Dr. Steve Chaney

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.

Do Whole Grains Reduce Inflammation?

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Are Low Carb Diets Healthy Long Term?

Author: Dr. Stephen Chaney 

InflammationInflammation is a bit like Dr. Jekyll and Mr. Hyde. Acute inflammation plays a valuable role in our immune response. But chronic inflammation is a scourge. Chronic inflammation:

  • Is a key component of all the “itis” diseases.
  • Can lead to autoimmune diseases.
  • Is thought to play an important role in heart disease.
  • Is associated with many other diseases, such as diabetes, cancer, Alzheimer’s disease, and inflammatory bowel diseases (IBS).

While there are many causes of chronic inflammation, diet plays an important role. In a previous issue of “Health Tips From the Professor” I have described how an anti-inflammatory diet can quell the fires of chronic inflammation.

Fiber from unprocessed plant foods is a key component of an anti-inflammatory diet. But are all plant fibers equally effective at reducing inflammation? Here is what we know:

  • Fiber from whole grains, vegetables, and fruits have different chemical and physical characteristics and support the growth of different species of friendly bacteria in our intestines.
  • Previous studies have shown that higher intakes of dietary fiber are associated with lower risk of heart disease.
    • Studies have suggested that fiber from whole grains may be more effective than fiber from fruits and vegetables at reducing heart disease risk.
  • Chronic inflammation is highly associated with the development of heart disease. This has led to the hypothesis that fiber from whole grains may be more effective than other plant fibers at reducing chronic inflammation.
    • Some studies have supported this hypothesis, but they have all been done with middle-aged participants, not with elderly participants who characteristically have higher levels of inflammation.

The study (R Shivakoti et al, JAMA Network Open, 5(3): e225012, 2022) I will describe today was designed to:

  • Test the hypothesis that whole grain fiber is more effective than vegetable or fruit fiber at reducing inflammation.
  • Determine how important reducing inflammation is at reducing the risk of heart disease.
  • Extending these findings to an older population group.

How Was The Study Done?

Clinical StudyThe data for this study was obtained from the Cardiovascular Health Study (CHS), a study designed to characterize factors influencing cardiovascular health in American adults aged 65 years or older. This study analyzed data from 4,125 participants (40% men, 95% white) who enrolled in the CHS study from 1989 to 1990.

These participants did not have heart disease at the time they were enrolled in the study. They had an average age of 72.6 at the beginning of the study and were followed for an average of 11.9 years. During that time 1,941 (47%) of them developed heart disease.

When the participants were enrolled in the study:

  • A food frequency questionnaire was administered to them by a trained dietitian to assess their long-term usual dietary intake. This information was used to assess:
    • Their total fiber intake and…
    • Their fiber intake from various dietary sources (whole grains, vegetables, and fruits).
  • Fasting blood samples were collected and used to analyze various markers of inflammation.

A follow-up via phone was conducted every 6 months to track an initial diagnosis of cardiovascular disease.

At the end of the study, the investigators analyzed:

  • The effect of total fiber and fiber from different food sources on the risk of developing heart disease.
  • The effect of total fiber and fiber from different food sources on inflammatory markers in the blood.
  • The extent to which decreased inflammation could explain the effect of whole grain fiber on reducing heart disease.

Do Whole Grains Reduce Inflammation?

With respect to inflammation:

  • Increased intake of total fiber was associated with healthier levels of the inflammatory markers CRP, IL-1RA, and sCD163.
    • Increased intake of fiber from whole grains was associated with healthier levels of the inflammatory markers CRP, IL-6, and IL-1RA.
    • Increased intake of vegetable fiber was not significantly associated with healthier levels of any inflammatory marker.
    • Increased intake of fiber from fruits was associated with healthier levels of the inflammatory marker sCD163.

With respect to cardiovascular disease:

  • Every 5g/day increase in total fiber decreased the risk of heart disease by 5%.
    • Every 5g/day increase in fiber from whole grains decreased the risk of heart disease by 14%.
    • Increased intake of fiber from vegetables and fruits did not have a statistically significant effect on the risk of heart disease.

Finally, when the investigators did a statistical analysis to determine to extent to which the effect of whole grain fiber on inflammation, could explain its effect on heart disease, they concluded:

  • The effect of whole grain fiber on inflammation could explain only about 16% of its effect on heart disease.

In the words of the authors, “In this prospective study of older adults, higher intakes of total fiber were associated with lower levels of various inflammatory markers, and this inverse association was primarily due to cereal fiber intake. Vegetable and fruit fiber intakes were not consistently associated with lower levels of inflammatory markers. These results suggest that specifically cereal fibers might be more effective in reducing systemic infection, which will need to be tested in interventional studies of specific populations.

