Tag: nutrition

Weight Loss Surgery Without Incisions: Bariatric Endoscopy

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Obesity is one of the most common health problems we face, and treatment has never kept pace with the need. More than 100 million U.S. adults meet criteria for obesity. Roughly 1% of patients who qualify for metabolic and bariatric surgery actually undergo it in a given year. Lifestyle change and medication help, and plenty of patients either get insufficient benefit or can’t sustain them. That leaves a wide gap, particularly for people with moderate obesity and for those who don’t qualify for surgery.

Bariatric endoscopy is starting to fill it. These are minimally invasive outpatient procedures sitting between lifestyle and pharmacotherapy on one side and surgery on the other. No incisions, lower risk, same-day discharge for most patients. They are also repeatable or reversible, which gives patients and clinicians room to change course.

Intragastric balloons are the simplest example. The device occupies space in the stomach, and patients feel full on less food. Studies consistently show 10 to 15% total body weight loss over six months alongside improvements in insulin resistance and liver health. In a prospective study of patients with NASH and early fibrosis who underwent balloon placement with paired liver biopsies, every patient who lost 10% or more of their weight showed a reduction in NAFLD activity score, 90% had resolution of NASH, and 45% showed fibrosis regression (Bazerbachi et al., Clin Gastroenterol Hepatol, 2021). Small study, striking numbers.

Endoscopic sleeve gastroplasty is the more durable option. An endoscopic suturing device reduces stomach volume, mimicking a surgical sleeve without incisions. MERIT, the first randomized trial of the procedure, compared ESG plus lifestyle modification against lifestyle alone in class 1 and 2 obesity and found the procedure safely induced and maintained weight loss with improvement in metabolic comorbidities (Abu Dayyeh et al., Lancet, 2022). Five-year data from a single-center cohort show mean total body weight loss around 16%, with roughly three-fifths of patients holding 10% or more (Sharaiha et al., Clin Gastroenterol Hepatol, 2021). Compared with surgery it means fewer complications, faster recovery, and preserved native anatomy.

Endoscopic revision is gaining traction too. Transoral outlet reduction addresses weight regain after gastric bypass by tightening the gastrojejunal anastomosis and the pouch, restoring restriction (Jirapinyo & Thompson, Endoscopy, 2018). For patients demoralized by regain, it is a far less invasive option than surgical revision.

Duodenal interventions work differently. Duodenal mucosal resurfacing and duodenal-jejunal bypass sleeves act less on restriction and more on metabolic signaling, with early data showing HbA1c reductions and weight loss in the 9 to 15% range. This is the least mature part of the field and should be described that way to patients.

Safety looks good. Serious adverse events run in the 0.2 to 4% range depending on the procedure. Most problems, nausea and abdominal discomfort, are mild and short-lived. FDA clearance of endoscopic suturing platforms reflects the accumulating evidence on both safety and efficacy.

So who are the candidates? Typically patients with BMI 30 to 50 who haven’t gotten results from diet and exercise alone. It is also an option for people who aren’t ready for surgery or not eligible. Patients who have regained weight after bariatric surgery may benefit, especially from TORe. Comorbidities like diabetes and MASLD factor in, since weight reduction directly improves their course.

The thing to stress is that bariatric endoscopy is a tool rather than a cure, and it doesn’t replace surgery or medication. Outcomes are best when procedures are combined with pharmacotherapy and lifestyle change, which is the same lesson obesity keeps teaching. It is a chronic, relapsing disease and it needs long-term management.

Scott Rennie, D.O.

References:

1. Bazerbachi F, et al. Intragastric Balloon Placement Induces Significant Metabolic and Histologic Improvement in Patients With Nonalcoholic Steatohepatitis. Clin Gastroenterol Hepatol. 2021;19(1):146-154.e4. https://pubmed.ncbi.nlm.nih.gov/32360804/

2. Abu Dayyeh BK, et al. Endoscopic sleeve gastroplasty for treatment of class 1 and 2 obesity (MERIT): a prospective, multicentre, randomised trial. Lancet. 2022;400(10350):441-451. https://pubmed.ncbi.nlm.nih.gov/35908555/

3. Sharaiha RZ, et al. Five-Year Outcomes of Endoscopic Sleeve Gastroplasty for the Treatment of Obesity. Clin Gastroenterol Hepatol. 2021;19(5):1051-1057.e2. https://pubmed.ncbi.nlm.nih.gov/32683103/

4. Jirapinyo P, Thompson CC. Endoscopic bariatric and metabolic therapies: surgical analogues and mechanisms of action. Endoscopy. 2018;50(4):371-377.

5. Ponce J, et al. Surg Obes Relat Dis. 2015;11(4):874-881.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Weight Loss Surgery Options for Obesity Explained

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Weight loss surgery, also called bariatric or metabolic surgery, is one of the most effective treatments available for severe obesity. Gastric bypass and sleeve gastrectomy are safer now than they have ever been, and demand keeps climbing. Surgery carries risk and requires a long-term commitment, and both belong in the conversation from the first visit.

Obesity affects more than 100 million U.S. adults, roughly 40.3% of the adult population, with 9.7% in the severe range (NCHS, NHANES August 2021 to August 2023). Type 2 diabetes, cardiovascular disease, cancer, and early death all track with excess weight. Lifestyle programs and medications help, and for many patients the results don’t hold. That is the gap surgery fills. The Swedish Obese Subjects study followed patients for over a decade and found surgery produced durable weight loss and lower mortality (Sjöström et al., NEJM, 2007), and a retrospective cohort found a 40% reduction in all-cause mortality after gastric bypass (Adams et al., NEJM, 2007).

