conflicted subtype) participants exhibited significantly greater activity in the left frontal EEG lead than did high shy–low social (the avoidant subtype) participants. A similar pattern of resting frontal EEG activity has been found in high shy–high social and high shy–low social 6-year-olds (Schmidt & Sniderman, 2001) […] These sets of findings, taken together, suggest that different types of shyness are distinguishable on behavioral, cortical, and autonomic levels during baseline conditions and in response to social challenge. […]
We speculate that genes that code for the transportation of serotonin may play an important role in the regulation of some components of the fear system, which includes the frontal cortex, forebrain limbic area, and HPA system. Serotonin has been implicated as a major neurotransmitter involved in anxiety and withdrawal (Westernberg, Murphy, & Den Boer, 1996). Some temperamentally shy individuals may possess a genetic polymorphism that contributes to a reduced efficiency of the transportation of serotonin. Such a genetic polymorphism has been noted in adults who score high on measures of neuroticism (Lesch et al., 1996). […] The reduction of serotonin contributes to overactivation of the amygdala and the HPA system in some individuals. The overactive amygdala stimulates the HPA system and the release of increased cortisol. This increase in cortisol may contribute to the pattern of frontal EEG activity noted early between shyness subtypes. […]
When the two shy subtypes encounter actual or perceived social stress, there is an increase in heart rate, cortisol, and frontal EEG activity. The two subtypes will differ, however, in the pattern of behavior and left frontal EEG activity. The shy–social subtype will experience an approach-avoidance conflict and a greater increase in left frontal EEG activity; the shy–low-social subtype will not experience the same conflict, as they do not have the same need to affiliate. Thus this subtype will tend to avoid social situations and will not present with the same pattern of left frontal EEG activity, although they may evidence an increase in cortisol and heart rate. […] we believe that the conflicted and avoidant subtypes may be on different pathways of developmental problems. Conflicted children are likely to be highly reticent, desiring to be a part of the peer group but having problems doing so and, we think, might be on a pathway to social anxiety; the avoidant child, on the other hand, may have problems simply engaging in any social situations and may avoid them all together, desiring instead to be alone, and, we think, on a pathway to social withdrawal and depression.”
As already mentioned, so far the book has been quite interesting. We’re complicated creatures and this kind of stuff is stuff you can add to the list of things you do not think about but which still have major consequences for how you live your life, what you feel about the life you live, and where you end up.
This book is crap, stay away from it. It’s very short, which was the only reason why I actually read it cover to cover. Kosso neglects some very important points you’d want to see in a publication like this; on the list of recommended reading he includes Kuhn but not Popper, and Popper’s name isn’t even mentioned. Presumably because he disagrees with Popper about the importance of falsification. Conceptually he doesn’t talk about and doesn’t seem to understand how crucial is the requirement in science that you restrict the (potential) outcome space when forming hypotheses. He picks out history and archaeology as examples of ‘social sciences’; maybe because that’s the closest he’s ever been to the social sciences? He talks about how experimental designs can play a role here, but doesn’t include a single word about the role of statistics in scientific disciplines.
I’d probably give it 1 out of 5 on amazon. He reads as if he doesn’t have a clue. The only good thing about the book is that it is quite short.
I have started reading Hoyt’s New Cyclopedia Of Practical Quotations and some of the quotes below are from that work. I may blog the book later, but I assume that given the amount of quotes in that work I may just decide to incorporate some of the good quotes from the book into future quotes posts without actually doing a lot of talking about the book itself here on the blog (I’ve handled other books of a similar nature in a similar manner in the past). Of course as you may be aware I’ve already used a lot of quotes which are also included in this book in past quotes posts; I should probably make clear – again – that I do try quite hard to avoid reposting quotes that I’ve already covered elsewhere. I should note also that I ‘read’ this book in a different way from how I read e.g. The Oxford Book of Aphorisms; there are a lot of crappy quotes in this book, and I’m not going to spend a lot of time reading about what religious nutters have said about Angels or Jesus, or perhaps what people who lived 200 years ago wrote about gardens, or butterflies, or mermaids. Especially as quite a few of the quoted writers had an annoying habit of being wearisomely verbose. Anyway, some quotes:
i. “Adversity is sometimes hard upon a man; but for one man who can stand prosperity, there are a hundred that will stand adversity.” (Carlyle)
ii. “I am certain there is too much certainty in the world.” (Michael Crichton)
iii. “We must daily decide whether the threats we face are real, whether the solutions we are offered will do any good, whether the problems we’re told exist are in fact real problems, or non-problems. Every one of us has a sense of the world, and we all know that this sense is in part given to us by what other people and society tell us; in part generated by our emotional state, which we project outward; and in part by our genuine perceptions of reality. In short, our struggle to determine what is true is the struggle to decide which of our perceptions are genuine, and which are false because they are handed down, or sold to us, or generated by our own hopes and fears.” (-ll-)
iv. “A politician is someone who promises you a bridge, even when there is no river.” (Gregory David Roberts, Shantaram)
v. “What makes old age so sad is, not that our joys but that our hopes cease.” (Jean Paul)
vi. “We all, when we are well, give good advice to the sick.” (Terence)
vii. “Affectation is an awkward and forced imitation of what should be genuine and easy, wanting the Beauty that accompanies what is natural.” (Locke)
viii. He who boasts of his descent, praises the deeds of another. (Seneca)
ix. “Nothing is more dishonourable than an old man, heavy with years, who has no other evidence of his having lived long except his age.” (-ll-)
x. “A crowd of fellow-sufferers is a miserable kind of comfort.” (-ll-)
xi. “Most people would succeed in small things if they were not troubled with great ambitions.” (Henry Wadsworth Longfellow)
xii. “Be always displeased at what thou art, if thou desire to attain to what thou art not; for where thou hast pleased thyself, there thou abidest.” (Francis Quarles)
xiii. “Ambition has but one reward for all:
A little power, a little transient fame,
A grave to rest in, and a fading name!” (William Winter, according to Hoyt’s… – often (seemingly) incorrectly attributed Walter Savage Landor)
xiv. “Predominant opinions are generally the opinions of the generation that is vanishing.” (Benjamin Disraeli)
xv. “Fear not the anger of the wise to raise;
Those best can bear reproof who merit praise.” (Pope)
xvi. “Apes are apes though clothed in scarlet.” (Ben Jonson)
xvii. ““We all know dogmatists who are more concerned about holding their opinions than about investigating their truth. … if they are mistaken, they will never discover it; they have condemned themselves to perpetual error. Human beings (including myself) sometimes use their beliefs for wish-fulfillment. Too often we believe what we want to be true.” (David Wolfe)
xviii. “That writer does the most, who gives his reader the most knowledge, and takes from him the least time.” (Charles Caleb Colton)
xix. “No author ever drew a character, consistent to human nature, but what he was forced to ascribe to it many inconsistencies.” (Edward Bulwer-Lytton)
xx. “As we advance in life we learn the limits of our abilities.” (James Froude)
By Edwards, Foster & Sanders. I’m currently finishing this book.
