Opinion

Many people who lose weight, whether through diet and lifestyle changes, medication, or bariatric surgery, recognize their body has changed. While they also experience improvements in quality of life and psychosocial areas, that’s not true for everyone. Some patients don’t “see” they’ve lost weight — a phenomenon referred to as “phantom fat,” “ghost fat,” or “vestigial body image.”

“Most people are happy with their appearance, or at least their body shape, after weight loss — although some are unhappy with the loose, sagging skin that can follow weight loss and seek plastic surgery to remedy that,” David B. Sarwer, PhD, director of the Center for Obesity Research and Education and professor of social and behavioral sciences, Temple University College of Public Health, Philadelphia, told this news organization. “There’s a subset of people who remain dissatisfied with their body image, including their shape.”

This body dissatisfaction of people who lose weight may be long-standing, predating the weight loss, or may be new because weight loss has catalyzed a host of previously unaddressed psychosocial issues. Some may show up at assessments on treatment onset, while others may be detected by monitoring changes during or after weight loss. “Mental health counseling after bariatric surgery is greatly underutilized,” Dr. Sarwer observed.
 

Ghost Fat

Research has corroborated the lingering self-perception of being “obese” vs “ex-obese.” In one study, patients who had undergone bariatric surgery reported being unable to see the difference in their size and shape 18-30 months following their procedure, despite substantial weight loss.

Some research suggests that rapid weight loss (eg, through bariatric surgery) is more likely to generate the perception of “phantom fat,” but additional research is needed to investigate whether the mode and speed of weight loss affect subsequent body image.

Being habituated to one’s former appearance may play a role, Dr. Sarwer suggested. “We see this not only with weight loss but with other body-altering procedures. It takes the brain time to catch up to the new appearance. In rhinoplasty, for example, it may take patients a while before they become accustomed to looking at their new face in the mirror after decades of looking at a more prominent nose.”
 

Years of Social Stigma

It may also take time for people to overcome years of enduring the stigma of obesity.

There are “pervasive” negative attitudes implying that individuals who are overweight and/or obese are “lazy, weak-willed, lacking in self-discipline and willpower” — a problem compounded by social media and media in general, which present unrealistic, glorified body images and disparaging messages about those with weight problems.

“Body image is a construct, rather than what you see in the mirror,” Sheethal Reddy, PhD, a psychologist at the Emory Bariatric Center, Emory University Hospital Midtown, Atlanta, told this news organization. “It’s the mental construct of our physical selves.”

According to Dr. Reddy, body image develops “within a broader societal context and is influenced by the person’s ethnic, racial, and cultural heritage.”

Adolescents are particularly vulnerable to body dissatisfaction. This is compounded in those with obesity, who often experience weight-based victimization and internalized weight-based stigma, compared with adolescents with lower weights. Weight stigma often takes the form of teasing and bullying.

“Appearance-related bullying and teasing during childhood and adolescence can reverberate into adulthood and persist throughout the lifespan,” Dr. Sarwer said. “When we see these patients and ask if they’ve ever been teased or bullied, not only do many say yes but it takes them back to those moments, to that origin story, and they remember someone saying something mean, cruel, and hurtful.”

Stigmatizing experiences can affect subjective body image, even after the weight has been lost and the person’s body is objectively thinner. Research comparing individuals who were overweight and lost weight to individuals who are currently overweight and haven’t lost weight and individuals who were never overweight suggests that “vestigial” body disparagement may persist following weight loss — especially in those with early-onset obesity.
 

The Role of Genetics

Genetics may contribute to people’s self-perception and body dissatisfaction, both before and after weight loss. A study of 827 community-based adolescents examined the association between polygenic risk scores (PRS) for body mass index (BMI) and type 2 diabetes and symptoms of body dissatisfaction and depression.

“Given the significant genetic role in BMI, we wanted to explore whether genetic risk for BMI might also predict body dissatisfaction,” lead author Krista Ekberg, MS, a doctoral candidate in clinical psychology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, told this news organization.

Genetic influences on BMI, as measured by PRS, were significantly associated with both phenotypic BMI and body dissatisfaction. “The association between PRS and body dissatisfaction was largely explained by BMI, suggesting that BMI itself accounts for much of the link between genetic risk and body dissatisfaction.”
 

Psychiatric History and Trauma

Adverse experiences, particularly sexual or physical abuse, may also account for body dissatisfaction after weight loss. “When some people with a history of this type of abuse lose a large amount of weight — typically after bariatric surgery — they often go through a period of emotional turbulence,” Dr. Sarwer said.

Childhood maltreatment can also be associated with body image disturbances in adulthood, according to a meta-analysis of 12 studies, encompassing 15,481 participants. Sexual abuse is “surprisingly common” among patients with obesity, according to Dr. Sarwer. A chart review of 131 patients revealed that 60% of those who reported a history of rape or sexual molestation were ≥ 50 pounds overweight vs only 28% of age- and sex-matched controls without a history of abuse. Other studies have corroborated these findings.

Excess weight can serve an “adaptive function,” Dr. Sarwer noted. It can be a self-protective mechanism that “insulates” them from sexual advances by potential romantic partners or abusers. Some may find that, after weight loss, repressed memories of a sexual assault surface as a result of the newer, more “attractive” appearance. Feeling vulnerable in their thinner bodies, they may need to regard themselves as overweight to maintain that feeling of “protection.” Weight loss may also trigger memories, flashbacks, or nightmares, as people return to a weight at which they were abused.

Dissociation is another mechanism linking trauma with post–weight loss body dysmorphia, Supatra Tovar, PsyD, RD, a clinical psychologist and registered dietitian with a practice in California, told this news organization. Dissociation from the body is often a coping mechanism for dealing with an overwhelming traumatic experience.

Individuals with a history of depression, anxiety, or posttraumatic stress disorder have higher levels of body dysmorphia, both before and after weight loss. One study found that patients undergoing bariatric surgery who had some type of psychopathology and other psychological risk factors were significantly more likely to report body image concerns 3 months after the surgery. Body image concerns were also more common in patients with preoperative depression, current psychotropic medication use, and a history of outpatient therapy or psychotropic medication use.

“Depression, anxiety, and trauma play a role in how you see yourself and how you carry yourself,” Dr. Reddy said. “This is wrapped up in any type of psychopathology. Being depressed is like looking at yourself through a cloud. It’s the opposite of ‘rose-colored glasses’ and instead, looking at yourself through a negative lens.”
 

Diagnosis and Interventions

Some helpful tools to assess the presence and extent of weight dissatisfaction and body dysmorphia include the Eating Disorder Inventory — Body Dissatisfaction Subscale and the Body Shape Questionnaire. It’s also important to take into account “the extent to which people are invested in their appearance psychologically,” Dr. Sarwer advised. The AO subscale of the Multidimensional Body-Self Relations Questionnaire generally assesses this. The Body Image Quality of Life Inventory assesses how and to what extent the perceived body image affects the person’s quality of life.

Experts recommend cognitive behavioral therapy (CBT) as an evidence-based intervention for body image issues, including those following weight loss.

“There’s an extensive CBT body image therapy program specifically tailored to the needs of overweight and obese individuals,” Dr. Sarwer said. “We don’t ignore historical variables that may have contributed to the problem, like early bullying, but we encourage people to think about what’s going on in their day-to-day life today. We drill down not only into the maladaptive behaviors but also the cognition and beliefs that may be erroneous but underlie these behaviors.”

The aim of CBT is to “modify irrational and dysfunctional thoughts, emotions, and behaviors through techniques such as self-monitoring, cognitive structuring, psychoeducation, desensitization, and exposure and response prevention.” The program laid out in Cash’s body image workbook includes eight steps. (Figure).

Weight Loss Doesn’t Automatically Equate With Happiness

Another realistic expectation runs counter to a common misperception that becoming thin will automatically translate into becoming happier. That’s not always the case, according to Dr. Tovar.

“If you haven’t worked deeply on addressing self-compassion and understanding that who you are at the core has nothing to do with your physical appearance, you can have an empty feeling once you’ve reached this point,” she said. “You still don’t know who you are and what you’re contributing to the world [because] you’ve been so focused on losing weight.”

Weight loss can also “unmask” questions about self-worth, even when receiving compliments about one’s “improved” appearance. “Praise and compliments after weight loss can be a double-edged sword,” Dr. Tovar observed. “You might think, ‘I wasn’t accepted or praised when I was overweight. The only way to be acceptable or validated is by losing weight, so I have to continue losing weight.’ ” This fuels fear of regaining the weight and can lead to continuing to see oneself as overweight, perhaps as a way to stay motivated to continue with weight loss. “Feeling that one’s value depends on remaining thin hampers body satisfaction,” she said.

Dr. Tovar, author of the book Deprogram Diet Culture: Rethink Your Relationship with Food, Heal Your Mind, and Live a Diet-Free Life, encourages people to shift the emphasis from weight loss to a holistic focus on self-worth and to explore obstacles to those feelings both before and after weight loss.

Endocrinologists and other medical professionals can help by not engaging in “weight and body shaming,” Dr. Tovar said.

She recommends physicians “encourage patients to tune in to their own bodies, helping them become more aware of how different foods affect their physical and emotional well-being.”

Set realistic expectations through “open, nonjudgmental conversations about the complexities of metabolism, weight, and health.”

Dr. Tovar advises rather than focusing on weight loss as the primary goal, physicians should focus on health markers such as blood glucose, energy levels, mental well-being, and physical fitness.

Prioritize “listening over lecturing.” Begin with empathy, asking questions such as “How do you feel about your health right now? What changes have you noticed in your body lately?” Doing this “creates space for the patient to express their concerns without feeling judged or shamed.”

Refer patients to a mental health professional when a patient exhibits signs of disordered eating or poor body image or when emotional factors are playing a significant role in the relationship with food and weight. “If a patient is caught in a cycle of dieting and weight gain, struggles with binge eating, or displays symptoms of depression or anxiety related to body, then psychological help is crucial.”

Ultimately, the goal of treatment “should be to provide a safe, supportive environment where patients can heal — not just physically but also emotionally and mentally,” Dr. Tovar added.

Dr. Tovar, Ms. Ekberg, and Dr. Reddy reported no relevant financial relationships. Dr. Sarwer received grant funding from the National Institute of Dental and Craniofacial Research and National Institute of Diabetes and Digestive and Kidney Diseases. He has consulting relationships with Novo Nordisk and Twenty30 Health. He is an associate editor for Obesity Surgery and editor in chief of Obesity Science & Practice.
 

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

Many people who lose weight, whether through diet and lifestyle changes, medication, or bariatric surgery, recognize their body has changed. While they also experience improvements in quality of life and psychosocial areas, that’s not true for everyone. Some patients don’t “see” they’ve lost weight — a phenomenon referred to as “phantom fat,” “ghost fat,” or “vestigial body image.”

“Most people are happy with their appearance, or at least their body shape, after weight loss — although some are unhappy with the loose, sagging skin that can follow weight loss and seek plastic surgery to remedy that,” David B. Sarwer, PhD, director of the Center for Obesity Research and Education and professor of social and behavioral sciences, Temple University College of Public Health, Philadelphia, told this news organization. “There’s a subset of people who remain dissatisfied with their body image, including their shape.”

This body dissatisfaction of people who lose weight may be long-standing, predating the weight loss, or may be new because weight loss has catalyzed a host of previously unaddressed psychosocial issues. Some may show up at assessments on treatment onset, while others may be detected by monitoring changes during or after weight loss. “Mental health counseling after bariatric surgery is greatly underutilized,” Dr. Sarwer observed.
 

Ghost Fat

Research has corroborated the lingering self-perception of being “obese” vs “ex-obese.” In one study, patients who had undergone bariatric surgery reported being unable to see the difference in their size and shape 18-30 months following their procedure, despite substantial weight loss.

Some research suggests that rapid weight loss (eg, through bariatric surgery) is more likely to generate the perception of “phantom fat,” but additional research is needed to investigate whether the mode and speed of weight loss affect subsequent body image.

Being habituated to one’s former appearance may play a role, Dr. Sarwer suggested. “We see this not only with weight loss but with other body-altering procedures. It takes the brain time to catch up to the new appearance. In rhinoplasty, for example, it may take patients a while before they become accustomed to looking at their new face in the mirror after decades of looking at a more prominent nose.”
 

Years of Social Stigma

It may also take time for people to overcome years of enduring the stigma of obesity.

There are “pervasive” negative attitudes implying that individuals who are overweight and/or obese are “lazy, weak-willed, lacking in self-discipline and willpower” — a problem compounded by social media and media in general, which present unrealistic, glorified body images and disparaging messages about those with weight problems.

“Body image is a construct, rather than what you see in the mirror,” Sheethal Reddy, PhD, a psychologist at the Emory Bariatric Center, Emory University Hospital Midtown, Atlanta, told this news organization. “It’s the mental construct of our physical selves.”

According to Dr. Reddy, body image develops “within a broader societal context and is influenced by the person’s ethnic, racial, and cultural heritage.”

Adolescents are particularly vulnerable to body dissatisfaction. This is compounded in those with obesity, who often experience weight-based victimization and internalized weight-based stigma, compared with adolescents with lower weights. Weight stigma often takes the form of teasing and bullying.

“Appearance-related bullying and teasing during childhood and adolescence can reverberate into adulthood and persist throughout the lifespan,” Dr. Sarwer said. “When we see these patients and ask if they’ve ever been teased or bullied, not only do many say yes but it takes them back to those moments, to that origin story, and they remember someone saying something mean, cruel, and hurtful.”

Stigmatizing experiences can affect subjective body image, even after the weight has been lost and the person’s body is objectively thinner. Research comparing individuals who were overweight and lost weight to individuals who are currently overweight and haven’t lost weight and individuals who were never overweight suggests that “vestigial” body disparagement may persist following weight loss — especially in those with early-onset obesity.
 

The Role of Genetics

Genetics may contribute to people’s self-perception and body dissatisfaction, both before and after weight loss. A study of 827 community-based adolescents examined the association between polygenic risk scores (PRS) for body mass index (BMI) and type 2 diabetes and symptoms of body dissatisfaction and depression.

“Given the significant genetic role in BMI, we wanted to explore whether genetic risk for BMI might also predict body dissatisfaction,” lead author Krista Ekberg, MS, a doctoral candidate in clinical psychology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, told this news organization.

Genetic influences on BMI, as measured by PRS, were significantly associated with both phenotypic BMI and body dissatisfaction. “The association between PRS and body dissatisfaction was largely explained by BMI, suggesting that BMI itself accounts for much of the link between genetic risk and body dissatisfaction.”
 

Psychiatric History and Trauma

Adverse experiences, particularly sexual or physical abuse, may also account for body dissatisfaction after weight loss. “When some people with a history of this type of abuse lose a large amount of weight — typically after bariatric surgery — they often go through a period of emotional turbulence,” Dr. Sarwer said.

Childhood maltreatment can also be associated with body image disturbances in adulthood, according to a meta-analysis of 12 studies, encompassing 15,481 participants. Sexual abuse is “surprisingly common” among patients with obesity, according to Dr. Sarwer. A chart review of 131 patients revealed that 60% of those who reported a history of rape or sexual molestation were ≥ 50 pounds overweight vs only 28% of age- and sex-matched controls without a history of abuse. Other studies have corroborated these findings.

