Dr. Steve Chaney

Can Artificial Sweeteners Make You Hungry?

by

Why Is There So Much Confusion About Artificial Sweeteners? 

Author: Dr. Stephen Chaney

Artificial SweetenersWhen artificial sweeteners were first introduced over 100 years ago, we were promised they would end obesity. We didn’t have to change our diets. We could just substitute calorie-free artificial sweeteners for sugar in all our favorite foods.

Since then, both consumption of artificial sweeteners and obesity have skyrocketed in this country. For example, in just the past 20 years:

  • The consumption of artificial sweeteners has increased by 54%, and…
  • The percentage of obese Americans has increased by 41%.

Today, over 40% of Americans are obese, and almost 10% of Americans are severely obese. That is a 4-fold increase since 1960!

Clearly, something isn’t working. Artificial sweeteners are not the magic solution we once thought they would be.

However, as I have told you before, association does not prove causation. Therefore, two important questions are:

  1. Are we consuming more artificially sweetened foods and drinks because more of us have become obese, or…

2) Do artificial sweeteners cause obesity?

Unfortunately, hundreds of clinical studies on this topic have not provided a definitive answer. For example, when we look at studies on diet sodas:

When the studies are tightly controlled by dietitians so that the people consuming diet sodas don’t add any extra calories to their diet, the results are exactly as expected. People consuming diet sodas lose weight compared to people drinking regular sodas.

However, the results are different in the real world where you don’t have a dietitian looking over your shoulder. In these studies, diet sodas are just as likely to cause weight gain as regular sodas.

As Barry Popkin, a colleague at the University of North Carolina, put it” “The problem is that we [Americans] areNo Fast Food using diet sodas to wash down our Big Macs and fries.” In short, people drinking diet sodas tend to increase their caloric intake by adding other foods to their diet. Even worse, the added foods aren’t usually fruits and vegetables. They are highly processed junk foods.

In other words, the suspicion is that artificial sweeteners may cause you to overeat. Various mechanisms for this effect have been proposed. For example, it has been proposed that artificial sweeteners may:

  • Increase your appetite.
  • Interfere with blood sugar control.
  • Increase your cravings for sweets.
  • Alter your gut bacteria.

Unfortunately, clinical studies designed to test these hypotheses have produced inconsistent results. So, we are left with the question:

3) Why are studies on artificial sweeteners so confusing? 

A recent clinical study (AG Yunker et al, JAMA Network Open, 4(9):e2126313, 2021) sheds light on all 3 of these important questions.

How Was This Study Done?

Clinical StudyThis study was called the “Brain Response to Sugar” study. It was designed to test the hypothesis that previous studies of artificial sweeteners may have provided misleading results because they didn’t account for the sex and BMI (a measure of obesity) of the study participants.

Many previous studies had primarily enrolled male, ideal weight participants. This study hypothesized that the response to artificial sweeteners might be different in female, overweight participants.

This study recruited 76 participants from the Southern California area between July 2016 and March 2020, when recruitment was halted because of the COVID-19 pandemic. The characteristics of the participants were:

  • 18-35 years old.
  • Weight stable for at least 3 months before the study.
  • Not taking medications and no history of eating disorders, diabetes, or other diseases.
  • 42% male and 58% female.
  • 37% healthy weight, 32% overweight, and 31% obese.
  • 40% included artificial sweeteners in their diet prior to the study, 60% did not.

The study was what is called a “within-participant randomized crossover trial”. Simply put, this means that each participant served as their own control. Here is how it worked:

  • Each participant came to the Dornsife Cognitive Neuroimaging Center three times. They arrived at the testing center at 8 AM after an overnight fast.
    • They drank either 75 grams of sucrose in 300 mL of water, enough sucralose in 300 mL of water to provide equivalent sweetness, or 300 mL of plain water at the beginning of each visit. The order in which the drinks were administered was randomized.
  • At 20 minutes after each drink, the participants were placed into an MRI machine shown various food and non-food images.
    • Four high-calorie food images (2 sweet and 2 savory), 4 low-calorie food images, and 4 non-food images were shown to the participants in random order.
    • As the images were shown, the MRI scanned the medial frontal cortex and orbitofrontal cortex, regions of the brain associated with appetite and hunger. Specifically, these are regions of the brain that affect:
      • Conditioned motivation to eat.
      • The reward value associated with food cues.
      • In addition, greater food cue reactivity in these regions of the brain has been shown to be associated with obesity.
  • At 125 minutes after each drink, the participants were allowed to select their meal from a buffet table, and the calories consumed was recorded.

Can Artificial Sweeteners Make You Hungry?

