PMOS and Skin Health

How does PMOS impact skin health?

According to the 2025 review of Cutaneous Manifestations in Polycystic Ovary Syndrome, acne and dark skin patches are some of the most common skin complaints in individuals with PMOS.

Individuals with PMOS are at increased risk of a number of skin conditions including acne, rosacea, skin tags (acrochordons), dark skin patches (acanthosis nigricans), dandruff (seborrheic dermatitis) and atopic dermatitis (the most common form of eczema). A variety of hormonal and cardiometabolic disruptions contribute to the risk of these conditions, in addition to low-grade inflammation and certain nutritional deficiencies. In this article we explore the link between PMOS and Skin Health.

At its core, PMOS is associated with abnormal functioning of the system of hormones that connects the hypothalamus, the pituitary gland and the ovaries (the HPO-axis).[1] PMOS is associated with hyperandrogenism (HA) or androgen excess (AE), elevated levels of androgens in individuals assigned female at birth.

Elevated androgens stimulate the skin glands to produce more sebum, an oily substance crucial for skin and hair lubrication.[2] Excess sebum alters Cutibacterium, a type of bacteria protecting the skin from harmful pathogens.[3] Changes in Cutibacterium lead to the buildup of Keratinocytes, special skin cells within pores that maintain the skin’s barrier properties.[4] Excess sebum and Keratinocytes cause pore blockage, triggering inflammation and, in severe cases, skin lesions.[5] As a result, individuals with PMOS are more than 2x as likely to develop acne compared to those without the condition.[6]

An increase in the level of circulating androgens disrupts the way that adipose tissue, the body fat or connective tissue that extends throughout your body,[7] metabolizes glucose.[8] The adipose tissue produces less adiponectin, a hormone that helps with insulin sensitivity and inflammation,[9] and more leptin,[10] a hormone that causes you to feel hungry in efforts to maintain enough fat stores for long-term health.[11] Reduced adiponectin leads to insulin resistance, whereby the body doesn’t respond as it should to the effects of insulin.[12] As a result, 65-70% of individuals with PMOS develop insulin resistance (IR).[13] In another study insulin resistance was shown to affect up to 95% of individuals with PMOS who are overweight and up to 75% of individuals who are lean.[14]

Insulin resistance leads to elevated production of insulin in the pancreas as a compensatory measure, leading to elevated levels of insulin in the blood or hyperinsulinemia[15] and, eventually, the pancreas is no longer able to produce enough insulin to maintain healthy levels of blood sugar and the individual develops hyperglycemia, or high blood sugar.

Insulin resistance stimulates the release of fatty acids into the blood[16][17] which then stimulate the liver to produce and secrete very low-density lipoprotein (VLDL).[18] The release of VLDL into the blood results in an increased level of lipids in the blood overall, hypertriglyceridemia, and stimulates the exchange of cholesteryl esters (a type of dietary fat that is a derivative of cholesterol)[19] from both high-density lipoprotein (HDL) and low-density lipoprotein (HDL).[20] The triglyceride (TG) enriched HDL then releases Apolipoprotein A-1 (ApoA-1) protein into the blood[21] to be rapidly cleared from the blood, partly through excretion via the kidney, leaving HDL less available to play a role in removing cholesterol from the body.[22] In parallel the TG enriched HDL undergoes lipolysis (the process through which lipids are broken down to access stored energy)[23] and becomes smaller and more dense.[24] There is a resulting low level of available HDL and high levels of small dense LDL.[25][26] As a result, individuals with PMOS are 2x more likely to have high cholesterol (also known as Dyslipidemia) than those without PMOS.[27]

The combination of increased sebum production and dyslipidemia creates conditions where the Malassezia yeast, a naturally-occurring yeast on our skin, thrives.[28] As a result, individuals with PMOS are prone to the development of dandruff or seborrheic dermatitis as it is believed to be caused by an inflammatory response to the Malassezia yeast.[29][30] Other proposed mechanisms include increased fatty acids on the skin surface, abnormal shedding of keratinocytes and epidermal barrier disturbances due to genetic factors.[31]

