Sara Szal MD
One of my patients is a woman who is 34 and doesn’t plan to have children. She has lost 28 pounds on a GLP-1 medication, her blood sugar and insulin resistance have improved, her jeans slide on without the usual struggle, and everyone from her sister to her trainer keeps telling her how amazing she looks.
By almost every conventional measure, her treatment is working, except she barely wants sex anymore.
She used to be the one who initiated but now desire rarely crosses her mind, and when her partner drops a hint, she feels polite indifference rather than appetite, which confuses her, because she loves him, finds him attractive, and can’t locate the switch that got turned off.
There’s something else, too. She tracks her heart rate variability (HRV), a measure of the variation in time between heartbeats that offers a window into the autonomic nervous system, and since she started the medication her morning number has dropped by 30 percent.
She’s losing weight but her body is telling a more complicated story.
Did the medication cause these changes? We don’t know for sure. Low desire and a falling HRV have many possible explanations (too little food, broken sleep, psychological stress, other medications, shifts in health or in the relationship itself), and any one of them could be responsible, or several could be braided together.
Still, I’m hearing versions of her story often enough now that it concerns me. Women on GLP-1s often tell me they want sex less. Some say arousal takes longer to build or arrives muted, as though someone turned down the volume on sensation. And several have confided that their vagina feels looser. They describe a laxity, a sense that things aren’t as snug or as responsive as they were before the weight came off.
I don’t yet know how common this is, or why it happens. It’s motivated me to ask every woman on these medications about desire, arousal, sensation, and pelvic floor function, ideally before her first dose and again each time the dose climbs or we have a follow-up visit.
What I can tell you is that the published evidence is astonishingly thin. I haven’t found a single randomized trial that used a validated measure of female sexual function, such as the Female Sexual Function Index (FSFI), as an endpoint in women taking GLP-1s, and I haven’t found a single study that measured pelvic floor strength. A July 2026 review from Mayo Clinic concluded that these drugs may paradoxically suppress desire and arousal through dopamine- and serotonin-related pathways in the brain, even as the weight comes down, while acknowledging that systematic clinical evidence in women is lacking.[1]
In other words, what I’m seeing in my patients is biologically plausible, and nobody has bothered to measure it yet. That brings us to today’s topic and a question for you: If you’re on a GLP-1, are you noticing a change in desire? Sensation? Pelvic floor function? HRV?
The great thing about Substack is that we can collect real world evidence instead of waiting for the people who fund the GLP research to step in and discover the more complete picture of what these medications may be doing to us, beyond reducing food noise, improving metabolism, lowering inflammation, and potentially reducing cognitive decline. I get it that these are wins for many of us, but only if we all get full informed consent.
I’ve spent more than 30 years caring for women, and I was trained, like most physicians of my generation, to treat the doctor’s scale as a vital sign and every lost pound as a small victory. Here’s what three decades in the exam room have taught me about that training.
We’ve become extraordinarily good at measuring how much weight a woman loses. We’re much less interested in what else she might lose along the way.
As GLP-1 medications reshape the treatment of obesity and get prescribed for other indications like bulimia, addiction, and diabetes, and as more women start them every month, that imbalance deserves scrutiny.
Note: The opening case is a clinical scenario illustrating questions that deserve investigation, not proof that GLP-1 treatment caused these symptoms. The patterns I describe from my practice are clinical observations, not study data. I wish we had the study data.
Let me be clear: I’m not opposed to GLP-1 medications. Semaglutide, liraglutide, tirzepatide, and the other incretin-based therapies represent an enormous advance in metabolic medicine; they can produce substantial weight loss and better glycemic control, and certain agents have demonstrated cardiovascular and other clinical benefits in appropriately selected populations. For women with obesity, type 2 diabetes, or significant metabolic dysfunction, they can be transformative. I’ve watched women fight insulin resistance for years with diet and exercise alone while their biology quietly worked against them, and I’ve seen how much changes, in their labs and in their faces, when that metabolic burden finally begins to lift.
So I want to ask a different question, one that sits underneath all the efficacy data: what should count as working, particularly for women?
