I’m bloated like four days a week. My stomach goes from flat in the morning to “are you pregnant” by evening for absolutely no reason I can identify. I’ve had random stomach pain that comes and goes. I’ve had weeks where I couldn’t poop and weeks where I couldn’t stop. I’ve Googled “why is my stomach always weird” more times than I’d like to admit.

And apparently I’m not alone, because #hotgirlshaveibs has over 112 million views on TikTok.

That number is funny to say out loud, but it’s also telling us something real: gut problems are so common in young women that we made a whole meme about it. Bloating, constipation, random stomach pain, IBS, these are being treated as an inherent part of having a female body, like cramps. Just a thing that happens. Nothing to do about it.

Except there’s actually a lot of research on why this is happening. And it’s more interesting than “women just have sensitive stomachs.” There’s a reason IBS affects women at twice the rate it affects men. There’s a reason your gut feels totally different in different weeks of the month. There’s a reason stress literally gives you stomach pain.

This short dive is the explanation your body has been waiting for. What’s actually going on, why it’s specifically worse for us, and what you can actually do about it.

1. Your Gut and Your Brain Are Basically in a Group Chat

2. Why Women Specifically Got the Worst Deal Here

3. What "Gut Health" Actually Means (And What It Doesn't)

4. The Bloating Chapter (Finally)

5. What to Eat (And What's Probably Making Things Worse)

6. Your Gut and Your Skin Are Talking To Each Other

7. The Cycle-Aware Gut Protocol

8. The Practical Guide: Probiotics Decoded and the Daily Habits

9. The Short Version of Everything

Chapter 1: Your Gut and Your Brain Are Basically in a Group Chat

Okay so picture this: you have a big exam coming up. Or a difficult conversation you’re dreading. And your stomach feels it before anything has even happened. The knot, the sudden need to run to the bathroom, the weird nausea that shows up when you’re stressed. That’s not a coincidence or a personality quirk. That’s biology.

Your gut and your brain are connected by something called the gut-brain axis, which is basically a direct communication highway between the two of them, running through a nerve called the vagus nerve. They’re constantly texting each other. The brain sends signals down to the gut (this is why stress and anxiety mess with your digestion). The gut sends signals back up to the brain (this is why gut problems affect your mood). It goes both ways, constantly.

Here’s what makes this even more interesting: your gut has its own nervous system. Like, an independent one. It has more nerve cells than your spinal cord, around 500 million of them and it can operate semi-independently of the brain. Scientists sometimes call it the “second brain,” which sounds dramatic but is actually just anatomically accurate. The gut is not just a tube that moves food. It’s a complex sensory organ that’s in constant conversation with everything else.

And living inside that gut? About 38 trillion bacteria, fungi, and other microorganisms that collectively make up your gut microbiome. These aren’t just sitting there. They’re actively producing neurotransmitters including about 90–95% of the body’s serotonin (yes, the mood chemical, mostly made in your gut, not your brain), GABA (the calming neurotransmitter your anxiety chapter covered), and dozens of other compounds that affect how you feel mentally and physically. The gut microbiome is, in a very real sense, part of your emotional regulation system.

This is why “gut health” isn’t a wellness trend invented to sell supplements. It’s a genuinely important area of research with implications that go way beyond digestion. When your gut bacteria are diverse and well-fed, the whole system tends to work. When they’re disrupted through a bad diet, antibiotics, chronic stress, not sleeping, the effects ripple outward into your mood, your skin, your hormones, and yes, your digestion.

The #hotgirlshavestomachissues meme exists because the gut-brain axis is more active in young women than most of us realise, in a hormonal environment that specifically makes it more reactive. Which brings us to chapter 2.

Chapter 2: Why Women Specifically Got the Worst Deal Here

Women are twice as likely to have IBS as men. Twice. And symptoms peak between ages 18 and 39.

For a long time, medicine didn’t have a great explanation for this. The assumption was that women were more likely to report symptoms, or that psychological factors explained the gap, or just that women had more “sensitive” guts in some vague way that nobody could really explain.

Then in December 2025, researchers at UC San Francisco published a study in the journal Science that finally gave us the mechanism. And it’s estrogen.

But not in the way you might think.

The estrogen finding that changed everything

The researchers were looking at a specific type of cell in the colon called L-cells. These cells normally release hormones related to appetite and gut movement. What the researchers found was that estrogen binds to receptors on these L-cells, and when it does, it triggers the release of a hormone called PYY, which then tells nearby pain-sensing cells to flood the area with serotonin.

Serotonin in the gut (not the mood version, a different mechanism) activates the pain-sensing nerve fibres that send “something’s wrong here” signals to your brain. So the chain looks like this:

To prove it was actually the estrogen doing this, they gave male mice estrogen doses equivalent to female levels. The male mice’s gut pain sensitivity immediately increased to match that of females.

Here’s the second part that explains so much: estrogen also caused those L-cells to produce more receptors for the byproducts of gut bacteria fermenting food specifically the fermentation of things like onions, garlic, beans, and wheat (what dietitians call FODMAPs). So estrogen isn’t just making the gut more pain-sensitive in general. It’s also making it more reactive to specific foods that produce gas and fermentation.

This is the mechanism behind two things that confuse a lot of women:

• Why your gut reacts to foods that don’t bother other people — estrogen has specifically made your gut more sensitive to those fermentation byproducts

• Why gut symptoms often change across your cycle — because estrogen levels change across your cycle, and so does gut sensitivity

The cycle-bloating connection

This is where it gets really specific and really useful.

In your follicular phase (after your period ends, leading up to ovulation), estrogen is rising. The gut is more sensitive because of the mechanism above. Some women notice their stomach is more reactive in this phase than they expect.

Around ovulation, estrogen peaks, this is when the gut is at its most sensitive, and some women have their worst gut pain here even though they don’t associate it with the premenstrual window at all.

