Dr. Steve Chaney

How Does Red Meat Cause Colon Cancer?

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How Can You Decrease Your Risk Of Colon Cancer? 

Author: Dr. Stephen Chaney

Grilled HamburgersBoth red meat and processed meat consumption are associated with increased risk of colon cancer. But the strength of that association differs between the two.

Processed meat has been classified as a carcinogen by the IARC*, indicating the evidence that processed meat causes colon cancer is definitive. Red meat, on the other hand, has been classified as a probable carcinogen by the IARC*. That means the evidence that red meat causes colon cancer is strong, but not definitive.

*[In case you were wondering, the IARC (International Agency for Research on Cancer) is an international agency charged by the WHO to, among other things, determine the risk of cancer from various foods, industrial chemicals, and environmental pollutants.]

As I said above, red meat consumption is associated with increased risk of colon cancer. But…

  • Not all studies agree (more about that later), and…
  • Association doesn’t prove cause and effect. It could be some other characteristic of red meat eaters that increases their risk of colon cancer.
  • Until recently we had no clear idea of how red meat might cause colon cancer.

Several mechanisms have been proposed. I will discuss each mechanism and ways to reduce the risk of colon cancer by that mechanism:

#1: When fat and juices from the meat drip onto an open flame, carcinogenic polyaromatic hydrocarbons (PAHs) Barbecue Gatheringare formed that stick to the surface of the meat. PAHs can be metabolized to cancer causing chemicals in our body.

  • PAH formation can be reduced by marinating the meat prior to cooking or by using cooking techniques that don’t involve an open flame.
  • PAH formation can be reduced, but not eliminated, by lower fat meat choices, such as grass-fed beef.
  • High fiber diets reduce exposure to PAHs by binding to them and flushing them through the intestine.
  • Cruciferous vegetables block the conversion of PAHs to cancer causing chemicals in our body.

#2: When red meats are cooked at high temperatures, amino acids in the meat combine with creatine, which is found in all red meats, to form heterocyclic amines (HCAs). HCAs can also be metabolized to cancer causing chemicals in our body.

  • HCA formation can be reduced by cooking the meat at lower temperatures.
  • Grass-fed beef does not reduce HCA formation because this mechanism is not dependent on the fat content of the meat.
  • High fiber diets and cruciferous vegetables reduce the danger of HCAs by the same mechanisms as for PAHs.

#3: The nitrates and nitrites used as preservatives in many processed meats react with amino acids from the meat to form carcinogenic N-nitrosamines in our intestines.

  • Antioxidant-rich fruits and vegetables can divert nitrates and nitrites into an alternative pathway that coverts them into nitric oxide, which is beneficial to our bodies. I have discussed this in a previous issue of “Health Tips From the Professor”.

#4: Heme, which is found in all red meats, combines with amino acids in the meat to form carcinogenic N-nitrosamines and similar N-nitroso compounds in our intestines.

  • This mechanism is inherent in all red meats and cannot be eliminated by choosing grass-fed beef or cooking at lower temperatures.
  • The formation of N-nitroso compounds from red meat appears to be carried out by gut bacteria. We know that meat eaters and vegetarians have very different populations of gut bacteria, but we don’t know whether this influences N-nitroso formation.

Mechanism #4 (formation of N-nitroso compounds from heme-containing red meat in our intestines) is the one I will be discussing in this article. But first, it’s time for Metabolism 101.

Metabolism 101: Why Should We Fear N-Nitroso Compounds?

ProfessorSimply put, N-nitroso compounds react with our DNA. They transfer methyl and ethyl groups to the nucleotides that make up our DNA sequence. The general term for these reactions is alkylation of the DNA.

  • In some cases, this causes the alkylated nucleotides to miscode during DNA replication. This can lead to cancer causing mutations.
  • In other cases, this causes genes to be permanently turned on or off.

To understand why this is a problem, you need to know a bit about cancer cell biology.

  • We have certain genes called “oncogenes”. These are genes that turn on processes like cell division. Normally these genes are tightly regulated so that cell division only occurs when it is needed. When these genes are permanently turned on, unregulated, continuous cell division occurs. In short, the cell becomes a cancer cell.
  • We have other genes called “tumor suppressor genes”. These are genes that do things like shutting down cell division when it is not needed. When these genes are permanently turned off, unregulated cell division can occur.

With this in mind, let us review what we know about red meat and colon cancer:

  • Red meat consumption is associated with increased risk of colon cancer.
  • Red meat consumption is also associated with increased concentrations of N-nitroso compounds in the colon. Studies also show:
  • The formation of N-nitroso compounds correlates with the heme content of the meat.
  • The formation of N-nitroso compounds in the colon is dependent on certain strains of gut bacteria.
  • The formation of N-nitroso compounds is reduced by diets high in fiber. It is likely this is because high fiber diets influence the types of bacteria in the colon, but that has not been proven yet.

What is missing is evidence that colon cancer cells contain the kind of DNA modifications (DNA alkylation) caused by N-nitroso compounds. That is what the current study (C Gurjao et al, Cancer Discovery, published online June 17, 2021) was designed to test.

How Was This Study Done?

Clinical StudyOne reason previous studies had not been able to demonstrate a clear correlation between red meat consumption and DNA modifications was that the studies were too small to obtain statistically significant results.

So, the authors of this study combined data from women in the Nurses’ Health Study, the Nurses’ Health Study II, and men in the Health Professionals Follow-Up Study. There were over 238,130 women and 51,529 men in these three studies.

None of the participants had cancer at the time they entered the studies. The participants were followed for at least 27 years. During that time 4855 participants developed colon cancer.

At the beginning of each study and every 4 years later the participants were asked to fill out a food frequency questionnaire to collect information about their usual diet over the past year. Validation studies showed that the diets of the participants changed little over the interval of the studies.

The participants in these studies were sent follow-up questionnaires every two years to collect information on lifestyle and newly diagnosed diseases like colon cancer.

For those who developed colon cancer, their medical records were reviewed to collect data on tumor size, tumor location, and disease stage.

The diagnoses of colon cancer often involves removing tissue from the cancer and from surrounding normal tissue and putting it in formalin-fixed paraffin-embedded tissue blocks. These were collected, and the DNA was extracted and sequenced to determine the extent and genetic location of alkylated DNA sequences.

How Does Red Meat Cause Colon Cancer?

colon cancerThis study measured the effect of red meat consumption on the extent and location of what the authors called “alkylation signatures”, which refers to the kinds of DNA modifications caused by N-nitroso compounds. Here is what they found:

  • Red meat consumption was positively associated with an increase in alkylation signatures caused by N-nitroso compounds in tumor tissue from patients with colon cancer.
    • This was true for both processed and unprocessed red meat.
    • There was no difference between men and women after adjusting for differences in red meat intake.
    • White meat (chicken and fish) did not cause an increase in alkylation damage in colon cells.
  • More importantly, there was an inverse association between alkylation damage in the tumor tissue and patient survival. Simply put, high levels of alkylation damage were associated with short survival times.

Previous studies have shown that processed red meat consumption was associated with increased levels of N-nitroso compounds and an increased risk of colon cancer in the distal colon.

  • This study showed colon cancer patients who had been consuming processed red meats had higher alkylation damage in tumors in the distal colon.

Previous studies have shown that certain oncogenes (genes that drive the conversion of normal cells to cancer cells) are activated in colon cancer cells and this activation is associated with alkylation damage to their DNA.

  • This study showed that tumors with activated oncogenes were enriched with the alkylation signature characteristic of N-nitroso compounds.

I realize this study is highly technical. It is not easy to understand, so let me simplify it.

  • Previous studies have shown that red meat consumption is associated with an increased risk of colon cancer.
  • Previous studies have also shown that red meat consumption is associated with an increased concentration of carcinogenic N-nitroso compounds in the colon.
  • This study shows that red meat consumption is associated with the kind of DNA damage caused by N-nitroso compounds in colon tumor cells. More importantly, this is the kind of damage that can lead to cancer-causing mutations. In addition:
    • The DNA damage occurs in the exact location of the colon predicted from earlier studies.
    • The DNA damage occurs in genes known to drive the conversion of normal colon cells to cancer cells.

In short, this study provides a plausible mechanism for the effect of red meat consumption on increased risk of colon cancer. It shows how red meat can cause colon cancer.

“In the words of the authors, “Our study has leveraged a comprehensive dataset with repeated dietary measures over years…and [DNA sequencing] on a large collection of colorectal tumors. It provides unique evidence supporting the direct impact of dietary behaviors on colorectal carcinogenesis…”

How Can You Decrease Your Risk Of Colon Cancer?

Steak SaladWhen this study is combined with previous studies, it provides a clear explanation of how red and processed meats can cause colon cancer. And, unfortunately, grass-fed beef is not a “Get Out Of Jail Free” card. This mechanism is equally applicable to grass-fed beef and conventionally raised beef.

Does this mean you need to become a vegan? While I have nothing against veganism, the answer appears to be no. As I discussed above whole, unprocessed plant foods are the antidote to the carcinogenic compounds formed from red meat. This is due to:

  • Their fiber, which sweeps some carcinogens out of the intestine before they can be absorbed.
  • Their antioxidants, which prevent some carcinogens from being formed.
  • Their phytonutrients, which block the activation of some carcinogens.
  • The friendly gut bacteria they support, which displace the bad bacteria that form some carcinogen precursors in the intestine.

The good news is that some red meat may be OK in the context of a primarily plant-based diet. For example, 3 ounces of red meat in a green salad or stir fry is less likely to increase your risk of colon cancer than an 8-ounce steak and fries.

The bad news is this is why not all studies have shown an association of red meat consumption and increased risk of colon cancer. Unfortunately, far too many of these studies have ignored other components of the diet.

The Bottom Line

A recent study looked at the effect of red meat consumption on DNA modifications in colon cells that are associated with the conversion of normal cells to cancer cells. It is a highly technical study, but the simplified version is:

  • Previous studies have shown that red meat consumption is associated with an increased risk of colon cancer.
  • Studies have also shown that red meat consumption is associated with an increased concentration of carcinogenic N-nitroso compounds in the colon.
  • This study shows that red meat consumption is associated with the kind of DNA damage caused by N-nitroso compounds in colon tumor cells – the kind of damage that can lead to cancer-causing mutations. In addition:
    • The DNA damage occurs in the exact location of the colon predicted from earlier studies.
    • The DNA damage occurs in genes known to drive the conversion of normal colon cells to cancer cells.

In short, this study provides a plausible mechanism for the effect of red meat consumption on increased risk of colon cancer. It shows how red meat can cause colon cancer.

