In June of 2013, the Cochrane Collaboration updated their meta-analysis of double-blinded, placebo-controlled randomized controlled trials testing whether zinc is useful in treating or preventing the common cold (1).

Their analysis included 16 trials for treating colds, with a total of 1,387 participants. Intake of zinc was associated with a significant reduction in the duration of the cold, reducing it by about one day. It did not show a benefit in reducing the severity of the symptoms.

Of the 16 trials, 11 showed benefit for zinc, while the others did not. The authors reported that trials showing no benefit have been criticized for using too little zinc or a form that is not bioavailable. (Zinc gluconate is a good choice for bioavailability; more on that in a future post.)

The analysis also included two preventive trials with a total of 394 participants. Both studies found a statistically significant benefit from zinc supplementation with the combined incidence of developing a cold reduced by 36% (0.64, 0.47-0.88).

As for how zinc helps treat or prevent colds, the authors had a few explanations. Zinc ions have an affinity for the receptor sites where the cold virus (rhinovirus) attaches to the nasal passages. It can bind both to the virus and to the nasal passages, thus blocking the ability of the virus to attach. Zinc might also prevent the formation of virus proteins, stabilize cell membranes, prevent histamine release, and inhibit prostaglandin metabolism.

The authors suggest treating a cold with 75 mg of zinc per day. They did not give an amount for preventing colds.

I have written before about the idea that some vegans might benefit from a zinc supplement for immune function and wound healing (see the VeganHealth.org article Zinc). A side benefit of zinc supplementation is that it can prevent cadmium absorption (see the Zinc and Alzheimer’s Disease section of the VeganHealth.org article Cadmium).

Personally, I have taken zinc for a number of years now and I have never had so few colds; those I’ve had have lasted less than a day rather than the usual week. So, whether it is a placebo or a coincidence, I continue to take zinc religiously, in two daily doses of 3.75 mg (as part of a Trader Joe’s calcium, magnesium, and zinc supplement).

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References

1. Singh M, Das RR. Zinc for the common cold. Cochrane Database Syst Rev. 2013 Jun 18;6:CD001364. | link

Dr. Michael Greger’s Latest in Clinical Nutrition Volume 17 DVD is now available.

Check it out at NutritionFacts.org!

It appears that I have exhausted the research on vitamin K2 and heart disease that measures direct outcomes in humans. I will summarize that research soon.

In the meantime, I have just finished reading a 2013 double-blinded, randomized, placebo-controlled trial on the MK-7 version of vitamin K2 conducted in The Netherlands (1).

The study included 244 healthy postmenopausal women who received either 180 µg of MK-7 or a placebo in one daily dose for 3 years. Bone measurements were taken after 1, 2, and 3 years.

There were so many measurements of bone health taken in the study at various parts of the skeleton that it would be tedious to read a list of each of them and what was found. Suffice it to say that there were some statistically significant reductions in bone deterioration in the treatment group that tended not to appear until the 3rd year. There was also a trend towards fewer moderate vertebral fractures in the treatment group, but the numbers were too small to determine statistical significance. To me, the trends seem too strong to be due simply to taking so many measurements that by chance some benefits were found from the treatment.

One caveat is that the trial was funded by Nattopharma, a company that makes an MK-7 supplement.

It should be noted that 180 µg of MK-7 is a much higher dose than you can get from animal products. In the Prospect-EPIC study, MK-7 intake from animal products ranged only from 0 – 2.2 µg (2). In contrast, the fermented soybean product, natto, has much higher amounts of MK-7 (about 775 µg per 100 g (3)).

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References

1. Knapen MH, Drummen NE, Smit E, Vermeer C, Theuwissen E. Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women. Osteoporos Int. 2013 Sep;24(9):2499-507. | link

2. Gast GC, de Roos NM, Sluijs I, Bots ML, Beulens JW, Geleijnse JM, Witteman JC, Grobbee DE, Peeters PH, van der Schouw YT. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovasc Dis. 2009 Sep;19(7):504-10. | link

3. Abstract of: Tsukamoto Y, Ichise H, Kakuda H, Yamaguchi M. Intake of fermented soybean (natto) increases circulating vitamin K2 (menaquinone-7) and gamma-carboxylated osteocalcin concentration in normal individuals. J Bone Miner Metab. 2000;18(4):216-22. | link

A reader pointed out an abstract of a cohort study looking at heart disease and vitamin K2 intake (1), the only one I’ve seen that was not from The Netherlands.

In this case it was the EPIC-Heidelberg cohort from Germany and their findings disagreed with The Netherlands studies depicted in the previous K2 posts.

