Dr. Steve Chaney

Update On Omega-3 Supplementation And Heart Disease

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How Much Omega-3s Do You Need?

Pendulum
Pendulum

In previous issues of “Health Tips From The Professor” I have described the medical consensus about omega-3 supplementation and heart disease as resembling a pendulum.

A few positive studies are published, and the pendulum swings in the positive direction. The medical consensus becomes, “Omega-3s may reduce heart disease risk.”

Then a few negative studies are published, and the pendulum swings in the other direction. The consensus becomes that omega-3 supplements are worthless. One review a few years ago went so far as to say that fish oil supplements were the modern-day version of snake oil.

Meta-analyses combine the data from multiple clinical studies to increase statistic power and minimize the effect of clinical studies that are outliers. They are supposed to provide clear answers to medical questions like the effect of omega-3 supplements on heart disease.

However, the meta-analyses published to date have also reached conflicting conclusions about the effectiveness of omega-3 supplementation. No wonder you [and the medical community] are confused!

In 2018 three large, well-designed, clinical studies looking at the effect of omega-3 supplementation on heart disease risk were published. They reached different conclusions. However, they covered a much wider range of omega-3 doses than previous studies. And the studies with the highest doses of omega-3s showed the most positive effect of omega-3 supplementation on the reduction of heart disease risk.

That lead a group of doctors and scientists from the United States and Finland to postulate that many previous studies had failed to find an effect of omega-3 supplements on heart disease risk because the dose of omega-3s they used was too low.

These scientists designed a very large meta-analysis (AA Bernasconi et al, Mayo Clinic Proceedings, doi.org/10.1016/j.mayocp.2020.08.034) to test their hypothesis. In short, their study was designed to:

  • Determine whether supplementation with the omega-3 fatty acids EPA and DHA resulted in reduced heart disease risk.
  • Quantify the relationship between the dose of EPA + DHA and the risk of heart disease outcomes.

How Was The Study Done?

Clinical StudyThis study was a meta-analysis of 40 randomized control clinical studies on the effect omega-3 supplementation on heart disease outcomes. Specifically:

  • It included all high-quality clinical studies of omega-3 supplementation published before August 2019.
  • It included a total of 135,267 participants.
  • It included participants at both low and high risk of developing heart disease.
  • It included studies of supplementation with EPA alone and with EPA + DHA.
  • It included omega-3 doses ranging from 400 mg/day to 5,500 mg/day.
  • It excluded dietary studies because:
    • It is difficult to measure the dosage of omega-3s that participants are consuming in dietary studies.
    • It is difficult to assure their compliance with dietary advice.
    • There is variation in the omega-3 content of various foods.
    • Participants in these studies are often advised to make other changes in diet. It then becomes difficult to know whether any benefits observed were from changes in omega-3s or from changes in other components of the diet.

Update On Omega-3 Supplementation And Heart Disease

omega-3 supplements and heart healthHere are the results of the meta-analysis. Supplementation with EPA or EPA + DHA reduced:

  • Coronary Heart disease (defined as diseases caused by atherosclerosis, such as angina, heart attack, and heart failure) by 10%.
  • Heart Attacks by 13%.
  • Coronary Heart disease deaths by 9%.
  • Heart attack deaths by 35%.

Because of the large number of participants in this meta-analysis, they were able to reach some other important conclusions:

  • Despite the claims you may have heard about a new drug consisting of highly purified EPA, this study found no evidence that EPA supplementation was superior to EPA + DHA supplementation.
  • Even though heart medications provide some of the same benefits as omega-3s, this study concluded that omega-3 supplementation reduced the risk of heart disease even for patients on multiple heart medications.
  • This study also concluded that omega-3 supplementation was likely to be effective for people at both low and high risk of heart disease. This means that omega-3 supplementation is likely to be beneficial for preventing heart disease.

The authors concluded: “The current study provides strong evidence that EPA + DHA supplementation is an effective strategy for the prevention of certain coronary heart disease outcomes…Considering the relatively low costs and side effect profiles of omega-3 supplementation and the low drug-drug interactions with other standard therapies…clinicians and patients should consider the potential benefits of omega-3 (EPA/DHA) supplementation…”

What Does This Study Mean For You?

Heart AttackThe most significant conclusions from this study are the reduction in heart attacks and heart attack deaths. That is because:

  • Approximately 1.5 million Americans suffer a heart attack each year. For those who survive their quality of life may be permanently altered.
    • A 13% reduction in heart attacks means that something as simple as EPA + DHA supplementation might prevent as many as 195,000 heart attacks a year.
  • Approximately 100,000 Americans will die from a heart attack each you.
    • A 35% reduction in heart attack deaths means that EPA + DHA supplementation might prevent as many as 35,000 deaths from heart attacks each year.
  • For many Americans sudden death from a heart attack is the first indication that they have heart disease.
    • As Benjamin Franklin said, “An ounce of prevention is worth a pound of cure”. That is why EPA + DHA supplementation makes sense for most people.

I can’t say that this study will be the final word on omega-3 supplementation and heart disease risk. However, several recent studies have supported the benefit of omega-3 supplementation at reducing heart disease risk. The pendulum has clearly swung in the direction of omega-3s being beneficial for heart health.

Of course, omega-3 supplementation is not a magic “Get Out of Jail Free” card. You can’t expect it to overcome the effects of a bad diet and lack of exercise with omega-3 supplementation alone. You need a holistic approach.

The American Heart Association recommends:

Doctor With Patient

  • If you smoke, stop.
  • Choose good nutrition.
    • Choose a diet that emphasizes vegetables, fruits, whole grains, low-fat dairy products, poultry, fish, legumes, non-tropical vegetable oils, and nuts.
    • Choose a diet that limits sweets, sugar-sweetened beverages, and red meats.
  • Reduce high blood cholesterol and triglycerides.
  • Reduce your intake of saturated fat, trans fat and cholesterol and get moving.
  • Lower High Blood Pressure.
  • Be physically active every day.
    • Aim for at least 150 minutes per week of moderate-intensity physical activity per week.
  • Aim for a healthy weight.
  • Manage diabetes.
  • Reduce stress.
  • Limit alcohol.
  • Have a regular physical checkup.

Add in omega-3 supplementation to these recommendations and you have a winning combination.

How Much Omega-3s Do You Need?

Question MarkAs I mentioned at the beginning of this article the omega-3 dosages used in the studies included in this meta-analysis ranged from 400 mg/day to 5,500 mg/day. More importantly, there were enough participants in these studies to obtain a fairly accurate estimate of dose response. This allow the authors to answer the question, “How much omega-3s do I need?”The study found that:

  • The protective effect of omega-3s for heart attack deaths and coronary heart disease deaths plateaued with dosages of EPA + DHA that exceeded 800 – 1200 mg/day.
  • The dose response of the protective effect of omega-3s for non-fatal heart attacks was linear over a wider range of dosages, with every increase 1,000 mg/day of EPA + DHA decreasing the risk of heart attack by 9%.

Based on the totality of their data, the authors concluded, “…clinicians and patients should consider the potential benefits of omega-3 supplementation, especially using 1,000 to 2,000 mg/day dosages, which are rarely obtained in most Westernized diets, even those including routine fish consumption.”

The Bottom Line

A recent meta-analysis combined the data from 40 clinical studies with over 135,000 participants looking at the effect of omega-3 supplementation on various types of heart disease. The study found that supplementation with EPA or EPA + DHA reduced:

  • Coronary Heart disease (defined as diseases caused by atherosclerosis, such as angina, heart attack, and heart failure) by 10%.
  • Heart Attacks by 13%.
  • Coronary Heart disease deaths by 9%.
  • Heart attack deaths by 35%.

Because of the large number of participants in this meta-analysis, they were able to reach some other important conclusions:

  • This study found no evidence that EPA supplementation was superior to EPA + DHA supplementation.
  • This study concluded that omega-3 supplementation reduced the risk of heart disease even for patients on multiple heart medications.
  • This study also concluded that omega-3 supplementation was likely to be effective for people at both low and high risk of heart disease. This means that omega-3 supplementation is likely to be beneficial for preventing heart disease.
  • The optimal dose of EPA + DHA appeared to be 1,000 – 2,000 mg/day.

The authors of the study concluded: “The current study provides strong evidence that EPA + DHA supplementation is an effective strategy for the prevention of certain coronary heart disease outcomes…Considering the relatively low costs and side effect profiles of omega-3 supplementation and the low drug-drug interactions with other standard therapies…clinicians and patients should consider the potential benefits of omega-3 (EPA/DHA) supplementation, especially using 1,000 to 2,000 mg/day dosages, which are rarely obtained in most Westernized diets, even those including routine fish consumption.”

For more details, including a more detailed discussion of what this study 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.

Do Antioxidants Reduce Diabetes Risk?

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What Diet Is Best For Reducing Your Risk Of Diabetes?

ConfusionI don’t need to tell you that nutrition is confusing. The headlines change day to day. One day antioxidants are good for you. The next day they are worthless. What are you to believe?

That is why I knew you would be skeptical when you saw recent headlines saying things like, “Antioxidants reduce your risk of diabetes” or “An antioxidant-rich diet may prevent diabetes”. You are probably waiting for the other shoe to drop.

You are waiting for the next headline telling you to ignore the previous headlines.

That is why I decided to analyze the study (FM Mancini et al, Diabetologia, 61: 308-316, 2018) behind the headlines and tell you whether the headlines were true or false. More importantly, I wanted to put the study into perspective so you could apply the findings to your life.

How Was The Study Done?

Clinical StudyThe data for this paper came from the Interaction of Genetic and Lifestyle Factors on the Incidence of Type 2 Diabetes (InterAct) study. French women born between 1925 and 1950 were enrolled in the study beginning in 1990.

Women were excluded from the study if they had pre-existing cardiovascular disease, diabetes, or cancer.

In June of 1993 a very extensive dietary questionnaire was mailed to all participants. The antioxidant capacity of each of the foods in the diet was estimated using an existing database, and the total antioxidant content of each woman’s diet was calculated.

A total of 64,223 women (average age = 52) completed the questionnaire and were followed for 15 years. During that time 1751 of the women developed type 2 diabetes.

The study correlated the total antioxidant content of the diet with the risk of developing type 2 diabetes. Coffee was excluded from the analysis because the antioxidants found in coffee are high molecular weight compounds, and it is not clear how well they are absorbed.

The major sources of antioxidants in the French diet were fruits (23%), vegetables (19%), wine (15%), tea (10%), and chocolate (2%). Whole grains and beans are also good sources of antioxidants, but the French (and Americans) don’t eat enough of them to influence their total antioxidant intake.

In case you were wondering why wine and chocolate were among the five top sources of antioxidants, remember this is the French diet we are talking about.

Do Antioxidants Reduce Diabetes Risk?

Diabetes and healthy die The authors of the study divided the women into 5 groups (quintiles) based on the antioxidant content of their diets. Quintile one had the lowest antioxidant intake, and quintile five had the highest antioxidant intake.

