How Does This Relate To Pregnancy, Labor, Birth, And The Postpartum Period?
Author: Carolyn Curtis, MSN, CNM, RN, FACNM, FAAN
Editor: Dr. Steve Chaney
Family History And Pregnancy
On the first prenatal appointment, an extensive history is taken that includes family history, personal medical history, gynecological history, pregnancy history; sexual history, social history.
Due to the many physiological changes that occur during pregnancy, birth and the postpartum period, one can be placed at increased risk for the development of health conditions that may not have been present prior to pregnancy.
A properly collected and granular family history may determine if a woman is at increased risk for disease, identify early warning signs of disease; and assist the provider in recommending treatments for reducing a woman’s risk for developing serious problems in during pregnancy, labor, birth and the postpartum period.
A recent study (D Rasooly et al, J Am Heart Assoc, 12(22): e030779, 2023) published in 2023 presents findings on the association between a comprehensive family history that includes parents, siblings and the self-reported personal history of obesity, diabetes, and heart and blood conditions.
How Was This Study Done?
The study involved 125,430 participants; 66.3% were women; 33.75 were men; 75.7% were White; 10.4% were Hispanic; 3.3% were Asian; 8.3% were Black and 2.4% were Other.
The study provided information on the possibility of someone developing a health problem based upon their family history. It also reported odds ratio (statistical probability) of other conditions developing when one health condition was present.
The Importance Of Family History For Maternal Health
The findings of the study were as follows. Of the 125,430 participants:
A family history of hypertension or high blood pressure was reported by 51.6% of the participants. When this was disaggregated by race, 60% of Blacks reported having a family history of hypertension and 54.4% of Asians reported having hypertension compared to 48.6% of Whites.
A family history of high cholesterol was reported by 38.7% of the participants.
A family history of heart attack was reported by 23.6% of the participants.
A family history of Type 2 diabetes was reported by 21.4% of the participants.
If one has a family history of a certain medical condition, there is an increased likelihood that this same condition can be passed on to the next generation (in this case, the pregnant mother). The statistical term “odds ratio” means the likelihood of this same condition occurring in the next generation when there is a family history vs when there is not a family history.
Passing the Same Disease Down To The Pregnant Mother
Compared to those who do not have a family history, here are the odds for passing down these same conditions to the mother.
Hypertension – 2.56 times the odds it can be passed down.
High cholesterol – 2.89 times the odds. If there is a family history of high cholesterol, there is 2.44 odds of Asians developing high cholesterol compared to 2.16 odds in the Black population.
Coronary Artery Disease – 3.54 the odds.
Type 2 diabetes – 3.79 times the odds.
Anemia – 2.66 times the odds.
Peripheral vascular disease – 6.60 times the odds.
Pulmonary embolism/deep vein thrombosis – 5.60 times the odds.
Obesity – 1.2 times the odds. If there is a family history of obesity, for Asian populations, there is 2.93 odds that obesity will be passed down to son or daughter. This ratio is 4.57 in the Black population.
Passing Another Disease Down To The Pregnant Mother
The study also reported the association of family history to someone’s personal health condition and the odds of the pregnant mother developing a different health condition pertaining to obesity, diabetes and heart and blood. On average there was 1.5 odds of developing a different condition from the condition reported in the family history. For example:
When there is a family history of Type 2 diabetes, there is 2.04 odds of developing obesity.
When there is a family history of pulmonary embolism/deep vein thrombosis; there is 3.25 odds of developing a bleeding disorder.
The two family health conditions that had the most evidence of association with other conditions were family history of stroke and heart attack.
When there is a family history of stroke, the odds of the pregnant mother developing other conditions are as follows:
Obesity (1.35).
Heart attack (1.7). There was almost double the odds ratio in the Hispanic population with 3.34 odds.
Hypertension (1.40). Whites reported 1.37 odds for developing hypertension compared to 1.55 for Blacks and 1.43 for underrepresented populations.
High cholesterol (1.33). When disaggregated by race, Whites had a 1.29 odds ratio; Black a 1.60 odds ratio and those underrepresented in biomedical research had a 1.33 odds ratio.
When there is a family history of heart attack, the odds of the pregnant mother developing related conditions are as follows:
Heart attack (2.17). These odds are decreased for Asians (1.92) and Hispanics (1.27).
Coronary artery disease (1.97).
Congestive heart failure (1.54).
High cholesterol (1.44).
When there is a family history of Type 2 diabetes, the odds of the pregnant mother developing other conditions are:
Heart attack (1.32).
Congestive heart failure (1.44).
Bleeding disorder (1.26).
Coronary artery disease (1.37 odds).
Asians with a family history of Type 2 diabetes have a 1.79 odds of developing heart valve disease.
How Does This Relate To Pregnancy, Labor, Birth, And The Postpartum Period?
The five main causes for pregnancy related death in the United States (defined as maternal death up until 12 months after giving birth) are:
Mental Health – 24%.
Hemorrhage – 14%.
Cardiovascular Disease – 13%.
Cardiomegaly (enlarged heart) – 9%.
Blood Clots – 9%
Many of these causes are related to the cardiovascular system. Based upon the data in this study, a family history of any of the following can contribute to the increased odds of developing health problems during pregnancy:
Stroke
Type 2 diabetes
Pulmonary embolism/deep vein thrombosis
Hypertension
Anemia
Once someone knows their family history, when planning for a pregnancy, they can work on any nutrition or lifestyle changes needed to reduce the incidence of problematic health conditions occurring during pregnancy and the health of the newborn.
The US Surgeon General has published My Family Health Portrait which will allow individuals to record and share their family history. It can be accessed at https://cbiit.github.io/FHH/html/index.html
The Bottom Line
When planning a pregnancy, a thorough family health and personal history is important.
Obesity, diabetes and heart and blood conditions can be passed from parents to children. Some of these conditions include anemia, peripheral vascular disease, pulmonary embolism/deep vein thrombosis, Type 2 diabetes, hypertension, coronary artery disease, and high cholesterol.
There is an association between a family history of stroke and heart attack and numerous other health conditions.
One’s family history can impact health conditions experienced during pregnancy that can result in pregnancy-related death up to 12 months after the baby is born.
The US Surgeon General’s My Family Health Portrait is an online tool that can help families to record their family health history and share with other family members.
For More Information
Feel free to visit my website, subscribe to my YouTube channel and learn more about my online coaching program, “Mastering Pregnancy and Birth”.
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.
The posts on this website and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
More than 40 years’ experience in the oversight of domestic and international programs and the provision of nursing and midwifery integrated service delivery in maternal child health, family planning, reproductive and women’s health care.
Twenty years’ experience in teaching, mentoring, and providing clinical oversight to undergraduate and graduate public health, medical, nursing and midwifery students.
About The Editor
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years.
Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
How do the myths of the food supplement industry originate? 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 scientific literature. However, it takes years of experience to get 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. When they make claims they know cannot be true, they are lying to you.
The saga of methylfolate 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
Let’s start with one of the “kernel of truth” that launched the whole methyl folate 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 methylfolate or 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 methylfolate 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 Methyl Folate 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
Our 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 later 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 methylfolate. Once you understand penetrance, you realize that individuals requiring methylfolate 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 Become A Myth?
Up to this point the hype around methyl folate 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 methylfolate 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 methylfolate 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.
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 cancer.
Suddenly, it was no longer about people with MTHFR deficiency. You were told that everyone should avoid folic acid and use methylfolate instead.
On 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 to 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. It is time for me to debunk the methylfolate myths.
The Methylfolate Myths
Myth: Methylfolate is natural. It comes from whole food. Folic acid is synthetic.
Fact: Methylfolate is chemically synthesized from folic acid. It is physically impossible to extract enough from whole foods. Here are the facts:
Methyfolate is only one of several naturally occurring folates in foods.
The best food sources of folates are beans, leafy greens, and broccoli.
To obtain the RDA of methyfolate for a single tablet you would need to start with 1 cup of lentils, two cups of cooked spinach, or 4 cups of broccoli.
You do the math! It just isn’t possible.
Myth: Methylfolate is better utilized by the body than folic acid.
Fact:This claim is based on levels of methylfolate in the blood after taking supplements providing equivalent amounts of methylfolate and folic acid. However, methylfolate has no biological activity in our blood. The measurement that matters is total folate levels (methylfolate plus other folates) in our cells.
If you take equivalent amounts of folic acid and methylfolate, you end up with identical folate levels in your cells (B.J. Venn et al, The Journal of Nutrition, 132: 3333-3335, 2002). In short, there is no difference in our ability to utilize methylfolate and folic acid.
Myth: If you have a mutation in the MTHFR gene, folic acid isn’t effective.
Fact: MTHFR slightly increases the need for folic acid (from 400 ug to between 600 and 800 ug), but multiple studies show that folic acid supplementation is effective in people with MTHFR mutations.
For example, homocysteine levels are easily measured and are a reliable indicator of methylfolate status.
That study also showed that folic acid was more effective than methylfolate at lowering homocysteine in people who were C677T heterozygotes and in people with normal MTHFR activity.
At present, lowering of homocysteine levels is the only indicator of methylfolate status for which methylfolate and folic acid have been directly compared. However, there are other studies suggesting that folic acid is likely to be effective for people with MTHFR defects. For example:
Fact: The few studies suggesting that folic acid supplementation might increase the risk of cancer were “outliers”. By that I mean they contradicted many other studies showing no increased risk.
Scientists are accustomed to this. We know that studies sometimes come up with conflicting results. In some cases, we can point to an error in experimental design or statistical analysis as the cause of the aberrant results.
In other cases, we never know the reason for the differences, so we go with the weight of experimental evidence (what the majority of studies show). The weight of evidence clearly supports the safety of folic acid.
However, that is not enough. If there is the slightest possibility that something causes cancer, we investigate it further. Consequently, the scientific community followed up with larger studies.
Those studies showed either reduced cancer risk or no difference in cancer risk with folic acid supplementation. None of the studies found any evidence that folic acid increased cancer risk. I have covered this in detail for folic acid and colon cancer risk in a previous issue of “Health Tips From The Professor”.
