Recently one of my favorite bloggers, Ferrett Steinmetz, had some chest pain, and as a precautionary measure went to the ER to get checked out. His initial tests came back normal, but the chest pain continued, and his blood work showed abnormal results. Ferrett had experienced a heart attack, and was immediately scheduled for surgery.
It got me thinking about heart disease.
Heart disease is incredibly common. It’s the leading cause of death in the United States.
So what can we do to prevent it?
For years the medical establishment told us that eating a low-fat, low-cholesterol diet was the best thing we could do to prevent heart disease. Even my last doctor tried to peddle this advice. I changed doctors.
Cardiologists who have been paying attention to the research now associate heart disease with factors like lack of exercise, diets high in refined carbohydrates, poor blood sugar control, inflammation, and sedentary lifestyle (lots of sitting — see infographic below). Dietary cholesterol doesn’t matter so much, and a moderate intake of saturated fat is probably not harmful (though monosaturated fats like olive oil may be preferable). Healthy fats (butter from grass-fed cows, olive oil, coconut oil, fatty fish) are a more “heart-healthy” source of fuel than grain products (even whole grains).
Bill Davis (author of Track Your Plaque and Wheat Belly) is one such forward-thinking cardiologist. Davis recommends a wheat-free, no refined vegetable oil (corn/sunflower/soy/canola), low-carbohydrate diet, as well as certain supplements (which he also sells) including vitamin D, fish oil, niacin, and coenzyme Q10. He also recommends foods such as olive oil, garlic, and tea (all associated with lower heart disease). Is he peddling products? Sure … but his approach is still leagues ahead of the conventional wisdom on heart disease.
Ferrett had to undergo triple bypass surgery. Thankfully, he survived, and is now recovering at home.
Cholesterol and Genetics
23andMe.com tracks fifteen SNP’s that are related to an increased or decreased risk of coronary heart disease (if you have a 23andMe account you can click here to see your heart disease risk profile).
The most significant SNP is rs3798220 (snpedia/23andMe). People carrying the C allele produce higher levels of lipoprotein(a), and have more than a twofold increased risk of heart disease. I feel fortunate to carry TT, but C carriers get a compliment from Dr. Davis. He calls them the “perfect carnivores” in this post, and claims this variant is more resistant to dehydration, tropical disease, and is more likely to be intelligent (I’m not sure what Davis is basing these claims on, but they’re interesting).
Heart disease risk for rs3798220-C carriers can be somewhat mitigated by low-dose aspirin therapy, at least in women. Estrogen HRT also lowers lipoprotein-a/Lp(a) levels. Among Bantu fishermen, higher fish intake was also associated with lower Lp(a).
Why are elevated Lp(a) levels associated with coronary heart disease? Lp(a) is similar to low-density lipoprotein (LDL), which is more likely to stick to arterial walls and clog them up (while the big HDL molecules bounce around harmlessly).
Environmental Risk Factors
In addition to genetic risk, these environmental risk factors are pretty well established. Unlike diet, there is little controversy around these risk factors for coronary heart disease:
We’re stuck with our genes, but these factors are avoidable. Don’t buy a house next to a freeway. If you smoke, making quitting a priority (if you’re under 40, the damage may be largely reversible). And get a standing desk (or convert — I added eight 12″ dowels to my IKEA desk — now it’s a standing desk).
Dietary Fat and Cholesterol
For decades, both fat intake and lipid cholesterol levels were associated with heart disease, but neither has been shown to be causative. The most famous high-fat diet correlation turned out to be Ancel Keys cherry-picking data for one of his presentations (though Keys may have been unfairly maligned by the paleo community, as this post explains).
What about cholesterol? As of 2010, the U.S. government was still recommending that we consume no more than 300mg of cholesterol a day (2 eggs contain about 370mg), even though a large body of research has failed to find any connection between dietary cholesterol and coronary heart disease. We’ll see if the 2015 guidelines update this recommendation.
Chris Kesser has written a number of articles debunking the idea that dietary cholesterol and saturated fat cause heart disease. I recommend his site.
