Oxford Handbook of Clinical Medicine (III)

Here are my first two posts about the book, which I have now finished. I gave the book three stars on goodreads, but I’m close to a four star rating and I may change my opinion later – overall it’s a pretty good book. I’ve read about many of the topics covered before but there was also quite a bit of new stuff along the way; as a whole the book spans very widely, but despite this the level of coverage of individual topics is not bad – I actually think the structure of the book makes it more useful as a reference tool than is McPhee et al. (…in terms of reference books which one might find the need to refer to in order to make sense of medical tests and test results, I should of course add that no book can beat Newman & Kohn). I have tried to take this into account along the way in terms of the way I’ve been reading the book, in the sense that I’ve tried to make frequent references in the margin to other relevant works going into more detail about specific topics whenever this seemed like it might be useful, and I think if one does something along those lines systematically a book like this one can become a really powerful tool – you get the short version with the most important information (…or at least what the authors considered to be the most important information) here almost regardless of what topic you’re interested in – I should note in this context that the book has only very limited coverage of mental health topics, so this is one area where you definitely need to go elsewhere for semi-detailed coverage – and if you need more detail than what’s provided in the coverage you’ll also know from your notes where to go next.

In my last post I talked a bit about which topics were covered in the various chapters in the book – I figured it might make sense here to list the remaining chapter titles in this post. After the (long) surgery chapter, the rest of the chapters deal with epidemiology (I thought this was a poor chapter and the authors definitely did not consider this topic to be particularly important; they spent only 12 pages on it), clinical chemistry (lab results, plasma proteins, topics like ‘what is hypo- and hypernatremia’, …), eponymous syndromes (a random collection of diseases, many of which are quite rare), radiology (MRI vs X-ray? When to use, or not use, contrast material? Etc.), ‘reference intervals etc.‘ (the ‘etc.’ part covered drug therapeutic ranges for some commonly used drugs, as well as some important drug interactions – note to self: The effects of antidiabetic drugs are increased by alcohol, beta-blockers, bezafibrate, and MAOIs, and are decreased by contraceptive steroids, corticosteroids, diazoxide, diuretics, and possibly also lithium), practical procedures (I was considering skipping this chapter because I’m never going to be asked to e.g. insert a chest drain and knowing how to do it seems to be of limited benefit to me, but I figured I might as well read it anyway; there were some details about what can go wrong in the context of specific procedures and what should be done when this happens, and this seemed like valuable information. Also, did you know that “There is no evidence that lying flat post procedure prevents headache” in the context of lumbar punctures? I didn’t, and a lot of doctors probably also don’t. You can actually go even further than that: “Despite years of anecdotal advice to the contrary, none of the following has ever been shown to be a risk factor [for post-LP headache]: position during or after the procedure; hydration status before, during, or after; amount of CSF removed; immediate activity or rest post-LP.”), and emergencies.

In this post I won’t cover specific chapters of the book in any detail, rather I’ll talk about a few specific topics and observations I could be bothered to write some stuff about here. Let’s start with some uplifting news about the topic of liver tumours: Most of these (~90%) are secondary (i.e. metastatic) tumours with an excellent prognosis (“Often ↑3yr survival to 59% from 13%; but ~50% have recurrence by 3yrs.[3] Liver transplant gives a 5yr survival rate of 70%.” It should be noted in a disease impact context that this type of cancer is far more common in areas of the world with poorly developed health care systems like Africa and China.

Alcoholism is another one of the causes of liver tumors. In the book they include the observation that the lifetime prevalence of alcoholism is around 10% for men and 4% for women, but such numbers are of course close to being completely meaningless almost regardless of where they’re coming from. Alcoholism is dangerous; in cases with established cirrhosis roughly half (52%) of people who do not stop drinking will be dead within 5 years, whereas this is also the case for 23% of the people who do stop drinking. Excessive alcohol consumption can cause alcoholic hepatitis; “[m]ild episodes hardly affect mortality” but in severe cases half will be dead in a month, and in general 40% of people admitted to the hospital for alcoholic hepatitis will be dead within one year of admission. Alcohol can cause portal hypertension (80% of cases are caused by cirrhosis in the UK), which may lead to the development of abnormal blood vessels e.g. in the oesophagus which will have a tendency to cause bleeding, which can be fatal.  Roughly 30% of cirrhotics with varices bleed, and rebleeding is common: “After a 1st variceal bleed, 60% rebleed within 1yr” and “40% of rebleeders die of complications.” Alcoholism can kill you in a variety of different ways (acute poisonings and accidents should probably also be included here as well), and many don’t survive long enough to develop cancer.

As mentioned in the first post about the book acute kidney injury is common in a hospital setting. In the following I’ve added a few more observations about renal disease. “Renal pain is usually a dull ache, constant and in the loin.” But renal disease don’t always cause pain, and in general: “There is often a poor correlation between symptoms and severity of renal disease. Progression [in chronic disease] may be so insidious that patients attribute symptoms to age or a minor illnesses. […] Serious renal failure may cause no symptoms at all.” The authors note that odd chronic symptoms like fatigue should not be dismissed without considering a renal function test first. The book has a nice brief overview of the pathophysiology of diabetic nephropathy – this part is slightly technical, but I decided to include it here anyway before moving on to a different topic:
“Early on, glomerular and tubular hypertrophy occur, increasing GFR [glomerular filtration rate, an indicator variable used to assess kidney function] transiently, but ongoing damage from advanced glycosylation end-products (AGE—caused by non-enzymatic glycosylation of proteins from chronic hyperglycaemia) triggers more destructive disease. These AGE trigger an inflammatory response leading to deposition of type IV collagen and mesangial expansion, eventually leading to arterial hyalinization, thickening of the mesangium and glomerular basement membrane and nodular glomerulosclerosis (Kimmelstiel–Wilson lesions). Progression generally occurs in four stages:
1 GFR elevated: early in disease renal blood flow increases, increasing the GFR and leading to microalbuminuria. […]
2 Glomerular hyperfiltration: in the next 5–10yrs mesangial expansion gradually occurs and hyperfiltration at the glomerulus is seen without microalbuminuria.
3 Microalbuminuria: as soon as this is detected it indicates progression of disease, GFR may be raised or normal. This lasts another 5–10yrs.
4 Nephropathy: GFR begins to decline and proteinuria increases.
Patients with type 2 DM may present at the later stages having had undetected hyperglycaemia for many years before diagnosis.”

Vitamin B12 deficiency is quite common, the authors note that it occurs in up to 15% of older people. Severe B12 deficiency is not the sort of thing which will lead to you feeling ‘a bit under the weather’ – it can lead to permanent brain damage and damage to the spinal cord. “Vitamin B12 is found in meat, fish, and dairy products, but not in plants.” It’s important to note that “foods of non-animal origin contain no B12 unless fortified or contain bacteria.” The wiki article incidentally includes even higher prevalence estimates (“It is estimated to occur in about 6% of those under the age of 60 and 20% of those over the age of 60. Rates may be as high as 80% in parts of Africa and Asia.”) than the one included in the book – this vitamin deficiency is common, and if severe it can have devastating consequences.

On bleeding disorders: “After injury, 3 processes halt bleeding: vasoconstriction, gap-plugging by platelets, and the coagulation cascade […]. Disorders of haemostasis fall into these 3 groups. The pattern of bleeding is important — vascular and platelet disorders lead to prolonged bleeding from cuts, bleeding into the skin (eg easy bruising and purpura), and bleeding from mucous membranes (eg epistaxis [nose bleeds], bleeding from gums, menorrhagia). Coagulation disorders cause delayed bleeding into joints and muscle.” An important observation in the context of major bleeds is incidentally this: “Blood should only be given if strictly necessary and there is no alternative. Outcomes are often worse after a transfusion.” The book has some good chapters about the leukaemias, but they’re relatively rare diseases and some of them are depressing (e.g. acute myeloid leukaemia: according to the book coverage death occurs in ~2 months if untreated, and roughly four out of five treated patients are dead within 3 years) so I won’t talk a lot about them. One thing I found somewhat interesting about the blood disorders covered in the book is actually how rare they are, all things considered: “every day each of us makes 175 billion red cells, 70 billion granulocytes, and 175 billion platelets”. There are lots of opportunities for things to go wrong here…

Some ways to prevent traveller’s diarrhea: “If in doubt, boil all water. Chlorination is OK, but doesn’t kill amoebic cysts (get tablets from pharmacies). Filter water before purifying. Distinguish between simple gravity filters and water purifiers (which also attempt to sterilize chemically). […] avoid surface water and intermittent tap supplies. In Africa assume that all unbottled water is unsafe. With bottled water, ensure the rim is clean & dry. Avoid ice. […] Avoid salads and peel your own fruit. If you cannot wash your hands, discard the part of the food that you are holding […] Hot, well-cooked food is best (>70°C for 2min is no guarantee; many pathogens survive boiling for 5min, but few last 15min)”

An important observation related to this book’s coverage about how to control hospital acquired infection: “Cleaning hospitals: Routine cleaning is necessary to ensure that the hospital is visibly clean and free from dust and soiling. 90% of microorganisms are present within ‘visible dirt’, and the purpose of routine cleaning is to eliminate this dirt. Neither soap nor detergents have antimicrobial activity, and the cleaning process depends essentially on mechanical action.”

Falciparum malaria causes one million deaths/year, according to the book, and mortality is close to 100% in untreated severe malaria – treatment reduces this number to 15-20%. Malaria in returning travellers is not particularly common, but there are a couple thousand cases in the UK each year. Malaria prophylaxis does not give full protection, and “[t]here is no good protection for parts of SE Asia.” Multidrug resistance is common.


November 8, 2015 Posted by | alcohol, Books, Cancer/oncology, Epidemiology, Infectious disease, Medicine, Nephrology | Leave a comment

A Systematic Review… (II)

Yesterday I gave some of the reasons I had for disliking the book; in this post I’ll provide some of the reasons why I kept reading. The book had a lot of interesting data. I know I’ve covered some of these topics and numbers before (e.g. here), but I don’t mind repeating myself every now and then; some things are worth saying more than once, and as for the those that are not I must admit I don’t really care enough about not repeating myself here to spend time perusing the archives in order to make sure I don’t repeat myself here. Anyway, here are some number from the coverage:

“Twenty-two high-burden countries account for over 80 % of the world’s TB cases […] data referring to 2011 revealed 8.7 million new cases of TB [worldwide] (13 % coinfected with HIV) and 1.4 million people deaths due to such disease […] Around 80 % of TB cases among people living with HIV were located in Africa. In 2011, in the WHO European Region, 6 % of TB patients were coinfected with HIV […] In 2011, the global prevalence of HIV accounted for 34 million people; 69 % of them lived in Sub-Saharan Africa. Around five million people are living with HIV in South, South-East and East Asia combined. Other high-prevalence regions include the Caribbean, Eastern Europe and Central Asia [11]. Worldwide, HIV incidence is in downturn. In 2011, 2.5 million people acquired HIV infection; this number was 20 % lower than in 2001. […] Sub-Saharan Africa still accounts for 70 % of all AIDS-related deaths […] Worldwide, an estimated 499 million new cases of curable STIs (as gonorrhoea, chlamydia and syphilis) occurred in 2008; these findings suggested no improvement compared to the 448 million cases occurring in 2005. However, wide variations in the incidence of STIs are reported among different regions; the burden of STIs mainly occurs in low-income countries”.

“It is estimated that in 2010 alone, malaria caused 216 million clinical episodes and 655,000 deaths. An estimated 91 % of deaths in 2010 were in the African Region […]. A total of 3.3 billion people (half the world’s population) live in areas at risk of malaria transmission in 106 countries and territories”.

“Diarrhoeal diseases amount to an estimated 4.1 % of the total disability-adjusted life years (DALY) global burden of disease, and are responsible for 1.8 million deaths every year. An estimated 88 % of that burden is attributable to unsafe supply of water, sanitation and hygiene […] It is estimated that diarrhoeal diseases account for one in nine child deaths worldwide, making diarrhoea the second leading cause of death among children under the age of 5 after pneumonia”

“NCDs [Non-Communicable Diseases] are the leading global cause of death worldwide, being responsible for more
deaths than all other causes combined. […] more than 60 % of all deaths worldwide currently stem from NCDs [3].
In 2008, the leading causes of all NCD deaths (36 million) were:
• CVD [cardiovascular disease] (17 million, or 48 % of NCD deaths) [nearly 30 % of all deaths];
• Cancer (7.6 million, or 21 % of NCD deaths) [about 13 % of all deaths]
• Respiratory diseases (4.2 million, or 12 % of NCD deaths) [7 % of all deaths]
• Diabetes (1.3 million, 4 % of NCD deaths) [4].” [Elsewhere in the publication they report that: “In 2010, diabetes was responsible for 3.4 million deaths globally and 3.6 % of DALYs” – obviously there’s a lot of uncertainty here. How to avoid ‘double-counting’ is one of the major issues, because we have a pretty good idea what they die of: “CVD is by far the most frequent cause of death in both men and women with diabetes, accounting for about 60 % of all mortality”].

