The first six months of 2014 are at an end, and I thought it made sense to make a post providing an overview of the books I’ve read during the first half of this year. I decided to be a bit more thorough in this post than I was when I wrote the 2013 book overview post; for example in this post I’ve at least tried to include in the links below all relevant posts I’ve written about the books on the blog, rather than just a subset of them. The corresponding goodreads list is here. Aside from links to relevant posts I’ve also added a bit of information about the books – the numbers in the parentheses are the goodreads ratings I have given the books (for information about how to interpret those ratings, see incidentally the comments here and here), whereas the various letters following those numbers indicate which ‘type’ of book it is – ‘f’ = fiction, ‘nf’ = non-fiction.
I was seriously considering adding other dimensions/categories to the categorization scheme as well, but in the end I decided against doing much of that because such things tend to get messy and I didn’t want to bother with figuring out which other categories might be interesting to include and which books fit into which categories. The only additional variables I added were the names of the publishers of the non-fiction books (it didn’t take any mental effort to add this variable and it seemed to me like it might be relevant information), as well as the names of the authors of the fiction books (-ll-). As people reading along here can’t be expected to necessarily know all the publishers included, I decided to also add a link to some information about each of the publishers featured on the list – the link is added the first place where they are mentioned – in order to make it easier to assess relatively fast which type of book it might be. Aside from these things I’ve written very little about each book; I have added a few other remarks here and there where they seemed relevant, but I’ve tried to keep such comments brief and to the point. If you don’t do this a post like this can get very long very fast.
I have not rated all the books on the list, but I have added the goodreads ratings in the great majority of cases where I have – usually the posts about the book will in the cases where no ratings are provided give you both some idea why I did not rate them and some idea as to what I think about those books. In general it’s safe to say that books I have not rated have some (to me) problematic features which I’ve felt somewhat ambivalent about. On a related note it should be clear from the list that I have not blogged all the books I’ve read this year; this is because I decided a while back to limit fiction blogging a bit – I have however covered all non-fiction books I’ve read this year so far, and many of them I have written more than one post about. Roughly two-thirds of the books I read were non-fiction; of the 53 books on the list there are 18 fiction books and 35 non-fiction books. There are 70 links to book-related posts below, and the great majority (64) deal with the non-fiction books, meaning that I’ve written slightly less than two blog posts about each non-fiction book on average.
On the list below I have only included books which I have read in full and have actually finished, meaning that as usual some books are left out – this is incidentally the reason, in case you were wondering, why the list below looks slightly different from the list on goodreads. The list may also look slightly different because although when writing an early draft of the post I organized the books according to how they were listed on goodreads – i.e. the books are not necessarily listed in the order they were read, or in the order they were covered here on the blog – I did not really care about this stuff when updating the draft later on to include new books I’d read (I should note that given the number of links you need to add and posts that you need to track down, a post like this actually takes a while to write). The category of books I’ve read significant chunks of this year but have not finished include books such as Microeconomic Theory, Ecological Dynamics, and Introduction to Quantum Mechanics, so ’20 pages of light reading’ is not in all cases an accurate characterization of the type of books excluded from the list.
I hope you’ll find the list helpful in terms of navigating the site and that it’ll make it easier for you to find stuff I’ve written here about things you consider interesting. I should note that I occasionally have a bit of trouble keeping track of the stuff I read myself, so this post was not only written for you guys..
Okay, here we go:
1. Pathophysiology of disease (5, nf. Lange medical text. Long, takes a lot of work compared to most of the other books on this list). I took a few quite long breaks from the book along the way, which is why the posts are somewhat spread out over time. I decided in the end to add all relevant posts about the book here, even the ones which were not written this year. Relevant links: 1, 2, 3, 4, 5, 6.
2. The Complete Maus (4, f). Art Spiegelman. I was seriously considering not including this one on the list at all (is this even a book?), but on the other hand it took me longer to read this than it took me to read Calvino so I figured I might as well add it to the list.
3. Why Women Have Sex (2, nf. Times Books. There are two non-fiction books on this list which are not either academic publications (the great majority) or technical publications (#40, 42 and 45) – this book is one of those two books. Don’t be fooled by the fact that the book is written by two university professors; the level of coverage here is much lower than that of pretty much every other non-fiction book on this list). Blog links: 1, 2.
6. Handbook of Individual Differences in Social Behavior (4, nf. Guilford Press psychology text. Long). Blog coverage here, here, and here. Note that I changed my mind about the goodreads rating after I’d written the last of my posts about the book.
7. Evolution of Island Mammals: Adaptation and Extinction of Placental Mammals on Islands (4, nf. Wiley-Blackwell biology text). Blog coverage here.
11. Death in the clouds (4, f). Agatha Christie.
14. Screening for Depression and Other Psychological Problems in Diabetes: A Practical Guide (2, nf. Springer). Blog coverage here.
16. The Daughter Of Time (4, f). Josephine Tey.
17. Cards on the Table (5, f). Agatha Christie.
18. A Practical Manual of Diabetic Retinopathy Management (2, nf. Wiley-Blackwell medical text). Blog coverage here.
19. The Cambridge Economic History of Modern Europe: Volume 1, 1700-1870 (3, nf. Cambridge University Press economics text). Blog coverage here and here.
21. Personality Judgment: A Realistic Approach to Person Perception (3, nf. An Academic Press psychology publication). Blog coverage here and here.
22. The Remains of the Day (5, f). Kazuo Ishiguro.
23. The Origin and Evolution of Cultures (5, nf. Oxford University Press. Takes a lot of work, but it’s an awesome book – “Highly recommended. Probably the best book I’ve read this year”). Blog coverage here, here, here, here and here.
24. What Did the Romans Know?: An Inquiry into Science and Worldmaking (2, nf. University of Chicago Press). Blog coverage here and here.
25. Bioterrorism and Infectious Agents: A New Dilemma for the 21st Century (3, nf. Springer medical text). Blog coverage here.
29. Lost in a Good Book (5, f). Jasper Fforde.
32. Do Androids Dream of Electric Sheep? (3, f). Philip K. Dick.
34. Military Geography: For Professionals and the Public (3, nf. Potomac Books/University of Nebraska Press). Blog coverage here, here and here.
36. To Kill a Mockingbird (2, f). Harper Lee. Overrated.
37. Impact of Sleep and Sleep Disturbances on Obesity and Cancer (5, nf. Springer medical text). Blog coverage here and here.
39. Something Rotten (5, f). Jasper Fforde.
41. Plant Animal Interactions: An Evolutionary Approach (5, nf. Blackwell Publishing biology text). A really great book, high average goodreads rating. Blog coverage here, here, and here.
43. Peril at End House (4, f). Agatha Christie.
48. Poirot Investigates (3, f). Agatha Christie. Unlike the other books by her on the list, this book is a collection of short stories, rather than a novel.
50. First Among Sequels (5, f). Jasper Fforde. Goodreads review: “(Maybe I shouldn’t give all these [Jasper Fforde] books five stars, but as long as they keep being awesome I’ll keep giving them five stars.)“. Blog coverage here.
53. Murder in Mesopotamia (4, f). Agatha Christie.
My first post about the book, which includes a few general remarks and observations, can be read here. In this post I’ll cover some stuff from the last 150 pages. I’ve bolded relevant key points here the same way I did in the first post about the book.
“Atherosclerosis-related disease, coronary heart disease (CHD), peripheral vascular disease (PVD), and thrombotic stroke are major complications in people with type 2 diabetes mellitus . A recent meta-analysis of 102 prospective studies demonstrated a hazard ratio of 2 for coronary death and non-fatal myocardial infarction (MI) and 2.5 for ischemic stroke . In the United Kingdom Prospective Diabetes Study (UKPDS), for each 1% increase in HbA1c there was a 28% increase in PVD . […] In the National Health and Nutrition Examination (NHANES III) performed in the USA, the prevalence of metabolic syndrome in diabetes was 86%. The prevalence of CHD in this group was 19.2%. In those with diabetes and no evidence of metabolic syndrome, CHD prevalence was 7.5%, which is comparable to those without diabetes or metabolic syndrome . Many studies in different populations have confirmed that dyslipidemia is a common finding in type 2 diabetes. […] A basic abnormality is the overproduction of large VLDL from the liver […] LDL-cholesterol concentrations are generally similar to those of the background population. However, LDL-cholesterol remains a major risk factor […] Qualitative changes in LDL particles increase their atherogenicity. The particles are smaller and denser with less lipid core. […] Statins are first-line pharmacotherapy for diabetic dyslipidemia. Their use is based on a wealth of data from robust, randomized trials for both primary and secondary prevention of CVD events. […] A large number of diabetic patients (n=2,912) was included in HPS. Simvastatin, which reduced LDL-cholesterol by 0.9 mmol/l, was associated with a 33% relative risk reduction in major CVD events (p = 0.0003). This benefit was independent of baseline lipids, diabetes duration, glycemic control, and age. The authors [of the HPS] calculated that simvastatin therapy over five years should prevent a first major cardiovascular event in about 45 people per 1,000 treated […] It is clear that patients with diabetes and CHD respond in a similar way to the nondiabetic population. However, a substantial residual vascular risk persists […] A contributory factor to the failure to achieve therapeutic goals is statin intolerance […] in practice there is a significant minority of patients who cannot tolerate statins at all, or can only tolerate a small dose, insufficient to achieve the LDL goal.”
“Subjects with both type 1 and type 2 diabetes are at increased risk of developing cardiovascular disease, with approximately three-quarters of patients with diabetes ultimately dying from vascular causes.” [In the first post I included this quote from a previous chapter: “Mortality from CVD accounts for more than 60% of deaths in patients with type 2 diabetes mellitus”. Estimates vary (and these estimates need technically not be in conflict with each other as 75% is more than 60%…), but regardless of the differences this is ‘the big one’.]
“Overall, the available data indicate that diabetes is associated with a range of metabolic abnormalities that adversely influence platelet function [I should note that they go into a lot of detail about these ‘metabolic abnormalities’, and this is stuff I deliberately excluded from the coverage because it’s very technical stuff]. Management of the platelet aspect of this prothrombotic state should involve normalization of the metabolic changes seen in diabetes and the appropriate use of antiplatelet therapy […] aspirin is used for secondary cardiovascular protection in diabetes [38, 39], a practice supported by two large meta-analyses [40, 41]. […] data indicate that aspirin may be less effective in secondary cardiovascular protection in diabetes […] there is no convincing evidence for the use of aspirin monotherapy for primary cardiovascular protection in diabetes, although some guidelines recommend its use in high-risk subjects. […] There is evidence to suggest that the type of hypoglycemic agent used may modulate predisposition to future ischemic events. Metformin is normally used as first-line therapy in subjects with type 2 diabetes. The UK Prospective Diabetes Study (UKPDS) has demonstrated reduced ischemic heart disease (IHD) risk in overweight patients using metformin compared with subjects not on this therapy […] Insulin is mainly used in type 2 diabetes after the failure of other hypoglycemic agents. Insulin-treated type 2 diabetes subjects are at a greater risk of cardiovascular events compared with noninsulin-treated subjects, which may simply be a reflection of longer disease duration, with a consequent increase in the risk of complications . In healthy individuals, insulin has antithrombotic effects, but it has the opposite effects in the presence of insulin resistance […] There are no clear guidelines for the treatment of diabetes with ACS and there is a great variability between countries and even centers in the same country, which is largely dependent on local resources and data interpretation of different trials. […] Antithrombotic therapy following ACS has been through major changes over the past decade. […] Despite major advances in therapy, atherothrombotic complications remain the main cause of morbidity and mortality in individuals with diabetes. […] Considered together, current evidence indicates that diabetes subjects have a differential response to antiplatelet and anticoagulant drug therapy compared to subjects with normal glucose metabolism. Further studies are still needed to clarify the optimal antithrombotic strategy in this high-risk population.”
“It is difficult, if not impossible, to assess directly the efficacy of individual dietary components on CVD risk because of the challenges, both practical and financial, in modifying the diets of a large group of people for long periods of time, as well as the difficulty that arises in studying individual dietary components within the context of habitual dietary patterns. Therefore, most dietary factors with the intent of reducing CVD risk are evaluated on the basis of short-term interventions (weeks or months) using biomarkers […] rather than hard endpoints. By combining data from different types of studies, dietary patterns have emerged that are associated with a lower risk of CVD […] Moderate fat intake (25% to 35% of energy) is associated with lower triglyceride concentrations than a low-fat diet. […] Current recommendations are to consume a diet containing 25%E [read: 25 percent of daily energy intake] to 35%E as total fat [3, 4]. For individuals with diabetes, the recommendation is to consume diets toward the higher end of this range [5, 6]. […] Low-fat diets are associated with elevated triglyceride concentrations and depressed high-density lipoprotein (HDL)-cholesterol concentrations resulting from what is commonly referred to as carbohydrate-induced hypertriglyceridemia […] Carbohydrate-induced hypertriglyceridemia, resulting in elevated triglyceride concentrations, is caused by an enhanced rate of hepatic fatty acid synthesis and is precipitated by an excess flow of glucose from the gut to the liver [14, 15] and subsequent production of hepatic triglyceride-rich particles, termed very low-density lipoprotein (VLDL) […]. In some cases delayed triglyceride clearance associated with low-fat diets has also been observed, contributing to the elevated triglyceride concentrations […] Within the context of a stable body weight, replacement of dietary fat with carbohydrate results in higher triglyceride and VLDL-cholesterol concentrations, lower HDL-cholesterol concentrations, and a higher (less favorable) total cholesterol to HDL-cholesterol ratio [20, 21, 22, 23, 24, 25].” [Eckel et al. pointed this out as well and I included coverage of this in my post about that book as well; but this is an important piece of information that I do not mind repeating here. Note that not all carbohydrates are the same, and that dietary fiber seems to have a protective effect. The chapter from which the above quote, and the paragraph below, was taken covered many of the same things covered in Barasi].
“a series of randomized controlled intervention trials […] have failed to demonstrate a benefit of supplemental vitamin E, beta-carotene, vitamin C, or folate on CVD risk reduction [156, 157]. Recently, interest has been focused on the potential effect of supplemental vitamin D in CVD risk reduction. In contrast to the prior vitamins, the relationship between vitamin D and CVD risk is focused on nutrient insufficiency rather than supplemental amounts [156, 158]. Until the results of randomized controlled trials with vitamin D become available, it is premature to make any recommendations.”
“Diabetics are more likely than nondiabetics to experience ACS, and diabetes is an independent predictor for mortality in ACS. Diabetics are also more likely to develop complications of ACS and its management such as heart failure and bleeding. With a few exceptions, the management of ACS is similar in patients with and without diabetes. In patients with diabetes, management does not differ between patients who are insulin dependent and patients who do not require insulin. […] The management of ACS begins with determining the appropriate timing for coronary artery reperfusion. Patients with STEMI [ST-elevation myocardial infarction – see this] or an equivalent should receive emergent reperfusion, preferably with PCI. Patients with UA/NSTEMI [see the link in the brackets above] can be risk stratified to determine the appropriate timing for coronary angiography. In these patients angiography is used to decide if medical therapy, PCI, or CABG [Coronary Artery Bypass Grafting] is the preferred treatment strategy. All patients with ACS should be treated with antiplatelet and antithrombin therapy, as well as adjuvant therapy with a statin, ACEI, and beta-blocker.” [there’s an entire chapter about these things where they go into quite a bit of detail, but I decided against covering this stuff here as most of it is once again highly technical stuff which is not easy to blog].
“Amputation of the lower limb is one of the most feared adverse health outcomes among patients with diabetes. […] PAD [Peripheral Artery Disease], referring to atherosclerotic occlusive disease of the lower limb arteries is a common, debilitating complication that correlates with cardiovascular disease mortality . Diabetes is a significant independent risk factor for PAD (odds ratio of 2–3) , together with hypertension, cardiovascular disease, hyperlipidemia, smoking, and obesity [3, 4]. The prevalence of PAD in patients with type 2 diabetes has been estimated at 23.5% in a UK population , and is strongly dependent on the duration of diabetes [6, 7]. Compared with men without diabetes, the adjusted relative risk of PAD among men with diabetes increased from 1.39 with diabetes duration of 1–5 years’ to 4.53 for diabetes of >25 years’ duration . […] a very high prevalence (71%) of PAD was recently reported in 1,462 elderly patients with diabetes (>70 years) in Spain as evaluated by a pathological ABI (ankle-brachial index) . […] A recent meta-analysis  including 94,640 participants and 1,227 LEA [Lower-Extremity Amputation] cases reported in 14 studies demonstrated a substantial increase in the risk of LEA associated with glycemia in individuals with diabetes. The overall risk reduction (RR) for LEA was 1.26 (95% CI 1.16–1.36) for each percentage point increase in HbA1c.”
“A Scottish study showed that after LEA diabetic subjects had a 55% greater risk of death than those without diabetes . […] Median time to death […] was 27.2 months with diabetes versus 46.7 months without diabetes (p<0.01) and survival rate 10 years after amputation was 22.9% in nondiabetic patients but only 8.4% in diabetic patients (p=0.0007). [I’ve read about these things before, and I should note that I do not believe these estimates are unique or aberrant. It’s not just that losing a leg sucks – when you’re so far along in the disease process that they have to start cutting off parts of you to keep you alive, you’re really quite likely not to live for a very long time. The prognosis of a diabetic who just had a LEA is much worse than that of the average breast cancer patient.] […] The clinical stage of symptomatic PAD can be classified using the Fontaine staging system . Fontaine stage I represents those who have PAD but are asymptomatic; stages IIa and IIb include patients with mild and moderate-to-severe intermittent claudication, respectively; those with ischemic rest pain are classified in Fontaine stage III; and patients with distal ulceration and gangrene represent Fontaine stage IV. Diagnosing PAD in patients with diabetes is of clinical importance for two reasons. The first is to identify a patient who has a high risk of subsequent MI or stroke regardless of whether symptoms of PAD are present. Indeed, patients with diabetes and PAD have a fivefold increased risk [of MI/stroke] compared to the presence of either disease alone [22, 23, 24, 25]. An observational study less then ten years ago demonstrated that patients with diabetes and PAD stage IV (=ulcer) have a 100% mortality within six years . The second reason is to elicit and treat symptoms of PAD, which may be associated with functional disability and limb loss.”
“PAD is often more subtle in its presentation in patients with diabetes than in those without diabetes […] Importantly, PAD in individuals with diabetes is usually accompanied by peripheral neuropathy with impaired sensory feedback […] The majority of patients with early PAD are either asymptomatic or have atypical leg symptoms, with “classical” claudication in only 10–35%, therefore detection is elusive unless actively sought. Given shared risk factors, it is axiomatic that there exists a high coprevalence of atherosclerosis in other vascular beds, including the coronary arteries in PAD patients . […] patients with PAD are at a high risk of cardiovascular events and therefore benefit from aggressive secondary prevention […] Many studies have documented that secondary prevention is underused in patients with PAD […] Antiplatelet drugs that have been shown to reduce the incidence of vascular death, nonfatal myocardial infarction, and nonfatal stroke in patients with PAD are aspirin, ticlopidine, and clopidogrel . Aspirin plus dipyridamole has not been proven to be more efficacious than aspirin alone in the treatment of patients with PAD .”
“Compared to patients with intermittent claudication (IC; stage II of PAD), patients with critical limb ischemia (CLI; stages III and IV after Fontaine) are in a more difficult situation: while amputation is rather infrequently necessary in patients with IC , amputation rates of 23% at 12 months were reported in patients with CLI . In patients with CLI, the incidence of diabetes mellitus and chronic renal insufficiency is 70.4% and 27.8%, respectively . Thus, patients with CLI are in the majority among patients with diabetes […] The prevalence of gangrene is about 20 to 30 times higher in patients with diabetes mellitus .” [In terms of the treatment options, they put it frankly in their recommendations in that chapter: “Primary amputations only in a leg-for-life situation”].
“Neoplasms include several hundreds of diseases, which can be distinguished by localization, morphology, clinical behaviour and response to therapy. […] Malignant neoplasms are characterized by progressive growth of tissue with structural and functional alterations with respect to the normal tissue. In some cases, the alterations can be so important that it becomes difficult to identify the tissue of origin. A peculiarity of most malignant tumours is the ability to migrate and colonize other organs (metastatization) via blood and lymph vessel penetration. The presence and extension of metastases are often the critical factors to determine the success of therapy and the survival of cancer patients. The pace of growth of malignant neoplasms varies widely, and asymptomatic neoplasms are often found at autopsy of individuals deceased from other causes. […] Most malignant neoplasms (about 90 %) in adults arise from epithelial tissues and are defined as carcinomas. […] Knowledge about the causes and the possible preventive strategies for malignant neoplasms has greatly advanced during the last decades. This has been largely based on the development of cancer epidemiology.”
I finished this book yesterday. I complained in my coverage of Managing Cardiovascular Complications in Diabetes that that book was full of formatting errors and that it seemed that nobody had proofread the book before publication, and I said in that post that ‘It’s much rarer, I think, to see stuff like that in Springer publications.’ I might be wrong about this, or at least I’ve updated my priors on that one; this specific book was even worse than the Managing Cardiovascular complications book in that respect – errors are all over the place. It’s odd and also slightly annoying, because if not for that problem I would consider this book to be a really nice little resource.
The book deals mainly with the data, and it is not a methodology text. Occasionally how we know what we know is important and the limits of our knowledge is important, so methodological questions are addressed here and there; but you certainly don’t need to have read a book like this to understand it, and although many specific details in the book presumably would not be understood by a random guy who’d just finished high school, most of the book is relatively easy to follow. This disease is this common in this area and that common in that area and the difference between these two areas may be due to these things; it kills this many people; these are some of the risk factors we know about, and the role they play is this – most of the book deals with questions such as these, and there are only so many ways you can make stuff like that impossible to understand by using a lot of fancy medical terms.
The book provides an excellent overview and the data and the level of coverage is actually quite excellent considering the length of the book – if not for the many errors and general sloppiness I’d feel tempted to give it a high rating. We know more than I thought we knew about these things, which is nice, and a few of the observations included were surprising to me. Of course a lot of details are missing but this is to be expected – people have written books about topics covered in a few pages here (e.g. this). If you read Mukherjee and this book, I think you’ll be off to a great start in terms of understanding cancer better; the obvious next step would be a book like this, but most people are probably not going to read stuff like that.
I should point out that perhaps I was a bit too hard on the lecture about the UK million women study in the recent Open Thread – I find it important to note in particular that specific topics also covered in this book, such as the role of birth control and hormone replacement therapy in cancer development, are covered in more detail in that lecture than they are in this book; so I refer you to that lecture, rather than covering that stuff below. Some of this stuff is the sort of stuff I’d probably want to know about if I were of the opposite gender. I should point out as well here that one of the reasons I did not think too highly of her lecture relates to her comments about cancer screening during the lecture (I think it’s around the 35 minute mark or so). Those comments annoyed me because I think she’s being intellectually dishonest during her lecture by not addressing the main problems with the pro-screening position, but only presents a weaker argument (to an audience unlikely to know any better) which is much easier to knock down – in the context of breast cancer screening the main argument against them, from what I’ve gathered, is not that these things do not save any lives (though there’s also a lively debate about how many lives are actually saved and how you should go about estimating this number), but rather that the costs – both monetary and non-monetary (the latter e.g. relating to the mental anguish experienced by the many, many women who get a false positive test result) – are not justified; there’s much more about these and related things in this book. In general it’s safe to say that it’s quite a bit harder to ‘properly justify’ screening programmes than many doctors often seem to think it is. Anyway the book doesn’t go into much detail about these things, and you’ll have to look elsewhere (e.g. Juth and Munthe) for detailed coverage of stuff like that.
I have added some observations from the book below and a few comments.
“Analytical studies (case–control and cohort) have shown the causal role of specific exposures in the aetiology of several malignant neoplasms. One limitation of the epidemiological approach, which may prove of critical importance in trying to detect comparatively small increases in risk, as in the case of environmental pollutants, is that even in the best conditions it is impossible to confidently identify by epidemiological means an increase in risk smaller than say 10–20 % (and serious problems arise in the interpretation of increases below 50 %), as the biases inherent in any observational study are of at least this order of magnitude (Adami et al. 2008).”
“In addition to lead-time bias, three types of bias are peculiar to the assessment of screening programmes. Because of self-selection, persons who elect to receive early detection may be different from those who do not: for instance, they may belong to better educated classes, be generally healthier and health conscious, and this could produce a longer survival independent of any effect of early detection. In addition, cancers with longer pre-clinical phases, which may mean less biological aggressiveness and better prognosis, are, in any case, more likely to be intercepted by a programme of periodical screening than cancers with a short pre-clinical phase, and a rapid, aggressive clinical course (length bias). Finally, because of criteria of positivity adopted to maximize yield of early cases, a number of lesions which in fact would never become malignant growths are included as ‘cases’, thus falsely improve the survival statistics (over-diagnosis bias).”
“The number of new cases of cancer which occurred worldwide in 2008 has been estimated at about 12,700,000 […]. Of these, 6,600,000 occurred in men and 6,000,000 in women. About 5,600,000 cases occurred in high-resource countries (North America, Japan, Europe including Russia, Australia and New Zealand) and 7,100,000 in low- and medium-resource countries. Among men, lung, stomach, colorectal, prostate and liver cancers are the most common malignant neoplasms […], while breast, colorectal, cervical, lung and stomach are the most common neoplasms among women […] The number of deaths from cancer was estimated at about 7,600,000 in 2008 […] No global estimates of survival from cancer are available: data from selected cancer registries suggest wide disparities between high- and low-resource countries for neoplasms with effective but expensive treatment, such as leukaemia, while the gap is narrow for neoplasms without an effective therapy, such as lung cancer […] The overall 5-year survival of cases diagnosed during 1995–1999 in 23 European countries was 49.6 % (Sant et al. 2009).”
“Survival from breast cancer has slowly increased in high-resource countries, where it now achieves 85 %, following improvements in screening practices and treatments. Survival in low-resource countries remains poor, in the order of 50–60 %. Breast cancer is the most common cancer among women worldwide: the estimated number of new cases in 2012 was 1,680,000” [I had no idea survival rates were that high in ‘high-resource countries’, though it’s a bit problematic that it is not spelled out what is actually meant by ‘survival’; I gather from this link that it’s the 5-year survival rate.]