Should a woman who loses 25 pounds while her strength slips, her HRV stays persistently low, and her desire fades be considered an uncomplicated treatment success? The answer depends on why those changes occurred, whether they last, and how they affect the life she’s trying to live, and yet those outcomes rarely make it into the conversation about weight-loss medications at all.
A 2025 review in Endocrinology took up the differences between women and men in how they respond to these drugs. Its authors, Stina Börchers and Karolina Skibicka, described quantitative differences in weight-loss response and possible interactions between GLP-1 signaling and estrogen, which will make sense to any woman who has noticed her appetite shift across her cycle. Their other finding was less reassuring: substantial gaps remain in the basic science involving women and female animals, especially research on brain function, behavior, and reproductive physiology.[2]
This is no small omission. These medications act on the pathways that govern appetite, metabolism, and reward, and the female hormonal environment, with its monthly tides and its midlife turn, may shape how those pathways respond. We’ve finally developed drugs that can bend the trajectory of metabolic disease. Now we owe the women taking them a full accounting of the consequences.
HRV is one of my favorite physiological measures, and one of the most misunderstood. It reflects the variation between successive heartbeats, and depending on how and when it’s measured, it offers a window into autonomic regulation, including the parasympathetic, vagal influences that let the heart slow down, settle, and recover. Higher HRV within the same person often tracks with better recovery and adaptability, though higher isn’t universally better; age, fitness, breathing, illness, medications, and measurement methods all push the number around, and I’m wary of anyone who turns a wearable score into a diagnosis.
Still, when a woman’s usual HRV drops substantially and stays down, I want to understand why, because the nervous system is where so much of a woman’s experience of her own body lives: her capacity to rest, to recover, to feel safe enough to soften into pleasure. GLP-1 medications may be part of that picture.
In a randomized, double-blind crossover trial published in Diabetes Care, 27 participants with type 2 diabetes and coronary artery disease received liraglutide or placebo. Compared with placebo, liraglutide:
• Reduced SDNN, a measure of HRV, by 33.9 milliseconds (P < 0.001).
• Reduced another HRV measure, RMSSD, by 0.3 log units (P = 0.025).
• Increased mean heart rate by 8.1 beats per minute (P = 0.003).
Those changes occurred even as weight and metabolic markers improved.[3] The finding deserves attention, though the participants looked nothing like a healthy 34-year-old woman, and the results can’t be stretched to cover every GLP-1 drug.
A newer study brought wearables into the picture. In 2025, researchers followed 66 people starting GLP-1 therapy for twelve weeks; participants lost roughly 10 percent of their body weight, and compared with matched controls, their resting heart rate rose by 3.2 beats per minute while their HRV ran 6.2 milliseconds lower at the twelve-week mark.[4] For someone whose baseline HRV is 60 milliseconds, six milliseconds may look trivial. For someone starting at 20, the same absolute drop takes a much bigger bite, which is why I care about a woman’s own baseline and trend far more than any universal target.
The evidence doesn’t all point one way, and I’d be doing you a disservice to pretend it does. In the large GRADE trial of adults with type 2 diabetes, liraglutide didn’t increase ECG-defined cardiovascular autonomic neuropathy relative to the comparison treatments, and one HRV measure, SDNN, was higher in the liraglutide group at two years (P = 0.02).[5] Meanwhile, a 2026 meta-analysis of randomized trials found that GLP-1-based medications raised resting heart rate overall, by about 3.5 beats per minute compared with placebo, with the size of the effect varying by agent and dose.[6]
Where does that leave us? Some GLP-1 medications can raise resting heart rate, and several studies show reductions in HRV, particularly early in treatment; but a lower reading doesn’t establish autonomic injury, and we don’t yet know the long-term meaning of every change we can observe.
A medication can improve cardiovascular outcomes while changing the autonomic signals your wearable measures, like resting heart rate and HRV.
What bothers me is how little sex-specific information we have. How much does HRV change in premenopausal women compared with postmenopausal women? Does estradiol status modify the response? Does the speed of weight loss matter more than the dose? And what happens to HRV when a woman is eating too little to support her training, a trap that’s easy to fall into when a drug has quieted hunger so effectively she forgets to eat lunch? These are answerable questions. For now, the studies I’ve described don’t give us reliable women-versus-men estimates of GLP-1-related HRV changes, so what we have is a research gap, and a gap is no evidence that the effect runs larger in women.
