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

Are High Fat Dairy Foods Good For You?

November 13, 2018 by Dr. Steve Chaney

Can You Have Your Cream And Eat It Too?

Author: Dr. Stephen Chaney

Dairy foods can play an important role in helping us get enough calcium in our diet and may provide some other benefits (discussed below). However, many dairy foods contain a lot of saturated fat. Thus, we have been told to select low-fat dairy foods. So, what should we make of the recent headlines and blogs telling us that high-fat dairy foods are good for us?

Are high fat dairy foods good for us?

To answer that question, I picked a recent article (F. Imamura et al, PLOS Medicine, doi: 10.1371/journal.pmed.1002670 ) claiming that dairy fats lower the risk of type 2 diabetes and did an in-depth analysis of the data behind the headlines.

Fat Chemistry 101

Before I get started, let me cover what I call “Fat Chemistry 101”. Sorry, professors never fully retire.

Fat Nomenclature: Let me briefly describe some of the nomenclature that chemists and biochemists use when they describe fats. Fats, or triglycerides, are generally defined as three fatty acids attached to a molecule of glycerol. The chemical nomenclature for fatty acids consists of a “C” followed by the number of carbons in that fatty acid. That, in turn, is followed by a colon (:) and the number of doubles bonds (0 for a saturated fatty acid, 1 for a monounsaturated fatty acid, and 2 or more for a polyunsaturated fatty acid). Let me give some examples, specifically the examples I will refer to in this article.

Saturated fatty acids:

C15:0 (pentadecanoic acid)
C16:0 (palmitic acid)
C17:0 (heptadecanoic acid)
C18:0 (stearic acid)

Monounsaturated fatty acids:

C18:1 (oleic acid)

C16:0, and C18:0 are referred to as even-chain fatty acids (They have an even number of carbon atoms). C15:0 and C17:0 are referred to as odd-chain fatty acids (They have an odd number of carbon atoms).

C16:0 (palmitic acid) is the most abundant saturated fatty acid in meats and dairy food. C18:0 (stearic acid) is the second most abundant saturated fatty acid in these foods. The odd-chain fatty acids C15:0 and C17:0 are primarily found in dairy fat although small amounts can also be found in meat and fish.

All saturated fats raise LDL cholesterol. However, the effect is not equally strong for all saturated fats. The effect on LDL cholesterol is strongest for palmitic acid (C16:0). It is weaker for stearic acid, possibly because stearic acid (C18:0) can be metabolized to oleic acid (C18:1), which has no effect on LDL cholesterol.

Foods Are A Complex Mixture Of Fats: We generally think of saturated fats coming from meat and dairy, monounsaturated fats coming from olive oil and avocados, and polyunsaturated fats as coming from vegetable oils, seeds, and nuts. However, that is an oversimplification. Meats also contain monounsaturated and polyunsaturated fats. Olive oil contains some saturated and polyunsaturated fats. Vegetable oils also contain monounsaturated and saturated fats.

Why do I even mention this? It is important because we tend to label a food “good” or “bad” based on its most abundant fat. Perhaps we would be better served if we considered all the major fats in that food before deciding whether it is good or bad for us.

How Was The Study Designed?

With that background in mind, let us turn our attention to the current study. The authors wished to test the hypothesis that high-fat dairy foods might decrease the risk of type 2 diabetes. The results of previous studies had been mixed, but the authors hypothesized that might have been due to the limitations of using dietary recalls to assess intake of high-fat dairy foods. Specifically, they theorized that dietary recalls tend to underestimate the less apparent sources of dairy fats such as creams, sauces, cheeses, and butter used as part of meal preparation or in prepared foods.

They postulated that blood and tissue concentrations of the odd-chain fatty acids (C15:0 and C17:0) would be a much better biomarker of dairy fat consumption than dietary recalls. They performed a meta-analysis of all studies that measured blood or tissue levels of odd-chain fatty acids and looked at type 2 diabetes as an outcome.

Their meta-analysis included 16 studies from 12 countries with a total of 63,682 participants (age range: 49 to 76 years). The participants were slightly overweight, but none of them had type 2 diabetes at the beginning of the studies. The participants were followed for an average of 9 years. By the end of the studies 15,180 (24%) had developed type 2 diabetes.

Are High Fat Dairy Foods Good For You?

When the authors compared the highest versus the lowest levels of odd-chain fatty acids in the subjects, the results of the study were as follows:

The highest level of C15:0 fatty acids was associated with a 20% lower incidence of type 2 diabetes.
The highest level of C17:0 fatty acids was associated with a 35% lower incidence of type 2 diabetes. This is consistent with several previous studies that have suggested C17:0 fatty acids are a better predictor of type 2 diabetes than C15:0 fatty acids.
When these data were combined the overall effect was a 29% lower incidence of type 2 diabetes.

The authors concluded: “These novel findings support the need for additional clinical and molecular research to elucidate the potential effects of [odd-chain] fatty acids on glucose-insulin metabolism and the potential role of selected [high-fat] dairy products for the prevention of type 2 diabetes.”

What Does This Study Mean For You?

On the surface, this looks like a very strong study. It is, after all, a meta-analysis with over 68,000 subjects. It also used biomarkers for dairy fat consumption rather than relying on less accurate dietary recalls. Finally, it is consistent with several earlier studies suggesting that high-fat dairy foods decrease the risk of type 2 diabetes and heart disease. What could go wrong?

The answer is “Plenty.”

Studies looking at the effect of high-fat dairy foods on the risk of heart disease and type 2 diabetes have been inconsistent. Some have shown benefit, but others have come up empty. Despite the inconsistent results, the idea that high-fat dairy foods might be good for us has gotten a lot of media attention. I suspect that is because this is the kind of news we really want to be true. After all, wouldn’t it be great news if we could eat all the cheese, cream, and butter we wanted?
Some studies have concluded that high-fat and low-fat dairy products were equally effective at decreasing the risk of heart disease and type-2 diabetes. If these studies are correct, they would suggest something else in dairy foods is protective, not the kind of fat.
The odd-chain saturated fatty acids are very minor constituents of dairy fat. Together, they represent 1.3% of the fatty acids in dairy fat. In contrast, even-chain saturated fatty acids make up 68% of the fatty acids in dairy fat. Palmitic acid (C16:0) makes up 30% or 23 times the concentration of odd-chain fatty acids. Stearic acid (C18:0) makes up 12% or 9 times the concentration of odd-chain fatty acids.
This study, and most previous studies, have just looked at the association between odd-chain fatty acids and type 2 diabetes. They do not prove cause and effect.
No mechanism has been proposed that would account for the proposed beneficial effects of odd-chain saturated fatty acids, especially in the presence of much higher concentrations of even-chain saturated fatty acids.
A study published last year (BJ Jenkins et al, Scientific Reports, 7:44845, doi: 10.1038/srep44845 ) reported that blood levels of C15:0 were dependent on intake of dairy foods, but that blood levels of C17:0 were independent of dairy intake. These authors presented evidence showing C17:0 in the human body resulted from metabolism of C18:0 (stearic acid) in our diet rather than coming from dairy fats.

In other words, the odd-chain fatty acid (C15:0) that comes from dairy foods is the one that has only a weak association with the risk of developing type 2 diabetes. The odd-chain fatty acid with a strong association with diabetes risk is synthesized in our bodies from stearic acid (C18:0), a fatty acid that is also found at high levels in meat.

So, are high fat dairy foods good for you? More studies are needed.

The Bottom Line

A recent study has reported that high-fat dairy products may reduce the risk of type 2 diabetes. This is consistent with a few other studies that have suggested high-fat dairy products may reduce the risk of diabetes and heart disease.

The idea that high-fat dairy foods might be good for us has gotten a lot of media attention. I suspect that is because this is the kind of news we really want to be true. After all, wouldn’t it be great news if we could eat all the cheese, cream, and butter we wanted?

However, the clinical results have been inconsistent. Some have shown benefit, but others have come up empty. Most of the studies also had significant limitations. I have discussed the limitations of the current study in the article above.

We can remain hopeful that high-fat dairy foods will eventually be shown to be good for us, but until we have stronger evidence for the proposed benefits of dairy fats, my recommendation is to consume high-fat dairy products sparingly.

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.

Is Our Microbiome Affected By Exercise?

November 6, 2018 by Dr. Steve Chaney

Microbiome Mysteries

Author: Dr. Stephen Chaney

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

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

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

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

How Was The Study Designed?

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

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

VO_2max (a measure of fitness) was determined at baseline and at the end of the exercise intervention. Stool samples for determination of gut bacteria and concentrations of short-chain fatty acids were taken at baseline, at the end of the exercise intervention, and again after the washout period.

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

Is Our Microbiome Affected By Exercise?

The results of the study were as follows:

Fitness, as assessed by VO_2max, increased for all the participants, and the increase in fitness was comparable for both lean and obese subjects.
Exercise induced a change in the population of gut bacteria, and the change was comparable in lean and obese subjects.
Exercise increased fecal concentrations of butyrate and other short-chain fatty acids in the lean subjects, but not in obese subjects.
The exercise-induced changes in gut bacteria and short-chain fatty acid production were largely reversed once exercise training ceased.

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

What Does This Study Mean For You?

There are two important take home lessons from this study.

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

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

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

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

The Bottom Line

A recent study has reported that:

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

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

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

Are Vitamin D Supplements Worthless?

October 30, 2018 by Dr. Steve Chaney

Are We Asking The Right Question?

Author: Dr. Stephen Chaney

We have been told that vitamin D is a miraculous “must have” vitamin. We have been told it’s not just important for healthy bones. It’s also important for a strong immune system, heart health, protection from cancer, and many other health benefits. We have been told that we should get our 25-hydroxy vitamin D levels tested and supplement with extra vitamin D if they are low.

Now, the latest headlines are saying all of that is wrong. They are telling us vitamin D supplements do not improve bone density or protect against falls and bone fractures. They are telling us to forget all the other claimed benefits of vitamin D. Those claims have been disproved. Forget about the 25-hydroxy vitamin D tests. They are a waste of money.

What is the truth? Why is it so confusing? Are vitamin D supplements worthless? Let me guide you through the claims and counterclaims so you can discover the truth for yourself.

How Did Vitamin D Become So Popular?

Let’s start with a brief history of vitamin D. It all started with the industrial revolution in Northern Europe. Suddenly, children and adults in the large cities were spending the bulk of their waking hours in dark factories rather than outdoors on the farm. They were already living in northern latitudes where sunlight was weak during the winter months. To make matters worse pollution from the factories was creating a haze that blocked the sunlight.