“Tobacco smoking is the main single cause of human cancer worldwide (IARC 2004) and the largest cause of death and disease. It is the key cause of lung cancer, and a major cause of cancers of the oral cavity, pharynx, nasal cavity, larynx, oesophagus, stomach, pancreas, uterine cervix, kidney and bladder, as well as of myeloid leukemia. In high-resource countries, tobacco smoking causes approximately 30 % of all human cancers (Doll and Peto 2005). […] A benefit of quitting tobacco smoking in adulthood has been shown for all major cancers causally associated with the habit. Smokers who stop around age 50 avoid over 50 % of overall excess mortality from all causes (Doll et al. 2004; Jha et al. 2013; Pirie et al. 2013), from lung cancers (Peto et al. 2000) and well as from other tobacco-related cancers (Bosetti et al. 2008a), and those who stop around age 40 or earlier avoid most of their tobacco-related cancer risk. […] “The risk of lung cancer among smokers relative to the risk among never-smokers is in the order of over 20-fold […] In the UK million women study, the RRs [relative risks] of lung cancer were 10.5 for current smokers of 10 cigarettes per day, 22.0 for 15, and 36.0 for ≥20 cigarettes per day. […] An association has been shown in many studies between exposure to involuntary smoking and lung cancer risk in non-smokers. The magnitude of the excess risk among non-smokers exposed to involuntary smoking is in the order 20 % (IARC 2004).” [You have a 20% risk increase from passive smoking and a twenty-fold increase from smoking. My conclusion from these observations would be that in terms of cancer risk passive smoking doesn’t really matter in the big picture, and that it is overhyped as a disease risk factor – the excess cancer risk attributable to smoking probably causes more than 100 cancers in smokers for each cancer case in a non-smoker, and most of the non-smokers who develop cancerous lesions will have been exposing themselves for years – questioning the assumption that they did not willingly take on this risk]. Lung cancer is “the most important cause of cancer death worldwide. It accounts for an estimated 1,250,000 new cases and 1,100,000 deaths each year among men and 580,000 cases and 500,000 deaths among women […]. Survival from lung cancer is poor (around 10 % at 5 years).”
“The role of dietary factors in causing human cancer remains largely obscure. For no dietary factor other than alcohol […] and aflatoxin (a carcinogen produced by some fungi in certain tropical areas) there is sufficient evidence of an increased or decreased risk of cancer. […] Alcohol drinking increases the risk of cancers of the oral cavity, pharynx, larynx, oesophagus and liver, colorectum and female breast (Baan et al. 2007). For all cancer sites, risk is a function of the amount of alcohol consumed […] The global burden of cancer attributable to alcohol drinking has been estimated at 3.6 and 3.5 % of cancer deaths (Boffetta 2006), although this figure is higher in high-resource countries (e.g., the figure of 6 % has been proposed for United Kingdom (Doll and Peto 2005) , and 9 % in Central and Eastern Europe). These included over 5 % of cancers and cancer deaths in men and about 1.5 % of cancers and cancer deaths in women. […] Systematic reviews have concluded that nutritional factors may be responsible for about one-fourth of human cancers in high-resource countries, although, because of the limitations of the current understanding of the precise role of diet in human cancer, the proportion of cancers known to be avoidable in practicable ways is much smaller (Doll and Peto 2005). The only justified dietary recommendation for cancer prevention is to reduce total caloric intake, which would contribute to a decrease in obesity, an established risk factor for human cancer […] There is sufficient evidence for a cancer preventive effect of avoidance of weight gain, based on a decreased risk of cancers of the colon, gallbladder, post- menopausal breast, endometrium, kidney and esophagus (adenocarcinoma) […] Estimates of the proportion of cancers attributable to overweight and obesity in Europe range from 2 % (Doll and Peto 2005) to 5 % (Bergstrom et al. 2001).”
“There is growing evidence that chronic infection with some viruses, bacteria and parasites represents a major risk factor for human cancer, in particular in low-income countries […] The population attributable fraction for infectious agents was 16.1 % in 2008, meaning that around two million new cancer cases were attributable to infections. HBV and HCV-related liver cancer, HPV-related cervical cancer and Helicobacter pylori-related stomach cancer overall are responsible for 95 % of the total number of infection-related cancers. The estimate of the attributable fraction is higher in less developed countries than in high-resource countries (22.9 % of total cancer versus 7.4 %). […] Cervical cancer is a major public health problem in many low and middle income countries. Incidence rates are high (20–40/100,000) in sub-Saharan Africa and Latin America countries, as well as in India and southern Asia. […] Chronic infection with HPV is a necessary cause of cervical cancer. Using sensitive molecular techniques, virtually all tumours are positive for the virus […]. Different types of HPV exist, and those associated with cervical cancer are mainly types 16, 18, 31, 45 and 58. In particular, HPV 16 is the main cervical carcinogen in most populations”.
“Approximately 40 occupational agents, groups of agents and mixtures have been classified as carcinogenic by IARC […] Estimates of the global burden of cancer attributable to occupation in high-income countries result in figures in the order of 1–5 % (Doll and Peto 2005 ; Schottenfeld et al. 2013). In the past, almost 50 % of these were due to asbestos alone, while in recent years the impact of asbestos on lung cancer […] is levelling off […] However, these cancers concentrate in some sectors of the population (mainly male blue-collar workers), among whom they may represent a sizable proportion of total cancers […] The available evidence suggests, in most populations, a small role of air, water, and soil pollutants. Global estimates are in the order of 1 % or less of total cancers (Doll and Peto 2005; Schottenfeld et al. 2013). This is in striking contrast with public perception, which often identifies pollution as a major cause of human cancer. However, in selected areas (e.g., residence near asbestos processing plants or in areas with drinking water contaminated by arsenic), environmental exposure to carcinogens may represent an important cancer hazard.”
“No precise estimates are available for the global contribution of drug use to human cancer. It is unlikely, however, that they represent more than 1 % in high-resource countries (Doll and Peto 2005). Furthermore, the benefits of therapies are usually much greater than the potential cancer risk.”
“A number of inherited mutations of a high-penetrance cancer gene increase dramatically the risk of some neoplasms. However, these are rare conditions in most populations and the number of cases attributable to them is rather small.” [An example: “breast cancer risk is greatly increased in carriers of mutations of several high-penetrance genes, in particular BRCA1, BRCA2, ATM, CHECK2 and p53. Although the cumulative lifetime risk in carriers of these genes is over 50 %, they are rare in most populations and explain only a small fraction (2–5 %) of total cases.”]
It’s been a while since I’ve posted one of these. This is where you share interesting stuff you’ve come across since the last time I posted one of these things (or perhaps it is where you don’t share interesting stuff; the latter is by far the most common decision, after all). I don’t really have anything interesting to share here myself, but I figured I should post something anyway, so… :
I was considering adding this lecture as well, but it’s not a particularly good lecture so that seemed like a bad idea.
A friend of mine recently made me aware of the existence of this resource, which one of two of you may consider to be worth checking out.
The last part had some interesting stuff, but I think I liked some of the chapters in the middle best. There are obvious parallels to be drawn between the coverage in a few of the last chapters and some of the work of Boyd and Richerson, though these guys’ approach and methodology is quite different.
I’ve included some stuff from the last part of the book below. Although I haven’t exactly read the works of a lot of moral philosophers (except perhaps random quotes of theirs – I’ve probably read quite a few of those over the years), I do think that some of the ideas and observations included in this part of the book are ideas and observations which many of them might benefit (/have benefited) from knowing (/more) about.
“The social interactions between two animals depend not only on their individual characteristics (e.g., age, sex, dominance rank, temperament) but also on the history of interactions between them, provided that they possess the capacity for individual recognition, have sufficient memory to remember the outcome of social interactions, and repeatedly meet each other. The two animals can thus be said to have developed a social relationship. This relationship is not directly visible. Observers decide it exists because the history of previous interactions allows them to predict the outcome of subsequent interactions between the same animals […]. Of course, it also allows the animals to predict the actions and responses of the partner with reasonable accuracy. This makes social intercourse much more efficient, obviating the need for thorough reassessment of the partner’s strength and possible other qualities every time they come close, which is why the establishment of relationships is adaptive for the participants. […] Social behavior is about conflict and cooperation, and relationships characterized by only one of these two probably do not exist. Even the most collaborative relationships tend to contain an element of competition — for instance, because collaborators need to decide on how to divide the benefits of their cooperative effort […] social relationships always contain elements of both cooperation and competition.”
“The partners in an established relationship need to communicate about their relative balance of power (i.e., physical strength and social influence) and about the exchange rate of services. The need for some form of communication is clear in even the simplest relationship. For example, individuals can alternate grooming each other and thus provide benefits in terms of hygiene […], tension reduction […], and endorphin release […] By varying the duration and frequency of their own grooming bouts, the partners can express their perceived relative power in the relationship and, through refusals of grooming invitations or variations in length, negotiate the actual power balance. Communication about the relationship is all the more important because the partners’ values change all the time. Individual qualities, such as strength or experience, change over time, as do their needs for services. External factors—for instance, group composition—may change the value of a partner because they affect the number of other group members who can offer the same service [these effects are termed ‘market effects’ in the literature] […] Changing assessments can be communicated by ceasing to support or share, by taking larger shares than before, or even by punishing partners after they failed to reciprocate […] Communication before engaging in the interaction […] is critical when interactions involve high risks, especially when the partners do not have reliable relationships. Agonistic support between males is a prime example because it involves high risks and because male alliances are fickle.”
“Given the dynamic nature of relationships, it is critical for one or both partners to establish whether the conflict signifies a growing mismatch in the assessments of each other’s value or whether it is a mere hiccup in an otherwise unchanged relationship. We believe this is why reconciliation evolved […] Reconciliation can be viewed as communication about the value of the relationship: it shows how much each partner is interested in the relationship and thereby is willing to repair it after the disturbance due to the conflict. According to this view, reconciliation is not only an effective way to end the conflict but is also a primary tool for relationship management […] The most important generalization to emerge from two decades of work on reconciliation (i.e., post-conflict friendly reunion between opponents) in primates is that individuals that reconcile are likely to have a strong social bond (de Waal, Chapter 2; Cords & Aureli, Chapter 9).”
“In primates, the benefits [of relationships] include selective tolerance around resources […], cooperative hunting […], food sharing […], services for mating privileges […], agonistic support, and protection against harassment. The last two are probably the most widespread and critical benefits related to relationship-dependent cooperation in primates. […] A coalition takes place when individuals support one another in an agonistic conflict […] An alliance is a type of relationship in which the two partners repeatedly form coalitions. Thus, coalitions are interactions that can be formed on a case-by-case basis, whereas alliances are enduring cooperative relationships […] The basic rule for coalitions and alliances is simple: they should be formed when they improve access to limiting resources for both partners […] The limiting resources are usually different for the two sexes because the fitness of males and females is limited by very different factors […] Male mammals […] usually contribute little to the development of the young. […] females usually compete for food or shelter, whereas males compete for mating opportunities (Emlen & Oring 1977).”
“Some of the most significant threats faced by female primates are social ones, in particular, sexual harassment and infanticide by males. Protective bonds between females, and especially those between males and females, may serve to reduce these social threats […] Species with lactational amenorrhea are vulnerable to infanticide by males unlikely to have fathered the infant, because this will speed up the female’s next conception. Many primates have lactational amenorrhea; male infanticide is reported for a remarkably high proportion of primate species […]. Yet male infanticide is rare in most of the species in which it occurs. Perhaps this is because of effective social counterstrategies […] Associations and social relationships can often be seen as strategies to reduce the negative impact of some challenge. Paradoxically, the selective forces that produced particular social behavior are often hard to discern because the behavior it has produced is effective in eliminating the fitness impact of these ultimate causes. Hence, their action is rarely apparent.”
“Among primate males, strong bonds to maintain alliances are expected to serve to improve mating access to females, and indeed they do. However, they are less common and shorter-lived than those among females […]. In various primate species, only a single male stays in a group of females, preventing the establishment of male bonds. But even in the all-male bands commonly found in these species […] or in many species with multimale groups, male bonds are not pervasive. The reasons for this are largely speculative at this stage. […] Most examples of male-female alliances are from species with limited sexual dimorphism, in which males and females can potentially provide mutual agonistic support.”
“When a group is faced with external threats, relationships within the group and with allies increase in importance. Group pressure is exerted on disputants to reconcile conflicts that threaten valued defensive alliances or solidarity. […] in-group/out-group distinctions are also a very salient dimension of nonhuman primate interactions.”
“we make two fundamental assertions regarding the evolution of morality: (1) there are specific types of behavior demonstrated by both human and nonhuman primates that hint at a shared evolutionary background to morality; and (2) there are theoretical and actual connections between morality and conflict resolution in both nonhuman primates and human development. […] the transition from nonmoral or premoral to moral is more gradual than commonly assumed. No magic point appears in either evolutionary history or human development at which morality suddenly comes into existence. In both early childhood and in animals closely related to us, we can recognize behaviors (and, in the case of children, judgments) that are essential building blocks of the morality of the human adult. […] The obvious common ground between current evolutionary and developmental approaches is that, instead of looking at human morality as coming from the outside — imposed by adults on the passive child, or imposed by culture on a fundamentally nasty human nature — it is generated from the inside. What we mean by “inside” is not that things happen in isolation from outside influences: evolution operates on the basis of ecological pressures, which come from the outside, and development takes place in constant interplay with the outside world. What we mean instead is that the decision making and emotions underlying moral judgments are generated within the individual rather than being simply imposed by society. They are a product of evolution, an integrated part of the human genetic makeup, that makes the child construct a moral perspective through interactions with other members of its species. […] Much research has shown that children acquire morality through a social-cognitive process; children make connections between acts and consequences. Through a gradual process, children develop concepts of justice, fairness, and equality, and they apply these concepts to concrete everyday situations (Killen & Hart 1995).”
“From our perspective, we assert that emotions such as empathy and sympathy provide an experiential basis by which children construct moral judgments. Emotional reactions from others, such as distress or crying, provide experiential information that children use to judge whether an act is right or wrong […] when a child hits another child, a crying response provides emotional information about the nature of the act, and this information enables the child, in part, to determine whether and why the transgression is wrong. Therefore, recognizing signs of distress in another person may be a basic requirement of the moral judgment process. The fact that responses to distress in another have been documented both in infancy and in the nonhuman primate literature provides initial support for the idea that these types of moral-like experiences are common to children and nonhuman primates. As an illustration, de Waal (1996) documents reactions to distressed individuals and the tendency to share food with others. Generally, it seems that our closest relatives, the great apes, go further in this regard than more distantly related primates, such as the monkeys. For example, “consolation” has thus far been demonstrated only in chimpanzees despite systematic attempts to find it in monkeys. Consolation is defined as friendly or reassuring contact provided by a bystander to a recipient of aggression […]. In the chimpanzee, this kind of interaction typically consists of putting an arm around the victim or patting him or her gently on the back or shoulder. Because of the contrast between monkeys and apes in this regard, de Waal & Aureli (1996) have recently speculated that consolation may require empathy. Since higher forms of empathy and sympathy require the ability to take someone else’s perspective, the difference may result from Hominoids (i.e., humans and apes) possessing this ability but not monkeys.”
“No biologist and few social scientists would deny that our species has natural aggressive potentials, but we possess many other natural tendencies as well, some of which serve to keep aggression in check. Thus, to call us naturally peaceful (which is, after all, a state observed far more often than war and strife) would be at least as justified as calling us naturally aggressive.”
“the “ought” question, which has occupied moral philosophers over the ages, may reach all the way back to rather mundane mechanisms of how to get along and when to repair relationships.”
I finished the book today. I wrote a brief review of the book on goodreads and gave it three stars. Many things covered in this book I’ve read about in detail elsewhere, e.g. in Sperling et al., Edwards et al., or, say, Eckel et al, but there was some new stuff in here as well. I really liked the first chapter, about ‘The Vascular Endothelium in Diabetes’; it covered some stuff which I’d never really gotten to the bottom of before (but due to the technical nature of that chapter I decided against covering it here). There are still a lot of details which I will not claim to fully understand, but I understand some of the main principles/mechanisms much better than I did. The book was occasionally difficult for me to read because it required knowledge about areas about which I didn’t know a great deal (e.g. haematology), and you should certainly not read this book if you don’t read more or less fluent medical textbook (“The focus of this book is to assist the physician or surgeon in preventing and managing CVD and CVD risk in diabetic patients”). As I pointed out in my goodreads review, the book was difficult for me to read for another reason as well. Authors of academic books should not use acronyms which they do not explain to the reader. Authors of such books should not explain unexplained acronyms five pages after they have used them for the first time. If they do, people might get angry at them.
I’m sure some people don’t care about such things, but this is the sort of stuff that can really piss me off, and it’s part of the reason why this book got three stars. Combining behaviour like that with some formatting errors and a few sentences which don’t make any sense because nobody seems to have proofread the damn thing, and you can end up with an academic publication which looks amateurish, even if it’s most certainly nothing of the sort. In terms of the formatting errors I will note that this is not the first Wiley-Blackwell publication like this I’ve seen – as I point out in my review of that book, the Edwards et al publication to which I link above had similar problems. It’s much rarer, I think, to see stuff like that in Springer publications.
I have added some observations from the book below. I plan to write another post about the book later on as I don’t think it’s fair to only give this book one post, considering how much stuff is in there. When I started out writing this post I was thinking that I’d make the quotes easier to read by adding relevant links where they might help. I realized quite fast that adding enough links to actually make a huge difference would most certainly not be worth it, though I have added a link here and there anyway in order to make the post more readable. I have also added a few bold sections below – I don’t like writing long posts and then have people not reading them because they’re long, so if you don’t particularly care about the topic covered below you might want to read the bolded parts in order to at least learn something from the post. There’s a lot more stuff about type 2 diabetes than about type 1 in this book, so when reading ‘diabetes’ below you should probably just think ‘type 2’.
I remember recently reading an article somewhere stating that there are many errors in medicine-related wikipedia articles and how that’s a problem, and I actually encountered an example of this while reading the book, though I can’t now remember which article it was. You should take it for granted that wiki articles to which I link in posts like these may have errors and inaccuracies (they may actually contain statements which are contradicted by the material covered in the book…), and I usually only link to them in posts like these to ‘translate’ the terms used without having to add a lot of additional text to the post in question. I’ll often not have read the articles to which I link when I link to as many as I do in this post, and a link to an article does not mean that I think all the stuff included in the article is correct. Okay, on to the book coverage:
“There is no doubt that diabetes is a significant contributor to the global burden of chronic non-communicable disease which accounts for over 36 million (63%) of deaths worldwide. Importantly, 80% of these deaths occur in low and middle income countries. [here’s a link to the source, the data above is from page 16. Note that “17.3 million (30%) [of all 57 million deaths worldwide] were due to CVDs.”] […] In an important contribution from the Global Burden of Metabolic Risk Factor of Chronic Disease Collaborating Group  national, regional and global trends in fasting plasma glucose and diabetes prevalence since 1980 were studied in a systematic analysis of health examination surveys involving over two and a half million participants and 370 country-years observations. They estimated that the number of people with diabetes increased from 153 (95% uncertainty interval 127–182) million in 1980 to 347 (314382) million in 2008 . [I included the quote partly because those numbers are interesting, partly because this quote from the introduction contains a good example of the kind of sloppiness I mention in the goodreads review; that last parenthesis was surely meant to say 314-382. But it doesn’t. And those kinds of small errors are all over the place.] […] In addition to increased risk of CVD patients with diabetes and established vascular disease have a poorer outcome than those without diabetes [7, 8]. Peripheral arterial disease is increased 2-4 fold in the diabetic population and lower limb amputations are at least 10 fold more common such that half of non-traumatic amputations are performed in diabetic patients [3, 7, 8].”
“a mean duration of diabetes of about a decade appears to confer an equivalent risk of CVD to a prior history of MI. In addition, recent work has shown that a history of DM results in six years of life years lost, mostly from CVD . […] 20% of all vascular events occur in patients without any traditional risk factors, necessitating the need for more precise clinical tools that aid clinicians in identifying those at highest risk . To help achieve this goal, there is growing interest in the development and exploitation of new biomarkers. […] A biomarker was defined by a National Institutes of Health (NIH) working group as “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention” . […] A biomarker should meet several criteria to be deemed clinically useful. This is structured around three fundamental questions : 1 Is the biomarker measurable? 2 Does the biomarker add new information? 3 Will the biomarker help the clinician to manage patients? Additional criteria include cost-effectiveness, safety, and replication of the biomarker in clinical scenarios. […] [Reclassification] is a relatively new concept, but potentially the most clinically relevant [of four criteria covered] as it assesses the ability of a test to reclassify individuals correctly into a different risk category; for example, an intermediate-risk subject into a high-risk subject, or a low-risk subject into an intermediate-risk subject […] The ability of the new test to achieve reclassification can be statistically examined by net reclassification improvement (NRI) or integrated discrimination improvement (IDI). The NRI method, which is determined by the proportion of individuals whose risk is correctly escalated or de-escalated, is more useful in primary prevention, where well-accepted categories of risk exist. The IDI estimates the change in predicted probability of an outcome between those with and without the outcome after the biomarker is added to the prediction model. The larger the value of the NRI or the IDI, the better the biomarker.”
Quite a few biomarkers are covered in the chapter, but I’d rather not talk too much about that stuff. There are various types of circulating biomarkers, imaging biomarkers and genetic biomarkers. A few have been included in national guidelines and the only class which does not seem to be useful in this context is the genetic one [“The AHA has given genomic testing in risk assessment in asymptomatic adults a Class III recommendation (no benefit)”]. Naturally reasons besides those related to assessing cardiovascular risk exist for doing genetic testing on diabetics, but if such tests are not useful in that respect then of course that limits their potential somewhat. Incidentally many biomarkers they talk about seem to measure similar things, meaning that adding them together don’t add a lot of information:
“It is logical to assume that if one biomarker measure gives a small incremental gain in risk prediction, multiple biomarkers would result in a larger one. However, trials of multiple biomarkers have disappointingly only shown at best a moderate improvement in usefulness when compared to standard risk factors .”
The biomarkers are assumed to hold most promise in the context of primary prevention, but “there is scant data on cost-effectiveness or differential benefit from specific treatments”. Okay, on to other stuff:
“Diabetic kidney disease […] is a clinical diagnosis and is defined by the presence of albuminuria, often with associated abnormal kidney function (an increase in creatinine or a decrease in creatinine clearance or estimated glomerular filtration rate [eGFR]) […] Diabetic nephropathy is a histological diagnosis, characterized by typical histopathological features including mesangial expansion, glomerular basement membrane thickening, and glomerulosclerosis with Kimmelstiel–Wilson lesions. Diabetic kidney disease is most commonly caused by diabetic nephropathy, but other kidney pathologies may be present […] Diabetic kidney disease is a chronic complication of diabetes and affects approximately one third of all diabetic patients [1, 2]. It is the most common cause of kidney failure requiring renal replacement therapy in Western countries  and can occur in both type 1 and type 2 diabetes with equivalent risks . The natural history and prognosis of diabetic kidney disease differ somewhat based on the type of diabetes and whether microalbuminuria is present […] In people with type 1 diabetes who have microalbuminuria, if left untreated, approximately 80% will develop macroalbuminuria (also called overt nephropathy) within 6–14 years [6, 7]. Subsequently, half of these will develop end-stage kidney disease (ESKD) over 10 years if there is still a lack of specific intervention. In contrast, approximately 20–40% of people with type 2 diabetes and microalbuminuria develop macroalbuminuria without intervention, and ESKD has been reported to develop in 20% of patients with overt nephropathy within 20 years . Some of these differences may relate to the older age and greater burden of comorbidity experienced by people with type 2 diabetes for a given duration of diabetes, meaning that more of them will die of cardiovascular and other complications before developing kidney disease.”
“Diabetic kidney disease has a heterogeneous presentation. Early stages are often asymptomatic and only detected by abnormal laboratory tests (albuminuria and changes in GFR). Albuminuria is one of the earliest detectable features of diabetic kidney disease […] As diabetes manifests as a systemic disease, patients with type 1 DM almost always have other signs of diabetic microvascular complications, such as retinopathy and neuropathy. Diabetic retinopathy usually precedes the onset of overt nephropathy, while the relationship between diabetic kidney disease and retinopathy is less predictable in type 2 diabetes. […] For people with type 1 diabetes, approximately 20–30% will have microalbuminuria after a mean duration of diabetes of 15 years [37, 38]. Similarly, 25% of individuals with type 2 diabetes have microalbuminuria after 10 years […] Proteinuria and abnormal kidney function are independent risk factors for renal outcomes in diabetes . […] As with treatment strategies for end-stage kidney disease secondary to other causes, dialysis and renal transplantation are both options for treatment for ESKD caused by diabetes. Lower survival rates have been observed for people with ESKD caused by diabetic kidney disease, with five years’ survival of 30%, according to USRDS data.”
“Cardiovascular disease (CVD) including coronary heart disease (CHD) is the major cause of mortality in patients with diabetes […] no more than 25% of the excess CHD risk in diabetes can be accounted for by established risk factors […] Hyperglycemia as a risk factor for CVD has been established for many years. Mortality from CVD accounts for more than 60% of deaths in patients with type 2 diabetes mellitus and clearly accounts for this ultimate complication of diabetes [3, 8]. The association between differing degrees of hyperglycemia and CVD risk has been an area of debate. The United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that the incidence of myocardial infarction rose by 14% per 1% rise in HBA1c . This is in line with other studies showing that glucose is a continuous risk factor in people with both type 1 and type 2 diabetes. […] There is also evidence that glucose fluctuations (the highs and lows) are associated with increased oxidative stress […] Increased oxidative stress results from an imbalance between oxidant production and antioxidant defenses […] Diabetes mellitus, obesity, micro- and macrovascular complications have been consistently associated with increased oxidative stress [37, 38, 39] and several studies have demonstrated that hyperglycemia per se is associated with increased oxidative stress [39, 40]. […] Hypoglycemia is also associated with increased cardiovascular mortality [58, 59], although the mechanisms behind this remain unclear. […] As well as being associated with increased oxidative stress , hypoglycemia also has pro-inflammatory effects on the vasculature. […] These changes contribute to a hypercoagulable state associated with increased platelet aggregation and plasma concentrations of coagulation factors […] Acute hypoglycemia has also been associated with long QT syndrome, which is associated with an increased risk of sudden cardiac death .”
“The majority of people with type 2 DM [diabetes mellitus] are hypertensives […] There is no question about the need to treat hypertension in either the primary prevention or secondary prevention settings for cerebrovascular disease, irrespective of the presence of diabetes. A systematic review of the effects of different BP-lowering drug regimens in people with hypertension, diabetes, or vascular disease found that the relative risks of stroke and other major vascular outcomes were proportional to the BP reduction achieved . […] there is a general consensus that ACE inhibitors or ARB are the first-line drugs of choice in both diabetes and metabolic syndrome. In primary prevention, the only question is the level of BP above which treatment is indicated. […] The recommended threshold for treatment in primary prevention is currently under discussion in both diabetics and nondiabetics. […] there is increasing uncertainty about the use of absolute thresholds of BP to determine the need for treatment […] Although “lower should be better,” the results of recent clinical trials examining the benefits of normalizing risk-factor levels have been counter-intuitive and, sometimes, disconcerting, and have called into question this belief […] Many hypertensive patients in clinical practice receive more than one antihypertensive drug, and the use of combination therapy is widely recommended in hypertension guidelines. Combinations may be especially important for patients with diabetes, for whom recommended BP targets are challenging.”
