Category: animal fat

The Evolution of Lactose Tolerance and My Butter Discoveries

Seth Roberts30 Comments

From a BBC documentary called Are We Still Evolving? I learned that after the development of farming there was intense selection in Europe for “lactose tolerance” — meaning the ability to digest lactose as an adult, which requires the enzyme lactase. (The technical name is lactase persistence.) The necessary gene spread rapidly. Now most Europeans have the gene. In Ireland almost everyone has the gene. Mark Thomas, an evolutionary geneticist interviewed on the show, who does research on lactose tolerance, said this:

It’s probably the most advantageous characteristic that Europeans have evolved in the last 30,000 years.. . . The advantage that’s been measured is just incredible, absolutely incredible, how big an advantage it was for these early farmers in Europe.

“Why would drinking milk into adulthood be so strongly selected for?” asked Alice Roberts, the presenter. Thomas replied,

Milk has got lots of energy in it, it’s very nutrient dense, it’s got lots of other goodies, like various vitamins, calcium, and so on. Also, it’s a relatively clean fluid, so it’s much better than drinking stream water or river water or well water or something like that. Another advantage is if you’re growing crops you have a boom and bust in terms of the food supply.

Not a word about butterfat — “lots of energy” is true of all fats. The rapid spread, the “incredible” advantage, suggests that milk supplied something resembling a necessary nutrient. As if everyone had been suffering from scurvy and the new gene allowed them to eat citrus — something like that. Such a gene would spread rapidly.

Does milk supply a necessary nutrient? My results suggest that butter — half a stick (60 g)/day — provides two clear benefits: 1. Better brain function. 2. Less risk of heart disease (probably). As far as I can tell, roughly everyone in America would get these benefits because their diets now lack enough of whatever it is. Both benefits reflect invisible problems. Like everyone else, I had no idea my brain function could be substantially improved and had no idea of my rate of progression (narrowing of arteries) toward atherosclerosis. Only because of unusual tests (the arithmetic test and a “heart scan”) did I notice sudden large improvements when I started eating lots of butter — what you’d expected from addition of a missing necessary nutrient. This explains why Thomas and almost everyone else is unaware of these benefits.

Keep in mind that before I started eating butter, I already ate a high-fat low-carbohydrate diet. Yet I wasn’t getting enough of something in butter. I already ate lots of pork fat. Perhaps the saturated fat in butter is better digested than the saturated fat in pork. Or perhaps the fat profile is better.

If lactose tolerance is so helpful, why are most Asians lactose intolerant? My work suggests two answers: 1. Yogurt. Long ago, Asians ate lots of yogurt. I know the Mongols did. There are present-day indications of this. The Chinese appreciate the value of yogurt more than Americans. Yogurt is more common in Chinese supermarkets than American ones. Yogurt makers are better and more common in China than Europe and America. Lots of Chinese make their own yogurt; as far as I can tell, home yogurt making is more popular in China than America. You can buy a cheap good yogurt maker many places in Beijing, unlike San Francisco. Yogurt provided butterfat. 2. Pork. The Chinese, of course, eat far more pork than Europeans. Unlike cows, pigs supply a cut with a large amount of fat: pork belly. I found it easy to get plenty of pork belly in China and eat it as the main course. Difficulty getting pork belly in the Bay Area is what pushed me to eat butter. This view predicts that European farmers raised more cows than pigs.

Anyway, to summarize, the great advantage conferred by lactose tolerance suggests the great value of something in milk if you eat a European-farmer-like diet. My work supports this; it suggests the crucial ingredient is butterfat. Which many Americans carefully avoid!

Note: The danger posed by the high level of AGEs (advanced glycation endproducts) in butter I don’t know about — but of course this danger has nothing to do with why lactose tolerance was so beneficial. My experience so far (the heart-scan improvement) suggests that that ordinary butter is not “artery-constricting”. Presumably AGEs are formed when milk is pasteurized so I would prefer to eat unpasteurized butter.

How Rare My Heart Scan Improvement?

Seth Roberts21 Comments


In 2009, I had a heart scan — a three-dimensional X-ray. The scan was used to calculate an Agatston score, a measure of arterial plaque. Higher scores mean a higher risk of heart attack. A few months after that, I discovered that butter improves how fast I do arithmetic.

Because butter was good for my brain, I started eating half a stick of butter (66 g) every day. Surely the butter was improving overall brain function. The effect of butter on the rest of my body I didn’t know. However, I thought it was highly unlikely that a food that greatly improves brain function is going to damage the rest of the body. The food you eat, after digestion, goes to the whole body (leaving aside the blood-brain barrier). Every part of the body must have been optimized to work well with the same food.