That lead directly to the discovery that sunlight was crucial to our body’s ability to synthesize vitamin D and that vitamin D was essential for building strong bones. The solution to the public health crisis of rickets and osteomalacia was to fortify dairy products with vitamin D. The almost universal adaptation of vitamin D fortification virtually eliminated rickets and osteomalacia except in association with certain rare diseases. The two important lessons learned from this experience were:

Vitamin D is essential for healthy bone formation.
Vitamin D supplementation improves bone health for individuals who are deficient in vitamin D

As we discuss the latest findings, we need to keep in mind that these fundamental principles have not changed.

In the late 20^th century our understanding of vitamin D took another leap with the discovery that vitamin D receptors were not restricted to bone cells. Almost every cell in our body contained vitamin D receptors. That lead to studies showing that people with low vitamin D intakes were more likely to experience heart disease, cancer, some autoimmune diseases, and infectious diseases such as flu than people with high vitamin D intakes.

The final leap in our understanding of vitamin D took place when the medical profession started routinely testing blood levels of 25-hydroxy vitamin D. That is when we discovered that some people who appeared to have adequate intake of vitamin D and/or adequate exposure to sunlight had low blood levels of 25-hydroxy vitamin D. Furthermore, follow-up studies showed that low 25-hydroxyvitamin D levels correlated with an increased risk of heart disease, cancer, and infectious disease. The important lessons learned from these experiments were:

Vitamin D deficiency is associated with increased risk of multiple diseases.
25-hydroxy vitamin D tests are the best way to measure vitamin D deficiency.

Once again, these fundamental principles have not changed.

What Did The Study Show?

The study (MJ Bolland et al, Lancet Diabetes Endocrinology 2018) behind the headlines was a meta-analysis of 81 randomized, placebo-controlled studies with a total of 53,537 subjects that looked at the effect of vitamin D supplementation in elderly populations on bone mineral density, bone fractures, and falls.

The meta-analysis only included studies in which vitamin D intake was the sole variable. In many cases the subjects were not taking a calcium supplement. If they were taking a calcium supplement, both the vitamin D group and placebo group were taking the same amount of calcium.

The results were unequivocal. In this study vitamin D supplementation had no effect on bone mineral density, bone fractures, or falls in elderly populations. The authors concluded “There is little justification to use vitamin D supplements to maintain or improve musculoskeletal health.”

Is this conclusion justified? Let’s put the findings of this study into a broader perspective.

Are We Asking The Right Questions?

Before throwing out our vitamin D supplements let’s ask whether this study is asking the right question. I have covered this topic in detail in my new book “Slaying The Supplement Myths” (https://slayingthesupplementmyths.com) with respect to similar studies that had called into question the value of calcium supplements for bone health. Let me cover the highlights here.

In my book I created the graphic on the right to put the question of who benefits from supplementation into perspective. For the purposes of this discussion, I will just focus on poor diet (or, in the case of vitamin D, poor exposure to sunlight). As I discussed above, science shows that people who are not getting enough vitamin D from diet and sunlight benefit from vitamin D supplementation. Unfortunately, vitamin D enthusiasts and some supplement companies have muddied the waters by going beyond what good science shows and suggesting or implying that everyone will benefit from vitamin D supplementation.

This is part of the problem. Once you have created a paradigm that everyone will benefit from vitamin D supplementation, that paradigm is easy to disprove. If someone already has adequate, or nearly adequate, levels of 25-hydroxy vitamin D, would we expect additional vitamin D to make a difference? Of course not, but that is exactly the question the most recent study was asking.

In discussing the limitations of their study, the authors said: “It is possible that trials of populations with low baseline 25-hydroxy vitamin D might produce different results because only 4 trials, involving 831 participants (1.6% of all participants), reported mean baseline 25-hydroxy vitamin D levels lower than 25 nmol/L (the level indicating vitamin D deficiency).

In other words, the study did not measure the effect of vitamin D supplementation for people who were vitamin D deficient. The only take-home lesson from this study is that people with adequate, or near adequate, vitamin D status do not benefit from vitamin D supplementation. That is a “no-brainer.”

Vitamin D And A Bone Healthy Lifestyle

The other glaring deficiency of this study is that it was only measuring the effect of vitamin D on bone health. They purposely excluded any other factor that might influence bone health. That was a fatal flaw because healthy bone requires a holistic approach, not individual nutrients. In my book Slaying the Supplement Myths I refer to this as a “bone healthy lifestyle.”

The most important feature of a “bone healthy lifestyle” is this:

Calcium, vitamin D, and resistance (weight bearing) exercise are all essential for healthy bones.
However, none of them is sufficient by itself. You need all three. You need a holistic approach if you wish to build strong bones.

Simply put, that means unless you include adequate calcium and exercise there is no reason to expect vitamin D supplementation to help build strong bones. Unfortunately, none of the studies included in the recent meta-analysis took a holistic approach to bone health. Some included calcium, but many didn’t. Resistance exercise was never considered. The studies were doomed to failure.

When you include flawed studies in your meta-analysis, you have what computer programmers call “Garbage in. Garbage out.” A meta-analysis can never be stronger than the individual studies it includes.

Other features of a “bone healthy lifestyle” include:

We need more than calcium and vitamin D for strong bones. We need magnesium, zinc, copper, manganese, vitamin C and vitamin K. If we are deficient in any of these, calcium will not be utilized as efficiently.
The foods we eat are also important. Our bones serve as a buffer system to keep our bodies slightly alkaline. Every time we eat acid-forming foods a little bit of bone is dissolved to neutralize the acid. For optimal bone health we need to minimize acid-forming foods and eat more alkaline-forming foods. That means we need to avoid sodas, sweets and refined grains. We also need to minimize meats, eggs, and dairy. Instead, we should focus on fruits, vegetables, peas, beans, lentils, seeds, and nuts.
Beware of drugs. The list of common medications that dissolve bones is a long one. Some of the worst offenders are anti-inflammatory steroids such as cortisone and prednisone, drugs to treat depression, drugs to treat acid reflux, and excess thyroid hormone. I am not suggesting that you should avoid properly prescribed medications. I would suggest you ask your doctor or pharmacist whether the drugs you are taking adversely affect bone density. If they do, you should pay a lot more attention to the other aspects of a “bone healthy lifestyle.”

Are Vitamin D Supplements Worthless?

Now we can come back to the question “Are vitamin D supplements worthless?” as the recent headlines have suggested. If you phrase the question as “Does everyone benefit from vitamin D supplementation?” or “Is vitamin D supplementation alone sufficient to build strong bones?” the answer is a clear no.

However, those are the wrong questions. If you ask: “Does vitamin D supplementation benefit people who are vitamin D-deficient?” the answer is a clear yes. If you ask: “Does a holistic approach that includes resistance exercise, adequate calcium, and adequate vitamin D improve bone health?” the answer is likely to be yes as well.

What about the headlines claiming that vitamin D is also worthless for strengthening the immune system and reducing the risk of heart disease, cancer, and auto-immune diseases? The studies on which these claims are based suffer from the same flaws. They are asking the same wrong questions.

My recommendations:

Have your blood levels of 25-hydroxy vitamin D tested on a regular basis. I have them tested each year when I get my physical.
If your blood levels of 25-hydroxy vitamin D are below 25 nmol/L (which the NIH considers deficient), you are likely to benefit from vitamin D supplementation. If they are above 50 nmol/L (which the NIH considers sufficient), vitamin D supplementation is unlikely to provide additional benefit. However, that level of vitamin D doesn’t guarantee that you will have strong bones. You also need sufficient calcium and resistance exercise.
If your blood levels are in the insufficient range (between 25 nmol/L and 50 nmol/L), the situation is more complicated. If you are close to 50 nmol/L, you may benefit slightly from adding a vitamin D supplement, but the benefit will be too small to show up in a clinical study such as the one that resulted in the recent headlines. My advice is to look at your diet and medication use. If they put you at risk for low bone density, my recommendation would be to add a vitamin D supplement – along with adequate calcium and resistance exercise, of course. If you are closer to 25 nmol/L, you will likely benefit from a vitamin D supplement along with adequate calcium and exercise.
Don’t think of vitamin D supplementation as a “magic bullet” that will solve all your ills. Instead, think of it as just one component of a holistic approach to a bone healthy lifestyle.

The Bottom Line

A recent meta-analysis concluded that vitamin D supplementation did not improve bone mineral density, reduce bone fractures, or reduce falls in the elderly. While this conclusion was definitive, the study was asking the wrong questions.

We know that vitamin D improves bone health for people who are vitamin D-deficient. However, only 1.6% of the people in this study were vitamin D-deficient at the beginning of the study. That means the study was really asking: “If people have adequate, or near adequate, vitamin D status, does vitamin D supplementation provide any additional benefit?” The answer to that question is a “no-brainer.” There is no reason to expect that additional vitamin D would provide benefit.
We know that while vitamin D is essential for building strong bones, it is not sufficient by itself. Strong bones require a holistic approach that includes resistance exercise, adequate calcium, and adequate vitamin D. However, this study only looked at the effect of vitamin D on bone health. Calcium and exercise were excluded from consideration. That means the study was really asking: “Is vitamin D a “magic bullet” that can build strong bones by itself?” Again, there is no reason to expect vitamin D to provide much benefit under those conditions.

My recommendations:

Have your blood levels of 25-hydroxy vitamin D tested on a regular basis. I have them tested each year when I get my physical.
If your blood levels of 25-hydroxy vitamin D are low, you are likely to benefit from vitamin D supplementation. If they are already optimal, vitamin D supplementation is unlikely to provide additional benefit.
Don’t think of vitamin D supplementation as a “magic bullet” that will keep your bones strong by itself. Instead, think of it as just one component of a holistic “bone healthy lifestyle.”

For more details and to see my detailed recommendations, 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.

How Long Do the Benefits of Supplements Last?

October 23, 2018 by Dr. Steve Chaney

Can Supplements Set You On A Path Towards A Healthier Life?

Author: Dr. Stephen Chaney

A recent study (U Alehagen et al, PLOS One, April 11, 2018, 1-15 ) reported that the heart benefits of supplementation with coenzyme Q10 and selenium persisted for 12 years after supplementation ended. You would have thought a story like that would have made the headlines. Nope. Hardly a mention. Perhaps it did not match the narrative of the media and health professionals that supplements are worthless.

This study broke new ground. Most studies last a year or two and report whether there were any benefits of supplementation. A few studies have been extended a few years beyond the original supplementation period and have reported continued benefits of supplementation. However, in those studies the intervention group was still taking supplements. The intervention period was simply extended.

