Microdosing GLP-1's is going mainstream

Online clinics like Noom, Hims, Found Health, Maximus and many others are promoting micro-dosing of GLP-1 medications like Ozempic and Mounjaro.

Isn’t that ridiculous?

Why take a lower dose of a medication when we know the dose that already works? We spent billions studying high-dose GLP-1s to treat diabetes and obesity. Those doses work amazingly well.

But we never asked the question: What’s the minimum effective dose for inflammation? for decreasing cravings? for improving metabolic dysfunction? for longevity?

Not the max dose.The minimum dose that still triggers biology.

Yes, higher doses produce more dramatic effects. That’s not controversial.

We’re seeing consistent reports of benefits WITHOUT any weight loss at all. Normal-weight individuals reporting reduced joint pain, improved autoimmune symptoms, improved metabolic labs, decreased brain fog, decreased cravings, and normalized menstrual cycles.

Suddenly, “micro-dosing” doesn’t sound ridiculous anymore.

What GLP-1s Actually Do

GLP-1 is a hormone your gut produces after you eat. Here is what it does:

• signals fullness to the brain

• slows stomach emptying

• stabilizes blood sugar

• reduces inflammation

• improves endothelial function

• modulates reward pathways

• influences liver fat and insulin sensitivity

GLP-1 receptors are everywhere in the body—pancreas, liver, brain, fat tissue, immune cells. This explains why GLP-1 medications affect much more than appetite.

The question is do micro-doses activate any of this? Or is it all placebo and wishful thinking?

Let’s break it down.

How Micro-dosing Works—At Least on Paper

Micro-dosing is simply taking a lower dose than the prescription strength off the shelf. The concept: if 3 tablets of Advil decrease your back pain, could 1 tablet help with milder pain?

A typical micro-dose of semaglutide (Ozempic) is 0.1 mg weekly—below the usual 0.25 mg starter dose.

A typical micro-dose of tirzepatide (Mounjaro) is 1 mg weekly—below the usual 2.5mg starter dose.

Wait, isn’t this off label use?

Yes. And off-label prescribing is standard, safe, and happens every single day.

In ophthalmology, we inject bevacizumab (Avastin) off-label for retinal diseases like wet macular degeneration and diabetic macular edema every single day.

It’s not just accepted—it’s the standard of care. Despite never having been FDA-approved for any eye disease.

Off-label is not fringe. Off-label is commonplace in medicine.

Some examples of off-label use of medications:

• Gabapentin for nerve pain

• Trazodone for insomnia

• Clonidine for ADHD

The fact that GLP-1 micro-dosing is off-label doesn’t invalidate it. It simply means we’re in that familiar territory where clinical judgment fills the gaps left by industry-funded research.

What the Science Actually Shows

When evaluating any treatment there are two main issues to consider

1. Is it safe

2. Is it effective?

Regarding safety, the side effect profile of full strength GLP-1’s is known. The first generation of these drugs was FDA-approved in 2005, so we have 20 years of data.

The most common side effects are GI related: nausea (20-40%), vomiting, constipation, diarrhea, abdominal discomfort, and fatigue. Less common side effects include gallstones and pancreatitis. With microdosing, these side effects should occur less.

Regarding efficacy, the most common criticism I hear is “There are no published studies supporting lower doses of GLP-1’S.”

Wrong.

Novo Nordisk and Eli Lily published phase 2 studies that included lower doses.

For low dose semaglutide (0.1mg), they reported 0.6% drop in HbA_1c and fasting blood glucose droped by 9 points (reference). A study in fatty liver patients demonstrated sustained reductions in liver enzymes and 40% achieved fatty liver resolution (reference).

For low dose tirzepatide (1 mg), they reported that HbA_1c dropped 1 percentage point and fasting blood glucose dropped 7 points (reference).

Bottom line:Microdosing is scientifically plausible and partially supported.

Where the Hype Gets Ahead of the Evidence

Now for the skeptical side.

We do not have rigorous data showing microdosing reliably treats:

• autoimmune disease

• chronic pain

• PCOS

• long COVID

• ADHD

• osteoarthritis (we might with Eli Lily's new drug)

Could it? Maybe.

Anecdotes are interesting. Mechanisms are interesting. But interesting is not the same as proven.

Where Microdosing Does Make Sense

✔ People who can’t tolerate higher doses

Nausea and vomiting rise with as you increase the dose. Lower doses can help.

✔ Mild metabolic dysfunction

Pre-diabetes, early insulin resistance, borderline elevated A1c, high visceral fat.

✔ Patients who want sustainability

Sometimes the best dose is the one you can stay on.

Where Microdosing Doesn’t Make Sense

✘ Severe obesity

Higher therapeutic doses are usually required.

✘ Advanced diabetes

A1c >8% usually needs more than 0.1 mg.

✘ People expecting rapid weight loss

Microdosing is slow by design.

My Take: Curious and Open

Where I land:

• The biology supports the idea

• Some data supports the idea

• Safety at low doses is excellent

• Off-label is normal—when done responsibly

• Placebo could explain some—but not all—reported benefits

If you try it, get baseline labs (fasting glucose, HbA1c, hsCRP, liver function tests) and a DEXA scan. Track your numbers over time.

The truth is probably this:

Microdosing is not magic.

It’s not useless.

It’s not proven.

It’s simply under studied.

And unstudied territory is often where the interesting questions live.