So who qualifies? Under the 2022 ASMBS and IFSO guidelines, surgery is recommended for people with BMI over 35 regardless of comorbidity, and for BMI 30 to 34.9 in patients with metabolic disease that has not responded to medical therapy (Eisenberg et al., Surg Obes Relat Dis, 2022). That is a meaningful loosening from the 1991 NIH thresholds most clinicians still carry in their heads. There is no strict age cutoff, though surgeons approach adolescents and older adults with extra care.

Before surgery, patients go through a thorough workup: nutrition and psychology evaluations, cardiac and pulmonary assessment, sometimes a sleep study and endoscopy. Smoking cessation is required. Most insurers still ask for documentation of six months of supervised weight management, a requirement with no good evidence behind it that delays care for people who need it. That time does get used for preparation and education, which is the one argument in its favor.

Several procedures are available. Sleeve gastrectomy is the most common worldwide. About 80% of the stomach is removed, limiting intake and changing hunger hormones. Patients typically lose 55 to 60% of excess weight. The operation is shorter than bypass and hospital stays run one to two days. Worsening reflux is the main downside (Peterli et al., JAMA, 2018).

Roux-en-Y gastric bypass has decades of long-term data behind it. A small pouch connects to the small intestine, bypassing part of the digestive tract. Average weight loss runs 60 to 70% of excess weight, diabetes remission rates are high, and reflux often improves. Risks include vitamin deficiencies, marginal ulcers, and internal hernias (Higa et al., Surg Obes Relat Dis, 2011).

One anastomosis gastric bypass simplifies the technique and shows promising results for weight and comorbidities, with higher risk of bile reflux and deficiencies. Duodenal switch and SADI combine a sleeve with intestinal rerouting. These are the most powerful options for diabetes remission and weight loss and they demand the most careful long-term monitoring. Gastric banding is now rare. It once looked appealing because it was reversible and low-risk, and the weight loss proved modest while long-term reoperation rates ran high (Genco et al., Surg Obes Relat Dis, 2016).

The randomized evidence is strong. Trials by Mingrone, Schauer, and Ikramuddin all demonstrated higher diabetes remission with surgery than with medical therapy alone, and the Schauer and Mingrone cohorts held those differences out to five and ten years (Schauer et al., NEJM, 2012 and 2017; Mingrone et al., Lancet, 2015 and 2021; Ikramuddin et al., JAMA, 2018).

Weight regain happens. About one in five patients regains some weight after bypass, from changes in anatomy or lapses in eating and activity. Surgeons can offer revision: re-sleeving, converting sleeve to bypass, or tightening pouches. These get tailored to the individual.

Long-term success depends on follow-up. Regular labs, nutrition counseling, ongoing team support. Lifelong vitamin and mineral supplementation is required rather than optional. Behavioral support matters, because habits carry as much weight as anatomy over years.

Weight loss surgery is one of the most powerful tools we have for a disease that is otherwise progressive and difficult to manage. With careful preparation, modern technique, and sustained follow-up, patients see improvements in weight, health, and quality of life that few other interventions produce.

Scott Rennie, D.O.

References:

1. National Center for Health Statistics. Prevalence of Overweight, Obesity, and Severe Obesity Among Adults Age 20 and Older: United States, August 2021–August 2023. https://www.cdc.gov/nchs/data/hestat/obesity-adult-17-18/obesity-adult.htm

2. Sjöström L, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med. 2007;357(8):741-752. https://pubmed.ncbi.nlm.nih.gov/17715408/

3. Adams TD, et al. Long-term mortality after gastric bypass surgery. N Engl J Med. 2007;357(8):753-761. https://pubmed.ncbi.nlm.nih.gov/17715409/

4. Eisenberg D, et al. 2022 American Society for Metabolic and Bariatric Surgery (ASMBS) and International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO) Indications for Metabolic and Bariatric Surgery. Surg Obes Relat Dis. 2022;18(12):1345-1356. https://pubmed.ncbi.nlm.nih.gov/36280539/

5. Schauer PR, et al. N Engl J Med. 2012;366(17):1567-1576; and N Engl J Med. 2017;376(7):641-651.

6. Mingrone G, et al. Lancet. 2015;386(9997):964-973; and Lancet. 2021;397(10271):293-304.

7. Ikramuddin S, et al. JAMA. 2018;319(3):266-278.

8. Peterli R, et al. Effect of Laparoscopic Sleeve Gastrectomy vs Laparoscopic Roux-en-Y Gastric Bypass on Weight Loss in Patients With Morbid Obesity: The SM-BOSS Randomized Clinical Trial. JAMA. 2018;319(3):255-265. https://pubmed.ncbi.nlm.nih.gov/29340679/

9. Higa K, et al. Surg Obes Relat Dis. 2011;7(4):516-525.

10. Genco A, et al. Surg Obes Relat Dis. 2016;12(10):1783-1788.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

How the Gut Affects Diabetes and Metabolic Disease

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

When we think about metabolic disease, attention goes to blood sugar, insulin, and fat. Another organ drives much of the process quietly, and it is the gut.

Calling the gut a digestive tube undersells it badly. It is a complex, dynamic system that shapes how we handle nutrients, regulate hormones, and respond to infection. Researchers now treat it as central to metabolic health, and that shift has opened new thinking about both prevention and treatment.

Consider what it actually contains. Its own nervous system, sometimes called the second brain. An endocrine system producing GLP-1, PYY, and ghrelin. A major site of immune defense. And constant interaction with the trillions of microbes living inside it. Together these systems determine how food gets processed, when fullness registers, and how glucose is regulated (Seeley et al., Cell Metab, 2015).

The gut-brain conversation is the powerful part. Signals move both directions. Hormones, nerve messages, and bacterial metabolites all feed into how the brain regulates appetite and metabolism. This is a large part of why simple calorie counting fails so often. The gut can override willpower, and the brain listens closely to what it says.