In the luteal phase (after ovulation, the two weeks before your period), progesterone takes over. And here’s what progesterone does to your gut: it slows everything down. Literally. It slows the contractions that move food through your intestines. This is why constipation is specifically worse in the two weeks before your period, progesterone is basically putting the brakes on your digestion.

Then as you get close to your period, prostaglandins kick in, the compounds that drive uterine contractions to start your period. They also affect your intestines. Which is why, right when your period starts, many women swing from constipation to diarrhea. Your intestines are responding to the same signal your uterus is.

And throughout all of this: the composition of your gut microbiome itself changes across your cycle. The bacteria that thrive in different hormonal environments are actually different bacteria, which is why your stomach can feel so variable month to month even if you’re eating the same things.

The anxiety loop

There’s one more piece that rounds out the “why women” picture. Women experience anxiety at twice the rate of men (covered in the anxiety short dive). And anxiety directly activates the gut-brain axis. The stress response tells the gut to change how fast things move, which changes the bacterial environment, which changes which signals go back to the brain.

This is why the TikTok meme exists. It’s not a coincidence that “hot girls have stomach issues” overlaps almost exactly with “young women have the worst mental health of any demographic.” The anxiety is activating the gut. The gut is feeding back into the anxiety. It’s a loop.

And once you understand that the loop exists, you can start intervening at both ends of it.

Chapter 3: What “Gut Health” Actually Means (And What It Doesn’t)

“Gut health” has become one of those wellness terms that means everything and nothing simultaneously. Let’s sort it out.

What it actually means

Your gut microbiome is healthy meaning it’s diverse, when it contains a wide variety of bacterial species that are collectively able to:

• Ferment dietary fibre into short-chain fatty acids (these are the compounds that reduce inflammation, maintain the gut lining, and communicate with the immune system)

• Metabolise estrogen properly through the estrobolome (so hormones are cleared correctly rather than recirculating)

• Produce adequate GABA and serotonin precursors for the gut-brain axis

• Maintain the integrity of the gut lining (preventing the “leaky gut” situation where compounds that shouldn’t cross into the bloodstream do)

All of these are extremely common in the 15–35 age group.

What “gut health” doesn’t mean

It doesn’t mean your gut is a glass that you can “clean” or “detox.” Your gut is not dirty. You cannot flush it. Juice cleanses and “gut reset” programmes don’t remove bacteria, they temporarily change the environment, and your bacteria largely return to their previous composition within a few weeks because bacteria adapt quickly.

It doesn’t mean that fermented food alone fixes everything. Kefir is great. It is not going to compensate for a diet with almost no fibre.

It doesn’t mean every gut problem has a dietary solution. Some gut conditions like Crohn’s disease, ulcerative colitis, coeliac disease, SIBO, gastroparesis, are medical conditions that require medical diagnosis and management. Persistent, severe, or new-onset gut symptoms that affect your quality of life should be investigated by a doctor, not just managed with probiotics. The TikTok meme normalises talking about gut issues, which is good. It should not normalise ignoring symptoms that need investigation.

The fibre gap you probably have

The single most impactful thing for gut microbiome diversity is dietary fibre specifically the variety of fibres that comes from eating a range of plant foods. Current recommendations are 25–38g of fibre daily. Most people in Western countries eat less than half of this.

This isn’t about eating more salad. It’s about variety. Different plant fibres feed different bacterial species. The research consistently shows that the most diverse gut microbiomes come from people who eat the widest variety of plant foods and not the people who eat the most of one specific “gut health” food. The goal is 30 different plant types per week, including vegetables, fruits, legumes, nuts, seeds, herbs, and wholegrains. This sounds like a lot until you realise that three different colours of bell pepper count as three, and a handful of mixed seeds counts as several.

That’s Part 1. Part 2 is where I get into the specific stuff: the bloating chapter with what actually makes it worse and what actually helps, what to eat (and stop eating), how your gut and your skin are connected in ways that explain a lot, the cycle-aware gut protocol, and the practical guide to probiotics that doesn’t just say “take a probiotic.”

So now you know what’s actually going on. Your gut and your brain are in a constant two-way conversation that affects your mood, your skin, your digestion, and your hormones. Estrogen specifically makes your gut more pain-sensitive through a mechanism that researchers only fully mapped in December 2025, meaning the “why does this hurt me more than everyone else” question finally has a real answer. And “gut health” isn’t a vibe. It’s a specific biological state with specific things that support or disrupt it.

Part 2 is the practical half.

Chapter 4 is the bloating chapter. The actual causes of each type of bloating (they’re different), what makes them worse, what the research says actually helps, and why most of the bloating advice you’ve seen is addressing the wrong thing.

Chapter 5 is what to eat. Not a meal plan. The specific foods and eating patterns with actual research behind them for gut health and the specific things that are probably making your gut worse right now.

Chapter 6 is the gut-skin connection, for anyone whose skin problems haven’t fully responded to topicals. The route from gut bacteria to estrogen to jawline acne is documented, and this is the chapter that explains it properly.

Chapter 7 is the cycle-aware gut protocol. What to do differently in each phase because your gut is genuinely different in each phase.

Chapter 8 is the practical guide: probiotics decoded (the strain thing matters and most people don’t know this), what supplements actually have evidence, and the daily habits that make the most difference.

Subscribe to read Part 2 →

Sources & Further Reading

UCSF — Do Hormones Explain Why Women Experience More Gut Pain? December 2025

Venkataraman et al. A cellular basis for heightened gut sensitivity in females — Science, December 2025

MedicalXpress — IBS affects women more than men — here’s why, October 2025

Digestive Diseases and Sciences — It’s a Women’s World: Sex Differences in IBS, March 2025

Mayo Clinic Proceedings — Sex and Gender Differences in Functional Gastroenterologic Disorders, 2021

Evelyn Health — PMS and gut health: what your digestive symptoms are telling you, June 2026

PMC meta-analysis. Effects of probiotics on depression and anxiety in clinically diagnosed patients, 2025

Frontiers in Microbiology. Psychobiotics in mental health: gut-brain axis insights, March 2026

Osprey Polyclinic. The gut-hormone connection for women, February 2026

Fortune — The hot girls have stomach issues social media trend makes sense, 2023

Part 1 ended with the evidence hierarchy, which established that CBT and resistance training have the strongest evidence, that magnesium and omega-3s have genuinely good supporting evidence, and that most of what’s being sold in the anxiety supplement space has weaker evidence than its marketing suggests.

