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Omega-3s Reduce Preterm Births

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Do Omega-3s Make For A Healthy Pregnancy?

Author: Dr. Stephen Chaney 

omega-3s during pregnancy is healthyThe role of omega-3s on a healthy pregnancy has been in the news for some time. Claims have been made that omega-3s reduce preterm births, postnatal depression, and improve cognition, IQ, vision, mental focus, language, and behavior in the newborn as they grow.

The problem is that almost all these claims have been called into question by other studies. If you are pregnant or thinking of becoming pregnant, you don’t know what to believe.

  • Should you eat more fish?
  • Should you take omega-3 supplements?
  • Or should you just ignore the claims about omega-3s and a healthy pregnancy?

These are not trivial questions. Let’s consider preterm births as an example. The medical profession has made enormous advances in keeping premature babies alive. However, premature babies are still at higher risk of several health conditions including:

  • Visual impairment.
  • Developmental Delay.
  • Learning difficulties.

Plus, it is expensive to keep premature babies alive. One recent study estimated that increasing omega-3 intake during pregnancy could reduce health care costs by around $6 billion in the United Stated alone.

Unfortunately, it’s not just omega-3s and pregnancy. The same is true for almost all nutritional health claims. One day a study comes out claiming that nutrient “X” cures some disease or has some miraculous benefit. The bloggers and news media hype that study. Suddenly you see that health claim everywhere. It becomes so omnipresent that you are tempted to believe it must be true.

But wait. A few months later another study comes to opposite conclusion. Now the media is telling you that health claim is false. The months come and go, and new studies keep coming out. Some support the health claim. Others refute it.

Pretty soon the nutrition headlines just become “noise”. You don’t know what to believe. If you want the truth, “Who ya gonna call?”

Who Ya Gonna Call?

ghost bustersIt’s not Ghostbusters. It not Dr. Strangelove’s health blog. It’s a group called the Cochrane Collaboration.

The Cochrane Collaboration consists of 30,000 volunteer scientific experts from across the globe whose sole mission is to analyze the scientific literature and publish reviews of health claims so that health professionals, patients, and policy makers can make evidence-based choices about health interventions.

The Cochrane Collaboration reviews all the relevant studies on a topic, exclude those that are biased or weak, and make their recommendations based on only the strongest studies. Their reviews are considered the gold standard of evidence-based medicine.

If you are of a certain age, you may remember that TV commercial “When EF Hutton talks, people listen.” It is the same with the Cochrane Collaboration. When they talk, health professionals listen.

This week we will examine the Cochrane Collaboration’s review titled “Omega-3 Fatty Acid Addition During Pregnancy”.

How Was The Study Done?

Clinical StudyFor this analysis the Cochrane Collaboration reviewed 70 randomized controlled trials which compared the effect of added omega-3s on pregnancy outcomes with either a placebo or a diet no added omega-3s. These trials included almost 19,927 pregnant women.

In one sense, Cochrane reviews are what is called a “meta-analysis”, in which data from numerous studies are grouped together so that a statistically significant conclusion can be reached. However, Cochrane Collaboration reviews differ from most meta-analyses found in the scientific literature in a very significant way.

Many published meta-analyses simply report “statistically significant” conclusions. However, statistics can be misleading. As Mark Twain said: “There are lies. There are damn lies. And then there are statistics”.

The problem is that the authors of most meta-analyses group studies together without considering the quality of studies included in their analysis. This creates a “Garbage In – Garbage Out” effect. If the quality of individual studies is low, the quality of the meta-analysis will also be low. Simply put, the conclusions from some published meta-analyses are not worth the paper they are written on.

The Cochrane Collaboration also reports statistically significant conclusions from their meta-analyses. However, they also carefully consider the quality of each individual study in their analysis. They look at possible sources of bias. They look at the design and size of the studies. Finally, they ask whether the conclusions are consistent from one study to the next. They clearly define the quality of evidence that backs up each of their conclusions as follows:

  • High-quality evidence. Further research is unlikely to change their conclusion. This is generally reserved for conclusions backed by multiple high-quality studies that have all come to the same conclusion. These are the recommendations that are most often adopted into medical practice.
  • Moderate-quality evidence. This conclusion is likely to be true, but further research could have an impact on it.
  • Low-quality evidence. Further research is needed and could alter the conclusion. They are not judging whether the conclusion is true or false. They are simply saying more research is needed to reach a definite conclusion.

Omega-3s Reduce Preterm Births

clinically provenHere are the conclusions that the Cochrane Collaboration said were supported by high-quality evidence:

  • Omega-3s reduce the risk of preterm births.
  • Omega-3s reduce the risk of low-birth-weight infants.

The authors concluded: “Omega-3 supplementation during pregnancy is an effective strategy for reducing the risk of preterm birth…More studies comparing omega-3s and placebo are not needed at this point.”

In other words, they are saying this conclusion is definite. Omega-3 supplementation should become part of the standard of medical care for pregnant women.

However, they did say that further studies were needed “…to establish if, and how, outcomes vary by different types of omega-3s, timing [stage of pregnancy], doses [of omega-3s], or by characteristics of women.”

That’s because these variables were not analyzed in the Cochrane study. Their review and meta-analysis included clinical trials:

  • Of women at low, moderate, and high risk of poor pregnancy outcomes.
  • With DHA alone, with EPA alone, and with a mixture of both.
  • Omega-3 doses that were low (˂ 500 mg/day), moderate (500-1,000 mg/day), and high (> 1,000 mg/day).

Do Omega-3s Make For A Healthy Pregnancy?

What about the effect of omega-3s on other pregnancy outcomes?

The conclusions the Cochrane Collaboration said were supported by moderate quality evidence included reductions in:

  • Perinatal death.
  • Admissions to the neonatal intensive care unit.

There was not enough high or moderate quality data to determine the effect of omega-3s on other pregnancy outcomes such as postnatal depression. More research is still needed in those areas. However, if you do receive any of these benefits from omega-3 supplementation, you can just consider them as side benefits.

What Does This Report Mean For You?

pregnant women taking omega-31) The proven effect of omega-3 supplementation on preterm births is significant because preterm births increase the risk of:

  • Visual impairment.
  • Developmental Delay.
  • Learning difficulties.

2) The likely effect of omega-3s on admission to neonatal intensive care units is significant because those units are very expensive.

3) The Cochrane study did not determine whether omega-3 supplementation was equally important for women at low, moderate, and high likelihood of poor pregnancy outcomes.

  • Therefore, omega-3 supplementation should be considered for all pregnant women.

4) The Cochrane study did not determine whether omega-3 supplementation was equally important during the first, second, or third trimester.

  • Therefore, omega-3 supplementation should be considered by all women of childbearing age who might become pregnant and throughout pregnancy.

5) The Cochrane study did not determine whether DHA, EPA, or a mixture of the two was most effective.

  • Therefore, your omega-3 supplement should probably contain both DHA and EPA. A group of experts recently recommended  that adults consume at least 650 mg/day of omega-3s with ≥ 220 mg of that coming from DHA and ≥ 220 mg/day coming from EPA.
  • Since most pregnant women in this country consume around 89 mg/day of DHA + EPA, omega-3 supplementation is warranted.

The Bottom Line 

The effect of omega-3s on pregnancy outcomes have been confusing. Some studies conclude that omega-3s are important for a healthy pregnancy. Other studies suggest they are ineffective. What are you to believe?

Fortunately, a group called the Cochrane Collaboration recently conducted a comprehensive review of this topic. This is significant because Cochrane Reviews are internationally recognized as the highest standard in evidence-based health care. They influence the treatment protocols recommended by the medical community.

This Cochrane Review concluded that omega-3 supplementation during pregnancy:

  • Reduces preterm births and low birth weight infants.
  • Likely reduces perinatal death and admissions to the neonatal intensive care unit.

The authors of the review said: “Omega-3 supplementation during pregnancy is an effective strategy for reducing the risk of preterm birth…More studies comparing omega-3s and placebo are not needed at this point.”

In other words, they are saying this conclusion is definite. Omega-3 supplementation should become part of the standard of medical care for pregnant women.

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

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

Vitamin D And ADHD

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Can ADHD Be Prevented?

Author: Dr. Stephen Chaney 

vitamin dIf you are pregnant, or of childbearing age, should you be supplementing with vitamin D? Increasingly, the answer appears to be yes.

  1. Based on blood 25-hydroxy vitamin D levels (considered the most accurate marker of vitamin D status):
    • 8-11% of pregnant women in the US are deficient in vitamin D (<30 nmol/L).
    • 25% of pregnant women have insufficient vitamin D status (30-49 nmol/L).

In short, that means around 1/3 of pregnant women in the US have insufficient or deficient levels of vitamin D. The effect of inadequate vitamin D during pregnancy is not just an academic question.

2) The Cochrane Collaboration (considered the gold standard for evidence-based medicine) has recently concluded that supplementation with vitamin D reduces the risk of significant complications during pregnancy.

