Not all chapters give me a lot of new insights – for example I know a lot more about the topic covered in the chapter about the Relationship Between Metabolic Control and Complications in Diabetes than what is covered in the book, and the ten-page chapter on The Diabetic Foot which I’ll soon read will not match the detailed coverage in Edmonds et al. – but anything else would be very surprising, and most chapters contain some stuff which I did not know. I understand the mechanisms driving microvascular complications better now than I did, but I’m still fuzzy on some of the details; like some of the genetics stuff in the first chapters that part of the book is very technical, and so I decided against covering that stuff in detail here. If you’re curious about that stuff, here’s a relevant link covering some of what the book has on that topic, in what seems from a brief skim to be a roughly similar amount of detail. To people who know nothing about this stuff (i.e., people who haven’t read my posts on related topics in the past…), diabetes in the long term causes damage to small and large blood vessels and may cause various forms of nerve damage (neuropathies) – here’s a brief and non-technical overview article. The connection between hyperglycemia – too high blood glucose – and small vessel disease is better established (and very well established at this point) than is the connection between hyperglycemia and large vessel disease, and although it may not sound too bad that small blood vessels are damaged, the consequences can be dire; long-term diabetes may among other things cause blindness and kidney failure. How precisely the blood vessels are damaged in diabetics was not very well understood for a very long time, but significant progress seems to have been made over the last couple of decades, and a ‘unifying theory’ of sorts – which brings together four separate mechanisms – seems to have been developed at this point (though I’m still not completely sure about how well this theory explains the neurological symptoms). As mentioned you can have a look at ‘the relevant link’ above if you want to know more about the details.
Age is an important factor in treatment, as different age groups will respond in dissimilar manners to treatment and will face different problems (biological factors, behavioural factors), so the book has separate chapters on diabetes management in very young children, adolescents, etc. Though the level remains high throughout the book, I’d incidentally note that I don’t believe these chapters on special management issues in specific patient subgroups are that technical, and I think many diabetics would be able to benefit from reading those chapters. To a diabetic, much of the stuff covered in the treatment part will be well known although there’ll also be some new stuff. I was continually bothered throughout some of those chapters by the fact that when comparing treatment outcomes of patients on intensive treatment regimes with subcutaneous insulin injections and patients on insulin pumps, the obvious problems with selection into treatment in the latter group were not commented upon when comparing outcomes (though it must be said that one of the authors do comment on this aspect in a later chapter).
Below I’ve selected out some stuff from the middle 200 pages or so of the book. I’ve not completely ignored passages which may be a bit hard to understand for people without any knowledge of this disease – this is also a post written in order to make it easier for myself to remember what was covered in some of those chapters – however as mentioned above I’ve left out the really technical stuff. I have also bolded some key concepts and a few observations for the ‘lazy’ readers who can’t be bothered to read all of it, in order to make the post easier to navigate.
“Since its introduction, insulin has been life sustaining for patients with type 1 diabetes [...] Although it is relativly inexpensive in the developed world, in many developing countries with limited health care resources, it is not routinely available (9). Indeed, children with type 1 diabetes in sub-Saharan Africa often do not live longer than 1 yr (10).” (I was wondering if this was an observation based on very old data (data access is a notorious problem when dealing with developing countries), but that seems not to be the case: “A child diagnosed with type 1 diabetes in sub-Saharan Africa has a life expectancy that varies between 7 months and 7 years, depending on the country” - link, original source is this article which I haven’t found an ungated copy of).
“[A] major risk of insulin therapy is weight gain. Insulin promotes fat storage in adipocytes and protein synthesis in muscles. [...] [In the Diabetes Control and Complications Trial (DCCT)] the body mass index (BMI) increased approx 2 more units with intensive than with conventional treatment in both genders. In the whole DCCT cohort, the risk of becoming overweight was almost twofold greater with IT [intensive treatment - US] [...] on average, adult subjects achieving a mean HbA1c of 7.2% gained 4.8 kg more during a 6-yr follow-up than their conventionally controlled counterparts” [my HbA1c is below 7.2% - US.]
“Exposure to a mean HbA1c of 11% for less than 3 yr yields the same rate of retinopathy as exposure to a HbA1c of 8% for 9 yr. The message is clear: The less time we allow a patient to be exposed to high levels of blood glucose, the better [...] The adverse hyperglycemic effects on the eyes and kidneys exhibit a carryover effect manifested by a kind of “metabolic memory” displayed by these target organs. [...] there is a momentum factor in retinopathy and nephropathy contributed to by the combination of glycemic level and time. The process of tissue damage builds up slowly, but in an accelerated fashion at higher HbA1c levels [...], it decelerates slowly at lower HbA1c levels [...], but also resumes its progression slowly after a period of time at lower HbA1c levels”
“It has long been recognized that treating and controlling diabetes is difficult. Diabetes is not an illness where a pill, an injection, or a particular diet is a cure. At best, there is hope to control it well. Optimal treatment demands dedication, motivation, energy, and knowledge. [...] Dealing with these issues on a daily basis can be a psychological burden [...] Thus, it is common for those with diabetes and/or close members of their families to have guilt, sorrow, and depression [...] Although depression is not a complication of diabetes, it frequently is a consequence of the illness. The prevalence of depression in adults varies. Levels of diagnosable depression among those with diabetes are approximately three times the estimated prevalence in the population at large (8). Depression also might be more severe in people with diabetes and has especially adverse effects. Difficulty evolves in treatment when clinical depression contributes to poor self-care, worsened glycemia, and deepened depression (9).”
“Hyperglycemia before eating slows gastric emptying and results in a more prolonged glycemic response (8), whereas hypoglycemia speeds emptying and results in a faster, higher, and earlier peak response (9).” [I was not aware of this!]
“Persons with type 1 diabetes may attempt to substitute protein for carbohydrates to attenuate postprandial glucose response. A large cross-sectional study in type 1 diabetes found that protein intakes greater than 20% of total energy intake were associated with higher albumin excretions than <20% dietary protein (43). Concern over the role protein intake plays in renal function suggests that consuming more than 20% protein in the diet is unwise.” [As I've pointed out before (the second paper in the post), salt intake seems like a more obvious place to intervene - but protein intake is not irrelevant].
“Diabetes is less frequent in preschool children than in older ages. In a large survey in Europe, age-specific incidence was compared among 3 age groups in more than 3000 cases during 1989–1990 (1). Eighteen percent of the cases were observed in children younger than 4 yr, 34% between 5 and 9 yr, and 48% in children aged 10–14 yr. Similar results have been obtained in North America (2). [I got diagnosed at the age of 2 - US] [...] A major characteristic of metabolic control in type 1 preschool children is the unstable glycemic control with its accompanying risk of severe hypoglycemia [...] In young children, severe and recurrent hypoglycemias are of major concern because they may impair normal brain development. When tested during adolescence, patients who presented with early-onset diabetes and/or a history of severe hypoglycemia showed global or selective neuropsychological dysfunction such as impairment of visual–spatial skills, psychomotor efficiency, attention, or memory (28–32). As early as 2 yr after disease onset, evidence exists for mild neuropsychological dysfunction (33). Onset of diabetes early in life (before 5 yr of age) predicted negative changes in neuropsychological performances over the first 2 yr of the disease (34).” [I've talked about this aspect of the disease before. Below's a bit more on this stuff:]
“The long-term risk of recurrent severe episodes of hypoglycemia, involving coma or convulsions, on the development of permanent cognitive impairment remains controversial. [...] There continue to be concerns about young children with type 1 diabetes, particularly those diagnosed less than 5 yr of age in whom defects in tests of cognitive function have consistently been found (126–131). [...] It is likely that the developing brain is more susceptible to damage during episodes of metabolic derangement. Deficiencies have been found in a number of cognitive domains but especially those that are more likely to be those originating in the frontal lobe. Not all of these studies have found a link with prior episodes of severe hypoglycemia, although more recent investigations have shown links between hypoglycemia and cognitive impairment.”
“The pubertal growth spurt is induced by sex hormones in both boys and girls, leading to increased amplitude of growth hormone (GH) pulses, and a rise in circulating insulinlike growth factor-1 (IGF-1) (26). Both the sex hormones and GH contribute to insulin resistance (27) and worsening glycemic control (28) [...] Insulin also plays an important anabolic role during puberty. Failure to adequately increase insulin doses during this period has adverse effects on diabetic control, leading to the impairment of growth and pubertal development [...] The GH/IGF axis, which plays a central role in the growth acceleration of puberty, can be significantly disordered in the diabetic adolescent with poor diabetic control, contributing to both growth impairment and greater insulin resistance (30).” [Incidentally both my brothers are higher than I am, though I can't be absolutely certain this has anything to do with my diabetes... - US] [...]
“In a retrospective, longitudinal study of 118 adolescent 18-yr-olds with type 1 diabetes, studied at three-monthly intervals between 8 and 18 yr, we found a significant deterioration in metabolic control throughout the period of adolescence (52). [...] Quality of life may also deteriorate during this time (53) [...] Adolescents with diabetes, unlike younger children, were reported by their parents as having poorer emotional and behavioral outcomes and poorer self-esteem outcomes than the nondiabetic adolescents.”
“Few diabetic women lived to childbearing age before the advent of insulin in 1922. Until then, less than 100 pregnancies were reported in diabetic women and most likely these women had type 2 and not type 1 diabetes. Even with this assumption, these cases of diabetes and pregnancy were associated with a greater than 90% infant mortality rate and a 30% maternal mortality rate (1,2). As late as 1980, physicians were still counseling diabetic women to avoid pregnancy (3). [...] There is an increased prevalence of congenital anomalies and spontaneous abortions in diabetic women who are in poor glycemic control during the period of fetal organogenesis, which is nearly complete by 7 wk postconception. A woman may not even know she is pregnant at this time. It is for this reason that prepregnancy counseling and planning is essential in diabetic women of childbearing age. Because organogenesis is complete so early on, if a woman presents to her health care team and announces that she has missed her period by only a few days, there is still a chance to prevent cardiac anomalies by swiftly normalizing the glucose levels. However, potential neural tube defects are probably already established by the time the menstrual period is missed. [...] HbA1c values early in pregnancy are correlated with the rates of spontaneous abortion and major congenital malformations [...] normalizing blood glucose concentrations before and early in pregnancy can reduce the risks of spontaneous abortion and congenital malformations nearly to that of the general population (6–12).”
“The life expectancy for patients with diabetic end-stage renal failure is only 3 or 4 yr.” [I was wondering if perhaps this statement was based on old data (you never know), so I had a look around. It doesn't seem to be - this is really how 'well' people do today. See e.g. the figure on page 6 of this study published earlier this year - half of the diabetics with end-stage renal failure were dead after 3 years, and only about a third survived 5 years. Yes, sometimes people get lucky - they 'get a transplant and live for decades'. But most diabetics don't; they just die, quite fast.]
“Although all cells in a person with diabetes are exposed to elevated levels of plasma glucose, hyperglycemic damage is limited to those cell types, such as endothelial cells, that develop intracellular hyperglycemia. Endothelial cells develop intracellular hyperglycemia because, unlike most other cells, they are unable to downregulate glucose transport when exposed to extracellular hyperglycemia [...] vascular smooth muscle cells, which are not damaged by hyperglycemia, show an inverse relationship between extracellular glucose concentration and subsequent rate of glucose transport [...] In contrast, vascular endothelial cells show no significant change in subsequent rate of glucose transport after exposure to elevated glucose concentrations”
“Diabetic ketoacidosis (DKA) is a potentially life-threatening medical emergency that reflects a state of metabolic decompensation in patients with insulin-dependent diabetes mellitus (IDDM) [...] At least 25% of patients with new-onset diabetes mellitus type 1, especially children, will present in ketoacidosis (1–6). [...] The cardinal hormonal alteration that triggers the metabolic decompensation of DKA is insulin deficiency accompanied by an excess of glucagon and the stress hormones epinephrine, norepinephrine, cortisol, and growth hormone (2,3,6). Insulin stimulates anabolic processes in liver, muscle, and adipose tissues and thereby permits glucose utilization and storage of the energy as glycogen, protein, and fat [...] Concurrent with these anabolic actions, insulin inhibits catabolic processes such as glycogenolysis, gluconeogenesis, proteolysis, lipolysis, and ketogenesis. Insulin deficiency curtails glucose utilization by insulin-sensitive tissues, disinhibits lipolysis in adipose tissue, and enhances protein breakdown in muscle. Glucagon acting unopposed by insulin causes increased glycogenolysis, gluconeogenesis, and ketogenesis. Although insulin and glucagon may be considered as the primary hormones responsible for the development of DKA, increased levels of the stress hormones epinephrine, norepinephrine, cortisol, and growth hormone play critical auxiliary roles. Epinephrine and norepinephrine activate glycogenolysis, gluconeogenesis, and lipolysis and inhibit insulin release by the pancreas. Cortisol elevates blood glucose concentration by decreasing glucose utilization in muscle and by stimulating gluconeogenesis. Growth hormone increases lipolysis and impairs insulin’s action on muscle. The catabolic and metabolic effects of each of these counterregulatory hormones are accentuated during insulin deficiency [...] the effects are synergistic and not merely additive. Even in normal persons, high concentrations of these counterregulatory hormones can induce hyperglycemia and ketonemia” (see also this and this – US)
“The classical patient with DKA is characterized by dehydration, acidosis with hyperventilation, with varying degrees of cerebral obtundation, and peripheral circulatory compromise [...] the most common precipitating factors following initial presentation are omission of insulin, infection, and, in adults, typical or atypical myocardial infarction (1,7). [...] In children, the major complication of concern during treatment for DKA is cerebral edema and related intracerebral complications [...] [children are] at a disproportionately higher risk for developing clinical cerebral edema as compared to adults with DKA. Clinically relevant cerebral edema is estimated to occur in 0.7–1.0% of episodes of diabetic ketoacidosis in children (26–28). [...] Once clinically obvious, cerebral edema is associated with a mortality of about 70% and only 7–14% of these patients escape permanent impairment of neurological function (31).”
i. “They tell us that Suicide is the greatest piece of Cowardice… That Suicide is wrong; when it is quite obvious that there is nothing in this world to which every man has a more unassailable title than to his own life and person.” (Arthur Schopenhauer)
ii. “When I am dead I would rather people thought me better than I was instead of worse; but if they think me worse, I cannot help it and, if it matters at all, it will matter more to them than to me.” (Samuel Butler) [I'd personally prefer a third option: That people didn't think of me/about me at all after my death. If I were completely forgotten right after my death, rather than 50 or 100 years later as is usually the case, my death would cause other people still alive
much less harm and grief.]
iii. “To me it seems that those who are happy in this world are better and more lovable people than those who are not.” (-ll-)
iv. “The inert mind is a greater danger than the inert body, for it overlays and stifles the desire to live.” (Robertson Davies)
v. “No snowflake in an avalanche ever feels responsible.” (Stanisław Lec)
vi. “Do not put your faith in what statistics say until you have carefully considered what they do not say” (William Watt)
vii. “Most people get a fair amount of fun out of their lives, but on balance life is suffering, and only the very young or the very foolish imagine otherwise.” (George Orwell)
viii. “One of the main reasons that it is so easy to march men off to war is that each of them feels sorry for the man next to him who will die.” (Ernest Becker)
ix. “Wisdom comes from experience. Experience is often a result of lack of wisdom.” (Terry Pratchett)
x. “Wisdom doesn’t necessarily come with age. Sometimes age just shows up all by itself.” (Tom Wilson)
xi. “I like work. It fascinates me. I can sit and look at it for hours.” (Jerome K. Jerome)
xii. “It is impossible to enjoy idling thoroughly unless one has plenty of work to do. There is no fun in doing nothing when you have nothing to do. Wasting time is merely an occupation then, and a most exhausting one. Idleness, like kisses, to be sweet must be stolen.” (-ll-)
xiii. “There’s nothing worse than being an ageing young person.” (Richard Pryor)
xiv. “Whenever two people meet there are six present. There is the man as he sees himself, each as the other person sees him, and each man as he really is.” (William James)
xv. “The real persuaders are our appetites, our fears and, above all, our vanity. The skillful propagandist stirs and coaches these internal persuaders.” (Eric Hoffer)
xvi. “It is doubtful if the oppressed ever fight for freedom. They fight for pride and power — power to oppress others. The oppressed want above all to imitate their oppressors; they want to retaliate.” (-ll-)
xvii. “A man is likely to mind his own business when it is worth minding. When it is not, he takes his mind off his own meaningless affairs by minding other people’s business.” (-ll-)
xviii. “We can be absolutely certain only about things we do not understand. A doctrine that is understood is shorn of its strength.” (-ll-)
xix. “The awareness of their individual blemishes and shortcomings inclines the frustrated to detect ill will and meanness in their fellow men. Self-contempt, however vague, sharpens our eyes for the imperfections of others. We usually strive to reveal in others the blemishes we hide in ourselves.” (-ll-)
xx. “To believe that if we could have but this or that we would be happy is to suppress the realization that the cause of our unhappiness is in our inadequate and blemished selves. Excessive desire is thus a means of suppressing our sense of worthlessness.” (-ll-)
A few lectures from Gresham College:
An interesting lecture on symmetry patterns and symmetry breaking. A lot of the discussion of the relevant principles takes animal skin patterns and -movement patterns as the starting point for the analysis, leading to interesting quotes/observations like these: ”Theorem: A spotted animal can have a striped tail, but a striped animal cannot have a spotted tail”, and “…but it can’t result in a horse, because a horse is not spherically symmetric”.
He also talks about e.g. snowflakes and sand dunes and this does not feel like a theoretical lecture at all – he’s sort of employing an applied maths approach to this topic which I like. Despite the fact that it’s basically a mathematics lecture it’s quite easy to follow and I enjoyed watching it.
He takes a long time to get started and he doesn’t actually ever say much about the non-Euclidian stuff (he never even explicitly distinguishes hyperbolic geometry from elliptic geometry using those terms). He’s also not completely precise in his language during the entire lecture; at one point he emphasizes the fact that three specific choices used in a proof were ‘mutually exclusive’ as though that was what was the key, even though what’s actually critical is that they were also collectively exhaustive – a point he fails to mention (and I’d assume it would be easy for a viewer not reasonably well-versed in mathematics to mix up these distinctions if they were not already familiar with the concepts). But maybe you’ll find it interesting anyway. It wasn’t a particularly bad lecture, I’d just expected a little more. I know where to go look if one wants a more complete picture of the things briefly touched upon in this lecture and I’ve looked at that stuff before, but I’m certainly not going to read Penrose again any time soon – that stuff’s way too much work considering the benefits of knowing that stuff in details (if I’m even theoretically able to obtain knowledge of the details – some of that stuff is really hard).
It’s been a while since I read stuff from this book, but I’m behind on the blogging so I decided to have a second look at some of that stuff. I never really got to talking much about chapter 14 (about liver disease) in my last post, and since then I’ve also read about disorders of the exocrine pancreas (chapter 15), renal disease (chapter 16), disorders of the parathyroids and calcium metabolism (chapter 17), and disorders of the endocrine pancreas (chapter 18). In this post I’ll limit my coverage to liver disease – it’s a fairly long chapter and these posts take quite a bit of time.
Before I start out with the main coverage, I should note that the one main take-away from this chapter is that the liver does a huge amount of different stuff. There’s a reason we can’t live without this organ (or perhaps a better way to think about this is that there are rather lots of reasons).
