Can Artificial Sweeteners Make You Hungry?

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.

Is Diabetes Increasing In Our Children?

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://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?

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.

Why Do Diet Sodas Make You Fat?

Is Mixing Diet Sodas With Carbs Bad For You?

Why Do Sodas Cause Obesity?Many people, and many doctors, believe that diet sodas and artificially sweetened foods are a healthy choice. After all:

  • Cutting calories by drinking diet sodas and eating artificially sweetened foods should help you lose weight.
  • If sugar is the problem for diabetics, diet sodas and artificially sweetened foods should be a healthier choice.

On the surface, these ideas appear to be self-evident. They seem to be “no-brainers”. The truth, however, is more complicated.

When 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, as I have described in an earlier issue of “Health Tips From the Professor”, the results are different in the real world where you don’t have a dietitian looking over your shoulder. In those 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] are 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.

Why is that? The short answer is that nobody knows (more about that later). However, a recent study (JR Dalenberg et al, Cell Metabolism, 31: 493-502, 2020) suggests an unexpected mechanism for the weight gain associated with diet soda consumption. Let’s look at that study.

How Was The Study Done?

Clinical StudyThe study recruited 45 healthy young adults (ages 20-45) who habitually consumed less than 3 diet sodas a month. They were randomly assigned to three groups. The participants in each group came into the testing facility seven times over a span of 2 weeks. Each time they were given 12 ounces of one of three equally sweet tasting beverages in a randomized, double-blind fashion.

  • Group 1 received a sucralose-sweetened drink contained 0.06 grams of sucralose (equivalent to two packets of Splenda).
  • Group 2 received a sugar-sweetened drink contained 7 teaspoons of sucrose (table sugar).
  • Group 3 received a combo drink contained 0.06 grams of sucralose plus 7 teaspoons of maltodextrin. Maltodextrin is a water-soluble carbohydrate that does not have a sweet taste.

o   Maltodextrin was used because Splenda and most other commercial sucralose products contain it along with sucralose. You need something to fill up those little sucralose-containing packets.

o   This drink was included as a control. The expectation was that it would give the same results as the sucralose-sweetened drink.

Three measurements were performed prior to and following the 2-week testing period:

  • An oral glucose tolerance test in which participants drink a beverage containing a fixed amount of glucose. Then their blood sugar and blood insulin levels are measured over the next two hours.

o   This is a measure of how well they were able to control their blood sugar levels.

  • A test in which they were given samples that had either a sweet, sour, salty, or savory taste. Then:

o   They were asked to identify each taste and report how strong the taste was.

o   MRI scans of their brains were performed to determine how strongly their brains responded to each of the tastes.

Is Mixing Diet Soda With Carbs Bad For You?

The results were surprising. The first surprise came when the investigators unblinded the results of the oral glucose tolerance test:

  • Blood sugar and blood insulin responses were unaffected by the 2-week exposure to sugar-sweetened drinks.

o   This was expected.

  • Blood sugar and blood insulin were relatively unaffected by the 2-week exposure to sucralose-sweetened drinks. If anything, the control of blood sugar levels was slightly improved at the end of two weeks.

o   This was a disappointment for the investigators. One of the prevailing theories is that artificially sweetened beverages alter the blood sugar response. The investigators found no evidence for that idea.

  • Following the 2-week exposure to the combo drinks (sucralose plus maltodextrin), blood sugar levels were unaffected, but blood insulin levels were increased. This implies that more insulin was required to control blood sugar levels. In other words, these participants had developed insulin resistance.

o   This result was unexpected. Remember the investigators had included this drink as a control.

o   The investigators pointed out that the insulin resistance associated with the sucralose-maltodextrin combo could increase the risk of type 2 diabetes and obesity.

  • Because of this unexpected result, the investigators did a follow-up study in which participants were given a maltodextrin-only drink using the same study protocol. The oral glucose tolerance test was unchanged by the 2-week exposure to maltodextrin-only drinks.

When the investigators conducted taste tests, the ability of participants to taste all four flavors was unchanged by a 2-week exposure to any of the drinks.

However, when the investigators did MRI scans to measure the brain’s response to these flavors:

  • A two-week exposure to the sucralose plus maltodextrin drinks reduced the brain’s response to sweet but not to any of the other flavors.

o   In other words, the subjects could still taste sweet flavors, but their brains were not responding to the sweet taste. Since sweetness activates pleasure centers in the brain this could lead to an increased appetite for sweet-tasting foods.

o   This might explain the weight gain that has been observed in many previous studies of diet sodas.

  • Two-week exposures to the other drinks had no effect on the brain’s response to any of the flavors. Once again, this effect was only seen in the sucralose-maltodextrin combination.

The investigators concluded:

  • “Consumption of sucralose combined with carbohydrates impairs insulin sensitivity…and…neural responses to sugar.
  • Insulin sensitivity is not altered by sucralose or carbohydrate consumption alone.
  • The results suggest that consumption of sucralose in the presence of a carbohydrate dysregulates gut-brain regulation of glucose metabolism.”

The investigators pointed out that this could have several adverse consequences. Again, in the words of the authors:

“Similar exposure combinations (artificial sweeteners plus carbohydrates) almost certainly occur in free-living humans, especially if one considers the consumption of a diet drink along with a meal. This raises the possibility that the combination effect may be a major contributor to the rise in incidence of type 2 diabetes and obesity. If so, addition of artificial sweeteners to increase the sweetness of carbohydrate-containing food and beverages should be discouraged and consumption of diet drinks with meals should be counseled against.”

Why Do Diet Sodas Make You Fat?

As I mentioned at the start of this article, there are a lot of hypotheses as to why diet sodas make us fat. These hypotheses break down into two classifications: psychological and physiological.