Part 2 is the practical half: the specific biological mechanisms of the interventions that work, and how to build them into a routine that’s actually manageable.

Table of contents

4. Your Gut and Your Anxiety: The Connection Is More Direct Than You Think

5. The Sleep-Anxiety Loop, And How to Break It

6. The Nutrition Chapter: Specific Mechanisms, Not Vague Advice

7. The Cycle-Aware Anxiety Protocol

8. The Complete Practical Guide

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Part 1 ended on the mineral-versus-chemical question, which is the debate most sunscreen content spends all its energy on. Part 2 is about the things that matter just as much and get almost no attention: how much you’re actually applying, whether your protection routine is quietly making you vitamin D deficient, what to do if your skin doesn’t tolerate standard formulas well, and the hormonal layer of pigmentation that no amount of perfect SPF technique alone will fully solve.

Table of Contents

4. How Much to Actually Apply. The Gap Is Bigger Than You Think

5. The Vitamin D Balance: Protecting Skin Without Becoming Deficient

6. SPF for Acne-Prone, Sensitive, and Reactive Skin

7. The Hormonal Pigmentation Connection: Melasma and Your Cycle

8. The Complete Practical Guide

9. Conclusion: The Habit That Outperforms Almost Everything Else in Skincare

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That’s not a knock on anyone’s intelligence. It’s a knock on where the information has been coming from. The same survey found that 36% of Gen Z say influencers are their primary source of skincare information and a lot of what’s circulating is confidently wrong. A tan being a sign of “healthy” skin. SPF only mattering on sunny days. A higher SPF number meaning you can apply less. These aren’t fringe beliefs. They’re common enough to show up in a national survey.

Meanwhile, “skin longevity” has become the defining skincare conversation of 2026, the shift from fixing damage after it happens to keeping skin functioning well for decades. Which makes this the perfect, slightly ironic moment to point out: the single most powerful skin longevity tool already exists, it’s been sitting in your bathroom cabinet the whole time, and most people are using it wrong or not using it enough.

This short dive is the sunscreen guide that should have existed years ago. What UV radiation is actually doing to your skin at a cellular level. Which myths are costing you the most. The honest, current state of the mineral-versus-chemical debate, including a few 2026 developments that haven’t filtered into mainstream skincare content yet. And in Part 2, the practical guide: how much to actually use, the vitamin D balance, and what to do if your skin is acne-prone, sensitive, or prone to pigmentation.

Let’s start with the biology.

1. What UV Radiation Actually Does to Your Skin

2. The Myths Costing You the Most

3. Mineral vs. Chemical Filters. What the Evidence Actually Says in 2026

Chapter 1: What UV Radiation Actually Does to Your Skin

Two Types of Rays, Two Different Kinds of Damage

Sunlight that reaches your skin contains two types of ultraviolet radiation that matter for skin health: UVA and UVB. They’re often talked about as if they’re interchangeable. They’re not. They damage skin through different mechanisms, at different depths, with different consequences and understanding the difference is the foundation for understanding why SPF alone isn’t the whole story.

UVB is the shorter-wavelength ray. It mostly affects the outer layer of your skin (the epidermis). This is the ray responsible for sunburn, and it works by directly damaging your skin cells’ DNA. When UVB hits a skin cell, it causes specific kinds of DNA damage where the building blocks of your DNA fuse together incorrectly. Your body has repair systems for this kind of damage, but they’re not perfect and the damage that doesn’t get repaired correctly is the kind that’s strongly linked to skin cancer development over time.

UVA is the longer-wavelength ray, and it penetrates much deeper, all the way into the dermis, the layer of skin where collagen and elastin live. This is the layer responsible for your skin’s structure, firmness, and bounce. UVA’s main damage pathway isn’t direct DNA breakage. It’s oxidative stress: UVA exposure generates reactive oxygen species inside skin cells, which then activate enzymes called MMPs (matrix metalloproteinases) that actively break down collagen. Research comparing UVA and UVB damage at the cellular level found that UVA specifically promotes the breakdown of dermal collagen fibres and triggers inflammation, while UVB primarily affects the surface cells. UVA penetrates roughly 1.6 times deeper into skin than UVB, which is exactly why it’s the ray most responsible for wrinkles, sagging, and loss of elasticity, while UVB is more associated with burning and surface damage.

Here’s the part that matters most: UVA is present at consistent intensity all day, every day, all year round, including through clouds and through glass windows. UVB intensity varies much more by time of day and season. This is why “I’m not getting sun damage, it’s cloudy” or “I’m inside all day” are two of the most common and most costly misunderstandings about sun protection. The ray responsible for collagen breakdown doesn’t care whether you can feel the heat.

Why the Damage Is Invisible Until It Isn’t

This is the part of “skin longevity” content that often gets skipped: by the time photoageing is visible; fine lines, uneven texture, brown spots, looser skin, the damage has usually been accumulating for years, sometimes decades.

The collagen breakdown triggered by UVA exposure happens immediately at a cellular level, every time skin is exposed without protection. But collagen is abundant, and the visible effects of its breakdown only become apparent once a critical threshold has been crossed. Research using collagen gels found that UVA radiation specifically causes hardening and loss of elasticity in collagen, more so than UVB and that this effect compounds with cumulative exposure over time. This is why someone who’s 24 and never worn SPF consistently doesn’t look damaged yet, but the cellular process that produces visible photoageing at 35 or 40 has already been running for years.

