Author: Dr. Scott Rennie

Dr. Rennie is board certified by the American Board of Obesity Medicine and the American Board of Family Medicine. He is also an active member of The Menopause Society. He is located in Nevada, licensed to practice medicine in all 50 U.S. states and Guam. His focus is on providing expert medical care with personalized service in the realms of telemedicine, weight loss without the use of medication, urgent care, primary prevention, and whole-body wellness.

GLP-1 Skin and Nerve Pain: Ozempic, Wegovy, Mounjaro

On By Dr. Scott RennieIn Weight Loss & Metabolic Health2 Comments

Originally published June 6, 2025. Revised August 2026 to reflect evidence that was not available when this was first written, including the STEP UP trial of semaglutide 7.2 mg, pharmacovigilance data from VigiBase and EudraVigilance, and a Mayo Clinic case-control study.

Semaglutide, sold as Ozempic and Wegovy, changed how we handle type 2 diabetes and obesity. Tirzepatide, sold as Mounjaro and Zepbound, pushed it further. I prescribe both routinely and the benefits are not in question. What follows applies to the class rather than to any one brand.

What has changed since I wrote this originally is the quality of the evidence underneath the complaints. In June 2025 the nerve and muscle problems I described were a handful of case reports. They are now in three national pharmacovigilance databases and one controlled study, and one of those findings has changed how I dose.

The skin pain is real, and it is a class effect

The original signal was small. Four patients, described by Stark and colleagues, all of whom developed allodynia after reaching the 2.4 mg weekly dose. Pain from light touch. A shirt hurting. Two stopped and resolved, one of the two who continued resolved at about four months, and all four scored as probable on the Naranjo scale.

Three things have happened since.

The first is tirzepatide, the molecule in Mounjaro and Zepbound. Ahern published two cases in October 2025, one on semaglutide and one on tirzepatide, and Chakrabarti and colleagues published the first tirzepatide-specific series in May 2026. Two patients with severe obesity, moderate to severe allodynia, onset tracking with dose escalation, resolution after stopping. So this is not a semaglutide quirk. It follows the receptor.

The second is that the pharmacovigilance data caught up. Laroche and colleagues ran a disproportionality analysis on VigiBase and found semaglutide and tirzepatide both significantly associated with hyperaesthesia, and semaglutide specifically with dysesthesia and burning sensation. Dose dependent, worse with the more potent agents, resolving on discontinuation, and with positive rechallenge in some cases. A separate EudraVigilance analysis found a dysesthesia signal as well.

The third is the detail I find most interesting. The Laroche paper opens by noting that the reports started on social media and medical blogs before they reached the literature, and that the signal was already visible in the trial data for semaglutide, tirzepatide and retatrutide. Patients described this accurately, in public, for a couple of years before anybody wrote it up.

I mention that because of what it means in a visit. When someone tells me their skin burns and nothing is there to see, that is now a recognized adverse effect with a database signal behind it, not a somatic complaint to be reassured away. I was too slow to that conclusion in 2025.

The 7.2 mg dose changes the arithmetic

Everything above came from case reports and spontaneous reporting databases. Those tell you that something happens. They cannot tell you how often. A randomized trial can, and one has now reported.

Wharton and colleagues published STEP UP in Lancet Diabetes and Endocrinology in November 2025. They randomized 1,407 adults with obesity and without diabetes to semaglutide 7.2 mg, semaglutide 2.4 mg, or placebo, in a five to one to one split, for 72 weeks. The weight loss result is the part that got covered: 18.7 percent on the high dose against 15.6 percent on 2.4 mg and 3.9 percent on placebo.

Here is the part that did not get covered. Dysesthesia occurred in 230 of the 1,004 patients on 7.2 mg. That is 22.9 percent. On 2.4 mg it was 6.0 percent. On placebo it was 0.5 percent, which is one person.

Read those three numbers again, because they are a dose-response curve in a randomized double-blind trial with over 1,400 people in it. Everything in the case series literature, and everything the pharmacovigilance databases hinted at, is confirmed by that single line in a phase 3b safety table.

The FDA approved the 7.2 mg dose as Wegovy HD in March 2026, through a 54-day accelerated review under the National Priority Voucher program, and has said it is looking further into the dysesthesia signal. I have written separately about who should actually consider the 7.2 mg dose.

In fairness to the drug, these events generally settled on their own or with a dose reduction, and serious adverse events were actually lower on 7.2 mg than on 2.4 mg, 6.8 percent against 10.9 percent. The trial authors concluded that 7.2 mg retained a favourable risk-benefit profile, and for weight loss that is defensible.

I would still put the sensory finding differently than they did. Almost one in four is not a rare adverse effect. It is a common one. It belongs in the conversation before the first injection, not in a footnote somebody reads after their shirt starts hurting.

