Celiac and Fat-Soluble Vitamins

One of the things I've been thinking about lately is the possibility that intestinal damage due to gluten grains (primarily wheat) contributes to the diseases of civilization by inhibiting the absorption of fat-soluble vitamins. If it were a contributing factor, we would expect to see a higher incidence of the common chronic diseases in newly-diagnosed celiac patients, who are often deficient in fat-soluble vitamins. We might also see a resolution of chronic disease in celiac patients who have been adhering faithfully to a long-term, gluten-free diet.

One thing that definitely associates with celiac disease is bone and tooth problems. Celiac patients often present with osteoporosis, osteopenia (thin bones), cavities or tooth enamel abnormalities (thanks Peter).

An Italian study showed that among 642 heart transplant candidates, 1.9% had anti-endomyosal antibodies (a feature of celiac), compared with 0.35% of controls. That's more than a 5-fold enrichment! The majority of those patients were presumably unaware of their celiac disease, so they were not eating a gluten-free diet.

Interestingly, celiac doesn't seem to cause obesity; to the contrary. That's one facet of modern health problems that it definitely does not cause.

The relationship between cancer and celiac disease is very interesting. The largest study I came across was conducted in Sweden using retrospective data from 12,000 celiac patients. They found that adult celiac patients have a higher overall risk of cancer, but that the extra risk disappears with age. The drop in cancer incidence may reflect dropping gluten following a celiac diagnosis. Here's another study showing that the elevated cancer risk occurs mostly in the first year after diagnosis, suggesting that eliminating gluten solves the problem. Interestingly, celiac patients have a greatly elevated risk of lymphoma, but a lower risk of breast cancer.

There's a very strong link between celiac and type I diabetes. In a large study, 1 in 8 type I diabetic children had celiac disease. This doesn't necessarily tell us much since celiac and type I diabetes are both autoimmune disorders.

One last study to add a nail to the coffin. Up to this point, all the studies I've mentioned have been purely observational, not able to establish a causal relationship. I came across a small study recently which examined the effect of a high-fiber diet on vitamin D metabolism in healthy (presumably non-celiac) adults. They broke the cohort up into two groups, and fed one group 20g of bran in addition to their normal diet. The other group got nothing extra. The bran-fed group had a vitamin D elimination half-life of 19.5 days, compared to 27.5 for the control group. In other words, for whatever reason, the group eating extra bran was burning through their vitamin D reserves 30% faster than the control group.

Unfortunately, the paper doesn't say what kind of bran it was, but it was probably wheat or oat (**Update- it's wheat bran**). This is important because it would determine if gluten was involved. Either way, it shows that something in grains can interfere with fat-soluble vitamin status, which is consistent with the staggering negative effect of refined wheat products on healthy non-industrialized cultures.

Add to this the possibility that many people may have some degree of gluten sensitivity, and you start to see a big problem. All together, the data are consistent with gluten grains interfering with fat-soluble vitamin status in a subset of people. As I discussed earlier, this could contribute to the diseases of civilization. These data don't prove anything conclusively, but I do find them thought-provoking.

Thanks to Dudua for the CC photo

Two Things That Get on My Nerves, Part II

Confusing Correlation and Causation

Recently, a paper was published that examined the association between sleep duration and the risk of death. Ferrie et al. showed that in their study population, subjects who slept either more or less than 7 hours a night had an increased overall risk of death. Here's how it was reported in Medical News Today:

Too Little Or Too Much Sleep Increases Risk Of Death

And here's a gem of a quote from one of the study's authors (excerpt from the article above):

In terms of prevention, our findings indicate that consistently sleeping around 7 hours per night is optimal for health and a sustained reduction may predispose to ill-health.

There's only one small problem: the study indicated no such thing. What the study showed is that people who sleep more or less than 7 hours tend to die more often than people who don't, not that the lack or excess of sleep caused the increased mortality. Have you ever noticed that you sleep more when you're not feeling well? Have you ever noticed that you sleep less when you're stressed? Could the increased mortality and sleep disturbances both be caused by some other factor(s), rather than one causing the other? We don't know, because the nature of the study doesn't allow us to answer that question!

