A folded white towel beside a plain bar of soap in a ceramic dish and a safety razor on a sunlit wooden bathroom shelf

Why Do I Keep Getting Boils?

On August 29, 2026August 30, 2026 By Dr. Scott RennieIn Skin & Wound CareLeave a comment

“Boil” is not a diagnosis. It is a word patients use for a painful lump that came up, hurt, and either drained or had to be opened. Underneath that one word sit at least four different problems with four different answers, and the reason people keep getting them is usually that nobody has said which one they have.

So the useful question is not what to put on it. It is where they keep happening.

Location does most of the diagnostic work

A furuncle is an infected hair follicle. It can turn up anywhere hair grows, it is usually staph, and a person who gets one is not necessarily a person who will get another.

Hidradenitis suppurativa lives in specific places. Armpits, groin, under the breasts, inner thighs, buttocks, around the anus. The same sites, over and over, often on both sides.

A pilonidal sinus sits in the cleft at the top of the buttocks and essentially nowhere else.

An inflamed epidermoid cyst comes back in exactly the same spot every time, because the sac is still there.

Four sites, four answers. If your lumps keep appearing in your armpits and groin, the working diagnosis is not recurrent boils.

The one that gets missed for years

Hidradenitis suppurativa is the diagnosis I most want people to know the name of, because the delay in getting it is measured in years rather than visits, and misdiagnosis is one of the biggest drivers of that delay (1).

What separates it from recurrent furuncles:

The same locations, repeatedly. Tunnels under the skin connecting one lesion to the next, which patients often describe as the drainage coming out somewhere other than where it went in. Rope-like scarring that builds up over years. Blackheads appearing in pairs, which is a small finding and quite specific. A family history, which is present often enough to be worth asking about.

Cultures from HS lesions frequently grow something, which is how it keeps getting called an infection. It is an inflammatory disease of the follicle, and antibiotics in it are working as anti-inflammatories more than as antimicrobials.

If you have been given six courses of antibiotics for boils in the same two places, you probably have HS and nobody has said so.

What actually treats an abscess

Drainage. Not antibiotics.

The IDSA guideline on skin and soft tissue infection puts incision and drainage as the treatment for a drainable abscess, with antibiotics as an adjunct in defined situations rather than a substitute (2). An abscess that is not opened does not resolve because someone took cephalexin.

This is why, practising by video, my rule is that a suspected abscess goes out to be drained rather than getting a prescription from me. I am firmer about that than some colleagues are, and I have not regretted it. A camera cannot tell me whether something is fluctuant, and a prescription that delays drainage by four days makes the eventual procedure bigger.

Why they keep coming back

For genuine recurrent furunculosis, the usual driver is staph colonization. The organism lives in the nose, the axillae, the groin, and it seeds new follicles.

Decolonization is the standard answer: intranasal mupirocin, chlorhexidine washes, attention to towels and razors. What is worth knowing is that treating the whole household beats treating the individual. Fritz and colleagues randomized exactly that comparison in children with community-associated staph infection and found household-wide decolonization more effective at eradication than treating the index patient alone (3).

That matters practically, because the patient who keeps recurring is often the one person in a house of four getting treated.

The part that belongs to my day job

Obesity, smoking and diabetes all sit behind recurrent skin infection, and they sit behind HS particularly hard.

Friction and skin folds are part of it, and plenty else is going on besides. Higher glucose impairs neutrophil function. Adipose tissue is metabolically active and inflammatory. Skin folds hold moisture and macerate. And the inflammatory biology of HS overlaps with metabolic disease in a way that is more than coincidence of body habitus.

What has changed recently is that we have a drug class that moves several of those levers at once. Multiple cohorts and case series now report reduced HS disease activity, fewer flares and less pain in patients treated with GLP-1 receptor agonists (4), and a cross-sectional survey found roughly two thirds of respondents reporting improvement in HS-specific measures (5).

I want to be careful here, because the enthusiasm is ahead of the evidence. These are retrospective cohorts and patient-reported surveys, not randomized trials with standardized background therapy. I take the signal seriously in a patient who has both conditions and would be a candidate for the drug anyway. I would not start an incretin in someone whose only indication is their skin.