The psychological hypothesis is easiest to explain. Essentially, it goes like this: We feel virtuous for choosing a zero-calorie sweetener, so we allow ourselves to eat more of our favorite foods. It is unlikely that this hypothesis holds for all diet soda drinkers. However, it is also hard to exclude it as at least part of the explanation for the food overconsumption associated with diet soda use.

There are multiple physiological hypotheses. Most of them are complicated, but here are simplified explanations of the three most popular hypotheses:

  • The sweet taste of artificial sweeteners tricks the brain into triggering insulin release by the pancreas. This causes blood sugar levels to plummet, which increases appetite.
  • The sweet taste of artificial sweeteners is not appropriately recognized by the brain. This diminishes release of hormones that suppress appetite.
  • Artificial sweeteners interfere with insulin signaling pathways, which leads to insulin resistance.

There is some evidence for and against each of these hypotheses.

However, this study introduces a new physiological hypothesis – namely that it is the combination of artificial sweeteners and carbohydrates that results in a dysregulation of the normal mechanisms controlling appetite and blood sugar.

What Does This Study Mean For You?

Diet Soda DangersLet’s start with the obvious. This is just a hypothesis.

  • This was a very small study. Until it is confirmed by other, larger studies, we don’t know whether it is true.
  • This study only tested sucralose. We don’t know whether this applies to other artificial sweeteners.
  • The study only tested maltodextrin in combination with sucralose. We don’t know whether it applies to other carbohydrates.

Therefore, in discussing how this study applies to you, let’s consider two possibilities – if it is true, and if it is false.

If this hypothesis is true, it is concerning because:

  • We often consume diet sodas with meals. If, for example, we take the earlier example of a diet soda with a Big Mac and fries, both the hamburger bun and the fries are high carbohydrate foods.

 

  • Sucralose and other artificial sweeteners are used in low calorie versions of many carbohydrate rich processed foods.

If this hypothesis is false, it does not change the underlying association of diet soda consumption with weight gain and type 2 diabetes. It is merely an attempt to explain that association. We should still try to eliminate diet sodas and reduce our consumption of artificially sweetened, low calorie foods.

My recommendation is to substitute water and other unsweetened beverages for the diet drinks or sugar sweetened beverages you are currently consuming. If you crave the fizz of sodas, drink carbonated water. If you need more taste, try herbal teas or infuse water with slices of lemon, lime, or your favorite fruit. If you buy commercial brands of flavored water, check the labels carefully. They may contain sugars or artificial sweeteners. Those you want to avoid.

The Bottom Line

Many studies have called into question the assumption that diet sodas and diet foods help us lose weight. In fact, most of these studies show that diet soda consumption is associated with weight gain rather than weight loss.

There are many hypotheses to explain this association, but none of them have been proven at present.

This study introduces a new hypothesis – namely that the combination of artificial sweeteners and carbohydrates results in a dysregulation of the normal mechanisms controlling appetite and blood sugar. In particular, this study suggested that combining sucralose with carbohydrates caused insulin resistance and reduce the ability of the brain to respond appropriately to sweet tastes.

The authors concluded: “Similar exposure combinations (artificial sweeteners plus carbohydrates) almost certainly occur in free-living humans, especially if one considers the consumption of a diet drink along with a meal. This raises the possibility that the combination effect may be a major contributor to the rise in incidence of type 2 diabetes and obesity. If so, addition of artificial sweeteners to increase the sweetness of carbohydrate-containing food and beverages should be discouraged and consumption of diet drinks with meals should be counseled against.”

If this hypothesis is true, it is concerning because:

  • We often consume diet sodas with meals. If, for example, we take the example of a diet soda with a Big Mac and fries, both the hamburger bun and the fries are high carbohydrate foods.
  • Artificial sweeteners are used in low calorie versions of many carbohydrate rich processed foods.

If this hypothesis is false, it does not change the underlying association of diet soda consumption with weight gain and type 2 diabetes. It is merely an attempt to explain that association. We should still try to eliminate diet sodas and reduce our consumption of artificially sweetened, low calorie foods.

My recommendation is to substitute water and other unsweetened beverages for the diet drinks or sugar sweetened beverages you are currently consuming. If you crave the fizz of sodas, drink carbonated water. If you need more taste, try herbal teas or infuse water with slices of lemon, lime, or your favorite fruit. If you buy commercial brands of flavored water, check the labels carefully. They may contain sugars or artificial sweeteners. Those you want to avoid.

For more details, read the article above.

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

Does Intermittent Fasting Work?

Will Intermittent Fasting Help You Lose Weight?

Author: Dr. Stephen Chaney

intermittent fastingIf you are like millions of Americans, one of your New Year’s resolutions is to lose weight. Now your dilemma is how to accomplish that. You have tried various diets before – Atkins, paleo, keto, Whole 30, etc. You lost some weight, but it came right back. You are looking for something new, something different from anything you have tried before.

What about intermittent fasting? It’s hot right now. It’s probably different from what you have tried in the past. It doesn’t require radical changes to what you eat. Some of your friends are singing its praises. Could this be the one that solves your weight problem forever?

A Primer On Intermittent Fasting

professor owlLet’s start by defining intermittent fasting and reviewing what we already know about it. There are several variations of what the mass media refers to as intermittent fasting, but the two most popular versions are:

  • Time-restricted fasting which limits daily intake of food to a 4 to 12-hour period. The most popular version of this restricts food intake to 8 hours followed by 16 hours of fasting.
  • Intermittent fasting in which there is a day or more of fasting or decreased food intake between periods of unrestricted eating. The most popular version of this allows 5 days of unrestricted eating followed by 2 days of fasting.

A major review (Di Francesco et al, Science, 362: 770-775, 2018) of time-restricted and intermittent fasting was published a little over a year ago. At the time that review was published, there were lots of studies comparing time-restricted fasting with continuous caloric restriction. I summarized those findings in a previous issue of “Health Tips From the Professor” last January.

