The Coronary Heart Disease Epidemic: Possible Culprits Part II

In the last post, I reviewed some of the factors that I believe could have contributed to the epidemic of heart attacks that began in the 1920s and 1930s in the U.S. and U.K., and continues today. I ended on smoking, which appears to be a major player. But even smoking is clearly trumped by another factor or combination of factors, judging by the unusually low incidence of heart attacks in France, Japan and on Kitava.

One of the major changes in diet that I didn't mention in the last post was the rise of industrial liquid vegetable oils over the course of the 20th century. In the U.S. in 1900, the primary cooking fats were lard, beef tallow and butter. The following data only include cooking fats and spreads, because the USDA does not track the fats that naturally occur in milk and meat (source):

Animal fat is off the hook. This is the type of information that makes mainstream nutrition advice ring hollow. Let's see what happened to industrial vegetable oils in the early 1900s:

I do believe we're getting warmer. Now let's consider the composition of traditional American animal fats and industrial vegetable oils:
It's not hard to see that the two classes of fats (animal and industrial vegetable) are quite different. Animal fats are more saturated (blue). However, the biggest difference is that industrial vegetable oils contain a massive amount of omega-6 (yellow), far more than animal fats. If you accept that humans evolved eating primarily animal fats, which is well supported by the archaeological and anthropological literature, then you can begin to see the nature of the problem.

Omega-6 and omega-3 fats are polyunsaturated fatty acids that are precursors to a very important class of signaling molecules called eicosanoids, which have a hand in virtually every bodily process. Omega-6 and omega-3 fats compete with one another for the enzymes (desaturases and elongases) that convert them into eicosanoid precursors. Omega-6-derived eicosanoids and omega-3-derived eicosanoids have different functions. Therefore, the balance of omega-6 to omega-3 fats in the diet influences the function of the body on virtually every level. Omega-6 eicosanoids tend to be more inflammatory, although the eicosanoid system is extraordinarily complex and poorly understood.

What's better understood is the fact that our current omega-6 consumption is well outside of our ecological niche. In other words, we evolved in an environment that did not provide large amounts of omega-6 all year round. Industrial vegetable oils are a product of food processing techniques that have been widespread for about 100 years, not enough time for even the slightest genetic adaptation. Our current level of omega-6 intake, and our current balance between omega-6 and omega-3, are therefore unnatural.
The ideal ratio is probably very roughly 2:1 omega-6:omega-3. Leaf lard is 6.8, beef tallow is 2.4, good quality butter is 1.4, corn oil is 45, cottonseed oil is 260. It's clear that a large qualitative change in our fat consumption occurred over the course of the 20th century.

I believe this was a major factor in the rise of heart attacks from an obscure condition to the primary cause of death. I'll be reviewing the data that convinced me in the next few posts.

The Coronary Heart Disease Epidemic
The Coronary Heart Disease Epidemic: Possible Culprits Part I
The Omega Ratio
A Practical Approach to Omega Fats
Polyunsaturated Fat Intake: Effects on the Heart and Brain
Polyunsaturated Fat Intake: What About Humans?
Vegetable Oil and Homicide

Vitamin D: It's Not Just Another Vitamin

If I described a substance with the following properties, what would you guess it was?

-It's synthesized by the body from cholesterol
-It crosses cell membranes freely
-It has its own nuclear receptor
-It causes broad changes in gene transcription
-It acts in nearly every tissue
-It's essential for health

There's no way for you to know, because those statements all apply to activated vitamin D, estrogen, testosterone and a number of other hormones. Vitamin D, as opposed to all other vitamins, is a steroid hormone precursor (technically it's a secosteroid but it's close enough for our purposes). The main difference between vitamin D and other steroid hormones is that it requires a photon of UVB light for its synthesis in the skin. If it didn't require UVB, it would be called a hormone rather than a vitamin. Just like estrogen and testosterone, it's involved in many processes, and it's important to have the right amount.

The type of vitamin D that comes from sunlight and the diet is actually not a hormone itself, but a hormone precursor. Vitamin D is converted to 25(OH)D3 in the liver. This is the major storage form of vitamin D, and thus it best reflects vitamin D status. The kidney converts 25(OH)D3 to 1,25(OH)D3 as needed. This is the major hormone form of vitamin D. 1,25(OH)D3 has profound effects on a number of tissues.

