Clinical Evidence

The Research Behind TAKE

Every citation on this page has been checked against the primary source. Where the evidence is strong, we say so. Where it is thin, contested, or absent, we say that too. A research page that only lists supportive studies is marketing with footnotes.

One mechanism

The clinical picture on a GLP-1 medication begins with a single change: appetite falls, and intake falls with it. Understanding that one mechanism explains most of what follows.

The class-wide range in caloric intake. Mozaffarian D, Agarwal M, Aggarwal M, et al. Nutritional priorities to support GLP-1 therapy for obesity: A joint Advisory from the American College of Lifestyle Medicine, the American Society for Nutrition, the Obesity Medicine Association, and The Obesity Society. Obesity (Silver Spring). 2025;33(8):1475-1503. Key finding: individuals using GLP-1 medications for obesity experience caloric reductions of 16 to 39 percent. Note on interpretation: this is a range assembled across the whole drug class. The lower figure comes from liraglutide studies and the upper figure from oral semaglutide. It should not be read as the range for any one medication.

Semaglutide 2.4mg, the closest measurement to our customer. Friedrichsen M, Breitschaft A, Tadayon S, et al. The effect of semaglutide 2.4 mg once weekly on energy intake, appetite, control of eating, and gastric emptying in adults with obesity. Diabetes, Obesity and Metabolism. 2021;23(3):754-762. Key finding: ad libitum energy intake was 35 percent lower than placebo at 20 weeks in 72 adults with obesity. Note on interpretation: intake was measured at supervised test meals, not across months of ordinary eating.

Tirzepatide. Martin CK, Carmichael OT, Carnell S, et al. Tirzepatide on ingestive behavior in adults with overweight or obesity: a randomized 6-week phase 1 trial. Nature Medicine. 2025;31(9):3141-3150. Key finding: tirzepatide reduced energy intake by an estimated 524.6 kcal at a test meal compared with placebo in 114 adults. Note on interpretation: the authors report this in calories, not as a percentage. No published percentage for tirzepatide exists.

The mechanism is reduced intake, not malabsorption. Sibal R, Balamurugan G, Langley J, Graham Y, Mahawar K. Macronutrient, micronutrient supplementation and monitoring for patients on GLP-1 agonists: Can we learn from metabolic and bariatric surgery? Nutrients. 2025;17(23):3659. Key finding: unlike bariatric surgery, which reduces both intake and absorption, GLP-1 receptor agonists typically lead to nutritional shortfalls through reduced intake alone. This distinction matters. It is why post-surgical supplementation protocols are not directly transferable, and why the answer here is nutritional adequacy rather than corrective dosing.

What happens to nutrient intake when energy intake falls

Micronutrient adequacy at 1,400 calories. Gardner CD, Kim S, Bersamin A, et al. Micronutrient quality of weight-loss diets that focus on macronutrients: results from the A TO Z study. American Journal of Clinical Nutrition. 2010;92(2):304-312. Key finding: when women reduced intake from roughly 1,900 to between 1,373 and 1,478 calories a day, the proportion at risk of inadequacy rose sharply and varied by diet pattern, reaching 51 percent for thiamine, 55 percent for folate, 70 percent for magnesium and 49 percent for zinc in individual groups. This is the clearest measurement of the energy range most GLP-1 patients now occupy.

What has been measured in GLP-1 patients specifically. Urbina J, Salinas-Ruiz LE, Valenciano C, Clapp B. Micronutrient and Nutritional Deficiencies Associated With GLP-1 Receptor Agonist Therapy: A Narrative Review. Clinical Obesity. 2026;16(1):e70070. Key finding: a structured search covering 2019 to 2025 identified only six qualifying studies. Vitamin D deficiency was the most common, at 7.5 percent at six months and 13.6 percent at twelve. The authors state that causality cannot be definitively established from observational data. Note on interpretation: six studies is the entire evidence base. Anyone claiming more certainty than that is overstating it.

Baseline vitamin D status in US adults. Herrick KA, Storandt RJ, Afful J, et al. Vitamin D status in the United States, 2011-2014. American Journal of Clinical Nutrition. 2019;110(1):150-157. Key finding: in 16,180 people, 5.0 percent were at risk of deficiency and 18.3 percent at risk of inadequacy. We cite this rather than older estimates because the earlier NHANES figures used a laboratory method the CDC has since replaced, and the two sets of numbers are not comparable.