There have also been a couple of small studies suggesting that folic acid might increase the risk of prostate and breast cancer. Although these were small, individual studies, they have been widely hyped by the methylfolate advocates. Once again, the definitive study has been done (S.E. Vollset et al, The Lancet, 381: 1029-1036, 2013).
It was a meta-analysis of 13 placebo-controlled studies involving over 50,000 subjects. The results were clear cut. Folic acid supplementation caused no increase in overall cancer risk, and no increase in the risk of colon cancer, prostate cancer, breast cancer, or any other individual cancer. Moreover, the average dose of folic acid in those studies was 2 mg/day, which is 5 times the RDA.
Of course, the bloggers and the companies selling methylfolate supplements ignore the definitive studies showing folic acid does not increase cancer risk. The myths and lies continue.
Myth: Folic acid can mask a B12 deficiency.
Fact: True but irrelevant if you use a supplement with folic acid and B12 in balance.
The Lies Of The Supplement Industry
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 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, it has not been shown to be superior to folic acid for any clinical application.
They may offer a methylfolate option for people who believe they need it. But they make no claim that it is superior to their products containing folic acid.
Less reputable companies, however, sensed money to be made by capitalizing on the buzz around methyl folate. They repeated the myths of the bloggers and claimed 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.
Let me give you an example. In preparing for this article, I looked at the claims of several companies that were promoting their methylfolate supplements. One in particular claimed they had studies showing:
1) Their methylfolate supplement was effective at reducing the risk of adverse pregnancy outcomes.
2) Their methylfolate supplement was twice as bioavailable as folic acid.
3) Their methylfolate supplement was able to lower homocysteine levels better than conventional folic acid supplementation.
All three studies were bogus.
With respect to the first study, it was likely true that their methylfolate supplement decreased adverse pregnancy outcomes. But there are dozens of studies showing that folic acid does the same thing.
And because they did not compare methylfolate and folic acid supplementation in their studies, they have no basis for claiming their supplement was superior.
The second study compared levels of methylfolate and folic acid in the blood. As I mentioned above, methylfolate has no biological activity in our blood. The measurement that matters is total folate levels (methylfolate plus other folates) in our cells. And previous studies have shown that equivalent amounts of methylfolate and folic acid give identical amounts of methyfolate in our cells.
The third study compared their supplement, which contained B6, B12, zinc, and betaine in addition to methylfolate, to folic acid alone. That’s comparing apples to oranges. That is because there are three pathways for lowering homocysteine levels, and B6, B12, and betaine play important roles in each of these pathways.
B12 is an integral part of the enzyme methionine synthase, an enzyme that converts homocysteine to the amino acid methionine. Methylfolate transfers its methyl group to the enzyme-bound vitamin B12, and methyl B12 transfers the methyl group to homocysteine, which converts it to methionine. In other words, methylfolate cannot lower homocysteine levels by itself. It needs vitamin B12.
Betaine also serves as a methyl donor in another pathway for converting homocysteine to methionine by an enzyme called betaine-homocysteine methyltransferase.
B6 is essential for yet another pathway that lowers homocysteine levels by converting homocysteine to the amino acid cysteine.
You might argue that the company was simply ignorant of the importance of B6, B12, and betaine for lowering homocysteine levels. However, that is unlikely. Why else would they have included B6, B12, and betaine in their supplement?
They must have known the study they designed was bogus. That suggests they conducted the study with the sole purpose of deceiving you, the consumer. I call that lying.
Finally, in case you were wondering, I am not recommending you select a single supplement with folic acid, B6, and B12. I do recommend you get your folic acid from a multivitamin or B complex supplement that provides all three B vitamins in balance.
Betaine deficiency is very rare, so I don’t include betaine in my recommendations.
What Does This Mean For You?
MTHFR mutations only result in partial loss of activity. Most individuals with MTHFR defects remain symptom free with the RDA, or slightly above the RDA, of folic acid.
However, there may be some individuals with a MTHFR defect and additional gene defects in metabolic pathways involving methylation who might benefit from methylfolate. This is due to a phenomenon that geneticists call penetrance and would likely represent a small subset of the population with MTHFR defects.
Finally,the claims that everyone would benefit from methylfolate instead of folic acid are false. They are contradicted by human metabolism and multiple published clinical studies.
In short, folic acid has been used for over 80 years. There are hundreds of clinical studies showing it is safe and effective, even in most individuals with a MTHFR deficiency. I can’t tell you whether the companies selling methylfolate are ignorant of basic metabolism and the published studies refuting their claims or whether they are purposely trying to deceive the public—but neither is a good thing.
The Bottom Line
Some supplement manufacturers are claiming that methylfolate is more natural and more effective than the folic acid that has been used in supplements for the past 80 years. In this issue of “Health Tips From the Professor” I debunk the methylfolate myths used by the supplement manufacturers to sell their methylfolate products.
I can’t tell you whether the companies selling methylfolate are ignorant of basic metabolism and the published studies refuting their claims or whether they are purposely trying to deceive the public—but neither is a good thing.
For more specifics, 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years. Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry textbooks for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
Vitamin B12 (also called cobalamin) is a complex molecule whose structure is shown on the left. It has a cobalt atom in its center which is essential for its functioning (more about that in a minute).
It was first discovered in 1947 and shown to be an essential nutrient for humans in 1948. It has been used in nutritional supplements since then.
The deficiency of vitamin B12 leads to a disease called pernicious anemia.
The initial symptoms are like other forms of anemia, namely:
Fatigue and weakness.
Pale skin.
Low red blood cell count.
If the deficiency persists long enough, neurological symptoms also appear including:
Numbness and tingling in hands and feet.
Lack of fine motor skills.
Difficulty maintaining balance and coordination.
Cognitive issues and mood changes.
Vitamin B12 is found naturally in animal foods such as meat (liver is a particularly good source), fish, poultry, eggs, and dairy.
Vitamin B12 deficiency is most frequently observed in vegetarians (Plant foods contain no vitamin B12) and the elderly (As we age, we tend to lose a protein called intrinsic factor in our intestine that is important for vitamin B12 absorption).
In our bodies, vitamin B12 occurs in two forms, methylcobalamin (popularly referred to as methyl B12) and adenosylcobalamin.
Adenosylcobalamin is important for energy production, especially the generation of energy from protein and fat.
Methylcobalamin is important for nerve function, DNA and RNA synthesis, and gene regulation among other things.
Both adenosylcobalamin and methylcobalamin are required to produce red blood cells.
How Is The Vitamin B12 For Supplements Produced?
While it is theoretically possible to extract enough vitamin B12 for a B12 supplement from B12-rich foods such as liver, the extraction process is complex and inefficient. If a supplement company claims their methyl B12 supplement comes from food, they are probably lying to you.
And the structure of vitamin B12 is so complex it is almost impossible to synthesize chemically.
For years most of the vitamin B12 (cobalamin) for supplements has been generated by growing certain B12-producing bacteria and related organisms in large vats and purifying the vitamin B12 they produce. However, these bacteria were inefficient at incorporating cobalt into the cobalamin they made resulting in an excess of cobalt in the growth medium. Since large amounts of cobalt can be toxic, the remaining liquid had to be treated as a hazardous material and disposed of properly.
Recently this problem has been solved by genetically engineering the bacteria so they are more efficient at utilizing cobalt. This is fast becoming the method of choice for making vitamin B12 for supplements.
In either case, the cobalamin is usually precipitated out of the growth medium as cyanocobalamin crystals and the crystals washed to remove impurities. Cyanocobalamin has been the primary source of vitamin B12 in supplements for the past 77 years (since 1948).
The methylcobalamin in most methyl B12 supplements is produced by reducing cyanocobalamin with sodium borohydride followed by the addition of methyl iodide or by directly adding methyl iodide to the bacterial cultures and using an alternate purification process.
The Methyl B12 Myths
Some supplement manufacturers are now claiming that methyl B12 (methylcobalamin) is more natural and more effective than the cyanocobalamin that has been used in supplements for the past 77 years. Let’s look at the myths propagated by methyl B12 supplement manufacturers and compare them to the facts.
Myth: Methyl B12 (methylcobalamin) is more natural than cyanocobalamin. We get the methyl B12 in our supplements from foods.
Fact: As I said above, it would be impossible to extract enough methylcobalamin from foods, so this claim is false.
Some of the methylcobalamin in supplements is chemically synthesized from cyanocobalamin. It can never be more natural than its starting ingredients.
However, in today’s world both cyanocobalamin and methylcobalamin are most likely to be made by chemically altering the cobalamin produced by genetically modified bacteria. In one case a cyano group is added. In the other case a methyl group is added.
Myth: Cyanocobalamin is toxic.
Fact: You get much more cyanide from common foods such as almonds, lima beans, any fruit with a pit such as peaches, and even some fruits with seeds, such as apples. For example, a single almond contains 200 times more cyanide than a supplement providing the RDA of cyanocobalamin.
Does that mean you need to avoid almonds and other cyanide-containing foods? The answer is no. God has designed our bodies to thrive on the natural foods He created for us. We have an enzyme called rhodanese in our mitochondria that can convert the small amounts of cyanide found naturally in foods to thiocyanate. And thiocyanate can be harmlessly excreted in the urine.
In short, we can eat almonds safely and we can take cyanocobalamin supplements safely. Our bodies are designed to handle them.
Myth: Because methylcobalamin is one of the active forms of B12 inside cells (adenosylcobalamin is the other), it is better utilized by cells than cyanocobalamin.
Fact: Cyanocobalamin and methylcobalamin are equally well absorbed by the intestine and equally well transported to our cells. At the cell membrane, the cyano and methyl groups are stripped off and cobalamin (B12) binds to a transport protein called transcobalamin II. Once inside the cell either a methyl group or adenosyl group is added back to cobalamin.
In short, methylcobalamin offers no advantage over cyanocobalamin because its methyl group is removed before it enters our cells. Once the methyl and cyano groups have been removed, the cell has no way of knowing whether B12 started out in the methyl or cyano form.