However, this study was unique in that supplementation was discontinued after 4 years. However, the positive effects of supplementation during that four-year period persisted for another 12 years without additional supplementation.

How Was The Study Done?

In this study 443 elderly individuals (average age =78) were recruited from a rural village in Sweden. They were given either supplements providing 200 mg/day of coenzyme Q10 and 200 mcg/day of selenium yeast or placebo pills. They were followed for four years. At this point the intervention phase of the trial ended, and the participants were followed for another 12 years without supplementation.

Cardiovascular deaths and all-cause mortality were recorded at 4 years (the end of the original intervention period), 10 years, and 12 years. The Swedish health care system is incredibly efficient. None of the participants were lost to follow-up.

Note on study design: Both coenzyme Q10 and selenium have heart health benefits and they compliment each other. Coenzyme Q10 was included in this study because our bodies lose the ability to make coenzyme Q10 as we age. By the time we reach age 80, we only make around half the coenzyme Q10 we made when we were younger. Selenium was included in the study because most Swedes are selenium deficient.

This study measured selenium levels and confirmed that all participants were selenium deficient at the beginning of the study. Selenium levels increased to near optimal in the supplemented group during the 4-year intervention period. In contrast, the placebo group remained selenium deficient.

How Long Do the Benefits of Supplements Last?

The results of the study were truly amazing.

When you compared the group that had received coenzyme Q10 and selenium during the first 4 years of the study with the placebo group:

Cardiovascular mortality was 38% less and all-cause mortality was 24% less 12 years later in the supplement group.
The decrease in cardiovascular mortality lessened slightly with time (53% lower at 4 years, 46% lower at 10 years, and 38% lower at 12 years.
In contrast, the decrease in all-cause mortality remained relatively constant.
The effect was greater for women (who have lower coenzyme Q10 levels than men) than it was for men.
The decrease in cardiovascular mortality was 57% for women and 22% for men.
Cardiovascular mortality was decreased by 40-50% for people at high risk of cardiovascular death because of atherosclerosis, diabetes, high blood pressure, or impaired heart function.

Putting This Study Into Perspective

I don’t want to read too much into this study. It has multiple limitations:

It is a very small study.
It is the first study I am aware of that has followed study participants years after supplementation has ended. More studies like this are clearly needed before any firm conclusions can be drawn.
It may be unique to Sweden where selenium deficiency is widespread. Selenium deficiency is much less prevalent in some other countries such as the United States.
It is possible that once the study population heard about the results of the initial 4-year study they started self-supplementing with coenzyme Q10 and selenium. However, since the participants did not know whether they were in the supplement or placebo group, that would likely affect both groups equally.

However, it is the implications of the study that fascinate me.

The authors of the study speculated that the improvement in endothelial cell function (Endothelial cells line the arteries and play an important role in arterial health) and/or decreased inflammation may have persisted long after supplementation stopped.
A more interesting idea is that supplementation (or the effects of supplementation) caused modifications to the DNA that were persistent (something we refer to as epigenetics). Moreover, those DNA modifications may have altered gene expression in a manner that reduced heart disease risk.

Much more work needs to be done before we know whether epigenetic modifications were responsible for the persistent benefit of supplementation in this, or any other, study. However, the ramifications of this idea are substantial. We think of supplementation as something that provides benefit only while we are taking the supplement. What if, under the right conditions, supplementation could send us down an entirely different path to better health? That would be worth major headlines.

The Bottom Line

A recent study in Sweden looked at the effects of supplementation with coenzyme Q10 and selenium on heart health 12 years after supplementation had ended.

The study reported that cardiovascular mortality was 38% less and all-cause mortality was 24% less 12 years later in the group that supplemented during the first 4 years.

The study has multiple limitations and needs to be repeated before drawing any definite conclusions. However, if true, it has interesting implications. What if the benefits of supplementation didn’t stop when you stopped supplementing? What if supplementation sent you down an entirely different path, a path towards better health?

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.

High Protein Diets and Weight Loss

October 16, 2018 by Dr. Steve Chaney

Do High Protein Diets Reduce Fat And Preserve Muscle?

Author: Dr. Stephen Chaney

Are high protein diets your secret to healthy weight loss? There are lots of diets out there – high fat, low fat, Paleolithic, blood type, exotic juices, magic pills and potions. But recently, high protein diets are getting a lot of press. The word is that they preserve muscle mass and preferentially decrease fat mass.

If high protein diets actually did that, it would be huge because:

It’s the fat – not the pounds – that causes most of the health problems.

Muscle burns more calories than fat, so preserving muscle mass helps keep your metabolic rate high without dangerous herbs or stimulants – and keeping your metabolic rate high helps prevent both the plateau and yo-yo (weight regain) characteristic of so many diets.

When you lose fat and retain muscle you are reshaping your body – and that’s why most people are dieting to begin with.

So let’s look more carefully at the recent study that has been generating all the headlines (Pasiakos et al, The FASEB Journal, 27: 3837-3847, 2013).

The Study Design:

This was a randomized control study with 39 young (21), healthy and fit men and women who were only borderline overweight (BMI = 25). These volunteers were put on a 21 day weight loss program in which calories were reduced by 30% and exercise was increased by 10%. They were divided into 3 groups:

One group was assigned a diet containing the RDA for protein (about 14% of calories in this study design).
The second group’s diet contained 2X the RDA for protein (28% of calories)
The third group’s diet contained 3X the RDA for protein (42% of calories)

In the RDA protein group carbohydrate was 56% of calories, and fat was 30% of calories. In the other two groups the carbohydrate and fat content of the diets was decreased proportionally.

What Did The Study Show?

Weight loss (7 pounds in 21 days) was the same on all 3 diets.

The high protein (28% and 42%) diets caused almost 2X more fat loss (5 pounds versus 2.8 pounds) than the diet supplying the RDA amount of protein.

The high protein (28% and 42%) diets caused 2X less muscle loss (2.1 pounds versus 4.2 pounds) than the diet supplying the RDA amount of protein.

In case you didn’t notice, there was no difference in overall results between the 28% (2X the RDA) and 42% (3X the RDA) diets.

Pros And Cons Of The Study:

The con is fairly obvious. The participants in this study were all young, healthy and were not seriously overweight. If this were the only study of this type one might seriously question whether the results were applicable to middle aged, overweight coach potatoes. However, there have been several other studies with older, more overweight volunteers that have come to the same conclusion – namely that high protein diets preserve muscle mass and enhance fat loss.

The value of this study is that it defines for the first time the upper limit for how much protein is required to preserve muscle mass in a weight loss regimen. 28% of calories is sufficient, and there appear to be no benefit from increasing protein further. I would add the caveat that there are studies suggesting that protein requirements for preserving muscle mass may be greater in adults 50 and older.

The Bottom Line:

1) Forget the high fat diets, low fat diets, pills and potions. High protein diets (~2X the RDA or 28% of calories) do appear to be the safest, most effective way to preserve muscle mass and enhance fat loss in a weight loss regimen.

2) That’s not a lot of protein, by the way. The average American consumes almost 2X the RDA for protein on a daily basis. However, it is significantly more protein than the average American consumes when they are trying to lose weight. Salads and carrot sticks are great diet foods, but they don’t contain much protein.

3) Higher protein intake does not appear to offer any additional benefit – at least in young adults.

4) Not all high protein diets are created equal. What some people call high protein diets are laden with saturated fats or devoid of carbohydrate. The diet in this study, which is what I recommend, had 43% healthy carbohydrates and 30% healthy fats.

5) These diets were designed to give 7 pounds of weight loss in 21 days – which is what the experts recommend. There are diets out there promising faster weight loss but they severely restrict calories and/or rely heavily on stimulants, they do not preserve muscle mass, and they often are not safe. In addition they are usually temporary. I do not recommend them.

6) This level of protein intake is safe for almost everyone. The major exception would be people with kidney disease, who should always check with their doctor before increasing protein intake. The only other caveat is that protein metabolism creates a lot of nitrogenous waste, so you should drink plenty of water to flush that waste out of your system. But, water is always a good idea.

7) The high protein diets minimized, but did not completely prevent, muscle loss. Other studies suggest that adding the amino acid leucine to a high protein diet can give 100% retention of muscle mass in a weight loss regimen – but that’s another story for another day.

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.

Are Probiotics Bad For You?

October 9, 2018 by Dr. Steve Chaney

Are Probiotics Worthless?

Author: Dr. Stephen Chaney

Probiotics (friendly gut bacteria) are all the rage. There is big money to be made, so the internet is ablaze with all the amazing things probiotics can do for you. Of course, most of those articles are posted by companies wanting to sell you their miracle mixture of probiotic bacteria.

In the last few weeks, you may have seen headlines proclaiming that probiotics are worthless. You just poop them out. Even worse, they may be upsetting the natural balance of bacteria in your gut. Are probiotics bad for you? They may be.

As usual, the truth is somewhere in the middle. Before I start sorting out fact from fiction, let me remind you of some important facts about gut bacteria that I covered in a recent article of “Health Tips From The Professor”:

The composition of bacteria in our gut is influenced by what we eat. For example, meat eaters have a completely different composition of gut bacteria than vegetarians.
Fiber from whole plant foods is a major food source for healthy gut bacteria.
Each plant-based food group and each food within that group has a unique blend of fibers. We should probably aim for a wide variety of whole plant foods in our diet.

Are Probiotics Worthless?

Let’s start with the study (N. Zmora et al, Cell 174, 1388-1405, 2018 ) that generated the headlines proclaiming that probiotics were worthless.

The characteristics of the study with my comments are as follows:

The study had 15 subjects who were given either a commercially available probiotic supplement or a placebo containing cellulose. It was a very small study.
The probiotic supplement contained 25 billion colony forming units of 11 commonly used strains of bacteria. Its manufacturer claimed the bacteria survived stomach acid and colonized the intestine, but no references were given for published clinical studies backing up that claim. It is buyer beware in the supplement industry. I would not believe any claims about a probiotic supplement that were not backed up by published clinical studies.
The investigators measured bacterial colonization of the mucosal cells lining the intestine rather than the population of bacteria that ended up in the feces. This is the “gold standard” for measuring colonization of the intestine by probiotic bacteria. However, it requires a colonoscopy before the study started and a second colonoscopy 3 weeks later. As any of you who have had a colonoscopy can attest, this is a very invasive procedure. It probably accounts for the small size of the study. In fact, the study started with 28 subjects and 13 dropped out, one after suffering a serious adverse reaction to the first colonoscopy. My point is simply that I don’t expect to see a lot of this type of study.

