Latest Study on Vitamin K and Coronary Heart Disease

A Dutch group led by Dr. Yvonne T. van der Schouw recently published a paper examining the link between vitamin K intake and heart attack (thanks Robert). They followed 16,057 women ages 49-70 years for an average of 8.1 years, collecting data on their diet and incidence of heart attack.

They found no relationship between K1 intake and heart attack incidence. K1 is the form found in leafy greens and other plant foods. They found that each 10 microgram increase in daily vitamin K2 consumption was associated with a 9% lower incidence of heart attack. Participants consumed an average of 29 micrograms K2 per day, with a range of 0.9 to 128 micrograms. That means that participants with the highest intake had a very much reduced incidence of heart attack on average. Vitamin K2 comes from animal foods (especially organs and pastured dairy)and fermented foods such as cheese, sauerkraut, miso and natto. Vitamin K is fat-soluble, so low-fat animal foods contain less of it. Animal foods contain the MK-4 subtype while fermentation produces longer menaquinones, MK-5 through MK-14.

There's quite a bit of evidence to support the idea that vitamin K2 inhibits and possibly reverses arterial calcification, which is possibly the best overall measure of heart attack risk. It began with the observations of Dr. Weston Price, who noticed an inverse relationship between the K2 MK-4 content of butter and deaths from coronary heart disease and pneumonia in several regions of the U.S. You can find those graphs in Nutrition and Physical Degeneration.

The 25% of participants eating the most vitamin K2 (and with the lowest heart attack risk) also had the highest saturated fat, cholesterol, protein and calcium intake. They were much less likely to have elevated cholesterol, but were more likely to be diabetic.

Here's where the paper gets strange. They analyzed the different K2 subtypes individually (MK-4 through MK-9). MK-7 and MK-6 had the strongest association with reduced heart attack risk per microgram consumed, while MK-4 had no significant relationship. MK-8 and MK-9 had a weak but significant protective relationship.

There are a few things that make me skeptical about this result. First of all, the studies showing prevention/reversal of arterial calcification in rats were done with MK-4. MK-4 inhibits vascular calcification in rats whereas I don't believe the longer menaquinones have been tested. Furthermore, they attribute a protective effect to MK-7 in this study, but the average daily intake was only 0.4 micrograms! You could get that amount of K2 if a Japanese person who had eaten natto last week sneezed on your food. I can't imagine that amount of MK-7 is biologically significant. That, among other things, makes me skeptical of what they're really observing.

I'm not convinced of their ability to parse the effect into the different K2 subtypes. They mentioned in the methods section that their diet survey wasn't very accurate at estimating the individual K2 subtypes. Combine that with the fact that the K2 content of foods varies quite a bit by animal husbandry practice and type of cheese, and you have a lot of variability in your data. Add to that the well-recognized variability inherent in these food questionnaires, and you have even more variabiltiy.

I'm open to the idea that longer menaquinones (K2 MK-5 and longer, including MK-7) play a role in preventing cardiovascular disease, but I don't find the evidence sufficient yet. MK-4 is the form of K2 that's made by animals, for animals. Mammals produce it in their breast milk and other animals produce it in eggs all the way down to invertebrates. I think we can assume they make MK-4, and not the longer menaquinones, for a reason.

MK-4 is able to play all the roles of vitamin K in the body, including activating blood clotting factors, a role traditionally assigned to vitamin K1. This is obvious because K2 MK-4 is the only significant source of vitamin K in the diet of infants before weaning. No one knows whether the longer menaquinones are able to perform all the functions of MK-4; it hasn't been tested and I don't know how you could ever be sure. MK-7 is capable of performing at least some of these functions, such as activating osteocalcin and clotting factors.

I do think it's worth noting that the livers of certain animals contain longer menaquinones, including MK-7. So it is possible that we're adapted to eating some of the longer menaquinones. Many cultures also have a tradition of fermented food (probably a relatively recent addition to the human diet), which could further increase the intake of longer menaquinones. The true "optimum", if there is one, may be to eat a combination of forms of K2, including MK-4 and the longer forms. But babies and healthy traditional cultures such as the Masai seem to do quite well on a diet heavily weighted toward MK-4, so the longer forms probably aren't strictly necessary.