As I have already mentioned, I really liked this book. Below I have covered some of the parts of the book which I have not yet talked about here on the blog, and in particular I’ve included stuff about how plants and animals cooperate with each other. I have of course had to leave a lot of stuff out.
“The lack of mobility in plants creates a physical obstacle in the dispersal of their genes. In a majority of all plants, this obstacle has been alleviated through the formation of mutualisms with animals that transport pollen grains between stigmas and also disperse seeds. In the case of pollination, the goal for the plant is to receive pollen on its stigma and to have pollen picked up and deposited on conspecific stigmas of other plants. The animal most commonly seeks a food reward. It is important to appreciate that mutualisms such as these represent reciprocal exploitation with an underlying evolutionary conflict. Selection in mutualisms favours selfish behaviour […] One manifestation of such selection […] is the widespread phenomenon of plant species that no longer reward pollinators but instead attract visitors by deception. […] Non-rewarding plants species constitute a substantial portion of all angiosperms, especially among orchids, but they are mostly minor components of the plant community in which they grow. […] Likewise, many flower-visitors (if not most) do not contribute to pollination but do remove floral resources such as nectar and pollen. […] A fair number of plants mimic not flowers but rather pollinator mates or oviposition sites. Flowers of the well-studied European fly orchids (Ophrys) and caladeniine Australian hammer orchids provide visual, olfactory and tactile cues mistaken by naïve wasp males for conspecific females (Stowe 1988), and pollination happens as males attempt copulation with the flowers.” [This sentence made me laugh!]
“pollination mutualisms evolve amid simultaneous antagonistic interactions; the plant is under selection to maximize the net fitness of attracting potentil mutualists at the lowest net cost while minimizing the detrimental effects of non-mutualists or low-quality mutualists. This tradeoff does not exist in antagonistic interactions […] Floral traits are likely to be as much the result of selection for avoidance of some animals as for attraction of others. […] The vast majority of all extant pollination mutualisms […] involve flowering plants, which dominate most biota on earth today.”
“Given that the benefit to plants of animals as pollen vectors is transport across longer distances, it is not surprising that the three extant groups of animals that have evolved flight – insects, birds and bats – contain a very large proportion of all pollinators. Among the insects, flower-visiting species are particularly frequent within the large orders Hymenoptera (bees and wasps), Lepidoptera (moths and butterflies), Diptera (flies) and Coleoptera (bettles). […] The Lepidoptera alone, whose coiling tongues make them flower specialists and effective consumers of nectar, constitute 11% of all described species on Earth […] Among birds, six phylogenetically independent groups have diversified as flower-visitors and often as pollinators […] Together these groups constitute over 10% of all recognized bird species. […] Flowers offer an extraordinary range of shapes, colours and scents, reflecting high rates of evolutionary change in these traits. […] Almost any flower part or even adjacent leaves are modified for the purpose of attracting pollinators. There is arguably more plasticity in these secondary reproductive traits in plants than in any other organismal groups, with the possible exception of birds.”
“Specificity among visitors is a necessity for effective pollination; if animals visit flowers of different species indiscriminately, heterospecific pollen transfer will result, which reduces the probability of pollen reaching a conspecific stigma […] The number of plant species visited varies greatly among flower-visiting species. […] Individual visitors often tend to specialize on a subset of potential flowers during any one foraging bout; in bees perhaps 90% of all visits may be made to a given species, with occasional visits to other species. This short-term specialization is referred to as floral constancy. The dominant flower may vary among simultaneously foraging conspecifics, and within individual visitors on successive foraging bouts. Reasons for such short-term selectivity have been explored in insects, and focus on the effects of foraging rate as a result of memory constraints. Insects must learn by trial and error how to effectively access a reward such as nectar in more complex flowers, as the rewards are concealed and most quickly accessed using a particular approach. Minimum handling time may be approached only after as many as 100 visits to a given zygomorphic flower […] visitors may be unable to keep more than one sensorimotor protocol in active memory, thus making it a superior strategy to focus on one food source at a time […] Specialization is often not in the evolutionary interest of a flower-visiting animal, as its ultimate interest is to optimize the reward harvesting rate over time. A foraging pattern that maximizes the harvesting rate of commodities such as nectar and pollen can include two or more coexisting plant species, especially if their floral structure is fairly similar so that the visitor can use a single visit behaviour protocol. […] The vast majority of all plants are pollinated by two or more species”
“With the […] exception of ants […], invertebrates play only an anecdotal role as seed-dispersers […] All major lineages of vertebrates take part in fruit consumption and seed dispersal, but their importance as dispersal agents is very unequal. Birds and mammals are the only or main dispersers of the vast majority of vertebrate-dispersed plants […] About 36% of 135 extant families of terrestrial birds, and 20% of 107 families of non-marine mammals, are partly or predominately frugivorous […] Fruit consumption by vertebrate dispersers […] has selected for fruit traits that enhance detectability by frugivores […] Although exceptions abound, fruits that are green or otherwise dull-coloured when ripe tends to be associated with seed dispersal by mammals, whereas fruits dispersed by birds tend to be brightly pigmented. The partial dichotomy between ‘bright’ and ‘dull’ ripe fruits has probably been selected for by the contrasting sensory capacities of birds and mammals […] Size is an important attribute of fruits, because it sets limits to ingestion by relatively small-sized dispersers that swallow them whole, like birds. […] Fruits eaten by mammals tend to be larger than those eaten by birds […] Fruit pulp is the reward offered by plants to dispersers, and its nutritional value is a critical element in the plant-disperser interaction. Compared to other biological materials, fruit pulp is characterized, on average, by high water and carbohydrate content, and low protein and lipid content. […] the occurence of secondary metabolites within ripe pulp presumably represents a tradeoff with respect to defence from damaging agents and palatability for dispersers […] A number of studies provide unequivocal support for the ‘palatability-defence tradeoff hypothesis’. […] increased frugivory is quite often associated with increased intestinal length, as an adaptive response for increasing intestinal absorption of the water-diluted nutrients in fruit juice. […] Most fruits are very deficient in nitrogen, which perhaps represents the most important nutritional constraint that frugivorous animals must cope with. Regular ingestion of small amounts of animal food seems to be the commonest way of complementing the poor protein intake associated with frugivory.”
“Abundance of fruit varies markedly among years and seasons, and within as well as between habitats, which generally leads to patchy and unpredictable distributions in time and space […] A distinct suite of behavioural and physiological traits allow frugivores to withstand or escape from temporary situations of fruit scarcity and efficiently locate unpredictable fruit sources. Seasonal migration and habitat shifts are the two most common generalized responses of frugivores to fluctuations in fruit availability. […] Plant-vertebrate dispersal systems are characterized not only by the absence of obligate partnershipts, but also by weak mutual dependence between species of plants and animals, and by the prevalence of unspecific relationships. […] the general picture is one of loose interdependence between species of plants and species of dispersers. […] pollen and seed dispersal by animals are fundamentally dissimilar […], and their differences have manifold evolutionary implications. The two most important distinctions are (i) that a definite target exists for dispersing pollen grains (the conspecific stigma) but not for dispersing seeds; and (ii) that the plant can control pollinators movements by providing incentives at the target site (nectar, pollen), but there are no similar incentives for seed dispersers to drop seeds in appropriate places. These differences are best framed in terms of the departure-related versus arrival-related advantages of dispersal [You can say that seed-dispersal systems work on the basis of ‘advance payment’ alone, whereas pollen dispersal mechanisms also include ‘payment upon delivery’ aspects].”
Finally, ants! Ants are awesome…
“Ants are one of the most abundant, diverse and ecologically dominant animal groups in the world. They make up from 10 to 15% of the entire animal biomass in many habitats, and in the Amazonian rainforest, for example, one hectare of soil may contain 8 million individuals. The impact of ants on the terrestrial environment is correspondingly great. In most habitats they are among the leading predators of other insects and small invertebrates, and in some environments they are the principal herbivores and seed predators. Ants can alter their physical environment profoundly, moving more soil than earthworms, and being major channellers of energy and cyclers of nutrients. […] It is probably fair to say that no other animal group interacts with plants in such diverse ways. Indeed, the fact that ants are the only specific taxa mentioned in the chapter headings of this book reflects their ecological importance in the lives of most plant species. Ants can protect plants directly from herbivores or from competition with other plants. They can also affect plant-community composition and dynamics by selective weeding or ‘gardening’, altering nutrient availability, pollinating flowers, or dispersing and harvesting seeds. Plants provide ants with food and shelter […]. Some relationships between ants and plants appear to be highly coevolved mutualisms and it is these interactions that have received the most study. But the majority of ant and plant species interact in more generalized ways, often through the influence of ants on the chemical and physical properties of soil. […] The oldest ant species, Sphecomyrma freyi, has been dated from amber to be about 80 million years old. [….] there is evidence that ants have been both remarkably diverse and ecologically successful for at least 50 million years”
“Cultivation of fungus by attine ants originated about 50 million years ago. The relationship between the higher attine ants and the symbiotic fungus they cultivate is obligate. Foundress queens propagate the fungus clonally by carrying a pellet of fungus in their mouths during their nuptial flight to establish new colonies. […] The relationship between the attines and their fungus has been termed an ‘unholy alliance’ because it combines the ants’ ability to circumvent plants’ anti-fungal defences with the ability of the fungus to subvert plants’ anti-insect defences. The ants benefit because the fungus breaks down plant tissue such as cellulose, starch and xylan, and possibly detoxifies insecticidal plant compounds. The fungus thus enable them to make use of plant material that would otherwise be unavailable and allows the ants to be truly polyphagous in the midst of diverse flora. […] the relationship between the ants and the fungus has recently been found to be a triumvirate, with evidence that an antibiotic-producing bacterium is an important component of the symbiosis. […] fungus gardens are particularly prone to infection by a group of closely related, highly specialized parasites in the fungal genus Escovopsis. […] Escovopsis is found in gardens of virtually all species of fungus-growing ants, but not elsewhere. The parasite is usually found at low levels, but if the health of the garden is compromised it can quickly take over and destroy the fungal crop. In healthy gardens, Currie et al. (1999) have shown that the fungus is kept in check by specific antibiotics produced by Streptomyces bacteria living on the bodies of the ants […] The bacterium can also promote the growth of the cultivated fungi. The position of the bacterium on the ant integument is genus-specific, indicating that the association with the ants is both highly evolved and of ancient origin […] Attine symbiosis appears to be a coevolutionary arms race between the garden parasite Escovopsis on the one hand, and the tripartite association of the actinomycete, the ant hosts and the fungus on the other. The relationship raises the interesting question of how the attine antibiotics have remained effective against the fungus-garden pathogens for such a long time, given that resistance to antibiotics is a well known problem in human and other populations.”
“The coevolution of ants and plants involving systems of rewards and services has resulted in a variety of elaborate and complex mutualistic interactions collectively known as ant-guard systems. Here the rewards are extra-floral nectar, specialized food bodies and nest sites, while the service is the protection of the plants from herbivory. […] Plant structures known as domatia are developmentally determined and appear to be specific adaptions for ant occupation. They are often formed by the hypertrophy of internal tissue at particular locations in the plant, creating internal cavities attractive to ants […] the plant species that bear them are known as myrmecophytes. […] Some myrmecophytes are actually ‘fed’ by the ants they house. Experiments have shown that two genera in the family Rubiaceae […] absorb nutrients from the wastes of the Iridomyrmex colonies they house in tunnels inside large tubers […] A variety of field studies have shown there is strong competition among ants for dormatia […] Ant-guard systems involving extra-floral nectaries are often complicated by the presence of Homoptera or lepidopteran larvae that secrete nectar-like fluids collectively known as honeydew. In such situations, the ants have a choice of food and the outcome of these three-way interactions between plants, ants and herbivores appears to be extremely variable. The Homoptera include herbivores such as aphids, leafhoppers, scale insects and coccids. Each animal is armed with a proboscis that penetrates plant vascular tissue, tapping into the nutrient supply. With little apparent effort, the sap enters the front end of the homopteran gut, later appearing at the back end as droplets, somewhat depleted in quality but still containing many nutrients, where it is ejected as honeydew. Many ant species harvest the honeydew and, in return, protect the homopterans from predators and parasites […] As a result, ant activity can increase levels of herbivory as well as other forms of damage […] Ant interactions with plant species that produce extra-floral nectaries, food bodies and domatia have evolved both in the presence of homopterans and lepidopteran larvae and the ant behaviour that protects them. For example, homopterans of various kinds are routinely maintained within domatia and they frequently feed on plants that bear extra-floral nectaries. This leads to the situation where plants are providing rewards for ant-guards that attack some of the plant’s enemies but protect others. A solution to this apparent conflict of interest was first proposed by Janzen (1979) who suggested that the presence of homopterans was part of the cost of the ant-guard system […] The evoluation of extra-floral nectaries has itself been viewed as a defence against homopteran attack, weaning ants away from the herbivores […] Homopterans are common herbivores and have been around for a very long time; thus, given their ubiquity, selection for extra-floral nectaries may have resulted in the plants exerting greater control over the ant-guards, provided ants preferred nectar to honeydew.”
When it’s easy for me to blog a novel and it makes sense to do it because it has a lot of quoteworthy stuff, I can justify doing it here. This blog is perhaps a little dry at times.
I’ve given Fforde’s book five stars on goodreads, just like the four previous books I’ve read by him. I pointed out in a brief review on goodreads that perhaps I should stop giving all of his books five stars, but as long as they keep being awesome I’ll keep giving them that rating. And this stuff is awesome. It’s also a bit silly, but that’s the price you pay. I saw many of the major plot-developments coming, but even so it was a very entertaining read.
I have added some quotes from the book below – I don’t think there are any spoilers in the stuff I have included:
“I opened a small parcel that contained a copy of the third book in my series: The Well of Lost Plots. I showed it to Landen, who pulled a face. ‘Are they still selling?’ ‘Unfortunately.'”
“Since I’d made it into print I’d been naturally curious about meeting the fictional me”
“‘I’m barely eighty-two,’ she said indignantly, ‘I’m not on the scrapheap yet. […] I’ve got a few friends coming around, and after we’ve discussed who is the most unwell, we’ll agree voluably with one another about the sorry state of the nation and then put it all to rights with poorly thought-out and totally impractical ideas.” [that passage reminded me of this]
“we are finding that more and more minor classics and a lot of general fiction are going for long periods of time without even being opened. Because of this, Text Grand Central are worried that bored characters in lesser books might try and move to more popular novels for work, which will doubtless cause friction.’
We were all silent. The inference was not lost on any of us – the fictional characters in the BookWorld could be a jittery bunch and it didn’t take much to set off a riot. […] The last thing we need right now is a band of disgruntled bookpeople besieging the Council of Genres, demanding the right to be read.”
“the Health and Safety Inspectorate are coming in to make sure we’re up to speed.’
‘On safety procedures?’
‘Good Lord, no! On how to fill the forms in properly.'”
“A chunk of burning Camembert on your doorstep meant only one thing – a warning from the Swindon Old Town Cheese Mafia”
“‘You’ll forgive me for saying this,’ said Webastow, looking over his spectacles, ‘but this is the most hare-brained piece of unadulterated stupidity that any government has ever undertaken anywhere.’
‘Thank you very much, replied Ms Yogert courteously. ‘I’ll make sure your compliments are forwarded to Mr Van de Poste.'”
“The young girl came and sat down next to me. She patted my hand reassuringly.
‘I didn’t want to be rescued anyway,’ she announced. ‘If I survive, the whole point of the poem is lost – Henry will be furious.’
‘Don’t worry,’ I said, ‘it’ll all be repaired.’
‘And everyone keeps on giving me their jackets,’ she continued in a huffy tone. ‘Honestly, it gets harder and harder to freeze to death these days.'”
“We were standing in the opening chapter of The Eyre Affair, or at least, the refurbished first chapter.”
“there was room on the hangar floor for not only Darcy’s country home of Pemberley, but also Rosings, Netherfield and Longbourn as well. They had all been hoisted from the book by a massive overhead crane so the empty husk of the novel could be checked for fatigue cracks before being fumigated for nesting grammasites and repainted. At the same time an army of technicians, plasterers, painters, chippies and so forth were crawling over the houses, locations, props, furnishings and costumes, all of which had to be removed for checking and maintenance.”
I took a short break from this book, but now I’ve started reading it again and I’ll probably finish it later today. Here’s the first post I wrote about the book. This is not going to be the last post about the book and I still have some chapters to go, so I’ll refrain from passing judgment on it just yet; but I must say that I find the book very interesting, and based on the coverage so far I’d probably give it four stars. It’s a bit too speculative at times, but aside from that it’s really good. People with a ‘science approach’ to life and other stuff may say that ‘we’re just apes’ (or ‘monkeys’, if they’re confused about the terminology), but precisely what this actually implies may even so still not be completely clear to them, because most people probably don’t know a great deal about how, say, chimpanzees behave and live their lives. This book will enlighten you about some of the ways in which common human behavioural patterns have close analogues in other species, and some of the patterns will probably surprise you (…and fascinate you, if you’re like me). We really are quite a bit like those other guys, in ways many of us probably have never even thought about. The book has certainly tempted me to explore the field of ethology in more detail later on.
Before moving on to the main coverage I feel the need to once again (I did this in my first post about the book as well) point out that this book is not in any way a book about strategies for how to make your aggressive colleague back off, or something like that. Quite a few of the chapters of this book are about conflict resolution/conflict management behaviours and strategies seen applied by primates in nature, and none of them are about behavioural strategies applied in the office. You’ll probably gain some valuable insights as to how humans may behave in a conflict setting as well from the book, but how many such insights you’ll take away from the book will surely depend on how confident you feel about extrapolating and drawing inferences from studies conducted on members of species related to us. There’s stuff on humans as well – there was indeed enough of that kind of stuff in the first part of the book for me to have no problem limiting my coverage in the first post about the book to the results of studies on humans alone – but the focus is decidedly different from the focus I imagine people are forced to apply when participating e.g. in anger management classes; this book is a different kettle of fish, this is mainly about understanding why animals behave the way they do, and specifically it is about understanding how they deal with conflict.
I have added some stuff from the book below. There’s a lot of good stuff in this book.
“Displacement activities are behavior patterns (often body care activities) exhibited by an animal that are “apparently irrelevant” to its ongoing activity […] and are thought to occur in situations of motivational conflict. […] displacement activities may be used as a behavioral measure of anxiety […] [Reviewing our results] [t]wo patterns emerge […] First, all group-living species show increased post-conflict affiliation between former opponents; second, all species for which information is available show increased post-conflict displacement activities. Out of four non-primate species studied thus far—the bottlenose dolphin, spotted hyena, domestic goat, and domestic cat—only the last did not show any evidence of post-conflict affiliation between former opponents. Dolphins, hyenas, and goats are all group-living animals that form stable social groups or fission/fusion societies […]. The domestic cat, on the contrary, is an opportunistic species that may aggregate at rich food sources (as seems to be the case for urban stray cats) but probably cannot be considered as a truly social species […]. Accordingly, cats lack the mechanisms of conflict regulation typical of social species […]. The observation of post-conflict affiliation in species as phylogenetically distant as primates, dolphins, hyenas, and goats implies that conflict-regulation mechanisms must have evolved independently several times in association with the rise of social life. Whether group life and the consequent inevitable frictions are invariably linked to the evolution of conflict-regulation mechanisms or whether only a fraction of group-living species have evolved post-conflict conciliatory behaviors is a question that awaits further theoretical […] and empirical studies. […] The observation of conciliatory behaviors in species that differ widely in their cognitive capacities suggests that reconciliation does not require special abilities such as introspection and self-awareness but that good memory and individual recognition probably suffice (see de Waal & Yoshihara 1983). Obviously, stating that high cognitive abilities are not necessary does not imply that they cannot actually be involved in the process of reconciliation, at least in a few species. In other words, it is unlikely that the cognitive mechanisms underlying reconciliation are entirely the same in goats and chimpanzees (Pan troglodytes). Similar functions do not imply similar mechanisms. […] All species for which information is available (several primates, goats, and cats) show an increase in the frequency of displacement activities after a conflict. Furthermore, in both goats and primates reconciliation caused a faster return of displacement activities to their baseline frequency. These results suggest that the post-conflict increase in displacement activities may be a general phenomenon and that one of the functions of post-conflict friendly reunions may be a reduction in the anxiety and arousal experienced by the recipient of aggression (see Aureli & Smucny, Chapter 10). […] cognitive or ecological constraints may […] limit the complexities of the social life of non-primates, but we are certainly very far from having identified such limits.”
“Across the five cultures girls and boys did not differ significantly in their peacemaking tendency […]. However, girls and boys sometimes differed in the acts and gestures they used to make peace. […] Acting silly to make others laugh may be a male strategy […] girls may be especially responsive to clowning by boys. Research in adults has shown that women laugh and smile more often when they are observers rather than actors, especially when the speaker is male (Provine 1993). […] Children classified as acquaintances interact differently than those classified as friends. […] acquaintances engaged in more intense conflicts and were less likely to use conciliatory resolution strategies than friends. The distinction between friends and acquaintances is thus an important one. […] Perhaps the simplest way of explaining [the] results is to suggest that both interactions and relationships matter to young children and that young children’s peacemaking reflects children’s motivation to repair damage to both. Friends may be motivated to protect their existing relationship from damage caused by conflict, whereas nonfriends may be motivated to restore peaceful interaction simply because playing together is more fun than playing alone. […] Our studies [on children] showed that reunions between former opponents generally occurred within the first two minutes after the end of the conflict. This timing is remarkably similar to the timing of post-conflict peacemaking in most nonhuman primate species”
“Tantrums are a common, if not ubiquitous, phenomenon of early childhood. Tantrums also occur in infant and juvenile nonhuman primates […]. Trivers (1985) proposes that tantrums may be a solution to a basic intergenerational conflict: the young benefit by maintaining parental nurturance as long as possible while parents’ inclusive fitness is eventually better served in other ways. When a juvenile primate has a tantrum following maternal rejection (e.g., while being weaned), its mother usually accepts it […]. Historically, the “terrible twos” are the age of weaning in Western culture, as it remains in other cultures to this day. A disposition to have tantrums that develop at an age when weaning occurred over most of human history might well reflect an evolutionary strategy to retain parental attention. […] the majority of post-tantrum reconciliations are initiated by the child. […] The great similarity between children’s temper tantrums and those of young primates, and the similarity in response by the caregiver (initial distancing but eventual affiliation), suggest a shared developmental underpinning of reconciliation.”
“if a conflict-provoking situation arises between two animals and one grooms the other, then aggression may be less likely than when no affiliative behavior is exchanged. One method for evaluating such conflict management is to observe primate groups in contexts known to increase social tension and the potential for aggression. If submission, tension-regulating behavior, and friendly responses increase in such competitive situations, then animals may be attempting to reduce escalation of conflict. Two such contexts have been investigated in primate groups: scheduled feeding and crowding. Scheduled feeding of provisioned groups produces a tense situation in anticipation of competition for food and does elicit attempts to reduce conflict beforehand […]. Crowding produces another situation in which increased competition for space produces a context in which aggression may be reduced through behavioral mechanisms. With respect to crowding, two main questions arise: Does crowding increase aggression, and do animals modify behavior under crowded conditions to reduce the potential for conflict? The answer to both questions is a qualified yes”
“In addition to post-conflict reconciliation (the focus of many chapters in this volume), nonhuman primates also use other, more powerful pre-conflict methods to maintain peace and harmony within their group. They adopt specific strategies to dissipate tension and reduce conflict before it erupts, suggesting that they possess the ability to anticipate these events and plan their behavior accordingly […] it may be naive to expect a simple relationship between density and aggression in primates because primates have complex and flexible social behavior and advanced cognitive abilities. They do not react passively to changing situations, such as increases in density, but may actively change their behavior to cope with adverse situations. […] Results indicate that different species may have unique reactions to short-term crowding and that more than one strategy may be used in response to increased density […] there is evidence that primates adopt different strategies (e.g., inhibition, conflict avoidance, or tension reduction) depending on the duration of crowding, the species studied, and the individual characteristics of the interacting partners (i.e., the age, sex, and kinship of particular dyads). […] Mongoose responses to crowding indicate that species other than primates modify behavior under high density and that the behavioral changes may be adaptive strategies to manage conflict. […] The behavioral reactions of humans to crowding are variable […], but the most common result is an increase in aggression […] and a decrease in affiliative interactions under higher density […] The decrease in social interaction has generally been interpreted as a withdrawal strategy to cope with the increased social stimulation at higher density […]. Remarkably, the pattern of response is quite similar to the conflict-avoidance strategy observed in macaques under short-term crowding […] individuals differ in their responses to crowding. Increased aggression during crowding appears to be more likely in males than in females […] Individual personality traits may also influence reactions to crowding. […] Such differential effects preclude describing a singular human pattern of response to crowding. […] [the results] appear to show some behavioral similarities between humans and other animals. Freedman (1979) argues that we should not assume that the reactions of human and non-human primates to crowding differ until data indicate otherwise.”
“young animals especially are highly motivated to form attachments for their own safety, and when they perceive themselves to be at risk, they react strongly when separated from attachment figures. Although a dramatic protest-despair reaction may be less marked in older individuals whose attachments are less strong […], we think that even among adults there are likely to be detectable signs of distress upon separation, and relief from distress upon reunion, when an individual values its relationship with a particular partner. Indeed, Cubicciotti & Mason (1975) showed such effects in adult titi and squirrel monkey (Saimiri sciureus) pair mates that were separated from each other for only 90 minutes and then reunited. Similarly, adult humans with close relationships often report emotional reactions (such as loneliness, anxiety, or even despair) to physical separation (Feeny 1998). […] Studies of attachment in humans have used mother-infant separations and reunions as a way of assessing the security of the attachment bond. The separation is itself a stressful experience for the infant, and the infant’s response to separation, and especially reunion with the mother, is characteristically different for infants with secure versus ambivalent attachments […]. Analogous results have been reported for nonhuman primates (e.g., Dettling et al. 1998).”
