Natural Approaches For Controlling ADHD

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Are Natural Approaches Better Than Drugs?

Author: Dr. Stephen Chaney 

diet for children with adhdSeveral years ago, I came across a headline in our local newspaper that said, “Try Nutrition, Not Drugs, for ADHD”. The article made claims like “No good evidence exists to support the ADHD disease hypothesis” and “…on numerous occasions we have seen ADHD symptoms completely disappear without medication”.

As a scientist, I am always a little skeptical about bold claims that run counter to established scientific wisdom. However, the authors of this article implied that their claims were based on a 2012 article in Pediatrics, which is a highly respected journal in its field, so I decided to investigate the article (Millichap and Yee, Pediatrics, 129: 1-8, 2012).

The article was written by two pediatricians with extensive experience treating children with ADHD. The article turned out to be a thorough review of the literature on nutritional approaches for controlling ADHD. It did not approach the rigor of a meta-analysis study. Rather, it is what I refer to as an “interpretive review”. By that I mean that the clinical studies were interpreted in part based on their clinical experience in treating children with ADHD.

Interpretive reviews can be either good or bad, depending on the objectiveness of the reviewers. In this case, I was familiar with many of the clinical studies they reviewed and found their interpretations to be accurate, so I decided to share their conclusions with you. But first I should probably talk about our ADHD epidemic and ask two important questions:

  1. Is ADHD over diagnosed?
  1. Are drugs always the best solution for controlling ADHD symptoms?

Are Natural Approaches Better Than Drugs? 

Increase 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. But let me point out what many experts miss.

Is ADHD Over Diagnosed?

Perhaps we should be asking whether teachers and parents might be tempted to overestimate the severity of the symptoms.

For parents,

  • Parents don’t have the time they used to have to supervise their kids.
    • 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.

For teachers,

  • Class sizes are large, and there aren’t enough teachers’ 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.

Why is the increase in ADHD diagnoses a concern?

drug side effectsThe 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.
  • Many children don’t like how the drugs make them feel. They make them feel irritable, depressed, anxious, or tense.
  • 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.

Natural Approaches For Controlling ADHD 

The pediatricians reviewed all the major nutritional approaches that have been used over the years to control ADHD. Let me start by saying that they are not wild-eyed proponents of “a nuts and berries diet cures all”. In fact, they use medications as the primary intervention for most of their ADHD patients. They advocate dietary approaches when:

  • Medicines fail or there are adverse reactions (side effects).
  • The parents or the patients prefer a more natural approach.
  • There are symptoms or signs of a mineral deficiency (more about that below).
  • There is a need to substitute an ADHD-free healthy diet for an ADHD-linked diet (Simply put, if the child’s diet is bad enough, there are multiple benefits from switching to a healthier diet – a possible reduction in ADHD symptoms is just one of them.)

I will summarize their key findings below: 

Omega-3 Fatty Acids

Child Raising HandThe authors reported that many studies have shown that children with ADHD tend to have low levels of essential fatty acids, especially the omega-3 fatty acids. They cite several studies which showed significant improvement in reading skills and reductions in ADHD symptoms when children with ADHD were given omega-3 supplements but also noted that other studies showed no effect. They postulated that some children may benefit more from omega-3 supplementation than others.

They routinely use doses of 300-600 mg of omega-3s with their ADHD patients. They find that this intervention reduces ADHD symptoms in many children but does not completely eliminate the need for medications.

My Two Cents: I have recently reported) on a study that strengthens the association between omega-3 supplementation and a reduction in ADHD symptoms. Whether omega-3 supplements will help your child is anyone’s guess. However, it is a natural approach with no side effects. It is certainly worth trying.

Food Additives

The current interest in food additives and ADHD originated with the Feingold diet. The Feingold diet eliminated

food additives, foods with salicylates (apples, grapes, luncheon meats, sausage, hot dogs and drinks containing artificial colors and flavors), and chemical preservatives (e.g. BHA and BHT).

It was popularized in the 1970s when some proponents claimed that it reduced ADHD symptoms in 50% of the children treated. After clinical studies showed that only a small percentage of children benefitted from this diet, it rapidly fell out of favor.

However, Millichap and Yee pointed out that more recent studies have shown that the subset of children who responded to the Feingold diet were not a “statistical blip”. A recent review of the literature reported that when children with suspected sensitivities to food additives were challenged with artificial food colors, 65–89% of them displayed ADHD symptoms.

My Two Cents: I have recently reported) on more recent studies documenting the effects of artificial food colors on ADHD. The studies I reviewed in that article reported that up to 28% of children with ADHD were sensitive to the amount of artificial food colors in the typical western diet and that removing those food colors resulted in a significant improvement in ADHD symptoms. Plus, those studies were just looking at food colors – not the hundreds of other food additives in the average American child’s diet.

I consider food additives to be problematic for many reasons. Even if removing them doesn’t reduce their ADHD symptoms, eliminating as many of those food additives as possible is probably a good idea. It doesn’t need to be complicated. Just replacing processed foods and sodas with fresh fruits and vegetables and with low fat milk and natural fruit juices diluted with water to reduce their sugar content might make a significant difference in your child’s ADHD symptoms.

Food Sensitivities

Even natural foods can be a problem for children with food sensitivity, and it appears that there may be a large percentage of hyperactive children with food sensitivities. Millichap and Yee reported that elimination diets (diets that eliminate all foods which could cause food sensitivity) improve behavior in 76-82% of hyperactive children.

Even though this approach can be very effective Millichap and Yee don’t normally recommend it for their patients because it is difficult and time-consuming. The elimination diet is very restrictive and needs to be followed for a few weeks. Then individual foods need to be added back one at a time until the offending food(s) are identified. (They reported that antigen testing is not a particularly effective way of identifying food sensitivities associated with hyperactivity)

My Two Cents: I have previously reported on the link between food sensitivities and hyperactivity. I agree with Millichap and Yee that elimination diets are difficult and view this as something to be tried after all other natural approaches have failed. However, if there is a particular food that causes hyperactivity in your child, identifying it and eliminating it from their diet could just be something that will benefit them for the rest of their life.

Sugar

sugar cubesThis is a particularly interesting topic. Many parents are absolutely convinced that sugary foods cause hyperactivity in their children, but the experts are saying that clinical studies have disproven that hypothesis. They claim that sugar has absolutely no effect on hyperactivity.

Millichap and Yee have an interesting perspective on the subject. They agree that clinical studies show that a sugar load does not affect behavior or cognitive function in small children, but they point to numerous clinical studies showing that the reactive hypoglycemia that occurs an hour or two after a sugar load adversely affects cognitive function in children, and that some children are more adversely affected than others.

My Two Cents: Reducing intake of refined sugars in your child’s diet makes sense for many reasons, especially considering the role of sugar intake in obesity. If your child has a tendency towards reactive hypoglycemia, it may also reduce ADHD symptoms.

Iron and Zinc Deficiency

Millichap and Yee reported some studies suggested that iron and zinc deficiencies may be associated with ADHD symptoms and recommend supplementation with an iron or zinc supplement when there is a documented deficiency.

My Two Cents: A simpler and less expensive approach would be a children’s multivitamin to prevent the possibility of iron or zinc deficiency. Of course, I would recommend that you choose one without artificial colors, preservatives and sweeteners.

A Healthy Diet

Millichap and Yee closed their review by discussing a recent study in Australia that reported a significant reduction in ADHD symptoms in children eating “Healthy” diets (fish, vegetables, tomato, fresh fruit, whole grains & low-fat dairy products) compared to children eating “Western” diets (Fast foods, red meat, processed meats, processed snacks, high fat dairy products & soft drinks). This is the dietary approach, along with omega-3 supplementation, that they recommend most frequently for their patients.

My Two Cents: I wholeheartedly agree. In fact, if you and your family were to follow a “Healthy” diet instead of a “Western” diet it would likely have numerous health benefits. Plus, you are automatically removing ADHD triggers like food additives and sugar from your child’s diet.

The Bottom Line

This review of natural approaches for controlling ADHD symptoms (Millichap and Yee, Pediatrics, 129: 1-8, 2012) is both good news and bad news. The good news is that there are multiple natural approaches that can significantly reduce ADHD symptoms. These include:

  • Use of omega-3 supplements. They recommended 300-600 mg/day.
  • Removal of food additives (particularly food colors) from the diet.
  • Identification of food sensitivities and removal of those foods from the diet.
  • Reducing the amount of simple sugars in the diet.
  • Elimination of iron and zinc deficiencies if they exist (Iron deficiency is relatively common in American children. Zinc deficiency is not.) Alternatively, I recommend a children’s multivitamin to prevent iron and zinc deficiencies in the first place.
  • Eating a healthy diet rather than a Western diet. This also has the benefit of reducing the amount of food additives and sugars in the diet.

The bad news is that each of these approaches seems to work only in a subset of children with ADHD.

  • If you are a parent who is interested in a natural alternative to ADHD stimulant medications this means you may need to be patient and try several natural approaches until you find the one(s) that work(s) best for your child. The benefit of making the effort is that all these approaches will also improve the health of your child in other important ways, and none of them have any side effects.
  • Unfortunately, physicians with only about 10 minutes to spend with each patient (which is increasingly the medical model in this country), may not have time to explore natural options. Medications are much easier to prescribe. You may need to be the one who takes the responsibility of exploring natural alternatives for your child.

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

 _____________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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 text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

 

 

Are GLP-1 Users Getting Enough Nutrients?

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What Does This Mean For Your Future Health?

Author: Dr. Stephen Chaney

Most people want to lose weight so they can get trimmer and healthier. I don’t know of anyone who wants to be leaner and less healthy. But if they are not getting the essential nutrients their body needs while they are losing weight, they may well end up both lean and unhealthy.

I don’t need to tell you that GLP-1 (glucagon-like peptide 1) drugs are all the rage. Total spending on GLP-1 drugs in the United States exceeded $71 billion in 2023, a 500% increase in just 5 years. There are 15 million Americans on GLP-1 drugs at any one time. And most of this increase has been driven by the weight-loss market.

GLP-1 drugs do work. They target the intestine and the brain, increasing satiety (feeling of fullness) and decreasing appetite.

However, like any other drug, they have side effects. The most frequent are:

  • Nausea
  • Vomiting
  • Diarrhea
  • Constipation
  • Increased heart rate.
  • Hypoglycemia
  • Allergic reactions

In a previous issue of “Health Tips From the Professor” I discussed a serious side effect that is often overlooked, namely increased risk of depression, anxiety, and suicidal thoughts. My recommendations were:

  • If you suffer from depression, anxiety, or suicidal thoughts, GLP-1 drugs may not be the best choice for you. At the very least you should discuss the risks and benefits with your doctor before using them.
  • If you are using GLP-1 drugs and experience an increase in depression, anxiety, or suicidal tendencies, you should discontinue the drug immediately and report your side effects to your doctor.

Another question that has not been addressed previously is whether people using GLP-1 drugs are getting the essential nutrients their bodies need for optimal health. Today’s study (B Johnson et al, Frontiers in Nutrition, published online in April 2025) was designed to measure the nutritional adequacy of GLP-1 user’s diets.

How Was This Study Done? 

clinical studyThe investigators enrolled 69 people who had been using a GLP-1 drug for at least a month in their study using an online research platform through the University of Turin in Italy.

The characteristics of the study participants were:

  • Weight:
    • 5% normal weight
    • 27% overweight
    • 18% Obese Class I
    • 20% Obese Class II
    • 30% Morbidly Obese
  • Age = 49.6 ± 12.3
  • Ethnicity:
    • 82% Caucasian
    • 6% Hispanic
    • 8% African American
    • 1% Asian
    • This is similar to the ethnic distribution of GLP-1 users in this region.
  • Length of GLP-1 use:
    • 7% <3 months
    • 29% 4-6 months
    • 25% 7-12 months
    • 39% >1 year

The participants were trained on how to use an online dietary recall instrument and then recorded their dietary intake for 3 consecutive days.

Are GLP-1 Users Getting Enough Nutrients?

Question MarkThe results of the 3-day dietary recalls from the GLP-1 users were:

  • Their diets were high in fat (39% of calories) and saturated fat (13%).
  • Their diets were low in fruit, vegetables, grains, and dairy foods.
  • Their diets were low in fiber (14 grams). This is half the recommended intake of fiber.
  • Their diets were sufficient for B-vitamins, copper, phosphorous, selenium, and zinc.
  • Their diets were deficient for calcium, iron, magnesium, potassium, choline, vitamin A, vitamin C, vitamin K, vitamin D, vitamin E, and fiber. For example:
    • 99% of participants were not getting enough Vitamins D and K from their diet.
    • 94% weren’t getting enough choline.
    • 90% weren’t getting enough magnesium.
    • 88% weren’t getting enough iron.

