Caroline Apovian, MD

Many patients with obesity blame weight gain on their metabolism. The reality is that metabolism can be blamed for weight regain after people try to lose weight! As we age, our metabolism does slow down; sometimes we think it stops working.

Metabolism, or resting energy expenditure, is directly related to how much muscle mass we have. As we age, we lose muscle, which is called sarcopenia.

What happens to our metabolism when we try to lose weight? Let’s first discuss what metabolism is.
 

What Is Metabolism?

Metabolism refers to the chemical reactions in the body’s cells that convert food into energy for sustaining life, cellular processes, and as storage for a rainy day.

Total energy expenditure (TEE) is broken down into resting energy expenditure (REE), thermic effect of food (TEF), and nonresting expenditure (NREE) or physical activity, and is made up of: TEE = 60% REE + 10% TEF + 30% NREE.

An elegant study performed by Dr. Rudy Leibel explored the effects of weight loss or weight gain on metabolism in 23 lean and 18 patients with obesity who were placed in a metabolic chamber. Weight loss of 10% or 20% body weight led to a decrease in TEE roughly equal to about 300 kcal/d, and an increase in body weight of 10% caused an increase in TEE of about 500 kcal/d. These changes led to the patient reverting to the prior weight (before weight loss or gain). In other words, Dr. Leibel postulated a feedback mechanism for the effect of fat mass decrease or increase on energy metabolism. The feedback mechanism or signal from fat was subsequently found to be leptin.

In a later study, Dr. Leibel and colleagues investigated the effects of body fat mass change on TEE and found that a 10% reduction in weight caused a decrease of TEE by 21%, comprising a decrease in NREE of 37.5% and a decrease in REE of 11.6%.

Therefore, the biggest change in TEE comes from NREE or exercise energy expenditure. The 35% variance in NEE change was accounted for by a decrease in muscle work efficiency in generating 10 watts or low levels of work such as walking.

In other words, when persons with obesity or lean persons lose weight, the efficiency of muscle at low levels of work increases such that one burns less energy when walking than one normally would. This helps conserve energy and tends to cause the body to go back to the higher weight.
 

So, How Can One Change Metabolism?

Let’s say one did lose weight and wants to counteract this TEE loss and increased muscle efficiency at low levels of work.

To counteract this effect, one should increase muscle work beyond low level so that more energy is expended. Another way would be to increase muscle mass so that there is more muscle that can do work.

This is exactly how metabolism can be altered or increased. What can be changed most readily, and what we have the most power over in our bodies, is the NREE.

To do this, muscles need anabolic power — the power to heal and build muscle mass. Anabolic power comes from eating healthy protein sources such as lean chicken, fish, beef, and eggs as well as dry beans, tofu, and dairy products.. It seems that older adults (> 60 years) need more protein than younger adults to build muscle mass, due to the body’s natural aging process which leads to sarcopenia. How much more? Studies show between 1.2 and 1.5 g/kg of body weight per day, whereas younger persons need 0.80 g/kg.

Developing sarcopenia with age involves muscle losing the ability to use protein and amino acids to rebuild injured tissue.

Let’s put this in perspective for treating obesity.

Obesity is brought on by the body’s defense of a higher body weight by interaction with the environment of highly processed foods that work on the reward pathway, leading to weight gain and resistance to satiety. Weight loss via diet, exercise, and medications works, but this weight loss is also accompanied by a decrease in TEE.

Weight loss is primarily fat mass loss, but depending on the degree of protein intake and muscle resistance training, 20%-50% of the total weight loss is muscle mass loss. Therefore, higher-protein diets and resistance exercise can be useful in preserving muscle mass and counteracting the decrease in TEE, maintaining energy expenditure. In older patients, an additional factor is the muscle’s lack of ability to use protein as an anabolic agent to protect muscle mass and thus the need for higher protein loads to do this.

All in all, can doctors help patients boost their metabolism, especially as they lose weight and maintain that loss? Yes — through protein intake and resistance exercise training.

Here are some tips to help your patients get cardio and resistance exercise into their routine.

First find out whether your patient prefers a social exercise interaction or solo training. If social, then the gym or classes such as cycling or boot camps at those gyms may work for them, especially if they can go with a friend. If solo is better, than a gym in the home might work. Peloton bikes are expensive but the interaction is all on the website!

A personal trainer may help motivate the patient if they know someone is waiting for them.

Let’s hit the gym!

Another note: There are agents in the obesity treatment pipeline that purport to change body composition while helping patients lose weight. Some of these agents are myostatin antagonists and antibodies that inhibit the activity of myostatin to break down muscle. These agents have been found to build muscle mass, but whether the quality of the muscle mass leads to an increase in muscle strength or functionality remains controversial. The next frontier in obesity treatment will be about decreasing fat mass and increasing muscle mass while making sure that increased muscle mass leads to improved functionality.

In the meantime, aside from new agents on the horizon, the best and healthiest way to keep metabolism on the up and up is to eat healthy lean proteins and exercise. How much exercise? The recommendation is 30-60 minutes of moderate to vigorous physical activity at least 5 days per week; plus 20 minutes of resistance exercise training 2-3 days per week for upper- and lower-extremity and core strength.

Again, let’s hit the gym!
 

Dr. Apovian is in the department of medicine, and codirector, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, at Brigham and Women’s Hospital, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis, Srl, L-Nutra, and NeuroBo Pharmaceuticals, and Novo Nordisk. She received research grant from the National Institutes of Health, Patient-Centered Outcomes Research Institute, and GI Dynamics.

A version of this article appeared on Medscape.com.

Many patients with obesity blame weight gain on their metabolism. The reality is that metabolism can be blamed for weight regain after people try to lose weight! As we age, our metabolism does slow down; sometimes we think it stops working.

Metabolism, or resting energy expenditure, is directly related to how much muscle mass we have. As we age, we lose muscle, which is called sarcopenia.

What happens to our metabolism when we try to lose weight? Let’s first discuss what metabolism is.
 

What Is Metabolism?

Metabolism refers to the chemical reactions in the body’s cells that convert food into energy for sustaining life, cellular processes, and as storage for a rainy day.

Total energy expenditure (TEE) is broken down into resting energy expenditure (REE), thermic effect of food (TEF), and nonresting expenditure (NREE) or physical activity, and is made up of: TEE = 60% REE + 10% TEF + 30% NREE.

An elegant study performed by Dr. Rudy Leibel explored the effects of weight loss or weight gain on metabolism in 23 lean and 18 patients with obesity who were placed in a metabolic chamber. Weight loss of 10% or 20% body weight led to a decrease in TEE roughly equal to about 300 kcal/d, and an increase in body weight of 10% caused an increase in TEE of about 500 kcal/d. These changes led to the patient reverting to the prior weight (before weight loss or gain). In other words, Dr. Leibel postulated a feedback mechanism for the effect of fat mass decrease or increase on energy metabolism. The feedback mechanism or signal from fat was subsequently found to be leptin.

In a later study, Dr. Leibel and colleagues investigated the effects of body fat mass change on TEE and found that a 10% reduction in weight caused a decrease of TEE by 21%, comprising a decrease in NREE of 37.5% and a decrease in REE of 11.6%.

Therefore, the biggest change in TEE comes from NREE or exercise energy expenditure. The 35% variance in NEE change was accounted for by a decrease in muscle work efficiency in generating 10 watts or low levels of work such as walking.

In other words, when persons with obesity or lean persons lose weight, the efficiency of muscle at low levels of work increases such that one burns less energy when walking than one normally would. This helps conserve energy and tends to cause the body to go back to the higher weight.
 

So, How Can One Change Metabolism?

Let’s say one did lose weight and wants to counteract this TEE loss and increased muscle efficiency at low levels of work.

To counteract this effect, one should increase muscle work beyond low level so that more energy is expended. Another way would be to increase muscle mass so that there is more muscle that can do work.

This is exactly how metabolism can be altered or increased. What can be changed most readily, and what we have the most power over in our bodies, is the NREE.

To do this, muscles need anabolic power — the power to heal and build muscle mass. Anabolic power comes from eating healthy protein sources such as lean chicken, fish, beef, and eggs as well as dry beans, tofu, and dairy products.. It seems that older adults (> 60 years) need more protein than younger adults to build muscle mass, due to the body’s natural aging process which leads to sarcopenia. How much more? Studies show between 1.2 and 1.5 g/kg of body weight per day, whereas younger persons need 0.80 g/kg.

Developing sarcopenia with age involves muscle losing the ability to use protein and amino acids to rebuild injured tissue.

Let’s put this in perspective for treating obesity.

Obesity is brought on by the body’s defense of a higher body weight by interaction with the environment of highly processed foods that work on the reward pathway, leading to weight gain and resistance to satiety. Weight loss via diet, exercise, and medications works, but this weight loss is also accompanied by a decrease in TEE.

Weight loss is primarily fat mass loss, but depending on the degree of protein intake and muscle resistance training, 20%-50% of the total weight loss is muscle mass loss. Therefore, higher-protein diets and resistance exercise can be useful in preserving muscle mass and counteracting the decrease in TEE, maintaining energy expenditure. In older patients, an additional factor is the muscle’s lack of ability to use protein as an anabolic agent to protect muscle mass and thus the need for higher protein loads to do this.

All in all, can doctors help patients boost their metabolism, especially as they lose weight and maintain that loss? Yes — through protein intake and resistance exercise training.

Here are some tips to help your patients get cardio and resistance exercise into their routine.