I’m pretty sure nobody who’s reading this blog semi-regularly will want to read this book; unless you’re a diabetic or a health care provider working with diabetics I guess it’s not easy to come up with a lot of good reasons why you should read it. But I decided to blog it anyway. If you do decide to read it, unless you’re used to medical textbooks I’d advise you to schedule your reading so that you only open this book when it’s been a while since you’ve last eaten; unless you’re at least somewhat desensitized to this kind of stuff (like I am at this point..) you’ll probably want to vomit after looking at some of the pictures in this book. This book covers everything from ‘Stage 1: The normal foot’ to ‘Stage 6 – The unsalvageable foot’. Good luck guessing what the latter looks like – if you don’t want to guess you can go here for images of a similar nature.
I know a lot more about the subject than I used to do at this point, but not all of this was new stuff to me – I’ve covered related matters before here on the blog, for instance here. However most of the stuff I’ve read in the past related to ‘epidemiology’, whereas I have not spent much time dealing with the actual disease process – what’s going on when the foot ‘goes bad’, how it may happen, what can be done about it, etc. – and here the book most certainly delivers.
I figure some curious diabetic googlers may stumble upon this article later on, and so it makes sense here to emphasize one thing before going any further – a point the authors of the book emphasize as well: There is no such thing as a trivial lesion of the diabetic foot; all foot problems need early diagnosis and appropriate intervention. If you’re a diabetic even a small wound/ulcer on your foot indicate that you’re (at least…) in stage 3 of their 6 stage categorization system. Next step after that is the infected foot, and the step after that one involves necrosis. You do not want to go there. What I found really surprising was the asymmetry between the time it takes for damage to be caused and the time it takes to heal that damage afterwards; necrosis can develop really fast, but healing may on the other hand take a very long time, especially if rapid and effective intervention is not undertaken at the early stage of the disease process – for example: “The average amount of time spent in a cast by diabetic patients with Charcot’s osteoarthropathy is 6 months but some patients may need a cast for over a year.” And here’s another related fact: “In our experience, fractures in stage 2 and higher stage diabetic feet take two or three times as long to heal as they do in low-risk or normal feet. Many health-care professionals appear to be unaware of this.”
I found the patient case studies particularly interesting, because they somehow make it all much more concrete and tangible. Of course it’s nice to know that: “Throughout their lifetime 15% of patients will develop ulceration; 85% of amputations result from non-healing ulcers” – but the case studies somehow makes all of this a bit more ‘real’. I have posted some of them below. I would like to remind you that I am 27 years old and that I have had diabetes for over 25 years at this point.
“A 17-year-old girl with type 1 diabetes of 4 years’ duration was referred to the diabetic foot clinic for education. A paternal uncle had type 1 diabetes and neuropathic ulceration. Her background was a chaotic one of great poverty and social deprivation with a history of truanting and running away from home. Her HbAlc was 14%. She had frequent admissions to hospital for ketotic episodes and traumatic lesions to her heels and her navel which became infected. She was educated in foot care and footwear but continued to wear unsuitable shoes; she also frequently missed appointments at the diabetic clinic and diabetic foot clinic. However, she agreed to attend the clinic in emergency and to take antibiotics if her foot lesions became infected. She had no more admissions for foot problems, but subsequently developed severe neuropathy, proliferative retinopathy and end-stage renal failure and is currently on dialysis.” [Usually we think of chronic complications to diabetes mellitus as disease processes that only rear their ugly heads after many years, if not decades, with the illness; this case study is a good reminder that even relatively short time periods with poor metabolic control/compliance can have catastrophic consequences for the individual in question.]
“A 62-year-old lady with type 1 diabetes of 40 years’ duration, retinopathy and neuropathy went on holiday to Blackpool, removed her shoes and socks and sat in a deckchair on the beach for 3 h. Her head and torso were shaded by an umbrella but her feet and legs were exposed to the sun. She suffered a full-thickness burn on the dorsum of her right foot (Fig. 3.10). She was admitted to hospital for debridement and skin grafting and the foot healed in 6 weeks.”