The study did not report the intake of omega-3 fats, but the participants were likely deficient in that as well.

The study participants averaged 0.8 gm/kg of protein, which is the recommended intake for sedentary adults who are not on a weight loss diet. However, 0.8 gm/kg of protein is not sufficient for maintaining muscle mass on weight loss diets, especially weight loss diets aided by GLP-1 drugs. Most experts recommend 1.2gm/kg to 1.6 gm/kg to prevent loss of muscle mass, with a few recommending as high as 2 gm/kg.

Most of the participants in this study did not meet the increased protein recommendations for weight loss.

  • Only 43% consumed at least 1.2 gm/kg of protein.
  • Only 10% consumed at least 1.6 gm/kg of protein.
  • Only 5% consumed at least 2.0 gm/kg of protein.

The authors concluded, “Participants on a GLP-1 drug are not meeting the DRI [daily recommended intake] for several vital nutrients through their diet or the higher protein needs during weight loss. Patient-centered nutritional guidance is essential to optimize health outcomes and prevent unintended health consequences.

What Does This Mean For Your Future Health?

QuestionsThe results of this study are both appalling and expected. Weight loss diets often result in nutritional insufficiencies. However, GLP-1-aided weight loss is worse.

That’s because GLP-1 is a drug, not a diet plan. It’s dispensed like any other drug.

  • Your doctor gives you a GLP-1 prescription. If you are lucky, they may give you a “one-size-fits-all” handout on how to lose weight while you are using it. For example, in this study:
    • Only 51% of participants received information from their doctor on how to manage side effects of GLP-1.
    • Only 20% were referred to a dietitian. The other 80% received no information on how to change their diet and lifestyle.
  • When you pick up the drug from the pharmacy, you get a package insert listing the side effects but no information on how to change your diet.

The results were predictable:

From a medical point of view the results were a big success:

  • The participants in the study reduced their caloric intake by 20%.
  • Most of the participants in the study felt the GLP-1 drug was helping them lose weight.

But from a nutritional point of view the study raises a red flag. Most of the participants were not told to change their diet or lifestyle, and they didn’t. Their diet was still:

  • High in total fat and saturated fat and probably low in healthy fats, although that was not assessed.
  • Low in fruits, vegetables, grain, dairy, and fiber.

The typical American diet is bad enough as it is. But when you eat the same diet and decrease calories, the nutritional inadequacies of the American diet are magnified. That is why the diets of the GLP-1 users were deficient in fiber plus 10 essential vitamins and minerals and did not contain enough protein to prevent loss of muscle mass.

Most (52%) of the participants were planning to be on GLP-1 drugs for a short period of time – just long enough to reach their weight loss goals. But the reality is far different.

Studies show that when people lose weight on GLP-1 drugs without changing their diet and lifestyle, the weight comes roaring back as soon as they get off the drugs. The reality is that those people will need to stay on GLP-1 drugs for a lifetime if they want to keep the weight off.

That’s when the nutritional inadequacies shown in this study start to have real health consequences. For example,

  • Long term inadequacies of calcium, magnesium, and vitamin D increase the risk of osteoporosis.
  • Long term muscle loss due to inadequate protein intake leads to frailty and metabolic diseases as we age.

I could go on, but you get the point. GLP-1 drugs are not a panacea. Without diet and lifestyle change, they are just a temporary and expensive solution to weight loss.

The Bottom Line

A recent study looked at the nutritional intake of GLP-1 users. It found:

  • Their diets were high in fat (39% of calories) and saturated fat (13%).
  • Their diets were low in fruit, vegetables, grains, and dairy foods.They were deficient in fiber plus 10 essential vitamins and minerals.

 

  • They were not getting enough protein to prevent the loss of muscle mass associated with GLP-1 use for weight loss.

The authors concluded, “Participants on a GLP-1 drug are not meeting the DRI [recommended intake] for several vital nutrients through their diet or the higher protein needs during weight loss. Patient-centered nutritional guidance is essential to optimize health outcomes and prevent unintended health consequences.

For details about the study and the health consequences of these nutrient deficiencies, read the article above.

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

______________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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 text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 53 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

The Methylfolate Myths

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The Lies Of The Supplement Industry

Author: Dr. Stephen Chaney

Pinochio

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.

MTHFR ReactionThe 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 Methylfolate Were Misleading

MTHFR mutants only have a partial loss of activity.

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

We Don’t Need 100% MTHFR Activity

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 methylfolate could be chalked up to an honest misunderstanding.

  • The doctors who published the original papers may not have known that MTHFR mutations only resulted in a partial reduction in enzyme activity.
  • They probably didn’t know the concepts of redundancy (our cells don’t need 100% enzyme activity) or penetrance (the same mutation may cause severe symptoms in some patients and have no effect in others).
  • It seemed logical to assume that everyone with a MTHFR mutation might do better with 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.cherry picking studies

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 Versus FactsMyth: 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.

Clinically ProvenFact: 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).

 

CancerMyth: 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

deceptionIf 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 methylfolate. 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:

  • Their methylfolate supplement was effective at reducing the risk of adverse pregnancy outcomes.
  • Their methylfolate supplement was twice as bioavailable as folic acid.
  • 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?

Questioning WomanMTHFR mutations only result in partial loss of activity. Most individuals with MTHFR defects remain symptom free with the RDA, or slightly above the RDA, of folic acid.

However, there may be some individuals with a MTHFR defect and additional gene defects in metabolic pathways involving methylation who might benefit from methylfolate. This is due to a phenomenon that geneticists call penetrance and would likely represent a small subset of the population with MTHFR defects.

Finally,the claims that everyone would benefit from methylfolate instead of folic acid are false. They are contradicted by human metabolism and multiple published clinical studies.

In short, folic acid has been used for over 80 years. There are hundreds of clinical studies showing it is safe and effective, even in most individuals with a MTHFR deficiency. I can’t tell you whether the companies selling methylfolate are ignorant of basic metabolism and the published studies refuting their claims or whether they are purposely trying to deceive the public—but neither is a good thing.

The Bottom Line

Some supplement manufacturers are claiming that methylfolate is more natural and more effective than the folic acid that has been used in supplements for the past 80 years. In this issue of “Health Tips From the Professor” I debunk the methylfolate myths used by the supplement manufacturers to sell their methylfolate products.

I can’t tell you whether the companies selling methylfolate are ignorant of basic metabolism and the published studies refuting their claims or whether they are purposely trying to deceive the public—but neither is a good thing.

For more specifics, read the article above.

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

 _____________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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.

Is Extra Protein Important For Seniors?

by

The Role Of Muscle Protein In Energy Metabolism 

Author: Dr. Stephen Chaney 

We’ve been told, “It’s all downhill after 30.” That may or may not be true depending on the lifestyle choices we make.

But for muscle mass, “It’s all downhill after 50!” Simply put, we start to lose muscle mass at an accelerating pace after 50, a process scientists call sarcopenia.

Sarcopenia should be a major concern for everyone over 50. Loss of muscle mass:

  • Causes unsteadiness which can lead to falls, bone fractures, and death.
  • Increases the risk of obesity because muscle burns more calories than fat. That increases our risk of obesity-related diseases such as heart disease, diabetes, some cancers, osteoarthritis, and other inflammatory diseases.
  • Robs us of the fun activities we would like to enjoy in our golden years.

But sarcopenia is not inevitable. As I have discussed in previous issues of “Health Tips From the Professor”, there are three things we can do to minimize sarcopenia as we age.

  • Get adequate weight-bearing exercise. In other words, pump iron or use your body weight for exercise on a regular basis.
  • Get adequate protein.
  • Get adequate amounts of the branched-chain amino acid leucine.

In this article I will focus on the last two, especially the fact that we need more protein and leucine to prevent loss of muscle mass as we age. To help you understand why that is, I am going to share my favorite topic – Metabolism 101 (Once a biochemistry professor, always a biochemistry professor).

Metabolism 101: The Role Of Muscle Protein In Energy Metabolism 

ProfessorMost people associate muscle mass with strength and endurance. Many understand the important role muscle mass plays in burning off excess calories and keeping us slim. But few people understand the important role that muscle protein plays in our everyday energy metabolism.

Let’s start with an overview of metabolism [Note: If you are not interested the details, you can just skip over the bullets and read the take-home message at the bottom of this section.]

  • We get energy from the carbohydrate, fat, and protein we consume. Excess carbohydrate, fat, and protein in our meals are stored to provide the energy our body needs between meals and during prolonged fasting.
    • We have a virtually unlimited ability to store fat, as some of you may have noticed.
    • We have a very limited ability to store carbohydrates in the form of glycogen in our liver.
    • Muscles are our largest organ system, and we can store some of the protein we eat as increased muscle mass, especially when protein intake is coupled with exercise. But muscle protein plays other very important functions. It is a precious resource.
  • In the fed state most of our energy is derived from blood glucose. This is primarily controlled by insulin. As blood glucose levels fall, we move to the fasting state and start to call on our stored energy sources to keep our body functioning. This process is primarily controlled by a hormone called glucagon.
    • In the fasting state most tissues easily switch to using fat as their main energy source, but…
      • Red blood cells and a few other tissues in the body are totally dependent on glucose as an energy source.
      • Initially our brain is totally dependent on glucose as an energy source, and our brains use a lot of energy. [Note: Our brain can switch to ketones as an energy source with prolonged starvation or prolonged carbohydrate restriction, but that’s another story for another day.]
  • Because our brain and other tissues need glucose in the fasting state, it is important to maintain a constant blood glucose level between meals.
    • Initially, blood glucose levels are maintained by calling on the glycogen reserves in the liver.
    • But because these reserves are limited, our body starts to break down muscle protein and convert it to glucose as well – even in the normal dinner/sleep/breakfast cycle.

You may have found the explanation above was excessive, but I couldn’t think of a simpler way of helping you understand that in addition to its other important role in the body, muscle protein is also an energy store.

When we eat, we make a deposit to that energy store. Between meals we withdraw from that energy store. When we are young the system works perfectly. Unless we fast for prolonged periods of time, we are always adding enough muscle protein in the fed state to balance out the withdrawals between meals.

But as we age, our ability to build muscle in the fed state becomes less efficient. Withdrawals exceed deposits, and we experience age-related muscle loss (sarcopenia).

What We Know About Preventing Age-Related Muscle Loss

As I said above, there are three things needed to prevent age-related muscle loss:

  • Adequate resistance exercise.
  • Adequate amounts of protein.
  • Adequate amounts of the essential, branched-chain amino acid called leucine.

And, as I said above, I am going to focus on the last two.

In previous issues of “Health Tips From the Professor” I have shared articles showing that the amount of both protein and leucine needed to maximize the gain in muscle mass following a meal or a workout increase as we age. For example.

  • For someone in their 30s, 15-25 grams of protein with 1.7 grams of leucine per meal is optimal.
  • But someone in their 60’s and 70s needs 25-30 grams of protein and 2.5-2.7 grams of leucine per meal to achieve the same effect.
  • Most of these studies have been done with men, but a recent study showed the results are identical with post-menopausal women.

However, previous studies have not addressed whether we need protein supplementation to achieve adequate protein intake or what kind of protein supplements were best. The studies I will discuss today were designed to answer these questions.

How Were These Studies Done? 

clinical studyStudy #1: As I said above, previous studies have suggested that 25-30 grams of protein per meal is optimal for preventing age-related loss of muscle mass in seniors. However, many seniors get most of their protein in their evening meal. On average, seniors consume

8-15 grams of protein at breakfast, 15-20 grams of protein at lunch, and 30-40 grams of protein at dinner.

This study (C Norton et al, The Journal of Nutrition, 146: 65-67, 2016) was designed to ask whether optimizing protein intake at each meal by adding a protein supplement at breakfast and lunch would increase lean muscle mass in seniors over a 24 week period.

The investigators recruited 60 adults, aged 50-70 (average age = 61) from the city of Limerick, Ireland. The participants were 73% women and had an average BMI of 25.8 (slightly overweight).

The participants were randomly assigned to receive either a milk-based supplement or an isocaloric, non-protein-containing, maltodextrin control. The protein supplement provided 20 grams of protein. The participants were instructed not to change any other aspect of their diet or activity level.

The protein supplement and placebo were provided in identical sachets, and the participants were told to mix them with water and consume them with breakfast and lunch. The protein supplement and placebo looked and tasted identical, so the subjects did not know which group they were in. Compliance was assessed by collecting the used sachets at the end of the study.

