Why do fat chicks always have those weird dark ring shaped marks on their ass?
Are those marks like, from friction?
I wondered about that too. Although some people with certain complexions seem to be discolored areas like that, even normal weight people
Tess has the same issue
View attachment 2962827
As this user pointed out…
I'm pretty sure it's just
acanthosis nigricans, a common skin condition afflicting fatties in areas where their skin tends to rub together a lot like around the neck, under the arms, between the folds, etc. It causes the skin to thicken, and darken in color.
… which makes sense. It often forms rings - like the ones you’re seeing - or bands in skin folds such as the gluteal crease, inner thighs, groin, neck, and armpits. It’s associated with associated with:
- Insulin resistance
- Prediabetes or type 2 diabetes
- Obesity
There’s
also friction-related hyperpigmentation, which is caused by chafing, pressure, and skin-on-skin rubbing. Basically, over time, friction leads to post-inflammatory hyperpigmentation (PIH), which can look like a ring or band.
The term for the rash / mild chronic inflammation is intertrigo, which is caused by moisture and friction. It’s worsened by heat, sweat, and prolonged sitting, and the PIH it helps induce can remain even after the inflammation goes away.
Finally, there’s pressure and compression marks. These are blemishes caused by the pressure associated with sitting, tight clothing, swimwear, and elastic seams. All of these conditions are more common in fatties because fatties have more skin folds. Skin folds mean more friction and more moisture than normal. Fat people have higher rates of insulin resistance and the excess weight means more pressure on said folds.
Why do these conditions cause this darkening of the skin? Well, skin darkening (aka hyperpigmentation) happens when melanocytes (pigment-producing cells in the basal epidermis) are stimulated to: (1) produce more melanin, and / or (2) transfer more melanin to surrounding keratinocytes. Inflammation, hormones, and growth factors all affect and trigger melanocytes.
Mechanical pressure is another explanation. Friction+ pressure + moisture = repeated micro-injury. Keratinocytes release inflammatory cytokines (ex. IL-1, TNF-α, prostaglandins), and this causes low-grade chronic inflammation. Even when you don’t see redness anymore, inflammatory signaling persists, and so mast cells and macrophages release mediators, which in turn upregulate tyrosinase, a key enzyme in melanin synthesis. Melanocytes increase melanin output as a
protective response. Keep fucking with your skin by turning it into a swamp or rubbing it vigorously, and it will start to prepare itself for your nonsense.
There’s also pigment “leakage”. Basically, there is damage to the skin’s basal layer, so melanin drops down into the dermis. Macrophages engulf them, and now we have dermal melanophages giving in your dermis. This makes pigmentation darker and longer-lasting. It also thickens skin, changes the skin colour to brown, and can produce a rough texture. In this situation, the pigment fades away slowly, but
only if the irritation stops.
By contrast, acanthosis nigricans is
not caused by inflammation of the skin. The core mechanism is hormonal, and relates to insulin resistance. Blood insulin levels rise - aka hyperinsulinemia, and so insulin begins binding to IGF-1 receptors on skin cells. This causes keratinocytes to proliferate and thicken the epidermis. Fibroblasts proliferate, melanocytes are indirectly stimulated, and pigmentation is increased incidentally. The darkness comes from thickness + light absorption + mild pigment increase, but not from melanocyte overreaction to injury like PIH described above.
Skin folds are more affected because they have higher insulin receptor density. Friction accentuates visibility, but is not the root cause, because this is a metabolic signaling disorder, not a damage response. Furthermore, they’re moist. Moisture macerates the stratum corneum, weakens barrier proteins in the skin (ex. filaggrin, loricrin), increases cytokine penetration, and allows microbial overgrowth (which, again, causes more inflammation).
Basically:
- Friction/moisture hyperpigmentation is where melanocytes respond to injury and inflammation.
- Acanthosis nigricans is where skin cells panic while responding to hormonal overdrive.
They create the same aesthetic symptom, but they start in different biological systems. The first is reactive / trauma-induced and the latter is endocrine-driven. That’s why weight loss helps acanthosis but is less useful in treating PIH. You can also have both conditions simultaneously and have them
both darken the skin. Why is it on her butt? Because she sits down a lot.
I want to know, but I also really don't want to know.