“Behavioural risk factors such as physical inactivity, tobacco use and unhealthy diet explain nearly 80 % of the CVD burden”

“nearly 80 % of NCD deaths occur in low- and middle-income countries [4], up sharply from just under 40 % in 1990 […] Low- and lower-middle-income countries have the highest proportion of deaths from NCDs under 60 years. Premature deaths under 60 years for high-income countries were 13 and 25 % for upper-middle-income countries. […] In low-income countries, the proportion of premature NCD deaths under 60 years is 41 %, three times the proportion in high-income countries [7]. […] Overall, NCDs account for more than 50 % of DALYs [disability-adjusted life years] in most counties. This percentage rises to over 80 % in Australia, Japan and the richest countries of Western Europe and North America […] In Europe, CVD causes over four million deaths per year (52 % of deaths in women and 42 % of deaths in men), and they are the main cause of death in women in all European countries.”

“Overall, age-adjusted CVD death rates are higher in most low- and middle-income countries than in developed countries […]. CHD [coronary heart disease] and stroke together are the first and third leading causes of death in developed and developing countries, respectively. […] excluding deaths from cancer, these two conditions were responsible for more deaths in 2008 than all remaining causes among the ten leading causes of death combined (including chronic diseases of the lungs, accidents, diabetes, influenza, and pneumonia)”.

“The global prevalence of diabetes was estimated to be 10 % in adults aged 25 + years […] more than half of all nontraumatic lower limb amputations are due to diabetes [and] diabetes is one of the leading causes of visual impairment and blindness in developed countries [14].”

“Almost six million people die from tobacco each year […] Smoking is estimated to cause nearly 10 % of CVD […] Approximately 2.3 million die each year from the harmful use of alcohol. […] Alcohol abuse is responsible for 3.8 % of all deaths (half of which are due to CVD, cancer, and liver cirrhosis) and 4.5 % of the global burden of disease […] Heavy alcohol consumption (i.e. ≥ 4 drinks/day) is significantly associated with an about fivefold increased risk of oral and pharyngeal cancer and oesophageal squamous cell carcinoma (SqCC), 2.5-fold for laryngeal cancer, 50 % for colorectal and breast cancers and 30 % for pancreatic cancer [37]. These estimates are based on a large number of epidemiological studies, and are generally consistent across strata of several covariates. […] The global burden of cancer attributable to alcohol drinking has been estimated at 3.6 and 3.5 % of cancer deaths [39], although this figure is higher in high-income countries (e.g. the figure of 6 % has been proposed for UK [9] and 9 % in Central and Eastern Europe).”

“At least two million cancer cases per year (18 % of the global cancer burden) are attributable to chronic infections by human papillomavirus, hepatitis B virus, hepatitis C virus and Helicobacter pylori. These infections are largely preventable or treatable […] The estimate of the attributable fraction is higher in low- and middle-income countries than in high-income countries (22.9 % of total cancer vs. 7.4 %).”

“Information on the magnitude of CVD in high-income countries is available from three large longitudinal studies that collect multidisciplinary data from a representative sample of European and American individuals aged 50 and older […] according to the Health Retirement Survey (HRS) in the USA, almost one in three adults have one or more types of CVD [11, 12]. By contrast, the data of Survey of Health, Ageing and Retirement in Europe (SHARE), obtained from 11 European countries, and English Longitudinal Study of Aging (ELSA) show that disease rates (specifically heart disease, diabetes, and stroke) across these populations are lower (almost one in five)”

“In 1990, the major fraction of morbidity worldwide was due to communicable, maternal, neonatal, and nutritional disorders (47 %), while 43 % of disability adjusted life years (DALYs) lost were attributable to NCDs. Within two decades, these estimates had undergone a drastic change, shifting to 35 % and 54 %, respectively”

“Estimates of the direct health care and nonhealth care costs attributable to CVD in many countries, especially in low- and middle-income countries, are unclear and fragmentary. In high-income countries (e.g., USA and Europe), CVD is the most costly disease both in terms of economic costs and human costs. Over half (54 %) of the total cost is due to direct health care costs, while one fourth (24 %) is attributable to productivity losses and 22 % to the informal care of people with CVD. Overall, CVD is estimated to cost the EU economy, in terms of health care, almost €196 billion per year, i.e., 9 % of the total health care expenditure across the EU”

“In the WHO European Region, the Eastern Mediterranean Region, and the Region of the Americas, over 50 % of women are overweight. The highest prevalence of overweight among infants and young children is in upper-to-middle-income populations, while the fastest rise in overweight is in the lower-to-middle-income group [19]. Globally, in 2008, 9.8 % of men and 13.8 % of women were obese compared to 4.8 % of men and 7.9 % of women in 1980 [27].”

“In low-income countries, around 25 % of adults have raised total cholesterol, while in high-income countries, over 50 % of adults have raised total cholesterol […]. Overall, one third of CHD disease is attributable to high cholesterol levels” (These numbers seem very high to me, but I’m reporting them anyway).

“interventions based on tobacco taxation have a proportionally greater effect on smokers of lower SES and younger smokers, who might otherwise be difficult to influence. Several studies suggest that the application of a 10 % rise in price could lead to as much as a 2.5–10 % decline in smoking [20, 45, 50, 56].”

“The decision to allocate resources for implementing a particular health intervention depends not only on the strength of the evidence (effectiveness of intervention) but also on the cost of achieving the expected health gain. Cost-effectiveness analysis is the primary tool for evaluating health interventions on the basis of the magnitude of their incremental net benefits in comparison with others, which allows the economic attractiveness of one program over another to be determined [More about this kind of stuff here]. If an intervention is both more effective and less costly than the existing one, there are compelling reasons to implement it. However, the majority of health interventions do not meet these criteria, being either more effective but more costly, or less costly but less effective, than the existing interventions [see also this]. Therefore, in most cases, there is no “best” or absolute level of cost-effectiveness, and this level varies mainly on the basis of health care system expenditure and needs [102].”

“The number of new cases of cancer worldwide in 2008 has been estimated at about 12,700,000 [3]. Of these, 6,600,000 occurred in men and 6,000,000 in women. About 5,600,000 cases occurred in high-resource countries […] and 7,100,000 in low- and middle-income countries. Among men, lung, stomach, colorectal, prostate and liver cancers are the most common […], while breast, colorectal, cervical, lung and stomach are the most common neoplasms among women […]. The number of deaths from cancer was estimated at about 7,600,000 in 2008 […] No global estimates of survival from cancer are available: Data from selected cancer registries suggest wide disparities between high- and low-income countries for neoplasms with effective but expensive treatment, such as leukaemia, while the gap is narrow for neoplasms without an effective therapy, such as lung cancer […]. The overall 5-year survival of cases diagnosed during 1995– 1999 in 23 European countries was 49.6 % […] Tobacco smoking is the main single cause of human cancer worldwide […] In high-income countries, tobacco smoking causes approximately 30 % of all human cancers [9].”

“Systematic reviews have concluded that nutritional factors may be responsible for about one fourth of human cancers in high-income countries, although, because of the limitations of the current understanding of the precise role of diet in human cancer, the proportion of cancers known to be avoidable in practicable ways is much smaller [9]. The only justified dietary recommendation for cancer prevention is to reduce the total caloric intake, which would contribute to a decrease in overweight and obesity, an established risk factor for human cancer. […] The magnitude of the excess risk [associated with obesity] is not very high (for most cancers, the relative risk (RR) ranges between 1.5 and 2 for body weight higher than 35 % above the ideal weight). Estimates of the proportion of cancers attributable to overweight and obesity in Europe range from 2 % [9] to 5 % [34]. However, this figure is likely to be larger in North America, where the prevalence of overweight and obesity is higher.”

“Estimates of the global burden of cancer attributable to occupation in high-income countries result in the order of 1–5 % [9, 42]. In the past, almost 50 % of these were due to asbestos alone […] The available evidence suggests, in most populations, a small role of air, water and soil pollutants. Global estimates are in the order of 1 % or less of total cancers [9, 42]. This is in striking contrast with public perception, which often identifies pollution as a major cause of human cancer.”

“Avoidance of sun exposure, in particular during the middle of the day, is the primary preventive measure to reduce the incidence of skin cancer. There is no adequate evidence of a protective effect of sunscreens, possibly because use of sunscreens is associated with increased exposure to the sun. The possible benefit in reducing skin cancer risk by reduction of sun exposure, however, should be balanced against possible favourable effects of UV radiation in promoting vitamin D metabolism.”

March 30, 2015 Posted by | alcohol, Books, Cancer/oncology, Cardiology, Data, Diabetes, Epidemiology, Infectious disease, Medicine | Leave a comment

The Psychology of Lifestyle (III)

Again, I refer to the first post in the series for general comments and observations related to the book‘s coverage. Below some more stuff from the book and some observations:

“92 per cent of men and 86 per cent of women in Britain drink alcohol (DoH 2002a).”

I sort of liked the chapter about alcohol more than I did at first after I’d yesterday read some stuff in Boccia et al. dealing with the same topic (their coverage is much poorer in regards to some key issues). When thinking about how to blog this chapter I was considering including a table from the book, table 5,1, in full, even if it’s rather large, but I decided against it as I might as well report what it’s talking about myself here. The observation that addiction and physical dependence should be treated as separate entities is not included in the coverage, although Clark & Treisman considered this to be a very important point to keep in mind (see also this post: “It is very important to realize that addiction and physical dependence are different phenomena with different underlying brain substrates”), but the coverage is still much more detailed than the public health review text alluded to above. It should be noted that some of the shortcomings of the chapter is presumably due to the intended scope of the coverage which makes the omission of some of the important distinctions seem understandable, sort of; the authors note early on that they mostly focus on volitional rather than dependent drinking, because the book deals with lifestyle behaviours over which individuals have some level of control (but if you’re covering smoking and illegal substance abuse in your book, why not cover dependent drinking as well? I still find their coverage of some of these issues sort of puzzling…). Anyway, table 5,1 includes the ICD-10 diagnostic criteria for alcohol dependence, and these criteria include (my bold):

Evidence of tolerance (need more alcohol to get the same effect); physiological withdrawal when alcohol use is reduced or ceased (or use of a closely related substance with the intention of relieving or avoiding withdrawal symptoms); persisting with alcohol use despite clear evidence of harmful consequences; preoccupation with alcohol use (important other pleasures/interests given up or reduced because of alcohol, much time spent on activities such as procuring alcohol, consuming it, or recovering from its effects); difficulty controlling drinking behaviour in terms of onset-, termination or level of use – evidenced by alcohol being consumed in larger amounts or over a longer period than intended, or by any unsuccessful effort or persistent desire to cut down; and lastly a strong desire or compulsion to use alcohol.

“The majority of people who drink alcohol have not been diagnosed as dependent drinkers. Orton (2001) reported that 7.5 per cent of men and 2.1 per cent of women in Britain in the 1990s could be classified as dependent on alcohol. […] Nonresponse bias is a particular problem in drinking surveys. […] Issues of response bias are a common concern and one that afflicts many of the lifestyle surveys reported throughout this text. […] An important issue for measurement of drinking is the validity and reliability of the instrument in question and unfortunately many widely used measures of alcohol consumption have not been tested for such psychometric properties. […] Probably the most convincing evidence that self-report measures of drinking in any one study do, at the very least, place people in an appropriate place on the drinking continuum compared to their peers is the relationship between self-reported drinking and proven increased risk for a number of alcohol related conditions (Room et al. 2005).”

“Men drink more alcohol than women and they are more likely to exceed their daily and/or weekly guidelines, even though those guidelines are higher than those recommended for women […]. This gender difference in alcohol consumption is consistently reported in the national surveys and elsewhere […] and furthermore is similar to the gendered drinking patterns of previous decades […] There are few clear socio-economic trends in alcohol consumption evident from the National Surveys”

“People under the influence of alcohol are more likely to behave aggressively and this can lead to physical violence that can harm themselves and others […]. Offenders are believed to be under the influence of alcohol in 46 per cent of incidents of domestic violence and 44 per cent of acquaintance violence. […] 15 per cent of rape victims recorded by the 2001 British Crime Survey were raped when they were under the influence of alcohol [I was actually really surprised the number was that low…] […] People under the influence of alcohol are also more likely to have accidents. […] The World Health Organisation (2002) estimates that 20 per cent of motor vehicle accidents worldwide are alcohol related.”

