Tag: obesity

Digital scale showing weight comparison of green and purple capsules in milligrams

Foundayo vs. the Wegovy Pill: Comparing the Two New Weight Loss Pills

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

For years, if you asked me “is there a pill version of these weight-loss drugs?”, the honest answer was no, not really. That changed twice in the past eight months. If you haven’t been following the news closely, the options today look very different than they did just a year ago.

A quick note on names first, since patients ask me this a lot. The Lilly drug some people have heard called “Fonday-o” is actually called orforglipron. Its brand name is official now, not a guess. The FDA approved it on April 1, 2026, under the brand name Foundayo. Before that, on December 22, 2025, the FDA approved a 25 mg oral semaglutide tablet under the Wegovy name. GLP-1 medicines help control appetite and blood sugar, and this was the first pill version of one approved for long-term weight management. Both pills are real, both are approved, and both can be prescribed today.

Why the two pills work so differently in your body

Semaglutide is a peptide, which is a small chain of amino acids, the building blocks of proteins. Your stomach is very good at breaking down peptides, which is exactly why semaglutide originally had to be given as a shot instead of a pill.

Novo Nordisk’s solution was to add an ingredient called SNAC that helps the drug get absorbed before your stomach destroys it. According to a review in the medical journal Clinical Diabetes, SNAC does three things at once. It changes the local acidity around the tablet as it dissolves, it briefly protects the drug from a stomach enzyme called pepsin that would otherwise break it down, and it helps the drug pass through the stomach lining into your bloodstream. This absorption happens in the stomach itself, not the intestines, which is unusual for a pill. The drug essentially enters your body right where the tablet is sitting against your stomach wall.

That clever trick comes with a catch. You have to take oral semaglutide on an empty stomach with no more than about four ounces of plain water, and you can’t eat or drink anything else, including coffee or other medications like thyroid pills, for at least 30 minutes afterward. Taking it too close to breakfast or your other pills can reduce how much of the drug actually gets into your system. This isn’t a small detail. It can be the difference between the medicine working well and not working at all.

Orforglipron works completely differently. It’s what’s called a small molecule, meaning it’s a simple, stable chemical rather than a fragile peptide chain. It belongs to the same family of drugs as semaglutide. GLP-1 receptor agonists mimic a natural gut hormone that reduces appetite, and because orforglipron has no peptide to protect, it doesn’t need any special absorption booster and doesn’t come with a strict timing routine. Lilly describes it as the only GLP-1 weight-loss pill you can take at any time of day, with or without food or water. In real life, that means someone who works night shifts, or who already takes six other pills each morning, doesn’t need a complicated schedule to make it work.

What the study results actually show

Here’s where I want you to slow down before drawing conclusions, because it’s easy to misread these numbers.

In a 64-week study called OASIS 4, which tested the drug in 307 adults with obesity or being overweight who did not have diabetes, oral semaglutide 25 mg led to about 17% average weight loss in people who stayed on the medicine the whole time, compared with about 3% for those taking a placebo (an inactive pill used for comparison). When you count everyone in the study, including people who stopped early, the numbers were about 14% versus 2%. Seventy-six percent of people lost at least 5% of their body weight, compared with 31% on placebo.

In a separate study called ATTAIN-1, published in the New England Journal of Medicine, orforglipron was tested at three different doses (low, medium, and high) over 72 weeks. Average weight loss was 7.8%, 9.3%, and 12.4% at those doses, compared with 2.1% on placebo. At the highest dose tested in the trial, 36% of people lost 15% or more of their body weight, and 18.4% lost 20% or more, compared with 5.9% and 2.8% on placebo.

If you compare those numbers side by side, it looks like semaglutide wins, and I don’t think that comparison holds up. These are two separate studies, different patients, different lengths of time, different ways of measuring results, and nobody has run them head-to-head in the same people at the same time. What I can say confidently is that both pills produce weight loss that’s meaningful and far beyond anything we had in pill form before 2025.

One more detail worth knowing, because it can be confusing if you read news coverage of the studies. The doses of Foundayo that actually got approved are 0.8, 2.5, 5.5, 9, 14.5, and 17.2 mg, and your doctor increases your dose gradually, about every 30 days. Those numbers are different from the 6, 12, and 36 mg doses mentioned in the New England Journal of Medicine study. That’s because the trial used a different capsule formula than the one that ended up on the market. The 17.2 mg tablet you can actually get prescribed is equivalent to the 36 mg dose used in the trial. So if you notice your maximum dose sounds much smaller than what you saw in the news, that’s why.