HungryHere are the results of the study:

  • There was no overall difference in brain activity in the regions of the brain associated with appetite, hunger, and desire for high-calorie foods following the sucralose and sucrose drinks. However:
    • For participants who were obese, high-calorie savory food images elicited greater brain activity in participants who had consumed sucralose than in participants who had consumed sucrose drinks. This difference was not seen in patients who were normal weight or overweight.
    • For female participants, high-calorie sweet and savory food images elicited greater brain activity in participants who had consumed sucralose than in participants who had consumed sucrose drinks. This difference was not seen in male patients.
    • These differences were not small. The effect of sucralose on brain activity in regions that control appetite and hunger was several-fold greater than the effect sucrose on brain activity in these regions.
    • And as you might expect, the different response to sucralose and sucrose was greatest for women who were obese.
  • Participants consumed more calories at the buffet table after the sucralose drink than after the sucrose drink.
    • There was no significant effect of weight on the differential response to sucralose and sucrose. However:
    • The differential response to sucralose and sucrose was larger for female participants than for the whole group.
  • These results are consistent with previous studies suggesting that appetite responses to food cues might be greater in females and individuals with obesity. However, this was the first study designed to directly test this hypothesis.

The authors concluded, “Our findings indicate that female individuals and those who are obese, and especially female individuals with obesity, might be particularly sensitive to greater neural responsivity elicited by sucralose compared to sucrose consumption. This study highlights the need to consider individual biologic factors in research studies and potentially dietary recommendations regarding the use and efficacy of non-nutritive sweeteners [artificial sweeteners] for body weight management.”

[Note: You may have noticed that the authors extrapolated from their data on sucralose to all artificial sweeteners. Is this extrapolation valid? The short answer is, “We don’t know”. Most of the mechanistic studies have been done with sucralose, but some studies suggest these same effects may be seen with other artificial sweeteners.]

Why Is There So Much Confusion About Artificial Sweeteners?

confusionIt seems like a “no brainer” that zero calorie drinks and reduced calorie foods would reduce weight gain and promote weight loss. But that just doesn’t seem to happen in the real world. Why is that?

  • Is it psychological? Do we feel so virtuous about consuming artificially sweetened foods and drinks that we allow ourselves to splurge on high-calorie junk foods?
  • Or is it physiological? Do artificial sweeteners increase our appetite for high-calorie junk foods?

Unfortunately, clinical studies have not been much help. Some studies suggest that artificial sweeteners increase our appetite for high-calorie foods, while others suggest they don’t. Clinical studies are supposed to resolve questions like these. Why have they been so confusing?

Part of the problem is that some of the studies on artificial sweeteners have been too small and/or too poorly designed to provide clear-cut answers. However, even well-designed clinical studies have two fundamental flaws:

  • Clinical studies are based on averages. They assume everyone is the same.
    • This study, and others like it, show the flaw in that assumption.
      • It appears that artificial sweeteners affect the appetite for high calorie foods more in individuals who are obese than in individuals who are normal weight or slightly overweight.
      • Artificial sweeteners also affect the appetite for high calorie foods more for females than for males.
      • What about age and ethnicity? Is the effect of artificial sweeteners on the appetite for high calorie foods affected by age or ethnicity? No one knows.
      • What about genetics? Is the effect of artificial sweeteners dependent on our genetic background? No one knows.
      • What about our microbiome? Again, no one knows.
  • Gold standard clinical studies only change one variable at a time. In studies of artificial sweeteners, the variable is artificial sweetener versus sugar. But we don’t eat just artificial sweeteners or sugar. We eat foods containing artificial sweeteners or sugar. Do the foods we eat alter the effect of the artificial sweeteners on appetite?
    • One recent study) suggests they might. It found that consumption of sucralose plus easily digested carbohydrate (such as might be found in artificially sweetened junk foods) may increase the craving for sweets more than consumption of either sucralose or sucrose alone.

What Does This Study Mean For You?

Simply put, the initial promise of artificial sweeteners as a solution to the obesity epidemic and the alarming increase in diabetes has not been borne out by either clinical studies or real-life experience.

And I have not addressed the potential risks of artificial sweeteners in this article. However, in my opinion, something that has potential risks, no matter how small, and no proven benefit is something to avoid.

But don’t take my word for it. As I reported in a previous “Health Tips From the Professor” article, an international consortium of scientists recently reviewed all the pertinent literature and published a position paper on whether artificially sweetened beverages were of value in responding to the global obesity crisis. They concluded:

  • “In summary, the available evidence…does not consistently demonstrate that artificially-sweetened beverages are effective for weight loss or preventing metabolic abnormalities [pre-diabetes and diabetes]. Evidence on the impact of artificially-sweetened beverages on child health is even more limited and inconclusive than in adults.”
  • “The absence of evidence to support the role of artificially sweetened beverages in preventing weight gain and the lack of studies on their long-term effects on health strengthen the position that artificially-sweetened beverages should not be promoted as part of a healthy diet.”

