Dr. Steve Chaney, Author at Health Tips From The Professor

Do Artificial Food Colors Cause ADHD?

June 17, 2025 by Dr. Steve Chaney

Is This Just The Tip Of The Iceberg?

Author: Dr. Stephen Chaney

Artificial colors are in the news again. And, unfortunately, what should solely be a health question has become political. Politics aside, most people fall into one of 3 camps:

Artificial colors are bad for us and should be removed from the food supply.

The fears about artificial colors are overblown.

What are artificial colors and why should I care?

Let me start with the third camp. Every nutrition expert worth their salt will tell you that whole, unprocessed foods are best for us. The problem is that they have a low profit margin.

The food industry makes most of their money from highly processed foods (50-60% profit from highly processed foods versus 8.5% for unprocessed foods).

And the market for highly processed foods is very competitive. Let me give you some metrics to help you understand just how competitive the market is:

In the average supermarket, unprocessed foods are located around the edge. The vast interior is mostly highly processed foods.

The most recent studies report that 60-70% of the foods Americans consume are highly processed.

With so much competition, the food industry needs to make their brand of processed foods stand out.

There are artificial preservatives to give processed foods long shelf life.

There are artificial flavors and flavor enhancers to make them taste yummy.

There are ingredients added to give them mouth appeal (how they feel in your mouth).

And finally, there are artificial colors (also known as synthetic food dyes) for eye appeal. Those are added to make them “pop” – to make them say “eat me”.

The seven most common food colors are Blue #1, Blue #2, Green #3, Red #3, Red #40, Yellow #5, and Yellow #6. They make processed foods look good.

But there are also health concerns associated with artificial food colors. The two most common are:

Cancer. Several studies have suggested that artificial food colors may increase the risk of cancer. However, because artificial food colors are added to foods of low nutritional value (candy, soft drinks, sugary cereals, etc.), it has been difficult to determine whether the increased cancer risk is due to the artificial colors or the foods they are found in.

ADHD. The studies are a bit stronger for this category. Because artificial colors can be hidden in chocolate cookies (when you mix all the colors together you get brown anyway), it has been possible to perform double-blind, placebo-controlled studies. And since both the food color and placebo groups are getting chocolate cookies, the only difference between the groups is whether the cookies contain artificial colors.

So, in today’s “Health Tips From the Professor” I will summarize what we know about artificial food colors and ADHD. But first, let’s start with a brief overview of ADHD

A Brief Overview Of ADHD

What is ADHD? ADHD is a broad term that encompasses two types of behaviors.

The AD portion of ADHD stands for attention deficit.

- Children with attention deficit have difficulty focusing and staying on task.

- This can affect their learning in standard classroom settings. I underlined standard classroom settings for a reason, which I will come back to later.

The H portion of ADHD stands for hyperactivity.

- Children with hyperactivity “bounce off walls” (I will define hyperactivity more precisely below.)

- This can lead to problems at home, in the classroom, and in relationships.

Some children have both. If you are their parents, I can only say, “Lucky you”.

The final D stands for disorder, implying that these conditions are not normal.

The ADHD epidemic.

ADHD has increased by 89% in the United States in just 25 years (1997-2022).

In 2022 11.5% of US children aged 3-17 were diagnosed with ADHD. That’s 7.1 million children.

Some experts claim that’s because of better diagnosis. Let’s examine that claim.

How is ADHD diagnosed?

The American Psychiatric Society diagnoses attention deficit based on 3 or more of the following criteria:

Has problems staying focused.
Doesn’t pay attention to details.
Doesn’t seem to listen.
Doesn’t follow instructions.
Has problems organizing tasks.
Avoids sustained mental effort.
Is easily distracted.

For those of you who are parents or grandparents, I would simply ask, “Does any of this sound familiar?”

The American Psychiatric Society diagnoses hyperactivity based on 3 or more of the following criteria:

Fidgets, taps hands, squirms in seat.
Not able to stay seated.
Runs around where it is inappropriate.
Unable to play quietly.
Always “on the go”.
Talks too much.
Has difficulty waiting for their turn.
Interrupts or intrudes on others.

Again, for those of you who are parents or grandparents, I would simply ask, “Does any of this sound familiar?”

Even worse, the final diagnosis is based primarily on the subjective reporting of symptoms by teachers and parents. The psychiatric evaluation is done primarily to eliminate other mental or physical diseases as causes of the symptoms.

Is ADHD Overdiagnosed?

So. perhaps we should ask whether teachers and parents might be tempted to overestimate the severity of the symptoms.

For teachers,

Class sizes are large, and there aren’t enough teacher’s aides.

They don’t have the time to deal with a child that requires extra attention.

It is easier to request an ADHD assessment, so that child can be put on drugs.

But there are other options. There are schools in which children with ADHD thrive, and many public schools have programs set up for ADHD children.

For parents,

Parents don’t have the time they used to have.

In most cases, both parents are working.

Some are working from home. In theory that could give them flexibility to take care of their children. But remote work often involves online meetings and strict deadlines that leave little time for their children.

And then there is social media. In today’s world, many parents are glued to their phones 24/7.

It’s easier to request a hyperactivity assessment, so that child can be put on drugs.

Could the increase in ADHD diagnoses be real?