The participants completed 4-day diet recalls under the supervision of a dietitian before and during the study. Lean muscle mass was determined prior to and at the end of the 24-week study.

protein shakesStudy #2: This study (J McKendry et al, The American Journal Of Clinical Nutrition, doi: 10.1016/j.ajcnut.2024.05.009) was designed to determine whether the ability to stimulate muscle protein synthesis depended on the type of supplemental protein.

This study was built on the results of the first study. Specifically, the investigators compared the effect on muscle protein synthesis of adding 25 grams of whey, pea, or collagen protein to breakfast and lunch meals.

The investigators enrolled 31 healthy, older (average age = 72) subjects from the Hamilton, Ontario area. Subjects were excluded from the study if:

  • They had a medical condition or were taking any medication that might influence the results.
  • They used tobacco or tobacco related products.
  • They consumed a vegan or vegetarian diet
  • They used a walking device or were inactive for any reason.

The participants were placed on a standardized diet consisting of prepackaged meals (breakfast, lunch, and dinner) and a mix of fruits, vegetables, snacks, and drinks. They were instructed to only eat the foods provided to them and to maintain their normal activity levels.

The diet was designed to provide the RDA for protein (0.8 gram of protein/kilogram of body weight) and to mimic the habitual dietary patterns of seniors in the United States and Canada.

  • Around 55% carbohydrate, 30% fat, and 15% protein.
  • Uneven distribution of protein throughout the day (19% at breakfast, 26% at lunch, and 55% at dinner).

After one week on the control diet, participants were randomly assigned to receive 25-gram protein supplements of either whey, pea, or collagen protein and instructed to add them to their standardized diet for breakfast and lunch (total daily protein intake was increased by 50 grams/day). They followed this regimen for 7 days.

On day one and 7 of the control phase and day 7 of the intervention phase (when the participants were consuming additional protein) muscle biopsies were obtained 90 minutes after breakfast for determination of the effect of the meal on muscle protein synthesis.

[Note: The participants were consuming a protein supplement containing an additional 25 grams of protein at both breakfast and lunch. But the effect of this additional protein on muscle protein synthesis was only determined after the breakfast meal.]

Is Extra Protein Important For Seniors? 

OptimizeEach of the studies provided important insights for anyone wanting to minimize age-related muscle loss.

Study #1: The effect of the 20-gram whey protein supplement for breakfast and lunch as follows:

  • Protein supplementation at breakfast and lunch resulted in a 1.3-pound gain in lean body mass over 24 weeks compared to the control group using an isocaloric, non-protein containing maltodextrin supplement.

The authors concluded, “Protein supplementation at breakfast and lunch for 24 weeks in healthy older adults resulted in a positive (1.3 pound) difference in lean muscle mass compared with an isoenergetic, non-nitrogenous maltodextrin control. These observations suggest that an optimized and balanced distribution of [supplemental] protein intakes could be beneficial in the preservation of lean tissue mass in the elderly.”

Note:

  • This study did not show that these protein levels were optimal. It only showed that using a protein supplement to increase protein intake at breakfast and lunch was beneficial for seniors consuming most of their protein at dinner.

Study #2: The effect of the three 25-gram protein supplements at breakfast and lunch on protein intake was as follows:

  • Adding 25 grams of either whey or pea protein to a relatively low-protein (15 grams) breakfast increased muscle protein synthesis by ~9%.
  • Adding 25 grams of collagen to the same low-protein breakfast had no effect on muscle protein synthesis.

Note: This study did not measure the effect of adding supplemental protein to lunch meal, but the results were probably similar.

The authors concluded, “We discovered that the RDA [for protein] was insufficient to support higher rates of MPS [muscle protein synthesis] in older adults. Manipulating dietary protein to increase daily consumption of higher quality – whey and pea but not collagen – proteins by targeting the lowest protein-containing meals offers a viable strategy to enhance…MPS [muscle protein synthesis] in older adults.”

“Consuming protein much closer to expert group consensus recommendations [1.2 gm/kg instead of the current 0.8 gm/kg for adults over 50] may help to increase…MPS [muscle protein synthesis] with advancing age and extend health-span – compressing the years of disease and disability commonly experienced by older individuals closer to the end of life.”

My comments are:

  • You may recall from the previous discussion that age-related muscle loss occurs because muscle protein synthesis (MPS) becomes less efficient as we age.
    • Therefore, an increase in muscle protein synthesis following each meal will lead to an increase in muscle mass over time, as was seen in the first study.
  • In our 60’s and beyond we require higher amounts of both protein and leucine to maximize muscle protein synthesis.
    • The collagen supplement used in this study provided enough supplemental protein. But it probably was ineffective because it only provided 0.86 grams of leucine.
      • The amount of leucine in the control diet was not specified, but with only 15 grams of protein for breakfast there was probably enough leucine to make up for the lack of leucine in the collagen supplement.
    • In contrast the whey and pea supplements provided 2.7 and 2.1 grams of leucine, respectively. When added to the leucine in the control diet, this would be more than enough to drive muscle protein synthesis.
  • Not every pea protein supplement may be as effective as the one used in this study. When I looked it up, it was described as an “enriched pea protein designed as a soy and milk alternative.” The manufacturer did not say how it was “enriched”, but I suspect it was enriched by adding extra leucine.

What Do These Studies Mean For You? 

Don’t Leave Out Resistant Exercise. These studies were focused on the timing and quality of protein. But don’t forget that adequate protein and leucine are only two of the requirements for preventing age-related muscle loss. The third, and arguably the most important, is resistance exercise.

Aim for at least three 30-minute resistance exercise sessions per week. If you have physical limitations consult with your health professional about the type, duration, and intensity of resistance exercise that is right for you.

Forget What You Have Been Told About Protein. You have been told that American consume too much protein. That’s probably true for the average couch potato. But it is not true for seniors. The average American does consume too much of the wrong kind of protein, but that’s another story for another day.

You have been told that the average woman only needs 46 grams of protein per day, and the average man needs only 56 grams of protein per day. That’s based on the RDA of 0.8 gm/kg (0.36 gm/pound) and an average weight of 127 pounds for women and 155 pounds for men.

We haven’t weighed that since the 50’s. Today the average woman weighs 170 pounds, and the average man weighs 201 pounds. That means protein intake should be at least 61 gm/day for women and 72 gm/day for men.

But that’s only if you are in your twenties or thirties. The consensus among those who study protein needs in seniors is that the RDA should be 1.2 gm/kg (0.54 gm/pound) for adults over 50. That’s 91 gram/day and 108 grams/day, respectively, for average weight women and men.

With that perspective, it is easy to understand the recommendation that seniors get 25-30 grams of protein and 2.5-2.7 grams of leucine per meal.

These studies did not address leucine intake, but they suggest that optimal protein intake may be closer to 30-40 grams of protein per meal. That’s 90-120 grams of protein day. But that is probably not what you are hearing from your doctor.

Why Is Supplemental Protein Important? It’s easy to say that seniors should get 30-40 grams of protein per meal, but that’s not the way most seniors eat.

When I was a child growing up in Alabama the standard breakfast was eggs, ham, grits with ham gravy and biscuits. I’m not saying that it was a healthy breakfast, but it was the standard breakfast where I lived at the time. And it provided plenty of protein.

In today’s world most seniors have been told to avoid eggs and red meat. Breakfasts are more likely to be some type of cereal with a fruit garnish and perhaps some toast. That’s a much healthier breakfast, but it’s a low-protein breakfast. That’s why most seniors only get 8-15 grams of protein at breakfast time.

I won’t go into lunches, but similar transformations have taken place at lunch time, which is why most seniors only get 15-20 grams of protein at lunch.

CerealAnd many seniors get even less protein at breakfast and lunch. For example:A cup of coffee and a croissant or a “healthier” bowl of cornflakes and skim milk at breakfast only provides 6 grams of protein.

  • A healthy green salad at lunch only provides 2 grams of protein.

In cases like this, the protein supplements may need to provide 30-40 grams of protein rather than the 20-25 grams of protein used in these studies.

So, if you want to avoid age-related muscle loss you have two choices:

  • Completely change your diet and incorporate more healthy protein foods into your breakfast and lunch menus or…
  • Add a protein supplement to your low-protein meals. The studies I have described above suggest that 20-25 grams of supplemental protein may be sufficient to transform a low-protein meal into one that will support muscle protein synthesis and minimize age-related muscle loss.
  • And if your breakfast and lunches are very low in protein, 30-40 grams of supplemental protein may be necessary to optimize protein intake.

Why Is Protein Quality Important? The second study shows that having enough protein is not sufficient to stimulate muscle protein synthesis. It must be high quality protein.

The authors of the study suggested that collagen did not stimulate muscle protein synthesis due to its low leucine content.

And, as I mentioned earlier, the pea protein used in the study was “enriched” so it could be used as a “whey or soy alternate”, and the “enrichment” probably included adding extra leucine.

So, if you are planning to use a plant protein supplement with your low-protein meal(s), I would recommend choosing one with added leucine.

How Much Protein Is Too Much? That depends on your age. If you are in your 20s or 30s, the ability of a protein meal and/or supplement to stimulate muscle protein synthesis begins to plateau at around 30 grams of protein, so there is little advantage to protein intakes above 30 grams at one time.

But if you are a senior, you use protein less efficiently. These and other studies with seniors suggest that 30-40 grams of protein per meal may be optimal.

However, high protein intake can be risky for some. The risk is smaller than you have been told, but it is not zero. Here are my recommendations:

  • If your physician has told you to limit protein intake, follow their advice.
  • If you are unsure about the health of your kidneys, consult with your physician before increasing your protein intake.
  • Keep adequately hydrated. Byproducts of protein metabolism can stress your kidneys if you are dehydrated.

What About An After-Workout Supplement? Previous studies have shown that the numbers are about the same for after-workout supplements.

  • For someone in their 30s, 15-25 grams of protein with 1.7 grams of leucine per meal is enough to maximize muscle gain after a workout.
  • But someone in their 60s or 70s needs at least 25-30 grams of protein and 2.5-2.7 grams of leucine per meal to maximize muscle gain.

One Final Pearl

At the very beginning of this article, I told you that the breakdown of muscle protein to keep blood sugar levels constant during fasting and starvation was driven by a hormone called glucagon.

And the active ingredient in the latest weight loss drugs like Wegovy, Ozempic, and Trulicity is GLP-1, which stands for glucagon-like peptide 1.

So, it should be no surprise that those drugs cause loss of muscle mass. That’s a side effect you probably haven’t been told about.

But the good news is that properly designed protein supplements can help you maintain and (with resistance training) increase muscle mass and also boost GLP-1 levels naturally. When choosing your protein supplement, ask for clinical studies showing that they increase GLP-1 levels.

The Bottom Line 

It’s all downhill after age 50! That’s when we start to experience age-related muscle loss, something called sarcopenia.

Age-related muscle loss can be prevented with resistance exercise, adequate protein, and adequate leucine. And the amount of both protein and leucine we need to prevent muscle loss increases as we age.

Previous studies have defined the amount of protein and leucine we need to prevent muscle loss in our 60s and 70s. The studies described in today’s “Health Tip” show the benefit of adding a protein supplement to our low-protein meals and the importance of a high-quality protein supplement for minimizing age-related muscle loss.

The authors of one of these studies concluded, “Consuming protein much closer to the expert group consensus recommendations [1.2 gm/kg instead of the current 0.8 gm/kg for adults over 50] may help to increase…MPS [muscle protein synthesis] with advancing age and extend health-span – compressing the years of disease and disability commonly experienced by older individuals closer to the end of life.”

For more information on these studies, how much protein you need, and what they mean for you, read the article above.

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

_____________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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 text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

 

For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

 

 

Are Seed Oils Inflammatory?

by

Rethinking Seed Oils

Author: Dr. Stephen Chaney

You can’t believe everything you read on the internet. Food myths abound. And they sound so convincing. The articles you read quote clinical studies supporting their food myth. And they offer plausible sounding explanations for why their food myth is accurate.

I have written a book, “Slaying the Food Myths”, to help you recognize and avoid food myths.

I started that book by sharing “secrets only scientists” know. The top 2 are particularly relevant.

  • Scientists design their studies to disprove existing paradigms. That guarantees there will be studies on both sides of every issue.
  • Every study has its flaws. But some have more flaws (are lower quality) than others.

Unfortunately, many of the online posts you read “cherry pick” the studies that support their belief.