In addition, cereal fiber was associated with a lower risk of CVD, although inflammation mediated less than 20% of the observed inverse association between cereal fiber and CVD. This suggests that the association of cereal fiber is primarily due to factors … other than systemic inflammation.”

Note: This conclusion underplays the role of fruit fiber in reducing inflammation. The statement is correct in saying only whole grain fiber reduces the inflammatory markers CRP, IL-6, and IL-1RA. However, both total fiber and fruit fiber increase the anti-inflammatory marker sCD163. That is why I chose to use the term “healthier levels” rather than lower or higher levels when describing the effects of whole grain and fruit fibers on markers of inflammation.

What Does This Study Mean For You?

confusion#1: The biggest takeaway from this study is that whole grains are good for you.

  • This study shows that whole grain fiber decreases our risk of developing heart disease.
    • This is fully consistent with multiple previous studies showing that whole grains decrease the risk of heart disease.
    • Previous studies have also shown that whole grains reduce the risk of cancer and diabetes.
  • This study also suggests that whole grain fiber reduces chronic inflammation.

There are also some takeaways from this and previous studies that may not be so obvious.

#2: Fiber has many important benefits beyond its effect on inflammation. For example:

  • This study concluded that the reduction in inflammation only explained a small part of the beneficial effect of whole grain fiber on reducing heart disease risk.
  • That is because whole grain fiber also:
    • Feeds friendly bacteria that improve gut function.
    • Provides satiety that can result in reduced fat and calorie intake.
    • Binds cholesterol, which improves blood cholesterol level.
    • Slows the rate at which dietary sugar enters the bloodstream, which improves blood sugar control.

#3: Whole plant foods have many benefits beyond their fiber content.

  • This study concluded that whole grain fiber was more beneficial than fiber from fruits and vegetables at reducing inflammation and reducing the risk of heart disease.
  • Previous studies have also shown that fruit and vegetables significantly decrease the risk of heart disease, stroke, and cancer.
  • That is because whole grains and unprocessed fruits and vegetables:
    • Displace sugar, refined flour, and highly processed foods from the diet.
    • Have a lower caloric density than processed foods, making it easier to achieve a healthy weight.
    • Provide nutrients and phytonutrients not found in processed foods.
    • Support a wide variety of healthy gut bacteria.

Are Low Carb Diets Healthy Long Term?

low carb dietconfusionWhen you consider all the benefits of whole grains, fresh fruits, and vegetables, it brings us to the final take home message.

#4: Despite what Dr. Strangelove has told you, low-carb diets may not be healthy long term.

  • There are no long-term (10 or 20-year) studies of low-carb diets. We simply have no evidence to support the claim that they are healthy long term.
  • Most low-carb diets eliminate or severely limit fruits and whole grains. Considering the many health benefits they provide, it is unlikely that any diet that restricts them is healthy long term.

The Bottom Line 

A recent study looked at the effect of plant fiber on inflammation and on heart disease.

With respect to inflammation the study found:

  • Increased intake of total fiber was associated with healthier levels of the inflammatory markers CRP, IL-1RA, and sCD163.
    • Increased intake of fiber from whole grains was associated with healthier levels of the inflammatory markers CRP, IL-6, and IL-1RA.
    • Increased intake of vegetable fiber was not significantly associated with healthier levels of any inflammatory marker.
    • Increased intake of fiber from fruits was associated with healthier levels of the inflammatory marker sCD163.

With respect to cardiovascular disease:

  • Every 5g/day increase in total fiber decreased the risk of heart disease by 5%.
  • Every 5g/day increase in fiber from whole grains decreased the risk of heart disease by 14%.
    1. The biggest takeaway from this study is that whole grains are good for you.

 Other takeaways from this and previous studies are:

2) Fiber has many important benefits beyond its effect on inflammation.

3) Whole plant foods have many benefits beyond their fiber content.

4) Despite what Dr. Strangelove has told you, low-carb diets may not be healthy long term.

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

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

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.

Do High Protein Diets Reduce Testosterone?

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What Does This Study Mean For You?

Author: Dr. Stephen Chaney

protein foodsLow carb diets are all the rage. Everywhere you turn you see articles proclaiming how healthy they are.

When you remove carbohydrates from the diet, you need to replace them with something. So, many of these diets are high in protein. And many people are choosing the high protein versions of low carb diets. For example:

  • High protein, low carb diets have become popular for weight loss.
  • And in our society, high protein diets are considered a good thing. We associate protein consumption with strength, energy, and virility. So, many athletes also include high protein, low carb diets as part of their training regimen.

