Unreported Side Effects of Powerful Drugs (part 3)

A comment on the previous post in this series — thanks, Vesna! — led me to a horrifying story about what happened to someone whose doctor prescribed statins (an expensive and nearly worthless class of drugs) because his cholesterol numbers were bad. (My friend and collaborator Norman Temple has written about the true value of statins.) The doctor did not warn him of the dangers, which were great. When his troubles began, he should have simply stopped the drug. What actually happened was that his doctor prescribed another dangerous drug. And his troubles got worse. Shades of Jane Brody!

I know a similar story. The elderly mother of a friend of mine was taken to the emergency room of a hospital because she had some sort of attack. It was the third such attack in a year. Her children were concerned. She was not of sound mind. Heroic measures to help her? Or a peaceful death? They chose a peaceful death. She was moved to a hospice. By mistake, her six prescriptions failed to be transferred. A clerical error. So she wasn’t able to take her usual drugs. She soon got better! Within a week or two she returned home. The drugs her doctor had prescribed had been killing her. Nobody had noticed.

First do no harm is a scary motto because it shows that those who take it seriously — supposedly the entire medical profession — aren’t thinking clearly, as I’ve heard Robin Hanson point out. It’s like English teachers having a motto with a word spelled wrong. And the consequences of doctors not thinking clearly — not doing something as obvious as stopping dangerous drugs when the patient gets worse — can be terrible. My suggested replacement motto: Learn something from everyone who comes to you for help.

This is closely related to self-experimentation, of course, which is all about figuring out for oneself what effect something has. I got a lot more interested in self-experimentation when it showed me that an acne drug I’d been prescribed was worthless.

Part 1.

How Should We Fight Infections?

In the latest New Yorke r, an article by Jerome Groopman is about the emergence of even-more-antibiotic-resistant bacteria.

I asked him what we should do to combat these new superbugs. “Nobody has the answer right now,” he said. “The fact of the matter is that we have found all the easy targets” for drug development. He went on, “So the only other thing we can do is continue to work on antibiotic stewardship.”

All the easy targets, huh? Here’s an easy target that hasn’t been exploited: Why are colds more common in the winter? Many diseases are more common in the winter. I believe it’s because sleep is worse in the winter. While you are asleep is when your body does its best job of fighting off infection. When I vastly improved my sleep — by standing much more, and by getting more morning light — I vastly reduced the number of easy-to-notice colds that I got. I still got cold infections, I think, but they merely caused me to sleep more than usual for a few days.

Several years ago I noticed an introductory epidemiology course in the UC Berkeley School of Public Health was taught by someone I knew. I called him. “Is your course going to cover what makes our ability to fight off infection go up or down?” I asked. No, he said. That is the usual answer. The question of why colds are more common in the winter is not part of the traditional study of epidemiology.

The connections between sleep and fighting off infection are so strong I’m pretty sure I’m right about this (that colds are more common in the winter because sleep is worse). Why, then, haven’t sleep researchers looked into this? Strangely enough, they may not have thought of it; I haven’t come across this idea in any book about sleep I’ve read. (If you’ve seen it somewhere, please let me know!) Justifications of sleep research tend to revolve around car accidents, which are often caused by too little sleep.

More. My point is not that poorer sleep causes more colds in the winter; it’s that it’s an easy target. Suppose you think the colds/winter connection is caused by less Vitamin D in the winter. An experiment in which one group gets Vitamin D supplements in the winter and another group doesn’t is easy to do, given the great health implications.

My Humor Research


[Rosie Shuster] did have one quality she could privately lord over her classmates: her father was a comedian. . . A life in comedy meant that Frank Shuster nodded, rather than laughed, at jokes that worked.

From American Nerd: The Story of My People by Benjamin Nugent, pp. 62-3. When I was in college I came up with a theory: Laughter is caused by sudden pleasure. Obviously we enjoy jokes, and jokes have punchlines. People laugh in lots of situations not involving humor and as far as I can tell they always involve sudden pleasure — unexpectedly seeing an old friend, for example.

Which is only to say, as this passage implies, there should be a limited number of joke categories and they should be far from mysterious. I once wrote a bunch of jokes from the TV show Cheers on cards and sorted them into categories. Later I classified six months of New Yorker cartoons and Spy accepted it. It was my first submission and I was thrilled.