Here is a brief summary of the key findings from that review:

  • If you read the blogs about time-restricted fasting, you will come across all sorts of metabolic mumbo-jumbo about ketone bodies, adiponectin, leptin, IGF-1, and blood glucose levels. It sounds so convincing. Don’t get sucked in by these pseudo-scientific explanations. At this point they are mostly speculation.
  • Although there is no conscious effort to control calories, time-restricted fasting result in an inadvertent reduction in food intake by restricting the time allowed for eating and by eliminating late night snacking. This reduction in caloric intake is likely responsible for most of the weight loss associated with intermittent fasting. When you control for calories, there is no difference in weight loss between time-restricted fasting and continuous caloric restriction (your typical reduced calorie diet).

However, at the time the review was published, far less was known about the relative benefits of intermittent fasting and simple caloric restriction. Since that time, two studies have rigorously compared the effectiveness of intermittent fasting and continuous caloric restriction on weight loss. I review those studies below

Will Intermittent Fasting Help You Lose Weight?

The first study (YM Roman et al, International Journal of Obesity, 43: 2017-2027, 2019) was a systematic review and meta-analysis of 9 clinical studies comparing intermittent fasting with continuous caloric restriction. Total caloric reduction was controlled and was the same for both intermittent fasting and continuous caloric reduction.

The studies ranged from 12 weeks to 52 weeks with most of them in the 20 to 30-week range. This meta-analysis found:

·       There was no difference between intermittent fasting and continuous caloric restriction in terms of weight loss, waist circumference, or body fat loss.

·       Loss of lean body mass, on the other hand, was greater for intermittent fasting than for continuous caloric restriction.

The authors concluded: “Since it is ultimately fat mass loss that improves health indices, and not the loss of muscle, the significantly greater loss of lean mass in the intermittent dieting group versus the continuous dieting group is concerning and needs to be further assessed.”

I would add, it is also concerning because lean mass muscle burns calories faster than fat mass. Loss of lean muscle mass could lead to a lower metabolic rate. That would make maintenance of the weight loss more difficult.

The second study (ML Headland et al, International Journal of Obesity, 43: 2028-2036) compared intermittent fasting versus continuous calorie restriction for 12 months in a group of 332 healthy overweight or obese adults. Again, total caloric reduction was the same for the two groups. In this study:

·       There was no significant difference between intermittent fasting and continuous caloric restriction for weight loss, body fat loss, and lean body mass loss. [Note: The retention of lean body mass in this study differs from the loss of lean body mass reported in the previous study. Additional studies will be required before we become overly concerned about potential loss of lean body mass with intermittent fasting.]

·       There were also no significant differences between the groups for blood levels of glucose, total cholesterol, triglycerides, HDL, and LDL.

Does Intermittent Fasting Work?

does intermittent fasting workThese studies make it clear there is no “magic” associated with either time-restricted or intermittent fasting.

·       If either time-restricted or intermittent fasting allows you to reduce your daily caloric intake by restricting the time that you are eating, you will lose weight and keep it off. However, if you compensate for the fasting periods by consuming additional calories when you are eating, all bets are off.

·       In clinical studies that restrict calories to the same extent in the various diets, neither time-restricted nor intermittent fasting results in greater weight loss than continuous caloric restriction (your typical reduced calorie diet).

o   In addition, neither time-restricted nor intermittent fasting results in better improvement in blood parameters (glucose, total cholesterol, triglycerides, HDL, and LDL) than continuous caloric restriction.

·       Intermittent fasting may result in greater loss of lean muscle mass than continuous caloric reduction. If confirmed by subsequent studies, this would be concerning.

This also means:

·       If you happen to read the blogs about time-restricted or intermittent fasting, you can forget all the metabolic mumbo-jumbo about ketone bodies, adiponectin, leptin, IGF-1, and blood glucose levels.

o   At this point this metabolic information comes mostly from animal studies. Its application to humans is purely speculation.

o   Since time-restricted and intermittent fasting offer no advantage over continuous caloric restriction, there is no evidence that changes in any of those metabolic markers has any effect on weight loss in humans.

Finally, you need to ask whether time-restricted and intermittent fasting are something you can maintain in the real world.

·       Your friends are unlikely to be on the same schedule. It won’t be easy to fit your diet around socializing, travel, and holidays.

The Bottom Line

There are several variations of what the mass media refers to as intermittent fasting, but the two most popular versions are:

  • Time-restricted fasting which limits daily intake of food to a 4 to 12-hour period. The most popular version of this restricts food intake to 8 hours followed by 16 hours of fasting.
  • Intermittent fasting in which there is a day or more of fasting or decreased food intake between periods of unrestricted eating. The most popular version of this allows 5 days of unrestricted eating followed by 2 days of fasting.

The latest studies make it clear there is no “magic” associated with either time-restricted or intermittent fasting.

·       If either time-restricted or intermittent fasting allows you to reduce your daily caloric intake by restricting the time that you are eating, you will lose weight and keep it off. However, if you compensate for the fasting periods by consuming additional calories when you are eating, all bets are off.

·       In clinical studies that restrict calories to the same extent in the various diets, neither time-restricted nor intermittent fasting results in greater weight loss than continuous caloric restriction (your typical reduced calorie diet).

o   In addition, neither time-restricted nor intermittent fasting results in better improvement in blood parameters (glucose, total cholesterol, triglycerides, HDL, and LDL) than continuous caloric restriction.

·       Intermittent fasting may result in greater loss of lean muscle mass than continuous caloric reduction. If confirmed by subsequent studies, this would be concerning.

Finally, you need to ask whether time-restricted and intermittent fasting are something you can maintain in the real world.

·       Your friends are unlikely to be on the same schedule. It won’t easy to fit your diet around socializing, travel, and holidays.

For more details, read the article above.

