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

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

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

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

Beef Tallow: a Good Source of Fat-Soluble Vitamins?

Suet is a traditional cooking fat in the US, which is a country that loves its cows. It's the fat inside a cow's intestinal cavity, and it can be rendered into tallow. Tallow is an extremely stable fat, due to its high degree of saturation (56%) and low level of polyunsaturated fatty acids (3%). This makes it ideal for deep frying. Until it was pressured to abandon suet in favor of hydrogenated vegetable oil around 1990, in part by the Center for Science in the Public Interest, McDonald's used tallow in its deep fryers. Now, tallow is mostly fed to birds and feedlot cows.

I decided to make pemmican recently, which is a mixture of pulverized jerky and tallow that was traditionally eaten by native Americans of many tribes. I bought pasture-raised suet at my farmer's market. It was remarkably cheap at $2/lb. No one wants it because it's so saturated. The first thing I noticed was a yellowish tinge, which I didn't expect.

I rendered it the same way I make lard. It turned into a clear, golden liquid with a beefy aroma. This got me thinking. The difference between deep yellow butter from grass-fed cows and lily-white butter from industrial grain-fed cows has to do with the carotene content. Carotene is also a marker of other nutrients in butter, such as vitamin K2 MK-4, which can vary 50-fold depending on what the cows are eating. So I thought I'd see if suet contains any K2.

And indeed it does. The NutritionData entry for suet says it contains 3.6 micrograms (4% DV) per 100g. 100g is about a quarter pound of suet, more than you would reasonably eat. Unless you were really hungry. But anyway, that's a small amount of K2 per serving. However, the anonymous cow in question is probably a grain-finished animal. You might expect a grass-fed cow to have much more K2 in its suet, as it does in its milkfat. According to Weston Price, butter fat varies 50-fold in its K2 content. If that were true for suet as well, grass-fed suet could conceivably contain up to 180 micrograms per 100g, making it a good source of K2.

Tallow from pasture-raised cows also contains a small amount of vitamin D, similar to lard. Combined with its low omega-6 content and its balanced n-6/n-3 ratio, that puts it near the top of my list of cooking fats.

Beef Tallow: a Good Source of Fat-Soluble Vitamins?

Suet is a traditional cooking fat in the US, which is a country that loves its cows. It's the fat inside a cow's intestinal cavity, and it can be rendered into tallow. Tallow is an extremely stable fat, due to its high degree of saturation (56%) and low level of polyunsaturated fatty acids (3%). This makes it ideal for deep frying. Until it was pressured to abandon suet in favor of hydrogenated vegetable oil around 1990, in part by the Center for Science in the Public Interest, McDonald's used tallow in its deep fryers. Now, tallow is mostly fed to birds and feedlot cows.

I decided to make pemmican recently, which is a mixture of pulverized jerky and tallow that was traditionally eaten by native Americans of many tribes. I bought pasture-raised suet at my farmer's market. It was remarkably cheap at $2/lb. No one wants it because it's so saturated. The first thing I noticed was a yellowish tinge, which I didn't expect.

I rendered it the same way I make lard. It turned into a clear, golden liquid with a beefy aroma. This got me thinking. The difference between deep yellow butter from grass-fed cows and lily-white butter from industrial grain-fed cows has to do with the carotene content. Carotene is also a marker of other nutrients in butter, such as vitamin K2 MK-4, which can vary 50-fold depending on what the cows are eating. So I thought I'd see if suet contains any K2.

And indeed it does. The NutritionData entry for suet says it contains 3.6 micrograms (4% DV) per 100g. 100g is about a quarter pound of suet, more than you would reasonably eat. Unless you were really hungry. But anyway, that's a small amount of K2 per serving. However, the anonymous cow in question is probably a grain-finished animal. You might expect a grass-fed cow to have much more K2 in its suet, as it does in its milkfat. According to Weston Price, butter fat varies 50-fold in its K2 content. If that were true for suet as well, grass-fed suet could conceivably contain up to 180 micrograms per 100g, making it a good source of K2.

Tallow from pasture-raised cows also contains a small amount of vitamin D, similar to lard. Combined with its low omega-6 content and its balanced n-6/n-3 ratio, that puts it near the top of my list of cooking fats.

Beef Tallow: a Good Source of Fat-Soluble Vitamins?

Suet is a traditional cooking fat in the US, which is a country that loves its cows. It's the fat inside a cow's intestinal cavity, and it can be rendered into tallow. Tallow is an extremely stable fat, due to its high degree of saturation (56%) and low level of polyunsaturated fatty acids (3%). This makes it ideal for deep frying. Until it was pressured to abandon suet in favor of hydrogenated vegetable oil around 1990, in part by the Center for Science in the Public Interest, McDonald's used tallow in its deep fryers. Now, tallow is mostly fed to birds and feedlot cows.

I decided to make pemmican recently, which is a mixture of pulverized jerky and tallow that was traditionally eaten by native Americans of many tribes. I bought pasture-raised suet at my farmer's market. It was remarkably cheap at $2/lb. No one wants it because it's so saturated. The first thing I noticed was a yellowish tinge, which I didn't expect.

I rendered it the same way I make lard. It turned into a clear, golden liquid with a beefy aroma. This got me thinking. The difference between deep yellow butter from grass-fed cows and lily-white butter from industrial grain-fed cows has to do with the carotene content. Carotene is also a marker of other nutrients in butter, such as vitamin K2 MK-4, which can vary 50-fold depending on what the cows are eating. So I thought I'd see if suet contains any K2.