This delay between cause and visible effect is precisely why prevention has to start before there’s anything to see. It’s the same logic that applies to bone density, as covered in a previous Between Saturdays; peak collagen density and skin structural integrity are being built and maintained right now, in your teens, 20s, and early 30s, whether or not you’re paying attention to it.

The DNA Damage Layer: Why This Isn’t Just About Wrinkles

It’s worth being direct about the more serious side of this conversation, because most skincare content focused on “skin longevity” and ageing tends to underplay it.

UVB radiation directly forms specific DNA lesions; cyclobutane pyrimidine dimers and related photoproducts, that are strongly associated with skin cancer development when they aren’t correctly repaired. UVA contributes too, primarily through oxidative DNA damage, and has its own documented association with melanoma risk. The cumulative, unprotected exposure that produces visible photoageing over years is the same cumulative exposure that raises skin cancer risk over the same period.

Even mild psychological stress appears to amplify UV damage at the cellular level. A 2024 study found that stress occurring during UVB exposure degraded collagen function by suppressing its production, compounding the damage already happening from the UV exposure itself. This is a genuinely interesting finding: the stress-skin connection covered in earlier Simply Salvia content isn’t separate from sun damage, it appears to interact with it directly.

None of this is meant to be alarming for its own sake. It’s meant to explain why “I’ll start caring about sunscreen when I’m older” is backwards. The damage that shows up later is being determined now.

Chapter 2: The Myths Costing You the Most

This is the chapter built directly around the specific gaps the 2026 AAD survey identified, the beliefs that are common, confidently held, and wrong.

“A Tan Means Healthy Skin”

This is the single most damaging misconception in the survey results, and it’s worth being completely clear about: there is no such thing as a healthy tan. Any visible tan is a sign of UV damage that has already occurred, it’s your skin’s melanin-producing cells responding to DNA damage by producing more pigment as a protective (and imperfect) response. A tan is your skin’s distress signal, not a sign of vitality.

This doesn’t mean sunlight itself is the enemy, sensible sun exposure has real benefits, covered in Chapter 5 of Part 2. It means that the specific outcome of “getting a tan” visible skin darkening from UV exposure is, by definition, evidence of damage having occurred, not a wellness goal to pursue.

“SPF Is Only Necessary on Sunny Days”

UV radiation, particularly UVA, isn’t meaningfully reduced by cloud cover. Up to 80% of UV rays can penetrate cloud cover, meaning a grey, overcast day can deliver nearly as much UVA exposure as a clear one. This is one of the more counterintuitive facts in sun safety, because cloud cover reduces the heat you feel, which intuitively (and wrongly) reads as reduced UV exposure.

The practical implication: daily SPF isn’t a summer habit or a beach-day habit. It’s a daily habit, regardless of forecast, because the ray most responsible for long-term collagen damage doesn’t fluctuate with visible weather conditions.

“Higher SPF Means I Can Apply Less”

This is backwards, and it’s a genuinely costly misunderstanding. SPF protection doesn’t scale linearly with the number, it scales logarithmically, and crucially, the SPF rating on any bottle is only achieved at a specific application amount (2mg per cm² of skin, which works out to roughly a nickel-sized amount for the face). Most people apply somewhere between a quarter and half of this amount in real-world use, which means an SPF 50 product applied at half the recommended amount delivers closer to SPF 10–15, not SPF 25.

A higher SPF number gives you more margin for under-application, not permission to under-apply. The number on the bottle is a ceiling you only reach with the correct amount.

“My Foundation/Moisturiser Has SPF, So I’m Covered”

Multi-purpose products with SPF built in are genuinely useful as a layer of protection, but they’re rarely sufficient as the only layer, for two reasons. First, people apply far less foundation or tinted moisturiser to their face than the amount needed to achieve the labelled SPF, typically a fraction of a nickel-sized amount, when full SPF protection requires significantly more. Second, many of these products aren’t reapplied through the day the way a dedicated sunscreen would be, even though SPF protection degrades with time and UV exposure regardless of the product format.

The practical guidance dermatologists give consistently: treat SPF-containing makeup as a bonus layer on top of a dedicated sunscreen applied properly underneath, not as a replacement for one.

“Sunscreen Causes More Harm Than the Sun Itself”

This belief has gained traction from genuine, evolving research on chemical sunscreen absorption, covered honestly in Chapter 3 but it’s frequently overstated into “sunscreen is dangerous,” which isn’t what the evidence supports. The honest research distinguishes between specific chemical filters with documented absorption and hormonal interaction concerns, and the category of sunscreen as a whole, which has decades of evidence supporting its role in reducing photoageing and skin cancer risk. The next chapter goes into this distinction properly.

Chapter 3: Mineral vs. Chemical Filters. What the Evidence Actually Says in 2026

This is the part of the sunscreen conversation that’s evolved the most recently, and it deserves a more current and more nuanced treatment than most existing content gives it.

How Each Type Works

Mineral (physical) sunscreens use zinc oxide and/or titanium dioxide. These work primarily by sitting on the skin’s surface and physically reflecting and scattering UV radiation, rather than absorbing it into the skin. Studies using isotopically labelled zinc oxide have found minimal systemic absorption through intact human skin meaning very little of it enters the bloodstream. Zinc oxide also has independent anti-inflammatory and barrier-supportive properties, which is part of why it’s frequently recommended for sensitive or reactive skin.

Chemical (organic) sunscreens use compounds like oxybenzone, octinoxate, octocrylene, homosalate, octisalate, and avobenzone. These work by absorbing UV radiation and converting it to heat, which is then released from the skin. They tend to feel lighter, blend more easily, and are less likely to leave a visible cast, which has historically made them the more popular choice, particularly on deeper skin tones.

The Absorption Question: What 2026 Research Actually Shows

This is where the conversation has shifted meaningfully in the past few years, and it’s worth being precise rather than alarmist.