Side effects

Both drugs work in a similar way in the body, and both come with similar side effects: nausea, vomiting, diarrhea, and constipation.

The ATTAIN-1 study reported specific numbers for orforglipron. Nausea occurred in 28.9% to 35.9% of people across the different doses, compared with 10.4% on placebo. Constipation occurred in 21.7% to 29.8%, versus 9.3% on placebo. Vomiting occurred in 13.0% to 24.0%, versus 3.5% on placebo. The number of people who stopped taking the drug because of side effects went up with higher doses, from 5.3% at the lowest dose to 10.3% at the highest, compared with 2.7% on placebo. Most side effects were mild to moderate.

Novo Nordisk reported that oral semaglutide’s side effects looked similar to what we already know from the injectable version of semaglutide, including the same warnings about pancreas inflammation, gallbladder problems, and allergic reactions. If you’ve taken injectable semaglutide before, this side effect pattern will likely feel familiar.

How I think about choosing between them

If you’re already doing well on injectable semaglutide and want to get away from needles, the oral tablet is the more natural next step. It’s the same active medicine, has a familiar side effect pattern, and carries the same approved benefit for heart health in people with existing heart disease.

If your biggest obstacle is fitting a medicine into a busy or unpredictable schedule, orforglipron tends to be more forgiving. That 30-minute waiting period for oral semaglutide sounds minor when we talk it through on a video visit, but in real life it trips people up. I’ve seen patients struggle with oral semaglutide not because it didn’t work, but because busy weekday mornings made it hard to follow the timing rules.

Cost is the third thing to consider, and it’s changing quickly. Novo Nordisk launched the 1.5 mg starting dose at $149 per month, with savings programs available. Lilly is offering self-pay pricing through its LillyDirect program, with commercially insured patients paying as little as $25 per month, and some Medicare Part D patients paying $50 starting as soon as July 1, 2026. These programs get updated often, so it’s worth checking the current terms before assuming a specific price applies to you. I haven’t run into a prior-authorization fight or a stocking problem with Foundayo yet. Most of what I prescribe goes through LillyDirect, cash pay, because it’s one of the cheaper options on the table. Patients who have insurance coverage tend to ask for injectable Wegovy or Zepbound instead.

We finally have two pill options, and each one tends to fail for a different reason, whether that’s the timing rules or something else. Figuring out which failure point matters most for your life is really the key to choosing the right one.

Scott Rennie, D.O.

Sources

FDA approves Novo Nordisk’s Wegovy pill, the first and only oral GLP-1 for weight loss in adults (PR Newswire): https://www.prnewswire.com/news-releases/fda-approves-novo-nordisks-wegovy-pill-the-first-and-only-oral-glp-1-for-weight-loss-in-adults-302648344.html
FDA Approves Oral Semaglutide as First GLP-1 Pill for Weight Loss (AJMC): https://www.ajmc.com/view/fda-approves-oral-semaglutide-as-first-glp-1-pill-for-weight-loss
Current Understanding of SNAC as an Absorption Enhancer: The Oral Semaglutide Experience (Clinical Diabetes, ADA): https://diabetesjournals.org/clinical/article/42/1/74/153538/Current-Understanding-of-Sodium-N-8-2
FDA approves Lilly’s Foundayo (orforglipron) (Eli Lilly investor release): https://investor.lilly.com/news-releases/news-release-details/fda-approves-lillys-foundayotm-orforglipron-only-glp-1-pill
FDA Approves First New Molecular Entity Under National Priority Voucher Program (FDA): https://www.fda.gov/news-events/press-announcements/fda-approves-first-new-molecular-entity-under-national-priority-voucher-program
Orforglipron, an Oral Small-Molecule GLP-1 Receptor Agonist for Obesity Treatment (New England Journal of Medicine, ATTAIN-1): https://www.nejm.org/doi/full/10.1056/NEJMoa2511774
Complete ATTAIN-1 results published in NEJM (Eli Lilly): https://lilly.gcs-web.com/news-releases/news-release-details/lillys-oral-glp-1-orforglipron-demonstrated-meaningful-weight
FOUNDAYO (orforglipron) tablets, US prescribing information (FDA): https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/220934Orig1s000lbl.pdf
Approved dosing for Foundayo for weight management (Lilly Medical): https://medical.lilly.com/us/products/answers/what-is-the-approved-dosing-for-foundayo-orforglipron-for-weight-management-320858
Foundayo now available in the U.S. (Eli Lilly investor release): https://investor.lilly.com/news-releases/news-release-details/foundayotm-orforglipron-lillys-new-oral-glp-1-pill-weight-loss

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.