Most experts agree that the causes of ADHD are complex, with the top 4 causes being genetics, diet, family & social environment, and physical environment (environmental pollutants).

The simplest way to think about it is that genetics cocks the gun and one or more of the other causes pulls the trigger.

With that in mind, we need to ask ourselves, “Has diet, family and social environment, or our physical environment gotten worse over the past 25 years?” The answer is a clear yes for all three.

So, while part of the increase in ADHD could be due to overdiagnosis, part of it is likely to be real.

Why is the increase in ADHD diagnoses a concern?

The answer is simple. The use of ADHD drugs has increased by 58% since 2012. Today over 50% of children diagnosed with ADHD are put on drugs. That’s a concern because:

Most of these drugs are stimulants.

Many are amphetamines.

They have serious side effects. For example:

Loss of appetite and weight loss.

Difficulty sleeping.

Upset stomach and nausea.

Feeling irritable, depressed, anxious, or tense.

- Many children don’t like how the drugs make them feel.

They can be gateway drugs.

They lose effectiveness over time. So, unless you have figured out the cause of the problem, the symptoms will return.

Because of this many parents are searching for natural solutions. One approach is to change their child’s diet. In today’s “Health Tips From the Professor” I will discuss the effect of one dietary change – the removal of artificial food colors from the diet.

Do Artificial Food Colors Cause ADHD?

The idea that food additives – specifically artificial colors and preservatives – might be responsible for hyperactivity was first raised by Dr. Ben Feingold 50 years ago. He devised the Feingold Diet – a diet that was free of artificial food colors and preservatives.

Some small-scale clinical studies suggested that the diet might be successful, and millions of parents used the diet for their hyperactive children with great success.

But the medical authorities pooh-poohed the Feingold Diet. They pointed out that when parents are putting their child on a special diet, they are also giving that child more attention – and it might be the parent’s increased attention that decreased the child’s hyperactive behavior.

They also pointed out that when you eliminate food additives from the diet you are decreasing the “junk” food and increasing fresh fruits and vegetables – in short, the child’s diet is much healthier.

They did a double-blind, placebo-controlled study and reported only 5% of the children with an ADHD diagnosis benefited from removing artificial food colors and preservatives from the diet. They considered 5% to be an artifact – just random noise in the statistical analysis of the data. Headlines proclaimed, “The Feingold Diet doesn’t work.”

So eventually the Feingold Diet lost popularity – but the idea that artificial food colors & preservatives might trigger hyperactivity has refused to go away.

The first inkling that the Feingold hypothesis might hold some water came from studies looking at the 5% of children whose ADHD symptoms improved when artificial colors were removed. When these children were evaluated in a second double-blind, placebo-controlled study, over 85% of them showed improvement in symptoms when artificial food colors were removed from their diet.

In short, this told us that artificial food colors and preservatives do cause ADHD symptoms in some children. The percentage of children is small, but these children are true responders.

This has led to further studies designed to provide a better estimate of the percentage of children whose ADHD symptoms are triggered by artificial food colors.

In 2004 a meta-analysis of 15 double-blind, placebo-controlled studies (DW Schah et al, Journal of Developmental & Behavioral Pediatrics, 25: 423-434, 2004) estimated that 11-28% of children with ADHD benefited from removal of artificial colors from their diet.

A more recent meta-analysis (IT Nigg et al, Journal of the American Academy of Child and Adolescent Psychiatry, 51: 86-97, 2012) estimated that 8% of ADHD children benefited from removal of artificial food colors from their diet.

And a pilot study published three years ago (AE Kirkland et al, Nutritional Neuroscience, 25: 159-168, 2022) suggests the effect of artificial food colors on ADHD symptoms may not be limited to children. They found a similar effect of artificial food colors on college students with ADHD.

In summary, the current evidence suggests:

Artificial food colors (and other artificial ingredients) can trigger ADHD symptoms in both children and adults.

The percentage of children and adults with ADHD who will benefit from removing artificial food colors from their diet is small (5-28%) but reproducible.

If you or your child happen to be sensitive to artificial food colors, relief from ADHD symptoms could be as simple as eliminating artificial food colors from their diet.

Is This Just The Tip Of The Iceberg?

Earlier in this article I used the analogy that genetic predisposition to ADHD cocked the gun, but it was diet, family & social environment, and/or physical environment that pulled the trigger.

Then I summarized the evidence that artificial colors are one dietary component that “pulls the trigger” (causes ADHD) in sensitive individuals. But that leads to two questions:

Is that all there is, or is that just the “tip of the iceberg”?

Have there been changes in our diet that might explain the rapid increase in ADHD cases?

Let’s examine the data:

In the 1970s when Dr. Feingold introduced his diet food additives were used sparingly.

- Today over 50% of the foods in the American diet contain more than 3 food additives.

In the 1970s there were a few thousand food additives in the American food supply.

- Today there are more than 10,000 additives, and less than 5% of them have been tested for their effects on brain development in children.

In the 1970s 10-15% of foods in the American diet were ultra-processed.

- Today 60-70% of the foods Americans eat are ultra-processed.

In short, in 1975 Dr. Feingold showed that artificial food colors and a handful of other additives triggered ADHD symptoms in a small percentage of children. Today our children’s diets are far worse, and they are exposed to thousands of untested food additives that did not exist in the 1970s.

