Why do humans require vitamin B12 supplementation while herbivores do not?

This question came about from reading the comments of this (very unclear) question, which the author did not properly clarify.

Vegans are often recommended to take vitamin B12 supplements, as the vitamin is not present in sufficient quantities within vegan food. This implies that plants do not produce (or need) vitamin B12 in their metabolic processes.

However, herbivorous animals do not require any vitamin B12 supplementation, yet contain significant amounts of vitamin B12 in their food products.

What, then, is so different about the digestive tracts of humans and other herbivores that prevent humans from obtaining sufficient vitamin B12 from bacterial sources? Can humans be supplemented with gut bacteria from herbivores, allowing them to obtain sufficient vitamin B12 while on a vegan diet without requiring supplementation?

The bacteria in the foregut of cud chewing animals (e.g. cows) provide enough B12 and other B vitamins. Uptake of B12 happens mainly in the small intestine. There are lots of bacteria in the human intestine but most fermentation of plant matter happens in the hindgut.

Hindgut fermentation also produces B12 but since this happens past the small intestine it is not sufficient to provide enough B12. Therefore non foregut fermenting herbivores (e.g. rabbits) get their B12 when they consume their own feces, which they do anyway to obtain higher digestion efficiency of plant matter. I would not recommend this process to any vegan human though.

As mentioned by bonCodigo, these animals need to take up enough cobalt, and their requirements for this element are higher than our own.

Source: Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients C. EDWARD STEVENS , IAN D. HUME Physiological Reviews Published 1 April 1998 Vol. 78 no. 2, 393-427

The Top Five Vitamins You Should Not Take

I used to take vitamin supplements almost every day. Taking vitamins seemed like a good idea: after all, we know that vitamins are essential for life, and vitamin deficiencies can definitely hurt you. I always thought that vitamins were an inexpensive way to get a little bit healthier.

Millions of Americans apparently agree with me. Close to half of the population in the U.S. takes vitamins, with multi-vitamins being the most popular.* Vitamins are sold in virtually every grocery store, ranging from mega-markets like Wegmans to the organic Whole Foods chain.

The vitamin and supplements industry, which is immensely profitable, relies on the intuition that if a little bit of something is good for you, a bit more can't hurt. Right?

Wrong. If you don't have a serious vitamin deficiency, taking supplemental vitamins doesn't provide any benefit, in almost all cases that have been studied. What's even more surprising is this: routinely taking mega-doses of vitamins might actually harm you.

So here are the top 5 vitamins that you should not take (unless your doctor recommends it):

1. Vitamin C. Perhaps the most popular single vitamin supplement, vitamin C occurs in plentiful amounts in many fresh fruits and vegetables. In the early days of global exploration, sailors often died from scurvy, caused by the lack of vitamin C. Way back in the 1700's, Scottish doctor James Lind famously conducted an experiment that proved that citrus fruit cured scurvy, although vitamin C itself wasn't discovered until the 1930s.

Vitamin C gained its current popularity through the woefully misguided efforts of Linus Pauling, who published a book in 1970 recommending mega-doses of C to prevent the common cold. Although Pauling was a brilliant chemist (and Nobel laureate), he was completely wrong about vitamin C, as Paul Offit explains in detail in his new book, "Do You Believe in Magic?"

Vitamin C doesn't prevent or cure colds. This question has been studied exhaustively: a review in 2005 covering 50 years worth of research concluded that

"the lack of effect . throws doubt on the utility of this wide practice."

Although Vitamin C is generally safe, megadoses of 2000 mg or more can increase the risk of kidney stones, which can be excruciatingly painful.

2. Vitamin A and beta carotene. Vitamins A, C, and E are all anti-oxidants, which have been promoted for their supposed anti-cancer properties. The evidence doesn't support this: for example, in a large study supported by the National Cancer Institute*, smokers who took vitamin A were more likely to get lung cancer than those who didn't.

Vitamin A plays an important role in vision, but too much vitamin A can be toxic, causing multiple serious side effects. Perhaps the most famous cases of vitamin A toxicity occurred in early polar explorers, who ate the livers of their sled dogs, not realizing that the livers had excessively high amounts of vitamin A. Antarctic explorer Douglas Mawson barely survived, and his companions died, probably of vitamin A poisoning.

3. Vitamin E. Long touted as an anti-cancer agent, vitamin E is a very popular supplement. A large study last year, of 35,533 men, looked at vitamin E and the risk of prostate cancer. The authors found that the risk of cancer increased for men taking vitamin E. In an even larger review done at Johns Hopkins University, Edgar Miller and Lawrence Appel found that the overall risk of death was higher in people who took vitamin E. The Mayo Clinic summarizes the evidence this way:

"Evidence suggests that regular use of high-dose vitamin E may increase the risk of death from all causes by a small amount."

4. Vitamin B6. The B vitamins, including B6 and B12, are present in many foods, and deficiencies are rare. But taking B6 supplements for a long time can be harmful, as NIH's website explains*:

"People almost never get too much vitamin B6 from food. But taking high levels of vitamin B6 from supplements for a year or longer can cause severe nerve damage, leading people to lose control of their bodily movements."

5. Multi-vitamins. This is the big one. With nearly 40% of Americans taking a multi-vitamin, they must be good for you, right? But a huge study that I wrote about last year, looking at 38,772 women over 25 years, found that the overall risk of death increased with long-term use of multivitamins, vitamin B6, folic acid, iron, magnesium, zinc, and copper. Death, one must admit, is a pretty bad outcome.

