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

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.

Are ADHD Symptoms Reduced by Omega-3s?

September 4, 2018 by Dr. Steve Chaney

Can Natural Approaches Cure ADHD?

Author: Dr. Stephen Chaney

You keep seeing headlines saying that omega-3 fatty acids can help children with ADHD. But your pediatrician doesn’t recommend them. Why not? Is the story about omega-3s helping with ADHD symptoms just another myth created by supplement companies wanting to lighten your wallet? Or, is your doctor not keeping up with the latest scientific advances? As usual, the truth lies somewhere in between.

This week I will discuss the latest study (J.P-C. Chang et al, Neuropyschopharmacology, 43: 534-545, 2018) on omega-3s and ADHD symptoms. It provides an excellent update on the role of omega-3s in reducing ADHD symptoms.

How Was The Study Done?

The study was a meta-analysis. Meta-analyses combine the data from multiple studies. Their strength comes from the fact that they include data from subjects of different backgrounds and ethnicity. However, a meta-analysis can never be stronger than the studies it includes in its analysis. Simply put, if it combines data from poorly designed studies, it is no better than the weakest study.

The problem is that there have been a lot of poorly designed studies in this area of research. Some studies have included both children and adults. Others included subjects with psychiatric diagnoses other than ADHD. Still others combined omega-3 supplementation with other vitamins and nutrients. Finally, some used inadequate measures of ADHD symptoms and cognitive function. Because the design of previous studies has been so varied, the results have been conflicting. Some studies have found that omega-3 supplementation reduced ADHD symptoms. Others found no benefit.

Because of the confusion arising from poorly designed studies, the authors of this study applied very rigorous criteria in selecting the studies to be included in their meta-analysis. Their criteria were:

The studies were randomized, double-blind, placebo-controlled trials of mega-3 supplementation with DHA or EPA alone or in combination.
Participants were school-aged children (4-12 years) and adolescents (13-17 years) who had a diagnosis of ADHD.
The study measured clinical symptoms of ADHD as reported by parents. Some also included reports by teachers. When cognitive data were included, the studies relied on well-established cognitive tests.
The data allowed a calculation of effect size (this is a statistical requirement that simply says the quality of the data were good enough to reliably calculate the difference between the supplemented and control groups).
The publications were in peer reviewed journals.

They ended up with seven studies with a total of 534 subjects (318 received omega-3s and 216 received a placebo).

They also performed a separate metanalysis of studies that have measured omega-3 levels in school-aged children and adolescents who had been diagnosed with ADHD. The criteria for inclusion in this metanalysis were similarly rigorous. They ended up including nine studies totaling 558 subjects, 297 with ADHD and 261 controls in this meta-analysis.

Do Omega-3s Reduce ADHD Symptoms?

The results from the first meta-analysis were:

Omega-3 supplementation significantly improved parental reports of total ADHD symptoms scores as well as scores of inattention and hyperactivity.
When the children were given cognitive performance tests, the omega-3 supplemented group performed better than the placebo group when tested for omission errors (for example, a number or word left out in a memory test) and commission errors (an incorrect number or word in a memory test).
A dose of EPA + DHA of 500 mg/day or greater appeared to be optimal.

The results from the second meta-analysis were:

Children and adolescents with ADHD had significantly lower levels of DHA, EPA, and total omega-3s in their red blood cells (a good measure of omega-3 status) than controls.

The authors concluded: “In summary, there is evidence that omega-3 supplementation improves clinical symptoms and cognitive performances in children and adolescents with ADHD, and that these youth have a deficiency of omega-3 levels. Our findings provide further support to the rationale for using omega-3s as a treatment option for ADHD.”

The authors went on to say: “In the context of ‘personalized medicine,’ it is tempting to speculate that a subpopulation of youth with ADHD and low levels of omega-3s may respond better to omega-3 supplementation, but there are no studies to date attempting this stratification approach [looking at the effect of omega-3 supplementation in the subpopulation with both ADHD and omega-3 deficiency]…Therefore, stratification of ADHD children by omega-3 levels…could be one approach to optimize the therapeutic effects of omega-3 supplementation.”

Basically, they are suggesting that the benefits of omega-3 supplementation are likely to be greatest for those children with ADHD who are also omega-3 deficient. They are also saying that future studies should measure omega-3 status before and after supplementation so that the true benefit of omega-3 supplementation can be determined. I agree

What Does This Mean For You?

This study was very well done. By including only the best designed studies in their meta-analysis, the authors have provided good evidence that omega-3s can be of benefit in reducing ADHD symptoms. The authors also pointed out that low-dose omega-3 supplementation is virtually free of side effects. Thus, this is an option that should be tried first, before considering medications to control ADHD symptoms.

On the other hand, I wouldn’t expect miracles. This was not a huge effect. Not all the ADHD symptoms improved with omega-3 supplementation. Teacher’s reports did not show the same benefits as parent’s reports.

There are two ways to interpret the limitations of omega-3 benefits seen in this meta-analysis.