Binge Eating Disorder Signs and Treatment in Adults and Kids

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

Binge Eating Disorder, or BED, is one of the eating disorders I screen for most often in practice. Clinicians define it as repeated episodes of eating a large amount of food in a short period of time while feeling a loss of control during the episode. BED involves episodes that feel compulsive: the person cannot stop eating even when full or uncomfortable. This goes well beyond a second helping at dinner or an indulgent dessert.

The diagnostic criteria for BED require both that large amounts of food are consumed in a discrete time frame and that there is a sense of loss of control while eating. The episodes are also linked to behaviors such as eating more rapidly than normal, eating until uncomfortably full, eating when not hungry, eating alone because of embarrassment, and feeling disgusted or guilty afterward. At least three of those behaviors must be present. The episodes need to occur at least once a week for three months, cause distress, and they are not followed by purging behaviors like in bulimia.

Here’s a hypothetical that illustrates the pattern: someone sits down in the evening and works through an entire pizza and a half-gallon of ice cream in under two hours, not from hunger but because they can’t stop. They feel physically ill afterward. Ashamed, too. The cycle repeats weekly or more often. I’ve seen a real version of this on video visits. One of my patients was managing things with intermittent fasting, and it worked in the sense that the scale moved, but every time the eating window opened back up, they took in way more calories than they needed. The fast itself was setting up the binge.

Children complicate this picture. For kids under 12, researchers have proposed a related diagnosis called Loss of Control Eating Disorder, or LOC-ED (Tanofsky-Kraff et al., 2008). The issue is that children may not consume amounts of food that adults would consider objectively large, but they still experience the same loss of control. In this group, the definition focuses on the subjective sense of being unable to stop eating. The proposed criteria mirror those of BED but apply specifically to children younger than 12. The episodes still need to happen at least once a week for three months and cause distress.

Picture a hypothetical case in pediatrics: a 10-year-old who sneaks into the kitchen at night, eats snack foods quickly, and can’t stop once started. The amount might look modest by adult standards. For a child, it’s significant. What matters is the loss of control, not the portion size. Wrappers hidden in the trash. A refusal to eat breakfast the next morning. Those are often the only clues a parent gets.

Treatment is available for both BED and LOC-ED. For adults with BED, the most evidence supports cognitive behavioral therapy, which helps patients identify triggers, restructure eating patterns, and address guilt and shame. Interpersonal therapy has also been shown to help, especially when social stress is a driver. Some patients benefit from medications. SSRIs have modest benefit for binge frequency, and lisdexamfetamine is the only medication currently approved by the FDA for BED in adults. Nutritional counseling and structured meal planning are usually part of the approach.

I should be direct about where I actually fit into this picture. I don’t manage BED treatment myself. Real treatment leans heavily on behavioral health, and in my current telemedicine positions I don’t have the coordination with a therapist or eating-disorder specialist that this really requires. What I do is screen for it on video visits: ask the direct questions, name what I’m seeing, and refer out from there.

For children with LOC-ED, treatment recommendations are less formalized since the diagnosis itself is still considered research-based. The focus is often on family-based behavioral therapy, involving parents in setting up structured eating schedules and reducing situations where loss of control is most likely to occur. Addressing mood or anxiety symptoms is important, since these are often linked to eating episodes. Nutrition support is also key, both for the child and for parents trying to guide food choices. Medications are not first-line in children.

Recognizing BED or LOC-ED is important because both conditions are linked to higher rates of obesity, depression, and medical complications if untreated. Many people don’t come forward because of shame or because they don’t realize their pattern is a diagnosable disorder. Asking direct questions about eating behaviors, especially around loss of control, can uncover these conditions and open the door to treatment.