Are high protein, low carb diets the best choice? Perhaps not, if the latest study is correct. This study (J Whittaker and M Harris, Nutrition And Health, 1-12, March 2022) claims that high protein, low carb diets decrease testosterone levels.

So, you are probably wondering, “Is this claim accurate?” To answer this question, I will evaluate the study and put it into perspective for you.

How Was This Study Done?

Clinical StudyThis study was a meta-analysis of 27 studies with a total of 309 participants looking at the effect of low carb diets on cortisol and testosterone levels. The participants were young (average age = 27.3), healthy, non-obese (BMI = 24.8), active males.

The selection criteria for studies included in the meta-analysis were:

  • Measurements of resting and post-exercise cortisol and testosterone levels. For simplicity, I will focus only on the testosterone results for this discussion.
  • Young, healthy male participants to minimize variation in steroid hormone metabolism due to age, sex, or disease.
  • Comparison of a low carb and high carb diets. The low carb and high carb diets averaged 18% and 58% carbohydrate, respectively.
  • Elimination of studies containing confounding variables that might affect steroid hormone metabolism such as:
    • Weight change of more than 6 pounds
    • Use of hormones, phytoestrogens, or medications.

In analyzing the data, they also compared:

  • Duration of <3 weeks or longer duration because it takes about 3 weeks for the body to fully adapt to ketone body utilization.
  • Moderate protein (average intake = 23.1% of calories) versus high protein (average intake = 48.8% of calories) intake. [Note: For comparison, the average protein intake for adults in this country is ~16%, with some experts recommending 17-21% to prevent weight loss as we age.]

Do High Protein Diets Reduce Testosterone?

Question MarkThis study looked at the effect of low carb diets on both resting and post-exercise testosterone levels.

  • Moderate protein, low carb diets had no consistent effect on either resting or post-exercise testosterone levels.
  • However, high protein, low carb diets reduced both resting and post-exercise testosterone levels.
    • The effect on resting testosterone was highly significant. High-protein, low carb diets caused a 37% decrease in resting testosterone levels.
    • The effect on post-exercise testosterone was smaller, but still significant.

In the words of the authors, “High-protein, low carb diets greatly decreased resting and post-exercise total testosterone…Individuals consuming such diets may need to be cautious about adverse endocrine effects.”

Is There A Good Metabolic Rationale For These Results?

ProfessorAs a biochemist, I always like to look at the metabolic rationale for the results. And there is a good metabolic rationale for the effect of high protein diets on testosterone levels:

  • When protein is metabolized ammonia is released, and excess ammonia is toxic.
  • To combat ammonia toxicity the body has a metabolic pathway called the urea cycle. It removes ammonia from the bloodstream and converts it to urea, which is excreted in the urine.
  • The ability of the urea cycle to remove ammonia from the bloodstream is limited. High protein intakes can overwhelm the ability of the urea cycle to remove ammonia. This typically occurs when protein intake exceeds 35% of calories.
    • In situations like this, the body produces cortisol, and cortisol upregulates the urea cycle so it can handle the excess ammonia.
    • For reasons that aren’t entirely clear, cortisol and testosterone are regulated oppositely. Whenever cortisol goes up, testosterone goes down.

To be clear, I am not saying this is what is happening. I am merely saying this is a plausible mechanism for explaining the fall in testosterone levels on a high protein diet, and many popular low carb diets are also high protein diets.

What Does This Study Mean For You?

questionsLast week I expressed skepticism about a recent study that had excellent experimental design but did not have a plausible metabolic rationale.

This week’s study is the opposite. It has an excellent metabolic rationale, but the study is weak. Specifically, several of the individual studies included in this meta-analysis are weak.

The authors considered this as a hypothesis-generating study. The authors went on to say this study shows where we should focus our attention in future studies, namely on the possible health consequences of high protein, low carb diets.

I agree. I am not ready to tell you unequivocally that high protein, low carb diets will lower your testosterone levels. However, if you are consuming a high protein, low carb diet for either weight loss or because you are a body builder or weightlifter, this study is a potential red flag. It is not a definitive study, but the results are metabolically plausible. They might just be true.

You should also keep in mind that all the “benefits” of high protein, low carb diets are based on short-term studies. There are no long-term studies on the benefits and risks of high protein, low carb diets. There is also no historical precedent for life-long adherence to a high protein, low carb diet.