3) Another recent study found that inadequate vitamin D status during pregnancy delayed several neurodevelopmental milestones in early childhood, including gross motor skills, fine motor skills, and social development.

If neurodevelopmental milestones are affected, what about ADHD? Here the evidence is not as clear. Some studies have concluded that vitamin D deficiency during pregnancy increases the risk of ADHD in the offspring. Other studies have concluded there is no effect of vitamin D deficiency on ADHD.

Why the discrepancy between studies?

  • Most of the previous studies have been small. Simply put, there were too few children in the study to make statistically reliable conclusions.
  • Most of the studies measured maternal 25-hydroxyvitamin D levels in the third trimester or in chord blood at birth. However, it is during early pregnancy that critical steps in the development of the nervous system take place.

Thus, there is a critical need for larger studies that measure maternal vitamin D status in the first trimester of pregnancy. This study (M Sucksdorff et al, Journal of the American Academy of Child & Adolescent Psychiatry, 60: 142-151, 2021) was designed to fill that need.

How Was The Study Done?

Clinical StudyThis study compared 1,067 Finnish children born between 1998 and 1999 who were subsequently diagnosed with ADHD and 1,067 matched controls without ADHD. There were several reasons for choosing this experimental group.

  • Finland is among the northernmost European countries, so sun exposure during the winter is significantly less than for the United States and most other European countries. This time period also preceded the universal supplementation with vitamin D for pregnant women that was instituted in 2004.

Consequently, maternal 25-hydroxyvitamin D levels were significantly lower than in most other countries. This means that a significant percentage of pregnant women were deficient in vitamin D, something not seen in most other studies. For example:

  • 49% of pregnant women in Finland were deficient in vitamin D (25-hydoxyvitamin D <30 nmol/L) compared to 8-11% in the United States.
  • 33% of pregnant women in Finland had insufficient vitamin D status (25-hydroxyvitamin D 30-49.9 nmol/L) compared to 25% in the United States.
  • Finland, like many European countries, keeps detailed health records on its citizens. For example:
    • The Finnish Prenatal Study collected data, including maternal 25-hydroxyvitamin D levels during the first trimester), for all live births between 1991 and 2005.
    • The Care Register for Health Care recorded, among other things, all diagnoses of ADHD through 2011.

Thus, this study avoided the limitations of earlier studies. It was ideally positioned to compare maternal 25-hydroxyvitamin D levels during the first trimester of pregnancy with a subsequent diagnosis of ADHD in the offspring. The long-term follow-up was important to this study because the average age of ADHD diagnosis was 7 years (range = 2-14 years).

Vitamin D And ADHD 

Child With ADHDDoes maternal vitamin D affect ADHD in the offspring? The answer to this question appears to be a clear, yes.

If you divide maternal vitamin D levels into quintiles:

  • Offspring of mothers in the lowest vitamin D quintile (25-hydroxyvitamin D of 7.5-21.9 nmol/L) were 53% more likely to develop ADHD than offspring of mothers in the highest vitamin D quintile (49.5-132.5 nmol/L).

When you divide maternal vitamin D levels by the standard designations of deficient (<30 nmol/L), insufficient (30-49.9 nmol/L), and sufficient (≥50 nmol/L):

  • Offspring of mothers who were deficient in vitamin D were 34% more likely to develop ADHD than children of mothers with sufficient vitamin D status.

The authors concluded: “This is the first population-based study to demonstrate an association between low maternal vitamin D during the first trimester of pregnancy and an elevated risk for ADHD diagnosis in offspring. If these findings are replicated, they may have public health implications for vitamin D supplementation and perhaps changing lifestyle behaviors during pregnancy to ensure optimal maternal vitamin D levels.”

Can ADHD Be Prevented? 

Child Raising HandI realize that this is an emotionally charged title. If you have a child with ADHD, the last thing I want is for you to feel guilty about something you may not have done. So, let me start by acknowledging that there are genetic and environmental risk factors for ADHD that you cannot control. That means you could have done everything right during pregnancy and still have a child who develops ADHD.

Having said that, let’s examine things that can be done to reduce the risk of giving birth to a child who will develop ADHD, starting with vitamin D. There are two aspects of this study that are important to keep in mind.

#1: The increased risk of giving birth to a child who develops ADHD was only seen for women who were vitamin D deficient. While vitamin D deficiency is only found in 8-11% of pregnant mothers in the United States, that is an average number. It is more useful to ask who is most likely to be vitamin D deficient in this country. For example:

  • Fatty fish and vitamin D-fortified dairy products are the most important food sources of vitamin D. Fatty fish are not everyone’s favorite and may be too expensive for those on a tight budget. Many people are lactose intolerant or avoid milk for other reasons. If you are not eating these foods, you may not be getting enough vitamin D from your diet. This is particularly true for vegans.
  • If you have darker colored skin, you may have trouble making enough vitamin D from sunlight. If you are also lactose intolerant, you are in double trouble with respect to vitamin D sufficiency.
  • Obesity affects the distribution of vitamin D in the body. So, if you are overweight, you may have low 25-hydroxyvitamin D levels in your blood.
  • The vitamin D RDA for pregnant and lactating women is 600 IU, but many multivitamin and prenatal supplements only provide 400 IU. If you are pregnant or of childbearing age, it is a good idea to look for a multivitamin or prenatal supplement that provides at least 600 IU, especially if you are in one of the high risk groups listed above.
  • Some experts recommend 2,000 to 4,000 IU of supplemental vitamin D. I would not recommend exceeding that amount without discussing it with your health care provider first.
  • Finally, for reasons we do not understand, some people have a difficult time converting vitamin D to the active 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D in their bodies. If you are pregnant or of childbearing age, it is a good idea to have your blood 25-hydroxyvitamin D levels determined and discuss with your health care provider how much vitamin D you should be taking. Many people need more than 600 IU to reach vitamin D sufficiency status.

#2: Maternal vitamin D deficiency has a relatively small effect (34%) on the risk of the offspring developing ADHD. That means assuring adequate vitamin D status during pregnancy should be part of a holistic approach for reducing ADHD risk. Other factors to consider are:No Fast Food

  • Low maternal folate and omega-3 status.
  • Smoking, drug, and alcohol use.
  • Obesity.
  • Sodas and highly processed foods.

Alone, each of these factors has a small and uncertain influence on the risk of your child developing ADHD. Together, they may play a significant role in determining your child’s risk of developing ADHD.

In closing, there are three take-home lessons I want to leave you with:

  1. The first is that there is no “magic bullet”. There is no single action you can take during pregnancy that will dramatically reduce your risk of giving birth to a child who will develop ADHD. Improving your vitamin D, folate, and omega-3 status; avoiding cigarettes, drugs, and alcohol; achieving a healthy weight; and eating a healthy diet are all part of a holistic approach for reducing the risk of your child developing ADHD.

2) The second is that we should not think of these actions solely in terms of reducing ADHD risk. Each of these actions will lead to a healthier pregnancy and a healthier child in many other ways.

3) Finally, if you have a child with ADHD and would like to reduce the symptoms without drugs, I recommend this article.

The Bottom Line 

A recent study looked at the correlation between maternal vitamin D status during the first trimester of pregnancy and the risk of ADHD in the offspring. The study found:

  • Offspring of mothers who were deficient in vitamin D were 34% more likely to develop ADHD than children of mothers with sufficient vitamin D status.

The authors concluded: “This is the first population-based study to demonstrate an association between low maternal vitamin D during the first trimester of pregnancy and an elevated risk for ADHD diagnosis in offspring. If these findings are replicated, they may have public health implications for vitamin D supplementation and perhaps changing lifestyle behaviors during pregnancy to ensure optimal maternal vitamin D levels.”

In the article above I discuss what this study means for you and other factors that increase the risk of giving birth to a child who will develop ADHD.

For more details read the article above.

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

 

Is It The Sugar Or Is It The Food?

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Is Fructose Bad For You?

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 us?

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:

Sugar ComparisonsVirtually 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?

Apple With Nutrition LabelThis 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. It is taken up by the liver, converted to glucose, and then slowly metered back into the bloodstream. This provides our brain and other tissues with the glucose they need for energy without blood sugar spikes. This is how fructose is supposed to be metabolized by our bodies.

Sodas and junk foods, on the other hand, have little to slow the absorption of fructose. When lots of 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 a recent 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.

Is Fructose Bad For You?

intestine & liverThe 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 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.

Despite what Dr. Strangelove tells you, fructose is not bad for you. It isn’t the problem. It is sodas and junk foods containing high-fructose corn syrup that are the problem. And substituting other sugars for high-fructose corn syrup doesn’t make them any better. As I showed you above, the so called “healthy” sugars are chemically and biologically indistinguishable from high-fructose corn syrup.

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.”

This study needs to be confirmed, and the mechanism may be entirely different in humans. However, whether 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.

Despite what Dr. Strangelove tells you, fructose is not bad for you. It isn’t the problem. It is sodas and junk foods containing high-fructose corn syrup that are the problem. And substituting other sugars for high-fructose corn syrup doesn’t make them any better. As I showed you above, the so called “healthy” sugars are chemically and biologically indistinguishable from high-fructose corn syrup.

