Saturday, April 17, 2010

White House Hosts Summit on Childhood Obesity

First Lady Michelle Obama met with task force members on Friday at the White House to tackle the weighty issue of childhood obesity. The task force will be preparing a report that will “serve as a very important road map, with goals, benchmarks, [and] measurable outcomes…” she said.

With one in three children falling into the overweight/obese category, this issue is approaching crisis mode. To stem the tide, and hopefully improve the health of our nation’s youth, the legislature, with the support of the White House, has been implementing programs, instituted the task force, and stumping for an improvement in our food delivery system overall and in our schools.

Back in February the White House announced the Healthy Food Financing Initiative, a $400 million/year initiative aimed to expand access to fresh, healthy food to all underserved urban and rural communities across the country within seven years, creating jobs in the process. During the same month, the First Lady launched her own childhood obesity initiative, “Let’s Move.” The program is quite ambitious, with the goal of developing workable ideas to help end childhood obesity within one generation.

The task force meeting, about 100 strong, was composed on senior Administration officials, doctors, teachers, activists, and other individuals who are committed to ending childhood obesity. Initial discussions focused on the cost of childhood obesity, the lack of playgrounds in neighborhoods around the country, and more esoteric issues such as behavioral economics. Melody Barnes, chairman of the task force and director of the Domestic Policy Council, broke the members into groups with a very specific task: "Come up with three to five of the best ideas, the important actions, the task force should recommend to the president."

It will be interesting to see what recommendations spring from this group of well-researched, knowledgeable individuals. Not only to they have to think outside the box, they need to think within a budget and at a level that works for children, parents, schools, and communities as a whole.

HealthNews Dozen: 12 Tips for Spring Allergies

With the onset of spring, allergens seem to be floating everywhere and attacking innocent people who were - until all of the sneezing and sniffling - happy to see the season change. It is the time of the year that many people find that they have allergic reactions to particular things, and for others, it is that unavoidable time to stock up on tissues and medications that might alleviate the pain and discomfort.

But there are things one can do to minimize allergic reactions and the presence of allergens in many parts of one’s life. If the body’s immune system refuses to cooperate and fend off the allergy-causing substances, it is up to the person to change parts of their environment. Though it is humanly impossible to form a cocoon and hide there until summer, Prevention Magazine has some more realistic suggestions.

The first thing to do is engage in some spring cleaning. Wearing a mask while doing it may keep from being bombarded with dust during the process, but the cleaning is necessary. The artificial heat of winter and lack of fresh air often allows much dust to build in closets and in corners, and ridding the home of it all is the best way to start. However, it is necessary for allergy sufferers to continue to keep the home clean. Once the major scouring process is complete, a weekly surface-clean will keep the home a safe place for overly sensitive senses.

Spring cleaning might be the time to change things about one’s bed to make it an allergy-free zone as well. Special allergen-proof pillows are available at most home stores. And for those who have severe allergic reactions, there are mattresses and box springs that have tight fabric weaves to keep dust mites out.

Another change to the home is to add throw rugs. Even in a carpeted room, buying throw rugs can not only enhance the look of the room but allow the carpet to stay allergen free. And rugs can be easily cleaned in hot temperatures on a regular basis to kill dust mites.

Speaking of laundry, linens, towels, and the like should be washed in water that is at least 130 degrees, something that can be tested with a meat thermometer. If the home washer doesn’t reach a high enough temperature, a laundromat can wash to your specification.

Surrounding oneself with clean air is not always possible, but there are some things to do to make surroundings more allergy-free. In the car, use air conditioning rather than letting the wind blow allergens into the vehicle. Stay away from smoking and smokers, and if one must smoke, doing it outside to keep the home and vehicles free of smoke will help immensely. And in the house, a dehumidifier can stop many dust mite problems, as they don’t thrive in humidity below 45 percent. But if that doesn’t work, installing an air filter or air purifier can alleviate some of the problems.

A less ideal solution is to isolate pets in exchange for not getting rid of them altogether, but that is not realistic for most people who love their animals. There can be “safe” rooms, like the bedroom, however, where the pets are prohibited, which will allow some literal breathing room for those with allergies.