  • We are omnivores. Our ancestors ate whatever nature provided. There were times when our paleolithic ancestors ate high protein, low carb meals, but it is unlikely any of them had the luxury of eating that way for a lifetime. That is a 21st century luxury.
  • If you plan to consume a high protein, low carb diet for an extended period of time, you are part of an uncontrolled experiment with an uncertain outcome.

In case you were wondering whether this applies to any high protein (>35% of calories from protein), diet which exceeds the ability of the urea cyclic to remove a toxic byproduct of protein metabolism, the answer is “We don’t know”. However, the typical American diet is around 55% carbohydrate and 20-35% fat. It would be extremely difficult to exceed 35% protein without significantly reducing carbohydrate intake. 

The Bottom Line

A recent study looked at the effect of high protein, low carb diets on testosterone levels. It found:

  • Moderate protein, low carb diets had no consistent effect on either resting or post-exercise testosterone levels.
  • However, high protein, low carb diets reduced both resting and post-exercise testosterone levels.
    • The effect on resting testosterone was highly significant. High-protein, low carb diets caused a 37% decrease in resting testosterone levels.
    • The effect on post-exercise testosterone was smaller, but still significant.

In the words of the authors, “High-protein, low carb diets greatly decreased resting and post-exercise total testosterone…Individuals consuming such diets may need to be cautious about adverse endocrine effects.”

I am not ready to tell you unequivocally that high protein, low carb diets will lower your testosterone levels.

However, if you are consuming a high protein, low carb diet for either weight loss or because you are a body builder or weightlifter, this study is a potential red flag. It is not a definitive study, but the results are metabolically plausible. They might just be true.

You should also keep in mind that all the “benefits” of high protein, low carb diets are based on short-term studies. There are no long-term studies on the benefits and risks of high protein, low carb diets. There is also no historical precedent for life-long adherence to a high protein, low carb diet.

If you plan to consume a high protein, low carb diet for an extended period of time, you are part of an uncontrolled experiment with an uncertain outcome.

For more details, read the article above.

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

 

Does Red Meat Cause Frailty In Older Women?

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Which Proteins Are Best?

Author: Dr. Stephen Chaney

Fatty SteakThe ads from the meat lobby say, “Red meat does a body good”. Are the ads true?

If we consider the health consequences of regularly eating red meat, the answer appears to be a clear, “No”. Multiple studies have shown a link between red meat consumption and:

  • Coronary heart disease.
  • Stroke
  • Type 2 diabetes.
  • Colon cancer, prostate cancer, and breast cancer.

And, if we consider the environmental consequences of red meat production, the answer also appears to be, “No”. I have discussed this in a recent issue of “Health Tips From the Professor”.

But what about muscle mass and strength? Red meat is a rich source of protein, and we associate meat consumption with an increase in muscle mass. Surely, red meat consumption must help us build muscle mass and strength when we are young and preserve muscle mass and strength as we age.

This is why the recent headlines claiming that red meat consumption increases the risk of frailty in older women were so confusing. I, like you, found those headlines to be counterintuitive. So, I have investigated the study (EA Struijk et al, Journal of Cachexia, Sarcopenia and Muscle, 13: 210-219, 2022) behind the headlines. Here is what I found.

How Was The Study Done?

Clinical StudyThis study utilized data acquired from the Nurses’ Health Study (NHS). The NHS began in 1976 with 121,700 female nurses aged 30 to 55. This study followed 85,871 nurses in the NHS once they reached age 60 for an average of 14 years.

Dietary intake was assessed using a food frequency questionnaire that was administered to all participants in the study every four years between 1980 and 2010. The long-term intake of red meat and other protein sources was based on a cumulative average of all available diet questionnaires for each participant.

The participants also filled out a Medical Outcomes Short Report every four years between 1992 and 2014. Data from this survey was used to calculate something called the FRAIL scale, which includes the following frailty criteria:

  • Fatigue
  • Low muscle strength.
  • Reduced aerobic capacity.
  • Having ≥5 of the following chronic diseases:
    • Cancer
    • High blood pressure
    • Type 2 diabetes
    • Angina
    • Myocardial infarction (heart attack)
    • Congestive heart failure
    • Asthma
    • COPD (chronic obstructive pulmonary disease)
    • Arthritis
    • Parkinson’s disease
    • Kidney disease
    • Depression
  • Greater than ≥5% weight loss in two consecutive assessments.

Frailty was defined as having met 3 or more criteria in the FRAIL scale. The study looked at the effect of habitual consumption of red meat or other protein sources on the development of frailty during the 14-year follow-up period.

Does Red Meat Cause Frailty In Older Women?