Well if you've made it this far, you're a hero (or a nerd)! Now for some humor. From the paper:

The concept of proposing beneficial effects to vitamin K2 seems to have different basis as for vitamin K1. Vitamin K1 has been associated with a heart-healthy dietary pattern in the earlier work in the USA and this attenuated their associations with CHD. Vitamin K2 has different sources and relate to different dietary patterns than vitamin K1. This suggests that the risk reduction with vitamin K2 is not driven by dietary patterns, but through biological effects.

They seem confused by the fact that people who ate foods high in saturated fat and cholesterol had less CHD, yet people consuming green vegetables didn't.  Here's more:

Thus, although our findings may have important practical implications on CVD prevention, it is important to mention that in order to increase the intake of vitamin K2, increasing the portion vitamin K2 rich foods in daily life might not be a good idea. Vitamin K2 might be, for instance more relevant in the form of a supplement or in low-fat dairy. More research into this is necessary.

Translation: "People who ate the most cheese, milk and meat had the lowest heart attack rate, but be careful not to eat those things because they might give you a heart attack. Get your K2 from low-fat dairy (barely contains any) and supplements."

Lawan Kanker Hati Dengan Kulit Apel

JANGAN KUPAS: Kulit apel kandung antioksidan 4,7 kali lebih banyak dari buah apel dan memiliki zat quarcetin untuk lawan penyakit hati


JAKARTA - Mengkonsumsi satu apel setiap hari sudah terbukti menjadikan tubuhsehat. Namun itu tak berlaku jika anda memakan apel dengan mengupas kulitnya terlebih dahulu. Sebaiknya, buanglah kebiasaan tersebut karena anda akan kehilangan zat quercetin yang berpotensi melawan kanker dan penyakit hati.

Kulit apel memiliki aktivitas antioksidan dan bioaktivitas yang lebih tinggi dari pada buah apel karena mengandung antisoksidan yaitu quercetin. Vitamin C yang terdapat pada daging buah apel hanya mempunyai aktivitas antioksidan 1, sedangkan quercetin mempunyai aktivitas antioksidan hingga 4,7 kali.

Tentunya zat gizi yang terkandung dalam satu butir buah apel bukan hanya itu. Kemampuan apel sebagai pencegah penyakit juga terletak pada kandungan karoten dan pektinnya. Karoten memiliki aktivitas sebagai vitamin A dan juga antioksidan yang berguna untuk menangkal serangan radikal bebas penyebab berbagai penyakit degeneratif seperti kanker dan diabet melitus.

Sedangkan pektin merupakan satu tipe serat pangan yang bersifat larut dalam air. Karena merupakan serat yang berbentuk gel, pektin dapat memperbaiki otot pencernaan dan mendorong sisa makanan pada saluran pembuangan.

Pektin juga dikenal sebagai antikolesterol karena dapat mengikat asam empedu yang merupakan hasil akhir metabolisme kolesterol. Makin banyak asam empedu yang berikatan dengan pektin dan terbuang ke luar tubuh maka makin banyak kolesterol yang termetabolisme.

Selain itu pektin juga dapat menyerap kelebihan air dalam usus, memperlunak feses, serta mengikat dan menghilangkan racun dari usus. Konsumsi apel secara teratur juga dapat menjaga keseimbangan gula darah serta menurunkan tekanan kolesterol darah.

Semua zat-zat yang dikandung apel selain yang tersebut diatas juga mempunyai khasiat mencegah pembentukan tumor usus dan mencegah serangan tumor. Zat gizi tersebut tentunya tidak hanya terkandung di daging buah saja tapi juga kulitnya. Dengan demikian mengkonsumsi apel dengan kulit lebih baik dibandingkan tanpa kulit.

Namun beberapa apel impor biasanya dilapisi lilin dengan tujuan menghambat laju proses pembusukan. Karena lebih baik dimakan beserta kulitnya perlu upaya untuk menghilanhkan lapisan lilin tersebut dengan cara mencelupkan apel ke dalam air hangat agar lapisan lilin mencair kemudian digosok hingga bersih dan kering.

Saat membeli apel pun harus diperhatikan kondisi buah. Pilihlah apel yang kulitnya mengkilap, ujung buah bekas kelopak tampak merenggang dan bila dijentikan dengan jari akan terdengar suara nyaring.