Clinical studies report the average results for all the children in the study. Your child may not be average. If your child doesn’t like fish, especially the oil, cold-water fish that are rich in omega-3s, they may experience a greater benefit from omega-3 supplementation.
The benefit of omega-3s seen in this meta-analysis is just one facet of a holistic, natural approach for controlling ADHD without drugs. One of the best reviews on natural approaches for controlling ADHD was written by two pediatricians with years of experience dealing with ADHD. I wrote about their review in a previous issue, adhd diet vs medication, of “Health Tips From the Professor”. You should check it out. There was a lot of wisdom in their advice.

The Bottom Line

A recent meta-analysis has reported that omega-3 supplementation improves clinical symptoms and cognitive performances in children and adolescents with ADHD.
The optimal dose appeared to be 500 mg/day or above.
The authors also reported that children with ADHD were more likely to be omega-3 deficient than children without ADHD and suggested that omega-3 supplementation is most likely to be effective for those children who are omega-3 deficient.
The authors also pointed out that low-dose omega-3 supplementation had negligible side-effects, so it should be tried before the child is put on medication.
Omega-3s are just one facet of a holistic, natural approach for reducing ADHD symptoms.

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.

Red Meat and Heart Health

August 28, 2018 by Dr. Steve Chaney

Can Red Meat Be Part Of A Heart Healthy Diet?

Author: Dr. Stephen Chaney

What about red meat and heart health?

It is so confusing. One recent headline proclaimed “Plant-based foods decrease the risk of heart disease and cancer.” Another headline read: “Including beef with the Mediterranean diet improves heart health.” You are probably wondering which of these studies is correct. More importantly, you are probably wondering whether you should include more meat or less meat in your diet.

If you read the articles, you will find that the dueling headlines are deceptive. Both studies reached essentially the same conclusion. The first study (K.S. Petersen et al, Current Developments in Nutrition, 2017; 1:e001289 ) concluded that plant-based diets significantly decreased the risk of heart disease and diabetes. It also concluded that you can include small amounts of animal protein in a plant-based diet without losing its health benefits. The second study (L.E. O’Connor et al, American Journal of Clinical Nutrition, 108: 1-8, 2018 ) concluded that the Mediterranean diet, which is a primarily plant-based diet, significantly decreased the risk of heart disease and diabetes. It also concluded that you could include small amounts of lean, unprocessed red meat in the Mediterranean diet without losing its health benefits.

You might be wondering how it is possible to go from a study showing that small amounts of lean, unprocessed red meat did not reduce the heart-health benefits of the Mediterranean diet to a headline claiming: “Including Beef With A Mediterranean Diet Improves Heart Health.” Did I mention that the study was funded by money from the beef industry and the headlines came from an online issue of Beef Magazine? That might explain it.

Let’s look at:

How the studies were designed.
The study results in detail.
What these studies mean for you.

How Were The Studies Done?

Study #1: The first study (K.S. Petersen et al, Current Developments in Nutrition, 2017; 1:e001289 ) was a systematic review of over 50 recent studies looking at the relative contribution of plant-based foods and animal products to healthy dietary patterns.

Study #2: The second study (L.E. O’Connor et al, American Journal of Clinical Nutrition, 108: 1-8, 2018 ) was, in the words of the authors, an investigator-blinded, randomized, crossover, controlled feeding trial. That is probably Greek to most of you, so let me explain.

A “controlled feeding study” is one in which subjects are given diets designed by dietitians to contain precise amounts of macronutrients and micronutrients. In this case, both diets were Mediterranean diets. One of the diets was the standard Mediterranean diet with 1 ounce/day of lean, processed red meat. This diet was referred to as Med-Control. The other diet was a version of the Mediterranean diet containing 2.47 ounces/day of red meat. It was referred to as Med-Red. (More about the design of these diets below). The diets were prepared for the subjects by the Indiana Clinical Research Center Bionutrition Facility at Purdue University. The subjects completed weekly menu check-off lists and met with staff weekly to monitor compliance.
A “crossover study” is one in which subjects are given one experimental diet, followed by a “washout period” when they consume their normal diet, followed by the second experimental diet. In this case both experimental diets were followed for 5 weeks and the washout period was 4 weeks. In this type of study each subject serves as their own control.
The term “randomized” simply means that some subjects consumed the Med-Control diet first and others consumed the Med-Red diet first.
The term “investigator-blinded” simply means the investigators did not know the order of the experimental diets each subject received. It is, of course, impossible to conduct a double-blind study when you are conducting a dietary intervention study, such as this one. The subjects know which diet they are consuming.

Other important features of the study were:

The study included 41 middle-aged (46±2 years), obese (BMI=30.5±0.6) adults from West Lafayette, Indiana.
Fasting blood samples were taken at entry into the study and during the last week of both experimental diets and the washout period. The investigators measured total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, ApoB, C-reactive protein, insulin, and blood glucose levels.
Blood pressure was also measured at the same times.