The results of the study with my comments are as follows:

Overall, the particular probiotic supplement used in this study didn’t work very well. There was minimal colonization of the intestinal mucosal cells by the bacteria in the probiotic supplement. Some did better than others, but the net colonization was small. We don’t know whether the results would have been the same with other probiotic supplements, but this is the finding that generated all the headlines. However, it is the rest of the study that is interesting.
The probiotic supplement worked better for some subjects than for others. Some of the subjects in the study were “permissive.” The probiotic cells colonized their intestinal mucosal cells with high efficiency. Other subjects were “resistant.” Probiotic bacteria had a great deal of difficulty colonizing their intestinal mucosal cells. This doesn’t surprise me. Most clinical studies report an average result. They don’t report individual variations. This is one of the first studies to report on individual variation of probiotic colonization. As such, it has important implications. It means that even though you may be taking a probiotic supplement that has been “clinically proven” to survive stomach acid and colonize the intestine, it may not work well for you. But, wait, the study gets even more interesting.
How well the probiotic supplement worked depended on the population of bacteria in the intestine to begin with. “Permissive” and “resistant” subjects had very different species of bacteria in their intestine at the beginning of the trial. There was a characteristic grouping of bacteria in “permissive” subjects and a different characteristic grouping of bacteria in “resistant” subjects. This is the part of the study that should have generated headlines. Let’s put this part of the study into perspective.

We each have around 38 trillion bacteria in our intestines. Let’s assume that all 25 billion bacteria in the probiotic supplement make it into the intestine intact. You have just dropped them into hostile territory where they are outnumbered 1,000 to 1. We know that some bacteria secret substances that support the growth of “like-minded” bacteria. That’s why certain species of bacteria tend to cluster together. We also know that bacteria secret toxins, so they can out-compete bacteria they don’t like. So, it is no wonder the survival of the probiotic bacteria depends on which species of bacteria are already populating the intestine when they arrive on the scene.

This study leaves a lot of unanswered questions:

What determined the original population of gut bacteria? Was it the genetics or health of the subject? Or, was it the food they were eating? We simply don’t know.
We were sending these probiotic bacteria into hostile territory. Were we giving them the food they needed to survive? Would the results have been different for the “resistant” subjects if they had been eating a different kind of fiber-rich foods, or taken a prebiotic supplement? Again, we just don’t know.

If we want to optimize the results of probiotic supplementation, these are the questions we should be asking.

Are Probiotics Bad For You?

Now, let’s turn to the study (J. Suez et al, Cell 174, 1406-1423, 2018) generating the headlines saying that probiotic supplements may be bad for you. This study was looking specifically at the use of probiotics following antibiotic use.

The study reported when probiotics are used following antibiotic use, they delay, rather than enhance, the recovery of intestinal bacteria back to the same number and type of bacteria that existed prior antibiotic use. That’s the finding that generated all the headlines. Let’s put that into perspective.

Both the headlines and interpretation of the data were inaccurate.

Probiotics actually had a relatively small effect on the ability to regain your “normal” population of intestinal bacteria. The headlines made it sound as if the delay was significant and that you never regained your “normal” population of intestinal bacteria. In fact by one measure, the population of intestinal bacteria was 70% normal by 5 days, 80% normal by 20 days, and 95% normal by 90 days.
Poop pills work better but will probably never be popular. When the investigators extracted intestinal bacteria from the subject’s poop and put them into pills prior to the study, the poop pills restored the “normal” population of intestinal bacteria much more quickly. However, I doubt that poop pills will become popular any time soon.
Your “normal” population of intestinal bacteria may not be the optimal population of intestinal bacteria. The headlines implied that the fact you never recovered your “normal” population of intestinal bacteria was a bad thing. That assertion assumes that all of us have the optimal population of intestinal bacteria to begin with, an assertion that almost any expert in the field would find absurd. The last time I checked, one of the major reasons for taking probiotic supplements was to change our population of intestinal bacteria for the better.

The study ignores the major reasons for taking a probiotic supplement after antibiotic use. Most people are not taking the probiotic supplement to restore their original population of intestinal bacteria. They are taking it to:

Prevent “bad guys” like yeast from filling the void caused by the antibiotics.
Improve digestion. Some strains of intestinal bacteria play an important role in digestion. Because antibiotics wipe out those bacteria, they often cause gas, diarrhea, and bloating. After antibiotic use, people are taking probiotic bacteria with digestive benefits to eliminate those digestive issues as quickly as possible.
Strengthen the immune system. People are generally taking antibiotics to fight some sort of infection. Some strains of intestinal bacteria play an important role in immunity. Because antibiotics wipe out those bacteria, they weaken the immune system. After antibiotic use, people are taking probiotics to strengthen the immune system as quickly as possible

In short, taking probiotic supplements that are proven to improve digestion and strengthen the immune system play an important role in minimizing the side effects of antibiotic use.

What Does This Mean For You?

At the beginning of this article I said; “The truth lies somewhere in between.” The first study is a perfect example.

It was valuable in that it challenged the assertion by some manufacturers that their probiotics survive stomach acid and work equally well for everyone. At the very least, it suggests that we should demand clinical proof that any probiotic supplement colonizes the intestine and provides a health benefit before we use it.
The most interesting finding from the first study is that probiotics work much better for some people than for others, and how well they work depends on the population of bacteria in our gut prior to taking the antibiotic. We have much more to learn about this individual variability, and how to control it.

Until we know more, my best advice is to eat a fiber-rich, primarily plant-based diet with as many different varieties of fruits, vegetables, whole grains, and legumes as possible. Providing a variety of fibers is important because at least some of them will likely support the growth of the bacteria in the probiotic supplement. Prebiotics may be of some help, but only if they have been shown to be effective for the particular strains of probiotic bacteria they are paired with.

The second study was much less enlightening. It reported that taking a probiotic after antibiotic use slowed the return to the original population of intestinal bacteria. My response to that is: “So what?”

The effect was minimal.
The purpose of probiotics is to improve on the population of intestinal bacteria, not to return to the same population of bacteria you had prior to antibiotic use.
Probiotics are taken after antibiotic use for reasons that have nothing to do with restoring the original population of intestinal bacteria.

The Bottom Line

Two recent studies have challenged the benefits of probiotic use.

The first study provided some valuable insights.

It reported that a particular probiotic supplement did a very poor job of colonizing the intestine. We have no idea whether that would apply to other probiotic supplements, but that was the result that generated all the headlines. At the very least, it suggests that we should demand clinical proof that any probiotic supplement colonizes the intestine and provides a health benefit before we use it.
However, the most interesting finding from the first study is that probiotics work much better for some people than for others, and how well they work depends on the population of bacteria in our gut prior to taking the antibiotic. We have much more to learn about this individual variability, and how to control it.

The second study was much less enlightening. It reported that taking a probiotic after antibiotic use slowed the return to the “normal” population of intestinal bacteria that were present before antibiotic use. My response to that is: “So what?”

The purpose of probiotics is to improve on the population of intestinal bacteria, not to return to the same population of intestinal bacteria you had prior to taking an antibiotic.
Probiotics are taken after antibiotic use for reasons that have nothing to do with restoring the original population of intestinal bacteria.

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 Omega-3s Reduce Heart Disease Risk

October 2, 2018 by Dr. Steve Chaney

Omega-3 Confusion

Author: Dr. Stephen Chaney

This article includes updates as of October 2, 2018. First, here is the earlier information.

Do omega-3s reduce heart disease risk?

The controversy around omega-3s and heart disease risk is part of the larger controversy around supplementation. It is omega-3 supplements that are controversial, not omega-3-rich fish. Of course, that completely ignores the fact that many omega-3-rich fish are contaminated with PCBs and/or heavy metals.

Why is omega-3 supplementation so controversial? The problem is that proponents of omega-3 supplementation often seize on a single study as “proof” that everyone should supplement with omega-3s. Opponents of omega-3 supplementation take the opposite approach. They pick studies showing that not everyone benefits from omega-3 supplementation as “proof” that nobody benefits. As usual, the truth is in between.

I have a section in my book, “Slaying The Food Myths,” called “None of Us Are Average.” In that section I point out that clinical studies report the average results of everyone in the study, but nobody in the study was average.

For example, let’s say the study reported that (on average) there was no heart health benefit from omega-3 supplementation. That is what makes the headlines. That is what opponents of omega-3 supplementation cite as “proof” omega-3 supplementation doesn’t work.

However, some of the people in the study may have benefited from omega-3 supplementation, while others did not. Thus, the important question is not “Does everyone benefit from omega-3 supplementation?” It is “Who benefits from omega-3 supplementation?” and “Why do the results vary so much from study to study?”

Omega-3 Confusion

I have a chapter in my book called “What Role Does Supplementation Play?” which helps put this omega-3 controversy into perspective. I created the graphic on the left to answer the question “Who needs supplementation?”

The concept is simple. Poor diet, increased need, genetic predisposition, and pre-existing disease all increase the likelihood that supplementation will be beneficial. However, the benefit will be most obvious in the center of the diagram where two or more of these factors overlap.

Let’s take this concept and apply it to studies of omega-3 fatty acids and heart disease risk. In particular, let’s use this concept to understand what I call “omega-3 confusion” – why some studies give negative results and others give positive results:

Poor Diet: Again, the concept is simple. You are most likely to see a benefit of omega-3 supplementation when the dietary intake of omega-3 fatty acids is low. Put another way, if the subjects in a study are already getting plenty of omega-3s from their diet, supplementing with omega-3s is unlikely to provide any benefit.

Until recently, dietary surveys were the standard method for assessing dietary omega-3 intake. However, dietary surveys can be inaccurate. The best of recent studies, measure the omega-3 levels in cellular membranes. The omega-3 levels at the beginning of the study reflect your diet. The omega-3 levels at the end of the study reflect how effective supplementation was at improving your omega-3 status. In short, this is the gold standard for omega-3 clinical studies. Subjects can lie about how many omega-3-rich foods they eat and whether they take their supplements, but the omega-3 levels in their cell membranes reveal the truth.

When you read the methods section, it turns out that most negative studies did not ask how much omega-3s their subjects were getting from their diet. Almost none of the negative studies measured omega-3 levels in cell membranes.

Increased Need: In terms of heart disease, we can think increased need as the presence of risk factors for heart disease such as:

Age
Obesity
Inactivity
Elevated cholesterol or triglycerides
Dietary factors like saturated fats and/or sugar and refined carbohydrates
Smoking

What does this mean in terms of clinical studies?

