Flaxseed Lowers Blood Pressure

A new study found that ground flaxseed powerfully lowers blood pressure:

A patient population with peripheral artery disease (PAD) was selected as ideal to benefit from dietary flaxseed. . . . Patients received 30g of milled flaxseed (or placebo) each day over 6 months. [I eat 50 g/day — Seth] . . . No significant adverse events were associated with flaxseed ingestion. . . . SBP in the placebo group increased by ~3 mmHg and DBP remained the same over the experimental period. However, SBP levels were ~10 mmHg lower (P<0.04) and DBP was ~8 mmHg lower (P<0.004) in the flax group compared to placebo. In the flaxseed group, patients with a SBP <140 mmHg at baseline did not receive an anti-hypertensive effect but patients who entered the trial with a SBP > 140 mmHg at baseline obtained a sustained and significant 15 and 7 mmHg reduction in SBP and DBP, respectively, during the six months. . . . one of the most potent anti-hypertensive effects ever observed by a dietary intervention.

This supports my belief that we can improve our overall health by trying to improve our brains (which are more sensitive than the rest of the body). I have blogged about flaxseed oil many times. I became interested in it when I noticed it improved my balance. Balance measurements showed that the optimal dose (2-4 T/day) was higher than flaxseed oil manufacturers suggested. Then I and others noticed that taking this amount of flaxseed oil produced big improvements in gum health. Tyler Cowen, for example, no longer needed gum surgery. Go home, said the surgeon.

Thanks to Grace Liu.

Assorted Links

Thanks to Anne Weiss and Dave Lull.

How Useful is Personal Genomics? A Case Study

How much can you help yourself by getting your genome sequenced? A lot, a little, not at all? Scenario 1 (big help): You discover you have a greatly elevated risk of Disease X. You do various things to reduce that risk that actually reduce it. Scenario 2: (a little help): You discover you have a greatly elevated risk of Rare Disease X. You do various things to reduce that risk but they don’t help. At least, when Disease X starts, you will be less upset. Scenario 3 (no help): You discover that you have a greatly elevated risk for a common easily-noticed disease (such as obesity). You already watched your weight, this changes nothing. Scenario 4 (harm): You discover that you have a greatly elevated risk of Scary Disease X (e.g., bipolar disorder). It is depressing news. Later studies show that the gene/disease association was a mistake. (Many gene/disease associations have failed to replicate.)

A recent Wired article tries to answer this question for one person: Raymond McCauley, a bioinformatics scientist who had his genome sequenced four years ago and learned he was “four or five times more likely than most people to develop age-related macular degeneration (AMD)”. The article says “of all the ailments described in the 23andme profile, AMD has one of the strongest genetic associations”. If I found this in my genetic profile, I would want to know the confidence interval of the increased risk. Is it a factor of 4.5 plus or minus 1? Or 4.5 plus or minus 8? This isn’t easy to figure out. In addition to the question of variability, there can easily be bias (= estimate is too high). Let’s say I do 100 gene/disease association studies. Then I scan these studies to pick the one with the strongest gene/disease association. It should be obvious that this particular association is likely to be too high and, depending on the details, could plausibly be pure chance (i.e., true association is zero). I have been unable to find out how replicable the gene/AMD association is. According to Wikipedia, “the lifetime risk of developing late-stage macular degeneration is 50% for people that have a relative with macular degeneration, versus 12% for people that do not have relatives with macular degeneration.” (Until it was eliminated via better diet, pellagra also ran in families.) The Wired article does not say whether any of McCauley’s relatives have/had AMD — a huge omission, given the uncertainty of gene/disease associations.

It wasn’t obvious what McCauley should do, according to the article:

McCauley read that there were a few preventative measures he could take to reduce the chances of AMD one day rendering him blind: don’t smoke and avoid ultraviolet light, for instance. Also, it seemed, he could try taking a special combination of vitamins, including B12 and lutein. But when he consulted the research, he could find little evidence to support the effectiveness of the regime, based on his genotype.

The article says nothing about quitting smoking but he does wear glasses that reduce ultraviolet light and takes certain vitamins. It is very hard for him to determine whether they help.