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.

Relief From Shin Splints

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What Causes Shin Splints?

Author: Julie Donnelly, LMT – The Pain Relief Expert

Editor: Dr. Steve Chaney

HotJuly is here and Florida is hot! The “Snowbirds” have gone north to the cooler weather (a goal of mine!) and life is moving in the slow lane.

For me, the slow down time is giving me the opportunity to work on some big projects that are planned to bring my work to massage therapists all over the USA.  If your massage therapist is interested in expanding their techniques, please tell them to contact me so we can chat.

I’m also finishing up the editing of my newest book: “Pain-Free Golf. The Secret to Your Best Golf Game Ever!”  I’m grateful and want to give a shout out to John Ma and Rebecca Saggau for their help in making this a much better book.

This month’s topic is on Shin Splints, and next month I’ll be talking about something most people aren’t aware of…bone bruises.

I hope you enjoy all the outdoor activities that go with the month of July.

What Are Shin Splints?

If you are a runner, play any sport that involves a lot of running, or if you drive for long distances, you may have experienced pain &/or burning along the front of your leg, next to your shin bone.  This pain is commonly called Shin Splints.

I’ve searched all through the internet and while I’ve found LOTS of articles about the cause of shin splints, the definition of shin splints, and treatments such as rest, ice, various meds, etc., I’ve never found anything that resembles the self-treatment I’ve been teaching for years and that is in each of my books.

I’m going to share that self-treatment with you. A plus is the treatment for the muscle that causes shin splints is also one of the main muscles that cause plantar fasciitis.  So, you may get some pain relief that you weren’t even expecting.

What Causes Shin Splints?

The Tibialis Anterior muscle cause shin splints. The tibialis anterior muscle runs along the outside of your shin bone (the tibia bone), merges into a tendon at your lower leg, crosses over your ankle and then inserts into your arch.  When it contracts, it lifts your foot and rolls it toward the outside.  Because of these attachments, it is also a key muscle in a sprained ankle and in plantar fasciitis, but these are topics for different newsletters.

The muscle fibers are directly on your shin bone, so when they are tightening due to a repetitive strain, such as running or pressing down on the gas pedal while driving long distances, they start to tear off the bone.  You can visualize this by considering how you rip meat off a bone while eating a steak or spareribs.

As the muscle is slowly tearing away from the bone you feel pain along the entire length of the bone, and it really hurts!  Fortunately, it’s easy to release the tension in the muscle. Plus, as you’re doing the self-treatment I’m showing you, you are pressing the fibers back on to the bone, so it stops them from ripping away completely.

Relief From Shin Splints

You can get immediate relief from shin splint pain by treating your tibialis anterior muscle.

Begin to warm up the muscle by putting your leg straight out and running your opposite heel down the length of the muscle.

Right at the point where the picture is showing the model’s heel on her leg is the point where you’ll find the most sensitive trigger point.

Continue from just below your knee to just above your ankle joint.

Next kneel down as shown in the picture on the right, placing the ball at the top of the muscle and right next to your shin bone.

Notice the way his toes are bent.  This will help prevent your arch from feeling like it’s going to cramp as the muscle pulls on the insertion point

Begin to move your leg so the ball is rolling down toward your ankle.  Stop when you find a tight point.

When you get to your ankle you can roll back up toward your knee again.  Ultimately it won’t hurt, but if it’s especially painful in the beginning just lighten up on the pressure.  You may even need to lift your leg off the ball at first which will allow blood to come into the muscle fiber and help lessen the tension.

This technique has helped so many people over the years, I know it will help you too!

How To Treat Yourself For Pain Relief

I’ve written several books and programs that teach you how to self-treat for pain from your head to your feet. The Shin Splint treatment is just one technique, and if you’ve been receiving this newsletter for a long time, you’ve seen many others.

My books are a good resource and will explain why muscles are causing your pain or discomfort, and how you can stop it fast.

Wishing you well,

Julie Donnelly

www.FlexibleAthlete.com

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 Low Vitamin D Make You Weak?

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Why Is Vitamin D Research So Controversial?

Author: Dr. Stephen Chaney

vitamin dMillions of Americans lose muscle strength as they age, something called sarcopenia. This is not a trivial matter. Loss of muscle mass:

  • Leads to loss of mobility. It can also make it difficult to do simple things like lifting your grandchild or carrying a bag of groceries.
  • Increases your risk of falling. This often leads to serious fracture which increases your of dying prematurely. In fact, bone fractures increase your risk of dying by 3-fold or more. Even in those who recover their mobility and quality of life may never be the same.
  • Lowers your metabolic rate. This increases your risk of obesity and all the diseases that are associated with obesity.

Loss of muscle strength as we age is preventable. There are several things we can do to preserve muscle strength as we age, but in today’s article I will focus on the effect of vitamin D on muscle strength.

What if something as simple as preventing vitamin D deficiency could improve muscle strength as we age? That idea has been around for a decade or more. But, for reasons I will detail below, it has proven controversial. Let me start by sharing a recent study on vitamin D and muscle strength (N Aspell et al, Clinical Investigations in Ageing, volume 2019:14, pages 1751-1761).

How Was The Study Done?

Clinical StudyThe data for this study came from 4157 adults who were enrolled in the English Longitudinal Study On Aging. Participants in this study were all over the age of 60 and were still living in their own homes. The general characteristics of the study population were:

  • Their average age was 69.8 with 45% male and 55% female.
  • While 76% of the participants rated their health as “good” or above
    • 73% were overweight or obese.
    • 54% had a longstanding disease that limited mobility.
    • 29% were taking multiple medications.

Serum 25-hydroxy vitamin D levels were determined as a measure of vitamin D status.

  • 22% of the participants were vitamin D deficient (<30 nmol/L 25-hydroxy vitamin D).
  • 34% of the participants were vitamin D insufficient (between 30 and 50 nmol/L 25-hydroxy vitamin D).
  • 46% of the participants had adequate vitamin D status (>50 nmol/L 25-hydroxy vitamin D).

Muscle strength was assessed by a handgrip strength test with the dominant hand. Muscle performance was assessed with something called the short physical performance battery (SPPB), consisting of a walking speed test, a repeated chair raise test, and a balance test.

Does Low Vitamin D Make You Weak?

When the data on handgrip strength were analyzed:

  • Only 22% of the participants who had adequate vitamin D status had low handgrip strength.
  • 40% of participants who were vitamin D deficient had low handgrip strength. That’s almost a 2-fold difference.
  • Handgrip strength increased linearly with vitamin D status.
    • The relationship between vitamin D status and handgrip strength was highly significant (p<001).
    • The beneficial effect of vitamin D status on handgrip strength plateaued at around 55-69 nmol/L 25-hydroxy vitamin D. In other words, you need adequate vitamin D status to support muscle strength, but higher levels provide no additional benefit.

When the data on muscle performance (the SPPB test) were analyzed:

  • Only 8% of the participants who had adequate vitamin D status scored low on this test.
  • 25% of participants who were vitamin D deficient scored low on this test. That’s a 3-fold difference.
  • Muscle performance also increased linearly with vitamin D status.
    • The relationship between vitamin D status and muscle performance was also highly significant (p<001).
    • The beneficial effect of vitamin D status on muscle performance also plateaued at around 55-69 nmol/L 25-hydroxy vitamin D.

The authors concluded: “Vitamin D deficiency was associated with impaired muscle strength and performance in a large study of community-dwelling older people. It is generally accepted that vitamin D deficiency should be reversed to prevent bone disease. This strategy may also protect skeletal muscle function in aging.”

Why Is Vitamin D Research So Controversial?

ArgumentYou can be forgiven if you are saying to yourself: “I’ve heard this sort of thing before. I see a blog or headline claiming that vitamin D has a certain benefit, but it’s usually followed by later headlines saying those claims are false. Why can’t the experts agree? Is all vitamin D research bogus?”

The relationship between vitamin D status and muscle strength is no different.

  • Many, but not all, studies looking at the association between vitamin D status and muscle strength find that vitamin D status affects muscle strength.
  • However, many randomized, placebo-controlled clinical trials looking at the effect of vitamin D supplementation on muscle strength have come up empty.

A meta-analysis (L Rejnmark, Therapeutic Advances in Chronic Disease, 2: 25-37, 2011) of randomized, placebo-controlled clinical trials of vitamin D supplementation and muscle strength provides insight as to why so many of them come up empty.

The meta-analysis combined data from 16 clinical trials. The conclusions were similar to what other meta-analyses have found:

  • Seven of the studies showed a benefit of vitamin D supplementation on muscle strength. Nine did not.
  • When the data from all 16 studies were combined, there was only a slight beneficial effect of vitamin D supplementation on muscle strength.

However, it was in the discussion that the reason for these discrepancies became apparent. There were three major deficiencies in study design that were responsible for the discrepancies.

1) There was a huge difference in study design.