Smoking is the other lever, and in HS it is a big one. If someone with HS smokes, that is the highest-yield conversation available, and it is not close.

For patients

Notice where they happen. If it is armpits, groin, under the breasts or the buttocks, and it is the same places repeatedly, ask your clinician about hidradenitis suppurativa by name. Naming it is often what gets the diagnosis moving.

If you have a painful lump with a pocket of pus in it, it needs draining. An antibiotic on its own will not finish the job.

If you get recurrent boils and there are other people in your house, ask whether the whole household should be treated rather than just you.

For colleagues

Ask where, not what. Location sorts furuncle from HS from pilonidal faster than any other question, and it is the question that shortens the diagnostic delay.

Household decolonization outperforms individual decolonization, and we mostly still prescribe the individual version.

The GLP-1 and HS literature is worth knowing and worth being careful with. When a patient with both asks whether the drug will help their skin, name the study designs and stop short of promising.

The Bottom Line

Recurrent boils in the armpits, groin, under the breasts or the buttocks are usually hidradenitis suppurativa, and the average person with it waits years for someone to say the word. A true abscess is treated by drainage, with antibiotics as an adjunct rather than a substitute. Recurrent furunculosis is usually a colonization problem, and treating the whole household beats treating the patient. And if the same person has recurrent skin infection, obesity and smoking, the skin is the symptom being presented and the other two are what is driving it.

Sources

1. Murray N, et al. Equity and Outcome Events in Hidradenitis Suppurativa: Exploring Effect Modifiers Associated with Diagnostic Delay in the Real World. Dermatol Ther (Heidelb). 2024;14(12):3211-3227. PMID 39487935. https://pubmed.ncbi.nlm.nih.gov/39487935/

2. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-52. PMID 24973422. https://pubmed.ncbi.nlm.nih.gov/24973422/

3. Fritz SA, Hogan PG, Hayek G, et al. Household versus individual approaches to eradication of community-associated Staphylococcus aureus in children: a randomized trial. Clin Infect Dis. 2012;54(6):743-751. PMID 22198793. https://pubmed.ncbi.nlm.nih.gov/22198793/

4. Rao S, et al. Skin Impacts and Tradeoffs of GLP-1 Therapy: Improved Patient-Reported Outcomes of Inflammatory Skin Disease. Dermatol Ther (Heidelb). 2026. PMID 42579223. https://pubmed.ncbi.nlm.nih.gov/42579223/

5. Javaheri ED, et al. Impact of GLP-1 Receptor Agonists on Hidradenitis Suppurativa: A Cross-Sectional Survey. Int J Dermatol. 2026 Jul 16. PMID 42461155. https://pubmed.ncbi.nlm.nih.gov/42461155/

6. DermNet. Hidradenitis suppurativa. https://dermnetnz.org/topics/hidradenitis-suppurativa

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 July 31, 2026November 7, 2026 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, four months apart. If you haven’t been following closely, the options today look nothing like they did two years 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 orforglipron. The FDA approved it on April 1, 2026, under the brand name Foundayo (1). Before that, on December 22, 2025, the FDA approved a 25 mg oral semaglutide tablet under the Wegovy name (2). GLP-1 medicines help control appetite and blood sugar, and that tablet was the first pill version of one approved for long-term weight management. Both are real, both are approved, and both can be prescribed today.

Both full prescribing labels are now public, and they differ in ways that decide the choice for a lot of people. Most of those differences have nothing to do with how much weight each one takes off.

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.

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 journal Clinical Diabetes, SNAC does three things at once (3). It changes the local acidity around the tablet as it dissolves, it briefly protects the drug from a stomach enzyme called pepsin, and it helps the drug cross the stomach lining into your bloodstream. The absorption happens in the stomach itself rather than 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 trick comes with a catch, and the label is specific about it (4). You take the tablet on an empty stomach in the morning with no more than four ounces of plain water. No other liquids. Swallow it whole, and wait at least 30 minutes before you eat, drink anything, or take any other oral medication.

Thirty minutes. Every morning. Before coffee.

Orforglipron works completely differently. It is a small molecule, meaning a stable chemical rather than a fragile peptide chain. It belongs to the same drug family, mimicking a natural gut hormone that reduces appetite, but with no peptide to protect it needs no absorption booster and carries no timing ritual. Its label says to take it once daily with or without food, and specifies no water restriction and no waiting period (5). For someone who works nights, or who already swallows six other pills at breakfast, that is the whole ballgame.