More. Mike Kenny put it better than me. That I was able to get my research published in a magazine I adored was “ a fusing of the intellectual with the practical.” I was going to say it was a practical application of pure research.

The Bechdel Test and Denise Richards

I loved Alison Bechdel’s Fun Home. It was one of the best books I read in 2007. So I was pleased to learn of the Bechdel Test, which can be applied to TV and movies:

To pass it your movie [or TV show] must have the following:

1) there are at least two named female characters, who

2) talk to each other about

3) something other than a man.

Few movies or TV shows pass it, said Jennifer Kesler.

I came across this test after spending a pleasant morning analyzing data while listening to the first six episodes of Denise Richards: It’s Complicated which I found on YouTube. (Such as part 1 of Episode 1.) The show consisted mainly of two named female characters — Denise and sister, Denise and friend, Denise and daughter — talking to each other about something other than a man.

I was surprised how much I liked it. When Denise and her dad (who lives with her) interview people to be her assistant, it was amusing (Denise has about 20 pets; one applicant said she didn’t like pets); when she gets mad at an entertainment journalist, it was forgivable; when she enters her nephew’s room to find him and his friends looking at a Playboy with her on the cover, it was unforgettable. The entertainment journalist wants to know why she is doing the reality show. “My [recently dead] mom wanted me to do it,” Denise says. The journalist can barely keep from laughing. “A deathbed wish?” she says. Denise got upset, so let me answer: The better you know almost anyone, the more you like them.

How to avoid demonization.

More. Gillian Flynn, one of Entertainment Weekly‘s TV reviewers, hated the show — gave it a D. Could reviewers be overly negative because they are forced to watch?

More about Unreported Side Effects of Powerful Drugs

A few days ago I blogged about how Tim Lundeen, via careful and repeated measurement — let’s call it self-experimentation — uncovered a serious and previously-unreported side effect of a drug he was taking. Tim’s example illustrates an important use of self-experimentation: discovering unreported side effects, which I believe are common.

By coincidence today I came across a talk about the very subject of unmentioned side effects: Alison Bass speaking about her new book, Side Effects: A Prosecutor, a Whistleblower, and a Bestselling Antidepressant on Trial. Near the end, Bass said,

It’s not the just the antidepressants, it’s not just the antipsychotics. This is happening with a lot of other drugs. With Vioxx, with Vytorin, an anti-cholesterol drug, with Propries [?] and Marimet [?], anti-anemia drugs. Where again and again the drug companies know that there are more severe side effects and they’re not letting the public know about that. It just keeps happening, unfortunately.

Just as it would be foolish to think the problem is limited to mental-health drugs, it would be foolish to think the problem is limited to side effects, that drug company researchers do everything right except fail to report side effects. Tim’s example shows how hard it is to learn about unreported side effects — so it is only realistic to think that there are other big problems with drug company research we don’t know about. Bass mentioned one I didn’t know about. A company did a clinical trial of Paxil. The goal was to see if the drug helped with Measures of Depression A and B. Turns out it didn’t: no effect. So the company changed the measures! They shifted to reporting different measures that the drug did seem to improve. Creating the hypothesis to be tested after the data supposedly supporting that hypothesis had already been collected. Without making this clear. (Which I presciently mentioned here, in response to an interesting comment by Andrew Gelman.) And if you think that drug companies do research like this — in ways that seriously damage people’s lives — but everyone else, such as academia, is really good, that is as realistic as thinking the problem with drug company research is restricted to side effects. Self-experimentation has all sorts of limitations, yes, but (a) you know what they are and (b) it is cheap enough so that you can gather more data to deal with the problems. Drug company research and lots of other research is too expensive to fail — or even be honest about shortcomings.

This is an aspect of scientific method that scientists rarely discuss: the effect of cost on honesty. Is there an economic term (a Veblen good, perhaps?) for things whose quality goes down as their cost goes up?