“Alcohol has been implicated in more than 60 medical conditions, predominantly with negative, but occasionally with positive, consequences […] the relationship between alcohol consumption and health is not always linear. […] Episodic heavy drinking, even when the overall volume of alcohol intake is low, has been found to increase the risk for a number of cardiovascular conditions. […] This association is physiologically consistent with the increased clotting, lower threshold for ventricular fibrillation and elevation of low density lipoproteins that occur after heavy drinking (Room et al. 2005). […] Breast cancer risk increases linearly with increased alcohol consumption: 10 grams of alcohol a day (an average UK unit) increases the relative risk of breast cancer by 9 per cent. A daily consumption of between 30 and 60 grams a day increases the relative risk by 41 per cent […] In England and Wales alcohol-related injury or illness accounts for 180,000 hospital admissions a year (HM Government 2007).”

“Alcohol serves an important social function. It enhances social integration and facilitates the development of relationships (Kuther and Timoshin 2003). It is hardly surprising that people drink most at a period in their lives [teen-age years, early twenties] which is normally associated with the development of stable adult relationships (Paglia and Room 1999). Increased levels of drinking in newly divorced people may be in part due to the breakdown of stable relationships and the desire to establish new relationships (HM Government 2007). Social isolation is a key factor in poor health outcomes […] so the positive social function of alcohol in enabling people to develop social relationships should not be overlooked.”

“In contrast to other lifestyle behaviours where social norms have been argued to play little or no part in the explanation for variations in behaviour, social norms are consistently reported to be useful in explaining variations in drinking behaviour”

“it is well established that the earlier a person starts to drink, smoke or use illegal drugs the higher the risk of later abuse […] There is evidence that people drink less if the price of alcohol increases […] and that those of particular concern, heavy drinkers and young people, both respond to price increases by drinking less […] Many interventions to encourage sensible drinking are aimed at adolescents and young people with the goal of preventing the establishment of unhealthy drinking habits. The rationale for a predominance of interventions for this age group includes the indisputable fact that young people are the heaviest drinkers in society […] Many early drinking interventions are educational in nature. In essence these are risk communication messages and the evidence from psychological research is that improving risk perceptions will have little impact on levels of drinking. Unsurprisingly then, there is little evidence that alcohol education and health promotion have any positive effect on drinking habits in Britain […] These campaigns are heard and understood because knowledge increases in targeted populations […] so it is not that the message is failing to reach the designated audience, rather the message has no impact on behaviour. […] Foxcroft et al. (2003) reviewed the effectiveness of programmes designed to prevent excessive drinking in young people. Worryingly, [they] found very little evidence that any of these programmes were effective. Among the studies with medium-term followup that met the methodological guidelines the majority, 19 studies, found no evidence of intervention effectiveness. Several of these studies had previously reported short-term effectiveness which demonstrates the importance of longer term follow-up. […] There are two concerns from these studies on early drinking interventions. First, there are a wealth of studies that report no reduction in any measure of drinking. Second, research has failed to consistently test and tease out what is effective.”

Next, smoking:

“There is considerable variation in the prevalence of smoking worldwide. In sub-Saharan Africa less than 10 per cent of the population smoke, whereas in Japan this figure rises to above 50 per cent, and in Indonesia 69 per cent, with almost three-quarters of the Vietnamese population smoking (Edwards 2004).” [I had no idea the numbers were that high anywhere… (and I’m perhaps slightly skeptical, in particular about the Japanese estimate; a 50+% smoking prevalence seems to not fit very well with the very high Japanese life expectancy)]

“Despite the health effects of smoking being known since the 1960s, and the health impact being publicised, some 12 million individuals still smoke in the UK: 25 per cent of men and 23 per cent of women (ONS 2007). These figures have shown a substantial decrease since the early 1970s: for example in the 1970s the comparable figures were 51 per cent of men and 41 per cent of women smoking.” [If you’re curious about Danish figures, I blogged some Danish alcohol and smoking stats some years back here (the post is in Danish)] […] smoking is the highest in the 20–24 year age group (about 36 per cent) and the lowest in the over 65 years (about 15 per cent). This reflects both the fact that many former smokers will have quit and also that about a quarter of smokers die before reaching retirement age (ONS 2007). […] in the UK it is suggested that annually some 120,000 people die as a result of their smoking habit (440,000 in the United States). Every year, tobacco smoking kills 5 million people worldwide (Perkins et al. 2008) […] Deaths caused by tobacco smoking in the UK are higher than the number of deaths caused by road traffic accidents (3,500), other accidents (8,500), poisoning and overdose (900), alcoholic liver disease (5,000), suicide (4,000) and HIV infection (250). Almost a half of all regular smokers will be killed by their habit. A man who smokes cuts short his life by 13.2 years and female smokers lose 14.5 years (ASH 2008).”

“It is usually teenagers who experiment with smoking, with very few smokers starting after the age of 25 years […]. There are a number of reasons why people start smoking, but these are mainly related to psychosocial motives […] One of the major reasons for experimenting with cigarettes is social pressure from peers or older siblings […] adolescents are more likely to smoke cigarettes if their parents smoke […] Research has also indicated that teenagers underestimate the health risk of smoking […] and they also believe that they will quit before they do themselves serious damage […]. Hence, they smoke in spite of knowing the health damage effects of smoking: they know of them, they just don’t think it will impact upon them. […] of all the lifestyle behaviours discussed in this book smoking has the simplest relationship with social class and is the only behaviour to demonstrate a totally linear relationship with class.”

“One of the major attempts to reduce smoking has been the introduction of graphic warning labels on cigarette packets or on posters and billboards. […] there is very little evidence of the success of this form of approach. When politicians are asked for the evidence of such approaches there is much filibustering and some reference to dated research which does not stand up to scrutiny (Ruiter and Kok 2005). […] the evidence can be described as, at best, insubstantial. […] there are a large number of studies that highlight that some type of in-person or telephone behavioural support with NRT [nicotine replacement therapy] increases quit rates, especially those using nicotine gum […]. This support works by increasing motivation for quitting and remaining tobacco-free. However, most quitters attempt to stop smoking by use of NRTs alone and overlook the behavioural and psychological support required to enhance and maintain the necessary motivation”

The stuff below is from the smoking chapter, but might easily have been found in a very different chapter (or even in a different book?):

“Motivational interviewing can be defined as ‘a client-centred, directive method for enhancing intrinsic motivation to change by exploring and resolving ambivalence’ (Miller and Rollnick 2002). Motivational interviewing has as its goal the simple expectation that increasing an individual’s motivation to consider change rather than showing them how to change should be the key step. If a person is not motivated to change then it is irrelevant if they know how to do it or not. […] Motivational interviewing (MI) is a technique based on cognitive-behavioural therapy which aims to enhance an individual’s motivation to change health behaviour. The whole process aims to help the patient understand their thought processes and to identify how their thought processes help produce the inappropriate behaviour and how their thought processes can be changed to develop alternative, health-promoting behaviours. Motivational strategies include eight components that are designed to increase the level of motivation the person has towards changing a specific behaviour. […] The eight components are: *giving advice (about specific behaviours to be changed) *removing barriers (often about access to particular help) *providing choice (making it clear that if they choose not to change that is their right and it is their choice […] *decreasing desirability (of the ambivalence towards change or the status quo) *practising empathy *providing feedback […] *clarifying goals (feedback should be compared with a standard (an ideal) *active helping”.

“The definition of ‘lapse’ and ‘relapse’ has been debated in various forums […] but simply a ‘lapse’ is a slip into smoking behaviour, whereas ‘relapse’ refers to long-term failure. Most smokers who attempt to quit do so through self-quitting […] but the rates of success are very low with reports suggesting that only about 3–5 per cent of those self-quitting attain long-term abstinence at 6–12 months (Hughes et al. 2004). More recently, self-quitters have been aided by being able to purchase over the counter NRT and although this can double the rate of success this is still a paltry 6–10 per cent success rate. […] Although the majority of smokers want to stop smoking and predict that they will have stopped in twelve months, only 2–3 per cent actually stops permanently a year (Taylor et al. 2006).”

Unsafe sex:

“In London, the area with the highest prevalence of HIV in the UK, 30 per cent of people did not know HIV could be transmitted through unprotected sex (National AIDS Trust 2006; UNAIDS 2006). [first thought: Some of these have got to be joke responses] […] [in the UK] the number of women diagnosed with HIV has increased in recent years and in 2007 it was some 40 per cent of the total (compared to 10 per cent of all diagnoses in 1990). […] 95 per cent of 16–24 year olds who use a condom do so in order to prevent pregnancy whereas only 71 per cent report using a condom in order to prevent infection. Furthermore, less than half (48 per cent) of men and only 37 per cent of women report using a condom ‘always’. […] At least 50 per cent of sexually active men and women acquire genital HPV infection at some point in their lives […] Regarding HIV it is estimated that one-quarter of people living with the disease do not know that they have it and are therefore at risk of transmitting the virus to others (CDC 2006e).”

“The pharmacological effects of alcohol and various other non-prescription substances tend to have the effect of reducing inhibitions, boosting confidence, intensifying emotions and increasing the importance of immediate cues such as sexual desire, at the expense of more future-oriented considerations such as STIs. As a result, users have been shown to engage in more risky sexual behaviours [related link (well, sort of related – if you skip the first paragraph and see link i. and ii…)] […] Alcohol use and sexual activity often co-occur and more than one-quarter of sexually active teens used alcohol or drugs during their last sexual experience […] However, not only does the condom have to be used, but also it has to be used effectively (i.e. properly). Hatherall et al. (2007) report that a sizeable minority (between 12 and 40 per cent) applied a condom imperfectly. […] it is well documented that the earlier first sex occurs the less likely it is that contraception will be used […] Reviews have shown that school-based sex education leads to improved awareness of risk and knowledge of protection strategies, and increases intention to adopt safer sex behaviours. It has also been found to delay sexual debut (Kirby et al. 2006).”

March 24, 2015 Posted by | alcohol, Books, Epidemiology, Medicine, Psychology | Leave a comment

The Psychology of Lifestyle (II)

For general comments about the book, see my first post. In this post I’ll add some more observations of interest from the book.

“[M]any [children] show fear and avoidance of novel foods. The tendency to reject novel foods has been termed neophobia. Research has begun to reveal how early experience and learning can reduce the neophobic response to new foods, thereby enhancing dietary variety. For example, Birch and Marlin (1982) found that when 2 year olds were given varying numbers of opportunities to taste new fruits or cheeses, their preferences increased with frequency of exposure. Researchers found that between five and ten exposures to a new food were necessary before preference for that food increased. In another study, Gerrish and Mennella (2001) investigated the acceptance of a novel taste (pureed carrot) by infants who had previously experienced a range of tastes that included many vegetables but not carrot. Exposure to fruit, carrots alone or a variety of vegetables resulted in an increased acceptance of pureed carrot. Furthermore, those who had been exposed to a variety of vegetables were also more likely to eat other novel foods. Researchers concluded that familiarity with a variety of flavours increased the acceptance of novel foods. The implication was that parents should expose their children to a wide variety of tastes to encourage the acceptance of novel foods. […] exposure is a major factor in encouraging consumption. […] during childhood, the neophobic response to new foods decreases with age […]. Although repeated opportunities to taste and eat new food has been found to reduce neophobia and enhance acceptance, merely smelling or looking at the food has no such effect (Birch et al. 1987). This finding is consistent with the learned safety hypothesis which suggests that neophobia is only reduced as we learn that the food is safe to eat and does not cause illness […]. Further evidence suggests that watching others consume the food may provide a form of ‘exposure by proxy’ or modelling which could also reduce rejection […] observing a parent eating energy dense food could potentially encourage a child to establish similar food preferences. The effectiveness of the role model has been found to differ depending on the relationship between the child and the model. […] Birch (1980) and Duncker (1938, cited in Birch 1999) report that older children are more effective role models than younger children; Harper and Sanders (1975) report that mothers are more effective than strangers; and for older preschool children, adult heroes are more effective than ordinary adults (Birch 1999).”

“Promise of a reward is a time-honoured parental tactic for promoting consumption of healthy food. Nevertheless, it has been argued that treating food consumption in this way may actually decrease liking for that food. Lepper and Greene’s (1978) overjustification theory argues that offering a reward for an action devalues it for the child. In support of this a number of studies have reported decreased liking for foods when children are rewarded for eating them […] Horne et al. (2004) argue that in order for rewards to be effective, it is important that they are highly desirable and that they indicate to the child that they are for behaviour which is enjoyable and high status. Other studies have investigated the impact of using food as a reward. For example, Birch et al. (1980) presented children with foods either as a reward, a snack or in a non-social situation and found that acceptance increased if the food was presented as a reward. It is easy to generalise this finding to real life situations. High fat and sweet items are used repeatedly in positive contexts, for example on special occasions. The consumption of already pleasurable items in this way is reinforced. If children are given foods as rewards for approved behaviour, preference for those foods is enhanced (Benton 2004).”

