Oxytocin for....Fat Loss?

Happy Tuesday!

Today, I released a brand-new episode on oxytocin for fat loss.

It’s live on Spotify now if you want to check it out.

In the video, I walk through what oxytocin is, how it impacts appetite and metabolism, why some studies look wildly promising, and the exact protocol I’m testing for body recomposition.

Today’s email will be the written companion to my best practices around oxytocin for fat loss.

At a high level, oxytocin is a naturally occurring peptide hormone/neuropeptide made in the hypothalamus and released from the posterior pituitary.

It’s famous for social bonding and childbirth, BUT it also talks to brain circuits that govern reward and satiety and to receptors on fat cells themselves.

That dual action is why researchers started testing it for obesity.

It can reduce how much you eat while nudging your body to burn a higher fraction of fat for fuel.

Think of it as a gentle “eat a bit less, burn a bit more fat” driver that pairs well with training, protein, and proper nutrition. 

How it Works for Fat Loss

Mechanistically, oxytocin binds the oxytocin receptor (OXTR), a GPCR found in the brain, gut, heart, skeletal muscle, and adipose tissue.

In the brain, it modulates hypothalamic and brainstem satiety pathways and dampens reward-driven eating.

People don’t necessarily feel less hungry, but they spontaneously consume fewer calories and less dietary fat.

In controlled feeding studies, a single 50mcg intranasal dose reduced test-meal intake by ~120–150 kcal and shifted behavior away from high-fat foods while increasing the satiety hormone CCK.

In the body, oxytocin activates lipolysis (breaking stored triglycerides into free fatty acids + glycerol) and increases fat oxidation, with gene-level signals pointing toward PPAR-α activation and downstream fatty-acid β-oxidation.

This results in fewer calories in, more fat burned, and less fat storage. 

Studies

In rodent diet-induced obesity models, chronic oxytocin infusions produced dose-dependent reductions in weight gain, increased adipose lipolysis and β-oxidation, and improved glucose tolerance/insulin sensitivity.

Interestingly, weight loss was preferentially from fat mass, with lean mass preserved, precisely what we want from a recomposition lens.

Acute, crossover meal-test studies in humans show reduced energy intake after a single 50mcg intranasal dose (roughly ~120–150 kcal less at the next meal), with improved insulin handling and a shift toward fat oxidation.

Over 8–12 weeks, early small trials and targeted populations suggested meaningful body-comp benefits.

In older adults with sarcopenic obesity, intranasal oxytocin over 12 weeks increased lean mass by ~2 kg and lowered LDL-C while reducing fat mass.

On the other hand, a larger randomized, double-blind trial (50mcg, four times daily for 8 weeks) did not reduce body weight vs placebo, even though it again confirmed lower meal intake on lab tests.

This seems to confirm that even if people didn’t lose scale weight, they still consumed less calories across the board.

Muscle Mass

One of the most compelling angles (and why I like oxytocin as a recomp tool) is its lean-tissue profile.

In animal studies, fat-selective loss with preserved skeletal muscle is a repeated finding.

In humans, the sarcopenic-obesity pilot resulted in an increase of 2.0 kg lean mass over 12 weeks with concomitant fat-mass reduction and better lipids.

Mechanistically, part of this may be reduced reliance on carbohydrate oxidation (sparing glycogen/protein), improved insulin sensitivity, and possibly indirect effects on training enjoyment/adherence via oxytocin’s pro-social/anti-stress signaling.

You still need to lift, prioritize protein, and sleep.

Oxytocin isn’t as strong as a GLP, but it’s one of the few tools that reliably supports fat loss while helping you maintain or even build muscle.

My Dosage Protocol

Here is my suggested dosing protocol.

• Dose: 50 mcg per dose, 3–4× daily (≈ 30–40 IU per dose by strict conversion).

• Route: Intranasal or subcutaneous (I like both. Intranasal is more convenient if you’re dosing multiple times per day).