Benfotiamine and Self-Experimentation: Surprising Results

Tim Lundeen, whose fish oil/arithmetic results impressed me, recently tried taking benfotiamine (a fat-soluble version of thiamine) to reduce damage caused by high blood sugar. Things did not go as he expected:

I bought 100mg capsules from Life Extension Foundation, and starting taking 1 per day in the morning with breakfast. Over the course of 3-4 weeks, the two small dead spots on the bottoms of my big toes started to feel normal, and I didn’t notice them anymore when I went walking. My energy and general mood were good, and my fasting blood sugar readings were basically unchanged, staying in the 85-95 range. Scores on my daily math speed test were good, possibly slightly better than before.

Unfortunately, I started to gain weight, gaining about 10 pounds over the 10 weeks I took benfotiamine, without any other major changes to my regimen.

Weight gain was not a known side effect. For example, a 2005 study in which 20 patients received the drug for three weeks reported: “No side effects attributable to benfotiamine were observed.” This is on a web page that is trying to sell benfotiamine but there’s nothing unusual about the situation. Studies of drug efficacy are almost always done by drug companies that want to sell the tested drug. What is the term for such a side-effects reporting system? The fox guarding the hen house, perhaps?

It isn’t easy to measure side effects in conventional studies of treatment vs placebo. If you measure the rates of 100 possible side effects, and use a 5% level of significance, one or two true positives will go unnoticed against a background of five or so false positives. So a drug company can paradoxically assure that they will find nothing by casting a very wide net. And there is a larger and more subtle problem that statistics such as the mean do not work well for detecting a large change among a small fraction of the sample. If soft drinks cause 2% of children to become hyperactive and leave the other 98% unchanged, looking at mean hyperactivity scores is a poor way to detect this. A good way to detect such changes is to make many measurements per child. Many did-a-drug-harm-my-chlld? cases come down to parents versus experts. The experts are armed with a a study showing no damage. But this study will inevitably have the weaknesses I’ve just mentioned — especially, use of means and few measurements per subject. The parents, on the other hand, will have used, informally, the more sensitive measurement method.

For these reasons, I suspect drug side effects are woefully underreported. Here is the story of a child with a neurodegenerative disease that might have been caused by “the Gardasil vaccine (or perhaps some other vaccine with key similarities, such as an aluminum adjuvant).” Her parents are trying to find other children with similar symptoms.

Slow Weed


Guthrie said that the quasi-legal status of smaller growing arrangements, combined with consumers’ preference for potent, high-maintenance weed, has shifted the balance of the pot business away from large-scale farms. “There’s a lot more people doing little scenes,” he said. The welter of laws pertaining to medical marijuana in California has offered careful operators like Guthrie the best of both worlds: prosecution for growing and selling has become much less likely, while federal busts and seizures keep prices high.

Too bad David Samuels, the author of this well-reported article, doesn’t use the term artisanal marijuana. Artisanal cheesemakers, etc., might learn something helpful from this. For example, maybe it helps that raw milk is slightly illegal. After he wrote Fast Food Nation, Eric Schlosser wrote about underground economies. Maybe he’ll eventually write Slow Food Nation.

A friend of mine spent a year growing pot in her California basement in response to the economic trends described in Samuel’s article. She stopped when her business partner became too unreliable.

Errors in The Queen of Fats

Susan Allport’s The Queen of Fats is the best introduction to omega-3 fatty acids and their importance that I know of. I learned a lot from it (and interviewed the author). This is why its errors are interesting; they shed light on the big nutritional misconceptions of our time (as Weston Price, the subject of yesterday’s post, did in a different way). Joel Kauffman, a chemist, made a list:

1. On p1 low-carb bread and beer are ridiculed despite evidence (see Nielsen JV, Joensson EA, Low-carbohydrate diet in type 2 diabetes. Stable improvement of body weight and glycaemic control during 22 months follow-up, Nutrition & Metabolism 2006;3(22) doi:10.1186/1743-7075-3-22) to the contrary. There are at least 10 studies supporting Nielsen. Low-carb means low insulin demand. Insulin converts carb to fat. Allport’s claim that the world’s leanest peoples mostly eat carbs neglects to mention that they are malnourished.

