There’s no RDA for vitamin K but there’s mounting evidence that it’s essential for both cardiovascular health and prostate health.
This is big, really big. It’s so big that I’m not going to mess around and force you to scroll a couple of hundred yards down to get to the pertinent information.
Here’s what you need to know right now:
- There’s an intriguing theory that suggests benign prostate hyperplasia (BPH) isn’t initiated by a hormonal imbalance but by a simple vitamin K insufficiency.
- There’s a lot of evidence that the vascular calcification that’s to blame for a lot of coronary heart disease (atherosclerosis) might be thwarted by taking supplemental vitamin K.
A lot of the time, I’ll report on some new findings or theories just because they’re interesting to me, but what I research and write about doesn’t always provoke any changes in my behavior or eating. Not so with what I’m about to present here. I am now taking a vitamin K supplement, and I think you should too.
Let me present my case.
Okay, this “get to know vitamin K” stuff might be a snore, but it’s important. First off, “vitamin K” isn’t a single compound but a family of compounds with the common chemical structure of 2-methyl-1,4-napthoquinone.
These compounds include phylloquinone, commonly known as vitamin K1, and a series of menaquinones, which are commonly grouped together as vitamin K2.
Vitamin K1 is found primarily in green leafy vegetables and plant oils, while K2 is predominantly of bacterial origin and found in small amounts in various animal meats and fermented foods.
The average physician knows about vitamin K because it’s instrumental in making four of the 13 proteins needed for blood clotting, and without enough of it, any wound to your skin will cause you to shoot out blood like a punctured garden hose. Well, maybe not that bad, but you get the idea.
Otherwise, vitamin K gets short shrift. It’s monitored in people who are taking anticoagulants or have bleeding disorders, but that’s about it. That’s hugely unfortunate because vitamin K appears to play a giant role in the health of the cardiovascular system and the prostate.
Atherosclerosis is a treacherous thing. A lot of the time, you don’t even know you have it until you’re lying on a table in some medical school while curious first-year med students slice into your carotid and start teasing apart the fats, cholesterol, and other substances that gummed up your artery walls and killed you. And even then, you don’t know it because, well, you’re dead.
All that organic garbage, collectively called plaque, narrowed your arteries and blocked the blood flow. It’s like when you used to use a paper straw to suck up your Slurpee and it eventually collapsed and left your mouth Slurpee-less.
Alternately, these plaques can burst, causing a blood clot that deprives your brain of oxygen and condemns you to a life of going to Halloween parties as Hector Salamanca.
One of the hallmarks of atherosclerosis is vascular calcification. It’s literally the deposition of mineral deposits in the vascular system. These deposits can, unimpeded, make the inner walls of your arteries look like the inside of a White Castle restaurant. Hold the onions.
Here’s where vitamin K comes in. Vascular calcification is an inflammation-mediated process where macrophages (a type of large white blood cell that not only kills microorganisms, but also stimulates the production of pro-inflammatory cytokines) promote the “mineralization” of arteries (the right kind of macrophages can also clean up arterial walls, but that’s another story).
Vitamin K (K1, specifically), however, has been shown to suppress the expression of these pro-inflammatory cytokines. Yeah, in other words, it’s a powerful anti-inflammatory, but so are a lot of vitamins and nutrients in general.
More importantly, vitamin K also affects something called “matrix GLA protein” (MGP). The molecule is a potent inhibitor of vascular calcification and its actions are vitamin K-dependent. MGP’s importance has been demonstrated in MGP-deficient animals, all of whom died of massive arterial calcifications within two months of birth (Luo, et al., 1997).
As far as human evidence, a Dutch observational study of 564 postmenopausal women found that dietary K2 (but not K1) was inversely associated with severe aortic calcification (Beulens, et al., 2009). K1 was also inversely associated with coronary calcification in another Dutch study involving 4,807 men and women over the age of 55 (Geleijnse, et al., 2004).
Other studies point to, or at least suggest, the urgency of ensuring adequate levels of vitamin K1. Perhaps surprisingly, the relationship between K1 and coronary heart disease (and, specifically, coronary artery calcium scoring, or CAC) is a dog that few researchers have, for whatever reason, chosen to chase.
The same appears to be true of the role of vitamin K in prostate health.
A fascinating and, for me, pulse-quickening paper was released in 2015. It noted, regarding benign prostate hyperplasia (BPH), that “there is no biological, mechanistic explanation for dealing with the root causes and progression of this very common disorder in men.”
It further noted that “All treatments to date are based on symptomatic relief, not a fundamental understanding of the cause of the disease.”
The paper was titled “Vitamin K: The Missing Link to Prostate Health” and the author, Michael Donaldson, Ph.D., made a compelling case for the need for supplemental vitamin K.
Donaldson theorized that varicose veins in the “pampiniform venous plexus” (varicoceles) are the direct cause of BPH. He cited research that found these varicoceles, even subclinical ones (those that don’t present observable symptoms), to cause “retrograde blood flow” from the testes past the prostate gland, causing the amount of free testosterone in the veins adjacent to the prostate to increase by 130 times.
If you then treat the varicoceles by embolization (blocking the blood vessel) of the internal spermatic vein and its tributary vessels, you Dorian Gray the prostate and restore it to its normal-sized, youthful form.
But that brings us to the question, “But what causes varicoceles?”
Donaldson pointed to research regarding the role that vitamin K plays in the calcification of varicose veins (also described in the section above concerning the role of vitamin K in cardiovascular health in general).