As I have posted earlier, I had a second heart scan, producing a second Agatston score, about a year after the first one. Amazingly, the second score was better (lower) than the first score. The woman in charge of the testing center said this was very rare — about 1 time in 100. The usual annual increase is about 20 percent.

Now I have gotten more information about the annual rate of change in Agatston scores. The graph above (thanks to Harry Rood) shows data from 40 people who listed their scores at the Track Your Plaque site. It is based on pairs of consecutive scores: it plots change versus level (average?). Because some people provided more than two scores, the data allowed 77 points to be plotted. My two scores were 38 (log 38 = 1.58) and 29 (log 29 = 1.46). So the decrease in log units was 0.12. If you look at the graph, you can see what an outlier this is — as I was told, it really is about 1 in 100.

Here we have the conjunction of two unusual things: 1. Eating half a stick of butter per day. Almost no one eats so much butter. 2. An extremely rare drop in the Agatston score over the same period. A principle of reasoning called Reichenbach’s Common Cause Principle says if two rare events might reflect cause and effect, they probably do. You can think of it like this: Lighting doesn’t strike twice in one place for two different reasons. Indeed, there is other evidence that high levels of saturated fat cause heart-scan improvement (even though this contradicts everything you’ve been told). Mozzafarian et al. (2004) found that in postmenopausal women, “a greater saturated fat intake is associated with less progression of coronary atherosclerosis.” So it is quite plausible that my butter intake improved my Agatston score.

Assorted Links

Seth Roberts1 Comment

Thanks to Craig Fratrik, Tom George and Sean Curley.

Podcast: Play in new window | Download

The Buttermind Experiment

Seth Roberts35 Comments

In August, at a Quantified Self meeting in San Jose, I told how butter apparently improved my brain function. When I started eating a half-stick of butter every day, I suddenly got faster at arithmetic. During the question period, Greg Biggers of genomera.com proposed a study to see if what I’d found was true for other people.

Eri Gentry, also of genomera.com, organized an experiment to measure the effect of butter and coconut oil on arithmetic speed. Forty-five people signed up. The experiment lasted three weeks (October 23-November 12). On each day of the experiment, the participants took an online arithmetic test that resembled mine.

The participants were randomly assigned to one of three groups: Butter, Coconut Oil, or Neither. The three weeks were divided into three one-week phases. During Phase 1 (baseline), the participants ate normally. During Phase 2 (treatment), the Butter participants added 4 tablespoons of butter (half a stick of butter) each day to their usual diet. The Coconut-Oil participants added 4 tablespoons of coconut oil each day to their usual diet. The Neither participants continued to eat normally. During Phase 3 (baseline), all participants ate normally.

After the experiment was finished. Eri reduced the data set to participants who had done at least 10 days of testing. Then she made the data available. I wanted to compute difference scores (Phase 2 MINUS average of Phases 1 and 3) so I eliminated someone who had no Phase 3 data. I also eliminated four days where the treatment was wrong (e.g., in the sequence N N N N N B B N N B, where N = Neither and B = Butter, I eliminated the final Butter day). That left 27 participants and a total of 443 days of data.

Because the scores on individual problems were close to symmetric on a log scale, I worked with log solution times. I computed a mean for each day for each participant and then a mean for each phase for each participant.

2011-01-26 buttermind averages This figure shows the means for each phase and group. The downward slopes show the effect of practice. The separation between the lines shows that individual differences are large. (There was no reliable difference between the three groups during Phase 1.)

The point of the baseline/treatment/baseline design is allow for a large practice effect and large individual differences. It allows a treatment effect to be computed for each participant by computing a difference score: Phase 2 MINUS average of Phases 1 and 3. The average of Phases 1 and 3 estimates what the results would be if the treatment made no difference.

2011-01-29 buttermind difference scores

This graph shows the difference scores. There are clear differences by group. A Wilcoxon test comparing the Butter and Neither groups gives one-tailed p = 0.006.

The results support my idea that butter improves brain function. They also suggest that coconut oil does not. In the next post I’ll discuss what else I learned from this experiment.

Different Effects of Omega-3 and Omega-6 on Heart Disease

Seth Roberts5 Comments

You have probably read hundreds of recommendations to eat more polyunsaturated fatty acids (PUFAs), which in practice means omega-6 and omega-3. If you shop at Whole Foods, you may see Udo’s Blend, a blend of PUFAs which includes both omega-3 and omega-6, as if someone isn’t getting enough omega-6. It is unquestionable that omega-3 is beneficial but there is plenty of evidence that omega-6 is harmful, starting with the Israeli Paradox. Why are they lumped together?