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

Can Gut Bacteria Make You Fat?

bacteria

bacteria

Gut Bacteria, Diet and Obesity

Author: Dr. Stephen Chaney

 

 

Can gut bacteria make you fat? It has been known for some time that the types of bacteria found in the intestines of obese people are different than those found in the intestines of lean individuals. But no one really knew the significance, if any, of that observation. Did obesity favor certain types of intestinal bacteria, or did certain types of intestinal bacteria favor obesity?

Obese individuals are often insulin resistant, and insulin resistance can cause higher sugar levels in the blood, urine and intestine. So it was easy to assume that obesity simply favored the growth of different types of bacteria in the intestine. However, recent studies have suggested that certain types of bacteria in our intestines may actually cause obesity.

Can Gut Bacteria Make You Fat?

For example, one study (Vijay-Kumar et al, Science, 328: 228-231, 2010) compared a strain of mice that are genetically predisposed to obesity with wild type (genetically lean) mice. They first looked at the intestinal bacteria. It turned out that the obese mice and lean mice had the same differences in intestinal bacteria that obese and lean humans have. And just like obese humans the obese mice ate more, displayed insulin resistance, and had elevated levels of triglycerides, cholesterol and blood sugar (They were pre-diabetic).

The investigators then decided to test the hypothesis that the particular bacterial strains found in the intestines of genetically obese mice might be causing their insulin resistance and obesity.

In the first experiment they killed off the intestinal bacteria in the genetically obese mice by putting high dose antibiotics in their food. Depleting the intestinal bacteria created some health problems for the mice, but it completely prevented the insulin resistance, overeating and obesity normally observed with this strain of mice.

In the second experiment they sterilized the intestines of the genetically lean mice and then colonized their intestines with intestinal bacteria from the genetically obese mice. When they did this, the genetically lean mice developed many of the characteristics of the genetically obese mice including insulin resistance, overeating, obesity and hyperglycemia.

insulin resistanceIn short, when their guts became colonized with bacteria from obese mice, the genetically lean mice became overweight and developed diabetes. Based on these experiments and other studies the scientists hypothesized that the wrong kinds of intestinal bacteria can make a significant contribution to insulin resistance, which in turn can lead to overeating and obesity. In short, they concluded that bad gut bacteria may make you fat.

The Battle of The Bacteria

In a second study (Walker et al, Science, 341: 1079-1089, 2013) the intestines of germ free mice were colonized with gut bacteria from lean and obese humans. The results were essentially the same as in the first study. That is, the mice who received gut bacteria from lean humans stayed lean and those who received gut bacteria from obese humans became obese.

But then the investigators asked two really interesting questions:

1) If you mixed the two types of bacteria, which one would win “the battle of the bacteria”?

For this experiment they took mice that had received gut bacteria from lean humans and mice that had received gut bacteria from obese humans and put them in the same cage. It turns out that since mice eat each other’s poop, they pick up each other’s intestinal bacteria. (No, I am not suggesting that you…)

The results of this experiment were (envelop please): The “lean” bacteria won out. They became the predominant bacteria in the intestines of all of the mice in the cage. Furthermore, none of the mice became obese – even the ones that had originally been inoculated with gut bacteria from obese humans.

2) Are the types of bacteria in the intestine influenced by diet?

In the previous experiment the mice were eating standard mouse chow – which is pretty healthy if you are a mouse. So the investigators decided to ask what would happen if they ate foods that were similar to really good and really bad human diets. They devised two types of diets for the mice – one that was high in fresh fruits & vegetable and low in fat (the good diet) and one that was high in fat and low in fresh fruits and vegetables (the bad diet).

On the good diet, the results were the same as in the previous experiment. On the bad diet the “lean” bacteria never grew in the intestines of the mice inoculated with bacteria from obese humans and those mice went on to become obese.

This study confirmed that the wrong kind of gut bacteria can cause obesity, but it also showed that diet can influence the type of bacteria that can grow in the intestine – something I talked about in an earlier issue of “Health Tips From the Professor”  Our Gut Bacteria Are What We Eat.

The Bottom Line

1) Does this mean that you should rush out and buy some probiotics (good bacteria) as part of your weight loss strategy? The simple answer is no. That would be premature. These studies were performed in mice. Although similar results have been reported in humans (for example, Jumpertz et al, Am. J. Clin. Nutr., 94: 58-65, 2011), those studies are very preliminary at present. In addition, genetics and diet obviously played a role in the results. In short, we are a long way from knowing to what extent intestinal bacteria might contribute to obesity in humans.

2) However, there are many very good reasons to make sure that you supply friendly bacteria to your intestinal track on a regular basis. For example, we know that bad bacteria in your intestine can compromise your immune system, convert foods that you eat to cancer causing chemicals, and cause chronic inflammation – which contributes to a number of major diseases.  Can gut bacteria make you fat?  We can’t yet say whether good bugs will help keep you slim, but we do know that they can help keep you healthy.

3) Finally, while we can’t yet say whether probiotic supplements can help you lose weight, it is becoming increasing clear that healthy diets (low fat, high fiber diets with lots of fresh fruits and vegetables) support the type of intestinal bacteria that can make you slim. This is yet one more reason why a healthy diet is so important if you want to stay slim and healthy.

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.

Our Gut Bacteria Are What We Eat

We Grow What We Eat

Author: Dr. Stephen Chaney

BacteriaThe subtitle of this week’s “Health Tips From the Professor” is “We Grow What We Eat”.

No, this is not about each of us starting a backyard garden and literally growing what we eat – although that would probably be a good idea for most of us. I’m actually talking about the bacteria that we “grow” in our intestine.

Most of you probably already know about the concept of “good” and “bad” intestinal bacteria.