The Bottom Line

When artificial sweeteners were first introduced over 100 years ago, we were promised they would end obesity. We didn’t have to change our diets. We could just substitute calorie-free artificial sweeteners for sugar in all our favorite foods.

Since then, both consumption of artificial sweeteners and obesity have skyrocketed in this country. Clearly, something isn’t working. Artificial sweeteners are not the magic solution we once thought they would be.

In recent years some studies have suggested that the reason that artificial sweeteners have failed us is that they stimulate our appetite for high calorie foods. However, this idea has been controversial. Some studies have supported it. Others have not.

Why have the clinical studies been so confusing? The study I describe in this article was designed to test the hypothesis that previous studies of artificial sweeteners may have provided misleading results because they didn’t account for the sex and BMI (a measure of obesity) of the study participants.

Many previous studies had primarily enrolled male, ideal weight participants. This study hypothesized that the response to artificial sweeteners might be different in female, overweight participants. The study found:

  • There was no overall difference in brain activity in the regions of the brain associated with appetite, hunger, and desire for high-calorie foods following consumption of drinks containing sucralose or sucrose. However:
    • For participants who were obese, high-calorie savory food images elicited greater brain activity in participants who had consumed sucralose than in participants who had consumed sucrose drinks.
    • For female participants, high-calorie sweet and savory food images elicited greater brain activity in participants who had consumed sucralose than in participants who had consumed sucrose drinks.
    • These differences were not small. The effect of sucralose on brain activity in regions that control appetite and hunger was several-fold greater than the effect sucrose on brain activity in those regions.
  • Participants consumed more calories at the buffet table after the sucralose drink than after the sucrose drink.
    • The differential response to sucralose and sucrose was larger for female participants than for the whole group.
  • These results are consistent with previous studies suggesting that appetite responses to food cues might be greater in females and individuals with obesity. However, this was the first study designed to directly test this hypothesis.

The authors concluded, “Our findings indicate that female individuals and those who are obese, and especially female individuals with obesity, might be particularly sensitive to greater neural responsivity elicited by sucralose compared to sucrose consumption. This study highlights the need to consider individual biologic factors in research studies and potentially dietary recommendations regarding the use and efficacy of non-nutritive sweeteners [eg, artificial sweeteners] for body weight management.”

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

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

Relief From Holiday Stress Headaches

by

Treatment For Pain In Your Temples 

Author: Julie Donnelly, LMT –The Pain Relief Expert

Editor: Dr. Steve Chaney 

Happy Thanksgiving. A Time To Count Our Blessings

It’s hard to believe that the holidays are upon us, this year just flew by!  I imagine we have all had ups and downs this year.  COVID is still here, albeit changing form and intensity.

Fortunately, many of us are vaccinated and the stats are showing that these people are having a milder case of the new variant.

I like to keep my vision on the idea that ultimately this will end, and we’ll be back to a semblance of normality again.  Let’s pray it’s happening sooner, rather than later!

2021 – A Year Of Vision And Determination For Me

For me, this time of COVID gave me the opportunity to focus more time on creating a course to teach my techniques to licensed massage therapists (LMTs). It’s something I’ve been wanting to do for many years, but I was so busy with therapy clients that I only dabbled in teaching.  Now I’m moving full speed ahead, with a goal of teaching nationwide to as many LMT’s as are willing to learn.

I’m also working with a golfer-client to edit a book I wrote several years ago. If it wasn’t for his curiosity about the book, and his excellent suggestions, this book would have lived it life out in my computer. The title is “The Secret to Your Best Golf Game EVER!”  If you aren’t flexible, your golf game will suffer.  But, if you release the knots in your joints, you’ll enjoy the game more, and your score will improve.  What a double-headed benefit!

There are other incredible projects that are in various stages of creation.  I know they will all materialize eventually. While 2021 has been a very trying year, it is also looking like an extremely productive and creative year!

What Do You Have To Be Grateful For This Year?

November is a great time of year to start to recap what has happened and be grateful for all the good that has come your way.  It’s the perfect opportunity before the real hectic season that December brings our way.  I hope you will enjoy revisiting your year, even if the primary gratitude you have is that it’s almost over!

 

Relief From Holiday Stress Headaches

headacheIt’s wonderful to have the holiday season before us, so many fun events to attend, time with family and friends, and delicious foods that are special for this time of year.

On the other hand, the holidays can also bring stress … and headaches!

You can read what seems like hundreds of articles about handling holiday stress, so we won’t go into that here. What we will focus on is a quick treatment you can do for yourself when you are having a headache.

pain free living book

In my book, Treat Yourself to Pain-Free Living I share several techniques to stop headache pain, and I’d like to share one with you right now.  This is one of my favorite techniques because it brings relief quickly.