• Timing: 15–30 minutes before meals (breakfast, lunch, dinner, optional at bedtime).

• Duration: 8–12 weeks on, then re-evaluate. Consider cycling 4–6 weeks off.

• Context: Pair with a modest calorie deficit, resistance training 3–4×/week, and adequate protein.

Reconstitution

Important: The following is educational information for research contexts. Use sterile technique. Not medical advice.

SubQ Injectable (target 1 mg/mL, 50 mcg = 0.05 mL = 5 “insulin units” on a U-100 syringe):

1. Start with a 10 mg lyophilized oxytocin vial that physically holds 3 mL. Add 3 mL bacteriostatic water to dissolve.

2. Withdraw the entire 3 mL solution into a sterile syringe and transfer it into a sterile empty vial.

3. Add 7 mL more bacteriostatic water to the new vial, bringing the total to 10 mL. Your concentration is now 10 mg / 10 mL = 1 mg/mL.

4. Dose: 50 mcg = 0.05 mL = 5 insulin “units” on a U-100 syringe. (3–4×/day.)

Intranasal Spray (target 500 mcg/mL, 1 pump ≈ 0.1 mL → 50 mcg per pump):

1. Add 3 mL of sterile saline nasal spray to the 10 mg powder vial and dissolve.

2. Withdraw the 3 mL and transfer it into a clean, empty nasal spray bottle (20 mL capacity is common).

3. Add 17 mL additional sterile saline nasal spray to reach 20 mL total volume.

4. Your concentration is 10 mg / 20 mL = 0.5 mg/mL = 500 mcg/mL. If your sprayer dispenses ~0.1 mL per pump, 1 pump ≈ 50 mcg.

5. Dose: 1 pump per nostril (≈ 100 mcg) or 1 pump total (≈ 50 mcg) depending on your preferred per-dose target, repeat 3–4×/day. (Always verify your specific bottle’s pump volume.)

NOTE: You can get Oxytocin from BioLongevity Labs using code HUNTERW at checkout for 15% off.

You can also buy a nasal spray version from Soma Chems and use code HUNTER20 at checkout.

Safety

Short-term intranasal oxytocin has been well tolerated in trials (most common issues are mild nasal irritation or headache).

The large NEJM Evidence RCT reported no significant safety signals versus placebo across 8 weeks.

We don’t have definitive long-term data in metabolic users.

As with most hormones, a sensible on/off cycling strategy is prudent.

Final Thoughts

Oxytocin shines as an adjunct.

It smooths out binge eating, subtly shrinks meal size, and tilts substrate use toward fat.

That makes it a natural complement to GLP-1s (or an off-cycle bridge when you’re reducing GLP-1 dose), to L-carnitine, and to mitochondrial support like SS-31.

Compared with stimulant-based weight loss drugs, oxytocin’s profile is calmer.

Better cravings, less conscious struggle, and pro-lean-mass data in older adults.

If you’re already training and eating decently, oxytocin’s effect can be exactly the nudge that keeps progress steady without white-knuckling hunger. 

Best,

Hunter Williams

Further Reading

• Blevins & Ho (2021) – Oxytocin as an Anti-Obesity Treatment

• Zhang et al. (2011) – Mechanisms of the Anti-Obesity Effects of Oxytocin in Diet-Induced Obese Rats

• Plessow et al. (2024) – Intranasal Oxytocin for Obesity: A Randomized Controlled Trial

• Espinoza et al. (2021) – Intranasal Oxytocin Improves Lean Muscle Mass and Lowers LDL in Older Adults with Sarcopenic Obesity

• Lawson et al. (2015) – Oxytocin Reduces Caloric Intake in Men

• Lawson (2017) – The Effects of Oxytocin on Eating Behaviour and Metabolism in Humans

• National Institute for Biological Standards and Control (NIBSC) Reference Standard for Oxytocin