In this week’s episode I looked at what your skin might be flagging about your blood sugar. Here I want to go a layer deeper, into why an internal, invisible thing like insulin would ever show up on the outside of you, and, just as importantly, when that might not be the case.
Let’s start with the mechanism, because once you see it, the skin signs stop looking random.
Insulin isn’t only a blood sugar hormone. It’s a growth signal. When it runs high for a long time (the state we call insulin resistance, where the body pumps out more and more insulin to get the same job done), it no longer stays in your bloodstream. It talks to your skin. One of the clearest examples is acanthosis nigricans, which is a velvety, darker thickening that appears in skin folds. High insulin drives skin cells (keratinocytes) to proliferate faster than usual, and the visible result is that thickened, pigmented patch that people so often mistake for dirt. The same paper notes that skin tags (acrochordons) often go with it, both recognised as cutaneous markers of insulin resistance, sometimes appearing well before glucose looks abnormal on a standard test.
Adult acne runs on a related wire. When insulin is elevated, it raises a cousin signal called IGF-1, and the two together stimulate the sebaceous glands to produce more oil, while also nudging androgen activity upward: a combination that feeds exactly the kind of breakouts that show up along the jaw in adulthood. This isn’t fringe thinking: a randomised controlled trial found that shifting people to a lower-glycaemic way of eating measurably lowered their IGF-1 levels. The dietary lever and the skin are wired to the same board.
Here’s the part that matters most: these signs can appear in people whose blood tests still read “normal”. Skin signals track with insulin, and insulin can be quietly elevated for years while glucose and HbA1c sit inside the reference range. That’s the whole “normal range problem”. The body posting an early notice on the outside while the standard test on the inside hasn’t caught up yet.
Now here’s the honest boundary.
Skin signs are markers, not diagnostic tests. Plenty of people have a skin tag or two for reasons that have nothing to do with metabolism, including friction, age, pregnancy, and genetics. A single tag is not a verdict. The signal is in the pattern: clustering, recurrence, and especially co-occurrence, like skin tags turning up alongside acanthosis nigricans. That combination is a stronger flag than either alone, but it’s still a prompt to ask a question, never an answer in itself.
And some skin conditions aren’t a blood sugar story at all. Eczema is the one I know personally, and it’s a useful example precisely because it doesn’t fit the pattern. Atopic dermatitis is fundamentally a skin-barrier and immune condition driven by barrier proteins like filaggrin and a particular immune response, with genetics and environmental triggers layered on top. Hand eczema that flares when you handle particular materials looks even more like a direct contact reaction than anything metabolic. Reaching for “it must be my blood sugar” there would be the wrong tool. Discernment - knowing which skin thing is which, is the actual skill.
But there is a thread that runs underneath almost all of it, and it surprised me when I first read into it: your skin keeps time.
Since the 2017 Nobel Prize in Physiology or Medicine went to the scientists who mapped the body’s molecular clock, we’ve learned that the skin runs its own peripheral version of it. Skin barrier function isn’t constant through the day. Studies measuring transepidermal water loss and barrier properties find a clear daily rhythm, with the barrier more permeable in the evening and overnight. That’s part of why itch and irritation tend to worsen at night, and why repair, cell turnover and hydration all follow the clock rather than ignoring it. Disrupt sleep and rhythm, and the barrier feels it.
Matsui et al., 2016
Matsui et al., 2016
Which is where the two halves of this newsletter meet. Whether a skin issue is metabolic (like acanthosis nigricans) or immune (like eczema), it sits on shared ground: inflammation, sleep, and the steadiness of your daily rhythm. That’s not a claim that fixing your sleep clears your skin. I can’t promise you that, and I wouldn’t. It’s an observation that the unglamorous foundations show up in more places than we’re usually told, skin included.
So the useful takeaway isn’t a diagnosis you give yourself in the bathroom mirror. It’s a better question to bring to your GP: if my skin is showing a cluster of these signs, is it worth looking at my blood sugar, and a fasting insulin test alongside the usual HbA1c? That’s a reasonable thing to ask, it changes nothing about your medical care, and it might surface a pattern earlier than a single glucose reading ever would.
Your skin is the readout you didn’t know you were carrying. Most of us were only ever taught to treat its surface. It’s worth learning to read it too, alongside your medical care, never instead of it.
Thank you for being here.
See you next week,
Frances x
Frances Norgate
Qualified Nutrition and Lifestyle Advisor