The finding that actually changed my practice

Here is the part that was not in the original post, and it is the most clinically useful thing in this update.

Triplett and colleagues at Mayo published a case-control study in Neurology in August 2025 looking at two specific neuropathies in GLP-1 users. Diabetic lumbosacral radiculoplexus neuropathy, which is severe asymmetric leg pain followed by weakness and wasting, and common fibular neuropathy, which is a foot drop.

They found 26 patients with 27 episodes of DLRPN. Median onset was six months after starting the drug, with a range of three to thirty five. At onset those patients had dropped a median of 2.4 percentage points of HbA1c, with a range up to 8.5, and lost a median of 13.9 percent of body weight. Nerve biopsy showed microvasculitis in four of five cases. For common fibular neuropathy there were 77 patients and 82 episodes, with a smaller median HbA1c drop of 1.2 percent and a slightly larger median weight loss of 15.7 percent.

Against matched controls, GLP-1 users were 51 percent more likely to develop DLRPN, odds ratio 1.5 with a confidence interval of 1.2 to 1.9, and 30 percent more likely to develop common fibular neuropathy, odds ratio 1.3 with an interval of 1.0 to 1.5. Every episode in the series occurred after 2015, and cases rose roughly sevenfold and ninefold between the 2015 to 2019 period and 2020 to 2024.

The interesting split is what predicted which neuropathy. DLRPN tracked with the size of the HbA1c reduction. Common fibular neuropathy tracked with weight loss, which makes sense for a nerve that gets compressed at the fibular head once the fat pad over it disappears.

That first association has a name that predates these drugs. Treatment-induced neuropathy of diabetes, described decades ago after aggressive insulin initiation, where a fast correction of chronic hyperglycemia produces an acute, severe, painful small fiber neuropathy. Nobody expected to see much of it from a weekly injection. We are seeing it because these drugs drop an A1c faster than anything we had before.

So the honest reframing is this. Some of what gets called Ozempic nerve pain is probably not a drug toxicity at all. It is the metabolic correction happening faster than the nerve can tolerate.

Rhabdomyolysis and muscle loss

The rhabdomyolysis report stands where it was. Billings and colleagues described a 47-year-old woman with diffuse muscle pain, weakness and a raised creatine kinase after starting semaglutide, improving after discontinuation. It remains a single case.

Muscle mass is the more common problem and it is not rare at all. Mohamad reported a 74-year-old man who used semaglutide for two years, lost eight kilograms, and turned up with fatigue, weakness and visible wasting. Dose reduction and resistance training recovered some of it. Sarcopenia is an expected consequence of large, fast weight loss, and older adults absorb almost all of that risk. I treat this as something to prevent from day one rather than something to detect later. I go through the evidence in more depth in my piece on whether GLP-1 drugs cause muscle loss.

The eye signal has moved, at least outside the United States

The 2024 JAMA Ophthalmology cohort from Hathaway and colleagues reported a markedly higher rate of non-arteritic anterior ischemic optic neuropathy in patients prescribed semaglutide, with a 36-month cumulative incidence of 6.7 percent against 0.8 percent. Subsequent work has been mixed, with a large Danish and Norwegian cohort finding a smaller but real elevation and other analyses finding none.

Regulators have moved since. The European Medicines Agency’s safety committee reviewed it in June 2025 and concluded NAION is a very rare side effect of semaglutide, affecting up to 1 in 10,000 people, and EU product information was updated on 30 September 2025. The WHO issued its own statement in June 2025. As of this revision the FDA has not added NAION to the US labels for Ozempic, Wegovy or Rybelsus and describes the evidence as under evaluation.

Worth noting that the EudraVigilance analysis also picked up optic ischemic neuropathy reports for tirzepatide and liraglutide, so the eye question may not stay a semaglutide question either.

The absolute risk is still low. I tell patients what it is and what sudden painless vision loss in one eye looks like, and I move on.

What I do differently now

I run a telemedicine practice, so all of this happens over video, and none of it needs a physical exam to get right.

The rate of change matters as much as the destination. If someone comes down four points of A1c in three months I now treat that as a reason to slow the titration rather than a win to celebrate. That is a genuine change in how I practice and it comes directly from the Mayo data.

I ask specifically about skin pain rather than waiting for it. The question that finds it is whether clothing or bedsheets hurt, not whether they have numbness or tingling.

Anyone going to 7.2 mg hears the number before they start. Twenty three percent is high enough that being warned about it is much better than being blindsided by it, and a patient who expects the sensation is far more likely to ring me than to quietly stop the drug.

Severe asymmetric leg pain in someone on a GLP-1 is not a titration side effect and it does not get a watchful waiting plan. That is a neurology referral, and the pain usually arrives weeks before the weakness does.

I check B12 in anyone with neurologic complaints, since slowed gastric emptying can reduce absorption.