Excess weight can serve an “adaptive function,” Dr. Sarwer noted. It can be a self-protective mechanism that “insulates” them from sexual advances by potential romantic partners or abusers. Some may find that, after weight loss, repressed memories of a sexual assault surface as a result of the newer, more “attractive” appearance. Feeling vulnerable in their thinner bodies, they may need to regard themselves as overweight to maintain that feeling of “protection.” Weight loss may also trigger memories, flashbacks, or nightmares, as people return to a weight at which they were abused.

Dissociation is another mechanism linking trauma with post–weight loss body dysmorphia, Supatra Tovar, PsyD, RD, a clinical psychologist and registered dietitian with a practice in California, told this news organization. Dissociation from the body is often a coping mechanism for dealing with an overwhelming traumatic experience.

Individuals with a history of depression, anxiety, or posttraumatic stress disorder have higher levels of body dysmorphia, both before and after weight loss. One study found that patients undergoing bariatric surgery who had some type of psychopathology and other psychological risk factors were significantly more likely to report body image concerns 3 months after the surgery. Body image concerns were also more common in patients with preoperative depression, current psychotropic medication use, and a history of outpatient therapy or psychotropic medication use.

“Depression, anxiety, and trauma play a role in how you see yourself and how you carry yourself,” Dr. Reddy said. “This is wrapped up in any type of psychopathology. Being depressed is like looking at yourself through a cloud. It’s the opposite of ‘rose-colored glasses’ and instead, looking at yourself through a negative lens.”
 

Diagnosis and Interventions

Some helpful tools to assess the presence and extent of weight dissatisfaction and body dysmorphia include the Eating Disorder Inventory — Body Dissatisfaction Subscale and the Body Shape Questionnaire. It’s also important to take into account “the extent to which people are invested in their appearance psychologically,” Dr. Sarwer advised. The AO subscale of the Multidimensional Body-Self Relations Questionnaire generally assesses this. The Body Image Quality of Life Inventory assesses how and to what extent the perceived body image affects the person’s quality of life.

Experts recommend cognitive behavioral therapy (CBT) as an evidence-based intervention for body image issues, including those following weight loss.

“There’s an extensive CBT body image therapy program specifically tailored to the needs of overweight and obese individuals,” Dr. Sarwer said. “We don’t ignore historical variables that may have contributed to the problem, like early bullying, but we encourage people to think about what’s going on in their day-to-day life today. We drill down not only into the maladaptive behaviors but also the cognition and beliefs that may be erroneous but underlie these behaviors.”

The aim of CBT is to “modify irrational and dysfunctional thoughts, emotions, and behaviors through techniques such as self-monitoring, cognitive structuring, psychoeducation, desensitization, and exposure and response prevention.” The program laid out in Cash’s body image workbook includes eight steps. (Figure).

Weight Loss Doesn’t Automatically Equate With Happiness

Another realistic expectation runs counter to a common misperception that becoming thin will automatically translate into becoming happier. That’s not always the case, according to Dr. Tovar.

“If you haven’t worked deeply on addressing self-compassion and understanding that who you are at the core has nothing to do with your physical appearance, you can have an empty feeling once you’ve reached this point,” she said. “You still don’t know who you are and what you’re contributing to the world [because] you’ve been so focused on losing weight.”

Weight loss can also “unmask” questions about self-worth, even when receiving compliments about one’s “improved” appearance. “Praise and compliments after weight loss can be a double-edged sword,” Dr. Tovar observed. “You might think, ‘I wasn’t accepted or praised when I was overweight. The only way to be acceptable or validated is by losing weight, so I have to continue losing weight.’ ” This fuels fear of regaining the weight and can lead to continuing to see oneself as overweight, perhaps as a way to stay motivated to continue with weight loss. “Feeling that one’s value depends on remaining thin hampers body satisfaction,” she said.

Dr. Tovar, author of the book Deprogram Diet Culture: Rethink Your Relationship with Food, Heal Your Mind, and Live a Diet-Free Life, encourages people to shift the emphasis from weight loss to a holistic focus on self-worth and to explore obstacles to those feelings both before and after weight loss.

Endocrinologists and other medical professionals can help by not engaging in “weight and body shaming,” Dr. Tovar said.

She recommends physicians “encourage patients to tune in to their own bodies, helping them become more aware of how different foods affect their physical and emotional well-being.”

Set realistic expectations through “open, nonjudgmental conversations about the complexities of metabolism, weight, and health.”

Dr. Tovar advises rather than focusing on weight loss as the primary goal, physicians should focus on health markers such as blood glucose, energy levels, mental well-being, and physical fitness.

Prioritize “listening over lecturing.” Begin with empathy, asking questions such as “How do you feel about your health right now? What changes have you noticed in your body lately?” Doing this “creates space for the patient to express their concerns without feeling judged or shamed.”

Refer patients to a mental health professional when a patient exhibits signs of disordered eating or poor body image or when emotional factors are playing a significant role in the relationship with food and weight. “If a patient is caught in a cycle of dieting and weight gain, struggles with binge eating, or displays symptoms of depression or anxiety related to body, then psychological help is crucial.”

Ultimately, the goal of treatment “should be to provide a safe, supportive environment where patients can heal — not just physically but also emotionally and mentally,” Dr. Tovar added.

Dr. Tovar, Ms. Ekberg, and Dr. Reddy reported no relevant financial relationships. Dr. Sarwer received grant funding from the National Institute of Dental and Craniofacial Research and National Institute of Diabetes and Digestive and Kidney Diseases. He has consulting relationships with Novo Nordisk and Twenty30 Health. He is an associate editor for Obesity Surgery and editor in chief of Obesity Science & Practice.
 

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

Many people who lose weight, whether through diet and lifestyle changes, medication, or bariatric surgery, recognize their body has changed. While they also experience improvements in quality of life and psychosocial areas, that’s not true for everyone. Some patients don’t “see” they’ve lost weight — a phenomenon referred to as “phantom fat,” “ghost fat,” or “vestigial body image.”

“Most people are happy with their appearance, or at least their body shape, after weight loss — although some are unhappy with the loose, sagging skin that can follow weight loss and seek plastic surgery to remedy that,” David B. Sarwer, PhD, director of the Center for Obesity Research and Education and professor of social and behavioral sciences, Temple University College of Public Health, Philadelphia, told this news organization. “There’s a subset of people who remain dissatisfied with their body image, including their shape.”

This body dissatisfaction of people who lose weight may be long-standing, predating the weight loss, or may be new because weight loss has catalyzed a host of previously unaddressed psychosocial issues. Some may show up at assessments on treatment onset, while others may be detected by monitoring changes during or after weight loss. “Mental health counseling after bariatric surgery is greatly underutilized,” Dr. Sarwer observed.
 

Ghost Fat

Research has corroborated the lingering self-perception of being “obese” vs “ex-obese.” In one study, patients who had undergone bariatric surgery reported being unable to see the difference in their size and shape 18-30 months following their procedure, despite substantial weight loss.

Some research suggests that rapid weight loss (eg, through bariatric surgery) is more likely to generate the perception of “phantom fat,” but additional research is needed to investigate whether the mode and speed of weight loss affect subsequent body image.

Being habituated to one’s former appearance may play a role, Dr. Sarwer suggested. “We see this not only with weight loss but with other body-altering procedures. It takes the brain time to catch up to the new appearance. In rhinoplasty, for example, it may take patients a while before they become accustomed to looking at their new face in the mirror after decades of looking at a more prominent nose.”
 

Years of Social Stigma

It may also take time for people to overcome years of enduring the stigma of obesity.

There are “pervasive” negative attitudes implying that individuals who are overweight and/or obese are “lazy, weak-willed, lacking in self-discipline and willpower” — a problem compounded by social media and media in general, which present unrealistic, glorified body images and disparaging messages about those with weight problems.

“Body image is a construct, rather than what you see in the mirror,” Sheethal Reddy, PhD, a psychologist at the Emory Bariatric Center, Emory University Hospital Midtown, Atlanta, told this news organization. “It’s the mental construct of our physical selves.”

According to Dr. Reddy, body image develops “within a broader societal context and is influenced by the person’s ethnic, racial, and cultural heritage.”

Adolescents are particularly vulnerable to body dissatisfaction. This is compounded in those with obesity, who often experience weight-based victimization and internalized weight-based stigma, compared with adolescents with lower weights. Weight stigma often takes the form of teasing and bullying.

“Appearance-related bullying and teasing during childhood and adolescence can reverberate into adulthood and persist throughout the lifespan,” Dr. Sarwer said. “When we see these patients and ask if they’ve ever been teased or bullied, not only do many say yes but it takes them back to those moments, to that origin story, and they remember someone saying something mean, cruel, and hurtful.”

Stigmatizing experiences can affect subjective body image, even after the weight has been lost and the person’s body is objectively thinner. Research comparing individuals who were overweight and lost weight to individuals who are currently overweight and haven’t lost weight and individuals who were never overweight suggests that “vestigial” body disparagement may persist following weight loss — especially in those with early-onset obesity.
 

The Role of Genetics

Genetics may contribute to people’s self-perception and body dissatisfaction, both before and after weight loss. A study of 827 community-based adolescents examined the association between polygenic risk scores (PRS) for body mass index (BMI) and type 2 diabetes and symptoms of body dissatisfaction and depression.

“Given the significant genetic role in BMI, we wanted to explore whether genetic risk for BMI might also predict body dissatisfaction,” lead author Krista Ekberg, MS, a doctoral candidate in clinical psychology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, told this news organization.

Genetic influences on BMI, as measured by PRS, were significantly associated with both phenotypic BMI and body dissatisfaction. “The association between PRS and body dissatisfaction was largely explained by BMI, suggesting that BMI itself accounts for much of the link between genetic risk and body dissatisfaction.”
 

Psychiatric History and Trauma

Adverse experiences, particularly sexual or physical abuse, may also account for body dissatisfaction after weight loss. “When some people with a history of this type of abuse lose a large amount of weight — typically after bariatric surgery — they often go through a period of emotional turbulence,” Dr. Sarwer said.

Childhood maltreatment can also be associated with body image disturbances in adulthood, according to a meta-analysis of 12 studies, encompassing 15,481 participants. Sexual abuse is “surprisingly common” among patients with obesity, according to Dr. Sarwer. A chart review of 131 patients revealed that 60% of those who reported a history of rape or sexual molestation were ≥ 50 pounds overweight vs only 28% of age- and sex-matched controls without a history of abuse. Other studies have corroborated these findings.

Excess weight can serve an “adaptive function,” Dr. Sarwer noted. It can be a self-protective mechanism that “insulates” them from sexual advances by potential romantic partners or abusers. Some may find that, after weight loss, repressed memories of a sexual assault surface as a result of the newer, more “attractive” appearance. Feeling vulnerable in their thinner bodies, they may need to regard themselves as overweight to maintain that feeling of “protection.” Weight loss may also trigger memories, flashbacks, or nightmares, as people return to a weight at which they were abused.

Dissociation is another mechanism linking trauma with post–weight loss body dysmorphia, Supatra Tovar, PsyD, RD, a clinical psychologist and registered dietitian with a practice in California, told this news organization. Dissociation from the body is often a coping mechanism for dealing with an overwhelming traumatic experience.

Individuals with a history of depression, anxiety, or posttraumatic stress disorder have higher levels of body dysmorphia, both before and after weight loss. One study found that patients undergoing bariatric surgery who had some type of psychopathology and other psychological risk factors were significantly more likely to report body image concerns 3 months after the surgery. Body image concerns were also more common in patients with preoperative depression, current psychotropic medication use, and a history of outpatient therapy or psychotropic medication use.

“Depression, anxiety, and trauma play a role in how you see yourself and how you carry yourself,” Dr. Reddy said. “This is wrapped up in any type of psychopathology. Being depressed is like looking at yourself through a cloud. It’s the opposite of ‘rose-colored glasses’ and instead, looking at yourself through a negative lens.”
 

Diagnosis and Interventions

Some helpful tools to assess the presence and extent of weight dissatisfaction and body dysmorphia include the Eating Disorder Inventory — Body Dissatisfaction Subscale and the Body Shape Questionnaire. It’s also important to take into account “the extent to which people are invested in their appearance psychologically,” Dr. Sarwer advised. The AO subscale of the Multidimensional Body-Self Relations Questionnaire generally assesses this. The Body Image Quality of Life Inventory assesses how and to what extent the perceived body image affects the person’s quality of life.

Experts recommend cognitive behavioral therapy (CBT) as an evidence-based intervention for body image issues, including those following weight loss.

“There’s an extensive CBT body image therapy program specifically tailored to the needs of overweight and obese individuals,” Dr. Sarwer said. “We don’t ignore historical variables that may have contributed to the problem, like early bullying, but we encourage people to think about what’s going on in their day-to-day life today. We drill down not only into the maladaptive behaviors but also the cognition and beliefs that may be erroneous but underlie these behaviors.”

The aim of CBT is to “modify irrational and dysfunctional thoughts, emotions, and behaviors through techniques such as self-monitoring, cognitive structuring, psychoeducation, desensitization, and exposure and response prevention.” The program laid out in Cash’s body image workbook includes eight steps. (Figure).

Weight Loss Doesn’t Automatically Equate With Happiness

Another realistic expectation runs counter to a common misperception that becoming thin will automatically translate into becoming happier. That’s not always the case, according to Dr. Tovar.

“If you haven’t worked deeply on addressing self-compassion and understanding that who you are at the core has nothing to do with your physical appearance, you can have an empty feeling once you’ve reached this point,” she said. “You still don’t know who you are and what you’re contributing to the world [because] you’ve been so focused on losing weight.”

Weight loss can also “unmask” questions about self-worth, even when receiving compliments about one’s “improved” appearance. “Praise and compliments after weight loss can be a double-edged sword,” Dr. Tovar observed. “You might think, ‘I wasn’t accepted or praised when I was overweight. The only way to be acceptable or validated is by losing weight, so I have to continue losing weight.’ ” This fuels fear of regaining the weight and can lead to continuing to see oneself as overweight, perhaps as a way to stay motivated to continue with weight loss. “Feeling that one’s value depends on remaining thin hampers body satisfaction,” she said.

Dr. Tovar, author of the book Deprogram Diet Culture: Rethink Your Relationship with Food, Heal Your Mind, and Live a Diet-Free Life, encourages people to shift the emphasis from weight loss to a holistic focus on self-worth and to explore obstacles to those feelings both before and after weight loss.

Endocrinologists and other medical professionals can help by not engaging in “weight and body shaming,” Dr. Tovar said.

She recommends physicians “encourage patients to tune in to their own bodies, helping them become more aware of how different foods affect their physical and emotional well-being.”

Set realistic expectations through “open, nonjudgmental conversations about the complexities of metabolism, weight, and health.”

Dr. Tovar advises rather than focusing on weight loss as the primary goal, physicians should focus on health markers such as blood glucose, energy levels, mental well-being, and physical fitness.

Prioritize “listening over lecturing.” Begin with empathy, asking questions such as “How do you feel about your health right now? What changes have you noticed in your body lately?” Doing this “creates space for the patient to express their concerns without feeling judged or shamed.”

Refer patients to a mental health professional when a patient exhibits signs of disordered eating or poor body image or when emotional factors are playing a significant role in the relationship with food and weight. “If a patient is caught in a cycle of dieting and weight gain, struggles with binge eating, or displays symptoms of depression or anxiety related to body, then psychological help is crucial.”