Hormonal and cardiometabolic dysregulation often lead to chronic low-grade inflammation in individuals with PMOS:

Elevated androgens cause adipose tissue to decrease production of adiponectin, a hormone that helps with insulin sensitivity and inflammation;[32][33]
Anovulation, a core feature of PMOS, results in lower levels of progesterone[34][35][36] which leads to increased production of inflammatory cytokines and histamine;[37][38]
Similarly, anovulation (and the increased numbers of preantral and antral follicles) results in higher levels of Anti-Müllerian Hormone (AMH)[39] leading to increased levels of high-sensitivity C-reactive protein (hs-CRP), although the mechanism is not well understood;[40]
Disturbances in the bacterial flora in the bowel, common in PMOS, lead to increased permeability of the lining of the gut and therefore increased passage of gram-negative bacteria (GNB), microorganisms that are often resistant to antibiotics,[41] back into circulation in the body, activating an immune response;[42]
Insulin resistance is both a contributing factor and exacerbated by inflammation; insulin resistance leads to a build-up of glucose in the blood, resulting in the release of pro-inflammatory cytokines;[43]
Accumulation of body fat around the abdomen, commonly associated with PMOS, means that those fat cells enlarge, outgrowing their blood supply and leading to hypoxia (oxygen deficiency) within the adipose tissue; the enlarged fat cells release more free fatty acids (FFAs) into the bloodstream, produce more pro-inflammatory adipokines; (signaling molecules)[44] and less anti-inflammatory adiponectin, attract macrophages (a type of monocyte that has migrated from the bloodstream)[45] that then release inflammatory cytokines and chemokines;[46] and
Similarly to central adiposity, the expansion of fat cells generally contributes to inflammation.[47]

As a result, individuals with PMOS are at increased risk of inflammatory skin conditions, including 2x the risk of atopic dermatitis (the most common form of eczema) and rosacea, a very common skin condition that results in redness and/or pimples on the cheeks, nose and forehead.[48]

Similarly, a variety of these factors contribute to weight gain in individuals with PMOS:

Elevated androgens cause adipose tissue, body fat/connective tissue,[49] to produce more leptin, a hormone that causes you to feel hungry in efforts to maintain enough fat stores for long-term health;[50][51]
Hyperinsulinemia triggers increased fat storage and hinders fat breakdown;[52]
Hyperglycemia also causes the body to store rather than use body fat (lipolysis inhibition);[53]
Low-grade inflammation increases the energy “harvested” from food and stimulates the production of the hormones leptin and ghrelin (also stimulates hunger);[54][55] and
Individuals with PMOS are also 2.5-4.0x more likely to develop hypothyroidism,[56][57] with underactive thyroid leading to weight gain.[58]

As a result, individuals with PMOS are 2.0-2.8x more likely to have obesity than those without the condition and more than half accumulate fat around the middle, central adiposity.[59][60][61][62]

Obesity, hyperinsulinemia and insulin resistance contribute to an increased prevalence of dark skin patches, acanthosis nigricans, in individuals with PMOS.[63][64][65][66][67] These dark skin patches are areas of dark, velvety thick skin that commonly appear in folds in the skin such as your neck, armpits and groin and can become itchy and develop an odor.[68][69]

Androgen excess can stimulate sweat glands and cause hyperhidrosis, excessive sweating, in individuals with PMOS.[70] Hyperhidrosis, in addition to obesity, hyperinsulinemia and insulin resistance contribute to an increased prevalence of skin tags, acrochordons, in individuals with PMOS.[71][72][73][74][75][76][77] Skin tags are soft, skin-colored growths that usually appear where the skin rubs together or where there are folds in the skin such as your neck, eyelids, under your arms, under your breasts or under the buttocks.[78]

Individuals with PMOS may be at increased risk of poor skin health in general due to increased risk of dehydration[79][80] and increased risks of certain nutritional deficiencies, including Vitamin C.[81][82][83]

General risk factors for skin health include:[84][85]

Increasing age;
Exposure to air pollution, irritants and/or harsh chemicals;
Poor diet and/or malnutrition;
Heavy alcohol use;
Smoking;
Sun exposure;
Stress; and
Sleep disturbances.

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