A just-published paper in the British Journal of Nutrition makes several new points about the relation of PUFAs and heart disease. Its main point is a new look at experiments in which one group was given more PUFAs than another group. Those experiments — there are only about eight — can be divided into two groups: (a) experiments in which the treated group was given both omega-3 and omega-6 and (b) experiments in which the treated group was given only omega-6. The two groups of experiments seem to have different results. In the “both” experiments the treated group seems to benefit; in the “only omega-6″ experiments, the treated group seems to be worse off. Suggesting that omega-3 and omega-6 have different effects on heart disease. They have been lumped together because experiments have lumped them together (varied both at the same time).
Experiments that try to measure the effect of PUFAs usually say they are replacing saturated fats. More PUFAs, less butter. The paper points out that studies of the effect of PUFAs have at least sometimes confounded reduction in saturated fats with reduction in trans fats. Benefits of the change may be due to the reduction in trans fats, not the reduction in saturate fats.

The paper also makes several good points about the Finnish study, a classic in the fat/heart disease literature. Supposedly the Finnish study showed that PUFAs (replacing saturated fats) reduce heart disease. It had hundreds of subjects but they were not randomized separately. The subjects were divided by hospital. Everyone in one hospital got one diet, everyone in a second hospital got a different diet. This meant it was easy for there to be confoundings (i.e., the treatment wasn’t the only difference between the groups). Indeed, there were big differences in consumption of a certain dangerous medication and margarine between hospitals. (Margarine is high in trans fats.)

Perhaps the first author, Christopher Ramsden, who works at NIH, is responsible for the high quality of this paper.
Thanks to Susan Allport.

Food For Thought

Seth Roberts6 Comments

A perfectly good Economist article about food and brain function includes the following:

Many studies suggest that diets which are rich in trans- and saturated fatty acids, such as those containing a lot of deep-fried foods and butter, have bad effects on cognition. Rodents put on such diets show declines in cognitive performance within weeks.

Whereas I found butter improved my cognitive performance within a day. And pork fat improved my sleep within a day. On the other hand, I wouldn’t be surprised if foods deep-fried in plant oils, such as corn oil, are bad for the brain.

Epilepsy’s Big, Fat Miracle …

Seth Roberts3 Comments

… is the title of a New York Times Magazine article about the ketogenic diet, a treatment for childhood epilepsy, which I’ve blogged about several times (here, here, here, here, here). It’s a very-high-fat diet. It interests me for two reasons: (a) It connects a high-fat diet with proper brain function, as my self-experiments have done. A curious feature of the ketogenic diet is that it isn’t permanent. After several years the child can go off it. My self-experimentation suggests that Americans eat far too little of certain fats. Perhaps eating enough of these fats would prevent childhood epilepsy. (b) It shows how someone who cares enough — in this case, Jim Abrahams, whose son had epilepsy — can be more effective than professional researchers and doctors. Abrahams rediscovered the diet. He saw its value, the professionals didn’t. I’ve argued that this is part of why my self-experimentation found new solutions to common problems: because I had those problems. I cared more about finding a workable solution than researchers in those areas, who had several other concerns (publication, funding, acceptance, etc.).

The details of the article reminded me of something I learned in the BBC series The Story of Science. For hundreds of years, medical students were told, following Aristotle, that the liver has three lobes. It doesn’t. You might think that examination of thousands of actual livers would have dispelled the wrong idea, but it didn’t. The article contains many examples of doctors ignoring perfectly good evidence in favor of nonsense they read in a book or heard in a lecture. Epilepsy is easy to measure. If a child has 100 seizures per day, and has been having them at this rate for years, and this goes down to 5 shortly after he starts the ketogenic diet, and goes up again when the child goes off the diet, there is no doubt the diet works. As early as the 1930s, this had been observed hundreds of times. This was overwhelming evidence of effectiveness. Doctors ignored it, probably based on the modern equivalent of the three-lobed liver. They complained, according to the article, that there was “no evidence it worked” or that the evidence wasn’t “controlled” or “scientific” (whatever that means). A study published in 2008 “answered doubts about keto’s clinical effectiveness” — as if doctors needed the equivalent of a very-large-type book to be able to read what most of us can read with normal-sized type.

According to the article, “by 2000, more people were asking about keto, but most pediatric neurologists still would not prescribe it” — as if the parents needed the approval of their doctor to try it. You don’t need a prescription to buy food.

Thanks to Tim Beneke, Michael Bowerman, Alex Chernavsky, David Cramer, and Peter Couvares.

How Wonderful is Lipitor?