Of everything I’m raising here, this may be the least studied and the most personally consequential, and it’s the one I hear about most in my office. It also sits at the center of the work I care about most, because female desire has always behaved like the canary in the coal mine of women’s health: it’s often the first thing to dim when something in the body or the life goes wrong, and too often the last thing anyone in a white coat thinks to ask about.
One of the remarkable effects of GLP-1 medications is the lowering of what patients call food noise. Women describe walking past the refrigerator without a running internal debate about what’s inside it, sitting through a work lunch without counting bites, waking up without the morning bargain about what they will and won’t eat that day. For many, that silence feels like freedom. I get it. I’m in recovery from disordered eating and food addiction after suffering privately with it until age 40.
But food isn’t our only source of pleasure, and appetite was never only about food. GLP-1 receptors sit in the hypothalamus and in the mesolimbic reward circuits that drive “wanting,” the motivational pull toward food, sex, and other natural rewards, so the same mechanism that quiets the call of a second helping could plausibly quiet the pull toward sex.[1] Could medications that turn down food-related reward also turn down sexual desire? Possibly.
The July 2026 review in Menopause, led by Regina Castaneda and colleagues at Mayo Clinic, examined weight-loss interventions and sexual function in midlife women and described a paradox worth taking seriously. Obesity itself impairs female sexual function, and weight loss through lifestyle change or bariatric surgery tends to improve it, through better metabolic health, body image, mobility, and vascular function; so when women on GLP-1s report the opposite, weight loss alone can’t explain it. The authors proposed that these drugs may act on desire and arousal through central neuroendocrine pathways, including dopamine- and serotonin-related signaling, while emphasizing that clinical evidence in women remains limited, drawn mostly from case reports, preclinical observations, and biological hypotheses rather than large, well-controlled human trials. Their practical recommendation is one I endorse: assess sexual function with validated instruments before and during therapy.[1]
In February 2026, researchers reported another intriguing finding in Behavioural Brain Research. They gave several GLP-1 receptor agonists to sexually experienced female rodents. In female rats, exendin-4 reduced proceptive behaviors (the darts and hops a female uses to solicit a mate) along with the intensity of lordosis, the posture of sexual receptivity; in female mice, liraglutide and dulaglutide reduced the time females spent with males. The researchers pointed to the lateral septum and the nucleus tractus solitarius, a brainstem hub, as likely sites of action, and the effects varied by drug and species.[7]
This doesn’t prove that Ozempic or Mounjaro lowers libido in women. A rat’s hop is a long way from a woman’s longing, which is woven from hormones, relationships, cognition, physical comfort, personal history, stress, and the felt sense of emotional safety. But the findings support a question that deserves proper human research.
And men? A 2025 analysis of the FDA Adverse Event Reporting System found a signal for decreased libido among men taking GLP-1 medications, though the picture isn’t uniform (some users report the opposite, a rise in libido), and databases like this one can’t establish that a drug causes a symptom or how often it occurs.[8] The drugs may not all behave alike, either. A 2026 analysis of real-world adverse-event reports found that tirzepatide had lower reporting odds than other GLP-1 medications for decreased libido (adjusted reporting odds ratio 0.39) and for sexual dysfunction (0.16).[9] That analysis wasn’t specific to women, and voluntary reporting databases carry well-known biases, so I treat it as a question worth testing, nothing more.
Then there’s sensation. Some of my patients tell me that touch feels muted, that arousal needs more stimulation to build and fades faster than it used to. I haven’t found any study of genital sensation in women on GLP-1s. The closest signal comes from a 2026 pharmacovigilance analysis of the World Health Organization’s global adverse-event database and the French national database, in which semaglutide and tirzepatide were associated with abnormal or heightened skin sensation (dysesthesia and hyperesthesia), while exenatide was associated with reduced sensation (hypoesthesia); the effects appeared dose-dependent, often resolved when the drug was stopped, and in some cases returned when it was restarted.[10] Extending those findings to the vulva and clitoris is speculative. It’s still a good reason to ask.
We currently lack a reliable percentage of women who experience reduced libido on GLP-1 therapy, or a trustworthy comparison with men.