Myth: Methylcobalamin is better utilized than cyanocobalamin for people with methylation defects.
Fact: A methylation defect would only affect methylation of cobalamin once it is released from transcobalamin II inside the cell. Once again, because the methyl and cyano groups are removed before cobalamin binds to transcobalamin II, methylcobalamin offers no advantage over cyanocobalamin.
What Does This Mean For You?
The claims that everyone would benefit from methylcobalamin (methyl B12) instead of cyanocobalamin is outrageous. Anyone who takes the time to research how B12 enters our cells would realize that the claim is biochemically impossible.
In short, cyanocobalamin has been used for 77 years. There are hundreds of clinical studies showing it is safe and effective, even in individuals with a MTHFR deficiency. I can’t tell you whether the companies selling methyl B12 are ignorant of basic metabolism and the published studies refuting their claims or whether they are purposely trying to deceive the public—but neither is a good thing.
The Bottom Line
Some supplement manufacturers are now claiming that methyl B12 (methylcobalamin) is more natural and more effective than the cyanocobalamin that has been used in supplements for the past 77 years. In this issue of “Health Tips From the Professor” I debunk the methyl B12 myths used by the supplement manufacturers to sell their methyl B12 products.
I can’t tell you whether the companies selling methyl B12 are ignorant of basic metabolism and the published studies refuting their claims or whether they are purposely trying to deceive the public—but neither is a good thing.
For more specifics, 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years.
Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”.
Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
It seems like every time you turn around there are new headlines warning us that a particular food or supplement increases your risk of cancer. If you believe all those headlines, there would be little you could eat. You might starve to death trying to avoid eating anything that increases your risk of cancer.
So, it’s important to ask which of those warnings are true and which are just myths.
For example, a few days ago, a friend called me and said, “I just heard that resveratrol is estrogenic and causes breast cancer. Should I read the labels of the herbal supplements I take and avoid anything with resveratrol in it.”
I assured her that this was just a myth. The likelihood that resveratrol and related polyphenols cause breast cancer is very low. And if she was concerned about breast cancer, there were much more important things to worry about.
But as I started to explain why it was a myth, I realized the explanation was complex. I was able to explain it to my friend in a 20-minute discussion. But it was then I realized I needed to write a “Health Tips From the Professor” article to help explain it to the general public.
Why Are We Concerned?
You might be asking, “Why is this such a big deal? Why do we care if something has estrogenic properties?” Let me start at the beginning.
When I first started teaching medical students in 1972, hormone replacement therapy (a combination of estrogen and progesterone) was thought to be a safe and effective treatment for menopausal symptoms and post-menopausal bone loss, and it was very widely prescribed.
That practice came to a screeching halt in 2002 when the Woman’s Health Initiative study showed that it increased the risk of breast, endometrial, and ovarian cancer. Today,
The hormone composition of hormone replacement therapy has been changed.
It is only prescribed for severe menopausal symptoms. And drugs are the treatment of choice to reduce post-menopausal bone loss.
It is prescribed for the shortest possible time to limit exposure.
These simple changes in hormone replacement therapy represent the single most important intervention for reducing breast cancer risk in the past 50 years. Yes, you heard that right. These changes were more effective than any other medication or preventative strategy for reducing the number of women developing and dying from breast cancer.
This lesson made a big impression on the medical community. So, it is easy to understand why anything resembling estrogen is immediately suspected of increasing the risk of breast cancer. But the reality is far more complicated. So, it’s time for another of my “Biochemistry 101” segments.
Biochemistry 101: What Does Estrogenic Mean?
Let’s start at the beginning with what polyphenols are. They comprise a diverse group of compounds with these common features.
If you look at their structures, they contain multiple rings (A chemist would tell you they have more than one phenol group, hence the term polyphenol. But that terminology is only useful if you are a chemist).
They are found in plants. Specifically, they are found in fruits, vegetables, herbs, spices and beverages (coffee, tea, and cocoa, for example).
They have antioxidant properties.
Types of polyphenols include flavonoids, phenolic acids, lignans, and stilbenes. I mention this only because soy isoflavones, which I will talk about later, are flavonoids.
Some of these compounds have structures that resemble estrogen. If they bind to estrogen receptors and have the same effect as estrogen in cultured human cells, they are said to have “estrogenic properties”.
That’s why you see blogs warning about foods and herbal ingredients we should avoid because of their “estrogenic” properties. Some of these blogs are written by people with “Dr” on front of their name. But they aren’t biochemists and don’t know what biochemists know.
Let’s dig a little deeper. Here are some of the complexities that most bloggers either don’t know about or ignore.
There is more than one kind of estrogen receptor.
Different estrogen receptors have different effects in the cell. For example, some estrogen receptors activate pathways that increase cancer risk. Other receptors activate pathways that decrease cancer risk.
The same estrogen receptor can have different effects in different cell types. That’s why estrogen replacement therapy reduced menopausal symptoms and post-menopausal bone loss AND increased cancer risk in other tissues.
The Estrogenic Myth
A couple of weeks ago I talked about “The Soy Myth”, specifically the myth that soy isoflavones increase breast cancer risk. Of course, that myth was based on the observation that soy isoflavones have estrogenic properties and a simplistic interpretation of what that means. But in fact, soy isoflavones:
Are found naturally in most soy foods unless they are highly processed.
Bind strongly to the estrogen receptors that decrease cancer risk.
Bind weakly to the estrogen receptors that increase breast cancer risk.
In contrast, estrogen:
Binds strongly to the estrogen receptors that increase breast cancer risk.
Binds weakly to the estrogen receptors that decrease breast cancer risk.
Soy isoflavones compete with estrogen for binding to the receptors that increase breast cancer risks. This helps protect breast cells from the cancer-promoting effects of estrogen.
So, it is true that soy isoflavones bind to estrogen receptors, but on the balance, you would predict that soy isoflavones decrease, rather than increase breast cancer risk.
The key word here is “predict” breast cancer risk. If you are a woman, you don’t want a prediction, you want to know one way or the other.
That’s why multiple human clinical studies have been conducted to determine the effect of soy foods on breast cancer risk. As I told you two weeks ago:
Some studies showed no effect of soy consumption on the risk of getting breast cancer or breast cancer recurrence if you have previously had breast cancer.
Other studies found that soy consumption reduced the risk of breast cancer occurrence and recurrence.
No studies found that soy consumption increased the risk of breast cancer occurrence or recurrence.
So, for soy the answers are clear.
Yes, soy isoflavones have estrogenic properties.
No, soy consumption is not associated with an increased risk of breast cancer. That is a myth.
The situation with resveratrol is similar:
It is found naturally in grapes and many other fruits.
It has estrogenic properties.
Cell culture experiments show that it activates pathways that reduce cancer risk.
Animal studies predominantly show that it reduces cancer risk. The only exceptions are a few animal studies with very high doses of resveratrol.
The few clinical studies that have been done show that it either has no effect on breast cancer risk or reduces cancer risk.
No human clinical trials have shown that resveratrol increases cancer risk.
The take home lesson is clear. Knowing that a food or herbal ingredient has estrogenic properties is meaningless unless you have data from human clinical trials on cancer outcomes.
So, the next time you see headlines telling you that you should avoid a food or herbal ingredient because it has “estrogenic properties” treat them skeptically. Unless the claim is backed up by human clinical trials showing an increased cancer risk, the claim is probably a myth.
What Does Increase Breast Cancer Risk?
The take home lesson is clear. If you are concerned about your risk of breast cancer or any other form of cancer you should ignore the social media posts, podcasts, and blogs about the cancer risks of estrogenic foods and herbal ingredients.
Unless they are backed by human clinical trials showing they increase cancer risks, the claims are likely to be mythical rather than real.
If they have any effect on cancer risk, it is likely to be small. Instead, focus on the important risk factors.
According to the American Cancer Society, the top 5 risk factor for breast cancer, and most other cancers, are:
#1: Overweight and obesity. The American Cancer Society recommends that you get and stay at a healthy weight.
Let me put this in perspective for you. Even if things like soy and resveratrol increased your risk of breast cancer, their effect is very small compared to estrogen and you are only exposed to them briefly once or twice a day.
In contrast, fat cells produce estrogen, and if you are overweight, fat cells accumulate in your breasts. Those fat cells are bathing your breast cells in a bath of pure estrogen 24/7.
#2: Inactivity. The American Cancer Society recommends that adults get at least 150 to 300 minutes of moderate intensity or 75 to 150 minutes of vigorous intensity activity each week (or a combination of these), preferably spread throughout the week.
#3: Alcohol use. The American Cancer Society says it is best not to drink alcohol at all. For women who do drink, they should have no more than 1 alcoholic drink a day.
#4: Hormone use after menopause. The American Cancer Society recommends talking to your health care provider about non-hormonal options to treat menopausal symptoms.
#5: Poor diet. The American Cancer Society recommends a diet low in fat, processed and red meat, and sugary drinks, but high in fruits and vegetables.
The Bottom Line
It seems like every day you hear about another food or supplement you should avoid because it has “estrogenic properties” and is likely to cause cancer. I call this the estrogenic myth because those claims are generally mythological rather than factual. In this article:
I discuss why these claims are myths rather than facts using soy isoflavones and resveratrol as examples.
Tell you what the American Cancer Society tells you to focus on if you want to decrease your risk of breast cancer and other cancers.
For more details on these studies and what they mean for you, 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years. Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading Biochemistry textbooks for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
Earth Day is today. So, it is time for my annual reminder that what you eat affects a lot more than just your health. It affects the health of our planet. Once again, it’s time to ask yourself, “Is my diet destroying the planet?
This is not a new question, but a recent commission of international scientists has conducted a comprehensive study into our diet and its effect on our health and our environment. Their report (W. Willet et al, The Lancet, 393, issue 10170, 447-492, 2019) serves as a dire warning of what will happen if we don’t change our ways.
The commission carefully evaluated diet and food production methods and asked three questions:
Are they good for us?
Are they good for the planet?