All in all, there are ways to ease the pain of allergy season. Though it may require more work than getting a prescription, it may be worth the better overall health of living in a cleaner environment and protecting oneself from mites and germs.

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Thursday, April 15, 2010

Copper in Food

Sources of Copper

It isn't hard to get enough copper-- unless you live in an industrial nation. I've compiled a chart showing the copper content of various refined and unrefined foods to illustrate the point. The left side shows industrial staple foods, while the right side shows whole foods. I've incorporated a few that would have been typical of Polynesian and Melanesian cultures apparently free of cardiovascular disease. The serving sizes are what one might reasonably eat at a meal: roughly 200 calories for grains, tubers and whole coconut; 1/4 pound for animal products; 1/2 teaspoon for salt; 1 cup for raw kale; 1 oz for sugar.

Note that beef liver is off the chart at 488 percent of the USDA recommended daily allowance. I don't know if you'd want to sit down and eat a quarter pound of beef liver, but you get the picture. Beef liver is nature's multivitamin: hands down the Most Nutritious Food in the World. That's because it acts as a storage depot for a number of important micronutrients, as well as being a biochemical factory that requires a large amount of B vitamins to function. You can see that muscle tissue isn't a great source of copper compared to other organs, and this holds true for other micronutrients as well.

Beef liver is so full of micronutrients, it shouldn't be eaten every day. Think of it in terms of the composition of a cow's body. The edible carcass is mostly muscle, but a significant portion is liver. I think it makes sense to eat some form of liver about once per week.

Modern Agriculture Produces Micronutrient-poor Foods

The numbers in the graph above come from NutritionData, my main source of food nutrient composition. The problem with relying on this kind of information is it ignores the variability in micronutrient content due to plant strain, soil quality, et cetera.

The unfortunate fact is that micronutrient levels have declined substantially over the course of the 20th century, even in whole foods. Dr. Donald R. Davis has documented the substantial decline in copper and other micronutrients in American foods over the second half of the last century (1). An even more marked decrease has occurred in the UK (2), with similar trends worldwide. On average, the copper content of vegetables in the UK has declined 76 percent since 1940. Most of the decrease has taken place since 1978. Fruits are down 20 percent and meats are down 24 percent.

I find this extremely disturbing, as it will affect even people eating whole food diets. This is yet another reason to buy from artisanal producers, who are likely to use more traditional plant varieties and grow in richer soil. Grass-fed beef should be just as nutritious as it has always been. Some people may also wish to grow, hunt or fish their own food.

Tuesday, April 13, 2010

Interview with John Barban

I recently did a podcast interview with John Barban from the Adonis Lifestyle blog. We talked mostly about fat mass and the body fat "setpoint". As it turns out, what I said must have been at odds with John's philosophy, because he posted another podcast the next week that appears to be about why he disagrees with me!

Anyway, enjoy the interview.

I did another one recently with Jimmy Moore that's coming soon.

Monday, April 12, 2010

Gary Taubes Speaks this Thursday at UW

Gary Taubes will be giving a lecture this Thursday, April 15th, at the University of Washington in Seattle, titled "Why we get fat: adiposity 101 and an alternative hypothesis of obesity". It's free and open to the public. The talk is from noon to 1:00, followed by a question and answer session from 1:00 to 2:00.

The talk will take place in Hogness auditorium, which is room A420 of the Health Sciences building (1959 NE Pacific St). The whole area is difficult to navigate, so allow yourself time to park and find the auditorium. Here are directions to Hogness, including parking.

I'll be sitting near the front if anyone wants to say hi afterward.

Friday, April 9, 2010

Full-fat Dairy for Cardiovascular Health

I just saw a paper in the AJCN titled "Dairy consumption and patterns of mortality of
Australian adults
". It's a prospective study with a 15-year follow-up period. Here's a quote from the abstract:
There was no consistent and significant association between total dairy intake and total or cause-specific mortality. However, compared with those with the lowest intake of full-fat dairy, participants with the highest intake (median intake 339 g/day) had reduced death due to CVD (HR: 0.31; 95% confidence interval (CI): 0.12–0.79; P for trend = 0.04) after adjustment for calcium intake and other confounders. Intakes of low-fat dairy, specific dairy foods, calcium and vitamin D showed no consistent associations.
People who ate the most full-fat dairy had a 69% lower risk of cardiovascular death than those who ate the least. Otherwise stated, people who mostly avoided dairy or consumed low-fat dairy had more than three times the risk of dying of coronary heart disease or stroke than people who ate the most full-fat diary.