Is this a coincidence or is this deterioration in diet and explosion of food additives driving the ADHD epidemic. Nobody knows.

But Pediatrics Professor Dr. Herbert Needleman has been quoted as saying, “We are conducting a vast toxicologic experiment in our society, in which our children and our children’s children are the experimental subjects.”

What Does This Mean For You?

If you are the parent or grandparent of a child with ADHD, the simplest thing you can do is to remove foods with artificial colors and preservatives from their diet whenever possible. If the child is sensitive to food colors, that one simple change may reduce their symptoms dramatically.

But, as I said above, artificial food colors and preservatives may just be the tip of the iceberg. My recommendation is to switch to a whole, unprocessed food diet for the entire family. Everyone in the family will be healthier, and you will have an even better chance of reducing your child’s ADHD symptoms.

And if you are looking for more ideas on natural approaches for children with ADHD, you may want to read a “Health Tips From the Professor” article I wrote several years ago based on a much longer publication by a pair of pediatricians who specialized in ADHD treatment.

They used ADHD medications as front-line treatment but researched natural approaches for those children who experienced unacceptable side effects from the drugs or for parents seeking a natural, drug-free approach. Their article was the result of 20+ years of testing various natural approaches with their ADHD patients. They found what worked and what didn’t work.

The bad news is that every child was different. There was no silver bullet. There was no single natural approach that worked for every child.

The good news was that at least one of the natural approaches in their arsenal worked for most of the children. It just required some time to find which approach(es) worked best for each child.

If you are searching for natural approaches to help your child or grandchild reduce their ADHD symptoms, this article is a great place to start.

The Bottom Line

ADHD cases are skyrocketing. Drugs work, but they have serious side effects. If you are the parent or grandparent of a child with ADHD, you may be searching for natural approaches to help that child control their ADHD symptoms. In this article, I discuss:

The causes of ADHD and how it is diagnosed.

Whether the rapid increase in ADHD cases is caused by overdiagnosis or the deterioration of our children’s diets.

The evidence that artificial food colors and preservatives trigger ADHD symptoms in sensitive children.

Other natural approaches that may reduce ADHD symptoms.

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.

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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.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

______________________________________________________________________

About The Author

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 D Just Got More Complicated

June 10, 2025 by Dr. Steve Chaney

The Hidden Flaws Of Vitamin D Studies

Author: Dr. Stephen Chaney

If I can paraphrase a famous saying, the question is, “To D or not to D.” On the one hand, you are told that vitamin D is a miracle supplement. It cures all your ailments. On the other hand, you are told that vitamin D supplements are worthless. They are a waste of money.

The problem is that vitamin D studies are all over the map. Some have shown beneficial effects of vitamin D supplementation. Others have come up empty. That allows “experts” to cherry pick the studies that support their bias. No wonder you are so confused.

If you have read my books or previous issues of “Health Tips From the Professor”, you know there is no such thing as a perfect clinical study. They all have their flaws. Sometimes the flaws are obvious. But sometimes we never know the flaws. We just know those studies are outliers.

So, let’s delve a little deeper into vitamin D metabolism and the hidden flaws that may have prevented some studies from showing the benefits of vitamin D supplementation. Then we will look at new data suggesting that vitamin D supplementation is more complicated than anyone imagined.

A Vitamin D Primer

Let’s start with a brief review of vitamin D metabolism.

Vitamin D metabolism starts in the skin when 7-dehydrocholesterol (a metabolite of cholesterol) is converted to cholecalciferol (vitamin D3) in a reaction requiring sunlight.

- In this sense, vitamin D3 is a hormone produced by the body. It only became an essential nutrient (vitamin) when Homo sapiens migrated to Northern latitudes and started to spend most of their time indoors.

Vitamin D then travels to the liver where it is converted to 25-hydroxyvitamin D. This is the most abundant form of vitamin D in the blood.

25-hydroxyvitamin D next travels to the kidney where it is converted to 1,25-dihydroxyvitamin D. This is the active form of vitamin D. It is the form that binds to the vitamin D receptor.

Vitamin D was first discovered as an essential nutrient that was needed for adequate bone mineralization. It prevented rickets in children and osteomalacia in adults.

The role of vitamin D in building strong bones is well established.

However, a few decades ago, it was discovered that vitamin D receptors were found in many other tissues including skin, immune system, heart, muscle, brain and nerves, and fat cells. This revolutionized our understanding of vitamin D’s role in the body.

This led to suggestions that vitamin D played a role in immunity and autoimmune diseases, brain function and mood, heart health, muscle and fat metabolism, and much more. Here is where it started to get confusing.

- Some studies showed positive results. They found that vitamin D played an important role in each of these areas, and that vitamin D supplementation was beneficial

- Other studies showed negative results. They found no benefit of vitamin D supplementation.

So, the question arose, “Were the negative studies flawed?” In some cases, the answer was a clear, “Yes”. The flaws were easy to identify. In other cases, no obvious flaw could be discovered.

However, that has changed dramatically in recent years when some “hidden flaws” were discovered that invalidated many of the negative studies. That’s the topic of my next section.