First find out whether your patient prefers a social exercise interaction or solo training. If social, then the gym or classes such as cycling or boot camps at those gyms may work for them, especially if they can go with a friend. If solo is better, than a gym in the home might work. Peloton bikes are expensive but the interaction is all on the website!

A personal trainer may help motivate the patient if they know someone is waiting for them.

Let’s hit the gym!

Another note: There are agents in the obesity treatment pipeline that purport to change body composition while helping patients lose weight. Some of these agents are myostatin antagonists and antibodies that inhibit the activity of myostatin to break down muscle. These agents have been found to build muscle mass, but whether the quality of the muscle mass leads to an increase in muscle strength or functionality remains controversial. The next frontier in obesity treatment will be about decreasing fat mass and increasing muscle mass while making sure that increased muscle mass leads to improved functionality.

In the meantime, aside from new agents on the horizon, the best and healthiest way to keep metabolism on the up and up is to eat healthy lean proteins and exercise. How much exercise? The recommendation is 30-60 minutes of moderate to vigorous physical activity at least 5 days per week; plus 20 minutes of resistance exercise training 2-3 days per week for upper- and lower-extremity and core strength.

Again, let’s hit the gym!
 

Dr. Apovian is in the department of medicine, and codirector, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, at Brigham and Women’s Hospital, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis, Srl, L-Nutra, and NeuroBo Pharmaceuticals, and Novo Nordisk. She received research grant from the National Institutes of Health, Patient-Centered Outcomes Research Institute, and GI Dynamics.

A version of this article appeared on Medscape.com.

Many patients with obesity blame weight gain on their metabolism. The reality is that metabolism can be blamed for weight regain after people try to lose weight! As we age, our metabolism does slow down; sometimes we think it stops working.

Metabolism, or resting energy expenditure, is directly related to how much muscle mass we have. As we age, we lose muscle, which is called sarcopenia.

What happens to our metabolism when we try to lose weight? Let’s first discuss what metabolism is.
 

What Is Metabolism?

Metabolism refers to the chemical reactions in the body’s cells that convert food into energy for sustaining life, cellular processes, and as storage for a rainy day.

Total energy expenditure (TEE) is broken down into resting energy expenditure (REE), thermic effect of food (TEF), and nonresting expenditure (NREE) or physical activity, and is made up of: TEE = 60% REE + 10% TEF + 30% NREE.

An elegant study performed by Dr. Rudy Leibel explored the effects of weight loss or weight gain on metabolism in 23 lean and 18 patients with obesity who were placed in a metabolic chamber. Weight loss of 10% or 20% body weight led to a decrease in TEE roughly equal to about 300 kcal/d, and an increase in body weight of 10% caused an increase in TEE of about 500 kcal/d. These changes led to the patient reverting to the prior weight (before weight loss or gain). In other words, Dr. Leibel postulated a feedback mechanism for the effect of fat mass decrease or increase on energy metabolism. The feedback mechanism or signal from fat was subsequently found to be leptin.

In a later study, Dr. Leibel and colleagues investigated the effects of body fat mass change on TEE and found that a 10% reduction in weight caused a decrease of TEE by 21%, comprising a decrease in NREE of 37.5% and a decrease in REE of 11.6%.

Therefore, the biggest change in TEE comes from NREE or exercise energy expenditure. The 35% variance in NEE change was accounted for by a decrease in muscle work efficiency in generating 10 watts or low levels of work such as walking.

In other words, when persons with obesity or lean persons lose weight, the efficiency of muscle at low levels of work increases such that one burns less energy when walking than one normally would. This helps conserve energy and tends to cause the body to go back to the higher weight.
 

So, How Can One Change Metabolism?

Let’s say one did lose weight and wants to counteract this TEE loss and increased muscle efficiency at low levels of work.

To counteract this effect, one should increase muscle work beyond low level so that more energy is expended. Another way would be to increase muscle mass so that there is more muscle that can do work.

This is exactly how metabolism can be altered or increased. What can be changed most readily, and what we have the most power over in our bodies, is the NREE.

To do this, muscles need anabolic power — the power to heal and build muscle mass. Anabolic power comes from eating healthy protein sources such as lean chicken, fish, beef, and eggs as well as dry beans, tofu, and dairy products.. It seems that older adults (> 60 years) need more protein than younger adults to build muscle mass, due to the body’s natural aging process which leads to sarcopenia. How much more? Studies show between 1.2 and 1.5 g/kg of body weight per day, whereas younger persons need 0.80 g/kg.

Developing sarcopenia with age involves muscle losing the ability to use protein and amino acids to rebuild injured tissue.

Let’s put this in perspective for treating obesity.

Obesity is brought on by the body’s defense of a higher body weight by interaction with the environment of highly processed foods that work on the reward pathway, leading to weight gain and resistance to satiety. Weight loss via diet, exercise, and medications works, but this weight loss is also accompanied by a decrease in TEE.

Weight loss is primarily fat mass loss, but depending on the degree of protein intake and muscle resistance training, 20%-50% of the total weight loss is muscle mass loss. Therefore, higher-protein diets and resistance exercise can be useful in preserving muscle mass and counteracting the decrease in TEE, maintaining energy expenditure. In older patients, an additional factor is the muscle’s lack of ability to use protein as an anabolic agent to protect muscle mass and thus the need for higher protein loads to do this.

All in all, can doctors help patients boost their metabolism, especially as they lose weight and maintain that loss? Yes — through protein intake and resistance exercise training.

Here are some tips to help your patients get cardio and resistance exercise into their routine.

First find out whether your patient prefers a social exercise interaction or solo training. If social, then the gym or classes such as cycling or boot camps at those gyms may work for them, especially if they can go with a friend. If solo is better, than a gym in the home might work. Peloton bikes are expensive but the interaction is all on the website!

A personal trainer may help motivate the patient if they know someone is waiting for them.

Let’s hit the gym!

Another note: There are agents in the obesity treatment pipeline that purport to change body composition while helping patients lose weight. Some of these agents are myostatin antagonists and antibodies that inhibit the activity of myostatin to break down muscle. These agents have been found to build muscle mass, but whether the quality of the muscle mass leads to an increase in muscle strength or functionality remains controversial. The next frontier in obesity treatment will be about decreasing fat mass and increasing muscle mass while making sure that increased muscle mass leads to improved functionality.

In the meantime, aside from new agents on the horizon, the best and healthiest way to keep metabolism on the up and up is to eat healthy lean proteins and exercise. How much exercise? The recommendation is 30-60 minutes of moderate to vigorous physical activity at least 5 days per week; plus 20 minutes of resistance exercise training 2-3 days per week for upper- and lower-extremity and core strength.

Again, let’s hit the gym!
 

Dr. Apovian is in the department of medicine, and codirector, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, at Brigham and Women’s Hospital, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis, Srl, L-Nutra, and NeuroBo Pharmaceuticals, and Novo Nordisk. She received research grant from the National Institutes of Health, Patient-Centered Outcomes Research Institute, and GI Dynamics.

A version of this article appeared on Medscape.com.

A few weeks ago, I made a patient who lost 100 pounds following a sleeve gastrectomy 9 months prior feel bad because I told her she lost too much weight. As I spoke to her, I realized that she found it hard to make life changes and that the surgery was a huge aide in changing her life and her lifestyle. I ended up apologizing for initially saying she lost too much weight.

For the first time in her life, she was successful in losing weight and keeping it off. The surgery allowed her body to defend a lower body weight by altering the secretion of gut hormones that lead to satiety in the brain. It’s not her fault that her body responded so well!

I asked her to be on my next orientation virtual meeting with prospective weight management patients to urge those with a body mass index (BMI) > 40 to consider bariatric surgery as the most effective durable and safe treatment for their degree of obesity.

Metabolic bariatric surgery, primarily sleeve gastrectomy and Roux-en-Y gastric bypass , alters the gut hormone milieu such that the body defends a lower mass of adipose tissue and a lower weight. We have learned what it takes to alter body weight defense to a healthy lower weight by studying why metabolic bariatric surgery works so well. It turns out that there are several hormones secreted by the gut that allow the brain to register fullness.

One of these gut hormones, glucagon-like peptide (GLP)-1, has been researched as an analog to help reduce body weight by 16% and has also been shown to reduce cardiovascular risk in the SELECT trial, as published in The New England Journal of Medicine (NEJM).

It’s the first weight loss medication to be shown in a cardiovascular outcomes trial to be superior to placebo in reduction of major cardiovascular events, including cardiovascular deaths, nonfatal myocardial infarction, and nonfatal stroke. The results presented at the 2023 American Heart Association meetings in Philadelphia ended in wholehearted applause by a “standing only” audience even before the presentation’s conclusion.

As we pave the way for nutrient-stimulated hormone (NuSH) therapies to be prescribed to all Americans with a BMI > 30 to improve health, we need to remember what these medications actually do. We used to think that metabolic bariatric surgery worked by restricting the stomach contents and malabsorbing nutrients. We now know that the surgeries work by altering NuSH secretion, allowing for less secretion of the hunger hormone ghrelin and more secretion of GLP-1, glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), oxyntomodulin (OXM), and other satiety hormones with less food ingestion.

They have pleiotropic effects on many organ systems in the body, including the brain, heart, adipose tissue, and liver. They decrease inflammation and also increase satiety and delay gastric emptying. None of these effects automatically produce weight loss, but they certainly aid in the adoption of a healthier body weight and better health. The weight loss occurs because these medications steer the body toward behavioral changes that promote weight loss.