Evidence suggests that the “bad” bacteria and yeast in our intestine can cause all sorts of adverse health effects:

  • There is mounting evidence that they can compromise our immune system.
  • There is also evidence that they can create a “leaky gut” (you can think of this as knocking holes in our intestinal wall that allow partially digested foods to enter the circulation where they can trigger inflammation and auto-immune responses).
  • There is some evidence that they can affect brain function and our moods.
  • They appear to convert the foods that we eat into cancer causing chemicals which can be absorbed into the bloodstream.
  • Studies in mice even suggest that they can make us fat.

The list goes on and on…

The “good bacteria” are thought to crowd out the “bad” bacteria and prevent many of the health problems they cause.

In case you’re thinking that it seems a bit far-fetched to think that our intestinal bacteria could affect our health, let me remind you that we have about 100 trillion bacteria in our intestine compared to about 10 trillion cells in our body. They outnumber us 10 to 1.

For years we have thought of “bad” bacteria and yeast as originating from undercooked, spoiled or poorly washed foods that we eat and the “good” bacteria as originating from foods like yogurt and probiotic supplements.

But most of us have not thought that the kinds of foods we choose to eat on a daily basis can affect the kinds of bacteria we “grow” in our intestine – until now. You’ve heard for years that “We are what we eat”. Well it now appears that we also “grow what we eat”. I’m referring to a recent study by G. D. Wu et al (Science, 334: 105-108, 2011).

Our Gut Bacteria Are What We Eat

I’m going to get a bit technical here (Don’t worry. There won’t be a quiz). Scientists refer to the population of bacteria in our intestines as our “microbiome”. Previous studies have shown that people from all over the world tend to have one of two distinct microbiomes (populations of bacteria) in their intestines – Bacteroides or Prevotella. [Again, don’t let the specialized scientific terminology scare you. These are just the names scientists have given to these two distinctive populations of intestinal bacteria].

What this study showed was that people who habitually consumed high-fat/low-fiber diets (diets containing predominantly animal protein and saturated fats) tended to have the Bacteroides bacteria in their intestine, while people who habitually consumed low-fat/high-fiber diets (diets that are primarily plant based and are high in carbohydrate and low in meat and dairy) tended to have the Prevotella bacteria in their intestine. And surprisingly this appears to be independent of sex, weight and nationality.

Is This Important?

The research defining these two distinct microbiomes (populations of intestinal bacteria) and showing that they are influenced by what we eat is very new. At this point in time we know relatively little about the health benefits and risks associated with the Bacteroides and Prevotella microbiomes.

For example:

  • Most of the studies on the health effects of “bad intestinal bacteria” were based on the identification of one or two “bad bacteria” in the gut – not on the hundreds of bacterial species found in the Bacteroides microbiome. So we can’t say for sure that the Bacteriodes microbiome found in people with diets high in animal protein and saturated fats will cause the same health problems as the “bad bacteria”. Nor do we know for sure how important a role the Bacteriodes microbiome plays in the health consequences of consuming that kind of diet.
  • Similarly, many of studies on the health benefits of “good intestinal bacteria” have been based on probiotic supplements containing one or two bacterial species – not the hundreds of bacterial species found in the Prevotella microbiome. So we can’t really say if probiotics or even the Prevotella microbiome will convey the same health benefits seen in populations who consume vegetarian diets.

However, now that do we know that we “grow what we eat” there are numerous studies ongoing to define the benefits and risks associated with each type of bacterial population.

For example, I shared a study with you recently which shows that the intestinal bacteria in people who eat a lot of animal protein convert carnitine (which is also found in meat) to a compound called TMAO, which may increase the risk of heart attacks, and that the conversion of carnitine to TMAO does not occur in people who consume a vegetarian diet ( see “Does Carnitine Increase Heart Disease Risk”)

Stay tuned! I’ll keep you updated as more information becomes available.

The Bottom Line:

Most of the studies I report on are ones that you can act on right away. This one is different. This study introduces a whole new concept – one that raises as many questions as it answers. This makes us ask those “what if” questions.

1)     Previous studies have shown that most people have one of two different kinds of microbiomes (populations of bacteria) in their intestines. This study showed that diets high in animal protein and fat favored one kind of intestinal microbiome, while diets low in fat and high in fiber from fruits & vegetables favored another type of intestinal microbiome.

2)     With a few exceptions we don’t know yet how important a role these intestinal microbiomes play in determining the health consequences of different diets. However, because our intestinal bacteria outnumber the cells in our body by 10:1, it is tempting to ask “What if?”

3)     We also don’t yet know the extent to which probiotics (either from foods or supplements) can overcome the effects of a bad diet on our intestinal microbiome, but it is tempting to ask “What if?”

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

Can Diet Alter Your Genetic Destiny?

Disease Is Not Inevitable

Author: Dr. Stephen Chaney

Bad GenesMany people seem to have the attitude that if obesity [or cancer, heart disease or diabetes] runs in their family, it is their destiny. They can’t really do anything about it, so why even try?

Most of us in the field of nutrition have felt for years that nothing could be further from the truth. But our belief was based on individual cases, not on solid science. That is no longer the case.

Recent scientific advances have given us solid proof that it is possible to alter our genetic destiny. A family predisposition to diabetes, for example, no longer dooms us to the same fate.

I’m not talking about something like the discredited Blood Type Diet. I’m talking about real science. Let me start by giving you an overview of the latest scientific advances.

Can Diet Alter Your Genetic Destiny?

The answer to this question is YES, and that answer lies in a relatively new scientific specialty called nutrigenomics – the interaction between nutrition and genetics. There are three ways in which nutrition and genetics interact:

1)     Your genetic makeup can influence your nutrient requirements.

The best characterized example of this is methylene tetrahydrofolate reductase (MTHFR) deficiency.  MTHFR deficiency increases the requirement for folic acid and is associated with neural tube defects and other neurological disorders, dementia, colon cancer & leukemia.