On the evidence, supplementing your diet with any of these 5 vitamins carries little or no benefit, and may cause you harm. This is why we do science, people. Our intuitions aren't always right: just because a little bit of something is good for you does not mean that a lot of it is even better.

Vitamins don't "boost your immune system," they don't promote joint health, they don't reduce stress, and they don't help prevent colds or other common ailments.

So what should one do? Ignore the marketing, and treat supplements like you would any other medicine: take them with caution. If you are taking regular vitamin supplements, or thinking about it, ask your doctor before doing so.

And by the way, 100 grams of spinach has healthy amounts of vitamins A, C, E, K, several B vitamins, and essential minerals including iron and calcium.

So ditch the vitamins and eat your spinach. Or blueberries. Blueberries are great.


Vitamins are organic compounds that are essential to the health of an organism. Humans cannot synthesize vitamins but obtain vitamins through dietary intake. Cobalamin, or vitamin B12, refers to a group of corrinoid molecules that contains a corrin ring with a central cobalt molecule [1]. Cobalamin is a cofactor for the highly conserved enzymes methionine synthase (MetH) and methylmalonyl-CoA mutase (MCM), which function in amino acid synthesis and fatty- and amino acid breakdown, respectively, in both bacteria and mammals [1] therefore, cobalamin plays a key role in homeostatic functions. Indeed, in humans, cobalamin deficiency can lead to decreased activity of MetH and MCM and result in megaloblastic anemia in addition to severe neurological symptoms. Besides its role as a cofactor for MetH and MCM, cobalamin is also used by many bacteria as a cofactor for additional processes, including metabolism and gene regulation. Cobalamin impacts host–microbe interactions by altering host and bacterial physiology at intestinal and extraintestinal sites. We discuss the current understanding of cobalamin in host–microbiota–pathogen interactions, highlighting recent investigations that deepen our appreciation of this molecule.

How do mammals acquire cobalamin?

Only a limited number of bacteria and archaea generate cobalamin de novo [1]. Moreover, plants and fungi do not require cobalamin therefore, humans obtain cobalamin through consumption of animal products. During digestion, cobalamin is absorbed in the ileum. Although some colonic bacteria produce cobalamin, humans are not able to uptake cobalamin produced at this location, and thus, the small intestine is the sole site of absorption. The mammalian protein intrinsic factor (IF) is essential to bind and absorb cobalamin. IF is produced in the stomach and binds cobalamin in the small intestine, in which IF-bound cobalamin is subsequently absorbed into circulation [2] (Fig 1).

Ingested food containing cobalamin enters the stomach. IF is produced in the stomach and binds cobalamin in the small intestine. There, cobalamin–IF complexes are absorbed by host enterocytes in the terminal ileum (indicated by outward arrows in small intestine). In the colon, the microbiota take up unabsorbed cobalamin. Additionally, some members of the microbiota produce cobalamin, which can also be taken up by other microbiota members. Cobalamin that remains unabsorbed by the host and not taken up by the microbiota is excreted in stool (outward arrow in colon). IF, intrinsic factor.

Mammalian herbivores—including rabbits, mice, rats, and nonhuman primates—practice coprophagy, or eating of feces, to obtain cobalamin because these organisms do not obtain sufficient cobalamin from vegetarian dietary sources. Notably, animal products from ruminants, such as cattle, are excellent dietary sources of cobalamin for humans despite being noncoprophagic herbivores. Ruminants are heavily colonized with cobalamin-producing microbes in the rumen, a specialized organ that allows fermentation of ingested feed, and this cobalamin is later absorbed in the small intestine [3]. Therefore, unlike most mammals, cattle are able to use the cobalamin produced by bacteria that colonize their own gastrointestinal tract without the practice of coprophagy.

Do humans compete with bacteria for cobalamin?

The ileum harbors a low level of bacteria compared to the colon, and an abnormal expansion of small intestinal bacteria may result in direct host–bacterial competition for cobalamin. Small intestinal bacterial overgrowth (SIBO) is a condition in which the typically low level of 10 3 bacteria/mL in the small intestine increases to 10 5 to 10 6 bacteria/mL, causing chronic diarrhea and malabsorption [4]. Cobalamin deficiency is a common complication of SIBO, potentially resulting from poor nutrient absorption due to diarrhea or by competition for available cobalamin between host IF and resident bacteria. In support of the latter idea, during in vitro growth, members of the genus Bacteroides that are common intestinal bacteria outcompete IF for binding to cobalamin [5], suggesting that bacteria interfere with absorption in vivo. Moreover, broad-spectrum tetracycline antibiotic therapy resolves cobalamin deficiency in human subjects [6]. These studies offer proof-of-principle evidence that host–bacterial competition for cobalamin impacts human health.

What is the interplay among intestinal bacteria for cobalamin?