A 2019 FDA study found that several common chemical UV filters like oxybenzone, avobenzone, octocrylene, and others were absorbed into the bloodstream at levels significantly higher than previously understood, in some cases far exceeding the FDA’s own threshold for requiring further safety testing. A 2020 JAMA study found that a single day of using an oxybenzone-containing lotion produced plasma concentrations of 94.2 ng/mL, nearly 200 times the FDA’s 0.5 ng/mL threshold below which further testing typically isn’t required.

The important nuance: exceeding that threshold means the FDA wants more data, it does not automatically mean harm has been demonstrated. But the specific concern with oxybenzone has accumulated more weight over time. One fertility clinic cohort study found that higher oxybenzone levels were associated with lower antral follicle count in women under 35, and higher FSH (a hormone marker of declining ovarian reserve) in women over 35 suggesting a possible hormonal effect, though human research in this area remains limited and the clinical significance isn’t fully established. The National Toxicology Program also released findings linking oxybenzone exposure to increased thyroid tumour risk in female rats, and the European Commission’s safety review concluded oxybenzone is not considered safe at current permitted concentrations.

This research has had a real, measurable effect on the market: oxybenzone appeared in 70% of chemical sunscreens tested in 2016, and by 2026 that figure had dropped to just 5%, the industry has been actively reformulating away from it in response to the accumulating evidence, even ahead of any formal ban.

What This Means Practically, Without the Panic

The honest takeaway isn’t “chemical sunscreen is dangerous, switch to mineral immediately.” It’s more specific than that:

The strongest concern is specifically tied to oxybenzone, not chemical sunscreens as a category. If you check your sunscreen’s ingredient list and oxybenzone (sometimes listed as benzophenone-3 or BP-3) isn’t there, the absorption and hormonal concerns from the research above largely don’t apply to your product.

Some newer and more widely used in Europe chemical filters, bemotrizinol in particular have significantly better safety profiles, with minimal systemic absorption and no documented hormonal disruption concerns, and have been used safely across Europe, Asia, and Australia for over 20 years. The FDA approved bemotrizinol for use in the US for the first time in over two decades, with products expected to reach shelves in late 2026, a meaningful regulatory shift that’s been a long time coming.

Mineral sunscreen remains the most conservative choice for anyone wanting to minimise systemic absorption with the most established safety data, and is generally the first recommendation for sensitive skin, pregnancy, and younger users. The trade-off is cosmetic: mineral formulas can leave more of a visible cast, particularly on deeper skin tones, although tinted mineral formulas have improved significantly.

What’s not well supported by the evidence: avoiding sunscreen altogether because of these concerns. The documented risks of unprotected UV exposure; collagen breakdown, DNA damage, skin cancer risk are considerably better established and more serious than the absorption concerns around specific chemical filters. The right response to the oxybenzone research is switching to mineral sunscreen or a chemical sunscreen without oxybenzone, not abandoning sun protection.

Part 1 ends here. Part 2 covers exactly how much sunscreen to actually apply (the real-world gap is bigger than most people realise), how to balance sun protection with vitamin D, what to do if you’re acne-prone or dealing with pigmentation, the specific hormonal connection to melasma that almost no one explains properly, and the complete practical guide with product recommendations at every price point.

Now you understand what UV radiation is actually doing to your skin. The difference between UVA’s deep collagen damage and UVB’s surface-level burning and DNA damage, and why the visible effects show up years after the cellular damage begins. You know which myths are costing the most: the tan myth, the cloudy-day myth, the “higher SPF means less product” myth. And you have the current, nuanced picture on mineral versus chemical filters including the oxybenzone research specifically, rather than a blanket judgement on an entire category.

Part 2 turns all of this into something you can actually use.

Chapter 4 covers exactly how much sunscreen to apply and how often, including the research on just how large the real-world gap is between the SPF on the label and the protection most people are actually getting.

Chapter 5 is the vitamin D chapter. How to protect your skin without ending up deficient, and what the evidence actually supports as a reasonable middle ground.

Chapter 6 is specific to acne-prone, sensitive, and reactive skin, which formulas tend to work best and which ingredients to watch for.

Chapter 7 covers the hormonal dimension of sun damage that almost nobody explains properly: melasma, the menstrual cycle, and why pigmentation can worsen at specific hormonal points regardless of how diligent your SPF routine is.

Chapter 8 is the complete practical guide: product recommendations at every price point, the application cheat sheet, and the daily routine.

Subscribe to read Part 2 →

Sources & Further Reading

Comparison of the Biological Impact of UVA and UVB upon the Skin with Functional Proteomics and Immunohistochemistry — PMC

A comparative study of UVA and UVB radiation: Mechanisms of DNA damage and repair — Indonesia Journal of Biomedical Science

Analysis of UV Radiation Wavelengths Causing Hardening and Reduced Elasticity of Collagen Gels In Vitro — MDPI

Early stage UV irradiation damage to skin collagen suppressed by HPA axis control — ScienceDirect

Gen Z is most exposed to sunscreen misinformation on TikTok — EMARKETER, AAD survey data, January 2026

AAD: How to apply sunscreen — American Academy of Dermatology guidance

The Great Debate: Mineral vs Chemical Sunscreen — Dr. Heather Rogers, April 2026

What Sunscreen Is Safe? Mineral vs. Chemical Explained — ScienceInsights, April 2026

EWG’s Trouble with Sunscreen Chemicals report, 2026

EWG’s 20th Annual Guide to Sunscreens, May 2026

Targeting Melasma: Innovations in Pigment Deposition and Photoaging — Journal of Cosmetic Dermatology, January 2026

Mechanisms of Estrogen and Progesterone in Melasma — International Journal of Molecular Sciences, 2025

Dietary antioxidant intake in women with facial melasma — case-control study, October 2025

Part 1 ended at the evidence hierarchy, which told you that most of what’s being sold is not at the top of it, and what actually is.

Part 2 is the practical half. The specific blood tests to ask for and the numbers that actually matter for hair health. The treatment guide, including everything you need to know about minoxidil. What the supplements actually do in which situations. And the complete month-by-month guide to a recovery that has a realistic timeline attached to it.