  • The subjects were of different ages, genders, and ethnicity.
  • The dose of vitamin D supplementation varied.
  • Different measures of muscle strength and performance were used.

Until the scientific and medical community agree on a standardized study design it will be difficult to obtain consistent results.Garbage In Garbage Out

While this deficiency explains the variation in outcomes from study to study, there are two other deficiencies in study design that explain why many of the studies failed to find an effect of vitamin D on muscle strength. I call this “Garbage In, Garbage Out”. Simply put, if the study has design flaws, it may be incapable of detecting a positive effect of vitamin D on muscle strength.

2) Many of the studies did not measure vitamin D status of the participants at the beginning of the study.

  • The results of the study described above show that additional vitamin D will be of little benefit for anyone who starts the study with an adequate vitamin D status.
  • In the study above 46% of the participants had adequate vitamin D status. This is typical for the elderly community. When almost 50% of the participants in a study have adequate vitamin D status at the beginning of a study it becomes almost impossible to demonstrate a beneficial effect of vitamin D supplementation on any outcome.

It is essential that future studies of vitamin D supplementation focus on participants who have low vitamin D status. Otherwise, you are almost guaranteeing a negative outcome.

3) Most of the studies ignored the fact that vitamin D status is only one of three factors that are essential for muscle strength.

  • In the case of muscle strength, especially in the elderly, the three essentials are vitamin D, protein, and exercise. All three are needed to maintain or increase muscle strength. Simply put, if one is missing, the other two will have little or no effect on muscle strength. Unfortunately, you cannot assume that exercise and protein intake are adequate in older Americans:
  • Many older adults don’t get enough exercise because of physical limitations.

Unfortunately, many clinical studies on the effect of vitamin D supplementation and muscle strength fail to include exercise and adequate protein intake in the study. Such clinical trials are doomed to failure.

Now you know why vitamin D research is so controversial. Until the scientific and medical community get their act together and perform better designed experiments, vitamin D research will continue to be controversial and confusing.

What Does This Mean For You?

Old Man Lifting WeightsLoss of muscle mass as we age is not a trivial matter. As described above, it:

  • Leads to loss of mobility.
  • Increases your risk of falling. This often leads to serious fractures which increase your risk of disability and death.
  • Lowers your metabolic rate, which increases your risk of obesity and obesity-related diseases.

So, what can you do prevent loss of muscle mass as you age? The answer is simple:

  • Aim for 25-30 grams of high-quality protein in each meal.
    • That protein can come from meat, fish, eggs, or vegetable sources such as beans, nuts, and seeds.
    • That doesn’t mean you need to consume an 8-ounce steak or a half chicken. 3-4 ounces is plenty.
    • However, it does mean you can’t subsist on green salads and leafy greens alone. They are healthy, but you need to include a good protein source if you are going to meet your protein needs.
  • Aim for 150 minutes of moderate intensity exercise per week.
    • At least half of that exercise should be resistance exercise (lifting weights, for example).
    • If you have physical limitations, consult your doctor and work with a physical therapist or personal trainer to design resistance exercises you can do.
    • Aim for a variety of resistance exercises. You will only strengthen the muscles you exercise.
  • Aim for an adequate vitamin D status.
    • Start with a multivitamin containing at least 800 IU of vitamin D3.
    • Because there is large variation in the efficiency with which we convert vitamin D to 25-hydroxy vitamin D, you should get your serum 25-hydroxyvitamin D tested on a yearly basis. Your health professional can tell you if you need to take larger amounts of vitamin D3.
    • This study suggests that a serum 25-hydroxy vitamin D level of 55-69 nmol/L is optimal, and higher levels provide no additional benefit. That means there is no need to take mega-doses of vitamin D3 unless directed by your health professional.

The Bottom Line 

A recent study looked at the effect of vitamin D status on muscle strength and performance in a healthy population with an average age of 69.

When they looked at handgrip strength:

  • Only 22% of the participants with an adequate vitamin D status had low handgrip strength.
  • 40% of participants who were vitamin D deficient had low handgrip strength. That’s almost a 2-fold difference.
  • Handgrip strength increased linearly with vitamin D status.

When they looked at muscle performance:

  • Only 8% of the participants with an adequate vitamin D status scored low on this test.
  • 25% of participants who were vitamin D deficient scored low on this test. That’s a 3-fold difference.
  • Muscle performance also increased linearly with vitamin D status.

The authors concluded: “Vitamin D deficiency was associated with impaired muscle strength and performance in a large study of community-dwelling older people. It is generally accepted that vitamin D deficiency should be reversed to prevent bone disease. This strategy may also protect skeletal muscle function in aging.”

If we look at the research more broadly, there are three factors that are essential for maintaining muscle mass as we age: exercise, protein, and vitamin D. Therefore, my recommendations are to:

1)  Aim for 25-30 grams of high-quality protein in each meal.

2) Aim for 150 minutes of moderate intensity exercise per week. At least half of that exercise should be resistance exercise.

3) Aim for an adequate vitamin D status (>50 nmol/L of serum 25-hydroxy vitamin D). A good place to start is with a multivitamin providing at least 800 IU of vitamin D3.

For more details on my recommendations and a discussion of why studies on vitamin D supplementation are often confusing, 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

 

Treating A Calf Cramp

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Stretching Your Calf

Author: Julie Donnelly, LMT – The Pain Relief Expert

Editor: Dr. Steve Chaney

Do you ever jump up at night with your calf screaming in pain?

Do cramps curl your toes and send shock waves all the way up your leg?

Have you ever been exercising, running, or cycling, and suddenly your calf cramped and stopped you in your tracks?

What Causes Calf Cramps?

The National Institute of Health (NIH) states that “the cause of leg cramps is unclear.”  Isn’t that encouraging!  There are just so many potential causes of calf cramps that it’s impossible to narrow it down. Some common causes are pregnancy, exercise, dehydration, insufficient levels of certain key nutrients, and electrolyte imbalances.

Electrolytes are minerals that have an electric charge.  You get them from the foods you eat and fluids you drink.

I’ve learned that the vitamins and minerals that impact cramps are: B1, B12, D, magnesium, potassium, and calcium.

I’m not a nutritionist so I’m not going to expound on nutritional causes, deficiencies, or solutions.  For that advice I suggest you go to a highly trained nutritionist for advice.  I’ve learned a lot by watching John McDougall, MD and T. Colin Campbell, PhD on YouTube.

However, my world is muscles, so that’s where I focus my attention in today’s article.

Muscle Contractions, Spasms, And Cramps

A little clarification of terms.  A contraction is when the entire length of a muscle fiber shortens. A spasm is when a small section of the muscle fiber ties up into what is sometimes thought of as a knot. A spasm happens slowly, so you rarely realize that the spasm is occurring. However, a cramp is when 100% of the muscle suddenly contracts 100% of the way and becomes as hard as a rock and feels like it is all knotted up.

There is a very complicated set of actions that enable us to do something as simple as picking up our cell phone and calling a friend.  You don’t need (or want) to know all the steps, so just suffice to say that each muscle fiber pulls with exactly the right power to make the movement we want to perform.

For example, let’s say you want to pick up a pen, maybe 10% of the fibers in your lower arm (that move your fingers) will contract.  But if you want to pick up a bowling ball, maybe 25% of your muscle fibers will contract.  If you then need to pick up your refrigerator, maybe 100% of your fibers will contract. (All numbers are guesses just to demonstrate a principle).

Regardless of whether you are contracting 10% or 90% of your muscle fibers, they will always contract 100% of the way.  Muscles don’t start to contract and then make a U-turn and stretch – and that’s the problem. The muscle will always contract 100% of the way before it will allow you to stretch it.

If you try to stretch while the muscle is contracting, you are potentially tearing the fibers. So, the idea is to help the muscle fibers complete the contraction, and then stretch.

Treating A Calf Cramp

I suggest you try this now when nothing is happening.  You sure don’t want to be trying to figure it out while your calf is cramping.

  • Cross your leg as shown in this picture
  • Grab both ends of the muscle and push them together as hard as you can.
  • Hold the squeeze until you are breathing normally.
  • Release, breathe normally for a minute, and repeat.

 

The second time isn’t going to hurt.  You’re only doing the second squeeze in case there are some muscles that didn’t finish the contraction, so you’re helping them along.

After the cramp has stopped, then you can safely stretch your calf muscles.

This really hurts!  But then, a cramp also really hurts!

Stretching Your Calf

There are two muscles of your calf that you will be stretching: the gastrocnemius and the soleus.

To stretch your gastrocnemius, as shown in the picture to the left, put one leg straight behind you, and bend your opposite knee.

 

Lean forward, bending the knee in the front while keeping your back foot planted on the floor.

 

You’ll feel a nice stretch in your calf as the gastrocnemius is being gently lengthened.

 

To stretch your soleus muscle, follow the picture on the right and bend your back leg, again keeping your foot planted on the floor, and straighten your forward leg.

 

Hold each stretch for about 15 seconds to allow the muscles to slowly lengthen.