Anyway, on to the chapter coverage. The chapter starts out with a brief overview of how liver disease presents and some key concepts. Overview of the structure and function of the liver (anatomical- and histological features etc.) then follows, description of blood flow to the organ, and a description of the various functions the liver has (energy metabolism; protein synthesis; solubilization, transport and storage functions; protective and clearance functions). Then an overview of liver disease follows – what goes wrong, how it manifests, etc. Given how many functions the liver has, liver disease can cause a lot of problems with a lot of different things, and I decided to cover this part in a bit of detail below. First of all, problems with the liver can mess up all kinds of metabolic processes: Altered carbohydrate metabolism secondary to liver disease may cause hypo- or hyperglycemia, altered lipid metabolism may cause fat accumulation within the liver or elsewhere in the body, whereas altered protein metabolism may cause altered mental status and even coma (hepatic encephalopathy). Bile (a fluid produced by the liver to help with digestion) secretion failure, termed cholestasis, may cause various forms of malabsorption and deficiency states – classical signs of liver disease, jaundice and icterus (yellow discoloration of sclera (the whites of the eyes) and skin), are both caused by build-up of bilirubin caused by cholestasis. Most people are aware of the liver’s role in drug metabolism, and of course a failing liver will not clear drugs as well as a healthy liver will; a problematic aspect in particular here is that impaired clearance may make individuals abnormally sensitive to the toxic effects of drugs. Incidentally the liver clears drugs and other things through various phases, which means that different types of liver cells end up getting exposed to different types of compounds; the liver isn’t just a big clump of cells which tend to get harmed the same way by hepatotoxic substances. Rather what happens in cases of hepatotoxic exposures is that different liver cells are harmed by different compounds in foreseeable ways, so that direct poisons harm the first clearance zones hardest, whereas other hepatotoxic substances will harm cells ‘further down the line’ which are the ones that get exposed to the toxic metabolites generated earlier in the process – sometimes it’s not the stuff that goes in which is toxic, but rather the stuff the liver cells need to convert it into to get it out of the system. Anyway, aside from the stuff already mentioned the liver also has a role in storing various substances, which means that liver dysfunction may cause vitamin deficiency states. The liver produces proteins which have various functions throughout the body and when its function is impaired critical proteins may not be produced in the necessary quantities, causing problems such as hypoalbuminemia-related edema (fluid build-up in tissues). Clotting factors are also produced by the liver and lack of those may lead to various coagulopathic states (bleeding disorders). Altered hormone clearance in the liver may cause things like elevation of blood estrogens, which may cause physiological changes such as gynecomastia. Liver failure may cause the kidneys to retain salt and water as a defence mechanism, and so patients with severe liver disease may develop kidney failure as a result of these processes. Ascites, excess fluid build-up in the peritoneal cavity, may develop through a ‘complex and multifactorial’ process. A particularly awful type of bad breath called fetor hepaticus may develop in late-stage liver disease.
As you can probably tell from the comments above, all in all there are a lot of ways in which a bad liver can screw you over. It does a lot of good things, so a lot of things can go wrong.
After covering general aspects of liver disease, the pathophysiological aspects of a few specific liver diseases are covered in the last part of the chapter. This part deals with acute hepatitis, chronic hepatitis, and cirrhosis. Various specific disorders and disease processes may cause each of these (with huge variation in symptoms/presentation and severity of disease), so the extent to which specific disorders are dealt with in detail in this part of the chapter may be debatable – but it’s good stuff anyway. I decided not to cover the stuff in that part of the chapter in great detail but I do want to give a brief overview with some key points, and actually a pretty good big-picture short version of many of the relevant clinical distinctions is given in the beginning of the chapter:
“Although many different pathogenic agents and processes can affect the liver [...], they are generally manifested in individual patients in a limited number of ways that can be assessed by evaluation of some key parameters. Liver disease can be acute or chronic; focal or diffuse; mild or severe; and reversible and irreversible. Most cases of acute liver disease (eg, due to viral hepatitis) are so mild that they never come to medical attention. [...] The patient recovers without any lasting medical consequences. In other cases of acute liver injury, symptoms and signs are severe enough to call for medical attention. The entire range of liver functions may be affected or only a few [...] Occasionally, viral and other causes of acute liver injury occur in an overwhelming manner with massive liver cell death. This syndrome of fulminant hepatic failure carries a high mortality rate, but if the patient survives, liver function returns to normal and there is no residual evidence of liver disease.
Liver injury may continue beyond the initial acute episode or may be recurrent (chronic hepatitis). In some cases of chronic hepatitis, liver function remains stable or the disease process ultimately resolves altogether. In other cases, there is progressive and irreversible deterioration of liver function.
Cirrhosis is ultimately the consequence of progressive liver injury. Cirrhosis can occur in a subset of cases of chronic hepatitis that do not resolve spontaneously or after repeated episodes of acute liver injury, as in the case of chronic alcoholism. In cirrhosis, the liver becomes hard, shrunken, and nodular and displays impaired function and diminished reserve due to a decreased amount of functioning liver tissue. More importantly, the physics of blood flow is altered such that blood in the hepatic portal vein is diverted around the liver rather than being filtered through the liver. This phenomenon, termed portal-to-systemic shunting, has profound effects on the function of various organ systems and sets the stage for certain devastating complications of liver disease [...]
The consequences of liver disease can be either reversible or irreversible. Those arising directly from acute damage to the functional cells of the liver, most notably hepatocytes, without destruction of the liver’s capacity for regeneration, are generally reversible. Like many organs of the body, the liver normally has both a huge reserve capacity for the various biochemical reactions it carries out and the ability to regenerate fully differentiated cells and thereby recover completely from injury. Thus, only in the most fulminant cases or in end-stage disease are there insufficient residual hepatocytes to maintain minimal essential liver functions.”
Some related comments from the last half of the chapter:
Based on clinical, laboratory, and biopsy findings, chronic hepatitis is often divided into two classes: chronic persistent and chronic active hepatitis. Chronic persistent hepatitis is seldom progressive despite persistent biochemical abnormalities reflecting ongoing liver cell necrosis. The clinical course is relatively benign, often characterized by spontaneous resolution (eg, clearance of persistent viral infection). Chronic active (aggressive) hepatitis is typically progressive, often resulting ultimately in cirrhosis and its complications or liver failure and death.” [...] The complications of chronic active hepatitis are those of progression to cirrhosis – variceal bleeding, encephalopathy, coagulopathy, hyperspleenism, and ascites. These are largely due to portal-to-systemic shunting rather than diminished hepatocyte reserve” [...]
“Either type of chronic hepatitis can be caused by infection with several hepatitis viruses (eg, hepatitis B with or without hepatitis D superinfection and hepatitis C); a variety of drugs and poisons (eg, ethanol, isoniazid, acetaminophen), often in amounts insufficient to cause symptomatic acute hepatitis; genetic and metabolic disorders (eg, α1-antiprotease (α1-antitrypsin) deficiency, Wilson’s disease, and hemochromatosis); or immune-mediated injury of unknown origin. [...] A specific cause can be determined for only 10-20% of patients. [...]
“As with other presentations of liver disease, not all patients with cirrhosis develop life-threatening complications. Indeed, in nearly 40% of cases, cirrhosis is diagnosed at autopsy in patients who did not manifest obvious signs of end-stage liver disease.”
Share whatever you like – links, books, christmas present ideas (I’m planning on giving that whole thing a miss, but I’m not the only one reading the comments), …
My contributions to the discussion below:
i. Alcohol may not just be bad for the fetuses that make it out of the birth canal:
“Of the 186 pregnancies, 131 resulted in delivery of a child, and 55 (30 percent) were spontaneously aborted. Of the abortions, 34 were detected only by urinary hCG before or at 6 completed gestational weeks. The 21 clinically recognized abortions occurred in the interval after 6 and by 15 completed gestational weeks.
A high intake of alcohol by women or their partners was associated with a higher frequency of spontaneous abortions than was a low intake (table 1). Women who experienced a spontaneous abortion were older and had, on average, longer menstrual cycles, a higher caffeine intake, and partners with a higher caffeine intake than did women who gave birth (table 1). No association was found between spontaneous abortion and the partner’s smoking habits, partner’s age, body mass index, and partner’s reproductive illnesses; contraception last used; education for both man and woman; or hours at work for both partners.
The crude associations between female and male alcohol intakes and spontaneous abortion shown in figures 1 and 2 changed only slightly by adjustment for the confounders listed in table 2. Female alcohol intake was associated with a 2–3 times higher adjusted risk of spontaneous abortion compared with no intake, and male intake was associated with a 2–5 times increase in the adjusted risk. However, only the relative risks for male and female intakes of 10 or more drinks/week compared with no intake were statistically significant. We found a high correlation between male and female alcohol intakes. Additional adjustment for male intake revealed a lower risk of spontaneous abortion associated with female alcohol intake, whereas the higher risk associated with a high male alcohol intake changed only slightly following adjustment for female intake [...] women in this study with a moderate or high alcohol intake [also] have an increased waiting time to pregnancy”
The quotes above are from Alcohol Consumption at the Time of Conception and Spontaneous Abortion, by Henriksen, Hjollund et al.
I should note that I don’t know enough about this stuff to comment intelligently on the findings. I’m planning to read Principles and Practice of Clinical Trial Medicine at some point in the not-too-distant future, and so I figured I ought to wait until I have had a go at that book to comment on this stuff. I wanted to add the link anyway though, in part so that I’d remember it in case it’ll be a while until I read Chin & Lee’s book.
iii. On a more personal note, Monday evening I beat an International Master for the first time in my life. It was in a one-minute bullet game (each player gets one minute to play the entire game) so it was not a particularly well played game, but I consider this to be a somewhat significant milestone still – IMs are really good chess players (‘An International Master is usually in the top 0.25% of all tournament players at the time he or she receives the title’ – from the wiki-link above). Here’s my opponent’s Fide profile, here’s the game. There’s incidentally no doubt this was the guy I played – his full name is on his profile and his blitz rating was above 2600 when I played him (which is high – higher than some GMs on the site). It wasn’t a case of me getting outplayed but winning on time anyway – rather I had a mate in one in the game which he spotted after he’d made his move, and he resigned as a consequence of spotting the mate even though I missed it. When he resigned he had only 0.3 seconds left on his clock, so this may have been a contributing factor; if he’d not resigned he’d have lost on time. I had 3.6 seconds left which was of course the main reason why I didn’t spot the mate – I was too busy making moves in the time scramble in order not to lose on time to look for mates.. The time-trouble was incidentally also of course the reason why I was only up a piece when he resigned and why I did not take his queen when he blundered it a few moves earlier (bullet-chess can get pretty wild…).
Although it’s not like I haven’t read some stuff about my disease over the years, the amount of textbook reading on the topic I’ve done has so far been limited to just a couple of books (and none of these have really been ‘textbooks on type 1 diabetes’); most of the stuff I know I’ve learned from the scientific literature, e.g. Diabetes Care articles, Cochrane reviews and similar, and in general the books which have dealt with diabetes which I’ve read have not been all that concerned about the various distinctions one might choose to make between the somewhat heterogenous disorders all going under the common name of ‘diabetes’. In ‘random books’ I think it’s fair to say that ‘diabetes’ usually is best translated ‘type 2 diabetes’, and the specific aspects of that disease most interesting to many book authors on health and related stuff are precisely the aspects which are completely irrelevant to type 1′s (e.g. lifestyle stuff related to prevention and disease progression in type 2′s).
So I decided to read this book to get a more solid background. Which kind of book is it? Here’s a quote from the introduction:
“The aim of Type 1 Diabetes: Etiology and Treatment is to fuse [...] contemporary investigational and practical issues and make them available to those involved in the research and practice of type 1 diabetes. This volume is not intended to be a comprehensive or exhaustive treatise on the subject of diabetes. As in many such endeavors, the pace of discovery often exceeds the ability to incorporate the latest knowledge into printed text. Nevertheless, we believe that this volume presents contemporary information on contemporary issues by recognized authorities in the field. We hope it stimulates thought and action in the research and care of patients with type 1 diabetes mellitus.”
In case you were wondering, “make them available to those involved in the research and practice of type 1 diabetes” = this is not a book for patients and it’s not an undergraduate textbook; it’s mainly a book for PhD students and endocrinologists. I’d say that even if you skip the introduction you probably don’t need to read 10 pages to realize that. This is the kind of book where I’ll read all the words and then see how much of it I actually understand, occasionally looking up stuff which I’m particularly interested in; but I’ll not put in the work to actually understand all the details of what’s covered in all the chapters of this book. I don’t care enough about stuff like this to be willing to spend the time and effort it takes to understand all the details. I’ve tried to be very careful about getting at least some ‘take-away’ message out of all chapters covered so that e.g. even though I’ll not understand all the various processes which get you to the finish line, at least I know what’s at the starting line and where you end up on the other side. You may think that I’m lazy and that I’m just (mentally) skipping the hard stuff, but although this is certainly true to some extent I should add that I consider it justified to say that even though I’m mentally skipping a few steps occasionally while reading this book I’m still engaged in ‘learning in depth’ – most of the stuff covered in this book is knowledge at a level way beyond what the average patient knows about genetics, immunology, metabolic pathways etc. I actually feel reasonably sure at this point that I’d not have continued reading past the first chapter of this book if I had not read McPhee et al. first (I haven’t read that entire book yet, but I’ve read a lot of stuff relevant to the coverage here).
It would be wrong of me to only talk about the downsides to the coverage in this post, i.e. that it’s a hard book for most people to read; the flip side of course is that there are a lot of interesting details here. The book is full of stuff I didn’t know I didn’t know. Fortunately enough for my coverage of the book here, despite the fact that the book in general is somewhat inaccessible not all chapters are equally ‘bad’, and so there is also occasionally some stuff in there which I believe to be reasonably accessible even to people who don’t know a whole lot about type 1 diabetes (though I may be making assumptions about people’s background knowledge here which are not warranted). Anyway I’ve tried to pick out some of those passages in my coverage below, and on the other hand I’ve tried very hard to stay clear of stuff most readers could not possibly be expected to understand. Do ask questions if some of the stuff is unclear to you. I’ve read roughly the first 180 pages. Note that not all the stuff below is from the book; I decided to add some comments of my own towards the end of the post. I decided to bold some of the stuff below so that even people who only skim the post may get something out of it.
“By 1990, two international groups [the EURODIAB Project and the DiaMond Project] working on the epidemiology of type 1 diabetes had been developed. [...] Because of these two important projects, the descriptive epidemiology of type 1 diabetes has been mapped for most of the world, and we now know more about the international variation in the incidence of type 1 diabetes than practically any other chronic disease. Within a short 15-yr time period, the epidemiology of type 1 diabetes rose from a “black hole” of ignorance to one of the best characterized chronic diseases worldwide” [...]
“The variation in the incidence of type 1 diabetes worldwide is greater than that observed for any other chronic disease in children. [...] the global variation in risk is enormous. A child in Helsinki, Finland is almost 400 times more likely to develop diabetes than a child in Sichuan, China (8). To put this in perspective, consider the following example. If children in the United States had the same risk of developing type 1 diabetes as children in China, then instead of 13,000 newly diagnosed children each year, there would be only 56. In other words, over 99% of the annual new cases of type 1 diabetes in the United States would be avoided. [...] Interestingly, the other epidemiologic features of type 1 diabetes are remarkably similar across populations, despite the enormous variation in disease risk (9). Incidence rates among males and females do not differ significantly, and the peak age at onset for both sexes occurs near the time of puberty. Thus, compared to all other risk factors, including human leukocyte antigen (HLA) haplotypes, viral infections, or the presence of autoantibodies, the place where a child lives is the most potent determinant of type 1 diabetes risk, excluding genetic/racial differences. If we knew what was causing the geographic patterns of type 1 diabetes, we would be well on our way to preventing the disease.” [...]
“Temporal trends in chronic disease incidence rates are almost certainly environmentally induced. If one observes a 50% increase in the incidence of a disorder over 20 yr, it is most likely the result of changes in the environment because the gene pool cannot change that rapidly. Type 1 diabetes is a very dynamic disease. [...] the incidence of type 1 diabetes is rising [and] these findings indicate that something in our environment is changing to trigger a disease response. [...] The data [...] clearly indicate that environmental factors are involved in the etiology of type 1 diabetes. With the exception of a possible role for viruses and infant nutrition, the specific environmental determinants that initiate or precipitate the onset of type 1 diabetes remain unclear. Type 1 diabetes is also, in large part, genetically determined” [here's a relevant link, I won't go into the details here although they spend a lot of pages talking about that stuff in the book]
“Evidence that type 1 diabetes is an autoimmune disorder is based on the presence of lymphocytic infiltrates of the pancreas at the onset of the diseases (37), as well as the occurrence of autoantibodies to islet cell antigens (ICAs), tyrosine phosphatase IA-2 (IA-2), glutamic acid decarboxylase (GAD), and insulin autoantibodies (IAA) (38,39). The presence of these autoantibodies indicates that tissue damage has likely been initiated by other etiologic agents. Thus, they represent important preclinical markers rather than risk factors for the disease. [...] most type 1 diabetes cases have β-cell autoantibodies at disease onset, [however] not all autoantibody positive individuals develop the disease. [...] first-degree relatives who are positive for multiple autoantibodies appear to be at very high risk for developing type 1 diabetes. [...] about 90% of individuals who develop type 1 diabetes have a negative family history of the disease.“
“The autoimmune response in type 1 diabetes is [...] similar to most other organ-specific autoimmune disorders in that both T-cells and autoantibody-producing B-cells are involved in the immune abnormalities associated with, as well as predicting, the disease (24). The molecular biology of β-cell destruction is therefore both diverse and complicated and the detailed mechanisms are yet poorly understood. [...] At the time of clinical diagnosis of type 1 diabetes, about 80% of the β-cells have been specifically destroyed.”
“We currently know that for individuals with two HLA-DQ susceptibility haplotypes, the cumulative risk of type 1 diabetes in the general Caucasian population is approximately 5% (25). However, it may range from 0.1% to >90%, depending on one’s risk factor profile, which includes age, ethnic, familial, genetic, environmental, and autoimmune determinants.” [...] Diabetogenic alleles are not fully penetrant” [...] There is no simple “rule” for diabetes risk [...] the position of provisional loci found in T1DM colocalize or overlap with loci found in different autoimmune/inflammatory diseases [...] This is consistent with the hypothesis that, like the MHC, some of these provisional loci may involve common susceptibility genes or biochemical pathways that are central to normal immune function.”
“At present, the prediction of type 1 diabetes is not a major clinical issue outside of trials for diabetes prevention. Patients, especially children, usually present acutely with diabetes with a dramatic history of polyuria, polydipsia, and weight loss. Despite what in retrospect is almost always a clear-cut clinical history of diabetes, a significant number of children have a delay in diagnosis, which increases the risk of severe metabolic decompensation with diabetic ketoacidosis (DKA), cerebral edema, and death. [...] Overall in the United States, DKA occurs in 25–50% of children with new-onset diabetes, and symptomatic cerebral edema occurs in approx 1% of DKA episodes. Of those patients with clinically apparent cerebral edema, between 40% and 90% die (1). [...] In the United States [...] it is rare to find individuals presenting with diabetes with normal HbA1c [an indicator of average blood glucose over the last 3 months or so - US] and it is likely that the great majority have had hyperglycemia for months prior to diagnosis.”
“Diabetes mellitus is classified based on clinical criteria into type 1 and type 2 diabetes (98). Recently, a growing number of monogenic diabetes disorders have been identified (98). Type 1 diabetes develops acutely. Ketoacidosis and coma develop unless insulin is administered. Type 2 diabetes develops mostly as a result of insulin resistance associated with obesity and β-cell dysfunction and occurs insidiously, and most patients are successfully controlled by diet, exercise, or oral hypoglycemic agents. [...] the overall autoantibody frequency in type 2 patients varies between 6% and 10% (105). However, the positive predictive value that a GAD65Ab positive type 2 diabetes patient [that is, a type 2 diabetic with a specific genotype] will be treated with insulin within 5 yr is 100% [...] Diabetes will appear as a function of loss of β-cell mass and loss of β-cell function. Different clinical phenotypes may develop, dependent on the combination of loss of β-cell mass and loss of function. [...] A different severity of inflammation may lead to variable degree of β-cell inhibition and resulting hyperglycemia [...] the degree of insulin resistance is also critical (99). Some subjects may encounter a severe loss of β-cells but, despite this, may not develop diabetes because of their high insulin sensitivity [...] Other subjects may develop diabetes at modest β-cell loss because they are highly insulin resistant. Therefore, it is not surprising that type 1 diabetes or autoimmune diabetes is associated with a large number of different phenotypes [...] To complicate the heterogeneity of autoimmune diabetes even further, it has also been found that patients with diabetes may develop GAD65 autoantibodies after the clinical diagnosis [...] In contrast to [...] patients masquerading as type 2 diabetic patients [because of slow onset of disease], an acute onset of type 1 diabetes is also reported (113). These patients have lower glycosylated hemoglobin values, diminished urinary excretion of C peptide, a more severe metabolic disorder with ketoacidosis, as well as higher serum pancreatic enzyme concentrations, compared to type 1 patients with a less dramatic onset [...]
“All vertebrates use insulin-producing pancreatic β-cells to achieve fuel homeostasis (1). These cells are able to measure the nutrient levels of the blood on a moment-to-moment basis and secrete insulin at rates that are exactly appropriate for the maintenance of optimal fuel levels. Therefore, the levels of circulating nutrients such as glucose, fatty acids, and amino acids are precisely controlled in mammals during fasting and feeding alike. The role of the pancreatic β-cells in fuel homeostasis is thus analogous to that of the thermostat in heating and cooling systems (2,3).” [This sounds simple enough. However it gets 'not simple' very fast.]