Yes, you got that right – going to the beach for 3 hours lead to a burn that took 6 weeks to heal. Here’s a similar example:
“A 25-year-old male patient with type 1 diabetes mellitus of 14 years’ duration, profound neuropathy and endstage renal failure treated with dialysis, slept in a bed next to a central heating radiator. During the night, in his sleep, his leg slipped against the radiator. He sustained full-thickness burns to his leg, but only attended the diabetic foot clinic when these became malodorous. There was a moist leathery eschar with purulent discharge. He was admitted to hospital for intravenous antibiotics. The burns were surgically debrided and split-skin grafts applied from a donor site on his thigh. He healed in 5 months.”
Note how well the last three guys are doing – they’re all in their 40es:
“A 46-year-old man with type 1 diabetes of 33 years’ duration, end-stage renal failure treated by renal transplantation and severe neuropathy, received regular foot checks under a renal foot study protocol. Three days before he went on holiday to the Channel Islands his feet were routinely checked and nothing abnormal was discerned. Two weeks later he came to the clinic on his return from holiday to report that his foot was ‘a little swollen’. He reported no trauma to the foot, but had been walking more than usual on cobbled pavements. The foot was red, 5°C hotter than the contralateral foot and very swollen. X-ray revealed a Lisfranc’s fracture-dislocation and he developed a rockerbottom foot. He was treated in a total-contact plaster cast for 6 months following which he wore bespoke boots to accommodate his deformity.”
“A 40-year-old male with type 1 diabetes of 30 years’ duration, proliferative retinopathy treated with laser photocoagulation, sensory neuropathy and autonomic neuropathy including postural hypotension, developed an acute right mid-foot Charcot’s osteoarthropathy. Because of a previous episode of severe sepsis…”
“A 44-year-old woman with type 1 diabetes of 26 years’ duration, proliferative retinopathy, profound neuropathy and end-stage renal failure treated by renal transplant had her feet checked at monthly intervals at the renal unit as part of a research protocol. Her foot pulses were palpable. She was educated in foot care, foot inspections and early reporting of any problems. However, during a 3-year period she suffered nine separate episodes of foot trauma, none of which she reported early: they were detected at her renal unit appointment. Causes of trauma included blisters from ill-fitting shoes, picking at dry skin, pulling off pieces of nail and being ‘trodden on by a baby’. In the last episode she stubbed her toe while walking barefoot, did not report the injury and presented late to the renal unit with spreading cellulitis, wet necrosis and septicaemia. She was resuscitated and treated with intravenous antibiotics and underwent 1st ray amputation to remove the source of her sepsis. Despite this, her septicaemia progressed and became overwhelming and she suffered a cardiac arrest and could not be resuscitated.”
i. Better Colleges Failing to Lure Talented Poor, by David Leonhardt.
“Only 34 percent of high-achieving high school seniors in the bottom fourth of income distribution attended any one of the country’s 238 most selective colleges […] Among top students in the highest income quartile, that figure was 78 percent. […]
Among high-achieving, low-income students, 6 percent were black, 8 percent Latino, 15 percent Asian-American and 69 percent white […]
The researchers defined high-achieving students as those very likely to gain admission to a selective college, which translated into roughly the top 4 percent nationwide. Students needed to have at least an A-minus average and a score in the top 10 percent among students who took the SAT or the ACT.
Of these high achievers, 34 percent came from families in the top fourth of earners, 27 percent from the second fourth, 22 percent from the third fourth and 17 percent from the bottom fourth. (The researchers based the income cutoffs on the population of families with a high school senior living at home, with $41,472 being the dividing line for the bottom quartile and $120,776 for the top.) […]
If they make it to top colleges, high-achieving, low-income students tend to thrive there, the paper found. Based on the most recent data, 89 percent of such students at selective colleges had graduated or were on pace to do so, compared with only 50 percent of top low-income students at nonselective colleges.”
For people with access to nber papers, here’s the direct link to the study.
The p-value isn’t the only thing you should care about when evaluating small-N studies and larger N replication attempts. It shouldn’t be news, but lots of people get this stuff wrong. Do remember that even in the replication studies, N may be quite small.
“Seifert doubts we will ever have an injectable cocktail of molecules that triggers regeneration. There’s too much complexity in the transition from wound to blastema to new limb, he says. It will also be a lengthy process. […] “Even if a human could grow a limb back, it might take 15-20 years,” says Seifert. A finger might be more realistic.”
iv. New insights into differences in brain organization between Neanderthals and anatomically modern humans. Razib Khan’s blog has some comments in case you’re curious.
iv. ‘The 99% percent’ weren’t really all that representative, it seems: The Geospatial Characteristics of a Social Movement Communication Network:
“Social movements rely in large measure on networked communication technologies to organize and disseminate information relating to the movements’ objectives. In this work we seek to understand how the goals and needs of a protest movement are reflected in the geographic patterns of its communication network, and how these patterns differ from those of stable political communication. To this end, we examine an online communication network reconstructed from over 600,000 tweets from a thirty-six week period covering the birth and maturation of the American anticapitalist movement, Occupy Wall Street. We find that, compared to a network of stable domestic political communication, the Occupy Wall Street network exhibits higher levels of locality and a hub and spoke structure, in which the majority of non-local attention is allocated to high-profile locations such as New York, California, and Washington D.C. Moreover, we observe that information flows across state boundaries are more likely to contain framing language and references to the media, while communication among individuals in the same state is more likely to reference protest action and specific places and times. Tying these results to social movement theory, we propose that these features reflect the movement’s efforts to mobilize resources at the local level and to develop narrative frames that reinforce collective purpose at the national level.”