Kandungan zat gizi dalam 100 gram buah apel adalah 58 kkal energi, 4 g lemak, 3 g protein, 14,9 karbohidrat, 900 IU vitamin A, 7 mg tiamin, r mg riboflavin, 2 mg niacin, 5 mg vitamin C, 0,04 mg vitamin B, 6 mg kalsium, 3 mg zat besi, 10 mg fosfor dan 130 mg potasium./cr1/itz
sumber :http://republika.co.id/berita/34351/Lawan_Kanker_Hati_Dengan_Kulit_Apel

What Can Evolution Teach us About the Human Diet?

Vegetarians deserve our respect. They're usually thoughtful, conscientious people who make sacrifices for environmental and ethical reasons. I was vegetarian for a while myself, and I have no regrets about it.

Vegetarianism and especially veganism can get pretty ideological sometimes. People who have strong beliefs like to think that their belief system is best for all aspects of their lives and the world, not just some aspects of it. Many vegetarians believe their way of eating is healthier than omnivory. One of the classic arguments for vegetarianism goes something like this: our closest living relatives, chimpanzees and bonobos, are mostly vegetarian, therefore that's the diet to which we're adapted as well. Here's the problem with that argument:

Where are chimps (Pan troglodytes) on this chart? They aren't on it, for two related reasons: they aren't in the genus Homo, and they diverged from us 5-7 million years ago. Homo erectus diverged from our lineage about 1.5 million years ago. I don't know if you've ever seen a Homo erectus skull, but 1.5 million years is clearly enough time to do some evolving. Homo erectus  ate animals as a significant portion of its diet.

If you look at the chart above, Homo rhodesiensis (often considered a variant of Homo heidelbergensis) is our closest ancestor, and our point of divergence with neanderthals (Homo neanderthalensis). Some archaeologists believe H. heidelbergensis was the same species as modern Homo sapiens. I haven't been able to find any direct evidence of the diet of H. heidelbergensis from bone isotope ratios, but the indirect evidence indicates that they were capable hunters who probably got a substantial proportion of their calories from meat. In Europe, they hunted now-extinct megafauna such as wooly rhinos. These things make modern cows look like chicken nuggets.

H. heidelbergensis was a skilled hunter and very athletic. They were top predators in their ecosystems, judged by the fact that they took their time with carcasses, butchering them thoroughly and extracting marrow from bones. No predator or scavenger was capable of driving them away from a kill.

Our closest recent relative was Homo neanderthalensis, the neanderthal. They died out around 30,000 years ago. There have been several good studies on the isotope ratios of neanderthal bones, all indicating that neanderthals obtained most of their protein from meat. They relied both on land and marine animals, depending on what was available. Needless to say, neanderthals are much more closely related to humans than chimpanzees, having diverged from us less than 500,000 years ago. That's less than one-tenth the time between humans and chimpanzees.

I don't think this means humans are built to be carnivores, particularly since there is accumulating evidence of diverse plant consumption by neanderthals, but it certainly blows away the argument that we're built to be vegetarians. Historical human hunter-gatherers had very diverse diets, but on average were meat-heavy omnivores. 

Statistics

Ricardo just sent me a link to the British Heart Foundation statistics website. It's a goldmine. They have data on just about every aspect of health and lifestyle in the U.K. I find it very empowering to have access to this kind of information on the internet.

I've just started sifting through it, but something caught my eye. The U.K. is experiencing an obesity epidemic similar to the U.S.:
Here's where it gets interesting. This should look familiar:

Hmm, those trends look remarkably similar. Just like in the U.S, the British are exercising more and getting fatter with each passing year. In fact, maybe exercise causes obesity. Let's see if there's any correlation between the two. I'm going to plot obesity on the X-axis and exercise on the Y-axis to see if there's a correlation. The data points only overlap on three years: 1998, 2003 and 2006. Let's take a look:
By golly, we've proven that exercise causes obesity! Clearly, the more people exercise, the fatter they get. The R-value is a measure of how closely the points fall on the best-fit line. 0.82 isn't bad for this type of data. If only we could get all British citizens to become couch potatoes, obesity would be a thing of the past! OK, I'm kidding. The obesity is obviously caused by something else. I'm illustrating the point that correlations can sometimes be misleading. Even if an association conforms to our preconceived notions of how the world works, that does not necessarily justify saying one factor causes another.  Controlled experiments can often help us strengthen a claim of causality.

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