Contrary to popular belief, full-fat dairy, including milk, butter and cheese, has never been convincingly linked to cardiovascular disease. In fact, it has rather consistently been linked to a lower risk, particularly for stroke. What has been linked to cardiovascular disease is milk fat's replacement, margarine. In the Rotterdam study, high vitamin K2 intake was linked to a lower risk of fatal heart attack, aortic calcification and all-cause mortality. Most of the K2 came from full-fat cheese. In my opinion, artisanal cheese and butter made from pasture-fed milk are the ultimate dairy foods.

From a 2005 literature review on milk and cardiovascular disease in the EJCN:
In total, 10 studies were identified. Their results show a high degree of consistency in the reported risk for heart disease and stroke, all but one study suggesting a relative risk of less than one in subjects with the highest intakes of milk.

...the studies, taken together, suggest that milk drinking may be associated with a small but worthwhile reduction in heart disease and stroke risk.

...All the cohort studies in the present review had, however, been set up at times when reduced-fat milks were unavailable, or scarce.
The fat is where the vitamins A, K2, E and D are. The fat is where the medium-chain triglycerides, butyric acid and omega-3 fatty acids are. The fat is where the conjugated linoleic acid is. So the next time someone admonishes you to reduce your dairy fat intake, what are you going to tell them??

Tuesday, April 6, 2010

Copper and Cardiovascular Disease

In 1942, Dr. H. W. Bennetts dissected 21 cattle known to have died of "falling disease". This was the name given to the sudden, inexplicable death that struck herds of cattle in certain regions of Australia. Dr. Bennett believed the disease was linked to copper deficiency. He found that 19 of the 21 cattle had abnormal hearts, showing atrophy and abnormal connective tissue infiltration (fibrosis) of the heart muscle (1).

In 1963, Dr. W. F. Coulson and colleagues found that 22 of 33 experimental copper-deficient pigs died of cardiovascular disease. 11 of 33 died of coronary heart disease, the quintessential modern human cardiovascular disease. Pigs on a severely copper-deficient diet showed weakened and ruptured arteries (aneurysms), while moderately deficient pigs "survived with scarred vessels but demonstrated a tendency toward premature atherosclerosis" including foam cell accumulation (2). Also in 1963, Dr. C. R. Ball and colleagues published a paper describing blood clots in the heart and coronary arteries, heart muscle degeneration, ventricular calcification and early death in mice fed a lard-rich diet (3).

This is where Dr. Leslie M. Klevay enters the story. Dr. Klevay suspected that Ball's mice had suffered from copper deficiency, and decided to test the hypothesis. He replicated Ball's experiment to the letter, using the same strain of mice and the same diet. Like Ball, he observed abnormal clotting in the heart, degeneration and enlargement of the heart muscle, and early death. He also showed by electrocardiogram that the hearts of the copper-deficient mice were often contracting abnormally (arrhythmia).

But then the coup de grace: he prevented these symptoms by supplementing the drinking water of a second group of mice with copper (4). In the words of Dr. Klevay: "copper was an antidote to fat intoxication" (5). I believe this was his tongue-in-cheek way of saying that the symptoms had been misdiagnosed by Ball as due to dietary fat, when in fact they were due to a lack of copper.

Since this time, a number of papers have been published on the relationship between copper intake and cardiovascular disease in animals, including several showing that copper supplementation prevents atherosclerosis in one of the most commonly used animal models of cardiovascular disease (6, 7, 8). Copper supplementation also corrects abnormal heart enlargement-- called hypertrophic cardiomyopathy-- and heart failure due to high blood pressure in mice (9).