“we investigated the relation between cognitive performance and heart rate variability as a function of fitness level. We measured the effect of three cognitive tasks (the psychomotor vigilance task, a temporal orienting task, and a duration discrimination task) on the heart rate variability of two groups of participants: a high-fit group and a low-fit group. Two major novel findings emerged from this study. First, the lowest values of heart rate variability were found during performance of the duration discrimination task, compared to the other two tasks. Second, the results showed a decrement in heart rate variability as a function of the time on task, although only in the low-fit group. Moreover, the high-fit group showed overall faster reaction times than the low-fit group in the psychomotor vigilance task, while there were not significant differences in performance between the two groups of participants in the other two cognitive tasks. In sum, our results highlighted the influence of cognitive processing on heart rate variability. […] results suggested that the main benefit obtained as a result of fitness level appeared to be associated with processes involving sustained attention.”
N = 28, so it’s a small sample size. But at least the results “seem to support the idea that aerobic training produces selective benefits in cognitive performance.”
vi. How you behave online can tell (a lot? something? a bit? – people seem to disagree about how ‘impressive’ the findings are…) about who you are: Private traits and attributes are predictable from digital records of human behavior, by Kosinski, Stillwell & Graepel.
Figure 2 is probably the main figure from this paper – it “shows the prediction accuracy of dichotomous variables expressed in terms of the area under the receiver-operating characteristic curve (AUC), which is equivalent to the probability of correctly classifying two randomly selected users one from each class (e.g., male and female)”:
“Eighty percent of the antibiotics sold in the United States goes to chicken, pigs, cows and other animals that people eat, yet producers of meat and poultry are not required to report how they use the drugs — which ones, on what types of animal, and in what quantities. This dearth of information makes it difficult to document the precise relationship between routine antibiotic use in animals and antibiotic-resistant infections in people”
This is insane. I had no idea the problem in the US was this big.
viii. One of my guilty pleasures:
(If you just want to watch the chess, you can skip the first 3 minutes or so.)
i. Aedes Albopictus.
“The Tiger mosquito or forest day mosquito, Aedes albopictus (Stegomyia albopicta), from the mosquito (Culicidae) family, is characterized by its black and white striped legs, and small black and white striped body. It is native to the tropical and subtropical areas of Southeast Asia; however, in the past couple of decades this species has invaded many countries throughout the world through the transport of goods and increasing international travel. This mosquito has become a significant pest in many communities because it closely associates with humans (rather than living in wetlands), and typically flies and feeds in the daytime in addition to at dusk and dawn. The insect is called a tiger mosquito because its striped appearance is similar to a tiger. Aedes albopictus is an epidemiologically important vector for the transmission of many viral pathogens, including the West Nile virus, Yellow fever virus, St. Louis encephalitis, dengue fever, and Chikungunya fever, as well as several filarial nematodes such as Dirofilaria immitis. […]
Aedes albopictus also bites other mammals besides humans and they also bite birds. They are always on the search for a host and are both persistent and cautious when it comes to their blood meal and host location. Their blood meal is often broken off short without enough blood ingested for the development of their eggs. This is why Asian tiger mosquitoes bite multiple hosts during their development cycle of the egg, making them particularly efficient at transmitting diseases. The mannerism of biting diverse host species enables the Asian tiger mosquito to be a potential bridge vector for certain pathogens, for example, the West Nile virus that can jump species boundaries. […]
The Asian tiger mosquito originally came from Southeast Asia. In 1966, parts of Asia and the island worlds of India and the Pacific Ocean were denoted as the area of circulation for the Asian tiger mosquito. Since then, it has spread to Europe, the Americas, the Caribbean, Africa and the Middle East. Aedes albopictus is one of the 100 world’s worst invasive species according to the Global Invasive Species Database. […]
In Europe, the Asian tiger mosquito apparently covers an extensive new niche. This means that there are no native, long-established species that conflict with the dispersal of Aedes albopictus. […]
The Asian tiger mosquito was responsible for the Chikungunya epidemic on the French Island La Réunion in 2005–2006. By September 2006, there were an estimated 266,000 people infected with the virus, and 248 fatalities on the island. The Asian tiger mosquito was also the transmitter of the virus in the first and only outbreak of Chikungunya fever on the European continent. […]
Aedes albopictus has proven to be very difficult to suppress or to control due to their remarkable ability to adapt to various environments, their close contact with humans, and their reproductive biology.”
In case you were wondering, the word Aedes comes from the Greek word for “unpleasant”. So, yeah…
ii. Orbital resonance.
“In celestial mechanics, an orbital resonance occurs when two orbiting bodies exert a regular, periodic gravitational influence on each other, usually due to their orbital periods being related by a ratio of two small integers. The physics principle behind orbital resonance is similar in concept to pushing a child on a swing, where the orbit and the swing both have a natural frequency, and the other body doing the “pushing” will act in periodic repetition to have a cumulative effect on the motion. Orbital resonances greatly enhance the mutual gravitational influence of the bodies, i.e., their ability to alter or constrain each other’s orbits. In most cases, this results in an unstable interaction, in which the bodies exchange momentum and shift orbits until the resonance no longer exists. Under some circumstances, a resonant system can be stable and self-correcting, so that the bodies remain in resonance. Examples are the 1:2:4 resonance of Jupiter‘s moons Ganymede, Europa and Io, and the 2:3 resonance between Pluto and Neptune. Unstable resonances with Saturn‘s inner moons give rise to gaps in the rings of Saturn. The special case of 1:1 resonance (between bodies with similar orbital radii) causes large Solar System bodies to eject most other bodies sharing their orbits; this is part of the much more extensive process of clearing the neighbourhood, an effect that is used in the current definition of a planet.”
iii. Some ‘work-blog related links’: Local regression, Quasi-experiment, Nonparametric regression, Regression discontinuity design, Kaplan–Meier estimator, Law of total expectation, Slutsky’s theorem, Difference in differences, Panel analysis.
v. Hill sphere.