The message the public ends up hearing is that no matter what feels right for your body, 7 hours of sleep is the optimum for health. Even though you'll have to go to work with bags under your eyes, feeling like crap, it's healthy. Even though you have the flu, you'd better not sleep more because it might give you a heart attack. I find that conclusion difficult to swallow.

The only way we could say that 7 hours of sleep is the healthiest amount (for the "average" person), would be to do an "intervention study", in which the subjects are manipulated rather than simply observed. Here's how it would work: we would take a large group of people and randomly assign them to either 5, 7 or 9 hours of sleep a night. We would then look at mortality over the course of the next few years, and see who dies more.

Intervention studies are the only way to establish causality, rather than simple association. At the end of our study, we could rightfully say that X amount of sleep causes an increase or decrease in mortality. Obviously, these types of studies are challenging and expensive to conduct, so it's tempting to over-interpret observational studies like the one I mentioned initially.  These studies are useful, but should be taken with a grain of salt.

This has to be one of the gravest, most frequent mistakes in the realm of health research and reporting. So many of the health recommendations we get from the media, the government, and even scientists are entirely based on associations! 

Two Things that Get on My Nerves, Part I

The "Thrifty Gene" Hypothesis

The thrifty gene hypothesis is the darling of many obesity researchers. It was proposed in 1962 by the geneticist James V. Neel to explain the high rates of obesity in modern populations, particularly modernizing American Indians. It states that our species evolved under conditions of frequent starvation, so we're designed to store every available calorie. In today's world of food abundance, our bodies continue to be thrifty and that's why we're fat.  You practically can't read a paper on overweight without seeing an obligatory nod to the thrifty gene hypothesis. The only problem is, it doesn't make much sense.

The assumption that hunter-gatherers and non-industrial agriculturalists lived under chronic calorie deprivation isn't well supported. The anthropological evidence indicates that most hunter-gatherers had abundant food, most of the time. They did have fluctuations in energy balance, but the majority of the time they had access to more calories than they needed. Yet they were not fat.

The Kitavans are a good example. They are a horticultural society that eats virtually no grains or processed food. In Dr. Staffan Lindeberg's studies, he has determined that overweight is virtually nonexistent among them, despite an abundant food supply.

The cause of obesity is not the availability of excess calories, it's the deregulation of the bodyweight homeostasis system. We have a very sophisticated set of feedback loops that "try" to maintain a healthy weight. It's composed of hormones (leptin, insulin, etc.), certain brain regions, and many other elements, known and unknown. These feedback loops influence what the body does with calories, as well as feeding behaviors. When you throw a wrench in the gears with a lifestyle that is unnatural to the human metabolism, you deregulate the system so that it no longer maintains an appropriate "set-point".

Here's what Neel had to say about the thrifty gene hypothesis in 1982 (excerpts from Good Calories, Bad Calories):

The data on which that (rather soft) hypothesis was based has now largely collapsed.

And what does he think causes overweight in American Indians now?

The composition of the diet, and more specifically the use of highly refined carbohydrates.

RIP, thrifty gene.

The Seat of Power

Have you ever wondered why the buttocks is one of the most attractive parts of the body on both sexes? I've heard it said that a man with a nice posterior will be better at thrusting during sex. I've also heard that it's purely aesthetic and nonfunctional, like a baboon's. Neither of these make any sense.

The shape of the buttocks comes mostly from the gluteal muscles (maximus and medius), superimposed by a layer of fat. The 'glutes' are some of the strongest muscles in the body, due to their large size and efficient leverage. Thrusting doesn't even come close to tapping into the glutes' tremendous power. What does? Heavy lifting. Sprints. Jumps. In short, some of the most functional full-body movements we perform as humans.