As we delve into the SELECT trial results, a 20% reduction in major cardiovascular events was accompanied by an average weight loss of 9.6%, without a behavioral component added to either the placebo or intervention arms, as is usual in antiobesity agent trials.

Does this mean that primary care providers (PCPs) don’t have to educate patients on behavior change, diet, and exercise therapy? Well, if we consider obesity a disease as we do type 2 diabetes and dyslipidemia or hypertension, then no — PCPs don’t have to, just like they don’t in treating these other diseases.

However, we should rethink this practice. The recently published SURMOUNT-3 trial looked at another NuSH, tirzepatide, with intensive behavioral therapy; it resulted in a 26.6% weight loss, which is comparable to results with bariatric surgery. The SURMOUNT-1 trial of tirzepatide with nonintensive behavioral therapy resulted in a 20.9% weight loss, which is still substantial, but SURMOUNT-3 showed how much more is achievable with robust behavior-change therapy.

In other words, it’s time that PCPs provide education on behavior change to maximize the power of the medications prescribed in practice for the most common diseases suffered in the United States: obesity, type 2 diabetes, cardiovascular disease, and hypertension. These are all chronic, relapsing diseases. Medication alone will improve numbers (weight, blood glucose, A1c, and blood pressure), but a relapsing disease continues relentlessly as patients age to overcome the medications prescribed.

Today I made another patient feel bad because she lost over 100 pounds on semaglutide (Wegovy) 2.4 mg over 1 year, reducing her BMI from 57 to 36. She wanted to keep losing, so I recommended sleeve gastrectomy to lose more weight. I told her she could always restart the Wegovy after the procedure if needed.

We really don’t have an answer to this issue of NuSH therapy not getting to goal and bariatric surgery following medication therapy. The reality is that bariatric surgery should be considered a safe, effective treatment for extreme obesity somewhere along the trajectory of treatments starting with behavior (diet, exercise) and medications. It is still considered a last resort, and for some, just too aggressive.

We have learned much about the incretin hormones and what they can accomplish for obesity from studying bariatric — now called metabolic — surgery. Surgery should be seen as we see stent placement for angina, only more effective for longevity. The COURAGE trial, published in 2007 in NEJM, showed that when compared with medication treatment alone for angina, stent placement plus medications resulted in no difference in mortality after a 7-year follow-up period. Compare this to bariatric surgery, which in many retrospective analyses shows a 20% reduction in cardiovascular mortality after 20-year follow-up (Swedish Obesity Study). In the United States, there are 2 million stent procedures performed per year vs 250,000 bariatric surgical procedures. There are millions of Americans with a BMI > 40 and, yes, millions of Americans with angina. I think I make my point that we need to do more bariatric surgeries to effectively treat extreme obesity.

The solution to this negligent medical practice in obesity treatment is to empower PCPs to treat obesity (at least uncomplicated obesity) and refer to obesity medicine practices for complicated obesity with multiple complications, such as type 2 diabetes and cardiovascular disease, and to refer to obesity medicine practices with a surgical component for BMIs > 40 or > 35 with type 2 diabetes, sleep apnea, and/or cardiovascular disease or other serious conditions.

How do we empower PCPs? Insurance coverage of NuSH therapies due to life-saving properties — as evidenced by the SELECT trial — without prior authorizations; and education on how and why metabolic surgery works, as well as education on behavioral approaches, such as healthy diet and exercise, as a core therapy for all BMI categories.

It’s time.

Caroline Apovian, MD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Altimmune; Cowen and Company; Currax Pharmaceuticals; EPG Communication Holdings; Gelesis, Srl; L-Nutra; and NeuroBo Pharmaceuticals. Received research grant from: National Institutes of Health; Patient-Centered Outcomes Research Institute; and GI Dynamics. Received income in an amount equal to or greater than $250 from: Altimmune; Cowen and Company; NeuroBo Pharmaceuticals; and Novo Nordisk.

A version of this article appeared on Medscape.com.

A few weeks ago, I made a patient who lost 100 pounds following a sleeve gastrectomy 9 months prior feel bad because I told her she lost too much weight. As I spoke to her, I realized that she found it hard to make life changes and that the surgery was a huge aide in changing her life and her lifestyle. I ended up apologizing for initially saying she lost too much weight.

For the first time in her life, she was successful in losing weight and keeping it off. The surgery allowed her body to defend a lower body weight by altering the secretion of gut hormones that lead to satiety in the brain. It’s not her fault that her body responded so well!

I asked her to be on my next orientation virtual meeting with prospective weight management patients to urge those with a body mass index (BMI) > 40 to consider bariatric surgery as the most effective durable and safe treatment for their degree of obesity.

Metabolic bariatric surgery, primarily sleeve gastrectomy and Roux-en-Y gastric bypass , alters the gut hormone milieu such that the body defends a lower mass of adipose tissue and a lower weight. We have learned what it takes to alter body weight defense to a healthy lower weight by studying why metabolic bariatric surgery works so well. It turns out that there are several hormones secreted by the gut that allow the brain to register fullness.

One of these gut hormones, glucagon-like peptide (GLP)-1, has been researched as an analog to help reduce body weight by 16% and has also been shown to reduce cardiovascular risk in the SELECT trial, as published in The New England Journal of Medicine (NEJM).

It’s the first weight loss medication to be shown in a cardiovascular outcomes trial to be superior to placebo in reduction of major cardiovascular events, including cardiovascular deaths, nonfatal myocardial infarction, and nonfatal stroke. The results presented at the 2023 American Heart Association meetings in Philadelphia ended in wholehearted applause by a “standing only” audience even before the presentation’s conclusion.

As we pave the way for nutrient-stimulated hormone (NuSH) therapies to be prescribed to all Americans with a BMI > 30 to improve health, we need to remember what these medications actually do. We used to think that metabolic bariatric surgery worked by restricting the stomach contents and malabsorbing nutrients. We now know that the surgeries work by altering NuSH secretion, allowing for less secretion of the hunger hormone ghrelin and more secretion of GLP-1, glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), oxyntomodulin (OXM), and other satiety hormones with less food ingestion.

They have pleiotropic effects on many organ systems in the body, including the brain, heart, adipose tissue, and liver. They decrease inflammation and also increase satiety and delay gastric emptying. None of these effects automatically produce weight loss, but they certainly aid in the adoption of a healthier body weight and better health. The weight loss occurs because these medications steer the body toward behavioral changes that promote weight loss.

As we delve into the SELECT trial results, a 20% reduction in major cardiovascular events was accompanied by an average weight loss of 9.6%, without a behavioral component added to either the placebo or intervention arms, as is usual in antiobesity agent trials.

Does this mean that primary care providers (PCPs) don’t have to educate patients on behavior change, diet, and exercise therapy? Well, if we consider obesity a disease as we do type 2 diabetes and dyslipidemia or hypertension, then no — PCPs don’t have to, just like they don’t in treating these other diseases.

However, we should rethink this practice. The recently published SURMOUNT-3 trial looked at another NuSH, tirzepatide, with intensive behavioral therapy; it resulted in a 26.6% weight loss, which is comparable to results with bariatric surgery. The SURMOUNT-1 trial of tirzepatide with nonintensive behavioral therapy resulted in a 20.9% weight loss, which is still substantial, but SURMOUNT-3 showed how much more is achievable with robust behavior-change therapy.

In other words, it’s time that PCPs provide education on behavior change to maximize the power of the medications prescribed in practice for the most common diseases suffered in the United States: obesity, type 2 diabetes, cardiovascular disease, and hypertension. These are all chronic, relapsing diseases. Medication alone will improve numbers (weight, blood glucose, A1c, and blood pressure), but a relapsing disease continues relentlessly as patients age to overcome the medications prescribed.

Today I made another patient feel bad because she lost over 100 pounds on semaglutide (Wegovy) 2.4 mg over 1 year, reducing her BMI from 57 to 36. She wanted to keep losing, so I recommended sleeve gastrectomy to lose more weight. I told her she could always restart the Wegovy after the procedure if needed.

We really don’t have an answer to this issue of NuSH therapy not getting to goal and bariatric surgery following medication therapy. The reality is that bariatric surgery should be considered a safe, effective treatment for extreme obesity somewhere along the trajectory of treatments starting with behavior (diet, exercise) and medications. It is still considered a last resort, and for some, just too aggressive.

We have learned much about the incretin hormones and what they can accomplish for obesity from studying bariatric — now called metabolic — surgery. Surgery should be seen as we see stent placement for angina, only more effective for longevity. The COURAGE trial, published in 2007 in NEJM, showed that when compared with medication treatment alone for angina, stent placement plus medications resulted in no difference in mortality after a 7-year follow-up period. Compare this to bariatric surgery, which in many retrospective analyses shows a 20% reduction in cardiovascular mortality after 20-year follow-up (Swedish Obesity Study). In the United States, there are 2 million stent procedures performed per year vs 250,000 bariatric surgical procedures. There are millions of Americans with a BMI > 40 and, yes, millions of Americans with angina. I think I make my point that we need to do more bariatric surgeries to effectively treat extreme obesity.

The solution to this negligent medical practice in obesity treatment is to empower PCPs to treat obesity (at least uncomplicated obesity) and refer to obesity medicine practices for complicated obesity with multiple complications, such as type 2 diabetes and cardiovascular disease, and to refer to obesity medicine practices with a surgical component for BMIs > 40 or > 35 with type 2 diabetes, sleep apnea, and/or cardiovascular disease or other serious conditions.