Protein and resistance training start at the beginning, not after the wasting shows up. Adequate protein means a number I have actually calculated with the patient, not a general encouragement.

And when I do suspect the drug, holding or reducing the dose answers the question faster than any test will.

The Bottom Line

Most patients do well on these medications and the benefits are large. Nothing in the last year changes that.

What the last year changed is that skin pain from these drugs stopped being an oddity. It is a class effect, it is dose dependent, and at the 7.2 mg dose it reached 22.9 percent in a randomized trial. It is not rare at all.

The other change is that some of the serious nerve injury looks like it is driven by how fast we are correcting the metabolic problem rather than by the drug poisoning the nerve. That is the actionable one, because the fix is in the titration, and the titration is entirely under our control.

Scott Rennie, D.O.

References

Wharton S, Freitas P, Hjelmesaeth J, et al. Once-weekly semaglutide 7.2 mg in adults with obesity (STEP UP): a randomised, controlled, phase 3b trial. Lancet Diabetes Endocrinol. 2025;13(11):949-963. PMID: 40961952

Stark J, Klass MJ, Owen L. Allodynia (skin tenderness) associated with semaglutide: A case series. Am J Health Syst Pharm. 2025;82(9):e426-e430. PMID: 39862389

Ahern S. Allodynia and Dysesthesia Associated With Semaglutide and Tirzepatide. Cureus. 2025;17(10):e94126. PMID: 41210042

Chakrabarti MP, Han S, Campbell NM. Cutaneous Allodynia Associated With GLP-1RA Tirzepatide for Weight Management: A Case Series. Am J Case Rep. 2026;27:e952158. PMID: 42101979

Laroche ML, Geniaux H, Jardou M. Dysesthesia associated with GLP-1 agonist therapies: data-mining analysis and literature review. Eur J Clin Pharmacol. 2026;82(6):154. PMID: 42168638

Popa Ilie IR, et al. Incretin-Based Drugs for Obesity: Common and Drug-Specific Reporting Patterns of Adverse Drug Reactions. Pharmaceuticals (Basel). 2026;19(6):876. PMID: 42356493

Triplett JD, Pinto MV, Young NP, et al. GLP-1RA-Associated Diabetic Lumbosacral Radiculoplexus and Common Fibular Neuropathies: A Case-Control Evaluation. Neurology. 2025;105(3):e213916. PMID: 40694751

Billings SA, Felix HM, Prier CC, Hedges MS. Rhabdomyolysis Associated With Semaglutide Therapy: A Case Report. Cureus. 2023;15(12):e50227. PMID: 38192938

Mohamad AA. A case report of semaglutide induced sarcopenia: causes of fatigue in older adults. Korean J Fam Med. 2025;46(4):288-291. PMID: 40223309

Hathaway JT, et al. Risk of Nonarteritic Anterior Ischemic Optic Neuropathy in Patients Prescribed Semaglutide. JAMA Ophthalmol. 2024. PMID: 38958939

European Medicines Agency. Meeting highlights from the Pharmacovigilance Risk Assessment Committee (PRAC), 2-5 June 2025. https://www.ema.europa.eu/en/news/meeting-highlights-pharmacovigilance-risk-assessment-committee-prac-2-5-june-2025

World Health Organization. The use of semaglutide medicines and risk of non-arteritic anterior ischemic optic neuropathy (NAION). 27 June 2025. https://www.who.int/news/item/27-06-2025-27-06-2025-semaglutide-medicines-naion

North American Neuro-Ophthalmology Society and American Academy of Ophthalmology. Consensus statement on GLP-1 receptor agonists and the risk of NAION. https://www.aao.org/education/clinical-statement/glucagon-like-peptide-1-receptor-agonists-risk-of-

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.

COVID Variant NB.1.8.1: What Patients and Clinicians Know

On By Dr. Scott RennieIn Infectious DiseaseLeave a comment

We all hoped COVID would fade into background noise by 2025. The virus did not agree. A new Omicron subvariant, NB.1.8.1, has been identified, and while it is not labeled a Variant of Concern, it is moving quickly enough in several countries to be worth paying attention to.

It was first identified in China earlier this year, then appeared in Australia, India, and the United States. Local outbreaks are being reported in dense areas including parts of California and New York. Genomic surveillance shows it spreading independently of travel patterns, which suggests it does not need help.

The subvariant carries several spike protein mutations: T22N, F59S, G184S, A435S, V445H, and T478I. These may improve binding to ACE2 receptors and blunt neutralizing antibodies. The pattern resembles BA.5, though NB.1.8.1 looks more efficient at evading immunity.

Laboratory data suggest moderate to significant immune escape. Antibodies from people who received current boosters show reduced neutralizing activity. The T-cell response, which is what keeps people out of the ICU, appears largely intact. That distinction is the reason boosters still matter, particularly for older adults and immunocompromised patients, and manufacturers are already adjusting formulations.

