Tag: Insulin Resistance

A hand mirror, a pair of folded cotton socks and a home glucose meter with a lancet on a sunlit wooden table

What Does Diabetes Do to Your Skin?

On By Dr. Scott RennieIn Skin & Wound CareLeave a comment

Skin is the one organ I can actually see on a video visit. No stethoscope, no palpation, no reaching across the desk. Just a camera, whatever light the patient happens to have, and a screen. That limitation has made me pay closer attention to skin than I did when I worked in urgent care, because on video it is often the first physical evidence that something metabolic is going on.

Between 30 and 70 percent of people with diabetes develop a skin problem attributable to the disease at some point (1). That is an enormous range, which tells you the studies are measuring different populations and different definitions rather than anything precise. Take the range as what it is, a signal that this is common, not a statistic to quote back to anyone.

What follows is what I look for, why it matters, and where I think the usual advice is weaker than it sounds.

The velvet patch on the back of the neck

Acanthosis nigricans is the one I care about most, because it is visible, it is early, and patients almost never bring it up. Dark, thickened, velvety skin in the folds. Back of the neck, armpits, groin, under the breasts. Patients describe it as dirt that will not wash off, and some have been scrubbing at it for years.

The mechanism is insulin. Hyperinsulinemia drives IGF-1 receptor activation on keratinocytes and fibroblasts, which proliferate (2). So the plaque is a rough readout of how much insulin the pancreas has been pushing out to keep glucose in range. It shows up before the fasting glucose does. Sometimes years before.

Skin tags travel with it and share the same driver (2). A patient with acanthosis nigricans and a crop of acrochordons on the neck and axillae is telling you about their insulin resistance without a single lab drawn.

Here is where I differ from what patients are usually told. Dermatology handles acanthosis nigricans as a cosmetic complaint and offers topical retinoids, urea, sometimes laser. Those do something to the appearance. None of them touch the reason it is there. I follow the ADA rule and screen every adult from 35 regardless of BMI, and when I see that patch I do not wait for the birthday. I check an A1c.

It also improves. Not overnight, and not completely in everyone, but weight loss and improved insulin sensitivity soften the plaques over months. That is worth telling someone who has been scrubbing their neck since high school.

Skin tags carry information

I have a whole post on what skin tags are and what they look like, and it gets steady traffic from people worried about a lesion. What that post does not do is explain why someone in their thirties suddenly has fifteen of them.

Friction is part of it. Insulin is the rest.

What high glucose actually does to a wound

This one deserves its own post and is getting one. The short version: glycosylation impairs neutrophil and macrophage function, which prolongs the inflammatory phase instead of letting the wound move on to proliferation. Fibroblast activity drops, VEGF expression drops, matrix metalloproteinases go up, collagen density falls. Layer underlying vascular disease on top of that and you have a wound that stalls.

The practical consequence is that a cut on someone with an A1c of 11 is a different clinical problem than the same cut on someone with an A1c of 6, even though it looks identical on camera.

The infections that come with the territory

Candidal intertrigo lives in the skin folds, and the bigger the fold the more reliably it shows up. Beefy red, satellite lesions at the edge, itching or burning rather than pain. Patients treat it with hydrocortisone from the drugstore, which makes it worse, and then arrive convinced they have an allergy.

Tinea in all its addresses, feet, groin, nails. Onychomycosis in particular is stubborn and, in a diabetic foot, is not merely a nuisance: a thickened dystrophic nail is a pressure point and a portal.

Then cellulitis. Elevated glucose, impaired barrier, and a break in the skin from a fissure or a fungal infection between the toes. My rule for an abscess is that it goes out for drainage rather than getting empiric antibiotics from me over video, and I am firmer about that than some colleagues are.

Hidradenitis suppurativa, and what changed

HS has been badly served for a long time. Painful nodules and sinus tracts in the axillae, groin and under the breasts, frequently mistaken for recurrent boils for years before anyone names it. The association with obesity is strong and it is not a coincidence of body habitus alone; the inflammatory biology overlaps.

