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Vitamin K2 is intimately involved in calcium metabolism. Matrix Gla-protein (MGP) is a vitamin K-dependent protein that is secreted in cartilage, lung, heart, kidney and arteries. MGP prefers the MK-4 form of vitamin K2, the type that occurs almost exclusively in animal foods. Mice lacking MGP develop extensive arterial and soft tissue calcification (accumulation of calcium, as in bone). Same for humans with naturally occurring mutations in MGP (Keutel syndrome). It also happens in rats treated with warfarin, which inhibits vitamin K recycling. Let's hear what Dr. Cees Vermeer and his group have to say about MGP:Among the proteins involved in vascular calcium metabolism, the vitamin K-dependent matrix Gla-protein (MGP) plays a dominant role. Although on a molecular level its mechanism of action is not completely understood, it is generally accepted that MGP is a potent inhibitor of arterial calcification. Its pivotal importance for vascular health is demonstrated by the fact that there seems to be no effective alternative mechanism for calcification inhibition in the vasculature. An optimal vitamin K intake is therefore important to maintain the risk and rate of calcification as low as possible.
So why do we care about vessel calcification? It associates strongly with the risk of heart attack and total mortality, better than traditional markers like the Framingham risk index*. That's because it's actually a measure of the disease process, rather than a marker with an unclear connection to it.In my post on vitamin K2, I mentioned the Rotterdam study, which found that vitamin K2 intake is strongly associated with a lower risk of cardiovascular and total mortality. Vitamin K1, which is the type found in plants, was not associated with reduced mortality. I just came across another study in women selected from the PROSPECT cohort that showed something similar. Women with the highest K2 intake had the lowest level of coronary calcification. There was no association with K1. This suggests, yet again, that humans aren't very good at making the conversion from K1 to K2 MK-4. This is probably because during evolution, we always had a ready source of K2, so efficient conversion became unnecessary. Vitamin K2 MK-4 is found almost exclusively in animal foods.Notably absent from the main text body is a discussion of where the K2 is coming from. It's tucked away in one sentence of the methods section: "cheese contributed 54%, milk products 22% and meat 15% of menaquinone intake." Oops! These are the foods that are supposed to cause heart disease! And do you remember where the K2 is? In the fat-- double oops! Yet another important nutrient that's found in animal fat.Keep in mind that these Dutch women have an intake of K2 that is probably lower than what we would have eaten as hunter-gatherers. Most people in modern societies are verifiably K2 deficient. A focus on the organs (brain, pancreas) and fats of wild animals, shellfish, fish eggs and insects would have assured hunter-gatherers a high intake of vitamin K2 MK-4. This is precisely what Weston Price found in Nutrition and Physical Degeneration. He refers to vitamin K2 MK-4 as "activator X" in the book. In modern times, our most readily available source of vitamin K2 MK-4 is actually not a paleolithic food at all, it's butter from pasture-raised cows. It's how we can get away with not eating brain, pancreas and bugs. *I plugged my numbers into this Framingham risk index calculator and it gave me the message "Please go back and enter an HDL value in the range of 20-100."!! I can imagine if you follow NCEP dietary guidelines your HDL would never break 100 mg/dL!
Vitamin K2 is intimately involved in calcium metabolism. Matrix Gla-protein (MGP) is a vitamin K-dependent protein that is secreted in cartilage, lung, heart, kidney and arteries. MGP prefers the MK-4 form of vitamin K2, the type that occurs almost exclusively in animal foods. Mice lacking MGP develop extensive arterial and soft tissue calcification (accumulation of calcium, as in bone). Same for humans with naturally occurring mutations in MGP (Keutel syndrome). It also happens in rats treated with warfarin, which inhibits vitamin K recycling. Let's hear what Dr. Cees Vermeer and his group have to say about MGP:Among the proteins involved in vascular calcium metabolism, the vitamin K-dependent matrix Gla-protein (MGP) plays a dominant role. Although on a molecular level its mechanism of action is not completely understood, it is generally accepted that MGP is a potent inhibitor of arterial calcification. Its pivotal importance for vascular health is demonstrated by the fact that there seems to be no effective alternative mechanism for calcification inhibition in the vasculature. An optimal vitamin K intake is therefore important to maintain the risk and rate of calcification as low as possible.