Apparently, much like it does in heart-related matters, a vitamin K deficiency (but in the case of the prostate, a deficiency in K2 and not, apparently, K1) leads to calcification of the middle wall of veins around the prostate, laying the groundwork for these torturous vein formations.
But taking supplemental vitamin K, or getting adequate amounts through diet, might fix things: “By providing vitamin K in the right form and quantity, along with other supporting nutrients and phytochemicals, it is likely that excellent prostate health can be extended much longer, and perhaps poor prostate health can be reversed.”
Donaldson cites two main pieces of evidence to back up the vitamin K/BPH relationship. First, he offers work by Dr. Gat (2008) who studied the treatment of male infertility by repairing varicoceles by microsurgery or embolization.
Gat was the one who found the ridiculously high free testosterone concentrations (130 times normal) in the blood reaching the prostate from the testes in men with varicoceles, a level he thinks could at least partially explain the hyperplasia seen in the prostate gland.
When varicoceles were treated, the enlarged prostate was relieved, first from the physical pressure of all that backed-up blood, and secondly from the burden of those extremely high testosterone levels. (Donaldson doesn’t dismiss the role testosterone or its metabolites play in BPH; only that there’s something else, e.g., a vitamin K deficiency, that precipitates prostate growth.) Gat even found that BPH didn’t even occur without the presence of varicoceles (which can’t be detected by palpation, only sonography or thermography).
Several subsequent studies have confirmed this relationship between vitamin K insufficiency and BPH.
Then there’s the second line of evidence from a portion of the EPIC (European Prospective Investigation into Cancer and Nutrition) study. One team of contributors – Nimpstch et al (2010) – found an inverse relationship between dietary intakes of vitamin K2 and risk of prostate cancer in a survey of 24,340 participants.
While the Nimpstch study doesn’t prove an association specifically between vitamin K and BPH, it certainly suggests a relationship between the vitamin and prostate health in general.
Clearly, there are other factors involved in BPH. You’ve got obesity, diabetes, and metabolic syndrome all playing a potential role. Testosterone is also involved, and the fact that eunuchs don’t develop BPH is pretty solid proof of its culpability.
But then there’s the conundrum of age: as men get older, BPH increases while testosterone levels drop. And, as Donaldson points out, neither do serum testosterone concentrations correlate with the severity of the condition. In other words, someone could have relatively low free T levels and still have an enlarged prostate. The opposite is also often true.
But it’s not testosterone itself that promotes growth of the prostate, but the conversion of testosterone to its metabolite – dihydrotestosterone (DHT). This mechanism is, of course, the most well-known target of pharmaceutical intervention.
Donaldson has no disagreement with any of those alternate causes of BPH, but he stresses that none of them gives us a clue as to the origins of BPH. His observations about vitamin K, though, offer a tantalizing clue.
There is currently no RDA for vitamin K; there just isn’t enough evidence or research to establish one. We do, however, have an “adequate intake” (AI) for the vitamin. For men and women over the age of 19, the AI is 120 mcg. day for men and 90 mcg. a day for women.
Unfortunately, few foods are fortified with vitamin K. As far as obtaining it through natural foods, you can get vitamin K1 by eating certain green vegetables and plant oils. Think spinach, broccoli, iceberg lettuce, and soybean and canola oil.
These are the types of foods that would theoretically thwart calcification of the arteries.
Foods that contain vitamin K2, however, are not in the “healthy” categories like fruits, vegetables, nuts, seeds, and legumes. Instead, it’s found in egg yolks, some cheeses, some cultured dairy products, and meat – foods that many doctors tell men to restrict.
These are the types of foods that would theoretically thwart BPH.
However, obtaining vitamin K through food presents a problem: The bioavailability of the different forms of vitamin K through food is horribly limited. For instance, the absorption rate of phylloquinone (vitamin K1) in its free form is about 80%, but its absorption rate through food appears to be a lot less than that (K1 appears to cling to the chloroplasts in plants with fierce tenacity).
For example, the human body only absorbs about 4% of the K1 in spinach. Natural sources of K2 appear to fare better in the digestive tract, but specific absorption rate data is scarce.
That leaves supplementation. I use Super K from Life Extension. They make good stuff.
The daily dosage of Super K is one gel cap, and each one contains 1500 mcg. of K1 and a combined 1100 mcg. of two types of vitamin K2 (menaquinone-4 and -7). When you compare those numbers to the recommended AI, it looks to be a case of overkill, but remember, absorption rates are generally poor, so we have to go Battle of Thermopylae on the body and overwhelm its reluctance to sop up vitamin K.
Besides, there’s probably nothing to fear from these relatively high doses; no adverse effects have ever been associated with vitamin K consumption from food or supplements in humans or animals. Its use, however, is contraindicated in people taking blood thinners, antibiotics, bile acid sequestrants (a specific type of cholesterol medication), or the weight-loss drug Orlistat.
Regarding prostate health in general, I also take Biotest’s P-Well™, which I helped formulate. It tackles the phytochemical side of the equation that Donaldson believes plays an equally important role in the health of the prostate.
As I stressed in the article, the idea that a vitamin K2 deficiency is at the root of many cases of BPH is theoretical. More research is definitely needed. Even so, if Donaldson is right, taking supplemental K2 would be unlikely to override obesity, high blood pressure, insulin resistance, or any serious medical condition that aids and abets the development of BPH.
But if it could thwart BPH in the absence of those other contributing factors? Whoa.
High hopes about BPH aside, the research about K1 limiting calcification is much more solid and should be reason enough for every adult – man or woman – to consider supplementing with it (except where contraindications exist).
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