Ultimately, the goal of treatment “should be to provide a safe, supportive environment where patients can heal — not just physically but also emotionally and mentally,” Dr. Tovar added.

Dr. Tovar, Ms. Ekberg, and Dr. Reddy reported no relevant financial relationships. Dr. Sarwer received grant funding from the National Institute of Dental and Craniofacial Research and National Institute of Diabetes and Digestive and Kidney Diseases. He has consulting relationships with Novo Nordisk and Twenty30 Health. He is an associate editor for Obesity Surgery and editor in chief of Obesity Science & Practice.
 

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

Several months ago in a letter about healthcare providers and the decision to use alcohol and other mind-altering substances on the job, I waxed enthusiastically about the new wave of no alcohol (NA) and zero (00) alcohol beers that have come on the market. In the last 2 years our local grocery store’s cooler space for nonalcoholic beer has grown from less than 24 inches to something approaching the height of the average sixth grader.

In a bold act of chivalry at the beginning of the pandemic I accepted the mantle of designated grocery shopper and over the last 3 years have become uncommonly proud of my ability to bring home the groceries efficiently and cost effectively, without catching COVID in the process. I have developed a sixth sense of choosing which human checker/bagger combination is fastest or whether the self-checkout is the way to go.

For obvious reasons the human checkers don’t ask for my ID when I am buying adult beverages. However, the self-check register freezes up instantly when I scan my 12-pack of Run Wild nonalcoholic. This necessitates a search for the MIA store person assigned to patrol the self-check corral, ever on the lookout for shoplifters, underage drinkers, and other generally shifty looking characters.

When I find one of the grocery store detectives (who is likely to have been a former patient), I say: “You know, this doesn’t have any alcohol in it.” They invariably reply with a shrug. “I know. But, the rules are the rules.” Occasionally, they may add: “It doesn’t make sense, does it?”

At first blush checking IDs for a nonalcoholic beverage may sound dumb, certainly to someone who is just a few years on either side of the legal drinking age. Why are we trying to protect some crazy teenager from the futility of getting high on a six-pack of something that at worst will make him spend most of the next couple of hours peeing?

But, there is concern in some corners that nonalcoholic drinks pose a significant threat to teenagers. Two PhDs at Stanford University have recently published a paper in which they worry that the dramatic rise in US sales of nonalcoholic drinks from 15% to 30% since 2018 may be socializing “users of alcohol drinking experiences by exposing them to the taste, look, and even brands of alcoholic beverages”.

Is there evidence to support their concern? I could only find one brief report in the Japanese literature that states that among young people “who experienced the nonalcoholic beverage intake, interest in or motivation for drinking alcoholic beverages, and/or smoking is higher than [among] those who did not.” The study didn’t appear to clearly separate the exposure in a family setting from the actual intake.

Beer is an acquired taste. If someone offered you your first taste of beer after a hot-weather set of tennis most of you would reject it and ask for water or lemonade. I can recall my first taste of beer. For some reason my father thought at age 11 or 12 I might like to try some from his glass. I’m not sure of his motivation, but he tried the same thing with oysters. I didn’t drink beer again until I was 16, motivated at that time by a group dynamic. The oyster trial, however, backfired on him and from then on he had to share his coveted dozen with me. Alcohol, unless heavily disguised by a mixer, is also not a taste that most young people find appealing.

It is unlikely that the average thrill-seeking teenager is going to ask his older-appearing buddy with a fake ID to buy him some nonalcoholic beer. Nor would he go to the effort or risk of acquiring his own fake ID just to see how it tastes. It just doesn’t compute, especially to a self-check corral patroller.

I guess one could envision a scenario in which a teenager wanting to fit in with the fast crowd would ask a trusted adult (or clueless parent) to buy him some nonalcoholic beer to bring to a party. He is running a serious risk of being laughed at by his friends if they find he’s drinking the fake stuff. It also seems unlikely that a parent would buy nonalcoholic beer to introduce his teenager to the taste of beer.

So, if there is little evidence to make us consider nonalcoholic beer as a gateway drug, should we continue to prohibit its sale to minors?

Although it runs counter to my usual commitment to evidence-based decisions, making it difficult for adolescents to buy nonalcoholic beverages feels like the right think to do. As long as alcoholic and nonalcoholic beverages share the same display space and are packaged in nearly identical containers, there is ample opportunity for confusion. Recent evidence suggesting that even small amounts of alcohol increases some health risks should strengthen our resolve to minimize that confusion.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Several months ago in a letter about healthcare providers and the decision to use alcohol and other mind-altering substances on the job, I waxed enthusiastically about the new wave of no alcohol (NA) and zero (00) alcohol beers that have come on the market. In the last 2 years our local grocery store’s cooler space for nonalcoholic beer has grown from less than 24 inches to something approaching the height of the average sixth grader.

In a bold act of chivalry at the beginning of the pandemic I accepted the mantle of designated grocery shopper and over the last 3 years have become uncommonly proud of my ability to bring home the groceries efficiently and cost effectively, without catching COVID in the process. I have developed a sixth sense of choosing which human checker/bagger combination is fastest or whether the self-checkout is the way to go.

For obvious reasons the human checkers don’t ask for my ID when I am buying adult beverages. However, the self-check register freezes up instantly when I scan my 12-pack of Run Wild nonalcoholic. This necessitates a search for the MIA store person assigned to patrol the self-check corral, ever on the lookout for shoplifters, underage drinkers, and other generally shifty looking characters.

When I find one of the grocery store detectives (who is likely to have been a former patient), I say: “You know, this doesn’t have any alcohol in it.” They invariably reply with a shrug. “I know. But, the rules are the rules.” Occasionally, they may add: “It doesn’t make sense, does it?”

At first blush checking IDs for a nonalcoholic beverage may sound dumb, certainly to someone who is just a few years on either side of the legal drinking age. Why are we trying to protect some crazy teenager from the futility of getting high on a six-pack of something that at worst will make him spend most of the next couple of hours peeing?

But, there is concern in some corners that nonalcoholic drinks pose a significant threat to teenagers. Two PhDs at Stanford University have recently published a paper in which they worry that the dramatic rise in US sales of nonalcoholic drinks from 15% to 30% since 2018 may be socializing “users of alcohol drinking experiences by exposing them to the taste, look, and even brands of alcoholic beverages”.

Is there evidence to support their concern? I could only find one brief report in the Japanese literature that states that among young people “who experienced the nonalcoholic beverage intake, interest in or motivation for drinking alcoholic beverages, and/or smoking is higher than [among] those who did not.” The study didn’t appear to clearly separate the exposure in a family setting from the actual intake.

Beer is an acquired taste. If someone offered you your first taste of beer after a hot-weather set of tennis most of you would reject it and ask for water or lemonade. I can recall my first taste of beer. For some reason my father thought at age 11 or 12 I might like to try some from his glass. I’m not sure of his motivation, but he tried the same thing with oysters. I didn’t drink beer again until I was 16, motivated at that time by a group dynamic. The oyster trial, however, backfired on him and from then on he had to share his coveted dozen with me. Alcohol, unless heavily disguised by a mixer, is also not a taste that most young people find appealing.

It is unlikely that the average thrill-seeking teenager is going to ask his older-appearing buddy with a fake ID to buy him some nonalcoholic beer. Nor would he go to the effort or risk of acquiring his own fake ID just to see how it tastes. It just doesn’t compute, especially to a self-check corral patroller.

I guess one could envision a scenario in which a teenager wanting to fit in with the fast crowd would ask a trusted adult (or clueless parent) to buy him some nonalcoholic beer to bring to a party. He is running a serious risk of being laughed at by his friends if they find he’s drinking the fake stuff. It also seems unlikely that a parent would buy nonalcoholic beer to introduce his teenager to the taste of beer.

So, if there is little evidence to make us consider nonalcoholic beer as a gateway drug, should we continue to prohibit its sale to minors?

Although it runs counter to my usual commitment to evidence-based decisions, making it difficult for adolescents to buy nonalcoholic beverages feels like the right think to do. As long as alcoholic and nonalcoholic beverages share the same display space and are packaged in nearly identical containers, there is ample opportunity for confusion. Recent evidence suggesting that even small amounts of alcohol increases some health risks should strengthen our resolve to minimize that confusion.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Several months ago in a letter about healthcare providers and the decision to use alcohol and other mind-altering substances on the job, I waxed enthusiastically about the new wave of no alcohol (NA) and zero (00) alcohol beers that have come on the market. In the last 2 years our local grocery store’s cooler space for nonalcoholic beer has grown from less than 24 inches to something approaching the height of the average sixth grader.

In a bold act of chivalry at the beginning of the pandemic I accepted the mantle of designated grocery shopper and over the last 3 years have become uncommonly proud of my ability to bring home the groceries efficiently and cost effectively, without catching COVID in the process. I have developed a sixth sense of choosing which human checker/bagger combination is fastest or whether the self-checkout is the way to go.

For obvious reasons the human checkers don’t ask for my ID when I am buying adult beverages. However, the self-check register freezes up instantly when I scan my 12-pack of Run Wild nonalcoholic. This necessitates a search for the MIA store person assigned to patrol the self-check corral, ever on the lookout for shoplifters, underage drinkers, and other generally shifty looking characters.

When I find one of the grocery store detectives (who is likely to have been a former patient), I say: “You know, this doesn’t have any alcohol in it.” They invariably reply with a shrug. “I know. But, the rules are the rules.” Occasionally, they may add: “It doesn’t make sense, does it?”

At first blush checking IDs for a nonalcoholic beverage may sound dumb, certainly to someone who is just a few years on either side of the legal drinking age. Why are we trying to protect some crazy teenager from the futility of getting high on a six-pack of something that at worst will make him spend most of the next couple of hours peeing?

But, there is concern in some corners that nonalcoholic drinks pose a significant threat to teenagers. Two PhDs at Stanford University have recently published a paper in which they worry that the dramatic rise in US sales of nonalcoholic drinks from 15% to 30% since 2018 may be socializing “users of alcohol drinking experiences by exposing them to the taste, look, and even brands of alcoholic beverages”.

Is there evidence to support their concern? I could only find one brief report in the Japanese literature that states that among young people “who experienced the nonalcoholic beverage intake, interest in or motivation for drinking alcoholic beverages, and/or smoking is higher than [among] those who did not.” The study didn’t appear to clearly separate the exposure in a family setting from the actual intake.

Beer is an acquired taste. If someone offered you your first taste of beer after a hot-weather set of tennis most of you would reject it and ask for water or lemonade. I can recall my first taste of beer. For some reason my father thought at age 11 or 12 I might like to try some from his glass. I’m not sure of his motivation, but he tried the same thing with oysters. I didn’t drink beer again until I was 16, motivated at that time by a group dynamic. The oyster trial, however, backfired on him and from then on he had to share his coveted dozen with me. Alcohol, unless heavily disguised by a mixer, is also not a taste that most young people find appealing.

It is unlikely that the average thrill-seeking teenager is going to ask his older-appearing buddy with a fake ID to buy him some nonalcoholic beer. Nor would he go to the effort or risk of acquiring his own fake ID just to see how it tastes. It just doesn’t compute, especially to a self-check corral patroller.

I guess one could envision a scenario in which a teenager wanting to fit in with the fast crowd would ask a trusted adult (or clueless parent) to buy him some nonalcoholic beer to bring to a party. He is running a serious risk of being laughed at by his friends if they find he’s drinking the fake stuff. It also seems unlikely that a parent would buy nonalcoholic beer to introduce his teenager to the taste of beer.

So, if there is little evidence to make us consider nonalcoholic beer as a gateway drug, should we continue to prohibit its sale to minors?

Although it runs counter to my usual commitment to evidence-based decisions, making it difficult for adolescents to buy nonalcoholic beverages feels like the right think to do. As long as alcoholic and nonalcoholic beverages share the same display space and are packaged in nearly identical containers, there is ample opportunity for confusion. Recent evidence suggesting that even small amounts of alcohol increases some health risks should strengthen our resolve to minimize that confusion.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Hidden behind all of the new drugs and breakthroughs reported at the 2024 ECTRIMS meetings was one paper that caught my attention.

It was that, after several years of study, simvastatin had no benefit for multiple sclerosis.

Statins for MS (and for Alzheimer’s disease) have been bandied about for some time, with arguments based on theoretical ideas, and small studies, that they’d have a beneficial effect on the disease – maybe from anti-inflammatory and other properties. In addition, they offered the benefit of being widely available and comparatively inexpensive.

Because of those studies, 15-20 years ago I used them off label for MS in a handful of patients – sometimes as an adjunct to their current treatment (limited at that point to interferons and Copaxone), or in patients who couldn’t afford the FDA-approved drugs. Although not without their drawbacks, the statins are relatively well understood and tolerated.

At some point, for reasons I’ve long forgotten, they all came off of them (at least for MS purposes). Maybe for side effects, or lack of benefit, or because new medications, with much clearer efficacies, were rolling out.

Now it seems pretty clear that statins don’t work for MS.

So was it a bad idea to try? No. Without asking questions we don’t find answers. If they’d worked out it would have been great, another tool on the neurology workbench to reach for in the right situation. It might also have led us to new avenues in MS treatment.

But it didn’t, and that’s fine. Although they don’t get the attention, we learn as much (sometimes more) from negative studies as we do from positive ones. If we put people on every drug that initially showed promise for their conditions, my patients would have a pretty huge medication list. For Alzheimer’s disease alone I remember studies that once suggested ibuprofen, statins, estrogen, nicotine, and several vitamins might be effective (“might” being the key word). Today we’re looking at the PDE5 inhibitors and semaglutide. The jury is still out on them, but whichever way it goes we’ll still learn something.

The statins are good drugs. Their benefits in cardiac and cerebrovascular disease can’t be disputed (I’m sure someone would, but that’s not the point of this piece). But, like all drugs, they don’t work for everything.

Just like other sciences, everything we do now in medicine is based on both the successes and failures of what came before. We learn from both and keep moving forward.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Hidden behind all of the new drugs and breakthroughs reported at the 2024 ECTRIMS meetings was one paper that caught my attention.

It was that, after several years of study, simvastatin had no benefit for multiple sclerosis.

Statins for MS (and for Alzheimer’s disease) have been bandied about for some time, with arguments based on theoretical ideas, and small studies, that they’d have a beneficial effect on the disease – maybe from anti-inflammatory and other properties. In addition, they offered the benefit of being widely available and comparatively inexpensive.

Because of those studies, 15-20 years ago I used them off label for MS in a handful of patients – sometimes as an adjunct to their current treatment (limited at that point to interferons and Copaxone), or in patients who couldn’t afford the FDA-approved drugs. Although not without their drawbacks, the statins are relatively well understood and tolerated.

At some point, for reasons I’ve long forgotten, they all came off of them (at least for MS purposes). Maybe for side effects, or lack of benefit, or because new medications, with much clearer efficacies, were rolling out.

Now it seems pretty clear that statins don’t work for MS.

So was it a bad idea to try? No. Without asking questions we don’t find answers. If they’d worked out it would have been great, another tool on the neurology workbench to reach for in the right situation. It might also have led us to new avenues in MS treatment.

But it didn’t, and that’s fine. Although they don’t get the attention, we learn as much (sometimes more) from negative studies as we do from positive ones. If we put people on every drug that initially showed promise for their conditions, my patients would have a pretty huge medication list. For Alzheimer’s disease alone I remember studies that once suggested ibuprofen, statins, estrogen, nicotine, and several vitamins might be effective (“might” being the key word). Today we’re looking at the PDE5 inhibitors and semaglutide. The jury is still out on them, but whichever way it goes we’ll still learn something.