In the colon, cobalamin availability is determined by two sources—host dietary intake (approximately 50% is not absorbed by the host) [2] and cobalamin generated by select colonic bacteria. Only 25% of bacteria in the gastrointestinal (GI) tract synthesize cobalamin, whereas 80% of bacteria encode cobalamin-dependent enzymes [7]. Therefore, bacteria rely heavily on cobalamin-uptake mechanisms to acquire sufficient levels from the surrounding environment. For example, genome sequencing revealed that 41% of intestinal bacterial strains encode at least three cobalamin-uptake transporters, with some strains encoding up to 17 transporters [7]. To date, over 27 corrinoid transporters have been identified. The importance of encoding multiple transporters is not clear. The transporters were proposed to function redundantly however, Degnan and colleagues recently reported that B. thetaiotaomicron expresses three transporters that uptake distinct corrinoids [7]. Even so, not all are required for colonization because a colonization defect was measured only upon deletion of one of these transporters. The decrease in B. thetaiotaomicron levels in the gut only occurred in the absence of bacteria from the phyla Firmicutes and Actinobacteria [8], which include cobalamin producers, suggesting that cobalamin-generating bacteria support growth of other bacteria in the community. It is reasonable to speculate that interbacterial competition for cobalamin also occurs and influences the composition of the microbiota, though no evidence of this phenomenon has been shown directly.

Does cobalamin contribute to bacterial pathogenesis?

Although growth within a host is a requisite for pathogenesis, cobalamin influences the ability of a pathogen to infect a host and cause disease, independent of its role as a cofactor for MetH and MCM. For example, many bacteria encode the eut operon that enables growth on ethanolamine (EA), a ubiquitous metabolite in the human body. EA metabolism influences pathogen growth and/or virulence in the intestinal tract (Salmonella, Clostridium, Enterococcus), at sites of extraintestinal dissemination (Salmonella and Listeria), and in the urinary tract (uropathogenic Escherichia coli) [9–17] (Fig 2). In these organisms, the EA ammonia lyase EutBC catalyzes the first step in the breakdown of EA and requires the cobalamin derivative adenosylcobalamin (AdoCbl) for activity. AdoCbl is not a true cofactor because this molecule undergoes irreversible Co-C bond cleavage during EA catabolism, and each round requires a new or readenoslyated AdoCbl molecule for enzyme activity. Moreover, besides encoding metabolic genes, the eut operons of the Firmicutes and Enterobacteriaceae also carry distinct regulatory elements that require cobalamin to drive eut expression. In the Firmicutes, EA is the signal that initiates phosphorylation of the sensor kinase EutW. This phosphate is then transferred to the noncanonical response regulator EutV (noncanonical because EutV functions post-transcription initiation by binding RNA and preventing formation of transcription-termination structures as opposed to binding DNA). In the absence of cobalamin, the eut-encoded small RNA (sRNA) EutX/Rli55 sequesters EutV, thereby inhibiting EutV antitermination activity. The sRNA contains an AdoCbl-binding domain. AdoCbl binding causes a structural change in EutX/Rli55 that results in transcription termination and production of a truncated sRNA that cannot sequester EutV [10, 18]. In the Enterobacteriaceae, eut expression requires the transcription factor EutR. Although EutR binds the eut promoter in the absence of EA and AdoCbl, both molecules are required for transcription initiation [14, 19]. In enterohemorrhagic E. coli O157:H7 (EHEC) and Salmonella, EutR regulates expression of virulence factors required for host infection and dissemination [11, 13, 14], and, similar to EutR regulation of eut expression, transcriptional activation requires EA and AdoCbl. In an analogous manner, cobalamin is required for enzymatic activity of propanediol dehydratase, which breaks down 1,2-propanediol, a metabolite that enhances Salmonella growth [20]. Additionally, cobalamin-dependent degradation of 1,2-propanediol releases breakdown product propionate, which promotes Citrobacter rodentium virulence during infection of the mammalian gastrointestinal tract [21] (C. rodentium is a murine pathogen frequently used to model EHEC and enteropathogenic E. coli infections).

Exclusive breastfeeding may cause B12 deficiency in babies

There is a broad consensus that breastfeeding is good for babies. The WHO recommends that infants should be fed exclusively with breast milk in the first six months of their lives.

But now a new PhD project challenges this view. The study shows that breast milk alone does not appear to provide sufficient amounts of the essential vitamin B12 in infants four months after birth.

&ldquoBefore we start proposing changes in the breastfeeding recommendations, we need to have our results replicated in larger studies by other researchers. But B12 is so important that we believe it&rsquos worth considering whether infants should be given breast milk substitute or regular food after around four months of life,&rdquo says molecular biologist Eva Greibe, who conducted the study at Aarhus University.

The most important vitamin

Vitamin B12 is the collective term for a group of chemical substances also known as cobalamins. The vitamin is essential for cell division, the formation of red blood cells and the general functioning of the nervous system.

Immediately after birth, the B12 levels in the breast milk are high, but four months after birth the levels have dropped dramatically.

B12 is particularly important for infants, and a lack of B12 may ultimately slow down a baby&rsquos physical and mental development and may cause irreversible nerve damage.

But although scientists are aware of the importance of B12, they still lack knowledge about how humans absorb it. Only recently did it become possible to measure the B12 levels in breast milk and it&rsquos this new method that&rsquos the starting point for Greibe&rsquos PhD study.

Mothers should consider a food supplement

She measured the B12 levels in the blood of around 100 women during and after pregnancy. The B12 levels in some of the women&rsquos breast milk and in the new-born babies&rsquo blood were also monitored.

&ldquoImmediately after birth, the B12 levels in the breast milk are high, but four months after birth the levels have dropped dramatically. And when we look at the babies after four months, we see that their B12 levels are so low that we can conclude that they&rsquore not getting sufficient amounts of B12,&rdquo says the researcher.