3. On p2 and later Allport calls saturated fatty acid chains “straight,” then still later by the correct term “zigzag,” but never by the chemist’s term “unbranched.” She is not aware that a saturated fatty acid chain of 22 carbons has many more conformations than the 22-carbon DHA with 6 carbon-carbon double bonds, or that double bonds keep 4-carbon groups rigid. If DHA “is constantly on the move” there must be some other reason.

5. On p10 canola oil, which is not rapeseed oil, is not usually promoted for its linolenic acid content, but for its low saturated content, lower than olive oil. This is not a real advantage, according to all the books (except Sears’) I have listed above.

6. The conundrum of eating fish for its omega-3s despite the mercury content was not resolved on p11 or elsewhere. There are two long-term studies showing that there is not a big problem: The Chicago Western Electric Study followed the effects of fish consumption in 2,107 men aged 40-55, and followed for 30 years. Those who ate an average of *35 g daily (about 1 big fish dinner every 5 days) had only 9/10 of the all-cause mortality rate of men who ate no fish. The Nurses’ Health Study on 84,688 women aged 34-59 years and followed for 16 years for outcomes vs. fish and omega-3 fatty acid intake, had the following findings: women consuming fish five times weekly had only 7/10 the all-cause mortality rate of those eating fish once a month. Pregnant women have been cautioned to restrict their intake of fish (https://www.cbc.ca/storyview/CBC/2002/10/21/Consumers/mercuryfish_021021) despite evidence that children receive most of their mercury from vaccines. Hepatitis b vaccine carries 12.5 micrograms per dose; influenza and other common vaccines carry 25 micrograms per shot, over 830 times the amount in a can of tuna. It has been reported that vaccines said not to contain the mercury compound, thimerosal, still might have it. The long duration of the diet studies makes it very clear that the mercury content of fish, in general, is not shortening life.

7. On p14 eating fat in general was used as a straw man and implied to be the major cause of heart disease. Not so; see below (section titled More at bottom of post).

8. On p15 the Framingham Study was claimed to have shown a positive link between serum cholesterol and risk of heart disease. This was disproven by 1937 by experiments on cadavers. See The Cholesterol Myths and either Great Cholesterol Con [there are two books with this title]. See above for evidence that the Seven Countries Study was a fraud. A more recent study on free-living elderly in Manhattan showed the opposite — those with the highest cholesterol and LDL0C levels lived the longest. See Schupf N, Costa R, Luchsinger J, et al. (2005). Relationship Between Plasma Lipids and All-Cause Mortality in Nondemented Elderly. Journal of the American Geriatrics Society 53:219-226.

10. On p20 the excessive bleeding in Eskimos is said to be unimportant vs. lower heart attack rates than those of Danes, but external bleeding, as with aspirin, probably indicates internal bleeding.

11. On p21 it was written that polyunsaturated fats held down cholesterol levels. Actually HDL levels were held down and there was no drop in mortality: Rose GA, Thomson WB, Williams RT (1965). Corn Oil in Treatment of Ischaemic Heart Disease. British Medical Journal 12 Jun:1531-1533.

12. On p22 gas-liquid chromatography was said to have been developed in the 1950s by oil companies. A Google search showed its invention in the 1940s to separate fatty acids: see James A T & Martin A J P. Gas-liquid partition chromatography: the separation and microestimation of volatile fatty acids from formic acid to dodecanoic acid. Biochem. J. 50:679-90, 1952. [National Institute for Medical Research, Mill Hill, London, England]

13. On p22-3, 25 it is implied that the increase in heart disease in Eskimos who adopted aspects of a Western diet is solely due to differences in omega-x fat intake. No attention was paid to the effect of carbs on a very carb-sensitive population.

14. On p25 Allport insults Spam for being “highly saturated.” This is nonsense, since lard is only 40% saturated. See Know Your Fats by Mary G. Enig, 2000.

17. On p49 the “pure cholesterol” fed to rabbits has been shown to be oxycholesterol, which is not healthful.

18. On p51 Ancel Keys, MD, was said to link serum cholesterol to heart disease, but this link had already been shown to be false in 1937 by work on cadavers.

19. On p54 Allport wrote that EPA was responsible for low cholesterol in Eskimo blood on traditional diets, but linoleic acid based fats do this also, and human fat is 10% linoleic (lard 6%).
20. On p57 was written that pork and dairy fats are very saturated. Actually, the former is about 40% saturated and the latter 62%. See Know Your Fats.

