Methylfolate and Methyl B12 – Myths or Lies? Part 1

Written by Dr. Steve Chaney on . Posted in Methyl folate

How Did The Myths Arise?

Author: Dr. Stephen Chaney

 

methylated b liesHow did methylfolate become the center of a myth? 

How are the lies of the food supplement industry created? Some of them start innocently enough. They are often based on a kernel of truth which is misinterpreted by some well-meaning medical doctors. It’s not their fault. We teach future doctors what I call “metabolism light” in medical school. There simply isn’t room in the medical curriculum to teach all the details and nuances of human metabolism. We also try to teach them the basics of how to interpret the scientific literature. However, it takes years of experience to get really good at picking out the strengths and weaknesses of clinical studies.

The doctors form their hypothesis and test it on a few patients. If it works, they publish a paper. At that point their idea is picked up by the “sensationalist” bloggers. These are the bloggers who like to focus on the sensational. They delight in writing about “new findings” that go against what the medical profession has been telling you for years. The bloggers don’t stop there. They usually expand the claims. They ‘cherry pick” the scientific literature by quoting only studies that support their viewpoint, and ignoring studies that refute it. In short, they put together a very compelling story. Soon the story is picked up by other bloggers who embellish it further. After it appears in enough sites, people start believing it. A myth is born.

Then supplement companies get in the act. They sense there is money to be made. They manufacture supplements to provide nutrients supported by the myths. They embellish the mythology even more and put together a compelling story to market their products. This is where the mythology becomes deception. Companies have the responsibility to design their products based on the best science. They have an obligation to tell the truth about their products. They know, or should know, that all their claims are not true. When they make claims they know cannot be true, they are lying to you.

The saga of the methylated B vitamins is a perfect example of how observations based on a kernel of truth became myths and eventually became downright lies. Let me share that story with you.

 

The Kernel Of Truth About Methylfolate

 

methylated b folic acidLet’s start with the “kernel of truth” that launched the whole methylfolate saga. It started with a doctor who was having a very difficult time finding a solution for a patient with some significant health issues. The doctor ordered a genetic test and discovered the patient had a deficiency in the methylene tetrahydrofolate reductase (MTHFR) gene. The doctor remembered the reaction catalyzed by MTHFR, and a light bulb went off. “Eureka”, he said. His patient must be unable to make N5-methyltetrahydrofolate (commonly referred to as methyl folate), and methylfolate is required for some very important methylation reactions in the cell.

He gave his patient methylfolate, and the patient’s symptoms got better. The doctor leapt to the conclusion that other patients with MTHFR deficiency needed methyl folate as well. Many of those patients responded to methylfolate as well. He didn’t bother to check whether they responded equally well to folic acid. He just assumed methylfolate was the magic elixir. He wrote a paper on his clinical observations, and the methylfolate story was launched. It all seemed so logical. However, the story was not nearly as straight forward as the doctor and the people publicizing his findings assumed. Let me walk you through some “Metabolism 101”. Don’t worry. There won’t be a quiz.

 

Why The Original Assumptions About Methylfolate Were Misleading

 

MTHFR mutants only have a partial loss of activity.

  • Individuals with 2 copies of a mutation from A to C at position 1298 of the MTHFR gene(A1298C homozygotes) comprise about 5% of the US population. They have 60% enzyme activity and appear to be normal in clinical studies.
  • Individuals with 2 copies of a mutation from C to T at position 677 of the MTHFR gene (C677T homozygotes) have 30% enzyme activity. They comprise about 10% of the US population. C677T homozygotes often have elevated homocysteine levels. The homozygous C677T mutation is associated with depression, anxiety, and mood swings in some people, but not in others (I will come back to the significance of that qualifying statement later).
  • C677T heterozygotes (one mutant gene) have 65% activity and are normal.

We Don’t Need 100% MTHFR Activity

space shuttleOur human body is wonderfully designed. For many of our most essential metabolic reactions we have built in redundancy. We don’t require 100% activity of key enzymes. This helps protect us from bad effects of mutations as they arise.