  • Some of this is innocent. The authors aren’t scientists, so they may not know the studies they quote are of low quality. While their mistake may be innocent, the information they are sharing is still wrong.
  • But I am less tolerant of “experts” who base their posts on studies they know are of low quality. I call them “Dr. Strangeloves”.

New food myths arise every day. And recently, food myths about seed oils have started to proliferate. Seed oils have become the latest food villain. It has gotten to the point where many people scan every label to make sure that no seed oil touches their lips.

To help clarify the situation, I have written a recent “Health Tips From the Professor” article debunking the seed oil myths.

Among the myths I discussed was the “seed oils cause inflammation” myth. In today’s “Health Tips From the Professor”, I will delve into that topic more deeply and share the latest research with you.

But before I do that, I need to return to my professor mode and share some background information.

What Are Omega-6 Fatty Acids And Why Do They Matter?

Professor

  • There are two classes of essential fatty acids – omega-6 and omega-3.
  • In each case there is a shorter fatty acid found in plant foods which is converted to a longer fatty acid which, in turn, is converted to a group of regulatory molecules that control a variety of biological functions including blood clotting and inflammation.
    • For the omega-6 group the shorter fatty acid is linoleic acid (LA), and the longer one is arachidonic acid (AA). Linoleic acid is the major fatty acid found in seed oils.
    • For the omega-3 group, the shorter fatty acid is linolenic acid, and the longer ones are EPA and DHA.
  • Essential fatty acids are the only foods for which it is literally true that, “You are what you eat”.
    • The membrane composition of every cell in your body reflects the relative amount of omega-6 and omega-3 fatty acids in your diet.
    • This means the ratio of omega-6 to omega-3 fatty acids in your cell membranes are identical to the ratio of omega-6 to omega-3 fats in your diet.

The significance of these statements will become apparent as I describe the study and its significance below.

What Do We Know About Omega-6 Fatty Acids And Inflammation?

FlamesThis is an important question because the omega-6 fatty acid linoleic acid (LA) is the major fatty acid in seed oils. So, when someone makes the claim that seed oil causes inflammation, they are saying that omega-6 fatty acids cause inflammation. So, the question becomes, “Is that true?”

For years the answer to this question has been unclear. Some studies have concluded that omega-6 fats decrease inflammation, while other studies suggest they increase inflammation. And, of course, the influencers who warn of the dangers of seed oils have cherry picked the studies showing they increase inflammation while ignoring studies showing they decrease inflammation.

It turns out that studies claiming that omega-6 fats increase inflammation are mostly low-quality studies. So, perhaps we should ask what recent high-quality studies show.

  • In 2012 a systematic review of the effects of linoleic acid (LA) on inflammatory markers stated, “We conclude that virtually no evidence is available from randomized, controlled intervention studies among healthy, non-infant human beings to show that addition of LA to the diet increases the concentration of inflammatory biomarkers”.
  • Two major meta-analyses that pooled the data from multiple studies found that circulating LA levels were inversely correlated with cardiovascular disease and type 2 diabetes [That means that higher levels of LA correlated with lower levels of heart disease and diabetes].
  • A recent report from the UK Biobank study found a strong inverse association between plasma LA levels and both total and cause-specific mortality [Higher levels of LA correlated with a longer life].
  • Based on these and other studies, the American Heart Association concluded, “To reduce omega-6 fat intakes from their current levels [in the American diet] would be more likely to increase rather than decrease coronary heart disease.”

Clearly, recent research is trending towards the conclusion that the omega-6 fat found in seed oils reduces inflammation and the risk of major disease.

But the authors of the current study (HTM Lai et al, Nutrients, 17, 2076, 2025) wanted to test that hypothesis in a more rigorous manner.

They examined the association between red blood cell membrane levels of linoleic acid (LA) and arachidonic acid (AA) and 10 biomarkers representing different phases and pathways of inflammation in a large, community-based sample (The Framingham Offspring Study).

How Was This Study Done?

clinical studyThe investigators used data from the Framingham Offspring Study (children of the original Framingham participants) and the Framingham Omni Cohort (a more ethnically and racially diverse population representing the current Framingham community).

There were a total of 2777 participants (mean age 66 years, 54% women, 9.8% minorities). Blood and urine samples were obtained from these participants during their scheduled examinations between 2005 and 2008.

  • The levels of linoleic acid (LA) and arachidonic acid (AA) were determined from red blood cell membranes.
  • One urinary and nine serum biomarkers of inflammation representing multiple inflammation pathways were measured. (For a list of the biomarkers tested and the rationale for their inclusion in this study, read the article.

Finally, the correlation between the omega-6 fats and biomarkers of inflammation was calculated.

Are Seed Oils Inflammatory?

Question MarkThe results were as follows:

  • Linoleic acid and arachidonic acid combined were inversely correlated with 6 biomarkers of inflammation and had no effect on the other 4.
  • The inverse association of linoleic acid with inflammatory biomarkers was not affected by age, gender, or ethnicity.

The authors concluded, “Our community-based study identified small, but significant, inverse associations between red blood cell linoleic and arachidonic levels and six major biomarkers of inflammation…representing a wide variety of inflammatory pathways. Our results suggest that linoleic acid is more likely to be anti- than pro-inflammatory, and the present efforts to reduce its intake are ill advised.”

Revisiting Seed Oils

Assortment Of Salad Dressing Bottles

You might be wondering what this study has to do with seed oils.

  • The omega-6 fat linoleic acid is a major component of seed oils (60-75%).
    • So, claims that seed oils are inflammatory are based on the claim that omega-6 fats are inflammatory.
  • This study shows omega-6 fats are more likely to be anti-inflammatory than pro-inflammatory.
  • Based on their heart health benefits, the American Heart Association recommends that we not decrease the amount of omega-6 fats in our diet.
    • Seed oils are the major source of omega-6 fats in our diet.
    • So, the American Heart Association recommendation about not decreasing omega-6 fats in our diet means that decreasing our use of seed oils is not a good idea.

I have debunked the other myths about seed oils in my previous “Health Tips From the Professor” article.

The only true concerns about seed oils have to do with processing, storage, and purity.

  • Omega-6 fats are easily oxidized, and the oxidation process can create free radicals. Free radicals can be created through high heat processing and improper storage.
  • Some seed oils contain undesirable impurities in their natural form. So, both the purification process and quality control testing are important.
  • And, as with most foods and supplements, it is “buyer beware”. Some manufacturers use the cheapest source of seed oil rather than the highest quality source.

My recommendations are:

  • Choose your source carefully.
    • For seeds and nuts look for freshness. If they look or taste funny, throw them out.
    • For oils and salad dressings choose reputable brands and choose ones that use low-heat processing.
  • Don’t overheat them.
    • Most vegetable oils are only suitable for use as salad dressings and other room temperature uses.
    • The exceptions are vegetable oils with high smoke points – for example, olive oil for stir fries and avocado oil for higher temperature cooking.
  • Store them safely. Don’t give them a chance to become oxidized.
    • We store sunflower seeds and almonds in our refrigerator and walnuts in our freezer.
    • We buy unsaturated vegetable oils in small quantities (so they are used up quickly) and store them in the refrigerator.
  • For supplements containing seed oil ingredients choose brands with high quality control standards.

The Bottom Line 

Seed oils have become the latest food villain. In a recent “Health Tips From the Professor” I have debunked the seed oil myths.

In today’s article I share the latest studies showing that seed oils are more likely to be anti-inflammatory than pro-inflammatory.

For more information on this study and how to select and use seed oils safely, read the article above.

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

_____________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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.

 

The Seed Oil Myths

by

The Truth About Seed Oils 

Author: Dr. Stephen Chaney 

The Seed Oil Myths

Myth Versus FactsYou’ve seen the claims. “You should avoid all seed oils. They are toxic.”

Any time you see claims like, “Avoid all…[add the food villain of the day]” or “[a certain food] is toxic” your “truth-meter” should go on high alert. Claims like that are more likely to be hype than truth.

More specifically, the claims about seed oils are:

  • They are heavily processed.
  • They contain toxic ingredients.
  • They are genetically modified.
  • They cause inflammation and oxidative damage.
  • They increase your risk of inflammatory diseases, heart disease, and cancer.
  • A healthier option is to replace seeds oils with animal foods high in saturated fats.

Like any good food myth, there is a kernel of truth to each of these claims. In this article I will describe the kernel of truth associated with each of these claims, put them into perspective, and give practical guidelines for incorporating seed oils into your diet.

The topics I will cover are:

  • The truth about fats.
  • The truth about omega-6 fats.
  • The truth about saturated fats.
  • The truth about canola oil.
  • The truth about seed oils.

The Truth About Fats

The health authorities and media must think the American public is stupid. They oversimplify everything. They tell us:

  • Animal fats are saturated fat.
  • Olive oil is monounsaturated fat.
  • Vegetable oils are omega-6 polyunsaturated fat.
  • Fish oil is omega-3 polyunsaturated fat.

The truth is that every naturally occurring fat and oil is a mixture of all four kinds of fat. And each food contains a unique mixture of fats. The kernel of truth is:

  • Animal fats have a higher percentage of saturated fat than other fats and oils.
  • Olive oil has a higher percentage of monounsaturated fat than other oils.
  • Vegetable oils have a higher percentage of omega-6 polyunsaturated fat than other oils.
  • Fish oil has a higher percentage of omega-3 polyunsaturated fat than other oils.

 

But the full truth is that each food contains a unique mixture of fats. For example,

  • Meat and butter from grass-fed animals contain a greater percentage of omega-3 fats than meat and butter from animals which were fattened on corn.
  • Flaxseed oil has a higher percentage of omega-3 fats than other seed oils.
  • High-oleic sunflower oil has the highest percentage of monounsaturated fat than other seed oils.
    • Other vegetable oils with high monounsaturated fat content include olive oil, avocado oil, and canola oil. [Note: Although olive oil is the source of monounsaturated fat that we hear about most, avocado oil is equally high in monounsaturated fat and has a higher smoke point, which makes it a better choice for high-heat cooking.]
  • Walnuts have a higher percentage of omega-3 fats than other nuts.
  • Macadamia nuts and almonds have the highest percentage of monounsaturated fats than other nuts, with cashews and peanuts not far behind. Nut butters, of course, reflect the fat composition of the nuts.

The point I am making is that while myths are simple, the truth is much more complex.

Take Home Lesson: Every vegetable oil and every seed oil has a unique composition of fats. Each has its unique benefits and unique drawbacks.

That is something you will want to think about the next time you read an article about the dangers or the benefits of all seed oils. Every seed oil is unique. No generalization applies to all of them.

Biochemistry 101 – Essential Fats

ProfessorLet’s start with the most important point.

  • Omega-6 fats and omega-3 fats are essential. Simply put, that means:
  • We can’t make them.
  • They are essential for life.
  • We must get them from our diet.

If they are essential, the next question is, “Why do we need them?” Let me start with a little “Biochemistry 101” and talk about their role in cell membranes and cellular regulation.

Cell Membranes:

  • You might think of cell membranes as a solid protective armor around the cells, but nothing could be farther from the truth. A better analogy would be the ocean that covers vast areas of our planet. Our membranes are quite fluid.
  • And that membrane fluidity is important. Our cell membranes contain receptors like the cholesterol receptor and insulin receptor that must cluster together for cholesterol and insulin to be transported into the cell. Those receptors cluster best when cell membranes are very fluid.
  • Our membranes are most fluid when they contain high levels of polyunsaturated fats (For membrane fluidity it doesn’t matter if they are omega-6 or omega-3). Conversely, our membranes are less fluid when they contain high levels of saturated fats.
  • And here is the most important point. Because our bodies cannot make omega-6 and omega-3 polyunsaturated fats, this is the one time it is literally true that, “We are what we eat”. If our diets are high in saturated fats, our membranes are high in saturated fats. If our diets are high in polyunsaturated fats, our membranes are high in polyunsaturated fats.
    • And the ratio of omega-6 and omega-3 polyunsaturated fats in our membranes reflects the ratio of omega-6 and omega-3 polyunsaturated fats in our diet.

Take Home Lesson: Diets high in omega-6 and/or omega-3 fats help lower cholesterol levels and improve blood sugar regulation.

Cellular Regulation:

  • Our cells also use the polyunsaturated fats in our cell membrane to make hormone-like substances called prostaglandins and leukotrienes that exert profound effects on nearby tissues. [Note: For the sake of simplicity, I will just talk about prostaglandins for the rest of this article, but what I say applies equally to leukotrienes.]
  • The enzymes that make prostaglandins do not distinguish between omega-6 and omega-3 polyunsaturated fats. They just use whatever polyunsaturated fat they come across.
  • That’s important because the effects of omega-6 and omega-3 prostaglandins are often different and are sometimes opposite.
  • Here’s where the “We are what we eat” principle comes into play. The ratio of omega-6 and omega-3s in our diet determines the omega-6 and omega-3 content of our membranes. And that determines the type of prostaglandins our cells produce.