Compared to the women in quintile one (lowest antioxidant intake), the risk of developing type 2 diabetes was decreased by:

  • 15% for women in quintile two.
  • 30% for women in quintile three.
  • 38% for women in quintile four.
  • 39% for women in quintile five (highest antioxidant intake).
  • As you might guess from the data above, there was an inverse association between total antioxidant content of the diet and type 2 diabetes up until somewhere between the third and fourth quintiles.
  • Above that antioxidant level, the relationship between dietary antioxidant content and risk of developing type 2 diabetes plateaued.

The authors concluded, “Our findings suggest that the total antioxidant capacity of the diet may play a role in reducing the risk of type 2 diabetes in middle-aged women. As type 2 diabetes represents a high disease burden worldwide, our results may have important public health implications.”

What Diet Is Best For Reducing Your Risk Of Type 2 Diabetes?

While most of the headlines talked about the effect of antioxidant intake on the risk of developing type 2 diabetes, we need to remember that the study was done with antioxidant-rich foods. That raises 3 important questions.

#1: Is it the antioxidants or the foods that decrease the risk of developing type 2 diabetes?

Diabetes-&-Vitamin-CThis was a diet rich in fruits, vegetables, and tea with moderate amounts of wine and chocolate. Although they didn’t make it to the top 5 in this study, whole grains and beans are also a good source of dietary antioxidants. In short, this was a very healthy diet.

That represents a complicating factor. For example, fruits and vegetables are also good sources of non-antioxidant phytonutrients that appear to have health benefits. They are also a good source of fiber and the healthy gut bacteria that eat the fiber.

In short, this study shows that healthy foods reduce the risk of developing type 2 diabetes. Since oxidative stress is thought to play a role in the development of diabetes, it is logical that antioxidants in these foods may help prevent diabetes. However, in reality, we don’t know how much of the risk reduction is due to the antioxidant content of the foods and how much is due to other components of the foods.

#2: Is it healthy foods that decrease the risk of type 2 diabetes, or is it due to decreased intake of unhealthy foods?

food choiceThe skeptic in me wants to ask, “Is the diabetes risk reduction due to the healthy foods included in the diet or does it derive from the fact that those foods displaced unhealthy foods from the diet?” It is also legitimate to ask whether people who eat healthier foods also followed a healthier lifestyle.

Fortunately, the data from this study puts those questions to rest. Compared to women in the lowest quintile of antioxidant intake, women in the highest quintile of antioxidants intake from diet:

  • Drank more sugar-sweetened and artificially sweetened beverages.
  • Ate more processed meat.
  • Ate more calories.
  • Smoked more.
  • Were just as likely to be overweight.

These women were more physically active, but in other ways their diet and lifestyle were no better than women with much less antioxidant intake.

However, we do need to remember that these are French women. Their overall diet and lifestyle is much better than American women. For example, at their worst:

  • 30% were overweight or obese compared to >60% for American women.
  • Intake of processed meat was less than ½ serving/day.
  • Intake of sugar-sweetened beverages was less than 1 ounce/day and intake of artificially sweetened beverages was 1.3 ounces/day.

#3: How much healthy foods do your need to include in your diet to reduce the risk of type 2 diabetes?

fruits and vegetablesThe fact that the beneficial effect of adding antioxidant-rich foods to your diet reduced the risk of developing type 2 diabetes up to a point and then plateaued has important implications. It means you don’t need to be a vegan to reduce your risk of type 2 diabetes. You just need to include enough healthy foods in your diet.

“How much healthy foods”, you might ask. If we look at the point at which the benefit of eating antioxidant-rich foods plateaued in this study, the women were eating:

  • 5-6 servings of fresh fruits and vegetables per day.
  • 4 cups of tea/day.
  • 7 pieces of chocolate/day.
  • 1 glass of wine/day.

If you are an American who is consuming less tea, chocolate, and wine than the French, you will probably want to aim for 6 or more servings of fresh fruits and vegetables per day and include whole grains and beans in your diet.

In a previous issue of “Health Tips From the Professor” I reviewed a study that looked at the optimal intake of fruits and vegetables for various other diseases. That study reported:

  • 10 servings per day is optimal for reducing the risk of heart disease, stroke, and premature death.
  • 6 servings per day is optimal for reducing the risk of cancer.

This study suggests 6 servings of fruits and vegetable per day is likely to also be optimal for reducing the risk of developing type 2 diabetes.

The bad news is that the average American eats one serving of fruit and less than 2 servings of vegetables a day. The good news is that each added serving of fruits and vegetables reduces your risk of disease and premature death. The same is probably true for whole grains and beans, but they weren’t specifically included in these studies.

What About Supplementation?

vitamin COf course, some of you will be tempted to say, “Changing my diet is hard. I’ll just take antioxidant supplements.” Will that work. If we are talking about individual antioxidant supplements, the answer is a clear, “No”. Numerous clinical studies have shown that.

However, one study looked at a holistic approach to supplementation and found that it significantly decreased the risk of developing type 2 diabetes over a 20-year period. That is encouraging, but you need to know that the people in that study were not just consuming antioxidant supplements. They were also consuming:

  • Supplements containing B vitamins, calcium, magnesium, and trace minerals.
  • Plant-based protein supplements that replaced some of the animal protein in their diet.
  • Omega-3 supplements.
  • Probiotic supplements.

So, just as was true for the diet study discussed above, antioxidant supplements may be beneficial in reducing the risk of developing type 2 diabetes. However, it is not possible to separate the benefits of antioxidant supplements from the other supplements included in the study.

The Bottom Line

You may have seen recent headlines claiming, “Antioxidants reduce your risk of diabetes”. The study behind those headlines was actually looking at the effect of antioxidant-rich foods like fruits and vegetables at decreasing the risk of developing type 2 diabetes.

The study did show that increasing the amount of antioxidant-rich foods in your diet decreases your risk of developing type 2 diabetes.

Since oxidative stress is thought to play a role in the development of diabetes, it is logical that antioxidants in those foods may help prevent diabetes. However, in reality we don’t know how much of the risk reduction is due to the antioxidant content of the foods and how much is due to the phytonutrient and fiber content of the foods.

There was an inverse association between total antioxidant content of the diet and type 2 diabetes up until somewhere between the 5 and 6 servings per day of fresh fruits and vegetables. At that point. the beneficial effect of eating antioxidant-rich foods plateaued. Eating 6 servings per day of fresh fruits and vegetables appears to be optimal for reducing the risk of developing type 2 diabetes.

To put that into perspective, a previous study that looked at the optimal intake of fruits and vegetables for various other diseases reported:

  • 10 servings per day is optimal for reducing the risk of heart disease, stroke, and premature death.
  • 6 servings per day is optimal for reducing the risk of cancer.

The bad news is that the average American eats one serving of fruit and less than 2 servings of vegetables a day. The good news is that each added serving of fruits and vegetables reduces your risk of disease and premature death. The same is probably true for whole grains and beans, but they weren’t specifically included in these two studies.

Of course, if you really wish to prevent or reverse type 2 diabetes, a holistic approach including weight control, exercise, diet, and supplementation is best.

For more details, including a more detailed discussion of supplementation, 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.

 

Finally, you should also never think of supplementation as a replacement for a healthy diet. If you wish to reduce your risk of developing type 2 diabetes, I recommend a holistic approach that includes weight control, exercise, diet, and supplementation.

Is The Keto Diet Best For Endurance Exercise?

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Where Do Food Myths Come From?

ketogenic dietI don’t need to tell you that the keto diet is popular right now. It is touted for weight loss, mental sharpness, and improved health. I discuss the accuracy of those claims in my book, “Slaying the Food Myths”.

Perhaps more surprising has been the adoption of the keto diet by so many endurance athletes. As I point out in my book, there is a kernel of truth for that idea. Fats and ketone bodies are a very efficient energy source for low to moderate intensity exercise, and we have a virtually unlimited source of stored fat that can be converted to ketone bodies.

However, I always add this caveat, “The keto diet is perfect for endurance exercise – as long as you don’t care how fast you get there”. That is because high intensity exercise requires muscle glycogen stores, which come from the carbohydrates we eat. When you cut carbs from the diet, you deplete your glycogen stores.

And, if you are running a marathon and you want to sprint to the finish line, you will need those muscle glycogen stores. Or, if you are in a cycling event and you want to power up a mountain, you will need those glycogen stores.

Of course, you are probably asking, “Why do so many endurance athletes swear by the keto diet?” There is a dirty little secret behind athlete endorsements. I’m not talking about the money that top athletes get paid for endorsements, although that is also a problem.

I’m talking about the testimonials you hear from your friend who runs marathons or your personal trainer. Unfortunately, testimonials from athletes are notoriously unreliable. The problem is that the placebo effect approaches 70% for athletes.

Competitive athletes are strong willed. If they think a diet or sports nutrition product will help them, they will themselves to a higher level of performance. And this happens subconsciously. They aren’t even aware that their mind is influencing their performance.

So, just because your favorite athlete endorses the keto diet doesn’t mean it is the perfect diet for you. Testimonials can be very misleading.

The important question to ask is, “Do clinical studies support the keto diet as the best diet for endurance exercise?” But, before I answer that question, let me frame the question by asking. “Where do food myths come from?” because the belief that keto diets are best for endurance exercise is a classic food myth.

Where Do Food Myths Come From?

I discussed this question at length in my book, “Slaying The Food Myths”. Let me summarize it briefly here.

Secrets Only Scientists Know: First you need to know the secrets only scientists know. Here are the top 2:

#1: Scientists design their studies to disprove previous studies. There is no glory for being the 10th person to confirm the existing paradigm. The glory comes from being the first to show the existing paradigm might be wrong. While this may seem to be a contrary approach, it is actually the strength of the scientific method.

However, it means that there will be published clinical studies on both sides of every issue.

#2: Every study has its flaws. There is no perfect study.

This is why the scientific community doesn’t base their recommendations on 2 or 3 published studies. We wait until there are 10 to 20 good quality studies and base our recommendations on what 90% of them show.

Now, let me contrast the scientific approach with how food myths are born.

Where Do Food Myths Come From? Food myths usually originate on blogs or websites. Often the articles are written by people with no scientific credentials. But some of them are written by doctors (I will call them Dr. Strangelove to “protect the guilty”). The articles they write have these things in common:

cherry picking studies

  • The articles are based on the biases of the author. No effort is made to look at the other side of the story.
  • The authors “cherry pick” studies that support their bias and ignore studies that contradict them.
  • They use scientific-sounding mumbo jumbo to make their hypothesis sound credible.
  • Their articles are usually spectacular. For example, they say things like, “A particular diet, food, or supplement will either cure you or kill you”, and/or “The medical community is hiding the truth from you.”
  • They never let the facts get in the way of a good story.

Since the idea sounds credible it is picked up by other blogs and websites without any fact checking (social media at its worst). Once it has been repeated often enough, it becomes generally accepted as true. It becomes a food myth. From that point on, studies that disprove the myth are often ignored.