“Hypoglycemia is the limiting factor in the glycemic management of diabetes because it generally precludes maintenance of euglycemia [normal blood glucose levels, US]. [...] Were it not for the potentially devastating effects of hypoglycemia, particularly on the brain, glycemic control would be rather easy to achieve. Administration of enough insulin (or any effective medication) to lower plasma glucose concentrations to or below the nondiabetic range would eliminate the symptoms of hyperglycemia, prevent diabetic ketoacidosis and the nonketotic hyperosmolar syndrome, almost assuredly prevent retinopathy, nephropathy, and neuropathy, and likely reduce atherosclerotic risk. However, the devastating effects of hypoglycemia are real and the glycemic management of diabetes is therefore complex.” [much of chapter 7, from which the above and the following quotes originate, covers stuff I've covered before e.g. in this post, but there was some new stuff in that chapter as well and I actually think of this as the best of the chapters I've read so far]
“Iatrogenic hypoglycemia is the result of the interplay of therapeutic insulin excess and compromised physiological and behavioral defenses against falling plasma glucose concentrations in T1DM [...] Glucose is an obligate metabolic fuel for the brain under physiological conditions (4). (The brain can utilize other circulating substrates, including ketones such as β- hydroxybutyrate, but the blood levels of these seldom rise high enough for them to enter the brain in quantity and thus partially replace glucose, except during prolonged fasting.) Because of its unique dependence on glucose oxidation as an energy source and because it cannot synthesize glucose or store more than a few minute’s supply as glycogen, the brain requires a continuous supply of glucose from the circulation. At normal plasma glucose concentrations the rate of glucose transporter (GLUT-1) mediated blood-to-brain glucose transport down a concentration gradient exceeds that of brain glucose metabolism. However, when arterial glucose concentrations fall below the physiological range blood-to-brain glucose transport falls and ultimately becomes limiting to brain glucose metabolism and thus its functions and even its survival. Given the immediate survival value of maintenance of the plasma glucose concentration, it is not surprising that physiological mechanisms that very effectively prevent or rapidly correct hypoglycemia have evolved.”
I was considering covering these mechanisms in detail as well, but I reconsidered and decided to cut it short. However a few remarks should be included on this topic. One key point here is that one of the important reasons why diabetics are prone to hypoglycemia is that most of the normal physiological defence mechanisms against hypoglycemia are basically destroyed in diabetics. The first step in the body’s correction of low blood glucose is reduction of insulin production. This takes place way before symptoms ever occur in normal people. Type 1 diabetics who’ve taken insulin for a while don’t produce insulin on their own, so their body can’t regulate/lower insulin production – it’s already at zero. So step one in the process is deactivated. The second step in the natural process to reverse hypoglycemia involves increased glucagon secretion; glucagon is a hormone which tells the liver to convert its stores of glucogen (a type of sugar) into glucose and release them into the bloodstream. The authors note that although glucagon responses to other stimuli remain mostly intact in diabetics, the response to hypoglycemia is destroyed, for reasons not well known. So the first two defence mechanisms against hypoglycemia are completely out of the window in diabetics. The main one left is increased epinephrine secretion. Normally this one only sets in after the first two other responses have failed, but a very important point is that the set point for when this mechanism sets in depends on how often the diabetic is hypoglycemic; if hypoglycemia is common, the body will start tolerating lower blood glucose levels without initiating the remaining counterregulatory mechanism (there are a few other mechanisms at play, but they basically only apply to long-term hypoglycemia and will not play any significant role in a diabetic with acute hypoglycemia). The epinephrine response will still be initiated eventually, but the blood glucose level needed to initiate the process will be downregulated over time if hypoglycemic episodes occur often, which is problematic for reasons explained below. An important observation from the book regarding this counterregulatory mechanism:
“The development of an attenuated epinephrine response to falling glucose levels — loss of the third defense against hypoglycemia — is a critical pathophysiological event. Patients with T1DM who have combined deficiencies of their glucagon and epinephrine responses have been shown in prospective studies to suffer severe hypoglycemia at rates 25-fold (45) or more (46) higher than those with absent glucagon but intact epinephrine responses during aggressive glycemic therapy.”
The main reason things tend to go bad in these cases is presumably that if the epinephrine response is lost, the first manifestation of hypoglycemia is neuroglycopenia; the diabetic learns that she has a low blood glucose only when her brain stops working properly. This makes engaging in the correct behavioural responses (ingestion of glucose) problematic.
The concepts of hypoglycemia unawareness and what’s termed hypoglycemia-associated autonomic failure are closely related and important concepts to be familiar with:
“The concept of hypoglycemia-associated autonomic failure in T1DM [...] posits that (1) periods of relative or absolute therapeutic insulin excess in the setting of absent glucagon responses lead to episodes of hypoglycemia, (2) these episodes, in turn, cause reduced autonomic (including adrenomedullary epinephrine) responses to falling glucose concentrations on subsequent occasions, and (3) these reduced autonomic responses result in both reduced symptoms of, and therefore the behavioral response to, developing hypoglycemia (i.e., hypoglycemia unawareness) and — because epinephrine responses are reduced in the setting of absent glucagon responses — impaired physiological defenses against developing hypoglycemia (i.e., defective glucose counterregulation). Thus, a vicious cycle of recurrent hypoglycemia is created and perpetuated.”
A few more concluding remarks from the chapter:
“hypoglycemia risk reduction requires consideration of both the conventional risk factors that lead to episodes of absolute or relative insulin excess — insulin (or other drug) dose, timing, and type, patterns of food ingestion and of exercise, interactions with alcohol or other drugs, and altered sensitivity to or clearance of insulin — and the risk factors for compromised glucose counterregulation that impair physiological and behavioral defenses against developing hypoglycemia [...] The underlying principle is that iatrogenic hypoglycemia is the result of the interplay of insulin excess and compromised glucose counterregulation rather than insulin excess alone.”
I was well aware that diabetics can’t regulate insulin production (of course) and that this is a problem in terms of counter-regulation which makes hypoglycemia more likely, but I had no idea that ‘normal people’ had other natural counter-regulatory mechanisms which are also impacted by diabetes (to be clear, I was familiar with the concept of hypoglycemia unawareness but I’d never read about it in detail and the glycagon-response deactivation in diabetics I was not aware of. I knew that injections of glucagon is a treatment option in case of severe hypoglycemia – I’ve had such injections a few times, though fortunately not within the last decade – but I didn’t know that ‘normal people’ naturally secrete this stuff on their own if/when their blood glucose drops). In case you were wondering how to break the cycle:
“In a patient with hypoglycemia unawareness, a 2- to 3-wk period of scrupulous avoidance of iatrogenic hypoglycemia is advisable”.
Basically the idea is to avoid hypoglycemias for a while in order to change the threshold where the epinephrine response kicks in. Of course one shouldn’t change it too much in the other direction; poorly regulated diabetics tend to have thresholds higher than normal, so that they get symptoms of hypoglycemia even when their blood glucose is within the normal range. Something like that of course makes it harder for those individuals to achieve the therapeutic goals of reasonably low Hba-1c’s. I was wondering if I should mention this or not because it might get confusing but I decided to anyway; it should be noted that hypoglycemia-associated autonomic failure is a different form of nervous system dysregulation in diabetics than the one that takes place in long-term diabetics who develop diabetic autonomic neuropathy (DAN). Hypoglycemia-associated autonomic failure is reversible, whereas DAN most of the time isn’t, and DAN may have a lot of unpleasant effects aside from ‘just’ hypoglycemia unawareness – while covering the relevant chapter in McPhee not too long ago I noted that DAN may affect the enteric nervous system and cause problems with peristalsis, but this is but one of many problems caused by autonomic dysregulation; see the link above for more on this stuff. It should be noted that the authors in McPhee do not seem to be aware of the fact (at least they do not make it clear…) that not all hypoglycemia-unawareness in diabetics is related to DAN. On a different if related note it might be added that the autonomous nervous system is not the only part of the nervous system that is potentially affected by diabetes in the long run; for example sensorimotor polyneuropathy affecting the extremities is a far from uncommon complication.
I read the book yesterday.
It’s an easy book to read and most people who’ve read it seem to like it – it has a rating average of 4.04 on goodreads. I decided in the end to give it two stars. It’ll be the last popular science book of this type I’ll read in a while, and you should note that if I didn’t happen to feel sick and tired of popular science books at this point I might have given it a higher rating – I don’t really think it’s any worse than Miller’s The Mating Mind which I gave three stars, but the question remains if I ought to subtract a star from that one rather than give this one another star. The main problem with these books is that I at this point feel that I just don’t learn enough new stuff from them to justify reading them, and they often make me annoyed due to the authors’ relatively lax standards of evidence and imprecise language (compared to, say, the language of academic textbooks), both of which are more or less direct consequences of the format.
I think there’s generally in these types of books too much speculation and too little worry on part of the author about saying things which are not supported by the data. Funny enough, thinking back to the discussion I had with Miao when covering Miller I should note that Ridley also seemed to have trouble figuring out how large vocabularies people tend to have. But unlike Miller, Ridley didn’t even feel any need to source his hilariously wrong estimate (see below) and that’s not a point in his favour even though the estimate isn’t in any way critical to the coverage. There are interesting observations in the book, quite a few of them, but often it’s harder to trust the author than it ought to be because he also says things which are plain wrong in his book and occasionally it’s very hard to pinpoint the source of an interesting observation, or even figure out if a source exists, because whole paragraphs may be supported by one source which doesn’t necessarily cover all the material in the paragraph in question – there are no (authors X and Y, 20XX) references like in academic papers, only an occasional number and a source in the back of the book; and once you realize that he says unsourced things which are not true in the text, you start worrying about the existence of unsourced observations within the sourced paragraphs as well. Or at least I did. Of course the fact that a statement is sourced doesn’t necessarily mean it’s right, but it’s a better starting point than is the alternative. Another major problem is that there are a lot of sentences which would be improved greatly by probability indicators like ‘perhaps’, ‘it’s likely that’, and similar – this relates to the ‘imprecise language’ part above. There’s too little doubt, and he’s sometimes way too categorical in his statements and/or give a too simplified view of the problem at hand.
Stuff I’ve read which covers some of the same stuff as is covered in this book includes Miller, Bobbi Low, the first couple of chapters in Scarre, a few chapters from Majerus, and some of Dawkins’ work. I already knew about the sex-parasites thing because that idea has been covered elsewhere, though of course the book has more details on this stuff. Anyway I think it’s safe to say that if you’re reasonably well-informed there’ll be a lot of pages in this book covering stuff you already know.
I’ve focused mainly on the good stuff in the book below, but I didn’t think it was right to only include good stuff, so there are a few ‘bad quotes’ and related critical remarks here and there as well.
“Selection within the species is always going to be more important than selection between the species.” [The source given to this claim is 'Humphrey 1983'. This is a good example of the 'he's too categorical' - Always??? I wonder what the hundreds of species which went extinct in Lake Victoria following the introduction of the Nile Perch have to say about that? Or what about the Dodo? Important in what way and for whom?]
“If a population is small [...] or the number of genes in the creature is very large, [Muller's] ratchet has a severe effect on an asexual lineage. [...] being sexual was a prerequisite for being big (and therefore few), or, conversely, sex is unnecessary if you stay small.“
“among mammals, the amount of recombinations bears no relation to the number of young, little relation to body size, and close relation to age at maturity. In other words long-lived, late-maturing animals do more genetic mixing regardless of their size or fecundity than short-lived, early-maturing animals.”
“the probability that a family of animals will become extinct does not depend on how long that family has already existed. In other words, species do not get better at surviving [...] Their chances of extinction are random. [...] The struggle for existence never gets easier. However well a species may adapt to its environment, it can never relax, because its competitors and its enemies are also adapting to their niches. Survival is a zero-sum game.”
“Sex, according to the Red Queen theory, has nothing to do with adapting to the inanimate world [...] but is all about combating the enemy that fights back. Biologists have persistently overestimated the importance of physical causes of premature death rather than biological ones. [...] The things that kill animals or prevent them from reproducing are only rarely physical factors. Far more often they are other creatures – parasites, predators and competitors. [...] Parasites have a deadlier effect than predators for two reasons. One is that there are more of them. [...] The second reason, which is the cause of the first, is that parasites are usually smaller than their hosts while predators are usually larger. This means that the parasites live shorter lives and pass through more generations in a given time than their hosts.” [...] Parasites and their hosts are locked in a close evolutionary embrace. The more successful the parasite’s attack [...] the more the host’s chances of survival will depend on whether it can invent a defence. The better the host defends, the more natural selection will promote the parasites that can overcome the defence. So the advantage will always be swinging from one to the other: the more dire the emergency for one, the better it will fight. [...] the notion of a host-parasite arms race is one of the most basic and unavoidable consequences of evolution.”
“The advantage of sex [to fight parasites] can appear in a single generation. This is because whatever lock is common in one generation will produce among the parasites the key that fits it. So you can be sure that it is the very lock not to have a few generations later. For by then the key that fits it will be common. Rarity is at a premium. [...] many of the most notoriously polymorphic genes, such as the blood groups, the histocompatibility antigens and the like, are the very genes that affect resistance to disease – the genes for locks. Moreover, some of these polymorphisms are astonishingly ancient. [...] Some very powerful force is at work ensuring that most versions of each gene survive, and that no version changes very much. That force is almost certainly disease. [...] most asexual plants are short-lived annuals. Long-lived trees face a particular problem, because their parasites have time to evolve to their genetic defences – to evolve. [...] Disease might almost put a sort of limit on longevity: there is little point in living much longer than it takes your parasites to adapt to you.” [...this last sentence sort of conveys an old idea which I've had before, but the framing is different and the framing is important. When thinking about this aspect in the past I've usually tended to think only about the selective pressures imposed by predators, rather than e.g. those of diseases, but of course the latter are likely to play a major role as well.]
“larger, more intelligent and more social animals are generally more flexible in their mating systems than smaller, stupid or more solitary ones.”
“A female human being does not have to share her sexual favours with many males to prevent infanticide, but she may have a good reason to share them with one well-chosen male apart from her husband. This is because her husband is, almost by definition, usually not the best male there is – else how would he have ended up married to her? His value is that he is monogamous and will therefore not divide his child-rearing efforts among several families. But why accept his genes? Why not have his parental care and some other male’s genes? [...] the principle – marry a nice guy but have an affair with your boss, or marry a rich but ugly man and take a handsome lover – is not unknown among female human beings.” [...] [According to findings by Robin Baker and Mark Bellis] the typical woman’s pattern of infidelity [...] is exactly what you would expect to find if she were unconsciously trying to get pregnant by a lover, while not leaving a husband.” [I don't really know to which extent one should trust these findings, however, as other findings by them described by Ridley simply can't be true and to me indicate questionable methodology at best:] “In a block of flats in Liverpool, they found by genetic tests that less than four in every five people were the sons of their ostensible fathers. The rest were apparently fathered by somebody else. In case this was something to do with Liverpool, they did the same tests in southern England and got the same result.” [As I put it in the margin, 'these numbers are way too high.' See e.g. this post by Razib Khan.]
“Cuckoldry paranoia is deep-seated in men. [...] Cuckoldry is an asymmetrical fate. A woman loses no genetic investment if her husband is unfaithful, but a man risks unwittingly raising a bastard. [...] It is not that a woman need not mind about her husband’s infidelity: it might lead to him leaving her, or wasting his time and money on his mistress, or picking up a nasty disease. But it does imply that men are likely to mind even more about their wives’ infidelity than vice versa. History, and law, have long reflected just that.”
“There has been no genetic change since we were hunter-gatherers, but deep in the mind of modern man is a simple hunter-gatherer rule: strive to acquire power and use it to lure women who will bear heirs; strive to acquire wealth and use it to buy affairs with other men’s wives who will bear bastards.” ["There has been no genetic change since we were hunter-gatherers" - did he actually just say that? You just can't write stuff like that. Again, this is way too categorical - it's just plain wrong. There are plenty of recent genetic changes to be found (see e.g. this), if you care to look for it. Also, on a different matter the 'strive to acquire wealth' part of human behaviour today may well somehow be related to things which took place in hunter-gatherer times, but a male decision rule to strive for wealth in order to have more babies sure as hell isn't derived from hunter-gatherer times; as he himself points out in his book, "accumulation of wealth was not possible in hunter-gatherer societies" (this is a direct quote from the book). It's as if he's unable to connect the chunks of knowledge he has obtained, and although that may well occasionally be hard this is just borderline weird.]
“the evidence for the average male brain differing in certain ways from the average female brain is now all but undeniable. [...] There is no a priori reason for assuming that men and women have identical minds and no amount of wishing it were so will make it so if it is not so. [...] to assume the sexes are mentally identical in the face of evidence that they are not is just as unfair as to assume sexual difference in the face of evidence that they are the same. [...] mankind may be the mammal with the greatest division of sexual labour, and the greatest of mental differences between the sexes.” [He starts out well in that chapter. But then the politically correct crap shows its ugly face anyway...] “I think it is easy and, given the evidence, rational to believe that the [mental] differences between the natures of men of different races are trivial, while the differences between the natures of men and women of the same race are considerable.” [Yeah, well... IQ data shows a similar pattern to the one in the link: Good luck finding gender differences as large as the racial differences. I remember a finding from a paper from a course I took last year on the economics of education; they found that the average SAT score of black college-educated in their (US) sample was about the same as the average SAT score of a white high school graduate. I can't be bothered to find the link, but the link above tells a similar story; the differences are huge. Switch 'sexes' with 'races', 'males' an 'females'/'men' and 'women' with 'blacks' and whites' in the sentences quoted above and see where you end up. We didn't have as much data on that kind of stuff when Ridley wrote his book as we do now, but we did have data back then as well and given the observed differences Ridley cannot have had good reasons for holding the view that he does. I won't go so far as to call him a hypocrite, but he should at the very least consider reading Clifford.]
“True, we learn a lot more than bats and cuckoos do. We learn mathematics and a vocabulary of ten thousand words, and what people’s characters are like.” [No source in the book. Of course there isn't - this number is bullshit, it's not even close. See also this discussion. On the one hand the fact that he didn't even feel the need to source the estimate makes him look worse than Miller, but on the other hand this isn't an estimate which is as critical to the book or the chapter as it was to Miller. In Ridley's case it's likely just a number he drew out of a hat, not caring enough about whether it was right or not to actually try to find out. Intellectual laziness is the problem, not the fact that the number is wrong.]
“As Horace Barlow of Cambridge University has pointed out, the things of which we are conscious are mostly the mental events that concern social actions: we remain unconscious of how we see, walk, hit a tennis ball or write a word. Like a military hierarchy, consciousness operates on a ‘need to know’ policy.”
I’ve read about and blogged this topic before, but this is the first academic text on the topic I’ve read. I liked the book and gave it four stars on goodreads. It’s a typical Springer publication, i.e. it’s a collection of relevant studies/papers published on the topic; there are fourteen papers/chapters included in the book. Given the nature of the book there’s some overlap across chapters, but that’s to be expected and it doesn’t really matter much. The book was published in 2011 so it’s reasonably up to date even though things are happening fast in this area.
Some of the authors of the studies included in the book assume that the reader possesses a level of knowledge about microbiology which goes way beyond what you’d get from reading an intro text like Hardy, and although I’ve also previously browsed one of the books you’d actually need to have read in order to understand the details (Brooks, Butel & Morse), I’ve of course long ago forgotten much of that stuff and so occasionally felt a bit lost while reading the book. There’s some good stuff in there though, and many of the chapters I did not find that hard to read although some details eluded me. It’s my impression that you probably will not get much out of the book if you’ve never read a microbiology text before (I actually feel a bit sad having to write that as the topics covered are very important in terms of future public health, and so in a way I’d really wish as many people as possible actually read this book, or at the very least familiarized themselves in some other way with the problems covered in the book).
“This book serves a twin purpose in helping to construct a more informed evidence base for coherent policy making while, at the same time, providing practical advice for health professionals in the prevention and control of HAIs.”