Take Home Lessons:

  • Some of the benefits of omega-6s are unique because they are dependent on omega-6 prostaglandins. These benefits cannot be duplicated by diets high in omega-3s.
  • Because some effects of omega-6 and omega-3 prostaglandins are opposite, we need to look closely at the omega-6 to omega-3 ratio in the diet to optimize the health benefits of these two essential polyunsaturated fats.

Now, with Biochemistry 101 behind us, we are ready to look at the truth about omega-6 fats.

The Truth About Omega-6 Fats

Assortment Of Salad Dressing Bottles

Let’s start by looking at the pros and cons of omega-6 fats. 

Pros Of Omega-6 Fats:

Cellular Health: Omega-6 and fats are important for maintaining proper membrane fluidity. And omega-6 prostaglandins also regulate cell metabolism and cellular repair mechanisms.

Heart Health: Omega-6s are associated with lower risk of heart disease. This is caused by:

  • Lower cholesterol levels due to proper membrane fluidity which allows clustering of cholesterol receptors.
  • More flexible endothelial cells lining our arteries, which helps lower blood pressure and prevent blockage of the arteries by blood clots. This is most likely due to more fluid cell membranes and the production of beneficial prostaglandins.
  • Some of these benefits are duplicated by omega-3 fats, but the American Heart Association stated in a recent Health Advisory (WS Harris et al, Circulation, 119, 902-907, 2009) that omega-6 fats are essential for some heart health benefits. They cannot be replaced by omega-3s.

Brain Health: Omega-3s get most of the press here, but experts feel that omega-6s play an important and independent role as well.

Fetal Growth and Development: Omega-6 fats are essential for normal neural development and growth. The mechanism(s) for this benefit are ill-defined.

Other Benefits:

  • Omega-6 fats support healthy skin, hair, and bones. The mechanisms for these effects are unknown, but most experts feel they are independent of omega-3 fats.
  • Omega-6 fats are also important for reproductive health. Most experts think this is due to the production of omega-6 prostaglandins.

Take Home Lesson: Omega-6 fats are essential for a healthy heart, a healthy brain, and normal fetal growth and development.

Cons Of Omega-6 Fats:

Oxidation: Omega-6 (and omega-3) fats are very susceptible to oxidation, especially at high temperatures. This can lead to free radical formation, which can promote the formation of cancer cells.

You may have seen the statement that omega-6 fats cause cancer. This is an oversimplification. A more accurate statement would be, “Improperly used, any polyunsaturated fat may increase cancer risk. But this is largely avoidable. Here are the precautions I recommend:

  • Choose your source carefully.
  • For seeds and nuts look for freshness. If they look or taste funny, throw them out.
  • For oils choose reputable brands and choose ones that use low-heat processing. Also, look for ones with minimal processing. They may be cloudy rather than clear, but they will also contain naturally occurring antioxidants and polyphenols.
  • Don’t overheat them.
    • Most vegetable oils are only suitable for use as salad dressings and other room temperature cooking.
    • The exceptions are vegetable oils with high smoke points – for example, olive oil for stir fries and avocado oil for higher temperature cooking.
  • Store them safely. Don’t give them a chance to become oxidized.
    • We store sunflower seeds and almonds in our refrigerator and walnuts in our freezer.
    • We buy unsaturated vegetable oils in small quantities (so they are used up quickly) and store them in the refrigerator.

Take Home Lesson: Improperly used, omega-6 fats, like any unsaturated fat, can become oxidized and form free radicals (the kernel of truth). Choose your source carefully. Don’t overheat them. Store them safely.

FlamesInflammation: This is the one you hear the most about. You have been told that omega-6 vegetable oils (seed oils) cause inflammation. As a blanket statement, it is mostly untrue. But it does have a kernel of truth.

Let’s start with the kernel of truth:

  • Omega-6 fats are inflammatory only when compared to omega-3 fats. You have also been told that omega-6 fats are inflammatory when compared to saturated fats. This is false, as I will discuss below.

Let me elaborate on the first statement with a little more Biochemistry 101 (If you haven’t guessed, that’s my favorite topic. Once a professor, always a professor).

  • Omega-6 fats are converted into one inflammatory prostaglandin. Omega-3 fats are converted into several anti-inflammatory prostaglandins (This is an example of some omega-6 and omega-3 prostaglandins having opposite effects).
  • Because of their opposite effects on inflammation, some experts say that the optimal ratio of omega-6 to omega-3 fats is in the range of 1:1 to 4:1. But the typical American diet is around 15:1.

If the omega-6 to omega-3 ratio is important (and not every expert agrees that it is), the statement that we should avoid omega-6-containing vegetable oils (seed oils) because they are inflammatory is mostly untrue.

  • Every omega-6 oil has a different omega-6 to omega-3 ratio. For example,
    • Corn oil has a 50:1 ratio and sesame oil has a 42:1 ratio. If you are just going by omega-6 to omega-3 ratios, you might want to avoid these.
    • Soybean oil has a 7:1 ratio and extra virgin olive oil has a 5:1 ratio. They are almost in the optimal range.
    • Canola oil has a 2:1 ratio. It’s in the optimal range.
    • And flaxseed oil is the clear winner with a 1:4 ratio.

But the truth is also much more complex than you have been led to believe.

  • The kernel of truth is that omega-6 fats can be converted to an inflammatory prostaglandin.
  • But omega-6 fats can also be converted to anti-inflammatory prostaglandins. And some omega-6 fats such as GLA are anti-inflammatory.
  • Human clinical studies find that omega-6 fats either have no effect on inflammation or decrease it slightly (A Poli et al, International Journal of Molecular Sciences, 24, 4567, 2023).

Take Home Lesson: Omega-6 fats are converted into one inflammatory prostaglandin (the kernel of truth). But they are also converted to anti-inflammatory prostaglandins. The net effect in the human body is a slight anti-inflammatory effect.

The Truth About Saturated Fats

You have been told that saturated fats are anti-inflammatory and decrease the risk of heart disease. For many Americans those claims are enticing because it means they don’t have to change their diet. But are the claims true?

You have been told that these claims are based on science. There are clinical studies behind them. Is that true?

The problem is that there are a lot of bad studies on saturated fats in the literature, and the Dr. Strangeloves of the world cherry pick the ones that support their beliefs.

If you want to compare the effect of different kinds of fat on either inflammation or heart health, you must make sure that all other components of the diet are the same. Too many of these studies have compared a whole food diet high in saturated fat with the typical American diet high in omega-6 fats. The results are predictable. Anything is better than the typical American diet.

In a previous issue of “Health Tips From The Professor” I discussed the criteria for a good study of fats. High quality studies must:

  • Show the subjects stick with the new diet for the duration of the study. Subjects find it difficult to adhere to a diet to which they are not accustomed long term and often revert to their more familiar diet. This requires either very close monitoring of what the subjects are eating or measurement of fat membrane composition to verify diet adherence, or both.
  • Carefully control or measure what the saturated fats are replaced with. In good studies only the fat composition of the diet changes. All other components of the diet remain the same.
  • Last two years or more. The fats we eat determine the fat composition of our cell membranes, and that is what ultimately determines both inflammation in our bodies and our risk of dying from heart disease. While it is true to say, “We are what we eat”, changing the fat composition of our cell membranes does not occur overnight. It takes 2 years or more to achieve a 60-70% change in the fat composition of cell membranes.
  • Measures multiple markers of inflammation or actual cardiovascular end points such as heart attack, stroke, and deaths due to heart disease.

When studies are done that meet these criteria the results are as follows:

Inflammation (A Poli et al, International Journal of Molecular Sciences, 24: 4567, 2023):

  • Replacing saturated fats with omega-6 fats reduces inflammation by 8%.
  • Replacing saturated fats with omega-3 fats reduces inflammation by 48%

Heart Disease (FM Sacks et al, Circulation, 136, Number 3, 2017):

  • Replacing saturated fats with omega-6 from decreased the risk of heart disease by 24%.
  • Replacing saturated fats with a mixture of both omega-6 and omega-3 fats decreased the risk of heart disease by 29%. This is equivalent to statin therapy, without the side effects.
  • When the replacement of saturated fats with omega-6 and omega-3 fats occurred in the context of a heart healthy diet such as the Mediterranean diet, heart disease risk was reduced by 47%.

The Food and Nutrition Board of the Institute of Medicine recommends that Americans not exceed 10% of calories from saturated fat.

  • Two thirds of Americans exceed this limit.

The Food and Nutrition Board recommends that omega-6 fats be around 5-6% of calories. Because omega-6 fats play an important role in heart health, the American Heart Association recommends they be at 5-10% of calories.

  • Americans get around 6.5% of their calories from omega-6 fats.

Take Home Lesson: Replacing saturated fat with omega-6 fats reduces both inflammation and heart disease risk. Adding omega-3 fats reduces both even more. So, bringing omega-6 and omega-3 into a better balance is a good idea. But omega-6 fats are essential and are at the recommended intake for most Americans, so don’t do this by cutting back on healthy omega-6 fats. Instead, add some more omega-3s.

The Truth About Canola Oil

There are a lot of things to like about canola oil:

  • It is an excellent source of healthy omega-6 fats.
  • It has a good omega-6 to omega-3 ratio (2:1), which makes it anti-inflammatory.
  • It is also a good source of monounsaturated fats and has a moderate smoke point, which makes it suitable for low heat cooking.

So, why is it so unpopular? Unfortunately, it suffers from a lot of undeserved myths. Each has a kernel of truth. But like a secret passed around the room, the myths have grown with each repetition, and the truth has become unrecognizable.

So, let’s try to separate the myths from the truth.

Myth: It is genetically engineered.

Truth: It was created by old-fashioned plant breeding.

 

Myth: Canola oil contains toxic ingredients.

Truth:

  • Rapeseed oil comes from the oilseed rape plant (a relative of mustard).
  • Rapeseed oil contains erucic acid and glucosinolates, both of which can be toxic in large amounts (the kernel of truth).
  • Baldur Stefansson from the University of Manitoba bred a “double low” variety the oilseed rape plant which produces an oil that contains <2% of both erucic acid and glucosinolates and is safe for human consumption. This new oil was named canola oil (from Canada and ola for oil). This was achieved by conventional plant breeding. Not genetic engineering.
  • Both cultivars of the oilseed rape plant are still grown. Rapeseed oil is used for industrial purposes, and canola oil is used for human consumption.
  • Canola oil is tightly regulated in Canada, the US, and the EU to <2% erucic acid.
  • 98% of the canola oil sold in the US is grown in Canada and the northern US.

Myth: Canola oil is unhealthy.

Truth: Because it is one of the least expensive omega-6 oils, canola oil is often found as an ingredient in unhealthy, highly processed, food (the kernel of truth). The solution is simple. Avoid unhealthy foods. Adding a different kind of fat to unhealthy foods is not going to make them healthier.

The Truth About Seed Oils

By now I have covered most of the myths about seed oils in my sections on omega-6 fats, saturated fats, and canola oil, but here is a quick review.

Myth: All seed oils are…[add your favorite derogatory term here].

Truth: Every seed oil has a unique composition of fats. Each has its unique benefits and unique drawbacks.

 

Myth: Seed oils are genetically modified.

Truth: The plants producing canola oil and high oleic sunflower oil have been modified (the kernel of truth), but they were modified by conventional plant breeding rather than genetic engineering.

 

Myth: Seed oils contain toxic ingredients. This myth is most often directed at canola oil.

Truth: Rapeseed oil contains components that can be toxic at high levels (the kernel of truth). However, the rapeseed plant has been bred to produce canola oil with safe levels of those components.

 

Myth: Seed oils are inflammatory, which increases your risk of inflammatory diseases and heart disease.

Truth: Seed oils contain omega-6 fats which can be converted into one inflammatory prostaglandin (the kernel of truth). But they are also converted to anti-inflammatory prostaglandins. The net effect in well done human clinical trials is a slight anti-inflammatory effect.

 

Myth: Seed oils cause oxidative damage, which increases your risk of cancer.

Truth: Seed oils (like any polyunsaturated fat) are susceptible to oxidation, especially at high temperatures. This can lead to free radical formation and oxidative damage (the kernel of truth). But this is only true when you use them improperly. The solution is to chose your source wisely, store them safely, and to not overheat them when cooking.