Vitamin K1 was found to be inversely associated with a fatal heart attack (.49, .25-.94), while vitamin K2 was not associated with incidence (1.21, .81–1.80) or fatal (1.09, .46–2.62) heart disease.

Results were adjusted for smoking, body mass index, waist circumference, hypercholesterolemia, high blood pressure, aspirin use, physical activity, education, and intakes of energy, fat, alcohol, calcium, and folate.

In another short report, a letter to Lancet described a trial in which people on dialysis with osteoporosis were given 45 mg/day of vitamin K2 (2). After six months, their LDL cholesterol had gone from 225 to 195 mg/dl. After treatment was discontinued, cholesterol levels returned to normal.

A couple caveats about this: 45 mg/day of vitamin K2 is about 1,000 times more than a normal intake, and these are very high LDL levels in a rather ill population which might not apply to healthy people.

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References

1. Nimptsch K, Rohrmann S, Linseisen J, Kaaks R. Dietary intake of vitamin K and risk of incident and fatal myocardial infarction in the EPIC-Heidelberg cohort study Gesundheitswesen 2010; 72: V143-DOI: 10.1055/s-0030-1266323 | link

2. Nagasawa Y, Fujii M, Kajimoto Y, Imai E, Hori M. Vitamin K2 and serum cholesterol in patients on continuous ambulatory peritoneal dialysis. Lancet. 1998 Mar 7;351(9104):724. | link

Since my last request for support, these have been the more popular posts:

Eat Right for Your Type: Debunked Again?
Clinical Trial of Methylcobalamin
Austrian Vegetarians: Good News?

But the most popular post by far was…drum roll please…

Petition: Veggie Burger at McDonalds

I read a survey not long ago that found one of the main reasons people do not go vegan is from not having options in restaurants. So, my readers are apparently savvy about this importance of this issue.

By the way, that petition still needs 56,000 more people to sign, so please keep passing it on.

Wile my vitamin K2 series has some ardent followers, they are not many in number. Frankly, I’d much rather be beating up on the blood type diet, but K2 is a topic that anti-vegans bring up a lot and the research seems important, so I will plug on with it.

If you feel this work is worthy of support, please see how in the box below. Thank you!

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Circa 2003, McDonalds had a veggie burger in many of their Southern California locations (see the article McDonald’s launches Veggie Burger in Southern California). I had it a few times and it was quite good. McDonalds says that it was not a popular item, so they removed it.

Ten years later, maybe it’s time they tried it again. Kathy Freston is circulating a petition on Change.org, McDonald’s: It’s Time For A Healthy, Meatless Option (Please!).

I’m not getting behind this effort so that hardcore vegans have something to eat at McDonalds, but rather for the number of animals that could be spared a lifetime of suffering just from meat-eaters trying this burger and eating it occasionally. Why order two big macs, when you can lose weight and reduce your risk of heart disease and diabetes by ordering just one Big Mac and a McVeggie?

I’m taking another break from vitamin K2 to report on a study that a reader passed on regarding methylcobalamin (1).

There has been very little testing of methylcobalamin and so I normally recommend taking cyanocobalamin because it is a more stable form of vitamin B12 and there are anecdotal reports of people needing large doses of methylcobalamin to achieve results.

A 2011 clinical trial from Korea sheds some light on this issue. The study was done with people who had their stomachs removed (gastrectomy) due to cancer. Patients who have had a gastrectomy can no longer produce intrinsic factor, a molecule required for efficient B12 absorption, and they are typically given B12 injections.

In this trial, patients took 1,500 µg of methylcobalamin each day.

At baseline, their B12 levels were an average of 170 pg/ml and 24 out of 30 had tingling in their hands and feet, the traditional sign of vitamin B12 deficiency. Many had other indicators as well, including elevated homocysteine (an average of 17.5 µg/l). Over the course of the 3 month trial, vitamin B12 levels steadily increased to an average of 810 pg/ml, homocysteine steadily decreased to 11.4 µg/l, 28 patients experienced symptom relief, and 16 patients were free of all symptoms.

A drawback to this trial is that it did not have a placebo group; all the patients knew they were receiving vitamin B12. But these results are, in my opinion, too impressive to be due simply to placebo and based on the homocysteine and symptom improvement, it appears safe to say that 1,500 µg per day of methylcobalamin should be enough for just about anyone.

I have added a paragraph about this study to the Methylcobalamin & Adenosylcobalamin page at VeganHealth.org

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References

1. Kim HI, Hyung WJ, Song KJ, Choi SH, Kim CB, Noh SH. Oral vitamin B12 replacement: an effective treatment for vitamin B12 deficiency after total gastrectomy in gastric cancer patients. Ann Surg Oncol. 2011 Dec;18(13):3711-7. | link

In Vitamin K2: Part One and Vitamin K2: Part Two, I reported some weak associations suggesting that vitamin K2 (found in animals foods), but not vitamin K1 (found in plant foods), might play a role in protecting against heart disease.