What has changed recently is incretin therapy. Multiple cohorts and case series now report reduced disease activity, fewer flares and less pain in HS patients treated with GLP-1 receptor agonists, alongside the expected BMI reduction (3). A cross-sectional survey found roughly two thirds of respondents reporting improvement in HS-specific measures (4).

I want to be honest about the strength of that evidence, because the enthusiasm is running ahead of it. These are retrospective cohorts, case series and patient-reported surveys. There is no adequately powered randomized trial with standardized background therapy. The signal is consistent enough that I take it seriously in a patient who has both conditions and would be a candidate for the drug anyway. It is not a reason to start an incretin in someone whose only indication is HS.

The foot

Somewhere between 19 and 34 percent of people with diabetes will develop a foot ulcer in their lifetime (5). The number that changed how I talk to patients is not that one, though. It is what happens after the ulcer closes: roughly 40 percent recur within one year, close to 60 percent within three years, and 65 percent within five (5).

Armstrong and colleagues argued from that data that a patient whose wound has closed should be thought of as in remission rather than healed (5). I use that word deliberately with patients now, because a person who believes they are healed puts the mirror away and stops looking at the bottom of their feet, while a person who believes they are in remission keeps checking, keeps wearing the shoes that were fitted for them, and calls about a blister on the day it appears rather than three weeks later when it has become something else. Remission gets you daily foot checks. Healed gets you a pair of sandals and a summer of walking on hot pavement with neuropathy.

That framing does more work in a fifteen-minute visit than any amount of education about glycemic targets.

What I ask for on video

Skin over a camera is genuinely hard. Autofocus hunts, phone processing smooths texture, and the color balance depends on whether someone is under a kitchen light or a window.

So I ask for two photographs of anything I need to actually assess. One from a distance, far enough back to show where the lesion sits and what the surrounding skin looks like, and one macro, as close as the phone will focus without blurring. Multiple angles if there is any elevation to it. The blur problem is the single most common reason I have to ask twice, and it is almost always because the patient is closer than the lens can handle. Backing up six inches fixes it.

For anything in a fold, I want the fold held open in the shot. For feet, I want the sole and between the toes, which usually means someone else holds the camera.

For patients

If the skin on the back of your neck or in your armpits has gone dark and thick and will not scrub off, that is not hygiene, and it is worth an A1c. If you are getting skin tags in bunches, same. If you have painful recurring lumps in your armpits or groin that have been called boils for years, ask specifically about hidradenitis suppurativa by name, because that is often what gets the diagnosis moving.

And if you have diabetes, look at your feet every day. Every day, including between the toes, including the bottom, using a mirror or a family member if you cannot see them.

For colleagues

Acanthosis nigricans in an adult is a screening prompt, not a dermatology referral. Check the A1c and the lipids before you send them for cosmetic treatment of the plaque.

The GLP-1 and HS literature is worth knowing about and worth being careful with. When a patient with both conditions asks whether the drug will help their skin, the honest answer names the cohorts, names their design, and stops short of promising anything.

On the foot, adopt the remission language. It changes adherence in a way that repeating ulcer statistics does not.

The Bottom Line

Skin is where metabolic disease announces itself, often years before a lab does. A velvety patch behind the neck, a crop of skin tags, a yeast infection in a fold that keeps coming back, a nail that will not clear. None of those are dermatologic curiosities to be treated in isolation. They are all the same disease showing up at the surface, and treating the surface without asking why it is there wastes the information. Check the A1c. Look at the feet. And when a wound closes on a diabetic foot, say remission, not healed.

Related Reading

Diabetic Foot Care: How to Check and Protect Your Feet

What is Hidradenitis suppurativa?

Skin Tags (Acrochordons): What They Are and Look Like

Ringworm, Athlete’s Foot and Jock Itch and Fungal Nail Infections

Newly Diagnosed With Type 2 Diabetes: What You Should Know

How Do You Actually Lose Weight? A Doctor Explains

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.