And indeed it does. The NutritionData entry for suet says it contains 3.6 micrograms (4% DV) per 100g. 100g is about a quarter pound of suet, more than you would reasonably eat. Unless you were really hungry. But anyway, that's a small amount of K2 per serving. However, the anonymous cow in question is probably a grain-finished animal. You might expect a grass-fed cow to have much more K2 in its suet, as it does in its milkfat. According to Weston Price, butter fat varies 50-fold in its K2 content. If that were true for suet as well, grass-fed suet could conceivably contain up to 180 micrograms per 100g, making it a good source of K2.

Tallow from pasture-raised cows also contains a small amount of vitamin D, similar to lard. Combined with its low omega-6 content and its balanced n-6/n-3 ratio, that puts it near the top of my list of cooking fats.

Beef Tallow: a Good Source of Fat-Soluble Vitamins?

Suet is a traditional cooking fat in the US, which is a country that loves its cows. It's the fat inside a cow's intestinal cavity, and it can be rendered into tallow. Tallow is an extremely stable fat, due to its high degree of saturation (56%) and low level of polyunsaturated fatty acids (3%). This makes it ideal for deep frying. Until it was pressured to abandon suet in favor of hydrogenated vegetable oil around 1990, in part by the Center for Science in the Public Interest, McDonald's used tallow in its deep fryers. Now, tallow is mostly fed to birds and feedlot cows.

I decided to make pemmican recently, which is a mixture of pulverized jerky and tallow that was traditionally eaten by native Americans of many tribes. I bought pasture-raised suet at my farmer's market. It was remarkably cheap at $2/lb. No one wants it because it's so saturated. The first thing I noticed was a yellowish tinge, which I didn't expect.

I rendered it the same way I make lard. It turned into a clear, golden liquid with a beefy aroma. This got me thinking. The difference between deep yellow butter from grass-fed cows and lily-white butter from industrial grain-fed cows has to do with the carotene content. Carotene is also a marker of other nutrients in butter, such as vitamin K2 MK-4, which can vary 50-fold depending on what the cows are eating. So I thought I'd see if suet contains any K2.

And indeed it does. The NutritionData entry for suet says it contains 3.6 micrograms (4% DV) per 100g. 100g is about a quarter pound of suet, more than you would reasonably eat. Unless you were really hungry. But anyway, that's a small amount of K2 per serving. However, the anonymous cow in question is probably a grain-finished animal. You might expect a grass-fed cow to have much more K2 in its suet, as it does in its milkfat. According to Weston Price, butter fat varies 50-fold in its K2 content. If that were true for suet as well, grass-fed suet could conceivably contain up to 180 micrograms per 100g, making it a good source of K2.

Tallow from pasture-raised cows also contains a small amount of vitamin D, similar to lard. Combined with its low omega-6 content and its balanced n-6/n-3 ratio, that puts it near the top of my list of cooking fats.

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 shown beneficial and sometimes striking effects on cancer, hypertension, type 1 diabetes, bone fracture and athletic performance. Vitamin D is a fundamental building block of health.

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 is impossible. Sunlight is also the most effective natural way to obtain vitamin D. To determine the optimal blood level of vitamin D, it's instructive to look at the serum 25(OH)D3 levels of people who spend a lot of time outdoors. The body seems to stabilize between 55 and 65 ng/mL 25(OH)D3 under these conditions. This is probably near the optimum. 30 ng/mL is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.

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; 3,000- 5,000 IU per day should be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested). I feel it's preferable to stay on the low end of this range. 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 on a fundamental level.

Thanks to horizontal.integration for the CC photo.

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 shown beneficial and sometimes striking effects on cancer, hypertension, type 1 diabetes, bone fracture and athletic performance. Vitamin D is a fundamental building block of health.

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 is impossible. Sunlight is also the most effective natural way to obtain vitamin D. To determine the optimal blood level of vitamin D, it's instructive to look at the serum 25(OH)D3 levels of people who spend a lot of time outdoors. The body seems to stabilize between 55 and 65 ng/mL 25(OH)D3 under these conditions. This is probably near the optimum. 30 ng/mL is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.

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; 3,000- 5,000 IU per day should be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested). I feel it's preferable to stay on the low end of this range. 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 on a fundamental level.

Thanks to horizontal.integration for the CC photo.

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 shown beneficial and sometimes striking effects on cancer, hypertension, type 1 diabetes, bone fracture and athletic performance. Vitamin D is a fundamental building block of health.

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 is impossible. Sunlight is also the most effective natural way to obtain vitamin D. To determine the optimal blood level of vitamin D, it's instructive to look at the serum 25(OH)D3 levels of people who spend a lot of time outdoors. The body seems to stabilize between 55 and 65 ng/mL 25(OH)D3 under these conditions. This is probably near the optimum. 30 ng/mL is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.

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; 3,000- 5,000 IU per day should be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested). I feel it's preferable to stay on the low end of this range. 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 on a fundamental level.

Thanks to horizontal.integration for the CC photo.

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 shown beneficial and sometimes striking effects on cancer, hypertension, type 1 diabetes, bone fracture and athletic performance. Vitamin D is a fundamental building block of health.

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 is impossible. Sunlight is also the most effective natural way to obtain vitamin D. To determine the optimal blood level of vitamin D, it's instructive to look at the serum 25(OH)D3 levels of people who spend a lot of time outdoors. The body seems to stabilize between 55 and 65 ng/mL 25(OH)D3 under these conditions. This is probably near the optimum. 30 ng/mL is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.

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; 3,000- 5,000 IU per day should be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested). I feel it's preferable to stay on the low end of this range. 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 on a fundamental level.

Thanks to horizontal.integration for the CC photo.