Here is a study that found greater omega-3 consumption associated with lower risk of AMD. Here is a study that found AMD associated with inflammation (too little omega-3 increases inflammation). Here is a study that found no association between vitamin and mineral intake and AMD. Based on this, if 23andme told me I had an increased risk of AMD, I would make sure to optimize my intake of flaxseed oil (or other omega-3 source) using some sort of brain test. I have documented in other posts that brain function is sensitive to omega-3 intake and (probably) most people don’t get enough. Of course, just as it is foolish to smoke (a lot) regardless of whether you have genetic risk of AMD, it is foolish to not optimize one’s omega-3 intake, whether or not you have genetic risk of AMD. In other words: everyone should optimize their omega-3 intake. If the 23andme results cause McCauley to do something wise like this that he would otherwise not have done, they have helped him.

The omega-3 study appeared after the Wired article so I don’t know how McCauley reacted to it. A puzzle about the story is that it isn’t even clear that the gene/AMD associations are true. Consider McCauley’s older relatives: parents, grandparents. Did/do any of them have AMD? If not, it is more plausible that all of them were at 12% risk of the disease than at 50% risk. Suppose all of them had, according to 23andme, the same increased risk as McCauley (at least some of them have the risk-bearing genes). Now it becomes more plausible that something is wrong with the 23andme risk estimate. If some of McCauley’s older relatives do have AMD, it is not clear why the 23andme results would make much difference. He should have already have known he was at increased risk of AMD.

The upshot is that in this particular case, I cannot even rule out Scenario 4 (does harm). All four scenarios strike me as plausible. Based on this article, we are a long way from learning the value of personal genomics.

Previously I used the example of Aaron Blaisdell to make the possibly counter-intuitive point that if you have a genetic disease something is wrong with your environment. Well, I do not have any obvious genetic disease. But I discovered, via self-experimentation, that my environment was terrible — meaning it could be improved in all sorts of ways: stop eating breakfast, drink flaxseed oil, eat butter, look at faces in the morning, take Vitamin D in the morning, and so on, not to mention eat fermented foods (which I figured out via psychology, not self-experimentation). My findings about what is optimal are so different than the way anyone now lives (except people who read this blog) that I believe everyone‘s environment can be vastly improved. If so, the value of discovering you have a genetically elevated risk of this or that is not obvious — you should already be trying to improve your environment. At least that is what my data has taught me. On the other hand, maybe genetic info (even wrong genetic info!) will give you a kick in the pants. Maybe that has happened with McCauley.

 

Assorted Links

Thanks to David Cramer and Nadalal.

Assorted Links

Thanks to Tim Beneke.

Assorted Links

Thanks to Robin Barooah and Mike Bowerman.

Two Years on the Shangri-La Diet

Alex Chernavsky, who often comments here, has updated his Shangri-La Diet (SLD) page. It now shows his weight over four years: two years before he started SLD and two years that he has been doing it.

Before he started SLD he was slowly gaining weight. After he started SLD, he went from 220 pounds (BMI = 32) to 193 pounds. He slowly gained a few pounds. Then (on my advice) he added a tablespoon of nose-clipped coconut butter and the steady climb stopped. Ffor about nine months has been steady at 195 pounds (BMI = 28). In other words, there is no sign that he is regaining the lost weight.

Because Alex has added a lot of omega-3 to his diet (via flaxseed oil), I’m sure his health has improved in other ways. Because he is a vegan, he had no interest in a conventional (Atkins) low-carb diet.

Alex reminded me that a doctor named Quigley left the following comment:

I’ve tried to find data that your diet works for SUSTAINED weight reduction in a study that would be applicable to a generalizable population. As you know, temporary weight loss is relatively easy. Sustained weight loss (wt loss > 2 yrs), is hard. If your diet can do it, I’d prescribe it every day.