 

 

Let Me Show You How You Can Treat Yourself

I’ve been teaching people how to self-treat since 1989.  As you know, I’ve written several books to show you how to self-treat to release tight muscles from your head to your feet, and I also have an MP4 program called the Julstro System that shows you how to release every muscle that causes the symptoms of carpal tunnel syndrome and trigger finger.

Did you know that I also do Zoom Consultations?  I work with people all over the world.  Zoom allows me to demonstrate to them what needs to be done, and then watch them to see if they are doing it correctly.

If you would like to work with me on a one-on-one basis from the comfort of your own home, just go to https://julstromethod.com/product/private-consultation/.  We’ll set up a date and you’ll be off to getting the relief you are seeking.

Wishing you well,

Julie Donnelly

www.FlexibleAthlete.com

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 Calcium Supplements Increase Deaths From Heart Valve Disease?

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What Did This Study Get Wrong?

Author: Dr. Stephen Chaney

Aortic Stenosis“Killer calcium” is back. Once again, we are seeing headlines saying that calcium supplementation increases our risk of dying from heart disease. If you have seen these headlines, you are probably confused.

After all, there have been three major clinical studies looking at the effect of calcium supplementation on heart disease risk. These studies followed close to 100,000 Americans for 10-20 years. And none of the studies found any increase in the risk of developing or dying from heart disease for people taking calcium supplements. For more information on this topic, see an article from “Health Tips From the Professor”.

You are probably wondering, “What is going on? I thought this issue was settled”.

In the first place, this study did not look at heart disease in general, but on a very specific form of heart valve disease called aortic stenosis. Aortic stenosis is a narrowing of the heart valve leading to the aorta. And it is often associated with calcification of the heart valve.

The cause of aortic stenosis is complex, but it is associated with:

  • Chronic inflammation.
  • High cholesterol levels.
  • Tobacco use.
  • Dysregulation of calcium metabolism caused by things like elevated parathyroid levels and end-stage kidney disease.
  • Elevated blood levels of calcium and/or vitamin D.

Because of the role of calcium and vitamin D in aortic stenosis, the current study (N Kassis et al, Heart, Epub ahead of print, 1-9, 2022) was designed to ask whether calcium and vitamin D supplementation influenced the risk of dying from aortic stenosis.

How Was This Study Done?

Heart Disease StudyThe Cleveland Clinic scanned their Echocardiography Database for patients aged 60 years or more who had been diagnosed with mild to moderate aortic stenosis. 2,657 patients met these criteria (average age = 74, 58% men) and were followed for an average of 59 months in their database.

In terms of calcium and vitamin D supplementation:

  • 49% did not supplement.
  • 12.5% supplemented with vitamin D (dose not defined).
  • 38.5% supplemented with calcium (500 – 2,000 mg/day) ± vitamin D.

The study looked at the correlation between vitamin D supplementation and calcium supplementation with:

  • Aortic valve replacement surgery.
  • All-cause mortality* with and without aortic valve replacement surgery.
  • Cardiovascular mortality* with and without aortic valve replacement surgery.

*Note: Since all the patients had aortic stenosis at the beginning of the study, both all-cause and cardiovascular mortality were primarily due to aortic stenosis.

Do Calcium Supplements Increase Deaths From Heart Valve Disease?

Before I describe the results of the study, there are two things you need to know:

  • Vitamin D supplementation did not have a significant effect on any outcome studied, so I will not mention vitamin D in the rest of this article.
  • In the calcium supplementing group, there were only a few people taking calcium supplements without vitamin D. However, their outcomes were the same as for people taking calcium + vitamin D supplements. Therefore, the authors discussed their results in terms of calcium supplementation, not calcium + vitamin D supplementation. I will do the same.

With those two things in mind, here is what the study found.

With respect to the need for aortic valve replacement surgery:

  • Calcium supplementation increased the need for surgery by 50%.

With respect to all-cause mortality:

  • Calcium supplementation increased the risk of death by 31%. When you divided the results into patients who did and did not have aortic valve replacement surgery within the 59-month follow-up of this study:
    • Those who received aortic valve replacement surgery did not have a statistically significant increase in risk of death.
    • Those who did not receive aortic valve replacement surgery had a 38% increased risk of death.

With respect to cardiovascular mortality:

  • Calcium supplementation doubled the risk of death. When you divided the results into patients who did and did not have aortic valve replacement surgery within the 59-month follow-up of this study:
    • Those who received aortic valve replacement surgery did not have a statistically significant increase in risk of death.
    • Those who did not receive aortic valve replacement surgery had a 205% increased risk of death.

The authors concluded, “Supplemental calcium … is associated with lower survival and greater AVR [aortic valve replacement surgery] in elderly patients with mild to moderate AV [aortic stenosis].”

What Did This Study Get Wrong?

thumbs down symbolLet me start by looking at the limitations of this study.

#1: This is a single study. It is a well-designed study, but it is only one study. And, as the authors acknowledge, previous studies have come down on both sides of this issue. Until we have more well-designed studies that come to the same conclusion, we cannot be confident this study is correct.

#2: The results of this study could have been significantly influenced by confounding variables.

For example:

  • End-stage kidney disease is associated with a dysregulation of calcium metabolism that can lead to aortic valve calcification. Patients in the calcium supplementation group had a 2-fold higher incidence of chronic kidney disease and a 10-fold higher incidence of kidney dialysis.
  • There were also significant differences in several diseases and drugs that influence the risk of developing aortic stenosis between the groups.

In the words of the authors, “Given the degree of clinical differences between the groups, there was a risk of residual confounding that may have impacted our findings; we attempted to mitigate this with our statistical model.”

However, as Mark Twain is quoted as saying, “There are lies. There are damn lies. And then there are statistics.”

That is a humorous way of saying we should not put too much faith in statistical manipulations of the data.

#3: They did not measure parathyroid levels. That is a serious omission because elevated parathyroid levels are a major driver of the type of dysfunctional calcium metabolism that could lead to calcification of the aortic valve.

#4: Serum calcium and vitamin D levels were slightly lower in the calcium supplementation group. This is unexpected because aortic stenosis is usually associated with higher serum calcium and vitamin D levels.

The authors speculated this might be due to transient increases in serum calcium levels following supplementation. This is possible for some calcium supplements, but not others.

Specifically, some calcium supplements are marketed on how quickly they get into the bloodstream. But those same supplements often do not provide all the nutrients needed for bone formation. There is always the possibility that excess calcium not used for bone formation might be deposited where we do not want it (such as in the aortic valve).

What Did This Study Get Right?

thumbs up#1: It was a larger, longer lasting study than previous studies on the effect of calcium supplementation on aortic stenosis. Even though it has limitations, we shouldn’t discount it. It might just be correct.

#2: It doesn’t necessarily conflict with the earlier studies showing that calcium supplementation doesn’t increase cardiovascular disease risk. That’s because the design of these studies is very different.

  • The health of the people studied was very different.
    • The earlier studies started with healthy adults and asked whether calcium supplementation increased their risk of developing cardiovascular disease.
    • This study started with people who already had a form of cardiovascular disease associated with abnormal calcium metabolism and asked whether calcium supplementation increased their risk of dying from the disease.
  • The age of the people studied was very different.
    • The earlier studies started with middle-aged adults and followed them for 10-20 years
    • This study started with people in their mid-70’s and followed them for almost 6 years.
  • The type of cardiovascular disease studied was different.
    • The earlier studies included all types of cardiovascular disease.
    • This study focused on a very minor type of cardiovascular disease, aortic stenosis. Aortic stenosis accounts for about 10% of all cardiovascular disease 17% of cardiovascular deaths. There may not have been enough deaths from aortic stenosis in the previous studies to have had a statistically significant effect on the results.

Given all these differences, the results of this study may not be incompatible with the results of previous studies

What Does This Study Mean For You?

There are three important takeaways from this and previous studies:

1) For most Americans calcium supplementation does not increase the risk of cardiovascular disease. That has been shown in three major clinical studies.

2) However, if you have been diagnosed with aortic stenosis, calcium supplementation may increase your risk of needing heart valve replacement or of dying from the disease. This study is not definitive, but I would advise caution.

You may wish to discuss with your doctor how to best balance:

    • The need for calcium supplementation to prevent osteoporosis…
    • With the need to limit calcium supplementation to prevent adverse outcomes from your aortic stenosis.

3) Finally, the authors did not discuss a very significant observation from this study, namely that heart valve replacement reduced the risk of dying from aortic stenosis in people taking calcium supplements.

Aortic valve replacement is the only proven treatment for aortic stenosis. If your doctor recommends aortic valve replacement, you should consider it.

The Bottom Line

A recent study looked at the effect of calcium supplementation for people with aortic stenosis, a rare form of heart disease.

The study found:

  • Calcium supplementation increased the need for aortic valve replacement surgery by 50%.
  • Calcium supplementation increased the risk of all-cause mortality* by 31%. When you divided the results into patients who did and did not have aortic valve replacement surgery during the study:
    • Those who received aortic valve replacement surgery did not have a statistically significant increase in risk of death.
  • Calcium supplementation doubled the risk of cardiovascular mortality*. When you divided the results into patients who did and did not have aortic valve replacement surgery within the 59-month follow-up of this study:
    • Those who received aortic valve replacement surgery did not have a statistically significant increase in risk of death.