“In the words of the authors, “Our study has leveraged a comprehensive dataset with repeated dietary measures over years…and [DNA sequencing] on a large collection of colorectal tumors. It provides unique evidence supporting the direct impact of dietary behaviors on colorectal carcinogenesis…”

For more details about this study and how you can eat red meat and still reduce your risk of colon cancer, 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 Groin Pain

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The Pectineus Muscle And Groin Pain 

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney 

Fall, Glorious Fall

Happy WomanFall is glorious in my book.  I was up in New York a few weeks ago, and the trees were just changing – I was about a week too early for the best colors, but it was still beautiful. The air was crisp and clean, and I loved all the fall decorations.

In Florida we are entering our most wonderful time of year. It’s starting to get cooler, the humidity is going down, and hurricane season is over. Hooray!  It’s great to be outdoors again!

And now that the weather has turned cooler in all parts of the USA, more people are exercising outdoors.  Are you?  Be sure to warm up your muscles before you go running or cycling.

Treating the Muscles That Cause Groin Pain and Impact Walking.

I have a client who had a pain pattern I hadn’t seen before, so it was a challenge to figure out what needs to be treated to get success. We’ll call my client “Bob” although that’s not his real name.

Bob had a shooting pain just to the left of his pubic bone whenever he tried to take a wide step.  As a runner it was definitely causing him issues whenever he tried to take a long step, like while running.

There are so many muscles that are involved in moving your legs so you can walk or run that I won’t be going into them all in this newsletter.  If it’s something you want to explore, please get either of my books by going to https://julstromethod.com/shop/

The Pectineus Muscle And Groin Pain

pectineus muscleThe muscle we’re concerned with today is the Pectineus.

The Pectineus is a small muscle that runs from the front of your pubic bone to the top of the inside of your thigh bone (femur).

It’s one of the large group of muscles called Adductors.  All the Adductors originate on your pubic bone and insert along the length of your femur, all the way to the inside of your knee.  When they contract, they pull your leg in toward midline (like crossing your legs).

However, when they are tight you can’t bring your leg out to the side.  And in the case of the Pectineus, you will have pain and limited range-of-motion moving your leg forward to take a big step.

If you look at the graphic above, consider what would happen if the muscle was so tight that it won’t stretch, and the bone was being pulled forward. You can see that it will pull on both the pubic bone and the top of the thigh bone. The Pectineus muscle is so small that the pain would be in a circle that encompasses both the origination and the insertion of the muscle.

Relief From Groin Pain

That’s what was happening to “Bob.”  First you release the “knots” from the Pectineus muscle, so that it can be stretched. The treatment is easy to explain, but impossible to show in a picture because it just looks like someone lying face down on the floor.  You couldn’t see the ball or where it’s located.

Take the Perfect Ball (or a tennis ball if you don’t have the Perfect Ball) and put it exactly where you see the muscle in the graphic.

Lie down on the floor, on top of the ball.  It should be pressing into the Pectineus muscle and the top of your thigh.  Ease into it because if the Pectineus muscle is tight, it will be really painful.  Just start by pressing gently into the ball and then add more of your body weight as the tension lessens.

To stretch the muscle, you can do an adaptation of the picture to the left.

Stand up straight and put your leg behind you.

For example, if you are stretching your left Pectineus, you can have your left leg back so your right leg is straight and your toe is on the ground, or you can do a more advanced stretch by picking up your leg and putting your foot on a step or a chair.

Be sure to hold on to something secure so you won’t lose your balance and fall.

If you turn your body slightly toward the right, you’ll get an even better stretch.

This treatment and stretch helped “Bob” relieve the pressure and he was able to get back to running again!

Have a happy month, and please feel free to contact me if you have any questions about the instructional program for massage therapists.

Wishing you well,

Julie Donnelly 

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

Is It Too Late To Change Your Diet?

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You Can Improve Your Health At Any Age

Author: Dr. Stephen Chaney

Fast Food ExamplesIf you are like most Americans, your dietary preferences as an adult are based on the foods your family ate while you were growing up.

  • Your favorite foods…
  • Your comfort foods…
  • The foods you always avoid…

…are based on your family heritage, not on your genes. And if you are like most Americans, your diet isn’t healthy.

  • It’s high in fat and cholesterol…
  • It’s high in sugar and refined carbohydrates…
  • It’s high in processed foods…
  • It’s low in whole, unprocessed foods…
  • It’s high in calories, so your waistline keeps growing.

You know your diet isn’t healthy, but you keep coasting along through your 30’s and 40’s until…the unthinkable happens. You are diagnosed with a deadly disease, like heart disease, high blood pressure, or diabetes, and your doctor says that unless you change your diet, you are doomed to a short unhealthy life. You have reached a fork in Food Choicesthe road.

Changing the diet you grew up with, the diet you love, is a daunting task. It’s tempting to think, “Why bother…

  • It’s probably too late to change my diet…
  • The damage has already been done…
  • I can’t reverse it now.”

If this scenario describes you or someone you love, you aren’t alone. There are millions of Americans just like you. You want to know whether changing your diet is worth the trouble. You want to know whether it is too late, or whether you can still change your health for the better.

Most clinical studies don’t answer this question. Most clinical studies do a diet assessment at the beginning of the study and look at health outcomes 20 or 30 years later. If they do more than one diet assessment during the study, the purpose of these assessments is to show that most people stick to the same diet throughout the study.

These studies measure the effect of habitual diets on health outcomes. They tell you that good diets lead to good health outcomes, and bad diets lead to bad health outcomes. But they don’t tell you whether changing your diet from bad to good in your 30’s or 40’s can have a significant effect on your health.

Fortunately, a recent study has answered this question. This study (Y Choi et al, Journal of The American Heart Association, 10e020718, 2021) started with people in their mid-20s. It looked at whether changing their diet from bad to good in their 30s and 40s had any effect on their risk of developing heart disease in their 50s and 60s.

How Was This Study Done?

Clinical StudyThe data for this study were obtained from the CARDIA study (Coronary Artery Risk Development in Young Adults). The study enrolled 4946 young adults (average age = 25, 55% female and 45% male, 50% black and 50% white) and followed them for 32 years (average age of participants at the end of the study = 57).

Diet was assessed by a trained interviewer at year 0, year 7 (average age of participants = 32), and year 20 (average age of participants = 45).

Adherence of the participants to a healthy, plant-centered diet was assessed using an analytical tool called APDQS that divided the foods eaten by the participants into 3 groups based on their known influence on heart disease:

1) Beneficial.

    • These foods included fruit, avocado, beans/legumes, green vegetables, yellow vegetables, tomatoes, other vegetables, nuts and seeds, soy products, whole grains, vegetable oil, fatty fish, lean fish, poultry, moderate alcohol, coffee, tea, and low-fat milk/cheese/yogurt.
    • This is what the investigators considered a plant-centered diet. It encompasses diets ranging from vegan to Mediterranean and DASH.

2) Adverse.

    • These foods included fried potatoes, refined grain desserts, salty snacks, pastries, sweets, high-fat red meats, processed meats, organ meats, fried fish/poultry, sauces, soft drinks, whole fat milk/cheese/yogurt, and butter.
    • This could be considered a typical American diet.

3) Neutral.

    • These foods included potatoes, refined grains, margarine, chocolate, meal replacements, pickled foods, lean meats, shellfish, eggs, soups, and fruit juices.
    • These foods are not the healthiest, but the evidence that they have a negative effect on health disease risk is inconclusive.

The participants were divided into 5 quintiles based on adherence to a plant-centered diet, with quintile 1 having the lowest adherence and quintile 5 having the highest adherence to a plant-centered diet.

The effect of diet on heart disease was measured in two ways:

1) The dietary data from years 0, 7 and 20 were averaged and the effect of average adherence to a plant-centered diet on the risk of developing heart disease by the time the participants were 57 was measured. This is similar to the design of most other studies looking at the effect of diet and heart disease.

2) The effect of an improvement in adherence to a plant-centered diet between ages of 32 and 45 on the risk of developing heart disease by age 57 was also measured. This is what makes this study unique. Basically, the investigators were asking if you could eat a bad diet for 30 years or more and still reduce your risk of heart disease by switching to a good diet by the age of 45. That is the question that millions of American are asking themselves right now.

Is It Too Late To Change Your Diet?

Heart Healthy DietAs I described above this study asked two distinct questions:

1) What effect does your habitual diet have on your risk of developing heart disease?

For this portion of the study, the investigators averaged the dietary data collected in years 0, 7, and 20 of the study and ranked the participants diet from 1 to 5 based on their adherence to a plant-centered diet. When they compared the group with best adherence (group 5) with the group with worst adherence (group 1):

    • Adherence to a plant-centered diet reduced their risk of developing heart disease by 48%.
    • This is consistent with previous studies looking at the beneficial effects of plant-centered diets on heart disease.

2) What effect does changing your diet from bad to good when you are in your 30s or 40s have on your risk of developing heart disease? 

For this portion of the study, the investigators compared the dietary data collected at years 7 and 20 (corresponding to average ages 32 and 45 for the participants) and ranked the participants from 1 to 5 based on improved adherence to a plant-centered diet. When they compared the group with best improvement in adherence (group 5) with the group with worst improvement in adherence (group 1):

    • Improved adherence to a plant-centered diet reduced the risk of developing heart disease by 39%.
    • This answers the questions I posed at the beginning of this article. In short, it is never too late to change your diet for the better.

The authors concluded, “In summary, our study shows that long-term consumption of a nutritionally rich plant-centered diet is associated with a lower risk of heart disease. Furthermore, increased [adherence to a] plant-centered diet in young adulthood is associated with a lower subsequent risk of heart disease throughout middle age, independent of the earlier diet quality” [In short, they are saying that changing to a more plant-centered diet in your 30s and 40s reduces your risk of heart disease.]

You Can Improve Your Health At Any Age

I titled this section, “You Can Improve Your Health At Any Age” for a reason. I wanted to make the point that it is never too late to change your diet, and your health, for the better.

Yes, I realize that the study I described above only shows:

  • The effect of changing to a more plant-centered diet in your 30s and 40s.
  • The benefit of changing to a more plant-centered diet on heart disease outcomes.

However, we have ample evidence that changing to a more plant-based diet at any age is likely to reduce the risk of many diseases. For example:

  • There are multiple reports in the literature of people in their 60s and 70s who had a health scare, changed to a more plant-centered diet, and dramatically improved their health.

While neither type of study can be considered definitive by itself, together they suggest it is never too late to change your diet for the better.

But what changes should you make? As I said above, anything from Vegan to Mediterranean or DASH fits the definition of a plant-centered diet (something I have previously referred to as a primarily plant-based diet).