“Cognitive models of eating behaviour explore the extent to which cognitions predict and explain behaviour. Most research from a cognitive perspective has drawn on social cognition models and several models have been developed […] All […] share the assumption that attitudes and beliefs are major determinants of eating behaviour, however they vary in terms of the cognitions they include and whether they use behavioural intentions or actual behaviour as their outcome measure […] Some research using the TRA and TPB has focused on predicting behavioural intentions. Research suggests however, that behavioural intentions are not that successful in predicting actual behaviour.”

“Traditionally habit has been measured by the number of times behaviour has been performed in the past […] Nevertheless behavioural recurrence does not constitute direct evidence for habitual processes. Verplanken and Orbell (2003) argue that habit is a psychological construct rather than behavioural recurrence and involves lack of awareness, difficulty to control, mental efficiency and repetition. Although repetition is a necessary requirement for a habit to develop, subsequent research has supported the hypothesis that frequency of past behaviour and habit are separate constructs [I also pointed this out elsewhere recently, but I think it’s an important insight. Revisiting my coverage of Buskirk et al.’s text after posting that comment I incidentally realized that Eysenck and Keane‘s coverage may well in some respects be more relevant/useful than the former.] […] It may be […] useful to conceptualise habits as established patterns of behaviour that may once have been initiated by rational choice but which are now under the control of specific situational cues that trigger the behaviour without cognitive effort. […] Reasoned action as represented in social cognition models and habit can be considered as two extremes of a conscious decision-making continuum. In between may lie a number of heuristic decision-making strategies that involve varying degrees of cognition.”

“Foltin et al. (1988) gave volunteers two cigarettes containing active marijuana or a placebo and found that active marijuana increased total caloric intake by 40 per cent. […] studies exploring the relationship between alcohol and food intake have been contradictory. In a mini-review Gee (2006) found that among eight studies reviewed, only one showed a significant difference in appetite ratings between the alcohol and no alcohol pre-load. […] Gee (2006) concluded that the effect of alcohol on appetite appears to be unsubstantiated; however alcohol’s effect on energy intake does appear significant. As well as recreational drugs, anti-psychotics and antidepressants have also been shown to influence hunger and satiety.” [Of course there are a large number of variables involved, but they don’t actually go into much detail in their coverage. To add to the list, sleep can also be quite important].

“According to Bourn (2001) approximately two-thirds of the UK’s population visit their GP at least annually, so primary care provides an unparalleled opportunity for health promotion and preventive interventions.” (This number is old, but a number like this one seems relevant to a wide variety of topics so even if it’s dated I decided to include it here anyway in order to increase the likelihood that I’ll remember the context of the estimate later).

“Despite considerable efforts over a number of years, there is limited evidence to suggest that educational approaches to dietary change (that is providing basic information about what constitutes a ‘healthy’ diet) alter children’s eating habits […] Hundreds of interventions to combat the obesity epidemic are currently being introduced worldwide, but there are significant gaps in the evidence base for such interventions and few been evaluated in a way that enables any definitive conclusions to be drawn about their effectiveness. Those that have shown an impact are limited to easily controlled settings and it remains unclear how promising small-scale initiatives would be scaled up for whole population impact (Butland et al. 2007). […] NICE recommends that interventions to improve diet should be multicomponent (i.e. including dietary modification, targeted advice, family involvement and goal setting), tailored to the individual, provide ongoing support, include behaviour change strategies and include awareness raising promotional activities as part of a longer term, multicomponent intervention rather than a one off activity.”

“The Office for National Statistics (2003) reported that distances walked annually dropped by 63 miles between 1975 and 2003 [I was actually sort of surprised the number wasn’t higher…]. Similarly, distances cycled dropped by 16 miles in the same period [I must admit part of the reason why I picked out the quote was that I wanted to illustrate once again why I gave this book a low rating on goodreads; the book here clearly gives you the impression that people walk less and bicycle less than they used to do. But try to look at those numbers and divide each of them with 365. There’s no way in hell those 16 miles of bicycling *per year* per person makes any measurable difference on any semi-relevant health variable of interest – this is something like 40 meters per day per person, or 10 seconds of bicycling per day, assuming an average speed of 15 km/hour…]. The proportion of people who travel by walking or cycling has declined by 26 per cent (Department of Health, Physical Activity, Health Improvement and Prevention 2004). [This number on the other hand seems much more likely to have health-relevance. But then you immediately start asking yourself: if that number is true, why are the other numbers so low? And the inclusion of all of the above numbers in the coverage actually illustrates perfectly a recurring issue I had with the coverage; there are a lot of numbers here, and they don’t all tell the same story, and the authors aren’t always making it the least bit easier to make sense of them because they seem to treat many of them quite uncritically. Maybe fewer people cycle, but those that do put in more kilometers – but the authors aren’t suggesting this in the text, so you sort of need to come up with these sorts of explanations for the semi-weird constellation of research results yourself]. Consequently, it has been argued that active transport is a key factor in the achievement of healthy levels of physical activity […] All four national surveys demonstrate the same sex difference in activity levels. Physical activity is the only lifestyle behaviour where men are more likely to achieve government guidelines than women […]. Sport is a traditional male activity which may contribute to this finding.”

“The relationship between [physical] activity and social class as measured by the National Statistics Socio-Economic Classification (NS-SEC) […] is complex. […] The relationship between NS-SEC and physical activity can be described by an inverted U-shaped curve, with those at either end of the NS-SEC scale being the least likely to be active. […] Compared to the general population, South Asian and Chinese men and women were much less likely to participate in physical activity of any kind. Bangladeshi men and women were the most inactive and were almost twice as likely as the general population to be classified as sedentary. […] Physical activity reduces the risk of premature mortality for everyone, regardless of their age, sex or ethnicity […] In England, the Department of Health, Physical Activity, Health Improvement and Prevention (2004) has estimated that adults who are physically active have a 20–30 per cent reduced risk of premature death. Warburton et al. (2006) have suggested that a 50 per cent reduction in risk from death is possible for the physically fit. The effect of physical activity on health manifests itself by its influence on a wide range of diseases. In particular, people who are physically active can achieve up to a 50 per cent reduced risk of developing the major lifestyle diseases: coronary heart disease, stroke, diabetes and cancers […] not only do inactive people face shorter lives, but also they face poor quality of life in the years preceding death. While the relationship of physical activity to each disease is important in its own right, what makes physical activity so important is the strength of its effect over such a wide range of conditions. […] Associations with health are generally stronger for measured cardiorespiratory fitness than for reported physical activity […] but a self-reported physical activity is still convincingly associated with reduced mortality […]. In short, cardiorespiratory fitness will benefit health but levels of physical activity that may not be of an intensity to alter physical fitness parameters may still have health benefits. […] Obesity is the main visible sign of inactivity, yet obesity is just one of possibly 20 chronic diseases and disorders for which low activity levels are a known contributory factor. […] it is easier to influence the energy intake–output balance through diet than through activity […] The evidence suggests that for physical activity to have a significant effect on bodyweight and in particular on weight loss then 30 minutes of moderate activity for five days a week is unlikely to be a high enough level of activity.”

“Social cognition theory has identified self-efficacy and perceived behavioural control as key factors in the practice of healthy levels of physical activity, but at best such models can predict 50 per cent of the variation in physical activity […] Extensive evaluation of social cognition models’ ability to predict uptake of physical activity leads to the conclusion that a perception of the risks of non-activity and the benefits of activity for health has at best a small impact of overall variation in physical activity behaviour. […] Kahn et al. (2002) in their review of informational campaigns found no evidence that informational only media-based campaigns were effective, in line with the theoretically derived conclusion that attempts to inform people of the benefits and costs of activity and inactivity are unlikely to facilitate substantial changes in behaviour. Similarly, Ogilvie et al. (2004) found no evidence that informational campaigns to increase active transport were successful. […] Behavioural interventions are more likely to be at a small group or individual level of intervention. Kahn et al. (2002) found that individually adapted behavioural change programmes were effective in increasing physical activity levels. Ogilvie et al. (2004) found that targeted behavioural change programmes were the most effective way to promote walking and cycling. […] Many public health interventions to increase physical activity in the community are not individualised, do not recognise the role of psychological processes in effective behavioural change and are carried out by professionals with no psychological training”.



March 20, 2015 Posted by | alcohol, Books, Epidemiology, Medicine, Pharmacology, Psychology | Leave a comment

100 Cases in Clinical Pathology

This book is another publication from the 100 Cases … series which I’ve talked about before – I refer to these posts for some general comments about what this series is like and some talk about the other books in the series which I’ve read. The book is much like the others, though of course the specific topics covered are different in the various publications. I liked this book and gave it 3 stars on goodreads. The book has three sections: a section dealing with ‘chemical pathology, immunology and genetics’; a section dealing with ‘histopathology’; and a section dealing with ‘haematology’. As usual I knew a lot more about some of the topics covered than I did about some of the others. Some cases were quite easy, others were not. Some of the stuff covered in Greenstein & Wood’s endocrinology text came in handy along the way and enabled me for example to easily identify a case of Cushing’s syndrome and a case of Graves’ disease. I don’t think I’ll spoil anything by noting that two of the cases in this book involved these disorders, but if you plan on reading it later on you may want to skip the coverage below, as I have included some general comments from the answer sections of the book in this post.

As someone who’s not working in the medical field and who will almost certainly never need to know how to interpret a water deprivation test (also covered in detail in Greenstein and Wood, incidentally), there are some parts of books like this one which are not particularly ‘relevant’ to me; however I’d argue that far from all the stuff included in a book like this one is ‘stuff you don’t need to know’, as there are also for example a lot of neat observations included about how specific symptoms (and symptom complexes) are linked to specific disorders, some related ideas about which other medical conditions might cause similar health problems, and which risk factors are potentially important to have in mind in specific contexts. If you’ve had occasional fevers, night sweats and experienced weight loss over the last few months, you should probably have seen a doctor a while ago – knowledge included in books like this one may make the reader perhaps a bit less likely to overlook an important and potentially treatable health problem, and/or increase awareness of potential modifiable risk factors in specific contexts. A problem is however that the book will be hard to read if you have not read any medical textbooks before, and in that case I would probably advise you against reading it as it’s almost certainly not worth the effort.

I have added a few observations from the book below.

“After a bone marrow transplant (and any associated chemotherapy), the main risks are infection (from low white cell counts and the use of immunosuppressants, such as cyclosporin), bleeding (from low platelet counts) and graft versus host disease (GVHD). […] An erythematous rash that develops on the palms or soles of the feet of a patient 10–30 days after a bone marrow transplant is characteristic of GVHD. […] GVHD is a potentially life-threatening problem that can occur in up to 80% of successful allogeneic bone marrow transplants. […] Clinically, GVHD manifests like an autoimmune disease with a macular-papular rash, jaundice and hepatosplenomegaly and ultimately organ fibrosis. It classically involves the skin, gastrointestinal tract and the liver. […] Depending on severity, treatment of acute GVHD may involve topical and intravenous steroid therapy, immunosuppression (e.g. cyclosporine), or biologic therapies targeting TNF-α […], a key inflammatory cytokine. […] Prognosis is related to response to treatment. The mortality of patients who completely respond can still be around 20%, and the mortality in those who do not respond is as high as 75%.”

“The leading indication for a liver transplant is alcoholic cirrhosis in adults and biliary atresia in children. […] The overall one-year survival of a liver transplant is over 90%, with 10-year survival of around 70%. […] Transplant rejection can be classified by time course, which relates to the underlying immune mechanism: • Hyperacute organ rejection occurs within minutes of the graft perfusion in the operating theatre. […] The treatment for hyperacute rejection is immediate removal of the graft. • Acute organ rejection take place a number of weeks after the transplant […] The treatment for acute rejection includes high dose steroids. • Chronic organ rejection can take place months to years after the transplant. […] As it is irreversible, treatment for chronic rejection is difficult, and may include re-transplantation.”