The recommendation itself. Mozaffarian D, et al, 2025, as above. Key finding: the advisory states that dietary supplements can be proactively considered for at-risk nutrients such as vitamin D, calcium and B12, or a multivitamin-mineral tablet, at appropriate doses tailored to the individual. Four professional societies, writing about this exact population. TAKE Complete is formulated to support nutritional adequacy during reduced intake.*

Lean mass

The share of weight lost as lean mass varies by medication, which is why we quote a range and name the drug rather than a single headline figure. The first entry below is the primary source for every lean mass number on this site.

The figure TAKE cites. Eisa N, Barood O. Lean Mass Changes With Incretin Therapy Versus Lifestyle Intervention: A Systematic Review and Meta-Analysis of Randomised Controlled Trials. Diabetes, Obesity and Metabolism. 2026;28(6):4818-4827. Published online 24 March 2026. doi:10.1111/dom.70666. Key finding: across 20 randomised controlled trials and 15,782 participants, lean mass as a proportion of total weight lost ran 25 to 39 percent with incretin therapy, specifically 35.2 percent for semaglutide (95% CI 31.5 to 38.9), 26.8 percent for liraglutide (23.1 to 30.5) and 25.4 percent for tirzepatide (22.8 to 28.0). The same analysis measured lifestyle intervention without medication at 26.2 percent (24.1 to 28.3) and found no significant difference in proportional lean mass loss between incretin therapy and lifestyle intervention. Lifestyle intervention combined with resistance training was lowest, at 17.5 percent (14.2 to 20.8). Note on interpretation: the comparison is the most important part of this paper. Proportional lean mass loss on medication is not meaningfully different from proportional lean mass loss achieved without it, so the accurate reading is that substantial weight loss costs lean tissue however it is achieved, not that these medications uniquely destroy muscle. The lowest proportion was reported in lifestyle interventions that included resistance training. That is a comparison across intervention groups within a meta-analysis rather than a direct test of resistance training, so we treat it as consistent with the wider evidence for resistance movement rather than as establishing it as the causal variable.

Body composition on tirzepatide. Look M, Dunn JP, Kushner RF, et al. Body composition changes during weight reduction with tirzepatide in the SURMOUNT-1 study of adults with obesity or overweight. Diabetes, Obesity and Metabolism. 2025;27(5):2720-2729. Key finding: in a DXA substudy with 255 participants enrolled and 160 included in the efficacy analysis, the proportion of body weight reduction was 74 percent as fat mass and 26 percent as lean mass with tirzepatide, against 75 percent and 25 percent on placebo. This is consistent with the pooled tirzepatide figure above, and the placebo comparison points the same way as the lifestyle comparison.

An earlier and smaller synthesis. Laverde LP, Muñoz-Velandia OM, Alfonso D, Gómez Medina AM. Effect of GLP-1 receptor agonists at doses for obesity management on muscle health: systematic review and meta-analysis of randomized controlled trials. International Journal of Obesity. 2026;50(8):1638-1646. Key finding: pooling seven studies across 821 patients, approximately 30 percent of total weight loss with GLP-1 therapy corresponded to lean mass, with the proportion varying substantially by drug, liraglutide lowest and semaglutide highest. The authors conclude that lean mass loss should not be considered a limitation for the use of these medications, but that treatment should be accompanied by nutritional support. Note on interpretation: this analysis pools seven studies and 821 patients. The Eisa and Barood analysis above pools 20 trials and 15,782 participants and reports confidence intervals for each medication, so it is the source we use for the figures quoted on this site. We list Laverde here because it remains a relevant paper and because its conclusion about nutritional support is the one our product line is built on.

Function, not just mass. Alissou M, Demangeat T, Folope V, et al. Impact of Semaglutide on fat mass, lean mass and muscle function in patients with obesity: The SEMALEAN study. Diabetes, Obesity and Metabolism. 2025;28(1):112-121. Key finding: across 115 patients on semaglutide 2.4mg followed to twelve months, lean mass fell then stabilised, grip strength improved by 4.5kg, and the prevalence of sarcopenia fell from 49 percent to 33 percent. Physical function improved even as lean mass declined.