In interpreting the results of this study, it is important to know other features of the experimental diets. They are:

Overall macronutrient composition was identical for the two diets. It was 40% carbohydrate, 22% protein, and 40% fat. In other words, it was nether low-carb nor low-fat. Instead it consisted of healthy carbs and healthy fats.
The differences between the two diets was almost entirely based on the relative amount of red meat and poultry in the diets. The Med-Control had more poultry and less red meat. The Med-Red had more red meat and less poultry.
The red meat was lean beef or pork tenderloin. The poultry was chicken or turkey breast (white meat with the skin removed prior to cooking). All meats were low in fat and cholesterol (˂10% total fat, ˂5% saturated fat, ˂95 mg cholesterol). In short, none of the subjects were eating juicy steaks and burgers or fried chicken.
Fish intake was the same on both diets (22% of protein intake) so that omega-3 intake was similar.
Nuts, seeds, and legumes (primarily soy) were the same on both diets (40% of protein intake). When you include grains and other plant protein sources, plant-based protein probably constituted almost 50% of total protein intake.
Both diets included the same amount of olive oil. The overall fat profile of the diet (7% saturated, 20% monounsaturated, and 13% polyunsaturated) was very healthy.
Both diets were rich in fruits and vegetables (4 servings/day of fruit and 7-8 servings/day of vegetables). This is much more than you would find in the typical American diet.
Both diets were composed primarily of whole grains. There was almost no sugar or refined grain in either diet. Again, this is very different from what most Americans eat.

Red Meat and Heart Health?

Study #1: While the authors of this paper reviewed a variety of studies, I will focus on studies looking at the inclusion of red meat into otherwise healthy diets. For example, the authors reported on a recently published study looking at inclusion of 3 different levels (1 ounce/day, 4 ounces/day, and 5 ounces/day) of lean, red meat into the DASH diet, a diet specifically designed to reduce the risk of high blood pressure. That study showed:

Inclusion of up to 5 ounces/day of lean red meat did not reduce the effectiveness of the DASH diet at reducing heart disease risk factors. In fact, total and LDL cholesterol levels were slightly better than when red meat was limited to 1 ounce/day.
However, the authors noted that:
- The DASH diet is already fairly high in animal protein. The increase in red meat consumption was achieved by replacing other animal protein sources in the diet.

- These were very lean cuts of red meat. All 3 versions of the DASH diet were designed to limit saturated fat intake to ˂6% of total calories.

- Plant protein was about 50% of total protein intake in all 3 diets.

- All 3 diets eliminated “empty calorie” foods and provided lots of fruits and vegetables (8-10 servings/day).

- All 3 diets included 4-5 cups of low fat dairy products.
The authors also noted that dietary intake was closely controlled in this study and that similar results might be difficult to achieve in a free-living setting. For example, they pointed out that previous studies have shown:
- Higher meat consumption in the American population is associated with lower consumption of fruits, vegetables, legumes, nuts, seeds and soy products.

The authors concluded: “It is likely that consumption of animal products (excluding processed meats) at recommended amounts in the context of a dietary pattern that meets recommendations for fruits, vegetables, whole grains, nuts, seeds, and legumes, and does not exceed recommendations for added sugar, sodium, and saturated fat, may not adversely affect, and may benefit cardiometabolic risk [risk of heart disease and diabetes].”

The authors went on to say: “However, population adherence to these recommendations is markedly suboptimal. Therefore, improving intake patterns to align with dietary guidelines should be the focus of our efforts rather than engaging in debate about whether diets for cardiovascular disease prevention should be exclusively plant-based or include animal foods in recommended amounts.”

In case you think that was clear as mud, let me offer my translation: “Lean, unprocessed meat consumption does not increase the risk of heart disease or diabetes when consumed as part of an extremely healthy diet. However, the American diet is lousy. We should focus on eating a healthy diet rather than arguing about whether it should be completely plant-based or can include some meat.”

Study #2: This study found that:

Total and LDL cholesterol decreased more with Med-Red Meat than with Med-Control. However, the authors noted that the Mediterranean diet has little effect on total and LDL cholesterol levels, so its effect on reducing heart disease risk must be due to other factors.
The other parameters (HDL cholesterol, ApoB, triglycerides, C-reactive protein, insulin and blood glucose levels) were essentially the same on the Med-Red and Med-Control diets. However, the Med-Control diet also had little effect on these parameters compared to the normal diet of the subjects in the study. That probably reflected the short duration (5 weeks) of the diet intervention phase. Much longer dietary interventions would be required to adequately assess the effectiveness of either the Mediterranean diet or the Mediterranean diet with red meat at reducing disease risk.
Once again, the Med-Red diet was a carefully controlled diet that featured:
- Small amounts (2.5 ounces/day) of very lean (<10% fat, <5% saturated fat) red meat in place of very lean poultry with about 50% of the protein in the diet coming from plant sources.

- Lots of fruits, vegetables, whole grains, nuts, seeds, legumes, omega-3-rich seafood, and olive oil.

- Almost no sugar and refined carbs.

- A very healthy fat profile (7% saturated, 20% monounsaturated, and 13% polyunsaturated fat).
In short, this diet was radically different from the typical American diet.

The authors concluded: “Adults who are overweight or obese can consume 2.5 ounces/day as lean and unprocessed beef and pork when adopting a Mediterranean Pattern to improve cardiometabolic disease [heart disease and diabetes] risk factors.”

The authors went on to say: “Our results support previous observational and experimental evidence which shows that unprocessed and/or lean red meat consumption does not increase the risk of developing cardiovascular [heart] disease…”

As discussed below, the second conclusion is not supported by the data. We need to remember that this study was funded by money from the beef industry.

What Does This Mean For You?