The quote above is from the preface of the book. The papers included in the book cover a wide variety of topics; one chapter deals with the ‘total scale’ of the problem of healthcare associated infections (HAIs), another chapter deals with (among other things) how antibiotic treatment regimes and the development of resistant strains in the community and/or health care institutions are associated, one chapter deals with the epidemiology of drug resistant strains of bacteria and how to properly categorize drug resistance (which can take on many forms), and quite a few chapters focus on specific HAIs (C. difficile, MRSA, VRE, ESBL-producing bacteria, CRE, Acinetobacter baumannii, and MDR (multi-drug resistant) Pseudomonas all get a chapter each). Many intervention studies are covered and the focus is not just on identifying the extent of the problem but also on finding ways to counter the problems; one chapter deals specifically with antibiotic stewardship, which is one of the main ways to try to stop the spread of antibiotic resistance, but many other chapters cover that topic as well in the specific setting. Another key strategic element in any intervention strategy, infection control measures (hand hygiene, patient isolation, etc.), is likewise covered in many of the chapters, and as the studies included have a very ‘evidence-based medicine approach’ to these matters important but potentially embarrasing problems like compliance problems on the part of health care providers [it's harder to convince doctors to wash their hands than it is to convince nurses..] are not overlooked. The book is not US-centric; countless international studies are included, and a specific chapter is reserved to dealing with MDR infections in low-resource health care settings. The institutional setting is important and is covered in a few chapters, and included in that discussion are observations related to how things like reimbursement methodology may impact health care provider behaviours and how faulty incentive structures on the institutional level may aggravate the problems with resistance development e.g. by failing to address collective action problems in this area.
As might be inferred from the comments above, there’s way too much stuff in there for it to make sense for me to cover it all here. However I have added some observations from the book below, emphasizing some important points and observations along the way and adding a few comments here and there.
“What is required is tackling of the problem at its root cause, namely the gross over use of antibiotics.” [...let's just start out with that one, so that people will not falsely assume that this aspect is not covered in the book.]
“In broad terms, there are two means by which patients can develop multi-resistant infections—they can either develop their own resistant pathogen, or they can acquire someone else’s strain.
Emergence of new resistant pathogens is directly related to antimicrobial selection pressure either via the mutation of new resistance genes or the alteration of bacterial ecology (e.g. in the gut) that facilitates the transfer of naturally occurring or emergent resistance genes from one bacterial class to another [...] antibiotic use in food production can have the same effect as direct human antibiotic misuse, since it can select for both resistant pathogens (e.g. fluoroquinolone-resistant Campylobacter in chicken meat) or resistance genes such that food consumption results in either direct fecal colonisation or acquisition of resistance genes by routine gut flora [3,4]. Antibiotic stewardship is therefore not simply a hospital issue.” [...]
“The global burden of healthcare associated infections (HAI) is currently unknown, despite international efforts to fill this gap in our knowledge. Where the size of the burden of HAI has been quantified, the greatest impact is in those countries with least resources to measure and manage them. [...] 3.5–10.5% of hospitalised patients in industrialised countries may experience HAI (E.C.D.C. 2008), while greater than 25% of hospitalised patients in developing world nations may be affected (W.H.O. 2005). [...] While in 2000, 70 countries did not screen donated blood for HIV, hepatitis B or hepatitis C, currently the risk of bacterial infection from transfusion is greater than the risk of acquiring these viruses. Reuse of contaminated needles or syringes during injections in limited resource settings poses a major threat for transmission of infection, accounting for an estimated 21 million hepatitis B infections, 2 million hepatitis C infections and over 95,000 HIV infections. [...] Of the 8.8 million deaths in children under the age of 5 years, infectious diseases account for 5.5 million (63%) [...] clinicians in developing countries tend to diagnose and prescribe medication empirically. People with undetected resistance then receive antibiotics to which their isolate is not susceptible. For example, one study in western Kenya found that more than half of the patients treated empirically for bacterial diarrhea were given ineffective antibiotics. Among patients with shigella, this number exceeded 80% (Shapiro et al. 2001). [...] In developing countries, antibiotics are a scarce resource, and most clinics and hospitals can barely afford common first-line agents, much less second and third-line alternatives [...] variation in prices of antibiotics is considerable. The wholesale price differential between amoxicillin and co-amoxiclav, for example, is on the order of a factor of 20 (Forster 2010). This means that where resistant bacteria necessitate the use of co-amoxiclav, only 5% of the patients can be treated for the same budget as with amoxicillin. [...] In coastal Kenya, resistance to chloramphenicol, amoxicillin, cotrimoxazole, and gentamicin in Gram-negative sepsis is common, and susceptibility remains only to two rarely used drugs, ciprofloxacin and cefotaxime. The cost of treating a 15 kg child with sepsis would be $0.38–2.30 for gentamicin and chloramphenicol versus $73–108 for the effective drugs [...] In Thailand, only 9% of antibiotics administered in a teaching hospital were appropriate to the patient’s condition, and 36% of patients were given antibiotics without evidence of an infection [...]
“The underused vaccines that could have the biggest effect on antibiotic use in hospitals are against Streptococcus pneumoniae and Haemophilus influenzae type b. To these should be added one of the new vaccines against Rotavirus, the main cause of dehydrating diarrhea, which kills 400,000–500,000 infants and children in developing countries annually. Even though Rotavirus is, in fact, a virus, reducing its incidence will reduce antibiotic use. The most appropriate treatment for rotavirus and other causes of watery diarrhea is oral rehydration therapy, but since antibiotics are used inappropriately in many cases, reducing the number of cases will reduce antibiotic use.” [..vaccines against viruses may help decrease the number of bacteria resistant to antibiotics - yep, this stuff is complicated..]
“HAI are recognised as among the most common adverse outcomes from hospitalisation in the US; approximately 1.7 million HAI are reported across the US each year, which are associated with around 99,000 deaths per year. Around a third of HAI are urinary tract infections, one fifth are surgical site infections, 15% are pneumonia and 14% are bloodstream infections (C.D.C. 2010).” [...] Estimates in Europe are that approximately 4.1 million patients per year experience HAI, and that attributable deaths are of the order of 37,000 per year (E.C.D.C. 2005–2010).” [These estimates are somewhat uncertain and I'm not sure how much you should read into the fact that they differ in the way that they do, with fewer but more lethal HAIs in the US. Before you read a lot into it, you should certainly note that there is huge regional variation in the data here.] [...]
“Surgical prophylaxis is a common area of overuse as shown in many publications. Measured by total DDDs [defined daily doses], it can amount to around one third of a hospital’s total antibiotic use. This illustrates the potential for ecological damage although surgeons often ask whether 24 h or even single dose prophylaxis can really select for resistance. The simple answer is yes, but of course much of the problem is extension of prophylaxis beyond the perioperative period, often for several days in critical patients, perhaps until all lines and drains are removed. There is no evidence base in favour of such practices.” [...]
“Since 2002, increasing rates of CDI [Clostridium difficile Infection] with a more severe course, higher mortality (from 4.7 to 13.8%) and more complications (from 7.1 to 18.2%) have been reported in Canada [...] Of all patients who develop CDI in the hospital setting, approximately 80–90% have used antibiotics in the previous 3 months. [...] MRSA can survive for months in hospital environment [...] and it can be isolated on clinical equipment, as well as on general surfaces especially close to patient’s area, such as curtains, beds, lockers and over-bed tables [...] Before contact precautions are implemented, MRSA carriers may have already contaminated their environment with MRSA. [...] Cross-transmission between patients may occur via HCWs [health care workers'] hands after touching contaminated environmental surfaces [...] One study showed that 10% of HCWs fingertips were contaminated with MRSA after contact with MRSA positive patient’s environment [...] There is now reasonable evidence that rates of MRSA, C.difficile, VRE and multi resistant Gram-negatives can be reversed by modulating use of key agents such as cephalosporins and quinolones [...] The real problem for the future, of course, is how to do this without “squeezing the balloon”, transferring the resistance selection pressure to other classes of agents. This highlights another paradox, that of current antibiotic policies which tend to lead to a lack of diversity of use of different classes of antibiotics. Diversity of use is probably one of the best strategies to delay emergence of resistance, although a lack of choice of truly different drug classes makes its implementation problematic. Moreover, the holy grail, and the most difficult thing is to achieve total reduction in prescribing while not compromising patient outcomes. Again, this isn’t something current strategies are good at achieving.” [...]
“ESBL-producing bacteria are not only present in hospitals from endemic nosocomial sources but are introduced into the hospital from other health care facilities (particularly high rates occur in care of the elderly homes [...] but also from individuals coming
from the community (Ben-Ami et al. 2006). [...] This community carriage is an important facet of ESBL control [Again, what happens outside the hospitals matter a great deal...] [...]
“Carbapenems have the broadest antimicrobial spectrum of any beta-lactam antibiotic and are frequently used as first-line agents for the treatment of severe infections caused by multiresistant Gram-negative bacteria [...] The emergence and spread of carbapenem-resistant Enterobacteriaceae (CRE) are therefore a major concern for patient safety and public health. Infections due to CRE may lead to increased likelihood of treatment failure and growing reliance on third-line agents and combination therapy, with doubtful therapeutic efficacy and increased potential for toxic side-effects [...] It also increases the cost of treatment [...] CRE differ from most other multidrug-resistant bacterial pathogens in that there is no reliable treatment available (Schwaber and Carmeli 2008). [...] two cases of panresistant CRE were recently reported from a hospital in New York [...panresistant strains are basically untreatable, US.] [...] Patients with CRE infection are at high risk of treatment failure and adverse outcomes, including increased mortality and morbidity, longer length of hospital stay, and higher treatment costs when compared to infections caused by susceptible strains. Several studies have reported high percentages of crude in-hospital mortality— some over 50%—among patients infected with CRE [...] the magnitude of the excess mortality directly attributable to CRE is difficult to quantify [...] Overall, uncertainties persist in individual patient-level analyses regarding which prior antibiotic exposures are most important as risk factors for acquisition of, transmission of and infection with CRE. Similarly, ecologic studies using aggregate datalevel analyses do not show a clear-cut picture.” [...]
“Antibiotic policies are crucial but they cannot be effective without active infection control program[s]. A hospital with a strong infection control program without an antibiotic stewardship component would tackle transmission of multi-resistant organisms such as VRE but would not prevent individual patients from getting colonised or infected with resistant microbes. On the other hand, strong antibiotic stewardship would be expected to control the menace of multi-resistant organism but in absence of an infection control program, transmission of organisms (even if not multiply resistant) would be easy and would adversely affect patient care.” [...]
“A retrospective, risk-adjusted, cohort study of 80 patients with Acinetobacter bacteraemia conducted in Korea demonstrated that those infected with imipenemresistant strains had a significantly higher 30-day cumulative mortality rate than those infected with imipenem-susceptible strains (57.5% versus 27.5%) [...] This was mainly due to a higher rate of inappropriate antimicrobial therapy. [...] Carbapenems are the mainstay of treatment for severe infections. However, carbapenem-resistant A. baumannii strains have emerged worldwide. [...] A considerable proportion of multi-drug resistant A. baumannii strains are susceptible only to polymyxins, which prompted the use of an old antibiotic in recent years. [...] Polymyxins are polypeptide antibiotics that act as detergents on the bacterial cell wall. They were introduced in 1940 but they were abandoned in the 1980s due to the occurrence of nephrotoxicity and neurotoxicity. [...] Reported nephrotoxicity ranges between 8 and 36%. [...] Reported neurotoxicity ranges between 7 and 29%, with oral and perioral paresthesias, visual disturbances and polyneuropathy [...] [So basically what has happened is that doctors have been forced to restart using drugs they threw away 30 years ago because those drugs caused kidney failure and severe nerve damage. These old drugs are currently the only drugs that work against some MDR infections, and no new drugs are even close to being developed at this point]. [...]
P. aeruginosa is the second most common cause of health-care associated pneumonia, of hospital-acquired pneumonia and of ventilator-associated pneumonia (VAP). It is also reported as the cause of 9% of hospital-acquired urinary tract infections (UTIs). [...] It is estimated that the rate of colonization and/or infection by MDR P. aeruginosa is 0.5 episodes/1,000 patient-days in the general ward and 29.9 to 36.7/100 patients in the ICU (Agodi et al. 2007; Peňa et al. 2009). [...] infections by MDR P. aeruginosa have a significant impact on mortality. A retrospective study of our group in non-neutropenic hosts in the general ward disclosed 22.2% mortality of infections by MDR P. aeruginosa compared to 0% of infections by susceptible isolates [...]. For ICU infections caused by MDR P. aeruginosa mortality ranges between 22% and 77%; this ranges between 12% and 23% when ICU infections are caused by susceptible isolates (Shorr 2009).” [...]
“Antibiotic effectiveness can be viewed as a shared resource in which current use depletes future value and imposes costs on society in the form of longer hospitalization, higher mortality rates, and the diversion of resources into the provision of newer and more expensive drugs. In making treatment decisions, prescribers should weigh the favorable effects of applying antibiotics to improve a patient’s health against the negative consequences for the public and future drug effectiveness (Laxminarayan 2003b). However, clinicians usually ignore the future therapeutic risks to society associated with antibiotic use and instead focus on the direct benefits of antibiotic treatment to their patients. [...] In the absence of a good pipeline of new drugs, it is the balance between the individual patient and society as a whole, otherwise known as the ecological perspective, that has to be clearly established and debated. We need to get clever, quickly. [...] In the long term, new antibiotics are needed [...] However, as a gap of 10–15 years has been identified (European Centre for Disease Prevention and Control and European Medicines Agency 2009), immediate action is needed to conserve the power of the available arsenal.”
i. Some questions:
“Look for reasons for living and internal strengths for managing risk:
* ‘What’s important to you in your life?’
* ‘What do you feel connected to? Faith? Family? Community?’
* ‘What keeps you going?’
* ‘Do you have a sense of purpose or meaning?’
* ‘How do you manage stress?’
* ‘What do you do to take care of yourself?’
* ‘What has kept you from killing yourself?’
* ‘What do you do that helps you deal with thoughts of suicide?’
* ‘How do you manage to stay safe?’
* ‘What would keep you from killing yourself now?’”
(From Chehil’s book)
ii. Detecting Consciousness in the Vegetative. An interesting post.
From this collection of hilarious Chinese translation fails (via Razib Khan – re. RK, see also this). Curious though I’d be about how the fries would deliver the baby, I don’t really need an emergency C-section at this point. And I’m not quite willing to let go of what’s left of my inner child yet. So I’d probably go for the fried cat ear.
iv. When I grow up, I want to be a cartoonist. In other words, a mathematician. On a related matter, comics like this (and this – don’t miss the votey at the red button!) almost make me sad I won’t have children. I should perhaps point out that SMBC in general is a pure goldmine when it comes to such comics – see for instance also this, this, this, this, this, this, this and this. The best I can hope for is probably something like this.
What’s going on in your life? What have you learned recently? Links of interest? How would you answer Chehil’s questions?
I finished the book.
It’s a great read, I gave it four stars on goodreads (average rating: 4.03). The book covers aspects of human warfare all the way from ancient times to the war in Iraq, so it covers a lot of ground. It ‘only’ covers the (lives and) deaths of ground troops throughout the ages – this is a completely natural line to draw and I see no reason to criticize it, but I should note that it does mean that one has to remind oneself during the reading of the book that even though a lot of different ways to die are accounted for here, many war deaths (and strategically important aspects of warfare, like naval battles or aerial warfare) still go almost completely unaccounted for in this book (also, civilians tend to die in war as well – he does touch upon this aspect of warfare as there’s sometimes simply no way around it, but many of the ways civilians have died in war are not covered here). The chapter on World War 2 is not that dissimilar from Fussell’s book Wartime – Understanding and Behaviour in the Second World War (here are links to my coverage of that book) which I read a while back – he actually quotes Fussell in the chapter on World War 2 – but I liked Stephenson’s book significantly better. I think it’s better written, it covers more stuff (though less stuff about World War 2) and the ratio of interesting stuff to uninteresting stuff is much higher. The book is quite a pageturner; I went through this book faster than I do many books of comparable length. Although the book covers a lot of different time periods, the narrative is coherent and he’s good at pointing out both which things changed over time and how and why they changed, and which things didn’t change quite as much. The book is a good mix of interesting data and personal narratives and accounts; there are a lot of primary sources included in the book, and they generally do a good job of illustrating specific aspects of warfare of interest. I’m closer to five stars than three.
There’s way too much good stuff in the book to cover it all here on the blog, but some samples of the kind of stuff you’ll encounter in the book’s last 250 pages are included below:
“A Confederate officer, I. Herman, observed that most infantrymen went through their allocation of cartridges during an engagement of any length. Five thousand men might easily expend 200,000 rounds in a few hours (an average of 40 rounds per man), and in his experience it took 400 rounds for every enemy killed. General Rosencrans at Murfreesboro estimated 145 shots to inflict one casualty (and not necessarily a fatality). [...] at Gettysburg, the bloodiest Civil War battle in terms of the total number of casualties, 81 percent of Union and 76 percent of Confederate soldiers came through the three days unhurt” [...] Of the 246,712 wounds from weapons that were treated during the war, the vast majority (just over 231,000) were from small arms. Next came artillery-induced wounds (13,518), followed by a very small number (922) of bayonet wounds. Obviously, if the wounds were treated the soldier had not been killed outright, but the proportion is at least an indicator of the most likely causes of death. [...] In the Union army the ratio of officers to men was 1 to 28, but the ratio of officers to men killed in battle was 1 to 17. [...] Fifty-five percent (235 out of 425) of Confederate general officers became casualties, and of those 73* were killed [...] Fifty-four (70 percent) died leading their men in attacks.” [...]
“The men who died with Custer at the Little Big Horn were thoroughly mutilated after death. Almost all (except George Custer) were scalped; some were decapitated and their heads taken to the Indian encampment (the Indians maintained that no men were tortured) but others were posthumously burned and further mutilated in the ritual celebrations following the battle.21 The wounded were dispatched either by warriors or by the women and youngsters who combed the battlefield afterward—a commonplace of battle in Europe up until the end of the Napoleonic Wars. Faces and penises, as might be imagined, were often the centers of attention — the faces bashed in, the penises either cut off or otherwise mutilated.” [...]
“Gatling viewed his brutally efficient (if sometimes stuttering) killing machine as in some way making warfare more economical of lives. In 1877 he wrote:
["]It may be interesting to you to know how I came to invent the gun that bears my name.… In 1861, during the opening events of the [American Civil] war … I witnessed almost daily the departure of troops to the front and the return of the wounded, sick and dead. The most of the latter lost their lives, not in battle, but by sickness and sickness incident to the service. It occurred to me that if I could invent a machine—a gun—that would by its rapidity of fire enable one man to do as much battle duty as a hundred, that it would to a great extent, supersede the necessity of large armies, and consequently exposure to battle and disease would be greatly diminished.["]
The efficiencies of automated killing were particularly valued in colonial warfare, where the cost of maintaining armies far from the home base was onerous. Ironically, the very success of machine guns in killing cost-effective quantities of natives tainted them when it came to European warfare, where it was felt, particularly among the officer class, that mechanization would reduce combat to a competition between meat grinders [...] The resistance was adamant, and it would take the cataclysm of the First World War to kill off the ancient idea of heroic combat.” [...]
“[During World War 1] in France there were 34 deaths per 1,000 population; in Germany, 30; in Britain, 16.6 The ratio of killed to wounded for the whole war was 3 wounded for every combat death. [...] Officers were twice as likely to be killed as the men they led. [...] In the German army the infantry casualty rate as a whole was 13.9 percent, but for the officer class it was a staggering 75.5 percent. [...] The greatest killer [...] was artillery, hence the shockingly high proportion of men whose bodies were never recovered and who have no known grave. More than 300,000 British and British Empire dead of the Western Front — 40 percent of the total killed there—were never found. [...] In one representative British division, 58 percent fell to artillery, 37 percent to small arms, and 5 percent to other agents (bombs, gas, and bayonets, for example). Of those killed by bullets, about half fell to machine-gun fire, and of all casualties about 25 percent were inflicted by machine-gun fire.” [...] the incidence of bayonet-inflicted casualties was minuscule: .32 percent, for example, of one sample of 200,000 British casualties.” [...]
“In October 1942, only 1 in 1,000 US Army members became a casualty. In November, it rose to 4 per 1,000, reflecting the fighting in North Africa, Guadalcanal, and New Guinea. By June 1944, it had soared to 50 per 1,000, hitting its peak in January 1945 with about 56 per 1,000.91 [...] As a snapshot the statistics are interesting but hide a much grimmer picture. The rate per thousand is a percentage of the whole army. Unlike World War I, where a much larger proportion of the total armed services was exposed to combat, in World War II the logistical tail was fat and long and comparatively safe. [...] Of the roughly 10 million men in the US Army by the war’s end, only about 2 million, or 1 in 5, were in the 90 combat divisions (of which 68 were infantry divisions), and of these, about 700,000 were in the infantry: 1 in 14 for the whole Army but absorbing 70 percent of the casualties.” [...] a soldier hit by a machine-gun round [...] stood a 50 percent chance of dying, compared with 20 percent if hit by artillery. Of those hit by bullets, almost a quarter were killed, whereas slightly fewer than one-fifth of soldiers struck by artillery died, and only one in ten from mortars.” [...] More than 77 percent of Soviet tankers (310,000 out of 403,000) were killed. [...] Burning to death was the greatest fear and the common fate of many tankers of whichever army.” [...]