The Hidden Flaws Of Vitamin D Studies

Most previous studies simply measured vitamin D intake:

In dietary studies, vitamin D intake was measured using diet questionnaires.

In supplement studies, vitamin D intake was measured by tracking whether the participants took all the supplement pills they were provided.

It was assumed that a certain dose of vitamin D produced the same blood levels of 1,25-dihydroxyvitamin D in everyone.

Now we know that assumption was flawed. The absorption and conversion of vitamin D to 1,25-dihydroxyvitamin D varies widely from individual to individual.

That means that every vitamin D study that relied on vitamin D intake without measuring its effect on blood 1,25-dihydroxyvitamin D levels is flawed. Their conclusions may or may not be true. Their evidence is unreliable.

I’m willing to give the authors of these studies some grace. They didn’t purposely design a flawed study. At the time they designed their studies we didn’t know about individual variability in the conversion of vitamin D to 1,25-dihydroxyvitamin D.

However, there is another “hidden flaw” I’m less willing to excuse. There have been some recent papers that measured 1,25-dihydroxyvitamin D levels before and after supplementation and have concluded that vitamin D supplementation had no benefit.

However, they failed to mention that the group they were studying already had adequate 1,25-dihydroxyvitamin D levels in their blood prior to supplementation. Under those circumstances there is no reason to expect that vitamin D supplementation will have any significant benefit.

This is an obvious flaw. But I call it a “hidden flaw” because the authors hid it. They didn’t mention it in their abstract or conclusion.

That’s dishonest. Most people just read the abstract and conclusions, and that is the information that is shared in the media. Very few people read the study to see if the abstract and conclusions are accurate.

As if this weren’t complicated enough, our understanding of the effects of vitamin D just got a lot more complicated.

Vitamin D Just Got More Complicated

Two recent reports indicate that predicting who will benefit from vitamin D supplementation may be even more complicated than we thought.

Report #1 suggests that there is significant individual variability in how people respond to blood levels of 1,25-dihydroxyvitamin D. If true, this adds another level of complexity to studies of vitamin D supplementation.

Not only do the studies need to measure the 1,24-dihydroxyvitamin D levels before and after supplementation for everyone in the study.

But they would also need to measure the individual response to 1,25-dihydroxyvitamin D.

This report (C Carlberg and A Haq, Journal of Steroid Biochemistry & Molecular Biology, 175: 12-17, 2018) summarized the results of two clinical studies and used that information to develop what they called the, “Personal Vitamin D Response Index”.

The first study supplemented elderly men (average age = 71) for 5 months during the Finnish winter (when blood 1,25-dihydroxyvitamin D levels are lowest) with 0, 1600 IU, or 3200 IU per day.

The second study supplemented young (average age = 35) men and women with a single high dose of vitamin D (80,000 IU) and followed them for 30 days.

At the beginning and end of each study:

Blood levels of 1,25-dihydroxyvitamim D were measured.

The activity of 24 vitamin D-responsive genes was measured. (These are genes whose activity is controlled by a vitamin D receptor and whose activity was known to respond to vitamin D.)

In addition, more than 100 clinical and biochemical parameters that might be affected by vitamin D levels were measured. Of these, 12 were found to respond to vitamin D supplementation.

The authors of this report combined all 36 vitamin D-responsive biomarkers (24 genes and 12 biochemical parameters) into a single screening panel they called the “personal vitamin D response index” and correlated this index with the change in 25-dihydroxyvitamin D levels for each individual.

They discovered significant individual variability in how the subjects in these studies responded to increases in their 1,25-dihydroxyvitamin D levels. For example:

They were able to divide the study participants into low, mid, and high responders to an increase in 1,25-dihydroxyvitamin D levels.

- In the first study 23.9% were low responders, 50.7% were mid responders, and 25.4% were high responders.

- In the second study 28.6% were low responders, 31.4% were mid responders, and 40% were high responders.

This is a confounding variable for vitamin D studies because the authors of this report estimated:

Low responders might require 1,25-dihydroxyvitamin D blood levels of 75-100 nmol/L to see a benefit of supplementation. Most studies do not attain 1,25-dihydroxyvitamin D levels that high, so low responders would not appear to benefit from supplementation.

High responders may already experience optimal benefits of vitamin D at 1,25-dihydroxyvitamin D levels that are generally considered as inadequate. So, supplementation would offer no apparent benefit for this group either.

Only mid responders might be expected to show a clear benefit from vitamin D supplementation.

The authors concluded, “Individuals can be distinguished into high, mid, and low responders to vitamin D via measuring vitamin D sensitive molecular parameters…Thus, we suggest that the need for vitamin D supplementation depends on the vitamin D status relative to the personal vitamin D response index of an individual rather than on the vitamin D status alone.”

Report #2 (P Maissan and C Carlberg, Nutrients, 17, 1204, 2025)) suggests that the benefits of vitamin D supplementation might vary depending on the time of day the supplement was taken.

This phenomenon is known as circadian rhythm, which describes how time influences physiological and behavioral processes. A little background information is in order.

We have a “biological clock” that is reset every day by sunlight exposure. Hormone levels rise and physiological processes increase and decrease during the day in response to this biological clock.

For the most part, you have no knowledge that this is going on in your body but let me share one example you are probably aware of.