In spite of what some blogs and supplement manufacturers would have you believe, supplementation with around 400 IU of folic acid is usually sufficient to overcome the consequences of MTHFR deficiency. 5-methylene tetrahydrofolate (also sold as methyl folate or 5-methyl folate) offers no advantage in absorption, bioavailability or physiological activity (Clinical Pharmacokinetics, 49: 535-548, 2010; American Journal of Clinical Nutrition, 79: 473-478, 2004).

This is just one example. There are hundreds of other genetic variations that influence nutrient requirements – some known and some yet unknown.

2)     A healthy diet can reduce your genetic predisposition for disease.

This perhaps the one that is easiest to understand. For conceptual purposes let us suppose that your genetic makeup were associated with high levels of inflammation. That would predispose you to heart disease, cancer and many other diseases. However, a diet rich in anti-inflammatory nutrients could reduce your risk of those diseases.

This is just a hypothetical example. I’ll give some specific examples in the paragraphs below.

3)     Diet can actually alter your genes.

This is perhaps the most interesting scientific advance in recent years. We used to think that genes couldn’t be changed. What you inherited was what you got.

Now we know that both DNA and the proteins that coat the DNA can be modified, and those modifications alter how those genes are expressed. More importantly, we now know that those modifications can be inherited.

Perhaps the best characterized chemical modification of both DNA and proteins is something called methylation. Methylation influences gene expression and is, in turn, influenced by nutrients in the diet like folic acid, vitamin B12, vitamin B6, choline and the amino acid methionine.

Again this is just the “tip of the iceberg”. We are learning more about how diet can alter our genes every day.

Examples Of How Diet Can Alter Genetic Predisposition

Mature Man - Heart Attack Heart Disease

  • Perhaps the most impressive recent study is one that looked at the effect of diet on 20,000 people who had a genetic predisposition to heart disease (PLOS Medicine, October 2011, doi/10.1371/journal.pmed.1001106).

These people all had a genetic variant 9p21 that causes a 2 fold increased risk of heart attack. The study showed that a diet rich in fruits, vegetables and nuts reduced their risk of heart attack to that of the general population.

  • Another study, the Heart Outcomes Prevention Evaluation (HOPE) study (Diabetes Care, 27: 2767, 2004; Arteriosclerosis, Thrombosis and Vascular Biology, 24: 136, 2008), looked at genetic variations in the haptoglobin gene that influence cardiovascular risk. The haptoglobin 2-2 genotype increases oxidative damage to the arterial wall, which significantly increases the risk of cardiovascular disease.

When the authors of this study looked at the effect of vitamin E, they found that it significantly decreased heart attacks and cardiovascular deaths in people with the haptoglobin 2-2 genotype, but not in people with other haptoglobin geneotypes.

  • There was also a study called the ISOHEART study (American Journal of Clinical Nutrition, 82: 1260-1268, 2005; American Journal of Clinical Nutrition, 83: 592-600, 2006) that looked at a particular genetic variation in the estrogen receptor which increases inflammation and decreases levels of HDL. As you might expect, this genotype significantly increases cardiovascular risk.

Soy isoflavones significantly decreased inflammation and increased HDL levels in this population group. But they had no    effect on inflammation or HDL levels in people with other genotypes affecting the estrogen reception.

To put this in perspective, these studies are fundamentally different from other studies you have heard about regarding nutritional interventions and heart disease risks. Those studies were looking at the effect of diet or supplementation in the general population.

These studies are looking at the effect of diet or supplementation in people who were genetically predisposed to heart disease. These studies show that genetic predisposition [to heart disease] does not have to be your destiny. You can change the outcome!

Cancer

  • A healthy diet (characterized by high intakes of vegetables, fruits, whole grain products and low intakes of refined grain products) compared with the standard American diet (characterized by high intakes of refined grain products, desserts, sweets and processed meats) results in a pattern of gene expression that is associated with lower risk of cancer.  (Nutrition Journal, 2013 12:24).
  • A healthy lifestyle (low fat diet, stress management and exercise) in men with prostate cancer causes downregulation of genes associated with tumor growth (PNAS, 105: 8369-8374).
  • Sulforaphane, a nutrient found in broccoli, turns on genes that suppress cancer.

Diabetes

  • A study reported at the 2013 meeting of the European Association for the Study of Diabetes showed that regular exercise activated genes associated with a lower risk of type 2 diabetes

Cellular Stress Response

  • A diet rich in antioxidant fruits and vegetables activates the cellular stress response genes that protect us from DNA damage, inflammation and reactive oxygen species (BMC Medicine, 2010 8:54).
  • Resveratrol, a nutrient found in grape skins and red wine, activates genes associated with DNA repair and combating reactive oxygen species while it reduces the activity of genes associated with inflammation, increased blood pressure and cholesterol production.

To put these last three examples (cancer, diabetes and cellular stress response) in perspective, they show that diet and supplementation can alter gene expression – and that those alterations are likely to decrease disease risk.

Obesity

  • Finally, an animal study suggests that maternal obesity may increase the risk of obesity in the offspring by increasing their taste preference for foods with lots of sugar and fats (Endocrinology, 151: 475-464, 2010).

The Bottom Line:

The science of nutrigenomics tells us that diet and genetics interact in some important ways:

1)     Your genetic makeup can influence your requirement for certain nutrients.

    • For example, methylene tetrahydrofolate reductase (MTHFR) deficiency increases your requirement for folic acid.
    • Contrary to what many blogs would have you believe, folic acid is just as effective as 5-methylene tetrahydrofolate (also sold as methyl folate or 5-methyl folate) at correcting MTHFR deficiency.

2)     Healthy diet and lifestyle can overcome genetic predisposition to certain diseases. The best established example at present is for people genetically predisposed to heart disease, but preliminary evidence suggests that the risk of other diseases such as diabetes and cancer are altered by your diet.

3)     Diet can actually alter gene expression – for better or worse depending on your diet. Those alterations not only affect your health, but they may affect your children’s health as well.