You could choose the plant-centered diet that best fits your preferences and lifestyle and read books or go online to find details and recipes that will help you transition to that diet…or you could simply:

  • Eat more fruit, avocado, beans/legumes, green vegetables, yellow vegetables, tomatoes, other vegetables, nuts and seeds, soy products, whole grains, vegetable oil, fatty fish, lean fish, poultry, moderate alcohol, coffee, tea, and low-fat milk/cheese/yogurt.
  • Eat less fried potatoes, refined grain desserts, salty snacks, pastries, sweets, high-fat red meats, processed meats, organ meats, fried fish/poultry, sauces, soft drinks, whole fat milk/cheese/yogurt, and butter.
  • Eat these foods in moderation: potatoes, refined grains, margarine, chocolate, meal replacements, pickled foods, lean meats, shellfish, eggs, soups, and fruit juices.

The Bottom Line

If you are like most Americans, you know your diet is unhealthy. But it is the diet you grew up with. It’s the diet you love. So, you keep eating it anyway.

Then you have a wake-up call. You find yourself in your doctor’s office, and your doctor is advising you to change your diet. But giving up the diet you love is difficult, and you wonder if it is worth it. Can you really improve your health significantly by changing your diet now, or is it too late? Has the damage already been done?

Fortunately, a recent study has answered these questions. This study started with people in their mid-20s. And it looked at whether changing their diet from bad to good in their 30s and 40s had any effect on their health in their 50s and 60s. This is what the study found.

  • Improved adherence to a plant-centered diet in their 30s and 40s reduced their risk of developing heart disease in their 50s and 60s by 39%.

While this study was very specific in terms of age and disease, I have discussed in the article above why changing to a more plant-based diet at any age is likely to reduce your risk of multiple diseases. In short, it is never too late to change your diet, and your health, for the better.

For more details about this study and how to change your diet for the better, 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 DNA Testing Valuable?

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What Is The True Value Of DNA Tests? 

Author: Dr. Stephen Chaney

Genetic TestingDNA testing is hot! DNA testing companies claim they can tell you your disease risk and personalize your diet and supplement program – all based on the sequence of your DNA.

On the other hand, most reputable medical sources say these DNA testing companies overpromise and underdeliver. They tell you that diet, lifestyle, and supplement recommendations based only on your DNA sequence are often inaccurate.

So, what should you believe? At this point you are probably wondering:

  • Is DNA testing valuable or is it a waste of money?
  • Is there a way to make DNA testing more accurate?
  • What is the true value of DNA testing to you, the consumer?

I will consider these 3 questions in my article below. But first let me share two stories about DNA testing, one true and the other fictional.

Perspectives on DNA Testing

When the human genome was first sequenced in 2003, it took 13 years and cost millions of dollars. That was an nutrigenomicsexciting time. Many of us in the scientific community thought we were on the verge of a revolution in human health and longevity. We would soon be able to tell individuals their risk of developing various diseases.

Even better, we would be able to tell them the kind of diet and supplementation they needed to avoid those diseases. We would be able to personalize our nutritional recommendation for every individual based on their genome – something we called nutrigenomics.

How naive we were! It has turned out to be much more complicated to design personalized nutrition recommendations based on someone’s genome than we ever imagined.

Today an analysis of your genome requires hours and costs less than $200. That represents a tremendous advance in technology. However, we are no closer to being able to make personal nutrition recommendations based on our DNA sequence today than we were 18 years ago.

Why is that? Let me share a fictional story because it provides a clue. In 1997, when I was still a relatively young scientist, I saw a film called GAATACA. [If you are looking for an entertaining film to watch, it is still available on some streaming services.]

This film envisioned a future society in which parents had their sperm and eggs sequenced so that their children would be genetically perfect. In that society the term “love child” had been redefined as a child who had been conceived without prior DNA sequencing.

The hero of this film was, of course, a love child. He was born with a genetic predisposition for heart disease. He was considered inferior, a second-class citizen of this future world.

Without giving away the plot of the film (I don’t want to spoil the enjoyment for you if you are thinking of watching it), he overcame his genetic inferiority. With a strict regimen of diet and physical fitness he became stronger and healthier than many of his genetically perfect peers.

This is when I first began to realize that our DNA does not have to be our destiny. We have the power to overcome bad genetics. We also have the power to undermine good genetics.

You might be wondering, “How can this be? Why doesn’t our DNA determine our destiny” I will answer that question in two parts.

  • First, I will share what experts say about the value of DNA testing.
  • Then I will put on my professor hat and discuss “Genetics 101 – What we didn’t know in 2003” (When the genome was first sequenced).

Is DNA Testing Valuable?

SkepticAs I said above, most scientists are skeptical about the ability of DNA testing to predict our ideal diet and supplementation regimens. For example, here are two recent reviews on the current status of DNA testing. [Note: These scientists are using “science speak”. Don’t worry if you don’t understand all the terms. I will explain their message in simpler terms in the next section.]

One review (C Murgia and MM Adamski, Nutrients, 366, 2017) published in 2017 concluded: “The potential applications to nutrition of this invaluable tool [DNA sequencing] were apparent since the genome was mapped…However, fifteen years and hundreds of publications later, the gap between genome mapping and health practice is not yet closed.”

“The discovery of other levels of control, including epigenetics [modifications of DNA that affect gene expression] and the intestinal microbiome complicate the interpretation of genetic data. While the science of nutritional genomics remains promising, the complex nature of gene, nutrition and health interactions provides a challenge for healthcare professionals to analyze, interpret and apply to patient recommendations.”

Another review (M Gaussch-Ferre et al, Advances in Nutrition, 9: 128-135, 2018) published in 2018 concluded: “Overall, the scientific evidence supporting the dissemination of genomic information for nutrigenomic purposes [predicting ideal diet and supplement regimens] remains sparse. Therefore, additional knowledge needs to be generated…”

In short, the experts are saying we still don’t know enough to predict the best diet or the best supplements based on genetic information alone.

Genetics 101 – What We Didn’t Know In 2003

GeneticistIn simple terms the experts who published those reviews are both saying that the linkage between our DNA sequence and either diet or supplementation is much more complex than we thought in 2003 when the genome was first sequenced.

That is because our understanding of genetics has been transformed by two new areas of research, epigenetics and our microbiome. Let me explain.

  1. Epigenetics has an important influence on gene expression. When I was a graduate student, we believed our genetic destiny was solely determined by our DNA sequence. That was still the prevailing viewpoint when the human genome project was initiated. As I said above, we thought that once we had our complete DNA sequence, we would know everything we needed to know about our genetic destiny.

It turns out that our DNA can be modified in multiple ways. These modifications do not change the DNA sequence, but they can have major effects on gene expression. They can turn genes on or turn them off. More importantly, we have come to learn that these DNA modifications can be influenced by our diet and lifestyle.

This is the science we call epigenetics. We have gone from believing we have a genome (DNA sequence) that is invariant and controls our genetic destiny to understanding that we also have an “epigenome” (modifications to our DNA) that is strongly influenced by our diet and lifestyle and can change day-to-day.

2) Our microbiome also has an important influence on our health and nutritional status. microbiomeSimply put, the term microbiome refers to our intestinal microbes. Our intestinal bacteria are incredibly diverse. Each of us has about 1,000 distinct species of bacteria in our intestines. 

Current evidence suggests these intestinal bacteria influence our immune system, inflammation and auto-immune diseases, brain function and mood, and our predisposition to gain weight – and this may just be the tip of the iceberg.

More importantly, our microbiome is also influenced by our diet and lifestyle, and environment. For example, vegetarians and meat eaters have entirely different microbiomes.

Furthermore, the effect of diet and lifestyle on our microbiome also changes day to day. If you change your diet, the species of bacteria in your microbiome will completely change in a few days.

If you are wondering how that could be, let me [over]simplify it for you:

    • What we call fiber, our gut bacteria call food.
    • Different gut bacteria thrive on different kinds of fiber.
    • Different plant foods provide different kinds of fiber.
    • Whenever we change the amount or type of fiber in our diet, some gut bacteria will thrive, and others will starve.
    • Bacteria grow and die very rapidly. Thus, the species of bacteria that thrive on a particular diet quickly become the predominant species in our gut.
    • And when we change our diet, those gut bacteria will die off and other species will predominate.

Finally, our microbiome also influences our nutritional requirements. For example, some species of intestinal bacteria are the major source of biotin and vitamin K2 for all of us and the major source of vitamin B12 for vegans. Other intestinal bacteria inactivate and/or remove some vitamins from the intestine for their own use. Thus, the species of bacteria that populate our intestines can influence our nutritional requirements.

Now that you know the complexity of gene interactions you understand why we are not ready to rely on DNA tests alone. That science is at least 10-20 years in the future. Companies that tell you otherwise are lying to you.

What Is The True Value Of DNA Tests? 

The TruthBy now you are probably thinking that my message is that DNA tests are worthless. Actually, my message is a bit different. What I, and most experts, are saying is that DNA tests are of little value by themselves.

To understand the true value of DNA tests, let me start with defining a couple of terms you may vaguely remember from high school biology – genotype and phenotype.

  • Genotype is your genes.
  • Phenotype is you – your health, your weight, and your nutritional needs. Your phenotype is determined by your genes plus your diet and your lifestyle.

With that in mind, let’s review the take-home messages from earlier sections of this article.

  • The take-home message from the two stories in “Perspectives on DNA Testing” is that our DNA does not have to be our destiny. We have the power to overcome bad genetics. We also have the power to undermine good genetics.
  • The take-home message from “Genetics 101” is that while the genes we inherit do not change, the expression of those genes is controlled in part by:
    • Epigenetic modifications to the DNA. And those epigenetic modifications are controlled by our diet and our lifestyle.
    • Our microbiome (gut bacteria). And our microbiome is controlled by our diet and our lifestyle.

Now we are ready to answer the question, “What is the true value of DNA testing?” There are actually two answers to this question. You have probably guessed the first answer by now, but you will be surprised by the second.

  1. DNA testing can only indicate the potential for obesity, the potential for nutritional deficiencies, and the potential for disease. But whether that potential is realized depends on our diet and lifestyle. Therefore, the true value of DNA testing comes from adding a comprehensive analysis of diet and lifestyle to the DNA test results. That includes:
    • Questionnaires that assess diet, lifestyle, health goals, and health concerns.

For example, your genetics may indicate an increased need for vitamin D. This is a concern if your vitamin D intake is marginal but may not be a concern if you are getting plenty of vitamin D from your diet, supplementation, and sun exposure.

    • Direct measurements of obesity such as height and weight (from which BMI can be calculated) and waist circumference (belly fat is more dangerous to our health than fat stored elsewhere in our body).

For example, most Americans have a genetic predisposition to obesity, but not everyone is obese. If you are overweight or obese, your nutrition and lifestyle recommendations should include approaches to reduce your weight. If not, these recommendations are not needed, even if you have a genetic predisposition to obesity.