“[We embrace] MacLean’s (1952) view of emotions as brain functions involved in maintaining individual survival. His evolutionary approach to brain anatomy led him to point out that emotions are not uniquely human traits because most of the brain structures involved in emotions are essentially the same in all mammals and perhaps in all vertebrates. Escaping from danger, for example, is a basic survival response for all animals. […] MacLean’s conceptual framework is still at the basis of the current evolutionary view of emotion (LeDoux 1996), and significant advances in neurophysiology have supported this view […] [An] important class of indicators of emotion is self-directed behavior, such as self-touch, self-scratching, and self-grooming. Apart from the hygienic function of self-directed behaviors, recent ethological studies on nonhuman primates have documented their occurrence in situations of uncertainty, social tension, or impending danger […]. Similarly, high levels of self-directed behavior are characteristic of humans experiencing anxiety […] Measures of variation in hormones and neurotransmitters associated with the stress response (e.g., cortisol, norepinephrine) have provided biological support for individual differences in emotional profiles of children, baboons, and macaques […] Behavioral indicators of anxiety […] increase in frequency under […] conditions that are associated with high risk of aggressive conflict. In captive group-living chimpanzees (Pan troglodytes) vocalizations of neighboring groups increase the likelihood of intragroup aggression and, as a consequence, are followed by higher rates of self-scratching”
“Testosterone may influence aggressive tendencies, and serotonin may regulate the threshold and intensity of the behavioral expression of aggression. Individuals with low serotonin levels exhibit impaired impulse control and a low threshold to escalate when facing potential conflict […] Territorial disputes occur naturally in the wild in many species, and when staged in laboratories, they result in marked physiological differences between winners and losers. For example, the levels of hormones associated with the stress response, such as glucocorticoids, are higher in losers than in winners after dyadic confrontations in a variety of species (e.g., swordtail fish, […] guinea pigs […], tree shrews […] In rats (Rattus norvegicus) differences between winners and losers may persist for several hours, even when the two opponents are separated from each other after the encounter […] Interestingly, hostile behavior during marital conflict in otherwise happy human couples produces changes in blood pressure, immunological function, and hormonal concentration typical of the stress response […] Even if overt aggression is reduced by establishing dominance relationships, conflicts of interest are usually not resolved in favor of subordinate individuals. In addition, subordinates have less control over the social environment and are strongly constrained in their actions. Accordingly, dominant and subordinate individuals differ in their physiological states […] evidence from different sources supports the view that reconciliation has an emotional impact by reducing post-conflict anxiety. […] there is now evidence from a number of different species that many of the most common vocalizations given by nonhuman primates function to initiate and facilitate social interactions. Playback experiments with adult female baboons have demonstrated that vocalizations also serve to diminish the strength of recipients’ responses to former aggressors’ potentially threatening behavior. Most important, apparently reconciliatory vocalizations influence recipients’ willingness to approach and be approached by former aggressors.”
“The tendency of human beings to respond with distress to the end of a close relationship is a consistent phenomenon across different cultures and across the age span […]. Recent social psychology studies have concluded that threats to social bonds are a primary source of anxiety […] and that social exclusion is probably the most common cause of anxiety […]. Behavioral and physiological responses to the disturbance and restoration of social relationships emerge early in life. These responses have been extensively studied in nonhuman primates through experimental manipulations of the mother-infant relationship […] disturbance through experimental separation provokes strong responses, such as increased plasma cortisol and heart rate, in the infant and the mother; reunions of mothers with their infants restore their physiological responses to baseline [in both nonhuman primates and rodents] […]. Similar physiological changes also are found when adults of established pairs of the monogamous titi monkeys (Callicebus moloch) are separated from each other […], suggesting that the disruption of strong bonds has similar effects throughout the life span. […] The marked stress response normally evoked by stimuli, such as exposure to novel environments or objects, exposure to naturally occurring predators (e.g., snakes), or separation of infants from their mothers, is buffered by the presence of familiar conspecifics”
“The mediation of reunions and other forms of conflict resolution does not need to involve only “negative” emotions, such as anxiety, fear, or distress. Conflict resolution often occurs through affiliative contacts that are likely to be associated with positive sensations. Gentle touching causes relaxation and a reduction in heart rate in humans, rhesus monkeys, and horses […] Allogrooming in monkeys decreases heart rate […] Although the actions of endogenous brain opioids affect and are affected by several hormones and neurotransmitters, their involvement in mother-infant attachment and separation distress is certain […]. The experience of separation distress likely provides the basic motivation for social reunion, and the subsequent opioid release alleviates separation distress, replacing it with positive sensations. This is probably also true for relationships between adults. For example, adult talapoin monkeys (Miopithecus talapoin) that have been socially isolated show a significant increase in brain opioids following affiliative behavior with their peers upon reunion […] The perspective of emotional mediation of social processes, including conflict resolution, does not require the identification of specific humanlike emotions, especially when the conscious feeling is not considered. It is only necessary to characterize the conditions (e.g., post-escalation relationship disturbance), the various changes (e.g., increased self-scratching), and the factors affecting them (e.g., relationship quality). […] this perspective can explain the effects of relationship quality on reconciliation without necessarily implying conscious knowledge of relationship value.”
This is a Wiley-Blackwell publication about human nutrition. It is also perhaps the strangest W-B publication I’ve ever read, because of the combination of the following two facts: i. Each chapter is two pages long (the book has 62 chapters). ii. This is an academic text without a single source or reference. The latter of those two points is the main reason why I have not rated the book.
The chapters are denser than you’d think (they have a lot of information considering what you’d expect from two-page chapters), and many chapters ‘come in pairs’ or deal with related stuff; for example there are three main chapters dealing exclusively with proteins – one about the ‘chemistry and digestion’ of proteins, another one about the ‘functions of proteins in the body’, and a third one about the ‘needs and sources’ of proteins. Carbohydrates and fats also get multiple chapters each, and micronutrients get 7 chapters of ‘exclusive coverage’ dealing only with those things. The level of detail is reasonably high (again considering what you’d expect), but of course there’s only so much stuff you can cram into a chapter two pages long. I think in many ways it is a really neat book to have for looking up stuff in this area that you’re wondering about and/or can’t quite remember (‘what was the role of butyric acid in the colon again?’ ‘Which factors affect calcium absorption?’ ‘What are the roles of the various B-vitamins in metabolism? How might I get into trouble if I don’t get enough riboflavin, and what can I do to avoid that situation?’). Quite a few of the things she talks about I don’t really consider it too problematic that she does not source; she knows a lot more about which role folate plays in the regulation of homocysteine levels than I do, and I don’t think there’s a big risk involved in just taking her word for it that those things work the way she says they do. Much of the book covers stuff on a level where I could justify thinking along such lines; many of the chapters are a bit like book versions of short Khan Academy nutrition lectures (perhaps a bit like lectures like this and this, I guess without having watched those lectures), and I figure if I’m okay with watching lectures like those I should be okay with reading a book like this as well, which is a big part of the reason why I didn’t just throw it away the moment I realized that there was actually not a single page of references to be found anywhere.
As I didn’t rate the book because of it, the lack of sourcing of course bothered me. One thing which puzzled me is why she decided to write the book this way – I simply do not understand that decision at all. Given the current state of affairs of nutritional science (and the current state at the time the book was written in 2007), I will say that I think the way she has chosen to write this book is simply flabbergasting to me. Nothing tempts people to disregard your information like not telling them where it comes from. There is not a single sentence in this book with the words ‘[X & Y] found that…’ – she only ever writes ‘a study found that…’, and this is just infuriating. There are various recommendations of daily intake of various substances in the book, but you have no idea who came up with those recommendations or which evidence base they are based on – there’s not even a source indicated in the headings in those cases. I simply don’t understand why she’d write the book that way – the lack of sources makes much of the stuff look deeply suspect, regardless of whether or not it’s actually all of it based on ‘the best available evidence’, and occasionally it seems as if she’s gone out of her way to avoid adding a source even in situations where it would make a lot more sense to add it than to not do that. To add insult to injury, a couple of the reported estimates in the last half of the book were so out of line with other estimates I could find elsewhere that I seriously considered throwing the book away. So, yeah.
But the book has a lot of good stuff as well which presumably a lot of people would benefit from knowing about, so it’s really hard for me to know what to think about it. To take an example of what I’m talking about here, Rees et al. observed in their book – as I have pointed out – that: “Vegans who omit all animal products from their diet often have subclinical vitamin B12 deficiency.” They probably wouldn’t have if they’d read this book. Anemia is a very common condition worldwide, and iron deficiency is estimated to be the most common cause. An estimated 250 million preschool children are vitamin A deficient. We humans need a lot of different stuff to keep going, and the food we eat plays many roles most of us probably haven’t given any thought. Everybody needs to eat, so there aren’t many people who would not benefit from knowing more about how these things work; even people following ‘an ideal balanced diet’ can be at risk of developing deficiency states due to malabsorption syndromes or various disease states which may change nutritional requirements.
I’ve added some ‘sample observations’ from the book, as well as a few comments, below:
“There is a continuous turnover of protein in the body, which in healthy adults exhibits a balance between synthesis and breakdown, and amounts to 3–6 g/kg body weight per day. During growth there is an excess of synthesis over breakdown, and in wasting conditions (e.g. starvation, cancer and after surgery or trauma), breakdown exceeds synthesis. Protein synthesis is regulated principally by insulin, and catabolism by glucocorticoids. […] The body is unable to make nine of the amino acids used in protein synthesis […] Lack of any one of these will limit the synthesis of protein, even if all the other required amino acids are present in adequate amounts. […] In addition, there are a number of other amino acids that can be synthesised in the body under normal conditions, given the necessary supply of precursor molecules. In the absence of these precursors, the amino acids become ‘conditionally indispensable […] Protein synthesis is an energy-demanding process; it has been calculated that the energy requirement is 4.2 kJ (1 kcal)/g of protein synthesised. Protein synthesis occurs more rapidly after a meal than in the fasting state, due to the greater supply of amino acids. On average the energy used in protein synthesis accounts for 12% of the basal metabolic rate. […] The digestibility of proteins from animal sources is much greater than that from plant sources. Digestibility for egg is given as 97%. […] Poor digestibility, of between 60 and 80%, is found in legumes and cereals with tough cell walls, particularly when uncooked, and is a factor in diets that are low in protein. […] Worldwide, the availability of plant proteins is relatively consistent, at about 50 g/person/day. However, the availability of animal protein sources varies widely, from <5 to 50 g/head/day, highest in most Western countries. […] Inadequate protein intakes rarely occur alone, and are generally found within a wider picture of undernutrition. Insufficient intakes of energy cause protein to be used for energy, and make it unavailable for tissue maintenance or growth.”
“The most rapid period of brain growth occurs from mid-gestation to 18 months after birth. At birth the brain accounts for 10% of the body weight; an adult brain weighs about 1.4 kg, and comprises 2% of body weight. Different components of the brain grow at different rates and have ‘critical periods’ when growth is most rapid and vulnerable to adverse influence.”
‘Alcohol and folic acid’ would probably be two factors most people would know about in this context. But there’s of course a lot more to developing a human brain than these variables. Generalized undernutrition can lead to smaller brain and less extensive neural networks, long-chain polyunsaturated fatty acids are quite important for brain development, you need copper for myelin synthesis but too much of it may be toxic, iodine deficiency leads to cretinism, severe iron deficiency may lead to long-term reductions in cognitive performance whereas too much of it again may lead to toxicity, excess vitamin A intake may be teratogenic, pyridoxine deficiency may lead to seizures/neurologic symptoms, … Incidentally the arrow doesn’t just go from food intake to brain performance; the brain is also helping you figure out what to eat: “neurotransmitters acting within the brain are thought to regulate preferences for particular macronutrients. Serotonin may influence the balance between carbohydrate and protein intakes. Noradrenaline and opiates are also believed to have a role. […] Disturbances of neurotransmitter release, whether of endogenous (e.g. in disorders of brain function) or exogenous origin (e.g. by drugs), are likely therefore to affect food intake.”
Some more stuff about childhood growth from a few chapters on related matters:
“The fastest rate of growth is in the first 6 months of life, with a doubling of birth weight, and slows towards 12 months, to achieve about three times birth weight. Body weight only doubles between the ages of 1 and 5 years. Standard growth charts are useful to check that growth is progressing appropriately […] During the years of [school-age] childhood, mean growth is relatively constant, and averages 2.5 kg and 6 cm per year. During puberty, on average: • girls increase by 20 cm (height) and 20 kg (weight); • boys increase by 30 cm (height) and 30 kg (weight). These increases represent 40% of eventual adult weight. Growth is vulnerable to faltering if nutritional intakes do not keep pace with the demands. […] Body fat percentage levels increase rapidly in the first months of life, but start to fall after the first year. […] There is a further increase from about the age of 5 years (adiposity rebound), which may start earlier in larger, fatter children […] In boys, the fat content starts to fall during the pubertal growth spurt, but in girls it continues to increase, resulting in the average 10% fat content differential between the sexes seen in adults. […] Growth in infants and young children, usually recorded as weight, should progress along a centile line on standard growth charts. Reasons for centile crossing (moving from one centile line to another) need to be established. […] Infants of diabetic mothers, who are often born very large (>4.5 kg), may exhibit ‘catch-down’ growth during the first year of life. Once removed from the oversupply of nutrients in the womb, their growth rate slows. […] An infant undernourished in the womb may show ‘catch-up’ growth. This should be an increase in lean body mass, rather than fat; the latter is linked to risk of later disease.”
“It is now recognised that vitamin D is synthesised in the skin by the action of ultraviolet light on a precursor, and could strictly be termed a hormone rather than a vitamin. Further, niacin [vitamin B3] can be made in the body from the amino acid tryptophan, so a separate supply may not be needed if protein intakes are adequate. However, in both of these cases, there are situations where synthesis is insufficient, and so a dietary need remains.”
“Inadequate intakes of macronutrients will most obviously be reflected in disturbed growth in children and body weight changes in adults. […] Undernutrition in the elderly is poorly reported, but is believed to be widespread […] The consequences of undernutrition can manifest both in the short and long term, and may have intergenerational effects, through poor pregnancy outcome and low birth weight. […] Worldwide, deficiencies of iron, vitamin A and iodine affect the greatest numbers of people. […] Several other micronutrients may become deficient when diets lack specific food groups. These include: • vitamin B12, when vegan diets are consumed; • calcium, when dairy products are excluded from the diet; • riboflavin, when diets are low in green vegetables and dairy products.”
“The typical increase in weight (in the UK) during pregnancy is 11–16 kg but varies widely. Gains in the second and third trimesters should average 0.4 kg/week for normal weight women, less (0.3 kg/ week) for overweight women and more (0.5 kg/week) for women who are underweight. […] The extra energy costs of pregnancy are estimated at 310 MJ (77 000 kcal) […] The mother’s nutritional status is unlikely to affect the volume or the macronutrient content of her milk for the first few weeks of lactation. However, poorly nourished women will not be able to sustain the same level of nutrients for prolonged periods. The fat content of the milk correlates with the mother’s levels of body fat, and the pattern of fatty acids secreted in the milk partly reflects those in the mother’s dietary intake. Neither the fat-soluble vitamin content nor the mineral content of the milk fluctuates with maternal dietary intake.”
“ATP is the fundamental molecule that on breakdown to ADP provides energy for contracting muscle. ATP stores are very limited and require continual replenishment; the amount stored would fuel only about two seconds of exercise. […] CHO [Carbohydrate] stores in muscle (300–800 g) and liver (80 g) are limited; fats stored mainly in subcutaneous tissue are found in very much greater amounts (minimum 5 kg in males, more in females). • Lipids are considerably more energy dense than CHOs. Metabolism of one gram of fat will deliver considerably more ATP molecules than one gram of CHO; however, more oxygen is required to metabolise fats, and fats cannot be metabolised anaerobically […] An important principle is that carbohydrates are the preferred energy source particularly for more intense and prolonged exercise […] Most athletes already consume sufficient protein in a mixed diet […] With the exception of energy intake the evidence that normal dietary supplements enhance sporting performance is poor.”
I found the two chapters about nutrition and sport interesting in a way, but mostly because they helped me figure out what happens in normal people – a book like this (which I have considered reading in the past, but has never gotten around to actually reading) is probably better at elucidating relevant mechanisms in my case.
“Consumers generally believe that foods produced organically, often by more traditional agricultural methods, have superior nutritional quality. This is not currently supported by the scientific literature, in which studies find no difference in nutrient content between organic and non-organic produce; there is also no information about impact on human health.”
This is my second post about the book – you can read my first post about the book here; that post includes some more general comments and observations. In this post I’ll cover plant-insect interactions and mammalian herbivory.
“Herbivory, which is the consumption of plants by animals, encompasses many different types of interactions that differ in their duration and deadliness to the plant. Insect herbivores, like mammals, feed on plants in numerous ways. Seed and seedling herbivory are predatory interactions because herbivores immediately kill individuals in the plant population. Insect herbivores that feed on leaves and other parts of mature plants typically do not cause plant mortality. In the rare cases when they do, it usually requires much time to kill the host plant. Such relationships are closer to parasite-host than predator-prey relationships. […] Insect herbivores differ from mammalian herbivores in their size, numbers, and the kinds of damage they inflict. Because of their small size, insects often have an intimate, lifelong association with the host plant. Moreover, while their associations are lifelong, often their lives are rather short, predisposing them to rapid rates of evolution. On average, insect herbivores are much more specialized than their mammalian counterparts. […] There has long been debate over why specialist feeding habits are widespread in herbivorous insects. […] There are clearly a number of hypotheses, each with some empirical support […] Because specialization is a complex trait, we don’t necessarily expect a single hypothesis to explain the phenomenon.”
“Insect populations frequently fluctuate in size, and this fact has prompted a good deal of speculation as to what factors limit the size of herbivore populations. Hairston, Smith and Slobodkin (1960) reasoned that, since herbivores rarely consume all of their plant resources (the world is green), herbivore populations are likely to be limited by parasites and predators, but not by resource abundance […] However, whether herbivorous insect populations are limited by food (bottom-up forces in a food web) or by predators (top-down forces) remains a hotly debated topic […], and it is unlikely that either force dominates all insect populations”
“The first obstacle that an insect faces is the fact that, on average, only about 10% of the energy available to one trophic level makes it to the next trophic level. Sources of energy loss include the fact that not everything ingested can be assimilated (e.g. lignin, cellulose). […] the chemistry of plant and animal tissues is very dissimilar. Liebig’s law of the minimum states that growth is possible to the extent determined by the nutrient that is in shortest supply. For herbivores, one such nutrient is protein. Because nitrogen is relatively easy to measure and protein is not, protein content is often estimated by assaying organic nitrogen, which comprises from 15 to 18% of plant proteins […] sap-feeding insects, like cicadas and other homopterans, often eat 100 to 1000 times their body weight per day because amino acids make up only a tiny proportion of the sap […] In general, both micro- and macronutrients can limit the growth rate of insect herbivores.”
I want to interpose an observation here – I find it quite interesting how seemingly unrelated fields can so often become related in ways you do not expect them to. I’m currently reading Mary Barasi’s Nutrition at a glance (which despite its low page count is actually quite a bit of work, as I’ve found out..). It makes sense in retrospect that some things overlap here, but when I started reading Barasi I did not expect stuff covered in this book to be relevant to the coverage in that book (she only deals with humans). It turns out that the stuff above – and some other stuff covered elsewhere in the book as well – is quite relevant to Barasi’s coverage; I’d probably have been somewhat confused by the focus on nitrogen in the protein chapters of Barasi if I had not read the stuff covered in chapter three of this book. When you’re about to learn some new stuff you never really know how that new stuff you’re about to learn may relate to stuff you already know, or for that matter how it may relate to stuff you’ll learn later on. I always love making new connections like these and connect dots I didn’t even know could be connected.
Okay, moving on…
“Aside from nutritional hurdles and the limited availability of some plant parts, herbivores may also be prevented from feeding as a result of plant defences. […] Adaptions include physical barriers, toxins, anti-feedants, decoys and even other organisms [ants!]. Some defences are always present on the plant; we call these constitutive defences. Many others, including thorns and spikes, are inducible, that is, they are augmented only after the plant is attacked […] The list of chemicals that owe their defensive value to their ability to interfere with insect physiology or behaviour is a very long one. While the elaboration of thorns, spines and hairs is restricted largely to their size and shape, the number of possible combinations, principally of carbon, oxygen, hydrogen, nitrogen and sulfur, is enormous. […] These plant constituents are commonly referred to as ‘secondary’ compounds. […] When the role of a secondary compound is defensive, it is commonly referred to as an ‘allelochemical’. […] Synergists are chemicals that enhance the toxicity of chemicals with which they are mixed. […] Our current understanding is that the presence of secondary compounds can deter many herbivores from using plants, but that almost every plant species has a suite of specialized herbivores that are adapted to use these compounds as attractants, as feeding stimulants or as a source of toxins for use in defence against their enemies. […] As many means as plants have to deter insects, insects have ways of circumventing them. […] The overall responses of plants subjected to herbivory may be viewed as a tradeoff between growth and defence.” [my bold, US]
“As a group, insect herbivores tend to have larger effects than mammalian herbivores on plant growth and reproduction […] when a plant is attacked by one herbivore it may become more or less vulnerable to attack by others. […] the degree to which plants can evolve to become better defended, might be constrained by the preferences of beneficial pollinators. […] While it is clear that herbivores can affect plant community composition and species distribution, the reciprocal effect also exists: plant community composition affects insect herbivore loads. […] The ‘resource concentration hypothesis [states that] herbivores are more likely to find hosts that are concentrated, and herbivores remain longer on hosts growing in dense or pure stands. […] The ‘enemies hypothesis’ [states that] increased diversity of predators and parasitoids in diverse stands may limit population densities of herbivores in these stands. The idea that diverse plant community composition may result in reduced attack by herbivores has been called ‘associational resistance’. […] both community composition and the dispersal abilities of herbivores in relation to the scale of community diversity will affect the degree to which plants receive damage from herbivores.”
“In summary, insect herbivores respond to selection by plant defences and nutritional status. Plants strongly affect insect fitness so that, in general, insect herbivores are relatively specialized with respect to their diet breadth (in comparison with mammalian herbivores). […] Plants affect insect abundance through their defences, which often entail the actions of other species, such as predacious and parasitic enemies of herbivores.
Insects in turn affect plant fitness, and may exert selection on plant defences, both physical and chemical. There is a growing body of evidence suggesting that these defences come at some cost to the plant. On a larger ecological scale, insects affect plant distribution and abundance, as well as the species diversity of plant communities. Frass, honeydew and greenfall from insect outbreaks also alter nutrient cycling regimes in the soil and the availability of nutrients to plants.
Finally, many of the adaptions and counter-adaptions of plants and their insect herbivores support the idea that much of the biodiversity of the earth is a result of the arms race between insect herbivores and their host plants.” [my bold, US]
“The amount of food differs between biomes. The tundra has a primary production of only about 140 g m−2 yr–1, while swamps and marshes reach about 3000 g m−2 yr–1, i.e. a 20-fold difference between the extremes […] The plant biomass, or standing crop, shows an even greater range between the least and most productive biomes, i.e. a 75 fold difference from about 600 g m−2 in the tundra to 45 000 in tropical rainforests. Estimates of food resources are vital for understanding the relations between plants and herbivores […] and [there is a] need for estimates that capture both the static and dynamic situations of the food resources. […] Given the large spatial and temporal variation in food abundance and quality, mobility is a valuable trait and the migratory habits of many ungulates represents an adaptive response. There are no strictly sedentary herbivores […] Herbivores have the advantage of feeding on objects that cannot escape, but on the other hand plant food has low nutritive value (it is low in nitrogen and must be digested slowly). […] Diet composition is commonly used to classify animals into functional groups, e.g. predators, omnivores and herbivores. Mammals, like all other living organisms, have a perverse tendency to defy exact classification […] Sixteen different categories of dietary specialization have been proposed, and seven of them refer to herbivores […] a large majority of the [mammalian] herbivores have quite a mixed diet and also feed on animal matter. [my bold, US] […] It is increasingly clear that mammalian herbivory on a given plant species can result in a continuum of responses, depending on the characteristics of the plant, the type of herbivory and the environment. […] there is no simple typical response for a given plant species.”
“The metabolic requirements of mammals increase with (body mass)0.75 (Kleiber 1932), but the capacity of the gastrointestinal tract with (body mass)1.0 […] Smaller animals thus have higher mass-specific food requirements without any accompanying proportional increase in the gut capacity, which limits the volume of digesta retained and its passage […] There is a tradeoff between the rate of intake and the time allowed for chewing. […] The theory of optimal foraging is based on the assumption that an animal would forage in such a way that it optimizes its fitness […] Food, in terms of quantity or quality, is usually highly variable and is sometimes distributed in more or less discrete patches. Therefore, one crucial point in the optimal foraging concept will be the criteria for when to leave a feeding patch and move to another. The ‘marginal value theorem’ states that a herbivore should stay as long as the extraction rate is above the average for the environment as a whole. […] Understanding the decision rules used by a herbivore requires an understanding of its behavioural responses on various time-scales. It is less probable that an animal optimizes its diet at each bite, but rather that it bases future decisions on an integration over longer periods.” [I found these observations rather funny in a way – some of this stuff is a lot like microeconomic theory, it’s just that in this case the hypotheses made relate to the behaviours of non-human organisms, rather than humans..]
“The Tet Offensive of 1968 was the pivotal event of the long Vietnam War. Its outcome and meaning have been the subjects of a debate that has raged for more than thirty years. […] Regardless of their differing interpretations on motivations and outcomes, all agree that the Tet Offensive was a decisive moment that forever changed the nature of the U.S. commitment to the war. […] On January 21, 1968, twenty thousand Communist troops surrounded the Marine base at Khe Sanh and lay siege to it for the next seventy-seven days. Ten days after the initial attack at Khe Sanh, in the early morning hours of January 31, Viet Cong and North Vietnamese forces launched a massive countrywide attack on the cities and towns of South Vietnam. More than eighty thousand Communist troops mounted simultaneous assaults on thirty-six of forty-four provincial capitals, five of six major cities, including Saigon and Hue, sixty-four of 242 district capitals, and more than fifty hamlets. The ferocity and scope of the offensive stunned both the American public and President Lyndon B. Johnson. […] Tet convinced the president that military victory in Vietnam was not attainable and forced a reevaluation of American strategy. The Tet Offensive and its aftermath marked the beginning of a protracted American retreat from Vietnam that would not end until five years later. […] The events of the Tet Offensive demonstrate a vital aspect of contemporary wars: military operations are normally but one aspect of the struggle and may not, as can be seen in the case of the events of 1968 in Vietnam, be the most important factor in determining the war’s outcome […] The conflict in Vietnam always had a strong political component in addition to the military engagements that raged on the battlefield […] the Tet Offensive, although usually seen within a military context, had serious political implications, and, in the final analysis, it was in the political arena that the offensive had its greatest impact. This guide is meant to provide information and resources for further study of the 1968 Tet Offensive. It is not meant to be an exhaustive discussion of the entire war […] [It] focuses on the events leading up to the Tet Offensive, the conduct of the offensive itself, and its aftermath. It also seeks to discuss the various tactical, operational, and strategic interpretations of the offensive and the events that took place in its aftermath.”