4)     Nutrigenomics is a young science and many of the individual studies should be considered preliminary. However, the scientific backing is become stronger every day for what many experts in the field have believed for years.

“Your genes do not have to be your destiny. Healthy diet and lifestyle can overcome a genetic predisposition to many diseases.”

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

Does Obesity Begin In Kindergarten?

Is Obesity Caused By Bad Genes Or Bad Lifestyle?

 Author: Dr. Stephen Chaney

 In past issues of “Health Tips From the Professor” I have shared some common sense weight loss tips. But what if it is all for naught? What if there is nothing you can do about your weight?

Fat ChildYou may have seen the headlines suggesting that obesity in kindergarten is a very strong predictor of obesity later in life. If so, you are probably wondering what that means for your kids or grandkids – and what it means for you. You are probably asking questions like:

  • Should you be worrying about that your toddler’s baby fat?
  • What can you do as parents and grandparents to protect the ones you love from a lifetime of obesity and all of the health challenges that involves?
  • Is there anything you can do about overweight and obesity? Are some people just fated to be obese from childhood on?

What Does the Study Actually Show?

This was a very well done study. It followed 7738 children of all socioeconomic classes who were enrolled in kindergarten (mean age 5.6) in the US in 1998 and followed them through the 8th grade (mean age 14.1) (Cunningham et al, New England Journal of Medicine, 370: 403-411, 2014).

When the children entered kindergarten, 12.4% of them were obese, and another 14.9% of them were overweight. By the time they reached the 8th grade 20.8% were obese and 17% were overweight. Those results didn’t make the headlines. They are similar to many previous studies.

The results that made the headlines were:

  • Overweight 5 year olds were 4 times more likely to become obese by age 14 than normal weight 5 year olds.
  • 87% of obese 8th graders (14 year olds) had a body mass index above the 50th percentile in kindergarten, and 75% had a body mass index above the 70th percentile.
  • Only 13% of overweight 8th graders had been normal weight (<50th percentile) in kindergarten, and only 13% of the normal weight 8th graders had been overweight in kindergarten.

These results are fully consistent with earlier studies showing that overweight toddlers are likely to become overweight teens, and overweight teens are likely to become overweight adults. What was unique about this study (and generated the headlines) was the precision of the statistics.

Does Obesity Begin In Kindergarten?

The answer to that question is clearly yes. However, the more important question is what message we, as responsible health advocates, should be sharing with the general public. Let me break that down to some of the most important questions that you are probably asking.

Is Obesity Caused By Bad Genes Or Bad Lifestyle?

Bad GenesTaken on face value, the results of this study might seem to suggest that genetics is the primary cause of obesity. However, if that is the message we convey to the public, it is likely to simply fuel the perception that most overweight individuals are genetically destined to be obese. There is nothing they can do about it. So, why even bother trying?

However, the authors of the study also noted that the percentage of children aged 6 to 11 who are above the 95% percentile of weight has increased 4-fold between 1963 and 2000. Genetics does not change in a mere 37 years (37 generations maybe). That 4-fold increase in severe childhood obesity is clearly driven by lifestyle changes over the past 30 or 40 years.

While nobody knows the exact percentages, a reasonable interpretation of recent research in this area might be:

  • 10-15% of us are genetically destined to be obese. There is little we can do to change our weight, but a healthy lifestyle can significantly reduce our risk of disease.
  • 10-15% of us are genetically predestined to be lean no matter what we eat (Yes. Your suspicions are true). Once again, lifestyle has relatively little influence on our weight, but a healthy lifestyle can significantly reduce our risk of disease.
  • The other 70-80% of us are genetically predisposed to become obese if we adapt the typical American lifestyle. For most of us lifestyle choices can make a big difference in our weight as well as our health.

So the answer to this question is BOTH. For most of us, obesity is caused by bad genes AND bad lifestyle.

When Should We Intervene?

You probably already know that any extra fat cells we develop in childhood never go away. They are always with us, looking for those extra calories they can store as fat.

This study suggests that by the time we are in kindergarten, the die may already be cast. Those extra fat cells may have already developed.

And, for many people, the time to intervene may be even sooner. This study also showed that birth weight plays an important role as well. Children who weighed 9 pounds or more at birth were 2-fold more likely to be obese in kindergarten than children who weighed less than 9 pounds at birth.

Once again, a small percentage of overweight babies is due to genetics, but it is lifestyle choices during pregnancy that lead to the majority of overweight babies.

The authors of the study noted that most public health initiatives (school lunch programs, lifestyle education programs, etc.) are targeted at school aged children. The authors went on to say that by then it may be too late to have any significant effect on the incidence of obesity in our children.

They suggested that we need to place a stronger emphasis on influencing lifestyle changes that affect the weight of babies at birth and are likely to influence whether or not they become obese by the time they reach kindergarten.

That’s not the realm of public health policy. That’s our responsibility.

What Should We Do?

If You Are Pregnant:

  • The old adage “You are eating for two” was never true.
  • Aim for an extra 150 calories during the 1st trimester, 300 during the 2nd and 3rd trimesters (That’s 1 or 2 servings of healthy foods).
  • Aim for little or no weight gain during the 1st trimester and a total of 20-26 pounds during the last two trimesters (a bit less if you are overweight).

If You Have a Young Child Who Is Overweight:

  • Don’t restrict calories. Restricting calories can stunt growth and interfere with normal mental and physical development.
  • Encourage your kids to exercise rather than watching TV and playing video games. You may need to set the example, and that’s a good thing for you as well as for them.
  • Provide your kids with a healthy diet. For most kids, that means more fruits and vegetables and less sugary beverages, fruit juices, and processed snack foods. That may simply mean that you don’t bring those kinds of foods into your house. Again, that would probably be a good thing for everyone in the family.

I know some of you are saying “My kids won’t eat healthy stuff”. Let me give you my take on that.