How do you know whether a common belief is true, or just another myth? The only way to be sure is to take a balanced look at all the clinical studies, not just the studies that support the belief.

That is what the authors of a recent review paper (CP Bailey and E Hennessy, Journal of the international Society of Sports Nutrition, 17, Article number: 33, 2020) did for the belief that the keto diet is the best diet for endurance exercise.

Is The Keto Diet Best For Endurance Exercise?

CyclistsBefore I discuss the findings of the review article, there are two things you should know:

#1: There is little scientific research on the effectiveness of the keto diet on endurance exercise. After an exhaustive search of the literature, the authors were only able to find 7 published studies on the topic.

#2:Most sports nutrition studies are of poor quality. In general, they are very small studies, are of short duration, and do not use common test procedures to measure a successful outcome. These studies on keto diets were no different. For example:

    • The number of subjects in these studies ranged from 5 to 29 (average = 14).
    • The duration of time on the diet in these studies ranged from 3 weeks to 12 weeks (average = 5 weeks).
    • Tests used to measure the effectiveness of specific diets on endurance exercise were VO2max (the maximum amount of oxygen you can utilize during exercise), Time to exhaustion (how long you can exercise before you are exhausted), Rating of perceived exertion (feeling of fatigue at the end of the exercise), Race time (time required to complete an event), and Peak power output during the event.
    • Four studies used a treadmill to simulate endurance exercise. The other three used a stationary bike.
    • Five of the studies compared the keto diet to a high carbohydrate diet. Two studies used the keto diet only.

The results were all over the place:

Question Mark

  • Two studies reported an increase in VO2max for both the keto diet and the high carbohydrate diet. One study reported a decrease in VO2max for both diets. The other studies reported no change in VO2max. In short, there was no difference between the diets for VO2max.
  • One study reported a decrease in race time for the high carbohydrate diet and a non-significant increase in race time for the keto diet. Two other studies reported no effect of either diet on race time. In short, one study suggested the high carbohydrate diet was more effective at shortening race time. The other two studies found no effect of either diet.
  • Two studies showed an increase in time to exhaustion for both diets. One study showed a decrease in time to exhaustion for the keto diet (participants got tired more quickly). That study did not include the high carbohydrate diet for comparison. In short, there was no clear difference between the two diets for time to exhaustion.
  • One study showed that the group on the keto diet reported a higher rating of perceived exertion (were more tired) at the end of the endurance event than the group on the high carbohydrate diet. Another study found no difference between the two diets. In short, one study suggested the high carbohydrate diet was better with respect to perceived exertion (tiredness) at the end of the endurance event. Another study found no difference between the two diets.
  • One study reported that peak power was significantly greater for the group on the keto diet than the group on the high carbohydrate diet. One of the studies with the keto group reported that peak power decreased for 4 out of 5 subjects on the keto diet. In short, one study suggested that the keto diet was more effective at increasing peak power than the high carbohydrate diet. Another study suggested the keto diet decreased peak power.

The authors concluded: “When compared to a high carbohydrate diet, there are mixed findings for the effect of the keto diet on endurance performance…The limited number of published studies point to a need for more research in this field.” I would add that we need larger, better designed studies, with common measures of exercise performance.

What Does This Mean For You?

confusionYou may be wondering why I even bothered to talk about such poor-quality studies and a review that could not provide a definitive answer. In fact, that is exactly my point.

This is characteristic of the kind of “evidence” that Dr. Strangelove and his buddies present to support whatever food myth they are featuring on their website. They don’t know how to distinguish good studies from bad studies, and they “cherry pick” only the studies that support their food myth.

So, if you believe that the keto diet is best for endurance exercise, you can “cherry pick” the one published clinical study that supports your belief. You just need to ignore the other 6 published studies.

And, if you believe that a high carbohydrate diet is better for endurance exercise than the keto diet, you can “cherry pick” two clinical studies that support your belief. You just need to ignore the other 5 published clinical studies.

None of the studies are high-quality studies, and the effect of either diet on endurance exercise in these studies is miniscule.

In short, there is no convincing evidence that the keto diet is best for endurance exercise. Or, put another way, we do not have enough evidence to elevate that belief from a food myth to a recommendation we can confidently make for an endurance athlete.

The Bottom Line

A recent publication conducted an impartial review of the evidence for and against the popular belief that a keto diet is the best diet for endurance exercise. The review found only 7 poor-quality studies on this topic in the scientific literature, and the results of those studies were all over the map.

  • One study reported the keto diet was better than a high carbohydrate diet for endurance exercise.
  • Two studies reported that the high carbohydrate diet was better.
  • The other 4 studies were inconclusive.
  • None of the studies found a significant effect on endurance performance by either diet.

So, if you believe that the keto diet is best for endurance exercise, you can “cherry pick” the one published clinical study that supports your belief. You just need to ignore the other 6 published studies.

And, if you believe that a high carbohydrate diet is better for endurance exercise than the keto diet, you can “cherry pick” two clinical studies that support your belief. You just need to ignore the other 5 published clinical studies.

In short, there is no convincing evidence that the keto diet is best for endurance exercise. Or, put another way, we do not have enough evidence to elevate that belief from a food myth to a recommendation we can confidently make for an endurance athlete.

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.

Recovering From A Torn Meniscus

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Regain Full Flexibility And Get Back To The Sports You Love

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney

Happy WomanI love Florida, but I must say I really miss the changing of the leaves like I enjoyed when I lived in New York.  October was magical!  The trees painting a picture of red, gold, maroon, yellow, and green, and the smells that are so familiar to anyone who has ever lived in the north.

Fires burning to heat chilly homes, apple cider, baking pies and cookies because we could get back into the kitchen as the weather cooled down.  And of course, Halloween.

The world has changed so much.  Remember how we could go out in costume with our friends, no adults needed, and go from door to door, shouting “Trick or Treat!”  We’d come home with a pillowcase (or plastic pumpkin) filled with candy.  Such sweet memories..

What Is A Torn Meniscus?

Knee JointOne of my clients asked me to talk about a medial meniscus tear, and that is a topic that is “near and dear to me” because I had a severed medial meniscus from a ski accident.

The meniscus is something that many people aren’t familiar with, unless they have had a meniscus tear, then you definitely know all about it.  It hurts!

All of the major joints are complicated with many ligaments and other structures, each having an important function.

The knee joint is straightforward.

The lateral (outside of knee joint) and medial (inside of knee joint) meniscus cushion the femur (thigh) bone and tibia (shin bone) so your knee can bend and straighten without wearing down the bone.

Ligaments that surround the knee joint hold the bones together and form a tight, secure joint.

How Does A Meniscus Tear?

MeniscusTrauma to the knee joint, especially a twisting movement, will tear the meniscus.

In 1995 I had a ski accident where I severed the medial meniscus, but I didn’t have insurance at the time. I paid the $1000 for an MRI to find out why my knee was in so much pain, and why my knee felt like it was going to totally separate.

It turned out that I not only severed my left medial meniscus, I also tore my anterior cruciate ligament (ACL), The ACL holds your bones together from front to back. When this tore, I felt like whenever stepped down my upper leg still kept going forward.  It was a scary feeling, I felt like my leg was going to come apart at my knee. Yikes!

Recovering From A Torn Meniscus

I need to remind you that I am not a doctor, nor do I have medical training to advise you about what to do.  This message isn’t meant to replace your physician’s advice.

When I found myself with a severed medial meniscus and a torn ACL, and I didn’t have medical insurance, I didn’t know what to do!  Fortunately, I was working along with Zev Cohen, MD.  My therapy practice was in Dr Cohen’s office, and he would often ask me to see one of his patients who were in pain when he knew it wasn’t caused by any systemic or visceral problems.  I totally respected Dr. Cohen because he truly wanted his patients to get better, even if it meant he was going to bring in a massage therapist!

As a result, when Dr. Cohen told me that my meniscus would heal with scar tissue, I believed him. And it worked!  The only glitch was the scar tissue made my knee stiff, so I started to do a movement that I believed would stretch the scar tissue enough so I could bend my knee properly. And that worked too!

Regain Full Flexibility And Get Back To The Sports You Love

A Stretch for AFTER Your Meniscus Heals 

Caution: Do Not do this stretch until your knee is completely healed. 

Stretch For Stiff KneeStand with your feet directly under your hips. Hold on to a closed door, being sure you’re on the side of the door that pushes out so you are pulling it shut as you do the stretch.

While keeping your knees straight up from your ankle, squat down, stopping when you start to feel pain in your knee.  Stay there, and then go just a little bit further.  Don’t push, it’s better to go slowly so your muscles stretch safely.  Scar tissue is really dense, it doesn’t stretch easily (if at all) so you need to slowly allow the scar tissue to loosen.

I can’t guarantee that this will work for you but let me tell you what happened to me.  I was doing this stretch multiple times a day, stopping when it would be too painful – or when I just ran out of time. Then one day – success!

One day I was squatting down and suddenly something released and I ended up sitting on the floor with my knees totally bent!

Since then I’ve been able to get back to skiing, and I have ZERO pain!

Wishing you well,

Julie Donnelly 

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.

Does Vitamin D Prevent Depression?

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Why You Can’t Believe Everything You Read

depressionThe days are getting shorter and Seasonal Depression, often called the “winter blues”, will soon be upon us. Most of the research on Seasonal Depression has centered on the effect of sunlight on our hormones.

However, sunlight is also responsible for the synthesis of vitamin D in our skin cells. So, some experts have hypothesized that low levels of 25-hydroxyvitamin D, the active form of vitamin D, in our blood also play a role in the winter blues.

If so, that could have important implications for managing depression, especially in older adults. Depression is estimated to affect around 6.5 million of the 49 million adults over the age of 65 in our country. Treatment costs for older adults in this country are estimated at $9 billion/year.

If something as simple and inexpensive as a vitamin D supplement could reduce the risk of depression, it would be a huge boon to our health care system.

Association studies suggest that may be a possibility. For example, one recent meta-analysis of 6 clinical studies (H Li et al, The American Journal of Geriatric Psychiatry, 27: P1192-1202, 2019) reported that every 10 ng/mL increase in 25-hydroxyvitamin D was associated with a 12% decrease in the risk of depression in older adults.

However, association studies do not prove cause and effect.

Unfortunately, randomized, placebo controlled clinical trials have given mixed results. A few studies suggested that vitamin D might reduce depression risk, but most of the studies found no effect of vitamin D on depression risk. However, most of the published studies have been poorly designed They were too small, too short, or did not use validated methods for measuring depression.

This was the genesis of the current study (OI Okerke et al., JAMA, 324: 471-480, 2020). It was designed to be a definitive study that would avoid the defects of previous studies.

The study concluded that vitamin D supplementation does not decrease the risk of depression in older adults, and those were the headlines you have probably seen. But is that conclusion true? Let’s take a peek behind the curtain and analyze the study.