We definitely agree that the women should continue with their breastfeeding, but we believe it’s worth considering whether to introduce supplements in the shape of regular food or breast milk substitute rich in B12 when the babies reach the age of 3-4 months.

&rdquoThis is a bit strange because breastfeeding and breast milk are regarded as the best thing you can do for babies. We definitely agree that the women should continue with their breastfeeding, but we believe it&rsquos worth considering whether to introduce supplements in the shape of regular food or breast milk substitute rich in B12 when the babies reach the age of 3-4 months.&rdquo

The cause remains a mystery

The researcher is unable to say anything about the cause of the dramatic drop in B12 levels in breast milk over the first months of a baby&rsquos life.

&rdquoWe don&rsquot know why the B12 levels drop. Maybe it&rsquos hormonal maybe it&rsquos nature&rsquos way of forcing the babies to eat more &ndash we don&rsquot know,&rdquo she says.

&ldquoBut we can see that babies who are fed with breast milk substitute have higher B12 levels. We also do not know whether exclusive breastfeeding in the first six months is harmful for the baby.&rdquo

Exclusive breastfeeding means that an infant receives only breast milk with no additional foods or liquids, not even water.

And that&rsquos why there&rsquos such a great need for further studies, she adds.

&rdquoB12 is extremely important for a child&rsquos development and we really need to look further into this. And moreover, it&rsquos not only the B12 levels that drop in the breast milk in the first 4-6 months, but also iron, copper, potassium and zinc &ndash and that just adds to the importance of carrying out further studies in this field.&rdquo

But the researcher is keen to point out that the conclusions need to be confirmed in follow-up studies before we can start talking about making changes to the recommendations.

Bottom Line:

  • Most individuals can get all of the necessary vitamins and minerals through a healthy eating pattern of nutrient-dense foods. The Dietary Guidelines for Americans 2015-2020 provides recommendations for specific populations, including women who are or may become pregnant, women who breastfeed, and people ages 50 and over.
  • Taking an MVM increases overall nutrient intake and helps some people get the recommended amounts of vitamins and minerals when they can’t or don’t get them from food alone. But taking an MVM can also raise the chances of getting too much of some nutrients, like iron, vitamin A, zinc, niacin, and folate/folic acid, especially when a person takes more than a basic, once-daily product that provides one hundred percent of the Daily Value (DV) of nutrients.
  • The Age-Related Eye Disease Study (AREDS), which was led by NIH’s National Eye Institute and concluded in 2001, showed that daily high doses of vitamins C and E, beta-carotene, and the minerals zinc and copper—called the AREDS formulation—can help slow the progression to advanced age-related macular degeneration (AMD), a blinding eye disease.
  • Data from the later AREDS2 study showed that removing beta-carotene from the AREDS formulation didn’t lessen its protective effect against developing advanced AMD. AREDS2 also showed that neither omega-3 fatty acids nor lutein/zeaxanthin, when added to the original AREDS formulation, affected the need for cataract surgery.
  • There’s no standard or regulatory definition for MVMs, or any dietary supplement, as to what nutrients they must contain or at what levels. Manufacturers choose which vitamins, minerals, and other ingredients, as well as their amounts, to include in their products. Simply stated, dietary supplements aren’t required to be standardized in the United States. However, they are required to bear a Supplement Facts label and ingredient list describing what’s in the product.
  • Read the Supplement Facts label to identify MVMs in your supplement product. Be sure to check the percent daily value (%DV) to see what proportion of your daily allotment you’re getting.
  • People with healthier diets and lifestyles are more likely to take dietary supplements, making it hard to identify any benefits from their use. There’s no convincing evidence that MVMs help prevent chronic disease.

Are supplements necessary?

One of the more common questions is whether I recommend any supplements. I recommend very few of them.

For longer fasts, I recommend a general multivitamin, although there is scant evidence that it is beneficial. In fact, almost all vitamin supplements have been proven to not be beneficial in large population based studies. In some cases, like vitamin B, they may even be harmful.

All vitamins go through periods of of popularity and unpopularity. It’s worse than high school. One minute, you’re the most popular kid in class, then next you’re the laughingstock.

Vitamin C

In the 1960’s, the king of vitamins was vitamin C. Linus Pauling is the only person to have won two unshared Nobel Prizes – once for chemistry and once for peace. He had the firm unshakeable belief that many of the problems of modern nutrition could be cured by mega doses of vitamin C. He suggested that high dose vitamin C could prevent or cure the common cold, the flu and even cancer. He even suggested that 󈬻% of all cancer can be prevented and cured by vitamin C alone”. That, of course is wildly optimistic.

Many studies were done over the next few decades that suggested that most of these vitamin C claims were simply false hopes. Turns out the only disease vitamin C cures is scurvy. As I don’t treat many 15th century pirates, it’s not too useful for me.

Vitamin E

Once vitamin C supplementation was proven largely useless to prevent disease, the next great hope was vitamin E. Its main claim to glory was as an ‘antioxidant’. Supposedly, vitamin E would neutralize all the nasty free radicals that were causing untold damage to our vascular system. Taking vitamin E would prevent heart disease, we were told. Except, of course, it did nothing of the sort.

The HOPE trial, best remembered now as one of the trials to establish the use of the ACEI class of medication in cardiovascular protection. However, this randomized controlled trial also tested whether vitamin E could prevent disease. Unfortunately, the answer was no.