“Chronic kidney disease (CKD) is characterized by a reduction in GFR over a period of 3 or more months (normal GFR is >90–120 mL/min). It arises from a progressive impairment of renal function with a decrease in the number of functioning nephrons; generally, patients remain asymptomatic until GFR reduces to below 15 mL/min (stage V CKD). Common causes of CKD are (1) diabetes mellitus, (2) hypertension, (3) glomerulonephritis, (4) renovascular disease, (5) chronic obstruction or interstitial nephritis, and (6) hereditary or cystic renal disease”

“The definition of an aneurysm is an abnormal permanent focal dilatation of all the layers of a blood vessel. An AAA [abdominal aortic aneurysm] is defined when the aortic diameter, as measured below the level of the renal arteries, is one and a half times normal. Women have smaller aortas, but for convenience, more than 3 cm qualifies as aneurysmal. The main risk factors for aneurysm formation are male gender, smoking, hypertension, Caucasian/European descent and atherosclerosis. Although atherosclerosis is a risk factor and both diseases share common predisposing factors, there are also differences. Atherosclerosis is primarily a disease of the intima, the innermost layer of the vessel wall, whereas in aneurysms there is degeneration of the media, the middle layer. […] The annual risk of rupture equals and begins to outstrip the risk of dying from surgery when the aneurysm exceeds 5.5 cm. This is the size above which surgical repair is recommended, comorbidities permitting. […] Catastrophic rupture, as in this case, presents with hypovolaemic shock and carries a dismal prognosis.” [The patient in the case history died soon after having arrived at the hospital]

“Stroke refers to an acquired focal neurological deficit caused by an acute vascular event. The neurological deficit persists beyond 24 hours, in contrast to a transient ischaemic attack (TIA) where symptoms resolve within 24 hours, although the distinction is now blurred with the advent of thrombolysis. […] Strokes are broadly categorized into ischaemic and haemorrhagic types, the majority being ischaemic. The pathophysiology in a haemorrhagic stroke is rupture of a blood vessel causing extravasation of blood into the brain substance with tissue damage and disruption of neuronal connections. The resulting haematoma also compresses surrounding normal tissue. In most ischaemic strokes, there is thromboembolic occlusion of vessels due to underlying atherosclerosis of the aortic arch and carotid arteries. In 15–20% of cases, there is atherosclerotic disease of smaller intrinsic blood vessels within the brain[…]. A further 15–20% are due to emboli from the heart. […] The territory and the extent of the infarct influences the prognosis; [for example] expressive dysphasia and right hemiparesis are attributable to infarcts in Broca’s area and the motor cortex, both frontal lobe territories supplied by the left middle cerebral artery.”

“The stereotypical profile of a gallstone patient is summed up by the 4Fs: female, fat, fertile and forty. However, while gallstones are twice as common in females, increasing age is a more important risk factor. Above the age of 60, 10–20% of the Western population have gallstones. […] Most people with cholelithiasis are asymptomatic, but there is a 1–4% annual risk of developing symptoms or complications. […] Complications depend on the size of the stones. Smaller stones may escape into the common bile duct, but may lodge at the narrowing of the hepatopancreatic sphincter (sphincter of Oddi), obstructing the common bile duct and pancreatic duct, leading to obstructive jaundice and pancreatitis respectively. […] In most series, alcohol and gallstones each account for 30–35% of cases [of acute pancreatitis]. […] Once symptomatic, the definitive treatment of gallstone disease is generally surgical via a cholecystectomy.”

“Breast cancer affects 1 in 8 women (lifetime risk) in the UK. […] Between 10 and 40% of women who are found to have a mass by mammography will have breast cancer. […] The presence of lymphovascular invasion indicates the likelihood of spread of tumour cells beyond the breast, thereby conferring a poorer outlook. Without lymph node involvement, the 10-year disease-free survival is close to 70–80% but falls progressively with the number of involved nodes.”

“Melanoma is a cancer of melanocytes, the pigmented cells in the skin, and is caused by injury to lightly pigmented skin by excessive exposure to ultraviolet (UV) radiation […] The change in colour of a pre-existing pigmented lesion with itching and bleeding and irregular margins on examination are indicators of transformation to melanoma. Melanomas progress through a radial growth phase to a vertical growth phase. In the radial growth phase, the lesion expands horizontally within the epidermis and superficial dermis often for a long period of time. Progression to the vertical phase is characterized by downward growth of the lesion into the deeper dermis and with absence of maturation of cells at the advancing front. During this phase, the lesion acquires the potential to metastasize through lymphovascular channels. The probability of this happening increases with increasing depth of invasion (Breslow thickness) by the melanoma cells. […] The ABCDE mnemonic aids in the diagnosis of melanoma: Asymmetry – melanomas are likely to be irregular or asymmetrical. Border – melanomas are more likely to have an irregular border with jagged edges. Colour – melanomas tend to be variegated in colour […]. Diameter – melanomas are usually more than 7 mm in diameter. Evolution – look for changes in the size, shape or colour of a mole.”

“CLL [chronic lymphocytic leukaemia] is the most common leukaemia in the Western world. Typically, it is picked up via an incidental lymphocytosis in an asymptomatic individual. […] The disease is staged according to the Binet classification. Typically, patients with Binet stage A disease require no immediate treatment. Symptomatic stage B and all stage C patients receive chemotherapy. […] cure is rare and the aim is to achieve periods of remission and symptom control. […] The median survival in CLL is between four and six years, though some patients survive a decade or more. […] There is […] a tendency of CLL to transform into a more aggressive leukaemia, typically a prolymphocytic transformation (in 15–30% of patients) or, less commonly (<10% of cases), transformation into a diffuse large B-cell lymphoma (a so-called Richter transformation). Appearance of transformative disease is an ominous sign, with few patients surviving for more than a year with such disease.”

“Pain, swelling, warmth, tenderness and immobility are the five cardinal signs of acute inflammation.”

“Osteomyelitis is an infection of bone that is characterized by progressive inflammatory destruction with the formation of sequestra (dead pieces of bone within living bone), which if not treated leads to new bone formation occurring on top of the dead and infected bone. It can affect any bone, although it occurs most commonly in long bones. […] Bone phagocytes engulf the bacteria and release osteolytic enzymes and toxic oxygen free radicals, which lyse the surrounding bone. Pus raises intraosseus pressure and impairs blood flow, resulting in thrombosis of the blood vessels. Ischaemia results in bone necrosis and devitalized segments of bone (known as sequestra). These sequestra are important in the pathogenesis of non-resolving infection, acting as an ongoing focus of infection if not removed. Osteomyelitis is one of the most difficult infections to treat. Treatment may require surgery in addition to antibiotics, especially in chronic osteomyelitis where sequestra are present. […] Poorly controlled diabetics are at increased risk of infections, and having an infection leads to poor control of diabetes via altered physiology occurring during infection. Diabetics are prone to developing foot ulcers, which in turn are prone to becoming infected, which then act as a source of bacteria for infecting the contiguous bones of the feet. This process is exacerbated in patients with peripheral neuropathy, poor diabetic control and peripheral vascular disease, as these all increase the risk of development of skin breakdown and subsequent osteomyelitis.” [The patient was of course a diabetic…]

“Recent onset fever and back pain suggest an upper UTI [urinary tract infection]. UTIs are classified by anatomy into lower and upper UTIs. Lower UTIs refer to infections at or below the level of the bladder, and include cystitis, urethritis, prostatitis, and epididymitis (the latter three being more often sexually transmitted). Upper UTIs refer to infection above the bladder, and include the ureters and kidneys. Infection of the urinary tract above the bladder is known as pyelonephritis [which] may be life threatening or lead to permanent kidney damage if not promptly treated. UTIs are also classified as complicated or uncomplicated. UTIs in men, the elderly, pregnant women, those who have an indwelling catheter, and anatomic or functional abnormality of the urinary tract are considered to be complicated. A complicated UTI will often receive longer courses of broader spectrum antibiotics. Importantly, the clinical history alone of dysuria and frequency (without vaginal discharge) is associated with more than 90% probability of a UTI in healthy women. […] In women, a UTI develops when urinary pathogens from the bowel or vagina colonize the urethral mucosa, and ascend via the urethra into the bladder. During an uncomplicated symptomatic UTI in women, it is rare for infection to ascend via the ureter into the kidney to cause pyelonephritis. […] Up to 40% of uncomplicated lower UTIs in women will resolve spontaneously without antimicrobial therapy. The use of antibiotics in this cohort is controversial when taking into account the side effects of antibiotics and their effect on normal flora. If prescribed, antibiotics for uncomplicated lower UTIs should be narrow-spectrum […] Most healthcare-associated UTIs are associated with the use of urinary catheters. Each day the catheter remains in situ, the risk of UTI rises by around 5%. Thus inserting catheters only when absolutely needed, and ensuring they are removed as soon as possible, can prevent these.”

September 24, 2014 Posted by | alcohol, Books, Cancer/oncology, Cardiology, Diabetes, Immunology, Medicine, Microbiology, Nephrology, Neurology | Leave a comment

100 Cases in Clinical Medicine

This book is another book in the same series as the 100 Cases in Acute Medicine book. Here’s part of the preface:

“Most doctors think that the most memorable way to learn medicine is to see patients. It is easier to recall information based on a real person than a page in a textbook. Another important element in the retention of information is the depth of learning. Learning that seeks to understand problems is more likely to be accessible later than superficial factual accumulation. This is the basis of problem-based learning, whereby students explore problems with the help of a facilitator. The cases in this book are designed to provide another useful approach, parallel to seeing patients and giving an opportunity for self-directed exploration of clinical problems. They are based on the findings of history taking and examination, together with the need to evaluate initial investigations such as blood investigations, X-rays and electrocardiograms.

These cases are no substitute for clinical experience with real patients, but they provide a safe environment for students to explore clinical problems and their own approach to diagnosis and management. Most are common problems that might present to a general practitioner’s surgery, a medical outpatients clinic or a session on call in hospital. There are a few more unusual cases to illustrate specific points and to emphasize that rare things do present, even if they are uncommon. The cases are written to try to interest students in clinical problems and to enthuse them to find out more. They try to explore thinking about diagnosis and management of real clinical situations.”

As for the ‘interest students in clinical problems and to enthuse them to find out more’-part they certainly succeeded, but I approached this book in a slightly different manner than I did the first one in the series. When I read the acute medicine book, I’d occasionally think to myself while reading the patient history and/or the reported lab results that ‘hey, this sounds a bit like…’ and I’d look up the diagnosis/condition I was considering in order to decide if I wanted to ‘guess’ at that, before moving on to reading the answer part of the case. I did this a few times as well here, but actually most of the pre-answer wiki peeks were related to the interpretation of specific lab results (‘how to interpret some of the arterial blood gas test results’). The reason why I tried to limit myself from looking up stuff before reading the answer was that I wanted to know a little bit about how much of the pathophysiology text (and stuff covered in related texts, such as e.g. Hall’s Handbook and Rogers et al., as well as various medical lectures e.g. from Khan Academy) I could remember. I actually realized when reading the first 100 cases book that there were very few conditions covered there which I had not already read about, or at least seen mentioned, elsewhere; the problem was figuring out which patients had which specific problems. Part of the reason why I often had trouble with that part was incidentally related to the fact that there are some other relevant books I have not read – books such as this one or this one (I’m not planning on reading these, just in case you were wondering). A related point is that doctors have a lot more information available to them than do the people who are sick, and that this is certainly a (small) part of the explanation for why they are better at figuring out what’s wrong than are the people who are sick – symptoms can be non-specific, but if so lab results will often tell you more about where to look and what to look for. I decided beforehand when reading this book that I’d try for fun to keep score and figure out in how many cases I guessed the correct diagnosis; it turned out that I guessed the right diagnosis in roughly one-fifth of the cases and in a few other cases the guess I made was a very plausible differential diagnosis which needed to be ruled out anyway. In a few of them I didn’t get ‘the complete picture’, and I learned something from many of the cases where I knew the (‘diagnosis’-part of the-) right answer. I feel quite certain I would have guessed more of them if I’d spent more time on individual cases; I read the entire book yesterday, and this is not a book you can read in a few hours (I think it took me 12 hours, at least, but I’m not really sure as I didn’t keep track and did take breaks occasionally. Ratios like these – me spending easily 5-10 hours or more on stuff which leads to a post which you’ll read in perhaps 10-15 minutes – are incidentally one reason why I sometimes feel that people reading along here are ‘cheating’ in a way. On the other hand I really can’t complain as long as I’m enabling such ‘cheating’ in the first place…). I got far most of my guesses correct, as in many cases I didn’t guess at all because I wasn’t completely sure what was going on. Of course treatment and management aspects I didn’t ‘guess at’, and that’s an important aspect of the book as well. The conditions I recognized spanned a rather broad range; from colon cancer over HIV seroconversion illness (main differential was malaria – I knew this as well) to COPD, rheumatoid arthritis, bacterial meningitis, obstructive sleep apnea, peripheral neuropathy secondary to undiagnosed type 2 diabetes mellitus, dementia, small cell lung cancer with associated paraneoplastic syndrome, and Parkinson’s disease. As you can probably tell from those diagnoses, like the acute medicine book this book also has some rather depressing cases. Some cases, e.g. a case of cerebral toxoplasmosis secondary to HIV infection (this is actually an AIDS-defining illness, so she had AIDS at the time of admission) and a diet-related vitamin B12 deficiency, were really obvious in retrospect, but in medicine there’s a lot of stuff to remember.