Sources

1. Vâță D, et al. Cutaneous Manifestations Associated with Diabetes Mellitus: A Retrospective Study. Diseases. 2023;11(3). PMID 37606477. https://pubmed.ncbi.nlm.nih.gov/37606477/

2. Marchand L, et al. All about skin manifestations of insulin resistance and type 2 diabetes: acanthosis nigricans and acrochordons. Postgrad Med J. 2020;96(1134):237. PMID 31611265. https://pubmed.ncbi.nlm.nih.gov/31611265/

3. 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/

4. 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/

5. Armstrong DG, Boulton AJM, Bus SA. Diabetic Foot Ulcers and Their Recurrence. N Engl J Med. 2017;376(24):2367-2375. PMID 28614678. https://www.nejm.org/doi/10.1056/NEJMra1615439

6. International Working Group on the Diabetic Foot. IWGDF Guidelines on the prevention and management of diabetes-related foot disease, 2023. https://iwgdfguidelines.org/guidelines-2023/

A wooden table in warm morning light with a coiled cloth tape measure, a small hand weight and a folded linen cloth

Does Menopause Cause Weight Gain, or Is It Just Aging?

On By Dr. Scott RennieIn Menopause & Women's Health, Weight Loss & Metabolic HealthLeave a comment

Your weight has been climbing about a pound a year since your early forties. Then something else changed. Same body, rearranged. The jeans that caught at the hip now catch at the waist.

Aging put the weight on. Menopause moved it.

The scale was never the menopause story

The Study of Women’s Health Across the Nation tracked women through the transition with repeated DXA scans. Weight and BMI gains that begin in premenopause “continue on an unaltered trajectory” through it, then flatten after the final period (1). Menopause does not bend the weight curve. The curve was already bending.

Two SWAN numbers circulate and both are real. In the full cohort of 3,064 women aged 42 to 52, weight rose 2.1 kg over three years, about 0.7 kg a year (2). In the smaller DXA sub-cohort, inside the 3.5-year window around the final period, 0.25 kg a year (1). Call it a pound to a pound and a half a year through midlife, none of it accelerated by menopause.

Where the fat goes

In 380 SWAN women with serial DXA, visceral fat drifted down before the transition at 1.85% a year, then climbed 6.24% a year inside the transition window (95% CI 4.31 to 8.17), settling at 1.47% after (3). Android fat went from 1.21% to 5.54%; the hip and thigh depot only to 2.03%. Lean mass flips sign in the same window, from gaining 0.2% a year to losing 0.2% (1), on top of the 3% to 8% per decade women lose after 30 (4).

Waist girth, meanwhile, rises 0.55% a year before the transition and 0.96% during it (3). Visceral fat moves six times faster than the tape can see, which is why a stable BMI and an unchanged waist are not reassurance.

Your metabolism did not crash at 50

Doubly labeled water, the reference method for what a human actually burns, was applied to 6,421 people across 29 countries. Total expenditure, basal expenditure and fat-free mass were “all stable from age 20 to 60” (5). The break point for adjusted total expenditure sits at 63.0 years, and the decline after it runs 0.7% a year (5).

The estradiol-specific effect is real and modest. Forty-five premenopausal women were randomized to ovarian suppression with placebo or transdermal estradiol add-back. Resting expenditure fell 54 kcal a day on placebo and did not fall at all with estradiol (6). Fifty-four calories. Measurable. Not a collapse.

Why it happens, and how much of that is known

Less than the confidence of the explanations would suggest. Estradiol loss lowers resting expenditure, since add-back prevented it in a randomized design (6), and the redistribution is time-locked to the final period rather than to birthdays (3). Past that it thins out fast. The one randomized ovarian-suppression trial measuring body composition and free-living expenditure together, 34 women over 24 weeks, found no endpoint that differed between groups (7). The Menopause Society says estrogen regulation of energy intake and expenditure “has not been well studied,” with “a paucity of studies” on estrogen and skeletal muscle (8). Falling estradiol, rising FSH, the androgen-to-estrogen shift: nobody has sorted out which drives it.