Why lean mass is not the same as muscle. Tinsley GM, Heymsfield SB. Fundamental Body Composition Principles Provide Context for Fat-Free and Skeletal Muscle Loss With GLP-1 RA Treatments. Journal of the Endocrine Society. 2024;8(11):bvae164. Key finding: fat-free mass measured by DXA includes water, glycogen, connective tissue and organ mass, and changes in it should not be conflated with changes in skeletal muscle. This applies to every proportion quoted above. A figure of 35.2 percent lean mass is not a figure of 35.2 percent skeletal muscle, and we do not present it as one anywhere on this site.

Protein

Intake targets for older adults. Bauer J, Biolo G, Cederholm T, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. Journal of the American Medical Directors Association. 2013;14(8):542-559. Key finding: at least 1.0 to 1.2g of protein per kilogram of body weight daily for healthy older adults, and 1.2 to 1.5g where acute or chronic illness is present.

The European position. Deutz NE, Bauer JM, Barazzoni R, et al. Protein intake and exercise for optimal muscle function with aging: recommendations from the ESPEN Expert Group. Clinical Nutrition. 2014;33(6):929-936. Key finding: the same 1.0 to 1.2g per kilogram floor, with the recommendation explicitly paired with physical activity rather than treating protein alone as sufficient.

Does higher protein preserve lean mass during restriction. Wycherley TP, Moran LJ, Clifton PM, Noakes M, Brinkworth GD. Effects of energy-restricted high-protein, low-fat compared with standard-protein, low-fat diets: a meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition. 2012;96(6):1281-1298. Key finding: across 24 trials and 1,063 participants, higher protein preserved 0.43kg more fat-free mass. The authors describe the benefit as modest, and we will use their word rather than a better one.

In older adults specifically. Kim JE, O'Connor LE, Sands LP, Slebodnik MB, Campbell WW. Effects of dietary protein intake on body composition changes after weight loss in older adults: a systematic review and meta-analysis. Nutrition Reviews. 2016;74(3):210-224. Key finding: across 20 randomized trials in adults over 50 during energy restriction, higher protein intake was associated with greater retention of lean mass and proportionally greater fat loss.

Fava bean protein quality. Itkonen ST, Calvez J, Airinei G, et al. True Ileal Amino Acid Digestibility and Protein Quality of 15N-Labeled Faba Bean in Healthy Humans. Journal of Nutrition. 2024;154(4):1165-1174. Key finding: true ileal amino acid digestibility of 84.1 percent and a DIAAS of 0.67, limited by histidine. Note on interpretation: this was measured in cooked whole faba beans rather than an isolate, and 0.67 sits below the threshold for a high-quality single protein source. This is why TAKE Nourish combines fava bean isolate with fermented yeast protein rather than relying on either alone.

Digestion and the gut

Gastrointestinal effects at obesity doses. Wharton S, Calanna S, Davies M, et al. Gastrointestinal tolerability of once-weekly semaglutide 2.4 mg in adults with overweight or obesity. Diabetes, Obesity and Metabolism. 2022;24(1):94-105. Key finding: pooled across the STEP trials, nausea occurred in 43.9 percent of participants versus 16.1 percent on placebo, diarrhea in 29.7 versus 15.9 percent, vomiting in 24.5 versus 6.3 percent, and constipation in 24.2 versus 11.1 percent. Most were mild to moderate and concentrated during dose escalation.

Gastric emptying. Hiramoto B, McCarty TR, Lodhia NA, et al. Quantified Metrics of Gastric Emptying Delay by Glucagon-Like Peptide-1 Agonists: A Systematic Review and Meta-Analysis. American Journal of Gastroenterology. 2024;119(6):1126-1140. Key finding: solid gastric emptying half-time was delayed by a pooled 36 minutes. Liquid emptying, measured by acetaminophen absorption, showed no significant difference.

Fiber and the microbiome. So D, Whelan K, Rossi M, et al. Dietary fiber intervention on gut microbiota composition in healthy adults: a systematic review and meta-analysis. American Journal of Clinical Nutrition. 2018;107(6):965-983. Key finding: across 64 randomized trials, fiber supplementation increased Bifidobacterium and Lactobacillus and raised faecal butyrate. Note on interpretation: the same analysis found no effect on microbial diversity. Claims that fiber increases gut diversity are not supported by this evidence, and we do not make them.