Early modeling puts NB.1.8.1 at 20 to 30 percent more transmissible than subvariants circulating in late 2024 such as JN.1, with possibly higher viral loads in the first two days. The practical translation is to test early and isolate immediately rather than waiting to see how it develops.

Symptoms are the ones we already know: sore throat, congestion, fatigue, dry cough, headache, fever. Some reports add hoarseness and mild GI upset such as nausea or abdominal discomfort, especially early on. That is not definitive yet, but on a video visit those two together are worth a second look, since I cannot examine a throat the way an in-person clinician can.

So far NB.1.8.1 has not been tied to more severe illness, and hospitalizations remain stable in vaccinated populations. The risk here is volume rather than severity. A variant that makes no one sicker can still overwhelm a health system if enough people get it at once, and places with fewer beds or lower booster uptake will feel it first.

What to do about it is not complicated. Prioritize updated boosters for high-risk groups. Consider masking indoors in long-term care settings when cases climb. Improve ventilation where you can. Test early, isolate early. Wastewater monitoring and sequencing give useful warning. Staffing, protective equipment, and telehealth capacity should all be ready to scale.

This is not 2020 again. It is the ordinary business of a virus that keeps evolving, and the response is the same as it has been: stay current, give patients clear guidance, and adjust when the data does.

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.

Why the Scale Isn’t the Best Measure of Weight Loss

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

When patients bring up weight loss, the number on the scale is almost always the first thing out of their mouth. The scale is a poor narrator. What is being lost, fat or muscle or some mix of the two, matters as much as how much of it is gone. That distinction is body composition, and it drives health, function, and what happens years down the line.

Research from Dr. Dympna Gallagher and colleagues has mapped how body composition shifts during weight loss, and how activity, resistance training in particular, protects muscle through it.

Not all weight loss is the same. Weight comes off as a mix of fat and fat-free mass, the latter including muscle, water, and bone. Work from the 1980s estimated that 20 to 30 percent of the weight lost on a standard diet comes from lean mass (Webster et al., 1984). That fraction is not fixed. Age, diet quality, activity, and the speed of loss all move it. Steady loss of about half a kilogram a week protects muscle better than anything faster (Council on Scientific Affairs, JAMA 1988). This matters because Framingham data link muscle loss to higher mortality while fat loss lowers risk (Allison et al., 1999).

Exercise changes the arithmetic. Gallagher’s review and work from Beavers and colleagues found that structured exercise cuts muscle loss during weight reduction nearly in half. In one trial in older adults, resistance training brought lean mass loss down from 16 percent to 10 percent (Beavers et al., 2017). Resistance work beat aerobic exercise at preserving muscle even when both groups lost similar total weight, and combining them produced the best result: more fat lost, better strength, better mobility (Davidson et al., 2009).

Body composition also drifts with age even when the scale holds steady. The Health ABC study found people gradually losing skeletal muscle and subcutaneous fat while gaining visceral fat and fat within muscle tissue (Newman et al., 2005). Less muscle with more central fat raises metabolic risk and costs mobility, and it is a large part of why sarcopenic obesity shows up in older adults.

Bariatric surgery offers a natural experiment in what happens under very large weight loss. Gallagher’s group found that surgical patients lost substantial fat while holding onto muscle long term, provided nutrition stayed adequate and they resumed activity afterward (Davidson et al., 2018). Skeletal muscle remained relatively stable at five years despite major reductions in fat mass.

What I tell patients comes down to this. Do not manage your health by the scale alone. Protect the muscle. Resistance training two or three times a week, adequate protein while calories are restricted, and goals you can actually sustain. A 5 to 10 percent reduction over roughly 20 weeks improves metabolic risk and is realistic for most people (Wadden et al., 1996). I would rather track grip strength or how many chair stands someone can do than watch the scale week to week, because those numbers tell me whether the weight coming off is the weight we wanted to lose.

That is the whole point of paying attention to composition. Losing fat while holding muscle buys better health, more independence, and better metabolic outcomes. Resistance training is not an optional extra here. It belongs in the treatment plan alongside everything else.

Scott Rennie, D.O.

References

Gallagher D. Body Composition Changes with Weight Loss, Including Physical Activity Regimens. Columbia University, 2022.

Wadden TA et al. Am J Clin Nutr. 1996;63(3 Suppl):294S-298S.

Council on Scientific Affairs. JAMA. 1988;260(17):2547-2551.

Webster JD et al. Can J Appl Sport Sci. 1984;9(3):111-118.

Allison DB et al. Int J Obes Relat Metab Disord. 1999;23(1):1-7.

Beavers KM et al. Obesity. 2017;25(9):1476-1483.