I’ve added some quotes, observations and key points from the book below.

“Cystic fibrosis should always be considered when there is a story of repeated chest infections in a young person. Although it presents most often below the age of 20 years, diagnosis may be delayed until the 20s, 30s, 40s or later in milder cases.”

“Patients with a chronic persistent cough of unexplained cause should have a chest X-ray. When the X-ray is clear the cough is likely to be produced by one of three main causes in non-smokers. Around half of such cases have asthma or will go on to develop asthma over the next few years. Half of the rest have rhinitis or sinusitis with a postnasal drip. In around 20 per cent the cough is related to gastro-oesophageal reflux […] Cough is a common side effect in patients treated with angiotensin-converting enzyme (ACE) inhibitors.”

“This man has signs of chronic liver disease with ascites and oedema. […] The most common cause of chronic liver disease is alcohol. […] However, his alcohol intake is too low to be consistent with the diagnosis of alcoholic liver disease [15-20 units/week, according to the patient history. This was why I initially rejected alcohol-related pathology in this case and (very briefly) considered other causes instead, without coming up with anything (this was another one of those aforementioned obvious ones in retrospect)…]. When the provisional diagnosis is discussed with him, though, he eventually admits that his alcohol intake has been at least 40–50 units per week for the last 20 years. His alcohol intake has increased further during the last year after his marriage had ended.” [Patients sometimes lie to their doctors. This one did. In case you were wondering he died three years later from an esophageal variceal bleed.]

“Patients often become symptomatic due to renal failure only when their glomerular filtration rate (GFR) is less than 15 mL/min [normal range is 90+, US] and thus may present with end-stage renal failure.” [This is an example of a more general point in many medical contexts; our bodies often have a lot of ‘excess capacity’ and redundancies implemented in order to make us less likely to get sick/get symptoms which may decrease our likelihood of survival even if things aren’t optimal. The book actually has other examples illustrating this point, e.g. this: “Patients with central diabetes insipidus typically describe an abrupt onset of polyuria and polydipsia. This is because urinary concentration can be maintained fairly well until the number of AVP-secreting neurones in the hypothalamus decreases to 10–15 per cent of the normal number, after which AVP levels decrease to a range where urine output increases dramatically.”]

“Petechiae are small capillary haemorrhages that characteristically develop in crops in areas of increased venous pressure, such as the dependent parts of the body. Petechiae are the smallest bleeding lesions (pinhead in size), and suggest problems with platelet number or function. Purpura are larger in size than petechiae with variable shape and involve bleeding into subcutaneous tissues. Purpura can be seen in a variety of bleeding disorders […] AML is the most common acute leukaemia in adults with a mean age at presentation of 65 years. Patients with AML generally present with symptoms related to complications of pancytopenia (eg, anemia, neutropenia, and thrombocytopenia), including weakness, breathlessness and easy fatigability, infections of variable severity, and/or haemorrhagic findings such as gingival bleeding, ecchymoses, epistaxis, or menorrhagia.”

“Vegans who omit all animal products from their diet often have subclinical vitamin B12 deficiency […] Vitamin B12 deficiency may occur in strict vegetarians who eat no dairy products. […] Typical neurological signs are position and vibration sense impairment in the legs, absent reflexes and extensor plantars.”

“Malaria prophylaxis is often not taken regularly. Even when it is, it does not provide complete protection against malaria […] A traveller returning from a malaria endemic region who develops a fever has malaria until proven otherwise.”

“Peripheral oedema may occur due to local obstruction of lymphatic or venous outflow or because of cardiac, renal, pulmonary or liver disease. Unilateral oedema is most likely to be due to a local problem […] Bilateral oedema may be due to cardiac, liver or renal disease. […] Pitting oedema needs to be distinguished from lymphoedema, which is characteristically non-pitting. This is tested by firm pressure with the thumb for approximately 10 s. If the oedema is pitting, an indentation will be present after pressure is removed. […] frothy urine is a clue to the diagnosis of nephrotic syndrome and is commonly noted by patients with heavy proteinuria.”

“80% of C. difficile infections occur in people aged over 65 years since a lower density and fewer species of gut bacteria make them more susceptible to colonisation by C. difficile […] 20% of hospital patients and those in long-term care facilities are colonised with C. difficile. […] C. difficile infection should be suspected in any hospital patient who develops diarrhoea.”

“ADPKD [Autosomal Dominant Polycystic Kidney Disease] is the most common inherited renal disease, occurring in approximately 1:600 to 1:1000 individuals. Although the name ‘ADPKD’ is derived from renal manifestations of cyst growth leading to enlarged kidneys and renal failure, this is a systemic disorder manifested by the presence of hepatic cysts, diverticular disease, inguinal hernias, mitral valve prolapse, intracranial aneurysms and hypertension. […] Patients with ADPKD are often asymptomatic. […] Flank pain is the most common symptom […] Hypertension occurs early in the course of this disease, affecting 60% of patients with normal renal function. Approximately 50% of ADPKD patients will develop end-stage renal failure.”

“Transient small nodes in the neck or groin are common benign findings. However, a 3 × 4 cm mass of nodes for 2 months is undoubtedly abnormal. […] Lymph nodes are normally barely palpable, if at all. The character of enlarged lymph nodes is very important. In acute infections the nodes are tender, and the overlying skin may be red. Carcinomatous nodes are usually very hard, fixed and irregular. The nodes of chronic leukaemias and lymphomas are non-tender, firm and rubbery.  […] The typical systemic symptoms of lymphoma are malaise, fever, night sweats, pruritus, weight loss, anorexia and fatigue.”

“Colonic diverticula are small outpouchings that are most commonly found in the left colon. […] Inflammation in a diverticulum is termed diverticulitis. […] Diverticular disease is a common finding in the elderly Western population and may be asymptomatic or cause irritable bowel syndrome-type symptoms. […] Diverticular disease is a common condition; its presence can distract the unwary doctor from pursuing a coincident condition.”

“Tension type headaches are the commonest headaches in the general population. The typical presentation is of mild to moderate headache, nonthrobbing, bilateral with no associated symptoms. Cluster headaches are characterised by attacks of severe unilateral orbital or temporal pain, accompanied by autonomic features such as nasal congestion, lacrimation and rhinorrhoea. Migraines are often preceded by characteristic symptoms such as flashing lights and are often unilateral. Nausea and photophobia may occur during an attack. Brain tumours cause headaches by causing raised intracranial pressure. The headache is worse after coughing and is often associated with nausea and vomiting. […] The sudden onset of a headache within seconds or a few minutes is characteristic of a subarachnoid haemaorrhage (SAH). […] Patients with SAH often describe the pain as ‘the worst headache in my life’. [And in many cases it’s also the last headache they ever will have:] SAH is associated with a mortality rate of up to 50%.”

“He drinks 35 units of alcohol per week and smokes 30 cigarettes per day.” [Aargh! Another one of those! But at least this one didn’t lie about his drinking habits. … But it gets worse:] “No history was available from the patient [she’s in a coma], but her partner volunteered the information that they are both intravenous heroin addicts. She is unemployed, smokes 25 cigarettes per day, drinks 40 units of alcohol per week and has used heroin for the past 4 years.” [Dammit! Some of these histories are depressing in more than one way. The woman had been found unconscious by her partner. My first thought when reading the case story about the woman and the lab results was that, ‘This reminds me of that movie I saw a while back, what’s it called..?’ – I can’t remember the name of the movie, but it’s not important. I want to quote a bit more extensively from the answer part of this case because I thought it was sort of fascinating in a way; it illustrates how a drug overdose isn’t always just a problem because of the drug overdose:]

“This patient has acute renal failure as a result of rhabdomyolysis. Severe muscle damage causes a massively elevated serum creatine kinase (CK) level and a rise in serum potassium and phosphate levels. In this case, she has lain unconscious on her left arm for many hours due to an overdose of alcohol and intravenous heroin. As a result, she has developed severe ischaemic muscle damage, causing release of myoglobin, which is toxic to the kidneys. […] Acute renal failure due to rhabdomyolysis causes profound hypocalcaemia in the oliguric phase due to calcium sequestration in muscle and reduced 1,25-dihydroxycalciferol levels, often with rebound hypercalcaemia in the recovery phase. This woman’s consciousness level is still depressed as a result of opiate and alcohol toxicity, and she has clinical and radiological evidence of aspiration pneumonia. She has mixed metabolic and respiratory acidosis (low pH, bicarbonate) due to acute renal failure and respiratory depression (pCO2 elevated). Her arterial oxygenation is reduced due to hypoventilation and pneumonia. She also has compartment syndrome in her arm due to massive swelling of her damaged muscles. This patient has life-threatening hyperkalaemia with electrocardiogram (ECG) changes. […] Emergency treatment involves intravenous calcium gluconate, which stabilizes cardiac conduction, and intravenous insulin/glucose, intravenous sodium bicarbonate and nebulized salbutamol, all of which temporarily lower the plasma potassium by increasing the cellular uptake of potassium. However, these steps should be regarded as holding measures while urgent dialysis is being organized. The chest X-ray and clinical findings indicate consolidation of the left lower lobe. This patient should initially be managed on an intensive care unit. She will require antibiotics for her pneumonia and will require a naloxone infusion or mechanical ventilation for her respiratory failure. The patient should have vigorous rehydration with monitoring of her central venous pressure. If a good urinary flow can be maintained, urinary pH should be kept greater than 7.0 by bicarbonate infusion, which prevents the renal toxicity of myoglobin. This patient also needs to be considered urgently for surgical fasciotomy to relieve the compartment syndrome in her arm.”

Back when I read the Acute Muscle Injuries text, compartment syndrome was sort of a worst-case-scenario. Here it’s just one of multiple problems, each of which on their own would be quite terrible. I should incidentally note in case you were wondering if all of the patients in this book are alcoholics that most of them are not – but that they mention in the coverage that: “In some surveys alcohol is linked directly to around 25% of acute medical admissions.” I looked around very briefly for those numbers because they sounded very high to me, but I didn’t find much. This paper had an estimate of 6%, but that’s out of all hospital admissions and you’d expect the proportion of all admissions involving alcohol to be significantly lower than the proportion of acute admissions. Note in that context that ‘the true number’ in the former case is to some extent unknowable – though you can try to estimate it, as people do – as e.g. alcohol’s role in certain cancers is quite difficult to figure out in general, and impossible to figure out at the individual level; it makes sense to say that drinking alcohol increases your risk of breast cancer (and perhaps that’s not even the best example as we’re quite sure alcohol has a role there, a level of certainty we in other areas of oncology do not have), but deciding with certainty whether patient X’s specific case of breast cancer was alcohol-related or not is impossible – ‘it may have been a contributing factor’ is probably the closest you can get, we don’t have a test for that. Same goes for a cardiovascular event – ‘alcohol may have played a role’, but that’s it. Perhaps also worth remembering here is incidentally that on a related note some epidemiological findings trying to have a closer look at precisely these sorts of things may have results which are partially explained by statistical artifacts unrelated to the ‘true’ associated risk; a smoker who drinks a lot is highly likely to die from various alcohol- and smoking-related causes at a relatively early age. Such early deaths may well make people with such habits less likely to get old enough to get prostate cancer (the risk of which increases dramatically with age), even if alcohol and smoking on their own perhaps actually increase the risk of prostate cancer, in the sense that the effects of both alcohol and smoking may be to make those cells more likely to turn malignant (I don’t know if this is actually the case or not, it’s just the sort of thing you need to watch out for). There are ways around such problems – a competing risks framework is important to have in mind here – but problems of this sort are sometimes hard to avoid and/or deal with.

They don’t talk about these things in the book, but they talk about a lot of other interesting stuff, and I can’t cover all of it. One thing I have yet to cover which I thought I should include as a small favour to a friend reading along is this part, from the very last pages of the book:

“Traditional Chinese medicine includes herbal therapy, acupuncture, massage and dietary therapy. There is potential for developing novel treatments for diseases such as asthma and food allergies with Chinese herbs. However, there is concern over the lack of standardization and controlled clinical trials. Chinese herbal medicines containing aristolochic acid have been implicated in a specific nephropathy characterised by extensive interstitial fibrosis with atrophy and loss of the tubules, with thickening of the walls of the interlobular and afferent arterioles. Blood pressure is generally normal or only modestly elevated. Patients presenting with a creatinine < 200 will generally stabilise their renal function after stopping the Chinese medications, but patients with worse kidney function will generally progress to end-stage kidney failure.”