Bariatric surgery demonstrates the whole system in action. Vertical sleeve gastrectomy and Roux-en-Y gastric bypass do far more than reduce stomach size. They produce wide-reaching changes in gut physiology that explain why they work so well for weight loss and diabetes control. After surgery, GLP-1 rises, insulin sensitivity improves, food preferences shift, and bile acid metabolism changes. The gut barrier tightens, which reduces inflammation. Most striking of all, patients often defend a new, lower body weight afterward, which suggests the whole regulatory system has reset (Stefater et al., Gastroenterology, 2010). Bile acid signaling appears central to that reset, and it holds across procedures (Myronovych et al., Obesity, 2014).

Nutrient signaling changes too. Iron metabolism is altered after surgery, and the change has been linked to HIF-2α signaling pathways that also improve glucose handling and GLP-1 release (Evers et al., Cell Rep, 2022). Adaptations like that are hard to explain with mechanical restriction alone.

The microbiome is another piece. Surgery shifts bacterial composition toward communities associated with healthier metabolism, and barrier function improves alongside it. Molecules like Reg3g strengthen the gut lining, increasing mucus and reducing leakiness, which lowers systemic inflammation and metabolic stress (Shin et al., Cell Metab, 2022).

These insights point toward treatments that skip the operating room. GLP-1 receptor agonists reproduce some of the hormonal effects seen after bypass or sleeve. Bile acid modulators, microbiome therapies, and strategies targeting iron signaling are all under study as ways into the same pathways.

Seen this way, the gut is where the body decides how to use energy, how to balance hormones, and how to regulate immunity. For patients, that science explains why surgery and gut-focused medications can make such a difference. For clinicians, it suggests the most effective treatment plans will be the ones that respect what the gut is actually doing.

Scott Rennie, D.O.

References:

1. Seeley RJ, Chambers AP, Sandoval DA. The role of gut adaptation in the potent effects of multiple bariatric surgeries on obesity and diabetes. Cell Metab. 2015;21(3):369-378. https://pubmed.ncbi.nlm.nih.gov/25662404/

2. Stefater MA, et al. Sleeve gastrectomy induces loss of weight and fat mass in obese rats, but does not affect leptin sensitivity. Gastroenterology. 2010;138(7):2426-2436. https://pubmed.ncbi.nlm.nih.gov/20226189/

3. Myronovych A, et al. Vertical sleeve gastrectomy reduces hepatic steatosis while increasing serum bile acids in a weight-loss-independent manner. Obesity (Silver Spring). 2014;22(2):390-400. https://pubmed.ncbi.nlm.nih.gov/23847068/

4. Evers SS, et al. Cell Rep. 2022;38(11):110487.

5. Shin JH, et al. Cell Metab. 2022;34(5):747-761.e6.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Why Stress Makes You Hungry: The Link to Obesity

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

One of the harder conversations I have with patients carrying overweight and obesity is about stress and eating. People tell me they reach for snacks when they are anxious or exhausted. That part is familiar to everyone. What is less obvious is how thoroughly stress rewrites the biology of appetite, and how far past willpower the problem sits.

Under ordinary circumstances, hunger runs on homeostatic systems responding to real energy needs. Stress shifts that balance toward non-homeostatic eating, meaning eating driven by something other than fuel. Cortisol rises. Brain reward pathways get stimulated. Cravings sharpen for calorie-dense, highly processed food. Over time the pattern feeds visceral fat gain and insulin resistance (Adam & Epel, Physiol Behav, 2007).

The affect regulation model explains the loop. Stress raises negative emotion, anxiety, sadness, tension. Eating reduces those feelings briefly. That behavior can escalate into binge episodes defined by loss of control and large quantities of food, and binge eating then reinforces itself psychologically and biologically (Heatherton & Baumeister, Psychol Bull, 1991; Telch & Agras, Int J Eat Disord, 1996). Cortisol rises further, abdominal fat increases, glucose spikes worsen insulin resistance.

Sleep and physical activity sit on top of this. Poor sleep increases cravings and erodes impulse control. Exercise works the other way, spending energy while lowering stress and improving mood, and patients who increase activity often find cravings less overwhelming. Food type matters too. Ultra-processed products are engineered to be hyper-palatable and push reward systems harder than whole foods do. Sugary drinks and fructose-rich snacks impair satiety and drive fat storage.

Identifying stress eating often starts with a plain question. I ask patients whether they feel they eat more than the people around them, or whether they ever feel out of control around food. Those two questions surface patterns people have struggled to put into words. Catching it early makes everything downstream more effective.

Patients with stress eating or binge eating disorder face additional obstacles. They drop out of weight programs at higher rates, regain faster, and need strategies reaching past diet and exercise. Emotional regulation, awareness of hunger and fullness cues, and methods for reducing stress responses all become part of the treatment rather than adjuncts to it. Emotion regulation deficits are well documented in binge eating disorder specifically (Czaja, Rief & Hilbert, Int J Eat Disord, 2009).

Mindfulness has trial support. The SHINE study found that a mindfulness-based intervention reduced reward-driven eating and improved fasting glucose in adults with obesity, with modest but real weight change and without strict calorie counting (Daubenmier et al., Obesity, 2016; Mason et al., J Behav Med, 2016). Cognitive behavioral therapy is the other well-supported tool, particularly for binge eating disorder. Both give patients skills for managing stress that don’t route through food.

Medication has a role. Lisdexamfetamine is FDA-approved for moderate to severe binge eating disorder. SSRIs and topiramate get used in selected cases. Continuous glucose monitoring has been explored as a way to show patients how binge episodes register physiologically in real time, and the work so far is early and promising rather than established (Presseller et al., Int J Eat Disord, 2024). Bariatric surgery remains an option, though outcomes may be less favorable when binge behaviors haven’t been addressed first.