I find that unacceptable as these drugs move from short courses toward long-term use. If sexual desire were a routine, predefined outcome in GLP-1 trials, we would already know whether these medications improve it, suppress it, or do both in different groups of women, and whether the answer shifts with menopausal status, the amount of weight lost, the type of drug, the dose, or the energy a woman has left after a day of eating very little. Instead we have a system that carefully records nausea and constipation and rarely asks a woman what has happened to her sexual life.
I want to point out something larger here, the cultural water we all swim in. Women have been offered a version of this bargain for generations: be smaller, and in exchange you’ll be acceptable, desirable, chosen. Many of us signed without reading the fine print, giving up hunger first, then rest, then pleasure, a little at a time, because thinness was the currency and our own desire was the price. I don’t want a brilliant new class of drugs to quietly renew that contract with better pharmacology and a weekly injection.
There’s another possibility to hold alongside the biology. A woman’s lower desire may have little to do with reward circuitry. She may be chronically under-fueled, exhausted, stressed, or worn down by gastrointestinal side effects, which are reported more often in women than in men on these drugs.[11] She may be in perimenopause or menopause, when falling estrogen reduces lubrication, sensation, and arousal all on its own. She may be taking an SSRI, struggling with her mood, or renegotiating her relationship with a body that looks different in the mirror and feels different under her partner’s hands. Those explanations matter because each calls for a different response.
So when a 34-year-old tells me she barely wants sex after losing weight, I won’t assume it’s psychological, and I won’t assume it’s the GLP-1. I want to investigate.
Here the evidence is stronger. When a person loses substantial weight, the loss usually includes both fat mass and lean mass, and the trouble is that most women are told how much weight they’ve lost rather than what they’ve lost.
In a 2025 systematic review and network meta-analysis published in Metabolism, researchers pooled data from 22 randomized controlled trials involving 2,258 participants. Compared with controls, GLP-1-based interventions produced average reductions of:
• 3.55 kilograms in total body weight
• 2.95 kilograms in fat mass
• 0.86 kilograms in lean mass
Roughly 25 percent of the weight lost was lean mass.[12]
Before that number becomes another frightening headline, a distinction worth making. Lean mass and skeletal muscle are different measures: lean mass also includes water, organs, blood, and other nonfat tissue, so a drop measured by DXA doesn’t mean the same amount of contractile muscle disappeared. Nor does a 25 percent lean-mass share mean the medication is uniquely toxic to muscle, since lean mass commonly falls with substantial weight loss by any route. What matters is how much is lost, what kind, and what happens to strength, function, and metabolic health along the way.
Still, it would be a mistake to wave the concern away. Skeletal muscle is the body’s largest site of insulin-stimulated glucose disposal, taking up most of the glucose that insulin clears from the blood after a meal (I think of it as the metabolic sink that keeps blood sugar in line).[13,14] It also underwrites mobility, metabolic resilience, and the physical independence we all hope to carry into our eighties. A 2025 review in The Journal of Clinical Endocrinology & Metabolism examined incretin-based therapies, fat-free mass, and cardiorespiratory fitness, and its authors highlighted the persistent question: how do we keep the metabolic benefits of substantial weight loss without compromising muscle and physical performance?[15] A 2026 safety review likewise flagged lean-mass loss as an area that needs better mitigation strategies and longer-term study.[16]
Another finding deserves more attention than it’s gotten. In a retrospective 2026 study published in The Journal of Nutrition, researchers examined body composition among patients using GLP-1-based medications with and without nutrition counseling. The group on medication without counseling had a mean muscle-mass reduction of 7.01 pounds, the largest loss among the groups studied; medication use was statistically associated with muscle-mass loss (P = 0.013), while those receiving nutrition counseling alongside therapy saw smaller average reductions.[17] The study was observational, so it can’t prove that counseling prevented muscle loss, and the groups may have differed in other important ways. But it reinforces a clinical principle I believe down to my bones.
A prescription that suppresses appetite is not a complete nutrition and muscle-preservation strategy.
Women losing weight need enough protein, enough total energy, resistance training, and real attention to strength and function, and the relative weight of each may shift across a woman’s reproductive life. A woman of 34, a woman of 46 entering perimenopause, and a postmenopausal woman of 63 aren’t physiologically interchangeable, yet the conversation about weight loss often treats them as though they were.