For more than three decades, Dr. Klevay has been a champion of the copper deficiency theory of cardiovascular disease. According to him, copper deficiency is the only single intervention that has caused the full spectrum of human cardiovascular disease in animals, including:
  • Heart attacks (myocardial infarction)
  • Blood clots in the coronary arteries and heart
  • Fibrous atherosclerosis including smooth muscle proliferation
  • Unstable blood vessel plaque
  • Foam cell accumulation and fatty streaks
  • Calcification of heart tissues
  • Aneurysms (ruptured vessels)
  • Abnormal electrocardiograms
  • High cholesterol
  • High blood pressure
If this theory is so important, why have most people never heard of it? I believe there are at least three reasons. The first is that the emergence of the copper deficiency theory coincided with the rise of the diet-heart hypothesis, whereby saturated fat causes heart attacks by raising blood cholesterol. Bolstered by some encouraging findings and zealous personalities, this theory took the Western medical world by storm, for decades dominating all other theories in the medical literature and public health efforts. My opinions on the diet-heart hypothesis aside, the two theories are not mutually exclusive.

The second reason you may not have heard of the theory is due to a lab assay called copper-mediated LDL oxidation. Researchers take LDL particles (from blood, the same ones the doctor measures as part of a cholesterol test) and expose them to a high concentration of copper in a test tube. Free copper ions are oxidants, and the researchers then measure the amount of time it takes the LDL to oxidize. I find this assay tiresome, because studies have shown that the amount of time it takes copper to oxidize LDL in a test tube doesn't predict how much oxidized LDL you'll actually find in the bloodstream of the person you took the LDL from (10, 11).

In other words, it's an assay that has little bearing on real life. But researchers like it because for some odd reason, feeding a person saturated fat causes their LDL to be oxidized more rapidly by copper in a test tube, even though that's not the case in the actual bloodstream (12). Guess which result got emphasized?

The fact that copper is such an efficient oxidant has led some researchers to propose that copper oxidizes LDL in human blood, and therefore dietary copper may contribute to heart disease (oxidized LDL is a central player in heart disease-- read more here). The problem with this theory is that there are virtually zero free copper ions in human serum. Then there's the fact that supplementing humans with copper actually reduces the susceptibility of red blood cells to oxidation (by copper in a test tube, unfortunately), which is difficult to reconcile with the idea that dietary copper increases oxidative stress in the blood (13).

The third reason you may never have heard of the theory is more problematic. Several studies have found that a higher level copper in the blood correlates with a higher risk of heart attack (14, 15). At this point, I could hang up my hat, and declare the animal experiments irrelevant to humans. But let's dig deeper.

Nutrient status is sometimes a slippery thing to measure. As it turns out, serum copper isn't a good marker of copper status. In a 4-month trial of copper depletion in humans, blood copper stayed stable, while the activity of copper-dependent enzymes in the blood declined (16). These include the important copper-dependent antioxidant, superoxide dismutase. As a side note, lysyl oxidase is another copper-dependent enzyme that cross-links the important structural proteins collagen and elastin in the artery wall, potentially explaining some of the vascular consequences of copper deficiency. Clotting factor VIII increased dramatically during copper depletion, perhaps predicting an increased tendency to clot. Even more troubling, three of the 12 women developed heart problems during the trial, which the authors felt was unusual:
We observed a significant increase over control values in the number of ventricular premature discharges (VPDs) in three women after 21, 63, and 91 d of consuming the low-copper diet; one was subsequently diagnosed as having a second-degree heart block.
In another human copper restriction trial, 11 weeks of modest copper restriction coincided with heart trouble in 4 out of 23 subjects, including one heart attack (17):
In the history of conducting numerous human studies at the Beltsville Human Nutrition Research Center involving participation by 337 subjects, there had previously been no instances of any health problem related to heart function. During the 11 wk of the present study in which the copper density of the diets fed the subjects was reduced from the pretest level of 0.57 mg/ 1000 kcal to 0.36 mg/1000 kcal, 4 out of 23 subjects were diagnosed as having heart-related abnormalities.
The other reason to be skeptical of the association between blood copper and heart attack risk is that inflammation increases copper in the blood (18, 19). Blood copper level correlates strongly with the marker of inflammation C-reactive protein (CRP) in humans, yet substantially increasing copper intake doesn't increase CRP (20, 21). This suggests that elevated blood copper is likely a symptom of inflammation, rather than its cause, and presents an explanation for the association between blood copper level and heart attack risk.