The beef industry and low carb enthusiasts are telling you that red meat consumption as part of a healthy diet is good for your heart. These claims are very misleading. That’s because most Americans assume that their diet is already healthy. In addition, some Americans are being misled into believing that low carb diets are healthy (As I document in my book, “Slaying The Food Myths” those claims are currently unproven). Finally, many Americans interpret these claims as telling them that the juicy steaks, burgers, and sausages they love are heart healthy. The reality is far different.

The studies the claims are based on looked at red meat consumption in the context of the heart healthy DASH and Mediterranean diets, not in the context of the typical American diet or low carb diets.
The only risk factors affected in most of the studies are total and LDL cholesterol, which have low reliability of predicting heart disease risk by themselves. Furthermore, they appear to have almost no effect on the heart healthy benefits of the Mediterranean diet. In addition, the studies have been too short (typically 5 weeks) to reliably assess the effect of red meat on other heart disease risk factors.
The effect of red meat on heart disease risk factors has been assessed in carefully controlled diets that feature:
- Small amounts of very lean (<10% fat, <6% saturated fat), unprocessed red meat in place of very lean poultry with about 50% of the protein in the diet coming from plant sources.

- Lots of fruits, vegetables, whole grains, nuts, seeds, legumes, omega-3-rich seafood, and vegetable oils.

- Almost no sugar and refined carbs.

- A very healthy fat profile (7% saturated, 20% monounsaturated, and 13% polyunsaturated fat).

The authors of one recent review accurately concluded: “It is likely that consumption of animal products (excluding processed meats) at recommended amounts in the context of a dietary pattern that meets recommendations for fruits, vegetables, whole grains, nuts, seeds, and legumes, and does not exceed recommendations for added sugar, sodium, and saturated fat, may not adversely affect, and may benefit cardiometabolic risk [risk of heart disease and diabetes]”.

How you extrapolate from that kind of conclusion to an unqualified claim that “Observational and experimental evidence shows that unprocessed and/or lean red meat consumption does not increase the risk of developing cardiovascular [heart] disease” is beyond me.

My summary would be: “Small amounts of lean, unprocessed meat do not appear to increase the risk of heart disease or diabetes when consumed as part of an extremely healthy plant-based diet. However, the American diet is lousy. Low carb diets leave out too many healthy foods. We should focus on eating a healthy diet [as defined above] rather than arguing about whether it should be low carb, low fat, completely plant-based or can include small amounts of lean, unprocessed meat.”

The Bottom Line

The studies the claims are based on looked at red meat consumption in the context of the heart healthy DASH and Mediterranean diets, not in the context of the typical American diet or low carb diets.
The only risk factors affected in most of the studies are total and LDL cholesterol, which have low reliability of predicting heart disease risk by themselves. In addition, they appear to have almost no effect on the heart healthy benefits of the Mediterranean diet. The studies have been too short (typically 5 weeks) to reliably assess the effect of red meat on other heart disease risk factors.
The effect of red meat on heart disease risk has been assessed in carefully controlled diets that feature:
- Small amounts of very lean (<10% fat, <6% saturated fat), unprocessed red meat in place of very lean poultry with about 50% of the protein in the diet coming from plant sources.

- Lots of fruits, vegetables, whole grains, nuts, seeds, legumes, omega-3-rich seafood, and vegetable oils.

- Almost no sugar and refined carbs.

- A very healthy fat profile (7% saturated, 20% monounsaturated, and 13% polyunsaturated fat).

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 Stretches For Sciatica Nerve Pain Work?

August 21, 2018 by Dr. Steve Chaney

Sciatica Treatment

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney

Stretches for sciatica nerve pain work,
but only when muscle spasms are released first!

Most people have been told to stretch tight muscles, but they haven’t been told that muscle spasms (trigger points) shorten the fibers and tie the muscles into tiny micro knots.

Here is an analogy that helps explain how muscle spasms cause pain.

Consider what happens if you have two trees, a big strong one and one that easily moves. Tie a rope straight across from tree to tree. If you pull on the rope it’s easy to see that the flexible tree bends.

However, if you tie several knots in the rope the flexible tree leans over toward the strong tree. Now if you try to stretch the rope to make the flexible tree stand up straight the knots put a strain on the points where the rope is tied.

Trying to stretch the rope causes the knots to tighten and overstretches the rope on either side of the knot.

This is what happens with your muscles.

In the case of sciatica, the muscle that crosses over your sciatic nerve is the piriformis. When the piriformis is shortened by a muscle spasm, it places a downward pressure on the sciatic nerve, impinging the nerve. This gets complicated because other muscles cause your pelvis to rotate and press the bone up into your sciatic nerve.

If you try to stretch the piriformis muscle, it causes the tight muscle to press down onto the sciatic nerve and can potentially tear the muscle.

Release the Muscle Knots Before Beginning Stretches for Sciatica Nerve Pain

Before stretching, it’s easy and essential to release the muscle that causes sciatica pain.

Lie on the floor, place the Trigger Point Therapy Ball or a new tennis ball onto the piriformis muscles (pictured left).

Ease onto the ball until it doesn’t hurt. Then move the ball just a bit to search for other tender points. Hold 30-60 seconds on each tender point to release the muscle knots.

Stretches for Sciatica Nerve Pain Can Now Commence Safely !

This seated spinal twist is a great stretch for sciatica.

Make sure you are seated tall and exhale as you twist. Hold for a minute and switch sides.