Studies in which most of the subjects have a poor diet, are over 65, and have multiple risk factors for heart disease are more likely to show a beneficial effect of omega-3s on heart disease risk.
Studies in which most of the subjects are young and healthy are unlikely to show a measurable benefit of omega-3s on heart disease risk. You would need to follow this population group 20, 30, or 40 years to demonstrate a benefit.

Genetic Predisposition: There is a lot we don’t know about genetic predisposition for heart disease. The only exception is family history. If you have a family history of early heart disease, you can be pretty certain you are at high risk for heart disease. As you might suspect:

Studies focused on populations with genetic predisposition to heart disease are more likely to show a benefit of omega-3 supplementation.
Studies that just look at the general population without consideration of genetic predisposition to heart disease are less likely to show a benefit of omega-3 supplementation.

Disease: Diseases like diabetes and high blood pressure increase heart disease risk. And, of course, pre-existing heart disease, especially a recent heart attack, dramatically increase the risk of a subsequent heart attack or stroke. Studies focusing on subjects with diabetes have been inconsistent. However, studies focusing on patients with pre-existing heart disease are more clear-cut:

Studies focused on populations with pre-existing heart disease and/or a recent heart attack are more likely to show a benefit of omega-3 supplementation.
Studies that just look at the general population without consideration of genetic predisposition to heart disease are less likely to show a benefit of omega-3 supplementation.

Interestingly, the situation is very similar with statin drugs. As I reported in a recent issue of “Health Tips From the Professor” on cholesterol lowering drugs, studies done with patients who had recently had a heart attack show a clear benefit of statin drugs, while studies with the general population show little or no benefit of statin drugs.

One More Factor: There is one more confounding factor that is somewhat unique to the omega-3-heart disease studies and, therefore, not included in the figure at the beginning of this section. Ethical considerations dictate that the placebo group in a double-blind, placebo controlled clinical study receive the “standard of care” for that disease. In the case of heart disease, the standard of care is 4-5 drugs which provide most of the same benefits as omega-3 fatty acids (although with many more side effects).

Thus, these studies are no longer asking whether omega-3s reduce heart disease risk. They are asking whether omega-3s have any additional benefits for heart disease patients already on 4-5 drugs. I have discussed this in more detail in a previous issue of “Health Tips From the Professor” on omega-3 and heart disease.

Why Are Omega-3 Studies Conflicting? In summary, the likelihood that clinical studies show a beneficial effect of omega-3 fatty acids on heart disease risk is highly dependent on study design and the population group included in the study. Many of the studies currently in the scientific literature are flawed in one way or another. Once you understand that, it is obvious why there are so many conflicting studies in the literature.

Unfortunately, meta-analyses that combine data from many studies are no better than the individual studies they include in the analysis. It is the old “Garbage in – garbage out” principle.

What Does An Ideal Study Look Like? In my opinion, an ideal study to evaluate the effect of omega-3s on heart disease risk should (at minimum):

Determine omega-3 levels in cellular membranes as a measure of omega-3 status (dietary intake of omega-3s plus their utilization by the body). The percentage of omega-3 fatty acids in cell membranes is referred to as Omega-3 Index. Based on previous studies (W.S. Harris et al, Atherosclerosis, 262: 51-54, 2017, most experts consider an Omega-3 Index of 4% to be low and an Omega-3 Index of 8% to be optimal.
Focus on a population group at high risk for heart disease or include enough subjects in the study so that you can determine the effect of omega-3s on high risk subgroups.
Measure cardiovascular outcomes (heart attack, stroke, cardiovascular deaths, etc.).
Perform the study long enough so that you can accumulate a significant number of cardiovascular events.
Include enough subjects for a statistically significant conclusion.

Do Omega-3s Reduce Heart Disease Risk?

Most of you have probably heard of the Framingham Heart Study. It was started in 1941 with a large group of residents of Framingham Massachusetts and surrounding areas. The data from this study over the years has shaped much of what we know about cardiovascular risk factors. The original participants have passed on, but the study has continued with their offspring, now in their 60s.

A recent study (W. H. Harris et al, Journal of Clinical Lipidology, doi: 10.1016/j.jacl.2018.02.010 ) with 2500 subjects in the Offspring Cohort of the Framingham Heart Study incorporates many of characteristics of a good omega-3 clinical study.

The average age of the subjects was 66. While none of the subjects enrolled in the study had been diagnosed with heart disease at the time the study began, this is a high-risk population. At this age a significant percentage of them would be expected to develop heart disease over the next few years.
The subjects did have other risk factors for heart disease. 13% of them had diabetes, 44% had high blood pressure, and 40% of them were on cholesterol medication. However, those risk factors were corrected for in the data analysis, so they did not influence the results.
The Omega-3 Index was measured in their red blood cell membranes at the beginning of the study.
The study was long enough (7.3 years) for cardiovascular disease to develop.

When they compared subjects with the highest Omega-3 Index (>6.8%) with those with the those with the lowest Omega-3 Index (<4.2%):

Death from all causes was reduced by 34%
Incident cardiovascular disease was reduced by 39% (Remember that none of the subjects had been diagnosed with heart disease at the beginning of the study. This terminology simply means that they received a new diagnosis of heart disease during the study.)
Cardiovascular events (primarily heart attacks) were reduced by 42%
Strokes were reduced by 55%.

There were two other interesting observations from the study:

There was no correlation between serum cholesterol levels and heart disease in this study.
The authors estimated that it would require an extra 1300 mg of omega-3s/day, either from a serving of salmon or from fish oil supplements, to bring the membrane Omega-3 Index from the lowest level in this study to an optimal level.

The authors cited three other recent studies performed in a similar manner that have come to essentially the same conclusion. These studies are not perfect. They are all association studies, so they do not prove cause and effect.

However, the authors concluded that Omega-3 Index should be measured routinely as a risk factor for heart disease and should be corrected if it is low.

The Bottom Line:

Perhaps there is nothing more controversial in nutrition today than omega-3 fatty acids and heart disease risk. It is so confusing. One day you are told they reduce heart disease risk. The next day you are told they are worthless. I have discussed the reasons for the conflicting results and the resulting omega-3 confusion in the article above.

I shared a recent study that escapes many of the pitfalls of previous studies because it measures the Omega-3 Index of red blood cells as an indication of omega-3 status.

When the study compared subjects with the highest Omega-3 Index (>6.8%) with those with the those with the lowest Omega-3 Index (<4.2%):

Death from all causes was reduced by 34%
Incident cardiovascular disease was reduced by 39% (Remember that none of the subjects had been diagnosed with heart disease at the beginning of the study. This terminology simply means that they received a new diagnosis of heart disease during the study.)
Cardiovascular events (primarily heart attacks) were reduced by 42%
Strokes were reduced by 55%.

There were two other interesting observations from the study:

There was no correlation between serum cholesterol levels and heart disease in this study.
The authors estimated that it would require an extra 1300 mg of omega-3s/day, either from a serving of salmon or from fish oil supplements, to bring the membrane Omega-3 Index from the lowest level in this study to an optimal level.

The authors concluded that Omega-3 Index should be measured routinely as a risk factor for heart disease and should be corrected if it is low.

Are Omega-3s Worthless?

Recommendations from the medical industry changes often. The following updates are in response to some of those changes concerning omega-3 and heart disease. These updates were added on October 2, 2018.

The internet is abuzz with headlines saying things such as “Omega-3 Supplements Don’t Protect Against Heart Disease” and “Forget Omega-3s”. Are those headlines true? Should we throw our omega-3 supplements in the trash?

If the recent headlines are true, it is confusing, to say the least. In the late 90s and early 2000s we were being told of clinical studies showing that omega-3s reduced the risk of heart attack and stroke. At that time the American Heart Association was recommending omega-3 supplements for patients at high risk of heart attack or stroke. What has changed?

It turns out that a lot has changed. The design of clinical studies has changed dramatically in the past 10-15 years. I have covered the changing omega-3 story in detail in my upcoming book “Slaying The Supplement Myths.” Let me just summarize a few key differences between the year 2000 and today.

The definition of “high risk of heart attack and stroke” has changed dramatically since 2000. Clinical studies today include subjects who have a much lower risk of heart attack and stroke. That makes it more difficult to see any benefits of omega-3s.
Most studies do not measure the omega-3 status of their subjects. That means they do not know whether their patients were omega-3 deficient at the beginning of the study. It also means they have no objective measure of how faithfully the subjects took their omega-3 capsules.
We are asking a totally different question today than we were in the year 2000. It is considered unethical to withhold “standard medical care” from the control group. In 2000 the standard of care was one or two heart medications and often did not include a statin. Back then we were asking “Do omega-3s reduce the risk of heart attack and stroke?” Today, the standard of care is 3-5 heart medications, each of which provides some of the same benefits as omega-3s. Today we are asking the question “Do omega-3s provide any additional benefit for people who are already taking 3-5 heart medications?”

Let me start by analyzing a recent study that illustrates these points perfectly.

How Was The Study Done?

On the surface the study appeared to be a well-designed study. The study (The ASCEND Study Collaborative Group, New England Journal Of Medicine, DOI: 10.1056/NEJMoa1804989, 2018 ) was conducted by scientists from the University of Oxford. They used a national diabetes registry and contacted general practitioners from all over England to identify 15,480 patients who had diabetes, but no evidence of heart disease and were willing to participate in the study. Participants were at least 40 (average age 63) and 60% male.

The participants were mailed a six month’s supply of capsules containing either 1 gram of omega-3s or olive oil as a placebo. Each 6 months the participants were mailed a questionnaire to report on whether they took the capsule daily and whether they had any adverse side effects. If they returned the questionnaire, they were given another 6 month’s supply of omega-3s or placebo. The patients were followed for an average of 7.4 years and “adverse vascular events” (simple definition: non-fatal and fatal heart attack or stroke) were recorded.

Omega-3 and Heart Disease?

The authors of the study reported:

Omega-3 supplementation had no significant effect on either serious vascular events or death from any cause.

The authors concluded “These findings, together with results of earlier randomized trials involving patients with and without diabetes, do not support the current recommendations for routine dietary supplementation with omega-3 fatty acids to prevent vascular events.”

On the surface, this appears to be a strong study and the results were conclusive. What could go wrong? The answer is “Plenty.”

What Are The Weaknesses Of The Study?

The study contains multiple weaknesses that have been ignored by the medical community and the press.