    • Blood pressure and blood markers of disease risk (cholesterol, triglycerides, and blood sugar).

For example, you may have genetic predisposition to high blood pressure or high cholesterol. If either of these are high, your recommendations should include nutrition and lifestyle approaches to lower them. However, if you are already keeping them under control through diet and lifestyle, no further changes may be necessary.

2) While the scientific community now knows the limitations of DNA testing, this information has not filtered down to the general public. This brings me to the second value of DNA testing. Several recent studies have shown that people are much more likely to follow recommendations based on DNA testing than recommendations based on dietary questionnaires, blood markers of disease, or even recommendations from their physician.

The Bottom Line

DNA testing is hot! DNA testing companies claim they can tell you your disease risk and personalize your diet and supplement program – all based on the sequence of your DNA.

On the other hand, most reputable medical sources say these DNA testing companies overpromise and underdeliver. They tell you that diet, lifestyle, and supplement recommendations based only on your DNA sequence are often inaccurate. They are of little value if they are only based on DNA testing.

So, what is the true value of DNA testing? To answer that question, we need to know two things:

1) Our DNA is not our destiny. We have the power to overcome bad genetics. We also have the power to undermine good genetics.

2) While the genes we inherit do not change, the expression of these genes is controlled in part by:

    • Epigenetic modifications to the DNA. And those epigenetic modifications are controlled by our diet and our lifestyle.
    • Our microbiome (gut bacteria). And our microbiome is controlled by our diet and our lifestyle.

With this information in mind, we are ready to answer the question, “What is the true value of DNA testing?” The true value of DNA testing is tw0-fold:

1) It comes from adding a comprehensive analysis of diet and lifestyle to the DNA test results. This includes:

    • Questionnaires that assess diet, lifestyle, health goals, and health concerns.
    • Direct measurements of obesity such as height and weight (from which BMI can be calculated) and waist circumference (belly fat is more dangerous to our health than fat stored elsewhere in our body).
    • Blood pressure and blood markers of disease risk (cholesterol, triglycerides, and blood sugar).

2) In addition, several recent studies have shown that people are much more likely to follow recommendations based on DNA testing than recommendations based on dietary questionnaires, blood markers of disease, or even recommendations from their physician.

For more details and explanations of the statements in “The Bottom Line”, read the article above.

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

What Is The Truth About Melatonin?

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Why Are There So Few High-Quality Melatonin Studies? 

Author: Dr. Stephen Chaney

Insomnia is a major problem in our world. The reasons are not hard to see:

  • We live in troubled times. Conflicts abound and the days of reasoned discussions and compromise have become distant memories.
  • We live in difficult times. Many of us have lost jobs or loved ones. We have all lost our freedoms. We live in forced isolation. The consoling hug of a friend or neighbor has become a distant memory.
  • We live in fast-paced times. We are constantly “on” from the moment our feet hit the floor in the morning to the moment our head hits the pillow at night. We are also on our devices until the time we go to bed, and most of the news on those devices is bad.

The reasons are also physiological:

  • When we turn off the lights our pineal gland produces a hormone called melatonin that calms our brain and prepares us for sleep.
  • However, as we age our body produces less melatonin because:
    • Our pineal gland produces less melatonin.
    • Many medications commonly prescribed to older Americans suppress melatonin synthesis.

Whatever the reason, insomnia has become a major problem for millions of Americans.

  • One third of all Americans and 69% of older Americans suffer from insomnia. That is a concern because severe insomnia:
  • Affects their quality of work.
  • Affects their quality of life.
  • Increases the risk of accidents.

Medications abound, but they have a long list of side effects. Plus, long term drug use can result in tolerance (the drug loses its effectiveness) and/or dependence (sleep without the drug becomes impossible).

It is no wonder melatonin supplements have become popular among people who have trouble getting a good night’s sleep.

People have been asking me about melatonin supplements. “Do they work? Are they safe?”

It turns out that these aren’t easy questions to answer. Most published studies on melatonin are poor quality and/or have been performed by the company that wants to sell you their melatonin supplement. This raises the question, “What is the truth about melatonin?”

Fortunately, I came across a recent study (F Auld et al, Sleep Medicine Reviews, 34: 10-22, 2017) which is a review and meta-analysis that included only high-quality studies in its analysis. This is the one I will discuss today.

How Was This Study Done?

Clinical StudyThe scientists in charge of this review and meta-analysis started by identifying 5030 studies of the effect of melatonin on various aspects of sleep that had been performed between 1990 and May 2015. Next, they excluded all poor-quality studies from their analysis.

I will list the exclusion criteria below with comments on why these exclusion criteria are important.

#1: Commercially sponsored research: You will often see clinical studies of melatonin supplements reported on their company’s website. The graphs look impressive. The website will say something like. “Our scientists found…” My question is, “If the scientists had not found that their company’s product worked, would they have a job tomorrow?”

Sometimes the research has been done by outside scientists who were supported by funding from the company. These studies are sometimes biased in favor of the company’s product.

#2: Unpublished research: Many companies will cite unpublished “white papers” showing their products work. Often these studies have been done by scientists not directly affiliated with the company. While that sounds impressive, my questions are, “What weaknesses in the study are they trying to hide? Why are they afraid to submit their study to the rigors of peer review so it can be published?”

#3: Research that did not use well established criteria and measurements of sleep disorders: There is an international classification system and rigorous protocols for evaluating sleep disorders. Studies using subjective measurements of sleep quality instead of internationally- recognized protocols are considered low-quality. [For example, a subjective measurement of sleep quality would be to ask subjects, “Did you sleep better?” Whereas, the gold standard objective protocol for sleep quality measures brain waves, heart and breathing rates, and eye and leg movements.]

#4: Research design that was not placebo-controlled. Many of the published clinical studies just gave melatonin to their subjects and asked if sleep quality improved. The placebo effect for something as subjective as sleep quality can be huge. Without a placebo control those studies are worthless.

#5: Research design that was not blinded: The investigators only included double- and single-blinded studies in their analysis. In the single-blinded studies the subjects did not know whether they got melatonin or the placebo. This is the most important aspect of blinding because it avoids the placebo effect.

In double-blinded studies, neither the subjects nor the investigators know who got melatonin and who got the placebo. This is considered the “gold standard” of clinical studies, but investigator blinding is only important when investigators are using subjective criteria to measure outcomes.

#6: Research design that was not randomized. Randomization simply means that the subjects were randomly assigned to the melatonin and placebo groups. This assures that the two groups are alike in every characteristic except whether they received melatonin or placebo.

Once they had excluded all low-quality studies, the investigators were left with 12 high-quality studies. [You didn’t misread that. They started by identifying 5030 studies on melatonin and, after carefully analyzing those studies, ended up with only 12 high-quality studies.] I can’t resist making two comments here.

  • Now you understand why many scientists are skeptical about the value of melatonin. There are too many low-quality studies.
  • Now you understand why I chose this particular paper to report on in today’s “Health Tips From the Professor”.

Most of the high-quality studies were small (had relatively few subjects), so the investigators combined studies of similar design in their meta-analysis.

They were able to assess the effect of melatonin supplements on something called sleep latency (the time it takes to fall asleep). This can be a problem at any age but is most common in the elderly.

What Is The Truth About Melatonin?

The TruthThe investigators identified five high-quality randomized, blinded, placebo-controlled clinical studies with a total of 1,113 subjects that addressed sleep latency (the time it takes to fall asleep). Subjects were given 2-3 mg of melatonin and the studies lasted 4-5 weeks.

When they combined the data from all 5 studies, there was a highly significant reduction in the time to fall asleep for melatonin-treated subjects compared to placebo. The p value was 0.004 (For comparison, p values <0.05 are considered significant, and p values <0.01 are considered highly significant.)

There were a few high-quality studies addressing the effect of melatonin on other sleep disorders. There appeared to be a beneficial effect of melatonin on some of those disorders, but there were not enough subjects in these studies for the effect of melatonin supplementation to be statistically significant.

The investigators concluded, “These findings highlight the potential importance of melatonin in treating certain sleep disorders. Meta-analysis of the data emphasized in particular the improvement in sleep latency [time it takes to fall asleep] with melatonin in these patients.”

Why Are There So Few High-Quality Melatonin Studies?

ConfusionThe investigators went on to say, “The development of large-scale, randomized, placebo-controlled trials is recommended to provide further evidence for therapeutic use of melatonin in a variety of sleep difficulties.” However, they acknowledged that future large-scale studies of melatonin supplements are unlikely.

In the words of the authors, “Future research may be hindered by the…lack of financial incentives that may decrease motivation to undertake such trials. Funding agencies are more likely to support research on novel medications, which leads to new treatments and increased revenue for pharmaceutical companies, than to supply funding for a supplement (melatonin) that has been easily purchased over the counter since the 1990’s.”

Finally, someone has pointed out the elephant in the room. There is a good reason that it is so hard to find large, high-quality studies on supplements – and it is called money. It takes lots of money to fund large high-quality clinical studies. Companies don’t make enough money from supplement sales to justify those kinds of studies.

Let me give you an example. There is a sleep disorder called “Non 24-hour sleep wake syndrome” in blind patients. Simply put, the pineal gland relies on the transition from light to darkness to regulate when melatonin is released. If a blind person cannot distinguish between light and darkness, they have no signal for melatonin release. They have no physiological signal that it is time to sleep.

Sometimes they can overcome this with a set bedtime every day. However, some blind people really struggle falling asleep and waking up on a regular schedule.

In the review I described above, two very small high-quality studies were identified that suggested melatonin supplementation may help blind people normalize their sleep and wake times. However, the studies were too small to be statistically significant.

On the other hand, a drug company spent hundreds of thousands of dollars developing and testing a drug which mimics the effect of melatonin. Because the drug does not occur in nature, they could patent it. And because they could afford to pay for large-scale, randomized, placebo-controlled clinical trials of the drug, the FDA approved it. They will probably make millions from this drug. You may have even seen it advertised on TV.

How Can You Get A Good Night’s Sleep?

SleepThe study described above confirms that melatonin is effective at reducing sleep latency (the time it takes to fall asleep). It may be useful for other sleep disorders, but the evidence to support those uses is inconclusive at present.

However, holistic approaches are always best. If you toss and turn at night, you might want to start by trying these “sleep hygiene” tips from the CDC:

  • Be consistent. Go to bed at the same time each night and get up at the same time each morning, including on the weekends.
  • Make sure your bedroom is quiet, dark, relaxing, and at a comfortable temperature.
  • Remove electronic devices, such as TVs, computers, and smart phones, from the bedroom.
  • Avoid large meals, caffeine, and alcohol before bedtime.
  • Get some exercise. Being physically active during the day can help you fall asleep more easily at night.