Collins’ book covered related stuff in one of his chapters, in that he dealt in some detail with e.g. some of the logistical challenges the US army was confronted with while fighting in Vietnam, and that coverage had made me curious to learn more – so I decided in the end to have a go at this book. Wikipedia has some stuff (see e.g. here), but books are nice and I liked Willbanks’ book, though I must admit I liked Collins’ coverage better; Collins’ coverage is in a sense of a much more technical nature than is Willbanks’, in that the latter talks a lot about e.g. US presidents and senators and how they reacted to military developments and stuff like this. You need to cover that kind of stuff to contextualize and understand what happened, but I don’t like politics and I was seriously considering skipping some of the primary sources included in the book for that reason (I did decide to read them in the end, but some of them I did not read too carefully). The book has an unconventional structure in the sense that many of the roughly 300 pages provide ‘secondary coverage’: Primary sources (intelligence reports, presidential speeches, news items), lists of important terms, concepts and people, as well as many pages of suggestions for further reading. The main body of the book doesn’t actually take very long to read, even though of course it has a lot more details than does the wiki.
I’ve added some observations from the book below.
“On March 8, 1965, elements of the U.S. 9th Marine Expeditionary Force came ashore in Vietnam at Da Nang, initially to provide security for the U.S. air base there. A month later, President Lyndon Johnson authorized the use of U.S. ground troops for offensive combat operations in Vietnam […] With the arrival of the Marines, a massive U.S. buildup ensued; by the end of the year, 184,300 American troops were in Vietnam. This number would rapidly increase until there were more than 485,000 in country by the end of 1967. […] By the middle of 1967, the war in Vietnam had degenerated into a bloody stalemate. U.S. and South Vietnamese operations had inflicted heavy casualties and disrupted Communist operations, but Hanoi continued to infiltrate troops into South Vietnam, and the Viet Cong still controlled the countryside in many areas in the south. […] Facing the Americans, South Vietnamese, and their allies was a formidable combination of PAVN and Viet Cong troops. There were two types of forces within the Viet Cong: main force units that by early 1968 numbered about sixty thousand soldiers organized into regular combat units, and the paramilitary or guerrilla forces. Main force units engaged in full-scale combat and were usually made up of highly motivated, skilled fighters who were adept at ambushes, the use of mortars and rockets, and coordinated attacks on allied defensive positions. The paramilitary forces of the Viet Cong included regional, or territorial, guerrillas and local guerrillas. They provided logistical support, scouts, and guides and engaged in local hit-and-run tactics such as staging ambushes and laying mines. MACV [Military Assistance Command,
Vietnam] estimated in October 1967 that there were nearly 250,000 Viet Cong main force and paramilitary forces operating in South Vietnam […] about half of the 197 main-force enemy battalions in the south were PAVN regulars.”
“Before 1968, both sides in the war had observed Tet cease-fires over the holiday. Therefore, the North Vietnamese reasoned that half the South Vietnamese army and national police would be on leave when Tet began and Saigon would be unprepared for a countrywide attack. […] the plan, using secrecy and surprise, called for a series of simultaneous attacks against American bases and South Vietnamese cities. Giap specifically targeted previously untouched urban centers such as Saigon […] Giap’s plan called for a preparatory phase that would be conducted from September to December 1967. During this period, PAVN forces would launch attacks in the remote outlying regions along South Vietnam’s borders with Cambodia and Laos. The purpose of these operations, which were essentially a grand feint, would be to draw U.S. forces away from the populated areas. This would leave the cities and towns uncovered. […] Although there is some disagreement among American scholars about the phasing of the actual offensive, Tran Van Tra asserted some years after the war that the plan for the offensive called for three distinct phases […] It is clear that to Hanoi and the NLF, the Tet Offensive, which is usually seen to cover a much shorter period by many American historians, was a more prolonged offensive that lasted beyond the action immediately following the Tet holiday […] The Tet Offensive thus really began in 1967 with the preparatory phase that included the diversionary attacks on the outlying areas in South Vietnam. The bitter fighting that resulted would set the stage for the Tet Offensive that began in January 1968 and lasted into the fall of that year.”
“As the fighting mounted at Khe Sanh in the first part of January 1968, the Communists were making final preparations for launching the Tet Offensive. Since Tet typically brought a mutual cease-fire, Hanoi assumed that the South Vietnamese would be relaxed and unprepared for an assault. Taking advantage of the situation, the Communists smuggled men and equipment into and around South Vietnam’s cities and provincial capitals. Weapons arrived in trucks loaded with flowers, vegetables, and fruit destined for the holiday celebrations. “Mourners” carried coffins filled with weapons and ammunition and buried them at pagodas and churches where they could easily be dug up later. Explosives were concealed in baskets of tomatoes and rice. Viet Cong (VC) soldiers in civilian clothes, some even dressed in South Vietnamese Army (ARVN) uniforms, mingled with crowds of South Vietnamese civilians returning to the cities for the Tet celebrations. [Maybe it’s worth interposing a few remarks here in order to provide some context. Willbanks doesn’t mention this, but some of the actions described above walk a very fine line indeed, in that one person’s ‘military deception’ may well be another person’s ‘war crime’; I’m thinking specifically of the ‘dressed in ARVN uniforms’-part. See e.g. this – specifically Article 39,
2: “It is prohibited to make use of the flags or military emblems, insignia or uniforms of adverse Parties while engaging in attacks or to shield, favour, protect or impede military operations.” – and this. War crimes aren’t just massacres and similar stuff (more on that kind of stuff below); after WW2 some people wanted really badly to execute German soldiers who’d done similar stuff to what these people did in Vietnam, and presumably part of the reason why the rules were changed in 49 was that they had been unable to do that. Either way of course in Vietnam they had an approach where they dealt with many thing ‘out of court‘…] […] U.S. military intelligence analysts knew that the Communists were planning some kind of spectacular attack but did not believe it would come during Tet or that it would be nationwide.”
“The Tet Offensive began in full force shortly before 3:00 a.m. on January 31. More than eighty thousand Communist troops—a mixture of PAVN regulars and VC main-force guerrillas—began a coordinated attack throughout South Vietnam. The PAVN and Viet Cong targeted more than three-quarters of the provincial capitals and most of the major cities […] The scope of the Tet Offensive was stunning; everywhere there was confusion, shock, dismay, and disbelief on the part of the allies. […] As fighting erupted and increased in intensity in and around the capital city, it seemed as if the rest of South Vietnam was also in danger of falling to the Communists. It soon became clear that the Communists had launched a major countrywide offensive […] Communist troops captured Hue and intense battles raged [many other places] […] They also seized control of scores of district capitals […] The fighting in the [Mekong] delta was intense and resulted in severe damage to the cities and towns where it occurred. […] The U.S. and South Vietnamese forces had to fight city by city to dislodge the Communist troops. Although the Communists had taken the Americans and North Vietnamese by surprise, their attacks were not as well coordinated as they might have been. Overcoming their initial surprise, the allied forces reacted reasonably quickly in most cases, permitting little time for the attacking forces to establish solid defensive positions. ARVN [South Vietnam’s army] fought more effectively than most Americans had expected. Generally, the Communists were unsuccessful in maintaining their positions in the cities for very long, and South Vietnamese and U.S. troops inflicted heavy casualties and took many prisoners. […] Despite heavy fighting at some places, in general, the Communist offensive seemed to run out of steam by the end of the first week in February. In most cases, allied control was regained in less than a week and Communist forces were driven out of most of the cities with a few days, with the exceptions being Cholon in Saigon and Hue”
“The longest and bloodiest battle of the Tet Offensive occurred in Hue […] South Vietnam’s third-largest city, with a wartime population of 140,000. Hue was the old imperial capital and served as the cultural and intellectual center of Vietnam. […] [After] [h]aving captured most of the city, the VC cadre instituted a new political regime and established Revolutionary Committees to control the various neighborhoods. While the NVA and VC assault troops roamed the streets freely and consolidated their gains, political officers began rounding up the South Vietnamese and foreigners on the special lists. They marched through the Citadel, reading out the names on the lists through loudspeakers and telling them to report to a local school. Those who did not report were hunted down. Most of the detainees were never seen alive again. […] The ancient capital was almost sacred to the Vietnamese people, particularly so to the Buddhists. The destruction of the city would result in political repercussions that neither the United States nor the government of South Vietnam could afford. […] As a result, limitations were imposed on the use of artillery and close air support to minimize collateral damage. Eventually these restrictions were lifted when it was realized that both artillery and close air support would be necessary to dislodge the enemy from the city. […] The cost of the battle for the people of Hue was catastrophic. During the twenty-five days of intense fighting to retake the city, Hue was reduced to rubble […] Estimates tallied ten thousand houses either totally destroyed or damaged, roughly 40 percent of the city, and 116,000 civilians were made homeless (out of a pre-Tet population of 140,000). […] Aside from this battle damage, the civilian population suffered terrible losses from the fighting: some 5,800 were reported killed or missing. Many of the dead and wounded were trapped in the rubble of their homes and courtyards. The exact extent of the battle’s toll on the civilians in Hue would not become clear for some time. In late February, soldiers moving through the Gia Hoi schoolyard came across freshly turned earth; upon investigation, the soldiers discovered the hastily buried bodies of a number of civilians, most of whom had been bound and shot. This proved only the first instance of such graves, and more bodies would be found over the course of the next several months. In total, South Vietnamese authorities uncovered nearly three thousand corpses in mass graves in the Hue area. Most had been shot, bludgeoned to death, or buried alive, almost all with their hands tied behind their backs. The victims included soldiers, civil servants, merchants, clergymen, schoolteachers, intellectuals, and foreigners.”
“On the morning of January 31, 1968, when the Tet Offensive was launched, General William Westmoreland remained convinced that the enemy’s real goal was the conquest of the U.S. Marine base at Khe Sanh […] The attacks on Saigon and other cities, he declared, were designed to create “maximum consternation” in Vietnam and were “diversionary” to the main effort still to come at Khe Sanh and the northern part of the country. […] Thus, despite the fact that the fighting continued in Hue, the attention of both the White House and Westmoreland remained fixed on Khe Sanh. […] The fighting during the subsequent phases of Tet was intense. The United States lost 562 dead in the week ending May 11, the highest weekly total of the war; with the loss of nearly 2,000 dead during that month, May 1968 became the bloodiest month of the war for U.S. troops. […] American losses in the war by the end of 1968 stood at 30,610 killed. Of these, 14,589, nearly half the total number, had been killed in the past year.”
“In the wake of Tet, the media took an increasingly unfavorable view of U.S. policy, and the reporting on the situation in South Vietnam during and after Tet had a significant impact on public opinion. […] Westmoreland claimed that the failed Communist efforts during Tet represented the “last gasp” of a losing cause, but few Americans believed him. In November 1967, Westmoreland had reported that American forces were winning the war in Vietnam, but the surprise and ferocity of the Tet attacks strained his credibility to the breaking point. Many Americans could not reconcile Westmoreland’s new claims with what they had seen on their TV screens. After Tet, it was impossible for most Americans to believe Westmoreland’s renewed promise that victory was just around the corner. […] Gallup Poll data suggest that between early February and the middle of March 1968, nearly one person in five switched from “hawk” to “dove” on the war. […] In the end, part of the blame for the ultimate outcome of the Tet Offensive may lie in biased and erroneous reporting, but the earlier bursts of optimism from the highest levels of government that told Americans that the United States was winning in Vietnam did not square well with the stunning surprise of the Communists attacks. All the reports, news photos, and film footage, good or bad, only served to add velocity to a situation made bad by the credibility gap that had begun to develop well before the Communists launched their offensive in 1968. Having gained a victory in countering the Tet Offensive, there was no need to juggle the numbers this time, but the credibility gap had opened up too far. Journalists in Saigon looked for signs of defeat everywhere, and when they looked hard enough they seemed to find them.”
“Following his inauguration in January 1969, Nixon began to implement a new policy in South Vietnam. Called Vietnamization, it included improved training and a vast modernization effort for the South Vietnamese armed forces. Concurrently, Nixon began to withdraw American troops, a process that continued until almost all U.S. ground soldiers had left […] the Paris Peace Accords were signed in January 1973, and a cease-fire was initiated soon thereafter. By March of that year, all American military forces had been withdrawn from South Vietnam. […] On April 30, 1975, PAVN tanks crashed through the gates at the presidential palace in Saigon, and the war was over. All of Vietnam fell under Hanoi’s control, and Saigon was renamed Ho Chi Minh City.”
“The Tet Offensive resulted in huge casualty figures for the Communist forces. Estimates range from a total of 40,000 dead out of 80,000 Communists engaged to as high as more than 72,000 Communists dead, according to U.S. military records. While these numbers are certainly subject to debate, it is clear that the Communists failed to hold on to any of the major objectives that they had attacked and suffered horrendous casualties in the process […] Most historians agree that the National Liberation Front never completely recovered from Tet. The Viet Cong was badly crippled as a fighting force, and the NLF political organization was seriously damaged. […] Militarily, the Viet Cong were never again able to field full main-force battalions (with some exceptions, such as in the Mekong Delta). From this point on in the war, the war became more conventional and was fought mainly by PAVN forces controlled directly from Hanoi. […] The war became increasingly a conventional battle and less an insurgency. […] the dominant themes of the words, and film from Vietnam . . . added up to a portrait of defeat for the allies. Historians, on the contrary, have concluded that the Tet Offensive resulted in a severe military-political setback for Hanoi in the South.”
“The Tet Offensive was never a purely military campaign, and any analysis of the operation must include an assessment of the outcome of its strategic political objectives. Although the allies won most of the Tet battles and inflicted horrendous casualties on the Communist forces, the Tet Offensive “broke like a clap of thunder on an astonished world” and resulted in a stunning strategic victory for the Communists. […] Tet, whether by design or not, was “unique in that the side that lost completely in a tactical sense came away with an overwhelming psychological and hence political victory.” […] The Tet Offensive played a key role in the subsequent events that led to the long, protracted U.S. withdrawal under Richard Nixon. It marked the beginning of the end of U.S. involvement in Southeast Asia. […] in the end, the offensive had such an impact on the White House, media, and the American people that the Communists’ failure to achieve their original goals at the tactical and operational levels proved irrelevant. In the end, they won a great political victory at the strategic level.”
This book is the third book in the series I’m reading. It was much worse than the first two I read – I gave it two stars on goodreads, but I was significantly closer to one star than three.
In a way the format of this book is quite different from the format of the other books I’ve read so far, in the sense that pure management aspects, follow-up procedures, communication aspects and similar stuff play a much larger role. It’s still 100 cases and 100 answers, but the ‘how to deal with patients’ aspect of medicine played a much larger role in this book than it did in the ‘previous ones’ (I believe they were written later, but…), whereas e.g. aspects like diagnostics were not emphasized to nearly the same extent, though many cases do deal with such things as well. It probably makes a lot of sense to focus on stuff like that, given that this is a book written for GPs who probably spend a lot of time dealing with patients, including patients with which they build a relationship over time, compared to some other types of doctors. One downside is that I personally am much less interested in such stuff than I am in ‘the other stuff’. Some cases were in a way only marginally related to medicine at all; for example there’s a case where a doctor observes a colleague smoking cannabis after his shift has ended (‘how would you best deal with such a situation?’-type answer), and a case where a patient is offering gifts to his doctor, again with a ‘how should you handle that situation?’-angle (apparently gift-giving from patients to doctors is a quite common phenomenon: “Most doctors are given between one and five gifts per year and the most common items are chocolate and alcoholic beverages or other food items”).
None of the cases in the book are ‘real cases’, they state this explicitly in the preface; rather the cases have been written in order for the book to present common themes encountered in general practice. Some of the cases simply made me annoyed and that’s part of why the rating is not higher. One made me outright angry because it was obvious that not only was it made up, the details also served to make it clear that the authors are [redacted]. Setting: A statistician presents in the clinic and demands a medically unnecessary cervical smear. Here’s one key passage from the answer part:
“The GP is talking about the patient’s absolute risk of developing cervical cancer. He noticed the absence of all risk factors and the previous normal test results. The point at which low risk becomes medium or high risk is based on scientific evidence and expert opinion. The patient talks about relative risk. Relative risks can sound quite dramatic when used outside their context and doubling of risk can sound very worrying. The doctor’s role is to communicate risk in context.”
The patient is supposedly a statistician. It gets even better, they lecture on in the answer part and tell us that:
“Any screening programme aims to maximize benefits and minimize harm and cost. Through statistical modelling, experts have worked out that it is safe to offer cervical smears at certain intervals. Patients at risk, for example those with mild dyskaryosis, are offered more frequent testing. Possibly, more frequent testing for all is likely cause harm: women will be inconvenienced having to take time out to undergo the tests; the number of false positive tests will increase proportionally with the number of tests conducted, resulting in unnecessary fear and investigations; and the money spent doing these test will not be available to provide other services”
Again – the patient is a statistician. This is the sort of thing statisticians tell doctors, not the other way around. This case isn’t just implausible, it defies belief – this sure as hell is not how an encounter between a statistician and a doctor would go down. It almost made me laugh, after I’d cooled down and stopped wanting to hit the authors. It makes sense to include a case or two where a patient is confident he or she knows better than the doctor what’s wrong/what’s to be done/etc. and where the doctor knows that the patient is wrong and ill-informed, because I’m sure that happens all the time in general practice, but when writing a case like that at least give a moment’s thought as to how plausible the case is. You really don’t want the illustrating example in your book to be one where a doctor lectures a statistician about statistics – if you do you just end up looking like a [redacted].
Other great moments in the book that could be mentioned would be a case about a Somali asylum seeker who’s lived in the UK for 6 years yet somehow is still in need of a translator due to not having learned to speak English yet, and a case where some parents are asking their doctor how best to go about mutilating their newborn child (“it would be reasonable to advise the parents to contact the authorities at the local synagogue or mosque for a list of approved and trained circumcisers”).
Not all cases are bad – for example there was a rather interesting one about the family of a terminal patient, where the family basically demanded that the GP kill the patient (“The oldest son approaches the GP: ‘You can clearly see that my father is suffering. We want you to give my father more morphine to stop him breathing. If you don’t do it, I will speed up the syringe driver and say you did it’.”). Not an easy situation to handle, to put it mildly, and situations like these probably do occur occasionally. However while there’s certainly some good stuff in the book and quite a few cases which will teach you something you didn’t know about the kind of stuff a doctor working as a GP may have to deal with on a regular basis, this is still by far the weakest of the publications in this series I’ve read – I have in part for that reason decided not to quote extensively from the book in this post. I was actually considering not blogging the book at all, but it seemed to make sense to at least talk a little bit about it here; now I have.
i. “Truth emerges more readily from error than from confusion.” (Francis Bacon)
ii. “I should like to like Schumann’s music better than I do; I dare say I could make myself like it better if I tried; but I do not like having to try to make myself like things; I like things that make me like them at once and no trying at all.” (Samuel Butler)
iii. “The man who lets himself be bored is even more contemptible than the bore.” (-ll-)
iv. “All progress is based upon a universal innate desire on the part of every organism to live beyond its income.” (-ll-)
v. “Morality is the custom of one’s country and the current feeling of one’s peers. Cannibalism is moral in a cannibal country” (-ll-)
vi. “Moral influence means persuading another that one can make that other more uncomfortable than that other can make oneself.” (-ll-)
vii. “It is said of money that it is more easily made than kept and this is true of many things, such as friendship; and even life itself is more easily got than kept.” (-ll-)
viii. “There is no such thing as a weird human being. It’s just that some people require more understanding than others.” (Tom Robbins)
ix. “We waste time looking for the perfect lover, instead of creating the perfect love.” (-ll-)
x. “There are two kinds of people in this world: those who believe there are two kinds of people in this world and those who are smart enough to know better.” (-ll-)
xi. “It’s never too late to have a happy childhood.” (-ll-)
xii. “If you believe in peace, act peacefully; if you believe in love, acting lovingly; if you believe every which way, then act every which way, that’s perfectly valid — but don’t go out trying to sell your beliefs to the system. You end up contradicting what you profess to believe in, and you set a bum example. If you want to change the world, change yourself.” (-ll-)
xiii. “The unhappy person resents it when you try to cheer him up, because that means he has to stop dwelling on himself and start paying attention to the universe. Unhappiness is the ultimate form of self-indulgence. When you’re unhappy, you get to pay a lot of attention to yourself. You get to take yourself oh so very seriously.” (-ll-)
xiv. “Your friend insults the homeless by giving them no credit for having made the decisions that shaped their lives, and demeans them further by declaring them powerless to alter their situations. There’re many ways, my dear, to victimize people. The most insidious way is to persuade them that they’re victims.” (-ll-)
xv. “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.” (Max Planck)
xvi. “This is a pleasant surprise, Archie. I would not have believed it. That of course is the advantage of being a pessimist; a pessimist gets nothing but pleasant surprises, an optimist nothing but unpleasant.” (Nero Wolfe)
xvii. “In a world that operates largely at random, coincidences are to be expected, but any one of them must always be mistrusted.” (-ll-)
xviii. “People are entirely too disbelieving of coincidence. They are far too ready to dismiss it and to build arcane structures of extremely rickety substance in order to avoid it. I, on the other hand, see coincidence everywhere as an inevitable consequence of the laws of probability, according to which having no unusual coincidence is far more unusual than any coincidence could possibly be.” (Isaac Asimov)
xix. “A fool can always find a greater fool to admire him.” (Nicolas Boileau-Despréaux)
xx. “Guilt has very quick ears to an accusation.” (Henry Fielding)
I read the book yesterday. Here’s what I wrote on goodreads:
“I’m not rating this, but I’ll note that ‘it’s an interesting model.’
I’d only really learned (…heard?) about Kuhn’s ideas through cultural osmosis (and/or perhaps a brief snippet of his work in HS? Maybe. I honestly can’t remember if we read Kuhn back then…). It’s worth actually reading the book, and I should probably have done that a long time ago.”
I was thinking about just quoting extensively from the work in this post in order to make clear what the book is about, but I’m not sure this is actually the best way to proceed. I know some readers of this blog have already read Kuhn, so it may in some sense be more useful if I say a little bit about what I think about the things he’s said, rather than focusing only on what he’s said in the work. I’ve tried to make this the sort of post that can be read and enjoyed both by people who have not read Kuhn, and by people who have, though I may not have been successful. That said, I have felt it necessary to include at least a few quotes from the work along the way in the following, in order not to misrepresent Kuhn too much.
So anyway, ‘the general model’ Kuhn has of science is one where there are three states of science. ‘Normal science’ is perhaps the most common state (this is actually not completely clear as I don’t think he ever explicitly says as much (I may be wrong), and the inclusion of concepts like ‘mini-revolutions’ (the ‘revolutions can happen on many levels’-part) makes things even less clear, but I don’t think this is an unreasonable interpretation), where scientists in a given field has adopted a given paradigm and work and tinker with stuff within that paradigm, exploring all the nooks and crannies: “‘normal science’ means research firmly based upon one or more past scientific achievements, achievements that some particular scientific community acknowledges for a time as supplying the foundation for it further practice.” Exactly what a paradigm is is still a bit unclear to me, as he seems to me to be using the term in a lot of different ways (“One sympathetic reader, who shares my conviction that ‘paradigm’ names the central philosophical elements of the book, prepared a partial analytic index and concluded that the term is used in at least twenty-two different ways.” – a quote from the postscript).
So there’s ‘normal science’, where everything is sort of proceeding according to plan. And then there are two other states: A state of crisis, and a state of revolution. A crisis state is a state which comes about when the scientists working in their nooks and crannies gradually come to realize that perhaps the model of the world they’ve been using (‘paradigm’) may not be quite right. Something is off, the model has problems explaining some of the results – so they start questioning some of the defining assumptions. During a crisis scientists become less constrained by the paradigm when looking at the world, research becomes in some sense more random; a lot of new ideas pop up as to how to deal with the problem(s), and at some point a scientific revolution resolves the crisis – a new model replaces the old one, and the scientists can go back to doing ‘normal science’ work, which is now defined by the new paradigm rather than the old one. Young people and/or people not too closely affiliated with the old model/paradigm are, Kuhn argues, more likely to come up with the new idea that will resolve the problem which caused the crisis, and young people and new people in the field are more likely than their older colleagues to ‘convert’ to the new way of thinking. Such dynamics are actually, he adds, part of what keeps ‘normal science’ going and makes it able to proceed in the manner it does; scientists are skeptical people, and if scientists were to question the basic assumptions of the field they’re working in all the time, they’d never be able to specialize in the way they do, exploring all the nooks and crannies; they’d be spending all their time arguing about the basics instead. It should be noted that crises don’t always lead to a resolution; sometimes the crisis can be resolved without it. He also argues that sometimes a revolution can take place without a major crisis, though the existence of such crises he seems to think important to his overall thesis. Crises and revolutions need not be the result of annoying data that does not fit – they may also be the result of e.g. technological advances, like the development of new tools and technology which can e.g. enable scientists to see things they did not use to be able to see. Sometimes the theory upon which a new paradigm is based was presented much earlier, during the ‘normal science’ phase, but nobody took the theory seriously back then because the problems that lead to crisis had not really manifested at that time.
Scientists make progress when they’re doing normal science, in the sense that they tend to learn a lot of new stuff about the world during these phases. But revolutions can both overturn some of that progress (‘that was not the right way to think about these things’), and it can lead to further progress and new knowledge. An important thing to note here is that how paradigms change is in part a sociological process; part of what leads to change is the popularity of different models. Kuhn argues that scientists tend to prefer new paradigms which solves many of the same problems the old paradigm did, as well as some of those troublesome problems which lead to the crisis – so it’s not like revolutions will necessarily lead people back to square one, with all the scientific progress made during the preceding ‘normal science’ period wiped out. But there are some problems. Textbooks, Kuhn argues, are written by the winners (i.e. the people who picked the right paradigm and get to write textbooks), and so they will often deliberately and systematically downplay the differences between the scientists working in the field now and the scientists working in the field – or what came before it (the fact that normal science is conducted at all is a sign of maturity of a field, Kuhn notes) – in the past, painting a picture of gradual, cumulative progress in the field (gigantum humeris insidentes) which perhaps is not the right way to think about what has actually happened. Sometimes a revolution will make scientists stop asking questions they used to ask, without any answer being provided by the new paradigm; there are costs as well as benefits associated with the dramatical change that takes place during scientific revolutions:
“In the process the community will sustain losses. Often some old problems must be banished. Frequently, in addition, revolution narrows the scope of the community’s professional concerns, increases the extent of its specialization, and attenuates its communication with other groups, both scientific and lay. Though science surely grows in depth, it may not grow in breadth as well. If it does so, that breadth is manifest mainly in the proliferation of scientific specialties, not in the scope of any single specialty alone. Yet despite these and other losses to the individual communities, the nature of such communities provides a virtual guarantee that both the list of problems solved by science and the precision of individual problem-solutions will grow and grow. At least, the nature of the community provides such a guarantee if there is any way at all in which it can be provided. What better criterion than the decision of the scientific group could there be?”