Omega-3 Supplements Reduced Vascular Deaths In This Study. To begin with, the study showed that omega-3 supplementation reduced vascular deaths (simple definition: fatal heart attacks and stroke) by 18%. That observation was reported as a single sentence in the Results section of the paper but did not appear in either the Discussion or Abstract. It was also not reported in any of the media reports telling you that omega-3s are worthless. Perhaps it did not match the preconceived beliefs of the authors.

This Study Was Not Really Looking At High Risk Patients. The studies in the late 90’s and early 2000’s showing a significant effect of omega-3s on heart attack risk were done with truly high-risk patients. For example, the best of these studies looked at the effect of omega-3 supplementation in patients who had suffered a heart attack in the past 6 months. Those patients were at high risk of a second heart attack in the next 6-12 months. They were in imminent danger.

This study looked at patients with diabetes. They have a 2 to 3-fold risk of heart attack or stroke over the next decade. That’s a big difference. In addition, this study only looked at patients with diabetes AND no evidence of heart disease. Their risk of heart attack and stroke is substantially less. In fact, if you look at the data in the study, 83% of the participants in their study were at low to moderate risk of heart disease. Only 17% were at high risk.

To put that into perspective, it has only been possible to prove the effectiveness of statins when they are tested in patients who have already suffered a heart attack. In low risk populations, their benefit is almost negligible. You will find details about those studies in my new book “Slaying The Supplement Myths.”

If you can’t prove statins are effective in low risk populations, why would you expect to be able to show omega-3s are effective in low risk populations.

The Subjects Were Already Getting Near Optimum Amounts of Omega-3s From Their Diet. The study analyzed the omega-3 index (a measure of omega-3 status) from a randomly selected subset of participants at the beginning and end of the study. They reported that the omega-3 index in their study participants increased from 7.1% at the beginning to 9.1% at the end, a 32% increase. They considered that to be a good thing because it showed that their participants were taking the omega-3 supplements faithfully.

However, let’s put that into perspective. An omega-3 index of 4% is associated with a high risk of heart disease. An omega-3 index of 8% is associated with a low risk of heart disease. It is considered optimum. With an omega-3 index of 7.1% at the beginning of the study, the subjects already had near optimum omega-3 status before the study even began.

If the subjects were already at near optimum omega-3 status, why would you expect additional omega-3 supplementation to be beneficial?

The Subjects Were On 3-5 Heart Medications. To discover this, you had to dig a little. Something only a science-wonk like me is willing to do. The Results section reported that 35% of the subjects were taking aspirin and 75% were on a statin. You have to go to the Supplementary Data online to discover that most of the subjects were on 3-5 heart medications in addition to 1 or 2 medications for diabetes. That is somewhat curious because nobody in the study had any detectable cardiovascular disease.

To understand the significance of this observation, we look at what the drugs do. Aspirin prevents blood clot formation in our arteries, which is one of the main benefits of omega-3s. For reasons nobody understands, statins decrease inflammation, which is another major benefit of omega-3s. Most of the subjects were also taking a medicine to decrease blood pressure, another major benefit of omega-3s.

If subjects are already on 3-5 heart medications that duplicate the benefits of omega-3s, why would you expect omega-3 supplementation to be beneficial?

As I said before, we are now asking a totally different question than we were in the studies performed in the late 90s and early 2000s. Back then we were asking whether omega-3s reduced the risk of heart disease. Today we are asking whether omega-3s have any additional benefits for someone who is already on 3-5 heart medications. That question may be of interest to your doctors, but it is probably not the question most of you are interested in.

Even worse, every one of those drugs has documented side effects. For example, the same group that published this paper also examined the role of aspirin in reducing heart attacks in the same patient population and concluded that the befits of aspirin were “largely counterbalanced by the bleeding hazard [caused by aspirin use],” (The ASCEND Study Collaborative Group, New England Journal Of Medicine, DOI: 10.1056/NEJMoa1804988, 2018). In contrast, they found no side effects in the group receiving 1 gram/day of omega-3s.

Garbage In Again, Garbage Out Again

Two recent meta-analyses (T Aung et al, JAMA Cardiology 3: 225-234, 2018 and Cochrane Database of Systematic Reviews ) have analyzed all the recent placebo-controlled studies and have concluded that omega-3s are of little or no use for reducing heart disease risk. However, those meta-analyses both suffered from what, in the computer programming world, is called “Garbage in. Garbage out.”

The meta-analyses included the studies from the late 90s and early 2000s, but the positive data from those studies was swamped out by all the recent negative studies, most of which suffered from the same flaws as the study I reviewed above. This is the “Achilles’ Heel” of meta-analysis. If they include flawed studies in their analysis, their conclusions will also be flawed. What the recent studies do tell us is that omega-3s are of little additional benefit if you are already taking multiple heart medications.

Don’t Throw The Baby Out With The Bathwater

The next time you visit your doctor you are likely to be told: “The evidence is in. We know that omega-3s don’t reduce the risk of heart attack.” Now you know the truth. What we can definitively conclude is that omega-3s offer little additional benefit if you are already taking multiple heart medications. As I said before, that question may be of interest to your doctor but is probably not the question you had in mind.

Unfortunately, because of the way clinical studies of omega-3 supplementation and heart disease risk are currently conducted, we may never have a definitive answer to whether omega-3s reduce heart disease risk for those of us who aren’t taking heart medications.

However, even if there is some controversy about omega-3s and heart disease risk, there are multiple other reasons for making sure that your omega-3 status is optimum. For example:

We know that omega-3s reduce triglycerides. This is non-controversial.
There is excellent evidence that omega-3s improve arterial health and reduce blood pressure.
There is good evidence that omega-3s reduce inflammation.

If they also reduce heart disease risk, consider that to be a side benefit.

The Bottom Line

A recent study has reported that that omega-3s do not reduce the risk of heart attack and stroke. However, the study suffered from multiple flaws.

Omega-3s reduced the risk of cardiovascular deaths in the study by 18%. That never got reported by the media.

The study was looking at subjects at relatively low risk of heart disease.

If you can’t even prove statins are effective in low risk populations, why would you expect to be able to show omega-3s are effective in low risk populations.

The subjects had near optimum omega-3 status before the study even began.

If the subjects were already at near optimum omega-3 status, why would you expect additional omega-3 supplementation to be beneficial?

The subjects were on 3-5 heart medications that provided many of the same benefits as omega-3s, but with side effects.

If subjects are already on 3-5 heart medications that duplicate the benefits of omega-3s, why would you expect omega-3 supplementation to be beneficial?

Two recent meta-analyses also concluded that omega-3s do not reduce the risk of heart disease. However, most of the studies in those meta-analyses suffered from the same flaws as the study I reviewed in this article. The meta-analyses are an excellent example of what computer programmers refer to as “Garbage in. Garbage out.”

The next time you visit your doctor you are likely to be told: “The evidence is in. We know that omega-3s don’t reduce the risk of heart attack.” Now you know the truth. What we can definitively conclude is that omega-3s offer little additional benefit if you are already taking multiple heart medications. That question may be of interest to your doctor, but that is probably not the question you had in mind.

Unfortunately, because of the way that clinical studies of omega-3 supplementation and heart disease risk are currently conducted, we may never have a definitive answer to whether omega-3s reduce heart disease risk for those of us who aren’t taking heart medications.

However, even if there is some controversy about omega-3s and heart disease risk, there are multiple other reasons for making sure that your omega-3 status is optimum. For example:

We know that omega-3s reduce triglycerides. This is non-controversial.
There is excellent evidence that omega-3s improve arterial health and reduce blood pressure.
There is good evidence that omega-3s reduce inflammation.

If they also reduce heart disease risk, consider that to be a side benefit.

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.

What Is Your Microbiome And Why Is It Important?

September 25, 2018 by Dr. Steve Chaney

Probiotics and Hero Bacteria

Author: Dr. Stephen Chaney

Suddenly the term “microbiome” is hot. It is featured in books, internet articles, and marketing materials produced by supplement companies wanting to sell their “magic” probiotic supplements. But, you are confused. You don’t know if what you read is true or just marketing hype. What is your microbiome anyway?

You have been asking me: “What is my microbiome? “Why is it important?” “How does it affect my health?” “Should I take a probiotic?” “What else should I do?”

I covered this topic in a section of my book, “Slaying The Food Myths” called “Our Mighty Microbiome.” However, this is an exploding area of scientific research. Published papers on our microbiome have increased by 600% in just the past 10 years. I already need to update the information in my book.

What Is Your Microbiome?

Your microbiome is defined as the community of microorganisms (bacteria, yeast and other fungi, and viruses) that live in and on you. Most of those microorganisms are bacteria, and most of them reside in your large intestine. Thus, the term “gut bacteria” is a useful and easier to understand approximation.

We are just beginning to understand just how complex and diverse our microbiome community is. Each of us harbor about 38 trillion microorganisms (give or take a few trillion). That means we each have slightly more microorganisms than we do cells in our body. However, it is not just the sheer number of microorganisms that is impressive. It is the number of different species we harbor in our bodies that indicates the true complexity of our microbiome.

For example, we each have more than 1,000 different species of bacteria in our large intestine. Collectively, these bacteria have around 750,000 unique genes. That is 30 times more than the human genome. Even so, understanding the health implications of our microbiome would be relatively simple if we all had the same species of bacteria in our intestines, but we don’t.

We are all unique. We all have different species in our intestines. The only simplifying principle is that these bacteria seem to exist as in distinct communities that generally group together. Even so, our microbiomes are amazingly complex.

We Are What We Eat

You have probably heard the phrase “We are what we eat” before and dismissed it. After all, we can eat carrots all day long, and we will never turn into a carrot. However, that phrase is literally true when we consider our microbiomes. For example, the microbiomes of meat-eaters have totally different families of microorganisms than microbiomes of vegetarians. We don’t yet fully understand the implications of these differences in gut bacteria. However, we think they may be responsible for some of the differences in health outcomes of meat eaters and vegetarians.

Our microbiomes are also influenced by individual foods in our diet. In part, that is because each food has a unique blend of fibers. To fully comprehend the significance of that statement, we need to understand what fibers do. Most of us think of fibers as the indigestible portion of foods. We think of it as “roughage” that helps keeps our intestines moving and binds toxins, so they can be eliminated safely. That is true, but fiber is much more.

While we can’t digest fiber, the microorganisms living in our intestine can digest much of it. That fiber becomes food for the microorganisms. We refer to food for our intestinal microorganisms as “prebiotics.” That means you probably need to rethink what the term prebiotic really means.