The investigators separated the participants into 5 quintiles based on total red meat consumption, unprocessed red meat construction, or processed red meat consumption. The range of intakes was as follows.

Total red meat: 0.4 servings per day to 1.8 servings per day.

Unprocessed red meat: 0.3 servings per day to 1.3 servings per day.

Processed red meat: 0.04 servings per day to 0.6 servings per day.

Clearly none of the women in this study were consuming either vegan or keto diets. As might be expected from a cross-section of the American public, there was a fairly narrow range of daily meat consumption.

Here are the results of the study:

  • Each serving per day of total red meat increased frailty by 13%.
  • Each serving per day of unprocessed red meat increased frailty by 8%.
  • Each serving per day of processed red meat increased frailty by 26%.
  • When each component of the frailty index was examined individually, all of them were positively associated with red meat consumption except for weight loss.

This was perhaps the most unexpected finding of the study. Not only did red meat consumption increased the risk of chronic diseases in these women, which would be expected from many previous studies. But red meat consumption also made these women more tired, weaker, and shorter of breath.

The authors concluded, “Habitual consumption of any type of red meat was associated with a higher risk of frailty.”

Which Proteins Are Best?

Red Meat Vs White MeatThe investigators then asked if replacing one serving/day of red meat with other protein sources was associated with a significantly lower risk of frailty. Here is what they found:

  • Replacing one serving per day of unprocessed red meat with a serving of:
    • Fish reduced frailty risk by 22%.
    • Nuts reduced frailty risk by 14%.
  • Replacing one serving per day of processed red meat with a serving of:
    • Fish reduced frailty risk by 33%
    • Nuts reduced frailty risk by 26%
    • Low-fat dairy reduced frailty risk by 16%
    • Legumes reduced frailty risk by 13%.

The authors concluded, “Replacing red meat with another source of protein including fish, nuts, legumes, and low-fat dairy may be encouraged to reduce the risk of developing frailty syndrome. These findings are in line with dietary guidelines promoting diets that emphasize plant-based sources of protein.” [I would note that fish and low-fat dairy are hardly plant-based protein sources.]

What Does This Study Mean For You?

Questioning WomanI am not yet ready to jump on the “eating red meat causes frailty” bandwagon. This is a very large, well-designed study, but it is a single study. It needs to be replicated by future studies.

And, as a biochemist, I am skeptical about any study that does not offer a clear metabolic rationale for the results. As I said earlier, increased protein intake is usually associated with an increase in muscle mass when we are young and a preservation of muscle mass as we age. There is no obvious metabolic explanation for why an increase in red meat consumption in older women would cause a decrease in muscle mass and other symptoms of frailty.

On the other hand, there are plenty of well documented reasons for decreasing red meat intake. Consumption of red meat is bad for our health and bad for the health of the planet as I have discussed in an earlier issue of “Health Tips From the Professor”. And substituting other protein sources, especially plant proteins, is better for our health and the health of our planet.

Finally, we also need to consider the possibility that this study is correct and that future studies will confirm these findings. Stranger things have happened.

As we age, we begin to lose muscle mass, a process called sarcopenia. Increased protein intake and resistance exercise can help slow this process. While I am not ready to say that red meat causes decreased muscle mass, I do think this study should make us think about which protein sources we use to prevent sarcopenia. At the very least we should not use age-related muscle loss as an excuse to increase our red meat intake. That might just be counterproductive.

The Bottom Line

A recent study looked at the effect of red meat consumption on frailty in older women. It came to the unexpected conclusion that:

  • Each serving per day of total red meat increased frailty by 13%.
  • Each serving per day of unprocessed red meat increased frailty by 8%.
  • Each serving per day of processed red meat increased frailty by 26%.
  • The increase in frailty could be reduced by replacing one serving/day of red meat with a serving of fish, nuts, low-fat dairy, or legumes.

I am not yet ready to jump on the “eating red meat causes frailty” bandwagon. This is a very large, well-designed study, but it is a single study. It needs to be replicated by future studies. And, as a biochemist, I am skeptical about any study that does not offer a clear metabolic rationale for the results.

On the other hand, there are plenty of well documented reasons for decreasing red meat intake. Consumption of red meat is bad for our health and for the health of the planet.

Finally, we also need to consider the possibility that this study is correct and that future studies will confirm these findings. Stranger things have happened.

As we age, we begin to lose muscle mass, a process called sarcopenia. Increased protein intake and resistance exercise can help slow this process. This study should make us think about which protein sources we use to prevent sarcopenia. At the very least we should not use age-related muscle loss as an excuse to increase our red meat intake. That might just be counterproductive.

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.

Health Tips From The Professor