When I was a kid, my mom had a pretty simple policy. If I didn’t like what she cooked, I didn’t have to eat it. I could simply wait until the next meal – when she would be serving the same kinds of healthy foods again.

I got the message pretty quick. It wasn’t eat healthy or eat junk food. It was eat healthy or go hungry. I decided early on that healthy was better than hungry.

Now, let me step down from my soapbox and summarize.

The Bottom Line:

1)     The latest research suggests that if a child is overweight by kindergarten, they are likely to be overweight for the rest of their lives. So if you want to spare your kids and grandkids  from a lifetime of obesity, you want to intervene early.

2)     A small percentage of those kids are destined to be obese no matter what they do. However, for the vast majority of them obesity can be prevented by a healthy lifestyle.

3)     If you are pregnant, don’t “eat for two”. That is terrible advice. If your pre-pregnancy weight is stable (neither increasing or decreasing), you only need to add a serving or two of healthy foods to your diet during pregnancy. Check with your doctor about the amount of weight gain that is right for you and follow their advice.

4)     If you have a young child who appears to be overweight, don’t restrict their calories. Instead, provide them with healthy food choices and encourage them to exercise.

5)     Finally, if you have been overweight since childhood, don’t despair. For most of us obesity is a combination of genetic predisposition and lifestyle choices. You can’t your genes, but you can change your lifestyle.

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 High Protein Diets Your Secret To Successful Weight Loss?

Do High Protein Diets Reduce Fat And Preserve Muscle?

Author: Dr. Stephen Chaney

Healthy Diet food group, proteins, include meat (chicken or turkAre high protein diets your secret to healthy weight loss? There are lots of diets out there – high fat, low fat, Paleolithic, blood type, exotic juices, magic pills and potions. But recently, high protein diets are getting a lot of press. The word is that they preserve muscle mass and preferentially decrease fat mass.

If high protein diets actually did that, it would be huge because:

  • It’s the fat – not the pounds – that causes most of the health problems.
  • Muscle burns more calories than fat, so preserving muscle mass helps keep your metabolic rate high without dangerous herbs or stimulants – and keeping your metabolic rate high helps prevent both the plateau and yo-yo (weight regain) characteristic of so many diets.
  • When you lose fat and retain muscle you are reshaping your body – and that’s why most people are dieting to begin with.

So let’s look more carefully at the recent study that has been generating all the headlines (Pasiakos et al, The FASEB Journal, 27: 3837-3847, 2013).

The Study Design:

This was a randomized control study with 39 young (21), healthy and fit men and women who were only borderline overweight (BMI = 25). These volunteers were put on a 21 day weight loss program in which calories were reduced by 30% and exercise was increased by 10%. They were divided into 3 groups:

  • One group was assigned a diet containing the RDA for protein (about 14% of calories in this study design).
  • The second group’s diet contained 2X the RDA for protein (28% of calories)
  • The third group’s diet contained 3X the RDA for protein (42% of calories)

In the RDA protein group carbohydrate was 56% of calories, and fat was 30% of calories. In the other two groups the carbohydrate and fat content of the diets was decreased proportionally.

Feet_On_ScaleWhat Did The Study Show?

  • Weight loss (7 pounds in 21 days) was the same on all 3 diets.
  • The high protein (28% and 42%) diets caused almost 2X more fat loss (5 pounds versus 2.8 pounds) than the diet supplying the RDA amount of protein.
  • The high protein (28% and 42%) diets caused 2X less muscle loss (2.1 pounds versus 4.2 pounds) than the diet supplying the RDA amount of protein.
  • In case you didn’t notice, there was no difference in overall results between the 28% (2X the RDA) and 42% (3X the RDA) diets.

Pros And Cons Of The Study:

  • The con is fairly obvious. The participants in this study were all young, healthy and were not seriously overweight. If this were the only study of this type one might seriously question whether the results were applicable to middle aged, overweight coach potatoes. However, there have been several other studies with older, more overweight volunteers that have come to the same conclusion – namely that high protein diets preserve muscle mass and enhance fat loss.
  • The value of this study is that it defines for the first time the upper limit for how much protein is required to preserve muscle mass in a weight loss regimen. 28% of calories is sufficient, and there appear to be no benefit from increasing protein further. I would add the caveat that there are studies suggesting that protein requirements for preserving muscle mass may be greater in adults 50 and older.

The Bottom Line:

1)    Forget the high fat diets, low fat diets, pills and potions. High protein diets (~2X the RDA or 28% of calories) do appear to be the safest, most effective way to preserve muscle mass and enhance fat loss in a weight loss regimen.

2)     That’s not a lot of protein, by the way. The average American consumes almost 2X the RDA for protein on a daily basis. However, it is significantly more protein than the average American consumes when they are trying to lose weight. Salads and carrot sticks are great diet foods, but they don’t contain much protein.

3)     Higher protein intake does not appear to offer any additional benefit – at least in young adults.

4)     Not all high protein diets are created equal. What some people call high protein diets are laden with saturated fats or devoid of carbohydrate. The diet in this study, which is what I recommend, had 43% healthy carbohydrates and 30% healthy fats.

5)    These diets were designed to give 7 pounds of weight loss in 21 days – which is what the experts recommend. There are diets out there promising faster weight loss but they severely restrict calories and/or rely heavily on stimulants, they do not preserve muscle mass, and they often are not safe. In addition they are usually temporary.  I do not recommend them.

6)    This level of protein intake is safe for almost everyone. The major exception would be people with kidney disease, who should always check with their doctor before increasing protein intake. The only other caveat is that protein metabolism creates a lot of nitrogenous waste, so you should drink plenty of water to flush that waste out of your system. But, water is always a good idea.

7)     The high protein diets minimized, but did not completely prevent, muscle loss. Other studies suggest that adding the amino acid leucine to a high protein diet can give 100% retention of muscle mass in a weight loss regimen – but that’s another story for another day.

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