By Natalie Howard, DNP, FNP-C — Johns Hopkins trained, metabolic medicine
Yes — skin tags are a documented marker of insulin resistance. Those soft flesh-colored growths on your neck, eyelids, and underarms (clinically called acrochordons) are strongly associated with high insulin, especially when they cluster. They are not just cosmetic, and they are not random. They are one of the most visible signs that your metabolic health is worth a closer look.
Here is the mechanism, what it does and does not tell you, and where treatments like GLP-1 medications fit in.
Prefer to watch? Here is the breakdown
A walkthrough of the insulin-to-skin-tag mechanism. The full written breakdown continues below.
Why does insulin cause skin tags?
When insulin stays chronically elevated (a state called hyperinsulinemia), it does more than manage blood sugar. Excess insulin activates IGF-1 (insulin-like growth factor) receptors in the skin. That activation drives overgrowth of the keratinocytes and fibroblasts — the cell types that build a skin tag.
In plain terms: high insulin tells skin cells to multiply, and skin tags are one result. This is why they tend to appear in friction zones like the neck and underarms, and why they often show up in groups rather than one at a time.
The association is documented in the literature. Tamega et al. (2010) found a direct association between skin tags and insulin resistance (PMID: 20464083). González-Saldivar et al. (2017) detailed the biochemical pathway connecting insulin resistance to skin changes, including the IGF-1 receptor mechanism (PMID: 27921251).
What is the difference between skin tags and acanthosis nigricans?
Skin tags and acanthosis nigricans often travel together, because they share the same underlying driver: elevated insulin.
Acanthosis nigricans is the darker, velvety thickening of the skin you may notice on the back of the neck, in the armpits, or in skin folds. When you see skin tags and these darkened patches in the same person, that co-occurrence is a stronger metabolic signal than either sign alone. Barbato et al. (2012) documented the association of both acanthosis nigricans and skin tags with insulin resistance (PMID: 22481657).
If you have both, that is worth a conversation about your metabolic markers.
Do skin tags go away if you treat insulin resistance?
This is where it is important to be precise. Skin tags are a marker and the product of a driver — they are not a validated test for whether insulin resistance is reversing.
What the science supports: chronically high insulin drives skin tag formation. As metabolic health improves and insulin comes down, that driver is reduced. What the science does not establish is that existing skin tags falling off proves your insulin resistance has reversed at the cellular level. Existing tags often need to be removed by a clinician; the metabolic improvement addresses the driver going forward, not the tags already there.
So the honest framing is: treat the metabolism, track the metabolic markers, and judge progress by labs — not by counting skin tags.
How do GLP-1 medications fit in?
GLP-1 receptor agonists (and dual GIP/GLP-1 agents like tirzepatide) improve insulin sensitivity and lower the chronically elevated insulin that drives skin tag formation. That means they act on the same root cause that produces these skin signs.
What that does not mean: a GLP-1 medication is not a skin tag treatment, and you should not expect tags to disappear as proof the medication is working. The point is the reverse — the skin signs are a prompt to evaluate the metabolic picture that GLP-1 therapy and other interventions are designed to address.
What should you do if you have clustering skin tags?
If your skin tags are multiplying or clustering, especially alongside acanthosis nigricans, it is worth getting your metabolic markers checked. The common workup includes fasting insulin, fasting glucose, HbA1c, and a lipid panel. Many people are told their glucose is “normal” while their fasting insulin is quietly elevated — which is exactly the state skin tags can flag.
You do not need to wait for a diabetes diagnosis to look at this. The skin is giving you early information.
Frequently asked questions
No. Skin tags can also come with age, weight, friction, pregnancy, and genetics. But when they cluster, recur, or appear with acanthosis nigricans, insulin resistance is one of the most documented associations and worth evaluating.
Yes. Insulin resistance is not limited to higher body weight. Lean people can have elevated fasting insulin, so skin tags can be a metabolic signal regardless of body size.
There is no single skin tag lab. The most informative starting markers are fasting insulin, fasting glucose, and HbA1c. Fasting insulin in particular often catches early insulin resistance that glucose alone misses.
No. Removal is cosmetic and addresses the individual tag. It does nothing to the insulin driver underneath, which is why tags can recur if the metabolic picture does not change.
Not necessarily. They are a risk marker, not a diagnosis. They are a reason to check your metabolic markers early, when changes are most reversible.
Educational content only. This is not medical advice and does not replace evaluation by your own licensed provider. If you have concerns about skin changes or metabolic health, consult a clinician.
Citations
- Tamega AdeA, Aranha AM, Guiotoku MM, Miot LD, Miot HA. Association between skin tags and insulin resistance. An Bras Dermatol. 2010 Jan-Feb;85(1):25-31. doi:10.1590/s0365-05962010000100003. PMID: 20464083.
- González-Saldivar G, Rodríguez-Gutiérrez R, Ocampo-Candiani J, González-González JG, Gómez-Flores M. Skin Manifestations of Insulin Resistance: From a Biochemical Stance to a Clinical Diagnosis and Management. Dermatol Ther (Heidelb). 2017 Mar;7(1):37-51. doi:10.1007/s13555-016-0160-3. PMID: 27921251.
- Barbato MT, Criado PR, Silva AK, Averbeck E, Guerine MB, Sá NB. Association of acanthosis nigricans and skin tags with insulin resistance. An Bras Dermatol. 2012 Jan-Feb;87(1):97-104. doi:10.1590/s0365-05962012000100012. PMID: 22481657.