31. On p66 a crack was made about an unbalanced diet. Since some populations have survived for centuries on all animal diets, a balanced diet turns out to be a fantasy designed to raise carb consumption despite a lack of evidence that there is any requirement for carb at all in the human diet. See the Ottoboni’s book. Also, there is vitamin C in fresh meat, so worrying about scurvy was not justified.

32. On p68 the claim that fats and carbs make up over 80% of the calories in every diet consumed by humankind is absurd, based on traditional Eskimo and Masai diets, among others.

33. On p 69: “so fat gives foods their distinctive aromas and tastes.” What about the odor of fresh bread, hot marshmallow, citral and neral in fruit, licorice, mint, wine, beer, etc.? These are not fats.
34. On p71 the statement that the increased energy in fats compared with carbs or proteins comes from their dense packing. The no-nonsense explanation is that carbs and proteins are partially oxidized because they contain oxygen and nitrogen, so oxidizing them the rest of the way to CO2 and water gives less energy than the all-hydrcarbon parts of fats.

35. Also on p71 is the fantasy that unsaturated fats contain less energy than than saturated because a double bond contains 10% less energy than a single bond. My old physical organic chemistry text has 80 kcal/mole for the C—C single bond, and 142 kcal for the C=C double bond, a far cry from Allport’s fantasy. And the energy available on digestion is given above — much less from mostly saturated fatty acids.

36. On p74 the slow melting of butter is not due to the melting points of the fatty acids in its triglycerides (fats), but the different melting points of the fats themselves.

37. On p78 and elsewhere Allport wrote of the high concentration of arachidonic acid and DHA in brain and nerve tissue. Her conflicted position on cholesterol is shown by her refusal to mention that the highest concentration of choleserol in the body is in the brain. But on p148 she writes that cholesterol is a necessary component of brain function

39. On p88 the fantasy begun by Ancel Keys that overconsumption of fats was the major health problem in the West was reiterated without any of the evidence from the books cited above that this was false.

40. On p89 domestic cow fat is said to be only 2% unsaturated. Know Your Fats says it is 42% unsaturated, and the CRC Handbook of 1983-4 says 52% unsaturated.
43. On p100: “In men, it [aspirin] cuts mortality from heart disease by more than half.” This is one of the most flagrant misquotations of the aspirin findings I have yet seen. Actually Bufferin cuts the number of non-fatal heart attacks by half with no change in mortality, and plain aspirin maybe by 1/3, also with no change in mortality.

44. On p104 a common omission characteristic of drug ads is found: “…mortality from heart disease goes up linearly with the increase in omega-6s…” does not include the crucial all-cause mortality, without which no amount of lowered mortality from some single cause has any meaning for action.

46. On p107 Allport implies that the incidence of heart disease in the US has not changed from 1909-1985. In Heart Frauds by Charles T. McGee (2001), p59, heart disease death rate was shown to have changed from 15/100,000 in 1910 to a peak of 331/100,000 in 1968, then falling to 194/100,000 by 1990. McGee shows that this drop corresponded well with an increase in vitamin C intake.

47. On p109 there is a disconnect between Allport’s generalization that seeds contain mostly omega-6s and leaves mostly omega-3s. Both canola and linseed oils are high in omega-3s which are in their seeds.

49. On p114 it was written that certain Nigerians with high omega-3 levels, presumably in blood, ate “a lot of greens” and most fat was palm oil, high in saturated fats, meaning that sat fats (and the other half of palm oil, the monounsaturated oleic acid 18:1*9) do not interfere with the transformation of linolenic acid from those greens into DHA and EPA. OK, then, why did she not relent on her anti-sat fat position?

50. On p118, Allport actually said that “…small amounts of saturated fats are better than large amounts of omega-6s.” This shows her conflict: such small amounts would require much less total fat consumption, and the value of this move has no positive evidence.