 

Flaxseed Oil Alleviates Psoriasis and Lichen Planus

Two months ago I wrote that camelina oil might be a good source of omega-3. A few days ago, a reader named Evelyn Majidi commented as follows:

Based on this suggestion, I ordered camelina oil from the good farmers in Saskatchewan and began taking it using the same dose (3T/day) that I had been taking of flaxseed oil for relief of psoriasis and lichen planus. Unfortunately, the slow but sure improvement I had been experiencing over the past year with flaxseed oil stopped immediately and after a week my skin and mouth began to deteriorate. After using about 1/4 of a bottle of the new oil I went back to flaxseed and am delighted to report that I am [again] having good results with it. Since both of my conditions wax and wane without any reason identified by medical science I cannot state that it was simply the flaxseed oil that has led to this success. Based on my experience, however, I intend to continue taking the oil regularly and I recommend that others with psoriasis or lichen planus try it. For me, two tablespoons a day were not enough, I needed three tablespoons of the oil to see a change. I don’t think it advisable to take capsules, you’d need to take too many to equal 3T of oil.[emphasis added]

Psoriasis is a skin disease that usually involves “thick, red skin with flaky, silver-white patches called scales”. Lichen planus is “an itchy rash on the skin or in the mouth”. To give some idea of how common they are, psoriasis has 36 million Google hits; lichen planus 1-2 million. (“Heart disease” has 64 million.)

Eveyln’s experience provides four pieces of evidence that suggest flaxseed oil (FSO) improved her psoriasis and lichen planus:

  1. When she started taking FSO at 3 T/day, they started improving. They did not improve with 2 T/day.
  2. Over the first year of FSO, she saw steady improvement in both in place of the usual up and down.
  3. When she replaced FSO with another oil, which she hoped would be better, the results were the opposite of what she wanted: The improvement stopped and the two conditions got worse.
  4. When she switched back to FSO, the improvement resumed.

I can think of no plausible alternative to the conclusion that FSO helped. There is plenty of other evidence that supports this conclusion: the evidence that omega-3 is anti-inflammatory, FSO is high in omega-3, most of us don’t get enough omega-3, and so on, including my own experience. You could write a book about the evidence that supports it. (Evelyn tried flaxseed oil because of reports on this blog that it improved/cured bad gums.)

In any case, the conclusion that FSO reduces psoriasis and lichen planus is new, in the sense that FSO (or another source of omega-3) is not a popular treatment for either condition. Here are about 16 treatments for psoriasis, including topical corticosteroids. None includes omega-3. Here are eight “lifestyle and home remedies” for psoriasis, including “take daily baths” (seriously, Mayo Clinic Staff?). None includes omega-3. After going through about forty-odd treatments, I found a reference to fish oil: “Other research has suggested that taking oral fish oil supplements containing 1.8 to 3.6 grams of eicosapentaenoic acid (EPA) a day may bring improvement.”

Same thing for lichen planus. FSO is not a popular treatment.

If you take flaxseed oil or other omega-3 source to treat psoriasis or lichen planus, I hope you will let me know what happens.

An Unbiassed View of What We Should Eat . . . From a Rat

In nature animals must choose a healthy diet based on what tastes good. This doesn’t work for modern humans — lots of people eat poor diets — but why it fails is a mystery. There are many possible reasons. Are the wrong (“unnatural”) foods available (e.g., too much sugar, too little omega-3, not enough fermented food)? Is something besides food causing trouble (e.g., too little exercise, too little attention to food)? Are bad cultural beliefs too powerful (e.g., “low-fat”, desire for thinness)? Is advertising too powerful? Is convenience too powerful? Lab animals are intermediate between animals in nature and modern humans. They are not affected by cultural beliefs, advertising, and convenience (the foods they are offered are equally convenient). Their choice of food may be better than ours.

Nutrition researchers understand the value of studying what lab animals choose to eat. In 1915, the first research paper about “dietary self-selection” was published, followed by hundreds more. The general finding is that in laboratory or research settings, animals choose a relatively healthy diet. There are two variations:

[1.] Cafeteria experiments with chemically defined [= synthesized] diets showed that some of these animals, when offered the separate, purified nutrient components of their usual diet, eat the nutrients in a balance that more or less resynthesizes the original diet and that is often superior to it. [2.] Other animals eat two or more natural foods in proportions that yield a more favorable balance of nutrients than will any one of these foods alone.

Both findings imply that housing an animal in a lab does not destroy the mechanism that tells it what to eat.