The best analogy I can think of is the US space program. Most space vehicles had built in redundancy so that if one system failed, the mission could go on. For example, you may remember the Hubble space telescope. It was launched with four gyroscopes to keep the telescope pointed in the right direction. After a few years, one gyroscope gave out. That was not a problem because there were three left. A few years latter the second gyroscope gave out. Again, there was no problem because there were still two gyroscopes left. It was only after the third gyroscope gave out that Hubble became a bit “wonky”, and a space shuttle was sent up to replace the gyroscopes. It is the same with MTHFR. Only when you get down to around 30% activity, does it become a bit wonky”. (That’s about as non-technical as I get.)

Not Everyone With MTHFR Deficiency Experiences Symptoms

This is due to a phenomenon my geneticist friends refer to as penetrance. Simply put, that means that not everyone with the same mutation experiences the same severity of symptoms. That is because the severity of a mutation is influenced by diet, lifestyle, and genetic background. Let me start with genetic background. In terms of MTHFR mutants you can think of genetic background as being mutations in a related methylation pathway. People who have a mutation in both MTHFR and a gene in a related pathway will experience more severe symptoms and are more likely to require methyl folate. Once you understand penetrance, you realize that individuals requiring methyl folate may represent only a small subset of people with MTHFR mutations.

Penetrance is a concept that most proponents of the methylfolate hypothesis completely ignore. The most severe MTHFR mutation (C677T homozygote) increases the probability that individuals will exhibit symptoms, but some individuals with that mutation are completely normal. Now that you understand the concepts of redundancy and penetrance, you can understand why that is.

 

When Did The Kernel of Truth About Methylfolate Become A Myth?

 

methylated b mythsUp to this point the hype around methylfolate could be chalked up to an honest misunderstanding. The doctors who published the original papers may not have known that MTHFR mutations only resulted in a partial reduction in enzyme activity. They probably didn’t know the concepts of redundancy (our cells don’t need 100% enzyme activity) or penetrance (the same mutation may cause severe symptoms in some patients and have no effect in others). It seemed logical to assume that everyone with a MTHFR mutation might do better with methyl folate supplementation. That was incorrect, but it was an honest mistake.

However, the message was picked up by the bloggers who specialize in sensational stories, especially stories that contradict what experts have been telling you for years. They picked up the methyl folate story and distorted it beyond recognition. They knew that “natural” is a buzz word, so they told you that methylfolate was natural and folic acid is synthetic (I exposed that lie earlier). They told you that methylfolate was better utilized than folic acid. They told you that methylfolate was more effective than folic acid. They told you folic acid was toxic. It was going to increase your risk of heart disease and cancer. Suddenly, it was no longer about people with MTHFR deficiency. You were being told that everyone should avoid folic acid and use methylfolate instead.

methylated b folicOn the surface, these pronouncements should not have passed the “If it sounds too good to be true…” test, or in this case, the “If it sounds too bad to be true…” test. You were being asked the believe that folic acid, which has been in use for over 80 years and is backed by hundreds of studies showing it is safe and effective, was neither safe nor effective. You were asked to believe that the government was poisoning you by fortifying foods with folic acid.

However, to make their blogs sound more convincing, they listed clinical studies supporting their stories. The problem is they “cherry picked” the studies that supported their story and ignored the rest. Their bias was particularly outrageous when it came to the “story” that folic acid increases cancer risks. They ignored 10 or 20 studies showing no cancer risk and reported one suggesting it might increase risk. I call that deceptive.

Unfortunately, the myths created by the bloggers have been repeated often enough that many people now believe they are true. I will debunk their myths next week, but first let me touch on how their deceptions became downright lies.

 

When Did The Myths About Methylfolate and Methyl B12 Become Lies?

 

If you are writing a blog, you are covered by “freedom of speech.” You can say whatever you want. It doesn’t have to be true. However, if you are a supplement manufacturer, you are held to a higher standard. Ignorance is no longer an excuse. You can no longer cherry pick the “facts” you like and ignore the rest. You are ethically obligated to research all the available literature and be guided by the best scientific evidence.

Reputable companies have been guided by the scientific evidence and have not jumped on the methylfolate bandwagon. They know folic acid is both safe and effective in a wide variety of clinical situations. They also know that, while methylfolate may be just as effective as folic acid, its potential is largely unproven at this point. It has not been tested in many clinical situations.

Less reputable companies, however, sensed money to be made by capitalizing on the buzz around methylfolate. They repeated the myths of the bloggers to claim that their products were superior to others on the market. They call it marketing. I call it lying. They have an obligation to fact check their claims, and only make claims that are true.