I liked the book and I gave it three stars on goodreads. You need to be fluent in ‘medical textbook’ in order to get much out of this book, but if you have some medical knowledge I believe you’ll be quite likely to find the books in this series quite interesting.

June 8, 2014 Posted by | alcohol, Books, Cancer/oncology, Epidemiology, Infectious disease, Medicine, Microbiology, Nephrology | Leave a comment

Random stuff

i. Effects of Academic Acceleration on the Social-Emotional Status of Gifted Students.

I’ve never really thought about myself as ‘gifted’, but during a conversation with a friend not too long ago I was reminded that my parents discussed with my teachers at one point early on if it would be better for me to skip a grade or not. This was probably in the third grade or so. I was asked, and I seem to remember not wanting to – during my conversation with the friend I brought up some reasons I had (…may have had?) for not wanting to, but I’m not sure if I remember the context correctly and so perhaps it’s better to just say that I can’t recall precisely why I was against this idea, but that I was. Neither of my parents were all that keen on the idea anyway. Incidentally the question of grade-skipping was asked in a Mensa survey answered by a sizeable proportion of all Danish members last year; I’m not allowed to cover that data here (or I would have already), but I don’t think I’ll get in trouble by saying that grade-skipping was quite rare even in this group of people – this surprised me a bit.

Anyway, a snippet from the article:

“There are widespread myths about the psychological vulnerability of gifted students and therefore fears that acceleration will lead to an increase in disturbances such as anxiety, depression, delinquent behavior, and lowered self-esteem. In fact, a comprehensive survey of the research on this topic finds no evidence that gifted students are any more psychologically vulnerable than other students, although boredom, underachievement, perfectionism, and succumbing to the effects of peer pressure are predictable when needs for academic advancement and compatible peers are unmet (Neihart, Reis, Robinson, & Moon, 2002). Questions remain, however, as to whether acceleration may place some students more at risk than others.”

Note incidentally that relative age effects (how is the grade/other academic outcomes of individual i impacted by the age difference between individual i and his/her classmates) vary across countries, but are usually not insignificant; most places you look the older students in the classroom do better than their younger classmates, all else equal. It’s worth having both such effects as well as the cross-country heterogeneities (and the mechanisms behind them) in mind when considering the potential impact of acceleration on academic performance – given differences across countries there’s no good reason why ‘acceleration effects’ should be homogenous across countries either. Relative age effects are sizeable in most countries – see e.g. this. I read a very nice study a while back investigating the impact of relative age on tracking options of German students and later life outcomes (the effects were quite large), but I’m too lazy to go look for it now – I may add it to this post later (but I probably won’t).

ii. Publishers withdraw more than 120 gibberish papers. (…still a lot of papers to go – do remember that at this point it’s only a small minority of all published gibberish papers which are computer-generated…)

iii. Parental Binge Alcohol Abuse Alters F1 Generation Hypothalamic Gene Expression in the Absence of Direct Fetal Alcohol Exposure.

Nope, this is not another article about how drinking during pregnancy is bad for the fetus (for stuff on that, see instead e.g. this post – link i.); this one is about how alcohol exposure before conception may harm the child:

“It has been well documented that maternal alcohol exposure during fetal development can have devastating neurological consequences. However, less is known about the consequences of maternal and/or paternal alcohol exposure outside of the gestational time frame. Here, we exposed adolescent male and female rats to a repeated binge EtOH exposure paradigm and then mated them in adulthood. Hypothalamic samples were taken from the offspring of these animals at postnatal day (PND) 7 and subjected to a genome-wide microarray analysis followed by qRT-PCR for selected genes. Importantly, the parents were not intoxicated at the time of mating and were not exposed to EtOH at any time during gestation therefore the offspring were never directly exposed to EtOH. Our results showed that the offspring of alcohol-exposed parents had significant differences compared to offspring from alcohol-naïve parents. Specifically, major differences were observed in the expression of genes that mediate neurogenesis and synaptic plasticity during neurodevelopment, genes important for directing chromatin remodeling, posttranslational modifications or transcription regulation, as well as genes involved in regulation of obesity and reproductive function. These data demonstrate that repeated binge alcohol exposure during pubertal development can potentially have detrimental effects on future offspring even in the absence of direct fetal alcohol exposure.”

I haven’t read all of it but I thought I should post it anyway. It is a study on rats who partied a lot early on in their lives and then mated later on after they’d been sober for a while, so I have no idea about the external validity (…I’m sure some people will say the study design is unrealistic – on account of the rats not also being drunk while having sex…) – but good luck setting up a similar prospective study on humans. I think it’ll be hard to do much more than just gather survey data (with a whole host of potential problems) and perhaps combine this kind of stuff with studies comparing outcomes (which?) across different geographical areas using things like legal drinking age reforms or something like that as early alcohol exposure instruments. I’d say that even if such effects are there they’ll be very hard to measure/identify and they’ll probably get lost in the noise.

iv. The relationship between obesity and type 2 diabetes is complicated. I’ve seen it reported elsewhere that this study ‘proved’ that there’s no link between obesity and diabetes or something like that – apparently you need headlines like that to sell ads. Such headlines make me very, tired.

v. Scientific Freud. On a related note I have been considering reading the Handbook of Cognitive Behavioral Therapy, but I haven’t gotten around to that yet.

vi. If people from the future write an encyclopedic article about your head, does that mean you did well in life? How you answer that question may depend on what they focus on when writing about the head in question. Interestingly this guy didn’t get an article like that.

March 1, 2014 Posted by | alcohol, Diabetes, Genetics, Personal, Psychology, Studies, Wikipedia | 2 Comments

Query plus ‘stuff’

i. My birthday is in two months, so I’ll probably be sending out a wish list in a couple of weeks (the kinds of books I usually want have to be sent from other parts of the world and that takes a lot of time…). Which means that now is a good time for you to recommend books and other stuff to me.

After reading this article on ‘The Real War 1939-1945’, (it’s quite long, don’t start reading it if you have but 5 or 10 minutes at your disposal – and thanks for linking to it Gwern!) I decided to add this book to my list. The author died just 6 days ago.

ii. A very good chess ressource. Also, this.

iii. Maybe the ‘good cholesterol’ isn’t all that good after all.

iv. A paper on the effects of alcohol on behaviour which some readers might find interesting.

v. Another one of Steven Farmer’s pharmacology lectures – Antimicrobial Agents 1:

vi. I read two whole chapters in The Human Past today, as well as part of a third. It’s a textbook, so (2,3-2,4?) chapters corresponds to ~10 hours of reading or so (one of the chapters was quite short). I decided to just add some related links from wikipedia below, in no particular order. This is some of the stuff I’ve been reading about:

Domestication of the pig
Terrace (agriculture)
Talheim Death Pit

City formation
Post-glacial rebound
Younger Dryas
Maglemosian culture
Beaker culture
Varna Cemetery
Linearbandkeramik (LBK) / Linear Pottery Culture (LPC)
Hallstatt culture
Lindow Man (featured article)
Ötzi the Iceman (people who read Razib Khan regularly will probably remember his posts on this one)

The climate-related stuff I found fascinating, but there’s only so much of that kind of stuff you can put into a book about ‘the human past’ so naturally the treatment of this subject was not as detailed as I’d perhaps have liked. Did you know that before the end of the last ice age, Japan wasn’t separated from the Asian mainland? Or that Tasmania was part of Australia? That you could walk from Britain to France? Do also read the articles on Sundaland and Doggerland and recall that not that long ago, you could walk from Asia to America… Also, “faunal evidence indicates the presence of domesticated cattle in the central Sahara by at least the 5th millenium BC. Only during the 3rd millenium BC did climate patterns change and the Sahara begin to take on the desert-like character it has today” (p.181) The world isn’t what it was, it’s very different, and you don’t actually need to go very far back in time to get very surprised at what has happened and how much things have changed.

Sorry for the infrequent updates.

May 29, 2012 Posted by | alcohol, Anthropology, Archaeology, Books, Chess, Geology, History, Infectious disease, Lectures, Medicine, Microbiology, Personal, Pharmacology, Wikipedia | Leave a comment

The Neuropathology of Alcohol-Related Brain Damage

“Excessive alcohol use can cause structural and functional abnormalities of the brain and this has significant health, social and economic implications for most countries in the world. Even heavy social drinkers who have no specific neurological or hepatic problems show signs of regional brain damage and cognitive dysfunction. Changes are more severe and other brain regions are damaged in patients who have additional vitamin B1 (thiamine) deficiency (Wernicke–Korsakoff syndrome). Quantitative studies and improvements in neuroimaging have contributed significantly to the documentation of these changes but mechanisms underlying the damage are not understood.”

From the abstract of this paper. Some more stuff from the paper:

“It has long been accepted that excessive alcohol use can cause structural and functional abnormalities of the brain and other organs (Courville, 1955; Victor et al., 1959; Dreyfus and Victor, 1961). In the brain, this has been demonstrated clinically, with imaging techniques and pathologically. Many alcoholics can also develop cirrhosis of the liver that can impact on brain structure and function and others develop nutritional deficiency states (vitamin B1 deficiency) that can cause severe brain damage and dysfunction. These latter two groups of alcoholic cases are often defined as ‘complicated alcoholics’ to differentiate them from those who do not have liver disease or nutritional deficiency states (uncomplicated alcoholics). Nevertheless, ‘uncomplicated alcoholics’ who are cognitively impaired have abnormalities (Pfefferbaum et al., 1997). The risks of ‘moderate’ alcohol consumption are more difficult to assess. Ding and colleagues showed that the more alcohol consumed, the larger the cerebrospinal fluid-filled spaces of the brain became (Ding et al., 2004). This data correspond with a neuropathological study that showed an increase in the cerebrospinal fluid-filled spaces covering the brain (pericerebral space) in men drinking more than eight standard drinks per day and a similar distinctive trend in those drinking five to eight standard drinks per day (Harper et al., 1988). […]

The first quantitative neuropathological study on brain weights in alcoholics (Harper and Blumbergs, 1982) was inspired by the various reports of ‘brain shrinkage’ seen on CT scans in alcoholics (Cala et al., 1978; Ron et al., 1980). Alcoholics have a reduced brain weight compared to controls and the degree of brain atrophy has been shown to correlate with the rate and amount of alcohol consumed over a lifetime (Harding et al., 1996). […]

As noted above, the mechanism for alcoholism-related white matter loss, restoration with alcohol abstinence and disruption of micro structural integrity still remains unclear but probably involves changes in both myelination and axonal integrity. This has been inferred from in vivo human and experimental MR diffusion tensor imaging studies (Pfefferbaum et al., 2006b, 2007) and may explain why tissue volume recovery appears incomplete with abstinence. Thus, alcoholic brain pathology may have two components, one reflecting permanent change and one a transient change. Regarding permanent effects, alcohol-related neuronal loss has been documented in specific regions of the cerebral cortex (superior frontal association cortex), hypothalamus and cerebellum (Harper, 1998). Such loss will result in axonal (Wallerian) degeneration and a permanent reduction in white matter volume. Structural changes in myelin, however, could explain the reversible white matter shrinkage that has been documented with serial MRI studies following periods of abstinence from alcohol (Shear et al., 1994; Pfefferbaum et al., 1995; Gazdzinski et al., 2005). […]

Analysis of the types of neurons lost from the frontal cortex revealed that they were the larger ones with a somal area >90 μm (Harper and Kril, 1989). This population of neurons is also more vulnerable in both Alzheimer’s disease (Terry et al., 1981) and normal aging (Terry and Hansen, 1987). There does not appear to be any link between alcohol-related brain damage and Alzheimer’s disease (Morikawa et al., 1999), although there is some work that suggests a relationship between alcohol and aging (Harper et al., 1998a).”

April 9, 2012 Posted by | alcohol, Medicine, Neurology, Studies | Leave a comment


1. A blitz chess game. I had black against a german player, Gerhard Richter. According to FIDE, there’s a guy with that name who has an ELO rating of 1949. I assume that was the guy I played against though I can’t know for certain – he had a quite high ‘slow rating’ so it was a strong player either way. In the game he drops a pawn at one point and I basically just run him over (though he does have some counterplay) after that – very satisfying to get a win like that against a strong opponent.

2. Will we ever restore sight to the blind?

It’s interesting how far medical science has advanced in some areas – to some degree we do ‘live in the future’, so to speak. I thought it was a bit funny that Ed would post this on the same day that I had a scheduled follow-up related to the medical trial in which I’m participating – I spent two hours today having my eyes looked at and measured in all kinds of ways.