Which is why I was fascinated to recently learn what Mr. T (pictured above), the pet rat of Alexandra Harney, the author of The China Price, and her husband, liked to eat. It wasn’t obvious. “We tried so many foods with him and always thought it made a powerful statement that even a wild rat turned his nose up at potato chips,” says Alexandra. “He hated most processed food. He also hated carrots, though.” Here are his top three foods:

  1. pate
  2. salmon sashimi
  3. scrambled eggs

Pate = protein, animal fat, complex flavors (which in nature would have been supplied by microbe-rich, i.e., fermented, food). Salmon sashimi = protein, omega=3. Scrambled eggs = ??

He liked beer in moderation, but not yogurt. “Owners of domestic rats say they love yogurt,” says Alexandra, “but Mr T only liked it briefly and then hated it, even lunging to bite a friend who brought him some. [Curious.] He loved cheese, stored bread for future consumption (but almost never ate it). Loved pesto sauce and coconut.” Note the absence of fruits and vegetables. Alexandra and her husband have no nutritional theories that I am aware of. They did not shape this list to make some point.

For me the message is: Why scrambled eggs? I too like eggs and eat them regularly and cannot explain why.

More Alex Tabarrok’s Thanksgiving post shows the connection between libertarian ideas (economies work better when more choice is allowed) and dietary self-selection.

Brain Surprise! Why Did I Do So Well?

For the last four years or so I have daily measured how well my brain is working by means of balance measurements and mental tests. For three years I have used a test of simple arithmetic (e.g, 7 * 8, 2 + 5). I try to answer as fast as possible. I take faster answers to indicate a better-functioning brain.

Yesterday my score was much better than usual. This shows what happened.

My usual average is about 550 msec or more; my score yesterday was 525 msec. An unexplained improvement of 25 msec.

What caused the improvement? I came up with a list of ways that yesterday was much different than usual, that is, was an outlier in other ways. These are possible causes. From more to less plausible:

1. I had 33 g extra flaxseed last night. (By mistake. I’m not sure about this.)

2. The test came at the perfect time after I had my afternoon yogurt with 33 g flaxseed. When I took flaxseed oil (now I eat ground flaxseed), it was clear that there was a short-term improvement for a few hours.

3. Many afternoons I eat 33 g ground flaxseed with yogurt. Yesterday I ground the afternoon flaxseed an unusually long time, making made the omega-3 more digestible.

4. I did kettlebells swings and a kettlebell walk about 2 hours before the test. These exercises are not new but usually I do them on different days. Yesterday was the first time I’ve done them on the same day. I’m sure ordinary walking improves performance for perhaps 30 minutes after I stop walking.

5. I had duck and miso soup a half-hour before the test. Almost never eat this.

6. I had a fermented egg (“thousand-year-old egg”) at noon. I rarely eat them.

7. I had peanuts with my yogurt and ground flaxseed. Peanuts alone seem to have no effect. Perhaps something in the peanuts improves digestion of the omega-3 in the flaxseed.

8. I started watching faces at 7 am that morning instead of 6:30 am or earlier.

Here are eight ideas to test. Perhaps one or two will turn out to be important. Perhaps none will.

After I made this list, I read student papers. The assignment was to comment on a research article. One of the articles was about the effect of holding a warm versus cold coffee cup. Holding a warm coffee cup makes you act “warmer,” said the article. Commenting on this, a student said she thought it was ridiculous until she remembered going to the barber. She sees the person who washes her hair (in warm water) as friendly, the barber as cold. Maybe this is due to the warm water used to wash her hair, she noted. This made me realize another unusual feature of yesterday: I had washed my hair in warm water longer than usual. I think I did it at least 30 minutes before the arithmetic test but I’m not sure. In any case, here is another idea to test. I found earlier that cold showers slowed down my arithmetic speed.

This illustrates a big advantage of personal science (science done for personal gain) over professional science (science done because it’s your job): The random variation in my life may suggest plausible new ideas. As far as I can tell, professional scientists have learned almost nothing about practical ways to make your brain work better. You can find many lists of “brain food” on the internet. Inevitably the evidence is weak. I’d be surprised if any of them helped more than a tiny amount (in my test, a few msec). The real brain foods, in my experience, are butter and omega-3. Perhaps my tests will merely confirm the value of omega-3 (Explanations 1-3). But perhaps not (Explanations 4-8 and head heating).