It gets worse. Since lots of people already believed they needed methylfolate, why not extend the claim to one of the methylated B vitamins, methyl B12? That would boost sales even more. The claims for methyl B12 were even more outrageous than for methylfolate. There wasn’t even a “kernel of truth” like MTHFR deficiency to serve as a foundation. The claim was the methyl B12 was needed because of some sort of ambiguous “methylation deficiency”. The lies had become whoppers.

Next week I will debunk the methylfolate and methyl B12 myths. Stay tuned.

 

The Bottom Line

 

This week I have shared the story about how the myths about methylfolate and methyl B12 arose and how they eventually became lies. Next week I will debunk the myths.

 

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

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Comments (3)

  • Caroline

    |

    I can remember in my DAOM doctoral studies one presenter was talking about methylation and everyone but me knew nothing, so he asked if our Shaklee was methylated and knowing how our B Complex is made, I said yes because I knew he would discuss it as not because of your article. Love our B Complex and sell lots of it, and I even call it a “cheap drunk” for lighting the spirit, energy and well being. I do enjoy your articles because of your educational teaching/history and that always helps me.

    Reply

  • Fran

    |

    I am a person who almost died because of MTHFR. Because my ability to detox was so poor, chemical pollution built up to extreme levels. All this happened while I was taking Shaklee B complex for thirty years prior to becoming sick. I contend that I would not have become so deathly ill if the B vitamins I was taking had been the correct methyl form!! I also will say that your “scientific” research is flawed and gives the wrong answer because you tested blood, not what actually gets into the cells. It does not matter what is in the blood, if it cannot get into the cells. That is the case with folic acid. Contact Dr. Ben Lynch. He has been researching this for many years. He has the correct answers. YOU do not.
    Thank you for giving me the opportunity to tell you about this. I’d be happy to speak directly with you regarding my severe experience with MTHFR, and how the methyl forms of folate and B12 saved my life.

    Reply

    • Dr. Steve Chaney

      |

      Dear Fran,

      I have consistently said that there are a few people who need methylfolate. These are individuals with several other mutations affecting pathways involving methylation reactions in addition to MTHFR. Situations like yours are exceedingly rare because multiple mutations are required. Published clinical studies show that most people with MTHFR deficiency do quite well with folic acid.

      Folic acid gets into cells quite easily and is immediately converted to folates, including methylfolate – even in individuals with MTHFR deficiency. Again, this is based on published clinical studies.

      I have been in touch with Dr. Ben Lynch and have pointed out the errors in his assertions. Many of his “answers” are contradicted by published clinical studies.

      Dr. Chaney

      Reply

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Latest Article

Is Our Microbiome Affected By Exercise?

Posted November 6, 2018 by Dr. Steve Chaney

Microbiome Mysteries

Author: Dr. Stephen Chaney

is our microbiome affected by exerciseIn a recent post,  What is Your Microbiome and Why is it Important,  of “Health Tips From The Professor” I outlined how our microbiome, especially the bacteria that reside in our intestine, influences our health. That influence can be either good or bad depending on which species of bacteria populate our gut. I also discussed how the species of bacteria that populate our gut are influenced by what we eat and, in turn, influence how the foods we eat are metabolized.

I shared that there is an association between obesity and the species of bacteria that inhabit our gut. At present, this is a “chicken and egg” conundrum. We don’t know whether obesity influences the species of bacteria that inhabit our gut, or whether certain species of gut bacteria cause us to become obese.

Previous studies have shown that there is also an association between exercise and the species of bacteria that inhabit our gut. In particular, exercise is associated with an increase in bacteria that metabolize fiber in our diets to short chain fatty acids such as butyrate. That is potentially important because butyrate is a primary food source for intestinal mucosal cells (the cells that line the intestine). Butyrate helps those cells maintain the integrity of the gut barrier (which helps prevent things like leaky gut syndrome). It also has an anti-inflammatory effect on the immune cells that reside in the gut.

However, associations don’t prove cause and effect. We don’t know whether the differences in gut bacteria were caused by differences in diet or leanness in populations who exercised regularly and those who did not. This is what the present study (JM Allen et al, Medicine & Science In Sports & Exercise, 50: 747-757, 2018 ) was designed to clarify.  Is our microbiome affected by exercise?