What the labels actually say, and why the number in your news feed is wrong

Most of the figures circulating online come from journal publications and press releases rather than from the approved labels. The label numbers are the ones your prescription is based on, so those are the ones I use.

For Wegovy tablets, the label reports a 64-week trial in 205 adults on the tablet against 102 on placebo, all with obesity or overweight plus a weight-related condition, with diabetes excluded (4). Average weight change was 13.6 percent down on the tablet and 2.4 percent down on placebo, a difference of 11.2 percentage points. Broken out by how much people lost: 76.3 percent lost at least 5 percent of their body weight versus 31.3 percent on placebo, 59.8 percent lost at least 10 percent versus 14.4 percent, 47 percent lost at least 15 percent versus 5.5 percent, and 27.9 percent lost at least 20 percent versus 3.1 percent.

For Foundayo, the label reports a 72-week trial in 3,127 adults without diabetes (5). Average weight change was 7.4 percent down at the 5.5 mg dose, 8.3 percent down at 9 mg, and 11.1 percent down at the maximum 17.2 mg dose, against 2.1 percent down on placebo. At 17.2 mg, 35.9 percent of patients lost at least 15 percent of their body weight, compared with 6 percent on placebo.

Put those side by side and the semaglutide tablet looks better, and I would be careful with that read. Different patients, different trial lengths, different placebo responses, and nobody randomized the same people to both. What is harder to wave away is the size of each evidence base. The semaglutide tablet’s label efficacy rests on 205 treated patients. Foundayo’s rests on 3,127. Both cleared the FDA, so both met the bar, but I have more confidence in how a drug behaves across a wide range of real people when the number in the trial is measured in thousands.

Here is the detail that confuses almost everyone who reads the news coverage. The approved Foundayo strengths are 0.8, 2.5, 5.5, 9, 14.5, and 17.2 mg, stepped up roughly every 30 days. The trial used a capsule at 1, 3, 6, 12, 24, and 36 mg. Those map onto each other in order, so the 17.2 mg tablet you can actually be prescribed is the 36 mg dose you read about. If your maximum dose sounds far smaller than the headline, that is why.

One thing I noticed reading the Foundayo label closely: the 14.5 mg strength is approved and dispensable, and it does not appear in the label’s efficacy table at all. You can be prescribed a dose with no published average weight loss attached to it. Not dangerous, just worth knowing if you end up parked there.

The only comparison anyone has run, and who paid for it

There is still no head-to-head trial of these two drugs in obesity. There is now an indirect comparison, published in Diabetes, Obesity and Metabolism in August 2026, which pulled individual patient data from the semaglutide tablet trial and aggregate data from the orforglipron trial and statistically adjusted for differences in sex, body weight and glucose status between the two populations (6).

It found oral semaglutide 25 mg ahead by 3.2 percentage points of body weight (95% confidence interval 5.9 to 0.4) and reported higher discontinuation with orforglipron, with an odds ratio of 4.1 for stopping due to any adverse event and 13.9 for stopping due to gastrointestinal side effects.

Five of the authors are Novo Nordisk employees and shareholders, two more work for a consultancy Novo paid to run the analysis, and Novo makes the drug that won. That does not make the result false. It does mean I apply a discount. The direction is plausible and roughly matches the gap between the two labels. The magnitude I would not quote to a patient as fact. And that gastrointestinal odds ratio of 13.9 has a confidence interval running from 2.0 to 96.0, which is another way of saying the study could not pin it down.

There is one true head-to-head, and it points the other way. In adults with type 2 diabetes, orforglipron beat oral semaglutide on weight loss (7). That trial used semaglutide at 7 mg and 14 mg, well under the 25 mg weight-management dose, in a different population, for a different purpose. It answers a different question than the one you are asking.

Birth control is the difference nobody mentions

This is the most actionable difference between the two drugs and it almost never comes up in the coverage.

The Foundayo label instructs patients on oral hormonal contraceptives to switch to a non-oral method, or to add a barrier method for 30 days after starting the drug and for 30 days after every dose escalation (5). Count the escalations. With six strengths, somebody climbing to the top dose is looking at several separate 30-day windows where their pill alone is not considered reliable. Non-oral hormonal contraception is not expected to be affected.