*Note: Since all the patients enrolled in this study had aortic stenosis at the beginning of the study, these deaths were primarily due to aortic stenosis.

The authors concluded, “Supplemental calcium … is associated with lower survival and greater AVR [aortic valve replacement surgery] in elderly patients with mild to moderate AV [aortic stenosis].”

There are three important takeaways from this and previous studies:

1) For most Americans calcium supplementation does not increase the risk of cardiovascular disease. That has been shown in three major clinical studies.

2) However, if you have been diagnosed with aortic stenosis, calcium supplementation may increase your risk of needing heart valve replacement or of dying from the disease. This study is not definitive, but I would advise caution.

  • You may wish to discuss with your doctor how to best balance:
    • The need for calcium supplementation to prevent osteoporosis…
    • With the need to limit calcium supplementation to prevent adverse outcomes from your aortic stenosis.

3) Finally, the authors did not discuss a very significant observation from this study, namely that heart valve replacement reduced the risk of dying from aortic stenosis in people taking calcium supplements.

Aortic valve replacement is the only proven treatment for aortic stenosis. If your doctor recommends aortic valve replacement, you should consider it.

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.

The Truth About Soy And Breast Cancer

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Why Is There So Much Confusion About Soy?

Author: Dr. Stephen Chaney

soyWhat is the truth about soy and breast cancer? If you are a woman, particularly a woman with breast cancer, it is an important question.

Some experts say soy should be avoided at all costs. They say that soy will increase your risk of breast cancer. Other experts say soy is perfectly safe and may even reduce your risk of breast cancer. Who is right?

If you are a breast cancer survivor, the question of whether soy increases or decreases your risk of disease recurrence is even more crucial. You have already endured surgery, chemotherapy, and/or radiation. You never want to go through that again.

Why Is There So Much Confusion About Soy?

soy confusionSoy isoflavones decrease estrogen production, strengthen the immune system, inhibit cell proliferation, and reduce the production of reactive oxygen species. These are all effects that might reduce breast cancer risk.

On the other hand, soy isoflavones also bind to estrogen receptors and exhibit weak estrogenic activity. This effect has the potential to increase breast cancer risk.

Cell culture and animal studies have only confused the issue. Soy isoflavones stimulate the growth of breast cancer cells in a petri dish. Soy isoflavones also stimulate breast cancer growth in a special strain of mice lacking an immune system. However, in studies in both mice and rats with a functioning immune system, soy isoflavones decrease breast cancer risk.

The confusion has been amplified by claims and counterclaims on the internet. There are bloggers who are more interested in the spectacular than they are in accuracy (Today we call this fake news). They have taken the very weak evidence that soy isoflavones could possibly increase breast cancer risk and have blown it all out of proportion.

Their blogs claim that soy definitely increase breast cancer risk and should be avoided at all costs. Their claims have been picked up by other web sites and blogs. Eventually, the claims have been repeated so many times that people started to believe them. A “myth” was created. I call it a myth because it was never based on convincing scientific evidence.

In the meantime, scientists looked at the cell culture and animal studies and took a more responsible approach. They said “If this is true, it is an important public health issue. We need to do clinical trials in humans to test this hypothesis.”

What Have Previous Clinical Studies Shown?

breast cancerThe question of whether soy consumption increased the risk of developing breast cancer was settled a long time ago. Some studies have shown no effect of soy consumption on breast cancer risk. Others have reported that soy consumption decreased breast cancer risk. A meta-analysis of 18 previous clinical studies found that soy slightly decreased the risk of developing breast cancer (J Natl Cancer Inst, 98: 459-471, 2006). None of those studies found any evidence that soy increased the risk of breast cancer.

What about recurrence of breast cancer in women who are breast cancer survivors? Between 2006 and 2013 there have been five major clinical studies looking at the effects of soy consumption on breast cancer recurrence in both Chinese and American populations. Once again, the studies have shown either no effect of soy on breast cancer recurrence or a protective effect. None of them have shown any detrimental effects of soy consumption for breast cancer survivors.

A meta-analysis of all 5 studies was published in 2013 (Chi et al, Asian Pac J Cancer Prev., 14: 2407-2412, 2013). This study combined the data from 11,206 breast cancer survivors in the US and China. Those with the highest soy consumption had a 23% decrease in recurrence and a 15% decrease in mortality from breast cancer.

What Did The Latest Study Show?

Clinical StudyIn previous clinical studies the protective effect of soy has been greater in Asian populations than in North American populations. This could have been because Asians consume more soy. However, it could be due to other population differences as well. To better evaluate the effect of soy consumption on breast cancer survivors in the North America, a group of investigators correlated soy consumption with all-cause mortality in breast cancer survivors in the US and Canada (Zhang et al, Cancer, DOI: 10.1002/cncr.30615, March 2017).

The data were collected from The Breast Cancer Family Registry, an international research infrastructure establish in 1995. The women enrolled in this registry either have been recently diagnosed with breast cancer or have a family history of breast cancer.

This study included 6235 breast cancer survivors from the registry who lived in the San Francisco Bay area and the province of Ontario in Canada. The women represented an ethnically diverse population and had a median age of 51.8 at enrollment. Soy consumption was assessed either at the time of enrollment or immediately following breast cancer diagnosis. The women were followed for 9.4 years, during which time 1224 of them died.

The results were as follows:

  • There was a 21% decrease in all-cause mortality for women who had the highest soy consumption compared to those with the lowest soy consumption.
    • The protective effect of soy was strongest for those women who had receptor negative breast cancer. This is significant because receptor-negative breast cancer is associated with poorer survival rates than hormone receptor-positive cases.
    • The protective effect was also greatest (35% reduction in all-cause mortality) for women with the highest soy consumption following breast cancer diagnosis. This suggests that soy may play an important role in breast cancer survival.
  • The authors concluded “In this large, ethnically diverse cohort of women with breast cancer, higher dietary intake of [soy] was associated with reduced total mortality.”

In an accompanying editorial, Omer Kucuk, MD, of the Winship Cancer Institute of Emory University, noted that the United States is the number 1 soy producer in the world and is in a great position to initiate changes in health policy by encouraging soy intake.  He said “We now have evidence that soy foods not only prevent breast cancer but also benefit women who have had breast cancer. Therefore, we can recommend women to consume soy foods because of soy’s many health benefits.”

The Truth About Soy And Breast Cancer

Myth Versus FactsEvery clinical study has its limitations. If there were only one or two studies, the question of whether soy increases breast cancer risk might still be in doubt. However, multiple clinical studies have come to the same conclusion. Either soy has no effect on breast cancer risk and breast cancer recurrence, or it has a protective effect.

Not a single clinical study has found any evidence that soy increases breast cancer risk. It is clear that consumption of soy foods is safe, and may be beneficial, for women with breast cancer. The myth that soy increases breast cancer risk needs to be put to rest.

On the other hand, we should not think of soy as a miracle food. Breast cancer risk is also decreased by a diet that:

  • Contains lots of fruits and vegetables.
  • Is low in processed grains & sweets and high in whole grains.
  • Is low in saturated & trans fats and high in omega-3 and monounsaturated fats.
  • Is low in red & processed meats and high in beans, fish & chicken.

Furthermore, diet is just one component of a holistic approach for reducing the risk of breast cancer. In addition to a healthy diet, the American Cancer Society recommends that you:

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

The Bottom Line

1) It is time to put the myth that soy increases breast cancer risk to rest. This myth is based on cell culture and animal studies, and those studies were inconclusive.

2) Multiple clinical studies have shown that soy either has no effect on breast cancer risk, or that it reduces the risk.

3) Multiple clinical studies have also shown that soy either has no effect on breast cancer recurrence in women who are breast cancer survivors, or that it reduces recurrence.

4) The latest clinical study is fully consistent with previous studies. It reports:

    • There was a 21% decrease in all-cause mortality for women who had the highest soy consumption compared to those with the lowest soy consumption.
    • The protective effect of soy was strongest for those women who had receptor negative breast cancer. This is significant because receptor-negative breast cancer is associated with poorer survival rates than hormone receptor-positive cases.
    • The protective effect was also greatest (35% reduction in all-cause mortality) for women with the highest soy consumption following breast cancer diagnosis. This suggests that soy may play an important role in breast cancer survival.

5) No clinical studies have provided any evidence to support the claim that soy increases either breast cancer risk or breast cancer recurrence.

6) On the other hand, we should not think of soy as a miracle food. Breast cancer risk is also decreased by a diet that:

    • Contains lots of fruits and vegetables.
    • Is low in processed grains & sweets and high in whole grains.
    • Is low in saturated & trans fats and high in omega-3 and monounsaturated fats.
    • Is low in red & processed meats and high in beans, fish & chicken

7) Finally, diet is just one component of a holistic approach for reducing the risk of breast cancer. In addition to a healthy diet, the American Cancer Society recommends that you:

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

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.