“An astronomical body‘s Hill sphere is the region in which it dominates the attraction of satellites. To be retained by a planet, a moon must have an orbit that lies within the planet’s Hill sphere. That moon would, in turn, have a Hill sphere of its own. Any object within that distance would tend to become a satellite of the moon, rather than of the planet itself.
In more precise terms, the Hill sphere approximates the gravitational sphere of influence of a smaller body in the face of perturbations from a more massive body. It was defined by the American astronomer George William Hill, based upon the work of the French astronomer Édouard Roche. For this reason, it is also known as the Roche sphere (not to be confused with the Roche limit). The Hill sphere extends between the Lagrangian points L1 and L2, which lie along the line of centers of the two bodies. The region of influence of the second body is shortest in that direction, and so it acts as the limiting factor for the size of the Hill sphere. Beyond that distance, a third object in orbit around the second (e.g. Jupiter) would spend at least part of its orbit outside the Hill sphere, and would be progressively perturbed by the tidal forces of the central body (e.g. the Sun), eventually ending up orbiting the latter. […]
The Hill sphere is only an approximation, and other forces (such as radiation pressure or the Yarkovsky effect) can eventually perturb an object out of the sphere. This third object should also be of small enough mass that it introduces no additional complications through its own gravity. Detailed numerical calculations show that orbits at or just within the Hill sphere are not stable in the long term; it appears that stable satellite orbits exist only inside 1/2 to 1/3 of the Hill radius.”
I found myself looking up quite a few other astronomy-related articles when I was reading Formation and Evolution of Exoplanets (technically the link is to the 2010 version whereas I was reading the 2008 version, but it doesn’t look as if a whole lot of stuff’s been changed and I can’t find a link to the 2008 version). I haven’t mentioned the book here because I basically gave up reading it midway into the second chapter. The book didn’t try to hide that I probably wasn’t in the intended target group but I decided to give it a try anyway: “This book is intended to suit a readership with a wide range of previous knowledge of planetary science, astrophysics, and scientific programming. Expertise in these fields should not be required to grasp the key concepts presented in the forthcoming chapters, although a reasonable grasp of basic physics is probably essential.” I figured I could grasp the key concepts even though I’d lose out on a lot of details, but the math started getting ugly quite fast, and as I have plenty of ugly math to avoid as it is I decided to give the book a miss (though I did read the first 50 pages or so).
vi. Grover Cleveland (featured).
“Stephen Grover Cleveland (March 18, 1837 – June 24, 1908) was the 22nd and 24th President of the United States. Cleveland is the only president to serve two non-consecutive terms (1885–1889 and 1893–1897) and therefore is the only individual to be counted twice in the numbering of the presidents. He was the winner of the popular vote for president three times—in 1884, 1888, and 1892—and was the only Democrat elected to the presidency in the era of Republican political domination that lasted from 1861 to 1913.
Cleveland was the leader of the pro-business Bourbon Democrats who opposed high tariffs, Free Silver, inflation, imperialism and subsidies to business, farmers or veterans. His battles for political reform and fiscal conservatism made him an icon for American conservatives of the era. Cleveland won praise for his honesty, independence, integrity, and commitment to the principles of classical liberalism. Cleveland relentlessly fought political corruption, patronage, and bossism. Indeed, as a reformer his prestige was so strong that the reform wing of the Republican Party, called “Mugwumps“, largely bolted the GOP ticket and swung to his support in 1884. […]
Cleveland took strong positions and was heavily criticized. His intervention in the Pullman Strike of 1894 to keep the railroads moving angered labor unions nationwide and angered the party in Illinois; his support of the gold standard and opposition to Free Silver alienated the agrarian wing of the Democratic Party. Furthermore, critics complained that he had little imagination and seemed overwhelmed by the nation’s economic disasters—depressions and strikes—in his second term. Even so, his reputation for honesty and good character survived the troubles of his second term. […]
Cleveland’s term as mayor was spent fighting the entrenched interests of the party machines. Among the acts that established his reputation was a veto of the street-cleaning bill passed by the Common Council. The street-cleaning contract was open for bids, and the Council selected the highest bidder, rather than the lowest, because of the political connections of the bidder. While this sort of bipartisan graft had previously been tolerated in Buffalo, Mayor Cleveland would have none of it, and replied with a stinging veto message: “I regard it as the culmination of a most bare-faced, impudent, and shameless scheme to betray the interests of the people, and to worse than squander the public money”. The Council reversed themselves and awarded the contract to the lowest bidder. For this, and several other acts to safeguard the public funds, Cleveland’s reputation as an honest politician began to spread beyond Erie County. […] [As a president…] Cleveland used the veto far more often than any president up to that time. […]
In a 1905 article in The Ladies Home Journal, Cleveland weighed in on the women’s suffrage movement, writing that “sensible and responsible women do not want to vote. The relative positions to be assumed by men and women in the working out of our civilization were assigned long ago by a higher intelligence.””
Here’s how his second cabinet looked like – this was how a presidential cabinet looked like 120 years ago (as always you can click the image to see it in a higher resolution – and just in case you were in doubt: Cleveland is the old white man in the picture…):
vii. Boeing B-52 Stratofortress (‘good article’).