Are they sustainable? Will they be able to meet the needs of the projected population of 10 billion people in 2050 without degrading our environment.
The commission described the typical American diet as a “lose-lose-lose diet”. It is bad for our health. It is bad for the planet. And it is not sustainable.
In its place they carefully designed their version of a primarily plant-based diet they called a “win-win-win diet”. It is good for our health. It is good for the planet. And it is sustainable.
In their publication they refer to their diet as the “universal healthy reference diet” (What else would you expect from a committee?). However, it has become popularly known as the “Planetary Diet”.
I have spoken before about the importance of a primarily plant-based diet for our health. In that context it is a personal choice. It is optional.
However, this report is a wake-up call. It puts a primarily plant-based diet in an entirely different context. It is essential for the survival of our planet. It is no longer optional.
If you care about our environment…If you care about saving our planet, there is no other choice.
How Was The Study Done?
The publication (W. Willet et al, The Lancet, 393, issue 10170, 447-492, 2019) was the report of the EAT-Lancet Commission on Healthy Diets from Sustainable Food Systems. This Commission convened 30 of the top experts from across the globe to prepare a science-based evaluation of the effect of diet on both health and sustainable food production through the year 2050.
The Commission included world class experts on healthy diets, agricultural methods, climate change, and earth sciences. The Commission reviewed 356 published studies in preparing their report.
Can Diet Affect The Health Of Our Planet?
When they looked at the effect of food production on the environment, the Commission concluded:
“Strong evidence indicates that food production is among the largest drivers of global environmental change.” Specifically, the commission reported:
Agriculture occupies 40% of global land (58% of that is for pasture use).
Food production is responsible for 30% of global greenhouse gas emissions and 70% of freshwater use.
Conversion of natural ecosystems to croplands and pastures is the largest factor causing species to be threatened with extinction. Specifically, 80% of extinction threats to mammals and bird species are due to agricultural practices.
Overuse and misuse of nitrogen and phosphorous in fertilizers causes eutrophication. In case you are wondering, eutrophication is defined as the process by which a body of water becomes enriched in dissolved nutrients (such as phosphates from commercial fertilizer) that stimulate the growth of algae and other aquatic plant life, usually resulting in the depletion of dissolved oxygen. This creates dead zones in lakes and coastal regions where fish and other marine organisms cannot survive.
About 60% of world fish stocks are fully fished and more than 30% are overfished. Because of this, catch by global marine fisheries has been declining since 1996.
“Reaching the Paris Agreement of limiting global warming…is not possible by only decarbonizing the global energy systems. Transformation to healthy diets from sustainable food systems is essential to achieving the Paris Agreement.”
The world’s population is expected to increase to 10 billion by 2050. The current system of food production is unsustainable.
When they looked at the effect of the foods we eat on the environment, the Commission concluded:
Beef and lamb are the biggest contributors to greenhouse gas emissions and land use.
The concern about land use is obvious because of the large amount of pastureland required to raise cattle and sheep.
The concern about greenhouse gas emissions is because cattle and sheep are ruminants. They not only breathe out CO2, but they also release methane into the atmosphere from fermentation in their rumens of the food they eat. Methane is a potent greenhouse gas, and it persists in the atmosphere 25 times longer than CO2.
The single most important thing we can do as individuals to reduce greenhouse gas emissions is to eat less beef and lamb. [Note: grass fed cattle produce more greenhouse gas emissions than cattle raised on corn because they require 3 years to bring to market rather than 2 years.]
In contrast, plant crops reduce greenhouse gas emissions by removing CO2 from the atmosphere.
In terms of energy use beef, lamb, pork, chicken, dairy, and eggs all require much more energy to produce than any of the plant foods.
In terms of eutrophication of our lakes and oceans, beef, lamb, and pork all cause much more eutrophication than any plant food. Dairy and eggs cause more eutrophication than any plant food except fruits.
Eating For A Healthy Planet
In the words of the Commission: “[The Planetary Diet] largely consists of vegetables, fruits, whole grains, legumes, nuts, and unsaturated oils. It includes a low to moderate amount of seafood, poultry, and eggs. It includes no or a very low amount of red meat, processed meat, sugar, refined grains, and starchy vegetables.”
When described in that fashion it sounds very much like other healthy diets such as semi-vegetarian, Mediterranean, DASH, and Flexitarian. However, what truly distinguishes it from the other diets is the restrictions placed on the non-plant portion of the diet to make it both environmentally friendly and sustainable. Here is a more detailed description of the diet:
It starts with a vegetarian diet. Vegetables, fruits, beans, nuts, soy foods, and whole grains are the foundation of the diet.
It allows the option of adding one serving of dairy a day (It turns out that cows produce much less greenhouse emissions per serving of dairy than per serving of beef. That’s because cows take several years to mature before they can be converted to meat, and they are emitting greenhouse gases the entire time).
It allows the option of adding one 3 oz serving of fish or poultry or one egg per day.
It allows the option of swapping seafood, poultry, or egg for a 3 oz serving of red meat no more than once a week. If you want a 12 oz steak, that would be no more than once a month.
This is obviously very different from the way most Americans currently eat. According to the Commission:
“This would require greater than 50% reduction in consumption of unhealthy foods, such as red meat and sugar, and greater than 100% increase in the consumption of healthy foods, such as nuts, fruits, vegetables, and legumes”.
“In addition to the benefits for the environment, “dietary changes from current diets to healthy diets are likely to substantially benefit human health, averting about 10.8-11.6 million deaths per year globally.”
What Else Did The Commission Recommend?
In addition to changes in our diets, the Commission also recommended several changes in the way food is produced. Here are a few of them.
1) Reduce greenhouse gas emissions from the fuel used to transport food to market.
2) Reduce food losses and waste by at least 50%.
3) Make radical improvements in the efficiency of fertilizer and water use. In terms of fertilizer, the change would be two-fold:
In developed countries, reduce fertilizer use and put in place systems to capture runoff and recycle the phosphorous.
In third world countries, make fertilizer more available so that crop yields can be increased, something the Commission refer to as eliminating the “yield gap” between third world and developed countries.
4) Stop the expansion of new agricultural land use into natural ecosystems and put in place policies aimed at restoring and re-foresting degraded land.
5) Manage the world’s oceans effectively to ensure that fish stocks are used responsibly and global aquaculture (fish farm) production is expanded sustainability.
What we can do: While most of these are government level policies, we can contribute to the first three by reducing personal food waste and purchasing organic produce locally whenever possible.
What Does This Mean For You?
If you are a vegan, you are probably asking why the Commission did not recommend a completely plant-based diet. The answer is that a vegan diet is perfect for the health of our planet. However, the Commission wanted to make a diet that was as consumer friendly as possible and still meet their goals of a healthy, environmentally friendly, and sustainable diet.
If you are eating a typical American diet or one of the fad diets that encourage meat consumption, you are probably wondering how you can ever make such drastic changes to your diet. The answer is “one step at a time”. If you have read the Forward to my books “Slaying The Food Myths” or “Slaying the Supplement Myths”, you know that my wife and I did not change our diet overnight. Our diet evolved to something very close to the Planetary Diet over a period of years.
The Commission also purposely designed the Planetary Diet so that you “never have to say never” to your favorite foods. Three ounces of red meat a week does not sound like much, but it allows you a juicy steak once a month.
Sometimes you just need to develop a new mindset. As I shared in my books, my father prided himself on grilling the perfect steak. I love steaks, but I decided to set a few parameters. I don’t waste my red meat calories on anything besides filet mignon at a fine restaurant. It must be a special occasion, and someone else must be buying. That limits it to 2-3 times a year. I still get to enjoy good steak, and I stay well within the parameters of the Planetary diet.
Develop your strategy for enjoying some of your favorite foods within the parameters of the Planetary Diet and have fun with it.
The Bottom Line
Is your diet destroying the planet? This is not a new question, but a recent commission of international scientists has conducted a comprehensive study into our diet and its effect on our health and our environment. Their report serves as a dire warning of what will happen to us and our planet if we don’t change our ways.
The Commission carefully evaluated diet and food production methods and asked three questions:
Are they good for us?
Are they good for the planet?
Are they sustainable? Will they be able to meet the needs of the projected population of 10 billion people in 2050 without degrading our environment.
The Commission described the typical American diet as a “lose-lose-lose diet”. It is bad for our health. It is bad for the planet. And it is not sustainable.
In its place they carefully designed their version of a primarily plant-based diet they called a “win-win-win diet”. It is good for our health. It is good for the planet. And, it is sustainable.
In their publication they refer to their diet as the “universal healthy reference diet” (What else would you expect from a committee?). However, it has become popularly known as the “Planetary Diet”.
The Planetary Diet is similar to other healthy diets such as semi-vegetarian, Mediterranean, DASH, and Flexitarian. However, what truly distinguishes it from the other diets is the restrictions placed on the non-plant portion of the diet to make it both environmentally friendly and sustainable (for details, read the article above).
I have spoken before about the importance of a primarily plant-based diet for our health. In that context it is a personal choice. It is optional.
However, this report is a wake-up call. It puts a primarily plant-based diet in an entirely different context. It is essential for the survival of our planet. It is no longer optional.
If you care about global warming…If you care about saving our planet, there is no other choice.
For more details 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years.
Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”.
Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
What is the truth about soy and breast cancer? Does it increase the risk of breast cancer, or is that just a myth? If you are a woman, particularly a woman with breast cancer, it is an important question.
Some experts say soy should be avoided at all costs. They say that soy will increase your risk of breast cancer. Other experts say soy is perfectly safe and may even reduce your risk of breast cancer. Who is right?
If you are a breast cancer survivor, the question of whether soy increases or decreases your risk of disease recurrence is even more crucial. You have already endured surgery, chemotherapy, and/or radiation. You never want to go through that again.
Why Is There So Much Confusion About Soy?
Soy isoflavones decrease estrogen production, strengthen the immune system, inhibit cell proliferation, and reduce the production of reactive oxygen species. These are all effects that might reduce breast cancer risk.