If this description fits you or someone you know, talk with a healthcare provider. Early recognition, especially in children, can change the trajectory and reduce the risk of chronic problems.

Scott Rennie, D.O.
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.

References:

Allison KC, Tarves EP. Treatment of night eating syndrome. Psychiatr Clin North Am. 2011;34(4):785-796. doi:10.1016/j.psc.2011.08.002

McCuen-Wurst C, Ruggieri M, Allison KC. Disordered eating and obesity: associations between binge-eating disorder, night-eating syndrome, and weight-related comorbidities. Ann N Y Acad Sci. 2018 Jan;1411(1):96-105. doi: 10.1111/nyas.13467. PMID: 29044551; PMCID: PMC5788730

Tanofsky-Kraff M, Marcus MD, Yanovski SZ, Yanovski JA. Loss of control eating disorder in children age 12 years and younger: proposed research criteria. Eat Behav. 2008;9(3):360-365. doi:10.1016/j.eatbeh.2008.03.001

Why Do I Eat at Night? Night Eating Syndrome Explained

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

Night Eating Syndrome (NES) is one of those conditions that many patients, and even some clinicians, overlook. NES is a recognizable eating disorder where the timing of food intake shifts into the evening and nighttime hours, distinct from occasional snacking after dinner. Patients often feel embarrassed and dismiss it as a bad habit. It has real consequences for weight, sleep, and overall health.

The diagnosis of NES is based on established criteria. To meet the definition, at least 25 percent of daily food intake occurs after the evening meal or there are at least two episodes of nocturnal eating per week. These episodes are not explained by social or cultural norms. People with NES are aware of what they are eating at night, unlike sleep-related eating disorders where the behavior may happen without recall. The condition also needs to cause significant distress or impairment in functioning (Allison & Tarves, 2011).

In practice, this can look two different ways. Some patients skip breakfast, eat a small lunch, and end up consuming half their calories after dinner. Others wake almost every night around 1 or 2 a.m., head to the kitchen, and eat before they can fall back asleep. Over time, the pattern disrupts sleep and drives weight gain.

NES also overlaps with mood and sleep disorders. Patients often report insomnia, depression, or evening stress. Eating becomes a way to cope with anxiety or to induce sleep. That’s why treatment has to be more than calorie restriction. Cognitive behavioral therapy focused on both eating and sleep habits has shown promise, and selective serotonin reuptake inhibitors (SSRIs) have been helpful in some patients (Allison & Tarves, 2011). I prefer CBT-I, but in practice medications often end up being what gets prescribed. I don’t treat night eating syndrome myself. I screen for it before prescribing weight loss medications, then refer out.

The tie between NES and obesity is important. McCuen-Wurst and colleagues (2018) have shown that NES is associated with higher rates of metabolic problems such as type 2 diabetes and hypertension. Timing matters. Eating late into the night throws off circadian rhythms and glucose metabolism, so the impact is greater than just extra calories.

On a video visit, NES surfaces only if you ask about it directly. Within the past six months, one patient told me, “I can’t sleep unless I eat something at midnight.” That single line was the diagnosis: Night Eating Syndrome. We had her follow up with behavioral health.

Treatment is best when it’s individualized. Weight loss alone won’t fix NES if the underlying behaviors and triggers aren’t addressed. Collaboration between primary care, psychiatry, nutrition, and sleep medicine can make a real difference. For colleagues, the key is asking when patients eat as closely as how much. For patients, understanding that this is a recognized condition with treatment options can take away some of the shame and open the door to better care.

Scott Rennie, D.O.
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.

References:

Allison KC, Tarves EP. Treatment of night eating syndrome. Psychiatr Clin North Am. 2011;34(4):785-796. doi:10.1016/j.psc.2011.08.002

McCuen-Wurst C, Ruggieri M, Allison KC. Disordered eating and obesity: associations between binge-eating disorder, night-eating syndrome, and weight-related comorbidities. Ann N Y Acad Sci. 2018 Jan;1411(1):96-105. doi: 10.1111/nyas.13467. Epub 2017 Oct 16. PMID: 29044551; PMCID: PMC5788730

Does Chronic Stress Cause Weight Gain? A Doctor Explains

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

Obesity gets described as a balance of diet and exercise, and stress plays a far larger role in it than most people are told. I have seen patients who eat well and stay active and still lose ground the moment their stress rises. Research from Dr. Rajita Sinha at Yale explains a good deal of why. Chronic stress produces measurable biological change, well past anything you would call a mood.