Still, certain types of lipid cholesterol measurements are associated with an increased risk of coronary heart disease, specifically LDL-P (low-density-lipoprotein particle number). We don’t want large numbers of tiny cholesterol particles floating about in our bloodstreams — they tend to clog up the works.
What raises LDL levels? While Lp(a) levels (discussed above) are related primarily to genetics, LDL levels are highly influenced by diet. High carbohydrate/high sugar diets seem to be the main culprit.
Cholesterol, Vitamin D, Sunlight, and Nitric Oxide
Some researchers believe that high cholesterol levels are merely a biomarker for coronary heart disease risk, and don’t cause heart disease at all. Chris Masterjohn explains how cholesterol is converted to vitamin D, and that sunlight is necessary for this process. So high lipid cholesterol might simply indicate that you aren’t getting enough sun, and that your vitamin D levels are too low. Low vitamin D levels are associated with a higher risk of coronary heart disease.
So all we have to do is take supplemental vitamin D, and we should reduce our risk of heart disease, right?
Not so fast.
In terms of heart disease, blood levels of vitamin D may be a red herring biomarker, just like high cholesterol levels.
Dermatologist Richard Weller has done some fascinating research in this area. He found that people from northern latitudes with less sun exposure generally experience more heart disease. Even after controlling for smoking, diet, and socioeconomic factors, people from sunnier areas experience markedly less heart disease.
Weller discovered that the skin stores large amounts of nitrates and nitrites, which are converted to nitric oxide by exposure to sunlight. Nitric oxide released into the bloodstream lowers blood pressure and dilates (relaxes and opens) blood vessels. Weller showed that this effect was not related to vitamin D levels; the amount and intensity of sunlight (about 30 minutes of sun in Edinburgh, during the summer) was not sufficient to raise vitamin D levels. But it was enough to convert skin nitrates and nitrites into nitric oxide, and lower blood pressure.
It’s not that vitamin D isn’t good for you. We know vitamin D increases calcium absorption, prevent rickets, and reduces the risk of many cancers (especially colon cancer). But in terms of heart disease, low vitamin D may just be a biomarker for low sun exposure, and therefore low plasma nitric oxide levels.
What about skin cancer risk? Weller, a dermatologist, points out that heart disease is a much bigger killer than skin cancer (by a factor of 100). And thirty minutes of Scottish sunlight is probably not going to cause much skin damage.
I live in the Bay Area and we get plenty of sun, but I’m rarely in it. My calves are British-schoolboy white. Moving forward, that’s going to change. According to Weller, even ten minutes of California winter sunshine is enough to activate nitric oxide (NO) release. I won’t be sporting a tan anytime soon, but I might be moving into a light beige.
Other Ways To Raise Nitric Oxide Levels
What if sunlight exposure isn’t an option, either due to latitude or lifestyle?
There are other ways to boost nitric oxide. The primary one is exercise, which has shown to be heart-protective.
Dark chocolate also boosts NO levels and reduces blood pressure.
So there are options to boost nitric oxide levels. And more than heart health is at stake; adequate NO levels are vital for sexual response in both men and women.
What About Supplements and Medications?
Which supplements and medications have the best evidence for protecting against heart disease?
Niacin has a decent track record, though a large trial by Merck combining statins and niacin showed no benefit. Personally I can’t tolerate large doses of niacin — the flush response is too much, and it messes with my digestion. Niacin may be especially effective for rs3798220-C carriers who produce higher levels of Lp(a), but low-dose aspirin is also effective.
Statins are often prescribed, but show no benefit for people who don’t already have coronary heart disease. Low-dose daily aspirin is just as (or more) effective, and much cheaper. Both statins and low-dose aspirin can have serious side effects, including internal bleeding and increased risk of macular degeneration for the latter.
Coenzyme Q-10 may be heart protective, and can help lower blood pressure. Oily fish like salmon is a good source, but since levels decrease with age, those of us over 40 might consider taking supplemental CoQ10. Statins tend to lower levels of coenzyme Q-10, and supplemental CoQ10 may protect against some of the side effects of statins.