Vitamin E supplements did not prevent heart disease or stroke. Indeed, more patients in the vitamin group died, had heart attacks and strokes although this was not statistically significant. Vitamin C was a bust, and so was vitamin E. But the list of shame would not stop there.

B vitamins

The next great hope was vitamin B. In the early 2000s, there was a great flurry of interest in a blood test called homocysteine. High homocysteine levels were correlated with increased risk of heart disease. Vitamin B could lower homocysteine levels, but whether this would translate into better health outcomes was unknown. Several large scale trials were launched with this hope. One of these was the NORVIT trial, published in 2006 in the prestigious New England Journal of Medicine.

The news was stunning. Stunningly bad, that is. Compared to taking placebo (sugar pills), supplementation with folate, vitamin B6 and B12 was giving people more heart attacks and strokes. Yes. The vitamin group was not doing better, it was doing worse. But worse news was still to come, if you can believe it.

In 2009, researchers studied the two randomized controlled trials of vitamin B supplementation and found that in addition to raising the risk of cardiovascular disease, the risk of cancer was increased by 21%! Aw snap! The risk of dying from cancer increased by 38%. Taking useless vitamins is one thing, taking vitamins that are actively harmful is something else.

The use of vitamin B supplements for kidney disease was similarly dismal. The DIVINe study randomized two groups of patients with chronic kidney disease (CKD) to either placebo or vitamin B supplements with the hope of slowing down the progression of kidney disease. Homocysteine levels are high in CKD and the vitamins were able to lower these levels. But did they make any real difference? Sure did. The use of vitamin B made things worse. It doubled the incidence of poor outcomes. Another nail in the coffin of the homocysteine story and vitamin B supplements. Another 10 years of research money wasted.

The ironic part of this flawed knowledge is that we are still paying the price. Enriched wheat flour, for example is wheat with all the goodness extracted and then certain vitamins replaced. So almost all the vitamins were removed, and replaced with huge doses of iron and vitamin B. So what we got was a huge surplus of vitamin B.

Not that I believe this was malicious. People were mostly concerned about nutrient deficiencies like beri beri, iron deficiency anemia and not so much with anything else. The problem, of course, is that we now have data that show that giving large doses of vitamin B may increase rates of cancer and heart attacks.

But why should vitamin B supplements be bad? After all, folate supplements have reduced the incidence of neural tube defects in pregnancy significantly.

Like everything else in medicine, it’s a question of context. Vitamin B is needed for growth of cells. During growth periods, like pregnancy and childhood, this is a good thing.

The problem is completely different during adulthood. Excessive growth is NOT good. The fastest growing cells are cancer cells, so they potentially love, love, love the extra vitamin B. Not so good for us people.

Even for regular cells, the excessive growth is not good, because it leads to scarring and fibrosis. This could explain the increased risk of heart attacks, strokes and kidney disease.


Calcium supplements, of course have been recommended by doctors for decades as a preventative strategy against osteoporosis. I explained everything in this lecture from a few years ago “The Calcium Story“. Almost every doctor has recommended calcium supplements to prevent osteoporosis.

Why? The rationale is that bones have lots of calcium so eating calcium must make bones stronger. This is, of course, the reasoning that a third grader might use, but that’s besides the point. Eating brains makes us smarter. Eating kidneys improves kidney function. Right…. But anyhow, this puerile reasoning lasted for about 50 years.

We pretend that we live in a world of evidence based medicine. Just as we discussed with calories, it seems that evidence is not needed for the status quo, but only for ‘alternative viewpoints’. They finally did a proper randomized controlled trial on calcium supplementation and published it in 2006. The Women’s Health Initiative randomized over 36,000 women to calcium and vitamin D or placebo. Then they followed them for over 7 years and monitored them for hip fractures. Did taking calcium every day for 7 years give women super-strong bones that never crack?

Hardly. There was no difference in total fractures, hip, vertebral or wrist fractures. In other words, calcium supplements were useless. Actually, that’s not true. There was a significant difference. Those people taking calcium had significantly more kidney stones. So, they were actually harmed by taking these pills. Nice. Are these women glad they faithfully took their pills every day for the last 7 years?

The problem with vitamin supplementation

What is the reason why these supplements are not beneficial and mostly harmful? It’s really quite simple. You must understand the root cause (the aetiology) of disease in order to prescribe rational treatment. The diseases that we face today – obesity, type 2 diabetes, osteoporosis, cancer, heart disease etc. ARE NOT VITAMIN DEFICIENCY DISEASES. If these are not diseases caused by a lack of vitamins, why would we expect supplementation to make a difference?

Let’s take an analogy. Suppose our car does not run because the engine has exploded. Somebody then says “Oh, hey, I had a time where our car did not run because it was out of gas. Therefore you should put more gas into the car”. But it doesn’t work. Because you must treat the root cause. The problem was that the engine exploded. I don’t really care how much gas is in the car in this situation.

So, if we are treating vitamin deficiency disease (scurvy, beri beri, osteomalacia) then replacing vitamins is very logical and effective. If we are treating obesity, then replacing vitamins is potentially useless. I don’t worry about nutrient density of foods, because I am not treating a nutrient deficiency disease. However, people love trying to sell you the latest greatest weight-loss supplement (green coffee, raspberry ketones, PGX, fibre, Sensa etc).