“The Boeing B-52 Stratofortress is a long-range, subsonic, jet-powered strategic bomber. The B-52 was designed and built by Boeing, which has continued to provide support and upgrades. It has been operated by the United States Air Force (USAF) since the 1950s. The bomber carries up to 70,000 pounds (32,000 kg) of weapons.
Beginning with the successful contract bid in June 1946, the B-52 design evolved from a straight-wing aircraft powered by six turboprop engines to the final prototype YB-52 with eight turbojet engines and swept wings. The B-52 took its maiden flight in April 1952. Built to carry nuclear weapons for Cold War-era deterrence missions, the B-52 Stratofortress replaced the Convair B-36. Although a veteran of several wars, the Stratofortress has dropped only conventional munitions in combat. Its Stratofortress name is rarely used outside of official contexts; it has been referred to by Air Force personnel as the BUFF (Big Ugly Fat/Flying Fucker/Fellow). […]
Superior performance at high subsonic speeds and relatively low operating costs have kept the B-52 in service despite the advent of later aircraft, including the cancelled Mach 3 North American XB-70 Valkyrie, the variable-geometry Rockwell B-1B Lancer, and the stealthy Northrop Grumman B-2 Spirit. The B-52 marked its 50th anniversary of continuous service with its original operator in 2005 and after being upgraded between 2013 and 2015 it will serve into the 2040s.[N 1] […]
B-52 strikes were an important part of Operation Desert Storm. With about 1,620 sorties flown, B-52s delivered 40% of the weapons dropped by coalition forces while suffering only one non-combat aircraft loss, with several receiving minor damage from enemy action. […]
The USAF continues to rely on the B-52 because it remains an effective and economical heavy bomber, particularly in the type of missions that have been conducted since the end of the Cold War against nations that have limited air defense capabilities. The B-52 has the capacity to “loiter” for extended periods over (or even well outside) the battlefield, and deliver precision standoff and direct fire munitions. It has been a valuable asset in supporting ground operations during conflicts such as Operation Iraqi Freedom. The B-52 had the highest mission capable rate of the three types of heavy bombers operated by the USAF in 2001. The B-1 averaged a 53.7% ready rate and the Northrop Grumman B-2 Spirit achieved 30.3%, while the B-52 averaged 80.5% during the 2000–2001 period. The B-52’s $72,000 cost per hour of flight is more than the $63,000 for the B-1B but almost half of the $135,000 of the B-2.”
I’ll just repeat that: $72,000/hour of flight. And the B-2 is at $135,000/hour. War is expensive.
I just finished the book, which is published by Britannica Educational Publishing and edited by Kara Rogers.
It’s a little bit repetitive, but it’s really quite good. I knew a lot about the subject already, but this is my first textbook dealing specifically with this topic and there were a few places where I had ‘aha-moments’ and suddenly understood everything a lot better – I really enjoy reading books that give me such experiences.
I should point out that Khan Academy has a lot of good stuff on this subject, and the videos there go into a lot more detail than does the book – I haven’t seen all those videos, but I’ve seen enough of them to know that this is mostly good stuff. I should perhaps also point out that each link above is to a topic covered at Khan Academy, each with multiple videos of coverage. Wikipedia also has some stuff on this subject.
As an intro textbook to the subject I think the book is a decent choice, though the illustrations are somewhat lacking. All concepts are properly introduced and defined, and definitions will sometimes be repeated other places in the book (which is part of what makes it repetitive) so you don’t necessarily need to memorize everything to keep track of what’s going on. My main points of criticism would be the unnecessary amount of repetition and the fact that it doesn’t actually go into much detail. The latter point of criticism can however also be considered a plus if you don’t know very much about the subjects covered, and of course the somewhat superficial treatment of the material also means that this is by no means a hard textbook to read.
I found it hard to blog stuff from the book, because most of it is just definitions, ‘how does it all work?’, ‘what can go wrong and how does it go wrong?’, disease progression, treatment options, etc. Not a lot of numbers in there, or a lot of stuff that can easily be quoted ‘out of context’. But I figured I couldn’t blog the book without at least posting a few bits from the book, so below a few quotes (none of these are ‘old numbers’; the book was published in 2011):
“of those likely to die during the first two weeks after a major heart attack, nearly half will die within one hour of the onset of
“less than half of the persons who die from heart attacks each year in the United States survive long enough to reach the hospital.”
“While life expectancy following a heart transplant is difficult to predict, the average recipient will live 8 to 10 years.” […] The survival rate at one year is now about 84 percent and at three years about 77 percent.”
“The renal arteries deliver to the kidneys of a normal person at rest 1.2 litres (2.5 pints) of blood per minute, a volume equivalent to approximately one-quarter of the heart’s output. Thus, a volume of blood equal to all that found in the body of an adult human is processed by the kidneys once every four to five minutes.”
“In general, the rate of heartbeat varies inversely with the size of the animal. In elephants it averages 25 beats per minute, in canaries about 1,000. In humans the rate diminishes progressively from birth (when it averages 130) to adolescence but increases slightly in old age. The average adult rate is 70 beats at rest.”
A big part of the book is available at the link.
I assume that not all of the five videos below are equally easy to understand for people who’ve not watched the previous ones in the various relevant playlists, but this is the stuff I’ve been watching lately and you should know where to look by now if something isn’t perfectly clear. I incidentally covered some relevant background material previously on the blog – if concepts from chemistry like ‘oxidation states’ are a bit far away, a couple of the videos in that post may be helpful.
I stopped caring much when I reached the 1 million mark (until they introduced the Kepler badge – then I started caring a little again until I’d gotten that one), but I noticed today that I’m at this point almost at the 1,5 million energy points mark (1.487.776). I’ve watched approximately 400 videos at the site by now.