Omega-3s And Congestive Heart Failure

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We Have Been Asking The Wrong Questions 

Author: Dr. Stephen Chaney

Confusion Clinical StudiesToday’s Health Tip is a follow-up to the article I published last month on omega-3s and heart disease risk. In that article I pointed out the reasons why studies of the effect of omega-3s and heart disease risk have been so confusing.

One of the reasons is that many of the studies have been asking the wrong questions.

  • They were asking whether omega-3s reduced the risk of heart disease for everyone. Instead, they should have been asking who benefited from omega-3 supplementation.
  • They were asking whether omega-3s reduced the risk of all forms of heart disease combined. Instead, they should have been asking whether omega-3s reduced the risk of specific kinds of heart disease.

I also discussed a large clinical trial, the VITAL study, that was designed to answer those two questions.

The study I will describe today (L Djoussé et al, JACC Heart Failure, 10: 227-234, 2022) mined the data from the VITAL study to evaluate the effect of omega-3 supplementation on congestive heart failure, a form of heart disease that was not discussed in the VITAL study.

Everything You Need To Know About Congestive Heart Failure

Congestive Heart FailureCongestive heart failure is a killer. The term congestive heart failure simply means that your heart no longer pumps blood well. The initial symptoms are relatively non-specific and include things like.

  • Shortness of breath.
  • Fatigue and weakness.
  • Reduced ability to exercise.
  • Rapid or irregular heartbeat.
  • Persistent cough or wheezing.

However, as it progresses, the symptoms get much worse. Fluid builds up in your tissues.

  • Fluid buildup in your legs, ankles, and feet can make it difficult to walk.
  • Fluid buildup in your lungs makes it difficult to breathe. In advanced stages it can feel like you are drowning in a room full of air.

According to the CDC:

  • 4 million Americans have congestive heart failure (CHF).
    • It leads to ~380,000 deaths/year.
  • 83% of patients diagnosed with CHF will be hospitalized at least once.
    • 67% will be hospitalized two or more times.
  • CHF costs >$30 billion per year in health care costs and lost wages.

The risk of congestive heart failure is not spread evenly across the American population. Black Americans and Americans with type 2 diabetes are at increased risk.

According to the Framingham Heart Study:

  • Type 2 diabetes increases the risk of CHF 2-fold in men and 5-fold in women. The reasons are not entirely clear. However:
    • High blood sugar is thought to either damage cells in heart muscle, weakening it, or damage small blood vessels within the heart, making it more difficult for the heart to pump blood.
    • Some diabetes drugs that lower blood sugar also appear to increase the risk of congestive heart failure.

According to the CDC:

  • Black Americans are 2-fold more likely to develop CHF than White Americans. Again, the reasons are not clear. However:
    • Some experts feel it could be due to the higher incidence of untreated high blood pressure in Black Americans.

In summary:

  • Congestive heart failure is a serious disease. Its symptoms affect your quality of life, and it can lead to hospitalizations and death.
  • Black Americans and Americans with type 2 diabetes are at higher risk of developing congestive heart failure.

How Was The Study Done?

The VITAL study, from which these data were extracted, was a placebo-controlled clinical trial designed to measure the effects of 1,000 mg omega-3 supplementation on the risk of developing heart disease. It enrolled 25,871 Americans aged 55 years or older and followed them for an average of 5.3 years.

The participants enrolled in the VITAL study represented a cross-section of the American population. Most were at low risk of heart disease, but there were subsets of the study group who were at higher risk of heart disease. A strength of the VITAL study was that it was designed so the high-risk subgroups could be evaluated separately.

The current study utilized data from the VITAL study to look at the effect of omega-3 supplementation on hospitalizations due to congestive heart failure. It also evaluated the effect of type 2 diabetes and race on the risk of hospitalizations.

Omega-3s And Congestive Heart Failure

Omega-3s And Heart DiseaseWhen the investigators looked at the whole population, most of whom were at low-risk of congestive heart failure, they did not see any effect of omega-3 supplementation on the risk of hospitalizations due to congestive heart failure.

However, when they looked at high risk groups, the story was much different.

In patients with type-2 diabetes:

  • Omega-3 supplementation reduced the risk of the initial hospitalization for congestive heart failure by 31%
  • Omega-3 supplementation reduced the risk of multiple hospitalizations due to congestive heart failure by 47%.

The effect of omega-3 supplementation on hospitalizations was greatest for the Black participants in the study.

In the words of the authors, “Our data show beneficial effects of omega-3 fatty acid supplements on the incidence of heart failure hospitalizations in participants with type 2 diabetes but not in those without type 2 diabetes, and such benefit appeared to be stronger in Black participants with type 2 diabetes.”

We Are Asking The Wrong Questions

ScientistAs I said above, there is so much confusion about the effect of omega-3s on heart disease because we scientists have been asking the wrong questions:

  • We have been asking whether omega-3s reduce the risk of heart disease for everyone. Instead, we should have been asking who benefits from omega-3 supplementation.
  • We have been asking whether omega-3s reduced the risk of all forms of heart disease combined. Instead, we should have been asking whether omega-3s reduced the risk of specific kinds of heart disease.

In my “Health Tip” last month I discussed a large clinical study, the VITAL study, that was specifically designed to answer the right questions. Like so many other studies it found that omega-3 supplementation did not significantly reduce the risk of all kinds of heart disease for everyone.

However, what it did find was more important than what it did not find:

  • When they looked at the effect of omega-3s on heart disease risk in high-risk groups, they found that major cardiovascular events were reduced by:
    • 26% in African Americans.
    • 26% in patients with type 2 diabetes.
    • 17% in patients with a family history of heart disease.
    • 19% in patients with two or more risk factors of heart disease.
  • When they looked at the effect of omega-3s on heart disease risk in people with low omega-3 intake, they found that omega-3 supplementation reduced major cardiovascular events by:
    • 19% in patients with low fish intake.
  • When they looked at the effect of omega-3s on the risk of different forms of heart disease, they found that omega-3 supplementation reduced:
    • Heart attacks by 28% in the general population and by 70% for African Americans.
    • Deaths from heart attacks by 50%.
    • Deaths from coronary heart disease (primarily heart attacks and ischemic strokes (strokes caused by blood clots)) by 24%.

In other words, when they asked the wrong questions, they got the wrong answer. If they had just looked at the effect of omega-3 supplementation on all forms of heart disease for everyone (like most other omega-3 studies), they would have concluded that omega-3s are worthless.

However, when they asked the right questions, they found that omega-3s were very beneficial for high-risk populations and for certain types of heart disease.

The current study utilized the same data to analyze the effect of omega-3 supplementation on hospitalizations due to congestive heart failure. And the results were similar.

If they had asked the wrong question, “Does omega-3 supplementation reduce congestive heart failure hospitalizations for everyone?”, they would have concluded that omega-3 supplementation was worthless.

However, instead they asked, “Does omega-3 supplementation reduce congestive heart failure hospitalizations for certain high-risk groups” and were able to show that omega-3 supplementation significantly reduced congestive heart failure hospitalizations for people with type 2 diabetes and for Blacks.

We need to change the paradigm for clinical studies of supplements. The old paradigm asks the wrong questions. If we really want to know the role of supplementation for our health, we need to start asking the right questions.

The Bottom Line

There is perhaps nothing more confusing to the average person than the “truth” about omega-3 supplementation and heart disease risk. Much of the confusion is because we have been asking the wrong questions:

  • We have been asking whether omega-3 supplementation reduces the risk of heart disease for everyone. Instead, we should have been asking who benefits from omega-3 supplementation.
  • We have been asking whether omega-3 supplementation reduces the risk of all forms of heart disease combined. Instead, we should have been asking whether omega-3 supplementation reduces the risk of specific kinds of heart disease.

A recent study on the effect of omega-3 supplementation on hospitalizations due to heart disease is a perfect example.

If they had asked the wrong question, “Does omega-3 supplementation reduce congestive heart failure hospitalizations for everyone?”, they would have concluded that omega-3 supplementation was worthless.

However, instead they asked, “Does omega-3 supplementation reduce congestive heart failure hospitalizations for certain high-risk groups” and were able to show that omega-3 supplementation significantly reduced congestive heart failure hospitalizations for people with type 2 diabetes and for Blacks.

We need to change the paradigm for clinical studies of supplements. The old paradigm asks the wrong questions. If we really want to know the role of supplementation for our health, we need to start asking the right questions.

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.

Can Diet Add Years To Your Life?

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Which Foods Have The Biggest Effect On Longevity? 

Author: Dr. Stephen Chaney

Fountain Of YouthEveryone over 50 is searching for the elusive “Fountain Of Youth”.

  • We want to look younger.
  • We want to feel younger.
  • We want the energy we had in our 20s.
  • We want to be rid of the diseases of aging.

The list goes on!

But how do we do that? Pills and potions abound that claim to reverse the aging process. Most just reverse your wallet.