 

Myth: Saturated fats are healthier than seed oils. Replacing saturated fat with the omega-6 fats found in seed oils increases inflammation and heart disease risk.

Truth: Many studies in this area of research are poorly designed. Well-designed studies show that replacing saturated fat with the omega-6 fats found in seed oils reduces both inflammation and heart disease risk.

 

Myth: Omega-3 fats are healthier than the omega-6 fats found in seed oils, so we should replace seed oils with omega-3 fats.

Fact: Omega-3 fats are more effective than omega-6 fats at reducing inflammation and heart disease risk (the kernel of truth). However, omega-6 fats are essential for a healthy heart, a healthy brain, and normal fetal growth and development. We can’t make them, so we must get them from our diet. Americans are currently consuming the recommended amount of omega-6 fats. So, we should not decrease the amount of omega-6 fats in our diet. Instead, we would benefit from adding more omega-3s to our diet.

 

Myth: Seed oils are highly processed. High heat processing alters the oils. Processing also removes beneficial antioxidants and polyphenols from the oils.

Truth: This is mostly true. The solution is to choose your brands carefully.

  • For oils choose reputable brands and choose ones that use low-heat processing. Also, look for ones with minimal processing. They may be cloudy rather than clear, but they will also contain naturally occurring antioxidants and polyphenols.
  • It’s not easy to choose your source carefully. But this difficulty is not unique to seed oils. For example:
    • The term EVO is supposed to mean extra virgin olive oil was used, but cheaper oils are sometimes blended into the olive oil to save money.
    • If a company wishes to use the term “grass fed” on their product, they must file a certification with the USDA, but the USDA does not inspect to determine whether the certification is accurate.
    • Seed oils are also found as an ingredient in unhealthy, highly processed foods. The solution here is simple. Avoid unhealthy foods. Adding a different kind of fat to unhealthy foods is not going to make them healthier.

For more details about each of these Truth statements, read the article above.

The Bottom Line

There are many myths about seed oils. Each myth has a kernel of truth but is mostly false. In this week’s “Health Tips From the Professor” I discuss the myths and truths about seed oils. Because this is a complex subject, I have broken it down into individual topics that address one or more seed oil myths before talking about seed oil myths directly.

The topics I covered are:

  • The truth about fats.
  • The truth about omega-6 fats.
  • The truth about saturated fats.
  • The truth about canola oil.
  • The truth about seed oils.

For more details read the article above.

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

_____________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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 text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

 

 

 

The News About Omega-3s Just Got Better

by

What Does This Study Mean For You? 

Author: Dr. Stephen Chaney 

good newsA recent meta-analysis (AA Bernasconi et al, Mayo Clinic Proceedings, 96: 1365-1375, 2021) of randomized clinical studies with over 150,000 patients showed that omega-3s reduced the risk of heart attacks by 13% and fatal heart attacks by 35%. Another major clinical study (T Chao et al, Nutrition, Metabolism and Cardiovascular Disease, 34: 537-547, 2024) with 30,000 patients found that omega-3s reduced all-cause mortality by 10%, cardiovascular mortality by 18%, heart attacks by 33%, and sudden cardiac death by 33%.

In short, the evidence that omega-3s reduce the risk of heart attacks and other forms of cardiovascular disease keeps getting stronger. However, the effect of omega-3s on heart failure is not as clear. Some studies suggest that omega-3s reduce the risk of heart failure and heart failure deaths. But other studies find little or no effect.

That’s unfortunate because heart failure is responsible for 45% of cardiovascular deaths and 14% of all deaths in the United States. In 2023 6.7 million Americans had heart failure, and that number is expected to increase to 8.5 million in 2030.

But numbers don’t tell the whole story. It is the trend in heart failure deaths that is truly concerning. Heart failure deaths per 100,000 Americans decreased by 20% between 1999 and 2012. Then the trend abruptly reversed. By 2021 heart failure deaths per 100,000 people was greater than in 1999. And the increase in heart failure deaths shows no signs of slowing down.

Nobody knows what is causing this rapid increase in heart failure deaths. But clearly the miracles of modern medicine are not working. And because the clinical studies on omega-3s and heart failure risk have been confusing, omega-3s are not currently recommended for heart failure patients.

This study (M A Jawad et al, Mayo Clinic Proceedings, 99: 1895-1904, 2024) was designed to clear up the confusion about omega-3s and heart failure risk.

How Was This Study Done?

clinical studyThis utilized data from the UK Biobank study. The UK Biobank study is an ongoing study that enrolled 502,366 subjects, aged 40-69, from the United Kingdom between April 1, 2007, and December 31, 2010. It regularly collects environmental, lifestyle, and genetic data on these individuals and tracks their health outcomes.

Within the study 273,033 participants had their blood levels of omega-3s determined by mass spectrometry. These measurements were used to calculate the Omega-3 Index (% of membrane fatty acids that are omega-3s) of these participants.

Of these participants:

  • 271,794 did not have a heart failure diagnosis at the time the omega-3 levels were determined. This group was used to evaluate the effect of omega-3s on the risk of developing heart failure.
  • 1,239 had a heart failure diagnosis at the time the omega-3 levels were determined. This group was used to determine whether omega-3s reduced the risk of death in heart failure patients.
  • 20,000 from this group had a repeat measurement of omega-3 levels around 4 years after the first measurement to determine the consistency of omega-3 levels. On average the repeat measurements were slightly lower, but the differences were small.

These participants were followed for an average of 13.7 years.

  • A diagnosis of heart failure was based on international diagnosis standards.
  • Deaths were identified by using the central death registry in the United Kingdom.

The News About Omega-3s Just Got Better

Omega-3s And Heart DiseaseThe data were clear. When participants with an Omega-3 Index in the top 20% were compared to those with an Omega-3 Index in the bottom 20%:

  • The risk of developing heart failure during the 13.7-year follow-up period was reduced by 21%.

When participants with a heart failure diagnosis prior to omega-3 measurement were compared in the same manner:

  • All-cause mortality was reduced by 48%
  • Cardiovascular mortality was reduced by 43%.

When the investigators looked at the effect of omega-3 supplementation in this population:

  • The risk of developing heart failure was 5% lower for those who reported omega-3 supplement use. I will discuss the reason for the discrepancy between comparisons based on omega-3 supplement use and comparisons based on blood levels of omega-3s below.

The authors concluded, “Higher plasma levels of marine omega-3 fatty acids were associated with a lower incidence of heart failure. Furthermore, among patients with preexisting heart failure, higher omega-3 levels were associated with lower risks of all-cause mortality and cardiovascular mortality. These findings suggest that increasing plasma omega-3 levels, whether by diet or supplementation, could reduce both risk for development of heart failure and death in those with prevalent heart failure.”

What Are The Strengths And Weaknesses Of This Study?

strengths and weaknessesThis was a very large, very well-done study. There is the usual caveat for this type of study, namely that it looks at associations and cannot prove cause and effect. However, it would be impossible to perform a double blind, placebo-controlled study with that many people for almost 14 years.

And heart failure does not happen overnight. Studies of the size and length are required to show meaningful effects of diet and/or supplementation on health outcomes like heart failure are not feasible.

Another major strength of this study is that it measured blood levels of omega-3s and showed those blood levels were relatively stable over time rather than relying on participants remembering what they ate and/or what supplements they used.

  • In terms of supplement use, studies like this one simply ask whether omega-3 supplements were used. They do not ask what the dose was, how frequently they were taken, the form of the omega-3 supplement (fish oil, EPA-only, DHA-only), and whether they were consumed with food or not (which affects absorption).
  • Studies that rely on diet recall and/or supplement use also have another weakness, namely individual differences in the absorption and utilization of omega-3 fatty acids. Simply put, two individuals getting the same dose of omega-3s from diet and supplementation may have different levels of omega-3s in their cellular membranes.
  • The authors felt it was these differences that explained why they saw a much stronger and more accurate effect of omega-3s on heart failure when they based their comparison on blood levels of omega-3s rather than omega-3 supplement use.

In short, this study significantly strengthens the evidence that omega-3s reduce the risk of heart failure and improve survival for those with heart failure.

What Does This Study Mean For You?

confusionHere are the take-home lessons from this study:

As I said above, this study significantly strengthens the evidence that omega-3s reduce the risk of heart failure and improve survival for those with heart failure. That means:

  • Optimizing your intake of omega-3s may be a good strategy for reducing your risk of heart failure. More importantly, optimizing omega-3 intake may also be a good strategy for improving your survival if you have been diagnosed with heart failure.
  • The authors said, “Because omega-3 is a well-tolerated over-the-counter nutrient…it is perplexing why this safe and affordable therapy…has not been widely incorporated into guideline-directed medical therapy for heart failure. Omega-3s…should be considered as add-on therapy to the standard regimen in the prevention and treatment of heart failure.” I agree.

But what is the optimum intake of omega-3s? This is what the authors had to say about that:

  • The top 20% of participants in this study had a blood Omega-3 Index of >5.45%, but this is not necessarily optimal.
  • Previous studies have suggested that an Omega-3 Index of 8% is the optimal target for reducing the risk of death from other forms of heart disease, and the authors feel this is also the optimal target for reducing the risk of heart failure.
  • The average American has an Omega-3 Index of 4-5%, which is associated with a high risk of heart disease.
  • Previous studies have indicated that an average intake of 1.4 g/day of EPA + DHA is required to move from an Omega-3 Index of 4% to 8%.

But the key word here is “average”.

  • None of us are average. We all absorb and retain omega-3s with different efficiencies. Many people will do great with 1.4 g/day. But some may need more to achieve an Omega-3 of 8%. And others will need less.
  • That’s why I recommend that you request blood tests of your Omega-3 Index and use those to guide you to an optimal 8% rather than relying on dosage of omega-3 supplements or frequency of omega-3-rich fish consumption alone.
  • However, I recognize that Omega-3 Index determinations are expensive and not all doctor’s offices are equipped to provide them. On average, an intake of 1-2 g/day of EPA + DHA is safe and likely effective at reducing risk of heart failure and other forms of heart disease. But it may not be optimal for you.

The Bottom Line 

Previous studies have shown that an optimal intake of omega-3s is likely to reduce the risk of heart attacks and deaths from heart disease. But the news about omega-3s just got better. A recent study strengthened the evidence that omega-3s also reduce the risk of heart failure and improve survival for those with heart failure.

The authors concluded, “Higher plasma levels of marine omega-3 fatty acids were associated with a lower incidence of heart failure. Furthermore, among patients with preexisting heart failure, higher omega-3 levels were associated with lower risks of all-cause mortality and cardiovascular mortality. These findings suggest that increasing plasma omega-3 levels, whether by diet or supplementation, could reduce both risk for development of heart failure and death in those with prevalent heart failure.”

For more details on this study and what it means for you, read the article above.

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

_______________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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 text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

 

Why Is Keeping Weight Off So Hard?

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Can You Achieve Permanent Weight Loss? 

Author: Dr. Stephen Chaney 

Why is the dreaded yo-yo rearing its ugly head again? You tried a new diet this year, and it worked really well. The weight came off easily. But the diet is over, and the pounds are starting to creep up once again.

You are beginning to wonder if this diet was just like all the other yo-yo diets you’ve tried in the past. You are wondering whether those pounds you lost will come back and bring their friends with them. If so, you’ll be like 156 million Americans who lose weight and gain it all back each year.

And it’s so frustrating. You are trying to be good. You are still exercising and trying to eat healthily. Why isn’t it working?

Could it be that your fat cells have a memory? Could it be they like to be big and bulky with lots of stored fat? While that description is a bit fanciful, a new study (LC Hinte et al, Nature Online, 2024) suggests your fat cells may have a memory, which could explain why it is so hard to keep the weight off.

This is a highly technical study. So, before I discuss how the study was done, I should perhaps review a little bit of Biochemistry 101.

Biochemistry101: Epigenetics and Gene Activity

EpigeneticsWhat Is Epigenetics? When I was a young graduate student (which is more than just a few years ago), I was taught that all genetic information resided in our DNA. During conception, we picked up some DNA from our dad and some from our mom, and that DNA was what made us a unique individual.

In recent years, the hype has centered on DNA sequencing. It seems like everyone is offering to sequence your genome and tell you what kind of diet is best for you, what foods to eat, and what supplements to take. But can DNA sequencing fulfill those promises?

The problem is that DNA sequencing only tells you what genes you have. It doesn’t tell you whether those genes are active. Simply put, it doesn’t tell you whether those genes are turned on or turned off.