In the past you have probably thought of prebiotics as supplements designed to support the growth of certain bacteria in our intestines. Now you know that prebiotic also refers to the fibers in the foods we eat. Because each food has a unique blend of fibers, each food supports the growth of slightly different populations of intestinal bacteria. This helps explain why the human microbiome is so complex.

We don’t fully understand the health consequences of these differences in our microbiome, but we think they are huge (see below). This is one reason I do not recommend any diet that eliminates whole food groups. It is easy to say we can replace the missing nutrients with a multivitamin. But, what about the missing fiber? We know that will affect our microbiome. We simply don’t know enough about the long-term health consequences of altering our microbiome to recommend eliminating high fiber foods from our diet. It’s not nice to fool with Mother Nature.

For example, in “Slaying The Food Myths” I discussed the evidence that meat-based low-carb diets are less healthy long term than primarily plant-based low-carb diets. That could be because of saturated fats and excess consumption of red meat. However, it might also be caused by the effect on the microbiome of the food groups that are eliminated in meat-based, low-carb diets.

Finally, as if all of this weren’t complex enough, there is some evidence that our microbiome is influenced by lifestyle (particularly obesity and exercise) and environment (particularly toxins in the environment). But, that’s another topic for another day.

Why Is Your Microbiome Important?

Now you know that our microbiome is incredibly complex. You also know “We are what we eat.” Why are those two things important? While there is a lot we don’t yet know, it appears that our microbiome has a powerful influence on our health.

For example, we know that our gut bacteria can convert components of the foods we eat into compounds that are absorbed into our bloodstream and either have a positive or negative effect on our health. Let me give you some specific examples:

“Good” intestinal bacteria produce butyrate in the process of digesting fiber. Butyrate, in turn, is thought to support intestinal health and activate genes that lower blood cholesterol levels.
“Bad” intestinal bacteria convert carnitine (a normal human metabolite found in meat, particularly red meat) into trimethylamine-N-oxide or TMAO, which is thought to increase the risk of heart disease. In a cruel twist of fate, these particular “bad” bacteria seem to be prevalent in the microbiome of meat-eaters, but absent from the microbiome of vegetarians.
We have been told that polyphenols are good for us. However, polyphenols are poorly absorbed. Fortunately, polyphenols are rapidly metabolized by our microbiome into metabolites that are more easily absorbed. Many experts think it is those microbiome-produced metabolites that are responsible for the health benefits of polyphenols. If everyone’s microbiome is different, how does that affect the health benefits of polyphenols. A recent study puts this into perspective. The authors fed an apple extract to 12 individuals and measured 110 polyphenol metabolites in their blood over the next 5 hours. The pattern of blood metabolites was different for every individual in the study. Furthermore, the pattern of blood metabolites correlated with differences in the species of bacteria in their intestine.

I have given examples of 3 different kinds of food-microbiome interactions here. There are more examples of each type of food-microbiome interaction in the literature. This just adds another layer of complexity. Not only does the food we eat affect our microbiome, but our microbiome influences how we metabolize the foods we eat. We are just beginning to understand how these differences influence our health. However, based on what we currently know, here are some of the ways our microbiome can influence our health:

Current evidence suggests that “bad” bacteria and yeast in our intestines may:

Compromise our immune system.
Create a “leaky gut”, which allows partially digested foods to get into the bloodstream where they can trigger inflammation and auto-immune responses.
Adversely affect brain function and moods.
Convert components of the foods we eat into compounds which increase the risk of cancer and heart disease.
Perhaps, even make us fat.

In contrast, “good” bacteria:

Crowd out the bad bacteria and prevent the health problems they cause.
Break down undigested fiber into compounds that are beneficial to our health.

What About Probiotics?

Now you know how important our microbiome is to our health, you are probably wondering whether you should add one or more probiotic supplements to your health regimen. Let me give you a brief primer on probiotic supplements.

“Hero Bacteria”: We have over 1,000 species of bacteria in our microbiome, and they work together in families. With that complexity, you may be wondering how someone could hope to create a probiotic supplement that worked. Fecal transplants (all the intestinal bacteria from a healthy individual) have been used for some life-threatening conditions, but I don’t think that is an approach most of us want to consider.

For better or worse, modern science uses a reductionist approach. We focus on a single component of a system and test its effectiveness in clinical studies. In the probiotic world, we focus on an individual strain of bacteria. If it proves effective in clinical studies, it is given a name and is used in probiotic supplements. It becomes what I call a “hero bacteria.”

For example, if scientists were looking for a probiotic supplement to aid with digestion or immunity, they would test dozens of strains initially. They would then select the one strain for further study. It may have been selected because it performed best in the preliminary studies. However, it may have been selected based on other characteristics, such as how easy it was for the scientist to grow in a culture dish. That strain is then put through rigorous clinical trials. If it performs well there, it becomes a “hero bacteria” suitable for a probiotic supplement. It has been “proven” to provide a specific benefit to our health.

However, it is not the only bacteria to provide that benefit. It might not have even been the “best” bacteria. It may have simply been the one that grew best in the lab.

Rule #1: Look for one or more named “hero bacteria” in your probiotic supplement. They have been proven to provide a specific health benefit.

Not All “Hero Bacteria” Are Created Equal: In some cases, companies that have developed a particular strain of “hero bacteria” have published the clinical studies supporting their claims in peer-reviewed journals. In other cases, they make the study claims, but say their data is “proprietary.” I am a skeptic. If they haven’t published their data, I assume it wasn’t good enough to be published.

Rule #2: Avoid any probiotic supplements that do not provide you with studies published in peer-reviewed scientific journals showing that studies with their “hero bacteria” support their product claims.

Some Companies Get Ahead Of What Good Science Supports: Their claims sound amazing, but they aren’t supported by clinical proof. They call it marketing. I call it lying.

In some cases, the lying is clear because they don’t provide you with clinical studies published in peer-reviewed journals.

However, if their claims sound too good to be true and they have provided clinical studies published in peer-reviewed journals, my advice is to read the studies. You don’t need to be an expert. The abstracts for every published article are available online. Read the abstract and see what health claims it makes. [Reviewers of peer-review articles generally insist that the claims match the evidence.] If a company’s marketing claims exceed the claims from the published studies backing their product, they are probably lying to you.

Rule #3: If a company’s marketing claims exceed the claims from the published studies backing their product, run the other direction. They are lying to you.

It Takes A Village: While it is useful to have one or more “hero bacteria” in your probiotic supplement, don’t assume that is all you need. Remember that you have many more than one or two bacteria in your gut. You have a thousand or more different species. For every “hero bacteria” that has gone through the clinical review process, there are dozens more that provide the same benefit, and they all work together. More importantly, they work by different mechanisms. You need a holistic approach to creating a healthier microbiome.

My recommendation is to choose probiotic supplements that contain several species that work together rather than just a single “hero bacteria.” I also recommend following a diet that supports a healthy microbiome. Based on what we currently know, that would be a primarily plant-based diet containing all five food groups.

Rule #4: Choose probiotic supplements that contain several species that work together rather than a single “hero bacteria”.

The Bottom Line

Because I know how confusing the term “microbiome” is to most of you I have written a brief overview of our microbiome and what it does. Topics I have covered are:

What is our microbiome?
How do the foods we eat influence our microbiome?
How does our microbiome influence the metabolism of the foods we eat?
How does our microbiome influence our health?
How do you select a good probiotic supplement?

If any of these topics interest 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.

How to Relieve Stress Naturally

September 18, 2018 by Dr. Steve Chaney

Try A Mental Massage

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney

Want to know how to relieve stress naturally?

Stress is rampant in the lives of many people, whether it be from work, homelife, or things we can’t control such as the weather or traffic. And stress is a killer! Even if it doesn’t kill, it sure makes life unpleasant.

This short article will explain an easy technique that will massage your stomach and other organs, enabling you to release stress from your body.

The first time you do this technique I suggest you lie down in bed, but afterward you can do it anyplace. It’s especially good to do while you’re experiencing a stressful situation.

How to Relieve Stress Naturally Step by Step

Start by breathing deeply at your normal pace, paying attention to the rise and fall of your abdomen and chest. Visualize tension like a block of ice that you are melting with the warmth of your breath.

Next, breathe in through your nose to the count of four.

Hold your breath to the count of five.

Slowly breath out through your mouth, to the count of six.

Do this several times and then return to breathing at a normal pace, but still filling and emptying your lungs fully.

While breathing, see the “ice” melting from your scalp all the way through your face, neck, lungs, heart and stomach. “Feel” it flowing out through your fingertips.

Continue by “feeling” the ice melting from your hips, legs and feet, flowing out through your feet.

Relax and visualize the tension melting and flowing out of your body.

Next, visualize soft fluffy blue mittens cradling your face, your throat, your lungs, heart and stomach. Visualize the mittens moving down and softly rubbing your arms, legs and feet.

Keep breathing slowly and deeply, relaxing into this comforting vision.

Finally, visualize pure, positive energy in the form of diamond dust, sparkling and flowing into your head, filling your body, and flowing out through your fingers and toes.

When you have the time, allow this to take as much time as you like. And when you are living your busy life, realize that you can do this entire relaxation meditation in 30 seconds. Just see it as waves of energy passing from your head to your feet.

This simple exercise is one that I’ve taught people for years, and it really works! It’s like a mini-spa treatment for your mind and nerves.

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.

About The Author

Julie Donnelly is a Deep Muscle Massage Therapist with 20 years of experience specializing in the treatment of chronic joint pain and sports injuries. She has worked extensively with elite athletes and patients who have been unsuccessful at finding relief through the more conventional therapies.

She has been widely published, both on – and off – line, in magazines, newsletters, and newspapers around the country. She is also often chosen to speak at national conventions, medical schools, and health facilities nationwide.

How Much Carbohydrates Should We Eat?

September 11, 2018 by Dr. Steve Chaney

The “Goldilocks Effect”

Author: Dr. Stephen Chaney

How much carbohydrates should we eat?

The low-carb wars rage on. Low-carb enthusiasts claim that low-carb diets are healthy. Many health experts warn about the dangers of low-carb diets. Several studies have reported that low-carb diets increase risk of mortality (shorten lifespan).

However, two recent studies have come to the opposite conclusion. Those studies reported that high carbohydrate intake increased mortality, and low carbohydrate intake was associated with the lowest mortality.