How Was The Study Done?

Clinical StudyThis study was an offshoot of the VITAL (VITamin D and OmegaA-3 TriaL) clinical study, so let me start by describing the characteristics of that study.

The VITAL study (JE Manson et al, New England Journal of Medicine, DOI: 10.1056/NEJMoa1811403) enrolled 25,871 healthy adults (average age = 67) in the United States. The study participants were 50% female, 50% male, and 20% African American. None of the participants had preexisting cancer or heart disease.

Study participants were given questionnaires on enrollment to assess clinical and lifestyle factors including dietary intake. Blood samples were taken from about 65% of the participants to determine 25-hydroxyvitamin D levels (a measure of vitamin D status) at baseline and at the end of the first year to assess the effectiveness of vitamin D supplementation. The participants were given either 2,000 IU of vitamin D/day or a placebo and followed for an average of 5.3 years.

This study consisted of 18,353 participants from the VITAL study. Ninety percent of the participants had no previous history of depression. Ten percent had previously been diagnosed or treated for depression but had been depression-free for over 2 years.

The participants filled out annual questionnaires to quantify the onset of depression by three criteria:

  • A diagnosis of depression by a physician.
  • Treatment for depression (medications, counseling, or both).
  • A questionnaire designed to evaluate symptoms of depression. The authors of the study referred to this as an assessment of their mood.

During the 5.3 year follow up period 3.6% of the participants reported the onset of diagnosed depression or a mood consistent with depression. This is consistent with previous studies showing that 1-5% of healthy, non-institutionalized older adults suffer from depression.

Does Vitamin D Prevent Depression?

thumbs down symbolThe results of the study were clear.

Treatment with 2,000 IU of vitamin D3 compared to placebo for 5.3 years did not have a statistically significant effect on:

  • The incidence or recurrence of depression diagnosis, or…
  • Treatment for depression, or…
  • Clinically relevant depressive symptoms.

The authors concluded, “These findings do not support the use of vitamin D3 in adults to prevent depression.”

Why You Can’t Believe Everything You Read

It would be tempting to say, “Case closed. We now know for certain that vitamin D has no effect on depression.”

After all, this was an excellent study. It was large (18,353 participants), lasted a long time (5.3 years), and used well established measures of depression. What’s not to like?

Peek Behind The CurtainUnfortunately, even well-designed studies can give misleading results. Let’s take a peek behind the curtain and see where this study went astray.

There were two glaring deficiencies in this study.

#1: Most of the participants had adequate vitamin D status at the beginning of the study. The average 25-hydroxyvitamin D level of participants at the beginning of the study was 31 ng/mL (78 nmol/L). The NIH considers 20-50 ng/mL (50-125 nmol/L) to be an adequate level of 25-hydroxyvitamin D for most physiological functions. This means that study participants started in the middle of the adequate range with respect to vitamin D status.

This was not a failure of study design. In fact, the authors of the study are to be commended for measuring the vitamin D status of participants at the beginning of the study. Many previous studies have neglected to do that.

The problem is that vitamin D has become extremely popular. Many Americans are already taking multivitamins or vitamin D supplements. To recruit enough people for the study the authors were forced to allow participants to enter the study even if they were taking vitamin D supplements, as long as the amount did not exceed 800 IU/day.

In short, most of the participants in this study were already supplementing with up to 800 IU/day of vitamin D. If so, they were allowed to continue taking their vitamin D supplements. The 2,000 IU of vitamin D was added to what they were already taking.

The question then becomes, if people are already taking RDA levels of supplemental vitamin D and their blood levels of 25-hydroxyvitamin D are already in the adequate range, do we really expect additional supplemental vitamin D to have a beneficial effect?

The author’s answer to that question was, “The mean baseline 25-hydroxyvitamin D level was 30.8 ng/mL; this value is already at a threshold for extraskeletal health benefits [health benefits other than bone health], and so the ability to observe effects of vitamin D3 supplementation may have been attenuated. [To determine whether vitamin D supplementation reduces the risk of depression] large-scale studies would be required to address the effects of high-dose, long-term vitamin D3 supplementation among those with nutrient deficiency.”

My more direct answer would be, “This study provides no useful information on whether vitamin D3 supplementation reduces the risk of depression. What is needed are studies that start with a population that is deficient in vitamin D.”

An accurate conclusion from this study would have been, “If you are already taking vitamin D supplements and/or have an adequate vitamin D status, supplementation with an extra 2,000 IU of vitamin D3 provides no additional benefit with respect to the risk of developing depression.” But that is not what the headlines said.

#2: The study did not record the reason for the onset of depression. That is important because the top 3 causes of depression in adults 65 and older are:

  • Loss of a spouse or partner.
  • Chronic health issues.
  • Restricted blood flow to the brain.

It is unlikely that vitamin D supplementation would have much of an effect on these issues.

In contrast, seasonal depression, which is more likely to be affected by vitamin D supplementation, was not measured in this study.

The Bottom Line

You may have seen recent headlines saying that vitamin D supplementation has no effect on the risk of developing depression.

The study behind these headlines was a very well-designed study. It was large (18,353 participants), lasted a long time (5.3 years), and used well established measures of depression.

It would be tempting to say, “Case closed. We now know for certain that vitamin D supplementation has no effect on depression.”

Unfortunately, even well-designed studies can give misleading results. This one had a major flaw that made the data almost useless.

The problem is that most Americans are already taking multivitamins or vitamin D supplements. To recruit enough people for the study the authors were forced to allow participants to enter the study even if they were taking vitamin D supplements, as long as the amount did not exceed 800 IU/day.

That meant that most participants already had adequate blood levels of 25-hydroxyvitamin D at the beginning of the study.

The question then becomes, if people are already taking RDA levels of supplemental vitamin D and their blood levels of 25-hydroxyvitamin D are already in the adequate range, do we really expect additional supplemental vitamin D to have a beneficial effect? The answer is, “Probably not”.

Rather than saying that this study definitively shows that vitamin D supplementation has no effect on the risk of developing depression, I feel it would be more accurate to say, “This study provides no useful information on whether vitamin D3 supplementation reduces the risk of depression. What is needed are studies that start with a population that is deficient in vitamin D.”

An accurate conclusion from this study would have been, “If you are already taking vitamin D supplements and/or have an adequate vitamin D status, supplementation with an extra 2,000 IU of vitamin D3 provides no additional benefit with respect to the risk of developing depression.” But that is not what the headlines said.

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.

Do Processed Foods Increase Your Risk Of Diabetes?

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Why Do We Keep Eating Processed Foods?

Fast Food DangersUnless you are Rip Van Winkle and have been asleep for the past 20 years you probably know that the highly processed foods in the typical American diet are bad for your health. But perhaps you didn’t realize just how bad they were.

But first, let’s start with a bit of perspective. Scientists like to be precise. Even healthy foods go through some processing.

  • The oatmeal you ate this morning was either steel-cut or ground. That is processing.
  • The almond butter you put on your whole grain toast this morning was made by roasting and grinding. That is processing.

So, scientists have developed the term “ultra-processed food” to describe the worst of the worse. In short, ultra-processed foods:

  • Usually go through several physical and chemical processes, such as extruding, molding, prefrying, and hydrogenation that can lead to the formation of toxic contaminants. One example you may have heard about recently would be acrylamide in French fries.
  • Typically contain ingredients of no or little nutritive value, such as refined sugar, hydrogenated oils, emulsifiers, artificial sweeteners, thickening agents, and artificial colors. Some of these ingredients have been linked to cancer, heart disease, and premature death.
  • Have long shelf-lives because of added preservatives. This allows migration of chemicals such as bisphenol A from the packaging materials into the food.

Examples of ultra-processed foods include:

  • Sodas
  • Chips
  • Candy and packages of cookies or crackers
  • Most breakfast cereals
  • Boxed cake, cookie, and pancake mix
  • Chicken nuggets and fish sticks
  • Fast food burgers
  • Hot dogs and other processed meats
  • Infant formula
  • Instant noodles
  • Most store-bought ice cream
  • Flavored yogurt

In short, ultra-processed foods include sodas and the junk and convenience foods Americans hold so dear. Even things like infant formula and flavored yogurt make the list.

Evidence of the ill effects of ultra-processed foods on our health is becoming overwhelming. In previous issues of “Health Tips From the Professor” I have shared recent studies that have shown that heavy consumption of ultra-processed foods is linked to increased risk of obesity and cancer. Other studies have linked ultra-processed food consumption with increased risk of depression, heart disease, and premature death.

In this issue of “Health Tips From the Professor” I:

  • Ask the important question, “If we know these foods are so bad for us, why do we still keep eating them?”

How Was The Study Done?

Clinical StudyThe data from this study were taken from an ongoing study in France (the NutriNet-Sante study) looking at associations between nutrition and health. This study began enrolling French adults 18 and older in 2009.

This is a web-based study. Participants are prompted to go to a dedicated website and fill out questionnaires related to things like sex, age, height, weight, smoking status, physical activity, health status, and diet.

With respect to diet, participants filled out a series of 3 nonconsecutive 24-hour dietary records at the time of enrollment and every 6 months. This is a particularly strong feature of this study. Many studies of this type only analyze participant’s diets at the beginning of the study. Those studies have no way of knowing how the participant’s diets may have changed during the study.

Diagnosis of type 2 diabetes for study participants was obtained from the French centralized health records.

The study enrolled 104,708 participants, 20% men and 80% women, and followed them for an average of 6 years. The average age of the participants was 43 years.

Do Processed Foods Increase Your Risk Of Diabetes?

High Blood SugarIn this study the range of ultra-processed foods in the French diet ranged from 7% to 27% (average = 17%). High intake of ultra-processed foods was associated with:

  • Younger participants. Simply put, young people were more likely to drink sodas and eat junk food than older adults.
  • Increased caloric intake. Ultra-processed foods have a higher caloric density than whole, unprocessed foods.
  • No surprise here. Previous studies have shown that ultra-processed food consumption increases the risk of obesity.
  • Poorer diet quality. Again, no surprise. Junk foods tend to crowd healthier foods out of the dirt. Specifically, ultra-processed food consumption was associated with:
    • Higher intake of sugar and salt.
    • Lower intake of fiber.
    • Higher intake of sugary drinks, red and processed meats.
    • Lower intake of whole grains, yogurt, nuts, fruits, and vegetables.

However, even after statistically correcting for all these factors, there was a significant association between ultra-processed food consumption and the onset of type 2 diabetes in the 6-year follow-up period.

  • There was a linear relation between ultra-processed food consumption and the development of type 2 diabetes. Simply put, the more ultra-processed food the participants consumed the more likely they were to be diagnosed with type 2 diabetes.
  • There was a 15% increased risk of developing type 2 diabetes for every 10% increase in ultra-processed food consumption.

The authors concluded:

“In this large observational prospective study, a higher proportion of ultra-processed food in the diet was associated with a higher risk of type 2 diabetes. Even though these results need to be confirmed in other populations and settings, they provide evidence to support efforts by public health authorities to recommend limiting ultra-processed food consumption.”