Stress eating is biology, psychology, and environment colliding in ways that push people toward overeating, and weak discipline explains none of it. Naming it and treating both the triggers and the physiology is what breaks the cycle. Treatment combining stress management, emotional regulation, and behavioral support makes lasting change realistic.

Scott Rennie, D.O.

References:

1. Adam TC, Epel ES. Stress, eating and the reward system. Physiol Behav. 2007;91(4):449-458. https://pubmed.ncbi.nlm.nih.gov/17543357/

2. Heatherton TF, Baumeister RF. Binge eating as escape from self-awareness. Psychol Bull. 1991;110(1):86-108. https://pubmed.ncbi.nlm.nih.gov/1891520/

3. Telch CF, Agras WS. Do emotional states influence binge eating in the obese? Int J Eat Disord. 1996;20(3):271-279. https://pubmed.ncbi.nlm.nih.gov/8912039/

4. Czaja J, Rief W, Hilbert A. Emotion regulation and binge eating in children. Int J Eat Disord. 2009;42(4):356-362. https://pubmed.ncbi.nlm.nih.gov/19040265/

5. Daubenmier J, et al. Effects of a mindfulness-based weight loss intervention in adults with obesity: A randomized clinical trial. Obesity (Silver Spring). 2016;24(4):794-804. https://pubmed.ncbi.nlm.nih.gov/26955895/

6. Mason AE, et al. Effects of a mindfulness-based intervention on mindful eating, sweets consumption, and fasting glucose levels in obese adults. J Behav Med. 2016;39(2):201-213. https://pubmed.ncbi.nlm.nih.gov/26563148/

7. Presseller EK, et al. Using Continuous Glucose Monitoring to Passively Classify Naturalistic Binge Eating and Vomiting Among Adults With Binge-Spectrum Eating Disorders: A Preliminary Investigation. Int J Eat Disord. 2024. https://onlinelibrary.wiley.com/doi/10.1002/eat.24266

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Eating Disorders in People With Obesity: Combining Care

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Working with patients who struggle with obesity, I see how often excess weight and disordered eating overlap. The two get treated as separate problems, sometimes as opposites. Plenty of people live at the intersection, and ignoring that connection makes treatment less effective and occasionally harmful.

Eating disorders are psychiatric conditions in which eating patterns or related behaviors disrupt health or functioning (APA, DSM-5-TR, 2022). They affect people across all ages, genders, and body sizes. The DSM-5-TR describes anorexia nervosa, bulimia nervosa, binge eating disorder, avoidant or restrictive food intake disorder, and others. Each has distinct features. All carry real medical and psychological risk.

Binge eating disorder matters most in this conversation. It is the most common eating disorder in the United States. Patients describe episodes of eating large amounts with a loss of control, followed by guilt, shame, or depression, without the vomiting or other compensatory behaviors seen in bulimia. Lifetime prevalence runs around 0.85% of U.S. adults, with 12-month prevalence near 0.44% (Udo & Grilo, Biol Psychiatry, 2018; Hudson et al., Arch Gen Psychiatry, 2007). Among patients seeking behavioral weight loss treatment, roughly one in ten meet criteria (Chao et al., Obesity, 2017). Among adults presenting for bariatric surgery, meta-analytic estimates using DSM-5 criteria put it near 14% (Hilbert et al., Int J Eat Disord, 2020).

Why does this matter? Untreated binge eating disorder makes weight loss programs harder to sustain. Patients drop out more often, regain faster, and carry higher rates of depression, anxiety, and substance use. The metabolic toll shows up as more diabetes and hypertension. Identifying it early lets us adapt care, often by starting with cognitive behavioral therapy or another evidence-based treatment before any weight loss effort.

Eating disorders leave physical findings, and a fair number of them are visible on a video call. Dry skin, thinning hair, and the fine body hair of anorexia are all things a patient can show on camera. Parotid enlargement in bulimia is visible. Dental enamel erosion isn’t, and neither are the electrolyte abnormalities that matter most, which is where labs and a low threshold for in-person referral come in. Severe cases can develop life-threatening arrhythmias. Binge eating disorder is more often associated with metabolic changes, elevated liver enzymes and worsening insulin resistance. Psychiatric comorbidity is frequent across the whole spectrum, including depression, anxiety, PTSD, and ADHD (Hilbert et al., Psychol Med, 2014).

It is a mistake to think only thin patients have eating disorders. Many patients with obesity have restrictive patterns, obsessive food thoughts, or emotional eating cycles. I have seen patients try extreme diets, binge during periods of stress, then spiral into weight cycling. Others present with nutrient deficiencies despite high calorie intake. Body size rules an eating disorder neither in nor out.

Screening is where this gets caught. The SCOFF questionnaire and the Eating Disorder Screen for Primary Care are short and practical. Even plain questions about body image, eating patterns, or feeling out of control with food will surface problems. When the psychiatric history includes depression, trauma, or substance use, suspicion should go up.

Treatment requires integration. For binge eating disorder, first-line options include cognitive behavioral therapy, interpersonal therapy, and dialectical behavior therapy (Brownley et al., Ann Intern Med, 2016; Grilo et al., Curr Obes Rep, 2023). Lisdexamfetamine, SSRIs, and topiramate help some patients. These approaches reduce binge episodes and rarely produce significant weight loss, which is worth saying to patients directly so nobody is disappointed by a treatment that is working. Obesity care gets layered in once eating behaviors stabilize. Dietitians, primary care, psychiatry, and behavioral health need to be working the same case. Heavy emphasis on BMI or food rules can backfire by reinforcing disordered thinking.