On the other hand, soy isoflavones also bind to estrogen receptors and exhibit weak estrogenic activity. This effect has the potential to increase breast cancer risk.
Cell culture and animal studies have only confused the issue. Soy isoflavones stimulate the growth of breast cancer cells in a petri dish. Soy isoflavones also stimulate breast cancer growth in a special strain of mice lacking an immune system. However, in studies in both mice and rats with a functioning immune system, soy isoflavones decrease breast cancer risk.
The confusion has been amplified by claims and counterclaims on the internet. There are bloggers who are more interested in the spectacular than they are in accuracy (Today we call this fake news). They have taken the very weak evidence that soy isoflavones could possibly increase breast cancer risk and have blown it all out of proportion.
Their blogs claim that soy definitely increases breast cancer risk and should be avoided at all costs. Their claims have been picked up by other web sites and blogs. Eventually, the claims have been repeated so many times that people started to believe them. A “myth” has been created. I call it a myth because it was never based on convincing scientific evidence.
In the meantime, scientists looked at the cell culture and animal studies and took a more responsible approach. They said “If this is true, it is an important public health issue. We need to do clinical trials in humans to test this hypothesis.”
What Have Previous Clinical Studies Shown?
The question of whether soy consumption increased the risk of developing breast cancer was settled a long time ago. Some studies have shown no effect of soy consumption on breast cancer risk. Others have reported that soy consumption decreased breast cancer risk. A meta-analysis of 18 previous clinical studies found that soy slightly decreased the risk of developing breast cancer (J Natl Cancer Inst, 98: 459-471, 2006). None of those studies found any evidence that soy increased the risk of breast cancer.
What about recurrence of breast cancer in women who are breast cancer survivors? There have been five major clinical studies looking at the effects of soy consumption on breast cancer recurrence in both Chinese and American populations. Once again, the studies have shown either no effect of soy on breast cancer recurrence or a protective effect. None of them have shown any detrimental effects of soy consumption for breast cancer survivors.
A meta-analysis of all 5 studies was published in 2013 (Chi et al, Asian Pac J Cancer Prev., 14: 2407-2412, 2013). This study combined the data from 11,206 breast cancer survivors in the US and China. Those with the highest soy consumption had a 23% decrease in recurrence and a 15% decrease in mortality from breast cancer.
What Did The Most Recent Study Show?
In earlier clinical studies the protective effect of soy has been greater in Asian populations than in North American populations. This could have been because Asians consume more soy. However, it could be due to other population differences as well.
To better evaluate the effect of soy consumption on breast cancer survivors in the North America, a group of investigators correlated soy consumption with all-cause mortality in breast cancer survivors in the US and Canada (Zhang et al, Cancer, DOI: 10.1002/cncr.30615, March 2017).
The data were collected from The Breast Cancer Family Registry, an international research infrastructure established in 1995. The women enrolled in this registry either have been recently diagnosed with breast cancer or have a family history of breast cancer.
This study included 6235 breast cancer survivors from the registry who lived in the San Francisco Bay area and the province of Ontario in Canada. The women represented an ethnically diverse population and had a median age of 51.8 at enrollment. Soy consumption was assessed either at the time of enrollment or immediately following breast cancer diagnosis. The women were followed for 9.4 years, during which time 1224 of them died.
The results were as follows:
There was a 21% decrease in all-cause mortality for women who had the highest soy consumption compared to those with the lowest soy consumption.
The protective effect of soy was strongest for those women who had receptor negative breast cancer. This is significant because receptor-negative breast cancer is associated with poorer survival rates than hormone receptor-positive cases.
The protective effect was also greatest (35% reduction in all-cause mortality) for women with the highest soy consumption following breast cancer diagnosis. This suggests that soy may play an important role in breast cancer survival.
The authors concluded “In this large, ethnically diverse cohort of women with breast cancer, higher dietary intake of [soy] was associated with reduced total mortality.”
In an accompanying editorial, Omer Kucuk, MD, of the Winship Cancer Institute of Emory University, noted that the United States is the number 1 soy producer in the world and is in a great position to initiate changes in health policy by encouraging soy intake. He said “We now have evidence that soy foods not only prevent breast cancer but also benefit women who have had breast cancer. Therefore, we can recommend women to consume soy foods because of soy’s many health benefits.”
The Soy Myth
Every clinical study has its limitations. If there were only one or two studies, the question of whether soy increases breast cancer risk might still be in doubt. However, multiple clinical studies have come to the same conclusion. Either soy has no effect on breast cancer risk and breast cancer recurrence, or it has a protective effect.
Not a single clinical study has found any evidence that soy increases breast cancer risk. It is clear that consumption of soy foods is safe, and may be beneficial, for women with breast cancer. The myth that soy increases breast cancer risk needs to be put to rest.
On the other hand, we should not think of soy as a miracle food. Breast cancer risk is also decreased by a diet that:
Contains lots of fruits and vegetables.
Is low in processed grains & sweets and high in whole grains.
Is low in saturated & trans fats and high in omega-3 and monounsaturated fats.
Is low in red & processed meats and high in beans, fish & chicken.
Furthermore, diet is just one component of a holistic approach for reducing the risk of breast cancer. In addition to a healthy diet, the American Cancer Society recommends that you:
1) It is time to put the myth that soy increases breast cancer risk to rest. This myth is based on cell culture and animal studies, and those studies were inconclusive.
2) Multiple clinical studies have shown that soy either has no effect on breast cancer risk, or that it reduces the risk.
3) Multiple clinical studies have also shown that soy either has no effect on breast cancer recurrence in women who are breast cancer survivors, or that it reduces recurrence.
4) The most recent clinical study is fully consistent with previous studies. It reports:
There was a 21% decrease in all-cause mortality for women who had the highest soy consumption compared to those with the lowest soy consumption.
The protective effect of soy was strongest for those women who had receptor negative breast cancer. This is significant because receptor-negative breast cancer is associated with poorer survival rates than hormone receptor-positive cases.
The protective effect was also greatest (35% reduction in all-cause mortality) for women with the highest soy consumption following breast cancer diagnosis. This suggests that soy may play an important role in breast cancer survival.
No clinical studies have provided any evidence to support the claim that soy increases either breast cancer risk or breast cancer recurrence.
For more information on this study and other things you can do to reduce the risk of breast cancer 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years. Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading Biochemistry textbooks for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
The low carb wars rage on. Low carb enthusiasts claim that low-carb diets are healthy. And they claim the lower you go, the healthier you will be. Let me start with some definitions:
The typical American diet is high carb. It gets about 55% of its calories from carbohydrates. [Note: The Mediterranean and DASH diets also get about 55% of their calories from carbohydrates. I’ll talk more about that later.]
Moderate carb diets get 26-46% of their calories from carbohydrates. Examples include the low carb Mediterranean diet and the Paleo, South Beach, and Zone diets.
Low carb diets get <26% of their calories from carbohydrates. The Atkins diet is the classic example of a low carb diet.
Very low carb diets get <10% of their calories from carbohydrates. Examples are the Keto and Carnivore diets.
And I don’t need to tell you that the Keto and Carnivore diets are receiving a lot of favorable press lately.
But some health experts warn that low carb and very low carb diets may be dangerous. Several studies have reported that low carb diets increase the risk of mortality (shorten lifespan).
As a consumer you are probably confused by the conflicting claims. Are low carb diets healthy, or is this another myth? In this issue of “Health Tips From the Professor” I am going to discuss two very large studies that came to opposite conclusions.
Both were what we call meta-analysis studies. Simply put, that means they combine the data from several smaller studies to obtain more statistically reliable data. But as Mark Twain said, “There are lies. There are damn lies. And then there are statistics.”
The first study, called the Prospective Urban Rural Epidemiology (PURE) study, was published a few years ago. It included data from 135,335 participants from 18 countries across 5 continents. That’s a very large study, and normally we expect very large studies to be accurate.
It showed a linear relationship between carbohydrate intake and mortality. Simply put, the more carbohydrate people consumed, the greater their risk of premature death. The results from the PURE study had low carb enthusiasts doing a victory lap and claiming it was time to rewrite nutritional guidelines to favor low carb diets.
Whenever controversies like this arise, reputable scientists are motivated to take another look at the question. They understand that all studies have their weaknesses and biases. So, they look at previous studies very carefully and try to design a study that eliminates the weaknesses and biases of those studies. Their goal is to design a stronger study that reconciles the differences between the previous studies.
And this study had two glaring weaknesses.
The percent carbohydrate intake ranged from 40% to 80%. It showed that a moderate carbohydrate intake might be healthier than a high carbohydrate intake, but it provided no information about low carb or very low carb diets.
The data was primarily from Asian countries. It was not clear whether it was relevant to the kind of diets consumed in North America and Europe.
This study was performed in two parts. This first part drew on data from the Atherosclerosis Risk in Communities (ARIC) study. That study enrolled 15,428 men and women, aged 45-64, from four US communities between 1987 and 1989. This group was followed for an average of 25 years, during which time 6283 people died.
Carbohydrate intake was calculated based on food frequency questionnaires administered when participants enrolled in the study and again 6 years later. The study evaluated the association between carbohydrate intake and mortality.
The second part was a meta-analysis that combined the data from the ARIC study with all major clinical studies since 2007 that measured carbohydrate intake and mortality and lasted 5 years or more. The total number of participants included in this meta-analysis was 432,179, and it included data from previous studies that claimed low carbohydrate intake was associated with decreased mortality.
The Low Carb Myth
The results from the ARIC study were:
The relationship between mortality and carbohydrate intake was a U-shaped curve.
The lowest risk of death was observed with a moderate carbohydrate intake (50-55%). This is the intake recommended by current nutrition guidelines.
The highest risk of death was observed with a low carbohydrate intake (<20%).
The risk of death also increased with very high carbohydrate intake (>70%).
When the investigators used the mortality data to estimate life expectancy, they predicted a 50-year-old participant would have a projected life expectancy of:
33.1 years if they had a moderate intake of carbohydrates.
4 years less if they had a very low carbohydrate intake.
1 year less if they had a very high carbohydrate intake.