- Some people suffer from “seasonal affective disorder” (SAD). It is a type of depression associated with the winter months, especially in regions with short days and long nights. For these individuals, bright lights that mimic sunlight are often an effective therapy.

Some aspects of circadian rhythm are mediated by the pineal gland which produces melatonin. Others are affected by the hypothalamus.

Since vitamin D synthesis requires sunlight, it makes sense that some vitamin D-responsive genes would also display a circadian rhythm.

This report used the data from the single high-dose vitamin D study described above. They found that:

Of 361 known vitamin D responsive genes, 87 of them show a clear circadian rhythm.

For 14 of these genes, there was significant individual variability in the response to vitamin D supplementation.

- Group 1 (36% of the population) had significantly higher expression of these genes following vitamin D supplementation than Group 2.

The authors concluded, “Overall, our findings emphasize the circadian nature of vitamin D target gene regulation and highlight interindividual variability in the…responses to vitamin D3 supplementation. These insights have important implications for personalized vitamin D3 supplementation strategies, suggesting that optimal dosing regimens may need to consider both circadian biology [the time of day the supplement is taken] and individual responsiveness to vitamin D.”

What Does This Mean For Clinical Studies?

The latest reports explain why vitamin D studies are so confusing – why some studies show benefits of vitamin D supplementation and other studies come up empty. Simply put, it’s because vitamin D metabolism is so complicated. Let me walk you through the complications.

1) There is significant individual variability in the conversion of vitamin D to its active 1,25-dihydroxyvitamin D form.

If vitamin D supplementation does not increase 1,25-dihydroxyvitamin D levels into the adequate range, it is likely that the results will be negative – meaning no benefit of vitamin D supplementation will be observed.

If 1,25-dihydroxyvitamin D levels are already in the adequate range prior to supplementation, the results may also be negative.

Fortunately, it is easy to determine blood levels of 1,25-dihydroxyvitamin D in study participants, and most good vitamin D studies are starting to do that.

But vitamin D metabolism just got more complicated. If recent studies are correct:

2) There may be significant individual variability in the biological response to 1,25-dihydroxyvitamin D.

If someone is a low responder, supplementation at the usual levels of vitamin D is unlikely to result in high enough 1,25-dihydroxyvitamin D levels to give a response.

If someone is a high responder, they will probably have maxed out their response without supplementation, so adding a vitamin D supplement is unlikely to provide any benefit.

Sorting participants in clinical studies into low, mid, and high responders is possible, but not easy. Currently the process of sorting individuals into these categories is based on 26 biomarkers. There is no single biomarker that predicts the vitamin D response level for any individual.

3) There may be a circadian rhythm for some beneficial effects of vitamin D. If this observation is confirmed by future research, the time of day vitamin D supplements should be taken may be important.

What Does This Mean For You?

By this point, you are probably more confused than ever. So, let me sum it up for you.

Many benefits of vitamin D supplementation are unclear. Some studies show benefits. Others come up empty. “Experts” cherry pick studies that support their beliefs.

Vitamin D metabolism is complicated. And each new study appears to introduce a new layer of complexity onto our understanding of how vitamin D works.

Many of the negative vitamin D studies were done before we understood the complexities of vitamin D metabolism or did not take known complexities into account.

But just because many of the negative studies are flawed doesn’t mean all the claims for vitamin D supplementation are true. Every study has its flaws – both positive and negative studies.

So, here is my advice to you.

#1: Be a cautiously optimistic consumer.

If your doctor or some internet guru tells you vitamin D supplementation is worthless, don’t believe them. But also, don’t believe claims for miraculous cures with vitamin D supplements.

We have fairly strong evidence that vitamin D supports healthy bones, a strong immune system, strong muscles, and a healthy brain. If you discover any other benefits of vitamin D supplementation, consider them to be unexpected side benefits.

#2: Base your intake of vitamin D on your blood 1,25-dihydroxyvitamin D levels. The NIH says that 1,25-dihydroxyvitamin D levels of:

<30 nmol/L indicate vitamin D deficiency

30 to <50 nmol/L indicate vitamin D insufficiency.

>50 nmol/L are adequate.

>125 nmol/L may be linked to adverse effects.

#3: Because you don’t know whether you are a low, mid, or high responder to 1,25-dihydroxyvitamin D, you may want to shoot for a 1,25-dihydroxyvitamin D level of somewhat greater than 50 nmol/L (the study said that low responders may need as much as 75-100 nmol/L).

Personally, I would aim for no more than 60-80 nmol/L because I would not want to risk vitamin D toxicity. I realize that 125 nmol/L is the lower limit set for toxicity, but I prefer to err on the side of caution.

#4: Be aware that there may be a circadian rhythm to the effectiveness of your vitamin D supplement.

Sunlight is required for synthesis of vitamin D. So, if there is a circadian rhythm to vitamin D effectiveness, vitamin D supplements might be more effective if taken in the morning than at night.

The Bottom Line

Why do so many studies on the benefits of vitamin D supplementation come up empty? Perhaps it’s because many investigators don’t understand the complexities of vitamin D metabolism. For example:

1) There is significant individual variability in the conversion of vitamin D to its active 1,25-dihydroxyvitamin D form.