Psyllium. van der Schoot A, Drysdale C, Whelan K, Dimidi E. The Effect of Fiber Supplementation on Chronic Constipation in Adults: An Updated Systematic Review and Meta-Analysis of Randomized Controlled Trials. American Journal of Clinical Nutrition. 2022;116(4):953-969. Key finding: psyllium improved stool consistency and reduced straining, with the authors concluding that doses above 10g daily for at least four weeks appear optimal. Psyllium requires substantial fluid, and it can delay the absorption of medicines taken alongside it.

Ginger and gastric motility. Wu KL, Rayner CK, Chuah SK, et al. Effects of ginger on gastric emptying and motility in healthy humans. European Journal of Gastroenterology and Hepatology. 2008;20(5):436-440. Key finding: 1,200mg of ginger halved gastric half-emptying time and increased antral contraction frequency in 24 healthy volunteers. Note on interpretation: this study measured motility. It did not measure nausea, and reported no difference in gastrointestinal symptoms. We cite it for what it found.

Ginger and nausea. Lete I, Allué J. The Effectiveness of Ginger in the Prevention of Nausea and Vomiting during Pregnancy and Chemotherapy. Integrative Medicine Insights. 2016;11:11-17. Key finding: a review of ginger for nausea in pregnancy and as an adjunct in chemotherapy, at doses of roughly 500 to 2,500mg daily. Note on interpretation: neither population is a GLP-1 population. No published trial of ginger for GLP-1-related nausea exists that we have been able to verify.

Probiotic delivery through stomach acid. Del Piano M, Carmagnola S, Andorno S, et al. Evaluation of the intestinal colonization by microencapsulated probiotic bacteria in comparison with the same uncoated strains. Journal of Clinical Gastroenterology. 2010;44 Suppl 1:S42-S46. Key finding: in 44 healthy volunteers, gastroprotected bacteria at one fifth the dose achieved colonisation kinetics comparable to uncoated strains at the full dose. Note on interpretation: this establishes the general principle that protecting cultures through the stomach matters. It is not a study of any particular proprietary delivery system, including ours.

What counts as a probiotic. Binda S, Hill C, Johansen E, et al. Criteria to Qualify Microorganisms as Probiotic in Foods and Dietary Supplements. Frontiers in Microbiology. 2020;11:1662. Key finding: a defining criterion is that the organism is alive at an efficacious dose throughout shelf life, not at the moment of manufacture. TAKE Flora is formulated to meet its stated count through the end of shelf life.

Hydration and electrolytes

Where electrolytes actually come from. Harnack LJ, Cogswell ME, Shikany JM, et al. Sources of Sodium in US Adults From 3 Geographic Regions. Circulation. 2017;135(19):1775-1783. Key finding: across 450 adults, roughly 95 percent of sodium intake came from food, while home tap water consumed as a beverage contributed under 0.5 percent. Because the large majority of daily sodium, potassium and magnesium comes from food rather than drink, a substantial reduction in food intake reduces electrolyte intake alongside it.*

Why this matters clinically. Ozempic (semaglutide) US Prescribing Information, section 5.6. Key finding: postmarketing reports of acute kidney injury, in some cases requiring hemodialysis, occurred mainly in patients who experienced gastrointestinal reactions leading to dehydration. The label advises monitoring renal function in patients reporting reactions that could lead to volume depletion, particularly during initiation and dose escalation. Fluid and electrolyte intake during a period of nausea, vomiting or diarrhea is not a comfort issue. Speak to your prescriber if these symptoms persist.

Hair

Shedding after weight loss. Kang DH, Kwon SH, Sim WY, Lew BL. Telogen Effluvium Associated With Weight Loss: A Single Center Retrospective Study. Annals of Dermatology. 2024;36(6):384-388. Key finding: among 140 patients presenting with weight-loss-associated shedding, mean weight loss was 15.2 percent of body weight at a mean rate of 3.5kg per month, and women developed it at lesser degrees of weight loss than men. Note on interpretation: retrospective and uncontrolled, so it describes who presents rather than how common this is.

The timing. Liyanage D, Sinclair R. Telogen Effluvium. Cosmetics. 2016;3(2):13. Key finding: shedding typically begins two to four months after the triggering event, and in acute cases resolves within three to six months with density recovering. This lag is why shedding tends to appear well after the change that caused it.