Here the data turn frustrating again. A 2026 systematic review in the International Journal of Obesity examined body-composition changes with GLP-1 therapy, and among the included studies, only one reported sex-stratified body-composition results. In that six-month liraglutide study, women had more pronounced reductions in waist circumference and trunk fat, while men showed significant changes in total fat and certain regional fat measures, particularly in the arms; the proportions reaching at least 5 or 10 percent weight loss were similar between the sexes.[18]
Interesting? Yes. Enough to say women lose more muscle than men on these drugs? Absolutely not. There’s evidence of sex-related differences in weight-loss response and fat distribution, but we don’t have robust comparative data on how much skeletal muscle women lose relative to men, and that distinction matters to me. I don’t want us replacing the historical neglect of women’s physiology with a fresh collection of unsupported claims about female fragility. I want the data.
This is the change my patients raise most hesitantly, often at the very end of a visit with one hand already on the doorknob, so I want to handle it with care.
Vaginal laxity is a subjective sense of looseness, usually noticed during sex. It can reflect changes in the pelvic floor muscles, in the connective tissue that supports the vagina, in the vaginal tissue itself, or some combination; it’s common after vaginal childbirth and with age, and most women never mention it unless someone asks. Nobody has studied pelvic floor strength in women taking GLP-1s, and the indirect evidence points in two directions.
Start with muscle. We’ve just seen that GLP-1s reduce lean mass, and a separate 2025 meta-analysis put the average lean-mass reduction at about 1.4 kilograms in people without diabetes.[19] In older adults on long-term semaglutide, longitudinal data suggest declining handgrip strength and faster progression of sarcopenia, the age-related loss of muscle mass and function.[20] The levator ani, the main muscle of the pelvic floor, is skeletal muscle. Whether it follows the same pattern is unknown.
Now the reassuring direction. Weight loss is one of the best-documented treatments for stress urinary incontinence, and in randomized trials of women with overweight or obesity, losing roughly 5 to 10 percent of body weight cut incontinence episodes by about half.[21,22] Less weight means less load bearing down on the pelvic floor every time a woman coughs, laughs, or lifts a toddler. Fewer symptoms and a stronger pelvic floor are different things, though. In one randomized trial of women with obesity, pelvic floor symptoms improved with weight loss, yet the improvement didn’t correlate with measured changes in pelvic anatomy.[22] Weight loss alone doesn’t appear to train these muscles; pelvic floor muscle training remains the active intervention, and researchers are now testing it in women losing weight on a low-calorie diet.[23]
Then there’s everything else that can make a vagina feel different. Falling estrogen in perimenopause and menopause thins and dries vaginal tissue and dulls sensation, a condition called genitourinary syndrome of menopause. And some women with pelvic floor complaints have too much muscle tone rather than too little, which changes how sex feels in its own way. “Looser” can mean weaker muscle, altered tissue, changed sensation, or several of these at once. We’re early in learning about the muscle signal in women on GLP-1s, and we need to track it carefully.
Here’s the evidence as it stands in October 2026. Notice how unevenly the evidence is distributed.
The body-composition concern rests on multiple randomized trials, even if the measurement of true skeletal muscle remains imperfect. The HRV findings are real but vary by study, drug, measurement method, and follow-up. The libido question is biologically plausible and clinically important, yet the human evidence is far too thin to support a confident causal claim. And sensation and the pelvic floor are the least studied of all; what I’m seeing in my practice is a signal worth measuring, and so far that’s all it is. I would rather sit with uncertainty, out loud and in front of you, than pretend we know what no one has measured.
I’m not suggesting women stop their GLP-1 medications because their HRV fell or their sex drive changed. Abrupt decisions can undo meaningful metabolic progress, and any change belongs in a conversation with the prescribing clinician. I’m suggesting we widen the lens. If you’re taking one of these medications, or considering one, here are the five questions I’d want on the table.
Beyond the number on the scale, consider body composition when it’s clinically appropriate. DXA can help distinguish fat from lean tissue, though it can’t perfectly quantify muscle. I also care whether you can lift, climb, carry, and move as well as you did before, because function is the outcome your life runs on.