“Particularly in battles like Okinawa, where flamethrowers were widely used to kill the Japanese in their cave redoubts, too many men would have witnessed scenes like this:
“Horst von der Goltz, Maine ’43, who would have become a professor of political science, was leading a flamethrower team … when a Nip sniper picked off the operator of the flamethrower. Horst had pinpointed the sniper’s cave. He had never been checked out on flamethrowers, but he insisted on strapping this one to his back and creeping toward the cave. Twenty yards from its maw he stood and did what he had seen others do: gripped the valve in his right hand and the trigger in his left. Then he pulled the trigger vigorously, igniting the charge. He didn’t know that he was supposed to lean forward, countering the flame’s kick. He fell backward, saturated with fuel, and was cremated within seconds.” [I decided against including a lot of these types of illustrative quotes in my coverage of the book, focusing instead mostly on the numbers, but I should note that there are a lot of these types of quotes in the book and they're very helpful when it comes to the problem of translating the numbers into real human experiences.] [...]
“A common way for a soldier to be killed “off the books,” as it were, was by his own comrades. The chaos of jungle warfare made friendly fire particularly lethal. On Bougainville, 16 percent of American deaths were attributable to friendly fire; and on Guadalcanal, it accounted for 12 percent of all casualties.” [...]
“The United States dropped three times as many bombs during the Vietnam War as it had during the whole of World War II. In 1968–69 alone it delivered one and a half times as many as the total dropped on Germany.” [...] “They [Viet Cong] booby-trapped our trucks and jeeps. They booby-trapped the trails they knew we’d take, because we always took the same trails, the ones that looked easy and kept us dry. They sniped at us. And every so often, when they felt called on to prove they were sincere guerrillas and not just farmers acting tough, they crowded a road with animals or children and shot the sentimentalists who stopped.
We did not die by the hundreds in pitched battles. We died a man at a time, at a pace almost casual. You could sometimes begin to feel safe, and then you caught yourself and looked around, and you saw that of the people you’d known at the beginning of your tour a number were dead … And you did some nervous arithmetic.” [...]
“In the first phase (“shock and awe”) of the Iraq War, starting in 2003, 148 US troops were killed in action, and of those a substantial number were from friendly fire; of the 24 British soldiers killed, 9 deaths were caused by US fire. By comparison the Iraqi army had an estimated 100,000 killed and 300,000 wounded. [...] In the chaos of insurgency warfare there are wrenching decisions to be made. Captain Ed Hrivnak, a member of a medevac team in Iraq, recalls that a wounded soldier “confides in me that he witnessed some Iraqi children get run over by a convoy. He was in the convoy and they had strict orders not to stop. If a vehicle stops, it is isolated and an inviting target for a rocket-propelled grenade. He tells me that some women and children have been forced out onto the road to break up the convoys so that the Iraqi irregulars can get a clear shot. But the convoys do not stop. He tells me that dealing with the image is worse than the pain of his injury.”” [...]
“During the American War of Independence [...] about a quarter of all patriot soldiers admitted to hospital died. In the Civil War it dropped to around 14 percent, but by the First World War the American soldier’s chances of surviving hospitalization for wounds had increased dramatically: Slightly over 6 percent were lost; in World War II, 4.5 percent; in Korea, 2.5 percent, and in Vietnam, 1.8 percent. [...] Several factors had to come together, each making a massive individual contribution but not a decisive one, until they acted in concert. They were the organization of medical services, the control of infection, blood transfusion, surgical procedures, and anesthetics. [...] Before the age of asepsis, antibiotics, anesthesia, and blood transfusion, military surgeons were caught between the devil and the deep blue sea. In order to prevent severe injuries to limbs from becoming gangrenous, amputation was widely considered prudent. However, the nonsterile conditions of the operation introduced its own risks [...] After the battle of Waterloo, 70 percent of amputees died, and during the Crimean War, 63 percent. [...] the losses to amputation during the Franco-Prussian War of 1870–71 were shocking [...] Of the 13,173 amputations (ranging from relatively minor operations to fingers up to major ones to limbs) undertaken by the French, 10,006 (76 percent) died of subsequent infection.“
“War is about many things, but at its core it is about killing or getting killed. It is not chess, or a computer game, or a movie, or a book about death. It is, implacably and nonnegotiably, the thing itself. [...] “Military history must never stray from the tragic story of killing,” says Victor Davis Hanson with characteristic forthrightness. “Wars are the sum of battles, battles the tally of individual human beings killing and dying.… To write of conflict is not to describe merely the superior rifles of imperial troops or the matchless edge of the Roman gladius, but ultimately the collision of a machine-gun bullet with the brow of an adolescent, or the carving and ripping of artery and organ in the belly of an anonymous Gaul. To speak of war in any other fashion brings with it a sort of immorality. Euphemism in battle narrative or the omission of graphic killing altogether is a near criminal offense of the military historian.””
From the introduction of the book. It’s quite interesting – I like it so far. Lots of interesting observations and details. Some more stuff from the first third of the book below:
“Whether atlatl or bow, the long-range missile weapon radically changed battlefield prospects. [...] It was the start of the great social leveling of combat killing. The ever-increasing sophistication of missile weaponry (the atlatl of the Aztecs defeated by the arquebuses of the conquistadors, the arquebus by the musket, the musket by the breech-loading rifle, and so on), and the concomitant reduction of high-risk, close-action shock combat is one of the core themes of warfare. Killing from a distance is invariably preferable to the riskiness of close combat. And so, over millennia the evolution of missile weaponry has all but rendered shock weapons redundant. [...] As a consequence, the battlefield has become “empty”: In most cases the warrior does not see whom he kills or is killed by. [...] Close-combat killing defined the heroic for millennia. There is a tension, constant for most of military history, between shock and missile tactics that arises from the constraints imposed by the physical properties of the weapons. Put simply, shock weapons—clubs, swords, stabbing spears, maces, et cetera—were more effective killers than missiles, but the warrior had to get close to his enemy, which is dangerous: “These very short ranges create severe psychological and social difficulties that render shock weapons the weapons of choice among only the more severely disciplined armies of high chiefdoms and states.… And more important, to reach this closure the warrior must pass through the killing zone of the enemy’s fire weapons.”” [...]
“In studies of forty-two primitive societies it has been found that the vast majority (thirty-nine) routinely killed all captured enemy warriors. Zapotecs removed hearts and genitals; the ancient Chinese bound and buried their defeated enemies and, like the Aztecs, much preferred to capture an enemy for later ritual sacrifice than kill him outright on the battlefield. Sometimes these acts of torture were carried out by noncombatant women and children (particularly young boys, for whom it was an initiation rite), as was the case among some of the American woodland Indian tribes [...] It was extremely rare that a captive warrior would be spared and incorporated into his captor’s tribe” [...]
“Ever since the introduction of relatively long-range missile weaponry, the tactical shape of battle has conformed to a fairly predictable pattern. First comes the “softening-up” barrage. It was arrows in the Bronze Age; high-explosive shells, delivered either by artillery or by aircraft, in ours. Following that there has to be a closure, a physical confrontation that claims territory. In the Bronze Age it would have been a combination of chariot-borne warriors and infantry; in ours it is soldiery borne in a variety of armored vehicles, delivered by aircraft (and parachute), or, occasionally, by helicopter.” [...]
“All bladed weapons—be they thrusting types like spears and certain swords and daggers, hacking types like axes and some swords, or missile types like arrows and javelins—employ a similar physics. The sharp point concentrates the delivered energy into a very small area for greatest possible penetration; the broader blade opens the wound for greatest possible tissue damage and blood loss [related link]. And if we look at the much broader tactical picture, we can see the same dynamic: The “physics” of attack tactics follows a similar transmission of force. The smaller, initial assault group punches the hole, and the larger follow-up force exploits the entry” [...]
“[Alexander of Macedon] was not just the commander of killers but a frontline killer himself. He was an inheritor of a heroic tradition of combat leadership. Greek generals and kings fought in the phalanx, and “there is not a single major Greek battle—Thermopylae, Delium, Mantinea, Leuctra—in which Hellenic generals survived the rout of their troops.” The Spartan king Cleombrotus was killed in the phalanx at Leuctra, for example, the usual fate of a defeated Spartan king. This exposure of commanders to the risks of the battlefield lasted until the nineteenth century [...], when it was replaced by the bureaucratization of leadership: the commander-as-manager.” [...]
“The practice of decimation, the execution of one man in ten in a unit that had performed particularly poorly, was not a Roman invention. Alexander had used it, and had himself borrowed the practice from earlier Near Eastern armies. [...]
“Our fascination with the mounted knight has somewhat distorted his importance in medieval battle. Not only did infantry play an important part, but an argument can be made that they were, in fact, the predominant element. During the main span of the medieval period (from around AD 500 to about 1400, when guns first made themselves felt on the battlefield), infantry outnumbered cavalry “by at least five to one.” Infantry was a cost-effective option compared with cavalry, and tactics, essentially through the mixed use of pikemen and missile firers (at first crossbowmen and archers, who were eventually superseded by arquebusiers and musketeers), developed to maximize the use of foot soldiers.” [...]
“Crossbows are known to have been used by Chinese infantry in the fourth century BCE and were used as hunting weapons by the Romans. Their reemergence in Europe during the tenth century seems to have been linked to an upsurge in siege warfare (the Roman siege ballista were essentially huge crossbows), but the Normans took to the crossbow with enthusiasm as an infantry weapon. The advantages to the user were enormous. A knight in whom years of training and a huge amount of money had been invested could be killed by a dolt with a bolt at about 200 yards or less.
The crossbow is a forerunner of machinelike weapons such as the rifle in that although it was relatively easy to use it was of fairly complex construction [...] The power of the crossbow, in one way, was considerably more than the longbow’s. It could “draw” about 750 pounds, compared with the longbow’s 70–150 pounds, but its released energy was comparatively inefficient because the span was short and its tips, whose whiplash movement turned stored energy into bolt speed and range, moved through a much shorter trajectory than the long and powerful expanse of the longbow’s. Also, the longbow’s arrow was heavier than a quarrel, which gave it greater penetrative power over a greater distance. [...] These characteristics molded the tactical use of both types of bow. The crossbow tended to be deployed in relatively close action where the flat trajectory would have a potentially devastating effect (the problem was, of course, that the closer the crossbowman was to the action, the greater his chances of being ridden down or shot down during the relatively lengthy periods of reloading). The longbow, on the other hand, tended to be used at longer distance in arcing trajectories where its high speed of reloading (about twelve shafts per minute, compared with perhaps three per minute for the crossbow—about the same rate as a black-powder musket) could inflict a storm of harm on the enemy. [...] The essential difference between the crossbow and the longbow had as much to do with relative cost as with relative lethality. A longbow, although mechanically simpler than the crossbow, was not necessarily cheaper. It was made from specialized wood, the supply of which presupposed land use dedicated to growing trees rather than more immediately profitable crops. The crossbow, even if made of wood, did not demand the exacting material of the longbow; in fact it could be, and was, made of a composite of materials. But perhaps more important, the crossbow also had a striking economic advantage that would be a preview of the age of the handgun: It did not take the great deal of training, practice, and physical strength to turn out a competent crossbowman that it took to turn out an archer.” [...]
“At first the small arms were less lethal than the bow and crossbow, but they were noisy—and noise has always been a potent factor on the battlefield, both raising or reducing morale depending on whose side was creating the din. [...] By the 1520s a handgun cost about 40 percent less than a crossbow.” [...]
“the flintlock [...] became the standard infantry gun for about 150 years (roughly 1700–1850) [...] Flintlocks were notoriously inaccurate at anything over about 50 yards. [...] Modern tests under laboratory conditions (that is, the guns were not fired by humans but clamped and electrically ignited) on actual eighteenth-century muskets have shown 60 percent hits on target at 75 yards; at 100 yards it was pretty much a fifty-fifty proposition. [...] Misfiring was also a significant problem. [...] As many as one in four discharge attempts were unsuccessful. [...] At the battle of Vitoria (1813) during the Peninsular War, contemporaries estimated that the British fired 60 rounds per man (usually the total allocation) for an expenditure of 3.5 million rounds or 450 per French casualty. [...] But mortality rates in combat become misleading when they are expressed as a percentage of total combatants or casualties vis-à-vis total rounds expended. Battle is not fought in the statistical median but at the hot spots of localized violence. In these hot spots, casualties could be far higher. [...] “It was by no means unusual,” writes Major General B. P. Hughes, for a unit to suffer 30 percent casualties in the close combat of the eighteenth century.” And the majority of those casualties would usually be taken among the first two ranks at distances of less than 50 yards, and probably within a few seconds of the opening volley” [...]
“A musket ball weighed about 1 ounce, and a hit at anything up to, say, 100 yards could inflict an appalling wound. Modern conoidal-shaped bullets make a clean entry but tend to tumble when they enter the body, leaving a trail of horrific damage, and create a large exit wound. A heavy round ball does not tumble but creates what in wound ballistics is known as “crushing” on initial impact. “Elastic” tissue such as muscle and skin is good at absorbing the kinetic energy of the projectile. A high-velocity bullet is not necessarily more lethal than a slower, heavier ball because kinetic energy is a function of mass. [...] An infantryman was most likely to be hit on his left side, as this was most often presented to the enemy (a right-handed shooter turns slightly to the right, exposing his left side). A full-velocity shot to the head or stomach invariably proved fatal. Stomach wounds were particularly feared (due in part to the almost inevitable death from peritonitis if the soldier was not killed outright).” [...]
“Some modern historians have looked to the records of types of wounds of those soldiers admitted to the French national military hospital, Les Invalides, in Paris. The records of 1762, for example, show that the great majority of men (68 percent) were hit by small arms; sword wounds accounted for 14.7 percent; 13.4 percent were wounded by artillery; and only 2.4 percent by the bayonet.” [...]
“Disease, as in all previous wars, was a greater killer of soldiers than combat (it accounted for 66 percent of all fatalities in the Civil War). Of the approximately 2,100,000 men who took up arms for the North, 360,000 died (17 percent of all who served), of whom about 110,000 (5.2 percent) were either killed outright in battle (67,058) or died from wounds (43,012). Although the high rate of death from disease is shocking, it was an improvement on the Mexican War of 1846–48, in which seven men died of disease for every one killed in battle. Of the approximately 880,000 Confederates who served, about 250,000 (28 percent) died from all causes. Of these Fox estimates that 94,000 (10.6 percent) were killed or mortally wounded [...] The numbers may be merely indicative, but they suggest that the South lost about 11 percent of its soldiers killed outright or died of wounds, compared with just over 7 percent for the North—a 30 percent greater killed rate for Confederate warriors. [...] It needs also to be borne in mind that the numbers of men killed outright or who died of wounds expressed as a percentage of those “who took up arms” needs to be tempered by the fact that not all who wore butternut or blue were involved in combat. Obviously, the death toll rises considerably when viewed as a percentage of combatants only”
My brief goodreads review of the book, which I read yesterday (I gave it two stars):
“Closer to one star than three. Multiple spelling errors, no inline citations, questionable coverage of the literature, the authors frequently repeat themselves. Not recommended.”
This is a poor book, and I was close to giving it one star. I was considering modifying the review above today, as I got started blogging the book; when I wrote the review I’d assumed they’d just put the sources in the back of the book because the idea never crossed my mind that somone might decide to write a book like this without providing any sources (…I mean, that would be insane – and they’re psychiatry professors..). See more details about this aspect below. Normally spelling errors don’t bother me that much, but I spotted four of them in the first 50 pages alone (plus two words that were not separated by a space) and that’s just completely unacceptable; if you make that many mistakes which make it into the final publication then you don’t care enough about your book. I have had good experiences with the Wiley-Blackwell publications I’ve read, but the fact that they allowed this book through is a strong point against them.
The book is not heavy on data, but they do talk quite a bit about various findings from the literature. The problem is that you have to take everything they talk about on faith, and I’m just not that kind of person. No specific studies are mentioned (sentences like, ‘we base this on X&Y’s publication (20XX)’ are completely absent), the number of studies used to establish the conclusions are unknown, effect sizes are rarely talked about except in a very general sense (and you’ve no idea where the numbers are coming from so often such estimates are not actually helpful), limitations of the studies on which the conclusions are based are not covered in any amount of detail. I have the distinct impression that the authors are really bad at math, due to coverage of some specific conditions and the reported risks associated with them, but I won’t go into that in detail here as I consider those specific findings uninteresting (and if they knew basic probability theory, so presumably would the authors). Some of the findings they talk about I’m sure are correct as they are well known and -established in the literature, but there are other claims in the book which contradict what has been found in studies I’ve read in the past on the topic, so I certainly see no great need to just take it for granted that the authors are right. The fact that they won’t go into the details of which studies they are basing their conclusions on and so on frankly just make them look bad, especially considering the overall data quality one has to work with in this area and the limitations imposed by this data quality problem – basically what they’ve ended up with is a book filled with postulates. They don’t even include a literature overview in the final pages of the book, like say in an appendix – the book has an index, but no literature list, so basically they just decided to publish a book in which they don’t even tell you which sources they’re basing their conclusions on. From the point of view of someone who’d only consider evidence which you can test/verify to be valid, this book would be completely worthless as they may just have made it all up. I’m sure they haven’t, but this approach really stinks. One might argue that given that the book’s main focus is on the clinical perspective (how to deal with patients), not epidemiology, lack of sourcing may not be that big of a deal – one major problem here, however, is that writing textbooks this way certainly isn’t the way to promote evidence-based approaches in the future. Given the problematic history of mental health care, this is sure as hell not an area where you get points in my book for not dealing with the data in some detail and dealing with questions related e.g. to how we know what we know, and how and why those conclusions we’ve drawn may be wrong.
As usual when reading this kind of material, I was mildly annoyed by the fact that the authors take for granted the view that all suicides should be prevented. There’s such a thing as a good suicide. I’m not exactly surprised that this notion is absent from the book, but I am still a bit annoyed.
Some observations from the book below:
“based on available data, globally suicide is believed to account for an average of 10–15 deaths for every 100 000 persons each year, and for each completed suicide there are believed to be up to 20 failed suicide attempts.” [believed by whom, you ask? I have no idea] [...] “in the USA and many other countries (particularly in wealthy or developed states), suicide continues to be one of the three leading causes of death in young people between the ages of 15 and 24.” [...]
“The majority of studies on risk factors for suicide have been conducted in developed countries using the psychological autopsy methodology. Psychological autopsy studies in the West have consistently demonstrated strong associations between suicide and mental disorder, reporting that 90% of people who die by suicide have one or more diagnosable mental illness [...] Using the same type of psychological autopsy methodology, studies conducted in developing countries have not demonstrated as robust an association between suicide and mental disorder as purported in the West.” [...] Other identified significant risk factors include current or past suicide behaviour, availability of and access to lethal means, exposure to trauma or abuse, severe psychosocial stressors, interpersonal loss, family history of suicide and mental disorder, alcohol and drug misuse, lack of significant relationships and social isolation, chronic physical illness, disabling pain, lack of internal coping abilities, and lack of access to health and social services and supports.” [...]
“In North America, studies indicate that the majority (up to two-thirds) of those who die by suicide have had contact with a health care professional for various physical and emotional complaints in the month before their death. [...] individuals at risk are often never identified” [...]
“In many parts of the world mental illness fails to be recognized as a legitimate health disorder and people with mental illness continue to be misunderstood as weak, lazy, attention seeking, crazy or stupid. Fear of being thought of or being labelled as mentally ill and fear of the ridicule, discrimination, social exclusion, loss of friends, loss of employment or loss of opportunity that may result likely contributes to the secrecy and silence that keeps people from reaching out and receiving help. [...] Regardless of the reasons, many of those who die by suicide do not seek help and do not inform others of their plans. Moreover, some who are contemplating suicide or who are committed to completing suicide may not reveal their thoughts or plans even when directly asked.” [...]
“Protective factors are those factors and experiences that are believed to reduce the risk for suicide and suicide behaviours and increase a person’s ability to cope with and manage stress and face life’s challenges. [...] Protective factors are less well established than are risk factors and the scientific data to support their notation is generally not very strong. [...] In the opinion of the authors of this manual, these factors have not been adequately demonstrated to prevent suicide. Many of them are simply negative restatements of known risk factors” [...]