If you are asking the question “What can I eat/ take/ supplement to help me lose weight?” then you are going in the wrong direction. The question you need to ask is “What can I NOT eat/take/supplement to help me lose weight?” The money to be made answering the latter question is orders of magnitude smaller than trying to answer the first.

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Folic acid IS NOT folate. It is a *precursor* to folate, and an artificial one at that.

Cyanocobalamin is NOT the form of B12 we get from food. METHYLcobalamin is.

Now if you can show me a study where they experimented with PROPER forms of folate and B12, OK, now you're cooking with gas. But until that happens, I'm going to continue to not worry about it because I'm more careful than the average bear with what supplements I buy. I won't say I'm perfect, I'm probably still missing something, but I do *not* go buy some cheap Centrum thing and content myself that it'll keep me healthy.

Here is why I posted my letter. Matching drugs to symptoms is easy and we could probably train a monkey to do it but finding the true cause of disease is much harder. I always start with a comprehensive four page blood test. I test for things like B12, Homocysteine, Vitamin D, Ferritin, thyroid antibodies, marine lipids and many more. No offence to the Cochrane data base but they are wrong. Most researchers never get near a patient and yet they run these flawed studies and publish the results. Heart disease remains the #1 cause of death in the US then Cancer and then the Medical Profession. Yes the medical profession is the #3 cause of death in the United States. Why don't we create a forum on that or is that study flawed or irrelevant? I personally think killing patients is a bad thing but I'm a littlie old fashioned. When Vioxx killed all those patients (close to 100,000 that they could find so it was likely far more) that was the risk you take.

Most medical doctors I know live and die by a lipid panel. If your cholesterol, HDL's and LDL's are within range that's the standard. Statins are supposed to be what will save planet Earth. I'm 66 and never see a medical doctor and why would I. I know more about what biomarkers matter than they ever will so I test myself. Rather than take one of the many statins that are very expensive and usually cause myalgias and arthralgias, I take Red Yeast Rice. I reduced my cholesterol from 277 to 154 in a week. I reduced my triglycerides from 240 to under 132 in a week. I lowered my LDL's from 184 to 85 in a week. Here's the kicker. This was done with ZERO side effects and for pennies a day. This is just ONE EXAMPLE of where nutritional supplements work and with less side effects and for bargain basement prices. I suggest when you make broad statements about how worthless supplements are you think outside the box. I forgot, you can't do that.

I really liked your site until I wandered into the area where medical doctors wrote opinions about nutritional supplements. I've never killed a patient in my 41 year career and that may be attributed to that I don't use drugs. So when your medical "experts" that received almost no nutritional training in medical school what their opinion is on supplements I have to laugh. You might as well ask a plumber how to fly the space shuttle.

Only looking at the cited studies for guidance on the effects of supplements is blinkered and not what I had expected for the seemingly open-minded and forward-thinking Dietdoctor site. The forms of the vitamins that those studies used were often artificial -- not the natural methylfolate, not the natural methylcobalamin, not natural Vitamin E, etc. Information written by reputable medical professionals on how problematic it is to take such studies as gospel is not that hard to find.
The typical cheaply-produced drugstore multivitamin has several ineffective (or worse) forms of vitamins/minerals. But that's not the only kind of supplement available.
My GP tested me for Vitamin D and I was very deficient - I have to take a D supplement to keep my level around 40. I have several variants of the MTHFR gene (gene test ordered by my gynecologist before a surgery) which cause me to have big problems with folic acid (artificial folate), and to do well with supplemental natural B9 and B12. Magnesium citrate helps with my endometriosis and migraines. Vitamin C helps with my general health and constipation. A moderate dose of calcium citrate (plus the D mentioned earlier) might help with my pre-menopausal osteopenia (scan ordered by my gynecologist). A moderate amount of iodine helps with my hypothyroidism (tested by my endocrinologist). My ferritin levels have been very low since I was 12 (tested by many of my MDs over the years) and the MDs have always recommend iron supplements. A low dose of niacin (nicotinic acid, not niacinamide) helps with my Raynaud's (tested by a physical medicine MD) and tiny blood vessel hemorrhages in my retina (scan by my ophthamologist). I have a genetic variant which means that my body does not really convert beta-carotene from vegetables or supplements into usable vitamin A, so I take a small amount of pre-formed vitamin A in a purified cod liver oil.
Aside from vitamins and minerals, I could mention the ginkgo that helps my Raynauds and vulnerable retinal blood vessels, the glutamine that helps my GERD (diagnosed by my gastroenterologist), the glutathione and SAM-e which help my mood and general health, the oregano oil that helps my SIBO and demodex mites, the fish oil that probably slightly lessens my increased Alzheimers risk from my APO-E E4 genetic variant, etc.
I could go on. but the point is that I actually get REAL benefits from many vitamin and mineral (and other types of) supplements, and this is based on actual physical conditions that I have, which have been confirmed by traditionally-trained US-based MDs, who have advised me to take many of these supplements, and who have witnessed the measurable benefits that I have gotten from many of them.
I'm actually so surprised that the Dietdoctor site's approach to supplements is so one-size-fits-all (more accurately, fits-none!), closed-minded, and unappreciative of the sorts of conditions (some of which I described above) which really can benefit from targeted, high-quality supplementation.