The statins are good drugs. Their benefits in cardiac and cerebrovascular disease can’t be disputed (I’m sure someone would, but that’s not the point of this piece). But, like all drugs, they don’t work for everything.

Just like other sciences, everything we do now in medicine is based on both the successes and failures of what came before. We learn from both and keep moving forward.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Hidden behind all of the new drugs and breakthroughs reported at the 2024 ECTRIMS meetings was one paper that caught my attention.

It was that, after several years of study, simvastatin had no benefit for multiple sclerosis.

Statins for MS (and for Alzheimer’s disease) have been bandied about for some time, with arguments based on theoretical ideas, and small studies, that they’d have a beneficial effect on the disease – maybe from anti-inflammatory and other properties. In addition, they offered the benefit of being widely available and comparatively inexpensive.

Because of those studies, 15-20 years ago I used them off label for MS in a handful of patients – sometimes as an adjunct to their current treatment (limited at that point to interferons and Copaxone), or in patients who couldn’t afford the FDA-approved drugs. Although not without their drawbacks, the statins are relatively well understood and tolerated.

At some point, for reasons I’ve long forgotten, they all came off of them (at least for MS purposes). Maybe for side effects, or lack of benefit, or because new medications, with much clearer efficacies, were rolling out.

Now it seems pretty clear that statins don’t work for MS.

So was it a bad idea to try? No. Without asking questions we don’t find answers. If they’d worked out it would have been great, another tool on the neurology workbench to reach for in the right situation. It might also have led us to new avenues in MS treatment.

But it didn’t, and that’s fine. Although they don’t get the attention, we learn as much (sometimes more) from negative studies as we do from positive ones. If we put people on every drug that initially showed promise for their conditions, my patients would have a pretty huge medication list. For Alzheimer’s disease alone I remember studies that once suggested ibuprofen, statins, estrogen, nicotine, and several vitamins might be effective (“might” being the key word). Today we’re looking at the PDE5 inhibitors and semaglutide. The jury is still out on them, but whichever way it goes we’ll still learn something.

The statins are good drugs. Their benefits in cardiac and cerebrovascular disease can’t be disputed (I’m sure someone would, but that’s not the point of this piece). But, like all drugs, they don’t work for everything.

Just like other sciences, everything we do now in medicine is based on both the successes and failures of what came before. We learn from both and keep moving forward.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

This transcript has been edited for clarity. 

One out of three American adults — about 100 million people in this country — have the metabolic syndrome. I’m showing you the official criteria here, but essentially this is a syndrome of insulin resistance and visceral adiposity that predisposes us to a host of chronic diseases such as diabetes, heart disease, and even dementia. 

Dr. Wilson

Dr. Wilson

Dr. Wilson

Annals of Internal Medicine

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

One out of three American adults — about 100 million people in this country — have the metabolic syndrome. I’m showing you the official criteria here, but essentially this is a syndrome of insulin resistance and visceral adiposity that predisposes us to a host of chronic diseases such as diabetes, heart disease, and even dementia. 

Dr. Wilson

Dr. Wilson

Dr. Wilson

Annals of Internal Medicine

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

One out of three American adults — about 100 million people in this country — have the metabolic syndrome. I’m showing you the official criteria here, but essentially this is a syndrome of insulin resistance and visceral adiposity that predisposes us to a host of chronic diseases such as diabetes, heart disease, and even dementia. 

Dr. Wilson

Dr. Wilson

Dr. Wilson

Annals of Internal Medicine

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Alzheimer’s disease (AD), the most common cause of dementia, is the fifth leading cause of death in the United States. An estimated 6.9 million Americans aged 65 years or older have AD. Comorbid conditions in AD may exacerbate the progression of dementia and negatively affect overall health.

Although the exact mechanisms remain unclear, systemic inflammation is thought to play a significant role in the development of many common comorbidities associated with AD. Among the most frequently observed comorbid conditions are hypertension, diabetes, and depression. The presence of these comorbidities affects the treatment and management of AD, underscoring the need to understand the mechanisms of their interrelationship and develop effective management strategies. 
 

Hypertension 

Hypertension is a well-established risk factor for numerous health conditions, including AD. A comprehensive review of five meta-analyses and 52 primary studies revealed that elevated systolic blood pressure (SBP) correlates with an 11 % increased risk of developing AD, raising the question of whether early intervention and control of blood pressure would mitigate the risk for AD later in life. 

Findings from the Northern Manhattan Study suggest that although elevated SBP contributes to cognitive decline in older patients, the use of antihypertensive medications can neutralize the effects of high SBP on certain cognitive functions. Furthermore, a systematic review and meta-analysis comprising 12 trials (92,135 participants) demonstrated a significant reduction in the risk for dementia and cognitive impairment with antihypertensive treatment.

Notably, a retrospective cohort study involving 69,081 participants treated with beta-blockers for hypertension found that beta-blockers with high blood-brain barrier permeability were associated with a reduced risk for AD compared with those with low blood-brain barrier permeability. Additionally, a secondary analysis of the SPRINT trial found antihypertensive medications that stimulate vs inhibit type 2 and 4 angiotensin II receptors were associated with a lower incidence of cognitive impairment. Although further clinical trials are necessary to directly assess specific medications, these findings emphasize the potential of antihypertensive treatment as a strategic approach to reduce the risk for AD.
 

Type 2 Diabetes 

The connection between AD and type 2 diabetes is such that AD is sometimes referred to as “type 3 diabetes.” Both diseases share some of the same underlying pathophysiologic mechanisms, particularly the development of insulin resistance and oxidative stress. A prospective cohort study of 10,095 participants showed that diabetes was significantly associated with a higher risk of developing dementia; this risk is even greater in patients who develop diabetes at an earlier age.

In an interview with this news organization, Alvaro Pascual-Leone, MD, PhD, a professor of neurology at Harvard Medical School, Boston, said, “In addition to being a comorbidity factor, diabetes appears to be a predisposing risk factor for AD.” This is supported by a comprehensive literature review showing an increased progression from mild cognitive impairment (MCI) to dementia in patients with diabetes, prediabetes, or metabolic syndrome, with a pooled odds ratio for dementia progression in individuals with diabetes of 1.53.

Owing to the overlapping pathophysiologic mechanisms in AD and diabetes, treating one condition may have beneficial effects on the other. A systematic umbrella review and meta-analysis that included 10 meta-analyses across nine classes of diabetes drugs found a protective effect against dementia with the use of metformin, thiazolidinediones (including pioglitazone), glucagon-like peptide 1 receptor agonists, and sodium-glucose cotransporter 2 inhibitors. Moreover, a cohort study of 12,220 patients who discontinued metformin early (ie, stopped using metformin without a prior history of abnormal kidney function) and 29,126 patients considered routine users found an increased risk for dementia in the early terminator group. Although further research is warranted, the concurrent treatment of AD and diabetes with antidiabetic agents holds considerable promise.
 

Depression and Anxiety

Anxiety and depression are significant risk factors for AD, and conversely, AD increases the likelihood of developing these psychiatric conditions. A systematic review of 14,760 studies showed dysthymia often emerges during the early stages of AD as an emotional response to cognitive decline. 

Data from the Australian Imaging Biomarkers and Lifestyle study showed a markedly elevated risk for AD and MCI among individuals with preexisting anxiety or depression. This study also found that age, sex, and marital status are important determinants, with men and single individuals with depression being particularly susceptible to developing AD. Conversely, a cohort study of 129,410 AD patients with AD, 390,088 patients with all-cause dementia, and 3,900,880 age-matched controls without a history of depression showed a cumulative incidence of depression of 13% in the AD group vs 3% in the control group, suggesting a heightened risk for depression following an AD diagnosis. 

These findings underscore the importance of targeted screening and assessment for patients with anxiety and depression who may be at risk for AD or those diagnosed with AD who are at risk for subsequent depression and anxiety. Although antidepressants are effective in treating depression in general, their efficacy in AD-related depression is of variable quality, probably owing to differing pathophysiologic mechanisms of the disease. Further research is necessary to explore both pharmacologic and nonpharmacologic interventions for treating depression in AD patients. Some studies have found that cognitive behavioral-therapy can be effective in improving depression in patients with AD.
 

Sleep Disorders

Research has shown a strong correlation between AD and sleep disorders, particularly obstructive sleep apnea, insomnia, and circadian rhythm disruptions. Additionally, studies suggest that insomnia and sleep deprivation contribute to increased amyloid beta production and tau pathology, hallmark features of AD. A scoping review of 70 studies proposed that this relationship is mediated by the glymphatic system (glial-dependent waste clearance pathway in the central nervous system), and that sleep deprivation disrupts its function, leading to protein accumulation and subsequent neurologic symptoms of AD. Another study showed that sleep deprivation triggers glial cell activation, initiating an inflammatory cascade that accelerates AD progression.

Given that the gold standard treatment for obstructive sleep apnea is continuous positive airway pressure (CPAP), it has been hypothesized that CPAP could also alleviate AD symptoms owing to shared pathophysiologic mechanisms of these conditions. A large systemic review found that CPAP use improved AD symptoms in patients with mild AD or MCI, though other sleep interventions, such as cognitive-behavioral therapy and melatonin supplementation, have yielded mixed outcomes. However, most studies in this area are small in scale, and there remains a paucity of research on treating sleep disorders in AD patients, indicating a need for further investigation.
 

Musculoskeletal Disorders

Although no direct causative link has been established, research indicates an association between osteoarthritis (OA) and dementia, likely because of similar pathophysiologic mechanisms, including systemic inflammation. Longitudinal analyses of data from the Alzheimer’s Disease Neuroimaging Initiative study found cognitively normal older individuals with OA experience more rapid declines in hippocampal volumes compared to those without OA, suggesting that OA may elevate the risk of cognitive impairment. Current treatments for OA, such as nonsteroidal anti-inflammatory drugs, glucocorticoids, and disease-modifying OA drugs, might also help alleviate AD symptoms related to inflammation, though the research in this area is limited.

AD has also been linked to osteoporosis. In a longitudinal follow-up study involving 78,994 patients with osteoporosis and 78,994 controls, AD developed in 5856 patients with osteoporosis compared with 3761 patients in the control group. These findings represent a 1.27-fold higher incidence of AD in patients with osteoporosis than in the control group, suggesting that osteoporosis might be a risk factor for AD.

Additionally, research has identified a relationship between AD and increased fracture risk and decreased bone mineral density, with AD patients exhibiting a significantly higher likelihood of bone fractures compared with those without AD. “Falls and fractures, aside from the risk they pose in all geriatric patients, in individuals with cognitive impairment — whether due to AD or another cause — have higher risk to cause delirium and that can result in greater morbidity and mortality and a lasting increase in cognitive disability,” stated Dr. Pascual-Leone. Current recommendations emphasize exercise and fall prevention strategies to reduce fracture risk in patients with AD, but there is a lack of comprehensive research on the safety and efficacy of osteoporosis medications in this population.
 

Implications for Clinical Practice

The intricate interplay between AD and its comorbidities highlights the need for a comprehensive and integrated approach to patient care. The overlapping pathophysiologic mechanisms suggest that these comorbidities can contribute to the evolution and progression of AD. Likewise, AD can exacerbate comorbid conditions. As such, a holistic assessment strategy that prioritizes early detection and management of comorbid conditions to mitigate their impact on AD progression would be beneficial. Dr. Pascual-Leone added, “The presence of any of these comorbidities suggests a need to screen for MCI earlier than might otherwise be indicated or as part of the treatment for the comorbid condition. In many cases, patients can make lifestyle modifications that improve not only the comorbid condition but also reduce its effect on dementia.” In doing so, healthcare providers can help improve patient outcomes and enhance the overall quality of life for individuals living with AD.

Alissa Hershberger, Professor of Nursing, University of Central Missouri, Lee’s Summit, Missouri, has disclosed no relevant financial relationships.

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

Alzheimer’s disease (AD), the most common cause of dementia, is the fifth leading cause of death in the United States. An estimated 6.9 million Americans aged 65 years or older have AD. Comorbid conditions in AD may exacerbate the progression of dementia and negatively affect overall health.

Although the exact mechanisms remain unclear, systemic inflammation is thought to play a significant role in the development of many common comorbidities associated with AD. Among the most frequently observed comorbid conditions are hypertension, diabetes, and depression. The presence of these comorbidities affects the treatment and management of AD, underscoring the need to understand the mechanisms of their interrelationship and develop effective management strategies. 
 

Hypertension 

Hypertension is a well-established risk factor for numerous health conditions, including AD. A comprehensive review of five meta-analyses and 52 primary studies revealed that elevated systolic blood pressure (SBP) correlates with an 11 % increased risk of developing AD, raising the question of whether early intervention and control of blood pressure would mitigate the risk for AD later in life. 

Findings from the Northern Manhattan Study suggest that although elevated SBP contributes to cognitive decline in older patients, the use of antihypertensive medications can neutralize the effects of high SBP on certain cognitive functions. Furthermore, a systematic review and meta-analysis comprising 12 trials (92,135 participants) demonstrated a significant reduction in the risk for dementia and cognitive impairment with antihypertensive treatment.

Notably, a retrospective cohort study involving 69,081 participants treated with beta-blockers for hypertension found that beta-blockers with high blood-brain barrier permeability were associated with a reduced risk for AD compared with those with low blood-brain barrier permeability. Additionally, a secondary analysis of the SPRINT trial found antihypertensive medications that stimulate vs inhibit type 2 and 4 angiotensin II receptors were associated with a lower incidence of cognitive impairment. Although further clinical trials are necessary to directly assess specific medications, these findings emphasize the potential of antihypertensive treatment as a strategic approach to reduce the risk for AD.
 

Type 2 Diabetes 

The connection between AD and type 2 diabetes is such that AD is sometimes referred to as “type 3 diabetes.” Both diseases share some of the same underlying pathophysiologic mechanisms, particularly the development of insulin resistance and oxidative stress. A prospective cohort study of 10,095 participants showed that diabetes was significantly associated with a higher risk of developing dementia; this risk is even greater in patients who develop diabetes at an earlier age.

In an interview with this news organization, Alvaro Pascual-Leone, MD, PhD, a professor of neurology at Harvard Medical School, Boston, said, “In addition to being a comorbidity factor, diabetes appears to be a predisposing risk factor for AD.” This is supported by a comprehensive literature review showing an increased progression from mild cognitive impairment (MCI) to dementia in patients with diabetes, prediabetes, or metabolic syndrome, with a pooled odds ratio for dementia progression in individuals with diabetes of 1.53.

Owing to the overlapping pathophysiologic mechanisms in AD and diabetes, treating one condition may have beneficial effects on the other. A systematic umbrella review and meta-analysis that included 10 meta-analyses across nine classes of diabetes drugs found a protective effect against dementia with the use of metformin, thiazolidinediones (including pioglitazone), glucagon-like peptide 1 receptor agonists, and sodium-glucose cotransporter 2 inhibitors. Moreover, a cohort study of 12,220 patients who discontinued metformin early (ie, stopped using metformin without a prior history of abnormal kidney function) and 29,126 patients considered routine users found an increased risk for dementia in the early terminator group. Although further research is warranted, the concurrent treatment of AD and diabetes with antidiabetic agents holds considerable promise.
 