Appetite suppression can make adequate nutrition surprisingly hard. Protein matters, and so do total energy intake, the quality of what you eat, and your ability to train and recover. Eating almost nothing is no sign the medication is working better.
If you track HRV and resting heart rate, look at the trends alongside sleep, hydration, training load, illness, stress, and symptoms. A persistent change deserves context, and calm curiosity will serve you better than panic.
Has desire improved, declined, or stayed the same? Have you noticed changes in arousal, lubrication, comfort, pleasure, or orgasm? Does your vagina feel different, looser, or less sensitive? Are you leaking urine more, or less, and do any of these changes distress you? Your answers matter whatever the scale says. If you can, ask your clinician to document your sexual function with a validated questionnaire such as the FSFI before you start and again as your dose increases.[1] Changes that track with dose increases are worth reporting, since some sensory side effects appear to be dose-related.[10] Clinicians seeing these changes can file a report with FDA MedWatch; female sexual side effects are badly under-captured, and the only way that changes is if we write them down.
I want to know about your metabolic markers. I also want to know whether you’re stronger, whether you have energy left for your life, whether you feel capable in your body, and whether pleasure still has a place in it. These outcomes are part of health, and they deserve a line in your chart.
I’ve practiced medicine long enough to remember when women were routinely told to eat less and exercise more, even when that advice ignored their insulin resistance, their hormonal shifts, and their metabolic disease, and when the woman who didn’t lose weight was quietly blamed for her own biology. I’m grateful we now have better tools. But I don’t want the weight-loss revolution to repeat the same cultural mistake with more sophisticated pharmacology.
For too long, a woman’s weight has stood in for her health, her discipline, her attractiveness, even her worth. A lower number became the goal, and the way she felt inside her body became an afterthought. This is personal for me. I’ve spent my career trying to define what can go right with the female body, and along the way I’ve watched too many women, patients and friends and women I love, shrink their appetites in every sense of the word to fit a shape someone else approved.
GLP-1 medications give us an extraordinary chance to change metabolic medicine. They also give us a chance to redefine what successful treatment means, and to start measuring the things that make a life feel worth living: strength, recovery, desire, sensation, a body that feels like home. Not every woman will lose meaningful muscle or see her HRV or desire decline. Some will grow stronger, recover better, and feel more sexually alive as their metabolic health improves, and that belongs in the story too. We need research that can tell those trajectories apart rather than assuming every woman who loses weight walks the same physiological path.
I keep returning to that 34-year-old woman, and to the women in my office who sound like her. Her blood sugar improved. She lost 25 pounds. Her metabolic health is better. Good; let’s celebrate all of it. But when she tells us she barely wants sex, that her HRV has fallen by 30 percent, or that her body no longer feels like her own, I want us to be curious enough to investigate, rather than waving her experience away because the scale delivered the expected number.
The future of women’s metabolic health cannot be measured in pounds alone.
It has to include strength, resilience, sexual health, and the capacity to inhabit fully the life she wants. We shouldn’t have to trade one dimension of health for another without even knowing the trade is happening, and we shouldn’t have to wait another generation for researchers to study the female body with the precision it deserves.
If you’ve taken a GLP-1 medication, tell me in the comments: beyond the weight you lost, what changed in your strength, recovery, desire, sensation, or pelvic floor? Is someone tracking your body composition, including muscle mass, and muscle strength? Did your prescriber ask about these things?
Your stories can’t establish causation or tell us how common a side effect is, but they can sharpen the questions researchers and clinicians need to ask.
xo, Dr. Sara
Notes
[1] Castaneda R, et al. Weight Loss Interventions and Sexual Function in Midlife Women: The Emerging Role of Glucagon-Like Peptide-1 Receptor Agonists. Menopause. 2026.
[2] Börchers S, Skibicka KP. GLP-1 and Its Analogs: Does Sex Matter? Endocrinology. 2025.
[3] Kumarathurai P, et al. Effects of Liraglutide on Heart Rate and Heart Rate Variability: A Randomized, Double-Blind, Placebo-Controlled Crossover Study. Diabetes Care. 2017.