How do we empower PCPs? Insurance coverage of NuSH therapies due to life-saving properties — as evidenced by the SELECT trial — without prior authorizations; and education on how and why metabolic surgery works, as well as education on behavioral approaches, such as healthy diet and exercise, as a core therapy for all BMI categories.

It’s time.

Caroline Apovian, MD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Altimmune; Cowen and Company; Currax Pharmaceuticals; EPG Communication Holdings; Gelesis, Srl; L-Nutra; and NeuroBo Pharmaceuticals. Received research grant from: National Institutes of Health; Patient-Centered Outcomes Research Institute; and GI Dynamics. Received income in an amount equal to or greater than $250 from: Altimmune; Cowen and Company; NeuroBo Pharmaceuticals; and Novo Nordisk.

A version of this article appeared on Medscape.com.

A few weeks ago, I made a patient who lost 100 pounds following a sleeve gastrectomy 9 months prior feel bad because I told her she lost too much weight. As I spoke to her, I realized that she found it hard to make life changes and that the surgery was a huge aide in changing her life and her lifestyle. I ended up apologizing for initially saying she lost too much weight.

For the first time in her life, she was successful in losing weight and keeping it off. The surgery allowed her body to defend a lower body weight by altering the secretion of gut hormones that lead to satiety in the brain. It’s not her fault that her body responded so well!

I asked her to be on my next orientation virtual meeting with prospective weight management patients to urge those with a body mass index (BMI) > 40 to consider bariatric surgery as the most effective durable and safe treatment for their degree of obesity.

Metabolic bariatric surgery, primarily sleeve gastrectomy and Roux-en-Y gastric bypass , alters the gut hormone milieu such that the body defends a lower mass of adipose tissue and a lower weight. We have learned what it takes to alter body weight defense to a healthy lower weight by studying why metabolic bariatric surgery works so well. It turns out that there are several hormones secreted by the gut that allow the brain to register fullness.

One of these gut hormones, glucagon-like peptide (GLP)-1, has been researched as an analog to help reduce body weight by 16% and has also been shown to reduce cardiovascular risk in the SELECT trial, as published in The New England Journal of Medicine (NEJM).

It’s the first weight loss medication to be shown in a cardiovascular outcomes trial to be superior to placebo in reduction of major cardiovascular events, including cardiovascular deaths, nonfatal myocardial infarction, and nonfatal stroke. The results presented at the 2023 American Heart Association meetings in Philadelphia ended in wholehearted applause by a “standing only” audience even before the presentation’s conclusion.

As we pave the way for nutrient-stimulated hormone (NuSH) therapies to be prescribed to all Americans with a BMI > 30 to improve health, we need to remember what these medications actually do. We used to think that metabolic bariatric surgery worked by restricting the stomach contents and malabsorbing nutrients. We now know that the surgeries work by altering NuSH secretion, allowing for less secretion of the hunger hormone ghrelin and more secretion of GLP-1, glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), oxyntomodulin (OXM), and other satiety hormones with less food ingestion.

They have pleiotropic effects on many organ systems in the body, including the brain, heart, adipose tissue, and liver. They decrease inflammation and also increase satiety and delay gastric emptying. None of these effects automatically produce weight loss, but they certainly aid in the adoption of a healthier body weight and better health. The weight loss occurs because these medications steer the body toward behavioral changes that promote weight loss.

As we delve into the SELECT trial results, a 20% reduction in major cardiovascular events was accompanied by an average weight loss of 9.6%, without a behavioral component added to either the placebo or intervention arms, as is usual in antiobesity agent trials.

Does this mean that primary care providers (PCPs) don’t have to educate patients on behavior change, diet, and exercise therapy? Well, if we consider obesity a disease as we do type 2 diabetes and dyslipidemia or hypertension, then no — PCPs don’t have to, just like they don’t in treating these other diseases.

However, we should rethink this practice. The recently published SURMOUNT-3 trial looked at another NuSH, tirzepatide, with intensive behavioral therapy; it resulted in a 26.6% weight loss, which is comparable to results with bariatric surgery. The SURMOUNT-1 trial of tirzepatide with nonintensive behavioral therapy resulted in a 20.9% weight loss, which is still substantial, but SURMOUNT-3 showed how much more is achievable with robust behavior-change therapy.

In other words, it’s time that PCPs provide education on behavior change to maximize the power of the medications prescribed in practice for the most common diseases suffered in the United States: obesity, type 2 diabetes, cardiovascular disease, and hypertension. These are all chronic, relapsing diseases. Medication alone will improve numbers (weight, blood glucose, A1c, and blood pressure), but a relapsing disease continues relentlessly as patients age to overcome the medications prescribed.

Today I made another patient feel bad because she lost over 100 pounds on semaglutide (Wegovy) 2.4 mg over 1 year, reducing her BMI from 57 to 36. She wanted to keep losing, so I recommended sleeve gastrectomy to lose more weight. I told her she could always restart the Wegovy after the procedure if needed.

We really don’t have an answer to this issue of NuSH therapy not getting to goal and bariatric surgery following medication therapy. The reality is that bariatric surgery should be considered a safe, effective treatment for extreme obesity somewhere along the trajectory of treatments starting with behavior (diet, exercise) and medications. It is still considered a last resort, and for some, just too aggressive.

We have learned much about the incretin hormones and what they can accomplish for obesity from studying bariatric — now called metabolic — surgery. Surgery should be seen as we see stent placement for angina, only more effective for longevity. The COURAGE trial, published in 2007 in NEJM, showed that when compared with medication treatment alone for angina, stent placement plus medications resulted in no difference in mortality after a 7-year follow-up period. Compare this to bariatric surgery, which in many retrospective analyses shows a 20% reduction in cardiovascular mortality after 20-year follow-up (Swedish Obesity Study). In the United States, there are 2 million stent procedures performed per year vs 250,000 bariatric surgical procedures. There are millions of Americans with a BMI > 40 and, yes, millions of Americans with angina. I think I make my point that we need to do more bariatric surgeries to effectively treat extreme obesity.

The solution to this negligent medical practice in obesity treatment is to empower PCPs to treat obesity (at least uncomplicated obesity) and refer to obesity medicine practices for complicated obesity with multiple complications, such as type 2 diabetes and cardiovascular disease, and to refer to obesity medicine practices with a surgical component for BMIs > 40 or > 35 with type 2 diabetes, sleep apnea, and/or cardiovascular disease or other serious conditions.

How do we empower PCPs? Insurance coverage of NuSH therapies due to life-saving properties — as evidenced by the SELECT trial — without prior authorizations; and education on how and why metabolic surgery works, as well as education on behavioral approaches, such as healthy diet and exercise, as a core therapy for all BMI categories.

It’s time.

Caroline Apovian, MD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Altimmune; Cowen and Company; Currax Pharmaceuticals; EPG Communication Holdings; Gelesis, Srl; L-Nutra; and NeuroBo Pharmaceuticals. Received research grant from: National Institutes of Health; Patient-Centered Outcomes Research Institute; and GI Dynamics. Received income in an amount equal to or greater than $250 from: Altimmune; Cowen and Company; NeuroBo Pharmaceuticals; and Novo Nordisk.

A version of this article appeared on Medscape.com.

A recent article hypothesized that fructose causes more metabolic disease than does sucrose when overfed in the human diet. Fructose intake as high-fructose corn syrup (HFCS) has risen since its use in soft drinks in the United States and parallels the increase in the prevalence of obesity.

The newest hypothesis regarding fructose invokes a genetic survival of the fittest rationale for how fructose-enhanced fat deposition exacerbates the increased caloric consumption from the Western diet to promote metabolic disease especially in our adolescent and young adult population. This theory suggests that fructose consumption causes low adenosine triphosphate, which stimulates energy intake causing an imbalance of energy regulation.

Ongoing interest in the association between the increased use of HFCS and the prevalence of obesity in the United States continues. The use of HFCS in sugary sweetened beverages (SSBs) has reduced the cost of these beverages because of technology in preparing HFCS from corn and the substitution of the cheaper HFCS for sugar in SSBs. Although SSBs haven’t been proven to cause obesity, there has been an increase in the risk for type 2 diabetes, cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), and even cancer. Research in HFCS, weight gain, and metabolic disease continues despite little definitive evidence of causation.

The relationship between SSBs consumption and obesity has been attributed to the increase in overall total caloric intake of the diet. These liquid calories do not suppress the intake of other foods to equalize the total amount of calories ingested. This knowledge has been gleaned from work performed by R. Mattes and B. Rolls in the 1990s through the early 2000s.

This research and the current work on HFCS and metabolic disease is important because there are adolescents and young adults in the United States and globally that ingest a large amount of SSBs and therefore are at risk for metabolic disease, type 2 diabetes, NAFLD, and CVD at an early age.

The concern over fructose stems from the association between the advent of increasing HFCS in SSBs and the increase in prevalence of obesity occurring at similar time periods in the United States, around 1970-1980.

Researchers noted the association and began to focus on potential reasons to pinpoint HFCS or fructose itself so we have a mechanism of action specific to fructose. Therefore, the public could be warned about the risk of drinking SSBs due to the HFCS and fructose ingested and the possibility of metabolic disease. Perhaps, there is a method to remove harmful HFCS from the food supply much like what has happened with industrially produced trans fatty acids. In 2018, the World Health Organization called for a total ban on trans fats due to causation of 500 million early deaths per year globally.