4. The Blood Tests to Request. And What the Numbers Actually Mean

5. The Full Treatment Guide. What the Research Supports and How to Use It

6. What the Supplements Actually Do, By Situation

7. The Cycle-Aware Approach. The Weeks Where Shedding Is Reliably Worse

8. The Complete Practical Guide

9. Conclusion: The Guide Your GP Probably Didn’t Have Time to Give You

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Then it was the shower drain. Then the pillow. Then the ponytail that felt noticeably thinner in my hand than it used to. By the time it was obvious enough to worry about, it had been happening for months.

This is how hair loss usually goes for women. Quietly at first, then all at once. And the information available when you finally start looking? Either terrifying, or trying to sell you something.

This short dive is the guide I wanted then. What’s actually happening. Why it happens to women specifically. What the research says works and what it says about the expensive supplements and serums that dominate this space. And, the practical framework: the blood tests to ask for, the treatments with real evidence, and the honest timeline.

Let’s start with the biology.

1. How Hair Actually Grows And Why That Determines Everything

2. The Most Common Causes in Women Under 35

3. The Evidence Hierarchy. What the Research Says Actually Works

Chapter 1: How Hair Actually Grows And Why That Determines Everything

The Hair Cycle

Every single hair on your head is going through its own independent cycle -completely separate from the hairs around it. And understanding this cycle is the key to understanding why hair loss happens the way it does: why it’s delayed, why it’s diffuse, and why recovery takes so much longer than you’d expect.

The cycle has three phases:

Anagen: the growth phase

This is when the hair is actively growing. Each strand spends between two and seven years in anagen, growing approximately 1cm per month. The length your hair can reach is largely determined by how long your follicles stay in anagen, which is partly genetic.

Catagen: the transition phase

A brief two-week window where the hair stops growing and the follicle starts to shrink and detach from its blood supply. Only about 1% of hairs are in this phase at any given time.

Telogen: the resting phase

The hair is no longer growing but is still attached to the follicle. It stays here for approximately three to four months before being shed and replaced by a new anagen hair growing underneath. About 10–15% of your hairs are in telogen at any one time.

Normally losing between 50 and 100 hairs per day is considered completely normal. These are the telogen hairs that have completed their cycle. The reason you don’t go bald is that only a small percentage of follicles are in this phase at any time, and the majority are actively growing.

Why Hair Loss Is Always Delayed

Here’s the thing that catches almost everyone off guard: whatever caused your hair loss happened two to three months before you noticed it.

When something goes wrong whether it’s a physical stressor, a hormonal shift, an illness, a period of severe restriction, a crash diet. The body’s response is to push a large number of hair follicles out of anagen and into telogen simultaneously. But those hairs don’t fall out immediately. They sit in the telogen resting phase for two to three months before they’re shed.

This means that by the time the hair is coming out in handfuls in the shower, the trigger already happened months ago. Which is why people so often struggle to identify what caused it. The event felt unrelated because it happened before the shedding started.

A 2025 review of 2,851 female telogen effluvium patients confirmed this two-to-three month delay as the consistent pattern across thousands of cases. The trigger and the shedding are temporally disconnected in a way that makes the cause genuinely difficult to identify without understanding the biology.

Normal Shedding vs. Actual Hair Loss - The Difference

The distinction matters because panic about normal shedding is common and it’s useful to know what you’re actually dealing with.

Normal shedding: Diffuse, even hair loss across the whole scalp. 50–100 hairs per day. The hair that comes out has a white bulb at the root (a telogen hair, it completed its cycle). No change in the density of your part or hairline. No patches.

Telogen effluvium (shedding disorder): More than 100–150 hairs per day, usually after a trigger. Often visible at the part line (which appears wider) or in the ponytail (which appears thinner). The hairs lost have white bulbs, they’re telogen hairs that were pushed out of their cycle early. Temporarily elevated, usually reversible.

Female pattern hair loss (androgenetic alopecia): Gradual thinning over months or years, primarily at the crown and widening of the part. The hairs lost are progressively finer and shorter, miniaturised by androgen activity at the follicle. Less diffuse than TE, more patterned. Responds to different treatments.

Alopecia areata: Patchy, often sudden hair loss in distinct circular areas. Autoimmune in origin, the immune system attacks hair follicles. Requires medical assessment.

Most young women experiencing sudden, diffuse hair shedding have telogen effluvium, which is reversible once the trigger is identified and addressed. The first job is identifying what caused it.

Chapter 2: The Most Common Causes in Women Under 35

Iron Deficiency - The Most Common and Most Missed

This is the one I most want you to know about because it’s the most common nutritional cause of hair loss in young women, the most consistently documented in research, and the most routinely missed by standard blood tests.

Iron plays a critical role inside the hair follicle. It’s required for DNA synthesis - the process that lets follicle cells divide and produce new hair. When iron stores are low, the follicle prioritises essential functions and hair production gets deprioritised. Follicles shift into telogen early, shedding increases, and new hair grows in finer and more slowly.

The important distinction: the blood test that GPs most commonly run is haemoglobin, which tests for anaemia. But you can be iron-deficient without being anaemic. Your haemoglobin can be completely normal while your iron stores are nearly empty. Only 32% of women with chronic telogen effluvium in one study were anaemic but 86% had low ferritin. Ferritin is the protein that stores iron, and it depletes long before haemoglobin falls.

A meta-analysis of 36 studies involving over 10,000 women found that those with hair loss had significantly lower ferritin levels than those without, on average 18 ng/mL lower. The critical threshold most dermatologists now use for hair loss specifically is ferritin below 40 µg/L but the standard lab reference range for “normal” ferritin often starts at 12 or 15 µg/L. This means you can receive a “normal” result while sitting at a level that’s driving hair loss.