You may also want to try relaxation techniques like yoga before bedtime.

When sleep hygiene fails, try melatonin to help you fall asleep. Here are a few things to know:

  • Melatonin is cleared from the body very rapidly (usually within 1-2 hours).
    • That means melatonin is much less likely to cause drowsiness the next morning than many of the insomnia drugs.
    • It also means that melatonin helps you fall asleep, as the review and meta-analysis described above confirmed. However, it doesn’t stick around long enough to help you stay asleep. Other herbs like valerian are more effective for that purpose.
  • Our ability to clear melatonin from our system declines as we age.
    • Therefore, doses of 2 or 3 mg are usually recommended for people over 50, while 5 or 10 mg are sometimes used for teenagers and young adults.
    • However, we are all different, so you may need to experiment to find the best dose for you.
  • Melatonin has remarkably few side effects compared to the widely prescribed insomnia drugs. It also appears less likely to create dependence.
  • Melatonin is often considered an occasional use supplement.
    • That is fine if you only have trouble falling asleep occasionally.
    • If you suffer from insomnia on a regular basis, you will be comforted to know that clinical studies have reported no side effects or dependency with daily use of low-dose melatonin for up to 6 months.
    • However, if you do have chronic insomnia, it is always a good idea to discuss your situation with your health professional to make sure it is not caused by an underlying medical condition.

The Bottom Line

Insomnia is a major problem in our world. Medications abound, but they have a long list of side effects. Plus, long term drug use can result in tolerance (the drug loses its effectiveness) and/or dependence (sleep without the drug becomes impossible).

It is no wonder melatonin supplements have become popular among people who have trouble getting a good night’s sleep. People have been asking me about melatonin supplements. “Do they work? Are they safe?”

It turns out these are not easy questions to answer. Most published studies on melatonin are poor quality and/or have been performed by the company that wants to sell you their melatonin supplement. This raises the question, “What is the truth about melatonin?”

Fortunately, I came across a recent review and meta-analysis that included only high-quality studies in its analysis. This study concluded that melatonin is effective at reducing sleep latency (the time it takes to fall asleep). It may be useful for other sleep disorders, but the evidence to support those uses is inconclusive at present.

For more details about this study, how to use melatonin, and a holistic approach to improve your quality of sleep 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 Restless Leg Syndrome

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Muscles, Nerves, And Restless Leg Syndrome 

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney 

Never-ending Summer

HotIt is starting to cool off in other parts of the country, but it’s still hot in Florida right now. Sometimes it feels like we have never-ending summer in Florida. Thank heaven for air conditioning!

For those of us who are old enough to remember the days before air conditioning, we are even more grateful for air conditioning.  I remember being pregnant with my son in 1967, when we were living in San Antonio, Texas.  Most people didn’t have air conditioning yet, and we certainly didn’t.  I came to realize why Southerners talk so slow (remember, I’m a New Yorker).  It was so hot we just didn’t talk at all. It took too much effort!

Fortunately, this time of year seems to pass quickly, and we’ll be getting back into cooler weather before we know it.  At least, that’s what I’m telling myself.

Restless Leg Syndrome (RLS)

confusionA reader asked me to talk about RLS this month.  Restless Leg Syndrome is a tricky topic, depending on which expert you read.  The Mayo Clinic said there isn’t a known cause of RLS, but it may be caused by an imbalance of the brain chemical dopamine.  The Mayo Clinic has also said RLS can be related to:

  • Peripheral neuropathy.
  • Iron deficiency.
  • Kidney failure.
  • Spinal cord conditions.

Yes, there isn’t a definitive cause for RLS.

A friend had RLS and told me that when she took iron supplements, and totally avoided flour and sugar that her symptoms disappeared.  Then I read that iron is the worst thing to take for RLS.  Go figure!

In any case, I’m not a doctor or a nutritionist, so I look at the possible muscular cause of RLS.

Muscles, Nerves, And RLS 

The nerves that go to your leg are the sciatic and femoral nerves, which are the continuation of your spinal cord, separating at your lumbar vertebrae to go down both of your legs.

The femoral nerve goes underneath and through your psoas muscle and under your inguinal ligament.  It innervates your anterior/medial thigh muscles. The importance in this pathway will be discussed, but please make note of how the nerve passes underneath the inguinal ligament.

Your sciatic nerve is the largest nerve in the body.  Its pathway is so big that we’ll just say it innervates your buttocks and the rest of your leg and foot that isn’t innervated by the femoral nerve.

After leaving your spine at your low back, these nerves pass under and through some powerful muscles, and this can be a problem when the muscles are tightened by a repetitive strain injury (RSI).  When a muscle contracts it pulls on the insertion point and you move a joint.

As you do something over and over (something as simple as sitting down and staying still for a long period of time) a phenomenon called “muscle memory” causes the muscle to shorten to a contracted length, and you have a problem when you go to move in the opposite direction.

For Example… 

Two muscles, the psoas and iliacus, connect your lumbar vertebrae and pelvis to your upper leg (femur).  When they contract you bend forward (psoas), lift your leg (iliacus) or sit down (both muscles).  When you sit for an extended period of time, muscle memory causes the muscles to change to the shorter length.

When you go to stand up these muscles are too short to easily lengthen enough for you to stand up, and you feel a strain at your low back.  Both your lumbar vertebrae and your pelvis rotate forward and down as the muscles are being strained while they are lengthening.

As the pelvis is rotating forward and down, several things happen that impact the sciatic and femoral nerves.

First the muscles tighten and since the nerves are passing through the muscles, the nerves are “pinched” in the pelvic area.  This can cause the nerves to send impulses to the lower leg and foot.

Next, as I mentioned above, the femoral nerve passes through the psoas muscle and is then directly underneath the inguinal ligament.  As the muscle tightens it presses the nerve up into the inguinal ligament, causing potential damage to the nerve, and also sending impulses to the quadriceps muscles.

As these nerves are impinged and sending impulses to the muscles, the muscle fibers may respond with itching, burning, and twitching.  You are experiencing the results in your thigh, but the cause of the problem is actually deep in your lower pelvic area.

[I realize this description is a bit confusing, and I’m not going into detail here. However if you are interested, or if you have low back pain, I suggest you consider getting my book The 15 Minute Back Pain Solution. This book will explain all of it in detail, and it will show you how to self-treat each muscle that impacts your low back, hips, sciatic nerve, groin, and knees.]

Relief From Restless Leg Syndrome 

Most times the order of treatment isn’t important, but when it comes to the pelvic muscles, and all the related muscles, the order is vital as one muscle can stop the entire treatment protocol from working.  This is why I wrote The 15 Minute Back Pain Solution. It gives you the exact order of treatment, and has photographs of doing each treatment, along with the explanation and a graphic of where that muscle refers pain/numbness.  To try to explain it here would require my putting the book into a newsletter, so that isn’t doable.

Start by treating your anterior thigh muscles. I’m going to show you how to treat just the anterior thigh muscles that can be impacting the femoral nerve.

Use a piece of 1” x 12” PVC pipe to slide (not roll) down your thigh from the very top of your leg to your knee. Cover your entire anterior thigh and out toward the outside of your leg.

Press deeply, it should feel like “hurts so good,” not “I think I’m going to faint!”  You are in control of the pressure so keep it at your tolerance level.

If you feel a bump, that’s a knot (spasm) that is pulling down on your pelvis.  Just stop on it and roll back and forth, trying to break it up.  Keep treating any knots you find in your thigh muscles.

A Good Stretch For Your Psoas Muscle 

Next stretch your psoas muscle. There is a yoga stretch that will help to stretch your psoas muscle, rotate your pelvis back into alignment, and take the pressure off both the sciatic and femoral nerves. The stretch is called the Sphinx.

Lie down with your pelvis firmly resting on the floor.

Put your bent elbows directly under your shoulders as shown in this picture.

Lean back, keeping your pelvis and elbows on the floor.

You are stretching the psoas muscle that is rotating your pelvis.

When you are comfortable doing this stretch, then you can do it standing up:

Put your calves up against the cabinet under your kitchen sink, and your butt gently pressing on the front of the sink.  These must stay still, don’t change the pressure at all or you have moved your pelvis.

Pivot at your lumbar vertebrae, leaning back with your upper back, while keeping your head as shown in the picture.

If you feel increased or decreased pressure on your butt, you have moved your pelvis.  Keep trying until you can lean back without moving your pelvis at all.

This is a start to treating the muscles that may be causing RLS.  Since muscles are the one thing the medical profession doesn’t look at, there’s a good chance this will help you!

Wishing you well,

Julie Donnelly 

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

A Diet To Die For

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Which Diet Is Best? 

Author: Dr. Stephen Chaney

Heart AttackMany clinical studies focus on the benefits or risks associated with individual components of our diet. For example, we have been told:

  • Saturated and trans fats are bad for us and monounsaturated and omega-3 fats are good for us.
  • Sugar and refined carbohydrates are bad for us, but complex carbohydrates are good for us.

However, we don’t eat saturated fats or sugars in isolation. They are part of a diet with many other foods. Do other foods in our diet affect the risks we associate with saturated fat or sugar? We don’t know.

Simply put, we don’t eat foods, we eat diets. We don’t eat saturated fats, we eat diets. It would be more helpful for the average person if research focused on which diets are good and bad for us instead of which foods are good and bad for us.

One recent study (JM Shikany et al, Journal of the American Heart Association, 10:e019158, 2021) did just that. It evaluated the effect of 6 different dietary patterns on the risk of sudden cardiac death (dropping dead from a stroke or heart attack).

  • It turns out that one of the diets significantly increases your risk of sudden cardiac death. I call that one, “A diet to die for”.
  • Another diet significantly decreases your risk of sudden cardiac death. I call that one, “A diet to live for”.
  • The other diets had no significant effect on the risk of sudden cardiac death.

You are probably wondering, “What were the diets?”; “Which diet is best?”; and “Which diet is worst?” I cover that below, but first we should look at how the study was designed.

How Was The Study Designed?

Clinical StudyThe study involved 21,069 participants in the REGARDS (Reasons for Geographical and Racial Differences in Stroke) clinical trial who were followed for an average of 10 years. This clinical trial enrolled:

  • 30% of its participants from what is called the “the stroke belt” (North Carolina, South Carolina, Georgia, Tennessee, Alabama, Mississippi, Arkansas, and Louisiana).
  • 20% of its participants from what is called “the stroke buckle” (the coastal plain of North Carolina, South Carolina, and Georgia).
  • 50% of its participants from elsewhere in the continental United States.

At the beginning of the study, participants were given a medical exam and filled out an extensive questionnaire on diet.

Based on the diet analysis, the participants were ranked for adherence to six dietary patterns.