Rosemary. Panahi Y, Taghizadeh M, Tahmasbpour Marzony E, Sahebkar A. Rosemary oil vs minoxidil 2% for the treatment of androgenetic alopecia: a randomized comparative trial. Skinmed. 2015;13(1):15-21. Key finding: 100 patients with androgenetic alopecia randomized to rosemary oil or minoxidil 2 percent for six months. Both groups increased hair count from baseline at six months, with no significant difference between them, and scalp itching was more frequent with minoxidil. Note on interpretation: there was no placebo arm, so improvement in both groups cannot be attributed to either agent with confidence, and a non-significant difference between two groups of 50 is not evidence of equivalence. The population was androgenetic alopecia, not shedding after weight loss.

Saw palmetto. Evron E, Juhasz M, Babadjouni A, Atanaskova Mesinkovska N. Natural Hair Supplement: Friend or Foe? Saw Palmetto, a Systematic Review in Alopecia. Skin Appendage Disorders. 2020;6(6):329-337. Key finding: nine studies and 381 participants, with reported improvements in hair count and density, and the finding that saw palmetto acts as a competitive inhibitor of both 5-alpha reductase isoforms. Note on interpretation: the authors report small samples, inadequate controls, industry sponsorship, and formulations containing multiple ingredients, so saw palmetto's individual contribution cannot be isolated. In the single head-to-head trial against finasteride, saw palmetto was inferior. Because it inhibits 5-alpha reductase, it is not suitable during pregnancy, while nursing, or while trying to conceive.

Biotin. Patel DP, Swink SM, Castelo-Soccio L. A Review of the Use of Biotin for Hair Loss. Skin Appendage Disorders. 2017;3(3):166-169. Key finding: every reported case of improvement with biotin involved an underlying pathology such as biotin deficiency or an inherited hair disorder. The authors conclude there is insufficient evidence for supplementation in people with normal biotin status. We include biotin as a nutrient in TAKE Complete, and we do not claim it will regrow hair.

Skin firmness and volume

DMAE and cutaneous tensile strength. Grossman R. The role of dimethylaminoethanol in cosmetic dermatology. American Journal of Clinical Dermatology. 2005;6(1):39-47. Key finding: in a randomized, placebo-controlled trial, 3% DMAE facial gel applied daily for 16 weeks produced statistically significant (p<0.05) improvement in forehead lines, periorbital wrinkles, lip fullness and overall skin appearance, with measurable increases in cutaneous tensile strength. An open-label extension found the gel well tolerated for up to one year, with no increase in erythema, peeling, dryness, itching, burning or stinging versus placebo. Note on interpretation: this is the primary published trial behind topical DMAE's cosmetic use, and it was conducted in a general aesthetic population rather than in people experiencing GLP-1-related facial volume loss specifically.

Hyaluronic acid and skin hydration and elasticity. Pavicic T, Gauglitz GG, Lersch P, et al. Efficacy of cream-based novel formulations of hyaluronic acid of different molecular weights in anti-wrinkle treatment. Journal of Drugs in Dermatology. 2011;10(9):990-1000. Key finding: in a randomized, split-face, placebo-controlled trial of 76 women aged 30 to 60 applying hyaluronic acid creams (molecular weights 50 to 2,000 kDa) twice daily for 60 days, all formulations significantly improved skin hydration and elasticity against placebo, with the lowest molecular weights (50 and 130 kDa) showing the greatest improvement in wrinkle depth. Note on interpretation: hyaluronic acid binds and retains water in the skin. It is not evidence that a topical ingredient can restore lost facial volume beneath the skin.

CoQ10 and periorbital wrinkle depth. Hoppe U, Bergemann J, Diembeck W, et al. Coenzyme Q10, a cutaneous antioxidant and energizer. BioFactors. 1999;9(2-4):371-378. Key finding: topical CoQ10 applied around the eyes for six months penetrated the skin, reduced markers of UV-induced oxidative stress, and reduced periorbital wrinkle depth, in a study of 20 subjects. The same paper reported reduced collagenase expression in UV-exposed dermal fibroblasts. Note on interpretation: this is a small, older study by current standards, and remains the most-cited published work behind topical CoQ10's cosmetic use.

What we do not claim

This section exists because a research page that only lists supportive findings is not a research page. These are the limits of our own evidence, stated plainly.

We do not claim that lean mass loss means muscle loss, and we do not claim one figure fits everyone. The proportions above are fat-free mass measured by DXA, which includes water, glycogen and connective tissue alongside muscle. The share also depends on the medication, and reported figures across the wider literature run from 20 to 50 percent. We quote the medication-specific figures with their confidence intervals rather than a single headline number, and we do not describe any of them as a measurement of skeletal muscle.