Vitamin D was originally identified as necessary for proper mineral absorption and metabolism. Deficiency causes rickets, which results in the demineralization and weakening of bones and teeth. A modest intake of vitamin D is enough to prevent rickets. However, there is a mountain of data accumulating that shows that even a mild form of deficiency is problematic. Low vitamin D levels associate with nearly every common non-communicable disorder, including obesity, diabetes, cardiovascular disease, autoimmune disease, osteoporosis and cancer. Clinical trials using vitamin D supplements have suggested that it may protect against cancer, hypertension, type 1 diabetes, bone fracture and enhance athletic performance. However, the evidence is pretty thin for most of these effects and requires more research.

It all makes sense if you think about how humans evolved: in a tropical environment with bright sun year-round. Even in many Northern climates, a loss of skin pigmentation and plenty of time outdoors allowed year-round vitamin D synthesis for most groups. Vitamin D synthesis becomes impossible during the winter above latitude 40 or so, due to a lack of UVB. Traditional cultures beyond this latitude, such as the Inuit, consumed large amounts of vitamin D from nutrient-rich animal foods like fatty fish.

The body has several mechanisms for regulating the amount of vitamin D produced from sunlight exposure, so overdose from this source appears to be impossible. Sunlight is also the most effective natural way to obtain vitamin D. How much vitamin D is optimal? 30 ng/mL 25(OH)D3 is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.  It's probably best to maintain at least 35 ng/mL 25(OH)D3.

Here's how to become vitamin D deficient: stay inside all day, wear sunscreen anytime you go out, and eat a low-fat diet. Make sure to avoid animal fats in particular. Rickets, once thought of as an antique disease, is making a comeback in developed countries despite fortification of milk (note- it doesn't need to be fortified with fat-soluble vitamins if you don't skim the fat off in the first place!). The resurgence of rickets is not surprising considering our current lifestyle and diet trends. In a recent study, 40% of infants and toddlers in Boston were vitamin D deficient using 30 ng/mL as the cutoff point. 7.5% of the total had rickets and 32.5% showed demineralization of bone tissue! Part of the problem is that mothers' milk is a poor source of vitamin D when the mother herself is deficient. Bring the mothers' vitamin D level up, and breast milk becomes an excellent source.

Here's how to optimize your vitamin D status: get plenty of sunlight without using sunscreen, and eat nutrient-rich animal foods, particularly in the winter. The richest food source of vitamin D is high-vitamin cod liver oil. Blood from pasture-raised pigs or cows slaughtered in summer or fall, and fatty fish such as herring and sardines are also good sources. Vitamin D is one of the few nutrients I can recommend in supplement form. Make sure it's D3 rather than D2; 2,000 IU per day hould be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested).  Vitamin D3 supplements are typically naturally sourced, coming from sheep lanolin or fish livers. A good regimen would be to supplement every day you get less than 10 minutes of sunlight.

People with dark skin and the elderly make less vitamin D upon sun exposure, so they should plan on getting more sunlight or consuming more vitamin D. Sunscreen essentially eliminates vitamin D synthesis, and glass blocks UVB so indoor sunlight is useless. Vitamin D toxicity from supplements is possible, but exceptionally rare. It only occurs in cases where people have accidentally taken grotesque doses of the vitamin. As Chris Masterjohn has pointed out, vitamin D toxicity is extremely similar to vitamin A deficiency. This is because vitamin A and D work together, and each protects against toxicity from the other. Excess vitamin D depletes vitamin A, thus vitamin D toxicity is probably a relative deficiency of vitamin A.

I know this won't be a problem for you because like all healthy traditional people, you are getting plenty of vitamin A from nutrient-dense animal foods like liver and butter. Vitamin K2 is the third, and most overlooked, leg of the stool. D, A and K2 form a trio that act together to optimize mineral absorption and use, aid in the development of a number of body structures, beneficially alter gene expression, and affect many aspects of health.

Thanks to horizontal.integration for the CC photo.

Okinawa and Lard

The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, sweet potatoes, exercise, and the fact that some of them may have been mildly calorie restricted for part of their lives.

The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat. Of course, they also eat the pork the lard came from.

I'm not saying lard will make you live to 100, but a moderate amount certainly won't stop you...

Real Food IV: Lard

Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.

The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.

If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.


Ingredients and Equipment:

• Lard
• Cheesecloth
• Baking dish
• Jars
  

1. Preheat the oven to 225 F.

2. Cut off any pieces of meat clinging to the fat.

3. Cut fat into small (~1-inch) cubes.

4. Place them into a non-reactive baking dish and then into the oven.

5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.

6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.

7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.

8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.

Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.