The Wegovy tablet label carries no equivalent instruction. Its pharmacokinetic studies found no clinically significant interaction with ethinyl estradiol and levonorgestrel (4).

For a woman in her twenties or thirties on a combined oral contraceptive who does not want a pregnancy, that single difference outweighs three percentage points of average weight loss. I bring it up before either drug gets prescribed, not after.

The other interactions that quietly decide this

Orforglipron is cleared through CYP3A4, and the label puts real fences around that (5). On a strong CYP3A4 inhibitor, the maximum Foundayo dose drops to 9 mg. Clarithromycin raised orforglipron exposure 3.5-fold in a study. Going the other way, carbamazepine cut exposure by 82 percent and efavirenz by 61 percent, so strong inducers are to be avoided and moderate ones need the dose pushed up while you watch whether it still works. Strong inhibitors that also block OATP1B, ritonavir being the example the label gives, are to be avoided outright. And simvastatin is capped at 20 mg a day alongside it.

The semaglutide tablet has a shorter list but one that matters in my practice. A single 600 mcg dose of levothyroxine taken with it produced a 33 percent rise in total thyroxine exposure (4). Add the 30-minute rule on top, which pushes every other morning medication back, and a patient on thyroid replacement plus a few other dailies has a genuine scheduling problem.

If someone comes to me on carbamazepine, or on ritonavir-boosted therapy, Foundayo is awkward enough that I start elsewhere. If someone is on levothyroxine and already struggles to take it correctly, I think hard before adding a second pill with its own empty-stomach window.

Side effects

Both drugs hit the gut, and both labels say so plainly.

Foundayo’s pooled safety data runs nausea at 26 percent, 34 percent and 35 percent across the 5.5, 9 and 17.2 mg doses against 10 percent on placebo (5). Vomiting climbs from 13 to 24 percent against 4 percent. Constipation runs 20 to 27 percent against 9 percent, and diarrhea 21 to 25 percent against 11 percent. Hair loss shows up at 4 to 5 percent against 2 percent, which patients ask me about more than the numbers would suggest.

The Wegovy tablet label describes side effects similar to the injection, and adds a few tablet-specific figures (4). Just under 7 percent of patients stopped the drug for an adverse reaction, against about 6 percent on placebo. Severe gastrointestinal reactions occurred in 2 percent of tablet patients and no placebo patients. Dysesthesia, meaning abnormal or unpleasant sensation, was reported in 5 percent of tablet patients and in nobody on placebo. That last one is not something I had on my radar before reading the label, and it is worth mentioning to a patient who calls about odd skin sensations rather than writing it off.

Both drugs carry a boxed warning about thyroid C-cell tumors and are contraindicated in anyone with a personal or family history of medullary thyroid carcinoma or MEN 2 (4)(5).

If you have heart disease, the answer is already made

Wegovy tablets carry an approved indication to reduce the risk of major adverse cardiovascular events, meaning cardiovascular death, non-fatal heart attack and non-fatal stroke, in adults with established cardiovascular disease and either obesity or overweight (4). The wording is identical to the injection’s.

Foundayo has no cardiovascular outcome indication. Its cardiovascular outcomes trial has not reported.

For a patient who has already had a heart attack or a stroke, that settles it. I go to semaglutide, and the only remaining question is tablet or injection.

How I actually choose

If you are the patient reading this, the useful question is not which drug is stronger. It is which one you will still be taking in a year. The 30-minute waiting period for the semaglutide tablet sounds minor when we talk it through on a video visit, and it trips people up in real life. I have watched patients lose ground on oral semaglutide because weekday mornings made the timing rules impossible to follow, and the drug cannot work from inside the bottle. If your mornings are chaotic, say so out loud when we talk. That is clinical information, not an excuse.

If you are a prescriber, I would frame the choice around four things before efficacy. Established cardiovascular disease points to semaglutide on the label. An oral contraceptive points away from orforglipron, or at least commits you to counseling a barrier method through every escalation. A CYP3A4 problem, especially an enzyme inducer, makes orforglipron hard to dose. Levothyroxine and a crowded morning pill box make the semaglutide tablet hard to take. What is left after those four filters is usually a clear answer, and in my experience the efficacy gap is the least useful thing to lead with.