So why do we care about vessel calcification? It associates strongly with the risk of heart attack and total mortality, better than traditional markers like the Framingham risk index*. That's because it's actually a measure of the disease process, rather than a marker with an unclear connection to it.In my post on vitamin K2, I mentioned the Rotterdam study, which found that vitamin K2 intake is strongly associated with a lower risk of cardiovascular and total mortality. Vitamin K1, which is the type found in plants, was not associated with reduced mortality. I just came across another study in women selected from the PROSPECT cohort that showed something similar. Women with the highest K2 intake had the lowest level of coronary calcification. There was no association with K1. This suggests, yet again, that humans aren't very good at making the conversion from K1 to K2 MK-4. This is probably because during evolution, we always had a ready source of K2, so efficient conversion became unnecessary. Vitamin K2 MK-4 is found almost exclusively in animal foods.Notably absent from the main text body is a discussion of where the K2 is coming from. It's tucked away in one sentence of the methods section: "cheese contributed 54%, milk products 22% and meat 15% of menaquinone intake." Oops! These are the foods that are supposed to cause heart disease! And do you remember where the K2 is? In the fat-- double oops! Yet another important nutrient that's found in animal fat.Keep in mind that these Dutch women have an intake of K2 that is probably lower than what we would have eaten as hunter-gatherers. Most people in modern societies are verifiably K2 deficient. A focus on the organs (brain, pancreas) and fats of wild animals, shellfish, fish eggs and insects would have assured hunter-gatherers a high intake of vitamin K2 MK-4. This is precisely what Weston Price found in Nutrition and Physical Degeneration. He refers to vitamin K2 MK-4 as "activator X" in the book. In modern times, our most readily available source of vitamin K2 MK-4 is actually not a paleolithic food at all, it's butter from pasture-raised cows. It's how we can get away with not eating brain, pancreas and bugs. *I plugged my numbers into this Framingham risk index calculator and it gave me the message "Please go back and enter an HDL value in the range of 20-100."!! I can imagine if you follow NCEP dietary guidelines your HDL would never break 100 mg/dL!
I was doing my usual journal rounds today when I came across an article in the American Journal of Hypertension that caught my eye. It's called "Metabolic Syndrome: Comparison of the Two Commonly Used Animal Models." Metabolic syndrome is a cluster of symptoms including large waist circumference, elevated triglycerides, elevated blood pressure, and insulin resistance. It's the quintissential modern metabolic disorder, and it affects 24% of Americans (NHANES III). So what are the two most commonly used animal models of metabolic syndrome?- A strain called the spontaneously hypertensive rat (SHR), fed a high-sucrose (table sugar, 50% fructose) diet.
- Sprague-Dawley (generic lab strain) rats fed a high-fructose diet.