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

Do Omega-3s Lower Blood Pressure in Young, Healthy Adults?

August 14, 2018 by Dr. Steve Chaney

What Is The Omega-3 Index And Why Is It Important?

Author: Dr. Stephen Chaney

Do omega-3s lower blood pressure in healthy adults?

The literature on the potential health benefits of omega-3s is very confusing. That’s because a lot of bad studies have been published. Many of them never determined the omega-3 status of their subjects prior to omega-3 supplementation. Others relied on dietary recalls of fish consumption, which can be inaccurate.

Fortunately, a much more accurate measure of omega-3 status has been developed and validated in recent years. It’s called the Omega-3 Index. Simply put, the Omega-3 Index is the percentage of EPA and DHA compared to 26 other fatty acids found in cellular membranes. Using modern technology, it can be determined from a single finger prick blood sample. It is a very accurate reflection of omega-3 intake relative to other fats in the diet over the past few months. More importantly, it is a measure of the omega-3 content of your cell membranes, which is a direct measure of your omega-3 nutritional status.

A recent extension of the Framingham Heart Study reported that participants with an Omega-3 Index >6.8% had a 39% lower risk of cardiovascular disease than those with an Omega-3 Index <4.2% (WS Harris et al, Journal of Clinical Lipidology, 12: 718-724, 2018 ). Although more work needs to be done, an Omega-3 Index of 4% or less is generally considered indicative of high cardiovascular risk, while 8% or better is considered indicative of low cardiovascular risk. For reference, the average American has an Omega-3 Index in the 4-5% range. In Japan, where fish consumption is much higher and cardiovascular risk much lower, the Omega-3 Index is in the 9-11% range.

Previous studies have suggested that omega-3 fatty acids lower blood pressure to a modest extent. Thus, it is not surprising that more recent studies have shown an inverse correlation between Omega-3 Index and blood pressure. However, those studies have been done with older populations, many of whom had already developed high blood pressure.

From a public health point of view, it is much more interesting to investigate whether it might be possible to prevent high blood pressure in older adults by optimizing omega-3 intake in a young, healthy population, most of whom had not yet developed high blood pressure. Unfortunately, there were no studies looking at that population. The current study was designed to fill that gap.

How Was The Study Done?

The current study (M.G. Filipovic et al, Journal of Hypertension, 36: 1548-1554, 2018 ) was based on data collected from 2036 healthy adults, aged 25-41, from Liechtenstein. They were participants in the GAPP (Genetic and Phenotypic Determinants of Blood Pressure) study. Participants were excluded from the study if they had been diagnosed with high blood pressure and were taking medication to lower their blood pressure. They were also excluded if they had heart disease, chronic kidney disease, other severe illnesses, obesity, sleep apnea, or daily use of non-steroidal anti-inflammatory medications.

Blood samples were collected at the time of their enrollment in the study and frozen for subsequent determination of Omega-3 Index. Blood pressure was also measured at their time of enrollment in two different ways. The first was a standard blood pressure measurement in a doctor’s office.

For the second measurement they were given a wearable blood pressure monitor that recorded their blood pressure over 24 hours every 15 minutes during the day and every 30 minutes while they were sleeping. This is considered more accurate than a resting blood pressure measurement in a doctor’s office because it records the variation in blood pressure, while you are sleeping, while you are exercising, and while you go about your everyday activities.

Do Omega-3s Lower Blood Pressure In Young, Healthy Adults?

None of the participants in the study had significantly elevated blood pressure. The mean systolic and diastolic office blood pressures were 120±13 and 78±9 respectively. The average Omega-3 Index in this population was 4.6%, which is similar to the average Omega-3 Index in the United States.

When they compared the group with the highest Omega-3 Index (average = 5.8%) with the group with the lowest Omega-3 Index (average = 4.6%):

The office measurement of systolic and diastolic blood pressure was decreased by 3.3% and 2.6% respectively
While those numbers appear small, the differences were highly significant.
The 24-hour blood pressure measurements showed a similar decrease.
Blood pressure measurements decreased linearly with increasing Omega-3 Index. [In studies of this kind, a linear dose-response is considered an internal validation of the differences observed between the group with the highest Omega-3 Index and the group with the lowest Omega-3 Index.]

The authors concluded: “A higher Omega-3 Index is associated with statistically significant, clinically relevant, lower systolic and diastolic blood pressure in normotensive, young and healthy individuals. Diets rich omega-3 fatty acids may be a strategy for primary prevention of hypertension.”

What Does This Mean For You?

Perhaps I should first comment on the significance of the relatively small decrease in blood pressure observed in this study.

These were young adults, all of whom had normal or near normal blood pressure.
The difference in Omega-3 Index was rather small (5.8% to 4.6%). None of the participants in the study were at the 8% or above that is considered optimal.
Liechtenstein is a small country located between Switzerland and Spain. Fish consumption is low and omega-3 supplement consumption is rare.

Under these conditions, even a small, but statistically significant, decrease in blood pressure is remarkable.

We should think of this study as the start of the investigation of the relationship between omega-3 status and blood pressure. Its weakness is that it only shows an association between high Omega-3 Index and low blood pressure. It does not prove cause and effect.