Stress acts on the brain circuits governing emotion, motivation, and self-control. Those circuits overlap with the ones handling food reward and craving, particularly for calorie-dense processed food (Sinha et al., 2022). Cortisol climbs under chronic stress. Ghrelin rises with it while leptin falls. What you end up with is a body primed to eat more, in an environment where high-calorie food is always within reach.

Calling that emotional eating undersells it. In Sinha’s lab work, people exposed to stress through guided imagery ate more snack food afterward, and participants who were already overweight were the most affected. Their cravings and calorie intake tracked with measured increases in cortisol and ghrelin. The stress reached past how they felt and changed how their brains and bodies handled food.

The pandemic ran this experiment at national scale. Nearly half of U.S. adults gained weight over that period, with worse effects among people who already had higher BMIs (Khubchandani et al., 2022). Children were not spared; CDC data showed the rate of BMI increase doubling against pre-pandemic years (Lange et al., 2021). The predictors of gain were emotional distress, having children at home, and how long it had been since someone last weighed themselves.

Work outside the pandemic points the same way. In one community study, people with higher baseline cortisol and greater insulin resistance were more likely to gain weight over the following six months (Chao et al., 2017). Those markers did more than correlate with obesity. They predicted it.

That has pushed researchers past the eat-less-move-more framing toward treatments aimed at the stress itself. Mindfulness-based stress reduction lowers food cravings, perceived stress, and blood pressure in people with obesity (Tuit et al., 2011). There is even evidence in parenting: a small study of low-income mothers found mindful parenting reduced parental stress and was associated with healthier BMI outcomes in their children (Jastreboff et al., 2018).

Medical and surgical treatment still matter, and the evidence suggests they perform best alongside strategies that reduce stress reactivity and support executive function. Stress management belongs in the treatment plan rather than tacked onto the end of it.

I have seen patients who feel defeated because they are certain the weight they gained under stress was a personal failure. The science says otherwise. Stress reshapes brain pathways, moves hormone levels, and changes eating behavior in ways we can measure. None of that makes change impossible. It does mean compassion is not optional in this conversation, and that treating stress as part of the disease moves the discussion off blame and onto something we can actually act on.

Scott Rennie, D.O.

References

Sinha R. Chronic Stress and Obesity. Yale School of Medicine, Columbia Obesity ABOM Virtual Course, 2022.

Chao A et al. High Cortisol and Insulin Resistance Predict Weight Gain. Obesity. 2017.

Khubchandani J et al. Depression and Anxiety Predict Weight Gain During the COVID-19 Pandemic. Diabetes & Metabolic Syndrome. 2022.

Lange SJ et al. Body Mass Index Increase in Children During COVID-19. MMWR Morb Mortal Wkly Rep. 2021.

Tuit K et al. Mindfulness and Stress Reduction in Obesity. Appetite. 2011.

Jastreboff AM et al. Mindful Parenting and Childhood Obesity Prevention. Journal of Pediatrics. 2018.

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 Parents Influence a Child’s Weight and Eating

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

Childhood obesity has little to do with a child’s willpower. Biology, environment, and daily routine shape it. Genetics matter. So does the household, and that is where parents hold real leverage: how they feed, how they structure the day, what they model.

None of what follows is about blame. It is about where the leverage actually sits.

The clearest example starts in infancy. Responsive feeding means reading hunger and fullness cues instead of pressuring or ignoring them, and it has been linked to healthier eating patterns and weight gain matched to a child’s needs (Ventura, Adv Nutr, 2017). A parent who notices a baby turning away from the bottle and respects that signal is teaching self-regulation. The “clean your plate” approach many of us grew up with does the opposite. It overrides the signal and sets up overeating later (Johnson & Birch, Pediatrics, 1994).

Breastfeeding is where the popular version of this claim outruns the evidence. Observational studies associate exclusive and longer breastfeeding with lower obesity risk, with reductions sometimes quoted around 24%. The review most often cited for that number argues the observational literature is heavily confounded by socioeconomic status, maternal weight, and the feeding practices that travel alongside breastfeeding, and that randomized and sibling-comparison designs show a far weaker effect (Woo & Martin, Curr Obes Rep, 2015). Breastfeeding is worth supporting on its own merits. Promising parents it will prevent obesity goes past what the data support.