 

Treatment For Pain In Your Temples

If your headache pain is in your temples, it is likely that your temporalis muscles are the culprits. The temporalis muscle is the cause of the throbbing you get in your temples when you have a headache.  Fortunately, it’s easy to find, and easy to self-treat.

Place your fingers as shown in this picture.  If you clench your teeth, you will feel the muscle “pop out.”  Then move your fingers up a little bit toward the top of your head and repeat the clenching movement.

To treat the muscle, just press your finger into a painful point and stay there without moving.  After a minute or so, continue pressing on the spot but move your fingers up and down on the same point.

To find other points, simply move your fingers and clench your teeth.  If you feel the muscle bulge, that’s a point to treat.

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 Diabetes Increasing In Our Children?

by

Why Is Diabetes Increasing In Our Children? 

Author: Dr. Stephen Chaney

Last week I shared a study documenting the alarming increase in ultraprocessed food consumption by our children and the effect it was having on their health (https://www.chaneyhealth.com/healthtips/are-we-killing-our-children-with-kindness/). For example, childhood obesity is closely linked to ultraprocessed food consumption.

In case you don’t understand why that is, here is what I said last week: “Because ultraprocessed foods are made in a factory, not grown on a farm:

  • They are high in fat, sugar, and refined carbohydrates. That means they have a high caloric density. Each bite has 2-3 times the calories found in a bite of fresh fruits and vegetables.
  • Even worse, the food industry has weaponized our natural cravings for sweet, salty, and fatty foods. They feed their prototypes to a series of consumer tasting panels until they find the perfect blend of sugar, salt, and fat to create maximum craving.
  • And if that weren’t enough, they add additives to create the perfect flavor and “mouth appeal”.
    • It is no wonder that clinical studies have found a strong correlation between high intake of ultraprocessed food and obesity in both children and adults.
    • It is also no wonder that the rate of childhood obesity has almost quadrupled in the last 40 years.”

Unfortunately, whenever you see an increase in obesity, type 2 diabetes is not far behind. Several studies have reported a dramatic increase in type 2 diabetes in our children over the last 20 years.

Because diabetics can manage their blood sugar levels with insulin and/or a variety of drugs, many people consider it as just an inconvenience. Nothing could be further from the truth. Diabetes is a deadly disease, and it is even deadlier when it appears early in life.

You probably already know that long-term complications of diabetes include heart disease and irreversible damage to nerves, kidneys, eyes, and feet. But you may not have known that childhood diabetes is more dangerous than diabetes in adults because:

  • It is more challenging to manage in children.
  • The complications of diabetes start to show up much earlier in life and affect quality of life at a much earlier age. For example:
    • Cardiovascular events occur 15 years earlier in someone with diabetes.
    • On average, a 50-year-old with diabetes will die 6 years earlier than someone without diabetes.
    • On average, a 10-year-old with diabetes will die 19 years earlier than a child without diabetes.

The study (JM Lawrence et al, JAMA, 326: 717-727, 2021) I will discuss today is the largest and most comprehensive study of childhood diabetes to date.

How Was This Study Done?

Clinical StudyThe data for this study were obtained from the SEARCH For Diabetes In Youth Study. This study collected data on physician-diagnosed cases of diabetes in 3.47 million children ages 19 or younger from 6 geographical areas in the US in 2001, 2009, and 2017.

The 6 geographical areas were:

  • Southern California (7 counties, including Los Angeles).
  • Colorado (14 counties, including Denver).
  • Ohio (8 counties, including Cincinnati)
  • South Carolina (4 counties, including Columbia).
  • Washington State (5 counties, including Seattle).
  • Indian Health Service users in select areas of Arizona and New Mexico.

The data on diabetes diagnoses were obtained by creating active surveillance networks composed of pediatric and adult endocrinologists, other clinicians, hospitals, and health plans in the study areas.

Is Diabetes Increasing In Our Children?

IncreaseTo answer this question let’s start with a historical perspective:

  • In 1950 obesity in US children was rare and type 2 diabetes in children was practically unknown.
    • Since then, obesity rates have skyrocketed, and type 2 diabetes has followed along behind it.
  • Between 1925 and 1950 the prevalence of type 1 diabetes in US children remained constant, but it has been steadily increasing since 1950.
    • Type 1 diabetes remains more prevalent than type 2 diabetes in our children, but the prevalence of type 2 diabetes has been increasing faster than type 1 diabetes.