This has been well characterized, and the best vitamin D studies are starting to incorporate 1,25-dihydroxyvitamin D measurements into their study design.

And recent studies have added to the complexity of vitamin D metabolism. Our understanding of vitamin D just got a lot more complicated. For example, these studies suggest that:

2) There may be significant individual variability in the biological response to 1,25-dihydroxyvitamin D levels.

3) There may be a circadian rhythm for some beneficial effects of vitamin D.

These observations have yet to be incorporated into clinical studies of vitamin D supplementation and may explain why some existing studies have failed to find beneficial effects of vitamin supplementation.

For more details on these studies and what they may 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.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

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.

Can Red Meat Be Good For You?

May 27, 2025 by Dr. Steve Chaney

Everything You Wanted To Know About Red Meat

Author: Dr. Stephen Chaney

Nutrition is a bit like politics and religion. Everyone has an opinion, and there is not much grace for those with different opinions.

And everything is black or white. There is no middle ground. Red meat is a perfect example. Cardiologists tell us the saturated fat and cholesterol in red meat increases our risk of heart disease. Oncologists tell us red meat increases our risk of colon, breast, prostate, and pancreatic cancer.

The association with red meat consumption and colon cancer is so strong that the World Health Organization has classified red meat as a probable carcinogen.

Vegans and vegetarians tell you to avoid red meat at all costs and substitute plant proteins in its place.

Keto and carnivore diet enthusiasts tell you that red meat is healthy if you avoid any plant foods containing carbohydrates (which is most plant foods).

Who is right? Is red meat good for you or bad for you? As usual, the answer is somewhere in the middle. We also need to stop looking at individual foods and start looking at the overall diet. We need to ask how our overall diet alters the effect of red meat on our health.

But first, let’s explore:

Why red meat is good for us.

Why red meat is bad for us.

How diet can help us minimize the bad and maximize the good.

I call this section, “Everything You Wanted To Know About Red Meat”.

Everything You Wanted To Know About Red Meat

Why Red Meat Is Good For Us.

Red meat is an excellent source of protein, iron, and vitamin B12. Plus, the iron in red meat is primarily found in the heme molecule and heme iron is absorbed much more efficiently than other forms of iron.

Red meat contains creatine, which powers our muscles. You can think of creatine molecules as little power packs that are charged when we eat and release a burst of energy whenever we begin to exercise.

Red meat contains carnitine, which helps our muscles use fat as an energy source. This is particularly important for heart muscle.

But both creatine and carnitine also have a dark side, which I will discuss below.

Why Red Meat Is Bad For Us.

When we think about heart disease:

The traditional view is that saturated fat and cholesterol are the problem, and we can reduce our risk of heart disease simply by choosing leaner cuts of meat.

Other experts feel the link between red meat and heart disease is more complicated. For example, some recent studies have suggested that the carnitine in red meat can be converted by gut bacteria to TMAO, and TMAO increases our risk of heart disease. I have discussed this in a previous issue of “Health Tips From the Professor”.

When we think about cancer:

When fat and juices from the meat drip onto an open ﬂame, carcinogenic polyaromatic hydrocarbons are formed that stick to the surface of the This can be reduced, but not eliminated, by lower fat meat choices.

When red meat is cooked at high temperatures, amino acids in the meat combine with creatine, which is found in all red meats, to form carcinogenic heterocyclic amines. This can be reduced, but not eliminated, by cooking the meat at lower temperatures.

The nitrates and nitrites used as preservatives in many processed meats react with amino acids from the meat to form carcinogenic N-nitrosamines in our intestines.

Heme iron, which is found in all red meats, also combines with amino acids in the meat to form carcinogenic N-nitroso compounds in our intestines. This mechanism is inherent in all red meats and cannot be eliminated by choosing lower fat cuts or cooking at lower temperatures.

Finally, diets high in red meat increase several markers of inflammation, and inflammation increases the risk of both heart disease and cancer.

How Diet Can Help Us Minimize The Bad And Maximize The Good.

I’m going to start this section with a provocative statement: “Plant foods are the antidote to all the bad effects of red meat.” Let me explain.

Plant foods are an excellent source of:

Antioxidants

Polyphenols and other phytonutrients

Fiber

Plus, the fiber and phytonutrients found in plant foods support the growth of beneficial gut bacteria.

Here is where it gets very complex:

Beneficial gut bacteria convert some of the foods we eat into compounds that are absorbed into the bloodstream and improve blood sugar control, reduce cholesterol synthesis, and reduce inflammation.

Polyphenols support the growth of certain gut bacteria, and those gut bacteria can convert these polyphenols into compounds that can be absorbed from the intestine. This necessary for many polyphenols to exert their beneficial effects in the body.

And, as you might expect, the gut bacteria of meat eaters and vegetarians is very different.

With this in mind, let’s come back to the concept of plant foods being the antidote for red meat.

In terms of heart health,

You may remember that I said above that the carnitine in red meat can be converted by gut bacteria into TMAO which increases the risk of heart disease. The operative wording here is “can be”. It turns out this only happens with the gut bacteria of habitual meat eaters. Here is the study that showed that:

- When habitual meat eaters were fed an 8-ounce sirloin steak, both carnitine and TMAO increased in their blood and urine.