Parents also teach by example. A child who regularly sees a parent eating vegetables or trying something unfamiliar is more likely to do it. Repeated exposure paired with parental modeling makes children more willing to accept foods they would otherwise refuse. Using food as a reward runs the other way. Saying “you can have dessert if you eat your broccoli” teaches a child that sweets are the prize and broccoli is the toll (Newman & Taylor, J Exp Child Psychol, 1992).

The home environment does quiet work. Fruit and vegetables visible and easy to grab, energy-dense snacks harder to reach, and children drift toward the better option without a rule being enforced. Family meals matter too. The link to diet quality is consistent even where the direct effect on weight is murkier. They add structure and cut down on distracted eating.

Sleep and activity belong in the same conversation. Short sleep and heavy screen time in early childhood both raise obesity risk. Parents who hold bedtimes, encourage active play, and set limits on screens are shaping energy balance in ordinary daily ways.

Some strategies backfire. Restriction is the main one. In a well-known experiment, restricting children’s access to a particular snack increased both their desire for it and how much they ate when it became available, compared with an unrestricted food (Fisher & Birch, Appetite, 1999). Using food to soothe emotion has a similar problem. It builds an association between eating and comfort that persists into adult life.

Genetics play their part. Some children are more sensitive to food cues and less attuned to satiety, and twin studies put real numbers on that heritability (Wardle, Carnell & Plomin, Am J Clin Nutr, 2008). Even so, a supportive home makes a measurable difference in children carrying that predisposition. Responsive feeding, structure, and consistent modeling buffer inherited risk.

For families already struggling, family-based behavioral treatment has trial evidence behind it. The model runs on collaborative goal-setting, structured monitoring, and positive reinforcement, and it improves child weight outcomes in ways that hold up over time (Wilfley et al., JAMA Pediatr, 2017). Parent-only versions of the same treatment perform comparably to parent-and-child versions, which matters for families who can’t get everyone to an appointment (Boutelle et al., Appetite, 2021).

Parents don’t cause obesity. They do hold leverage points that matter, from infancy through adolescence, in how food, sleep, stress, and activity get managed at home.

Scott Rennie, D.O.

References:

1. Ventura AK. Does Breastfeeding Shape Food Preferences? Links to Obesity. Adv Nutr. 2017;8(1):149-150.

2. Johnson SL, Birch LL. Parents’ and children’s adiposity and eating style. Pediatrics. 1994;94(5):653-661. https://pubmed.ncbi.nlm.nih.gov/7936891/

3. Woo JG, Martin LJ. Does Breastfeeding Protect Against Childhood Obesity? Moving Beyond Observational Evidence. Curr Obes Rep. 2015;4(2):207-216. https://pubmed.ncbi.nlm.nih.gov/26100032/

4. Newman J, Taylor A. Effect of a means-end contingency on young children’s food preferences. J Exp Child Psychol. 1992;53(2):200-216. https://pubmed.ncbi.nlm.nih.gov/1578198/

5. Fisher JO, Birch LL. Restricting access to foods and children’s eating. Appetite. 1999;32(3):405-419. https://pubmed.ncbi.nlm.nih.gov/10336797/

6. Wardle J, Carnell S, Haworth CM, Plomin R. Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment. Am J Clin Nutr. 2008;87(2):398-404. https://pubmed.ncbi.nlm.nih.gov/18258631/

7. Wilfley DE, et al. Dose, Content, and Mediators of Family-Based Treatment for Childhood Obesity. JAMA Pediatr. 2017;171(12):1151-1159. https://pubmed.ncbi.nlm.nih.gov/29084318/

8. Boutelle KN, et al. Appetite. 2021.

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 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 Risks and How to Lower Them

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

Bariatric surgery has become one of the most effective treatments for obesity and its complications. Roux-en-Y gastric bypass and sleeve gastrectomy are performed more often now as safety has improved and demand has grown. Surgery is still surgery, and the risks are worth knowing in detail.