“A number of risk factors have been strongly linked to both suicide and suicide behaviours. Distal risk factors can be understood as predisposing factors that may increase a person’s vulnerability to suicide. [...] Proximal risk factors include factors which augment current vulnerability for suicide as well as factors which may precipitate or trigger suicide or suicide behaviours.” [...]
“In North America, Western Europe (including the UK) and most other countries for which data are available, suicide rates generally increase with increasing age. Projected on top of this trend are three peaks representing periods of increased risk: adolescence/young adulthood, middle age and old age. In general, suicide rates rise sharply in late adolescence and early adulthood, before leveling off through early midlife, then rising again in middle age and then again after age 70. In developed countries the highest suicide rates are found in the elderly. [...] In general, suicide behaviours in the elderly are more likely to be lethal as compared to younger age groups. [...] In most countries, suicide deaths occur more frequently in men than in women. In the United States, suicide rates are four times higher in men. [...] In many Asian countries, including India for example, the rates of suicide death, particularly in rural areas, are almost equal for men and women. In China, female suicide rates are 25% higher than male suicide rates.” [Considering the kind of data likely to be available, I don't trust this finding very much but I thought the observation was still interesting. Cultural factors causing differences in reported rates is one of many potential drivers here which should at least be considered a potentially contributing factor (e.g. greater shame associated with the suicide of a son (/an heir) than a daughter).] [...]
“Suicidal ideation refers to thoughts, fantasies, ruminations and preoccupations about death, self-harm and self-inflicted death. Suicidal ideation can be both ‘passive’ and ‘active’. A person who is actively thinking about killing themselves and is having thoughts of initiating a suicide process that will lead to their death is experiencing active suicide ideation. A person who has thoughts about wanting to ‘disappear’, wishing they could just go to sleep and never wake up, or thoughts that they would rather not be alive, but who does not have thoughts of actively initiating a suicide process that would lead to their death, is experiencing passive suicide ideation. Active suicide ideation confers greater risk than passive suicide ideation and the greater the magnitude and persistence of the suicidal thoughts, the higher the risk for eventual suicide. [...] Suicide ideation occurs along a continuum of frequency (fleeting to persistent), intensity (manageable to intolerable or uncontrollable), duration (chronic to acute) and persistence (intermittent to persistent), and can be associated with different levels of intent (no wish or desire to die to strong desire to die) as well as motivation.” [...]
“In general, men tend to choose more violent means and women less violent means. Globally, hanging, firearms and poisoning are the most common lethal means for suicide – hanging being the most common in both genders. [...] In developing countries, particularly in agricultural areas, ingestion of pesticides is the most common method of suicide. [...] an estimated 30% of suicide deaths globally are attributable to the ingestion of pesticide.” [...]
“Suicide attempts are 10–20 times more prevalent than completed suicides and up to 50% of those who die by suicide have made at least one previous attempt. These figures are likely underestimates of the true prevalence of suicide attempts as many attempts likely go undetected [...] past suicide attempts are a major risk factor for suicide death. Up to one-fifth of people who attempt suicide will reattempt (most within a year) and reattempts are often associated with more lethal means, lower chance of rescue and survival, and higher likelihood of serious medical consequences.” [...]
“the suicide rate among single adults is twice that of married adults, and rates among those who are divorced, separated or widowed are four to five times higher than those for married individuals.” [...]
“Identification of ‘suicide risk factors’ does not allow a completely accurate prediction of when or if a specific individual will in fact die by suicide. Thus, suicide assessment scales that rely on the cataloguing of patient risk factors, although a useful clinical aid in the assessment of suicide risk, cannot by themselves be used successfully to predict who will commit suicide. [...] It is the weighting and confluence of specific suicide risk factors rather than the number of risk factors present that must be considered in determining risk” [...]
“Suicidal thoughts are relatively common amongst adolescents. [...] Suicidal ideation in and of itself does not indicate psychopathology or need for intervention in teenagers. In children, however, expression of suicidal ideation warrants serious attention. Young children may not appreciate the ‘finality’ of death and therefore may unwittingly commit suicide, not realizing that they will not come back. [...] Many [...] warning signs are nonspecific and ambiguous, and taken separately may be just a normal part of growing up. On the other hand, if these warning signs represent a clear change in a young person’s personality, behaviour or functioning they may be signals of a serious underlying problem.” [...]
“Although many universal and targeted interventions for suicide prevention have been implemented in countries and communities around the world, few have been empirically studied and evaluated in either developing or developed countries. Of those that have been evaluated, few have been shown to impact suicide rates. [...] A number of interventions popularly considered to be very effective in reducing suicide rates, including suicide telephone hotlines and school-based suicide-education programmes, have shown little or no substantial positive effect on decreasing suicide rates.” [...]
“suicide does not occur in a vacuum. Once the individual ends his or her life, there are clinicians, family members, friends and communities that may require support. [...] Experience of shock and disbelief is normal in the first few hours or days following the loss of a loved one. Once the initial shock of the loss has dissipated, most people slowly begin the process of recognizing and accepting the loss. Feelings of intense sadness, anger, hopelessness, helplessness and guilt often wax and wane throughout the day, with periods of extreme intensity becoming less overwhelming and less persistent over time. Thoughts about not wanting to be alive anymore, that life is not worth living, and of wanting to reunite with the deceased are not uncommon [...] After six months to one year, the pain associated with the grief generally becomes less intrusive, less intense and less persistent. Although there may be reexperiencing of intense grief when confronted with reminders of the loss, and periods of feeling sad, angry and empty, these grief experiences no longer prevent the person for moving on with their life and doing what they need to do, such as returning to work, returning to school, reconnecting in their personal relationships, participating in social and recreational activities, and caring for their families and children.” [...]
“Often the most meaningful way to help someone who has experienced loss is to simply listen to them. [...] Acknowledge and validate their feelings. [...] Do not tell them not to cry or get angry. [...] Do not tell them how you think they should feel. [...] Give them space and time to talk about their loss. [...] Assist problem-solving around practical issues and concerns.”
(Yes, as mentioned before I now know that Wang actually isn’t that unknown (neither is Richter for that matter, however the specific recording above really needs a wider audience..) – but this is wonderful stuff… I’ve put the rest of the Wang/Harrell concerto below the fold)
I finished the book. I ended up at two stars on goodreads – it didn’t improve towards the end. If I had to sum it up in just a few words, I’d say something like this: ‘You’ll learn a lot of stuff about the region from reading this book, but the book isn’t actually all that great.’ The first few chapters I’ve yet to talk about here covered economic factors, and the last ones were brief chapters about specific subregions, both regional entities of Russia (e.g. The Volga region, the Urals, Siberia, …) as well as other regional entitites of the FSU (e.g. the Central Asian republics, the Eastern European countries of Ukraine, Moldova and Belarus, a chapter about the Baltics, etc..). I’ve already talked a lot about the book here, so I’ll limit my coverage of the last part of the book to some observations from the remaining chapters which I’ve posted below.
“about one-third of all Russians now claim that they never read” [...]
“about 5% of Russia’s gross domestic product (GDP) is produced by agriculture and another 5% by forestry [...] In Russian society 100 years ago, 80% of the people were peasants. [...] Today 15% of workers in Russia are employed in forestry or agriculture; this remains a much higher rate than in the West, where it is under 3% [...] Because the collective farming was notoriously inefficient, people were tacitly encouraged by the authorities to take care of themselves and to grow their own food. Small plots of land (averaging 0.06 ha) were grudgingly given out by the Soviet authorities to the urban residents, so that some food could be grown around cities. [...] Villagers had slightly larger plots of land (usually 0.10–0.20 ha) immediately next to their houses to grow their own food. [...] These tiny plots yielded an astonishing 30% of the total agricultural produce in the country in 1980, and yield even more today. [...] Fewer than 20% of all vegetables are produced on large farms. [...]
“Because Soviet agriculture was so inefficient [...], the Soviet Union had to import about one-fifth of its total calories by the early 1980s, making it the largest single importer of food on earth [...] About one-quarter of all economic expenditures in the Soviet Union were on food. [...] In 2005 over $16 billion was spent by Russia to import food — almost 17% of all imports for the year. The cost went up to $35 billion by 2008 [...] Although for some African nations food constitutes one-third of all imports, for a typical European country food accounts for under 10% of imports (under 5% in the United States)”
“Russia is a country of heavy smokers; 65% of its men smoke, as compared to 35% in France or 22% in the United States. Fewer Russian women smoke (about 10%), but their number is increasing (World Health Organization, 2007).”
“The service sector was greatly underdeveloped in the Soviet Union, because the government always gave the highest priority to heavy industry. Although mass transit was well developed, other services lagged far behind Western norms. After World War II only 10% of all workers were in the service sector, and by 1990 only 25%, as compared to over 70% in the United States at that time. [...] recent years have seen a massive increase in the relative importance of services”
“about 80% of all those commuting to work in Russian cities do so by bus [...] In Russia only 14% of travel happens by plane, as compared to 40% by automobile and 33% by train. The proportion of air travel is higher than in the United States because a lot fewer people travel by private car in Russia (under 10% of all passenger-kilometers, as opposed to almost 85% in the United States).”
“Russia had over 44,000 km of petroleum pipelines and over 150,000 km of gas pipelines in 2008. [...] Although less glamorous than trains or planes, pipelines move more freight, about 55% of the total [...] Of these, 59% move natural gas and 41% move petroleum.”
“About 27% of the Russian population had online access in 2008 (38 million users) [...] Internet access is about as common in Russia now as it is in Turkey or Brazil, but not nearly as common as in developed Asia or Europe.”
“Not only were goods not necessarily available at the Soviet shops, but entire categories of stores simply did not exist. For example, there were no shopping malls with brand-name stores, because there were no brands; all clothing was made by the state, with minimal differences among the available models. There were no craft stores, no car dealerships, and no home improvement stores.” (reminded me of this)
“In Northern Eurasia or the former Soviet Union (FSU), there are 15 countries in four groups: the Baltic states; Russia, Belarus, Ukraine, and Moldova; the three states in the trans-Caucasus; and the five states of Central Asia. Russia is presently divided into seven regions, distinguished on the basis of political units.” Here’s a brief overview from the book, click to view full size:
[Again an illustration of why I don't always trust the author's numbers: The population figures here are completely off, as a lot of people seem to have been left out. If you add all the population figures they only add up to 84 million, even though the country has more than 140 million inhabitants. There is no explanation in the text for why these numbers don't add up. My motivation for including the table above both derived from my desire to once again illustrate this aspect and from the fact that it was easier to add the table than it would have been to list the Federal districts myself.] [...]
“The Russian Caucasus is included in the South federal district, which occupies 600,000 km2 and contains 23 million people in 13 subjects of federation [...] the South district of Russia is the second most densely populated territory after the Central district, with an average density of 40/km2. It is also the least urbanized region, with only 58% of its population living in cities. It leads the country in fertility [...] it is also the poorest region among the seven federal districts, with only half of Russia’s average gross regional product (GRP) per capita. [...] The poorest three republics in Russia are war-torn Chechnya (GRP unknown) and its neighbors Ingushetiya (about 15% of the national average) and Dagestan (about one-third of the national average). These are also the areas with the highest unemployment (24%), highest poverty rate, and highest fertility [...] Chechnya is years away from being a prosperous and stable society, and this is one area in Russia where travel is not advisable.”
“The Ural Mountains are a treasure trove of resources: coal, iron ore, manganese, titanium, chromium, gold, copper, nickel, vanadium, marble, and many other minerals. This is the richest area in all of Russia with respect to nonferrous metals and gemstones. Over 1,000 minerals are found in the Urals [...] Now that Tyumen Oblast and the two autonomous okrugs are included in the Urals district, the region has also become by far the richest area in Russia with respect to petroleum and natural gas, accounting for over 70% of all Russia’s oil and more than 80% of its natural gas reserves. [...] The oil and natural gas fields of what was then the West Siberia economic region were discovered in the 1960s and developed in the 1970s. In 1965 this area produced only 1 million metric tonnes (mmt) of petroleum, but by 1985 it was [...] 400 mmt [...] The production of oil in this area dropped dramatically in the 1990s because of the economic downturn, to about 200 mmt per year in 1995, but has since risen to about 320 mmt. This number is unlikely to increase farther, because the oil fields are rapidly being depleted.”
“Siberia is pivotal to Russia’s economic might. It is part of Asiatic Russia and is usually defined as [I thought this choice of words was problematic. See the wiki] the land east of the Urals and west of the Lena River, sometimes including the entire watershed of the Lena. Thus the territory west of Siberia is European Russia, and the land east of it is the Far East, also called the Russian Pacific. [...] Siberia thus defined (5.1 million km2) is just a little smaller than the largest (Far East) federal district, and is bigger than the European Union (EU) in size. Although it accounts for about one third of Russia’s territory, it has only 20 million residents, giving it an average population density of only 3.9 people/km2. [...] It has few people, plenty of natural resources, and a very cold continental climate. Like the rest of Russia, Siberia is losing population fast [...] The overall decline is about –0.6% per year, among the fastest in Russia.” [...]
“The [Russian Far East] has merely 6.7 million residents [spread out over 6.2 million km2], giving it a population density of 1.1/km2— the lowest average density in Russia, and only one-third of Canada’s density. To put it another way, this huge region is settled by only about half as many people as live in Moscow. [...] With respect to economic development, the southern part of the region along the Trans-Siberian Railroad is more or less contiguously settled. In the north, there are three isolated clusters of development (around Yakutsk, Magadan, and Petropavlovsk), with virtually untouched wilderness in between. [...] The Far East has lost about 1 million people since 1991.”
“The history of Ukraine’s statehood is a long and convoluted one, but essentially centers on internal struggles between pro-Russian and pro-Polish groups and on its emerging nationalism since the mid-18th century, with perpetually shifting affinities and borders. Areas of western Ukraine have seen hundreds of border adjustments in the past five centuries [...] Ukraine in this sense is a classic example of a political transition zone in perpetual search of an identity. Post-Soviet Ukraine remains in the same position today” [...]
“Close to a million Moldovans have left the country for employment in the construction, retail, food, and textile industries of Russia, Ukraine, Turkey, Italy, and France. [The current population of the country amounts to ~4 million people...]
“Uzbekistan’s leading export is not oil [like Kazakhstan], but cotton; its major industry is not machine building [-ll-], but textiles. It does have limited natural gas supplies, but very little petroleum. In short, it has relatively little to offer to the world [...] Uzbekistan has some of the worst corruption in the world as measured by Transparency International, and it also has one of the most brutal and least transparent judicial systems. In particular, opposition journalists are persecuted and sometimes disappear without a trace. [...] Kyrgyzstan is another struggling economy in the region. Although it was the first Central Asian state to launch market reforms and political democratization in the early 1990s, it soon fell out of pace with Kazakhstan and Russia because of internal political tensions. [...] a bloody revolt [...] deepening economic crisis [...] pervasive corruption [...] Tajikistan is the least developed, poorest, and most mountainous country in the FSU. [...] a bitter civil war [...] Islamist movements [...] an increasingly vocal Muslim population [...] unresolved border disputes [...] frequent border closures [...] Turkmenistan is the most closed society of Central Asia. Its development was severely hampered by 15 years of [...] autocratic rule [...] Its economy [...] is one of the least privatized in the FSU, with about 70% of all assets still state owned. [...] Central Asia remains one of the remotest areas of the world, far away from the economic powerhouses of Asia, Europe, or North America, and is entirely landlocked.” [Sounds like a great place to visit!]
Magnus Carlsen won the Chess World Championship today, in case you didn’t know. Anyway, on to the lectures:
I’ve now read roughly two-thirds of the book so I figured I might as well post another post about the book, even though I’m not actually particularly impressed with the stuff I’ve read since the last post. My current goodreads rating is now much closer to two stars than three. Topics which I’ve read about since the last post include: The Geopolitical Position of Russia in the World (chapter 9); Demographics and Population Distribution (chapter 10); Cities and Villages (chapter 11); Social issues – Health, Wealth, Poverty, and Crime (chapter 12); Cultures and Languages (chapter 13); Religion, Diet, and Dress (chapter 14); Education, Arts, Sciences, and Sports (chapter 15); Tourism (chapter 16); Oil, Gas, and Other Energy Sources (chapter 17, the first in Part IV, about economics); and Heavy Industry and the Military Complex (chapter 18).
The author applies a data-centered approach most of the time, and I love that! …which makes it harder for me to be critical of the stuff than it otherwise might have been. However critical I must be, and some chapters are much better than others. In one specific chapter he includes numbers which anyone with two brain-cells can tell are complete bullshit, without adding many critical remarks – according to the crime per capita estimates provided in that chapter, Russia’s crime/capita numbers are less than one-fourth of those of the UK. Yeah.. On a related note, an implicit assumption often rearing its ugly head in the text is that the economic data provided towards the end of the Soviet Era accurately reflected economic conditions. Stuff like that – numbers and the problem of how to interpret them and when in particular to be cautious – cause a few problems along the way. Even (semi-?)valid numbers and estimates are not always put into the proper context, so for example 2002 numbers and 2009 numbers (or numbers from the early 90es and numbers from the 2000s) are given in consecutive paragraphs without attention to the problem that these numbers may not be comparable. I’m not sure the author knows what a standard deviation is, so I am not sure this is the kind of person you want writing a book with a lot of data. He’s far from always uncritical, this must be said, but there’s still a trust issue here for me to deal with in that I often don’t think he’s nearly as skeptical and precise as he ought to be; he draws conclusions not fully supported by the data he uses to support the conclusions in question more than a few times. It should be mentioned that at least in part the trust problem arises due to the scope of the book; as can be inferred from the topics listed above nobody can claim to be an expert on all of this stuff, so you need to take some things on faith. But the problem is surely aggravated by some of the more ‘soft’, not-too-data centered chapters, where he’s just in my view way too uncritical of Soviet material (/propaganda) and seem to try to make Soviet life out to be better than you’d conclude that it had been if you were to just judge by the numbers he provides himself and not ignoring obvious less-than-flattering interpretations. Here’s an example of the kind of stuff I find problematic:
“By and large, the [health] care was decent. A Soviet worker who came down with flu, for example, just needed to dial the local clinic’s phone in the morning and stay in bed; the physician on call would come and visit the worker at home, usually later that same day. Physicians were accustomed to spending about half of their workday making house calls.”
My first thought: F..¤#$£ inefficient as hell, and probably hellishly expensive! Here’s a related observation:
“The Soviet Union also had one of the longest average hospital stays in the world, because home care was viewed as inherently inferior, while hospital beds were free. A typical hospitalization would last for 2–3 weeks, and frequently over a month.”
Given this kind of information, it really should be no surprise that:
“By the end of the Soviet period, the U.S.S.R. had the highest ratio of doctors to patients in the world”.
But here’s the thing – the word ‘inefficient’ isn’t mentioned once in that chapter. The lots of doctors/capita is interpreted as a great thing, not a serious problem indicating severe inefficiencies in health care delivery. The same chapter started out with some pure gold which really set the pace for the rest of that chapter:
“The Soviet Union had what was arguably one of the best health care systems in the world. Surprised? If you have seen Michael Moore’s film Sicko, you may not be: Moore depicts Cuba as an example of a socialist state with a free, universal health care system that has produced impressive results. This is something many Americans and even some Europeans have a hard time imagining.”
(Naturally) I was very close to stopping reading altogether there – ‘arguably’ indeed. He’s talking about a country where the life expectancy was below 70 years (in 1990), far from the top 10 percent of the world (but ‘within the best third’, which is the only observation regarding the relative performance he includes..). Instead of stopping reading there I decided instead to adjust my expectations downwards and to just start paying a lot more attention to the raw data (and where it was coming from) and a lot less attention to the author’s observations and interpretations of said data. I think this was a good decision. I don’t think the author always understands what he’s talking about although I’m sure he does sometimes. What I’m also sure of is that his standards of evidence are different from mine.
Another illustrative quote and some related observations from chapter 12 below:
“The health care system went through a major restructuring on short notice [in the 90s], with support from the state abruptly declining to a fraction of its former amount due to rising inflation rates and to unwillingness or inability to pay more.”