Here’s a semi-related link with some good news: Khan Academy Launches First State-Wide Pilot In Idaho.
i. Remember ‘the good old days’ of film-making? Here’s a reminder: The Hays Code.
“1. No picture shall be produced that will lower the moral standards of those who see it. Hence the sympathy of the audience should never be thrown to the side of crime, wrongdoing, evil or sin.
2. Correct standards of life, subject only to the requirements of drama and entertainment, shall be presented.
3. Law, natural or human, shall not be ridiculed, nor shall sympathy be created for its violation. […]
The sanctity of the institution of marriage and the home shall be upheld. Pictures shall not infer that low forms of sex relationship are the accepted or common thing.
1. Adultery, sometimes necessary plot material, must not be explicitly treated, or justified, or presented attractively.
2. Scenes of Passion
a. They should not be introduced when not essential to the plot.
b. Excessive and lustful kissing, lustful embraces, suggestive postures and gestures, are not to be shown.
c. In general passion should so be treated that these scenes do not stimulate the lower and baser element. […]
1. No film or episode may throw ridicule on any religious faith.
2. Ministers of religion in their character as ministers of religion should not be used as comic characters or as villains. […]
The reason why ministers of religion may not be comic characters or villains is simply because the attitude taken toward them may easily become the attitude taken toward religion in general. Religion is lowered in the minds of the audience because of the lowering of the audience’s respect for a minister.”
ii. I’d love to see some corresponding Danish numbers:
“Italians born in 1970, who are about 43 now, will pay 50% more in taxes as a percentage of their lifetime income than those born in 1952, according to research from the Bank of Italy and the University of Verona. The research also found they will receive half the pension benefits that Italy’s 60-somethings are getting or are poised to get.” (link, via MR)
iii. Longevity AmongHunter-Gatherers: A Cross-Cultural Examination. Some main findings and conclusions from the paper:
“Post-reproductive longevity is a robust feature of hunter-gatherers and of the life cycle of Homo sapiens. Survivorship to grandparental age is achieved by over two-thirds of people who reach sexual maturity and can last an average of 20 years.
Adult mortality appears to be characterized by two stages. Mortality rates remain stable and fairly low at around 1 percent per year from the age of maturity until around age 40. After age 40, the rate of mortality increase is exponential (Gompertz) with a mortality rate doubling time of about 6–9 years. The two decades without detectable senescence in early and mid-adulthood appear to be an important component of human life span extension.
The average modal age of adult death for hunter-gatherers is 72 with a range of 68–78 years. This range appears to be the closest functional equivalent of an “adaptive” human life span.
Departures from this general pattern in published estimates of life expectancy in past populations (e.g., low child and high adult mortality) are most likely due to a combination of high levels of contact-related infectiousdisease, excessive violence or homicide, and methodological problems that lead to poor age estimates of older individuals and inappropriate use of model life tables for deriving demographic estimates.
Illnesses account for 70 percent, violence and accidents for 20 percent, and degenerative diseases for 9 percent of all deaths in our sample. Illnesses largely include infectious and gastrointestinal disease, although less than half of all deaths in our sample are from contact-related disease.
Comparisons among hunter-gatherers, acculturated hunter-gatherers, wild chimpanzees, and captive chimpanzees illustrate the interaction of improved conditions and species differences. Within species, improved conditions tend to decrease mortality rates at all ages, with a diminishing effect at older ages. Human and chimpanzee mortality diverge dramatically at older ages, revealing selection for a longer adult period in humans. […]
Our results contradict Vallois’s (1961: 222) claim that among early humans, “few individuals passed forty years, and it is only quite exceptionally that any passed fifty,” and the more traditional Hobbesian view of a nasty, brutish, and short human life (see also King and Jukes 1969; Weiss 1981). The data show that modal adult lifespan is 68–78 years, and that it was not uncommon for individuals to reach these ages”
iv. What is it like when one of your parents gets Alzheimer’s? It’s not fun.
In people with impaired glucose tolerance interventions are clinically and cost effective
Screening for type 2 diabetes to allow early detection might be cost effective in certain groups
What this study adds
Modelling the whole screening and intervention pathway from screening to death shows that screening for type 2 diabetes and impaired glucose tolerance, followed by interventions, seems to be cost effective compared with no screening
Uncertainty still exists concerning the cost effectiveness of screening for type 2 diabetes alone
Screening populations with a higher prevalence of glucose intolerance might result in better clinical outcomes, although cost effectiveness seems unaffected”
vi. PLOS-ONE: Minimal Intensity Physical Activity (Standing and Walking) of Longer Duration Improves Insulin Action and Plasma Lipids More than Shorter Periods of Moderate to Vigorous Exercise (Cycling) in Sedentary Subjects When Energy Expenditure Is Comparable.
N is small but even so this is an interesting finding.
vii. “Commercial fishing operations in the past 40 years have precipitated a dramatic change in ocean fish stocks, with tuna and other big predators declining and small fish like anchovies and sardines surging. That’s the conclusion of the most ambitious study ever completed of fish populations in the Earth’s oceans, conducted by Villy Christensen of the University of British Columbia’s Fisheries Centre.In the past 100 years, 80% of the biomass of fish in the world’s oceans has been lost, Christensen says in a AAAS video that coincided with a symposium at the Annual Meeting. “Just in the last 40 years, we have lost 60% of the biomass,” he explained. “So we’ve seen some very serious declines, and there’s no doubt about what the cause is: We’re talking about overfishing—overfishing at the global scale.” […] Christensen’s team of scientists based their conclusions on more than 200 marine ecosystem models and more than 68,000 estimates of fish biomass from 1880 to 2007, the Vancouver Sun reported, citing a University of British Columbia news release.”