Only a few studies have looked at the relationship between more accurate markers of copper status and cardiovascular disease in humans. Leukocyte copper status, a marker of tissue status, is lower in people with cardiovascular disease (22, 23). People who die of heart attacks generally have less copper in their hearts than people who die of other causes, although this could be an effect rather than a cause of the heart attack (24). Overall, I find the human data lacking. I'd like to see more studies examining liver copper status in relation to cardiovascular disease, as the liver is the main storage organ for copper.

According to a 2001 study, the majority of Americans may have copper intakes below the USDA recommended daily allowance (25), many substantially so. This problem is exacerbated by the fact that copper levels in food have declined in industrial nations over the course of the 20th century, something I'll discuss in the next post.

Sunday, April 4, 2010

Magnesium and Vitamin D Metabolism

Ted Hutchinson posted a link in the comments section of my last post, pointing to a page on the Vitamin D Council's website where Dr. John Cannell discusses cofactors required for proper vitamin D metabolism. It's actually the site's home page, highlighting how important he feels this matter is. In this case, 'cofactor' simply means another nutrient that's required for the efficient production and use of vitamin D. They include:
  • Magnesium
  • Zinc
  • Vitamin K2
  • Vitamin A
  • Boron
And probably others we aren't yet aware of. On another page, Dr. Cannell links to two papers that review the critical interaction between magnesium status and vitamin D metabolism (1, 2). Here's a quote from the abstract of the second paper:
Magnesium... is essential for the normal function of the parathyroid glands, metabolism of vitamin D and adequate sensitivity of target tissues to [parathyroid hormone] and active vitamin D metabolites. Magnesium deficit is usually associated with hypoparathyroidism, low production of active vitamin D metabolites, in particular 1,25(OH)2 vitamin D3 and resistance to PTH and vitamin D. On the contrary, magnesium excess, similar to calcium, inhibits PTH secretion. Bone metabolism is impaired under positive as well as under negative magnesium balance.
Magnesium status is critical for normal vitamin D metabolism, insulin sensitivity, and overall health. Supplemental magnesium blocks atherosclerosis in multiple animal models (3, 4). Most Americans don't get enough magnesium (5).

The bottom line is that no nutrient acts in a vacuum. The effect of every part of one's diet and lifestyle is dependent on every other part. I often talk about single nutrients on this blog, but my core philosophy is that a proper diet focuses on Real Food, not nutrients. Tinkering with nutritional status using supplements is potentially problematic. Despite what some people might tell you, our understanding of nutrition and human health is currently rather crude-- so it's best to respect the accumulated wisdom of cultures that don't get the diseases we're trying to avoid.

Friday, April 2, 2010

Low Vitamin D: Cause or Result of Disease?

Don Matesz at Primal Wisdom put up a post a few days ago that I think is worth reading. It follows an e-mail discussion between us concerning a paper on magnesium restriction in rats (executive summary: moderate Mg restriction reduces the hormone form of vitamin D by half and promotes osteoporosis). In his post, Don cites several papers showing that vitamin D metabolism is influenced by more than just vitamin D intake from the diet and synthesis in the skin.

Celiac disease patients have low 25(OH)D3, the circulating storage form of vitamin D, which spontaneously corrects on a gluten-free diet. There are numerous suggestions in the medical literature that overweight and sickness cause low vitamin D, potentially confounding the interpretation of studies that find lower levels of illness among people with low vitamin D levels.

Don't get me wrong, I still think vitamin D is important in preventing disease. But it does lead me to question the idea that we should force down huge doses of supplemental vitamin D to get our 25(OH)D3 up to 60, 70 or even 80 ng/mL. When the dosage of supplemental D goes beyond what a tan Caucasian could conceivably make on a day at the beach (4,000 IU?), that's when I start becoming skeptical. Check out Don's post for more.