Depression and Anxiety

Anxiety and depression are significant risk factors for AD, and conversely, AD increases the likelihood of developing these psychiatric conditions. A systematic review of 14,760 studies showed dysthymia often emerges during the early stages of AD as an emotional response to cognitive decline. 

Data from the Australian Imaging Biomarkers and Lifestyle study showed a markedly elevated risk for AD and MCI among individuals with preexisting anxiety or depression. This study also found that age, sex, and marital status are important determinants, with men and single individuals with depression being particularly susceptible to developing AD. Conversely, a cohort study of 129,410 AD patients with AD, 390,088 patients with all-cause dementia, and 3,900,880 age-matched controls without a history of depression showed a cumulative incidence of depression of 13% in the AD group vs 3% in the control group, suggesting a heightened risk for depression following an AD diagnosis. 

These findings underscore the importance of targeted screening and assessment for patients with anxiety and depression who may be at risk for AD or those diagnosed with AD who are at risk for subsequent depression and anxiety. Although antidepressants are effective in treating depression in general, their efficacy in AD-related depression is of variable quality, probably owing to differing pathophysiologic mechanisms of the disease. Further research is necessary to explore both pharmacologic and nonpharmacologic interventions for treating depression in AD patients. Some studies have found that cognitive behavioral-therapy can be effective in improving depression in patients with AD.
 

Sleep Disorders

Research has shown a strong correlation between AD and sleep disorders, particularly obstructive sleep apnea, insomnia, and circadian rhythm disruptions. Additionally, studies suggest that insomnia and sleep deprivation contribute to increased amyloid beta production and tau pathology, hallmark features of AD. A scoping review of 70 studies proposed that this relationship is mediated by the glymphatic system (glial-dependent waste clearance pathway in the central nervous system), and that sleep deprivation disrupts its function, leading to protein accumulation and subsequent neurologic symptoms of AD. Another study showed that sleep deprivation triggers glial cell activation, initiating an inflammatory cascade that accelerates AD progression.

Given that the gold standard treatment for obstructive sleep apnea is continuous positive airway pressure (CPAP), it has been hypothesized that CPAP could also alleviate AD symptoms owing to shared pathophysiologic mechanisms of these conditions. A large systemic review found that CPAP use improved AD symptoms in patients with mild AD or MCI, though other sleep interventions, such as cognitive-behavioral therapy and melatonin supplementation, have yielded mixed outcomes. However, most studies in this area are small in scale, and there remains a paucity of research on treating sleep disorders in AD patients, indicating a need for further investigation.
 

Musculoskeletal Disorders

Although no direct causative link has been established, research indicates an association between osteoarthritis (OA) and dementia, likely because of similar pathophysiologic mechanisms, including systemic inflammation. Longitudinal analyses of data from the Alzheimer’s Disease Neuroimaging Initiative study found cognitively normal older individuals with OA experience more rapid declines in hippocampal volumes compared to those without OA, suggesting that OA may elevate the risk of cognitive impairment. Current treatments for OA, such as nonsteroidal anti-inflammatory drugs, glucocorticoids, and disease-modifying OA drugs, might also help alleviate AD symptoms related to inflammation, though the research in this area is limited.

AD has also been linked to osteoporosis. In a longitudinal follow-up study involving 78,994 patients with osteoporosis and 78,994 controls, AD developed in 5856 patients with osteoporosis compared with 3761 patients in the control group. These findings represent a 1.27-fold higher incidence of AD in patients with osteoporosis than in the control group, suggesting that osteoporosis might be a risk factor for AD.

Additionally, research has identified a relationship between AD and increased fracture risk and decreased bone mineral density, with AD patients exhibiting a significantly higher likelihood of bone fractures compared with those without AD. “Falls and fractures, aside from the risk they pose in all geriatric patients, in individuals with cognitive impairment — whether due to AD or another cause — have higher risk to cause delirium and that can result in greater morbidity and mortality and a lasting increase in cognitive disability,” stated Dr. Pascual-Leone. Current recommendations emphasize exercise and fall prevention strategies to reduce fracture risk in patients with AD, but there is a lack of comprehensive research on the safety and efficacy of osteoporosis medications in this population.
 

Implications for Clinical Practice

The intricate interplay between AD and its comorbidities highlights the need for a comprehensive and integrated approach to patient care. The overlapping pathophysiologic mechanisms suggest that these comorbidities can contribute to the evolution and progression of AD. Likewise, AD can exacerbate comorbid conditions. As such, a holistic assessment strategy that prioritizes early detection and management of comorbid conditions to mitigate their impact on AD progression would be beneficial. Dr. Pascual-Leone added, “The presence of any of these comorbidities suggests a need to screen for MCI earlier than might otherwise be indicated or as part of the treatment for the comorbid condition. In many cases, patients can make lifestyle modifications that improve not only the comorbid condition but also reduce its effect on dementia.” In doing so, healthcare providers can help improve patient outcomes and enhance the overall quality of life for individuals living with AD.

Alissa Hershberger, Professor of Nursing, University of Central Missouri, Lee’s Summit, Missouri, has disclosed no relevant financial relationships.

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

Alzheimer’s disease (AD), the most common cause of dementia, is the fifth leading cause of death in the United States. An estimated 6.9 million Americans aged 65 years or older have AD. Comorbid conditions in AD may exacerbate the progression of dementia and negatively affect overall health.

Although the exact mechanisms remain unclear, systemic inflammation is thought to play a significant role in the development of many common comorbidities associated with AD. Among the most frequently observed comorbid conditions are hypertension, diabetes, and depression. The presence of these comorbidities affects the treatment and management of AD, underscoring the need to understand the mechanisms of their interrelationship and develop effective management strategies. 
 

Hypertension 

Hypertension is a well-established risk factor for numerous health conditions, including AD. A comprehensive review of five meta-analyses and 52 primary studies revealed that elevated systolic blood pressure (SBP) correlates with an 11 % increased risk of developing AD, raising the question of whether early intervention and control of blood pressure would mitigate the risk for AD later in life. 

Findings from the Northern Manhattan Study suggest that although elevated SBP contributes to cognitive decline in older patients, the use of antihypertensive medications can neutralize the effects of high SBP on certain cognitive functions. Furthermore, a systematic review and meta-analysis comprising 12 trials (92,135 participants) demonstrated a significant reduction in the risk for dementia and cognitive impairment with antihypertensive treatment.

Notably, a retrospective cohort study involving 69,081 participants treated with beta-blockers for hypertension found that beta-blockers with high blood-brain barrier permeability were associated with a reduced risk for AD compared with those with low blood-brain barrier permeability. Additionally, a secondary analysis of the SPRINT trial found antihypertensive medications that stimulate vs inhibit type 2 and 4 angiotensin II receptors were associated with a lower incidence of cognitive impairment. Although further clinical trials are necessary to directly assess specific medications, these findings emphasize the potential of antihypertensive treatment as a strategic approach to reduce the risk for AD.
 

Type 2 Diabetes 

The connection between AD and type 2 diabetes is such that AD is sometimes referred to as “type 3 diabetes.” Both diseases share some of the same underlying pathophysiologic mechanisms, particularly the development of insulin resistance and oxidative stress. A prospective cohort study of 10,095 participants showed that diabetes was significantly associated with a higher risk of developing dementia; this risk is even greater in patients who develop diabetes at an earlier age.

In an interview with this news organization, Alvaro Pascual-Leone, MD, PhD, a professor of neurology at Harvard Medical School, Boston, said, “In addition to being a comorbidity factor, diabetes appears to be a predisposing risk factor for AD.” This is supported by a comprehensive literature review showing an increased progression from mild cognitive impairment (MCI) to dementia in patients with diabetes, prediabetes, or metabolic syndrome, with a pooled odds ratio for dementia progression in individuals with diabetes of 1.53.

Owing to the overlapping pathophysiologic mechanisms in AD and diabetes, treating one condition may have beneficial effects on the other. A systematic umbrella review and meta-analysis that included 10 meta-analyses across nine classes of diabetes drugs found a protective effect against dementia with the use of metformin, thiazolidinediones (including pioglitazone), glucagon-like peptide 1 receptor agonists, and sodium-glucose cotransporter 2 inhibitors. Moreover, a cohort study of 12,220 patients who discontinued metformin early (ie, stopped using metformin without a prior history of abnormal kidney function) and 29,126 patients considered routine users found an increased risk for dementia in the early terminator group. Although further research is warranted, the concurrent treatment of AD and diabetes with antidiabetic agents holds considerable promise.
 

Depression and Anxiety

Anxiety and depression are significant risk factors for AD, and conversely, AD increases the likelihood of developing these psychiatric conditions. A systematic review of 14,760 studies showed dysthymia often emerges during the early stages of AD as an emotional response to cognitive decline. 

Data from the Australian Imaging Biomarkers and Lifestyle study showed a markedly elevated risk for AD and MCI among individuals with preexisting anxiety or depression. This study also found that age, sex, and marital status are important determinants, with men and single individuals with depression being particularly susceptible to developing AD. Conversely, a cohort study of 129,410 AD patients with AD, 390,088 patients with all-cause dementia, and 3,900,880 age-matched controls without a history of depression showed a cumulative incidence of depression of 13% in the AD group vs 3% in the control group, suggesting a heightened risk for depression following an AD diagnosis. 

These findings underscore the importance of targeted screening and assessment for patients with anxiety and depression who may be at risk for AD or those diagnosed with AD who are at risk for subsequent depression and anxiety. Although antidepressants are effective in treating depression in general, their efficacy in AD-related depression is of variable quality, probably owing to differing pathophysiologic mechanisms of the disease. Further research is necessary to explore both pharmacologic and nonpharmacologic interventions for treating depression in AD patients. Some studies have found that cognitive behavioral-therapy can be effective in improving depression in patients with AD.
 

Sleep Disorders

Research has shown a strong correlation between AD and sleep disorders, particularly obstructive sleep apnea, insomnia, and circadian rhythm disruptions. Additionally, studies suggest that insomnia and sleep deprivation contribute to increased amyloid beta production and tau pathology, hallmark features of AD. A scoping review of 70 studies proposed that this relationship is mediated by the glymphatic system (glial-dependent waste clearance pathway in the central nervous system), and that sleep deprivation disrupts its function, leading to protein accumulation and subsequent neurologic symptoms of AD. Another study showed that sleep deprivation triggers glial cell activation, initiating an inflammatory cascade that accelerates AD progression.

Given that the gold standard treatment for obstructive sleep apnea is continuous positive airway pressure (CPAP), it has been hypothesized that CPAP could also alleviate AD symptoms owing to shared pathophysiologic mechanisms of these conditions. A large systemic review found that CPAP use improved AD symptoms in patients with mild AD or MCI, though other sleep interventions, such as cognitive-behavioral therapy and melatonin supplementation, have yielded mixed outcomes. However, most studies in this area are small in scale, and there remains a paucity of research on treating sleep disorders in AD patients, indicating a need for further investigation.
 

Musculoskeletal Disorders

Although no direct causative link has been established, research indicates an association between osteoarthritis (OA) and dementia, likely because of similar pathophysiologic mechanisms, including systemic inflammation. Longitudinal analyses of data from the Alzheimer’s Disease Neuroimaging Initiative study found cognitively normal older individuals with OA experience more rapid declines in hippocampal volumes compared to those without OA, suggesting that OA may elevate the risk of cognitive impairment. Current treatments for OA, such as nonsteroidal anti-inflammatory drugs, glucocorticoids, and disease-modifying OA drugs, might also help alleviate AD symptoms related to inflammation, though the research in this area is limited.

AD has also been linked to osteoporosis. In a longitudinal follow-up study involving 78,994 patients with osteoporosis and 78,994 controls, AD developed in 5856 patients with osteoporosis compared with 3761 patients in the control group. These findings represent a 1.27-fold higher incidence of AD in patients with osteoporosis than in the control group, suggesting that osteoporosis might be a risk factor for AD.

Additionally, research has identified a relationship between AD and increased fracture risk and decreased bone mineral density, with AD patients exhibiting a significantly higher likelihood of bone fractures compared with those without AD. “Falls and fractures, aside from the risk they pose in all geriatric patients, in individuals with cognitive impairment — whether due to AD or another cause — have higher risk to cause delirium and that can result in greater morbidity and mortality and a lasting increase in cognitive disability,” stated Dr. Pascual-Leone. Current recommendations emphasize exercise and fall prevention strategies to reduce fracture risk in patients with AD, but there is a lack of comprehensive research on the safety and efficacy of osteoporosis medications in this population.
 

Implications for Clinical Practice

The intricate interplay between AD and its comorbidities highlights the need for a comprehensive and integrated approach to patient care. The overlapping pathophysiologic mechanisms suggest that these comorbidities can contribute to the evolution and progression of AD. Likewise, AD can exacerbate comorbid conditions. As such, a holistic assessment strategy that prioritizes early detection and management of comorbid conditions to mitigate their impact on AD progression would be beneficial. Dr. Pascual-Leone added, “The presence of any of these comorbidities suggests a need to screen for MCI earlier than might otherwise be indicated or as part of the treatment for the comorbid condition. In many cases, patients can make lifestyle modifications that improve not only the comorbid condition but also reduce its effect on dementia.” In doing so, healthcare providers can help improve patient outcomes and enhance the overall quality of life for individuals living with AD.

Alissa Hershberger, Professor of Nursing, University of Central Missouri, Lee’s Summit, Missouri, has disclosed no relevant financial relationships.

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

Percutaneous endoscopic gastrostomy (PEG) was first introduced in the early 1980s by surgeons Michael Gauderer and Jeffrey Ponsky as a less-invasive alternative to surgical gastrostomy via open laparotomy. The concept was born after the pair observed that the light from an endoscope in an infant undergoing endoscopy caused the abdominal wall to glow in the darkened operating room.

In fact, PEG was among the first procedures that defined minimally invasive surgery, a concept that has now revolutionized the surgical field. Since that time, PEG has evolved as a preferred method for patients needing long-term nutritional support for various indications. By 2001, approximately 216,000 PEGs were placed annually in the United States. While the volume of PEG procedures has declined in recent years at some institutions as practice patterns have shifted toward interventional radiology–placed gastrostomy tubes, evaluation of patients for PEG insertion, removal, or management of PEG complications remains a core area of gastroenterology practice.

University of Michigan

Among the most important roles of the gastroenterologist in considering potential PEG candidates is to determine whether an appropriate indication exists, a decision that requires a detailed understanding of a patient’s overall clinical condition, goals of care, values, and preferences. This month’s Ethics Corner column provides important expert insights on navigating the complex ethical and clinical issues relating to PEG placement, a common GI consultation that deserves thoughtful consideration and demands effective communication among members of the multidisciplinary team and with patients.

Also in our October issue, we highlight a recently published large multicohort study from Gastroenterology elucidating clinical, serologic, and genetic factors associated with extraintestinal manifestations in IBD. We also review key updates to colonoscopy quality indicators, including modifications to existing indicators such as ADR and the addition of two new “priority indicators” — rate of inadequate bowel prep and sessile serrated lesion detection rate.

In this month’s Member Spotlight, Dr. Stephanie Pointer of Digestive & Liver Health Specialists in Nashville, Tennessee, shares the many ways in which she has given back to her community through music and mentoring while leading a thriving GI practice. We hope you enjoy this, and all the coverage included in our October issue.