In light of the data above it probably wouldn’t be outrageous to assume that said ‘unwillingness’ was presumably at least a little related to the fact that the system which was set up was inefficient and provided far from impressive health outcomes. Of course there were other reasons as well, relating to political economy stuff and so on. But he never comes close to even saying this. Even weirder, he talks about “fewer doctors” being one explanation for the worsened health outcomes during the post-Soviet period on the very same page that he provides data making it very clear that the number of doctors was not the problem. Judging from the data he provides himself on that page, the raw number of physicians in Russia was pretty much identical in 1990 and 2000 (though it was a little lower in 1995), and it was notably higher than both years in 2005 (and so the number of physicians/1000 people was if anything higher in 2000 than in 1990 judging from that data, as the nation underwent a significant population decline during the period – something he documents himself in the book and talks about in some detail).
Obvious conclusions from the data are not always drawn, and questionable conclusions from the same data sometimes seem to be. But there’s a lot of data and there’s a lot of good stuff as well, and so I felt I should add some data from the chapters mentioned above below. The book is a mixed bag at this point. I’m learning a lot, but I feel like I have to be a lot more cautious about trusting the information provided than I usually need to be when I’m reading a book. I have never felt any need to worry about the author lying to me about how kidneys work while reading McPhee et al, or about the author using very questionable data to draw conclusions without pointing out that there’s some uncertainty here. Blinnikov isn’t uncritical, but compared to some of the publications I have made a habit of reading at this point reading this book occasionally feels a bit like reading an elephant’s account of his brother’s trip to the porcelain shop – this stuff seems too close to politics for comfort, and the author isn’t as careful and unbiased in his coverage as I’d have liked. Anway, quotes below (my bold):
“Since 1992 [...] Russia has been steadily losing people to the tune of 500,000 or so per year, and this has become a firmly established phenomenon. [...] the average Russian man is expected to live only 61 years, and the average Russian woman 74. The reasons for this discrepancy are complex, but the factor most commonly cited is the high rate of alcoholism among Russian men [...] only about 100,000 legal migrants come to Russia each year, while about 500,000 people are lost per year due to the fertility–mortality imbalance. [...] About 16% of the Russian population has completed a college education (vs. 28% in the United States) [...] Only three-quarters of all households in Russia have running water, while only 71% have flush toilets. [...] 82% of urban dwellers have central heat provided by a power plant, while 50% of rural dwellers depend on wood-burning brick ovens or on coal boilers.” [...]
“sanitary norms set in 1922 dictated the size of the minimal livable space at 9 m2 [...] per person. This remained unchanged over the entire Soviet period and without respect to local needs [...] As illustrated in Bater (1996), the actual space available toward the end of the U.S.S.R. ranged from 13 m2 in Estonia to 7 m2 in Turkmenistan, with 10 m2 being the national average. [...] On average, one person has 19 m2 in which to live [today]. [...]
The level of urbanization rose through the 20th century: In 1900 almost 80% of the Russian Empire consisted of peasants; in 1950 the U.S.S.R. had an urbanization level of 52%; in 1970 it was 62%; and since 1990 Russia’s level has been 74%. [...] Even by 2005, only 7% of the total agricultural output in Russia was produced on private farms. The kolkhozy were restructured into joint-stock cooperative ventures, but their management practices remained essentially unchanged. Although the workers collectively own each enterprise now, the head manager typically has the controlling vote, and the enterprise continues to be inefficient. In 2005, the output of the Russian agricultural sector was 40% less than in 1990; the sown acreage had decreased at least 30%; and the number of cattle had decreased by 46%. Russia today imports a little less than half of the food it needs to feed its own population—one of the highest rates of foreign-food dependency in the world” [at least he commented upon the inefficiency here, otherwise I would have. I'll add here that it's likely that the 1990 numbers can't be trusted, so although this is not the impression you get from reading the book the extent to which this is a 'true decline' is probably still to some extent an open question.]
“there were 31,800 murders and attempted murders in Russia in 2000, versus only 22,200 in 2007. The majority of contract killings were perpetrated by the mob against prominent businessmen and journalists in the mid-1990s (Volkov, 1999); such attacks are now rare. Most domestic homicides happen between spouses and involve alcohol.” [...]
“Russia had over 1 million prisoners in 1995, and about 872,000 10 years later. Seven percent of the inmates in 2005 were women, and about 17% were repeat offenders.” [...]
“The Transparency International organization’s global Corruption Perception Index for 2007 ranked Russia very much near the bottom, in 143rd place out of 179 countries—right above Togo” [...]
“in Russia about 80% of people have been baptized in the Orthodox faith, but only 44% profess belief in a God, and merely 12% attend church on a monthly basis.” [...] 22% are agnostics who are not sure whether there is a God, and about 22% call themselves atheists. By comparison, in the United States about 75% of people consider themselves Christians, and about 40% attend a religious ceremony at least once a month.” [...] About 25% [of Russians] embrace a vague syncretic worldview that recognizes the existence of spirits, karma, and reincarnation, and affirms divination, talismans, tarot, and yoga as legitimate practices, while simultaneously professing adherence to the Russian Orthodox Church (which vehemently condemns all of these things).” [...]
“many universities are located in Moscow and St. Petersburg: In 2000, 171 (19%) were found in Moscow and 77 (8%) in St. Petersburg, with a total of 914 colleges and universities, public and private, in the entire country.” [...]
In the late 1970s, over 150 full-length movies were made in the U.S.S.R. per year. Russian film production practically ceased in 1992–1996 due to lack of funding, with merely 20–30 produced per year; it began again in the mid-1990s with Hollywood-wannabe gangster flicks sponsored by shady businessmen. [...] By comparison, Hollywood produced over 400 movies in 1996. [...] About 120 new movies come out every year in Russia now [...] The number of modern multiplex cinemas in Russia went up from 8 in 1995 to 185 in 2001″ [...]
“In real terms (after adjustment for inflation), the salary of a PhD-level senior researcher decreased by a factor of 10 between 1989 and 1999, whereas many other professions supported by state budgets did not see a comparable decline. Thus, if in the late Soviet period a Moscow city bus driver had a salary slightly lower than that of a physics professor, by the end of the Yeltsin period the bus driver was making five to seven times more than the professor. The result, predictably, was a drastic reduction in the number of scientists. [...]
By the end of the Soviet period, about 30 million people per year took advantage of resorts and sanatoria in the Russian Federation alone, not counting the other republics. Most were domestic tourists. The number of organized tourists in Russia abruptly plunged to a mere 8 million per year following the economic collapse of 1991, however. [...] In 2008 36.5 million Russians crossed the nation’s borders; 11 million of these crossings were for tourist trips, and 2 million business trips. [...] Russia sends five times as many tourists abroad as it receives.” [...]
“The U.S.S.R. was the largest producer of oil and natural gas in the world by the early 1980s, surpassing the United States and Saudi Arabia with production from the giant fields in western Siberia [...] [Russia] remains the world leader in natural gas production and is currently second in petroleum production [...] The share of [the energy] sector went up from only 12% of the total gross domestic product (GDP) in 1991 to 31% in 2002. [...] The distribution of energy production in Russia is very uneven. The oil and gas fields in western Siberia produce 69% of all the petroleum and 91% of all the natural gas [...] In 2007, 4 companies in the top 20 in Russia were engaged in metal production, heavy machinery production, or other heavy manufacturing” [...]
“Perhaps the heaviest legacy [...] of the Soviet economy was its military–industrial complex, called in Russian the [...] VPK. Its presence was pervasive: Entire cities were built around steel mills, aluminum smelters, tank manufacturers, chemical factories, or nuclear weapons facilities. Over 50% of the country’s industrial output in the 1980s was generated by this sector. [...] According
to some estimates, in the late Soviet period about one-quarter of all industrial workers in the country (5 million people) were employed by the VPK, including almost 1 million researchers at over 2,000 institutes and factories, and the sector accounted for almost 20% of the country’s gross domestic product (GDP). Hundreds of research labs, institutes, and factories were scattered over a few dozen small and medium-sized cities that did not appear on any maps [...] They were largely declassified, renamed, and finally put on maps by 2000. Most remain closed to casual visitors, however, and even Russia’s residents (let alone foreigners) require special permits to enter.”
I’m currently reading this book, and I like it so far. The book has stuff on physical geography (relief and hydrography, climate, biomes, and environmental stuff), the history and politics of the area/region, cultural and social geography (demographics and population distribution/structure, cultural stuff including religion and language etc.), some stuff about economic factors of interest, as well as some chapters providing more details about the specific regions towards the end of the book. The book mostly deals with Russia, but there’s stuff about other post-Soviet states as well.
Reading it feels a little like reading a very detailed wikipedia article (~450 pages long) and I must admit that I’ve probably lost a little more respect for humanities students along the way while reading this; again it’s not that the book is bad, far from it, but I feel pretty sure you don’t add much value to an education by including courses such as ones dealing with material like this. The ability of a university student to read and understand a book like this will tell you very little about their abilities as nine out of ten high schoolers technically ought be able to do that without problems. Also, reading the book will take a normal person at most a couple of days, so if an employer has a position that really requires one to know stuff like what’s in the book I don’t see how it could ever be a big deal if the applicant doesn’t – the situation is a bit different if the individual doesn’t know multi-variable calculus and that is a requirement. A depressing point is that even though this is an easy read, a course dealing with the stuff in this book is probably potentially a lot more useful than are many other courses those students might have taken instead (art history, Hebrew studies, theatre research, Indology (“In this course, students will be introduced to the basic Indian systems of Yoga, both in its ancient texts and practices and in its modern practice and will pay particular attention to the development of Yoga in Denmark in the 20th century.”),…) (all examples in the previous parenthesis taken directly from the University of Copenhagen course catalogue).
This is not the first book about Russia/USSR I read, but most of the stuff I’ve read so far has only dealt with the history of the country/region; this book adds a lot of stuff because it deals with a lot of other things as well. I think he actually handles the history part quite well, but of course it’s not a very detailed account.
Below I’ve added some observations from the first third of the book or so:
“Russia has over 120,000 rivers over 10 km long, which collectively create 2.3 million km of waterways. Fifty-four percent of their flow enters the Arctic Ocean, with only 15% entering the Pacific. Another 8% of water flows to the Atlantic Ocean via the Black and Baltic Seas, and 23% to the Aral-Caspian interior basin with no outlet to the ocean. [...] The [Volga] basin occupies only 8% of the country, but is home to 40% of its population. [...] The Volga loses 7% of its annual flow to human consumption. Its flow has been reduced by about 20% in the last 100 years. The Siberian rivers primarily flow north to the Arctic Ocean, with the exception of the Amur, which flows east into the Pacific.”
“Climatologists generally consider the following factors important in producing a particular climate type: Latitude, [...] Elevation above sea level [...] Proximity to the ocean [...] Presence of ocean currents [...] Prevalent wind direction [...] Position relative to a mountain range [...] Cloud cover and dust [...] Human infrastructure.” [there are further details in the book about how these factors impact the climate of the FSU, in broad terms, but I won't go into the details here...]
“Only a fraction of the Russian population (8%) lives near a seacoast [...] Compare this to the United States, where two-thirds of all people live within 200 km of a coast” [...] [I've previously blogged this map, and it's pretty handy if you want to know more about the details of where people live - more than three out of four Russians live in the European part of the country, and so Siberia is relatively empty. If you want to know more about the population density of the US, I've blogged that stuff before as well here.]
“The biomes of Northern Eurasia are similar to those of Europe or North America: tundra in the north; taiga and deciduous forests in the middle; steppe and desert in the south. The extreme south has deserts or subtropical Mediterranean-like shrub vegetation. [...] For millions of years, Northern Eurasia and North America were connected to each other [...] This resulted in an array of animals and plants that are shared by these two regions. [...] The flora and fauna of India (which is on the same continent as Russia), on the other hand, are completely dissimilar to Northern Eurasia’s; they are more like Africa’s. [...] Many animal genera or even species are identical in North America and Northern Eurasia [...] If an exact match is missing, there is usually a pretty good substitute/vicariant species” [...]
“The overall diversity of the plants and animals in Russia is not great, because of its northern location. For example, there are 11,000 species of vascular plants, 30 of amphibians, 75 of reptiles, 730 of birds, and 320 of mammals in the Russian Federation. By comparison, the United States (a more southern country half the size of Russia) has 19,000 species of vascular plants, 260 of amphibians, 360 of reptiles, 650 of birds, and 360 of mammals.”
“In Northern Eurasia, the taiga is a huge biome (covering over half of all Russia) [...] The boreal forests of Eurasia make up about 21% of the world’s total tree cover on 5.3 million km2 [...] Soils of the taiga are poor in nutrients and acidic [...] Steppe forms in areas with moisture deficit that precludes tree growth. Although steppes are on average warmer than most of the forested biomes to the north, it is really the lack of water that determines the tree boundary. [...] The classic Eurasian steppe is treeless [...] There are few places where virgin steppe can still be seen. As in North America, over 99% of this biome in Eurasia was plowed under in the 19th and 20th centuries.” [...]
“With its spacious, rainless interior, Eurasia is home to the northernmost deserts in the world. [...] The main deserts in North America are found at latitudes between 25º and 35ºN, whereas in Eurasia they occur between 38º and 44ºN. [...] Altogether, the Central Asian deserts occupy 3.5 million km2 — an area as large as Saudi Arabia and Iran combined.” [...]
“The exact sequence and elevation of the vegetation belts [of a mountain range] are determined by the direction of the slope (north-facing slopes are always colder and have a lower treeline) and by local climatic and biological factors. The treeline, for example, occurs at 300 m in the polar Urals and the Khibins in the Kola Peninsula in the Arctic, but at 2,000 m in the Carpathian mountains, 2,500 m in the Caucasus, and above 3,000 m in much of Central Asia” [...]
“The U.S.S.R. was one of the largest polluters of air on the planet, and Russia still is today [...] Between 2000 and 2005, an average big city in Russia saw a 30% increase in air pollutants. [...] Although there has been some increase in production since 2000, Russia generally pollutes less today than it did 20 years ago. However, a major new contributor to air pollution is car exhaust. Moscow, for example, had only 500,000 automobiles in the late 1980s. Today there are about 4 million cars and trucks in the city [...] In 2007, Russia as a whole had 195 passenger cars per 1,000 people [...] In the late Soviet period, Russia had only 50 cars per 1,000 people.” [...]
“Every spring, Moscow faucets run with brownish-tinged water smelling faintly of manure; it enters the Moscow water supply system from agricultural fields upstream.” [...]
“At the end of the Soviet period, the U.S.S.R. boasted over 40 [nuclear] reactors at 15 sites (today Russia has 31 reactors at 10 operating plants), not counting a few dozen small research reactors at scientific institutes. By comparison, the United States has slightly over 100 commercial reactors, Japan has 63, and France has 59. [...] Nuclear pollution is unevenly concentrated in the FSU, and much of the information about former accidents is still classified. [...] the highest levels of such pollution are found in and around Chernobyl (northern Ukraine, southeastern Belarus, and southwestern Russia); in the Novaya Zemlya islands and Semey, Kazakhstan; and at the production facilities in Sarov, Kyshtym, and a few cities near Krasnoyarsk. Furthermore, there are several submarine staging areas where offshore dumping of nuclear waste took place in the Far East and off the Kola Peninsula. Beyond these areas, there are a smattering of sites polluted by radiation—for example, in European Russia in Ivanovo and Perm Oblasts close to Moscow, as well as in the Komi Republic [...] Unlike in the United States, information on the actual location of [toxic waste] sites in Russia or other post-Soviet states is not readily available. [...] These sites number in the hundreds, if not in the thousands” [...]
“The eventual rise of Moscow to the preeminent position among Russian cities had to do with some pure luck and the political talents of the early princes there, but it also owed a good deal to geography: Originally an insignificant wooden fort (established in 1147), it was located at a perfect midpoint between the sources of the Dnieper and the Volga. It was situated on a tributary (the Moscow) of a tributary (the Oka) of the Volga—not on the main water artery, but close enough to Smolensk (100 km to the west in the Dnieper basin) that the Dnieper headwaters could be easily reached. In the age before highways, all transportation of goods took place by rivers. [...] The main exploratory push and the expansion of the Russian frontier across Siberia came in the mid-17th century with the new Romanov dynasty [...] in less than one century (from 1580 to 1650), the Russian state was extended from Tyumen in western Siberia all the way to Okhotsk on the Pacific Coast! Of course, this vast area was not fully settled by any means, but about two dozen forts were built at strategic locations. [...] Every major Siberian city that was established during this period is situated on a big river. The movement was somewhat analogous to the opening of the American West, except that it was driven less by farmers and more by fur traders [...] The early settlers were a highly mobile force, not interested in farming or other sedentary pursuits. [...] In comparison, the movement to the west, north, and south was much slower, because more developed states and tribes there made rapid expansion impossible.”
“By the start of World War I in 1914, the Russian Empire included most of Ukraine, Belarus, and Moldova (Bessarabia); Finland, Armenia, Azerbaijan, and Georgia; the Central Asian states (Russian Turkestan); Lithuania, Latvia, and Estonia; significant portions of Poland; and some Turkish cities in the Balkans. Only about 45% of its population consisted of ethnic Russians. The total population was 125 million in 1897, the time of the first Russian census. Alaska was sold in 1867 to the United States [...] After a bitter civil war [...] in 1917–1922 [...] U.S.S.R. [...] reconstituted itself within the former borders of the Russian Empire, with the
exceptions of Finland, Poland, the Baltic states, much of western Ukraine and Belarus, and Moldova. This may be explained by not only political and cultural but also geographic factors. [...] northern Eurasia forms a large, easily-defensible area bounded by some of the highest mountains in the world on the south, by the frozen Arctic Ocean on the north, and by the Pacific Ocean on the east. It is much more open and vulnerable in the west, and this is precisely where all the major wars were fought. Once these boundaries were reclaimed by the Soviets in the 1920s, there was relatively little change for 70 years.” [...]
“It is important to understand that the Russian Federation today is not merely a smaller U.S.S.R. It is qualitatively different from either the Russian Empire or the U.S.S.R. The latter two had fewer than 50% ethnic Russians and had external borders with nations of very different cultures (e.g., Hungary, Turkey, Iran, Afghanistan), whereas Russia is over 80% ethnically Russian and mainly borders other Russian-speaking territories in Ukraine, Belarus, or Kazakhstan [...] Although Russia remains the biggest state in the world by area, it is half of its original size and is now only 9th in terms of population” [...]
“The average Soviet citizen had less than 20% of the square footage available to the average American, and perhaps about 40% of the level available to the average European. In addition, over half of the country’s population had no access to indoor plumbing. [...] In the late 1980s, over 60% of the Soviet Union’s industrial output was in the form of heavy machinery (tractors, turbines, engines, etc.), thought to be necessary for the production of better goods and weapons. Less than 30% was accounted for by consumer goods.” [...]
“The important geographic outcome of 1991 was that a single, unitary state, the U.S.S.R., with its capital in Moscow, was replaced on the world maps by 15 newly independent states (NIS), each with its own capital, president, parliament, and so on. Twelve of these would soon form the Commonwealth of Independent States (CIS), a military and economic alliance; three others, the Baltics, would be admitted to the North Atlantic Treaty Organization (NATO) and the European Union (EU) in 2004. From 1991 on, the political and economic changes in each NIS were decoupled to a large extent from those in others, and proceeded along individualized trajectories. There were very rapid reforms in the Baltic states, almost no reforms in Uzbekistan and Belarus, and intermediate levels of reforms in others.”
i. “To expect a man to retain everything that he has ever read is like expecting him to carry about in his body everything that he has ever eaten.” (Schopenhauer)
ii. “It perpetually happens that one writer tells less truth than another, merely because he tells more truths.” (Lord Macaulay)
iii. “In great affairs men show themselves as they wish to be seen, in small things they show themselves as they are.” (Chamfort)
iv. “When a well-educated young man first enters society he is liable to commit many errors which the world term childish, simply because he has not yet learned how childish grown men really are.” (Leopardi)
v. “A man’s dying is more the survivors’ affair than his own.” (Thomas Mann)
vi. “We are most likely to get angry and excited in our opposition to some idea when we ourselves are not quite certain of our own position, and are inwardly tempted to take the other side.” (-ll-)
vii. “Opinions cannot survive if one has no chance to fight for them.” (-ll-)
viii. “Habit is overcome by habit.” (Thomas Kempis)
ix. “The sure conviction that we could if we wanted to is the reason so many good minds are idle.” (Georg Christoph Lichtenberg)
x. “To be content with life — or to live merrily, rather — all that is required is that we bestow on all things only a fleeting, superficial glance; the more thoughtful we become the more earnest we grow.” (-ll-)
xi. “Before one blames, one should always find out whether one cannot excuse. To discover little faults has been always the particularity of such brains that are a little or not at all above the average. The superior ones keep quiet or say something against the whole and the great minds transform without blaming.” (-ll-)
xii. ”Delight at having understood a very abstract and obscure system leads most people to believe in the truth of what it demonstrates.” (-ll-)
xiii. “There is no greater impediment to progress in the sciences than the desire to see it take place too quickly.” (-ll-)
xiv. “It takes in reality only one to make a quarrel. It is useless for the sheep to pass resolutions in favour of vegetarianism while the wolf remains of a different opinion.” (W. R. Inge)
xv. “Argument is generally waste of time and trouble. It is better to present one’s opinion and leave it to stick or no as it may happen. If sound, it will probably in the end stick, and the sticking is the main thing.” (Samuel Butler)
xvi. “If a person would understand either the Odyssey or any other ancient work, he must never look at the dead without seeing the living in them, nor at the living without thinking of the dead. We are too fond of seeing the ancients as one thing and the moderns as another.” (-ll-)
xvii. “An idea must not be condemned for being a little shy and incoherent; all new ideas are shy when introduced first among our old ones. We should have patience and see whether the incoherency is likely to wear off or to wear on, in which latter case the sooner we get rid of them the better.” (-ll-)
xviii. “The evil that men do lives after them. Yes, and a good deal of the evil that they never did as well.” (-ll-)
xix. “Silence is not always tact and it is tact that is golden, not silence.” (-ll-)
xx. “There is nothing which at once affects a man so much and so little as his own death.” (-ll-)
The book is a Springer publication by Niklas Juth and Christian Munthe. Here’s what I wrote in my goodreads review:
“I don’t think it’s a bad book, and it’s likely one of the best on the topic. I generally liked the book and I was at three stars throughout much of it. Different ethical approaches to problems in this area are described and applied to a variety of contexts.