Please note the disclaimer at the bottom of the article from our medical director Dr. Bret Scher. "At Diet Doctor, we agree with Dr. Fung that supplements are not beneficial for most people. However, we also recognize a role for specific supplements, such as vitamin D or omega 3 fatty acids, when someone struggles to get enough in their daily diet. Since we all have different food preferences and tastes, some of us may fall short on these valuable nutrients. In those select cases, supplementation may be of benefit."

Usual Test For Vitamin Deficiency Can Mislead Doctors

ST. LOUIS -- A test that generally is used to measure the amount of vitamin B12 in the body is not sensitive enough to detect a deficiency of the vitamin, which has been linked to several neurological conditions, according to Saint Louis University research. The findings were presented this month at a meeting of the American Neurological Association.

"B12 deficiency is associated with dementia, peripheral neuropathy and spinal cord disease," says Florian Thomas, M.D., Ph.D., associate professor of neurology at Saint Louis University School of Medicine and a researcher on the project.

"While it occurs at any age, B12 deficiency is more common in the elderly, may affect some vegetarians and their newborns, can be provoked by laughing gas anesthesia and also by a unique form of recreational drug use. Importantly, it is very easy to treat by taking one pill per day for life. We need to do a better job of detecting the problem."

Thomas and his Saint Louis University colleagues, Laurence J. Kinsella, M.D., associate professor of neurology, and Jamie T. Haas, M.D., a neurology resident, found that the standard test for B12 deficiency -- measuring its blood level -- may be too insensitive.

The scientists found that of 34 patients who had normal levels of B12, 26 had elevated levels of methylmalonic acid (MMA), which indicated B12 deficiency.

They are urging doctors who suspect their patients lack the vitamin to also test for levels of MMA, a natural compound in the body that increases when B12 is lacking.

"The usual way of diagnosing B12 deficiency may be inadequate because it underestimates the frequency of the problem, which is present in up to 20 percent of the elderly," Thomas says. "The problem is eminently treatable at pennies a day."

Dr. Kinsella has had a longstanding interest in B12 deficiency and its relationship to nitrous oxide, a general anesthetic in common use in dental offices and hospital operating rooms. A B12 deficiency can be caused by nitrous oxide, also known as laughing gas, by inhibiting the action of B12 when tissue stores are low.

"This becomes a public health problem in the elderly undergoing surgery or dental work who may have undiagnosed and untreated B12 deficiencies. It also occurs among dental personnel and others who repeatedly abuse nitrous oxide for its euphoric effects," he says.

Nitrous oxide abuse in the form of "whippets" or "whippits" occurs among medical personnel, teenagers and young adults who purchase nitrous oxide containers from baking supply stores or use the gas contained in whipped cream dispensers (hence the name), says Kinsella.

Thomas and colleagues earlier this year published the case of a young man who abused nitrous oxide and devastating neurological damage to the spinal cord and peripheral nerves. The link to nitrous oxide was recognized and the patient recovered with B12 replacement.

B12 deficiency also can be a consequence of stomach stapling bariatric surgery, which has become an increasingly common procedure for weight loss, because an intact stomach is important for B12 absorption, Thomas says.

Multiple sclerosis can be difficult to distinguish from B12 deficiency, cautioned a companion piece also presented at the conference.

Saint Louis University researchers Chitharanjan Rao, M.D., neurology resident, John Selhorst, M.D., chair of neurology, and Thomas found that patients with either condition can have pain, problems with vision and gait and similar MRIs.

The potential confusion makes careful search for B12 deficiency even more critical, Thomas says, since B12 deficiency can easily be reversed, while multiple sclerosis may be a life-long disease.

Thomas and Kinsella urge doctors to more rigorously check for B12 deficiency by measuring both serum B12 and MMA in patients before surgery and to test patients who are over 65 for the problem every two years. Nitrous oxide abuse resulting in B12 deficiency should be considered especially in younger adults presenting with unusual neurological conditions.

Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first M.D. degree west of the Mississippi River. Saint Louis University School of Medicine is a pioneer in geriatric medicine, organ transplantation, chronic disease prevention, cardiovascular disease, neurosciences and vaccine research, among others. The School of Medicine trains physicians and biomedical scientists, conducts medical research, and provides health services on a local, national and international level.

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Materials provided by Saint Louis University. Note: Content may be edited for style and length.

Are We Actually Meant to Eat Meat?

I think there are definitely benefits to becoming a vegetarian, but I don't necessarily believe a person has to go to that extreme to receive benefits. I think a lot of the times when we eat meat (especially as college students), the meat is not necessarily the healthiest sorts of meat: maybe it is ground beef with a high fat content, or fried chicken, etc. Personally, I feel much different when I eat good meat (lean chicken, turkey or beef) rather than when I eat meat such as fast food, fried chicken. By choosing to eat lean means and add a variety of healthy vegetables to our diet, I think we can be our healthiest.

AARON GREGORY ZERKEL | December 5, 2012 7:10 PM | Reply

If humans are not supposed to eat meat then why does the body require vitamin B12 which primarily comes animal products? Doctors also suggest that if you are considering a vegetarian diet to consult them first so you can be suggested vitamins to cover the nutrients you won't be receiving from veggies. Knowing this makes me wonder about poor Hindus in India who religiously don't consume meat and whether or not they suffer from any malnourishment or other effects from their diets or if their bodies have adjusted to their lifestyles. Have their been any studies done on this?