Megan A. Adams, MD, JD, MSc

Editor in Chief

Percutaneous endoscopic gastrostomy (PEG) was first introduced in the early 1980s by surgeons Michael Gauderer and Jeffrey Ponsky as a less-invasive alternative to surgical gastrostomy via open laparotomy. The concept was born after the pair observed that the light from an endoscope in an infant undergoing endoscopy caused the abdominal wall to glow in the darkened operating room.

In fact, PEG was among the first procedures that defined minimally invasive surgery, a concept that has now revolutionized the surgical field. Since that time, PEG has evolved as a preferred method for patients needing long-term nutritional support for various indications. By 2001, approximately 216,000 PEGs were placed annually in the United States. While the volume of PEG procedures has declined in recent years at some institutions as practice patterns have shifted toward interventional radiology–placed gastrostomy tubes, evaluation of patients for PEG insertion, removal, or management of PEG complications remains a core area of gastroenterology practice.

University of Michigan

Among the most important roles of the gastroenterologist in considering potential PEG candidates is to determine whether an appropriate indication exists, a decision that requires a detailed understanding of a patient’s overall clinical condition, goals of care, values, and preferences. This month’s Ethics Corner column provides important expert insights on navigating the complex ethical and clinical issues relating to PEG placement, a common GI consultation that deserves thoughtful consideration and demands effective communication among members of the multidisciplinary team and with patients.

Also in our October issue, we highlight a recently published large multicohort study from Gastroenterology elucidating clinical, serologic, and genetic factors associated with extraintestinal manifestations in IBD. We also review key updates to colonoscopy quality indicators, including modifications to existing indicators such as ADR and the addition of two new “priority indicators” — rate of inadequate bowel prep and sessile serrated lesion detection rate.

In this month’s Member Spotlight, Dr. Stephanie Pointer of Digestive & Liver Health Specialists in Nashville, Tennessee, shares the many ways in which she has given back to her community through music and mentoring while leading a thriving GI practice. We hope you enjoy this, and all the coverage included in our October issue.

Megan A. Adams, MD, JD, MSc

Editor in Chief

Percutaneous endoscopic gastrostomy (PEG) was first introduced in the early 1980s by surgeons Michael Gauderer and Jeffrey Ponsky as a less-invasive alternative to surgical gastrostomy via open laparotomy. The concept was born after the pair observed that the light from an endoscope in an infant undergoing endoscopy caused the abdominal wall to glow in the darkened operating room.

In fact, PEG was among the first procedures that defined minimally invasive surgery, a concept that has now revolutionized the surgical field. Since that time, PEG has evolved as a preferred method for patients needing long-term nutritional support for various indications. By 2001, approximately 216,000 PEGs were placed annually in the United States. While the volume of PEG procedures has declined in recent years at some institutions as practice patterns have shifted toward interventional radiology–placed gastrostomy tubes, evaluation of patients for PEG insertion, removal, or management of PEG complications remains a core area of gastroenterology practice.

University of Michigan

Among the most important roles of the gastroenterologist in considering potential PEG candidates is to determine whether an appropriate indication exists, a decision that requires a detailed understanding of a patient’s overall clinical condition, goals of care, values, and preferences. This month’s Ethics Corner column provides important expert insights on navigating the complex ethical and clinical issues relating to PEG placement, a common GI consultation that deserves thoughtful consideration and demands effective communication among members of the multidisciplinary team and with patients.

Also in our October issue, we highlight a recently published large multicohort study from Gastroenterology elucidating clinical, serologic, and genetic factors associated with extraintestinal manifestations in IBD. We also review key updates to colonoscopy quality indicators, including modifications to existing indicators such as ADR and the addition of two new “priority indicators” — rate of inadequate bowel prep and sessile serrated lesion detection rate.

In this month’s Member Spotlight, Dr. Stephanie Pointer of Digestive & Liver Health Specialists in Nashville, Tennessee, shares the many ways in which she has given back to her community through music and mentoring while leading a thriving GI practice. We hope you enjoy this, and all the coverage included in our October issue.

Megan A. Adams, MD, JD, MSc

Editor in Chief

As primary care physicians, we are often the first ones patients see when they become infected with influenza. According to Centers for Disease Control and Prevention statistics, approximately 5%-20% of the US population will be infected with influenza every year. Additionally, more than 200,000 of these patients will be hospitalized because of complications related to influenza.

Earlier in September, the World Health Organization (WHO) issued its latest clinical practice guidelines for influenza for the 2024-2025 season. This is a 213-page document aimed at healthcare providers who treat patients infected with influenza. It includes treatment for those with severe and nonsevere influenza infections, those in both the outpatient and hospitalized setting, as well as medication prophylaxis for those exposed to the virus. Additionally, it defines risk estimates for those who are at risk of being hospitalized or dying. In contrast, previous updates focused on management of severe influenza or those at risk of severe influenza.

These guidelines cover recommendations regarding all the antiviral medications for treating influenza used around the world. For the purpose of this article, we will focus on those most commonly used in the United States.

A newer medication discussed was baloxavir. It is recommended to be used for patients with nonsevere influenza who are at high risk for progression to severe disease. The advice is to not use it for those with little risk of progression to severe disease. Oseltamivir is recommended for those with severe infection.

The guidelines recommend against using antibiotics for those who have a low likelihood of having a bacterial coinfection. As primary care doctors, we often prescribe medications to help with symptoms. These guidelines recommend against the use of corticosteroids and antibiotics but did advise that NSAIDs could be used for symptom relief.

One of the important parts of these guidelines is prevention in patients who have been exposed but are asymptomatic. They recommend baloxavir or oseltamivir but only for those patients who are at high risk of being hospitalized if they were to become infected. Any of the antivirals can be used for patients who are exposed to the novel influenza A, which is associated with a higher mortality rate. Caution when prescribing antivirals is recommended in immunocompromised patients because there is more drug resistance seen in these patients.

These updates also discuss the use of different influenza tests. In the outpatient setting, primary doctors don’t have time for test results that may take 2 days to come back. Only rapid tests make the sense in the primary care setting. Additionally, in the age of COVID, it is important to make an accurate diagnosis so we should be testing patients. There is resistance seen with the antivirals we prescribe for influenza so prescribing them empirically without a confirmed diagnosis of influenza may be doing more harm than good.

One gap in these recommendations is vaccination. This topic was not covered at all. It would be helpful to have a strategy in place to prevent infection in populations rather than focusing just on exposed individuals. A discussion of when and who and to vaccinate would be helpful. Research into the effectiveness of vaccines is key and more accurate development of a season’s influenza vaccine would be beneficial. Currently, there is much vaccine misinformation being spread around. Education and information regarding influenza vaccines, especially coming from WHO, is crucial.

Another failure of these recommendations is that the guidelines apply only to those who present within a few days of becoming symptomatic. As family doctors, we know many of our patients self-treat or consult Google. They often don’t come for medical care until they’ve been sick for a week or longer. There are no guidelines for these patients.

In general, these guidelines are comprehensive and do a great job discussing the current medications available. However, more is needed to increase vaccination rates. Patients need to know that if they may be sick with influenza, they need to seek medical care as soon as possible. We, as family doctors, need to do a better job of risk-stratifying our patients and prescribing prophylactic medication when suitable. Every infection we prevent aids in the health of our community and the global population at large.

Dr. Girgis practices family medicine in South River, New Jersey, and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, New Jersey. She has no relevant conflicts of interest.

As primary care physicians, we are often the first ones patients see when they become infected with influenza. According to Centers for Disease Control and Prevention statistics, approximately 5%-20% of the US population will be infected with influenza every year. Additionally, more than 200,000 of these patients will be hospitalized because of complications related to influenza.

Earlier in September, the World Health Organization (WHO) issued its latest clinical practice guidelines for influenza for the 2024-2025 season. This is a 213-page document aimed at healthcare providers who treat patients infected with influenza. It includes treatment for those with severe and nonsevere influenza infections, those in both the outpatient and hospitalized setting, as well as medication prophylaxis for those exposed to the virus. Additionally, it defines risk estimates for those who are at risk of being hospitalized or dying. In contrast, previous updates focused on management of severe influenza or those at risk of severe influenza.

These guidelines cover recommendations regarding all the antiviral medications for treating influenza used around the world. For the purpose of this article, we will focus on those most commonly used in the United States.

A newer medication discussed was baloxavir. It is recommended to be used for patients with nonsevere influenza who are at high risk for progression to severe disease. The advice is to not use it for those with little risk of progression to severe disease. Oseltamivir is recommended for those with severe infection.

The guidelines recommend against using antibiotics for those who have a low likelihood of having a bacterial coinfection. As primary care doctors, we often prescribe medications to help with symptoms. These guidelines recommend against the use of corticosteroids and antibiotics but did advise that NSAIDs could be used for symptom relief.

One of the important parts of these guidelines is prevention in patients who have been exposed but are asymptomatic. They recommend baloxavir or oseltamivir but only for those patients who are at high risk of being hospitalized if they were to become infected. Any of the antivirals can be used for patients who are exposed to the novel influenza A, which is associated with a higher mortality rate. Caution when prescribing antivirals is recommended in immunocompromised patients because there is more drug resistance seen in these patients.

These updates also discuss the use of different influenza tests. In the outpatient setting, primary doctors don’t have time for test results that may take 2 days to come back. Only rapid tests make the sense in the primary care setting. Additionally, in the age of COVID, it is important to make an accurate diagnosis so we should be testing patients. There is resistance seen with the antivirals we prescribe for influenza so prescribing them empirically without a confirmed diagnosis of influenza may be doing more harm than good.

One gap in these recommendations is vaccination. This topic was not covered at all. It would be helpful to have a strategy in place to prevent infection in populations rather than focusing just on exposed individuals. A discussion of when and who and to vaccinate would be helpful. Research into the effectiveness of vaccines is key and more accurate development of a season’s influenza vaccine would be beneficial. Currently, there is much vaccine misinformation being spread around. Education and information regarding influenza vaccines, especially coming from WHO, is crucial.

Another failure of these recommendations is that the guidelines apply only to those who present within a few days of becoming symptomatic. As family doctors, we know many of our patients self-treat or consult Google. They often don’t come for medical care until they’ve been sick for a week or longer. There are no guidelines for these patients.

In general, these guidelines are comprehensive and do a great job discussing the current medications available. However, more is needed to increase vaccination rates. Patients need to know that if they may be sick with influenza, they need to seek medical care as soon as possible. We, as family doctors, need to do a better job of risk-stratifying our patients and prescribing prophylactic medication when suitable. Every infection we prevent aids in the health of our community and the global population at large.

Dr. Girgis practices family medicine in South River, New Jersey, and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, New Jersey. She has no relevant conflicts of interest.

As primary care physicians, we are often the first ones patients see when they become infected with influenza. According to Centers for Disease Control and Prevention statistics, approximately 5%-20% of the US population will be infected with influenza every year. Additionally, more than 200,000 of these patients will be hospitalized because of complications related to influenza.

Earlier in September, the World Health Organization (WHO) issued its latest clinical practice guidelines for influenza for the 2024-2025 season. This is a 213-page document aimed at healthcare providers who treat patients infected with influenza. It includes treatment for those with severe and nonsevere influenza infections, those in both the outpatient and hospitalized setting, as well as medication prophylaxis for those exposed to the virus. Additionally, it defines risk estimates for those who are at risk of being hospitalized or dying. In contrast, previous updates focused on management of severe influenza or those at risk of severe influenza.

These guidelines cover recommendations regarding all the antiviral medications for treating influenza used around the world. For the purpose of this article, we will focus on those most commonly used in the United States.

A newer medication discussed was baloxavir. It is recommended to be used for patients with nonsevere influenza who are at high risk for progression to severe disease. The advice is to not use it for those with little risk of progression to severe disease. Oseltamivir is recommended for those with severe infection.

The guidelines recommend against using antibiotics for those who have a low likelihood of having a bacterial coinfection. As primary care doctors, we often prescribe medications to help with symptoms. These guidelines recommend against the use of corticosteroids and antibiotics but did advise that NSAIDs could be used for symptom relief.

One of the important parts of these guidelines is prevention in patients who have been exposed but are asymptomatic. They recommend baloxavir or oseltamivir but only for those patients who are at high risk of being hospitalized if they were to become infected. Any of the antivirals can be used for patients who are exposed to the novel influenza A, which is associated with a higher mortality rate. Caution when prescribing antivirals is recommended in immunocompromised patients because there is more drug resistance seen in these patients.

These updates also discuss the use of different influenza tests. In the outpatient setting, primary doctors don’t have time for test results that may take 2 days to come back. Only rapid tests make the sense in the primary care setting. Additionally, in the age of COVID, it is important to make an accurate diagnosis so we should be testing patients. There is resistance seen with the antivirals we prescribe for influenza so prescribing them empirically without a confirmed diagnosis of influenza may be doing more harm than good.

One gap in these recommendations is vaccination. This topic was not covered at all. It would be helpful to have a strategy in place to prevent infection in populations rather than focusing just on exposed individuals. A discussion of when and who and to vaccinate would be helpful. Research into the effectiveness of vaccines is key and more accurate development of a season’s influenza vaccine would be beneficial. Currently, there is much vaccine misinformation being spread around. Education and information regarding influenza vaccines, especially coming from WHO, is crucial.

Another failure of these recommendations is that the guidelines apply only to those who present within a few days of becoming symptomatic. As family doctors, we know many of our patients self-treat or consult Google. They often don’t come for medical care until they’ve been sick for a week or longer. There are no guidelines for these patients.

In general, these guidelines are comprehensive and do a great job discussing the current medications available. However, more is needed to increase vaccination rates. Patients need to know that if they may be sick with influenza, they need to seek medical care as soon as possible. We, as family doctors, need to do a better job of risk-stratifying our patients and prescribing prophylactic medication when suitable. Every infection we prevent aids in the health of our community and the global population at large.

Dr. Girgis practices family medicine in South River, New Jersey, and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, New Jersey. She has no relevant conflicts of interest.

“Here’s my records.”

I hear that a lot, usually in the context of a patient handing me a flash drive or (less commonly) trying to plug it into my computer. (I have the USB ports turned toward me to keep that from happening.)

Uh, no.

I love flash drives. They definitely make data transfer easy, compared with the CDs, ZIPs, JAZZ, floppies, paper, and punch cards of past years (I should also, as a childhood TRS-80 user, include cassette tapes).

At this point an encrypted flash drive is pretty much the entire briefcase I carry back and forth to work each day.

But there is no patient I trust enough to plug in one they handed me.

I’m sure most, if not all, are well meaning. But look at how many large corporations have been damaged by someone slipping in a flash drive with a malicious program somewhere in their network. Once in, it’s almost impossible to get out, and can spread quickly.

Even if the patient is benign, I have no idea who formatted the gadget, or put the records on. It could be a relative, or friend, with other motives. It could even be a random flash drive and they don’t even know what else is on it.

My desktop is my chart system. I have to protect the data of all my patients, so I exercise caution about what emails I open and what I plug into it. Even the person offering me the flash drive wants the info guarded.

So I don’t, as a rule, plug in anything a patient hands me. All it takes is one malicious file to compromise it all. Yeah, I pay for software to watch for that sort of thing, but you still can’t be too careful.

This is where paper still shines. It’s readable and it’s transportable (at least for small things like an MRI report and lab results). I can scan it into a PDF without risking any damage to my computer. And it definitely shouldn’t be plugged into a USB drive unless you’re trying to start a fire.