#1: The Convenience Pattern. This dietary pattern relied heavily on pre-packaged or restaurant meals, pasta dishes, pizza, Mexican food, and Chinese food.

#2: The Plant-Based Pattern. This dietary pattern relied heavily on vegetables, fruits, fruit juice, cereal, beans, fish, poultry, and yogurt.

#3: The Sweets Pattern. This dietary pattern relied heavily on added sugars, desserts, chocolate, candy, and sweetened breakfast foods.

#4: The Southern Pattern. This dietary pattern relied heavily on added fats, fried food, eggs and egg dishes, organ meats, processed meats, and sugar-sweetened beverages.

#5: The Alcohol and Salad Pattern. This dietary pattern relied heavily on beer, wine, liquor, green leafy vegetables, tomatoes, and salad dressing.

#6: The Mediterranean Pattern. Adherence to the Mediterranean dietary pattern was based on the well-established Mediterranean Diet Score.

  • Points are added for beneficial foods (vegetables, fruits, legumes, whole grain cereals, nuts, and fish).
  • Points are subtracted for detrimental foods (meat and dairy).
  • Points are added for a high ratio of monounsaturated fats to saturated fats (think diets rich in olive oil).
  • One point is added for moderate alcohol consumption, Zero or excess alcohol consumption is assigned 0 points.

The study looked at the correlation of these dietary patterns with the incidence of sudden cardiac death during the 10-year study.

A Diet To Die For

deadThe results were striking.

  • The Southern Diet increased the 10-year risk of sudden cardiac death 2.2-fold. Basically, it doubled the risk.
    • In people with no previous history of heart disease at the beginning of the 10-year study, the Southern Diet increased the risk of sudden cardiac death by 2.3-fold.
    • In people with a previous history of heart disease at the beginning of the 10-year study, the Southern Diet increased the risk of sudden cardiac death by 2-fold.
  • The Mediterranean Diet decreased the 10-year risk of sudden cardiac death 41%.
    • In people with no previous history of heart disease at the beginning of the 10-year study, the Mediterranean Diet decreased the risk of sudden cardiac death by 51%. Basically, it cut the risk in half.
    • In people with a previous history of heart disease at the beginning of the 10-year study, the Mediterranean Diet decreased the risk of sudden cardiac death by 23%, but that decrease was not statistically significant.
  • None of the other diets had a significant effect on the 10-year risk of sudden cardiac death.

In the words of the authors, “We identified a trend towards an inverse association of the Mediterranean diet score and a positive association of adherence to the Southern dietary pattern with risk of sudden cardiac death.” [That is a fancy way of saying the Mediterranean diet decreased the risk of sudden cardiac death, and the Southern dietary pattern increased the risk of sudden cardiac death.]

Which Diet Is Best?

AwardThe Mediterranean Diet Is Best: In this analysis of the effects of 6 different dietary patterns on the risk of sudden cardiac death, it is obvious that the Mediterranean diet is best. It cut the risk of sudden cardiac death in half.

This should come as no surprise:

  • I have reported on a previous study showing that the Mediterranean diet decreases the risk of heart disease by 47%.
  • In the Woman’s Health Study the Mediterranean diet decreased the risk of sudden cardiac death by 36%.
  • In the Nurses’ Health Study there was an inverse association between the Mediterranean Diet Score and sudden cardiac death.

The Southern Dietary Pattern Was Worst. It doubled the risk of sudden cardiac death. As someone who grew up in the South, this comes as no surprise to me. Let me count the ways:

  • It starts with a breakfast of fried eggs, grits with “red-eye gravy” (a mixture of ham drippings and coffee), ham or sausage, and biscuits made with lots of lard and sugar.
  • When I was growing up, a snack might be an RC cola and moon pies (look that one up).
  • Dinner might be fried chicken and hushpuppies or fried fish and hushpuppies.
  • Instead of picnics we have pig pickins (which is pretty much what it sounds like).
  • And we boil our vegetables with fatback (pig fat) and sugar.

I could go on, but you get the picture. Don’t get me wrong, I have fond memories of the foods I ate while growing up in the South. I just don’t eat them much anymore.

Why Didn’t The Plant-Based Dietary Pattern Score Better? One of the surprises from this study was that the Plant-Based Dietary Pattern didn’t score better. After all, numerous studies have shown that mostly plant-based diets reduce the risk of heart disease. Why did it strike out in this study?Vegan Foods

My feeling is that the study did not adequately describe a true Plant-Based Dietary Pattern. As I described above, participants following the Plant-Based Dietary Pattern were identified as having above average consumption of vegetables, fruits, fruit juice, cereal, beans, fish, poultry, and yogurt compared to others in this study. I have two concerns with this classification.

  • As described, this is a semi-vegetarian diet, while the best results for reducing heart disease risk are seen with strict vegetarian and lacto-ovo-vegetarian diets.
  • However, my biggest concern is that we don’t know what other foods they were consuming. Were they also consuming convenience foods? Were they consuming sweets? We don’t know.

That is very different from the two dietary patterns that stood out in this study.

  • 50% of the participants in this study came the Southeastern region of the United States. So, when the study identified participants as following a Southern Dietary Pattern based on a few southern foods, it is likely that those participants ate many other southern foods as well.

If 50% of the participants in the study had come from the Loma Linda area of California where vegetarianism is much more common, the study might have done a better job of identifying participants consuming a plant-based diet.

  • While participants consuming the Mediterranean diet were more scattered geographically, the Mediterranean Diet Score used to identify people consuming a Mediterranean diet is much more detailed and has been validated in numerous previous studies.

In short, the Southern and Mediterranean Dietary Patterns may have stood out in this study because they provided a more precise distinction between those consuming a Southern or Mediterranean diet and those following other dietary patterns. If the Plant-Based Dietary Pattern had been more precisely described, it might have shown a statistically significant benefit as well.

The Bottom Line

Many clinical studies focus on the benefits or risks associated with individual components of our diet.

However, we don’t eat foods, we eat diets. It would be more helpful for the average person if research focused on which diets are good and bad for us instead of which foods are good and bad for us.

One recent study did just that. It evaluated the effect of 6 different dietary patterns on the risk of sudden cardiac death (dropping dead from a stroke or heart attack).

  • It turns out that the Southern diet doubles your risk of sudden cardiac death. I call that one, “A diet to die for”.
  • In contrast, the Mediterranean diet cuts your risk of sudden cardiac death in half. I call that one, “A diet to live for”.
  • The other diets had no significant effect on the risk of sudden cardiac death.

For more details on the study, why the Southern diet is so bad for us, and why the Mediterranean diet is so good for us, read the article above.

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

Best Way To Reduce Risk Of Breast Cancer

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What Does The American Cancer Society Say About Reducing Breast Cancer Risk? 

Author: Dr. Stephen Chaney

breast cancerBreast cancer is a scary disease. The American Cancer Society tells us:

  • 281,000 women will be diagnosed with invasive breast cancer in 2021.
  • 43,000 women will die from breast cancer in 2021.
  • The good news is that both prevention and treatment of breast cancer have gotten much better:
    • The 5-year survival rate is 90%.
    • The 10-year survival rate is 84%.
    • For women over 50 the death rate has decreased by 1%/year between 2013 and 2018 (mainly due to recognition that hormone replacement therapy is a risk factor for breast cancer).
  • The bad news is:
    • The cost of breast cancer treatment can range from $50,000 to over $180,000.
    • The side effects of breast cancer treatment can be brutal.
      • For example, there is an effective treatment to prevent breast cancer recurrence for some forms of breast cancer, but many women discontinue the treatment after a few years because of the side effects.

So, wouldn’t it be wonderful if there were some simple changes you could make that would dramatically reduce your risk of developing breast cancer in the first place? There are lots of options for reducing your risk of developing breast cancer, but which one(s) should you choose?

  • Dr. Strangelove and his friends are only too happy to recommend their favorite potion, food, or diet.
  • There are long lists of foods you should avoid if you want to reduce your risk of breast cancer.
  • There are also lists of harmful chemicals in cleaners and other household products that you should avoid.

It can become confusing. It can become overwhelming. It would be easy to just throw up your hands and say, “I give up. I don’t know what to do.”

You may be thinking, “Why doesn’t someone simplify things by identifying the top few lifestyle changes that are most effective for reducing my risk of developing breast cancer?”

It turns out someone has. Today I will share two recent studies that have identified the top 6 strategies for reducing your risk of breast cancer, and I have ranked them from 1 to 6 in order of effectiveness.

What Is The Best Way To Reduce Risk Of Breast Cancer?

AwardThe first study (RM Tamimi et al, American Journal of Epidemiology, 184: 884-893, 2016 was designed to identify the major modifiable risk factors for invasive, postmenopausal breast cancer (The term “modifiable risk factors” refers to those risk factors that are under your control.

The study utilized data collected from the Nurses’ Health Study between 1980 and 2010. During that time 8,421 cases of invasive breast cancer were diagnosed in 121,700 postmenopausal women in the study. The study looked at the effect of nonmodifiable and modifiable risk factors on the development of invasive breast cancer in these women.

  • Nonmodifiable risk factors included current age, age at which menstruation began, height, age of first birth, number of births, weight at age 18, family history of breast cancer, and prior benign breast disease.
  • Modifiable risk factors included weight change since age 18, alcohol consumption, physical activity level, breastfeeding, and postmenopausal hormone therapy use.

Here were the results from the study:

  • All the risk factors included in this study accounted for 70% of the risk of developing invasive breast cancer in postmenopausal women.
  • Modifiable risk factors accounted for 34.6% of the risk of developing invasive breast cancer in postmenopausal women.

When they analyzed the effect of modifiable risk factors on the risk of developing invasive breast cancer separately:

  • 44 pounds of weight gain since age 18 increased the risk by 50%.
  • Postmenopausal hormone replacement use increased the risk by 35%.
  • More than one alcoholic beverage/day increased the risk by 32%.
  • Low physical activity increased the risk by 7%.
  • Lack of breastfeeding increased the risk by 5%.

What About The Effect Of Diet On Breast Cancer Risk?

You may be wondering, “What about the effect of a healthy diet on my risk developing invasive breast cancer?” Unfortunately, the study I described above completely disregarded the effect of diet on breast cancer risk.

However, the second study (MS Farvid et al, International Journal of Cancer, 144: 1496-1510, 2019) I will discuss today partially addresses this issue. It uses the same database as the first study and looks at the effect of fruit and vegetable consumption on the risk of developing invasive breast cancer.

When this study compared high versus low intake of fresh fruits and vegetable on the risk of developing invasive breast cancer:

  • Women eating >5.5 servings/day of fruits and vegetables had a 11% lower risk than women consuming ≤2.5 servings/day.
  • Women consuming >2.5 servings/day of fruit had a 9% lower risk than women consuming ≤0.5 servings/day.
  • Women consuming >4.5 servings/day of vegetables had a 9% lower risk than women consuming ≤0.5 servings/day.