What shows up on your labs

SWAN modeled cardiovascular risk factors two ways in 1,054 women with a natural final period, once as chronological aging and once as ovarian aging. Only total cholesterol, LDL cholesterol and apolipoprotein B jumped inside the year before and after the final period (9). Glucose, insulin, blood pressure, fibrinogen and CRP fit the plain aging model (9), and the American Heart Association agrees (10).

So insulin resistance is not independently menopause-driven, whatever you have been told. The visceral fat is menopause-linked, and visceral fat drives insulin resistance on its own. A chain, not a shortcut, and it points at different treatment.

Here is where my own practice diverges from the cohort data. I screen lipids and apoB at intake, before starting any medication for weight loss, so my trigger is the visit rather than the menopausal stage. For hormone therapy I don’t routinely order them. I give the patient the options and tell her up front that insurance sometimes will not pay for apoB or apoA testing, which turns out to be a real constraint on what actually gets drawn.

Lift something heavy, then eat enough protein to use it

101 randomized trials, 5,697 postmenopausal women. Training raised fat-free mass 0.66 kg and cut fat mass 1.27 kg, and the modalities split: resistance work won for lean mass (+0.90 kg), aerobic for fat and waist (1.94 kg, 2.30 cm) (11).

Protein partners that work rather than replacing it. In 776 postmenopausal women aged 55 and older, whey improved lower-limb lean mass and strength when paired with resistance training, and had “no significant benefit on muscle strength or lean mass” without it (12). The powder is not the intervention.

Write down 1.2 g of protein per kilogram daily, 150 minutes of moderate activity weekly, strength training twice a week (4). On an incretin, higher: 1.2 to 1.6 g/kg/d, strength work three times weekly (13).

The strongest diet trial here is a prevention trial

The Women’s Healthy Lifestyle Project randomized 535 premenopausal women, mean age 47, and followed them 54 months through the transition. The intervention group finished 0.2 lb lighter. Controls gained 5.2 lb (14). Which diet matters less: 144 centrally obese postmenopausal women randomized to an energy-restricted Mediterranean or Central European diet both lost 7.6 kg and 24.6% of visceral fat in 16 weeks, with no difference between arms (15). Choose the one you will still be doing next year.

Hormone therapy, stated precisely in both directions

A Cochrane review of 28 randomized trials and 28,559 women found no evidence that estrogen alone or estrogen with progestogen affects body weight or prevents the BMI increase normally experienced at menopause (16). That review is old, last published in 2000, and still the largest pooled analysis of that endpoint. Hormone therapy does not cause weight loss, and it does not prevent menopausal weight gain.

What it does is narrower. The Menopause Society’s own key point: hormone therapy “may help attenuate abdominal adipose accumulation and weight gain associated with the menopause transition,” and “the effect is small” (8). In the WHI, no significant slowing of weight gain and a lesser waist increase over three years (8). On muscle, systematic reviews find neither benefit nor harm (8). A 2026 review is blunt: hormone therapy “should not be marketed or prescribed for weight loss or obesity treatment” (17).

Good drug. Vasomotor symptoms, genitourinary syndrome, bone. Abdominal fat is not on that list.

My own practice, stated plainly: I don’t prescribe MHT for patients who want to lose abdominal fat.

GLP-1s and the muscle question

Menopausal status does not blunt these drugs. A post hoc SURMOUNT analysis by reproductive stage found tirzepatide produced 23% weight reduction in postmenopausal women against 3% on placebo, matching premenopausal women at 26% versus 2% (18).