We do not claim GLP-1 medications uniquely cost you lean tissue. The analysis we cite found no significant difference in proportional lean mass loss between incretin therapy and lifestyle intervention. Substantial weight loss draws on lean tissue whether or not a medication is involved. What the evidence does support is that adequate protein and resistance movement are associated with a smaller proportion, and that is the basis on which our products exist.

We do not claim creatine preserves lean mass during reduced intake. The meta-analytic evidence puts the effect of creatine on lean body mass at approximately 1.10kg when combined with resistance movement, most pronounced with consistent training, and the effect in women did not reach statistical significance (Delpino FM, et al. Nutrition. 2022;103-104:111791). The study closest to this population, in women after bariatric surgery, was negative. Creatine is safe and well tolerated at 3 to 5g daily across long-term use (Kreider RB, et al. Journal of the International Society of Sports Nutrition. 2017;14:18), and a trial in GLP-1 users is currently underway. Until it reports, we will not claim more than that.

We do not claim topical growth-factor peptides regrow hair. Molecules above approximately 500 daltons do not meaningfully cross intact skin (Bos JD, Meinardi MMHM. Experimental Dermatology. 2000;9(3):165-169). The growth factors used in cosmetic hair serums range from roughly 6,000 to 45,000 daltons. The only independent clinical trial of a topical growth-factor hair serum reported that no participant achieved meaningful hair preservation (Mann K, et al. Journal of Cosmetic Dermatology. 2026;25(3):e70797). Studies showing benefit from growth factors use injection or microneedling, which bypasses the skin barrier entirely. The evidence in TAKE Root rests on rosemary and saw palmetto.

We do not claim TAKE Form restores lost facial fat. Facial volume loss during rapid weight loss is a loss of subcutaneous fat. None of DMAE, hyaluronic acid or CoQ10 has been shown to replace fat beneath the skin; their published evidence is for skin firmness, hydration and antioxidant activity at the surface. Form is formulated to support the appearance of the skin around that loss, not to reverse it.

We do not claim a higher culture count is better. A review of probiotic dose-response found a clear relationship only for antibiotic-associated diarrhea, and none for bowel function or general digestive outcomes (Ouwehand AC. Beneficial Microbes. 2017;8(2):143-151). Our count sits within the range used in clinical studies. That is the honest statement.

We do not claim GLP-1 medications damage the gut microbiome. A systematic review of 38 studies found only nine in humans, most reporting no change in diversity, and concluded that assertions of clinically significant microbiome modulation by these medications should be circumspect (Gofron KK, Wasilewski A, Małgorzewicz S. Nutrients. 2025;17(8):1303). The reasonable argument is narrower: eating substantially less means eating less fiber, and fiber is what feeds these organisms.*

We do not claim TAKE itself has been clinically tested. No trial has studied our products. What has been studied are the individual nutrients and ingredients, in the populations and at the doses described above. We formulate from that evidence. We do not pretend it is the same thing.

How to read this page

Sample sizes, populations and study designs are given wherever they change how a finding should be read. A study in young men under supervised conditions does not tell you what happens to a woman in her fifties eating 1,300 calories a day. A biomarker moving is not the same as a person feeling better. A comparison that finds no significant difference between two treatments has not shown they are equivalent. A difference between intervention groups within a meta-analysis is not the same as a trial designed to test that intervention. And a proportion calculated by someone else from a paper's numbers is not a finding of that paper.

Where a claim on this site is not supported by evidence we can point to, we would rather remove the claim than find a study that almost fits. If you find something on this page that does not hold up, tell us and we will correct it.

For questions about the research behind a specific product, contact care@takecomplete.com.

These statements have not been evaluated by the Food and Drug Administration. TAKE products are not intended to diagnose, treat, cure, or prevent any disease. Individual results vary. Always speak with your healthcare provider about medication side effects or medical concerns.
Ozempic® and Wegovy® are registered trademarks of Novo Nordisk A/S. Mounjaro® and Zepbound® are registered trademarks of Eli Lilly and Company. References to these names on this page are for informational and descriptive purposes only and do not imply affiliation, sponsorship, or endorsement by, or partnership with, Novo Nordisk A/S, Eli Lilly and Company, or any other GLP-1 medication manufacturer.