- When vegans were fed the same 8-ounce steak, only carnitine increased. No TMAO was detected.

- When the meat eaters were treated with an antibiotic that wiped out their gut bacteria prior to eating the steak, no TMAO was detected. This showed it was the gut bacteria in the meat eaters that were responsible for converting carnitine to TMAO.

Fiber from whole grains, fruits, and vegetables binds to cholesterol and flushes it out of the intestine, preventing its absorption into the bloodstream.

Plant-based diets are anti-inflammatory.

In terms of cancer,

The ﬁber found in fruits, vegetables and whole grains binds to polyaromatic hydrocarbons and heterocyclic amines and ﬂushes them out through the intestines.

Polyaromatic hydrocarbons require activation by the liver before they become carcinogenic. Indoles and isothiocyanates found in broccoli, cabbage, and other cruciferous vegetables inhibit the enzymes that catalyze this activation.

Antioxidants found in fruits, vegetables and whole grains reduce the formation of N-nitroso compounds in the intestines.

A largely plant-based diet appears to favor a population of intestinal bacteria that is less likely to convert compounds in meat into cancer-causing chemicals. [Note: This is a new area of research, so the data supporting this mechanism of cancer prevention are less deﬁnitive than for the other three mechanisms.]

These observations are based studies designed to identify the mechanisms by which plant-based diets negate the bad effects of red meat. For example, let me share a recent study (T Onali et al, Journal of Nutritional Biochemistry, 141, 109906, 2025) asking whether berries could negate the bad effects of adding red meat (pork) to a typical Finnish diet.

How Was This Study Done?

This study was conducted by a group of scientists at the University of Helsinki. They recruited 43 adults aged 20-68 and divided them into two groups. Each group was told to continue with their regular diet, except that consumption of any red meat or berries other than the foods they were provided with was prohibited.

Each group was given an extra 5 ounces of pork (minced pork, pulled pork, pork strips from fillet, cold cuts, sausages, and bacon) to eat each day.

One group was also given 1 cup of berries (bilberries, strawberries, cloudberries, raspberries, lingonberries, and blackcurrant) to eat each day.

- Note: These are the foods most familiar to people from Finland in each category.

- They were provided with these foods on a weekly basis.

This intervention portion of the study lasted four weeks.

Dietary intake was assessed in each group using 3-day food records (two weekdays and one weekend day) at the beginning and the end of the study.

Participants in the study collected stool samples on two consecutive days at the beginning and end of the study. These stool samples were analyzed in the following ways:

Bacterial DNA was extracted from the stool samples and used to determine which gut bacteria were present in the stools.

The stool samples were homogenized and filtered to:

- Determine the polyphenols and polyphenol metabolites present in the stool samples.

- Determine whether low molecular weight compounds present in the stool samples were able to inhibit the growth of human colon cancer cells in cell culture.

What Did The Study Show?

The dietary analysis found that total calories, protein, carbohydrate, fat, and saturated fat did not change significantly in either group. This indicates that the study participants likely substituted the pork they were given for other high-fat meats they were eating before the study.

However, in the group that was also given berries fiber, vitamin C, vitamin E, manganese, and several polyphenols increased significantly. This suggests that study participants likely substituted the berries for less healthy foods they were eating before the study.

The study found that:

In the red meat-only group the relative abundance of beneficial Roseburia and Fecalibacterium gut bacteria was decreased. This did not occur in the red meat + berries group.

In the red meat + berries group the concentration of several beneficial polyphenols and polyphenol metabolites was increased.

In the red meat + berries group, the filtrate obtained from stool samples inhibited the growth of several human colon cancer cell lines in cell culture experiments. These experiments did not identify which berry polyphenols were responsible for inhibiting the growth of cancer cells. It also did not determine whether the polyphenols came directly from the berries or were created when gut bacteria modified the polyphenol(s).

But these experiments did show that something in the intestines of people consuming a high berry diet inhibited colon cancer cell growth.

The author’s concluded, “Berry supplementation to a diet high in red and processed meat led to berry-derived polyphenolic metabolites in the feces, beneficially modified gut microbiota, inhibited the viability of colon cancer cells, collectively suggesting potential in cancer prevention.

The difference seen in gut metabolism was probably induced by the higher intakes of dietary fiber, vitamin C and E, manganese, and polyphenols by the berry diet.”

Can Red Meat Be Good For You?

This study is one piece of the puzzle to help us understand the effect of diet on the benefits and risks of red meat consumption. Here is what I mean by that.

We can think of scientific investigations in terms of solving a large puzzle with lots of little pieces. If you are a puzzle enthusiast, you know the best way to solve a complicated puzzle is to put the edge pieces together first and then fill in the rest of the puzzle.

In this context, the studies showing that small amounts of red meat are not harmful in the context of healthy, primarily plant-based diets like the DASH and Mediterranean diets are the edge of the puzzle. Smaller studies that define the mechanisms of this effect and provide proof these mechanisms are accurate are the interior pieces that fill out the puzzle. This study is one of those interior pieces.

So, what does that mean for you? It means that diet context is important.

Most of the studies showing the bad effects of red meat have been done in the context of the typical American diet. That might consist of an 8 or 12-ounce steak with fries and either a soft drink or iced tea. Fruits and vegetables, if present at all, are minimal. Dessert usually consists of some sugary treats.