Davidson LE et al. Arch Intern Med. 2009;169(2):122-131.

Davidson LE et al. Obesity. 2018;26(3):500-506.

Newman AB et al. Am J Clin Nutr. 2005;82(4):872-878.

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.

Is Yo-Yo Dieting Bad for You? Weight Cycling Explained

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

A lot of my patients describe the same arc. They work hard, lose weight, feel good for a while, and then months or years later it comes back. That repeated loss and regain is weight cycling. It is common, and it is hard on people both physically and emotionally.

The question I hear most often is whether it is even worth trying if the weight is coming back anyway. The research answers that more clearly than it used to, and the answer is yes.

Weight cycling generally means repeated intentional loss followed by unintentional regain. Some researchers set the bar at a 10 percent change in body weight occurring three or more times. Depending on the study, it affects 20 to 35 percent of men and up to half of women (Montani et al., 2015).

Why does the weight return? Biology pushes back harder than most people anticipate. After weight loss, resting energy expenditure falls further than body size alone would predict, and this metabolic adaptation can persist for years, meaning the body burns less than expected (Fothergill et al., 2016). Hormones move too. Leptin drops, hunger hormones climb, and patients end up hungrier and less satisfied by meals than they were before (Sumithran et al., 2011). The body also tends to compensate for exercise by raising appetite. Together these explain why maintenance is the hard part, not the losing (Thomas et al., 2012).

The real question is whether the cycling itself does damage. Large reviews and cohort studies have not found strong evidence that weight cycling raises mortality or major chronic disease risk when the weight loss is intentional and supervised (Mehta et al., 2014). Some work suggests regain may favor fat over muscle, visceral fat especially, though the findings are inconsistent (Mackie et al., 2017).

The psychological picture is better than most people assume. Foster and colleagues found that patients who regained weight still reported improvements in mood, hunger, and eating behavior after the loss phase (Foster et al., 1996). Other work has found no consistent long-term harm from the pattern itself (Osborn et al., 2011).

So should patients keep trying? The National Task Force on the Prevention and Treatment of Obesity concluded in 1994 that weight cycling should not deter people from attempting weight loss, and that position has held up (National Task Force, JAMA 1994). The benefits of intentional loss, lower blood pressure, better lipids, better glucose control, better quality of life, generally outweigh the risk of regaining.

One of my patients lost about 8 percent of her body weight through diet and walking. A year later most of it had come back. During the stretch she kept it off, though, her blood pressure normalized and she came off one of her antihypertensives. The weight returned. The benefit she got during that window was real and measurable, and the research says her experience is the rule rather than the exception.

What I steer patients toward is sustainable habit rather than another aggressive diet. Regular activity, consistent eating patterns, decent sleep, and watching the trend line instead of the daily number. A setback does not undo the progress. Staying connected to support, whether that is a clinician, a dietitian, or counseling, matters more than most people expect.

Weight cycling is real and it is discouraging. It is not a reason to stop. Even temporary weight loss buys real health, and the useful reframe is to treat weight management as ongoing care rather than a project with an end date.

Scott Rennie, D.O.

References

Montani JP et al. Obesity Reviews. 2015.

Fothergill E et al. Obesity. 2016.

Sumithran P et al. NEJM. 2011.

Thomas DM et al. Obesity. 2012.

Mehta T et al. Obesity Reviews. 2014.

Mackie GM et al. Obes Res Clin Pract. 2017.

Foster GD et al. J Consult Clin Psychol. 1996.

Osborn CY et al. Ethn Dis. 2011.

National Task Force on the Prevention and Treatment of Obesity. Weight cycling. JAMA. 1994;272(15):1196-1202.

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 Much Exercise Do You Need to Lose Weight?

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

Patients ask me all the time how much exercise really matters for weight loss. The honest answer is that it depends on what they are trying to do. Losing weight quickly, keeping it off, and staying healthy are three different goals, and exercise performs very differently against each one.

On one point the research is not ambiguous. Exercise on its own rarely produces large weight loss. Most trials show modest changes, roughly half a kilogram to three kilograms, and that is in people putting in 180 to 270 minutes a week (Jakicic et al., 2019). Below 150 minutes, most people do not lose much at all. I see the same thing on my schedule. Patients who start walking three times a week often feel noticeably better while the scale barely moves, and that gap is worth naming out loud before they get discouraged by it.

None of which makes exercise optional. It is among the best tools we have for preventing regain. Long-term data show that people sustaining higher volumes, often north of 250 minutes a week, are considerably more likely to hold onto a 10 percent loss (Jakicic et al., 2014). That is where the real return sits.

Paired with dietary change, the numbers improve. Adding exercise to calorie restriction increases short-term loss by about 20 to 25 percent over diet alone (Wing et al., 1998; Goodpaster et al., 2010). I had a patient who was cutting calories carefully and getting almost nothing for it until she added regular cycling. With both together she lost roughly twice as much and held it considerably longer.