One of those studies, called the Prospective Urban Rural Epidemiology (PURE) study was published just last year. It included data from 135,335 participants from 18 countries across 5 continents. That’s a very large study, and normally we expect very large studies to be accurate. The results from the PURE study had low-carb enthusiasts doing a victory lap and claiming it was time to rewrite nutritional guidelines to favor low-carb diets.

Whenever controversies like this arise, reputable scientists are motivated to take another look at the question. They understand that all studies have their weaknesses and biases. So, they look at previous studies very carefully and try to design a study that eliminates the weaknesses and biases of those studies. Their goal is to design a stronger study that reconciles the differences between the previous studies.

Such a study has just been published (SB Seidelmann et al, The Lancet, doi.org/10.1016/S2468-2667(18)30135-X ). This study resolves the conflicting data and finally answers the question: “How much carbohydrates should we be eating if we desire a long and healthy life?” The answer is “Enough.”

I call this “The Goldilocks Effect” You may remember “Goldilocks And The Three Bears.” One bed was too hard. One bed was too soft. But, one bed was “just right.” One bowl of porridge was too hot. One was two cold. But, one was “just right.” According to this study, the same is true for carbohydrate intake. High carbohydrate intake is unhealthy. Low carbohydrate intake is unhealthy. But, moderate carbohydrate intake is “just right.”

How Was The Study Done?

This study was performed in two parts. This first part drew on data from the Atherosclerosis Risk in Communities (ARIC) study. That study enrolled 15,428 men and women, aged 45-64, from four US communities between 1987 and 1989. This group was followed for an average of 25 years, during which time 6283 people died. Carbohydrate intake was calculated based on food frequency questionnaires administered when participants enrolled in the study and again 6 years later. The study evaluated the association between carbohydrate intake and mortality.

The second part was a meta-analysis that combined the data from the ARIC study with all major clinical studies since 2007 that measured carbohydrate intake and mortality and lasted 5 years or more. The total number of participants included in this meta-analysis was 432,179, and it included data from both studies that claimed low-carbohydrate intake was associated with decreased mortality.

How Much Carbohydrates Should We Eat?

The results from the ARIC study were:

The relationship between mortality and carbohydrate intake was a U-shaped curve.
The lowest risk of death was observed with a moderate carbohydrate intake (50-55%). This is the intake recommended by current nutrition guidelines.
The highest risk of death was observed with a low carbohydrate intake (<40%).
The risk of death also increased with very high carbohydrate intake (>70%).
When the investigators used the mortality data to estimate life expectancy, they predicted a 50-year old participant would have a projected life expectancy of:
1 years if they had a moderate intake of carbohydrates.
Their life expectancy was 4 years less if they had a low carbohydrate intake.
Their life expectancy was 1.1 year less if they had a very high carbohydrate intake.
The risk associated with low carbohydrate intake was affected by what the carbohydrate was replaced with.
When carbohydrate was replaced with animal protein and animal fat there was an increased risk of mortality on a low-carb diet. The animal-based low-carb diet contained more beef, pork, lamb, chicken and fish. It was also higher in saturated fat.
When carbohydrate was replaced with plant protein and plant fats, there was a decreased risk of mortality on a low-carb diet. The plant-based low-carb diet contained more nuts, peanut butter, dark or whole grain breads, chocolate, and white bread. It was also higher in polyunsaturated fats.
The effect of carbohydrate intake on mortality was virtually the same for all-cause mortality, cardiovascular mortality, and non-cardiovascular mortality.
There was no significant affect of carbohydrate intake on long-term weight gain (another myth busted).

The results from the meta-analysis were very similar. When the data from all studies were combined:

Both low carbohydrate diets and very high carbohydrate diets were associated with increased mortality.
Meat-based low-carb diets increased mortality, and plant-based low-carb diets decreased mortality.
Once again, the results were the same for total mortality, cardiovascular mortality, and non-cardiovascular mortality.

The authors concluded: “Our findings suggest a negative long-term association between life-expectancy on both low carbohydrate and high carbohydrate diets…These data also provide further evidence that animal-based low carbohydrate diets should be discouraged. Alternatively, when restricting carbohydrate intake, replacement of carbohydrates with predominantly plant-based fats and proteins could be considered as a long-term approach to healthy aging.”

Why Were Some Previous Studies Misleading?

This study also resolved the discrepancies between previous studies. The authors pointed out that the average carbohydrate intake is very different in Europe and the US than in Asian countries and low-income countries. In the US and Europe, mean carbohydrate intake is about 50% of calories and it ranges from 25% to 70% of calories. With that range of carbohydrate intake, it is possible to observe the increase in mortality associated with both low and high carbohydrate intakes.

White rice is a staple in Asian countries, and protein is a garnish rather than a main course. Consequently, overall carbohydrate intake is greater in Asian countries and very few Asians eat a low carbohydrate diet. High protein foods tend to be more expensive than high carbohydrate foods. Thus, very few people in developing countries can afford to follow a low carbohydrate diet, and overall carbohydrate intake also tends to be higher.

Therefore, in Asian and developing countries the average carbohydrate intake is greater (~61%) than in the US and Europe, and the range of carbohydrate intake is from 45% to 80% of calories. With that range of intake, it is only possible to see the increase in mortality associated with high carbohydrate intake.

Both the studies that low-carb enthusiast quote to support their claim that low-carb diets are healthy relied heavily on data from Asian and developing countries. In fact, when the authors of the current study overlaid the data from the PURE study with their ARIC data, there was an almost perfect fit. The only difference was that their ARIC data covered both low and high carbohydrate intake while the PURE study touted by low-carb enthusiasts only covered moderate to high carbohydrate intake. [I have given you my rendition of the graph on the left. If you would like to see the data yourself, look at the paper .]

Basically, low-carb advocates are telling you that diets with carbohydrate intakes of 30% or less are healthy based on studies that did not include carbohydrate intakes below 40%. That is misleading. The studies they quote are incapable of detecting the risks of low carbohydrate diets.

What Does This Mean For You?

There are several important take-home lessons from this study:

All major studies agree that very high carbohydrate intake is unhealthy. In part, that reflects the fact that diets with high carbohydrate intake are likely to be high in sodas and sugary junk foods. It may also reflect the fact that diets which are high in carbohydrate are inevitably low in protein or healthy fats or both.
All studies that cover the full range of carbohydrate intake agree that low carbohydrate intake is also unhealthy. It shortens life expectancy of a 50-year old by about 4 years.
The studies quoted by low carb enthusiasts to support their claim that low-carb diets are healthy don’t include carbohydrate intakes below 40%. That means their claims are misleading. The studies they quote are incapable of detecting the risks of low carbohydrate diets.
Meat-based low-carb diets decrease life expectancy while plant-based low carb diets increase life expectancy. This is consistent with previous studies. For more details on those studies, see my article “Are Any Low-Carb Diets Healthy?” in “Health Tips From The Professor” or my book, “Slaying The Food Myths.”

The health risks of meat-based low-carb diets may be due to the saturated fat content or the heavy reliance on red meat. However, the risks are just as likely to be due to the foods these diets leave out – typically fruits, whole grains, legumes, and some vegetables. Proponents of low-carb diets assume that you can make up for the missing nutrients by just taking a multivitamin. However, each food group also provides a unique combination of phytonutrients and fibers. The fibers, in turn, influence your microbiome. Simply put, whenever you leave out whole food groups, you put your health at risk.

Limitations Of This Study

My main concern with this study and all previous studies is that they lump all carbohydrates together, as if they were equally healthy or unhealthy. We should really be focusing on healthy carbohydrates versus unhealthy carbohydrates, healthy proteins versus unhealthy proteins, and healthy fats versus unhealthy fats. We should be focusing on foods.

For example, the plant-based low carbohydrate diets in this study probably had a higher percentage of healthy carbohydrates because those diets feature whole, plant-based foods. The very high carbohydrate diets in this study probably had a higher percentage of unhealthy carbohydrates. However, we have no idea whether the diets with moderate carbohydrate intake featured healthy carbohydrates or unhealthy carbohydrates. That is critical because moderate carbohydrate intake was the baseline to which all other diets were compared.

An important unanswered question is: “What is the relationship between carbohydrate intake and lifespan when most of the carbohydrates come from whole, plant-based foods?” Is low carbohydrate intake healthier or less healthy than moderate carbohydrate intake? Is high carbohydrate intake still less healthy? We have no idea. No studies have analyzed the data in that way.

Similarly, we know from multiple studies that meat-based, low-carb diets increase mortality and plant-based, low-carb diets decrease mortality when compared to moderate carbohydrate intake with no differentiation of protein source. But, what if the moderate carbohydrate group had also been subdivided into meat eaters and plant eaters? Would meat-based, low-carb diets still be less healthy than meat-based, moderate-carbohydrate diets? Would plant-based, low-carb diets still be healthier than plant-based, moderate-carb diets? We have no idea.

The Bottom Line

The low-carb wars are raging. Several studies have reported that low-carb diets increase risk of mortality (shorten lifespan). However, two recent studies have come to the opposite conclusion. Those studies have low-carb enthusiasts doing a victory lap and claiming it is time to rewrite nutritional guidelines to favor low-carb diets.

However, a study just published a couple of weeks ago resolves the conflicting data and finally answers the question: “How much carbohydrate should we be eating if we desire a long and healthy life?” The answer is “Enough.”

I call this “The Goldilocks Effect.” According to this study, high carbohydrate intake is unhealthy. Low carbohydrate intake is unhealthy. But, moderate carbohydrate intake is “just right.”

Specifically, this study reported:

Moderate carbohydrate intake (50-55%) is healthiest. This is also the carbohydrate intake recommended by current nutritional guidelines.
All major studies agree that very high carbohydrate intake (60-70%) is unhealthy. It shortens life expectancy of a 50-year old by about a year.
All studies that cover the full range of carbohydrate intake agree that low carbohydrate intake (<40%) is also unhealthy. It shortens life expectancy of a 50-year old by about 4 years.
The studies quoted by low carb enthusiasts to support their claim that low-carb diets are healthy don’t include carbohydrate intakes below 40%. That means their claims are misleading. The studies they quote are incapable of detecting the risks of low carbohydrate diets.
Meat-based, low-carb diets decrease life expectancy while plant-based, low carb diets increase life expectancy. This is consistent with the results of previous studies.

The authors concluded: “Our findings suggest a negative long-term association between life-expectancy and both low carbohydrate and high carbohydrate diets…These data also provide further evidence that animal-based low carbohydrate diets should be discouraged. Alternatively, when restricting carbohydrate intake, replacement of carbohydrates with predominantly plant-based fats and proteins could be considered as a long-term approach to healthy aging.”

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.