This is where epigenetics comes in. Epigenetics is the science of modifications that alter gene expression. In simple terms, both DNA and the proteins that bind to DNA can be modified. This does not change the DNA sequence. But these modifications can determine whether a gene is active (turned on) or inactive (turned off).

This sounds simple enough, but here is where it really gets interesting. These modifications are affected by our diet, our lifestyle (body weight and exercise, for example), our microbiome (gut bacteria), and our environment.

And if that weren’t complicated enough, some of these epigenetic changes (DNA modifications) can be transitory and others are long-lasting.

The authors of this study hypothesized that obesity causes long-lasting epigenetic changes to certain critical genes in our fat cells that slow metabolism and promote fat accumulation, even after we have lost weight. In other words, these epigenetic changes “prime” our fat cells to regain all the weight we’ve lost.

How Do You Measure the Effect of Epigenetic Changes? As you might expect this study measured epigenetic modifications to critical genes in fat cells. But that’s only part of the story. Epigenetic modification can turn genes on, turn them off, or have no effect on gene activity.

So, the investigators also needed to monitor the activity of the genes to determine the effect of the epigenetic modifications. Fortunately, one fact you may have learned in high school or college biology is mostly unchanged by the passage of time.

It is that the genetic sequence of DNA is translated into messenger RNA and that messenger RNA is used to code for proteins. If epigenetic modifications turned on a gene, we would expect higher levels of the corresponding messenger RNA and corresponding protein in those cells. Conversely, if epigenetic modifications turned off a gene, we would expect the opposite.

It turns out that it is much easier to measure changes in messenger RNA levels than individual protein levels that correspond to specific genes. So, the investigators used cellular messenger levels to measure the effect of epigenetic modifications on gene activity.

How Was This Study Done?

clinical studyThe investigators measured the effect of obesity and subsequent weight loss on fat cell gene expression in a limited set of human subjects and supplemented those results with a more expansive set of experiments with mice.

I don’t normally report on animal studies or very small human studies because these studies often lead to misleading results that are not supported by subsequent long-term, large clinical studies.

However, I am making an exception for this study because it leads to an interesting paradigm shift which, if true, changes the way we think about how to keep weight off long term.

Human Study: The investigators determined messenger RNA levels for key genes in fat cells from human volunteers who were:

  • At a healthy weight.
  • Obese both before and 2 years after bariatric surgery that resulted in at least 25% weight loss.

The groups were small (10-16 total), in part because obtaining fat cell samples is an invasive and painful procedure.

Mouse study: The investigators determined both messenger RNA levels and epigenic modifications for key genes in fat cells from 6-week-old male mice who were:

  • Fed either a low-fat or high-fat chow diet for 25 weeks. As expected, the mice fed the low-fat diet remained lean and the mice fed the high-fat diet became obese.
  • Subsequently, the obese mice were put on low-fat chow for 8 weeks during which time their weight returned to normal.
  • Finally, both the ‘always lean’ and ‘formerly obese’ mice were put on high-fat chow to compare how rapidly they gained weight.

What Happens To Fat Cells During Obesity And Weight Loss?

This study is best viewed as a story of what happens to fat cells during obesity and subsequent weight loss. There are two parts – what happens to human fat cells and what happens to mouse fat cells:

 Human Fat Cells: When obese individuals were compared to lean individuals:

  • Genes coding for fat storage and inflammation (which is known to be associated with obesity) were more active.
  • Fat-burning genes were less active.
  • These changes in gene expression were retained even after the obese individuals lost substantial weight through bariatric surgery.

[Note: The measurements of gene expression were based on the amount of messenger RNA produced by those genes.]

The human study had a couple of important limitations, which is why the investigators also did a similar study with mice.

#1: Because the study did not include a habitually lean group who became obese after going on a high-fat diet (no clinical review board would approve such a study), it could not determine whether the differences in gene expression were caused by the onset of obesity or whether they caused obesity.

Simply put, we know some individuals are genetically predisposed to obesity. The differences in gene expression between lean and obese individuals could have simply represented a genetic predisposition to obesity.

The mouse experiments did not suffer from that limitation because it was possible to put lean mice on a high fat diet until they became obese.

#2: The study did not measure epigenetic changes that may have caused the changes in gene expression. That is because humans are genetically heterogeneous. Consequently, you need population studies with hundreds of individuals to reliably determine epigenetic differences between groups.

The mouse experiments did not suffer from that limitation because laboratory mice are genetically homogeneous.

Mouse Fat Cells:

When the investigators looked at the physical effects of obesity:

  • When mice became obese on a high-fat diet:
    • Blood glucose levels rose.
    • Insulin levels rose, indicating the mice had become insulin resistant.
    • Fat accumulated in their livers.
  • When the obese mice lost the excess weight on a low-fat diet all these parameters returned to normal.
  • When the ‘always lean’ and ‘previously obese’ mice were put back on a high fat diet at the end of the study, the previously obese mice gained weight more quickly than the always lean mice.

In other words, mice responded to obesity in the same way that humans do except none of these effects could be explained by genetics. This strain of mice was genetically homogeneous.

When the investigators compared gene expression (as measured by messenger RNA levels) in mice who had become obese to ‘always lean’ mice:

  • Genes coding for fat storage and inflammation were more active.
  • Fat-burning genes were less active.
  • These changes in gene expression were retained even after the obese mice lost weight.

In other words, mice responded to obesity in the same ways as humans with respect to gene expression. However, in this case it was clear that obesity caused the changes in gene expression.

When the investigators looked at epigenetic modifications:

  • They identified epigenetic modifications to the regulatory regions of genes whose activity was increased or decreased when the mice became obese.
  • These epigenetic modifications were retained even after the mice lost weight.

These data suggest, but do not prove, that the epigenetic modifications were responsible for the changes in gene activity.

The authors concluded, “We show that both human and mouse adipose tissues retain transcriptional changes after appreciable weight loss.

Furthermore, we find persistent obesity induced alterations in the epigenome of mouse adipocytes that negatively affect their function and response to metabolic stimuli. Mice carrying this obesogenic memory show accelerated rebound weight gain…in response to high-fat diet feeding.

In summary, our findings indicate the existence of an obesogenic memory, largely on the basis of stable epigenetic changes, in mouse adipocytes and probably other cell types. These changes seem to prime cells for pathological response [weight gain] in an obesogenic environment, contributing to the problematic ‘yo-yo’ effect often seen with dieting.”

More simply put, the investigators concluded that obesity causes epigenetic modifications to the DNA of fat cells that prime them to regain their fat stores. They said that this may contribute to the ‘yo-yo’ effect often seen with dieting and explain why keeping weight off is so hard.

Why Is Keeping Weight Off So Hard?

Question MarkYou are not alone. You are like millions of other Americans. You lose weight effectively, but you struggle to keep it off. You just look at a donut and the fat jumps from the donut to your hips. You try to eat right, but the pounds keep creeping back on.

Experts have told us for years that our fat cells (and perhaps other cells in our body) are the culprit. Those cells have switched from a fat burning mode to a fat storage mode. There have been lots of attempts to explain that phenomenon, but my favorite is one that hypothesizes that our metabolism was designed for paleolithic times when it was either feast or famine.

Simply put, the theory is that our bodies were designed to store energy reserves in times of plenty and hold on to those energy reserves as long as possible in times of famine. Holding on to energy reserves was essential for prehistoric man to survive cold winters when food was hard to come by. And our number one energy reserve is, you guessed it, fat.

That is an appealing hypothesis, but it doesn’t tell us how our bodies manage to do that.

That’s what makes this study so intriguing. It may be wrong. It needs to be substantiated by large scale clinical trials. But the idea that epigenic changes occur during obesity and persist after substantial weight loss is novel. More importantly, it may explain the “feast or famine” response and why it is so hard to keep weight off after substantial weight loss.

Can You Achieve Permanent Weight Loss?

By now you may be thinking, “I thought my weight loss woes were due to my genetics. Now you’re telling me that they could be due to my epigenetics. Am I doubly cursed? Is there nothing I can do to keep my weight off?”

I can tell you science doesn’t have a simple answer, but there are two big clues that offer hope.

#1: Slow and steady wins the race. Obesity experts have known for years that slow weight loss often results in permanent weight loss.

  • If you are counting calories, that means a reduction of around 500 calories per week (That’s 71 calories per day, which is equivalent to one small apple, one hard-boiled egg, or 1.5 ounces of chicken breast). And a 500-calorie deficit maintained each week for a year can lead to a 20-25 pound weight loss.
  • If you are thinking of diets, it could amount to switching to a diet of unprocessed or minimally processed foods consisting of fruits, vegetables, whole grains, and primarily plant-based proteins without worrying about calories or serving sizes. Again, clinical studies show that switching from the typical American diet to this kind of diet can lead to substantial weight loss over a period of years.

Neither approach is popular in the weight loss world, but they work. Why do they work? It could be because the daily reduction in calories is so small that it never triggers the famine response.

If we look at the two parts of the study I reported on above:

  • In the human study weight loss was achieved through bariatric surgery which causes a huge reduction in caloric intake and rapid weight loss.
  • In the mouse study going from high-fat chow to low-fat chow represented a large decrease in calories. And again, weight loss was very rapid. It took the mice 25 weeks to become obese and only 4-8 weeks to lose the weight they had gained.

When viewed from this perspective, the epigenetic modifications observed after weight loss in this study may have been due to the famine response rather than a retention of the modifications observed during obesity.

And when you think about it, most popular diets feature major restrictions (calories, fats, carbs, forbidden foods, time of eating) and cause rapid weight loss. They are likely to trigger a famine response as well.

#2: The secrets of the National Weight Control Registry. There are some people who manage to keep their weight off and avoid the yo-yo effect. They don’t have any genetic or epigenetic advantage over the rest of us. They have lost weight on every diet imaginable – including rapid weight loss fad diets.

Yet they have managed to keep the weight off. What are their secrets? How did they avoid regaining their weight? How did they avoid the yo-yo diet effect?

An organization called the National Weight Control Registry was established to answer that question. It has enrolled more than 10,000 people who have lost weight and kept it off. On average people in this group have lost 66 pounds and kept it off for at least 5 years.

The National Weight Control Registry kept track of what they did to keep the weight off. Everyone’s approach was a little different, but the National Weight Control Registry summarized the ones that were most frequently mentioned. Here is what they do that you may not be doing:

#1: They consume a reduced calorie, whole food diet.

#2: They get lots of exercise (around 1 hour/day).

#3: They have internalized their eating patterns. In short, this is no longer a diet. It has become a permanent part of their lifestyle. This is the way they eat without even thinking about it.

#4: They monitor their weight regularly. When they gain a few pounds, they modify their diet until they are back at their target weight.

#5: They eat breakfast on a regular basis.

#6: They watch less than 10 hours of TV/week.

#7: They are consistent (no planned cheat days).

The good news is that participants in the National Weight Control Registry reported that while maintaining weight loss was difficult at first, it became easy after 2 years.

Of course, we don’t know whether is due to epigenic modifications being reset to “lean” by these behaviors or whether the new behaviors became automatic and overrode epigenetics.

It doesn’t matter. It means you can end the ‘yo-yo’ cycle forever. You can keep weight off, and you know how to do it.

The Bottom Line

A recent study in both humans and mice suggests that epigenetic modifications to key genes in your fat cells make it hard to keep weight off. These epigenetic changes may explain why so many people struggle with yo-yo dieting.

 

For more details on this study and how you may be able to override these epigenetic modifications and prevent weight regain read the article above.

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

 _____________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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 text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

Maternal Mortality In The United States

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Leading Causes Of Maternal Deaths

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

Editor: Dr. Steve Chaney

Maternal Mortality In The United States

Between 2018 and 2021, the maternal mortality (death) rate in the United States nearly doubled, placing the country last among developed nations in maternal health outcomes.  The maternal mortality ratio (MMR) is a key indicator of a nation’s overall health, making this rapid increase a cause for serious concern.

Understanding Maternal Mortality

Maternal mortality refers to the number of women who die during pregnancy or within 42 days (six weeks) after childbirth for every 100,000 live births. As per the Government Accounting Office, 25% of the increase in maternal mortality from 2020 to 2021 was due to Covid-19, which contributed to the doubling of the maternal mortality ratioi.

The maternal mortality ratio is used globally to assess the state of a country’s health. A rising MMR signals the need for urgent action.

In 2022, the U.S. recorded an overall maternal mortality ratio 22.3 deaths per 100,000 live birthsii. This decreased by about 10 deaths per 100,000 from 2021 (32 deaths per 100,000 live births in 2021). However, stark racial disparities continued to exist as demonstrated through 2018 to 2021.