If you want to know why I didn’t go higher [than 3 stars], here are some relevant points of criticism: 1) Some of the concluding analysis in the last chapter was so weak that I ended up writing some relatively nasty stuff in the margin of the book. I decided at one point to subtract a star because of that stuff, but I later decided that it was probably wrong to do that, and so I ended up back at three stars. However I still find their analysis and conclusions related to DTC genetic testing poorly argued. No, not poorly argued – stupid. 2) I also very much disagree with their take on prenatal screening in general, especially when it comes to the decision-relevant parameters to be included in a discussion like that.”
If I’d gone into more detail about 2, there would be more than 2 points of criticism, but the major problem I have is with the DTC genetic testing analysis – primarily because that’s what’s coming next, and so this is where you want the analysis to be as accurate as possible as it actually may have decision-impacting consequences. Razib Khan has written more than a few posts on that topic (23andme-posts) in the past, and as I’ve read him I broadly agree with him regarding the general principles; on the other hand these guys basically seem to consider an outcome where such services are regulated out of existence to be completely fine. The basic argument they present is that they believe (for various bad reasons) that similar principles should be applied to evaluate the ethical framework of these testing measures and the ethics of screening programmes containing tests such as the ones on offer by the private companies (this I incidentally find completely mindboggling, given their repeated emphasis on the differences between voluntary patient-directed health initiatives and screening – see also below), which would mean that counseling requirements would have to be quite strict to justify them – almost certainly too strict for it to make much sense for firms to stay in countries where such requirements are imposed (RK has talked about this aspect before as well). Here’s a relevant quote:
“There is no reason not to apply exactly the same ethical requirements to DTC genetic testing as to genetic screening programmes run by hospitals and other public health institutions. If DTC genetic testing providers can meet these requirements and still make a profit, fine. If not, we may conclude that the very idea of a sustainable business of DTC genetic testing was a fantasy to begin with.”
No thought is given to the problem that the level of counseling provided to actual people using these services may well go down with the formal counseling requirements required (because people buy the services abroad instead, where requirements are laxer). Close to no thought is given to intra-industry dynamics and if one were to take the implicit sketched incentives model of major industry players in chapter 6 seriously one would surely consider it a miracle that there’s such a thing as used car salesmen, or estate agents.
But enough with the criticism, there’s a lot of good stuff as well. They talk quite a bit along the way about the Wilson and Jungner criteria, which is a natural starting point for the analysis. Stuff like that you need to know about if you want to discuss such matters, so here is one version of the criteria, and here’s the 1968 paper (it’s quite long, I haven’t read it). I should point out that the formulation of the principles in the book diverges a bit from those in the link, but it seems that many of the key principles are preserved in the linked version (the book version has 10 points rather than 9, and is a bit more detailed). The main take-away I got from this book is that it’s actually quite a bit harder to justify screening programmes than I’d have thought beforehand – not all the reasons they provide for being cautious about these things I find convincing, but some of them are clearly worth having in mind. Some quotes from the book:
“we will in the rest of this book use the following working definition of the term “screening”:
The use of medical investigation or testing methods at the initiative of health care or society for the purpose of investigating the health status of individuals with the aim of selecting some of these for possible further treatment from a large population of people that is not united by previously recognised risk or symptoms of disease.” [...]
“roughly, there are three kinds of goals or values that can provide the rationale for introducing screening programmes:
1. Improvement of (physiological) health, reduction of disease or amelioration of symptoms of disease.
2. Improvement of psychological well-being or reduction of suffering.
3. Promotion of autonomy.
[...] these goals may conflict in various ways.” [...]
“The most straightforward way in which an individual may be better off regarding her psychological wellbeing is by having her anxiety or uncertainty regarding her future health status removed – e.g. by having an initial assessment of risk of disease adjusted by having some test. However, the appearance of this possible benefit presupposes that the individual in question has been suspecting that she (or her offspring) is at risk for the disease(s) screened for in the first place (otherwise, there is no initial risk assessment to adjust). Since, by definition, in the case of screening, the initiative to having the test does not come from the individual herself, this cannot be presupposed here. We do not question that reducing anxiety or worry is a valid objective of health care, but this objective is primarily an argument for health care to offer medical investigations if requested by individuals, not for screening. On the contrary, screening runs the evident risk of creating more anxiety than it reduces [...] Thus, in terms of well-being, screening programmes (in contrast to the offering of testing to concerned individuals approaching health care with some initial worry) must primarily be justified with reference to their potency for resulting in some kind of improvement of physiological health.”
“since screening programmes tend to target large and unprepared populations, setting up organisations for appropriate counselling is particularly complicated and challenging and usually requires substantial resources. Thus, the room for serious mistakes is larger, and meeting this challenge makes it more difficult for a screening programme to justify its costs compared to less proactive ways of organising the offering of health care services.”
“The line of reasoning underlying the idea that screening improves autonomy is roughly the following: if individuals possess the knowledge that they or their offspring have an increased risk of contracting some disease, they are in a better position to plan their lives in accordance with their own conception of a good life, to live in accordance with their own values [...] Traditionally in ethics, autonomy has not been considered primarily as a value to promote, but rather as something that gives rise to moral restrictions on how we are allowed to treat each other when trying to promote other things found valuable [...] according to this line of thought, there is a moral obligation to respect autonomy but not necessarily to promote it. [...] a central characteristic of screening is that the initiative to the investigation is not coming from the individuals themselves, but from society or large societal institutions. This is potentially problematic already from the point of view of the idea of respecting autonomy, since that idea makes pressure to accept or abstain from medical procedures at least questionable. Respect for autonomy is usually not only taken to mean that informed consent should be obtained in order for an investigation to be justified, but also that the individual should not be pressured or subjected to more subtle manipulative efforts. [...] The more that participation is taken for granted in the offer of entering a screening programme, the more pressure there is to participate. The more benefits are emphasised and the less drawbacks are mentioned, the more pressure to participate. The more active the patient has to be in order to refuse investigation, the more pressure to participate. And the more pressure to participate, the more problematic from the point of view of autonomy.35 Although pressure can be reduced in various ways, the general point remains: the very fact that the initiative comes from society always presents some problem from the point of view of autonomy. [...] there are practical problems related to screening regarding the need for counselling in order to promote autonomy. [...] There is, in effect, always a counter proportionality between pursuing the promotion of autonomy as a goal and economic viability in the context of screening.” [...]
“there is no empirical evidence in support of the position that more prenatal testing leads to more discrimination and stigmatisation of the disabled.20 Rather, the trend in many countries seems to be the opposite: in tandem with the development of prenatal diagnosis, more resources have been invested in improving both the quality of life and the societal opportunities of disabled people.” [But this observation did not stop them from arguing as if the stigmatisation argument was valid in chapter 5, while discussing non-invasive prenatal diagnosis, even though there's absolutely no reason to assume it's a problem. This fact annoyed me.] [...]
“Both prenatal and neonatal screening programmes [...] have good chances of being efficient in terms of uptake, i.e. testing a large part of the populations of foetuses and newborns respectively. This is so, since most (prospective) parents are in contact with health care during pregnancy and birth anyway [...] this is cost reducing and probably one contributing explanation of the fact that all developed countries have more or less ambitious pre- and neonatal screening programmes.” [...]
“regarding these kinds of tests, there always must be a tradeoff between sensitivity and specificity – one cannot increase the one without decreasing the other. [...] the case for the importance of high specificity is strengthened if there are no effective treatments [...] or if existing treatments are very burdensome [...] In contrast, it seems more reasonable to opt for high sensitivity if there is an effective treatment and there are severe consequences for the individual in terms of health without early diagnosis [...] Traditionally, among screening specialists, high sensitivity has been seen as a more important feature of a screening programme than high specificity. [...] Plausibly, the ethical assessment of how sensitivity and specificity should be balanced cannot be decided by a simple rule. Rather, such assessments would have to be done by careful consideration of each suggested screening programme in a broader context” [...] as a rule, the less predictive value, the stronger the reason to abstain to use the test in a screening program.” [...]
“These are very good reasons indeed not to use relative risk in the presentation of either what sort of information that may be provided by a screening test, or when informing about the actual result of a test. [...] What the patient needs to know both for deciding whether or not to enter a screening programme and what to do on the basis of the test result are the absolute risk figures. In spite of this, there is a widespread tendency in the practice of screening, as well as medical testing in general, for health professionals to press more strongly on relative risk figures when the absolute risks are low or uncertain. [...] Since different genes have different penetrance and expressivity [...] a genetic test [in many cases] cannot even result in a precise risk-figure. Rather, if a useful test can be construed at all, the result it will present will be in terms of a range of risk, like 5–35% increased risk in comparison to the general population. If the risk-level is low to begin with, the predictive value of such a test, and thus the value as a tool for guidance for health care measures or private decision-making, is virtually non-existing. [...] It is [...] safe to say, that the threat to the quality of screening programmes created by the fact that the methods for testing and analysis used provide unclear information potentially affects all types of screening programmes in terms of the groups and diseases targeted.” [...]
“The extent of false positives [in mammography screening] is debated [...] However, Cochrane Collaboration estimates that one in ten during a 10 year period of mammography screening is a false positive. [...] When treatment is initiated due to overdiagnosis,
it is called overtreatment. One question in the debate regards the magnitude of overtreatment. Figures cited vary from 10% increase of overtreatment due to the initiation of mammography screening programmes,52 to 30% [...] Our conclusion from all of this is that the debate regarding overdiagnosis and -treatment, while being cast in the language of scientific facts, is powered mainly by deep ethical disagreements. Positions with regard to this disagreement range from the idea that overdiagnosis and -treatment is not a great problem at all, to the notion that it is a conclusive argument against a screening programme. These positions can, of course, be upheld almost regardless of the magnitude of overtreatment. However, as pointed out, it is difficult to free oneself from the suspicion that this ethical disagreement has been allowed (by one or both parties) to leak into also what is supposed to be the purely scientific part of the discussion. [...] the debate would probably gain from bringing implicit value-judgements into the open.”
“the self-reinforcing nature of screening programmes has an important consequence: unless blatantly flawed, they will probably be very difficult to roll back once in place. This has nothing to do with what is medically or ethically well-founded, but follows from the pragmatics of institutions and realpolitik. This should be kept in mind when new screening programmes are proposed. [...] if we were to imagine the situation that mammography screening was proposed to be initiated today on the basis of present evidence (including the confusing scientific debate), it would not be an easy task to find it to be warranted. First, partly due to the lack of methodological consensus, the scientific basis of information is much too uncertain and difficult to interpret. Second, if counselling procedures of an appropriate nature were to be included, this would presumably seriously elevate the cost of the programme.” [...]
“In 2008, The Cochrane Collaboration published a review: Screening for prostate cancer.71 The review found only two trials that were eligible for inclusion to start with. [...] However, in recent years, this scientific vacuum is starting to be remedied. The most ambitious study is The European Randomized Study of Screening for Prostate Cancer (ERSPC), which was initiated in the early 1990s and includes 182,000 men from seven European countries between the ages of 50 and 74. Results published after a median of 9 years shows a reduced rate of death from prostate cancer of 20%.74 However, the absolute benefit (0.7/1000 reduction) was small and was associated with a 70% increase in prostate cancer diagnosis. In other words, 1410 men needs to be screened and 48 more cases needs to be treated in order to prevent one death, as compared to the non-screened population. [...] most men tested positive with PSA are subsequently shown not to have prostate cancer; only 25–35% of men who have a follow-up biopsy are diagnosed with cancer [...] new data suggest that the extent of the harms of being diagnosed with cancer have not been sufficiently appreciated in the debate. A large cohort study in USA indicates that a diagnosis of prostate cancer may increase the immediate risk of suicide and cardiovascular death. [...] there is relatively large agreement that standards of informed consent in PSA screening, at least in the United States, have been poor. A recent survey among test subjects revealed that a majority (71.4%) were told about the upside of PSA testing, while only a minority (32%) were informed about potential drawbacks.”
The Causes and Behavioral Consequences of Disasters: Models informed by the global experience 1950-2005
I finished the book, which is yet another Springer publication, yesterday. I gave it 2 stars on goodreads. If you want to work for FEMA or a similar organization at some point, this is probably the kind of book you’ll want to read. If you aren’t planning on doing that I’m not sure you need to read it.
Here’s part of what they write in the preface:
“Informed by a systematic study of a unique representative database of 360 disasters worldwide, spanning 1950–2005, we provide in this book a framework that can help us understand the causes of disasters. We also present a model of population behavior after these events. We intend these two inextricably linked models to be useful guides for public health disaster preparedness and response efforts.”
I think that in a way they promise more than they can keep. It turns out that no actual systematic testing of the ‘models’ takes place in the book; the ‘models’ are models in the sense that organizational design ‘models’ are models – these are not the type of models I usually talk about when I use the term ‘model’. There are no equations, no ways to test whether the models are any good or if factors are missing from the models. Most of the chapters deal only with one or two specific disasters. The second ‘model’, which deals with behavioural responses of populations to disasters, seems to me to be little but a bunch of (hard-to-test) postulates about how populations behave after a disaster has struck, supported by what basically amounts to little but anecdotal evidence. The only thing they use the data-base for is to pick out anecdotes to talk about. I should note that what’s bothering me is not mainly that I believe the models are necessarily wrong – I’m not sure they are, as they are general and comprehensive enough to be applied in a variety of contexts and seem to perform reasonably well in the contexts to which they are applied, in the sense that they provide one with a way of thinking about the matters at hand – it’s rather that the ‘models’ are too squishy. Naturally a huge problem here is that one disaster is very different from another (you try to come up with a good model which one might be able to use to compare a suicide bomb attack with an outbreak of cholera, identifying common elements and decision-relevant parameters…) and so if you want to say something about disasters in general you can’t really say all that much – this problem is hard to get around and I’m sure the authors have thought a great deal about it before starting out. Some might then argue that the authors were too ambitious, whereas others might argue that this level of analysis is the only kind you can even try to apply here so one should not fault them for at least trying.
It’s not all bad and some analytically important distinctions are made along the way which I had never given any thought. I learned some stuff from reading this book. Some quotes and a few comments:
“Several disciplines have come to agree that the initial hazard, whether it be natural, technological, or human-made, is not an isolated predictor of the events or outcomes to follow. Rather, preexisting characteristics of the affected region intersect with the hazard to shape the magnitude of the consequences of the hazard [1–3]. These preexisting characteristics can produce adverse consequences [4–6] but can also mitigate the consequences of hazards [3, 7–10]. We use here the term “vulnerabilities” for the former, and “capacities” for the latter. [...]
Our model of disaster development [...] consists of three stages. First, the context in which a disaster strikes is characterized by vulnerabilities and capacities. Features of the underlying context rest on a vulnerability–capacity continuum and their role as vulnerabilities or capacities depends on their influence in exacerbating, or protecting against, the adverse consequences of hazards that affect regions and populations. Second, a hazard occurs that intersects with existing vulnerabilities and capacities, defining the severity of the disaster. Temporally the vulnerabilities and capacities predate the hazard, although, in the case of chronic hazards, the hazards themselves may shape the underlying vulnerabilities and capacities. Third, intermittent stressors and intermittent protectors act coincident with, or soon after, the hazard. They become apparent only after the hazard initiates, and have the potential to enhance or mitigate the severity of disaster outcomes. [Intermittent stressors and intermittent protectors] are neutral preexisting characteristics that will act as a vulnerability or capacity only in the presence of an external stressor (the hazard).”
The book spends several chapters applying the framework outlined above to specific disasters (e.g. the Vargas tragedy; the New York City Subway Fire in December 1990; the 1950 earthquake in Cuzco, Peru) identifying specific vulnerabilities and capacities that played a role in the specific disasters as well as intermittent stressors and -protectors of importance (to give an example, during the 1950 Peru earthquake, almost a third of all of Cuzco’s inhabitants happened to be watching a soccer game in Cuzco’s brand new stadium when the earthquake hit. If not for that intermittent protector, the number of victims may well have been much, much higher – the stadium handled the earthquake very well, but many of those people’s homes were destroyed by the earthquake). The second half of the book adds to the analysis population behavioural response to disasters. Some more quotes:
“we argue here that rather than being chaotic or unpredictable, population behavior after disasters is rational and predictable and emerges from the interaction between a hazard and its context that has been discussed throughout this book. [...] 1960s. While early accounts of this behavior depicted post-disaster behavior as “panic” and “irrational,”  later analysts have shifted to recognize, as we do here, that post-disaster behavior is “organized” and “predictable” [2, 3].
Understanding the progression of population behavior after disasters represents an important element in disaster preparedness and response. Anticipating the timing and nature of population behavior could allow for better synchronization between institutional efforts to restore normalcy with a population’s immediate and long-term needs. [...]
We suggest that there are five progressive stages of post-disaster population behavior. We summarize each stage here and then discuss each stage in more detail in subsequent chapters. Stage one is characterized by group preservation behaviors. At this time the compact group, or the group of people directly affected by the hazard, is the focus. Initial reactions and behaviors are motivated by intimate contact with the hazard and will be characterized by fear and anxiety, information seeking and disseminating behavior, and actions toward group preservation. [...]
In stage two, population preservation and altruism emerge. During this period, members of the compact group, now reassured that their immediate safety is secured, work with persons who were not directly affected by the hazard to rescue and provide aid to the immediate victims. This stage moves beyond the initial group preservation behaviors of the compact group and engages a population that is only indirectly affected by the hazard. This latter group bridges the gap between the compact group and the general population, helping disseminate information about the hazard and developing disaster to the general community. Here too, information- seeking behaviors are prevalent, while population preservation actions manifest. [...]
At stage three, internalizing the disaster begins. Both members of the compact group and those in the general population begin to internalize the disaster, adapting to the post-hazard environment. Narratives of the hazard are constructed in an attempt to understand what transpired and why it did. What was previously considered a “normal” activity may not be appropriate in the post-disaster context, leading to changes in routine behaviors. Disaster survivors may ask themselves who or what was responsible for what they went through. [...]
Stage four marks the onset of externalizing. Externalizing is an attempt to address the emotions and vulnerabilities identified during the internalizing process. At this time, compensation and relief may be sought, and actions are taken against perceived perpetrators of the disaster. In addition, during this stage populations begin to address vulnerabilities identified during the internalizing stage. [...]
The final and fifth stage is marked by renormalization and adaptation. This is a potentially slow and protracted process in which the population identifies and acts according to new norms that are appropriate to the altered post-disaster context. At this point, group adaptation occurs. New modes of behavior become dominant, while external behaviors are normalized.” [...]
“It is [...] important to note here that the model proposed is a model of population behavior. We acknowledge that there will be a range of individual responses to hazards and we accept and expect there to be individuals in any disaster whose behaviors do not correspond with what we propose. In the subsequent chapters, we elaborate on each of these stages and present key case examples illustrating each stage of population behavior.”
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