I’d been meaning to read the book right after my exam last week, but in the end I made other plans.
After a tough start of the week with a lot of work (I had a presentation Wednesday which required a lot of preparation, among other things), I decided to read the book yesterday. It’s great – I was quickly reminded while reading this that some of the City Watch books in my mind really are among the most enjoyable of Pratchett’s books. A few quotes:
“They walked like men who had all day. They did have all day. They had chosen this particular street because it was busy and wide and you didn’t get too many trolls and dwarfs in this part of town. The reasoning was faultless: in lots of areas, right now, dwarfs or trolls were wandering around in groups or, alternatively, staying still in groups in case any of those wandering bastards tried any trouble in this neighbourhood. There had been little flare-ups for weeks. In these areas, Nobby and Fred considered, there wasn’t too much peace, so it was a waste of effort to keep what little was left of it, right? You wouldn’t try keeping sheep in places where all the sheep got eaten by wolves, right? It stood to reason. It would look silly. Whereas in big streets like Broadway there was lots of peace which, obviously, needed keeping. Common sense told them this was true.” [Nobby and Fred are ‘(Discworld) policemen’]
“‘The painting talked to him?’
Sir Reynolds made a face. ‘We believe that’s what he meant. We don’t really know. He did not have any friends. He was convinced that if he went to sleep at night he would turn into a chicken. He’d leave little notes for himself saying, “You are not a chicken”, although sometimes he thought he was lying. […]
He also hwrote his journal on random pieces of paper, you know, and never gave any indication as to the date or hwhere he hwas staying, in case the chicken found him. And he used very guarded language, because he didn’t want the chicken to find out.’
‘Sorry, I thought you said he thought he was the chick—‘ Colon began.
‘hWho can fathom the thought processes of the sadleah disturbed, sergeant?’ said Sir Reynold wearily. […] his handwriting was what might have been achieved by a spider on a trampoline during an earthquake.”
“‘He said the government hushed it up.’
‘Yeah, but your mate Dave always says the government hushes things up, Nobby,’ said Fred.
‘Well, they do.’
‘Except he always gets to hear about ’em, and he never gets hushed up,’ said Fred.
‘I know you like to point the finger of scoff, sarge, but there’s a lot goes on that we don’t know about.’
‘Like what, exactly?’ Colon retorted. ‘Name me one thing that’s going on that you don’t know about. There – you can’t, can you?'”
“‘We could handle them, though, couldn’t we, sir?’ said Carrot. ‘With the golem officers on our side too? If it came to it?’
Of course we couldn’t, Vimes’s mind supplied, not if they mean it. What we could do is die valiantly. I’ve seen men die valiantly. There’s no future in it.”
“he was not certain, not certain at all, what he’d do if the prisoner gave him any lip or tried to be smart. Beating people up in little rooms … he knew where that led. And if you did it for a good reason, you’d do it for a bad one. You couldn’t say ‘we’re the good guys’ and do bad-guy things.”
“‘I’ve never been on a Girls’ Night Out before,’ said Cheery, as they walked, a little uncertainly, through the night-time city. ‘Was that last bit supposed to happen?’
‘What bit was that?’ said Sally.
‘The bit where the bar was set on fire.’
‘Not usually,’ said Angua.”
“‘Our rations got lost in the excitement, sir. But the dwarfs will share theirs. They aren’t unfriendly, sir. Just cautious.’
‘Share? They have dwarf bread?’
‘I’m afraid so, sir.’
‘I thought it was illegal to give that to prisoners. I think I’ll wait, thanks.'”
At this point, right now while writing this, I’m too scared to go to sleep. It is not the first time, it’ll not be the last.
What’s there to be afraid of? Well, I should start out by pointing out that I always measure blood glucose before going to sleep. And I mean always. There are no exceptions to this rule, zero. I mean none – going to sleep without knowing my blood glucose just doesn’t happen. If I’m around others I may be discreet about the matter, but it’s non-negotiable. More than 90% of my lifetime hypoglycemia-related hospitalizations have been sleep-related. In the past I’ve fallen asleep in my own bed and woken up many hours after I should have in a hospital bed more than a few times, with no memory of how I got there. The fear that I’d one day just not wake up at all became much more real after I moved away from home.
I measured a blood glucose half an hour ago, just before going to sleep. The measured value was in the same neighbourhood as the highest of the ones measured here (2.3 mmol/l). I had zero awareness anything was wrong and if I’d not had a decision rule never to go to sleep without testing, I’d probably just have gone to bed without thinking anything might be wrong. The blood glucose level is now back in the normal range, but I’m hesitant to go to sleep until it has increased a bit more than it has – especially as it’s not completely clear to me what caused this in the first place (double dosis of the slow-acting insulin two days ago?).
If I had just gone to sleep, things could have been ‘interesting’. This is a part of diabetes normal people usually don’t get to see. The fact of the matter is that I’ll sometimes be afraid simply to go to sleep because the disease may kill me in my sleep. It almost did last year.
I should perhaps point out that this episode wasn’t really anything super special. These things happen, not ‘on a regular basis’; but they do happen.
I have friends (they may be reading along) who’ve pointed out that they consider my level of risk aversion to be excessive and who’ve advised me that I’d perhaps be happier if I was more willing to take on risk in general. I think growing up with diabetes changes how you think about risk. Nights like these are probably part of the reason why I have a hard time following that advice. The people giving advice should know this side of the equation too. Most people without the disease don’t.