Similar to the process of making HFCS, most trans fats are formed through an industrial process that alters vegetable oil and creates a shelf stable inexpensive partially hydrogenated oil. Trans fats have been shown to increase low-density lipoprotein (LDL) cholesterol and decrease high-density lipoprotein (HDL) increasing the risk for myocardial infarction and stroke.

The prevalence of obesity has increased worldwide, even in countries where SSBs do not contain HFCS.

Still, the proof that HFCS can override the satiety pathway and cause excess calorie intake is intriguing and may have teeth if we can pinpoint the increase in prevalence of obesity in children and adolescents on increased ingestion of HFCS in SSBs. There is no reason nutritionally to add sugar or HFCS to liquids. Plus, if HFCS has a metabolic disadvantage then all the more reason to ban it. Then, it becomes like trans fats: a toxin in the food supply.


Dr. Apovian is a Faculty Member, Department of Medicine; Co-Director, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts. She has disclosed financial relationships with Altimmune, Inc; Cowen and Company, LLC; Currax Pharmaceuticals, LLC; EPG Communication Holdings, Ltd; Gelesis, Srl; L-Nutra, Inc; NeuroBo Pharmaceuticals; and Novo Nordisk, Inc. She has received research grants from the National Institutes of Health; Patient-Centered Outcomes Research Institute; GI Dynamics, Inc.

A version of this article appeared on Medscape.com.

A recent article hypothesized that fructose causes more metabolic disease than does sucrose when overfed in the human diet. Fructose intake as high-fructose corn syrup (HFCS) has risen since its use in soft drinks in the United States and parallels the increase in the prevalence of obesity.

The newest hypothesis regarding fructose invokes a genetic survival of the fittest rationale for how fructose-enhanced fat deposition exacerbates the increased caloric consumption from the Western diet to promote metabolic disease especially in our adolescent and young adult population. This theory suggests that fructose consumption causes low adenosine triphosphate, which stimulates energy intake causing an imbalance of energy regulation.

Ongoing interest in the association between the increased use of HFCS and the prevalence of obesity in the United States continues. The use of HFCS in sugary sweetened beverages (SSBs) has reduced the cost of these beverages because of technology in preparing HFCS from corn and the substitution of the cheaper HFCS for sugar in SSBs. Although SSBs haven’t been proven to cause obesity, there has been an increase in the risk for type 2 diabetes, cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), and even cancer. Research in HFCS, weight gain, and metabolic disease continues despite little definitive evidence of causation.

The relationship between SSBs consumption and obesity has been attributed to the increase in overall total caloric intake of the diet. These liquid calories do not suppress the intake of other foods to equalize the total amount of calories ingested. This knowledge has been gleaned from work performed by R. Mattes and B. Rolls in the 1990s through the early 2000s.

This research and the current work on HFCS and metabolic disease is important because there are adolescents and young adults in the United States and globally that ingest a large amount of SSBs and therefore are at risk for metabolic disease, type 2 diabetes, NAFLD, and CVD at an early age.

The concern over fructose stems from the association between the advent of increasing HFCS in SSBs and the increase in prevalence of obesity occurring at similar time periods in the United States, around 1970-1980.

Researchers noted the association and began to focus on potential reasons to pinpoint HFCS or fructose itself so we have a mechanism of action specific to fructose. Therefore, the public could be warned about the risk of drinking SSBs due to the HFCS and fructose ingested and the possibility of metabolic disease. Perhaps, there is a method to remove harmful HFCS from the food supply much like what has happened with industrially produced trans fatty acids. In 2018, the World Health Organization called for a total ban on trans fats due to causation of 500 million early deaths per year globally.

Similar to the process of making HFCS, most trans fats are formed through an industrial process that alters vegetable oil and creates a shelf stable inexpensive partially hydrogenated oil. Trans fats have been shown to increase low-density lipoprotein (LDL) cholesterol and decrease high-density lipoprotein (HDL) increasing the risk for myocardial infarction and stroke.

The prevalence of obesity has increased worldwide, even in countries where SSBs do not contain HFCS.

Still, the proof that HFCS can override the satiety pathway and cause excess calorie intake is intriguing and may have teeth if we can pinpoint the increase in prevalence of obesity in children and adolescents on increased ingestion of HFCS in SSBs. There is no reason nutritionally to add sugar or HFCS to liquids. Plus, if HFCS has a metabolic disadvantage then all the more reason to ban it. Then, it becomes like trans fats: a toxin in the food supply.


Dr. Apovian is a Faculty Member, Department of Medicine; Co-Director, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts. She has disclosed financial relationships with Altimmune, Inc; Cowen and Company, LLC; Currax Pharmaceuticals, LLC; EPG Communication Holdings, Ltd; Gelesis, Srl; L-Nutra, Inc; NeuroBo Pharmaceuticals; and Novo Nordisk, Inc. She has received research grants from the National Institutes of Health; Patient-Centered Outcomes Research Institute; GI Dynamics, Inc.

A version of this article appeared on Medscape.com.

A recent article hypothesized that fructose causes more metabolic disease than does sucrose when overfed in the human diet. Fructose intake as high-fructose corn syrup (HFCS) has risen since its use in soft drinks in the United States and parallels the increase in the prevalence of obesity.

The newest hypothesis regarding fructose invokes a genetic survival of the fittest rationale for how fructose-enhanced fat deposition exacerbates the increased caloric consumption from the Western diet to promote metabolic disease especially in our adolescent and young adult population. This theory suggests that fructose consumption causes low adenosine triphosphate, which stimulates energy intake causing an imbalance of energy regulation.

Ongoing interest in the association between the increased use of HFCS and the prevalence of obesity in the United States continues. The use of HFCS in sugary sweetened beverages (SSBs) has reduced the cost of these beverages because of technology in preparing HFCS from corn and the substitution of the cheaper HFCS for sugar in SSBs. Although SSBs haven’t been proven to cause obesity, there has been an increase in the risk for type 2 diabetes, cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), and even cancer. Research in HFCS, weight gain, and metabolic disease continues despite little definitive evidence of causation.

The relationship between SSBs consumption and obesity has been attributed to the increase in overall total caloric intake of the diet. These liquid calories do not suppress the intake of other foods to equalize the total amount of calories ingested. This knowledge has been gleaned from work performed by R. Mattes and B. Rolls in the 1990s through the early 2000s.

This research and the current work on HFCS and metabolic disease is important because there are adolescents and young adults in the United States and globally that ingest a large amount of SSBs and therefore are at risk for metabolic disease, type 2 diabetes, NAFLD, and CVD at an early age.

The concern over fructose stems from the association between the advent of increasing HFCS in SSBs and the increase in prevalence of obesity occurring at similar time periods in the United States, around 1970-1980.

Researchers noted the association and began to focus on potential reasons to pinpoint HFCS or fructose itself so we have a mechanism of action specific to fructose. Therefore, the public could be warned about the risk of drinking SSBs due to the HFCS and fructose ingested and the possibility of metabolic disease. Perhaps, there is a method to remove harmful HFCS from the food supply much like what has happened with industrially produced trans fatty acids. In 2018, the World Health Organization called for a total ban on trans fats due to causation of 500 million early deaths per year globally.

Similar to the process of making HFCS, most trans fats are formed through an industrial process that alters vegetable oil and creates a shelf stable inexpensive partially hydrogenated oil. Trans fats have been shown to increase low-density lipoprotein (LDL) cholesterol and decrease high-density lipoprotein (HDL) increasing the risk for myocardial infarction and stroke.

The prevalence of obesity has increased worldwide, even in countries where SSBs do not contain HFCS.

Still, the proof that HFCS can override the satiety pathway and cause excess calorie intake is intriguing and may have teeth if we can pinpoint the increase in prevalence of obesity in children and adolescents on increased ingestion of HFCS in SSBs. There is no reason nutritionally to add sugar or HFCS to liquids. Plus, if HFCS has a metabolic disadvantage then all the more reason to ban it. Then, it becomes like trans fats: a toxin in the food supply.


Dr. Apovian is a Faculty Member, Department of Medicine; Co-Director, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts. She has disclosed financial relationships with Altimmune, Inc; Cowen and Company, LLC; Currax Pharmaceuticals, LLC; EPG Communication Holdings, Ltd; Gelesis, Srl; L-Nutra, Inc; NeuroBo Pharmaceuticals; and Novo Nordisk, Inc. She has received research grants from the National Institutes of Health; Patient-Centered Outcomes Research Institute; GI Dynamics, Inc.

A version of this article appeared on Medscape.com.

A recent study found that people with obesity have lower blood levels of vitamin D than people of healthy weight. This association of obesity with low vitamin D levels has led to much speculation on whether low vitamin D levels cause obesity or whether obesity causes low vitamin D levels. The interest in this topic is piqued by the possibility that if vitamin D deficiency causes obesity, perhaps treatment could be as simple as providing vitamin D supplementation to enhance weight loss.

What is known about vitamin D’s role in the body?

It’s well known that vitamin D is essential for bone health as well as balancing the minerals calcium and phosphorus, but what is its role in weight management? Approximately 80%-90% of vitamin D in the body is from the skin synthesis of cholecalciferol through ultraviolet B radiation from sun exposure. The normal range of 25-hydroxy vitamin D is measured as nanograms per milliliter (ng/mL). Most experts recommend a level between 20 and 40 ng/mL, but this has been a controversial topic of never-ending debate in the medical literature.