Now let’s look at the results from the SEARCH For Diabetes In Youth Study:

Prevalence of Type 2 Diabetes:

  • The prevalence of type 2 diabetes in US children aged 10-19 increased from 0.34/1000 youths in 2001, to 0.46/1000 youths in 2009, to 0.67/1000 youths in 2017.
    • This is a 94% increase between 2001 and 2017. Put another way, the prevalence of type 2 diabetes in our children has almost doubled in just 16 years!
    • The greatest increase was seen among Black (0.85/1000 youths), Hispanic (0.57/1000 youths), and American Indian (0.42/1000 youths) population groups.
  • These data are consistent with 3 previous studies reporting a doubling of type 2 diabetes in children over similar time periods.

Note: Since data collection ended in 2017, this study does not take into account the increase in type 2 diabetes caused by increased body weight and reduced activity in children during the pandemic. There are no firm data on the increase in type 2 diabetes in children during the pandemic, but some hospitals have reported increases of 50% to 300% in new diagnoses of type 2 diabetes in 2020.

Prevalence of Type 1 Diabetes:

  • The prevalence of type 1 diabetes in US children aged 19 and younger increased from 1.48/1000 youths in 2001, to 1.93/1000 youths in 2009, to 2.15/1000 youths in 2017.
  • This is a 45% increase between 2001 and 2017.
    • The greatest increase was seen among White (0.93/1000 youths), Black (0.89/1000 youths), and Hispanic (0.59/1000 youths) population groups.
    • These data are consistent with a similar study of type 1 diabetes in children in Holland.

In summary:

  • This study documents a dramatic increase in the prevalence of both type 1 and type 2 diabetes in US children between 2001 and 2017.
  • Type 2 diabetes is still less prevalent than type 1 diabetes in US children, but it is increasing twice as fast.

Why Is Diabetes Increasing In Our Children?

Question MarkWhen it comes to type 2 diabetes, the experts agree:

  • The increase in type 2 diabetes in children is directly related to the obesity epidemic, which is now impacting our children. The obesity epidemic is, in turn, caused by:
    • Decreased exercise. Video games and social media have replaced actual games played outside.

However, when it comes the increase in type 1 diabetes, the experts are perplexed. There is no easy explanation. Let’s start with the basics:

  • Type 1 diabetes is an autoimmune disease. With type 1 diabetics, their immune system starts attacking the insulin-producing beta cells in their pancreas. Consequently, they lose the ability to produce insulin.
  • The autoimmune response seen in type 1 diabetes is caused by a combination of genes and environment. Specifically:
    • Certain genes predispose to type 1 diabetes. However:
      • Only some people with those genes develop type 1 diabetes.
      • Our genetics doesn’t change with time, so genetics cannot explain the increases in type 1 diabetes we are seeing.
  • That leaves the environment. There are many hypotheses about how our children’s environment influences their risk of developing type 1 diabetes. However:
    • Some of these hypotheses involve things that have not changed over the last 15-20 years. They cannot explain the increase in type1 diabetes we are seeing in children.
    • Some of these hypotheses are not supported by good data. They are speculative.

With that in mind, I will list the top 5 current hypotheses and evaluate each of them.

#1: The viral infection hypothesis: Basically, this hypothesis states that type 1 diabetes can be triggered by child with flucommon viral infections such as the flu.

  • This is a plausible hypothesis. Whenever our immune system is stimulated by invaders it sometimes goes rogue and triggers autoimmune responses.
  • It is also supported by good data. The onset of type 1 diabetes is often associated with a viral infection in genetically susceptible children.
  • However, prior to the pandemic viral infections have been constant. They haven’t changed over time. Therefore, they cannot explain an increase in type 1 diabetes between 2001 and 2017.

#2: The hygiene hypothesis: Basically, this hypothesis states that when we raise our children in a sterile environment, their immune system doesn’t develop normally. Essentially the hypothesis is saying that it’s not a bad thing if your toddler eats some dirt and moldy fruits. However:

  • The data linking hygiene to food allergies is better than the data linking hygiene to autoimmune responses.
  • There is no evidence that hygiene practices have changed significantly between 2001 and 2017.

#3: The vitamin D hypothesis: Basically, this hypothesis states that vitamin D deficiency is associated with the autoimmune response that causes type 1 diabetes.

  • One of the functions of vitamin D is to regulate the immune system.
  • As I have reported previously, suboptimal vitamin D levels are associated with increased risk of developing type 1 diabetes.
  • While we know that up to 61% of children in the US have suboptimal vitamin D levels, we don’t know whether that percentage has changed significantly in recent years.

happy gut bacteria#4: The gut bacteria hypothesis: Basically, this hypothesis suggests that certain populations of gut bacteria increase the risk of developing type 1 diabetes. This is what we know.

  • Children who develop type 1 diabetes have a unique population of gut bacteria.
  • This population of gut bacteria also triggers inflammation, and chronic inflammation can lead to autoimmune responses.
  • A diet rich in highly processed foods supports growth of the same gut bacteria found in children with type 1 diabetes.
  • Consumption of highly processed foods has increased significantly in the last twenty years.