KELLY SARAH FITZPATRICK | December 5, 2012 7:35 PM | Reply

Both of them make good points and so do you. Personally I could never go through with being a vegetarian because I loveee meat! My sister and my cousin both tried it but neither of them could stay with it either. Maybe there is just something about humans that wants meat, which makes it hard for me to think we're not suppose to have it. But this article is very interesting. It compares the anatomy of carnivores, herbivores, and omnivores to the human anatomy and it makes good argument that we are supposed to be herbivores.

TAYLOR CARROLL | December 6, 2012 5:31 PM | Reply

There was a blog similar to this one, but it asked if becoming a vegan or vegetarian was actually less healthy. The findings were that since vegans cut anything made by animals from their diet that they need to take B12 vitamin supplements (this is usually found in animals).
I don't think we're not meant to eat meat because this certain vitamin that we need is found in it.


1. Study population

We consecutively included 40 first-ever lacunar stroke patients presenting at the Neurology Department of the Maastricht University Medical Centre between February 2009 and October 2010. Lacunar stroke was defined as an acute stroke syndrome with an ischemic lesion on brain MR compatible with the occlusion of a single perforating small artery (subcortical, demarcated, and a diameter <20 mm). Patients with severe co-morbidity, either neurological or psychiatric, were excluded. Patients were assessed at 3 months after stroke to exclude acute phase effects.

2. Ethics statement

The study was approved by the Medical Ethical Committee of the Maastricht University Medical Centre and all patients signed informed consent.

3. Assessments

Fatigue was measured by self-report with the Checklist Individual Strength (CIS) [7]. The questionnaire contains 20 statements with total scores ranging from 20 to 140. The patient has to indicate on a 7-point scale to what extent the statement is applicable for him/her. A score >76 indicates severe fatigue [7].

Symptoms of depression were measured by self-report with the Hospital Anxiety and Depression Scale-Depression subscale (HADS-D) [8]. This subscale consists of 7 items with 4 possible statements relating to the emotional aspects of depression. Total scores range from 0 to 21. This subscale does not include physical and cognitive symptoms, including fatigue. As such, it is suitable to use in somatic populations. Since suicidal items are lacking, the instrument is less appropriate to assess the severity of depression. However, a score >10 is considered clinically significant.

Stroke severity was measured with the National Institutes of Health Stroke Scale (NIHSS) [9] on admission.

4. Vitamin B12 level

Vitamin B12 was measured in serum using a solid-phase time-resolved fluoroimmunoassay. Vitamin B12 level <150 pmol/L was considered deficient [1], since this is clinically as well as scientifically used as a cut-off to decide for vitamin B12 deficiency [10]. Also, Pieters et al [1] used a cut-off of 2.5% at both ends, which resulted in reference values between 150 and 630 pmol/L. To further substantiate this lower reference value, they applied the Bhattacharya-technique and found the lower limit also to be at 150 pmol/L.

5. Brain MRI

On brain MRI (standard T2-weighted and FLAIR sequences), two experienced neurologists (JS and RvO) individually graded pWMLs based on the Fazekas scale [11]. Extensive white matter lesions were defined according to Fazekas classification as T-2 weighted irregular periventricular hyperintensities extending into the deep white matter. In case of disagreement, lesions were ascertained by consensus.

6. Statistical analysis

We used PASW Statistics 18 software. Differences between groups were analyzed with Mann-Whitney U-tests and Pearson Chi-square. We used logistic regression analyses to test associations between the presence of severe fatigue and clinically significant depression, and vitamin B12 status, adjusted for the presence of extensive pWMLs. Since depression is found to be related to low vitamin B12 levels in the elderly population [12], we also adjusted for age.

Sorting through nutritional myths

Unlike biological carnivores, we will not get sick or die from malnutrition if we stop eating dairy, eggs and flesh products. On the other hand, if we stop eating plant foods, we will likely become malnourished. On both a physical and psychological level, humans can thrive on a plant-based diet. Even many famous athletes perform at their peak on plant-based diets. And replacing animal foods with plant foods does not mean we are going against our biology, which is a popular view today. While statistics on the size of the global vegan population are sparse, there are estimated to be millions of vegans in the U.S. alone, and there is ample evidence of healthy populations of people all over the world who traditionally consume little to no animal products. The leading health authorities in the U.S., U.K., Canada and Australia all confirm that well-planned vegan diets are a safe, healthy and viable option for all age groups.

Still, some insist that a vegan diet isn’t for everyone or that some people fail to thrive on a vegan diet. Ex-vegans are often quick to blame a plant-based diet for a wide range of health problems while ignoring all of the other factors that can contribute to poor health, but correlation is not causation. According to nutrition expert Micaela Karlsen, the trend in thinking that says each person requires a highly personalized nutrition regimen, while good at selling books and diet plans, is completely inaccurate. As Karlsen explains, “Human beings are one species we are all the same animal, with the same digestive physiology. And, as is true of all species, we do not require personalized nutritional programs unless we are dealing with a specific disease or some other very unusual condition.”

For a concise reference to plant-based nutrition, we recommend Vegan for Life by Jack Norris and Virginia Messina, both registered dieticians. Vegan for Life will answer all of your concerns and questions. It is backed up by the best peer-reviewed scientific research, and includes a chapter on how to evaluate competing nutritional claims in an age of confusing and conflicting information, much of which is directly funded or heavily influenced by the meat, dairy and egg industries.