Its strength is that it is consistent with many other studies showing omega-3 fatty acids lower blood pressure. Furthermore, it suggests that the effect of omega-3s on blood pressure may also be seen in young, healthy adults who have not yet developed high blood pressure.

Finally, the authors suggested that a diet rich in omega-3s might reduce the incidence of high blood pressure by slowing the age-related increase in blood pressure that most Americans experience. This idea is logical, but speculative at present.

However, the GAPP study is designed to provide the answer to that question. It is a long-term study with follow-up examinations scheduled every 3-5 years. It will be interesting to see whether the author’s prediction holds true, and a higher Omega-3 Index is associated with a slower increase in blood pressure as the participants age.

Why Is The Omega-3 Index Important?

The authors of this study said: “The Omega-3 Index is very robust to short-term intake of omega-3 fatty acids and reliably reflects an individual’s long-term omega-3 status and tissue omega-3 content. Therefore, the Omega-3 Index has the potential to become a cardiovascular risk factor as much as the HbA1c is for people with diabetes…” That is a bit of an overstatement. HbA1c is a measure of disease progression for diabetes because it is a direct measure of blood sugar control.

In contrast, Omega-3 Index is merely a risk factor for cardiovascular disease. However, if it is further validated by future studies, it is likely to be as important for predicting cardiovascular risk as are cholesterol levels and markers of inflammation.

However, to me the most important role of Omega-3 Index is in the design of future clinical studies. If anyone really wants to determine whether omega-3 supplementation reduces cardiovascular risk, high blood pressure, diabetes or any other health outcome they should:

Start with a population group with an Omega-3 Index in the deficient (4-5%) range.
Supplement with omega-3 fatty acids in a double blind, placebo-controlled manner.
Show that supplementation brought participants up to an optimal Omega-3 Index of 8% or greater.
Look at health outcomes such as heart attacks, cardiovascular deaths, hypertension, stroke, or depression.
Continue the study long enough for the beneficial effects of omega-3 supplementation to be measurable. For cardiovascular outcomes the American Heart Association has stated that at least two years are required to obtain meaningful results.

These are the kind of experiments that will be required to give definitive, reproducible results and resolve the confusion about the health effects of omega-3 fatty acids.

The Bottom Line

An accurate measure of omega-3 status has been developed and validated in recent years. It’s called the Omega-3 Index. Simply put, the Omega-3 Index is the percentage of EPA and DHA compared to 26 other fatty acids found in cellular membranes.

Although more work needs to be done, an Omega-3 Index of 4% or less is generally considered indicative of high cardiovascular risk while 8% or better is considered indicative of low cardiovascular risk.

Previous studies have shown an inverse correlation between Omega-3 Index and blood pressure. However, these studies have been done with older populations, many of whom had already developed high blood pressure.

From a public health point of view, it is much more interesting to investigate whether it might be possible to prevent high blood pressure in older adults by optimizing omega-3 intake in a young, healthy population, most of whom had not yet developed high blood pressure. Until now, there have been no studies looking at that population.

The study described in this article was designed to fill that gap. The participants in this study were ages 25-41, were healthy, and none of them had elevated blood pressure.

When the group with the highest Omega-3 Index (average = 5.8%) was compared with the group with the lowest Omega-3 Index (average = 4.6%):

Both systolic and diastolic blood pressure were decreased
Blood pressure measurements decreased linearly with increasing Omega-3 Index.

Let me translate that last sentence into plain English for you. The authors were saying that optimizing omega-3 intake in young adults may slow the age-related increase in blood pressure and reduce the risk of them developing high blood pressure as they age. This may begin to answer the question “Do omega-3s lower blood pressure in young, healthy adults?”

Or even more simply put: Aging is inevitable. Becoming unhealthy is not.

For more details, read the article above.

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

Does Vitamin D Reduce Cholesterol In Children?

August 7, 2018 by Dr. Steve Chaney

Is Vitamin D Associated With Heart Disease Risk?

Author: Dr. Stephen Chaney

Not too many years ago, we thought of vitamin D as affecting bone density and little else. Then we discovered that almost every cell in our body has vitamin D receptors. This has lead to research suggesting that vitamin D affects our health in many ways that were unimaginable only a couple of decades ago.

For example, low vitamin D levels are associated with increased risk of heart disease. The linkage between vitamin D and heart disease has not been proven. Nor do we know the mechanism. However, this has lead to ongoing research asking if there is any relationship between vitamin D and cholesterol metabolism.

The answer appears to be yes. Several studies have suggested a correlation between low vitamin D levels and elevated total cholesterol, LDL cholesterol, and triglycerides – all risk factors for heart disease.

The next question is how early in life is this correlation found. Again, some studies have suggested that the same correlation between low vitamin D and high levels of unhealthy lipids are found in teens. But, what about pre-teens, children who haven’t gone through puberty yet? That’s what this study was designed to determine.

How Was The Study Done?

The current study was based on data collected from 419 children, ages 6-8, in the Physical Activity and Nutrition in Children (PANIC) Study in Eastern Finland. This was a lifestyle study that collected information on body weight, diet, and activity levels.