The risk associated with low carbohydrate intake was affected by what the carbohydrate was replaced with.
When carbohydrates were replaced with animal protein and animal fat there was an increased risk of mortality on a low-carb diet.
The animal-based low-carb diet contained more beef, pork, lamb, chicken, and fish. It was also higher in saturated fat.
When carbohydrates were replaced with plant protein and plant fats, there was a decreased risk of mortality on a low-carb diet. The plant-based low-carb diet contained more nuts, peanut butter, dark or whole grain breads, chocolate, and white bread. It was also higher in polyunsaturated fats.
The effect of carbohydrate intake on mortality was virtually the same for all-cause mortality, cardiovascular mortality, and non-cardiovascular mortality.
There was no significant effect of carbohydrate intake on long-term weight gain (another myth busted).
The results from the dueling meta-analyses were actually very similar in some respects. When the data from all studies were combined:
Very high carbohydrate diets were associated with increased mortality.
The results were the same for total mortality, cardiovascular mortality, and non-cardiovascular mortality.
The authors concluded: “Our findings suggest a negative long-term association between life-expectancy and both low carbohydrate and high carbohydrate diets…These data also provide further evidence that animal-based low carbohydrate diets should be discouraged.
Alternatively, when restricting carbohydrate intake, replacement of carbohydrates with predominantly plant-based fats and proteins could be considered as a long-term approach to healthy aging.”
Simply put, that means if a low carb diet works best for you, it is healthier to replace the carbs with plant-based fats and protein rather than animal-based fats and protein.
The “Goldilocks Effect”
This study also resolved the discrepancies between previous studies. The authors pointed out that the PURE study relied heavily on data from Asian and developing countries, and the average carbohydrate intake is very different in Europe and the US than in Asian and developing countries.
In the US and Europe mean carbohydrate intake is about 50% of calories and it ranges from 25% to 70% of calories. With that range of carbohydrate intake, it is possible to observe the increase in mortality associated with both very low and very high carbohydrate intakes.
The US and European countries are affluent, which means that low carb enthusiasts can also afford diets high in animal protein.
In contrast, white rice is a staple in Asian countries, and protein is a garnish rather than a main course. Consequently, overall carbohydrate intake is greater in Asian countries and very few Asians eat a truly low carbohydrate diet.
High protein foods tend to be more expensive than high carbohydrate foods. Thus, very few people in developing countries can afford to follow a very low carbohydrate diet, and overall carbohydrate intake also tends to be higher in those countries.
Therefore, in Asian and developing countries the average carbohydrate intake is greater (~61%) than in the US and Europe (~50%), and the range of carbohydrate intake is from 45% to 80% of calories instead of 25% to 70%. With this range of intake, it is only possible to see the increase in mortality associated with very high carbohydrate intake.
In fact, when the authors of the current study overlaid the data from the PURE study with their ARIC data, there was an almost perfect fit. The only difference was that their ARIC data covered both low and high carbohydrate intake while the PURE study touted by low carb enthusiasts only covered moderate to high carbohydrate intake.
[I have given you my rendition of the graph on the right. If you would like to see the data yourself, look at the paper.]
Basically, low carb advocates are telling you that diets with carbohydrate intakes of 26% or less are healthy based on studies that did not include carbohydrate intakes below 40%. That is misleading. The studies they quote are incapable of detecting the risks of low carbohydrate diets.
In short, the ARIC study finally answered the question, “How much carbohydrate should we be eating if we desire a long and healthy life?” The answer is “Enough”.
I call this “The Goldilocks Effect”. You may remember “Goldilocks And The Three Bears”. One bed was too hard. One bed was too soft. But one bed was “just right”. One bowl of porridge was too hot. One was two cold. But one was “just right”.
According to this study, the same is true for carbohydrate intake. High carbohydrate intake is unhealthy. Low carbohydrate intake is unhealthy. But moderate carbohydrate intake is “just right”.
What Does This Study Mean For You?
There are several important take-home lessons from this study:
1) All major studies agree that very high carbohydrate intake is unhealthy. In part, that reflects the fact that diets with high carbohydrate intake are likely to be high in sodas and sugary junk foods. It may also reflect the fact that diets which are high in carbohydrates are often low in plant protein or healthy fats or both.
2) All studies that cover the full range of carbohydrate intake agree that low and very low carbohydrate diets are also unhealthy. They shorten the life expectancy of a 50-year-old by about 4 years.
3) The studies quoted by low carb enthusiasts to support their claim that low-carb diets are healthy don’t include carbohydrate intakes below 40%. That means their claims are misleading. The studies they quote are incapable of detecting the risks of low carbohydrate diets. Their claims are a myth.
4) Not all high carb diets are created equally. As I noted above, the Mediterranean and DASH diets are just as high in carbohydrates as the typical American diet, but their carbohydrates come from whole fruits and vegetables, whole grains, beans, nuts, and seeds. And multiple studies show that both diets are much healthier than the typical American diet.
5) Not all low carb diets are created equally. Meat-based low-carb diets decrease life expectancy compared to the typical American diets while plant-based low carb diets increase life expectancy.
6) The health risks of meat-based low-carb diets may be due to the saturated fat content or the heavy reliance on red meat. However, the risks are just as likely to be due to the foods these diets leave out – typically fruits, whole grains, legumes, and some vegetables.
7) Proponents of low-carb diets assume that you can make up for the missing nutrients by just taking multivitamins. However, each food group also provides a unique combination of phytonutrients and fibers. The fibers, in turn, influence your microbiome. Simply put, whenever you leave out whole food groups, you put your health at risk.
The Bottom Line
The low-carb wars are raging. Several studies have reported that low carb diets increase risk of mortality (shorten lifespan). However, a study published a few years ago came to the opposite conclusion. That study had low carb enthusiasts doing a victory lap and claiming it is time to rewrite nutritional guidelines to favor low-carb diets.
However, a study published a year later resolves the conflicting data and finally answers the question: “How much carbohydrate should we be eating if we desire a long and healthy life?” The answer is “Enough”.
I call this “The Goldilocks Effect”. According to this study, high carbohydrate intake is unhealthy. Low carbohydrate intake is unhealthy. But moderate carbohydrate intake is “just right”.
Specifically, this study reported:
Moderate carbohydrate intake (50-55%) is healthiest. This is the carbohydrate intake found in healthy diets like the Mediterranean and DASH diets, and is the intake recommended by current nutritional guidelines.
2) All major studies agree that very high carbohydrate intake (60-70%) is unhealthy. It shortens the life expectancy of a 50-year-old by about a year.
3) All studies that cover the full range of carbohydrate intake agree that low carbohydrate intake (<26%) is also unhealthy. It shortens the life expectancy of a 50-year-old by about 4 years.
4) The studies quoted by low carb enthusiasts to support their claim that low-carb diets are healthy don’t include carbohydrate intakes below 40%. That means their claims are misleading. The studies they quote are incapable of detecting the risks of low carbohydrate diets.
5) Meat-based low-carb diets decrease life expectancy compared to the typical American diet while plant-based low carb diets increase life expectancy. This is consistent with the results of previous studies.
The authors concluded: “Our findings suggest a negative long-term association between life-expectancy and both low carbohydrate and high carbohydrate diets…These data also provide further evidence that animal-based low carbohydrate diets should be discouraged.”
Simply put, the latest study means that the supposed benefits of low carb diets are a myth.
For more details, 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years. Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry textbooks for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
Over the past couple of weeks” I have talked about one of the greatest strengths of the scientific method – namely that investigators constantly challenge, and occasionally disprove, existing paradigms. That allows us to discard old models of how things work and replace them with better ones.
Two weeks ago, I shared a study that disproved the myth that low to moderate alcohol consumption is healthier than total abstinence.
Last week I shared a study that disproved the myth about chocolate helping you lose weight weight.
This week I tackle the “good” cholesterol myth. I will share several studies that challenge the belief that HDL cholesterol is good for your heart.
The belief that HDL is good for your heart has all the hallmarks of a classic paradigm.
It is supported by multiple clinical studies.
Elaborate metabolic explanations have been proposed to support the paradigm.
It is the official position of most medical societies, scientific organizations, and health information sites on the web.
It is the recommendation of most health professionals.
It has been repeated so often by so many trusted sources that everyone assumes it must be true.
Once we accept the HDL/heart health paradigm as true, we can construct other hypotheses on that foundation. For example:
Raising your HDL levels naturally takes effort. Pharmaceutical companies have been pursuing the “magic pill” that raises HDL levels without any effort on your part.
Low carb diets like the Keto and Paleo diets are high in saturated fat. The low carb enthusiasts claim this is a good thing because saturated fat raises HDL levels, and HDL is good for your heart.
But what if the paradigm that HDL is good for your heart isn’t true? What if it is a myth? These hypotheses would be like the parable of a house built on a foundation of sand. They will be washed away as soon as the paradigm is critically tested.
Do Drugs That Increase HDL Levels Work?
The first hint that the HDL/heart health paradigm might be faulty happened when a pharmaceutical company developed a drug that selectively increased HDL levels.
The drug company thought they had found the goose that laid golden eggs. Just imagine. People wouldn’t have to lose weight, exercise, or change their diet. They could simply take a pill and dramatically decrease their heart disease risk. A drug like that would be worth billions of dollars.
The pharmaceutical company couldn’t believe it. Raising HDL levels just had to reduce heart disease risk. They concluded they didn’t have the right drug, and they continued to work on developing new drugs.
That was 18 years ago, and no HDL-increasing drug has made it to market. Have they just not found the right drug, or does this mean the HDL/heart health paradigm is incorrect?
Does Saturated Fat Decrease Heart Disease Risk?
Now let’s turn to two claims of low carb enthusiasts.
#1: Saturated fats decrease your risk of heart disease in the context of a low carb diet. I have debunked that claim in several previous issues of “Health Tips From The Professor”. But let me refer you to two articles here – one on saturated fat and heart disease risk and one on low-carb diets.
#2: Saturated fats decrease heart disease risk because they raise HDL levels. This is the one I will address today.