Of course, paper isn’t secure, either. If you have it piled up everywhere it’s pretty easy for an unsupervised person to walk off with it. That actually happened to a doctor I shared space with 20 years ago, albeit unintentionally. A patient had brought in a bunch of his records in a folder and set them down on the counter. When he left he grabbed another patient’s chart by mistake and didn’t realize it until the next day. Fortunately he returned them promptly, and there were no issues. But it had the potential to be worse.

Today my charts on roughly 20,000 patients can all fit on a gadget the size of my thumb instead of a multi-room shelving system and storage closet. That’s pretty cool, actually. But it also opens other vulnerabilities.

It ticks some patients off that I won’t plug in their flash drives, but I don’t care. Most of them understand when I explain it, because it’s to protect them, too.

The odds are that they don’t mean any harm, but I can’t take that chance.

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

“Here’s my records.”

I hear that a lot, usually in the context of a patient handing me a flash drive or (less commonly) trying to plug it into my computer. (I have the USB ports turned toward me to keep that from happening.)

Uh, no.

I love flash drives. They definitely make data transfer easy, compared with the CDs, ZIPs, JAZZ, floppies, paper, and punch cards of past years (I should also, as a childhood TRS-80 user, include cassette tapes).

At this point an encrypted flash drive is pretty much the entire briefcase I carry back and forth to work each day.

But there is no patient I trust enough to plug in one they handed me.

I’m sure most, if not all, are well meaning. But look at how many large corporations have been damaged by someone slipping in a flash drive with a malicious program somewhere in their network. Once in, it’s almost impossible to get out, and can spread quickly.

Even if the patient is benign, I have no idea who formatted the gadget, or put the records on. It could be a relative, or friend, with other motives. It could even be a random flash drive and they don’t even know what else is on it.

My desktop is my chart system. I have to protect the data of all my patients, so I exercise caution about what emails I open and what I plug into it. Even the person offering me the flash drive wants the info guarded.

So I don’t, as a rule, plug in anything a patient hands me. All it takes is one malicious file to compromise it all. Yeah, I pay for software to watch for that sort of thing, but you still can’t be too careful.

This is where paper still shines. It’s readable and it’s transportable (at least for small things like an MRI report and lab results). I can scan it into a PDF without risking any damage to my computer. And it definitely shouldn’t be plugged into a USB drive unless you’re trying to start a fire.

Of course, paper isn’t secure, either. If you have it piled up everywhere it’s pretty easy for an unsupervised person to walk off with it. That actually happened to a doctor I shared space with 20 years ago, albeit unintentionally. A patient had brought in a bunch of his records in a folder and set them down on the counter. When he left he grabbed another patient’s chart by mistake and didn’t realize it until the next day. Fortunately he returned them promptly, and there were no issues. But it had the potential to be worse.

Today my charts on roughly 20,000 patients can all fit on a gadget the size of my thumb instead of a multi-room shelving system and storage closet. That’s pretty cool, actually. But it also opens other vulnerabilities.

It ticks some patients off that I won’t plug in their flash drives, but I don’t care. Most of them understand when I explain it, because it’s to protect them, too.

The odds are that they don’t mean any harm, but I can’t take that chance.

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

“Here’s my records.”

I hear that a lot, usually in the context of a patient handing me a flash drive or (less commonly) trying to plug it into my computer. (I have the USB ports turned toward me to keep that from happening.)

Uh, no.

I love flash drives. They definitely make data transfer easy, compared with the CDs, ZIPs, JAZZ, floppies, paper, and punch cards of past years (I should also, as a childhood TRS-80 user, include cassette tapes).

At this point an encrypted flash drive is pretty much the entire briefcase I carry back and forth to work each day.

But there is no patient I trust enough to plug in one they handed me.

I’m sure most, if not all, are well meaning. But look at how many large corporations have been damaged by someone slipping in a flash drive with a malicious program somewhere in their network. Once in, it’s almost impossible to get out, and can spread quickly.

Even if the patient is benign, I have no idea who formatted the gadget, or put the records on. It could be a relative, or friend, with other motives. It could even be a random flash drive and they don’t even know what else is on it.

My desktop is my chart system. I have to protect the data of all my patients, so I exercise caution about what emails I open and what I plug into it. Even the person offering me the flash drive wants the info guarded.

So I don’t, as a rule, plug in anything a patient hands me. All it takes is one malicious file to compromise it all. Yeah, I pay for software to watch for that sort of thing, but you still can’t be too careful.

This is where paper still shines. It’s readable and it’s transportable (at least for small things like an MRI report and lab results). I can scan it into a PDF without risking any damage to my computer. And it definitely shouldn’t be plugged into a USB drive unless you’re trying to start a fire.

Of course, paper isn’t secure, either. If you have it piled up everywhere it’s pretty easy for an unsupervised person to walk off with it. That actually happened to a doctor I shared space with 20 years ago, albeit unintentionally. A patient had brought in a bunch of his records in a folder and set them down on the counter. When he left he grabbed another patient’s chart by mistake and didn’t realize it until the next day. Fortunately he returned them promptly, and there were no issues. But it had the potential to be worse.

Today my charts on roughly 20,000 patients can all fit on a gadget the size of my thumb instead of a multi-room shelving system and storage closet. That’s pretty cool, actually. But it also opens other vulnerabilities.

It ticks some patients off that I won’t plug in their flash drives, but I don’t care. Most of them understand when I explain it, because it’s to protect them, too.

The odds are that they don’t mean any harm, but I can’t take that chance.

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Over the last few decades the patient encounter has changed dramatically. Most recently fueled by the COVID pandemic, face-to-face events between patients and providers have become less frequent. The shift began years before with the slow acceptance of telemedicine by third-party payers.

As more practices have opened portals, the encounters between providers and patients via the internet have become more common, but received mixed reviews, often leaving both providers and patients with more questions than answers. Even more recently, the explosive arrival of generative artificial intelligence (AI) has promised, some might say threatened, to add a whole new complexity and uncertainty to patient encounters regardless of the venue or platform.

Still, among the growing collection of options, I think it is fair to say that a live face-to-face encounter remains the gold standard in the opinions of both patients and providers. Patients may have become increasingly critical and vocal when they feel their provider appears rushed or is over focused on the desktop computer screen. However, given all of the options, I suspect that for the moment patients feel a face-to-face meeting continues to offer them the best chance of being heard and their concerns answered.

Even when the image on the video screen is sharp and the intelligibility of the audio feed is crystal clear, I bet most providers feel they can learn more about the patient during a live face-to-face encounter than a Zoom-style encounter.

Nonetheless, there are hints that face-to-face visits maybe losing their place in the pantheon of patient-provider encounters. A recent study from England found that there were a significant number of patients who were more forthcoming in reporting their preferences for social care-related quality of life when they were surveyed by internet rather than face-to-face. It is unclear what was behind this observation, however it may be that patients were embarrassed and viewed these questions about their social neediness as too sensitive to share face-to-face.

There is ample evidence of situations in which the internet can provide a level of anonymity that emboldens the user to say things that are cruel and hurtful, using words they might be afraid to voice in a live setting. This license to act in an uncivil manner is behind much of the harm generated by chat rooms and other social media sites. While in these cases the ability to hide behind the video screen is a negative, this study from England suggests that we should be looking for more opportunities to use this emboldening feature with certain individuals and populations who may be intimidated during a face-to-face encounter. It is likely a hybrid approach may be the most beneficial strategy tailored to the individual patient.

One advantage of a face-to-face visit is that each participant can read the body language of the other. This, of course, can be a disadvantage for the provider who has failed to master the art of disguising his “I’m running behind” stress level, when he should be replacing it with an “I’m ready to listen” posture.

Portals have opened up a whole other can of worms, particularly when the provider has failed to clearly delineate what sort of questions are appropriate for an online forum, not informed the patient who will be providing the answer, and a rough idea of when this will happen. It may take several trips up the learning curve for patients and providers to develop a style of writing that make optimal use of the portal format and make it fit the needs of the practice and the patients.

Regardless of what kind of visit platform we are talking about, a lot hinges on the providers choice of words. I recently reviewed some of the work of Jeffrey D. Robinson, PhD, a professor of communication at the Portland State University, Portland, Oregon. He offers the example of the difference between “some” and “any.” When the patient was asked “Is there something else you would like to address today” almost 80% of the patient’s unmet questions were addressed. However, when the question was “Is there anything else ...” very few of the patient’s unmet questions were addressed. Dr. Robinson has also found that when the question is posed early in the visit rather than at the end, it improves the chances of having the patient’s unmet concerns addressed.

I suspect that the face-to-face patient encounter will survive, but it will continue to lose its market share as other platforms emerge. We can be sure there will be change. We need look no further than generative AI to look for the next step. A well-crafted question could help the patient and the provider choose the most appropriate patient encounter format given the patient’s demographic, chief complaint, and prior history, and match this with the provider’s background and strengths.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Over the last few decades the patient encounter has changed dramatically. Most recently fueled by the COVID pandemic, face-to-face events between patients and providers have become less frequent. The shift began years before with the slow acceptance of telemedicine by third-party payers.

As more practices have opened portals, the encounters between providers and patients via the internet have become more common, but received mixed reviews, often leaving both providers and patients with more questions than answers. Even more recently, the explosive arrival of generative artificial intelligence (AI) has promised, some might say threatened, to add a whole new complexity and uncertainty to patient encounters regardless of the venue or platform.

Still, among the growing collection of options, I think it is fair to say that a live face-to-face encounter remains the gold standard in the opinions of both patients and providers. Patients may have become increasingly critical and vocal when they feel their provider appears rushed or is over focused on the desktop computer screen. However, given all of the options, I suspect that for the moment patients feel a face-to-face meeting continues to offer them the best chance of being heard and their concerns answered.

Even when the image on the video screen is sharp and the intelligibility of the audio feed is crystal clear, I bet most providers feel they can learn more about the patient during a live face-to-face encounter than a Zoom-style encounter.

Nonetheless, there are hints that face-to-face visits maybe losing their place in the pantheon of patient-provider encounters. A recent study from England found that there were a significant number of patients who were more forthcoming in reporting their preferences for social care-related quality of life when they were surveyed by internet rather than face-to-face. It is unclear what was behind this observation, however it may be that patients were embarrassed and viewed these questions about their social neediness as too sensitive to share face-to-face.

There is ample evidence of situations in which the internet can provide a level of anonymity that emboldens the user to say things that are cruel and hurtful, using words they might be afraid to voice in a live setting. This license to act in an uncivil manner is behind much of the harm generated by chat rooms and other social media sites. While in these cases the ability to hide behind the video screen is a negative, this study from England suggests that we should be looking for more opportunities to use this emboldening feature with certain individuals and populations who may be intimidated during a face-to-face encounter. It is likely a hybrid approach may be the most beneficial strategy tailored to the individual patient.

One advantage of a face-to-face visit is that each participant can read the body language of the other. This, of course, can be a disadvantage for the provider who has failed to master the art of disguising his “I’m running behind” stress level, when he should be replacing it with an “I’m ready to listen” posture.

Portals have opened up a whole other can of worms, particularly when the provider has failed to clearly delineate what sort of questions are appropriate for an online forum, not informed the patient who will be providing the answer, and a rough idea of when this will happen. It may take several trips up the learning curve for patients and providers to develop a style of writing that make optimal use of the portal format and make it fit the needs of the practice and the patients.

Regardless of what kind of visit platform we are talking about, a lot hinges on the providers choice of words. I recently reviewed some of the work of Jeffrey D. Robinson, PhD, a professor of communication at the Portland State University, Portland, Oregon. He offers the example of the difference between “some” and “any.” When the patient was asked “Is there something else you would like to address today” almost 80% of the patient’s unmet questions were addressed. However, when the question was “Is there anything else ...” very few of the patient’s unmet questions were addressed. Dr. Robinson has also found that when the question is posed early in the visit rather than at the end, it improves the chances of having the patient’s unmet concerns addressed.

I suspect that the face-to-face patient encounter will survive, but it will continue to lose its market share as other platforms emerge. We can be sure there will be change. We need look no further than generative AI to look for the next step. A well-crafted question could help the patient and the provider choose the most appropriate patient encounter format given the patient’s demographic, chief complaint, and prior history, and match this with the provider’s background and strengths.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Over the last few decades the patient encounter has changed dramatically. Most recently fueled by the COVID pandemic, face-to-face events between patients and providers have become less frequent. The shift began years before with the slow acceptance of telemedicine by third-party payers.

As more practices have opened portals, the encounters between providers and patients via the internet have become more common, but received mixed reviews, often leaving both providers and patients with more questions than answers. Even more recently, the explosive arrival of generative artificial intelligence (AI) has promised, some might say threatened, to add a whole new complexity and uncertainty to patient encounters regardless of the venue or platform.

Still, among the growing collection of options, I think it is fair to say that a live face-to-face encounter remains the gold standard in the opinions of both patients and providers. Patients may have become increasingly critical and vocal when they feel their provider appears rushed or is over focused on the desktop computer screen. However, given all of the options, I suspect that for the moment patients feel a face-to-face meeting continues to offer them the best chance of being heard and their concerns answered.

Even when the image on the video screen is sharp and the intelligibility of the audio feed is crystal clear, I bet most providers feel they can learn more about the patient during a live face-to-face encounter than a Zoom-style encounter.

Nonetheless, there are hints that face-to-face visits maybe losing their place in the pantheon of patient-provider encounters. A recent study from England found that there were a significant number of patients who were more forthcoming in reporting their preferences for social care-related quality of life when they were surveyed by internet rather than face-to-face. It is unclear what was behind this observation, however it may be that patients were embarrassed and viewed these questions about their social neediness as too sensitive to share face-to-face.

There is ample evidence of situations in which the internet can provide a level of anonymity that emboldens the user to say things that are cruel and hurtful, using words they might be afraid to voice in a live setting. This license to act in an uncivil manner is behind much of the harm generated by chat rooms and other social media sites. While in these cases the ability to hide behind the video screen is a negative, this study from England suggests that we should be looking for more opportunities to use this emboldening feature with certain individuals and populations who may be intimidated during a face-to-face encounter. It is likely a hybrid approach may be the most beneficial strategy tailored to the individual patient.

One advantage of a face-to-face visit is that each participant can read the body language of the other. This, of course, can be a disadvantage for the provider who has failed to master the art of disguising his “I’m running behind” stress level, when he should be replacing it with an “I’m ready to listen” posture.

Portals have opened up a whole other can of worms, particularly when the provider has failed to clearly delineate what sort of questions are appropriate for an online forum, not informed the patient who will be providing the answer, and a rough idea of when this will happen. It may take several trips up the learning curve for patients and providers to develop a style of writing that make optimal use of the portal format and make it fit the needs of the practice and the patients.

Regardless of what kind of visit platform we are talking about, a lot hinges on the providers choice of words. I recently reviewed some of the work of Jeffrey D. Robinson, PhD, a professor of communication at the Portland State University, Portland, Oregon. He offers the example of the difference between “some” and “any.” When the patient was asked “Is there something else you would like to address today” almost 80% of the patient’s unmet questions were addressed. However, when the question was “Is there anything else ...” very few of the patient’s unmet questions were addressed. Dr. Robinson has also found that when the question is posed early in the visit rather than at the end, it improves the chances of having the patient’s unmet concerns addressed.