Type and volume both matter. For general health, 150 minutes of moderate activity a week is the baseline. For meaningful weight loss, 250 to 300 minutes is closer to what is needed. For maintenance, somewhere in the 200 to 300 range seems to work. None of this requires a gym. Walking, yard work, and even light activity like standing or slow walking accumulate, and a 2021 doctoral dissertation found that increasing light-intensity activity independently predicted weight loss at both 6 and 12 months (Jackson, 2021).

Practically, I tell patients to start from where they actually are. Adding steps, breaking up long stretches of sitting, and picking something they do not dread produces more consistency than any prescribed routine they will abandon in a month. Thirty to sixty minutes on most days works whether it comes in one block or four. And if weight loss is the goal, it has to be paired with dietary change; exercise alone will disappoint them.

Exercise is not a shortcut to weight loss, and patients who come in expecting it to be will be let down. What it does do is keep lost weight off, improve metabolic health, and protect function as people age. Move more, sit less, keep going.

Scott Rennie, D.O.

References

Jakicic JM et al. Physical Activity and the Prevention of Weight Gain in Adults: A Systematic Review. Med Sci Sports Exerc. 2019;51(6):1262-1269.

Jakicic JM et al. Obesity. 2014;22:2284-2292.

Goodpaster BH et al. JAMA. 2010;304(16):1795-1802.

Wing RR et al. Am J Clin Nutr. 1998;67(3):551-558.

Physical Activity Guidelines Advisory Committee. 2018 Scientific Report.

Jackson R. Doctoral dissertation, 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.

Does Fasting Slow Aging? What the Science Says

On By Dr. Scott RennieIn Longevity & Healthy AgingLeave a comment

Aging cannot be stopped. The pace of it may be influenced by what and when we eat, and that idea is old rather than new. Since the 1930s, animal studies have shown that cutting calories without causing malnutrition extends lifespan. Rodents held at a 30 percent reduction lived longer with less cancer and less heart disease.

The proposed mechanisms are lower oxidative stress, better mitochondrial function, and less inflammation. Less fuel in, less metabolic wear.

Then you move from mice to people and it gets complicated.

The CALERIE trials brought calorie restriction into human research. CALERIE II found that cutting roughly 15 percent of calories for two years improved blood pressure, cholesterol, and markers of oxidative stress, and those benefits appeared without major weight loss (Kraus et al., 2019). The obstacle is adherence. Sustained restriction is hard on mood, on social life, and on nutritional balance, and most people will not hold it.

Which is how fasting patterns entered the conversation. Intermittent fasting covers several approaches. Some people fast on alternate days. Others follow 5:2, eating normally five days a week and restricting on two. Time-restricted feeding, which confines eating to an 8 to 10 hour window, has drawn the most recent attention.

Alternate-day fasting does produce fat and weight loss, but hunger is a serious barrier and dropout rates run high. Modified versions have not clearly outperformed standard calorie restriction (Trepanowski et al., 2017).

Time-restricted feeding looks more workable. Sutton and colleagues tested an early schedule with all meals between 7 a.m. and 3 p.m. Participants did not lose weight, but insulin sensitivity, blood pressure, and oxidative stress markers all improved, and they reported less hunger through the evening (Sutton et al., 2018). Other short-term work points the same direction, particularly on appetite control and metabolic flexibility (Hatori et al., 2012; Varady et al., 2022).

What does that mean in practice? Calorie restriction has the strongest animal data and some genuinely promising human results, and almost nobody sustains it. Alternate-day fasting rarely survives contact with real life. Time-restricted feeding is the one most patients can actually keep, and even moving to a 10 hour window and dropping late-night meals is a defensible starting point.

When I talk this through with patients, I usually suggest starting at a 12 hour window and tightening it only if they tolerate the change well. What goes in the window still matters more than the window does, and nutrient density should not get lost in the enthusiasm about timing.

Fasting is one tool among several, and which one fits depends on the person, their health, and what they can hold onto for longer than a month.

Scott Rennie, D.O.

References

Ravussin E, Redman LM et al. 2015.

Kraus WE et al. Lancet Diabetes Endocrinol. 2019.

Sutton EF et al. Cell Metab. 2018.

Trepanowski JF et al. JAMA Intern Med. 2017.

Heilbronn LK et al. 2005.

Spadaro PA et al. 2022.

Hatori M et al. Cell Metab. 2012.

Varady KA et al. 2022.

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.

Do Weight Loss Supplements Work? What Research Shows

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

Patients ask me about supplements constantly. They have seen an ad promising fast results from something natural and want to know whether it is worth a try. The answer is duller than the advertising. The evidence behind most weight loss supplements is thin, and the safety problems are not.