The idea that saturated fats decrease heart disease risk because they raise HDL levels is based on a simplistic concept of HDL particles. The reality is more complex. Several clinical studies have shown:
The type of fat determines the property of the HDL particles.
When polyunsaturated fats predominate, the HDL particles have an anti-inflammatory effect. When saturated fats predominate, the HDL particles have a pro-inflammatory effect.
Anti-inflammatory HDL particles relax the endothelial cells lining our blood vessels. That makes the lining of our blood vessels more pliable, which improves blood flow and reduces blood pressure.
Anti-inflammatory HDL particles also help reduce inflammation of the endothelial lining. This is important because an inflamed endothelial lining is more likely to accumulate fatty plaques and to trigger blood clot formation that can lead to heart attacks and strokes.
So, the question becomes, “What good is it to raise HDL levels if you are producing an unhealthy, pro-inflammatory HDL particle that may increase the risk of high blood pressure, heart attacks, and strokes?”
In short, these studies suggest it isn’t enough to just focus on HDL levels. You need to ask what kind of HDL particles you are creating.
So, let’s look at experiments that have challenged the HDL/heart health paradigm.
Is HDL Good For Your Heart?
Once the studies were published showing that…
Drug-induced increase of HDL levels without any change in health habits is not sufficient to decrease heart attack risk, and…
Not all HDL particles are healthy. There are anti-inflammatory or pro-inflammatory HDL particles, which are likely to have opposite effects on heart attack risk…
…some people started to question the HDL/heart health paradigm. And one group came up with the perfect study to test the paradigm.
But before I describe the study, I need to review the term “confounding variables”. Here is a brief synopsis:
The studies supporting the HDL/heart health paradigm are association studies. Association studies measure the association between a single variable (in this case, increase in HDL levels) and an outcome (in this case, heart disease events, heart disease deaths, and total deaths).
Associations need to be corrected for other variables known to affect the same outcome (things like age, gender, smoking, and diabetes would be examples in this case).
Confounding variables are variables that also affect the outcome but are unknown or ignored. Thus, they are not used to correct the associations, which can bias the results.
The Good Cholesterol Myth
The authors of this study (M Briel et al, BMJ 2009:338.b92) observed that most interventions that increase HDL levels also lower LDL levels. Lowering LDL is known to decrease the risk of heart disease deaths. But this effect had been ignored in most studies looking at the association between HDL and heart disease deaths.
They hypothesized that the change in LDL levels was a confounding variable that had been ignored in previous studies and may have biased the results.
To test this hypothesis the authors searched the literature and identified 108 studies with 299,310 participants that:
Compared the effect of drugs, omega-3 fatty acids, or diet with either a placebo or usual care.
Measured both HDL and LDL levels.
Measured reduction in cardiovascular risk.
Had a randomized control design.
Lasted at least 6 months.
They found that every 10 mg/dl decrease in LDL levels in these studies was responsible for a:
1% reduction in heart disease events (both heart disease deaths and non-fatal heart attacks).
2% reduction in heart disease deaths.
4% reduction in total deaths.
After correcting for the effect of decreased LDL levels on these heart disease outcomes, the increase in HDL levels had no statistically significant effect on any of the outcomes.
The authors concluded, “Available data suggest that simply increasing the amount of circulating HDL cholesterol does not reduce the risk of coronary heart disease events, coronary heart disease deaths, or total deaths. The results support reduction in LDL cholesterol as the primary goal for lipid modifying interventions.”
In other words, this study:
Supports the author’s hypothesis that LDL levels were a confounding variable that biased the studies supporting the HDL/heart health paradigm.
Concludes that increasing HDL levels has no effect on heart disease outcomes, thus invalidating the HDL/heart health paradigm.
In short, this study destroyed the “good” cholesterol myth.
Is Everything You Knew About HDL Wrong?
Does that mean that everything you knew about HDL is wrong? Not exactly. It just means that you may need to change your perspective.
Don’t focus on HDL levels. Peek behind the curtain and focus on what’s behind the HDL levels. For example:
Losing weight when overweight increases HDL levels. But the decrease in heart disease outcomes is more likely due to weight loss than to the increase in HDL levels.
Exercise increases HDL levels. But the decrease in heart disease outcomes is more likely due to exercise than to the increase in HDL levels.
Reversing pre-diabetes or type 2 diabetes increases HDL levels. But the decrease in heart disease outcomes is more likely due to the reversal of diabetes than to the increase in HDL levels.
High-dose omega-3 fatty acids increase HDL levels. But the decrease in heart disease outcomes is more likely due to the omega-3 fatty acids than to the increase in HDL levels.
The Mediterranean diet increases HDL levels. But the decrease in heart disease outcomes is more likely due to the diet than to the increase in HDL levels.
And if you want to go the drug route:
Statins and some other heart drugs increase HDL levels, but the reduction in heart disease outcomes is probably due to their effect on LDL levels rather than their effect on HDL levels.
On the other hand:
Saturated fats increase HDL levels. But saturated fats increase heart disease risk and create pro-inflammatory HDL particles. So, in this case the increase in HDL levels is not a good omen for your heart.
Drugs have been discovered that selectively increase HDL levels. However, there is nothing of value behind this increase in HDL levels, so the drugs have no effect on heart disease outcomes.
The Bottom Line
In this article I discuss several studies that have challenged the good cholesterol myth – the belief that HDL is good for your heart.
For example, one group of investigators analyzed the studies underlying the HDL/heart health paradigm. They hypothesized that these studies were inaccurate because they failed to account for the effects of LDL levels on heart disease outcomes.
After correcting for the effect of decreased LDL levels on heart disease outcomes in the previous studies, the authors showed that increases in HDL levels had no significant effect on any heart disease outcome.
The authors concluded, “Available data suggest that simply increasing the amount of circulating HDL cholesterol does not reduce the risk of coronary heart disease events, coronary heart disease deaths, or total deaths. The results support reduction in LDL cholesterol as the primary goal for lipid modifying interventions.”
In other words, this study:
Supports the author’s hypothesis that LDL levels were a confounding variable that biased the studies supporting the HDL/heart health paradigm.
Concludes that increasing HDL levels has no effect on heart disease outcomes, thus invalidating the HDL/heart health paradigm.
Does that mean that everything you knew about HDL is wrong? Not exactly. It just means that you need to change your perspective. Don’t focus on HDL levels. Focus on what’s behind the HDL levels. For more information on that, read the article above.
For more information on this study, and what it means for you, 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years.
Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”.
Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
Sometimes you come across news that just seems too good to be true. The claims that you can lose weight just by eating chocolate are a perfect example. Your first reaction when you heard that was probably “Sure, when pigs fly!”
But it’s such an enticing idea – one might even say a deliciously enticing idea. And, in today’s world enticing ideas like this quickly gain a life of their own. Two popular books have been written on the subject.
Chocolate diet plans are springing up right and left. A quick scan of the internet even revealed a web site saying that by investing a mere $1,250 in a training course you could become a “Certified Chocolate Weight Loss Coach” earning $50,000/year.
If you like chocolate as much as most people you are probably wondering, “Could it possibly be true, or is it just another myth?
Can Chocolate Help You Lose Weight?
The idea that chocolate could help you lose weight does have some support. There are actually three published clinical studies suggesting that chocolate consumption is associated with lower weight (European Journal of Clinical Nutrition, 62: 247-253, 2008; Nutrition Research, 31: 122-130, 2011; Archives of Internal Medicine, 172: 519-521, 2012).
While that sounds impressive, they were all cross-sectional studies. That means they looked at a cross section of the population and compared chocolate intake with BMI (a measure of obesity). Cross sectional studies have a couple of very important limitations:
1) Cross sectional studies merely measure associations. They don’t prove cause and effect. Was it chocolate that caused the lower weight, or was it something else that those populations were doing? We don’t really know.
2) Cross sectional studies don’t tell us why an association occurs. In many ways, this is the old chicken and egg conundrum. Which comes first? In this case the question is whether the people in the studies became obese because they ate less chocolate – or did they eat less chocolate because they were obese and were trying to control their calories? Again, we have no way of knowing.
The Chocolate Myth
Chocolate is relatively rich in fat and high in calories. It’s not your typical diet food. On the surface, it seems implausible that eating chocolate could actually help you lose weight.
Scientists love to poke holes in implausible hypotheses, so it is no surprise that a recent study (JA Greenberg and B Buijsse, PLOS ONE, 8(8) e70271) has poked some huge holes in the “chocolate causes weight loss” hypothesis.
This study analyzed data from over 12,000 participants in the Atherosclerosis Risk in Community (ARIC) Study. This was also a cross-sectional study, but it was a prospective, cross-sectional study (That’s just a fancy scientific term which means that the study followed a cross section of the population over time, rather than just asking what that population group looked like at a single time point).
The authors of the study assessed frequency of chocolate intake and weight for each individual in the study at two separate times 6 years apart. The results were very interesting:
When they looked at a cross section of the population at either time point, their results were the same as the previous three studies – namely those who consumed the most chocolate weighed less. So, the cross-sectional data were consistent. Overweight people consumed less chocolate. But that still doesn’t tell us why they consumed less chocolate.
However, when they followed the individuals in the study over 6 years, those who consumed the most chocolate gained the most weight. The chocolate eaters were skinnier than the non-chocolate eaters at the beginning of the study, but they gained more weight as the study progressed. And the more chocolate they consumed the more weight they gained over the next 6 years. [No surprise here. Calories still count.]
When they specifically looked at the population who had developed an obesity-related illness between the first and second time point, they found that by the end of the study those participants had:
Decreased chocolate intake by 37%
Decreased fat intake by 4.5%
Increased fruit intake by 20%
Increased vegetable intake by 17%
In short, this study is more consistent with the “obesity causes reduced chocolate intake” model than the “reduced chocolate intake causes obesity” model. Simply put, if you are trying to lose weight, sweets like chocolate are probably among the first things to go.