In any full-body movement, the hips are the central source of power. The strongest muscles surround the hips, and muscle strength diminishes progressively as you move further from them. A shapely buttocks is typically a strong buttocks, and a strong buttocks generally means a strong person. So if you want to decide at a glance whether a person is capable of sprinting and jumping after large prey, and then carrying it home, the buttocks is a good place to look.

The buttocks is also a storage area for fat. Humans tend to store a disproportionate amount of fat near their center of gravity: in the abdominal cavity, on the hips and on the buttocks. The right amount of fat indicates a healthy individual. A shapely buttocks is typically attached to someone who is strong and well-nourished. It's not so hard to imagine why we find it attractive.

Teenagers Less Likely To Engage In Risky Sexual Behavior

The University of Washington study, recently published in the Journal of Adolescent Health, also compared risky sexual behavior of teens living at home and those who established their own residences and found no significant differences between the groups, said Jennifer Bailey, a research scientist with the UW's Social Development Research Group and lead author of the paper.

"No one has compared typical teens before, because we stop being so concerned about their sexual behavior after they leave high school," said Bailey. "But it is important that we know what they are doing because late adolescence and the early 20s are the peak times for acquiring a sexually transmitted infection.

"HIV is a big risk. Chlamydia can affect fertility. The prevalence of gonorrhea and chlamydia are increasing. And some forms of human papillomavirus are related to cervical and other cancers. So it is important that we know what puts young people at risk for these sexually transmitted infections and what social structures may help protect them."

The study found that college students were more likely to always use a condom and less likely to engage in casual sex or high-risk sex than teens who did not attend a two- or four-year college.

Adapted from materials provided by University of Washington

Real Food VIII: Ghee

All this talk about butter is making me hungry. Richard mentioned in the comments that he bought some ghee recently and has been enjoying it, so I thought I'd post a recipe. Ghee is the Hindi word for clarified butter. It's butter that has had everything removed but the fat. Rich in fat-soluble vitamins and lacking the sometimes problematic lactose and casein, ghee has rightfully been considered a health food in India since ancient times.

Another advantage of ghee is its high smoke point, which is higher than butter because it doesn't contain any protein or sugars. Consequently, food sauteed in ghee has a clean, rich taste.

The recipe is simple but touchy. I recommend using the best butter you can get your hands on. 100% grass-fed, unsalted cultured butter is the best.

Ingredient and materials

• Butter (1 lb minimum)
• Wide-mouth glass jars
• Cheesecloth
• Rubber bands
  

Recipe

1. Place the butter in a saucepan and turn the heat to medium until it's melted.
   
2. Once it begins to boil, turn the heat down to low. It's very important to calibrate the heat correctly. Typically, you will want the burner on its lowest setting. The idea is to evaporate the water without burning the oil. It should boil, but slowly.
3. The melted butter starts out cloudy but gradually clears up as the water evaporates. At the same time, a crust will form on the surface of the ghee and the bottom of the pan. Keep the heat very low.
   
4. Push a portion of the top crust to the side with a spoon to see inside of the saucepan. When the butter looks clear and bubbles only rise from the bottom every few seconds, it's done. You have to be very careful because once the water has evaporated, the fat heats up quickly and burns the crust. This gives the ghee an acrid flavor and color. Make sure to handle the pot cautiously, because hot oil can give severe burns.
   
5. Allow the ghee to cool until it's warm but not hot. Place a piece of cheesecloth over the lid of your jar. Secure it with a rubber band. Pour the ghee through the cheesecloth, into the jar.
   
6. Store ghee in the refrigerator or at room temperature. It keeps much longer than butter.

The picture above is of my last batch of ghee.

More Fat-Soluble Vitamin Musing

If vitamin A, D and K2 deficiency are important contributors to the characteristic pattern of chronic disease in modern societies (the 'disease of civilization'), we should see certain associations. We would expect to find a lower fat-soluble vitamin status along with the most prevalent chronic diseases: cancer, cardiovascular disease, diabetes, osteoporosis, tooth decay, etc. We would also expect that improving vitamin status could reduce the incidence or recurrence of these diseases, which would be more convincing than a simple association.