Now the counterintuitive part. In the SURMOUNT-1 DXA substudy, 160 participants scanned at baseline and week 72, tirzepatide produced 21.3% weight loss, 33.9% fat mass loss and 10.9% lean mass loss (19). Of the weight lost, roughly 75% was fat and 25% lean in both the tirzepatide and the placebo arms (19). The lean loss scales with the weight lost rather than with the drug.

DXA lean mass is also not muscle. It counts water, glycogen and organ mass, and modeling puts true muscle loss nearer 10% to 15% of weight reduction in women who are not strength training (13). In a 106-patient semaglutide cohort, grip strength rose 4.1 kg at a year and sarcopenic obesity fell from 49% to 33% (20). Function can improve while the DXA number falls.

Still, nobody has published incident sarcopenia or functional outcomes for postmenopausal women on these drugs. That gap is why protein and lifting belong in the prescription.

When I start a postmenopausal patient on an incretin, the instruction is 1.6 g of protein per kilogram of body weight a day, and strength training two to three times a week. That is the top of the range the evidence supports (13), and I put it there on purpose.

What is oversold

Supplements sold for menopausal weight loss. I looked for a randomized trial of any of them showing meaningful weight or visceral fat reduction and found none. Absence of evidence in one search is not proof of absence, so put it precisely: the marketing category exists; the trial literature does not. The Menopause Society does not recommend supplements or herbal remedies even for hot flashes (21).

Hormone therapy stacked on a GLP-1. Two retrospective cohorts, no randomized trial, and the 2026 review is unambiguous: do not start hormone therapy to boost an obesity medication (17).

And one asymmetry worth getting exactly right. Treating hot flashes or insomnia in order to lose weight has no trial behind it that I can find. The reverse direction is supported: the Menopause Society recommends weight loss for vasomotor symptoms, conceding those studies are small pilots and post hoc analyses (21).

If you are the patient reading this

Stop asking whether menopause made you gain weight. Ask where it went. Your BMI can sit still while visceral fat climbs 6% a year (3), so get lipids and apoB checked around your final period (9). Then put your effort where the randomized evidence is: resistance training, and a deficit you can hold for years.

Which raises the obvious question for a practice that runs entirely over video. So here is what I actually do. Patients get a Withings scale that syncs into the chart on its own and reports weight, BMI and body fat. A blood pressure cuff syncs the same way, automatically. The waist they measure themselves, with a tape, because the scale will not catch what the tape catches. Weight and blood pressure come in at least monthly and often more frequently than that, which means the trend is visible long before an annual visit would have found it.

For the clinicians

Screening beats explaining. The window runs roughly two years before to 18 months after the final period (1), and that is when lipids move and visceral fat accelerates (3)(9). Order the panel with apoB in it, and do not reassure a woman on a stable BMI or an unchanged waist; both understate a 6.24% per year visceral gain (3). When you start an incretin, write the protein target and the strength training into the plan (13). Hormone therapy earns its place on symptoms, bone and the diabetes signal (8), and no line at all on the weight plan.

The Bottom Line

Aging adds the weight, roughly a pound and a half a year through midlife, on a curve menopause does not bend (1)(2). Menopause moves the fat, visceral gain going from minus 1.85% to plus 6.24% a year inside a 3.5-year window (3). Metabolism holds steady to 60 (5). Hormone therapy treats symptoms and bone, not weight (8)(16). What changes the outcome is lifting, protein, a deficit you can sustain, and where indicated, a medication that works as well after menopause as before (11)(18).

Related Reading

Perimenopause and Menopause Symptoms and How to Manage Them FDA Removes Black Box Warning From Menopause Hormone Therapy Why Menopause Care Is Missing From Women’s Checkups Does Fasting Slow Aging? What the Science Says How Does Aging Change Your Metabolism? What Research Shows Why Exercise Matters for Obesity Beyond Weight Loss How Obesity in Pregnancy Affects the Baby and Placenta Why Is Losing Weight and Keeping It Off So Hard?

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.