 

How Was The Study Designed?

is our microbiome affected by exercise studyThis study was performed at the University of Illinois. Thirty-two previously sedentary subjects (average age = 28) were recruited for the study. Twenty of them were women and 12 were men. Prior to starting the study, the participants filled out a 7-day dietary record. They were asked to follow the same diet throughout the 12-week study. In addition, a dietitian designed a 3-day food menu based on their 7-day recall for the participants to follow prior to each fecal collection to determine species of gut bacteria.

The study included a two-week baseline when their baseline gut bacteria population was measured, and participants were tested for fitness. This was followed by a 6-week exercise intervention consisting of three supervised 30 to 60-minute moderate to vigorous exercise sessions per week. The exercise was adapted to the participant’s initial fitness level, and both the intensity and duration of exercise increased over the 6-week exercise intervention. Following the exercise intervention, all participants were instructed to maintain their diet and refrain from exercise for another 6 weeks. This was referred to as the “washout period.”

VO2max (a measure of fitness) was determined at baseline and at the end of the exercise intervention. Stool samples for determination of gut bacteria and concentrations of short-chain fatty acids were taken at baseline, at the end of the exercise intervention, and again after the washout period.

In short, this study divided participants into lean and obese categories and held diet constant. The only variable was the exercise component.

 

Is Our Microbiome Affected By Exercise?

is our microbiome affected by exercise fitnessThe results of the study were as follows:

  • Fitness, as assessed by VO2max, increased for all the participants, and the increase in fitness was comparable for both lean and obese subjects.
  • Exercise induced a change in the population of gut bacteria, and the change was comparable in lean and obese subjects.
  • Exercise increased fecal concentrations of butyrate and other short-chain fatty acids in the lean subjects, but not in obese subjects.
  • The exercise-induced changes in gut bacteria and short-chain fatty acid production were largely reversed once exercise training ceased.

The authors concluded: “These findings suggest that exercise training induces compositional and functional changes in the human gut microbiota that are dependent on obesity status, independent of diet, and contingent on the sustainment of exercise.” [Note: To be clear, the exercise-induced changes in both gut bacteria and short-chain fatty acid production were independent of diet and contingent on the sustainment of exercise. However, only the production of short-chain fatty acids was dependent on obesity status.]

 

What Does This Study Mean For You?

is our microbiome affected by exercise gut bacteriaThere are two important take home lessons from this study.

  • With respect to our gut bacteria, I have consistently told you that microbiome research is an emerging science. This is a small study, so you should regard it as the beginning of our understanding of the effect of exercise on our microbiome rather than conclusive by itself. It is consistent with previous studies showing an association between exercise and a potentially beneficial shift in the population of gut bacteria.

The strength of the study is that it shows that exercise-induced changes in beneficial gut bacteria are probably independent of diet. However, it is the first study to look at the interaction between obesity, exercise and gut bacteria, so I would interpret those results with caution until they have been replicated in subsequent studies.

  • With respect to exercise, this may be yet another reason to add regular physical activity to your healthy lifestyle program. We already know that exercise is important for cardiovascular health. We also know that exercise increases lean muscle mass which increases metabolic rate and helps prevent obesity. There is also excellent evidence that exercise improves mood and helps prevent cognitive decline as we age.

Exercise is also associated with decreased risk of colon cancer and irritable bowel disease. This effect of exercise has not received much attention because the mechanism of this effect is unclear. This study shows that exercise increases the fecal concentrations of butyrate and other short-chain fatty acids. Perhaps, this provides the mechanism for the interaction between exercise and intestinal health.

 

The Bottom Line

A recent study has reported that:

  • Exercise induces a change in the population of gut bacteria, and the change was comparable in lean and obese subjects.
  • Exercise causes an increase in the number of gut bacteria that produce butyrate and other short-chain fatty acids that are beneficial for gut health.
  • These effects are independent of diet, but do not appear to be independent of obesity because they were seen in lean subjects but not in obese subjects.
  • The exercise-induced changes in gut bacteria and short-chain fatty acid production are largely reversed once exercise training ceases.

The authors concluded: “These findings suggest that exercise training induces compositional and functional changes in the human gut microbiota that are dependent on obesity status, independent on diet, and contingent on the sustainment of exercise.”

For more details and my interpretation of the data, read the article above.

 

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

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