Paul R. Thomas at Columbia University’s Institute of Human Nutrition has reviewed this literature. What he and others find is that these products mostly do not work. The studies that exist tend to be small, short, and funded by the companies selling the product. Where a benefit shows up, it is small. Garcinia cambogia came in at under a kilogram of difference against placebo. That is not what patients are hoping for when they buy it, and it is not remotely close to what lifestyle change or an FDA-approved medication will do (Thomas, 2022).

The marketing claims sort into a few categories. Appetite suppression is credited to hoodia, glucomannan, and saffron. Metabolic or energy boosting gets attributed to caffeine, green tea extract, and bitter orange. Fat absorption blocking is the pitch for chitosan, and reduced fat synthesis for CLA and garcinia cambogia. The proposed mechanisms sound reasonable. The measured effects are close to nothing.

Safety is the more serious issue. Supplements do not have to be proven safe or effective before they are sold, because they are regulated closer to food than to drugs. The FDA can generally act only after harm is documented, which leaves a wide window. Independent testing has repeatedly turned up quality failures, including heavy metal contamination and doses that do not match the label. Some products have been found to contain banned or genuinely dangerous drugs, among them sibutramine, pulled from the market over cardiovascular risk, and phenolphthalein, a carcinogen (Tucker et al., 2018).

The harm is documented rather than theoretical. Roughly 23,000 emergency department visits a year in the United States are attributed to supplements, and weight loss and energy products account for most of them. The usual presentations are palpitations, chest pain, and tachycardia, and the patients are disproportionately young adults in their twenties and early thirties (Geller et al., 2015).

When patients ask what to do, I tell them to be careful. If they are going to use something, single-ingredient products from established national brands are the safer end of the pool, ideally with third-party verification such as USP or NSF. Avoid proprietary blends that will not disclose what is in them. Be suspicious of anything promising to melt fat. If they have a reaction, stop the product, keep the bottle, and report it to Poison Control and the FDA’s MedWatch program.

Supplements are everywhere and the evidence does not support them. Nutrition, physical activity, behavioral support, and where appropriate FDA-approved medication remain both more effective and considerably safer than whatever is currently being advertised.

Scott Rennie, D.O.

References

Thomas PR. Weight Loss Supplements. Columbia University Institute of Human Nutrition, 2022.

Geller AI et al. Emergency Department Visits for Adverse Events Related to Dietary Supplements. NEJM. 2015;373:1531-1540.

Tucker J et al. Unapproved Pharmaceutical Ingredients Included in Dietary Supplements Associated With US Food and Drug Administration Warnings. JAMA Network Open. 2018;1(6):e183337.

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.

Do Weight Loss Apps and Devices Really Help?

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

Patients ask me whether weight loss apps and digital programs actually work. It is a fair question, and the honest answer has a lot of qualifiers in it. Traditional obesity care runs into limited visit time, cost, and a shortage of places to refer people. Technology, whether an app, a web platform, or a hybrid program with human coaching, routes around some of that.

Dr. Bonnie Spring at Northwestern has studied how eHealth, mHealth, and telehealth are reshaping obesity treatment. Her finding is that these tools extend reach, lower cost, and deliver feedback in real time. The difficulty is holding anyone’s attention long enough for that to matter.

The trends in the research are reasonably clear. Web-based programs on their own produce small losses, around 2 to 3 percent of body weight. Better than nothing, and well short of the 7 to 8 percent that structured in-person programs achieve (Wieland 2014; Raaijmakers 2015; Tang 2014). Roughly half of users drop out.

Mobile approaches do better. In a review of U.S. trials, about 63 percent of studies found meaningful weight loss with mHealth interventions (Burke, Ma, Spring 2015). Texting on its own moved very little; outcomes improved when coaching or app-based monitoring was layered on. The catch is that most people abandon apps almost immediately, with more than three quarters stopping within three days of downloading.

Spring’s Opt-In Study used the Multiphase Optimization Strategy to build something cost-effective: remote sessions, structured self-monitoring, goal setting, and a trained buddy for support. Participants targeted a 7 percent loss, the threshold known to reduce diabetes and cardiovascular risk. More than half got there, at under $500 per person. That is comparable to the Diabetes Prevention Program at a fraction of the cost.

The buddy component turned out to matter most. Having a friend or family member reinforcing the changes between formal sessions kept people going, which lines up with what we already knew: social support is among the strongest predictors of durable results.

Access remains uneven. Reliable internet and comfort with digital tools are not evenly distributed, even though weight loss apps are among the most downloaded health apps in the world (Nikolaou & Lean, 2017). Owning a smartphone is the easy part. Cultural fit, affordability, and whether someone finds the technology tolerable all matter as much.

In my practice I have seen patients do well with commercial programs like Omada or Noom, which pair app-based tracking with remote coaching. Others get further with something simpler, MyFitnessPal being the usual example. These run somewhere between $40 and $130 a month, which is its own barrier and worth asking about before recommending one.