  • Black women: 49.5 deaths per 100,000 live births (more than 2.5 times the rate for white women)
  • White women: 19.0 deaths per 100,000 live births
  • Hispanic women: 16.9 deaths per 100,000 live births
  • Asian women: 13.2 deaths per 100,000 live births

Maternal Mortality versus Pregnancy Related Deaths

What Is The Difference?

While maternal mortality measures deaths that occur from the onset of pregnancy to six weeks post-delivery, pregnancy-related deaths extend further.  Pregnancy-related deaths are the number of deaths per 100,000 live births up to 12 months (one year) after birth or the first birthday.

Does The Age Of The Mother Make A Difference?

The age of the mother significantly affects the risk of dying during pregnancy. The ratio of deaths among women younger than 25 years of age is 14.4 deaths per 100,000 live births. Women aged 25 to 39 have a rate of 21.1/100,000 live births, while those aged 40 and older face a staggering 87.1 deaths per 100,000 live birthsiii. This means that women over 40 are dying at six times the rate of those under 25 and four times the rate of women aged 25 to 29iv.

When Are The Deaths Occurring?

Surprisingly, a little under half (47%) of maternal deaths occur during pregnancy or within the first week postpartum (Maternal Mortality).  And a little over half (53%) happen between one week and one year after childbirth or the baby’s first birthday (Pregnancy-Related Deaths).

Leading Causes Of Maternal Deaths

The primary causes of maternal mortality in the U.S. are largely preventablev. The six main causes of maternal death include:

  • Mental Health Conditions (23%) – Suicide, overdose, and substance-related poisoning are the leading causes, this affects White and Hispanic women more than Black or Asian women.
  • Hemorrhage (14%) – Severe postpartum bleeding remains one of the top causes of maternal deaths not only in the Unites States but throughout the world with Asian women being more susceptible. Hemorrhage is defined as bleeding about one half quart of blood.
  • Cardiac Conditions (13%) – Heart disease disproportionately affects Black women.
  • Blood Clots (9%) – A major contributor to maternal deaths.
  • Cardiomyopathy (9%) – A condition affecting the heart muscle, making it harder to pump blood efficiently.
  • Hypertensive Disorders of Pregnancy (7%) – relating to high blood pressure

Contributors to maternal death include familial, societal, health care system issues and one’s personal health. it is possible to reduce the risks of maternal death by understanding one’s personal health history and your family’s health history.

This information informs nutritional, behavioral and lifestyle changes that can be made prior to and during pregnancy to reduce health risks, enabling a healthier pregnancy outcome.

The Bottom Line

  • The United States has the highest maternal mortality rate amongst all developed countries in the world.
  • The maternal mortality rate in the U.S. has nearly doubled between 2018 and 2021; Covid-19 caused a 25% increase of maternal deaths from 2020 to 2021 which contributed to the doubling of maternal deaths. Black women have been disproportionately affected, with mortality rates 2.5x that of White women.
  • Women aged 40 and over die at four times the rate of women ages 25 to 39 and six times more than women under 25 years of age.
  • The leading causes of maternal deaths include mental health conditions, hemorrhage, cardiac conditions, blood clots, and cardiomyopathy— most of which are preventable.
  • Almost half of maternal deaths occur throughout pregnancy and the first week after childbirth. A little more than half of maternal deaths occur from the first week following birth up to the first year after birth.  It’s important to continue monitoring mothers with home visits once they return home from the hospital and up until one year after birth.

References

i General Accounting Office, Maternal Health: Outcomes Worsened and Disparities Persisted During the Pandemic.  Oct, 2022.

ii Hoyert DL.  Maternal mortality rates in the United States, 2022.  NCHS Health E-Stats.  2024.  DOI:https://dx.doi.org/10.15620/cdc/152992.

iii Ibid

iv Ibid.

vFour in five pregnancy related deaths in the US are preventable – https://www.cdc.gov/media/releases/2022/p0919-pregnancy-related-deaths.html.

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 – Over 80 videos exploring pregnancy, labor, birth, postpartum and contraception

www.thecarabcompany.com – Website with free downloadable pregnancy and birth information

Mastering Pregnancy and Birth Coaching Program –  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.

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 has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years.

Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

Eating For A Healthy Heart

by

What Does This Mean For You?

Author: Dr. Stephen Chaney

You may remember the nursery rhyme, “Jack Sprat could eat no fat. His wife could eat no lean…” You may know people who fit these extremes. And in terms of diets these extremes might represent the vegan and keto diets in today’s world.

The nursery rhyme assures us that, “…between them they licked the platter clean.” But were their diets equally healthy? Which of them would have been more likely to live a long and healthy life?

And, since this is Heart Health Month, we might ask, “Which diet would have been better for their hearts?”

If you search Mr. Google – even with AI assist – you might be confused. That’s because AI bases its recommendations on the quantity of posts, not the accuracy of posts. And lots of media influencers recommend both diets, and just about every popular diet in between for heart health.

But what does good science say on the topic of heart healthy diets? Fortunately, a recent comprehensive review and meta-analysis (G. Riccardi et al, Cardiovascular Research, 118: 1118-1204, 2022) has answered that question.

How Was The Study Done?

clinical studyThe investigators reviewed 99 clinical studies with tens of thousands of participants that looked at the associations between foods or food groups and heart disease risk.

Most of the studies were “prospective cohort” studies in which:

  • Populations are divided into groups (cohorts) based on the foods they consume…
  • …and followed for a number of years (this is where the term “prospective” comes from)…
  • …and at the end of the study, the association between food and heart outcomes is measured.

However, the review also included several major randomized controlled clinical trials, including:

  • The DASH diet study.
  • The Lyon Diet Heart study.
  • The PREDIMED study.

Eating For A Healthy Heart

strong heartHere are the findings of the study. Most will sound very familiar. But you will note some subtle differences based on recent data.

The overall summary was that for a healthy adult population:

  • Low consumption of salt and foods of animal origin…
  • …and increased intake of plant foods…
  • …are associated with reduced heart disease risk.

Of course, we have known that for years. It’s when they broke the data down further that it became more interesting.

Foods Of Animal Origin:

  • Processed meats increase heart disease risk. A single serving of processed meat is associated with a 27% to 44% increased risk of heart disease. This is not new.
  • Unprocessed red meat is also associated with increased risk of heart disease, but this association is not as Steakconsistent as for processed meats. The authors noted that some of this may be due to differences in saturated fat content or cooking methods of the red meats included in individual studies.

But this analysis also showed that the effect of red meat on heart disease risk may be dose dependent. For example:

    • The studies they reviewed suggested that consuming ≥2 servings per day of red meat is associated with a 27% increased risk of heart disease. However, consuming <3 servings per week may not increase risk.
    • The idea that the effect of red meat on heart disease risk may be dose-dependent is novel. However, the authors said we also need to ask what replaces red meat in the diet. They postulated that when red meat consumption is decreased, it is often replaced with healthier protein sources.
  • White meat such as poultry does not appear to affect heart disease risk. This has been predicted by earlier reports, but this analysis strengthens those predictions.
  • Fish consumption decreases heart disease risk. This is not new. But this review added precision about recommended fish intake (2-4 servings/week) and a couple of caveats:
    • The heart benefits of fish may be due to their omega-3 content and may not apply equally to fish with lower omega-3 content.
    • The authors also expressed concerns about the sustainability of high-omega-3 fish populations. I would also add that our oceans are increasingly polluted, so contamination is another concern.
  • Egg consumption up to one egg/day does not appear to increase heart disease risk. This is consistent with the are eggs good for youcurrent American Heart Association recommendations.

However, the authors noted that the effect of eggs on serum cholesterol, and hence heart disease risk depends on several factors.

    • Genetics, obesity, and diabetes can make it more difficult to regulate serum cholesterol levels. For these individuals, eggs may need to be eaten only sparingly.
    • Diets low in saturated fat and high in fiber from plant foods help the body regulate serum cholesterol. Several studies suggest that eggs may decrease heart disease risk in the context of this type of diet.
  • Dairy: Neither low-fat nor high-fat dairy foods appear to influence heart disease risk. This is different from the standard recommendation to consume low-fat dairy foods. But it is in line with the trend of recent research studies on dairy and heart disease.

Once again, there were a couple of caveats:

    • There is increasing evidence that fermented dairy foods may decrease heart disease risk which may explain why certain high-fat cheeses and other high-fat fermented dairy foods appear to have a neutral or slightly beneficial effect on heart disease risk.
    • As with eggs the effect of high-fat dairy foods on heart disease risk may be influenced by genetics and diet context.

Foods Of Plant Origin: The effect of plant foods have been known for some time, and the most recent studies included in this analysis have not changed those conclusions.

  • Fruits and Vegetables consistently reduce heart disease risk in multiple studies. In each case, the optimal Vegan Foodsintake appears to be about 2 servings of each per day which provides an 18-21% risk reduction for vegetables and a 21-32% risk reduction for fruits.
  • Legumes (beans and peas) also consistently reduce heart disease risk in multiple studies. At the optimal intake of around 4 servings per week the risk reduction is around 14%.
  • Nuts also consistently reduce heart disease risk. At the optimal intake of around one serving (a handful) per day, the risk reduction is around 25%.
  • Cereals (grains) were divided into 3 categories:
    • Refined carbohydrates with a high glycemic index (e.g., white rice, white bread) are associated with increased heart disease risk in multiple studies probably due to their effect on blood sugar levels. And the increased risk is significant (Around 66% higher risk for every 2 servings).
    • Refined carbohydrates with a low glycemic index (e.g., pasta, corn tortillas) show an inconsistent effect on heart disease risk.
    • Whole grains are consistently associated with a lower heart disease risk. Two servings of whole grains per day are associated with a 25%-34% decreased risk.

Miscellaneous Foods:

  • Soft Drinks are associated with increased heart disease risk. One serving per day increases the risk by around 15-22% and recent evidence suggests that artificially sweetened soft drinks offer no heart health benefits compared to sugar sweetened soft drinks.
  • Coffee and Tea are both associated with decreased heart disease risk. For coffee the optimal benefit may occur at around 3 cups/day. Higher levels may have an adverse effect on heart disease risk.

Summary of Heart Health Recommendations

ScientistIf you are thinking that was a lot of information, the authors provided a numerical summary of their recommendations for a heart-healthy diet. They are:

  • Two servings per day of vegetables, fresh fruits, and whole grains.
  • One serving per day of nuts and seeds, low-glycemic index refined cereals, extra-virgin olive oil or non-tropical vegetable oils, and yogurt.
  • Four servings per week of legumes and fish.
  • No more than 3 servings per week of white meat, eggs, cheese, and milk.
  • No more than 2 servings per week of high-glycemic index refined starchy foods, red meat, and butter.
  • Only occasional consumption of processed meats.

What Does This Study Mean For You?

QuestionsOf course, nobody wants to follow a “diet by the numbers”. If you are like most of us, you want flexibility and you want to be able to eat some of your favorite foods. So, let me put these recommendations into a more “user friendly” form.

If you want a healthy heart:

  • Whole, unprocessed or minimally processed, plant foods are your friends.
  • Your heart-healthy foundation should be fruits, vegetables, whole grains, nuts and seeds, healthy plant oils, and legumes.
  • Your heart-healthy foundation can also include fermented dairy foods and low-glycemic index refined grains.
  • Your “go-to” beverages should be water, tea (both caffeinated and herbal teas), and coffee. You should avoid soft drinks and other sugar-sweetened or artificially sweetened beverages.
  • Once you have achieved a heart-healthy foundation you can add a few servings per week of white meat, eggs, cheese, and dairy, even high-fat dairy.
  • If you have good adherence to the heart-healthy foundation described above and no genetic or health issues that increase your risk of heart disease, you can probably eat more of these foods.
  • Conversely, if your adherence to the heart-healthy foundation is poor and/or you are at high risk of heart disease, you may wish to consume less of these foods.
  • If you have good adherence to the heart-healthy foundation, you can also add up to 1-2 servings of high-glycemic index refined carbohydrates, red meat, or butter per week. With red meat, you may want to consider it as a garnish that adds flavor to a plant-based meal rather than the centerpiece of the meal.
  • You should eat processed meats seldom or never.

The Bottom Line

A new comprehensive review and meta-analysis of 99 clinical studies with tens of thousands of participants has updated the correlation between foods and heart disease risk.

Many of the recommendations based on this analysis are identical to previous recommendations for a heart-healthy diet.

But there are some subtle changes to those recommendations based on the latest data.

For more details about this study and what a heart-healthy diet might look like for you, read the article above.

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

_______________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

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

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 text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

Health Tips From The Professor