Fasting blood samples were also collected and analyzed for blood lipid levels (total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides) and for 25-hydroxyvitamin D (25(OH)D), which is considered the most accurate measure of vitamin D status. The National Institutes of Health considers:

<30 nmol/L of 25(OH)D an indicator of vitamin D deficiency.
30 to <50 nmol/L 25(OH)D an indicator of vitamin D insufficiency.
≥50 nmol/L 25(OH)D an indicator of adequate vitamin D status.

To put this study in perspective, vitamin D status is a major concern in Finland because of its proximity to the Arctic Circle. There is little sunlight in the winter, and, although the days are long in the summer, the sun is weak. The major sources of vitamin D in the Finnish diet are fish, vitamin D-fortified fluid milk products, vitamin D-fortified fat spreads, and vitamin D supplementation. Vitamin D fortification was introduced in Finland in 2003. Vitamin D supplementation has also become increasing popular. The number of people using vitamin D supplements has increased from 11% in 2000 to 41% in 2011.

A recent study looking a vitamin D status between 2000 and 2011 found that the combination of food fortification and vitamin D supplementation has been successful at improving vitamin D status in the Finnish population, increasing average 25(OH)D levels from 48 nmol/L to 65 nmol/L.

Does Vitamin D Reduce Cholesterol In Children?

In this study the mean serum 25(OH)D in the children was 68.1 nmol/L. 20% of the children had serum 25(OH)D below 50 nmol/L, and only 4 children (1%) had serum 25(OH)D below 30 nmol/L. When 25(OH)D levels were compared with blood lipid levels:

Higher serum 25(OH)D levels were associated with lower plasma levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides.
The association between higher 25(OH)D levels and lower blood levels of total cholesterol, LDL cholesterol, and HDL cholesterol remained after correcting for weight, physical activity, sedentary behavior, diet, daylight time, parental education, and genetic mutations known to affect vitamin D metabolism.

What Does This Mean For You?

I don’t want to overinterpret the study. Not all studies show an inverse association between 25(OH)D and cholesterol levels. Most of the previous studies have also indicated that higher 25(OH)D levels were associated increased HDL levels, while this study found higher 25(OH)D levels associated with decreased HDL levels. Much more research needs to be done.

However, this study is yet another indication that optimal vitamin D status may be important for heart health, even in young children. While the correlation between vitamin D status and heart health is not definitive at present, virtually everyone agrees that adequate vitamin D status is a good thing.

My recommendations are to:

Get as much vitamin D as possible from vitamin D-fortified foods, oily fish, and sensible sun exposure.
Get your serum 25(OH)D level determined and take vitamin D supplements if it is low.

The Bottom Line

A recent study of vitamin D status in Finnish children ages 6-8 found:

Higher vitamin D status was associated with lower plasma levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides.
The association between better vitamin D status and lower blood levels of total cholesterol, LDL cholesterol, and HDL cholesterol remained after correcting for weight, physical activity, sedentary behavior, diet, daylight time, parental education, and genetic mutations known to affect vitamin D metabolism.

This study is another indication that optimal vitamin D status may be important for heart health, even in young children. While the correlation between vitamin D status and heart health is not definitive at present, virtually everyone agrees that adequate vitamin D status is a good thing.

My recommendations are to:

Get as much vitamin D as possible from vitamin D-fortified foods, oily fish, and sensible sun exposure.
Get your serum 25-hydroxyvitamin D level determined and take vitamin D supplements if it is low.
Make sure your children are getting enough vitamin D in their diet and have optimal serum 25-hydroxyvitamin D.

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.

Why Is Fructose Bad For You?

July 31, 2018 by Dr. Steve Chaney

Is It The Sugar, Or Is It The Food?

Author: Dr. Stephen Chaney

I don’t usually report on studies done in mice, but this study sheds light on a particularly puzzling question: Why is fructose bad for you?

The studies are clear-cut. High fructose consumption is associated with inflammation, obesity, non-alcoholic liver disease, insulin resistance, type 2 diabetes, kidney disease, increased LDL cholesterol and triglycerides, and heart disease. Based on these associations, fructose appears to be deadly. Why would anyone want to consume it?

Yet fructose is found in virtually every fruit. In fact, fructose, also known as fruit sugar, was first isolated from fruits. Hence the name fructose. Humans have been eating fruits safely for thousands of years. Fruits are very good for us. That raises the question: “If fruits are good for us, how can fructose be bad for us?”.

An important clue can be found by looking at what the food industry has done to the American diet. Because fructose imparts a pleasurable, sweet taste to foods, the food industry keeps adding it to more and more foods. As a result, dietary intake of fructose has increased 100-fold over the past two centuries. It has reached the point where fructose now accounts for almost 10% of the caloric intake in the United States.

Is It The Sugar, Or Is It The Food?

Let me expand the discussion by using a couple of graphics I developed for my book, “Slaying The Food Myths.”

There Are No Sugar Villains. There Are No Sugar Heroes:

Virtually all sweeteners are primarily a mixture of fructose and glucose. The graphic on the left compares high fructose corn syrup (the current villain) with other “natural” sweeteners used in foods (our current heroes). High fructose corn syrup ranges from about 40% fructose to 55% fructose. The exact percentage depends on what kind of food product is being made with it. Honey and coconut sugar are about 45% fructose. Sucrose and grape juice concentrate are around 50% fructose. Apple juice concentrate is around 60% fructose, and agave sugar comes in at a whopping 80% fructose.