Vitamin D levels and obesity

A strong link exists between low vitamin D levels (serum 25[OH] vitamin D) and obesity. This has been noted for many years without identifying the underlying reasons beyond the sequestering of vitamin D in adipose tissue, although I’ll discuss other possibilities.

The inverse correlation between vitamin D and obesity has been seen in other diseases, such as cardiovascular disease, hypertension, prediabetes, and insulin resistance, as well as in sarcopenia and aging. Most studies emphasized the correlation between increasing adiposity with vitamin D deficiency in all ethnic and age groups. The causes and potential direct consequences of the vitamin D deficiency state in obesity are not well understood.
 

Vitamin D and adipose tissue

It’s been proposed that low vitamin D status in obesity might be due to increased vitamin D clearance from serum and enhanced storage of vitamin D by adipose tissue.

In adipose tissue, vitamin D exerts a variety of effects on inflammation, innate immunity, metabolism, and differentiation and apoptosis in many cell types. There is a stronger association between 25(OH)D and visceral fat as compared to subcutaneous adipose tissue, which suggests an influence of inflammation and components of the metabolic syndrome on vitamin D metabolism.

Because vitamin D has anti-inflammatory properties, it’s possible that low vitamin D status contributes to adipose tissue inflammation, a key link between obesity and its associated metabolic complications in obesity. A higher storage of vitamin D in adipose tissue, if accompanied by a parallel increase in the local synthesis of 1,25(OH)2D3 and action, may conceivably modulate adipocyte function as well as the activity of adipose tissue macrophages and hence the level of adipose tissue inflammation. In addition, it seems likely that 1,25(OH)2D3 also regulates the function of macrophages and other immune cell populations within adipose tissue.

It’s well known that vitamin D is stored in body fat, leading to the assumption that this was important in the evolution of vertebrates, including humans, who lived at latitudes where vitamin D could not be made in the winter and vitamin D stores had to be mobilized to maintain vitamin D sufficiency.
 

What is vitamin D’s role in obesity?

The main question that has eluded an answer so far is this one: Is vitamin D deficiency only a coincidental finding in obesity due to sequestration of the vitamin in fat, or does it have a role in the development of obesity and its complications, such as cardiovascular disease, type 2 diabetes, and hypertension?

Low vitamin D usually leads to impaired calcium absorption in the intestine and a lower calcium level, and eventually enhanced bone turnover and impaired bone mineral density (BMD).

However, it is known that in obesity there is greater BMD than in those who are lean. This leads to the conclusion that because there is a lack of vitamin D deficiency effects on bone in those with obesity, there is not really a vitamin D deficiency, and it may be that the sequestration in adipose tissue leads to a permanent supply that can maintain bone health.

An alternative explanation is that there is greater skeletal loading in obesity, and elevations in hormones such as estrogen and leptin could compensate for the vitamin D deficiency, leading to greater BMD in obesity.

Several other potential mechanisms besides sequestration of vitamin D in adipose tissue have been identified for low vitamin D and obesity. These include impaired hepatic 25-hydroxylation in nonalcoholic fatty liver disease, less sunlight exposure due to lower mobility and different clothing habits in people with obesity vs. their lean counterparts, and adverse dietary habits. For example, people with higher BMIs spend less time exercising outdoors and are more sedentary in general than their lean counterparts. Therefore, they are less likely to get sun exposure because of a decrease in time spent outdoors. Those with higher BMIs also tend to cover their bodies, showing less skin when outdoors than their leaner counterparts, and thus there is likely to be less conversion to vitamin D via skin and sun exposure in people with obesity.

Some studies suggest that an increased level of parathyroid hormone due to vitamin D deficiency promotes lipogenesis because of greater calcium influx in adipocytes. Another hypothesis is that the active form of vitamin D, 1,25(OH) D, inhibits adipogenesis through actions modulated by vitamin D receptors. These studies are promising, but prospective randomized trials are needed to determine whether vitamin D supplementation is a treatment option in preventing obesity. So far, vitamin D supplementation shows inconsistent results.

To conclude, there is a high prevalence of vitamin D deficiency in obesity, most likely because of dilution and sequestration in greater volumes of fat, blood muscle, and liver in obesity. Low vitamin D levels can’t be ruled out as a cause of obesity because of the research showing some interesting findings in vitamin D receptors in adipose tissue. Vitamin D deficiency in obesity doesn’t seem to affect bone mass but could have deleterious effects on other organ systems.

Weight loss improves obesity and complications, including the risk for cardiovascular disease and type 2 diabetes as well as vitamin D deficiency.
 

What do the guidelines say?

Treatment of vitamin D deficiency requires higher doses in obesity to achieve the same serum concentration compared with lean persons. Maintenance doses should not differ between those with obesity and lean persons.

The association of vitamin D and obesity remains elusive. Studies need to focus on vitamin D, vitamin D receptors, and actions of vitamin D in adipose tissue to investigate this relationship further.

In the meantime, media attention remains focused on the potential treatment and prevention of obesity with the mighty, all-purpose vitamin D, even though there is scant evidence.

Dr. Apovian is codirector at the Center for Weight Management and Wellness at Brigham and Women’s Hospital and professor of medicine in the division of endocrinology, diabetes and hypertension at Harvard University, Boston. She disclosed conflicts of interest with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.

A version of this article first appeared on Medscape.com.

A recent study found that people with obesity have lower blood levels of vitamin D than people of healthy weight. This association of obesity with low vitamin D levels has led to much speculation on whether low vitamin D levels cause obesity or whether obesity causes low vitamin D levels. The interest in this topic is piqued by the possibility that if vitamin D deficiency causes obesity, perhaps treatment could be as simple as providing vitamin D supplementation to enhance weight loss.

What is known about vitamin D’s role in the body?

It’s well known that vitamin D is essential for bone health as well as balancing the minerals calcium and phosphorus, but what is its role in weight management? Approximately 80%-90% of vitamin D in the body is from the skin synthesis of cholecalciferol through ultraviolet B radiation from sun exposure. The normal range of 25-hydroxy vitamin D is measured as nanograms per milliliter (ng/mL). Most experts recommend a level between 20 and 40 ng/mL, but this has been a controversial topic of never-ending debate in the medical literature.

Vitamin D levels and obesity

A strong link exists between low vitamin D levels (serum 25[OH] vitamin D) and obesity. This has been noted for many years without identifying the underlying reasons beyond the sequestering of vitamin D in adipose tissue, although I’ll discuss other possibilities.

The inverse correlation between vitamin D and obesity has been seen in other diseases, such as cardiovascular disease, hypertension, prediabetes, and insulin resistance, as well as in sarcopenia and aging. Most studies emphasized the correlation between increasing adiposity with vitamin D deficiency in all ethnic and age groups. The causes and potential direct consequences of the vitamin D deficiency state in obesity are not well understood.
 

Vitamin D and adipose tissue

It’s been proposed that low vitamin D status in obesity might be due to increased vitamin D clearance from serum and enhanced storage of vitamin D by adipose tissue.

In adipose tissue, vitamin D exerts a variety of effects on inflammation, innate immunity, metabolism, and differentiation and apoptosis in many cell types. There is a stronger association between 25(OH)D and visceral fat as compared to subcutaneous adipose tissue, which suggests an influence of inflammation and components of the metabolic syndrome on vitamin D metabolism.

Because vitamin D has anti-inflammatory properties, it’s possible that low vitamin D status contributes to adipose tissue inflammation, a key link between obesity and its associated metabolic complications in obesity. A higher storage of vitamin D in adipose tissue, if accompanied by a parallel increase in the local synthesis of 1,25(OH)2D3 and action, may conceivably modulate adipocyte function as well as the activity of adipose tissue macrophages and hence the level of adipose tissue inflammation. In addition, it seems likely that 1,25(OH)2D3 also regulates the function of macrophages and other immune cell populations within adipose tissue.

It’s well known that vitamin D is stored in body fat, leading to the assumption that this was important in the evolution of vertebrates, including humans, who lived at latitudes where vitamin D could not be made in the winter and vitamin D stores had to be mobilized to maintain vitamin D sufficiency.
 

What is vitamin D’s role in obesity?

The main question that has eluded an answer so far is this one: Is vitamin D deficiency only a coincidental finding in obesity due to sequestration of the vitamin in fat, or does it have a role in the development of obesity and its complications, such as cardiovascular disease, type 2 diabetes, and hypertension?

Low vitamin D usually leads to impaired calcium absorption in the intestine and a lower calcium level, and eventually enhanced bone turnover and impaired bone mineral density (BMD).

However, it is known that in obesity there is greater BMD than in those who are lean. This leads to the conclusion that because there is a lack of vitamin D deficiency effects on bone in those with obesity, there is not really a vitamin D deficiency, and it may be that the sequestration in adipose tissue leads to a permanent supply that can maintain bone health.

An alternative explanation is that there is greater skeletal loading in obesity, and elevations in hormones such as estrogen and leptin could compensate for the vitamin D deficiency, leading to greater BMD in obesity.

Several other potential mechanisms besides sequestration of vitamin D in adipose tissue have been identified for low vitamin D and obesity. These include impaired hepatic 25-hydroxylation in nonalcoholic fatty liver disease, less sunlight exposure due to lower mobility and different clothing habits in people with obesity vs. their lean counterparts, and adverse dietary habits. For example, people with higher BMIs spend less time exercising outdoors and are more sedentary in general than their lean counterparts. Therefore, they are less likely to get sun exposure because of a decrease in time spent outdoors. Those with higher BMIs also tend to cover their bodies, showing less skin when outdoors than their leaner counterparts, and thus there is likely to be less conversion to vitamin D via skin and sun exposure in people with obesity.