51. Also on p118 and 142, Allport minimized the dangers of trans fats, being totally unaware that controlled tests in human subjects showed serious adverse effects. Risérus U, Abner P, Brismar K, Vessby B (2002a). Treatment with Dietary trans10cis12 Conjugated Linoleic Acid Causes Isomer-Specific Insulin Resistance in Obese Men with the Metabolic Syndrome. Diabetes Care 25(9):1516-1521; Risérus U, Basu S, Jovinge S, Fredrikson GN, Årnlov J, Vessby B (2002b). Supplementation with Conjugated Linoleic Acid Causes Isomer-Dependent Oxidative Stress and Elevated C-Reactive Protein. A Potential Link to Fatty Acid-Induced Insulin Resistance. Circulation 106:1825-1929.

52. On p126 in an otherwise good discussion of bad aspects of leaky membranes, a bad simile was used: “…we all know what happens to engines when they run constantly…” Do we? It was found by the 1960s that most car engine wear occurred immediately after startup from cold, while there was no measurable wear during constant running at moderate rpms.

54. On p129 Allport notes that there was not a single known case of diabetes (no type given) in Eskimos of the Umanak district in 1971 on their traditional diet. The implication is that omega-3s did the job, but no airtime was ever given to the zero-carb diets.

55. On p134, again, diabetes (type not given) and obesity were equated to caloric intake, not, as so often demonstrated, carb intake.

56. On p135 one of the classic objections to the Atkins low-carb diet is given — that it causes kidney and liver failure due to higher protein consumption. This was twice false, since no such damage was seen by Atkins in his patients who did raise protein intake; but more important, the missing carbs are ideally to be replaced by fat, which has no glycemic index, unlike protein with a GI of 20 or so.

58. On p139 the blanket recommendations to eat “… lots (and lots) of fruits…” is very destructive to diabetics (both types) and pre-diabetics. Many kinds of fruit are high in sugars. Barry Groves, PhD, Nutrition, Richard K. Bernstein, MD, and William Cambell Douglass, Jr., MD, have avoided fruit for decades and are all in their seventies in good health.

59. Also on p139 the advice to avoid any high omega-6 oil is OK, but the advice to minimize butter is not. Not only is there no danger in butter, but its medium-chain fatty acids have antimicrobial properties. See Know Your Fats, above.

60. On p140 and 142 the advice to eat a wide variety of fish does not account for differences in EPA and DHA content, or differences in mercury content. Benefits of supplements of EPA and DHA have been shown in controlled trials.

61. On p143 saturated fats come in for another absurd hit, this time with the epithet “solid.” Phew! Of course lard and tallow are not solid at body temperature! And they do not cause heart disease: Ravnskov U (1998). The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology 51:443-60.

62. On p144 Allport reverses herself from her position on p138 and gives amounts of EPA and DHA supplements to take daily. She wisely cautions against supplements containing omega-6s since we get too much of them anyway. But she says that strict vegetarians need more linolenic acid as though they are not getting it from eating massive amounts of leafy vegetables.

65. On p149 a study within the Physicians’ Health Study (the one with the misquoted and misinterpreted info on aspirin) there was a finding that 94 of 15,000 of them who experienced sudden cardiac death were 90% less likely to do so if they had the highest omega-3 levels in their blood. First, in the absence of all-cause mortality, you cannot tell whether high omega-3 levels did any overall good. Next only 0.6% of the total or 1 in 170 had this cause of death, so the benefit is pretty small. Dietary intake of omega-3s was not even given.

66. On p151 it is not clear whether all omega-3s in blood are measured by the commercially available tests, or whether the individual ones are assayed and reported. If EPA and DHA levels are not reported, there will be little if any value in the tests.

67.On p192 Allport wrote that rapeseed oil “…has a high alpha linolenic acid content.” My CRC Handbook of 1983-4 lists 1%!! Such is the result of confusing rapeseed and canola.

You can see from the numbering I’ve omitted some of them; for the full list, contact Dr. Kauffman at kauffman at bee dot net. For more on health misconceptions, read his book Malignant Medical Myths, Infinity Publ., West Conshohocken, PA, 2006. ISBN 0-7414-2909-8 326 pp. $24.95.