What Does This Study Mean For You?

Questioning WomanYou might be tempted to say that a 15% increase in the risk of developing diabetes is a small price to pay for continuing to eat the foods you enjoy. However, you should be alarmed by this study. Here is why.

The French diet is much healthier than the American. Remember that ultra-processed foods only comprised 17% of the French Diet. In contrast, a recent survey found that:

  • Ultra-processed foods make up 58% of the average American’s diet.
  • Ultra-processed foods account for 90% of the added sugar in our diet.

It is no wonder that obesity and diabetes are reaching epidemic proportions in our country.

You might also be tempted to think that you can just take some medications and live with type 2 diabetes. However, you should think of type 2 diabetes as a gateway disease. It increases your risk of heart disease, high blood pressure, Alzheimer’s disease, kidney damage, and neuropathy, just to name a few. These are diseases that make your life miserable and ultimately kill you.

More importantly, type 2 diabetes is completely reversible if you catch it early enough. Just lose some weight, exercise more, give up the ultra-processed foods, and eat a healthy diet. I recommend a whole food, primarily plant-based diet.

Why Do We Keep Eating Processed Foods?

Fast FoodsWe all know that ultra-processed foods are bad for us. Study after study show that they make us sick. They kill us prematurely. And, unlike most topics in the field of nutrition, this is not controversial.

For example, there have been lots of bizarre diets that have come and gone over the years. There have been books written on “The Steak Lover’s Diet” and “The Drinking Man’s Diet”. But nobody has written a book on “The Junk Food Lover’s Diet”. It simply would not be believable.

So why do we Americans keep eating such unhealthy foods. Part of the answer is physiological. A preference for sweet, salty, and fatty foods is hardwired into our brain. That’s because they had great survival value in prehistoric times.

If we think back to the time when we were hunters and gatherers:

  • Fruits are healthy foods. They are a great source of antioxidants, phytonutrients, and fiber, but there were no orchards or grocery stores back then. We had to search for fruits in the wild. Our desire for sweet tasting foods provided the motivation to seek them out.
  • Game was seasonal and sometimes scarce. We had to be prepared to go for days or weeks without eating except for the leaves and roots we could gather. Our bodies are designed to store fat as the primary energy source to get us through the lean times. Our preference for fatty foods encouraged us to store as much fat as possible in times of plenty so we would be prepared for times of scarcity.
  • If we fast forward to our early recorded history, salt was scarce. It was worth its weight in gold. Yet some salt is essential for life. Our preference for salty foods encouraged us to search out supplies of salt.

Unfortunately, the food industry has weaponized these food preferences to create the ultra-processed foods we know today. Their ads entice us by associating these foods with youth and good times. And ultra-processed foods have become ubiquitous. There are fast food restaurants on almost every street corner and shopping mall in the country.

Fortunately, we do not have to let the food industry destroy our health. We can retrain our taste buds to appreciate the sweetness of fresh fruits and vegetables. We can substitute healthy fats for the kinds of fat found in most ultra-processed foods. We can also retrain our taste buds to appreciate herbs and spices with just a pinch of salt.

The Bottom Line

Ultra-processed foods, such as sodas, junk foods, and convenience foods have become the biggest food group in the American diet. A recent study found:

  • Ultra-processed foods make up 58% of the average American’s diet.
  • Ultra-processed foods account for 90% of the added sugar in our diet.

That is scary because ultra-processed foods are deadly. Previous studies have shown that consumption of ultra-processed foods is linked to obesity, heart disease, cancer, and Alzheimer’s disease.

The study discussed this week looked at the association between ultra-processed food consumption and type 2 diabetes. It showed:

  • There was a linear relation between ultra-processed food consumption and the development of type 2 diabetes. Simply put, the more ultra-processed food the participants consumed the more likely they were to be diagnosed with type 2 diabetes.
  • There was a 15% increased risk of developing type 2 diabetes for every 10% increase in ultra-processed food consumption.

You might be tempted to think that you can just take some medications and live with type 2 diabetes. However, you should think of type 2 diabetes as a gateway disease. It increases your risk of heart disease, high blood pressure, Alzheimer’s disease, kidney damage, and neuropathy, just to name a few. This are diseases that make your life miserable and ultimately kill you.

More importantly, type 2 diabetes is completely reversible if you catch it early enough. Just lose some weight, exercise more, give up the ultra-processed foods, and eat a healthy diet. I recommend a whole food, primarily plant-based diet.

For more details and a discussion of why Americans continue to eat ultra-processed food even though we know it is bad for us, 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.

The Truth About Vitamin D And Respiratory Diseases

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How Should You Prepare For This Winter?

deadSome health experts are making dire predictions for this fall when COVID-19 overlaps with our annual flu season. People are worried.

When people are worried, hucksters smell a quick buck and start coming out of the woodworks. They are touting all sorts of miracle pills and potions that will keep us safe this winter. The FDA is doing its best to shut them down, but it’s like the “Whack A Mole” game you may remember from the county fair. As soon as the FDA shuts one down, another pops up.

In the meantime, you are left trying to sort through the claims. I could write a whole book on the truth (and lies) about the claims you are seeing on the internet. But this week I will focus on vitamin D. I will give you unbiased answers to three questions.

1) What is the truth about vitamin D and respiratory disease?

2) Will vitamin D help protect you against COVID-19?

3) How should you prepare for this winter?

I am basing today’s “Health Tip” on a recently published study (H Brenner et al, Nutrients 2020, 12, 2488) looking at the effect of vitamin D status on deaths from respiratory disease in older German adults.

How Was The Study Done?

Clinical StudyThe data from this study were taken from an ongoing study in Germany looking at the effect of diet and lifestyle on health outcomes in older adults. In this case, 9548 adults, ages 50-75, from the region of Saarland in Germany were enrolled in the study between 2000 and 2002 and followed for an average of 15 years.

Blood samples were drawn at the time of enrollment and 25-hydroxyvitamin D levels were determined as a measure of vitamin D status. Deaths and cause of deaths over the 15 year period were obtain from German health records.

The basic characteristics of the study population were:

  • The gender breakdown was 43.8% men, 52.6% female.
  • The average age was 62.1 years.
  • Almost all participants were Caucasians of German or French descent.
  • 8% were vitamin D insufficient (25-hydroxyvitamin D of 30-<50 nmol/L)
  • 1% were vitamin D deficient (25-hydroxyvitamin D of <30 nmol/L)

Note: Almost 60% of this study group had an inadequate vitamin D status. The comparable figures for the US population are 42% with inadequate vitamin D status (34% vitamin D insufficient and 8% vitamin D deficient).

The reasons for this are likely two-fold:

  • Saarland is at the latitude of Newfoundland, Canada, so sun exposure is less than for most Americans.
  • Germans are less likely to consume supplements than Americans.

However, the fact that 60% of this study group has inadequate vitamin D status makes it a particularly good group to look at the effect of vitamin D status on health outcomes.

The Truth About Vitamin D And Respiratory Diseases

the truth signThis study found:

  • Vitamin D insufficiency (25-hydroxyvitamin D of 30-<50 nmol/L) increased the risk of dying from respiratory disease by 1.9-fold for men and 2.1-fold for women.
  • Vitamin D deficiency (25-hydroxyvitamin D of <30 nmol/L) increased the risk of dying from respiratory disease by 2.3-fold for men and 3.0-fold for women.

The authors pointed out that this was consistent with a recent meta-analysis of randomized clinical trials showing that supplementation with RDA levels of vitamin D reduced the risk of acute respiratory tract infections by 70% in people who were vitamin D deficient.

The authors concluded:

“Vitamin D insufficiency and deficiency are common and account for a large proportion of respiratory disease mortality in older adults…Our results, along with evidence from meta-analyses from RCTs [Randomized Placebo-Controlled Clinical Trials] regarding results of vitamin D3 supplementation on various outcomes, suggest that vitamin D3 supplementation could contribute to lowering mortality from respiratory and other diseases during and beyond the COVID-19 pandemic, particularly among women.”

How Should You Prepare For This Winter?

Winter WindNow it is time to answer the three questions I posed at the beginning of this article:

1) What is the truth about vitamin D and respiratory disease?

There have been many studies suggesting that inadequate vitamin D status increases the risk of “catching” respiratory diseases such as the seasonal flu. Some of those studies showed that supplementation with vitamin D3 reduced the risk of catching respiratory diseases. However, most of those were small studies.

This study and the meta-analysis the authors referred to were much larger, better designed studies. Other large, well designed studies are needed. But, taken together, these two studies strongly support the hypothesis that inadequate vitamin D status significantly increases the risk of developing and dying from respiratory diseases.

However, we do need to put this into perspective.

  • Supplementation with vitamin D primarily protects individuals with inadequate vitamin D status. It doesn’t appear to offer significant benefit for individuals with adequate vitamin D status (>50 nmol/L 25-hydroxyvitamin D).
  • Supplementation with vitamin D at doses of 2,000 IU or less appears to be sufficient for most people. There is little evidence that megadoses are beneficial unless you are severely vitamin D deficient (more about that below).

2) Will vitamin D help protect you against COVID-19?

vitamin dThe answer to this question is less clear. As we learn more about COVID-19 we have learned that it is much more than just a respiratory disease. On the other hand, cellular studies suggest that vitamin D may interfere with the mechanism by which COVID-19 attacks cells.

What do clinical studies say? We are just learning. Four small clinical trials and one large study have recently been published or posted online as preprints prior to being accepted for publication.

  • The second study (HW Kaufman et al, PLOS One, September 17, 2020) used data from a major national testing center (Quest Diagnostics) and linked COVID-19 test results with 25-hydroxyvitamin D test results for 191,779 patients. This study reported that vitamin D deficiency was associated with a 30% increased risk of testing positive for COVID-19.
  • The third study found that vitamin D deficiency was associated with hospital admissions for COVID-19.
  • The fourth study found that vitamin D deficiency was associated ICU admissions for COVID-19.

Taken together these 5 studies suggest that vitamin D deficiency may increase the risk of being infected by COVID-19 and on the severity of the disease if you are infected.

I should point out that these studies are preliminary. Normally we would say that they need to be confirmed by larger studies before becoming incorporated into the standard of care for COVID-19.

You might be saying to yourself, , “Why is the medical community paying so much attention to preliminary studies?” The answer is simple:

  • The need is urgent. We need all the tools at our disposal to fight this deadly disease, and we need them now.
  • Vitamin D3 supplementation at 2,000 IU or less is inexpensive and safe. Plus, even if further studies find that our vitamin D status has no effect on COVID-19 risk, we know that adequate vitamin D has many other potential health benefits.

To summarize:

  • Preliminary studies suggest that adequate vitamin D status may offer some protection for COVID-19. These studies are not definitive. No reputable scientist is ready to tell you that vitamin D will ward off COVID-19. However, supplementation with 2000 IU/day or less of vitamin D3 is safe and may have multiple health benefits.
  • Vitamin D should not be considered a “magic bullet”. It is just one aspect of a holistic approach to creating a healthy body that is less susceptible to respiratory diseases like COVID-19.