[4] Grosicki GJ, et al. Heart and Health Behavior Responses to GLP-1 Receptor Agonists: A 12-Wk Study Using Wearable Technology and Causal Inference. American Journal of Physiology-Heart and Circulatory Physiology. 2025.
[5] Pop-Busui R, et al. Differences in Prevalence and Incidence of Electrocardiogram Abnormalities and Cardiovascular Autonomic Neuropathy Among Randomized Glucose-Lowering Treatments in Early Type 2 Diabetes: The GRADE Cohort. Diabetes Care. 2025.
[6] Zhang Y, et al. Effect of Glucagon-Like Peptide-1 Receptor Agonists on Heart Rate in Non-Diabetic Individuals With Overweight or Obesity: A Systematic Review and Pairwise and Network Meta-Analysis of Randomized Controlled Trials. European Journal of Medical Research. 2026.
[7] Shevchouk O, et al. Short- and Long-Acting GLP-1 Receptor Agonists Decrease Female Sexual Behaviors in Experienced Rodents. Behavioural Brain Research. 2026.
[8] Pourabhari Langroudi A, et al. Male Sexual Dysfunction Associated With GLP-1 Receptor Agonists: A Cross-Sectional Analysis of FAERS Data. International Journal of Impotence Research. 2025.
[9] Lee N, Kim Y. Not All GLP-1 Receptor Agonists Are Alike: Real-World Evidence of Differential Endocrine and Dermatologic Safety. Diabetes/Metabolism Research and Reviews. 2026.
[10] Laroche M-L, et al. Dysesthesia Associated With GLP-1 Agonist Therapies: Data-Mining Analysis and Literature Review. European Journal of Clinical Pharmacology. 2026.
[11] Kantowski T, et al. Obesity Management: Sex-Specific Considerations. Archives of Gynecology and Obstetrics. 2024.
[12] Karakasis P, et al. Effect of Glucagon-Like Peptide-1 Receptor Agonists and Co-Agonists on Body Composition: Systematic Review and Network Meta-Analysis. Metabolism. 2025.
[13] Merz KE, Thurmond DC. Role of Skeletal Muscle in Insulin Resistance and Glucose Uptake. Comprehensive Physiology. 2020.
[14] Sylow L, et al. The Many Actions of Insulin in Skeletal Muscle, the Paramount Tissue Determining Glycemia. Cell Metabolism. 2021.
[15] Liu Z, et al. Incretin Receptor Agonism, Fat-Free Mass, and Cardiorespiratory Fitness: A Narrative Review. The Journal of Clinical Endocrinology & Metabolism. 2025.
[16] Kunutsor SK, et al. Safety and Tolerability of Glucagon-Like Peptide-1 Receptor Agonists: A State-of-the-Art Narrative Review. Drugs. 2026.
[17] Hoffman K, et al. Impact of Glucagon-Like Peptide-1/Glucose-Dependent Insulinotropic Polypeptide Therapy and Nutrition Counseling on Body Composition. The Journal of Nutrition. 2026.
[18] Sawicka-Gutaj N, et al. GLP-1 Agonists and Changes in Body Mass and Composition in Adults With Overweight or Obesity With or Without Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis. International Journal of Obesity. 2026.
[19] Anyiam O, et al. How Do Glucagon-Like Peptide-1 Receptor Agonists Affect Measures of Muscle Mass in Individuals With, and Without, Type 2 Diabetes: A Systematic Review and Meta-Analysis. Obesity Reviews. 2025.
[20] Prokopidis K. Glucagon-Like Peptide-1 Receptor Agonists and Muscle Strength Changes in Older Adults: Risks Beyond Muscle Mass Reductions. British Journal of Pharmacology. 2026.
[21] Wu JM. Stress Incontinence in Women. The New England Journal of Medicine. 2021.
[22] Gozukara YM, et al. The Improvement in Pelvic Floor Symptoms With Weight Loss in Obese Women Does Not Correlate With the Changes in Pelvic Anatomy. International Urogynecology Journal. 2014.
[23] Mendes PCS, et al. Effect of Pelvic Floor Muscle Training on Reports of Urinary Incontinence in Obese Women Undergoing a Low-Calorie Diet Before Bariatric Surgery: Protocol of a Randomized Controlled Trial. Trials. 2023.