Let's start with cancer. This one is like shooting fish in a barrel. There are consistent associations between low vitamin D status and numerous cancers, most notably breast and colon. And it doesn't just stop at associations. Here's a double-blind, placebo-controlled trial showing a 60% reduction of internal cancers in 1,179 American women taking 1,100 IU of D3 (and calcium) per day for 4 years. I won't go through the rest of the mountain of data linking low vitamin D to cancer, but if you want to see more science go here.

Vitamin K2 has been less well studied in this respect, but preliminary evidence is promising. Cancer patients are often vitamin K deficient. Supplementation with menatetrenone (K2 isoform MK-4) may reduce the recurrence of liver cancer. There's a strong inverse association between K2 intake and advanced prostate cancer, with the effect coming mostly from dairy.

In my post on K2 last week, I mentioned a study in which investigators found a strong inverse association between K2 consumption and cardiovascular as well as all-cause mortality. Patients with severe arterial calcifications tend to be K2 deficient, and K2 deficiency can induce arterial calcification in rodents. Marcoumar, a drug that interferes with K2 status, also causes calcification in humans. There's a mechanism behind K2's effect on CVD. There are several K2-dependent proteins that may protect the arteries from calcification, lipid accumulation and damage: matrix Gla protein, gas6, and protein S.

There is also a compelling association between vitamin D status and cardiovascular disease. Here's a quote from one study that struck me:

The adjusted prevalence of hypertension (odds ratio [OR], 1.30), diabetes mellitus (OR, 1.98), obesity (OR, 2.29), and high serum triglyceride levels (OR, 1.47) was significantly higher in the first than in the fourth quartile of serum 25(OH)D levels (P<.001 for all).

In other words, the 25% of people with the lowest D status are more likely to have hypertension and high triglycerides, and much more likely to be obese and/or have diabetes than the 25% with the highest D status. Keep in mind it's just an association, but that is nevertheless an impressive list of problems that are linked to low D status. Here's a large study that looked specifically at the association of vitamin D status and heart attack risk, and found a strong association even for people who are only mildly deficient. Supplementing elderly women with a modest amount of D3 improves hypertension.

The link between fat-soluble vitamins and bone/dental health is very strong. Vitamins D and K2 are required for proper formation and mineralization of the bones and teeth, and proper development of the cranium and face (this is exactly what Weston Price saw). K2 supplementation has a major protective effect on osteoporosis and fractures, according to several controlled trials. The salivary glands have the highest concentration of K2 MK-4 of any organ, and they secrete it into saliva along with K2-dependent proteins. Weston Price documented the dramatic protective effect of cod liver oil (A and D) and butter oil (A and K2) against tooth decay.

I couldn't find any consistent associations between vitamin A status and chronic disease. This may be because, as opposed to D and K2, few people in the US or Europe are deficient. It's interesting to note that grain-fed dairy is still a good source of vitamin A, while it loses most of the vitamin D and K2 that's found in grass-fed dairy.

Osteoporosis and arterial calcification are not due to a lack or an excess of calcium. In fact, the two problems often come hand-in-hand. Calcium supplements are unnecessary at best. The Japanese, who eat far less calcium than the average American, have a lower risk of osteoporosis and fracture. The problem with both osteoporosis and arterial calcification is that the body is not using its calcium effectively. The studies mentioned above show that the fat-soluble vitamins are critical for proper calcium use by the body, among other things.

I hope you can see that a deficiency of fat-soluble vitamins could well be a major contributor to the characteristic pattern of diseases that afflict industrialized nations. There are two more facts that we need to complete the picture. First of all, some research suggest a high prevalence of vitamin D and K deficiency (or insufficiency). A, D and K are synergistic. A and D have their own nuclear receptors that alter the transcription of hundreds of genes, while K activates many of these genes once they are translated into proteins. Thus, you'd expect that giving them together would have a much larger effect that giving them alone. This suggests that the studies using single vitamins may be falling far short of the protection afforded by optimal status of all three.