While all fresh fruits and vegetables contributed to this effect:

  • The most protective fruits were berries and cantaloupe & melons.
  • The most protective vegetables were yams & sweet potatoes, green leafy vegetables (such as kale, mustard greens, and chard), and cruciferous vegetables (such as Brussels sprouts).

The authors concluded, “Our findings support that higher intake of fruits and vegetables, and specifically cruciferous and yellow/orange vegetables, may reduce the risk of breast cancer, especially those that are more likely to be aggressive tumors.”

Now we are ready to answer your question, “Which lifestyle changes are most effective for reducing your risk of developing breast cancer?” If we combine the two studies and rank order the modifiable risk factors, it would look like this.

#1: Minimize weight gain during your adult years.

#2: Don’t use postmenopausal hormone replacement therapy unless absolutely necessary.

#3: Drink little or no alcohol.

#4: Eat a healthy diet with lots of fresh fruits and vegetables.

#5: Be physically active.

#6: Breastfeed when possible.

What Does The American Cancer Society Say About Reducing The Risk Of Breast Cancer?

American Cancer SocietyThe advice of the American Cancer Society is remarkably similar. Here are their recommendations:

  1. Get to and stay at a healthy weight.

After menopause, most of your estrogen comes from fat tissue. Having more fat tissue increases the amount of estrogen your body makes, raising your risk of breast cancer. Also, women who are overweight tend to have higher levels of insulin. Higher insulin levels have also been linked to breast cancer.

If you are already at a healthy weight, stay there. If you are carrying extra pounds, try to lose some. Losing even a small amount of weight can also have other health benefits and is a good place to start.

3) Be physically active and avoid time spent sitting.

Current recommendations are to get at least 150-300 minutes of moderate intensity or 75-150 minutes of vigorous intensity activity each week. Getting to or exceeding 300 minutes is ideal.

In addition, you should limit sedentary behavior such as sitting, lying down, watching TV, and other forms of screen-based entertainment. This is especially important if you spend most of your working day sitting.

3) Follow a healthy eating plan.

A healthy eating pattern includes a variety of vegetables, fiber-rich legumes (beans and peas), fruits in a variety of colors, and whole grains. It is best to avoid or limit red and processed meats, sugar-sweetened beverages, highly processed foods, and refined grain products. This will provide you with key nutrients in amounts that help you get to and stay at a healthy weight.

4) It is best not to drink alcohol.

Research has shown that drinking any alcohol increases the risk of breast cancer. If you choose to drink alcohol, the American Cancer Society recommends that women have no more than 1 alcoholic drink on any given day. A drink is 12 ounces of regular beer, 5 ounces of wine, or 1.5 ounces of hard liquor.

5) Think carefully about using hormone replacement therapy.

Studies show that HRT using a combination of estrogen and progestin increases the risk of breast cancer. This combination can also lead to increased breast density making it harder to find breast cancer on mammogram.

Talk with your doctor about all the options to control your menopause symptoms, including the risks and benefits of each. If you decide to try HRT, it is best to use it at the lowest dose that works for you and for as short a time as possible.

The Bottom Line

Breast cancer is a scary disease. The good news is that detection and treatment of breast cancer has improved over the past decade. The bad news is that treatment is expensive, and the side effects can be brutal.

There are lots of options for reducing your risk of developing breast cancer, but which one(s) should you choose?

  • Strangelove and his friends are only too happy to recommend their favorite potion, food, or diet.
  • There are long lists of foods you should avoid if you want to reduce your risk of breast cancer.
  • There are also lists of harmful chemicals in cleaners and other household products that you should avoid.

It can become confusing. It can become overwhelming. It would be easy to just throw up your hands and say, “I give up. I don’t know what to do.”

You may be thinking, “Why doesn’t someone simplify things by identifying the top few lifestyle changes that are most effective for reducing my risk of developing breast cancer?”

It turns out someone has. Today I will share two recent studies that have identified the top 6 strategies for reducing your risk of breast cancer, and I have ranked them from 1 to 6 in order of effectiveness in the article above.

For more details about these studies, my ranking of the top 6 strategies for reducing your risk of breast cancer, and the American Cancer Society recommendations, read the article above.

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

Is Low Omega-3 Intake As Bad For You As Smoking?

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

Author: Dr. Stephen Chaney

deadWe already know that smoking is one of the worst things we can do to our bodies. It dramatically increases our risk of cancer, heart disease, diabetes, and lung diseases, including chronic obstructive pulmonary disease (COPD).

It also leads to premature death. People who smoke regularly die 5 years earlier than those who don’t.

That is the bad news. The good news is that smoking is what is called a “modifiable risk factor”. Simply put, that means it is a risk factor we are in control of. The message has been clear for years.

  • If you don’t smoke, keep it that way.
  • If you do smoke, stop. If you are a smoker, quitting isn’t easy, but it is worth it. The damage caused by smoking can largely be reversed if you stay off cigarettes long enough.

Obesity and diabetes are also modifiable risk factors that have a huge effect on the risk of both heart disease and premature death. People with diabetes die 4 years earlier than those without diabetes. But obesity and diabetes are harder for most people to reverse than smoking.

Diet is another modifiable risk factor, but, in general, its effect on the risk of heart disease and premature death is not as great as smoking and diabetes. But what if there were one component of diet that had huge effect on both heart disease and premature death?

The long chain omega-3 fatty acids (EPA & DHA) might just fill that bill. We already know they significantly reduce the risk of heart disease (see below), but could they also help us live longer? This study (MI McBurney et al, American Journal of Clinical Nutrition, published online June 16, 2021) was designed to answer that question.

Metabolism 101: What Is The Omega-3 Index And Why Is It Important?

professor owlClinical studies on the benefits of omega-3s have been plagued by the question of how to best measure the omega-3 status of the participants.

  • You can ask the participants to fill out a dietary survey and calculate how many omega-3-rich foods they are eating, but:
    • Dietary recall is notoriously inaccurate. People don’t remember everything they ate and have a hard time estimating portion sizes.
  • You can measure omega-3 fatty acids in the blood, but:
    • Blood levels are transient. Omega-3 fatty acids enter the bloodstream from the intestine and then disappear from blood as they are taken up by the cells.
    • Different forms of omega-3s (esters versus acetate, for example) are absorbed from the intestine and taken up by cells at different rates.
  • You can measure the omega-3 content of cellular membranes. This is the best assay for omega-3 status because:
    • The long chain omega-3 fatty acids (EPA and DHA) that have the biggest effect on heart disease risk accumulate in our cell membranes.
    • Omega-3 fatty acids are essential (our bodies can’t make them). That means the omega-3 content of our cell membranes reflect the omega-3 content of our diet. This is one of the cases where the saying, “We are what we eat”, is literally true.
    • The omega-3 content of our cell membranes is relatively stable. It reflects the omega-3 content of our diet over the last few months.
  • In theory, you could measure the omega-3 content of cell membranes from any tissues in the body, but red blood cells can easily be obtained by a simple blood draw, so they are the tissue of choice.

A group lead by Dr. William H Harris standardized this measurement by creating something called the Omega-3 Index. Simply put, the Omega-3 Index is the percentage of EPA and DHA in red blood cell membranes.

It turns out that the Omega-3 Index is an excellent indicator of heart disease risk.

  • An Omega-3 Index of less than 4% is associated with a high risk of heart disease.
  • An Omega-3 Index of more than 8% is associated with a low risk of heart disease.

But could a low Omega-3 Index also be associated with an increased risk of premature death? This is what the current study was designed to find out.

How Was This Study Done?

Clinical StudyThe data for this study were obtained from the ongoing Framingham Offspring Heart Study.

To put this statement into perspective, the original Framingham Heart Study began in 1948 in Framingham Massachusetts with the goal of identifying the factors that contributed to heart disease. It was one of the first major studies to identify the role of saturated fats, elevated blood cholesterol, and elevated blood triglycerides on heart disease risk.

The study is continuing today with the second and third generation descendants of the original study participants. It has also been broadened to include other diseases and additional risk factors, such as the Omega-3 Index.

This study selected 2240 participants from the Framingham Offspring study who had no heart disease and also had Omega-3 Index measurements at the beginning of the study. The study then followed them for 11 years. The goal of the study was to compare the Omega-3 Index with the two most potent risk factors for heart disease (smoking and diabetes) in predicting the risk of premature death.

The characteristics of the participants at the beginning of the 11-year study were:

  • 43% male, 57% female.
  • Average age = 65.
  • 3% were smokers.
  • 8% were diabetic.
  • Average Omega-3-Index = 5.8%. This is slightly higher than the American average of ~5%.

Is Low Omega-3-Intake As Bad For You As Smoking?

omega-3 supplements and heart healthThe participants in the study were divided into 5 quintiles based on their Omega-3 Index.

  • The 20% of the group in the lowest quintile had an Omega-3 Index of <4.2%.
  • The 20% of the group in the highest quintile had an Omega-3 Index of >6.8%.

First, the scientists running the study did a direct comparison of the top three risk factors on the risk of premature death. Here is what they found.

  • The group with the lowest average Omega-3 Index died 4.74 years earlier than the group with the highest average Omega-3 Index.
  • Smokers died 4.73 years earlier than non-smokers.
  • People with diabetes died 3.90 years earlier than people without diabetes.

That means low omega-3 intake was just as bad for the participants in this study as smoking. Even the authors of the study were surprised by this result. They had expected omega-3 fatty acids to be beneficial, but they had not expected them to be as beneficial as not smoking.

Because omega-3 fatty acid intake and smoking were the two most potent risk factors for premature death, the authors looked at the interaction between the two. They found that the predicted 11-year survival was:

  • 85% for non-smokers with high omega-3 intake.
  • 71% for either…
    • Smokers with high omega-3 intake, or…
    • Non-smokers with low omega-3 intake.
  • Only 47% for smokers with low omega-3 intake.

Simply put, this study predicts if you were a 65-year-old smoker with low omega-3 intake, you could almost double your chances of surviving another 11 years by giving up smoking and increasing your omega-3 intake.

In the words of the authors, “Smoking and omega-3 intake seem to be the most easily modified risk factors [for premature death]…Dietary choices that change the Omega-3 index may prolong life.”

The Bottom Line

We know that smoking is deadly, but could low intake of omega-3 fatty acids be just as deadly?

A recent study compared omega-3 intake with the two most potent risk factors (smoking and diabetes) in predicting the risk of premature death. Here is what it found.

  • The group with the lowest average omega-3 intake died 4.74 years earlier than the group with the highest average omega-3 intake.
  • Smokers died 4.73 years earlier than non-smokers.
  • People with diabetes died 3.90 years earlier than people without diabetes.