In other words, if fructose is the culprit that everyone makes it out to be, “healthy” sugars are no better than high fructose corn syrup. Simply substituting a “healthy” sugar for high fructose corn syrup is unlikely to provide any meaningful benefit.

Is It The Sugar, Or Is The Food?

This graphic shows us what a nutrition label would look like on a medium apple. I am sure that label is a wake-up call for many of you. The amount of sugar and the percentage of fructose and glucose are about the same as in an 8-ounce soda sweetened with high fructose corn syrup. The same is true for virtually every other fruit you can think of.

Now let me share one more thing you won’t hear from what I refer to as “Dr. Strangelove’s Health Blog” (You probably know the ones I am referring to). Virtually all the studies showing the bad effects of fructose consumption have been done with sodas and sugary junk foods. They haven’t been done with apples.

In fact, virtually every study looking at fruit and vegetable consumption has shown they are incredibly good for us. They lower inflammation and reduce the risk of obesity, diabetes, heart disease, and cancer. And, the more the better. One study found that the health benefits of fruit and vegetable consumption topped out at around 10 servings a day.

With this background, you should now fully understand why the question “If fruits are good for us, how can fructose be bad for us?” is so perplexing.

My simplistic explanation has always been that whole foods like fruits have fiber, which slows the absorption of fructose from the intestine. Our bodies were designed to handle fructose in a safe manner when it enters the bloodstream slowly. Sodas and junk foods, on the other hand, have little to slow the absorption of fructose. When fructose enters the bloodstream rapidly, our “safe” metabolic pathways for handling it are overwhelmed, and it is forced into the pathways that are harmful. For example, the “excess” fructose is converted to fat by the liver, which causes inflammation, obesity, fatty liver disease, and triglyceride production.

This is, of course, simply my hypothesis for explaining the different effect of fructose in fruits and sodas. It is based on sound metabolic principles, but it is far from proven. That is why I found the current study (C. Jang et al, Cell Metabolism, 27: 351-361, 2018 ) so interesting. It provides a metabolic rationale for my hypothesis.

How Was The Study Done?

Mice were fed a 1:1 mixture of fructose and glucose at doses that approximated the ranges of typical human fructose consumption. The fructose was isotopically labeled so that fructose and its metabolites could be identified by LC-MS (liquid chromatography – mass spectrometry). After feeding the mice the labeled fructose, the investigator measured the amount of fructose and its metabolites in various organs and in the portal vein, which transports sugars from the intestine to the liver for additional metabolism before they enter the bloodstream.

Why Is Fructose Bad For You?

The first surprise was that most of the fructose was metabolized by the intestinal mucosal cells that line the small intestine rather than the liver. Previous reports had assumed that fructose was primarily metabolized by the liver because that was where most of the bad effects of fructose metabolism had been observed.

These investigators observed that fructose was primarily converted to glucose and small molecular weight metabolites by the intestinal mucosal cells before being released into the portal vein, where they were transported to the liver. However, there was a strong dose response effect.

At low fructose doses, 90% of fructose was metabolized by intestinal mucosal cells before being released to the liver.
At high fructose doses, only 70% of fructose was metabolized by intestinal mucosal cells.
That means at high fructose doses the amount of fructose reaching the liver unchanged increases from 10% to 30%. That is a 3-fold increase!

The authors concluded:

“Based on these findings, we propose that the small intestine shields the liver from fructose and that excessive doses of fructose overwhelm the small intestine, spilling over to the liver where they cause toxicity.”
“A key difference between the health effects of fiber-rich fruits (and perhaps even fiber-rich prepared foods) and juices/sodas is their rate of intestinal fructose release.”
“It is likely that the appearance rate of free fructose in the small intestine plays a critical role in dictating its metabolic fate. Like the lower doses in our experiments, a slower rate of fructose appearance will result in more complete intestinal clearance, whereas higher doses and faster rates result in fructose overflow to the liver.”

This study needs to be confirmed, and the mechanism may be entirely different in humans. However, whether the mechanism is the same in mice and humans is immaterial. We already know that fructose in sodas and junk foods exerts a very different effect on our health than fructose in fruits and other fiber-containing foods.

The Bottom Line

Previous studies have clearly shown that fructose in sodas and junk foods is bad for us, while fructose in fruits is good for us. A recent study in mice provides a metabolic explanation for this difference. The study found:

At low fructose doses, 90% of fructose was metabolized by intestinal mucosal cells before being released to the liver.
At high fructose doses, only 70% of fructose was metabolized by intestinal mucosal cells.
That means at high fructose doses the amount of fructose reaching the liver unchanged increases from 10% to 30%. That is a 3-fold increase!

The authors concluded:

“Based on these findings, we propose that the small intestine shields the liver from fructose and that excessive doses of fructose overwhelm the small intestine, spilling over to the liver where they cause toxicity.”
“A key difference between the health effects of fiber-rich fruits (and perhaps even fiber-rich prepared foods) and juices/sodas is their rate of intestinal fructose release.”
“It is likely that the appearance rate of free fructose in the small intestine plays a critical role in dictating its metabolic fate. Like the lower doses in our experiments, a slower rate of fructose appearance will result in more complete intestinal clearance, whereas higher doses and faster rates result in fructose overflow to the liver.”

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.