#5: The obesity hypothesis: Basically, this hypothesis suggests that obesity increases the risk of developing type 1 diabetes.

  • While the mechanism is not clear, childhood obesity is associated with both inflammatory and autoimmune diseases like type 1 diabetes.
  • Childhood obesity has increased dramatically in the past few years.

As you may have noticed, there are weaknesses to each of these hypotheses. This is why there is no current agreement among experts as to why type 1 diabetes is increasing in our children.

My guess is that none of these hypotheses can fully explain the increase in type 1 diabetes in our children, but that several of them may contribute to it.

What Can We Do?

Family Riding BicyclesWhatever the mechanism, the increase in both type 1 and type 2 diabetes in our children is troubling. Unless this trend is reversed, we may be dooming our children to short, unhealthy lives. So, what can we, as concerned parents and grandparents, do?

For type 2 diabetes, the answer is clear.

1) Reverse the dominance of ultraprocessed foods in children’s diets. Encourage the consumption of whole, unprocessed or minimally processed foods, and include lots of fresh fruits and vegetables. Set a good example as well.

2) Encourage more activity. Get them outside and moving. Create family activities that involve exercise.

3) Reverse the obesity epidemic. If we succeed in reversing the dominance of ultraprocessed foods in their diet and encouraging more activity, we can reverse the obesity epidemic without putting our children on crazy diets.

For type 1 diabetes, the answer is less clear because the cause for the increase in type 1 diabetes is uncertain. However, I will point out that:

1) Increased consumption of fresh fruits and vegetables, whole grains, and legumes supports the growth of friendly gut bacteria that reduce inflammation and the risk of autoimmune diseases. For more detail on an anti-inflammatory diet, click here.

2) Reversing the obesity epidemic also reduces inflammation and the risk of autoimmune diseases.

3) Adequate vitamin D levels reduce the risk of autoimmune diseases, including type 1 diabetes. My recommendation is to get your 25-hydroxyvitamin D levels tested and supplement with vitamin D3 as needed, especially during the winter months.

The Bottom Line

Last week I shared a study documenting the alarming increase in ultraprocessed food consumption by our children and the effect it was having on their health. For example, childhood obesity is closely linked to ultraprocessed food consumption, and the rate of childhood obesity has almost quadrupled in the last 40 years.

Unfortunately, whenever you see an increase in obesity, type 2 diabetes is not far behind. This week’s study looked at the prevalence of childhood diabetes in 3.47 million children from 6 geographical areas of the United States between 2001 and 2017. This study found:

  • The prevalence of type 2 diabetes in US children increased 94% between 2001 and 2017. It almost doubled.
  • The prevalence of type 1 diabetes in US children increased 45% between 2001 and 2017.

These statistics are tragic because diabetes is a deadly disease.

You probably already know that long-term complications of diabetes include heart disease and irreversible damage to nerves, kidneys, eyes, and feet. But you may not have known that childhood diabetes is more dangerous than diabetes in adults because:

  • It is more challenging to manage in children.
  • The complications of diabetes start to show up much earlier in life and affect quality of life at a much earlier age. For example:
    • Cardiovascular events occur 15 years earlier in someone with diabetes.
    • On average, a 50-year-old with diabetes will die 6 years earlier than someone without diabetes.
    • On average, a 10-year-old with diabetes will die 19 years earlier than a child without diabetes.

For more details about this study, why the prevalence of diabetes in US children is increasing, and what we can do about it, read the article above.

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

Are We Killing Our Children With Kindness?

by

The Danger Of Ultraprocessed Foods 

Author: Dr. Stephen Chaney

fast foodIt breaks my heart when I see a mom and her children in the checkout line of a supermarket with a cart filled with sodas, sweets, and convenience foods and devoid of fresh fruits and vegetables – or when I see fast food restaurants packed with parents and their children.

I get it. Our kids love these foods. It seems like an act of kindness to give them the foods they crave. But are we killing our children with kindness?

Let me explain. The human brain is hardwired to crave sweets, salt, and fat. In prehistoric times each of these cravings had a survival benefit. For example:

  • Mother’s milk is naturally sweet. It only makes sense that babies should crave the nutrition source that is essential for their early growth and development.
  • Fruits provide a cornucopia of vitamins, minerals, and phytonutrients. But fruits were scarce and seasonal in prehistoric times. Their sweetness provided an incentive for early man to seek them out.
  • Some salt is essential for life. Yet in early history it was scare. It was worth its weight in gold.
  • In prehistoric times it was feast or famine. The human body has an unlimited capacity to store fat in times of plenty, and those fat stores carried early man through times of famine.

Today most Americans live in a time of food abundance. There are fast food restaurants on almost every street corner and in every shopping mall. We think of famine as the days we skipped lunch because we were busy.