That means high omega-3 intake was just as beneficial for the participants in this study as not smoking. Even the authors of the study were surprised by this result. They had expected omega-3 fatty acids to be beneficial, but they had not expected them to be as beneficial as not smoking.

Because omega-3 fatty acid intake and smoking were the two most potent risk factors for premature death, the authors looked at the interaction between the two. They found that the predicted 11-year survival was:

  • 85% for non-smokers with high omega-3 intake.
  • 71% for either…
    • Smokers with high omega-3 intake, or…
    • Non-smokers with low omega-3 intake.
  • Only 47% for smokers with low omega-3 intake.

Simply put, this study predicts if you were a 65-year-old smoker with low omega-3 intake, you could almost double your chances of surviving another 11 years by giving up smoking and increasing your omega-3 intake.

In the words of the authors, “Smoking and omega-3 intake seem to be the most easily modified risk factors [for premature death]…Dietary choices that change the Omega-3 index may prolong life.”

For more details about this study, 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 Collagen Supplements Build Muscle?

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Could Collagen Supplements Make You Leaner? 

Author: Dr. Stephen Chaney

Sports SupplementsCollagen supplements have been considered “vanity products”. Their largest market is people who want to have younger, more beautiful skin. And for many people, collagen delivers on this promise.

However, collagen plays many other roles in the body. It also helps rebuild tendons and ligaments. Many people take collagen supplements to reduce joint pain.

But could collagen supplements coupled with resistance training also build muscle and reduce fat? If so, that would be huge.

A recent study (D Zdzieblik et at, British Journal of Nutrition, 114: 1237-1245, 2015) suggested collagen supplements may do just that. This study showed that a collagen supplement plus resistance training increased lean muscle mass and decreased fat mass in elderly men (average age = 72).

If this finding is duplicated in future studies, it has significant health implications. Both men and women in their 70s lose muscle mass at a rapid rate (a process called sarcopenia). Anything that slows or reverses this process has the potential to extend high quality life and prolong their golden years.

But what about younger adults? Could a collagen supplement plus resistance training also help them build muscle and lose fat? This study (D Zdzieblik et at, International Journal of Environmental Research and Public Health, 18: 4837-4855, 2021) was designed to answer that question.

It was a randomized, placebo-controlled study comparing 15 g of collagen peptides with 15 g of whey protein, and a placebo (silicon dioxide).

How Was This Study Done?

couch potatoThe study recruited 120 middle-aged (average age = 50), overweight (average BMI = 30) men who were untrained (<60 minutes of exercise per week over the previous year). [In other words, the study recruited middle-aged couch-potatoes.]

The participants were asked to fill out a three-day diet analysis at the beginning and end of the 12-week study with the assistance of a nutritionist.

  • Average caloric intake was 2,600 calories/day.
  • Average protein intake was 104 grams/day. That is 30% higher than the recommended protein intake for men of that age and weight.
  • The macronutrient content of the diet was 16% protein, 37% fat, and 43% carbohydrate.
  • These values were not significantly different between groups and did not change during the study.

All participants participated in a one-hour training program three times per week. The training began with a 10-minute cardio exercise to warm up. That was followed by a three-set program consisting of horizontal leg presses (both legs), reverse crunches, lat-pull exercise, sit-ups, and chest presses with 1 to 2 min rest periods between sets. The intensity of exercise was gradually increased over the 12-week study.

The participants were randomly divided into three groups. After each workout they were given sachets containing 15 g of collagen peptides, 15 g of whey isolate, or 15 g of silicon dioxide (placebo). They were instructed to dissolve the powder in 8 ounces of water and drink it within one hour of the workout. They were also given the same sachets and instructed to take them at the same time of day for the days they were not working out.

Finally, the participants were instructed not to change their diet or physical activity apart from the intake of the powder in the sachets they were given and the one-hour training sessions.

Do Collagen Supplements Build Muscle?

Collagen Supplement & Muscle MassAll three groups had statistically significant:

  • Increases in percent lean muscle mass.
  • Decreases in percent fat mass.
  • Increases in leg muscle strength.

No surprises here. If you take a group of middle-aged couch-potatoes and put them in a strength training program, you will see increases in lean muscle mass, decreases in fat mass, and increases in muscle strength.

The real question was what was the effect of the collagen and whey protein supplements? This is where the results got really interesting.

  • The collagen peptide supplement gave a significantly greater increase in lean muscle mass and decrease in fat mass than the placebo. The increase in leg muscle strength was also greater than the placebo, but this difference was not statistically significant.
  • The whey protein supplement also increased lean muscle mass and decreased fat mass compared to the placebo, but these differences were not statistically different.

In other words, at the doses used in this study (see next section for discussion), the collagen supplement worked better than the whey protein supplement. Here is the actual data from the study:

  • Increase in percent lean muscle mass: collagen supplement = 7.4%, whey protein supplement = 5.8%. placebo = 5.0%.
  • Decrease in percent fat mass: collagen supplement = 15%, whey protein supplement = 11.5%, placebo = 10%.

In the words of the authors, “In conclusion, collagen peptide supplementation combined with resistance training was associated with a significantly greater increase in fat free mass and a decrease in fat mass compared with placebo. Resistance training combined with whey protein also had a positive impact on body composition, but the respective effects were more pronounced following the collagen peptide administration.”

Could Collagen Supplements Make You Leaner?

strengths-weaknessesThis study leaves lots of questions. Let me handle the main ones here.

What Are The Strengths and Weaknesses Of The Study?

The strengths are obvious. This was a well-design, randomized, placebo-controlled clinical trial, which is the gold standard for determining the efficacy of a treatment.

The weaknesses are also obvious. This was a very small clinical study. There is one previous study that showed the same benefit of collagen in an older age group. However, both studies were published by the same group of scientists. And these scientists were funded by the manufacturer of the collagen product used in the study. More and larger studies performed by other laboratories are needed to confirm this finding.

How Do Resistance Exercise, Whey Protein, And Collagen Stimulate Muscle Growth?

Muscle growth is stimulated by a regulatory pathway called mTOR that (among other things) regulates protein Weight Trainingsynthesis in muscle cells. For the purposes of this article, I will discuss 3 mechanisms for activating mTOR and increasing muscle protein synthesis.

#1: Resistance exercise (weight training) activates mTOR. That should come as no surprise. The main reason people do weight training is to increase strength and muscle mass. mTOR is the pathway that makes this possible.

#2: Whey protein is rich in the essential amino acid leucine, and leucine also stimulates the mTOR pathway.

  • Leucine is one of three branched chain amino acids. While all three branched chain amino acids have been traditionally credited with stimulating muscle protein synthesis, recent research has shown that only leucine is needed. The other two branched chain amino acids just play a supportive role. You only need enough of the them to make a complete protein.
  • While whey protein gets all the attention in the sports world, any complete protein with high levels of leucine has the same effect.
  • The effect of leucine and resistance training on the mTOR pathway are additive. That is why whey and other leucine-rich proteins enhance the effect of resistance exercise on both muscle mass and strength.

#3: Collagen does not contain enough leucine to activate the mTOR pathway. However, the authors have proposed another mechanism to account for collagen activation of the mTOR pathway.

  • Most proteins we eat are digested to their individual amino acids before they are absorbed. However, collagen is rich in an unusual amino acid called hydroxyproline that makes collagen resistant to our digestive enzymes.
  • Thus, collagen is not digested to individual amino acids, but to small peptides that are absorbed from our intestine.
  • One of these breakdown products, a dipeptide composed of glycine and hydroxyproline, has been shown to stimulate the mTOR pathway.

While this mechanism has not been proven, collagen does appear to enhance the effect of resistance exercise on both muscle mass and strength.

Collagen Only Has 8 Essential Amino Acids. How Could It Stimulate The Synthesis Of Muscle Protein, Which Requires 9 Essential Amino Acids?

Question MarkThe answer is simple. The people in this study were consuming 30% more than the recommended amount of protein in their diet in addition to the collagen supplement. They already had all the essential amino acids needed to synthesize muscle protein. The collagen supplement simply stimulated the rate of muscle protein synthesis by activating the mTOR pathway.

However, there are situations in which the 9th essential amino acid could become important for muscle protein synthesis. Here are two examples

  • Vegans and strict vegetarians might not be getting enough protein in their diet. As I pointed out in a previous article vegan “experts” know how to get enough protein from their diet, but many vegan “novices” do not.
  • Older Americans are also at risk. They need extra protein in their diet to prevent sarcopenia (muscle loss) as they age. And some of them are on restrictive diets, either because of the latest fad or because of loss of income and/or mobility.

Why Did The Collagen Supplement Work Better Than Whey Protein In This Experiment? 

Again, the answer is simple. Both collagen and leucine-rich proteins like whey enhance muscle protein synthesis by activating the mTOR pathway (see above). This study used the same amount of protein (15 g/day) for both collagen supplement and the whey protein supplement.

While 15 g/day appears to be optimal for the collagen supplement, the authors pointed out that previous studies suggest that the optimal dose for whey protein is closer to 20 g/day for middle-aged men.

So, I would ignore the apparent difference in effectiveness of the collagen and whey protein supplements.

The important conclusion is that both collagen and leucine-rich proteins like whey enhance the effect of resistance exercise on lean muscle mass to a similar extent. But they appear to do so by slightly different mechanisms.

What Does This Mean For You?

This study is intriguing. It suggests that collagen may have some tricks up its sleeve we didn’t know about.

  • It may do more than give you a healthy, youthful looking skin.
  • It may do more than help with achy joints.
  • Coupled with resistance exercise it may also help you increase muscle mass and reduce fat mass. It may make you leaner.

The Bottom Line

Collagen supplements have been considered “vanity products”. Their largest market is people who want to have younger, more beautiful skin. And for many people, collagen delivers on this promise.

However, collagen plays many other roles in the body. It also helps rebuild tendons and ligaments. Many people take collagen supplements to reduce joint pain.

But collagen may have other tricks up its sleeve. A recent study suggests that collagen supplements may enhance the effect of resistance exercise on increased muscle mass and reduced fat mass. It may make you leaner.

The study also concluded that both collagen and whey protein enhance the effect of resistance exercise on lean muscle mass to a similar extent. But they appear to do so by slightly different mechanisms.

Let me be clear. I am not recommending you take a collagen supplement to help you build muscle mass. I consider these results as preliminary, and we have good evidence that leucine-rich proteins plus resistance exercise helps build muscle mass. 

However, if you are taking a collagen supplement for another reason and are working out, this could be an unexpected benefit.

For more details about this study and how collagen supplements may increase muscle mass, read the article above.

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

Health Tips From The Professor