3. U.S. Homicide Trends. The data are not completely up to date, but 2005 isn’t that long ago. Did you know that roughly 8 out of 9 (88,8%) of all homicides are committed by males? Or that males are almost 4 times more likely to get murdered? Here are some more data:

Females are much more likely to be killed by an intimate or a family member. If all else were equal (it’s not, but it’s probably worth pondering whether this changes the conclusion..), a female would be able to reduce her risk of getting killed significantly just by staying single instead of getting intimately involved with someone. Note that whereas something like one third of all female murder victims get killed by an intimate, the corresponding male number is just 3% (here’s another link adding more detail) – in terms of optimal strategies for lowering risk, the two genders should focus on different variables here. When dealing with the murders of females at the age of 25-50, approximately 40% of them are committed by an intimate (see previous link).

3a. I remember reading a study at one point (via MR?) where they looked at murder rates using BAC as an explanatory variable. I tried looking around in the archives but it seems that I did not blog it back then – I thought I had. Anyway, I’m not sure this study was the one I was thinking about but it covers the same subject and it was what popped up when doing a quick google – Alcohol, drugs and murder: A study of convicted homicide offenders. Abstract:

“Data on 1,887 convicted homicide offenders were examined to discern the relationships between alcohol and/or drug use and murder. Information obtained through confidential interviews at state prisons and local jails provided demographics and information on drinking and drug use immediately before the crime and relevant data on the offenders’ typical drinking style. About 50 percent of the offenders were under the influence of alcohol at the time of the crime, similar to the rate found by other studies. Substance use was more prevalent than nonuse before the homicide: 36 percent used alcohol only, 13 percent used both alcohol and drugs, 7 percent used drugs only, and 43 percent did not use either. A heavier style of drinking is much more prevalent among homicide offenders than in the general population. Blacks showed the least involvement with alcohol before homicide. A direct role for alcohol is indicated by the finding that homicides were associated with a heavier than usual episode of drinking and the large mean alcohol consumption contiguous to the crime (9.3 ounces of alcohol or about 18 drinks). Evidence also indicates that a unique relationship existed between drug use and homicide.”

A majority of people who commit murder, at least in the US, do so under the influence of drugs or alcohol.

March 12, 2012 Posted by | alcohol, Chess, Data, Demographics, Medicine | 10 Comments

Beer goggles, parties…

When I went to that party at uni a little while ago (I tweeted it at the time, but no blog posts) I felt a bit like Jane Goodall. At least during the time periods of it where I was not caught up in social interactions, but perhaps also during the rest of it – I was very aware of the social context. I came to realize that I’ll probably never feel the same way about being at a party as I did when I was younger (I’m not actually that old now, just ‘older’). I also came to realize that this particular method of meeting people of the opposite sex, though inefficient, is not actually necessarily as bad as I’ve been telling myself. Exposure rate is high, you have the potential to meet a lot of people over a short amount of time, and the likelihood of ‘something happening’ goes up quite a bit with the consumption of alcohol, some of the (party-related?) effects of which I’d forgotten all about. As a standard selection and pairing-mechanism, parties like these aren’t really totally stupid, though some people deal better with the setting than others and thus have higher returns from participating – from my own experience I conclude that my expected returns from participating are probably low, however given the right social setting participating in such a thing needn’t be a boring and unpleasant, or perhaps even painful, experience. Though I continue to believe that it’s a far from optimal method. Traditional dating is costly, but those costs could also be considered part of an implicit selection mechanism weeding out non-serious candidates – but a major problem with traditional dating is that you need to meet the potential partner first, which is (certainly part of) the whole point of (these kinds of) parties.

Anyway, below a little random stuff on the beer goggles phenomenon, alcohol and sexual behaviour, partnership and obesity risk ect.:

i. From Beer goggles: blood alcohol concentration in relation to attractiveness ratings for unfamiliar opposite sex faces in naturalistic settings, by Lyvers, Cholakians, Puorro & Sundram:

“The popular notion that alcohol intoxication enhances perceptions of the physical attractiveness of the opposite sex has been inconsistently supported. The current study tested intoxicated and non-intoxicated persons of both genders in naturalistic settings after measuring their blood alcohol concentration (BAC) by a breath test. A sample of 80 heterosexual university student social drinkers was recruited at a campus pub and campus parties over a 3 month period to take a survey rating the attractiveness of unfamiliar faces of the opposite gender presented in photographs. Attractiveness ratings were positively correlated with BAC. Analysis of covariance (ANCOVA) was conducted on attractiveness ratings with independent variables of gender and BAC group, with three levels of the latter: non-intoxicated (BAC = 0), moderately intoxicated (BAC .01%-.09%), and highly intoxicated (BAC .10%-.19%). Both intoxicated groups gave significantly higher attractiveness ratings than non-intoxicated controls. The findings confirm the “beer goggles” phenomenon of folk psychology for both genders, although the mechanism remains unclear.”

I think it’s interesting that the ‘beer goggles’ start kicking in at BACs well below .1% (if they did not, the evaluations of the ‘moderately intoxicated’ group would match those of the non-intoxicated group).

ii. From Alcohol intoxication and self-reported risky sexual behaviour intentions with highly attractive strangers in naturalistic settings :

“Objective: The present investigation examined the relationship between alcohol intoxication and risky sex intentions in naturalistic settings.

Methods: Heterosexual young adults (n == 72) were approached at a campus pub and at campus parties. Blood alcohol concentration (BAC) was measured by a breath test and ranged from 0 to 0.18%%. Participants rated their likely intent to have sex with 10 highly attractive unfamiliar models of the opposite gender, as depicted in photographs, if the opportunity arose. Photos varied in terms of accompanying information regarding risk, with three levels: slight risk, moderate risk and high risk.

Results: BAC was significantly positively correlated with self-reported likelihood of young adult men engaging in risky sex with highly attractive unfamiliar models at all risk levels, whereas in young adult women the relationship was significant only at the slight risk level. Men reported significantly higher intent to have risky sex than women did at all risk levels.”

iii. From Entry Into Romantic Partnership Is Associated With Obesity, by Natalie S. The & Penny Gordon-Larsen:


“BMI is highly correlated between spouses; however, less is understood about the underlying mechanism(s) by which the development of obesity in one individual increases the risk of obesity in his/her spouse. The objective of this study is to investigate whether romantic partnership and duration of cohabitation are related to incident obesity and obesity-promoting behaviors. We used two data sets from the National Longitudinal Study of Adolescent Health: (i) 6,949 US adolescents (wave II, 1996) followed into adulthood (wave III, 2001–2002) and (ii) 1,293 dating, cohabiting, and married romantic couples from wave III, including measured anthropometry and self-report behavior data. In the longitudinal cohort, we used sex-stratified logistic regression models to examine the risk of incident obesity by longitudinal romantic relationship status and duration of time spent living with a romantic partner. In the Couples Sample, we used multinomial logistic regression to predict concordance in outcomes: obesity, moderate-to-vigorous physical activity, and screen time by romantic partnership and duration of time living with a romantic partner. Individuals who transitioned from single/dating to cohabiting or married were more likely to become obese than those who were dating at both waves. Partner concordance for negative, obesity-related behaviors was strongest for married couples and couples who lived together greater than or equal to 2 years. The shared household environment may increase the likelihood of becoming obese, influence partner concordance, and may be an important target for obesity intervention.”

Some more details:

“Men living with a romantic partner for 1.00–1.99 years were twice as likely to become obese, compared to men not living with a romantic partner.” […]

“Concordant obesity was over threefold higher (prevalence ratio (PR) = 3.30, 95% CI: 1.97–5.55), and discordant obesity twofold higher (PR = 1.90, 95% CI: 1.37–2.63) than concordant nonobesity in married vs. dating partners (Figure 1a). Similarly, married couples were more likely to consist of one or two less physically active partners than dating couples (PR = 2.00, 95% CI: 1.29–3.12 and PR = 2.15, 95% CI: 1.39–3.31, respectively) (Figure 1b), while cohabiting couples were more likely to consist of two sedentary partners (PR = 1.98, 95% CI: 1.37–2.87) (Figure 1c).” […]

“Duration of relationship was strongly associated with concordant obesity. Romantic partners who lived together greater than or equal to 2 years were significantly more likely to consist of one or two obese, less physically active, and more sedentary partners” [To take an example, the Odds Ratio of both partners being obese is 1.18 for a couple that’s been together less than a year (1.0 corresponds to the obesity risk of individuals who’re not living together with a partner), whereas it’s 4.31 for a couple that’s been together for more than 2 years, US]” […]

“Several studies examining longitudinal changes in romantic relationship status report a differential sex effect of entry into marriage, with greater weight gain in women (9,10,30). Women may be differentially impacted by transitions in romantic relationship status; for example, through increased social obligations encouraging consumption of regular meals (31,32) and larger portion sizes (33), resulting in increased energy intake (30). Further, entry into cohabitation or marriage is associated with decreased physical activity (34) and a decline in desire to maintain weight for the purpose of attracting a mate (6). In contrast, obese women may be less likely to marry (35). Our longitudinal findings suggest that both men and women who enter marriage are more likely to become obese, consistent with findings from another large, racially diverse sample of young adults (36). Moreover, we found that individuals who lived with romantic partners for a longer duration had higher likelihood of incident obesity suggesting that shared household environmental factors may contribute to changes in obesity.”

It’s an American study, but I’m pretty sure some of the mechanisms driving the results apply as well in other parts of the world.

September 25, 2011 Posted by | alcohol, Data, dating, Personal, Psychology, Studies | Leave a comment

Alcohol consumption, a few numbers

Two great graphs, from gnxp (there’s more at the link):

The ‘wordsum’ variable above is a vocabulary test; a higher score indicates that an individual has a more extensive vocabulary.

This report (pdf) concludes that in Denmark, “there’s no (/significant? /clear? /obvious?) connection between average alcohol-consumption and length of education.”

(“Der er ingen tydelig sammenhæng mellem gennemsnitligt alkoholforbrug og
uddannelseslængde, men umiddelbart har skoleelever det højeste gennemsnitlige forbrug.”)

I’m not sure that’s the right conclusion to draw and they make no attempt to justify it, they just state it as if it was a fact without any further comments. Here’s a graph of the results:

I have excluded from the graph the two variables ‘skoleelev’ and ‘anden skoleuddannelse’ because I have no clue precisely what those varibles mean and who they include (both relate to people somewhere in the educational system, but that’s all I know). Does a high school student belong to the ‘skoleelev’ or the ‘anden skoleuddannelse’ segment? When is something a ‘skoleuddannelse’? I have no idea. Stuff like that can just really make me mad – the communication here is so damn poor that I’d rather throw away the results than post them here. Anyway, I was surprised that people with the shortest education drink (much) less than average and less surprised that people with a long education drink more than average. I’d assumed that the relationsship between education and alcohol consumption was v-shaped. Maybe selection bias is at work here, I don’t know, but these data certainly do not support the hypothesis of a v-shaped relationsship. The reason why I believe their conclusion (‘no connection btw…’) is incorrect is that there do seem to be a relationsship between education and alcohol consumption; it looks like people without much schooling drink much less than average and that people with a relatively long education drink more than average. No, you can’t draw a straight line, but who says the ‘relationsship’ should necessarily be a straight line? The fact that alcohol consumption varies widely across education levels is a clear sign that the two variables are in fact connected, even if we don’t know precisely how they are connected. Note that these numbers are not age-adjusted and that I’ve taken out people from the educational system. There are a lot more 20-30 year old plumbers who’re no longer in the educational system than there are people with phd’s. That’s another way to say that the group of people with long educations should actually be drinking less than the other groups, all else equal, because they’re on average a few years older (and ‘older’ here means ‘drink less’ for the relevant age demographic).

The report has a lot more data. Some of the results are quite surprising. Here’s one bit that took me by surprise: ‘41,9 % of the participants think that it is ok to drink alcohol in order to become inebriated. 58,1 % do not think it is ok.’ (41,9% af deltagerne i denne undersøgelse mener, at det er i orden at drikke alkohol for at blive beruset. Tilsvarende mener 58,1% at det ikke er i orden.). Ok – so more than half don’t think it’s ok to drink alcohol in order to get drunk? Seriously?

May 2, 2010 Posted by | alcohol, Data, Demographics | 10 Comments

Who knew?

According to a new study, Europeans get drunk to have sex.

The leader of the study, Mark Bellis:

Millions of young Europeans now take drugs and drink in ways which alter their sexual decisions and increase their chances of unsafe sex or sex that is later regretted.

Yet despite the negative consequences, we found many are deliberately taking these substances to achieve quite specific sexual effects.

They do? Seriously?

[banging my head against the wall…]

May 9, 2008 Posted by | alcohol, Studies | 2 Comments