I suspect that the face-to-face patient encounter will survive, but it will continue to lose its market share as other platforms emerge. We can be sure there will be change. We need look no further than generative AI to look for the next step. A well-crafted question could help the patient and the provider choose the most appropriate patient encounter format given the patient’s demographic, chief complaint, and prior history, and match this with the provider’s background and strengths.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Fatigue, nausea, acid reflux, muscle loss, and the dreaded “Ozempic face” are side effects from using glucagon-like peptide 1 (GLP-1) receptor agonists (RAs) such as semaglutide or the dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA tirzepatide to control blood sugar and promote weight loss. 

But what I’ve learned from working with hundreds of patients on these medications, and others, is that most (if not all) of these side effects can be minimized by ensuring proper nutrition. 

Setting patients up for success requires dietary education and counseling, along with regular monitoring to determine any nutritional deficiencies. Although adequate intake of all the macro and micronutrients is obviously important, there are five nutrients in particular that clinicians should emphasize with their patients on GLP-1 RAs or GIP/GLP-1 RSs.
 

Protein

My patients are probably sick of hearing me talk about protein, but without the constant reinforcement, many of them wouldn’t consume enough of this macronutrient to maintain their baseline lean body mass. The recommended dietary allowance (RDA) for protein (0.8 g/kg bodyweight) doesn’t cut it, especially for older, obese patients, who need closer to 1.0-1.2 g/kg bodyweight to maintain their muscle mass. For example, for a 250-lb patient, I would recommend 114-136 g protein per day. This is equivalent to roughly 15 oz of cooked animal protein. It’s important to note, though, that individuals with kidney disease must limit their protein intake to 0.6-0.8 g/kg bodyweight per day, to avoid overtaxing their kidneys. In this situation, the benefit of increased protein intake does not outweigh the risk of harming the kidneys.

It’s often challenging for patients with suppressed appetites to even think about eating a large hunk of meat or fish, let alone consume it. Plus, eating more than 3-4 oz of protein in one meal can make some patients extremely uncomfortable, owing to the medication’s effect on gastric emptying. This means that daily protein intake must be spread out over multiple mini-meals. 

For patients who need more than 100 g of protein per day, protein powders and premade protein shakes can provide 20-30 g protein to fill in the gaps. Although I always try to promote food first, protein supplements have been game changers for my patients, especially those who find solid food less appealing on the medication, or those who avoid animal protein. 

Clinicians should have their patients monitor changes in their lean body mass using a dual-energy x-ray absorptiometry scan or a bioelectrical impedance scale; this can be a helpful tool in assessing whether protein intake is sufficient. 
 

Fiber

Even my most knowledgeable and compliant patients will experience some constipation. Generally speaking, when you eat less, you will have fewer bowel movements. Combine that with delayed gastric emptying and reduced fiber intake, and you have a perfect storm. Many patients are simply not able to get in the recommended 25-35 g fiber per day through food, because fibrous foods are filling. If they are prioritizing the protein in their meal, they will not have enough room for all the vegetables on their plate. 

To ensure that patients are getting sufficient fiber, clinicians should push consumption of certain vegetables and fruits, such as carrots, broccoli, Brussels sprouts, raspberries, blackberries, and apples, as well as beans and legumes. (Salads are great, but greens like spinach are not as fibrous as one might think.) If the fruit and veggie intake isn’t up to par, a fiber supplement such as psyllium husk can provide an effective boost.
 

Vitamin B12

Use of these medications is associated with a reduction in vitamin B12 levels, in part because delayed gastric emptying may affect B12 absorption. Low dietary intake of B12 while on the medications can also be to blame, though. The best food sources are animal proteins, so if possible, patients should prioritize having fish, lean meat, eggs, and dairy daily. 

Vegetarians and vegans, who are at an increased risk for deficiency, can incorporate nutritional yeast, an excellent source of vitamin B12, into their daily routine. It is beneficial for patients to get blood work periodically to check on B12 status, because insufficient B12 can contribute to the fatigue patients experience while on the medication.
 

Calcium

Individuals should have calcium on their radar, because weight loss is associated with a decrease in bone mineral density. Adequate intake of the mineral is crucial for optimal bone health, particularly among postmenopausal women and those who are at risk of developing osteoporosis. The RDA for calcium is 1000-1200 mg/d, which an estimated 50% of obese individuals do not take in. 

Although dairy products are well-known for being rich in calcium, there are other great sources. Dark green leafy vegetables, such as cooked collard greens and spinach, provide nearly 300 mg per cup. Tofu and sardines are also calcium powerhouses. Despite the plethora of calcium-rich foods, however, some patients may need a calcium supplement.
 

Vitamin D

Vitamin D deficiency or insufficiency is common among individuals with obesity, so even before these patients start the medications, supplementation may be warranted. The vitamin’s role in promoting calcium absorption, as well as in bone remodeling, make adequate intake essential for patients experiencing significant weight loss.

Clinicians should emphasize regular consumption of fatty fish, such as salmon, as well as eggs, mushrooms, and vitamin D–fortified milks. But unfortunately, that’s where the list of vitamin D–rich foods ends, so taking a vitamin D supplement will be necessary for many patients.

Regularly monitoring patients on GLP-1 RAs through blood work to check vitamin levels and body composition analysis can be helpful in assessing nutritional status while losing weight. Clinicians can also encourage their patients to work with a registered dietitian who is familiar with these medications, so they can develop optimal eating habits throughout their health journey.

Ms. Hanks, a registered dietitian in New York City, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Fatigue, nausea, acid reflux, muscle loss, and the dreaded “Ozempic face” are side effects from using glucagon-like peptide 1 (GLP-1) receptor agonists (RAs) such as semaglutide or the dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA tirzepatide to control blood sugar and promote weight loss. 

But what I’ve learned from working with hundreds of patients on these medications, and others, is that most (if not all) of these side effects can be minimized by ensuring proper nutrition. 

Setting patients up for success requires dietary education and counseling, along with regular monitoring to determine any nutritional deficiencies. Although adequate intake of all the macro and micronutrients is obviously important, there are five nutrients in particular that clinicians should emphasize with their patients on GLP-1 RAs or GIP/GLP-1 RSs.
 

Protein

My patients are probably sick of hearing me talk about protein, but without the constant reinforcement, many of them wouldn’t consume enough of this macronutrient to maintain their baseline lean body mass. The recommended dietary allowance (RDA) for protein (0.8 g/kg bodyweight) doesn’t cut it, especially for older, obese patients, who need closer to 1.0-1.2 g/kg bodyweight to maintain their muscle mass. For example, for a 250-lb patient, I would recommend 114-136 g protein per day. This is equivalent to roughly 15 oz of cooked animal protein. It’s important to note, though, that individuals with kidney disease must limit their protein intake to 0.6-0.8 g/kg bodyweight per day, to avoid overtaxing their kidneys. In this situation, the benefit of increased protein intake does not outweigh the risk of harming the kidneys.

It’s often challenging for patients with suppressed appetites to even think about eating a large hunk of meat or fish, let alone consume it. Plus, eating more than 3-4 oz of protein in one meal can make some patients extremely uncomfortable, owing to the medication’s effect on gastric emptying. This means that daily protein intake must be spread out over multiple mini-meals. 

For patients who need more than 100 g of protein per day, protein powders and premade protein shakes can provide 20-30 g protein to fill in the gaps. Although I always try to promote food first, protein supplements have been game changers for my patients, especially those who find solid food less appealing on the medication, or those who avoid animal protein. 

Clinicians should have their patients monitor changes in their lean body mass using a dual-energy x-ray absorptiometry scan or a bioelectrical impedance scale; this can be a helpful tool in assessing whether protein intake is sufficient. 
 

Fiber

Even my most knowledgeable and compliant patients will experience some constipation. Generally speaking, when you eat less, you will have fewer bowel movements. Combine that with delayed gastric emptying and reduced fiber intake, and you have a perfect storm. Many patients are simply not able to get in the recommended 25-35 g fiber per day through food, because fibrous foods are filling. If they are prioritizing the protein in their meal, they will not have enough room for all the vegetables on their plate. 

To ensure that patients are getting sufficient fiber, clinicians should push consumption of certain vegetables and fruits, such as carrots, broccoli, Brussels sprouts, raspberries, blackberries, and apples, as well as beans and legumes. (Salads are great, but greens like spinach are not as fibrous as one might think.) If the fruit and veggie intake isn’t up to par, a fiber supplement such as psyllium husk can provide an effective boost.
 

Vitamin B12

Use of these medications is associated with a reduction in vitamin B12 levels, in part because delayed gastric emptying may affect B12 absorption. Low dietary intake of B12 while on the medications can also be to blame, though. The best food sources are animal proteins, so if possible, patients should prioritize having fish, lean meat, eggs, and dairy daily. 

Vegetarians and vegans, who are at an increased risk for deficiency, can incorporate nutritional yeast, an excellent source of vitamin B12, into their daily routine. It is beneficial for patients to get blood work periodically to check on B12 status, because insufficient B12 can contribute to the fatigue patients experience while on the medication.
 

Calcium

Individuals should have calcium on their radar, because weight loss is associated with a decrease in bone mineral density. Adequate intake of the mineral is crucial for optimal bone health, particularly among postmenopausal women and those who are at risk of developing osteoporosis. The RDA for calcium is 1000-1200 mg/d, which an estimated 50% of obese individuals do not take in. 

Although dairy products are well-known for being rich in calcium, there are other great sources. Dark green leafy vegetables, such as cooked collard greens and spinach, provide nearly 300 mg per cup. Tofu and sardines are also calcium powerhouses. Despite the plethora of calcium-rich foods, however, some patients may need a calcium supplement.
 

Vitamin D

Vitamin D deficiency or insufficiency is common among individuals with obesity, so even before these patients start the medications, supplementation may be warranted. The vitamin’s role in promoting calcium absorption, as well as in bone remodeling, make adequate intake essential for patients experiencing significant weight loss.

Clinicians should emphasize regular consumption of fatty fish, such as salmon, as well as eggs, mushrooms, and vitamin D–fortified milks. But unfortunately, that’s where the list of vitamin D–rich foods ends, so taking a vitamin D supplement will be necessary for many patients.

Regularly monitoring patients on GLP-1 RAs through blood work to check vitamin levels and body composition analysis can be helpful in assessing nutritional status while losing weight. Clinicians can also encourage their patients to work with a registered dietitian who is familiar with these medications, so they can develop optimal eating habits throughout their health journey.

Ms. Hanks, a registered dietitian in New York City, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Fatigue, nausea, acid reflux, muscle loss, and the dreaded “Ozempic face” are side effects from using glucagon-like peptide 1 (GLP-1) receptor agonists (RAs) such as semaglutide or the dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA tirzepatide to control blood sugar and promote weight loss. 

But what I’ve learned from working with hundreds of patients on these medications, and others, is that most (if not all) of these side effects can be minimized by ensuring proper nutrition. 

Setting patients up for success requires dietary education and counseling, along with regular monitoring to determine any nutritional deficiencies. Although adequate intake of all the macro and micronutrients is obviously important, there are five nutrients in particular that clinicians should emphasize with their patients on GLP-1 RAs or GIP/GLP-1 RSs.
 

Protein

My patients are probably sick of hearing me talk about protein, but without the constant reinforcement, many of them wouldn’t consume enough of this macronutrient to maintain their baseline lean body mass. The recommended dietary allowance (RDA) for protein (0.8 g/kg bodyweight) doesn’t cut it, especially for older, obese patients, who need closer to 1.0-1.2 g/kg bodyweight to maintain their muscle mass. For example, for a 250-lb patient, I would recommend 114-136 g protein per day. This is equivalent to roughly 15 oz of cooked animal protein. It’s important to note, though, that individuals with kidney disease must limit their protein intake to 0.6-0.8 g/kg bodyweight per day, to avoid overtaxing their kidneys. In this situation, the benefit of increased protein intake does not outweigh the risk of harming the kidneys.

It’s often challenging for patients with suppressed appetites to even think about eating a large hunk of meat or fish, let alone consume it. Plus, eating more than 3-4 oz of protein in one meal can make some patients extremely uncomfortable, owing to the medication’s effect on gastric emptying. This means that daily protein intake must be spread out over multiple mini-meals. 

For patients who need more than 100 g of protein per day, protein powders and premade protein shakes can provide 20-30 g protein to fill in the gaps. Although I always try to promote food first, protein supplements have been game changers for my patients, especially those who find solid food less appealing on the medication, or those who avoid animal protein. 

Clinicians should have their patients monitor changes in their lean body mass using a dual-energy x-ray absorptiometry scan or a bioelectrical impedance scale; this can be a helpful tool in assessing whether protein intake is sufficient. 
 

Fiber

Even my most knowledgeable and compliant patients will experience some constipation. Generally speaking, when you eat less, you will have fewer bowel movements. Combine that with delayed gastric emptying and reduced fiber intake, and you have a perfect storm. Many patients are simply not able to get in the recommended 25-35 g fiber per day through food, because fibrous foods are filling. If they are prioritizing the protein in their meal, they will not have enough room for all the vegetables on their plate. 

To ensure that patients are getting sufficient fiber, clinicians should push consumption of certain vegetables and fruits, such as carrots, broccoli, Brussels sprouts, raspberries, blackberries, and apples, as well as beans and legumes. (Salads are great, but greens like spinach are not as fibrous as one might think.) If the fruit and veggie intake isn’t up to par, a fiber supplement such as psyllium husk can provide an effective boost.
 

Vitamin B12

Use of these medications is associated with a reduction in vitamin B12 levels, in part because delayed gastric emptying may affect B12 absorption. Low dietary intake of B12 while on the medications can also be to blame, though. The best food sources are animal proteins, so if possible, patients should prioritize having fish, lean meat, eggs, and dairy daily. 

Vegetarians and vegans, who are at an increased risk for deficiency, can incorporate nutritional yeast, an excellent source of vitamin B12, into their daily routine. It is beneficial for patients to get blood work periodically to check on B12 status, because insufficient B12 can contribute to the fatigue patients experience while on the medication.
 

Calcium

Individuals should have calcium on their radar, because weight loss is associated with a decrease in bone mineral density. Adequate intake of the mineral is crucial for optimal bone health, particularly among postmenopausal women and those who are at risk of developing osteoporosis. The RDA for calcium is 1000-1200 mg/d, which an estimated 50% of obese individuals do not take in. 

Although dairy products are well-known for being rich in calcium, there are other great sources. Dark green leafy vegetables, such as cooked collard greens and spinach, provide nearly 300 mg per cup. Tofu and sardines are also calcium powerhouses. Despite the plethora of calcium-rich foods, however, some patients may need a calcium supplement.
 

Vitamin D

Vitamin D deficiency or insufficiency is common among individuals with obesity, so even before these patients start the medications, supplementation may be warranted. The vitamin’s role in promoting calcium absorption, as well as in bone remodeling, make adequate intake essential for patients experiencing significant weight loss.

Clinicians should emphasize regular consumption of fatty fish, such as salmon, as well as eggs, mushrooms, and vitamin D–fortified milks. But unfortunately, that’s where the list of vitamin D–rich foods ends, so taking a vitamin D supplement will be necessary for many patients.

Regularly monitoring patients on GLP-1 RAs through blood work to check vitamin levels and body composition analysis can be helpful in assessing nutritional status while losing weight. Clinicians can also encourage their patients to work with a registered dietitian who is familiar with these medications, so they can develop optimal eating habits throughout their health journey.

Ms. Hanks, a registered dietitian in New York City, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.