I quote this part also to focus in on an area where I am in disagreement with Kuhn – this relates to his implicit assumption that scientific paradigms (whatever that term may mean) are decided by scientists alone. Certainly this is not the case to the extent that the scientific paradigms equal the rules of the game for conducting science. This is actually one of several major problems I have with the model. Doing science requires money, and people who pay for the stuff will have their own ideas about what you can get away with asking questions about. What the people paying for the stuff have allowed scientists to investigate has changed over time, but some things have changed more than others and what might be termed ‘the broader cultural dimension’ seems important to me; those variables may play a very important role in deciding where science and scientists may or may not go, and although the book deals with sociological stuff in quite a bit of detail, the exclusion of broader cultural and political factors in the model is ‘a bit’ of a problem to me. Scientists are certainly not unconstrained today by such ‘external factors’, and/but most scientists alive today will not face anywhere near the same kinds of constraints on their research as their forebears living 300 years ago did – religion is but one of several elephants in the room (and that one is still really important in some parts of the world, though the role it plays may have changed).
Another big problem is how to test a model like this. Kuhn doesn’t try. He only talks about anecdotes; specific instances, examples which according to him illustrates a broader point. I’m not sure his model is completely stupid, but there are alternative ways to think about these things, including mental models with variables omitted from his model which likely lead to a better appreciation of the processes involved. Money and politics, culture/religion, coalition building and the dynamics of negotiation, things like that. How do institutions fit into all of this? These things have very important effects on how science is conducted, and the (near-)exclusion of them in a model of how to conceptualize the scientific process at least somewhat inspired by sociology and related stuff seems more than a bit odd to me. I’m also not completely clear on why this model is even useful, what it adds. You can presumably approximate pretty much any developmental process by some punctuated equilibrium model like this – it seems to me to be a bit like doing a Taylor expansion, if you add enough terms it’ll look plausible, especially if you add ‘crises’ as well to the model to explain the cases where no clear trend is observable. Stable development is normal science, discontinuities are revolutions, high-variance areas are crises; framed that way you suddenly realize that it’s very convenient indeed for Kuhn that crises don’t always lead to revolutions and that revolutions need not be preceded by crises – if those requirements were imposed on the other hand, the underling data-generating-process would at least be somewhat constrained by the model (though how to actually measure ‘progress’ and ‘variance’ are still questions in need of an answer). I know that the model outlined would not explain a set of completely randomly generated numbers, but in this context I think it would do quite well – even if it’s arguable if it has actually explained anything at all. Add to the model imprecise language – 22 definitions… – and the observation that the model builder seems to be cherry-picking examples to make specific points, what you end up with is, well…
The book was sort of interesting, but, yeah… I feel slightly tempted to revise my goodreads review after having written this post, but I’m not sure I will – it was worth reading the book and I probably should have done it a long time ago, even if only to learn what all the fuss was about (it’s my impression, which may be faulty, that this one is (‘considered to be’) one of the must-reads in this genre). Some of the hypotheses derived from the model seem perhaps to be more testable than others (‘young people are more likely to spark important development in a field’), but even in those cases things get messy (‘what do you mean by ‘important’ and who is to decide that? ‘how young?’). A problem with the model which I have not yet mentioned is incidentally that his model of how interactions between fields and the scientists in those fields take place and proceed to me seems to leave a lot to be desired; the model is very ‘field-centric’. How different fields (which are not about to combine into one), and the people working in them, interact with each other may be yet another very important variable not explored in the model.
As a historical narrative about a few specific important scientific events in the past, Kuhn’s account probably isn’t bad (and it has some interesting observations related to the history of science which I did not know). As ‘a general model of how science works’, well…
“This book, aimed at upper-division undergraduate students and those starting graduate studies, attempts to provide a manageable synthesis of recent developments in the field of terrestrial plant-animal interactions”, they write in the introduction. One of the amazon reviewers claimed that “This is a VERY easy read” – which was actually, in combination with the high ratings it’s got, a large factor leading me to give this book a try; I figured that I shouldn’t be too worried about the fact that this book is written for advanced undergraduates/graduate students in a field I’m not super familiar with.
The book is actually not terribly difficult to read – in the sense that most concepts/terms applied throughout the book are defined along the way, meaning that you’re unlikely to have major issues understanding what’s going on even if you’re not an evolutionary biologist (I’m not, so I should know). It also helps that many of the terms which are not defined along the way will be sort of obvious to you from the context (they never really tell you what coprolite is, but I should think a picture of a dinosaur turd would help… I incidentally read about those things last year, so that particular word did not cause me problems). Although not all ‘potentially problematic terms’ are defined in the book most of them are, and there are a lot of definitions in this book. It’s quite dense; it’s a book where my average reading speed will be around 10 pages per hour, when measured over multiple hours and including necessary reading breaks and so on – perhaps 13-15 when things are going really well. I recently started reading Christie’s Peril at End House, and I’m reasonably sure it’ll take me less time to read that entire book than it took me reading chapter 2 of this book (chapter 2 was, I should perhaps add, significantly longer than the average chapter). I’m well aware that some textbooks are worse than 10-15 pages/hour and I have my eyes on another text dealing with related stuff which I’m reasonably sure will be a bit more work than this one was, and I’m also aware that some books catering to a more advanced audience will presumably take familiarity with many of the terms defined in this book for granted; but even so, calling this ‘a very easy read’ is perhaps a bit much. I should note that although I don’t want to delude anyone into thinking this book is easier to read than it is, I also really don’t want to give people reading along here more excuses not to read this book than is strictly necessary, because I think it’s just a great book.
I have decided to give the book a couple of posts here on the blog, perhaps 3, but I don’t know when I’ll post the others – I have finished the book, and I’ve started reading Kuhn. I’m somewhat behind on the book blogging at the moment, which tends to happen when I’m reading stuff offline; in part because blogging books I’ve read offline is in general a lot more work, among other things because I can’t copy/paste relevant segments when quoting from the books.
I’ve given the book five stars on goodreads simply because as mentioned it’s a really great book – it’s the sort of book which does all those things I’ve been consistently annoyed about popular science books dealing with topics related to the ones covered in this book not doing, and it’s on the other hand also the sort of book which does none of those annoying things the other type of books tend to do. The book doesn’t spend a page talking about how butterflies look nice, ‘you could see the sun setting in the distance…’, or some anecdote about the uncle of the author or crap like that; you have definitions, functional relationships and dynamics explored in detail – a thoroughly analytical approach, without all the infuriating crud. Occasional appreciation, yes, but mainly just the data, the dynamics, the science.
In biology you have two major fields called zoology (dealing with animals) and botany (dealing with plants), but “the knowledge of these two groups of organisms has traditionally progressed along separate lanes, under the leadership of different researchers and independently of each other” (a quote from the introduction). What this means is that there haven’t been a lot of people who’ve done work on ‘the stuff in the middle’ – which is a shame, as “we will never fully understand the evolution of the morphology, behaviour and life history of plants and animals unless we understand in sufficient detail their reciprocal influences in ecological and evolutionary time” (another quote from the introduction). So they’ve written down some of the things they know about these things. The book has nine chapters written by 13 different contributors. The first two chapters are sort of ‘general’ chapters; the first one is about: ‘Species interactions and the evolution of biodiversity’, and the second (much longer) one is about: ‘The history of associations between plants and animals’. In part 2 of the book, dealing with ‘mostly antagonisms’, they talk about plant-insect interactions (chapter 3), mammalian herbivory (chapter 4) and granivory (chapter 5 – “Granivory describes the interaction between plants and the animals (termed granivores or seed-predators) that feed mainly or exclusively on seeds.”). In part 3, dealing with ‘mostly mutualisms’, they talk about pollination by animals (chapter 6) and seed dispersal by vertebrates (chapter 7). In the last part, ‘synthesis’, they talk about ant-plant interactions (chapter 8) and a little bit about ‘future directions’ in research on these matters (chapter 9). In my opinion there were no bad chapters in this book – this is a ‘pure’ five star rating, without any kind of ‘compensatory stuff’ going on. Other people may disagree, but my opinion is that the book is well written, deals with super interesting stuff, and that this stuff is just plain fascinating!
It would be easy to write one post dealing with each of the chapters but I’m not going to do that, and so my posts about this book are going to be another set of those posts where you’ll spend perhaps 10-15 minutes on perhaps 10 hours of material. The book has a lot of stuff I simply cannot cover here, and I highly recommend that you read it if you find the stuff I cover here interesting. It’s been hard to blog this book because it’s in general really difficult to know what to exclude, and very easy to find new things to add. The stuff below covers some of the material from the first two chapters, corresponding to roughly 75 pages.
“The majority of terrestrial organisms fly. […] The evolution of propelled and passive flight, and their consequences, may well be regarded as the most creative force in the development of biodiversity. Most plants fly at one stage of their life cycle or another, as pollen or as seeds or both. Spores of ferns and fungi fly. Pollen, spores and seeds are carried on the wind by a multitude of winged animals: insects, birds, bats and perhaps pterosaurs in their day. […] the vast majority of terrestrial organisms exist in trophic systems based on plants, be they the plant themselves, herbivores, carnivores, pollinators, frugivores or granivores […] as we climb the trophic ladder, species richness increases by orders of magnitude. A plant species, such as an oak, birch or willow, may be host to 200-300 insect herbivore species. Each herbivorous insect may be utilized by 10-20 carnivores, either predators or parasites. The plant provides both food and habitat for the associated fauna and many microhabitats are available for colonization […] Including undescribed species, there may be 10-100 million species of all kinds living today, over half of them insects, of which 99,5% can fly in the adult stage. […] Add to the insects about 9000 species of birds and 1000 bat species, together making up 80% of the warm-blooded vertebrates, and we see that conquest of the air has been an evolutionary ‘success’ of extreme proportions.”
“The basis for the spectacular radiations of animals on earth today is clearly the resources provided by the plants. They are the major primary producers, autotrophically energizing planet Earth. […] Well over 90% of energy in terrestrial systems is fixed by autotrophic plants (the remainder by algae and bacteria), and almost all terrestrial animals depend on autotrophic production, either directly as herbivores or saprophages, or for shelter and microhabitats, or indirectly as predators and parasites utilizing the second trophic level of herbivores. […] plant-animal interactions are both direct and indirect and ramify throughout the trophic system. […] multitrophic-level interactions are ubiquitous and important both for the understanding of natural interactions and for effective management of landscapes dominated by humans […] while plant hosts and their varied insect herbivores evolve and are constantly replaced in time and space, their associations nonetheless remain constant. A Paleozoic palaeodictyopterid insect imbibing vascular tissue sap from a marattialean tree fern is functionally playing the same role as an aphic today feeding on the same tissues in an angiosperm […] Given the taxonomic turnover of vascular plants and herbivorous insects and yet the survival of persistent ecological associations, the phenomenon of ecological convergence is an important long-term pattern […] multidisciplinary evidence from various geological disciplines, particularly those applied to the earlier part of the fossil record, indicate that the more ancient the ecosystem, the less it resembles the present.”
“Three hypotheses have been proposed for assessing how ecological units, such as functional feeding groups, dietary guilds and mouthpart classes, expand in macroevolutionary time […] The first hypothesis, the ecological saturation hypothesis (ESH), advocated by palaeobiologists, maintains that the total number of ecological positions, or roles, has remained approximately constant through time after an initial exponential rise […] Thus taxa enter and exit the ecological arena of the biological community […], but their associations or roles remain virtually level. By contrast, the expanding resource hypothesis (ERH) is favoured by biologists and states that there is a gradual increase in food resources and availability of niches through time […] the intrinsic trend of diversification hypothesis (ITDH) […] holds that the long-term patterns of ESH and ERH vary among groups of organisms […] This view would imply that the proportion of occupied ecological roles has a globally disjunct pattern according to group, time and space. Of these, the current data favors ESH, if one assumes that the ecological clock was set during the Pennsylvanian and the previous fossil record is too poor for analysis.”
“Taphonomy is the study of the physical, chemical and biotic events that affect organisms after death, including pre-burial processes that transform the original living community into an entombed death assemblage that may be encountered by paleobiologists many aeons later. The fidelity to which the preserved assemblage actually resembles the source community is an issue in dicussions of the quality of the fossil record […] A full appreciation of the fossil associational record [between insects and plants] requires an evaluation of the five major types of qualitative evidence: plant reproductive biology, plant damage, dispersed coprolites, gut contents, and insect mouthparts. […] Collectively, these five types of evidence range from the direct, ‘smoking gun’ of gut contents, where the consumer and consumed are typically identifiable, to the more remote and circumstantial evidence of floral reproductive biology and mouthparts, where inferences are based on functional understanding, usually from modern analogues. […] Of all types of evidence for plant-arthropod associations, plant damage has the most extensive fossil record […] gut contents are the rarest type of evidence for plant-animal associations”
“Functional feeding groups can be sorted into 14 basic ways that insects access food” [I had no idea! And yes, they talk about all of these in the book. Note that you can easily split up those ‘basic ways’ into more subcategories if you like:] “In well-preserved Cretaceous and Caenozoic angiosperm-dominated floras, there are approximately 30 distinct types of external foliage-feeding, ranging from generalized bite-marks on margins to highly stereotyped and often intricate patterns of slot-hole feeding: earlier floras have fewer recognizable types of damage. […] The history of arthropod feeding on plants began during the Late Silurian to early Devonian […] by the close of the Pennsylvanian, the expansion of arthropod herbivory had invaded all plant organisms and virtually all plant tissues […] This expansion of dietary breadth provided a modern cast to the spectrum of insect diets. […] while the overwhelming bulk of the 14 plant-associated diet types was in place during the late Pennsylvanian, it was followed by the addition of 4 novel diet types during the Mesozoic in conjunction with the establishment of freshwater ecosystems and the diversification of advanced seed plants. […] When expressed as a diversity curve spanning the past 400 million years, there is a linear but stepped rise in mouthpart class diversity from the Early Devonian to the Early Jurassic, where it reached a plateau, followed by only a few subsequent additions […] Thus virtually all basic mouthpart innovation, including plant-associated mouthpart classes, was established prior to the angiosperm ecological expansion during the Middle Cretaceous [this was when flowering plants really took off, US], suggesting that mouthpart classes are attributable to basic associations with seed plants, or vascular plants of the more remote past, rather than the relatively late-appearing angiosperms […] Arthropods have used plants extensively for shelter probably since the Early Devonian”
“The amount of live plant tissue assimilated by arthropods is significantly greater than that of vertebrates in virtually all biomes except grasslands […] The fossil evidence indicates that this arthropod dominance has probably been the case since the establishment of the earliest terrestrial ecosystems. In fact, it was not until the latest Devonian that vertebrates emerged on land […], for which evidence indicates obligate carnivory. […] Direct evidence for vertebrate herbivory does not occur until the latest Pennsylvanian to earliest Permian […], about 100 million years after it appeared among mid-Paleozoic arthropods. […] A consequence of large vertebrate size is that consumption of plant organs is frequently complete and not partial as it is among arthropods, leaving minimal evidence from leaves, seeds and other wholly-consumed items. Also, the rarity of vertebrates when compared to arthropods may result in an underestimate of vertebrate importance in their interactions with plants. […] An interesting aspect of Paleozoic tetrapod herbivores is that they were uniformly short-necked and short-limbed browsers that cropped plant material within a metre to perhaps two metres of the ground surface. This trend continued […] into the Late Triassic, at which time basal dinosaur lineages began their diversification into virtually all major terrestrial feeding niches […] While Paleocene to middle Eocene mammalian herbivores were dominated by small to medium-sized forms consuming fruit, seeds and leaves, later herbivores were much larger, and invaded the browsing and eventually grazing adaptive zones […] This shift is related to the mid-Caenozoic origin of savanna and grassland biomes concomitant with the ecological spread of grasses. The oldest grasses reliably documented in the fossil record occur at the Palaeocene/Eocene boundary [~56 mya, US] […], although the earliest evidence for a grassland-adapted mammalian fauna is from the middle Oligocene [~28 mya, US] of Mongolia […] During the Pleistocene (2.65 Ma to 10 000 yr BP), much of the Planet underwent severe climactic pertubations from five major episodes of continental and associated alpine glaciation. Continental faunas were considerably reorganized during and after this interval in terms of dominance and composition of species […] Much evidence now supports a view that continental species did not respond as cohesive assemblages to these major environmental shifts, but rather individualistically […] An important exception to this trend are insects with high host specificity, which responded differently, retaining ancestral plant associations to the present […] or becoming extinct. Herbivorous mammals have less obligate dependence on plant species […] and thus exhibit greater dietary flexibility during times of major environmental stress.”
“Most doctors think that the most memorable way to learn medicine is to see patients. It is easier to recall information based on a real person than a page in a textbook. Another important element in the retention of information is the depth of learning. Learning that seeks to understand problems is more likely to be accessible later than superficial factual accumulation. This is the basis of problem-based learning, whereby students explore problems with the help of a facilitator. The cases in this book are designed to provide another useful approach, parallel to seeing patients and giving an opportunity for self-directed exploration of clinical problems. They are based on the findings of history taking and examination, together with the need to evaluate initial investigations such as blood investigations, X-rays and electrocardiograms.
These cases are no substitute for clinical experience with real patients, but they provide a safe environment for students to explore clinical problems and their own approach to diagnosis and management. Most are common problems that might present to a general practitioner’s surgery, a medical outpatients clinic or a session on call in hospital. There are a few more unusual cases to illustrate specific points and to emphasize that rare things do present, even if they are uncommon. The cases are written to try to interest students in clinical problems and to enthuse them to find out more. They try to explore thinking about diagnosis and management of real clinical situations.”
As for the ‘interest students in clinical problems and to enthuse them to find out more’-part they certainly succeeded, but I approached this book in a slightly different manner than I did the first one in the series. When I read the acute medicine book, I’d occasionally think to myself while reading the patient history and/or the reported lab results that ‘hey, this sounds a bit like…’ and I’d look up the diagnosis/condition I was considering in order to decide if I wanted to ‘guess’ at that, before moving on to reading the answer part of the case. I did this a few times as well here, but actually most of the pre-answer wiki peeks were related to the interpretation of specific lab results (‘how to interpret some of the arterial blood gas test results’). The reason why I tried to limit myself from looking up stuff before reading the answer was that I wanted to know a little bit about how much of the pathophysiology text (and stuff covered in related texts, such as e.g. Hall’s Handbook and Rogers et al., as well as various medical lectures e.g. from Khan Academy) I could remember. I actually realized when reading the first 100 cases book that there were very few conditions covered there which I had not already read about, or at least seen mentioned, elsewhere; the problem was figuring out which patients had which specific problems. Part of the reason why I often had trouble with that part was incidentally related to the fact that there are some other relevant books I have not read – books such as this one or this one (I’m not planning on reading these, just in case you were wondering). A related point is that doctors have a lot more information available to them than do the people who are sick, and that this is certainly a (small) part of the explanation for why they are better at figuring out what’s wrong than are the people who are sick – symptoms can be non-specific, but if so lab results will often tell you more about where to look and what to look for. I decided beforehand when reading this book that I’d try for fun to keep score and figure out in how many cases I guessed the correct diagnosis; it turned out that I guessed the right diagnosis in roughly one-fifth of the cases and in a few other cases the guess I made was a very plausible differential diagnosis which needed to be ruled out anyway. In a few of them I didn’t get ‘the complete picture’, and I learned something from many of the cases where I knew the (‘diagnosis’-part of the-) right answer. I feel quite certain I would have guessed more of them if I’d spent more time on individual cases; I read the entire book yesterday, and this is not a book you can read in a few hours (I think it took me 12 hours, at least, but I’m not really sure as I didn’t keep track and did take breaks occasionally. Ratios like these – me spending easily 5-10 hours or more on stuff which leads to a post which you’ll read in perhaps 10-15 minutes – are incidentally one reason why I sometimes feel that people reading along here are ‘cheating’ in a way. On the other hand I really can’t complain as long as I’m enabling such ‘cheating’ in the first place…). I got far most of my guesses correct, as in many cases I didn’t guess at all because I wasn’t completely sure what was going on. Of course treatment and management aspects I didn’t ‘guess at’, and that’s an important aspect of the book as well. The conditions I recognized spanned a rather broad range; from colon cancer over HIV seroconversion illness (main differential was malaria – I knew this as well) to COPD, rheumatoid arthritis, bacterial meningitis, obstructive sleep apnea, peripheral neuropathy secondary to undiagnosed type 2 diabetes mellitus, dementia, small cell lung cancer with associated paraneoplastic syndrome, and Parkinson’s disease. As you can probably tell from those diagnoses, like the acute medicine book this book also has some rather depressing cases. Some cases, e.g. a case of cerebral toxoplasmosis secondary to HIV infection (this is actually an AIDS-defining illness, so she had AIDS at the time of admission) and a diet-related vitamin B12 deficiency, were really obvious in retrospect, but in medicine there’s a lot of stuff to remember.
I’ve added some quotes, observations and key points from the book below.
“Cystic fibrosis should always be considered when there is a story of repeated chest infections in a young person. Although it presents most often below the age of 20 years, diagnosis may be delayed until the 20s, 30s, 40s or later in milder cases.”
“Patients with a chronic persistent cough of unexplained cause should have a chest X-ray. When the X-ray is clear the cough is likely to be produced by one of three main causes in non-smokers. Around half of such cases have asthma or will go on to develop asthma over the next few years. Half of the rest have rhinitis or sinusitis with a postnasal drip. In around 20 per cent the cough is related to gastro-oesophageal reflux […] Cough is a common side effect in patients treated with angiotensin-converting enzyme (ACE) inhibitors.”
“This man has signs of chronic liver disease with ascites and oedema. […] The most common cause of chronic liver disease is alcohol. […] However, his alcohol intake is too low to be consistent with the diagnosis of alcoholic liver disease [15-20 units/week, according to the patient history. This was why I initially rejected alcohol-related pathology in this case and (very briefly) considered other causes instead, without coming up with anything (this was another one of those aforementioned obvious ones in retrospect)…]. When the provisional diagnosis is discussed with him, though, he eventually admits that his alcohol intake has been at least 40–50 units per week for the last 20 years. His alcohol intake has increased further during the last year after his marriage had ended.” [Patients sometimes lie to their doctors. This one did. In case you were wondering he died three years later from an esophageal variceal bleed.]
“Patients often become symptomatic due to renal failure only when their glomerular filtration rate (GFR) is less than 15 mL/min [normal range is 90+, US] and thus may present with end-stage renal failure.” [This is an example of a more general point in many medical contexts; our bodies often have a lot of ‘excess capacity’ and redundancies implemented in order to make us less likely to get sick/get symptoms which may decrease our likelihood of survival even if things aren’t optimal. The book actually has other examples illustrating this point, e.g. this: “Patients with central diabetes insipidus typically describe an abrupt onset of polyuria and polydipsia. This is because urinary concentration can be maintained fairly well until the number of AVP-secreting neurones in the hypothalamus decreases to 10–15 per cent of the normal number, after which AVP levels decrease to a range where urine output increases dramatically.”]
“Petechiae are small capillary haemorrhages that characteristically develop in crops in areas of increased venous pressure, such as the dependent parts of the body. Petechiae are the smallest bleeding lesions (pinhead in size), and suggest problems with platelet number or function. Purpura are larger in size than petechiae with variable shape and involve bleeding into subcutaneous tissues. Purpura can be seen in a variety of bleeding disorders […] AML is the most common acute leukaemia in adults with a mean age at presentation of 65 years. Patients with AML generally present with symptoms related to complications of pancytopenia (eg, anemia, neutropenia, and thrombocytopenia), including weakness, breathlessness and easy fatigability, infections of variable severity, and/or haemorrhagic findings such as gingival bleeding, ecchymoses, epistaxis, or menorrhagia.”
“Vegans who omit all animal products from their diet often have subclinical vitamin B12 deficiency […] Vitamin B12 deficiency may occur in strict vegetarians who eat no dairy products. […] Typical neurological signs are position and vibration sense impairment in the legs, absent reflexes and extensor plantars.”
“Malaria prophylaxis is often not taken regularly. Even when it is, it does not provide complete protection against malaria […] A traveller returning from a malaria endemic region who develops a fever has malaria until proven otherwise.”
“Peripheral oedema may occur due to local obstruction of lymphatic or venous outflow or because of cardiac, renal, pulmonary or liver disease. Unilateral oedema is most likely to be due to a local problem […] Bilateral oedema may be due to cardiac, liver or renal disease. […] Pitting oedema needs to be distinguished from lymphoedema, which is characteristically non-pitting. This is tested by firm pressure with the thumb for approximately 10 s. If the oedema is pitting, an indentation will be present after pressure is removed. […] frothy urine is a clue to the diagnosis of nephrotic syndrome and is commonly noted by patients with heavy proteinuria.”
“80% of C. difficile infections occur in people aged over 65 years since a lower density and fewer species of gut bacteria make them more susceptible to colonisation by C. difficile […] 20% of hospital patients and those in long-term care facilities are colonised with C. difficile. […] C. difficile infection should be suspected in any hospital patient who develops diarrhoea.”
“ADPKD [Autosomal Dominant Polycystic Kidney Disease] is the most common inherited renal disease, occurring in approximately 1:600 to 1:1000 individuals. Although the name ‘ADPKD’ is derived from renal manifestations of cyst growth leading to enlarged kidneys and renal failure, this is a systemic disorder manifested by the presence of hepatic cysts, diverticular disease, inguinal hernias, mitral valve prolapse, intracranial aneurysms and hypertension. […] Patients with ADPKD are often asymptomatic. […] Flank pain is the most common symptom […] Hypertension occurs early in the course of this disease, affecting 60% of patients with normal renal function. Approximately 50% of ADPKD patients will develop end-stage renal failure.”
“Transient small nodes in the neck or groin are common benign findings. However, a 3 × 4 cm mass of nodes for 2 months is undoubtedly abnormal. […] Lymph nodes are normally barely palpable, if at all. The character of enlarged lymph nodes is very important. In acute infections the nodes are tender, and the overlying skin may be red. Carcinomatous nodes are usually very hard, fixed and irregular. The nodes of chronic leukaemias and lymphomas are non-tender, firm and rubbery. […] The typical systemic symptoms of lymphoma are malaise, fever, night sweats, pruritus, weight loss, anorexia and fatigue.”
“Colonic diverticula are small outpouchings that are most commonly found in the left colon. […] Inflammation in a diverticulum is termed diverticulitis. […] Diverticular disease is a common finding in the elderly Western population and may be asymptomatic or cause irritable bowel syndrome-type symptoms. […] Diverticular disease is a common condition; its presence can distract the unwary doctor from pursuing a coincident condition.”
“Tension type headaches are the commonest headaches in the general population. The typical presentation is of mild to moderate headache, nonthrobbing, bilateral with no associated symptoms. Cluster headaches are characterised by attacks of severe unilateral orbital or temporal pain, accompanied by autonomic features such as nasal congestion, lacrimation and rhinorrhoea. Migraines are often preceded by characteristic symptoms such as flashing lights and are often unilateral. Nausea and photophobia may occur during an attack. Brain tumours cause headaches by causing raised intracranial pressure. The headache is worse after coughing and is often associated with nausea and vomiting. […] The sudden onset of a headache within seconds or a few minutes is characteristic of a subarachnoid haemaorrhage (SAH). […] Patients with SAH often describe the pain as ‘the worst headache in my life’. [And in many cases it’s also the last headache they ever will have:] SAH is associated with a mortality rate of up to 50%.”