When fed sugar, these rats develop insulin resistance, impaired glucose tolerance, elevated triglycerides and hypertension. Fructose causes leptin resistance in rats. Leptin resistance causes metabolic syndrome in rats. These studies trace a line directly from sugar to the metabolic syndrome. On to humans. Total sugar and fructose consumption have been increasing in the U.S. in recent decades, along with metabolic syndrome. I think the average numbers may hide some important information, because there is a fraction of the population that consumes far more than the average amount of sugar through soda. Leptin resistance seems to be central to the metabolic syndrome, and typically precedes the other symptoms. The evidence suggests that the rat research on metabolic syndrome is applicable to humans. I don't think sugar acts alone in causing the metabolic syndrome in humans. I believe the liver is a central player in the disorder, as many of the markers used to diagnose it are measures of processes that occur in the liver (triglyceride synthesis, glucose and insulin disposal). Insulin resistance in the liver is sufficient to cause many of the hallmarks of the metabolic syndrome in mice. The fructose portion of sugar and high-linoleic (omega-6) vegetable oils act synergistically to cause liver dysfunction in rats and probably humans. I also believe wheat contributes to the process, perhaps through its ability to cause hyperphagia (overeating) or intestinal damage. So we're back to the three big killers in the modern diet:- Refined vegetable oils
- Sugar
- Wheat
I was doing my usual journal rounds today when I came across an article in the American Journal of Hypertension that caught my eye. It's called "Metabolic Syndrome: Comparison of the Two Commonly Used Animal Models." Metabolic syndrome is a cluster of symptoms including large waist circumference, elevated triglycerides, elevated blood pressure, and insulin resistance. It's the quintissential modern metabolic disorder, and it affects 24% of Americans (NHANES III). So what are the two most commonly used animal models of metabolic syndrome?- A strain called the spontaneously hypertensive rat (SHR), fed a high-sucrose (table sugar, 50% fructose) diet.
- Sprague-Dawley (generic lab strain) rats fed a high-fructose diet.
When fed sugar, these rats develop insulin resistance, impaired glucose tolerance, elevated triglycerides and hypertension. Fructose causes leptin resistance in rats. Leptin resistance causes metabolic syndrome in rats. These studies trace a line directly from sugar to the metabolic syndrome. On to humans. Total sugar and fructose consumption have been increasing in the U.S. in recent decades, along with metabolic syndrome. I think the average numbers may hide some important information, because there is a fraction of the population that consumes far more than the average amount of sugar through soda. Leptin resistance seems to be central to the metabolic syndrome, and typically precedes the other symptoms. The evidence suggests that the rat research on metabolic syndrome is applicable to humans. I don't think sugar acts alone in causing the metabolic syndrome in humans. I believe the liver is a central player in the disorder, as many of the markers used to diagnose it are measures of processes that occur in the liver (triglyceride synthesis, glucose and insulin disposal). Insulin resistance in the liver is sufficient to cause many of the hallmarks of the metabolic syndrome in mice. The fructose portion of sugar and high-linoleic (omega-6) vegetable oils act synergistically to cause liver dysfunction in rats and probably humans. I also believe wheat contributes to the process, perhaps through its ability to cause hyperphagia (overeating) or intestinal damage. So we're back to the three big killers in the modern diet:- Refined vegetable oils
- Sugar
- Wheat
As winter approaches, there are steps you can take to preserve your health and well-being. Here's a list of things I find useful:-Eat in season. Root vegetables like beets, turnips, rutabagas and potatoes are in season and make a satisfying dish. Try baked beets with raw garlic, sage and butter. Winter squash are tasty, nutritious and colorful. They make excellent soups and mashes, and can be baked or steamed. My favorite varieties are butternut, kabochas, delicata and gold nugget. They pair well with sage or nutmeg. In some places, hardy greens such as kale and collards are available in winter. Many fruits such as apples, pears and citrus are in season during the winter (or stored from fall).-Prepare soup stocks. There's nothing like a long-simmered bone broth to drive away the winter chill. They are also rich in minerals and gelatin, which aids digestion and soothes the digestive tract.-Make sauerkraut or other fermented vegetables. Fermentation was once used as a means to preserve flavor and nutrition for the winter. Fermented vegetables are a powerful digestive aid. After the first frost, cabbage is at its sweetest. Sweet cabbage makes the best kraut.-Keep your vitamin D level high. This may protect against the typical winter ills, including flu and seasonal depression. Unless you live in a warm climate and spend time outside in the winter regularly, it's wise to seek out vitamin D. High-vitamin cod liver oil, pasture-raised animal fats, shellfish and fatty fish are good sources. Some people may wish to supplement with vitamin D3.