Part Three is on yet another study from The Netherlands, this time a component of the The Rotterdam Study published in 2004 (1). Unlike the other other two studies, this one had much stronger results.

The study had a prospective component in which 4,807 men and women aged 55 years and older were followed for an average of 7.2 years. At baseline, all participants were given an ECG to determine if they had heart disease and were excluded if they did.

Vitamin K2 intake was positively associated with the intake of total fat, saturated fat, and calcium, as well as body mass index, and diabetes; it was inversely associated with intake of polyunsaturated fatty acids.

For vitamin K1, the results once again showed it not to be associated with a reduced risk of heart disease (nor mortality).

In model 1, that adjusted for age, gender, and total energy intake, when comparing the group with the highest daily intake (> 33 µg) of vitamin K2 to the lowest (< 22 µg), K2 was associated with a reduced risk of heart disease (.71, .51-1.00), death from heart disease (.59, .35-.99), and overall mortality (.81, .67-.98). These findings are borderline statistically significant.

However, in model 2 that adjusted for factors in model 1 and also body mass index, smoking status and history, diabetes, education, and intake of alcohol, saturated fat, polyunsaturated fat, flavonols (a group of antioxidants), and calcium, the associations became much stronger for heart disease (.59, .40-.86), death from heart disease (.43, .24-.77), and overall mortality (.74, .59-.92).

There was also a cross-sectional component of the study in which 4,473 people were given x-rays at baseline to determine if they had aortic artery calcification. Vitamin K2 intake was inversely associated with severe calcification in model 1 (.56, .39-.80) and model 2 (.48, .32-.71).

As for the possibility of reverse causation (in which people with poor health decided to eat fewer foods high in K2), the authors said, “In contrast to phylloquinone [K1], intake of menaquinone [K2] (mainly MK-4 from eggs and meat, and MK-8 and MK-9 from cheese), is not related to a healthy lifestyle or diet, which makes it unlikely that the observed reduction in coronary risk is due to confounding. Subjects with a history of MI were excluded from the analysis to avoid bias that may arise from intentional changes in diet.”

They also said, “We hypothesize that menaquinones in cheese (MK-8 and MK-9) could exert a beneficial effect in the cardiovascular system and that the high cheese consumption in France and the Mediterranean countries may possibly account for lower prevalences of [heart disease].”

Although the results from this one study are fairly strong, it takes a lot more than one cohort study to justify recommendations for preventing chronic disease. You could combine these results with those for the studies reviewed in Vitamin K2: Part One and Part Two, but those studies are not nearly as strong. Finally, all of these studies included only older people from The Netherlands; we need data from other regions.

In a relatively quick search of PubMed, I could not find any other studies looking at the association between vitamin K2 and heart disease in humans. In fairness to me, the search was quick because so few results were returned. But I will be looking around some more and also reviewing more studies on vitamin K2 and other diseases in the upcoming days.

At this point in time, I am not going out to get vitamin K2 supplements. However, I’m also not dismissing the idea that in a few weeks from now, I might be.

Stay tuned.

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References

1. Geleijnse JM, Vermeer C, Grobbee DE, Schurgers LJ, Knapen MH, van der Meer IM, Hofman A, Witteman JC. Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. J Nutr. 2004 Nov;134(11):3100-5. | link

In Vitamin K2: Part One, I reported on a study from EPIC that followed 16,000 women for 8 years and found an arguably borderline statistically significant, beneficial association for vitamin K2 and the prevention of heart disease.

The same group of researchers, from The Netherlands, published another study of 564 post-menopausal women, comparing their vitamin K intakes to coronary artery calcification (1).

The theory is that vitamin K activates proteins that sequester calcium. Vitamin K1 is cleared from the bloodstream for use in the liver while vitamin K2 is much more likely to be found in the vessel walls where it can prevent calcium from being deposited in the vessel walls.

As predicted, the results showed that vitamin K1 was not associated with a reduced amount of coronary artery calcification. Vitamin K2, however, was associated with reduced risk in a borderline statistically significant manner.

In comparing the highest one-fourth of intake to the lowest, in the model adjusted only for age, the risk was barely statistically significant at 0.82 (0.68–0.99).

In the model adjusted further for smoking, diabetes, BMI, hypertension, educational attainment, HDL and LDL cholesterol, the risk was 0.85 (0.72–1.02); not statistically significant.