3) How Should You Prepare For This Winter?

Winter WindAs we approach the winter months, the days are getting shorter and sun exposure is decreasing. This is the time of year when your 25-hydroxyvitamin D levels will be at their lowest.

At the same time, we are likely to see a convergence of the seasonal flu, flu-like illnesses, and COVID-19 this winter. You will need a healthy body, a healthy immune system, and adequate vitamin D status more than ever.

When asked about vitamin D and COVID-19 in a recent interview, Dr. Anthony Fauci, Director of the National Institute of Allergy and Infectious Diseases, said, “If you’re deficient in vitamin D, that does have an impact on your susceptibility to infection. I would not mind recommending, and I do it myself, taking vitamin D supplements.”

I recommend supplementation with vitamin D3 to make sure your vitamin D status is adequate. The RDA for vitamin D is 600 IU for adults and 800 IU for seniors over the age of 70. However, because the efficiency with which we convert vitamin D3 to 25-hydroxyvitamin D varies from person to person, many experts recommend supplementing with 1,500-2,000 IU of vitamin D3.

I also recommend that you ask your health provider for a 25-hydroxyvitamin D test. If you are in the vitamin D deficient range, your health provider may recommend more than 2,000 IU/day of vitamin D3.

Finally, we should not rely on vitamin D alone. As I discussed in a previous issue of “Health Tips From The Professor”, I recommend a holistic approach for strengthening our immune systems, and I recommend the CDC guidelines for reducing the risk of catching both the flu and COVID-19.

I would note that social distancing, hand washing, and mask wearing are just as effective at reducing the risk of getting the flu as they are for getting COVID-19. In fact, some Asian countries practice mask wearing in public every flu season.

The Bottom Line

  • A recent study found that inadequate vitamin D status caused a 2-3-fold increased risk of dying from respiratory illnesses for seniors (ages 50-74).
  • A previous meta-analysis reported that supplementation with RDA levels of vitamin D reduced the risk of acute respiratory tract infections by 70% in people who were vitamin D deficient.
  • Taken together, these two studies strongly support the hypothesis that inadequate vitamin D status significantly increases the risk of developing and dying from respiratory diseases.
  • Preliminary studies suggest that adequate vitamin D status may offer some protection for COVID-19. These studies are not definitive. No reputable scientist is ready to tell you that vitamin D will ward off COVID-19. However, supplementation with 2000 IU/day or less of vitamin D3 is safe and may have multiple health benefits.
  • Vitamin D should not be considered a “magic bullet”. It just one aspect of a holistic approach to creating a healthy body that is less susceptible to respiratory diseases like COVID-19.

So, how should we prepare for this winter?

  • As we approach the winter months, the days are getting shorter and sun exposure is decreasing. This is the time of year when your 25-hydroxyvitamin D levels will be at their lowest.
  • At the same time, we are likely to see a convergence of the seasonal flu, flu-like illnesses, and COVID-19 this winter. You will need a healthy body, a healthy immune system, and adequate vitamin D status more than ever.
  • I recommend supplementation with vitamin D3 to make sure your vitamin D status is adequate. The RDA for vitamin D is 600 IU for adults and 800 IU for seniors over the age of 70. However, because the efficiency with which we convert vitamin D3 to 25-hydroxyvitamin D varies from person to person, many experts recommend supplementing with 1,500-2,000 IU of vitamin D3.
  • Finally, we should not rely on vitamin D alone. As I discussed in a previous issue of “Health Tips From The Professor”, I recommend a holistic approach for strengthening our immune systems, and I recommend the CDC guidelines for reducing the risk of catching both the flu and COVID-19.

I would note that social distancing, hand washing, and mask wearing are just as effective at reducing the risk of getting the flu as they are for getting COVID-19. In fact, some Asian countries practice mask wearing in public every flu season.

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.

Does Poverty Affect Nutritional Status?

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How Can We Improve Nutrition In Disadvantaged Communities?

Calcium FoodsRecently there has been increased focus on health disparities in disadvantaged communities. In our discussions of the cause of these health disparities, two questions seem to be ignored.

1. Does poverty play a role in poor nutrition?

2. Does poor nutrition play a role in the health disparities we see in disadvantaged communities?

The study (K Marshall et al, PLoS One 15(7):e0235042) I discuss in this week’s “Health Tips From The Professor” attempts to address both of these questions.

Before, I start, let me put this study into context.

  • Osteoporosis is a major health problem in this country. Over 2 million osteoporosis-related fractures occur each year, and they cost our health care system over 19 billion dollars a year. Even worse, for many Americans these osteoporosis-related fractures often cause:
    • A permanent reduction in quality of life.
    • Immobility, which can lead to premature death.
  • Inadequate calcium and vitamin D intakes increase the risk of osteoporosis.

While most studies simply report calcium and vitamin D intakes for the general population, this study breaks them down according to ethnicity and income levels. The results were revealing.

How Was The Study Done?

Clinical StudyThis study drew on data from the 2007-2010 and 2013-2014 National Health and Nutrition Examination Surveys (NHANES). These surveys are conducted by the National Center for Health Statistics, which is part of the CDC. They are designed to assess the health and nutritional status of adults and children in the United States and are used to produce health statistics for the nation.

The NHANES interview includes demographic, socioeconomic, dietary, and health-related questions. The examination component consists of medical, dental, and physiological measurements, as well as laboratory tests administered by highly trained medical personnel. All participants visit a physician. Dietary interviews and body measurements are included for everyone.

This study measured calcium intake, vitamin D intake, and osteoporosis for adults 50 and older. The data were separated by gender, ethnic group and income level. Four different measures of poverty were used. For purposes of simplicity, I will only use one of them, income beneath $20,000, for this article.

Does Poverty Affect Nutritional Status?

The Effect of Ethnicity And Gender On Calcium And Vitamin D Intake: 

FriendsWhen the authors looked at the effect of ethnicity and gender on calcium and vitamin D intake, in people aged 50 and older the results were (Note: I am using the same ethnic nomenclature used in the article):

Hispanics:

    • 66% (75% for women and 56% for men) were getting inadequate calcium intake.
    • 47% (47% for women and 47% for men) were getting inadequate vitamin D intake.

Non-Hispanic Blacks:

    • 75% (83% for women and 64% for men) were getting inadequate calcium intake.
    • 53% (51% for women and 54% for men) were getting inadequate vitamin D intake.

Non-Hispanic Whites:

    • 60% (64% for women and 49% for men) were getting inadequate calcium intake.
    • 33% (30% for women and 37% for men) were getting inadequate vitamin D intake.

For simplicity, we can generalize these data by saying:

Gender:

    • Women are more likely to be calcium-deficient than men.
    • Men are more likely to be vitamin D-deficient than women.

Ethnicity: For both genders and for both calcium and vitamin D:

    • The rank order for deficiency is Non-Hispanic Blacks > Hispanics > Non-Hispanic Whites.

The Effect Of Poverty On Calcium Intake, Vitamin D Intake, And Osteoporosis:

PovertyWhen looking at the effect of poverty, the authors asked to what extent poverty (defined as income below $20,000/year) increased the risk of calcium and vitamin D deficiency in adults over 50. Here is a summary of the data

Hispanics:

    • For both Hispanic women and Hispanic men, poverty had little effect on the risk of calcium and vitamin D deficiency.

Non-Hispanic Blacks:

    • For Non-Hispanic Black women, poverty had little effect on the risk of calcium deficiency, and vitamin D deficiency.
    • For Non-Hispanic Black men, poverty increased the risk of both calcium and vitamin D deficiency by 32%.

Non-Hispanic Whites:

    • For Non-Hispanic White women, poverty had little effect on the risk of calcium deficiency but increased the risk of vitamin D deficiency by 30%.
    • For Non-Hispanic White men, poverty increased the risk of both calcium deficiency and vitamin D deficiency by 18%.

For simplicity, we can generalize these data by saying:

    • Poverty increased the risk of both calcium and vitamin D deficiency for Non-Hispanic Black men, Non-Hispanic White women, and Non-Hispanic White men.

Other statistics of interest:

  • The SNAP program (formerly known as Food Stamps) had little effect on calcium and vitamin D intake. There are probably two reasons for this:
    • In the words of the authors, “While the SNAP program has been shown to decrease levels of food insecurity, the quality of the food consumed by SNAP participants does not meet the standards for a healthy diet.” In other words, the SNAP program ensures that participants have enough to eat, but SNAP participants are just as likely to prefer junk and convenience foods as the rest of the American population. The SNAP program provides no incentive to eat healthy foods.
    • We also need to remember that dairy foods are a major source of calcium and vitamin D in the American diet and that Hispanics and Non-Hispanic Blacks are more likely to be lactose-intolerant than the rest of the American population. There are other sources of calcium and vitamin D in the American diet. But without some nutrition education, most Americans are unaware of what they are.
  • An increased risk of osteoporosis was found in Non-Hispanic Black men, and Non-Hispanic Whites with incomes below $20,000/year.
    • This increased risk of osteoporosis was seen primarily for the individuals in each group who were deficient in calcium and vitamin D. There were other factors involved, but I will focus primarily on the effect of poverty on calcium and vitamin D intake in the discussion below.

How Can We Improve Nutrition In Disadvantaged Communities?

Questioning WomanLet’s start with the two questions I posed at the beginning of this article:

1. Does poverty play a role in poor nutrition?

2. Does poor nutrition play a role in the health disparities we see in disadvantaged communities?

In terms of calcium intake, vitamin D intake, and the risk of osteoporosis, the answer to both questions appears to be, “Yes”. So, the question becomes, “What can we do?”

It is when we start to ask what we can do to increase calcium and vitamin D intake and decreased the risk of osteoporosis in disadvantaged communities that we realize the complexity of the problem. There are no easy answers. Let’s look at some of the possibilities.

[Note: I am focusing on what we can do to prevent osteoporosis, not to detect or treat osteoporosis. The solutions for those issues would be slightly different.]

1. We could increase funding for SNAP. That would increase the quantity of food available for low income families, but, as noted above, would do little to improve the quality of the food eaten.

2. We could improve access to health care in disadvantaged communities. But unless physicians started asking their patients what they eat and start recommending a calcium and vitamin D supplement when appropriate, this would also have little impact on diet quality.

3. We could improve nutrition education. A colleague of mine in the UNC School of Public Health ran a successful program of nutrition education through churches and community centers in disadvantaged communities for many years. The program taught people how to eat healthy on a limited budget. Her program improved the health of many people in disadvantaged communities.

However, the program was funded through grants. When she retired, federal and state money to support the program eventually dried up. The program she started is a model for what we should be doing.

4. The authors suggested food fortification as a solution. In essence, they were suggesting that junk and convenience foods be fortified with calcium and vitamin D. That might help, but I don’t think it is a good idea.