In this context, red meat is bad for you.

In contrast, consider the place red meat occupies in a primarily plant-based diet. Red meat becomes a condiment rather than the main course. Think of 2-3 ounces of red meat as part of a green salad or stir fry with a variety of greens and other vegetables. You might have beans, whole grains, or another vegetable to round out your plate. Dessert would be whatever fruit is in season. And your beverage might be water, milk, or herbal tea.

In this context, the bad effects of red meat disappear. In short, there are no bad foods, only bad diets.

I started this blog with the question, “Can red meat be good for you?” You may be wondering if I have answered that question.

At the beginning of this article, I listed the good things about red meat, namely that it is a good source of protein, iron, vitamin B12, carnitine, and creatine.

If you remove the bad, only the good remain. So, the answer is, “Yes. In the right diet context red meat can be good for you”.

The Bottom Line

You have heard that red meat is bad for you. It increases your risk of heart disease and cancer. You should avoid it at all costs.

But is that true? In the article above I:

Describe both the benefits and risks of red meat.

Discuss how plant foods negate many of the bad effects of red meat.

Share a study providing proof of that concept.

Share how you can enjoy the benefits of red meat while avoiding the bad effects of red meat consumption.

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.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”.

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.

The Importance Of Family History For Maternal Health

May 20, 2025 by Dr. Steve Chaney

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”.

You-Tube Channel (https://www.youtube.com/channel/UCPMch7GamgUYYd9H3GonJZQ) – Over 80 videos exploring pregnancy, labor, birth, postpartum and contraception

www.thecarabcompany.com (https://www.thecarabcompany.com/) – Website with free downloadable pregnancy and birth information

Mastering Pregnancy and Birth Coaching Program (https://www.thecarabcompany.com/healthy-pregnancy-to-healthy-birth-accelerator) – A program that prepares Dads and Mom’s-to-be for a healthier pregnancy and safer birth. This course also provides information for Doulas to provide enhanced support to families.

Carolyn Curtis

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.

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

______________________________________________________________________

About The Author

Carolyn Curtis, MSN, CNM, RN, FACNM, FAAN, has:

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 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.

The Methylfolate Myths

May 13, 2025 by Dr. Steve Chaney

The Lies Of The Supplement Industry

Author: Dr. Stephen Chaney

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.

One study has shown that folic acid and methylfolate were equally effective at lowering plasma homocysteine in people who were MTHFR C677T homozygotes (P. Fohr et al, American Journal of Clinical Nutrition, 75: 275-282, 2002).

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.

Another study showed folic acid was just as effective as a diet providing equivalent quantities of folate from foods at lowering homocysteine levels in people with various MTHFR mutations (A. Ashfield-Watt et al, American Journal of Clinical Nutrition, 76: 180-186, 2002).

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:

Folic acid has been shown in multiple studies to be effective in preventing neural tube defects (M. De-Regil et al, Cochrane Database Systematic Reviews 2010 Oct 6;(10):CD007950. PMID: 20927767), which are highly associated with the C677T MTHFR gene defect.

Three studies have shown that supplementation with folic acid, B12, and B6 slowed cognitive decline in older people with elevated homocysteine levels ( Durga et al, The Lancet, 369: 208-216, 2007); A.D. Smith et al, PLoS ONE 5(9): e12244. doi:10.1371/journal.pone.0012244, 2010); G. Douaud et al, Proceedings of the National Academies of Sciences, 110: 9523-9528, 2013).

In contrast, the one study that substituted methylfolate for folic acid showed no effect (A. McMahon et al, New England Journal of Medicine, 354: 2764-2769, 2006).

Myth: Folic acid causes cancer.

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.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

The Methyl B12 Myths

May 6, 2025 by Dr. Steve Chaney

How Is The Vitamin B12 For Supplements Produced?

Author: Dr. Stephen Chaney

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.

_____________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_____________________________________________________________________

About The Author

Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”.

The Estrogenic Myth

April 29, 2025 by Dr. Steve Chaney

What Does Increase Breast Cancer Risk?

Author: Dr. Stephen Chaney

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.

____________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_____________________________________________________________________

About The Author

Eating For A Healthy Planet

April 22, 2025 by Dr. Steve Chaney

Can Diet Affect The Health Of Our Planet?

Author: Dr. Stephen Chaney

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.

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.

_____________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”.

The Soy Myth

April 15, 2025 by Dr. Steve Chaney

Why Is There So Much Confusion About Soy?

Author: Dr. Stephen Chaney

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:

Control your weight
Be physically active
Limit alcohol
Don’t smoke
Limit hormone replacement therapy unless absolutely necessary.
Reduce stress

The Bottom Line

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.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

The Low Carb Myth

April 8, 2025 by Dr. Steve Chaney

The “Goldilocks Effect”

Author: Dr. Stephen Chaney

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.

A second study published a year later (SB Seidelmann et al, The Lancet, doi.org/10.1016/S2468-2667(18)30135-X eliminated these weaknesses and resolved the conflicting data.

How Was The Second Study Done?

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.

Meat-based low-carb diets increased mortality, and plant-based low-carb diets decreased 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.

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.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

______________________________________________________________________