Sequencing depends on the condition. In anorexia, the priority is weight restoration and psychiatric treatment, never weight reduction. For bulimia, obesity treatment waits until binge-purge behaviors are controlled. In binge eating disorder, obesity treatment can follow once episodes are reduced and things are stable. For ARFID, individual assessment guides the approach. In every case the eating disorder comes first while symptoms are active. Starting weight loss treatment too early worsens the disorder, damages trust, and blocks recovery (Mehler et al., J Eat Disord, 2011).

Recognizing that obesity and eating disorders coexist changes how we practice. It moves the focus from weight to whole-person health. Patients need care addressing both the physical and psychological sides, which means helping them repair their relationship with food and body while long-term medical outcomes improve.

Scott Rennie, D.O.

References:

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). 2022.

2. Udo T, Grilo CM. Prevalence and Correlates of DSM-5-Defined Eating Disorders in a Nationally Representative Sample of U.S. Adults. Biol Psychiatry. 2018;84(5):345-354. https://pubmed.ncbi.nlm.nih.gov/29859631/

3. Hudson JI, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2007;61(3):348-358. https://pubmed.ncbi.nlm.nih.gov/16815322/

4. Chao AM, et al. Obesity (Silver Spring). 2017;25(4):713-720.

5. Hilbert A, et al. Meta-analysis on the long-term effectiveness of psychological and medical treatments for binge-eating disorder. Int J Eat Disord. 2020;53(9):1353-1376. https://pubmed.ncbi.nlm.nih.gov/32583527/

6. Hilbert A, et al. Psychol Med. 2014;44(15):3239-3250.

7. Brownley KA, et al. Binge-Eating Disorder in Adults: A Systematic Review and Meta-analysis. Ann Intern Med. 2016;165(6):409-420. https://pubmed.ncbi.nlm.nih.gov/27367316/

8. Grilo CM, et al. Curr Obes Rep. 2023.

9. Mehler PS, et al. J Eat Disord. 2011.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Does Poor Sleep Make You Gain Weight? Sleep and Obesity

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

When we talk about weight management, the conversation centers on diet and exercise. Both are critical. Sleep gets skipped. The research keeps showing it as a major player in metabolism, appetite, and energy balance, and for patients working on weight, the link is worth understanding.

Sleep is a biologic state touching nearly every system. The American Academy of Sleep Medicine and the Sleep Research Society jointly recommend seven or more hours a night for adults, and their consensus statement links shorter sleep to weight gain and obesity among other outcomes (Watson et al., Sleep, 2015). Too little of it throws off hormones, eating patterns, and decision-making around food.

Short sleep tracks consistently with higher obesity risk. In a controlled crossover study, adults restricted to four hours a night for five nights consumed roughly 300 calories more per day than the same people sleeping nine hours, with the excess weighted toward fat and carbohydrate (St-Onge et al., Am J Clin Nutr, 2011). Sleep restriction raises ghrelin, which drives hunger, and lowers leptin, which signals fullness (Spiegel et al., Ann Intern Med, 2004). Patients also snack more often and stretch their eating window across the day (Barragan et al., J Clin Sleep Med, 2023).

Brain imaging helps explain it. After sleep loss, reward centers light up in response to images of calorie-dense food. People report stronger cravings and are willing to pay more for high-calorie options after a single bad night (St-Onge et al., Am J Clin Nutr, 2012; Rihm et al., J Neurosci, 2019). I have seen patients describe exactly this. Their self-control, as they put it, vanishes after a bad night.

Does less sleep burn more calories? Slightly, and it doesn’t help. Insufficient sleep raises total daily energy expenditure by about 5%, roughly 100 calories a day, and participants in that work ate well past the deficit and gained weight (Markwald et al., PNAS, 2013). More hours awake means more hours eating. The net energy balance goes the wrong direction.

Poor sleep also undermines weight loss efforts directly. In a calorie restriction study, participants with short sleep lost more lean mass and less fat than those sleeping adequately (Nedeltcheva et al., Ann Intern Med, 2010). Variable sleep patterns predict weaker weight loss and worse food choices (Papandreou et al., Int J Obes, 2020). Running the other way, a randomized trial extending habitual sleep by just over an hour reduced daily intake by about 270 calories and produced modest weight loss with no diet changes at all (Tasali et al., JAMA Intern Med, 2022). That trial is the one I find most useful with patients, because it asks for something people can actually do.

The practical implication is that sleep is an active part of metabolism rather than optional recovery time. I suggest patients track it alongside food and steps, the same way they might track blood pressure or glucose.

Simple things help. Consistent bed and wake times support circadian rhythm. A cool, dark, quiet room improves quality. Avoiding caffeine, alcohol, or heavy meals before bed makes a measurable difference. When patients wake in the night, I tell them not to lie there clock-watching. Getting up briefly, reading, and returning to bed when sleepy works better. Small adjustments, and they shift the trajectory.

For providers, the take-home is to ask about sleep the way we ask about diet or exercise. For patients, prioritizing it changes appetite, energy, and weight in ways that show up on a scale. Nutrition and activity matter enormously, and without adequate sleep the system is working against both.

Scott Rennie, D.O.