If we want to improve the overall health of disadvantaged communities, we need to find ways to replace junk and convenience foods with healthier foods. Adding a few extra nutrients to unhealthy foods does not make them healthy.

5. The authors also said that a calcium and vitamin D supplement would be a cheap and convenient way to eliminate calcium and vitamin D deficiencies. Unfortunately, supplements are currently not included in the SNAP program. Unless that is changed, even inexpensive supplements are a difficult choice for families below the poverty line.

As I said at the beginning of this section, there are no easy answers. It is easy to identify the problem. It would be easy to throw money at the problem. But finding workable solutions that could make a real difference are hard to identify.

Yes, we should make sure every American has enough to eat. Yes, we should make sure every American has access to health care. But, if we really want to improve the health of our disadvantaged communities, we also need to:

  • Change the focus of our health care system from treatment of disease to prevention of disease.
  • Train doctors to ask their patients what they eat and to instruct their patients how simple changes in diet could dramatically improve their health.
  • Provide basic nutrition education to disadvantaged communities at places where they gather, like churches and community centers. This would cover topics like eating healthy, shopping healthy on a limited budget, and cooking healthy.

We don’t necessarily need another massive federal program. But those of us with the knowledge could each volunteer to share that knowledge in disadvantaged communities.

  • Cover basic supplements, like multivitamins, calcium and vitamin D supplements, and omega-3 supplements in food assistance programs like SNAP.

The Bottom Line

Osteoporosis is a major health problem in this country. Over 2 million osteoporosis-related fractures occur each year, and they cost our health care system over 19 billion dollars a year. Even worse, for many Americans these osteoporosis-related fractures often cause:

  • A permanent reduction in quality of life.
  • Immobility, which can lead to premature death.

We know that inadequate calcium and vitamin D intakes increase the risk of osteoporosis. But most studies simply report calcium and vitamin D intakes for the general population. At the beginning of this article, I posed two questions.

  1.  Does poverty play a role in poor nutrition?

2. Does poor nutrition play a role in the health disparities we see in disadvantaged communities?

A recent study looked at the effect of gender, ethnicity and income levels on calcium intake, vitamin D intake, and the risk of developing osteoporosis. The results of this study shed some light on those two questions.

When looking at the effect of gender and ethnicity on the risk of inadequate calcium and vitamin D intake, the study found:

  • Women are more likely to be calcium-deficient than men.
  • Men are more likely to be vitamin D-deficient than women.
  • For both genders and for both calcium and vitamin D, the rank order for deficiency is Non-Hispanic Blacks > Hispanics > Non-Hispanic Whites. [Note: Note: I am using the same ethnic nomenclature used in the study.]
  • Poverty (defined as incomes below $25,000/year) significantly increased the risk of both calcium and vitamin D deficiency for Non-Hispanic Black men, Non-Hispanic White women, and Non-Hispanic White men.
  • An increased risk of osteoporosis was also found in Non-Hispanic Black men, and Non-Hispanic White men and women with incomes below $20,000/year.
  • This increased risk of osteoporosis was seen primarily for the individuals in each group who were deficient in calcium and vitamin D.

In short, this study suggests that the answer to both questions I posed at the beginning of the article is, “Yes”.

For more information and a discussion of what we could do to correct this health disparity in disadvantaged communities, 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.

You Can Touch Your Toes Again

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sunOne more hot month to go!  This has been an exceptionally hot summer in many places around the USA. In fact, many times Florida was cooler (mid 90’s) than some of the cities up north.  Weird!

I hope you are doing well as this COVID19 problem keeps hanging around to make our lives a challenge. When the shutdown happened back in March, I didn’t know what I was going to do.  As you are well-aware, I don’t do relaxing massage, I work with people who are in real pain.  How do I tell people to just be in pain until this pandemic passes!

Fortunately for me, and for my clients, the first client I saw after the shutdown was a medical doctor. I asked her about people coming to me and she told me if everyone wears a mask, and I wash my hands before and after treating someone, that it would be fine.  So that’s what’s been happening. Plus, I wash everything down with a strong disinfectant after each client, and all is well.

I’m seeing less people, but I’m seeing people who are in a lot of pain and are desperate for help.  As my clients have told me, I am an essential worker, and I believe they are right.

With that said, I want to tell you about a man who drove 17 hours from southern Texas to work with me for a week. Let’s call him JT for privacy.

You Can Touch Your Toes Again

Pelvis Stiffness 1JT was stiffer than anyone I’d ever seen in the past, and after a 17-hour trip, we knew he needed to come in a LOT. He ended up coming in for 3 hours a day for the first 3 days, and 90 minutes on Thursday and Friday.

When JT arrived, it amazed me at how stiff his pelvis was, every muscle that moved his pelvis, legs and low back were tied up in multiple tight knots. He has given me permission to share his pictures with you so I can explain something really interesting that I found, and how it can help you to release tension in your low back.

Day 1: JT’s hips were so locked that when he bent forward his fingertips only went to 7” above his knees.  He couldn’t bend any further than this!

I’ve already shown you how to do the self-treatment for your quadriceps using a 12”x1” length of PVC pipe, and how to use the Perfect Ball on your low back muscle.  This is where we started so the muscles that rotate the pelvis down in the front can start to release.

Pelvis Stiffness 2Day 2: First I worked on all of the muscles that insert into his thigh bone where it inserts into his pelvis. Then JT used the Perfect Ball and working on the floor he went deeply into all of the muscles that connect his pelvis to his thigh bone.

At the end of the day his fingers were 5” below his knee joint.

On Day 3 there was a set-back, his fingers were still about 2” below his knee joint but we were questioning what we were missing.  When JT bent forward, he had pain in the front of his pelvis, just below the point of his hip bone.  That’s an area that definitely shouldn’t be hurting when JT bent forward.  I kept looking at my skeleton, Max, and my book of muscles/bones/joints, to try to figure it out, and looking at the muscles of the pelvis.  Then suddenly it was so clear!

Your hamstrings originate at the base of your posterior pelvis, and they insert just below the back of your knee.  Your thigh bone (femur) inserts into your hip at an area called the acetabulum, it looks like fitting a ball into a curved cup.

This is the part I want to share with you today.

How Your Hamstrings Impact Your Pelvis

On the afternoon of Day 3, I was frustrated at the set-back. After staring at Max and my book of muscles it finally dawned on me that it was JT’s hamstrings that were part of the problem, even though it was his rotating pelvis that was causing his hip joint to be out of alignment.

I had been working on all of the pelvic muscles and they all felt pretty good, and I had done a pass down the back of his thighs, but I hadn’t focused on JT’s hamstrings. And that made all the difference!

An important point to mention when talking about a long-standing problem with tight muscles is to discuss “muscle memory.”

Muscle memory is when a muscle that has been held shortened for an extended time (which could be just a few hours) it will shorten to that new length. The problem is, you release the tension in the muscles and get relief, but the muscle shortens again, and the strain is again placed on your joints.

As JT’s hamstrings shortened, they pulled down of the back of his pelvis, and this twisted the alignment of his hip joint. Because of this misalignment, he was feeling pain in the front of his hip, and that was the piece I’d been missing.

Pelvis Stiffness 3

 

After treating JT’s hamstrings (treatment shown below) he was able to bend almost all the way to his ankles!  Only three days before JT could only bend to not even the middle of his thigh, yet here he was almost to his ankles!

 

 

 

 

Treating Hamstrings To Relax The Pelvis

treat tight hamstringsIf you have been to my therapy office, you know that I always teach how to do 1-2 self-treatments.  The reason is you need to reverse muscle memory, and the only way to do that is to do the self-treatments frequently – every day is best.

A simple way of treating your hamstrings is to put a Perfect Ball on a wooden chair, or the corner of a desk, and put your hamstrings onto the ball.

Keep moving the ball until you find tender points as these are the knots (spasms) that are putting a strain on your pelvis.  Treat each point and then stretch 

Stretching Your Hamstrings

Hamstring Stretch

 

Lie on your back and put a rope under your arch.  Start with your knee bent and lift your leg up as high as you can go without seriously straining your hamstrings.

 

Slowly straighten your leg, stretching your hamstrings.

 

Day 5 – JT is Ready to Go Back to Texas

Pelvis Stiffness 4JT is now only 3” above the top of his foot. He’s not touching his toes yet, but he feels so much better.

The best news is that JT is thoroughly familiar with every self-treatment to release all of the muscles that have an impact on his pelvis.  He’s not 100% better yet, but he’s well on his way.

How Does This Affect You? 

The important part of this story for you is that you CAN learn how to self-treat, and the odds are excellent that you can get relief from even the most stubborn of chronic pains.

My goal is to help as many people as possible to eliminate chronic pain that is caused by tight muscles, and to show they how to self-treat!

Wishing you well,

Julie Donnelly 

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.

How Much DHA Is Needed To Prevent Alzheimer’s

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What Are We Missing?

Cognitive-DeclineWe are an aging population. As such, issues like cognitive decline, dementia, and Alzheimer’s Disease are of increasing concern. After all, what is the good of reaching your “Golden Years” with a healthy body if you lose your mind?

The ability of the omega-3 fatty acids DHA and EPA to reduce the risk of cognitive decline, dementia, and Alzheimer’s Disease is controversial. Some studies say yes. Others say no.

When studies are conflicting most experts simply conclude the treatment is unproven. I am sympathetic to that viewpoint, but I first like to ask the questions: “Why are the studies conflicting? What are we missing?”

I start by evaluating the strengths and weaknesses of the individual studies.

  • If the studies claiming the treatment works are weak, I am content to “join the chorus” and consider the treatment unproven.
  • If the studies claiming the treatment doesn’t work are weak, I am a strong advocate for more well-designed studies before we conclude that the treatment doesn’t work.
  • If both the “pro” and “con” studies are strong, I want to ask, “What are we missing?”

This is the situation with studies asking whether DHA reduces the risk of Alzheimer’s Disease and other forms of cognitive decline as we age.

  • Association studies show that greater intake and higher blood levels of the omega-3 fatty acids EPA and DHA are associated with lower risk of Alzheimer’s Disease.
  • However, most placebo-controlled clinical trials with either DHA alone or DHA + EPA have come up negative. Of course, one can always argue that most of the placebo-controlled clinical trials were too short or too small to show a statistically significant effect. But, my question remains, “What else are we missing?”

One recent study has provided an interesting clue. The authors of the study postulated that B vitamins were required to deliver omega-3 fatty acids to the brain, and their study showed that omega-3 fatty acids were only effective at decreasing the risk of cognitive decline in subjects who also had optimal B vitamin status.

In other words, this study suggested that studies on the effect of omega-3 supplementation and risk of developing Alzheimer’s are doomed to failure if a significant percentage of the subjects have sub-optimal B vitamin status.