Of all the supplements I have considered, vitamin K2 (found in fermented foods, aged cheeses, poultry liver, and grass-fed dairy products) seems to be the most promising in terms of actually preventing coronary heart disease. This study found an inverse relationships between dietary vitamin K2 and heart disease in older women.
I eat most of those foods, and recently I also started taking 50mcg of vitamin K2 (the Mk-7 form, derived from nattō) several times a week (I’ve tried actually eating nattō, but I can’t stand the taste).
Vitamin K2 controls where calcium goes in the body via modulation of the hormone osteocalcin. How exactly does this process work? Here’s a excerpt from this article.
The possible role of vitamin K2 in preventing coronary plaque development has emerged from observations of its effects on several bone proteins, whose main function is to keep calcium where it belongs in the body.
Osteocalcin is a calcium-regulating protein that is controlled by vitamin K2. When vitamin K is present, osteocalcin normally undergoes a process called carboxylation, which binds osteocalcin to the mineral portion of bone. However, in vitamin K2 deficiency, osteocalcin cannot perform this function, resulting in unrestrained calcium resorption (removal) from bone tissue that leads to osteoporosis.
The opposite situation seems to occur in the arteries. Calcium is deposited because another protein called matrix GLA-protein, which is a calcification inhibitor and is also K2-controlled, cannot undergo the process of carboxylation in a vitamin K-deficient state. Because only carboxylated matrix GLA-protein inhibits calcification, undercarboxylated matrix GLA-protein has been found to occur in unusually high concentration at the edge of calcified and atherosclerotic plaques, suggesting it plays an active role in depositing calcium in plaque.4 Impairment of the function of osteocalcin and matrix GLA-protein due to incomplete carboxy-lation results in an increased risk for developing osteoporosis and vascular calcification, respectively.
So if you want your arteries to remain uncalcified, you should absolutely make sure you are consuming enough vitamin K2.
What about fish oil? Consuming fatty fish multiple times a week is clearly associated with reduced risk of coronary heart disease, but it’s less clear if supplemental fish oil is beneficial. I do both, but use a lower dose of fish oil (only 2-3g on most days).
Linus Pauling hypothesized that arterial plaque is only created in the absence of adequate vitamin C levels. Researchers at the Linus Pauling Institute make a strong case for raising the RDA to 200mg a day (high enough not only to prevent scurvy, but to reduce mortality from a wide range of diseases). Other research has shown that vitamin C supplementation lowers levels of C-reactive protein (CRP is a biomarker of inflammation that is linked to heart disease). Population studies in the 1990′s found that vitamin C supplementation is associated with increased longevity, specifically from reduced cardiovascular disease. I’ve taken vitamin C for decades (though I no longer megadose, as very large doses of vitamin C can reduce copper absorption).
Heart disease is the biggest killer in the United States, and most other developed countries. We can reduce our risk by doing the following:
- - reduce sitting (get a standing desk and limit TV couch time)
- - exercise daily (long walks and taking the stairs count)
- - get some sun on your skin daily (but don’t burn)
- - eat dark chocolate and drink red wine
- - eat a low-grain, low refined vegetable oil, low-sugar diet (not necessarily low-carb; some foods containing carbohydrates like whole fruit and properly cooked beans probably have more benefits than drawbacks)
- - eat “good fats” including olive oil, butter from grass-fed cows, coconut oil
- - get enough dietary vitamin K2, and consider supplementing up to 100mcg/day
- - eat oily wild-caught fish multiple times a week (canned salmon is a less expensive source)
- - eat green leafy vegetables to supply nitrates for NO production
- - consume at least 200mg of vitamin C a day from food and supplements
- - have impeccable dental hygiene; periodontal disease is strongly linked to heart disease (brush and floss daily and thoroughly, don’t eat sticky carbs and acidic juice, chew xylitol gum, consume fat soluble vitamins [D, K2, A], and see a dentist on a regular basis — I’ll do a detailed post on this topic in the coming months)
Did I miss anything? May you all live long and prosper!