References:

1. Watson NF, et al. Recommended Amount of Sleep for a Healthy Adult: A Joint Consensus Statement of the American Academy of Sleep Medicine and Sleep Research Society. Sleep. 2015;38(6):843-844. https://pubmed.ncbi.nlm.nih.gov/26039963/

2. St-Onge MP, et al. Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals. Am J Clin Nutr. 2011;94(2):410-416. https://pubmed.ncbi.nlm.nih.gov/21715510/

3. Spiegel K, et al. Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med. 2004;141(11):846-850. https://pubmed.ncbi.nlm.nih.gov/15583226/

4. Barragan R, et al. J Clin Sleep Med. 2023;19(10):1785-1794.

5. St-Onge MP, et al. Sleep restriction leads to increased activation of brain regions sensitive to food stimuli. Am J Clin Nutr. 2012;95(4):818-824. https://pubmed.ncbi.nlm.nih.gov/22357722/

6. Rihm JS, et al. J Neurosci. 2019;39(5):888-899.

7. Markwald RR, et al. Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain. Proc Natl Acad Sci USA. 2013;110(14):5695-5700. https://pubmed.ncbi.nlm.nih.gov/23479616/

8. Nedeltcheva AV, et al. Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med. 2010;153(7):435-441. https://pubmed.ncbi.nlm.nih.gov/20921542/

9. Papandreou C, et al. Int J Obes (Lond). 2020;44(6):1279-1285.

10. Tasali E, et al. Effect of Sleep Extension on Objectively Assessed Energy Intake Among Adults With Overweight in Real-life Settings: A Randomized Clinical Trial. JAMA Intern Med. 2022;182(4):365-374. https://pubmed.ncbi.nlm.nih.gov/35129580/

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

New Obesity Drugs Beyond Ozempic and Zepbound Explained

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Obesity treatment is shifting fast. For years the standard toolkit was lifestyle counseling plus a handful of older medications. New drug classes now target the actual biology of the disease: hormonal signaling, metabolic rate, body composition. Three groups matter most right now. Nutrient-stimulated hormone-based therapies. Oral small molecule receptor agonists. And activin receptor pathway inhibitors.

NuSHs mimic or amplify the body’s own hormonal response to food. GLP-1 increases satiety, slows gastric emptying, and supports insulin secretion (Wilding et al., N Engl J Med, 2021). GIP regulates fat metabolism and glucose response (Frías et al., N Engl J Med, 2021). Amylin, co-secreted with insulin, works as its own satiety signal (Dehestani et al., J Obes Metab Syndr, 2021). PYY reduces appetite and energy intake (Schmidt et al., Am J Physiol Endocrinol Metab, 2014). Oxyntomodulin reduces intake too, and also raises energy expenditure (Wynne et al., Int J Obes, 2006).

Several drugs in this class are already in trials, and CagriSema pairs an amylin analogue with a GLP-1 receptor agonist, reducing body weight by 17.1 percent in 20 weeks in a Phase 1b trial, not Phase 3 (Enebo et al., Lancet, 2021). Survodutide, a GLP-1 and glucagon receptor agonist, produced weight loss of up to 18.7 percent over 46 weeks (Le Roux et al., Lancet Diabetes Endocrinol, 2024). Retatrutide, which hits GIP, GLP-1, and glucagon receptors together, produced a 24.2 percent reduction over 48 weeks in Phase 2 testing. Women lost about 28.5 percent of body weight, men about 21.9 percent (Jastreboff et al., N Engl J Med, 2023). Oral semaglutide at 50 mg reached 17.4 percent weight loss at 68 weeks, with 37 percent of participants losing more than a fifth of their body weight (Knop et al., Lancet, 2023). Mari-tide is still in Phase 2, with promising early results.

Small molecule receptor agonists are the other track, and their edge is simple: a pill instead of a needle. Orforglipron produced about 14.7 percent weight loss at 36 weeks, in range with the injectables (Wharton et al., N Engl J Med, 2023). Danuglipron is behind it. Early Phase 2 data, in patients with type 2 diabetes rather than obesity specifically, showed reduced appetite alongside improved glucose and weight outcomes (Saxena et al., Diabetes Obes Metab, 2023). Whether that holds up in an obesity-only population is still unclear.

Activin receptor pathway inhibitors take a different approach. They target pathways that preserve muscle while fat comes off, since traditional weight loss burns muscle right along with fat. These drugs try to change that ratio (Heymsfield et al., JAMA Netw Open, 2021).

Bimagrumab, a monoclonal antibody that blocks the activin type II receptor, reduced fat mass by 20.5 percent while increasing lean mass by 3.6 percent over 48 weeks in trials. Combine it with a GLP-1 drug like semaglutide or tirzepatide and the body-composition effect gets stronger still. Taldefgrobep, a myostatin inhibitor originally developed for Duchenne muscular dystrophy, is now being tested for obesity. SRK-439 is another myostatin-targeting antibody in development, aimed at fat loss without the lean-mass cost.

What sets these treatments apart is what the weight loss is made of: more muscle retained, metabolic markers that move too, alongside the pounds lost. That’s a real shift, for patients who may get more durable results and fewer complications, and for clinicians who get more tools to match therapy to the person in front of them.

Scott Rennie, D.O.

References:

Wilding JPH, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384:989-1002. PMID 33567185. https://pubmed.ncbi.nlm.nih.gov/33567185/

Frías JP, et al. Tirzepatide versus Semaglutide Once Weekly in Patients with Type 2 Diabetes (SURPASS-2). N Engl J Med. 2021. PMID 34170647. https://pubmed.ncbi.nlm.nih.gov/34170647/

Dehestani B, Stratford NR, le Roux CW. Amylin as a Future Obesity Treatment. J Obes Metab Syndr. 2021;30(4):320-325. PMID 34929674. https://pubmed.ncbi.nlm.nih.gov/34929674/

Schmidt JB, Gregersen NT, Pedersen SD, et al. Effects of PYY3-36 and GLP-1 on energy intake, energy expenditure, and appetite in overweight men. Am J Physiol Endocrinol Metab. 2014;306(11):E1248-56. PMID 24735885. https://pubmed.ncbi.nlm.nih.gov/24735885/