The authors of the current study ( IC Arellanes et al, EBioMedicine, doi.org/10.1016/j.ebiom.2020.102883) proposed two additional hypotheses for the negative results of previous clinical trials and designed an experiment to test their hypotheses. Their hypotheses were:

  • Uptake of DHA and EPA by the brain is very inefficient, and previous studies have not used sufficient doses of DHA or DHA plus EPA to see a significant effect on cognitive impairment.
  • The APOE4 gene further decreases the uptake of DHA and EPA by the brain.

Before I describe how the study was done, I should probably provide some context by describing how DHA and EPA reach the brain and the role of the apoE protein in the process. It’s time for my favorite topic: “Biochemistry 101”.

Biochemistry 101: What Does The ApoE Protein Do?

ProfessorIf you have ever tried to mix oil and water, it should come as no surprise to you that fats, including DHA and EPA, and cholesterol are not water soluble. That leaves our bodies with a dilemma. How do they get the fat and cholesterol we eat to pass through our bloodstream and get to our cells, where they are needed?

Our body’s solution is to incorporate the fat and cholesterol into particles called lipoproteins. Lipoprotein particles sequester the fat and cholesterol in their interior and surround them with water soluble phospholipids and proteins. Lipoproteins allow our bodies to transport fat and cholesterol through our bloodstream to the tissues that need them.

The next question, of course, is how the lipoproteins know which cells need the fat and cholesterol. This is where apoproteins like apoE come into play. We can think of the apoE protein as a zip code that directs lipoproteins to cells with an apoE receptor.

Our nervous system contains lots of apoE receptors, and binding of the apoE protein to its receptor is instrumental in the delivery of DHA, EPA, and cholesterol to our nervous system.

DHA and cholesterol are both important for brain health. That is because they are major components of the myelin sheath that wraps around our neurons and protects them. EPA may also be important for brain health because its anti-inflammatory effects are thought to prevent the accumulation of the amyloid plaques that are the hallmark of late-onset Alzheimer’s Disease.

There are three major versions of the APOE gene, APOE2, APOE3, and APOE4. Each of them plays slightly different roles in our body. However, it is the APOE4 version that is of interest to us. About 25% of us have the APOE4 version of the APOE gene and it increases our risk of developing Alzheimer’s Disease by a factor of two.

We do not know why this is, but one hypothesis is that lipoproteins with the apoE4 protein have more difficultly delivering much needed DHA, EPA, and cholesterol to the brain. This is one of the hypotheses that the authors set out to study.

How Was The Study Done?

Clinical StudyThere are two things you should know about this study.

  • This was a pilot study designed to test the author’s hypotheses and allow them to choose the correct dose of DHA to use for a subsequent study designed to test whether high-dose DHA can reduce the risk of developing Alzheimer’s Disease.
  • This was a very small study. That’s because the only way to determine how much DHA and EPA reaches the nervous tissue is to perform a lumbar puncture and obtain cerebrospinal fluid at baseline and again at the end of the study. Lumbar punctures are both painful and a bit risky. They were lucky to find 26 individuals who consented to the lumbar punctures.

This was a double-blind, placebo controlled clinical study.

  • Half the subjects were given 2,152 mg/day of DHA for 6 months, and half were given a daily placebo consisting of corn and soybean oil for 6 months.
  • Because previous studies have suggested that B vitamins were important for DHA and EPA uptake by nervous tissue, all subjects received a B vitamin supplement.
  • Levels of DHA and EPA were measured in both plasma and cerebrospinal fluid at baseline and again at the end of 6 months. Note: The subjects were only supplemented with DHA. The investigators were relying on the body’s ability to convert DHA into EPA.
  • All subjects were screened for APOE4

Other important characteristics of the study subjects were:

  • Average age was 69. They were 80% female.
  • All of them had a close family member who had previously been diagnosed with dementia, but none of them had been diagnosed with cognitive impairment at the time of entry into the study.
  • Around 45% of them had the APOE4 version of the APOE.

In other words, none of them currently had dementia, but most were at high risk of developing dementia.

How Much DHA Is Needed To Prevent Alzheimer’s?

fish and fish oilAfter 6 months of supplementing with over 2,000 mg/day of DHA:

  • DHA levels in the blood had increased by 200%.
  • However, DHA levels in cerebrospinal fluid had increased by only 28%.
  • Moreover, DHA levels in cerebrospinal fluid were 40% lower in subjects who had the APOE4 gene compared to subjects with the APOE2 and APOE3

EPA levels in cerebrospinal fluid averaged about 15-fold lower than DHA levels. When they looked at the effect of DHA supplementation on EPA levels.

  • EPA levels in plasma had increased by 50%.
  • EPA levels in cerebrospinal fluid had increased by 43%.
  • EPA levels in cerebrospinal fluid were 3-fold lower in subjects who had the APOE4 gene compared to subjects with the APOE2 and APOE3

The authors concluded:

“We observed only a modest (28%) increase in cerebrospinal fluid DHA levels with 2152 mg per day of DHA supplementation. This finding has implications for past clinical trials that have used lower doses (e.g. 1 g daily of DHA supplements or less) and were overwhelmingly negative. Using lower doses of omega-3 supplements may have resulted in limited omega-3 brain delivery.”

“Another aspect affecting the response to DHA supplementation is APOE4 status. Subjects with the APOE4 gene showed lower DHA levels and significantly lower EPA levels than subjects with other APOE genes”.

“In summary, our study suggests that higher doses of omega-3 fatty acids (2 or more g of DHA) are needed to ensure adequate brain delivery, particularly in APOE4 carriers…Past low dose (1 g per day or less) omega-3 supplementation trials in dementia prevention may not have provided adequate brain levels to fully evaluate the efficacy of omega-3 supplementation on cognitive outcomes.”

Based on the results from this study the authors are currently testing the effect of B vitamins and high dose DHA supplementation on cerebrospinal fluid fatty acid levels, brain imaging, and cognitive outcomes in a larger ongoing clinical trial.

What Does This Study Mean For You?

Questioning ManThe ability of the omega-3 fatty acids DHA and EPA to reduce the risk of cognitive decline, dementia, and Alzheimer’s Disease is confusing. Studies disagree.

In situations like this, most experts dismiss the hypothesis as “unproven”. However, I like to ask, “What are we missing?”

One recent study provided a clue. It suggested that omega-3s and B vitamins were interdependent. We need both to reduce cognitive decline. However, that might not be the complete answer.

This study gave both DHA and B vitamins to subjects and discovered another interesting clue. The study suggests we may not have been giving subjects enough omega-3s to see a significant effect on cognitive decline.

Let me start by saying this study did not test whether or not DHA supplementation prevents cognitive decline, dementia, and Alzheimer’s Disease. Nor does it tell us how much DHA is needed to prevent Alzheimer’s Disease, other than to show that anything less than 2 g per day is likely to be inadequate. 

However, the study did make two important advances:

#1: It showed just how difficult it is to deliver adequate amounts of DHA and EPA to the brain. This is important because it shows:

  • Most previous studies have not used high enough doses of DHA or DHA plus EPA to evaluate the effect of omega-3 fatty acids on cognitive decline. Those studies were not simply negative. They were doomed to failure. The studies were worthless.
  • That means we should stop saying that the ability of omega-3s to prevent cognitive decline and diseases like Alzheimer’s is unproven. Instead, we should say that hypothesis has not adequately been tested.
  • That also means future studies of the ability of DHA to reduce the risk of cognitive decline, dementia, and/or Alzheimer’s will need to use much higher doses or a better delivery system to get adequate amounts of DHA and EPA into the brain.

#2: It showed that the APOE4 gene significantly decreases the ability of the brain to accumulate DHA and EPA. This has several important implications.

  • Because both DHA and EPA are vital for brain health, this may explain why the APOE4 gene increases the risk of Alzheimer’s Disease.
  • It also means those at highest risk for Alzheimer’s Disease are the ones who are most likely to have difficulties accumulating DHA and EPA in their brain.
  • Once again, it means future studies of the ability of supplemental DHA to reduce the risk of Alzheimer’s Disease will need to use much higher doses of DHA.

The Bottom Line

We are an aging population. As such, issues like cognitive decline, dementia, and Alzheimer’s Disease are of increasing concern. After all, what is the good of reaching your “Golden Years” with a healthy body if you lose your mind?

The ability of the omega-3 fatty acids DHA and EPA to reduce the risk of cognitive decline, dementia, and Alzheimer’s Disease is controversial.

  • Association studies show that greater intake and higher blood levels of the omega-3 fatty acids EPA and DHA are associated with lower risk of Alzheimer’s Disease.
  • However, most placebo-controlled clinical trials with either DHA alone or DHA + EPA have come up negative.

In situations like this, most experts dismiss the hypothesis as “unproven”. However, I like to ask, “What are we missing?”

One recent study provided a clue. It suggested that omega-3s and B vitamins were interdependent. We need optimal amounts of both to reduce dementia. However, that might not be the complete answer.

This study gave both DHA and B vitamins to participants and discovered another interesting clue. The study suggests we may not have been giving subjects enough omega-3s to see a significant effect on cognitive decline.

The authors of the study hypothesized:

  • Uptake of DHA and EPA by the brain is very inefficient, and previous studies have not used sufficient doses of DHA or DHA plus EPA to see a significant effect on cognitive impairment.
  • The APOE4 gene, which is known to increase the risk of Alzheimer’s Disease, further decreases the uptake of DHA and EPA by the brain.

Their study confirmed their hypotheses and made two important advancements:

#1: It showed just how difficult it is to deliver adequate amounts of DHA and EPA to the brain. This is important because it shows:

  • Most previous studies have not used high enough doses of DHA or DHA plus EPA to evaluate the effect of omega-3 fatty acids on cognitive decline. Those studies were not simply negative. They were doomed to failure. The studies were worthless.
  • That means we should stop saying that the ability of omega-3s to prevent cognitive decline and diseases like Alzheimer’s is unproven. Instead, we should say that hypothesis has not adequately been tested.
  • That also means future studies of the ability of DHA to reduce the risk of cognitive decline, dementia, and/or Alzheimer’s will need to use much higher doses or a better delivery system to get adequate amounts of DHA and EPA into the brain.

#2: It showed that the APOE4 gene significantly decreases the ability of the brain to accumulate DHA and EPA. This has several important implications.

  • Because both DHA and EPA are vital for brain health, this may explain why the APOE4 gene increases the risk of Alzheimer’s Disease.
  • It also means those at highest risk for Alzheimer’s Disease are the ones who are most likely to have difficulties accumulating DHA and EPA in their brain.
  • Once again, it means future studies of the ability of supplemental DHA to reduce the risk of Alzheimer’s Disease will need to use much higher doses of DHA.

Based on the results from this study the authors are currently testing the effect of B vitamins and high dose DHA supplementation on DHA and EPA levels in the brain, brain imaging, and cognitive outcomes in a larger ongoing clinical trial.

For more details, read the article above. For a better understanding of the roles of DHA, EPA, and the APOE gene in brain health, you may want to read my “Biochemistry 101” section 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.

 

Health Tips From The Professor