Technology works when it carries evidence-based strategy inside it: goal setting, self-monitoring, timely feedback, social support. Without those it is a download that gets deleted on day three. Knowing which products have research behind them and which have marketing behind them is part of our job now, and steering a patient toward the right one is often what separates a few weeks of enthusiasm from an actual result.

Scott Rennie, D.O.

References

Spring B. Use of Technology in the Prevention and Treatment of Obesity. Northwestern University, 2024.

Wieland LS et al. Systematic Reviews. 2014.

Raaijmakers LGM et al. Obesity Reviews. 2015.

Tang J et al. Obesity Reviews. 2014.

Burke LE, Ma J, Spring BJ et al. Ann Behav Med. 2015.

Nikolaou CK, Lean MEJ. Int J Obes. 2017.

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 to Sleep Better: Practical Steps for Patients

On By Dr. Scott RennieIn Other Diseases and ConditionsLeave a comment

Sleep gets a fraction of the attention we give diet and exercise, and it should not. Research from Dr. Ari Shechter at Columbia University has shown that poor sleep feeds obesity, diabetes, hypertension, and heart disease. It costs people their daily functioning, and underneath that it is quietly setting long-term disease risk. It is not a secondary problem.

When I ask patients about sleep, I keep it practical. When did this start, and is it new or has it always been like this? What is the bedroom like, too warm or too bright or too loud? Do they snore, gasp, or stop breathing, which points toward apnea? Any crawling or tingling in the legs, which points toward restless legs? I ask about weekdays versus weekends, because an irregular schedule can look exactly like insomnia. And I ask about caffeine, alcohol, nicotine, and medications, which patients rarely volunteer.

Formal tools give the conversation structure. The Epworth Sleepiness Scale is quick for daytime sleepiness. The Pittsburgh Sleep Quality Index is broader. STOP-Bang and the Berlin questionnaire flag possible apnea. The Insomnia Severity Index tracks both severity and how much it is costing someone functionally.

For objective data, in-lab polysomnography remains the standard for apnea, limb movement disorders, narcolepsy, and REM sleep behavior disorder. Wrist actigraphy at home gives a more practical picture of sleep and wake patterns over time, which is often what I actually need.

Adults should target 7 to 9 hours, and children and teenagers need more. Hours alone do not settle it. Timing, efficiency, and how someone feels the next day all matter. Patients tell me constantly that they are in bed for eight hours and wake up unrested. That is the point where efficiency and awakenings become the more useful thing to look at.

The consequences of chronic short sleep are well documented. It shifts ghrelin and leptin in the direction of more hunger and weight gain (Spiegel et al., 2004). It degrades glucose control and raises diabetes risk (Tasali et al., 2022). Hypertension, coronary disease, and stroke all track with insufficient sleep, and long-standing sleep problems are associated with cognitive decline and dementia risk (Vorster et al., 2024).

Causes are usually layered. Behavior contributes: irregular schedules, screens late, heavy meals and alcohol close to bed. So do physiologic and psychological factors: apnea, restless legs, anxiety, chronic pain.

Practical work starts with sleep hygiene. A consistent schedule resets circadian rhythm. Bedrooms should be cool, dark, and quiet. Bright light late interferes with sleep onset. Evening caffeine and alcohol come down. A wind-down routine, reading or stretching or a warm shower, makes the transition easier.

Daytime habits matter more than patients expect. Morning light anchors circadian rhythm. Even ten minutes of aerobic activity improves sleep depth. And for anyone waking in the night, what they do next shapes the rest of it: awake more than twenty minutes, get up and do something quiet in dim light rather than lie there getting frustrated.

The behavioral approach I use most is stimulus control. The principle is simple, which is rebuilding the association between the bed and sleep. Go to bed only when sleepy. Use the bed for sleep. Leave it if sleep is not coming. I have watched patients with years of insomnia retrain themselves this way. One had been scrolling his phone in bed for hours every night; once he started leaving the room when sleep would not come and only returning when he felt drowsy, his sleep onset shortened within a few weeks and the nightly frustration went with it.

Sleep is a medical necessity, and it belongs in routine care alongside everything else we screen for. Taking it seriously improves rest, and it also improves cardiometabolic health, mental health, and how people feel about their days.

Scott Rennie, D.O.

References

Shechter A. Improving Sleep in Your Patients. Columbia Cornell Obesity Medicine Course, 2024.

Spiegel K et al. Ann Intern Med. 2004.

Tasali E et al. JAMA Intern Med. 2022.

Markwald RR et al. PNAS. 2013.

Vorster A et al. Clin Transl Neurosci. 2024.

Board Certified in Obesity Medicine and Family Medicine

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

Does 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.