Some studies suggest that an increased level of parathyroid hormone due to vitamin D deficiency promotes lipogenesis because of greater calcium influx in adipocytes. Another hypothesis is that the active form of vitamin D, 1,25(OH) D, inhibits adipogenesis through actions modulated by vitamin D receptors. These studies are promising, but prospective randomized trials are needed to determine whether vitamin D supplementation is a treatment option in preventing obesity. So far, vitamin D supplementation shows inconsistent results.

To conclude, there is a high prevalence of vitamin D deficiency in obesity, most likely because of dilution and sequestration in greater volumes of fat, blood muscle, and liver in obesity. Low vitamin D levels can’t be ruled out as a cause of obesity because of the research showing some interesting findings in vitamin D receptors in adipose tissue. Vitamin D deficiency in obesity doesn’t seem to affect bone mass but could have deleterious effects on other organ systems.

Weight loss improves obesity and complications, including the risk for cardiovascular disease and type 2 diabetes as well as vitamin D deficiency.
 

What do the guidelines say?

Treatment of vitamin D deficiency requires higher doses in obesity to achieve the same serum concentration compared with lean persons. Maintenance doses should not differ between those with obesity and lean persons.

The association of vitamin D and obesity remains elusive. Studies need to focus on vitamin D, vitamin D receptors, and actions of vitamin D in adipose tissue to investigate this relationship further.

In the meantime, media attention remains focused on the potential treatment and prevention of obesity with the mighty, all-purpose vitamin D, even though there is scant evidence.

Dr. Apovian is codirector at the Center for Weight Management and Wellness at Brigham and Women’s Hospital and professor of medicine in the division of endocrinology, diabetes and hypertension at Harvard University, Boston. She disclosed conflicts of interest with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.

A version of this article first appeared on Medscape.com.

A recent study found that people with obesity have lower blood levels of vitamin D than people of healthy weight. This association of obesity with low vitamin D levels has led to much speculation on whether low vitamin D levels cause obesity or whether obesity causes low vitamin D levels. The interest in this topic is piqued by the possibility that if vitamin D deficiency causes obesity, perhaps treatment could be as simple as providing vitamin D supplementation to enhance weight loss.

What is known about vitamin D’s role in the body?

It’s well known that vitamin D is essential for bone health as well as balancing the minerals calcium and phosphorus, but what is its role in weight management? Approximately 80%-90% of vitamin D in the body is from the skin synthesis of cholecalciferol through ultraviolet B radiation from sun exposure. The normal range of 25-hydroxy vitamin D is measured as nanograms per milliliter (ng/mL). Most experts recommend a level between 20 and 40 ng/mL, but this has been a controversial topic of never-ending debate in the medical literature.

Vitamin D levels and obesity

A strong link exists between low vitamin D levels (serum 25[OH] vitamin D) and obesity. This has been noted for many years without identifying the underlying reasons beyond the sequestering of vitamin D in adipose tissue, although I’ll discuss other possibilities.

The inverse correlation between vitamin D and obesity has been seen in other diseases, such as cardiovascular disease, hypertension, prediabetes, and insulin resistance, as well as in sarcopenia and aging. Most studies emphasized the correlation between increasing adiposity with vitamin D deficiency in all ethnic and age groups. The causes and potential direct consequences of the vitamin D deficiency state in obesity are not well understood.
 

Vitamin D and adipose tissue

It’s been proposed that low vitamin D status in obesity might be due to increased vitamin D clearance from serum and enhanced storage of vitamin D by adipose tissue.

In adipose tissue, vitamin D exerts a variety of effects on inflammation, innate immunity, metabolism, and differentiation and apoptosis in many cell types. There is a stronger association between 25(OH)D and visceral fat as compared to subcutaneous adipose tissue, which suggests an influence of inflammation and components of the metabolic syndrome on vitamin D metabolism.

Because vitamin D has anti-inflammatory properties, it’s possible that low vitamin D status contributes to adipose tissue inflammation, a key link between obesity and its associated metabolic complications in obesity. A higher storage of vitamin D in adipose tissue, if accompanied by a parallel increase in the local synthesis of 1,25(OH)2D3 and action, may conceivably modulate adipocyte function as well as the activity of adipose tissue macrophages and hence the level of adipose tissue inflammation. In addition, it seems likely that 1,25(OH)2D3 also regulates the function of macrophages and other immune cell populations within adipose tissue.

It’s well known that vitamin D is stored in body fat, leading to the assumption that this was important in the evolution of vertebrates, including humans, who lived at latitudes where vitamin D could not be made in the winter and vitamin D stores had to be mobilized to maintain vitamin D sufficiency.
 

What is vitamin D’s role in obesity?

The main question that has eluded an answer so far is this one: Is vitamin D deficiency only a coincidental finding in obesity due to sequestration of the vitamin in fat, or does it have a role in the development of obesity and its complications, such as cardiovascular disease, type 2 diabetes, and hypertension?

Low vitamin D usually leads to impaired calcium absorption in the intestine and a lower calcium level, and eventually enhanced bone turnover and impaired bone mineral density (BMD).

However, it is known that in obesity there is greater BMD than in those who are lean. This leads to the conclusion that because there is a lack of vitamin D deficiency effects on bone in those with obesity, there is not really a vitamin D deficiency, and it may be that the sequestration in adipose tissue leads to a permanent supply that can maintain bone health.

An alternative explanation is that there is greater skeletal loading in obesity, and elevations in hormones such as estrogen and leptin could compensate for the vitamin D deficiency, leading to greater BMD in obesity.

Several other potential mechanisms besides sequestration of vitamin D in adipose tissue have been identified for low vitamin D and obesity. These include impaired hepatic 25-hydroxylation in nonalcoholic fatty liver disease, less sunlight exposure due to lower mobility and different clothing habits in people with obesity vs. their lean counterparts, and adverse dietary habits. For example, people with higher BMIs spend less time exercising outdoors and are more sedentary in general than their lean counterparts. Therefore, they are less likely to get sun exposure because of a decrease in time spent outdoors. Those with higher BMIs also tend to cover their bodies, showing less skin when outdoors than their leaner counterparts, and thus there is likely to be less conversion to vitamin D via skin and sun exposure in people with obesity.

Some studies suggest that an increased level of parathyroid hormone due to vitamin D deficiency promotes lipogenesis because of greater calcium influx in adipocytes. Another hypothesis is that the active form of vitamin D, 1,25(OH) D, inhibits adipogenesis through actions modulated by vitamin D receptors. These studies are promising, but prospective randomized trials are needed to determine whether vitamin D supplementation is a treatment option in preventing obesity. So far, vitamin D supplementation shows inconsistent results.

To conclude, there is a high prevalence of vitamin D deficiency in obesity, most likely because of dilution and sequestration in greater volumes of fat, blood muscle, and liver in obesity. Low vitamin D levels can’t be ruled out as a cause of obesity because of the research showing some interesting findings in vitamin D receptors in adipose tissue. Vitamin D deficiency in obesity doesn’t seem to affect bone mass but could have deleterious effects on other organ systems.

Weight loss improves obesity and complications, including the risk for cardiovascular disease and type 2 diabetes as well as vitamin D deficiency.
 

What do the guidelines say?

Treatment of vitamin D deficiency requires higher doses in obesity to achieve the same serum concentration compared with lean persons. Maintenance doses should not differ between those with obesity and lean persons.

The association of vitamin D and obesity remains elusive. Studies need to focus on vitamin D, vitamin D receptors, and actions of vitamin D in adipose tissue to investigate this relationship further.

In the meantime, media attention remains focused on the potential treatment and prevention of obesity with the mighty, all-purpose vitamin D, even though there is scant evidence.

Dr. Apovian is codirector at the Center for Weight Management and Wellness at Brigham and Women’s Hospital and professor of medicine in the division of endocrinology, diabetes and hypertension at Harvard University, Boston. She disclosed conflicts of interest with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.

A version of this article first appeared on Medscape.com.

The unfortunate death of Lori McClintock, wife of northern California congressman Tom McClintock, shortly after consuming the herbal remedy white mulberry leaf on Dec. 15, 2021, gives us the opportunity to discuss how to better protect the American public from nutritional supplements with claims to aid health. Mulberry leaf has been purported to lower blood glucose levels, cholesterol, and inflammation as well as promote weight loss.

Many people desire to improve their health with concoctions purported to be “natural” or “from nature” instead of seeing a doctor and taking a medication or other therapy that is evidenced-based and backed by approval from the Food and Drug Administration. With the burgeoning prevalence of obesity and type 2 diabetes in this country (and worldwide) and the lack of a magic bullet that can stop the progression of these life-threatening diseases, many Americans turn to herbal and nutritional supplements that claim to promote weight loss and improve health.

Passed in 1994, the Dietary Supplement Health and Education Act (DSHEA) has allowed manufacturers of herbal and nutritional supplements to be “off the radar” of government regulators, unless their products have been shown to do harm – which is the government’s burden to prove.

A dietary supplement is defined as a product containing one or more vitamin, mineral, herb, or other botanical; amino acid; or other substance that would increase the total dietary intake of that product.

DSHEA exempted dietary supplements from the rigorous safety and efficacy testing that medications must undergo for various disease states, which is regulated by the FDA.
 