Seth Roberts6 Comments

John Cassidy, a staff writer at The New Yorker, understands clearly the poor judgment of economics professors. In How Markets Fail he said the Nobel Prize in Economics has made things worse, because it has often been given for worthless work. Outside of economics, however, he can write this:

during a period in which American companies have created iPhones, Home Depot, and Lipitor, the best place to work has been in an industry [the financial industry] that doesn’t design, build, or sell a single tangible thing.

That such a smart well-informed non-party-liner can believe Lipitor is wonderful shows Orwell was right: with enough repetition, people can be convinced war = peace. Here is the truth about Lipitor:

Statin therapy is extremely efficient in lowering cholesterol numbers, but unfortunately not without adverse effects on the body. To prevent a first heart attack, for every life that is saved – 1% over 10 years of use – statins cause an equal number of adverse deaths due to accidents, infection, suicide and cancer — 1% over 10 years’ use and significantly greater levels of serious side effects and suffering. . . . In a study to see the effects of raising the Lipitor levels from 10 to 80 mg (more sales) on patients, those taking 80 mg had increased liver problems, that is the rate of raised liver enzymes was six times higher than those given 10 mg of Lipitor. Even though the total deaths due to CVD in the 80 mg group was fewer (126) than in the 10 mg group (155), the total deaths due to other causes was higher in the 80 mg (158) than the 10 mg (127) group. There was no difference in the overall mortality rate.

Lipitor, the miracle drug. Taken by millions at a cost of billions. This is what happens when you — such as those in charge of health care — have little understanding of a problem: You aren’t good at solving it.

Cardiologists believe that high cholesterol causes heart attacks. Their depth of understanding was illustrated by the cardiologist at my Quantified Self talk about butter who said that the Framingham study showed that diet caused heart attacks (no, it found new correlations between heart disease and “risk factors” such as cholesterol — see also this) and that the recent reduction in heart attacks is evidence of our improved understanding (e.g., the science behind Lipitor). That a thousand other things changed over the same time period he apparently hadn’t considered. He simply couldn’t defend — at least then — his core belief that butter was bad. A cardiologist! How many thousands of people has he told to eat less butter?

Cassidy’s article about the harm done by the financial industry, from which that quote was taken, is excellent.

Effect of Flaxseed Oil on Arithmetic

Seth Roberts6 Comments

After I moved to China in September, I was surprised that my arithmetic speed went down. (That is, I got faster.) I had lowered it from about 630 msec/problem to 600 msec/problem by eating lots of butter. I had no idea how to lower it further. I didn’t deliberately change my diet in China but it was quite different. I kept some things the same: the amount and brand of butter/day, the amount and brand of flaxseed oil/day.

I failed to figure out why I had gotten faster. I reduced the amount of flaxseed oil from 3 T (tablespoons) per day to 2 T per day. It made no difference. (In the beginning of my interest in flaxseed oil, change from 2 T/day to 3 T/day had made a difference.) Perhaps because of the butter.

Surprised that the change from 3 T/day to 2 T/day hadn’t made a difference, I went down to 1 T/day for two weeks, then back to 2 T/day. Both changes made a difference:

Each point is a separate test. Each test had 32 arithmetic problems (e.g., 3+4, 11-3). In the beginning of the data shown in the figure I tested myself once per day. After 12 days I started doing two tests/day, one right after the other. I was curious about the repeatability of the numbers; it wasn’t hard; it was a way to get better measurements. Averaging over the tests for each day to get one value per day, combining the 19 2-T/day (before) days and the 11 2-T/day (after) days, and comparing the combination to the final 7 1-T/day days, t (38) = 6.5. If you’re not familiar with t values, t = 2 is a barely reliable difference, t = 4 is a very clear difference.

This is more evidence that flaxseed oil improves brain function. It interests me because it implies the optimum dose is close to 2 T/day. It cost about $20 and took 1 person-month. In contrast, the DHA-Alzheimer’s study I mentioned two days ago cost about $1 million and took about 7000 person-months. And used (a) a cruder something-versus-nothing comparison, b) a less-sensitive between-subjects comparison, and (c) a more ethically-problematic placebo-controlled design.

Stroke and Saturated Fat

Seth RobertsLeave a comment

A 1997 epidemiological study, which I just learned about, found that increases in saturated fat intake were associated with a lower risk of stroke. Sampling from among the papers that cited it, this study found a non-significant change in the same direction. This study found a significant change in the same direction in Japanese, who eat a low amount of saturated fat. This is especially interesting because many people assumed that the high rate of stroke among Japanese was due to high salt intake. This finding suggests it is due to low saturated fat intake.

As I said in a recent post, this sort of consistency across studies on a question of enormous interest argues against the severest critics of epidemiology, such as John Ioannidis.