Sources

1. Greendale GA, et al. Changes in body composition and weight during the menopause transition. JCI Insight 2019. https://pmc.ncbi.nlm.nih.gov/articles/PMC6483504/

2. Sternfeld B, et al. Physical activity and changes in weight and waist circumference in midlife women. Am J Epidemiol 2004. https://academic.oup.com/aje/article/160/9/912/86561

3. Greendale GA, et al. Changes in regional fat distribution and anthropometric measures. J Clin Endocrinol Metab 2021. https://pmc.ncbi.nlm.nih.gov/articles/PMC8372653/

4. The Menopause Society. MenoNote: Midlife Weight Gain, 2025. https://menopause.org/wp-content/uploads/for-women/MenoNote-Weight-Gain.pdf

5. Pontzer H, et al. Daily energy expenditure through the human life course. Science 2021. https://doi.org/10.1126/science.abe5017

6. Melanson EL, et al. Regulation of energy expenditure by estradiol in premenopausal women. J Appl Physiol 2015. https://pmc.ncbi.nlm.nih.gov/articles/PMC4628992/

7. Gavin KM, et al. Ovarian suppression in premenopausal women: no change in free-living energy expenditure. Obesity 2020. https://pmc.ncbi.nlm.nih.gov/articles/PMC7653843/

8. North American Menopause Society. 2022 hormone therapy position statement. Menopause 2022. https://menopause.org/wp-content/uploads/professional/nams-2022-hormone-therapy-position-statement.pdf

9. Matthews KA, et al. Chronological aging or the menopausal transition? J Am Coll Cardiol 2009. https://doi.org/10.1016/j.jacc.2009.10.009

10. El Khoudary SR, et al. Menopause transition and cardiovascular disease risk. Circulation 2020. https://doi.org/10.1161/CIR.0000000000000912

11. Khalafi M, et al. Exercise training and body composition in postmenopausal women. Front Endocrinol 2023. https://pmc.ncbi.nlm.nih.gov/articles/PMC10306117/

12. Kuo YY, et al. Whey protein supplementation in postmenopausal women. Nutrients 2022. https://pmc.ncbi.nlm.nih.gov/articles/PMC9572824/

13. Mozaffarian D, et al. Nutritional priorities to support GLP-1 therapy for obesity. Am J Clin Nutr 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC12612741/

14. Kuller LH, et al. Women’s Healthy Lifestyle Project: results at 54 months. Circulation 2001. https://doi.org/10.1161/01.cir.103.1.32

15. Bajerska J, et al. Energy-restricted Mediterranean and Central-European diets in postmenopausal women. Sci Rep 2018. https://pmc.ncbi.nlm.nih.gov/articles/PMC6057942/

16. Kongnyuy EJ, et al. Hormone replacement therapy: weight and body fat distribution. Cochrane Database Syst Rev CD001018. https://www.cochrane.org/evidence/CD001018_hormone-replacement-therapy-has-no-effect-body-weight-and-cannot-prevent-weight-gain-menopause

17. Younglove C. Menopause hormone therapy in weight management. Obesity Pillars 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC13010941/

18. Tchang BG, et al. Weight reduction with tirzepatide by reproductive stage: SURMOUNT post hoc analysis. Obesity 2025. https://doi.org/10.1002/oby.24254

19. Look M, et al. Body composition changes with tirzepatide in SURMOUNT-1. Diabetes Obes Metab 2025. https://doi.org/10.1111/dom.16275

20. Alissou M, et al. Semaglutide, fat mass, lean mass and muscle function: SEMALEAN. Diabetes Obes Metab 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC12673431/

21. North American Menopause Society. 2023 nonhormone therapy position statement. Menopause 2023. https://menopause.org/wp-content/uploads/professional/2023-nonhormone-therapy-position-statement.pdf

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.

Related Reading

Longevity Medicine: What Actually Works, and What Doesn’t Does Intermittent Fasting Work? A Doctor Explains Does Meal Timing Affect Your Metabolism and Health? Does Menopause Cause Weight Gain, or Is It Just Aging?

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.