Wynne K, Park AJ, Small CJ, et al. Oxyntomodulin increases energy expenditure in addition to decreasing energy intake in overweight and obese humans: a randomised controlled trial. Int J Obes (Lond). 2006;30(12):1729-1736. PMID 16619056. https://pubmed.ncbi.nlm.nih.gov/16619056/

Enebo LB, Berthelsen KK, Kankam M, et al. Lancet. 2021;397:1736-1748. Phase 1b trial. PMID 33894838. https://pubmed.ncbi.nlm.nih.gov/33894838/

Le Roux CW, et al. Lancet Diabetes Endocrinol. 2024;12:162-173. PMID 38330987. https://pubmed.ncbi.nlm.nih.gov/38330987/

Jastreboff AM, et al. N Engl J Med. 2023;389:514-526. PMID 37366315. https://pubmed.ncbi.nlm.nih.gov/37366315/

Knop FK, et al. Lancet. 2023 (OASIS 1). PMID 37385278. https://pubmed.ncbi.nlm.nih.gov/37385278/

Wharton S, Blevins T, Connery L, et al. N Engl J Med. 2023;389:877-888. PMID 37351564. https://pubmed.ncbi.nlm.nih.gov/37351564/

Saxena AR, Frias JP, Brown LS, et al. Tolerability, safety and pharmacodynamics of oral, small-molecule GLP-1 receptor agonist danuglipron for type 2 diabetes. Diabetes Obes Metab. 2023. PMID 37311722. https://pubmed.ncbi.nlm.nih.gov/37311722/

Heymsfield SB, Coleman LA, Miller R, et al. Effect of Bimagrumab vs Placebo on Body Fat Mass Among Adults With Type 2 Diabetes and Obesity. JAMA Netw Open. 2021;4(1):e2033457. PMID 33439265. https://pubmed.ncbi.nlm.nih.gov/33439265/

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Why Is Losing Weight and Keeping It Off So Hard?

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

As a physician, one of the most common questions I hear from patients is, “Why is it so hard to lose weight and keep it off?” The answer sits in how the body protects its energy stores. What once kept humans alive through scarcity now works against us, in a world of constant food access. The brain runs this system. Understanding its role is where treatment has to start.

Fat storage was never a flaw. Our biology stores energy as fat because that protected our ancestors when food access was unpredictable. Without it, surviving famine would have been unlikely (Schwartz et al., Endocr Rev, 2017).

The brain monitors and regulates fat mass much like a thermostat, a concept called the defended fat mass, or set point, and when fat stores rise, the brain senses the change through hormones like leptin and insulin and responds by increasing energy use while dialing down appetite. When fat stores fall, the brain reads that as a threat. It lowers energy use and ramps up hunger to rebuild the reserve.

That’s why weight loss so often gets followed by regain. The body works to hold on to defended fat mass, and it works at it actively (Rosenbaum & Leibel, Int J Obes, 2010).

The trouble is that our environment no longer matches our biology. Calorie-dense processed food, disrupted sleep, chronic stress, and sedentary living push fat mass higher than what was historically defended. Over time, this reset drives obesity at the population level (Hall & Guo, Gastroenterology, 2017).

Obesity is best understood as a neurometabolic disease. The body does exactly what it was built to do here: protect its energy reserves. In the modern world, though, that defense turns harmful, raising the risk of diabetes, cardiovascular disease, and hypertension (Heymsfield & Wadden, N Engl J Med, 2017).

The real goal of treatment is to recalibrate the defended fat mass. When the brain adapts to a lower set point, weight loss follows without a running fight against hunger.

This is where medications enter. Phentermine reduces appetite by stimulating the nervous system. Topiramate cuts cravings and helps stabilize mood. Bupropion/naltrexone targets reward pathways to blunt food cravings. Liraglutide, a GLP-1 receptor agonist, increases satiety and slows digestion. Newer agents, semaglutide and tirzepatide chief among them, are highly effective GLP-1 receptor agonists that produce sustained weight loss (Wilding et al., N Engl J Med, 2021).

Not every medication works on the brain. Orlistat blocks fat absorption in the gut. It helps some patients, but it doesn’t touch defended fat mass, which caps its long-term effect (Yanovski & Yanovski, JAMA, 2014).

The core point: weight regulation is hardwired. Not chosen. Patients live inside a system where the brain works hard to preserve fat stores. Treatments that respect that biology work better than the ones that ignore it.

Scott Rennie, D.O.

References:

Hall KD, Guo J. Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition. Gastroenterology. 2017;152(7):1718-1727. PMID 28193517. https://pubmed.ncbi.nlm.nih.gov/28193517/

Heymsfield SB, Wadden TA. Mechanisms, Pathophysiology, and Management of Obesity. N Engl J Med. 2017;376:254-266. PMID 28402780. https://pubmed.ncbi.nlm.nih.gov/28402780/

Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes (Lond). 2010;34 Suppl 1:S47-55. PMID 20935667. https://pubmed.ncbi.nlm.nih.gov/20935667/

Schwartz MW, et al. Obesity Pathogenesis: An Endocrine Society Scientific Statement. Endocr Rev. 2017;38:267-296. PMID 28898979. https://pubmed.ncbi.nlm.nih.gov/28898979/

Wilding JPH, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384:989-1002. PMID 33567185. https://pubmed.ncbi.nlm.nih.gov/33567185/

Yanovski SZ, Yanovski JA. Long-term Drug Treatment for Obesity: A Systematic and Clinical Review. JAMA. 2014;311:74-86. PMID 24231879. https://pubmed.ncbi.nlm.nih.gov/24231879/

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Which Medications Can Make Weight Loss Harder?