What this costs right now

Both manufacturers run tiered self-pay pricing that starts low at the smallest dose and rises as you titrate up, and both have promotional rates on their lower strengths that are scheduled to end on December 31, 2026. Because these terms change faster than I can keep a blog post current, check the two official pages directly rather than trusting a number you read anywhere, including here: LillyDirect for Foundayo (8) and NovoCare for Wegovy (9).

What I can tell you from prescribing both is operational. I haven’t run into a prior-authorization fight or a stocking problem with Foundayo yet. Most of what I prescribe goes through LillyDirect on cash pay, because it has been one of the cheaper options on the table. Patients who have real insurance coverage tend to ask for injectable Wegovy or Zepbound instead, and I do not talk them out of it. For a fuller breakdown of cash prices across the whole class, including the injections, see my separate post on cash pay options.

The Bottom Line

Two pills, both approved, both effective, and the deciding factors are mostly not about weight loss. The semaglutide tablet takes off a bit more weight in the label data, carries a cardiovascular indication, and demands an empty stomach and a 30-minute wait every single morning. Foundayo asks nothing of your schedule, has a far larger trial behind it, and brings a contraception instruction and a list of drug interactions that rule it out for some people entirely.

Bring your actual medication list and your actual morning routine to the visit. Those two things will pick the drug faster than any comparison chart.

Sources

1. FDA approves Lilly’s Foundayo (orforglipron), the only GLP-1 pill for weight loss (Eli Lilly): https://investor.lilly.com/news-releases/news-release-details/fda-approves-lillys-foundayotm-orforglipron-only-glp-1-pill

2. 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

3. Current Understanding of SNAC as an Absorption Enhancer: The Oral Semaglutide Experience (Clinical Diabetes, American Diabetes Association): https://diabetesjournals.org/clinical/article/42/1/74/153538/Current-Understanding-of-Sodium-N-8-2

4. WEGOVY (semaglutide) injection and tablets, US prescribing information (DailyMed): https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ee06186f-2aa3-4990-a760-757579d8f77b

5. FOUNDAYO (orforglipron) tablets, US prescribing information (Eli Lilly): https://uspl.lilly.com/foundayo/foundayo.html

6. Michalak W, Bøg M, Bendixen T, Chowdhury R, Cowley P, Laugesen C, et al. Oral Semaglutide 25 mg Versus Orforglipron 36 mg in Obesity: A Population-Adjusted Indirect Treatment Comparison. Diabetes, Obesity and Metabolism. 2026;28(8):7247-7256: https://pubmed.ncbi.nlm.nih.gov/42225305/

7. Orforglipron Outperforms Oral Semaglutide in Head-to-Head Type 2 Diabetes Trial (AJMC): https://www.ajmc.com/view/orforglipron-outperforms-oral-semaglutide-in-head-to-head-type-2-diabetes-trial

8. Foundayo self-pay pricing (LillyDirect): https://www.lilly.com/lillydirect/foundayo

9. Wegovy self-pay pricing (NovoCare): https://www.novocare.com/

10. 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

A table covered with many plates and bowls of food

Binge Eating Disorder Signs and Treatment in Adults and Kids

On September 17, 2025September 29, 2026 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.

Why Do I Eat at Night? Night Eating Syndrome Explained

On September 17, 2025September 11, 2026 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. The question that opens it up is whether a person is eating after they have gone to bed, and whether they believe they need to eat in order to get back to sleep.

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.

Does Chronic Stress Cause Weight Gain? A Doctor Explains

On April 25, 2025September 11, 2026 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.

How Parents Influence a Child’s Weight and Eating

On April 12, 2025September 29, 2026 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.

Weight Loss Surgery Without Incisions: Bariatric Endoscopy

On March 28, 2025September 11, 2026 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.

Weight Loss Surgery Risks and How to Lower Them

On March 28, 2025September 11, 2026 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.

Weight Loss Surgery Options for Obesity Explained

On March 27, 2025September 11, 2026 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.

Weight Loss Drug Side Effects and How Common They Are

On March 24, 2025September 29, 2026 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.

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