People with obesity may fall prey to dietary supplements’ claims

Persons suffering from obesity and its metabolic sequelae may be susceptible to the claims of dietary supplements because:

• The stigma associated with obesity, including the lack of understanding that obesity is a disease not under a person’s control, may make those with the disease wish to remedy it on their own out of shame and peer pressure.
• Clinicians and doctors traditionally have not been trained in obesity medicine so they aren’t comfortable treating obesity.
• It’s only fairly recently that obesity was recognized as a disease, so many insurance companies still don’t reimburse for obesity treatments, including the agents that can suppress appetite and result in weight loss.

For all of these reasons and more, only 2% or less of the millions of Americans suffering from obesity are treated with an antiobesity agent each year.

This has paved the way for the dietary supplement industry to prey on a desperate population, in much the same way that fad diets continue to attract multitudes of Americans. These supplements, however, carry much more risk than fad diets.

The solution, of course, is better regulation of the supplement industry, but it’s also improvement of how obesity is treated by the medical community.
 

How can clinicians and the community help?

Government, academic, community, clinical, and lay persons are more frequently recognizing obesity as a disease. Stigma will slowly come to a halt, as it has for other diseases such as depression and addiction to alcohol and drugs. Medications that have undergone rigorous testing for safety and efficacy eventually will be prescribed more and covered by healthcare insurance. Clinicians, and specifically physicians, are the most trusted persons in terms of giving medical advice. We need to ask patients whether they are taking supplements and be vocal about their lack of protection against harm, as allowed by DSHEA.

It would not be overkill to add prompts to the medical record to ask patients not only about smoking, alcohol, and drug use but also about supplements of all kinds. Some medical records do use these prompts but they are not as ubiquitous as those for smoking, alcohol, and drug use.

The supplement industry is powerful, but so is the medical industry when it comes to lobbying for change. It is ironic that Lori McClintock was the wife of a congressman. Perhaps the silver lining is future work toward legislation advocating for an end to these tragic deaths from poorly regulated supplements. Alignment with government in pushing for stricter regulations could save lives in the future.

Dr. Apovian is a faculty member, department of medicine, division of endocrinology, diabetes, and hypertension; and codirector, Center for Weight Management and Wellness, Boston. She disclosed ties with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.



A version of this article first appeared on Medscape.com.

The unfortunate death of Lori McClintock, wife of northern California congressman Tom McClintock, shortly after consuming the herbal remedy white mulberry leaf on Dec. 15, 2021, gives us the opportunity to discuss how to better protect the American public from nutritional supplements with claims to aid health. Mulberry leaf has been purported to lower blood glucose levels, cholesterol, and inflammation as well as promote weight loss.

Many people desire to improve their health with concoctions purported to be “natural” or “from nature” instead of seeing a doctor and taking a medication or other therapy that is evidenced-based and backed by approval from the Food and Drug Administration. With the burgeoning prevalence of obesity and type 2 diabetes in this country (and worldwide) and the lack of a magic bullet that can stop the progression of these life-threatening diseases, many Americans turn to herbal and nutritional supplements that claim to promote weight loss and improve health.

Passed in 1994, the Dietary Supplement Health and Education Act (DSHEA) has allowed manufacturers of herbal and nutritional supplements to be “off the radar” of government regulators, unless their products have been shown to do harm – which is the government’s burden to prove.

A dietary supplement is defined as a product containing one or more vitamin, mineral, herb, or other botanical; amino acid; or other substance that would increase the total dietary intake of that product.

DSHEA exempted dietary supplements from the rigorous safety and efficacy testing that medications must undergo for various disease states, which is regulated by the FDA.
 

People with obesity may fall prey to dietary supplements’ claims

Persons suffering from obesity and its metabolic sequelae may be susceptible to the claims of dietary supplements because:

• The stigma associated with obesity, including the lack of understanding that obesity is a disease not under a person’s control, may make those with the disease wish to remedy it on their own out of shame and peer pressure.
• Clinicians and doctors traditionally have not been trained in obesity medicine so they aren’t comfortable treating obesity.
• It’s only fairly recently that obesity was recognized as a disease, so many insurance companies still don’t reimburse for obesity treatments, including the agents that can suppress appetite and result in weight loss.

For all of these reasons and more, only 2% or less of the millions of Americans suffering from obesity are treated with an antiobesity agent each year.

This has paved the way for the dietary supplement industry to prey on a desperate population, in much the same way that fad diets continue to attract multitudes of Americans. These supplements, however, carry much more risk than fad diets.

The solution, of course, is better regulation of the supplement industry, but it’s also improvement of how obesity is treated by the medical community.
 

How can clinicians and the community help?

Government, academic, community, clinical, and lay persons are more frequently recognizing obesity as a disease. Stigma will slowly come to a halt, as it has for other diseases such as depression and addiction to alcohol and drugs. Medications that have undergone rigorous testing for safety and efficacy eventually will be prescribed more and covered by healthcare insurance. Clinicians, and specifically physicians, are the most trusted persons in terms of giving medical advice. We need to ask patients whether they are taking supplements and be vocal about their lack of protection against harm, as allowed by DSHEA.

It would not be overkill to add prompts to the medical record to ask patients not only about smoking, alcohol, and drug use but also about supplements of all kinds. Some medical records do use these prompts but they are not as ubiquitous as those for smoking, alcohol, and drug use.

The supplement industry is powerful, but so is the medical industry when it comes to lobbying for change. It is ironic that Lori McClintock was the wife of a congressman. Perhaps the silver lining is future work toward legislation advocating for an end to these tragic deaths from poorly regulated supplements. Alignment with government in pushing for stricter regulations could save lives in the future.

Dr. Apovian is a faculty member, department of medicine, division of endocrinology, diabetes, and hypertension; and codirector, Center for Weight Management and Wellness, Boston. She disclosed ties with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.



A version of this article first appeared on Medscape.com.

The unfortunate death of Lori McClintock, wife of northern California congressman Tom McClintock, shortly after consuming the herbal remedy white mulberry leaf on Dec. 15, 2021, gives us the opportunity to discuss how to better protect the American public from nutritional supplements with claims to aid health. Mulberry leaf has been purported to lower blood glucose levels, cholesterol, and inflammation as well as promote weight loss.

Many people desire to improve their health with concoctions purported to be “natural” or “from nature” instead of seeing a doctor and taking a medication or other therapy that is evidenced-based and backed by approval from the Food and Drug Administration. With the burgeoning prevalence of obesity and type 2 diabetes in this country (and worldwide) and the lack of a magic bullet that can stop the progression of these life-threatening diseases, many Americans turn to herbal and nutritional supplements that claim to promote weight loss and improve health.

Passed in 1994, the Dietary Supplement Health and Education Act (DSHEA) has allowed manufacturers of herbal and nutritional supplements to be “off the radar” of government regulators, unless their products have been shown to do harm – which is the government’s burden to prove.

A dietary supplement is defined as a product containing one or more vitamin, mineral, herb, or other botanical; amino acid; or other substance that would increase the total dietary intake of that product.

DSHEA exempted dietary supplements from the rigorous safety and efficacy testing that medications must undergo for various disease states, which is regulated by the FDA.
 

People with obesity may fall prey to dietary supplements’ claims

Persons suffering from obesity and its metabolic sequelae may be susceptible to the claims of dietary supplements because:

• The stigma associated with obesity, including the lack of understanding that obesity is a disease not under a person’s control, may make those with the disease wish to remedy it on their own out of shame and peer pressure.
• Clinicians and doctors traditionally have not been trained in obesity medicine so they aren’t comfortable treating obesity.
• It’s only fairly recently that obesity was recognized as a disease, so many insurance companies still don’t reimburse for obesity treatments, including the agents that can suppress appetite and result in weight loss.

For all of these reasons and more, only 2% or less of the millions of Americans suffering from obesity are treated with an antiobesity agent each year.

This has paved the way for the dietary supplement industry to prey on a desperate population, in much the same way that fad diets continue to attract multitudes of Americans. These supplements, however, carry much more risk than fad diets.

The solution, of course, is better regulation of the supplement industry, but it’s also improvement of how obesity is treated by the medical community.
 

How can clinicians and the community help?

Government, academic, community, clinical, and lay persons are more frequently recognizing obesity as a disease. Stigma will slowly come to a halt, as it has for other diseases such as depression and addiction to alcohol and drugs. Medications that have undergone rigorous testing for safety and efficacy eventually will be prescribed more and covered by healthcare insurance. Clinicians, and specifically physicians, are the most trusted persons in terms of giving medical advice. We need to ask patients whether they are taking supplements and be vocal about their lack of protection against harm, as allowed by DSHEA.

It would not be overkill to add prompts to the medical record to ask patients not only about smoking, alcohol, and drug use but also about supplements of all kinds. Some medical records do use these prompts but they are not as ubiquitous as those for smoking, alcohol, and drug use.

The supplement industry is powerful, but so is the medical industry when it comes to lobbying for change. It is ironic that Lori McClintock was the wife of a congressman. Perhaps the silver lining is future work toward legislation advocating for an end to these tragic deaths from poorly regulated supplements. Alignment with government in pushing for stricter regulations could save lives in the future.

Dr. Apovian is a faculty member, department of medicine, division of endocrinology, diabetes, and hypertension; and codirector, Center for Weight Management and Wellness, Boston. She disclosed ties with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.



A version of this article first appeared on Medscape.com.