And in the model adjusted even further for alcohol consumption and energy-adjusted intake of protein, calcium and fiber the risk was back to statistically significant at 0.80 (0.65–0.98).

Interestingly, the women in the highest intake of vitamin K2 also had the highest intake of calcium at 1,317 mg per day, and calcium and vitamin K2 intakes were significantly associated with each other. Ditto for protein (but not fiber).

Why would women with the highest calcium intake have the lowest amount of artery calcification? Well, as I have written about before, dietary calcium does not appear to cause calcification of the arteries until calcium intakes reach at least 1,400 mg per day, if at all (see Calcium Supplements – The Final Word?).

MK4 was the only vitamin K2 subtype that showed an individual trend towards less artery calcification.

People should keep in mind that this study was cross-sectional, making it a less reliable form of evidence than a prospective study (other things being equal).

In summary, vitamin K2 intake was weakly associated with a lower risk for artery calcification.

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References

1. Beulens JW, Bots ML, Atsma F, Bartelink ML, Prokop M, Geleijnse JM, Witteman JC, Grobbee DE, van der Schouw YT. High dietary menaquinone intake is associated with reduced coronary calcification. Atherosclerosis. 2009 Apr;203(2):489-93. | link

I have posted a number of times about the blood type diet, as described in the book Eat Right For Your (Blood) Type (1996), by Peter D’Adamo (see posts).

I lived in Atlanta during the late 1990s and it was quite popular there at the time. And why not? Who wouldn’t want to eat right for their blood type?!

While the diet and book are a stroke of marketing genius, in my humble opinion, it is also a very far-fetched piece of science. I’m talking way out there. La la land.

I should probably mention that this humble opinion is shared by every medical doctor, nutrition research scientist, and dietitian I’ve ever heard on the subject.

Most unfortunately, the blood type diet has never been tested with an actual clinical trial. Rather RDs, MDs, PhDs, and even WMDs, dismiss it by saying that there is simply no evidence to support it. And while I’m terribly sympathetic to the idea that there is no evidence to support it, I don’t think this is satisfying to a layperson who reads the book. When the subject comes up, I can almost see them thinking to themselves, “You silly dietitians are just brainwashed by the grain and dairy lobbies,” or whatever they think might be biasing that particular dietitian (such as the desire to promote veganism among people with all blood types).

We now have at least a cross-sectional study that provides more evidence about the (lack of) effectiveness of eating right for your blood type (1).

The participants were 993 women and 462 men, aged 20 to 29 years old, taking part in the Toronto Nutrigenomics and Health study.

Based on the food items listed in Eat Right for Your Type, subjects received a positive point for consuming a serving of a recommended food item for one’s blood type and a negative point for eating a food to avoid. The foods that were not listed either to consume or avoid were ignored.

Here is an idea of what the diets are like:

A – almost vegan (no meat, little dairy)
B – semi-vegetarian (low grains, more dairy)
AB – very similar to B with a little less fruits and vegetables and a little more meat
O – paleo (high-meat, high-vegetables, no grains and little dairy)

The data was analyzed in two different ways.

In the first, the entire population was separated into thirds according to their scores for each diet and regardless of their blood type. To make a long story short, the type A and type AB diets fared the best in terms of disease risk factors (see the abstract linked below for the details).

The second set of analyses had four separate sub-analyses in which everyone was divided according to how close they ate the particular blood type diet being examined. Then the people with that blood type were compared to the rest of the population. According to the authors, “no significant interaction effects were observed between diet adherence and blood group for most of the risk factors, suggesting that effects of following ‘Blood-Type’ diets is independent of an individual’s blood group.”

Note that they said no significant interaction was found for most of the risk factors. Given the number of data points they compared (hundreds), it is not surprising that they found some statistically significant, but still rather weak associations, and, in my opinion, the associations they found were inconsistent enough to be meaningless.

With this study, I think we finally have something that moves beyond “no evidence to support” to “evidence to disprove.” However, it still isn’t going to be very persuasive to a believer, especially given how hard it is to explain.

Clinical trials are expensive and since no researcher actually believes there’s anything behind the blood type diet, it’s no wonder that more money hasn’t been forked out to test it.

The diet seems to have gone out of fashion, but if it experiences a resurgence, it might be time to bite the bullet and spend the money on a clinical trial that, with little doubt, would finally allow us to show people that there is no need to eat according to your blood type.

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References

1. Wang J, García-Bailo B, Nielsen DE, El-Sohemy A. ABO Genotype, ‘Blood-Type’ Diet and Cardiometabolic Risk Factors. PLoS One. January 15, 2014.
DOI: 10.1371/journal.pone.0084749 | link