Science, especially health science, is so important yet it is remarkably hard to learn about. Part of the problem seems to be that those who can write well (such as journalists) don’t understand the science and those who understand the science (such as scientists) can’t write well. (Another part of the problem, as Veblen pointed out, is that among academics to write clearly is low status, to write mumbo-jumbo is high status.) This is why I like Leonard Mlodinow‘s work so much; he writes well and understands the science.

But don’t misunderstand this post. The Queen of Fats is an excellent book. The most impressive and hopeful thing about it is that it was written by a non-scientist — in other words, that a non-scientist was able to figure out that the common neglect of omega-3 fats was seriously wrong. (Omega-3 fats receive almost no attention in Eat Drink and Be Healthy by Walter Willett et al. for example. There is no RDA for them.) I like to think it’s some sort of turning point that non-scientists have become able to grasp how wrong the health establishment can be; another example is Taubes’s Good Calories, Bad Calories.

More. The list of errors unfortunately omitted some general comments:

The Seven-Country Study by Ancel Keys that was so influential (cholesterol and saturated fat being “bad”) was not presented as the fraud it was. For a great description, see The Great Cholesterol Con (GCC), by Anthony Colpo (2007). For an honest Fourteen Country Study see another GCC of 2007, this one by Malcolm Kendrick, in which Kendrick showed that the 7 countries with the lowest saturated fat consumption had the highest mortality from heart disease (450/100,000 per year), while the 7 countries with the highest saturated fat intake had the lowest mortality from heart disease (170/100,000). See also The Cholesterol Myths by Uffe Ravnskov, 2000. Low-carb high-fat diets were ridiculed from start to finish as destructive and a fad, despite overwhelming evidence that they are not. See Nielsen JV, Joensson EA, Low-carbohydrate diet in type 2 diabetes. Stable improvement of bodyweight and glycaemic control during 22 months follow-up, Nutrition & Metabolism 2006;3(22) doi:10.1186/1743-7075-3-22. While Allport may be correct in claiming that omega-3s will prevent or reverse diabetes (and she is not always clear on which type), the evidence is clear that type-1 is much more easily controlled with a low-carb high-fat diet, and type-2 may be controlled so well on a low-carb diet that no medication is needed. See Dr. Bernstein’s Diabetes Solution, rev. ed. by Richard K. Bernstein, MD, Boston, MA:Little, Brown, 2003. So Allport’s recommendation to eat large amounts of fruit (p139) could be a disaster for diabetics. Eskimos are often obese albeit healthy, so omega-3s for weight loss seems too much to claim. And she seems unaware of the prevalence of grain allergies. See Natural Health & Weight Loss, Barry Groves, 2007; Know Your Fats by Mary G. Enig, 2000. Also Allport seems to equate eating linolenic acid as the equivalent of eating EPA and DHA in fish, and does not recommend supplements of the latter two. Neither idea had any supporting evidence presented. Nor was the ideal range of omega-3 intake given. A study of the conversion of radioisotopically-labeled linolenic acid to EPA in humans showed poor conversion, and even poorer conversion to DHA. Adequate intakes of pre-formed DHA are needed for good health. See Burdge G, alpha-Linolenic acid metabolism in men and women: nutritional and biological implications, Curr Opin Clin Nutr Metab Care 2004;7:137-144.

Cheap vs. Expensive Wine

The Harvard Society of Fellows, I learned from this great post by Steve Levitt, drink expensive wine — like $60/bottle. Steve, who was a Fellow for 3 years, did a simple experiment that showed the other members couldn’t tell expensive wine from cheap wine. Although the other members had liked the idea of doing the experiment, they didn’t like the results:

There was a lot of anger when I revealed the results, especially the fact that I had included the same wine twice. One eminent scholar stormed out of the room stating that he had a cold — otherwise he would have detected my sleight of hand with certainty.

Stormed out of the room! Why were they so angry? I think they were embarrassed. And not just that. Steve doesn’t say it, but I think there had been lots of dinner table conversation about how great the wine was. Now all that conversation was revealed to be delusional. Noting the greatness of the wine was — to be crude about it — a way of noting the greatness of those assembled at the table. “We appreciate the finer things in life,” they were saying. “We deserve to be here.” Snobbery is reassuring. In a tiny voice, the results said, yes, you are here, congratulations, but the reason you are here is more complicated than “you deserved it”.