“He drinks 35 units of alcohol per week and smokes 30 cigarettes per day.” [Aargh! Another one of those! But at least this one didn’t lie about his drinking habits. … But it gets worse:] “No history was available from the patient [she’s in a coma], but her partner volunteered the information that they are both intravenous heroin addicts. She is unemployed, smokes 25 cigarettes per day, drinks 40 units of alcohol per week and has used heroin for the past 4 years.” [Dammit! Some of these histories are depressing in more than one way. The woman had been found unconscious by her partner. My first thought when reading the case story about the woman and the lab results was that, ‘This reminds me of that movie I saw a while back, what’s it called..?’ – I can’t remember the name of the movie, but it’s not important. I want to quote a bit more extensively from the answer part of this case because I thought it was sort of fascinating in a way; it illustrates how a drug overdose isn’t always just a problem because of the drug overdose:]
“This patient has acute renal failure as a result of rhabdomyolysis. Severe muscle damage causes a massively elevated serum creatine kinase (CK) level and a rise in serum potassium and phosphate levels. In this case, she has lain unconscious on her left arm for many hours due to an overdose of alcohol and intravenous heroin. As a result, she has developed severe ischaemic muscle damage, causing release of myoglobin, which is toxic to the kidneys. […] Acute renal failure due to rhabdomyolysis causes profound hypocalcaemia in the oliguric phase due to calcium sequestration in muscle and reduced 1,25-dihydroxycalciferol levels, often with rebound hypercalcaemia in the recovery phase. This woman’s consciousness level is still depressed as a result of opiate and alcohol toxicity, and she has clinical and radiological evidence of aspiration pneumonia. She has mixed metabolic and respiratory acidosis (low pH, bicarbonate) due to acute renal failure and respiratory depression (pCO2 elevated). Her arterial oxygenation is reduced due to hypoventilation and pneumonia. She also has compartment syndrome in her arm due to massive swelling of her damaged muscles. This patient has life-threatening hyperkalaemia with electrocardiogram (ECG) changes. […] Emergency treatment involves intravenous calcium gluconate, which stabilizes cardiac conduction, and intravenous insulin/glucose, intravenous sodium bicarbonate and nebulized salbutamol, all of which temporarily lower the plasma potassium by increasing the cellular uptake of potassium. However, these steps should be regarded as holding measures while urgent dialysis is being organized. The chest X-ray and clinical findings indicate consolidation of the left lower lobe. This patient should initially be managed on an intensive care unit. She will require antibiotics for her pneumonia and will require a naloxone infusion or mechanical ventilation for her respiratory failure. The patient should have vigorous rehydration with monitoring of her central venous pressure. If a good urinary flow can be maintained, urinary pH should be kept greater than 7.0 by bicarbonate infusion, which prevents the renal toxicity of myoglobin. This patient also needs to be considered urgently for surgical fasciotomy to relieve the compartment syndrome in her arm.”
Back when I read the Acute Muscle Injuries text, compartment syndrome was sort of a worst-case-scenario. Here it’s just one of multiple problems, each of which on their own would be quite terrible. I should incidentally note in case you were wondering if all of the patients in this book are alcoholics that most of them are not – but that they mention in the coverage that: “In some surveys alcohol is linked directly to around 25% of acute medical admissions.” I looked around very briefly for those numbers because they sounded very high to me, but I didn’t find much. This paper had an estimate of 6%, but that’s out of all hospital admissions and you’d expect the proportion of all admissions involving alcohol to be significantly lower than the proportion of acute admissions. Note in that context that ‘the true number’ in the former case is to some extent unknowable – though you can try to estimate it, as people do – as e.g. alcohol’s role in certain cancers is quite difficult to figure out in general, and impossible to figure out at the individual level; it makes sense to say that drinking alcohol increases your risk of breast cancer (and perhaps that’s not even the best example as we’re quite sure alcohol has a role there, a level of certainty we in other areas of oncology do not have), but deciding with certainty whether patient X’s specific case of breast cancer was alcohol-related or not is impossible – ‘it may have been a contributing factor’ is probably the closest you can get, we don’t have a test for that. Same goes for a cardiovascular event – ‘alcohol may have played a role’, but that’s it. Perhaps also worth remembering here is incidentally that on a related note some epidemiological findings trying to have a closer look at precisely these sorts of things may have results which are partially explained by statistical artifacts unrelated to the ‘true’ associated risk; a smoker who drinks a lot is highly likely to die from various alcohol- and smoking-related causes at a relatively early age. Such early deaths may well make people with such habits less likely to get old enough to get prostate cancer (the risk of which increases dramatically with age), even if alcohol and smoking on their own perhaps actually increase the risk of prostate cancer, in the sense that the effects of both alcohol and smoking may be to make those cells more likely to turn malignant (I don’t know if this is actually the case or not, it’s just the sort of thing you need to watch out for). There are ways around such problems – a competing risks framework is important to have in mind here – but problems of this sort are sometimes hard to avoid and/or deal with.
They don’t talk about these things in the book, but they talk about a lot of other interesting stuff, and I can’t cover all of it. One thing I have yet to cover which I thought I should include as a small favour to a friend reading along is this part, from the very last pages of the book:
“Traditional Chinese medicine includes herbal therapy, acupuncture, massage and dietary therapy. There is potential for developing novel treatments for diseases such as asthma and food allergies with Chinese herbs. However, there is concern over the lack of standardization and controlled clinical trials. Chinese herbal medicines containing aristolochic acid have been implicated in a specific nephropathy characterised by extensive interstitial fibrosis with atrophy and loss of the tubules, with thickening of the walls of the interlobular and afferent arterioles. Blood pressure is generally normal or only modestly elevated. Patients presenting with a creatinine < 200 will generally stabilise their renal function after stopping the Chinese medications, but patients with worse kidney function will generally progress to end-stage kidney failure.”
I liked the book and I gave it three stars on goodreads. You need to be fluent in ‘medical textbook’ in order to get much out of this book, but if you have some medical knowledge I believe you’ll be quite likely to find the books in this series quite interesting.
This will be my last post about the book. Go here for a background post and my overall impression of the book – I’ll limit this post to coverage of the ‘Simple Models of Complex Phenomena’-chapter which I mentioned in that post, as well as a few observations from the introduction to part 5 of the book, which talks a little bit about what the chapter is about in general terms. The stuff they write in the chapter is in a way a sort of overview over the kind of approach to things which you may well end up adopting unconsciously if you’re working in a field like economics or ecology and a defence of such an approach; I’ve as mentioned in the previous post about the book talked about these sorts of things before, but there’s some new stuff in here as well. The chapter is written in the context of Boyd and Richerson’s coverage of their ‘Darwinian approach to evolution’, but many of the observations here are of a much more general nature and relate to the application of statistical and mathematical modelling in a much broader context; and some of those observations that do not directly relate to broader contexts still do as far as I can see have what might be termed ‘generalized analogues’. The chapter coverage was actually interesting enough for me to seriously consider reading a book or two on these topics (books such as this one), despite the amount of work I know may well be required to deal with a book like this.
I exclude a lot of stuff from the chapter in this post, and there are a lot of other good chapters in the book. Again, you should read this book.
Here’s the stuff from the introduction:
“Chapter 19 is directed at those in the social sciences unfamiliar with a style of deploying mathematical models that is second nature to economists, evolutionary biologists, engineers, and others. Much science in many disciplines consists of a toolkit of very simple mathematical models. To many not familiar with the subtle art of the simple model, such formal exercises have two seemingly deadly ﬂaws. First, they are not easy to follow. […] Second, motivation to follow the math is often wanting because the model is so cartoonishly simple relative to the real world being analyzed. Critics often level the charge ‘‘reductionism’’ with what they take to be devastating effect. The modeler’s reply is that these two criticisms actually point in opposite directions and sum to nothing. True, the model is quite simple relative to reality, but even so, the analysis is difﬁcult. The real lesson is that complex phenomena like culture require a humble approach. We have to bite off tiny bits of reality to analyze and build up a more global knowledge step by patient step. […] Simple models, simple experiments, and simple observational programs are the best the human mind can do in the face of the awesome complexity of nature. The alternatives to simple models are either complex models or verbal descriptions and analysis. Complex models are sometimes useful for their predictive power, but they have the vice of being difﬁcult or impossible to understand. The heuristic value of simple models in schooling our intuition about natural processes is exceedingly important, even when their predictive power is limited. […] Unaided verbal reasoning can be unreliable […] The lesson, we think, is that all serious students of human behavior need to know enough math to at least appreciate the contributions simple mathematical models make to the understanding of complex phenomena. The idea that social scientists need less math than biologists or other natural scientists is completely mistaken.”
And below I’ve posted the chapter coverage:
“A great deal of the progress in evolutionary biology has resulted from the deployment of relatively simple theoretical models. Staddon’s, Smith’s, and Maynard Smith’s contributions illustrate this point. Despite their success, simple models have been subjected to a steady stream of criticism. The complexity of real social and biological phenomena is compared to the toylike quality of the simple models used to analyze them and their users charged with unwarranted reductionism or plain simplemindedness.
This critique is intuitively appealing—complex phenomena would seem to require complex theories to understand them—but misleading. In this chapter we argue that the study of complex, diverse phenomena like organic evolution requires complex, multilevel theories but that such theories are best built from toolkits made up of a diverse collection of simple models. Because individual models in the toolkit are designed to provide insight into only selected aspects of the more complex whole, they are necessarily incomplete. Nevertheless, students of complex phenomena aim for a reasonably complete theory by studying many related simple models. The neo-Darwinian theory of evolution provides a good example: ﬁtness-optimizing models, one and multiple locus genetic models, and quantitative genetic models all emphasize certain details of the evolutionary process at the expense of others. While any given model is simple, the theory as a whole is much more comprehensive than any one of them.”
“In the last few years, a number of scholars have attempted to understand the processes of cultural evolution in Darwinian terms […] The idea that uniﬁes all this work is that social learning or cultural transmission can be modeled as a system of inheritance; to understand the macroscopic patterns of cultural change we must understand the microscopic processes that increase the frequency of some culturally transmitted variants and reduce the frequency of others. Put another way, to understand cultural evolution we must account for all of the processes by which cultural variation is transmitted and modiﬁed. This is the essence of the Darwinian approach to evolution.”
“In the face of the complexity of evolutionary processes, the appropriate strategy may seem obvious: to be useful, models must be realistic; they should incorporate all factors that scientists studying the phenomena know to be important. This reasoning is certainly plausible, and many scientists, particularly in economics […] and ecology […], have constructed such models, despite their complexity. On this view, simple models are primitive, things to be replaced as our sophistication about evolution grows. Nevertheless, theorists in such disciplines as evolutionary biology and economics stubbornly continue to use simple models even though improvements in empirical knowledge, analytical mathematics, and computing now enable them to create extremely elaborate models if they care to do so. Theorists of this persuasion eschew more detailed models because (1) they are hard to understand, (2) they are difﬁcult to analyze, and (3) they are often no more useful for prediction than simple models. […] Detailed models usually require very large amounts of data to determine the various parameter values in the model. Such data are rarely available. Moreover, small inaccuracies or errors in the formulation of the model can produce quite erroneous predictions. The temptation is to ‘‘tune’’ the model, making small changes, perhaps well within the error of available data, so that the model produces reasonable answers. When this is done, any predictive power that the model might have is due more to statistical ﬁtting than to the fact that it accurately represents actual causal processes. It is easy to make large sacriﬁces of understanding for small gains in predictive power.”
“In the face of these difﬁculties, the most useful strategy will usually be to build a variety of simple models that can be completely understood but that still capture the important properties of the processes of interest. Liebenstein (1976: ch. 2) calls such simple models ‘‘sample theories.’’ Students of complex and diverse subject matters develop a large body of models from which ‘‘samples’’ can be drawn for the purpose at hand. Useful sample theories result from attempts to satisfy two competing desiderata: they should be simple enough to be clearly and completely grasped, and at the same time they should reﬂect how real processes actually do work, at least to some approximation. A systematically constructed population of sample theories and combinations of them constitutes the theory of how the whole complex process works. […] If they are well designed, they are like good caricatures, capturing a few essential features of the problem in a recognizable but stylized manner and with no attempt to represent features not of immediate interest. […] The user attempts to discover ‘‘robust’’ results, conclusions that are at least qualitatively correct, at least for some range of situations, despite the complexity and diversity of the phenomena they attempt to describe. […] Note that simple models can often be tested for their scientiﬁc content via their predictions even when the situation is too complicated to make practical predictions. Experimental or statistical controls often make it possible to expose the variation due to the processes modeled, against the background of ‘‘noise’’ due to other ones, thus allowing a ceteris paribus prediction for purposes of empirical testing.”
“Generalized sample theories are an important subset of the simple sample theories used to understand complex, diverse problems. They are designed to capture the qualitative properties of the whole class of processes that they are used to represent, while more specialized ones are used for closer approximations to narrower classes of cases. […] One might agree with the case for a diverse toolkit of simple models but still doubt the utility of generalized sample theories. Fitness-maximizing calculations are often used as a simple caricature of how selection ought to work most of the time in most organisms to produce adaptations. Does such a generalized sample theory have any serious scientiﬁc purpose? Some might argue that their qualitative kind of understanding is, at best, useful for giving nonspecialists a simpliﬁed overview of complicated topics and that real scientiﬁc progress still occurs entirely in the construction of specialized sample theories that actually predict. A sterner critic might characterize the attempt to construct generalized models as loose speculation that actually inhibits the real work of discovering predictable relationships in particular systems. These kinds of objections implicitly assume that it is possible to do science without any kind of general model. All scientists have mental models of the world. The part of the model that deals with their disciplinary specialty is more detailed than the parts that represent related areas of science. Many aspects of a scientist’s mental model are likely to be vague and never expressed. The real choice is between an intuitive, perhaps covert, general theory and an explicit, often mathematical, one. […] To insist upon empirical science in the style of physics is to insist upon the impossible. However, to give up on empirical tests and prediction would be to abandon science and retreat to speculative philosophy. Generalized sample theories normally make only limited qualitative predictions. The logistic model of population growth is a good elementary example. At best, it is an accurate model only of microbial growth in the laboratory. However, it captures something of the biology of population growth in more complex cases. Moreover, its simplicity makes it a handy general model to incorporate into models that must also represent other processes such as selection, and intra- and interspeciﬁc competition. If some sample theory is consistently at variance with the data, then it must be modiﬁed. The accumulation of these kinds of modiﬁcations can eventually alter general theory […] A generalized model is useful so long as its predictions are qualitatively correct, roughly conforming to the majority of cases. It is helpful if the inevitable limits of the model are understood. It is not necessarily an embarrassment if more than one alternative formulation of a general theory, built from different sample models, is more or less equally correct. In this case, the comparison of theories that are empirically equivalent makes clearer what is at stake in scientiﬁc controversies and may suggest empirical and theoretical steps toward a resolution.”
“The thorough study of simple models includes pressing them to their extreme limits. This is especially useful at the second step of development, where simple models of basic processes are combined into a candidate generalized model of an interesting question. There are two related purposes in this exercise. First, it is helpful to have all the implications of a given simple model exposed for comparative purposes, if nothing else. A well-understood simple sample theory serves as a useful point of comparison for the results of more complex alternatives, even when some conclusions are utterly ridiculous. Second, models do not usually just fail; they fail for particular reasons that are often very informative. Just what kinds of modiﬁcations are required to make the initially ridiculous results more nearly reasonable? […] The exhaustive analysis of many sample models in various combinations is also the main means of seeking robust results (Wimsatt, 1981). One way to gain conﬁdence in simple models is to build several models embodying different characterizations of the problem of interest and different simplifying assumptions. If the results of a model are robust, the same qualitative results ought to obtain for a whole family of related models in which the supposedly extraneous details differ. […] Similarly, as more complex considerations are introduced into the family of models, simple model results can be considered robust only if it seems that the qualitative conclusion holds for some reasonable range of plausible conditions.”
“A plausibility argument is a hypothetical explanation having three features in common with a traditional hypothesis: (1) a claim of deductive soundness, of in-principle logical sufﬁciency to explain a body of data; (2) sufﬁcient support from the existing body of empirical data to suggest that it might actually be able to explain a body of data as well as or better than competing plausibility arguments; and (3) a program of research that might distinguish between the claims of competing plausibility arguments. The differences are that competing plausibility arguments (1) are seldom mutually exclusive, (2) can seldom be rejected by a single sharp experimental test (or small set of them), and (3) often end up being revised, limited in their generality or domain of applicability, or combined with competing arguments rather than being rejected. In other words, competing plausibility arguments are based on the claims that a different set of submodels is needed to achieve a given degree of realism and generality, that different parameter values of common submodels are required, or that a given model is correct as far as it goes, but applies with less generality, realism, or predictive power than its proponents claim. […] Human sociobiology provides a good example of a plausibility argument. The basic premise of human sociobiology is that ﬁtness-optimizing models drawn from evolutionary biology can be used to understand human behavior. […] We think that the clearest way to address the controversial questions raised by competing plausibility arguments is to try to formulate models with parameters such that for some values of the critical parameters the results approximate one of the polar positions in such debates, while for others the model approximates the other position.”
“A well-developed plausibility argument differs sharply from another common type of argument that we call a programmatic claim. Most generally, a programmatic claim advocates a plan of research for addressing some outstanding problem without, however, attempting to construct a full plausibility argument. […] An attack on an existing, often widely accepted, plausibility argument on the grounds that the plausibility argument is incomplete is a kind of programmatic claim. Critiques of human sociobiology are commonly of this type. […] The criticism of human sociobiology has far too frequently depended on mere programmatic claims (often invalid ones at that, as when sociobiologists are said to ignore the importance of culture and to depend on genetic variation to explain human differences). These claims are generally accompanied by dubious burden-of-proof arguments. […] We have argued that theory about complex-diverse phenomena is necessarily made up of simple models that omit many details of the phenomena under study. It is very easy to criticize theory of this kind on the grounds that it is incomplete (or defend it on the grounds that it one day will be much more complete). Such criticism and defense is not really very useful because all such models are incomplete in many ways and may be ﬂawed because of it. What is required is a plausibility argument that shows that some factor that is omitted could be sufﬁciently important to require inclusion in the theory of the phenomenon under consideration, or a plausible case that it really can be neglected for most purposes. […] It seems to us that until very recently, ‘‘nature-nurture’’ debates have been badly confused because plausibility arguments have often been taken to have been successfully countered by programmatic claims. It has proved relatively easy to construct reasonable and increasingly sophisticated Darwinian plausibility arguments about human behavior from the prevailing general theory. It is also relatively easy to spot the programmatic ﬂaws in such arguments […] The problem is that programmatic objections have not been taken to imply a promise to deliver a full plausibility claim. Rather, they have been taken as a kind of declaration of independence of the social sciences from biology. Having shown that the biological theory is in principle incomplete, the conclusion is drawn that it can safely be ignored.”
“Scientists should be encouraged to take a sophisticated attitude toward empirical testing of plausibility arguments […] Folk Popperism among scientists has had the very desirable result of reducing the amount of theory-free descriptive empiricism in many complex-diverse disciplines, but it has had the undesirable effect of encouraging a search for simple mutually exclusive hypotheses that can be accepted or rejected by single experiments. By our argument, very few important problems in evolutionary biology or the social sciences can be resolved in this way. Rather, individual empirical investigations should be viewed as weighing marginally for or against plausibility arguments. Often, empirical studies may themselves discover or suggest new plausibility arguments or reconcile old ones.”
“We suspect that most evolutionary biologists and philosophers of biology on both sides of the dispute would pretty much agree with the defense of the simple models strategy presented here. To reject the strategy of building evolutionary theory from collections of simple models is to embrace a kind of scientiﬁc nihilism in which there is no hope of achieving an understanding of how evolution works. On the other hand, there is reason to treat any given model skeptically. […] It may be possible to defend the proposition that the complexity and diversity of evolutionary phenomena make any scientiﬁc understanding of evolutionary processes impossible. Or, even if we can obtain a satisfactory understanding of particular cases of evolution, any attempt at a general, uniﬁed theory may be impossible. Some critics of adaptationism seem to invoke these arguments against adaptationism without fully embracing them. The problem is that alternatives to adaptationism must face the same problem of diversity and complexity that Darwinians use the simple model strategy to ﬁnesse. The critics, when they come to construct plausibility arguments, will also have to use relatively simple models that are vulnerable to the same attack. If there is a vulgar sociobiology, there is also a vulgar criticism of sociobiology.”
“100 Cases in Acute Medicine presents 100 acute conditions commonly seen by medical students and junior doctors in the emergency department, or on the ward, or in the community setting. A succinct summary of the patient’s history, examination, and initial investigations, including photographs where relevant, is followed by questions on the diagnosis and management of each case. The answer includes a detailed discussion of each topic, with further illustration where appropriate, providing an essential revision aid as well as a practical guide for students and junior doctors.
Making clinical decisions and choosing the best course of action is one of the most challenging and difficult parts of training to become a doctor. These cases will teach students and junior doctors to recognize important clinical symptoms and signs, and to develop their diagnostic and management skills.”
The book is quite simple. There are 100 medical cases. Each case has a brief description of symptoms and what we know about the patient, plus a couple of questions. On the next page of the book there are then answers to the questions posed with (semi-?)detailed explanations. In many cases one of, or perhaps the only question, is: ‘what’s wrong with this person?’, but sometimes the management aspect is considered to be the key variable (‘obese hypertensive and hyperlipidemic type 2 diabetic with previous MI has just been admitted with cardiac symptoms. Here are the results of his blood-work and an ECG. How do you proceed?’ – not a quote, but close enough…), and in such cases there are e.g. questions about which particular aspects of this presentation you should be most concerned about, or perhaps an open question related to aspects such as how to optimize the follow-up process. I’ll never diagnose anyone with anything or set up a medical management plan, as that is for doctors to do, but I thought it looked like an interesting book, so I figured I’d give it a shot. Reading a book like this is a little bit like watching House, except that the medicine in here is actually trustworthy and you avoid all the drama (I know that I have remarked upon how reading medical textbooks will change your viewing experience of medical dramas before, but in the context of this book that particular aspect seems perhaps even more relevant than usual – all the patients in this book have presented to the ER because they are sick and we are told about their symptoms and perhaps some of the test results which have come back from the lab; this setting, I believe, is pretty much the default setting for medical dramas…).
The blog currently has 118 posts related to the topic of medicine so I have read some stuff and watched some lectures on these topics; I figured it’d be interesting to see if I could figure out some of the cases, and I felt reasonably sure I’d learn from both the ones I could figure out and the ones I couldn’t (as I considered them likely to add details I didn’t know, e.g. about differential diagnoses, in the anwers). I also thought more generally that it’d be nice to have a book with some ‘common/standard’ health complaint cases presented. Diagnostics is often more difficult than you’d think from reading about specific diseases, because people in many cases don’t present with all the textbook symptoms, and because certain symptoms present in a lot of very different situations. A confused old person with altered mental status might for example ‘just’ be dehydrated with nothing else going on (severe dehydration can be quite dangerous, thus the ‘just’) – but it could also be a brain tumour, or a subarachnoid hemorrhage, or a urinary tract infection (“Elderly people, particularly females, are more prone to urinary tract infections and often present with confusion”), or… Severe abdominal pain and vomiting in a young person isn’t always appendicitis; this book had a young woman with familial Mediterranean fever present that way.
There were more than a few cases where I ‘got it right’, including some quite obscure ones like a case of Stevens-Johnson syndrome (-SJS – this one is really rare, something like 1 in 200.000 rare – I only guessed it because I read the wiki on that one a while back and it stuck) and a patient with an insulinoma (this one also has a very low incidence, “estimated at 1 to 4 new cases per million persons per year” – my knowledge of diabetes helped here, as did my recall of the coverage of this condition in McPhee et al (at least I think that was where I read about it). There were quite a few more common ones I got right, for example cases of pre-eclampsia (Hall covered that one in quite a bit of detail, so I had no problems figuring out what was going on there), mumps, diabetic ketoacidosis, hyperosmolar hyperglycaemic state (I found it interesting that they included both a DKA case and a HHS case, and/but I had of course no problem recognizing either of these), malaria, alcohol withdrawal syndrome (obvious from the patient history, but not if you don’t know about the risk of seizures and -progression to DT associated with alcohol withdrawal – which the patient obviously didn’t…), Lyme disease, trypanosomiasis (well, I couldn’t remember that that’s what it was called, but I did guess ‘sleeping sickness’, which is good enough, I think – though of course I’d have no idea how to treat someone with that disease…), anorexia nervosa, and pulmonary oedema. There were a lot of them I didn’t get right or didn’t know the answer to, which is in a way to be expected (the insulinoma and SJS cases were not the only quite rare ones – who’s ever heard about Goodpasture syndrome anyway?). In more than a few cases you need, in order to get the diagnosis right, to be able to read and understand the results of an electrocardiogram, a CT scan, an MRI or a chest X-ray; I’ve seen these before in textbooks, but I’ve never received formal training in interpreting them – however at least in the case of the pulmonary oedema the X-ray results were obvious. ‘He’s having a heart attack’ was a sort of a diagnosis in a couple of cases, but not what they were going for – if they thought his heart was fine they probably wouldn’t have asked the lab for troponin levels or ordered an ECG..
I have added some observations from the book below, most of them from the ‘answer sections’. As I didn’t assume anyone reading along here would be likely to read the book later on I have not tried very hard to avoid ‘spoilers’:
“[Neurocysticercosis] is the most common parasitic infection of the central nervous system and the leading cause of adult-onset seizures in the developing world.”
“Mumps is the most common cause of unilateral acquired sensorineural hearing loss in children and young adults worldwide […] Suspect mumps in a patient who presents with parotitis and fever.” (I did. The included vaccination history helped.).
“A 19-year-old woman has presented to the emergency department complaining of fevers and malaise after returning from a holiday in South Africa two weeks earlier. Over the preceding 3–4 days she noticed a rash and sore throat and is now feeling generally tired and unwell. She has no significant medical history and does not take any regular medications or recreational drugs. She does not smoke, nor drink alcohol. She admits to several episodes of unprotected sexual intercourse with a man she met in South Africa.”
My first thought when reading the case history above: Immediate psychiatric consult and an IQ test. If you’re having unprotected sex with a South African whom you don’t know well on multiple occasions you’re either insane or a moron. More seriously, this one was one of several really depressing presentations. There were ways to make the patient history even worse (‘when she came back to receive the results of her (positive) HIV test she mentioned during the followup that she’d been gaining a bit of weight lately and that she had been feeling nauseous occasionally, especially during the morning hours…’), but this was quite bad enough. Do note however that there could be other explanations for her illness than just HIV, and that these should be considered as well: “This woman is likely to have a viral illness, considering her history of fevers, rash and sore throat. Infectious mononucleosis (glandular fever) secondary to Epstein–Barr virus is a common illness in young adults, presenting with fever, rash and lymphadenopathy following on from a sore throat.”