Yet these cravings remain, and the food industry has weaponized them. They are churning out an endless supply highly processed foods and beverages. These foods are not being designed to improve their nutritional value. They are designed to satisfy our cravings and lure us and our children into consuming more of them every year.

Scientists have developed a classification system that assigns foods in the American diet to different groups based on the degree of processing of that food. As you might expect, the best classification is unprocessed foods. The worst classification is called “ultraprocessed foods”. [I will describe this classification system in more detail in the next section.]

It is time we asked how much ultraprocessed foods our children are eating and what it is doing to their health. That is the topic of the study (L Wang et al, JAMA, 326: 519-530, 2021) I will discuss today.

How Was This Study Done?

Clinical StudyThe data for this study were obtained from NHANES (National Health and Nutrition Examination Survey) dietary data collected from 33,795 American children (ages 2-19, average age = 10) between 1999 and 2018.

NHANES is a program conducted by the CDC to survey the health and nutritional status of adults and children in the United States. The survey has been conducted on a continuous, yearly basis since 1999.

The dietary data are collected via 24-hour dietary recalls conducted by trained interviewers, with a second recall administered over the phone 3-10 days later to improve the accuracy of the data.

  • Children aged 12-19 completed the dietary survey on their own.
  • For children aged 6-11, a parent or guardian assisted them in filling out the survey.
  • For children aged 2-5, a parent or guardian filled out the survey for them.

The foods and beverages consumed by the children were divided into 4 major groups based on the extent of processing using a well-established classification system called NOVA. The 4 groups are:

1) Unprocessed Or Minimally Processed Foods.

  • This includes whole foods and foods that are minimally processed without the addition of oils, fats, sugar, salt, or other ingredients to the food.
  • Examples of minimally processed foods include things like oatmeal, nut butters, dried fruit, frozen fruits or vegetables, and dried beans.

2) Processed Culinary Ingredients.

  • This includes recipes from restaurants or in-home cooking that add small amounts of oils, fats, sugar, salt, and seasonings to whole foods.

3) Processed Foods

  • This includes foods made in factories by the addition of salt, sugar, oil, or other substances added to whole or minimally processed foods.
  • Examples include tomato paste, canned fruits packed in sugar syrup, cheese, smoked or cured meat.

4) Ultraprocessed Foods

  • These are industrial formulations created in factories mostly or entirely from substances extracted from foods (oils, fats, sugar, starch, and proteins), derived from food constituents (hydrogenated fats and modified starch), or synthesized in laboratories (flavor enhancers, colors, and food additives).
  • Examples include sugar sweetened beverages; sweet or savory packaged snacks; chocolates and candies; burgers, hot dogs, and sausages; poultry and fish nuggets, pastries, cakes, and cake mixes.

Are We Killing Our Children With Kindness?

Obese ChildAs I said above, the important question is, “Are we killing our children with kindness when we give them the sugary drinks, sweets, convenience foods, and fast foods they crave?” After all, the foods we give them when they are young are the ones they are most likely to select when they get older.

Let’s start by looking at how pervasive these foods have become. That was the purpose of the study I am discussing today, and the results of this study are alarming. When they looked at the changes in food consumption by our children between 1999 and 2018:

  • The percentage of calories from ultraprocessed foods increased from 61.4% to 67%. That means:
    • Today, more than 2/3 of the calories our children consume daily come from ultraprocessed foods!
  • The percentage of calories from unprocessed and minimally processed foods decreased from 28.8% to 23.5%. That means:
    • In the span of just 19 years the diets of our children have gone from bad to worse!
  • Ultraprocessed foods were more likely to be consumed away from home and at fast food restaurants.

When the investigators looked at individual categories of ultraprocessed foods:

  • The percentage of calories coming from ready to heat and eat dishes like frozen pizzas and other frozen meals or snacks increased from 2.2% to 11.2%.
  • The percentage of calories coming from sweet snacks and desserts increased from 10.7% to 12.9%.
  • The percentage of calories coming from sugar sweetened beverages decreased from 10.8% to 5.3%.
    • This is potentially the only good news from this study.

The authors concluded. “Based on NHANES data from 1999 to 2018, the estimated energy intake from consumption of ultraprocessed foods has increased among youths in the US and has consistently comprised the majority of their total energy intake.”

“These results suggest that food processing may need to be considered as a food dimension in addition to nutrients and food groups in future dietary recommendations and food policies.”

The Danger Of Ultraprocessed Foods

Fast Food DangersThis study clearly shows that ultraprocessed foods have become the mainstay of our children’s diets. Forget a balanced diet! Forget “Eat your fruits and vegetables”! Our children’s diets have been fundamentally transformed by “Big Food, Inc”.