  • Should we train for marathons or bodybuilding contests?
  • Should we meditate or do yoga to relieve stress?
  • Should we get serious about losing weight?
  • Should we get more sleep?
  • Is there some miracle diet that can slow the aging process?

All the above probably slow the aging process, but the evidence is best for the effect of diet on aging. Several recent meta-analyses have looked at the effect of diet on the risk of premature deaths. In this issue of “Health Tips From the Professor” I review a study (LT Fadnes et al, PLoS Medicine, February 8, 2022) that combines the best of these meta-analyses into a single database and provides a provocative insight into the effect of diet on longevity.

How Was This Study Done?

Clinical StudyThis study combined data from recent meta-analyses looking at the impact of various food groups on the risk of premature deaths with the Global Burden of Disease Study which provides population-level estimates of life years lost due to dietary risk factors.

The authors then developed a new algorithm that allowed them to estimate how different diets affect sex- and age-specific life expectancy.

They divided the population into three different diet categories based on their intake of whole grains, vegetables, fruits, nuts, legumes, fish, eggs, dairy, refined grains, red meat, processed meat, white meat, sugar-sweetened beverages, and added plant oils. The diet categories were:

  • Typical Western Diet (TW). This diet was based on average consumption data from the United States and Europe. This was their baseline.
  • Optimal diet (OD). This diet is similar to a vegan or semi-vegetarian diet. However, it was not a purely vegan diet nor a purely semi-vegetarian diet. Instead, it represented the best diet people in this study were consuming.
  • Feasibility diet (FA). This diet recognizes that few people are willing to make the kind of changes required to attain an optimal diet. It is halfway between the Typical Western Diet and the Optimal Diet.

To help you understand these diets based on the foods the study participants were eating, here are the comparisons in terms of daily servings:

Food TW Diet FA Diet OD Diet
Whole grains 1.5 servings 4.3 servings 7 servings
Vegetables 3 servings 4 servings 5 servings
Fruits 2.5 servings 3.75 servings 5 servings
Nuts 0 serving* 0.5 serving* 1 serving*
Legumes 0 serving** 0.5 serving** 1 serving**
Fish 0.25 serving 0.5 serving 1 serving
Eggs 1 egg 0.75 egg 0.5 egg
Dairy 1.5 servings 1.25 servings 1 serving
Refined grains 3 servings 2 servings 1 serving
Red meat 1 serving 0.5 serving 0 serving
Processed meat 2 servings 1 serving 0 serving
White meat 0.75 serving 0.6 serving 0 serving
Sugar-sweetened beverages 17 oz 8.5 oz 0 oz
Added plant oils 2 tsp 2 tsp 2 tsp

*1 serving = 1 handful of nuts

**1 serving = 1 cup of beans, lentils, or peas

Using their algorithm, the authors asked what the effect on longevity would be if people changed from a typical western diet to one of the other diets at age 20, 60, or 80 and maintained the new diet for at least 10 years. The 10-year requirement is based on previous studies showing that it takes around 10 years for dietary changes to affect the major killer diseases like heart disease, cancer, or diabetes.

Finally, the authors improved the accuracy of their estimates of the effect of diet on longevity by taking into account the quality of each study included in their analysis. I will discuss the importance of this below.

Can Diet Add Years To Your Life?

The results were impressive.

The authors estimated that if people in the United States were to change from a typical western diet to an “optimal diet” and maintain it for at least 10 years,

…starting at age 20, men would live 13 years longer and women would live 10.7 years longer.

…starting at age 60, men would live 8.8 years longer and women would live 8 years longer.

…starting at age 80, both men and women would live 3.4 years longer.

But what if you weren’t a vegan purist? What if you only made half the changes you would need to make to optimize your diet? The news was still good.

The authors estimated that people in the United States were to change from a typical western diet to a “feasibility diet” and maintain it for at least 10 years,

…starting at age 20, men would live 7.3 years longer and women would live 6.2 years longer.

…starting at age 60, men would live 4.8 years longer and women would live 4.5 years longer.

…starting at age 80, both men and women would live ~2 years longer.

The authors concluded, “A sustained dietary change may give substantial health gains for people of all ages for both optimized and feasible [diet] changes. [These health gains] could translate into an increase in life expectancy of more than 10 years. Gains are predicted to be larger the earlier the dietary changes are initiated in life.”

Which Foods Have The Biggest Effect On Longevity?

The algorithm the authors developed also allowed them to look at which foods have the biggest effect on longevity. The authors estimated when changing from a typical western diet to an optimal diet, the greatest gains in longevity were made by eating:

  • More legumes, whole grains, and nuts, and…
  • Less red and processed meat.

The authors concluded, “An increase in the intake of legumes, whole grains, and nuts, and a reduction in the intake of red meat and processed meats, contributed most to these gains [in longevity].”

However, this conclusion needs to be interpreted with caution. We also need to recognize that an “optimal diet” was defined as the best diet people in this study were eating. In addition, the effect of different foods on longevity depends on:

  • The quality of the individual studies with that food, and…
  • The difference in consumption of that food in going from a western diet to an optimal diet.

For example:

  • Legumes, whole grains, nuts, red & processed meat made the list because the quality of data was high and the difference in consumption between the typical western diet and optimal diet was significant.
  • The quality of data for an effect of fruits and vegetables was also high. For example, one major study concluded that consuming 10 servings a day of fruits and vegetables a day reduces premature death by 31% compared to consumption of less than 1 serving a day. However, the difference in consumption of fruits and vegetables between the western and optimal diets in this study was small, so fruits and vegetables didn’t make the list.
  • Eggs and white meat didn’t make the list because the quality of data was low for those foods. Simply put,  that means that there was a large variation in effect of those foods on longevity between studies.
  • Other foods didn’t make the list because the quality of data was only moderate and/or the difference in intake was small.

So, the best way to interpret this these data is:

  • This study suggests that consuming more legumes, whole grains, and nuts and less red & processed meats has a significant beneficial effect on health and longevity.
  • Consuming more fruits and vegetables is likely to have a significant benefit on health and longevity, but you would need to consume more than people did in this study to achieve these benefits. In the words of the authors, “Fruits and vegetables also have a positive health impact, but, for these food groups, the intake in a typical Western diet is closer to the optimal intake than for the other food groups.”
  • Other foods may impact health and longevity, but the data in this study are not good enough to be confident of an effect.

What Does This Study Mean For You?

This study is the best of many studies showing the benefit of a more plant-based diet on health and longevity. It particularly encouraging because it shows:

  • You can achieve significant benefit by switching to a more plant-based diet late in life. You get the biggest “bang for your buck” if you switch at age 20. But even making the switch at age 60 or 80 was beneficial.
  • You don’t need to be a “vegan purist”. While the biggest benefits were seen for people who came close to achieving a vegan or semi-vegetarian diet, people who only made half those changes saw significant benefits.

As I said above, this is a very strong study. However, the underlying data come from association studies, which can have confounding variables that influence the results.holistic approach

For example, people who eat more plant-based diets tend to weigh less and exercise more. And both of those variables can influence longevity. Each study attempted to statistically correct for those variables, but they still might have a slight influence on the results.

However, I don’t see that as a problem because, in my view, a holistic approach is always best. As illustrated on the right, we should be seeking a lifestyle that includes a healthy diet, weight control, and exercise.

As for supplementation, both the vegan and semi-vegetarian diets tend to leave out whole food groups. Unless you are married to a dietitian, that means your diet is likely to be missing important nutrients.

The Bottom Line

A recent study asked whether changing from the typical western diet to a healthier, more plant-based diet could influence longevity. The results were very encouraging. The study showed that:

  • Changing to a healthier diet could add up to a decade to your lifespan.
  • The improvement in lifespan was greatest for those whose diets approached a vegan or semi-vegetarian diet, but a significant improvement in lifespan was seen for people who made only half those dietary improvements.
  • The improvement in lifespan was greatest for those who switched to a healthier diet in their 20’s, but significant improvements in lifespan were seen for people who didn’t change their diet until their 60’s or 80’s.

In terms of the foods that have the biggest effect on longevity.

  • This study suggests that consuming more legumes, whole grains, and nuts and less red & processed meats has a significant beneficial effect on health and longevity.
  • Consuming more fruits and vegetables is likely to have a significant benefit on health and longevity, but you would need to consume more than people did in this study to achieve those benefits.
  • Other foods may impact health and longevity, but the data in this study are not good enough to be confident of an effect.

The authors concluded, “A sustained dietary change may give substantial health gains for people of all ages for both optimized and feasible [diet] changes. [These health gains] could translate into an increase in life expectancy of more than 10 years. Gains are predicted to be larger the earlier the dietary changes are initiated in life.

An increase in the intake of legumes, whole grains, and nuts, and a reduction in the intake of red meat and processed meats, contributed most to these gains. Fruits and vegetables also have a positive health impact, but, for these food groups, the intake in a typical Western diet is closer to the optimal intake than for the other food groups.”

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

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

Health Tips From The Professor