“Urinary tract infections can often present with non-specific symptoms, such as confusion and general malaise, particularly in elderly patients. […] Early treatment according to the Surviving Sepsis protocol is key to ensuring patients have the best chance of surviving a serious infection.”
I include this one at least in part because people reading my comments above about confusion perhaps being the result of a urinary tract infection may have thought that ‘okay, so not all of these cases are all that severe’, as a urinary tract infection is probably perceived of as belonging on ‘the opposite side of the scale’ as brain cancer. In the specific case that would be an incorrect way to think about the situation: “The patient is haemodynamically unstable […] The patient’s daughter should be informed that her mother is very unwell and may not survive.” Yes, this was another one of the depressing ones. Here’s a related quote from another case: “Most women will experience a urinary tract infection (UTI) at some time in their life, so education towards UTI prevention is important (e.g. wipe from front to back after a bowel movement or after urinating, and try to empty the bladder before and after sexual intercourse).”
“Tuberculosis should be suspected in anyone presenting with shortness of breath, fever, haemoptysis and weight loss. […] An important differential diagnosis to consider is lung malignancy.”
“Alcohol misuse increases the risk of intracerebral bleeds, because head injury is more likely to be sustained or as a result of deranged liver function. Sustained alcohol misuse can lead to deranged liver function and therefore reduced production of vitamin K, which is essential for normal blood clotting properties. […] Seizures are a common way for patients with alcohol withdrawal to present.”
“In patients who are vomiting and develop signs of a chest infection, an aspiration pneumonia should be considered.”
“Angiodysplasia is a condition where the small vessels in the bowel are dilated, very fragile and prone to bleeding. […] Angiodysplasia of the colon is the second most common cause of GI bleeding in patients over the age of 60 years (diverticular disease being the most common in that age group). The most common presentation is intermittent bleeding without pain.”
“There are common steps in the management of acute intoxication and poisoning. As with most medical emergencies, the airway, breathing and circulation (ABC) should be assessed and managed appropriately in the first instance. Neurological examinations should be carried out to look for lateralizing and/or cerebellar signs. It is also important to examine for abnormal ocular movements and papillary changes as it helps to give clues to the common drugs/toxins involved. […] Often a ‘drug screen’ is requested but this is rarely necessary. A typical drug screen is expensive and difficult to interpret. The results may take 1–2 weeks to become available and it is not possible to screen for all possible toxins. Therefore it does not alter immediate patient management in most instances. Neuroimaging, such as CT of brain, is only necessary when patients are suspected to have a structural brain lesion or significant head injury. A provoked seizure from poisoning or substance abuse does not necessitate neuroimaging in most circumstances. […] In most cases the treatment of poisonings requires supportive therapy only as specific antidotes are often not available.” (ABC arguably isn’t enough – in a different answer they add on D and E as well:) “The approach to any critically ill person should start with ABCDE (airway, breathing, circulation, disability, exposure). Each step should consist of an assessment and appropriate management before moving on to subsequent stages. This approach is a logical way of thinking through and dealing with an acutely ill person.”
“[Anorexia nervosa] is a psychiatric diagnosis characterized by a refusal to maintain normal weight for age and height, a fear of gaining weight, body image distortion and amenorrhoea. There are other subtypes, which include ‘restricting’ calorie intake, or ‘binge eating/purging’ behaviours which can include laxative, diuretic or enema use. She has evidence of a low bodyweight (formal diagnosis relies on an ideal body weight <85 per cent, body mass index <17.5 kg/m2). Her body image perception is altered. […] Most people with anorexia nervosa are female, with the onset highest during late adolescence.”
“IgA [Immunoglobulin A] nephropathy is the most common glomerular disease worldwide. It occurs most commonly in those of Asian or Caucasian origin and is more common in males (2:1). Most cases occur between the ages of 20 and 30. Most cases are sporadic and the cause is not identified, but it tends to occur following an upper respiratory tract infection or gastrointestinal infection. […] Cases can present in several ways. About half of all cases present as in this case with frank haematuria and flank pain after an upper respiratory tract infection. A third of patients can present with asymptomatic microscopic haematuria. Ten per cent of patients can present with a more severe process characterized by either the nephrotic syndrome or an acute rapidly progressive glomerulonephritis (oedema, hypertension, haematuria and renal failure).”
“Atrial fibrillation becomes more common with increasing age such that more than 10 per cent of those aged over 80 years have AF. The most common causes of AF are hypertension, heart failure, ischaemic heart disease and valvular disease. Hyperthyroidism is another cause and may not have obvious clinical signs in the elderly. […] Stroke risk can be estimated from a score (CHA2DS2VASc: Congestive heart failure, Hypertension, Age ≥75 (doubled), Diabetes, Stroke (doubled), Vascular disease, Age 65–74, and Sex category (female) […] A score of 2 predicts a 2.2 per cent per year adjusted stroke risk […] This is generally accepted to be the cut-off to starting treatment with an oral anticoagulant provided there are no contraindications. […] The main concern with anticoagulants is the risk of bleeding and an assessment of this risk should be made prior to starting treatment. A bleeding risk score such as HAS-BLED can be used to assess risk […] Warfarin is still the anticoagulant of choice.”
“The incidence of stroke after thrombolysis is around 1–1.5 per cent and most strokes occur within five days of the MI, with most cases of haemorrhage within 24 hours of MI and thrombolysis.”
This is a risk it makes sense to be aware of – lots of people die from MIs and understanding the details of the risks involved when treating these may in some cases be helpful; if a person dies from a hemorrhagic stroke shortly after receiving treatment for an MI, this should not be considered a major indication that the doctors screwed up. Medical science has advanced a lot over the years, but ‘the anticoagulant of choice’ they talk about above is rat poison so do be careful not to overestimate how much doctors can really do for you if you get sick.
“In the setting of a positive family history of early death due to chest disease and a history of deranged liver function tests, one should […] consider α1-antitrypsin deficiency. α1-Antitrypsin deficiency (A1AD) is a disease which has various phenotypes […] It is one of the most commonly inherited genetic disorders. […] The severity of lung disease differs even in siblings with the same allele. This is partially explained by environmental factors such as smoking and dust exposure; therefore it is paramount to educate patients with α1-antitrypsin deficiency not to smoke.” (yep, you guessed it – the patient was a smoker. Despite having been diagnosed with COPD 3 years earlier. Again, depressing.)
“CURB 65 is one of the most commonly used tools for assessment of community-acquired pneumonia severity. It is a useful adjunct but should not replace thorough clinical assessment. CURB 65 stands for: C = confusion; U = Urea ≥7 mmol/L; R = Respiratory rate >30/min; B = Blood pressure systolic <90 or diastolic <60 mmHg; 65 = age ≥65 years. Mortality approaches 83 per cent if all four CURB components are present. […] Most if not all atypical pneumonias present with classical pneumonic symptoms (fever, productive cough and shortness of breath), so it is hard to differentiate clinically. Atypical pneumonia is a term used to describe pneumonia caused by (i) Mycoplasma pneumoniae, (ii) Chlamydophila pneumoniae, (iii) Chlamydophila psittaci, (iv) Coxiella burnetii, (v) Legionella spp, or (vi) Francisella tularensi [I talked about this last one before, in a completely different context…]. The term ‘atypical pneumonia’ remains useful to describe these pathogens as their treatment and sometimes duration of antibiotic therapy is different from typical pathogens.”
“Subdural haematomas are bleeds that occur between the dura mater and the arachnoid mater, enveloping the brain. They usually develop following traumatic injury […] Older people are particularly prone to such injuries as the brain naturally atrophies and shrinks with age. Blood collects in the space and draws in water due to osmotic pressures. The area of bleeding increases in size, causing compression of the cerebral tissue. […] Cushing’s triad of systolic hypertension with a wide pulse pressure, bradycardia and irregular or rapid respiratory rate is a major sign of raised intracranial pressure. These features occur due to insufficient blood flow to the brain and compression of arterioles. Subacute and chronic subdural haematomas classically present days to weeks after the insult. Any patient who presents with neurological signs several days after a head injury should be investigated for a subdural bleed.”
“Fever, jaundice and right upper quadrant abdominal pain make up the Charcot’s triad which are the main signs and symptoms of acute cholangitis. If a patient presents with Charcot’s triad and altered mental status and shock, it is called Reynold’s pentad. […] The most common cause of acute cholangitis is gallstone disease. […] Acute cholangitis carries a high mortality.”
I liked the book and gave it three stars on goodreads.
“The first half of the book was not easy to read due to the technical nature of the coverage, and so I decided to put it away for a while. However I did pick it up again, and I’m really glad I did as there’s simply no way around the fact that this book is awesome. Some of the chapters in this book are chapters you need to read.
Highly recommended. Probably the best book I’ve read this year.”
I’ve finished the book – the above is my review of it on goodreads. I gave the book five stars.
The last part of it had (at least) two of those must-read chapters which I when I read them feel like I really ought to blog, and they both had a lot of stuff. The first of these chapters was an awesome chapter on agriculture. I wrote some stuff of my own about that stuff in my last post about the book (I’ve incidentally corrected a few minor inaccuracies in that post since it was posted – I thought I should mention this here), but I’m pretty sure I wouldn’t have done this if I’d known what was in that chapter; they cover this topic in a lot of detail and they do it really well. Many of the aspects they cover incidentally do not overlap with what I wrote though some of course do; you’ll surely get a lot out of reading this post despite having read my earlier comments on the topic (at least if you’re interested in these sorts of things). In my archaeology textbook, which is only a few years old, the idea that the dramatic climate change which took place around the Pleistocene/Holocene boundary was a crucial factor in the development of agriculture is taken for granted, but Boyd and Richerson’s coverage reminds us that archaeologists were not always so eager to accept this hypothesis (and it should be noted that other, weaker, hypotheses are mentioned/covered in the archaeology text as well – I was skeptical about some of these while reading the book (I wrote a couple of pretty harsh remarks in the margin) because they seemed implausible to me; Boyd and Richerson illustrates in the chapter e.g. through application of models of population dynamics that I had reason to be skeptical). I forgot to talk about climate in my last post on the topic probably because I assumed people knew this part, but it gets its fair share of the attention in this post anyway so I guess no harm is done.
The other chapter I consider to be best categorized as a ‘must-read’ chapter is chapter 19, on ‘Simple Models of Complex Phenomena’, which relates a little bit – but only a little – to a blog post of mine which has recently got some attention. When reading that chapter I was never in any doubt I’d cover that stuff here – this stuff is pure gold. The ‘Microevolutionary processes give rise to history’-chapter was also really interesting and the last chapter on memes there are probably more than a few people who’d benefit from reading, but I’ll not cover that stuff here; I don’t think I’d have problems writing 4 or 5 posts about the remaining parts of the book, and this is simply too much. I’ll talk about agriculture in this post and then I’ll probably cover the model chapter in a later post. It’s possible that the agriculture coverage in the book is less interesting to people with very limited knowledge of archaeology and human prehistory than it is to me (not that I’d say I know much about this stuff – actually on second thought I probably belong in the group of people with ‘very limited knowledge’ as well…), because a lot of things which relate closely to what they write about are perhaps hard to conceptualize without knowing anything about these things, but anyway I write about what I find interesting, so here we are.
Let’s move on to the book chapter coverage:
“Numerous subsequent investigations [after the Braidwood team] now provide a reasonably detailed picture of the origins of agriculture in several independent centers and its subsequent diffusion to almost all of the earth suitable for cultivation. These investigations have discovered no region in which agriculture developed earlier or faster than in the Near East, though a North Chinese center of domestication of millet may prove almost as early. Other centers seem to have developed later, or more slowly, or with a different sequence of stages, or all three. The spread of agriculture from centers of origin to more remote areas is well documented for Europe and North America [a major problem in relation to East Asia/China is incidentally the lack of ‘transitional sites’ dated around 8.000 to 6.000 years BC; we have very early sites and then we have “abundant and widespread evidence for sedentary Neolithic villages” by 6000 BC (Scarre et al.) – but we miss some evidence as to what happened in between – US]. Ethnography also gives us cases where hunters and gatherers persisted to recent times in areas seemingly highly suitable for agriculture, most notably much of western North America and Australia. Attempts to account for this rather complex pattern are a major focus of archaeology.”
“The processes involved in such a complex phenomenon as the origin of agriculture are many and densely entangled. Many authors have given climate change a key explanatory role […] The coevolution of human subsistence strategies and plant and animal domesticates must also play an important role […] Hunting-and-gathering subsistence may normally be a superior strategy to incipient agriculture […], and, if so, some local factor may be necessary to provide the initial impetus to heavier use of relatively low-quality, high-processing-effort plant resources that eventually result in plant domestication. Population pressure is perhaps the most popular candidate […] Quite plausibly, the complex details of local history entirely determine the evolutionary sequence leading to the origin and spread of agriculture in every region. Indeed, important advances in our understanding of the origins of agriculture have resulted from pursuit of the historical details of particular cases […] Nonetheless, we propose that much about the origin of agriculture can be understood in terms of two propositions:
Agriculture was impossible during the last glacial age. During the last glacial age, climates were variable and very dry over large areas. Atmospheric levels of CO2 were low. Probably most important, last-glacial climates were characterized by high-amplitude ﬂuctuations on timescales of a decade or less to a millennium. Because agricultural subsistence systems are vulnerable to weather extremes, and because the cultural evolution of subsistence systems making heavy, specialized use of plant resources occurs relatively slowly, agriculture could not evolve.
In the long run, agriculture is compulsory in the holocene epoch. In contrast to the Pleistocene climates, stable Holocene climates allowed the evolution of agriculture in vast areas with relatively warm, wet climates, or access to irrigation. Prehistoric populations tended to grow rapidly to the carrying capacity set by the environment and the efﬁciency of the prevailing subsistence system. Local communities that discover or acquire more intensive subsistence strategies will increase in number and exert competitive pressure on smaller populations with less intensive strategies. Thus, in the Holocene epoch, such intergroup competition generated a competitive ratchet favoring the origin and diffusion of agriculture.”
This is the basic idea. But the chapter has a lot more:
“For the last 400,000 years, very high-resolution climate proxy data are available from ice cores taken from the deep ice sheets of Greenland and Antarctica. Resolution of events lasting little more than a decade is possible in Greenland ice 80,000 years old, improving to monthly resolution 3,000 years ago. During the last glacial, the ice core data show that the climate was highly variable on time scales of centuries to millennia […] The last glacial period was arid and extremely variable compared to the Holocene. Sharp millennial-scale excursions occur in estimated temperatures, atmospheric dust, and greenhouse gases. The intense variability of the last glacial carries right down to the limits of the nearly 10-year resolution of the ice core data. […] Even though diffusion and thinning within the ice core progressively erases high-frequency variation in the core […] the shift from full glacial conditions about 18,000 years ago to the Holocene interglacial is accompanied by a dramatic reduction in variation on timescales shorter than 150 years. The Holocene (the last relatively warm, ice-free 11,600 years) has been a period of very stable climate, at least by the standards of the last glacial age. The climate ﬂuctuations recorded in high-latitude ice cores are also recorded at latitudes where agriculture occurs today. Sediments overlain by anoxic water that inhibits sediment mixing by burrowing organisms are a source of low- and mid-latitude data with a resolution rivaling ice cores. Events recorded in North Atlantic sediment cores are closely coupled to those recorded in Greenland ice […], but so are records distant from Greenland. Hendy and Kennett (2000) report on water temperature proxies from sediment cores from the often-anoxic Santa Barbara Basin just offshore of central California. This data shows millennial- and submillennial-scale temperature ﬂuctuations from 60–18 thousand years ago with an amplitude of about 8°C, compared to ﬂuctuations of about 2°C in the Holocene epoch. As in the Greenland cores, the millennial-scale events often show very abrupt onsets and terminations and are often punctuated by brief spikes of warmth and cold.”
“We expect that opportunism was the most important strategy for managing the risks associated with plant foods during the last glacial age. Annual plants have dormant seed that spreads their risk of failure over many years, and perennials vary seed output or storage organ size substantially between years as weather dictates. In a highly variable climate, the specialization of exploitation on one or a few especially promising species would be highly unlikely, because ‘‘promise’’ in one year or even for a decade or two would turn to runs of years with little or no success. However, most years would likely be favorable for some species or another, so generalized plant-exploitation systems are compatible with highly variable climates. […] Plant food-rich diets take considerable time to develop. Plant foods are generally low in protein and often high in toxins. Some time is required to work out a balanced diet rich in plant foods, for example, by incorporating legumes to replace part of the meat in diets. Whether intensiﬁcation and agriculture always lead to health declines due to nutritional inadequacy is debatable, but the potential for them to do so absent sometimes-subtle adaptations is clear […] The seasonal round of activities has to be much modiﬁed, and women’s customary activities have to be given more prominence relative to men’s hunting. Changes in social organization either by evolution in situ or by borrowing tend to be slow […] We doubt that even sophisticated last-glacial hunter-gatherers would have been able to solve the complex nutritional and scheduling problems associated with a plant-rich diet while coping with unpredictable high-amplitude change on timescales shorter than the equilibration time of plant migrations and shorter than actual Holocene trajectories of intensiﬁcation.”
“Low mean productivity, along with greater variance in productivity, would have greatly decreased the attractiveness of plant resources during the last glacial age. Lower average rainfall and carbon dioxide during the last glacial age reduced the area of the earth’s surface suitable for agriculture […] On present evidence we cannot determine whether aridity, low CO2 levels, millennial-scale climate variability, or submillennial-scale weather variation was the main culprit in preventing the evolution of agriculture. Low CO2 and climate variation would handicap the evolution of dependence on plant foods everywhere and were surely more signiﬁcant than behavioral or technological obstacles. Hominids evolved as plant-using omnivores (Milton, 2000), and the basic technology for plant exploitation existed at least 10 thousand years before the Holocene […] At least in favorable localities, appreciable use seems to have been made of plant foods, including large-seeded grasses, well back into the Pleistocene […] Signiﬁcantly, we believe, the use of such technology over spans of last-glacial time that were sufﬁcient for successive waves of intensiﬁcation of subsistence in the Holocene led to only minor subsistence intensiﬁcation, compared to the Mesolithic, Neolithic, and their ever-more-intensive successors. […] After 11,600 B.P., the Holocene period of relatively warm, wet, stable, CO2-rich environments began. Subsistence intensiﬁcation and eventually agriculture followed. Thus, while not perfectly instantaneous, the shift from glacial to Holocene climates was a very large change and took place much more rapidly than cultural evolution could track.”
“Might we not expect agriculture to have emerged in the last interglacial 130,000 years ago or even during one of the even older interglacials? No archaeological evidence has come to light suggesting the presence of technologies that might be expected to accompany forays into intensive plant collecting or agriculture at this time. Anatomically modern humans may have appeared in Africa as early as 130,000 years ago […], but they were not behaviorally modern. Humans of the last interglacial were uniformly archaic in behavior. Very likely, then, the humans of the last interglacial were neither cognitively nor culturally capable of evolving agricultural subsistence. However, climate might also explain the lack of marked subsistence intensiﬁcation during previous interglacials. Ice cores from the thick Antarctic ice cap at Vostok show that each of the last four interglacials over the last 420,000 years was characterized by a short, sharp peak of warmth, rather than the 11,600-year-long stable plateau of the Holocene (Petit et al., 1999).”
“Once a more productive subsistence system is possible, it will, over the long run, replace the less-productive subsistence system that preceded it. The reason is simple: all else being equal, any group that can use a tract of land more efﬁciently will be able to evict residents that use it less efﬁciently […] More productive uses support higher population densities, or more wealth per capita, or both. An agricultural frontier will tend to expand at the expense of hunter-gatherers as rising population densities on the farming side of the frontier motivate pioneers to invest in acquiring land from less-efﬁcient users. […] Thus, subsistence improvement generates a competitive ratchet as successively more land-efﬁcient subsistence systems lead to population growth and labor intensiﬁcation. Locally, huntergatherers may win some battles (e.g., in the Great Basin; Madsen, 1994), but in the long run the more intensive strategies will win wherever environments are suitable for their deployment. The archaeology supports this argument […] Societies in all regions of the world undergo a very similar pattern of subsistence efﬁciency increase and population increase in the Holocene, albeit at very different rates. Holocene hunter-gatherers developed local equilibria that, while sometimes lasting for thousands of years, were almost always replaced by more intensive equilibria.”
“Cohen’s (1977) inﬂuential book argued that slowly accumulating global-scale population pressure was responsible for the eventual origins of agriculture beginning at the 11,600 B.P. time horizon. He imagines, quite plausibly, that subsistence innovation is driven by increases in population density, but, implausibly we believe, that a long, slow buildup of population gradually drove people to intensify subsistence systems to relieve shortages caused by population growth, eventually triggering a move to domesticates. Looked at one way, population pressure is just the population growth part of the competitive ratchet. However, this argument fails to explain why pre-agricultural hunter-gatherer intensiﬁcation and the transition to agriculture began in numerous locations after 11,600 years ago […] Assuming that humans were essentially modern by the Upper Paleolithic, they would have had 30,000 years to build up a population necessary to generate pressures for intensiﬁcation. Given any reasonable estimate of the human intrinsic rate of natural increase under hunting-and-gathering conditions (somewhat less than 1% yr-1 to 3% yr-1, populations substantially below carrying capacity will double in a century or less […] If agricultural technologies were quick and easy to develop, the population pressure argument would lead us to expect Pleistocene populations to shift in and out of agriculture and other intensive strategies as they ﬁnd themselves in subsistence crises due to environmental deterioration or in periods of plenty due to amelioration. Most likely, minor intensiﬁcations and de-intensiﬁcations were standard operating procedure in the Pleistocene. However, the time needed to progress much toward plant-rich strategies was greater than the ﬂuctuating climate allowed, especially given CO2- and aridity-limited plant production.”
This part is really important to understand, and I know I’ve talked about this before but I’ll say it again: Humans living, say, 25.000 years ago were not stupid. They weren’t monkeys walking around looking for berries in the woods. They probably tried and tried repeatedly to make this kind of stuff work, explore all kinds of creative ways to obtain enough/more food, always slightly adjusting their strategies in order to stay alive and keep having kids – but the climate wouldn’t allow them to ever achieve ‘take off’. As they put it towards the end of the chapter: “If climate variation did not limit intensiﬁcation during the last glacial age to vanishingly slow rates compared to the Holocene epoch, the failure of intensive systems to evolve during the tens of millennia anatomically and culturally modern humans lived as sophisticated hunter-gatherers before the Holocene is a considerable mystery.” It seems climate is a big part of the explanation why we never got to where we are now before we did. Environmental constraints limit the activities of all lifeforms in all kinds of ways, and it would serve us well every once in a while to recall that we are in fact no different, even if we like to think we are, and that such effects may have played a crucial role in the history of our species.
I’ve added a bit more from the book. Some of the stuff below I talked about in the last post as well (do recall that I wrote that post before I read this chapter), but I figured it wouldn’t hurt to include it here anyway:
“The timing of initiation of agriculture varies quite widely […] The exact sequence of events also varies quite widely. For example, in the Near East, sedentism preceded agriculture, at least in the Levantine Natuﬁan sequence, but in Mesoamerica crops seem to have been added to a hunting-and-gathering system that was dispersed and long remained rather mobile […] For example, squash seems to have been cultivated around 10,000 B.P. in Mesoamerica, some 4,000 years before corn and bean domestication began to lead to the origin of a fully agricultural subsistence system […] Some mainly hunting-and-gathering societies seem to have incorporated small amounts of domesticated plant foods into their subsistence system without this leading to full-scale agriculture for a very long time. […] the path forward through the whole intensiﬁcation sequence varied considerably from case to case.”
“In all known cases, the independent centers of domestication show a late sequence of intensiﬁcation beginning with a shift from a hunter-gatherer subsistence system based upon low-cost resources using minimal technological aids to a system based upon the procurement and processing of high-cost resources, including small game and especially plant seeds or other labor-intensive plant resources, using an increasing range of chipped and ground stone tools […] The reasons for this shift are the subject of much work among archaeologists […] The shifts at least accelerate and become widespread only in the latest Pleistocene or Holocene. However, a distinct tendency toward intensiﬁcation is often suggested for the Upper Paleolithic more generally. […] Upper Paleolithic peoples often made considerable use of small mammals and birds in contrast to earlier populations. These species have much lower body fat than large animals, and excessive consumption causes ammonia buildup in the body due to limitations on the rate of urea synthesis […] Consequently, any signiﬁcant reliance on low-fat small animals implies corresponding compensation with plant calories, and at least a few Upper Paleolithic sites, such as the Ohalo II settlement on the Sea of Galilee […], show considerable use of plant materials in Pleistocene diets. Large-seeded annual species like wild barley were no doubt attractive resources in the Pleistocene when present in abundance and would have been used opportunistically during the last glacial age. If our hypothesis is correct, in the last glacial age no one attractive species like wild barley would have been consistently abundant (or perhaps productive enough) for a long enough span of time in the same location to have been successfully targeted by an evolving strategy of intensiﬁcation, even if their less intensive exploitation was common. The broad spectrum of species, including small game and plants, reﬂected in these cases is not per se evidence of intensiﬁcation (specialized use of more costly but more productive resources using more labor and dedicated technology), as is sometimes argued […] In most hunter-gatherer systems, marginal diet cost and diet richness (number of species used) are essentially independent […], and prey size is far less important in determining prey cost than either mode or context of capture […] For all these reasons, quantitative features of subsistence technology are a better index of Pleistocene resource intensiﬁcation than species used. We believe that the dramatic increase in the quantity and range of small chipped stone and groundstone tools only after 15,000 B.P. signals the beginning of the pattern of intensiﬁcation that led to agriculture.”
“Early intensiﬁcation of plant resource use would have tended to generate the same competitive ratchet as the later forms of intensiﬁcation. Hunter-gatherers who subsidize hunting with plant-derived calories can maintain higher population densities and thus will tend to deplete big game to levels that cannot sustain hunting specialists […] Once the climate ameliorated, the rate of intensiﬁcation accelerated immediately in the case of the Near East. In other regions changes right at the Pleistocene-Holocene transition were modest to invisible […] The full working out of agrarian subsistence systems took thousands of years. […] Fully agricultural subsistence systems in the sense of a dominance of domesticated species in the diet typically postdate the origin of agriculture [which they define as “dependence upon domesticated crops and animals for subsistence” – US] by a millennium or more. […] Zvelebil (1996) emphasizes the complexity and durability of frontiers between farmers and hunter-gatherers and the likelihood that in many places the diffusion of both genes and ideas about cultivation was a prolonged process of exchange across a comparatively stable ethnic and economic frontier.”