You might be saying to yourself, “So, they are eating their favorite processed foods. What’s the big deal? How bad can it be?” My answer is, “Pretty Bad”. I chose the title, “Are we killing our children with kindness”, for a reason.

When you look at what happens to children who eat a diet that is mostly ultraprocessed foods:

#1: Their nutrition suffers. When the investigators divided the children into 5 groups based on the percentage of calories coming from ultraprocessed foods, the children consuming the most ultraprocessed food had:

  • Significantly higher intakes of carbohydrates (mostly refined carbohydrates); total fats; polyunsaturated fats (mostly highly processed omega-6-rich vegetable oils); and added sugars.
  • Significantly lower intakes of fiber; protein; omega-3 polyunsaturated fatty acids; calcium; magnesium; potassium; zinc; vitamins A, C, D, and folate.
    • The low intake of fiber means our children will be less likely to have health-promoting friendly bacteria and more likely to have disease-promoting bad bacteria in their guts.
    • The low intake of calcium, magnesium, and vitamin D means they will be less likely to achieve maximum bone density as young adults and will be more likely to suffer from osteoporosis as they age.

#2: They are more likely to become obese. Remember, these are foods that are made in a factory, not grown on a farm.

  • They are high in fat, sugar, and refined carbohydrates. That means they have a high caloric density. Each bite has 2-3 times the calories found in a bite of fresh fruits and vegetables.
  • As I said earlier, the food industry has weaponized our natural cravings for sweet, salty, and fatty foods. They feed their prototypes to a series of consumer tasting panels until they find the perfect blend of sugar, salt, and fat to create maximum craving.
  • And if that weren’t enough, they add additives to create the perfect flavor and “mouth appeal”.
    • It is no wonder that clinical studies have found a strong correlation between high intake of ultraprocessed food and obesity in both children and adults.
    • It is also no wonder that the rate of childhood obesity has almost quadrupled (5% to 18.5%) in the last 40 years.

#3: They are more likely to become sick as adults and die prematurely.

  • Obesity; high intake of fat, sugar, and refined carbohydrates; and low intake of fiber, omega-3s, and essential nutrients all contribute to an increased risk of diabetes, heart disease, and some cancers.
    • It is no wonder that clinical studies have found a strong correlation between high intake of ultraprocessed food and increased risk of diabetes, heart disease, some cancers, and premature death in adults.
    • It is also no wonder a recent study found that type 2 diabetes in children has almost doubled between 2001 and 2017.

The data are clear. When we allow our children to subsist on a diet mostly made up of the ultraprocessed foods they crave, we may be giving them, not love, but a lifetime of obesity and declining health instead. And yes, we may be killing them with kindness.

Instead, my recommendations are:

  • expose your children to a variety of fresh fruits, vegetables, and minimally processed foods at an early age.
  • They will reject some of them, and that’s OK. Introduce others until you find whole, minimally processed foods they like. Reintroduce them to some of the foods they initially rejected as they get older.
  • Don’t keep tempting ultraprocessed foods in your house.
  • You may just succeed in putting your children on the path to a healthier diet and a healthier, longer life.

The Bottom Line

It breaks my heart when I see a mom and her children in the checkout line of a supermarket with a cart filled with sodas, sweets, and convenience foods and devoid of fresh fruits and vegetables – or when I see fast food restaurants packed with parents and their children.

I get it. Our kids love these foods. It seems like an act of kindness to give them the foods they crave. But are we killing our children with kindness?

It is time we asked how much ultraprocessed foods our children are eating and what it is doing to their health. A recent study did just that. When they looked at the changes in food consumption by our children between 1999 and 2018:

  • The percentage of calories from ultraprocessed foods increased from 61.4% to 67%. That means:
    • Today, more than 2/3 of the calories our children consume daily come from ultraprocessed foods!
  • The percentage of calories from unprocessed and minimally processed foods decreased from 28.8% to 23.5%. That means:
    • In the span of just 19 years the diets of our children have gone from bad to worse!

This study clearly shows that ultraprocessed foods have become the mainstay of our children’s diets. Forget a balanced diet! Forget “Eat your fruits and vegetables”! Our children’s diets have been fundamentally transformed by “Big Food, Inc”.

You might be saying to yourself, “So, they are eating their favorite processed foods. What’s the big deal? How bad can it be?” My answer is, “Pretty Bad”. I chose the title, “Are we killing our children with kindness”, for a reason.

When you look at what happens to children who eat a diet that is mostly ultraprocessed foods:

  • Their nutrition suffers.
  • They are more likely to become obese.
  • They are more likely to become sick as adults and die prematurely.

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.

How Does Red Meat Cause Colon Cancer?

by

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

by

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?

by

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?

by

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?

by

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

by

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.

Health Tips From The Professor