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

As a physician, I often meet patients who are discouraged by weight gain that doesn’t seem to make sense. They may be eating well, exercising regularly, and still the scale keeps moving up. Lifestyle choices matter a great deal. Medications and supplements can matter just as much, and knowing which ones affect weight is worth raising with your own doctor, because the cause can be hiding in plain sight.

Certain prescriptions are known to promote weight gain. Diabetes medications are a good example: insulin, sulfonylureas like glipizide, and thiazolidinediones like pioglitazone often push weight up. Metformin, GLP-1 receptor agonists like semaglutide, and SGLT-2 inhibitors tend to do the opposite and help with weight control.

I’ve also seen this pattern with antidepressants. Drugs like escitalopram, citalopram, or paroxetine can add pounds, as can tricyclics such as amitriptyline. Even trazodone or mirtazapine carry this risk. For some patients, switching to bupropion, fluoxetine, or sertraline makes a noticeable difference.

Atypical antipsychotics are another tricky class. Olanzapine, risperidone, and quetiapine are all associated with weight gain, while ziprasidone tends to have less impact. Anti-epileptic drugs split the same way. Same pattern, different receptors. Valproic acid and gabapentin tend to increase weight; topiramate and lamotrigine usually don’t.

Even medications outside psychiatry and neurology come up in this discussion. Lithium, commonly used as a mood stabilizer, often causes weight gain, and so do glucocorticoids like prednisone, especially with longer courses. Beta blockers such as metoprolol and propranolol carry the same issue, carvedilol usually has less effect, and antihistamines like diphenhydramine or cetirizine can shift weight too, though loratadine tends not to, which is worth remembering the next time an allergy prescription gets refilled without a second thought. Hormonal contraception adds another layer: depo-medroxyprogesterone is linked to weight gain, which can be genuinely frustrating for patients who are otherwise doing everything right. Non-hormonal methods are an option worth raising.

Over-the-counter medications and supplements belong in this conversation too, right alongside anything prescribed. Chronic antihistamine use may interfere with appetite regulation. Proton pump inhibitors, like omeprazole, can indirectly affect weight through changes in gut microbiota. Long-term NSAID use may lead to water retention. Some “energy” or “muscle gain” supplements hide hormones or steroids that work against weight control entirely.

This is why reviewing medications matters so much in a weight conversation. Weight gain gets blamed entirely on diet or activity when the real trigger may be sitting in the pillbox. Of course, no one should stop a medication on their own. Sometimes the benefit outweighs the side effect. Sometimes there’s a safer alternative that gets the same result without the tradeoff.

Bringing medications into the conversation gives us a fuller picture. It lets us make thoughtful adjustments while still focusing on lifestyle. It’s about tailoring a plan that actually supports long-term health, one a patient can live inside for years.

Scott Rennie, D.O.

Sources:

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

How Should Parents Limit a Child’s Food? Finding Balance

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

As a physician, I’ve seen how difficult it can be for families to set healthy eating patterns for their kids. Parents often ask me how to keep children from eating too much junk food without turning it into a daily battle. Research points to two main strategies: overt restriction and covert restriction. How they play out at home differs enormously.

Overt restriction is the one most people think of first. It’s when a parent sets clear rules like “No candy after dinner” or “You can only have one cookie.” Simple, on paper. In practice it often backfires: studies show that when kids are told they can’t have a certain food, that food becomes more appealing, and they get curious and start craving it more. I’ve had parents tell me that their child, once away from home, goes overboard on the very foods that were restricted. The literature backs this up, linking overt restriction to a higher risk of overeating and weight gain once children get access on their own (Ogden J, Reynolds R, Smith A. Appetite. 2006;47:100-106).

Covert restriction works differently. It doesn’t rely on direct rules; instead it shapes the environment. A parent might stock the pantry with fruits and vegetables, limit the chips and sweets that come into the house, and skip the frequent fast-food runs, so the child never feels denied anything even though the choices available are quietly healthier than they’d otherwise be. Research suggests this method reduces cravings and lowers the pull of high-sugar, high-fat foods (Boots SB, Tiggemann M, Corsini N. Appetite. 2019;135:54-60).

Between the two, covert restriction seems to have the better long-term track record. When the home is set up so the easiest option is also the healthiest, children develop preferences that last. That said, overt restriction isn’t always avoidable, since food allergies, medical diets, or severe obesity can make firm rules necessary. When that happens, pairing restriction with positive reinforcement and supportive communication limits the damage.

Another useful approach I’ve seen is what some call a junk food budget. Parents allow a set number of treats each week, maybe two or three small items, and the child decides when to spend them. Once they’re gone, that’s it until the following week. This gives kids some autonomy and teaches self-regulation. Research suggests it helps prevent binge eating or overvaluing restricted foods later in life (Ogden J, Reynolds R, Smith A. Appetite. 2006;47:100-106). Parents often tell me it lowers family conflict too.

The big picture: food habits are shaped more by environment and tone than by rigid control. When families make healthy foods visible and easy to reach, involve kids in cooking, and give them some freedom to manage their own indulgences, the results are usually better. For providers, guiding parents toward motivational interviewing, and helping them balance overt and covert strategies, supports healthier eating without adding to the power struggles.

Scott Rennie, D.O.

Sources:

  • 1. Ogden J, Reynolds R, Smith A. Expanding the concept of parental control: a role for overt and covert control in children’s snacking behaviour? Appetite. 2006;47(1):100-106. https://pubmed.ncbi.nlm.nih.gov/16682098/
  • 2. Boots SB, Tiggemann M, Corsini N. Pumpkin is “yucky”: correlates of avoidant/restrictive food intake in preschool children and their mothers. Appetite. 2019;135:54-60. https://pubmed.ncbi.nlm.nih.gov/30599153/

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.