Women aged 15–35 are disproportionately affected because of menstrual blood loss. Menstruation depletes iron monthly, and if dietary intake isn’t replacing what’s lost, which is genuinely difficult without red meat on a typical Western diet, ferritin gradually depletes over months or years. Iron deficiency affects approximately 72% of women experiencing hair loss, making it the single most common underlying factor.

What to do: Ask for ferritin specifically and not just a full blood count or haemoglobin. Ask what your result is rather than just whether it’s “normal.” If it’s below 40 µg/L, discuss iron supplementation with your GP.

Dietary iron: red meat is the most bioavailable source; lentils, chickpeas, spinach, pumpkin seeds, and sardines for plant-based sources. Always pair plant-based iron with vitamin C. Avoid tea and coffee within an hour of iron-rich meals.

Stress - The Mechanism Is More Specific Than You’ve Been Told

Stress-related hair loss is real, documented, and follows a predictable biological pattern. But “stress causes hair loss” is too vague to be useful. Here’s the specific mechanism.

Cortisol (the main stress hormone) affects hair follicles directly. A 2025 paper in JAAD Reviews detailed how cortisol, the HPA axis, inflammatory cytokines, and neuropeptides mediate telogen effluvium and found a particularly cruel feedback loop: stress triggers TE, but the psychological distress of watching your hair fall out maintains and amplifies the stress response that caused the shedding. The hair loss and the stress feed each other.

When the body is under significant stress, approximately 70% of anagen hairs can be pushed into telogen simultaneously far more than the usual 10–15%. This produces the alarming shower-drain level of shedding that most people don’t connect to the period of burnout or acute stress that happened two months earlier.

Both acute stress (a major life event, illness, surgery) and chronic stress (sustained work overload, long-term sleep disruption, ongoing emotional strain) can trigger TE but they do so through overlapping mechanisms. A 2025 Cureus review identified a newly understood pathway: chronic psychological stress impairs mitochondrial function in follicular cells, accelerating the shift out of the growth phase through oxidative stress. This is a structural cellular effect, not just a “stress response.”

The good news: Stress-triggered TE is almost always reversible. Once the trigger is removed and the body recovers, follicles return to anagen. Shedding typically slows within three to six months after the stressor resolves, and regrowth begins. Full cosmetic recovery takes 12 to 18 months, because hair grows slowly regardless of how well the follicles are functioning. The timeline is longer than most people expect, which creates the impression that recovery isn’t happening when it actually is.

Hormonal Shifts; Postpartum, Post-Pill, and the Cycle

Postpartum hair loss is the textbook example of hormonally triggered TE. During pregnancy, estrogen rises significantly and keeps a much higher percentage of hairs in the anagen (growth) phase, which is why many women’s hair is thicker and more lustrous when pregnant. After birth, estrogen drops sharply. The hairs that were held in anagen by elevated estrogen all transition to telogen simultaneously. Two to four months later, the shedding arrives and for new mothers in an already exhausted, depleted state, it can be severe.

Postpartum TE is almost universally self-resolving. The follicles are healthy. The trigger; the hormonal shift was a one-time event. Given adequate nutrition (particularly iron and protein, which are often depleted in the postpartum period), recovery is the expected outcome.

Post-pill shedding follows the same mechanism. The combined oral contraceptive pill maintains artificially elevated synthetic hormones. When it’s stopped, those hormones drop and the hair that was held in anagen by the pill’s hormonal environment transitions to telogen. The shedding typically begins six to twelve weeks after stopping the pill and can last three to six months. Again, self-resolving once the body establishes its natural hormonal rhythm.

The menstrual cycle and hair shedding is a less discussed but real phenomenon. Research published in the British Journal of Dermatology examining 17,009 women found significant skin and hair condition changes associated with menstrual cycle irregularity. The luteal phase (the two weeks before the period) is when estrogen is falling and progesterone is dominant. Some women notice increased shedding in this window. This is hormonal fluctuation affecting the follicle environment at a cycle level rather than a structural hair loss condition. Notably worse in the context of iron deficiency, which amplifies the follicular sensitivity.

PCOS creates chronic androgen excess (elevated testosterone and DHT) which miniaturises hair follicles on the scalp (androgenetic alopecia pattern) while simultaneously causing excess hair growth elsewhere. If hair loss follows a pattern of central and crown thinning with widening of the part, and you have other PCOS symptoms (irregular cycles, acne, excess body hair), this is the conversation to have with a GP.

Other Causes Worth Knowing

Thyroid dysfunction: Both hypothyroidism (underactive) and hyperthyroidism (overactive) are associated with diffuse hair loss. The thyroid regulates cellular metabolism, including the metabolic activity of hair follicles. Thyroid issues are more common in women than men and are frequently underdiagnosed. An October 2025 study of 100 women with hair loss found significantly different thyroid hormone profiles in the hair loss group compared to controls. TSH (thyroid-stimulating hormone) is the standard test; ask for this alongside ferritin if diffuse hair loss has no obvious trigger.

Rapid weight loss or severe calorie restriction: The body deprioritises hair production under significant energy deficit. This is one of the mechanisms behind TE in eating disorders and crash dieting. The follicles are not damaged, they’ve simply been put into conservation mode. Recovery requires restoring adequate nutrition and calorie intake.

Vitamin D deficiency: Increasingly documented as a contributing factor. Vitamin D receptors are present in hair follicles, and deficiency is associated with accelerated follicle miniaturisation and slower regrowth. Worth including in any hair loss blood panel.

Protein deficiency: Hair is made almost entirely of keratin - a protein. Inadequate dietary protein provides insufficient building material for hair production, particularly relevant for women on very low-calorie or low-protein diets.

Chapter 3: The Evidence Hierarchy. What the Research Says Actually Works

This chapter is the one that differs most from what’s being sold to you.

The hair loss supplement and serum industry is enormous. Biotin gummies, collagen powders, “hair growth vitamins,” scalp serums with seventeen ingredients. The marketing is compelling and the evidence behind most of it is thin. Here’s what the research actually ranks.