Of course, even prospective cross-sectional studies have their limitations. Double blind, placebo-controlled studies are clearly needed to resolve this question. The only published study of this type has reported a slight weight gain associated with 25 g/day of dark chocolate, but the study was too small and too short in duration to draw firm conclusions.
In summary, more studies are needed, but the current evidence does not support the “miracle diet food” claims for chocolate. This appears to be another food myth. Pigs are flying!
The Bottom Line:
Pigs still haven’t learned how to fly. As enticing as it may sound, the weight of current evidence does not support the claims that chocolate is a miracle diet food or that eating chocolate every day is a sensible strategy for losing weight.
On the other hand, dark chocolate is probably one of the healthier dessert foods. There is no reason not to enjoy an occasional bite of chocolate as part of a healthy, calorie-controlled diet.
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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years. Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
You have probably heard that moderate alcohol consumption is healthier than complete abstinence from alcohol. It is certainly a popular viewpoint.
It is also a scientific paradigm. By that I mean:
It is supported by multiple clinical studies.
Elaborate metabolic explanations have been proposed to support this paradigm.
It is the official position of most medical societies, scientific organizations, and health information sites on the web.
It is the recommendation of most health professionals.
It has been repeated so often from so many trusted sources that everyone assumes it must be true.
But is it a myth? You may have been surprised when you saw recent headlines saying, “Having an alcoholic drink or two per day is not healthier than abstaining.”
But first, I want to explain to you how the scientific method works. That’s because this study is a perfect example of the scientific method in action.
How Were We Lead Astray?
I have described the scientific method in detail in my books “Slaying The Food Myths” and “Slaying The Supplement Myths”, which you will find here.
Today, I will just give you a brief synopsis of the scientific method.
1) Most scientific studies are designed to disprove existing scientific paradigms. This is such a study.
In the scientific world, there is no glory in being the 10th person to prove that a scientific paradigm is correct. The glory comes from being the first person to disprove a scientific paradigm and create a new paradigm in the process.
This constant testing of existing paradigms is one of the most important strengths of the scientific method.
2) There is no perfect study. Every study has its flaws.
“Confounding variables” are flaws that can be the Achilles Heel of any association study.
Now let me explain the significance of these statements in the context of the current study:
All the studies supporting the current paradigm were association studies. Association studies measure the association between a selected variable and an outcome. For these studies, the selected variable was alcohol consumption, and the outcome was increased mortality.
Association studies try to statistically correct for other variables known to affect the outcome. For example, diseases like heart disease, diabetes, and cancer increase the risk of premature death. These are known variables that would be corrected for in any well-designed study of alcohol consumption and mortality.
“Confounding variables” are unknown variables that also affect the outcome of the study. But since they are unknown, they are not corrected for.
Let me give you a simplistic example of a confounding variable. Let’s say you were doing a study of dietary habits, and you found an association between ice cream consumption and mortality. You might conclude that ice cream consumption is bad for you. It increases your risk of dying.
But then you might remember that ice cream consumption increases during the summer. And then you might reason that people swim more during the summer, and there is a correlation between swimming and drowning deaths.
Swimming could be a confounding variable. To make sure that your initial conclusion that ice cream increases the risk of dying was correct, you would need to correct your data for swimming deaths during the summer and see if you still found a correlation between ice cream consumption and mortality.
Could The Current Paradigm Be Incorrect?
You might be thinking, “What does this have to do with studies on the correlation between alcohol consumption and increased mortality?” Let me explain.
The baseline group for these comparisons was the abstainers – the group consuming no alcohol. Previous studies have compared the mortality risk associated with various amounts of alcohol consumption with the mortality risk of the abstainer group. This sounds like a reasonable approach.
But the investigators challenging the current paradigm noted that the “abstainer group” in previous studies included both lifetime abstainers and former drinkers who had become abstainers. They hypothesized that the “former drinkers” group may have become abstainers because of health issues related to excess alcohol consumption.
In short, they hypothesized that the “former drinkers” group was a confounding variable that biased the results of the previous studies. They hypothesized that the “lifetime abstainers” group was a more appropriate baseline group for this kind of study. They then set out to prove their hypothesis.
How Was This Study Done?
The investigators searched the literature and found 107 studies with 4.8 million participants published between 1980 and July 21, 2021, that:
Assessed the correlation between alcohol consumption and mortality.
Had data that allowed the investigators to separate lifetime abstainers from former drinkers who had become abstainers.
The investigators divided alcohol consumption into low, moderate, high, and very high categories based on the ounces of alcohol consumed per day. Since ounces of alcohol is not an easy measure for most of us, I have converted ounces/day to drinks/day based on the CDC definition of a drink (a 12-ounce beer, 5-ounce glass of wine, or 1.5 ounces of a distilled spirit like gin or vodka). And to make it even simpler, I have rounded to the nearest whole number. With that said, here are the classifications.
Low alcohol intake = 1-2 drinks/day.
Moderate alcohol intake = 2-3 drinks/day.
High alcohol intake = 3-4 drinks/day.
Very high alcohol intake = >4 drinks/day.
The risk of death associated with each of these intake levels was compared the risk of death of their preferred baseline group, the “lifetime abstainers”.
Finally, the data were corrected for other variables known to influence the correlation between alcohol consumption and mortality, namely age, sex, heart health, social status, race, diet, exercise, BMI, and smoking status. [These are known variables and had been adjusted for in most previous studies.]
The Alcohol Myth
When the investigators compared the mortality risk of former drinkers who had become abstainers with lifetime abstainers:
The former drinkers were 31% more likely to die, and this difference was highly significant.
This is consistent with their hypothesis that the “former drinkers” group was a confounding variable that may have biased the conclusions of previous studies.
When they compared the mortality risk of various levels of alcohol consumption with lifetime abstainers instead of all abstainers, they found:
The risk of mortality associated with low (1-2 drinks/day) and moderate (2-3 drinks/day) alcohol intake was statistically identical to the risk of mortality for lifetime abstainers.
The high alcohol intake group (3-4 drinks/day) was 24% more likely to die than the lifetime abstainers.
The very high alcohol intake group (>4 drinks/day) was 39% more likely to die than the lifetime abstainers.
In short, when lifetime abstainers were used as the baseline group, low to moderate alcohol intake did not reduce the risk of dying, as previous studies had suggested. This study suggests the idea that low to moderate alcohol consumption is good for us may not be accurate. It may be a myth.
Finally, there was a significant gender difference in the effect of alcohol consumption on mortality.
For women:
Even moderate alcohol consumption was associated with an increased risk of mortality. Only low alcohol consumption posed no increase in mortality.
The increased risk of mortality for women was significantly higher than for men with every level of alcohol consumption.
The authors concluded, “In this…meta-analysis, daily low or moderate alcohol intake was not significantly associated with all-cause mortality risk, while increased risk was evident at higher consumption levels, starting at lower levels for women than for men.”
Of course, this isn’t the end of the story. The scientific method will continue. Old paradigms don’t die easily. Other investigators will challenge the conclusions of this study. Stay tuned. I will give you updates as future studies are published.
What Does This Study Mean For You?
If you like to imbibe, there are two important takeaways from this study.
The bad news is that you can no longer claim that a drink or two a day is healthier than total abstinence from alcohol.
The good news is that this and every study preceding it have found that a drink or two a day is no less healthy than total abstinence. The studies found no increase in mortality associated with low to moderate alcohol intake.
[However, low to moderate alcohol intake may increase your risk of specific diseases. For example, many studies suggest that even low alcohol intake is associated with an increased risk of breast cancer.]
This study also agrees with previous studies that high alcohol intake increases your risk of death, and women are more susceptible to adverse effects of alcohol intake than men.
So, while this study challenges the existing paradigm that low to moderate alcohol intake is beneficial, it does not change the current recommendations on alcohol intake by most health organizations.
Adults of legal drinking age should limit alcohol intake to 2 drinks or less per day for men and one drink or less per day for women.
Adults who do not drink alcohol should not start. [The current study strengthens this recommendation because it takes away the excuse that low to moderate alcohol consumption is healthier than abstinence.]
Drinking less is better than drinking more.
The CDC guidelines also note that the risk of some cancers increases even at very low levels of alcohol consumption.
Finally, the CDC recommends that some people never consume alcohol, including:
Women who are pregnant or might become pregnant.
Anyone younger than 21.
Anyone with medical conditions or medications that interact with alcohol.
Anyone recovering from an alcohol use disorder or who has trouble controlling the amount they drink.
The Bottom Line
A recent study is a perfect example of the scientific method in action. Scientists are constantly challenging the existing scientific paradigms, and this is an important strength of the scientific method.
A group of scientists recently published a study challenging the paradigm that low to moderate alcohol intake is healthier than total abstinence from alcohol.
They hypothesized that previous studies supporting this paradigm had a common methodological flaw, corrected for the flaw, and reanalyzed the data from 104 studies with a total of 4.8 million participants.
The revised data showed no health benefit of low to moderate alcohol consumption compared to total abstinence. When you look at the data more closely, the current paradigm may be a myth.
This is a major change to the existing paradigm because it removes the justification for low to moderate alcohol consumption.
However, the revised data did not differ from previous studies in the following ways:
There is no health risk associated with low to moderate alcohol intake compared to total abstinence.
High alcohol intake (>3 drinks/day) is associated with increased mortality.
Women are more sensitive to the adverse effects of alcohol than men.
So, this study does not change current guidelines for alcohol consumption.
For more information on this study, what it means for you, and the CDC guidelines on alcohol consumption 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.
My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.
My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.
For more detail about FTC regulations for health claims, see this link.
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years. Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading Biochemistry textbooks for medical students.
Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.
For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.
On the first prenatal appointment, an extensive history is taken that includes family history, personal medical history, gynecological history, pregnancy history; sexual history, social history.
The findings of the study were as follows. Of the 125,430 participants:
The two family health conditions that had the most evidence of association with other conditions were family history of stroke and heart attack. 
The five main causes for pregnancy related death in the United States (defined as maternal death up until 12 months after giving birth) are:
Carolyn Curtis, MSN, CNM, RN, FACNM, FAAN, has:
Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years.