The numbers are encouraging. In the LABS Consortium multicenter prospective study, 30-day mortality was 0.3% across 4,776 patients, and major adverse events including venous thromboembolism, reoperation, or extended hospitalization occurred in 4.3% (LABS Consortium, NEJM, 2009). For context, that mortality rate sits below several common major operations. Vigilance still matters, particularly in patients with prior VTE, untreated sleep apnea, poor functional status, or very high BMI.

Among early complications, leaks are what surgeons and patients fear most. Anastomotic leaks occur in about 1% of gastric bypass patients and 2 to 5% after sleeve gastrectomy (Sakran et al., Surg Endosc, 2013; Rosenthal et al., Surg Obes Relat Dis, 2012). Median time to diagnosis is around a week, which usually means the patient is already home. Treatment ranges from drainage and stents to reoperation. Endoscopic vacuum therapy is a newer approach with reported success rates up to 90% (Markus et al., Langenbecks Arch Surg, 2022).

Thrombosis is the other serious early risk. Deep vein thrombosis and pulmonary embolism account for a large share of postoperative deaths, and 70 to 80% of cases occur after discharge (O’Connor et al., Surg Obes Relat Dis, 2021). That timing is the whole problem. There is no universal agreement on extended prophylaxis, and weight-based dosing with enoxaparin is often considered for high-risk patients. Portal vein thrombosis is less common and has been reported almost exclusively after sleeve gastrectomy. These patients present with abdominal pain and are treated with anticoagulation (Parikh et al., Surg Obes Relat Dis, 2017).

Obstruction is a particular concern in bypass patients. Small bowel obstruction can follow adhesions, hernias, or clots, and internal hernias are the tricky ones. Symptoms may be vague, intermittent pain or nausea, or they may present as a full obstruction. Missing it leads to bowel ischemia. A high index of suspicion is the only real defense.

Nutritional problems arrive later and cause real harm when overlooked. Thiamine deficiency can produce Wernicke’s encephalopathy with confusion, ataxia, and nystagmus, and it develops in patients with vomiting or poor intake. Deficiencies in iron, calcium, vitamin D, and B12 are common. Routine supplementation and lab monitoring at three months, six months, and annually thereafter are the standard for good reason (Makarewicz et al., Obes Surg, 2007).

Weight regain is a reality rather than a failure. Roughly one in five patients regains some weight after gastric bypass. Sometimes the cause is behavioral, sometimes anatomical. Either way it is a signal to look more closely, and revisional surgery can be appropriate depending on anatomy and history.

For clinicians, the practical question is when to send a patient back to their bariatric team. Persistent abdominal pain, food intolerance, unexplained weight regain, or concerning deficiencies should all prompt referral. Imaging, endoscopy, or revision may follow.

Bariatric surgery can transform a patient’s life and substantially improve comorbidities. The benefits come attached to responsibilities: careful preoperative evaluation, surgical expertise, and long-term follow-up. Patients do best when both they and their providers understand what can go wrong and stay alert for the early signs.

Scott Rennie, D.O.

References:

1. Longitudinal Assessment of Bariatric Surgery (LABS) Consortium. Perioperative safety in the longitudinal assessment of bariatric surgery. N Engl J Med. 2009;361(5):445-454. https://pubmed.ncbi.nlm.nih.gov/19641201/

2. Sakran N, et al. Surg Endosc. 2013;27(1):240-245.

3. Rosenthal RJ, et al. International Sleeve Gastrectomy Expert Panel Consensus Statement. Surg Obes Relat Dis. 2012;8(1):8-19. https://pubmed.ncbi.nlm.nih.gov/22248433/

4. O’Connor EA, et al. Surg Obes Relat Dis. 2021;17(7):1218-1225.

5. Parikh M, et al. Surg Obes Relat Dis. 2017;13(11):1835-1839.

6. Markus PM, et al. Langenbecks Arch Surg. 2022;407(3):1039-1047.

7. Makarewicz W, et al. Wernicke’s syndrome after sleeve gastrectomy. Obes Surg. 2007;17(5):704-706. https://pubmed.ncbi.nlm.nih.gov/17658034/

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.

Weight Loss Drug Side Effects and How Common They Are

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

As more patients start anti-obesity medications, the question that comes up most is about side effects. These drugs are powerful tools for weight loss and metabolic health. They aren’t without risk. Knowing what to expect and how to manage it often decides whether someone stays on treatment or quits in month two.

