I mentioned earlier a vitamin K2 connection that may prove to be the most exciting and unexpected benefit of this long-misunderstood nutrient: diabetes prevention. In 2007, groundbreaking research shocked the scientific community by revealing that our skeleton, via the vitamin K2–dependent protein osteocalcin, has a significant impact on our body's production and sensitivity to insulin.1 With that radical discovery, our perception of the skeleton makes a quantum leap from it being an inert scaffolding to it being a dynamic endocrine gland. Writing in the prestigious journal Cell, researchers explained that osteocalcin, produced within our bones, has the capacity to improve the body's glucose tolerance. And that makes vitamin K2 critical for preventing an illness of epidemic proportions: insulin-resistant diabetes.
Insensitivity to insulin, otherwise known as insulin resistance, is the underlying cause of type 2 diabetes. Type 1 diabetes, also called juvenile-onset diabetes, is often diagnosed in childhood and occurs because the pancreas does not make insulin. Only about 10 percent of diabetics are type 1, and to date there is no known relationship between type 1 diabetes and vitamin K2. Ninety percent of diabetics are afflicted with type 2, also called adult-onset or non-insulin-dependent diabetes. Within the decade, this obesity-associated lifestyle illness will become the biggest cause of disease and death in North America, and account for the biggest expenditure of health care dollars of all illnesses.
Insulin is a hormone secreted by the pancreas every time we eat, but much more so when we eat high-glycemic-index foods. High-glycemic-index foods are those that cause blood sugar levels to spike—sugar, white flour, bread, pasta and baked goods, for example. Insulin acts like a key that unlocks our body's cells to let sugar move from the bloodstream into the cells to provide us with energy and lower our blood sugar. However, when blood sugar and in turn insulin levels are too high too often because of a diet that's high in sugary, starchy or processed food, the cellular “lock” gets jammed up and the insulin “key” doesn't work so well. Over time, insulin becomes less and less efficient at opening the cellular doors to let sugar in: the overexposure to insulin causes cells to become resistant (insensitive) to it. Eventually, blood sugar levels remain high even though the body is producing plenty of insulin.
The condition is referred to as “starvation in the midst of plenty” because the cells are starving for the energy from the sugar that circulates in the bloodstream but can't get in.
The second highest concentration of vitamin K2 in the body is in the pancreas, the organ that produces insulin and governs blood sugar levels. In animals and humans, it seems that a lack of vitamin K negatively affects the pancreas's insulin production. For example, animal studies show that vitamin K deficiency negatively impacts glucose tolerance by slowing insulin response. Sugar stays in the blood longer and insulin levels are ultimately higher—the worst possible outcome for type 2 diabetes—when vitamin K is lacking. Basically, when researchers induce vitamin K deficiency, test animals develop type 2 diabetes.2 Similar effects are seen in humans, although for ethical reasons human studies have focused on vitamin K intake rather than inducing vitamin K deficiency. Acute insulin response, the amount of insulin produced within 30 minutes of glucose intake, was found to be impaired in study subjects with low vitamin K intake.3
Only one week of vitamin K2 supplementation in healthy, nondiabetic trial participants significantly reduces their two-hour postmeal insulin production by half.4 Elevated insulin for hours after a meal is bad for diabetics, since it promotes insulin resistance. When insulin is functioning normally, it rises just enough in response to carbohydrate intake to get blood sugar levels back down again, then it declines so that it won't overexpose cells. The fact that K2 supplementation lowers late (two-hour postmeal) insulin levels indicates that menaquinone helps insulin work more efficiently. This is certainly in keeping with the groundbreaking findings of the 2007 Cell study that revealed osteocalcin impacts insulin activity. Since osteocalcin improves insulin
sensitivity and vitamin K2 activates osteocalcin, it stands to reason that K2 supplementation would improve insulin sensitivity.
Admittedly, changes in postmeal insulin levels are only an indirect measure of insulin resistance, and there are more specific markers to monitor this epidemic condition. Recent research from Japan shows that vitamin K2 status is inversely related to insulin-resistant diabetes.5 The more deficient diabetics are in vitamin K2, the worse their results on several specific tests to determine blood sugar control and insulin sensitivity. These included the hemoglobin A1c test, a measure of long-term blood sugar control, and the HOMA-IR test, a method that quantifies both insulin resistance and the function of pancreatic cells that produce insulin. Patients with more K2-activated osteocalcin have better results on all of these tests, and better glucose tolerance. Other studies show that, although elevated levels of both carboxylated and undercarboxylated forms of osteocalcin are associated with improved glucose tolerance, only the K2-activated form improves insulin sensitivity.6
Does taking vitamin K2 improve insulin sensitivity? So far the intervention research examining the effects of taking a vitamin K supplement instead of just monitoring vitamin K levels have used only K1, not K2. This was a North American study where, unlike Japanese and European research that now focuses primarily on K2, we're still fooling around with K1. Be that as it may, the results are still interesting. First of all, 36 months of vitamin K1 supplementation in people between 60 and 80 years of age slowed the progression of insulin resistance, although it didn't stop or reverse the disease.7 I'm not knocking this benefit; a proven slowing of the advancement of such a serious disease is a good enough reason on its own to take vitamin K. But, given that carboxylated osteocalcin plays such an important role in insulin sensitivity, you'd expect a better result. Remember, K1 isn't nearly as efficient at activating osteocalcin as K2. As such, it's not surprising that vitamin K1 supplementation had only a modest effect in this trial. Researchers should have looked at K2 as well, but it does prime the pump for further studies using menaquinone.
The more curious finding from this particular study was that three years of vitamin K supplementation had a beneficial effect on insulin resistance in older men but not in older women. Why might that be? Recall from Chapter 4 that undercarboxylated osteocalcin increases in postmenopausal women, so
they have greater requirements for vitamin K2 at that time. It is highly likely that the treatment dose in this study was sufficient to benefit men but insufficient for older women with higher vitamin K2 requirements. A similar trend is seen in cancer studies. Again, it's not that women can't reap all the benefits of vitamin K2 that men can. We just need more K2 to meet our greater demands for bone health, in addition to cancer and diabetes prevention requirements.
Type 2 diabetes has a couple of infamous cronies, heart disease and osteoporosis. Do those conditions sound familiar? Insulin-resistant diabetics are highly likely to develop those vitamin K2–deficiency diseases. Based on the emerging evidence from many scientific domains and the fact that type 2 diabetics are at the highest risk for two well-established menaquinone-deficiency diseases, osteoporosis and atherosclerosis, I recommend 240 micrograms of MK-7 to all of my diabetic, prediabetic and overweight patients.