Gastrointestinal effects are the ones I hear about most. Nausea leads the list. In STEP 1, which studied semaglutide 2.4 mg in adults without diabetes, nausea affected 44.2% of participants against 17.4% on placebo (Wilding et al., NEJM, 2021). In SCALE, the corresponding trial of liraglutide 3.0 mg, nausea affected 40.2% versus 14.7% on placebo (Pi-Sunyer et al., NEJM, 2015). Those two trials are the source of most of the numbers in this post, and they studied different drugs. Smaller meals, avoiding high-fat food, and slow dose titration usually get patients through it.

Constipation and diarrhea both follow the same pattern, common early and improving with time. Hydration, added fiber, and sometimes a stool softener handle most constipation. Diarrhea occasionally warrants a dose adjustment. Rarely, delayed gastric emptying can progress toward obstruction, which presents as bloating, pain, and vomiting and needs prompt evaluation.

Pancreatitis is uncommon and serious. In SCALE, acute pancreatitis occurred in a small number of liraglutide patients and none on placebo, at an incidence around 0.3%. Severe abdominal pain radiating to the back with nausea and vomiting should trigger immediate discontinuation and workup.

Gallbladder disease is a real risk and it is mostly a consequence of the weight loss itself. In SCALE, cholelithiasis occurred in 1.5% of liraglutide patients versus 1.1% on placebo, and acute cholecystitis in 0.8% versus 0.4%. Rapid weight loss and changes in bile concentration are the likely mechanism, which means the risk travels with any effective therapy rather than with this drug class specifically.

Hypoglycemia is uncommon with GLP-1 receptor agonists used alone in patients without diabetes, because these drugs stimulate insulin secretion in a glucose-dependent way. Risk climbs sharply in combination with insulin or a sulfonylurea. That combination is where monitoring and dose adjustment of the background agent become necessary, and it is worth addressing before starting rather than after the first low reading.

Thyroid cancer risk is rare and gets asked about constantly. GLP-1 receptor agonists carry a boxed warning for medullary thyroid carcinoma based on rodent C-cell tumor data, and they are contraindicated in anyone with a personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia type 2. Human data haven’t established a causal link, and a widely publicized French case-control study reporting an association drew substantial methodological criticism in the same journal (Bezin et al., Diabetes Care, 2023). I tell patients the contraindication is firm and the population-level risk remains unproven.

Kidney injury is rare and usually a consequence of dehydration after vomiting or diarrhea rather than a direct drug effect. Pushing fluids during dose escalation is an easy preventive step.

Heart rate increases are reported as well. Resting heart rate can rise by roughly one to four beats per minute on semaglutide or tirzepatide. Palpitations should always be reported.

Pregnancy deserves its own conversation. These medications aren’t recommended during pregnancy, and semaglutide should be stopped at least two months before conception. There is also an interaction with oral contraceptives, since delayed gastric emptying affects absorption. For tirzepatide, patients on oral contraceptives should switch to a non-oral method or add a barrier method for four weeks after starting and for four weeks after each dose increase.

Injection site reactions occur in a small percentage of patients, usually three to five percent. Redness, swelling, and itching are the usual complaints, and rotating sites with good technique resolves most of it.

None of this means patients should avoid these medications. Awareness and early management are what keep people on treatment. I often tell patients to call me if nausea or constipation is interfering with their day-to-day life rather than waiting for the next follow-up. Small changes in dosing or diet usually make the drug tolerable again.

Anti-obesity medications work, and they need thoughtful monitoring. With open communication, most side effects are manageable and most patients stay on track.

Scott Rennie, D.O.

References:

1. Wilding JPH, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity (STEP 1). N Engl J Med. 2021;384(11):989-1002. https://pubmed.ncbi.nlm.nih.gov/33567185/

2. Pi-Sunyer X, et al. A Randomized, Controlled Trial of 3.0 mg of Liraglutide in Weight Management (SCALE). N Engl J Med. 2015;373(1):11-22. https://pubmed.ncbi.nlm.nih.gov/26132939/

3. Bezin J, et al. GLP-1 Receptor Agonists and the Risk of Thyroid Cancer. Diabetes Care. 2023;46(2):384-390. https://pubmed.ncbi.nlm.nih.gov/36356111/

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.