What Has Strong Evidence

Minoxidil: the strongest evidence for hair growth in women

Minoxidil was originally developed as a blood pressure medication. One of its side effects was hair growth and that side effect became the treatment. It works by prolonging the anagen phase of the hair cycle and increasing blood flow to follicles, giving them a better nutrient supply.

5% topical minoxidil is FDA-approved for female hair loss. A 2025 meta-analysis of randomised clinical trials found that oral minoxidil at low doses (0.25–2.5mg daily for women) produced comparable or superior hair regrowth to topical minoxidil, with good tolerability at low doses. A JAMA Dermatology consensus statement in January 2025 from an international panel established best practice guidelines for low-dose oral minoxidil, signalling its acceptance as a mainstream treatment rather than a fringe one.

The honest caveats: minoxidil works while you use it. If you stop, hair that was maintained by it will shed again within a few months. It requires commitment to ongoing use. It also takes three to six months to show meaningful results - shorter than the recovery timeline from TE, but still requiring patience. And low-dose oral minoxidil requires a GP prescription and cardiac screening for anyone with a relevant medical history.

Addressing the underlying cause first. If hair loss is driven by iron deficiency, no topical treatment will fully compensate. Restoring ferritin is the primary intervention and once levels are adequate, the follicles resume normal function. Same logic applies to thyroid dysfunction, severe dietary restriction, and hormonal disorders. The treatment must match the cause.

What Has Reasonable Evidence

Iron supplementation (when deficient)

Not as a supplement for everyone (iron toxicity is a real risk) but for women with confirmed low ferritin, supplementation is well-evidenced for supporting hair regrowth. The form matters: ferrous fumarate or ferrous sulfate are well-absorbed; ferrous gluconate is gentler on the stomach if the others cause GI issues. Taken with vitamin C, away from tea and coffee.

Zinc

Hair loss patients consistently show lower zinc levels than controls. The October 2025 study of 100 women with hair loss found significantly lower zinc in the hair loss group. Zinc plays a role in follicle cell division and the hair growth cycle. However, excessive zinc supplementation suppresses copper absorption and can cause its own problems, supplementation should be guided by blood levels rather than taken speculatively.

Vitamin D

As above - worth testing, worth supplementing if deficient. 1,000–2,000 IU daily is well-evidenced as safe for most adults at low to moderate deficiency.

What the Research Doesn’t Strongly Support

Biotin

The biotin-hair growth connection is one of the most heavily marketed claims in the supplement industry.

The evidence: biotin deficiency (genuinely rare) is associated with hair loss, and correcting it helps. But supplementing biotin above adequate levels in people who are not deficient has no demonstrated effect on hair growth or retention. Most people consuming a typical diet are not biotin-deficient. Biotin supplements are being purchased on the basis of a mechanism (deficiency = hair loss) that doesn’t apply to the people buying them. They also interfere with thyroid and cardiac blood tests.

Collagen supplements for hair growth

Collagen provides amino acids that are building blocks for hair keratin. The indirect logic makes sense. The clinical evidence for oral collagen supplementation specifically producing measurable hair growth is thin. There are better and cheaper ways to get protein.

Most proprietary “hair growth vitamin” blends

Usually contain biotin (not evidenced for non-deficient individuals), some B vitamins (useful only if deficient), and various botanicals (saw palmetto, DHT-blocking herbs) at doses too low to produce the effects claimed. Save the money for ferritin testing or an actual treatment.

Scalp serums with “growth-stimulating” ingredients (rosemary oil, caffeine serums, peptides)

Some preliminary evidence exists for rosemary oil, one small study found it comparable to 2% minoxidil at 6 months. It’s not evidence of strong efficacy; it’s evidence that it might do something. Caffeine applied to the scalp has some in-vitro evidence for blocking DHT at the follicle. None of this is at the level of minoxidil evidence. These can be incorporated into a routine, but they are not treatments.

Part 1 ends here. Part 2 is the practical half: the blood tests to request, the full treatment guide, the supplement breakdown, how to build a recovery routine, and the cycle-aware approach for the weeks when shedding is reliably worse.

Now you understand what’s actually happening. The hair cycle and why loss is always delayed. The causes most common in women under 35; iron deficiency (the one most GPs miss), stress (with a more specific mechanism than you’ve been told), hormonal shifts, and thyroid. And the evidence hierarchy for treatment, which looks very different from what the supplement industry presents.

Part 2 takes all of this and makes it actionable.

Chapter 4 is the blood test guide. Exactly what to ask for, what the numbers mean, and what the targets are for hair health specifically versus the standard “normal” ranges.

Chapter 5 is the full treatment guide. Minoxidil in detail (topical versus oral, what to expect, the timeline), what the hormonal treatments do, and the honest assessment of every other intervention in the space.

Chapter 6 is the supplement chapter. What the evidence actually says about biotin, collagen, zinc, iron, vitamin D, and the “hair growth blends,” with the specific scenarios where each one makes sense and the ones where you’re wasting money.

Chapter 7 is the cycle-aware approach. How to support your follicles in the weeks where shedding is hormonally worse, what dietary and lifestyle interventions the research backs for the luteal phase specifically.

Chapter 8 is the complete practical guide: the daily routine for hair health, what to do in months one through twelve, and when to stop trying to manage this yourself and see a dermatologist or trichologist instead.

Subscribe to read Part 2 →

Sources & Further Reading

Karakoyun et al. Retrospective Review of 2851 Female Patients With Telogen Effluvium — Journal of Cosmetic Dermatology, February 2025

Sunil & Zacharia. Clinical profile of female patients with chronic telogen effluvium and its association with serum ferritin level — Asian Journal of Medical Sciences, December 2024

Iron deficiency and nonscarring alopecia in women — meta-analysis, Skin Appendage Disorders, 2022 (36 studies, 10,000+ women)

Mdanat et al. Quantitative analysis of circulating biomarkers in females with hair loss — Nutrients, October 2025

Hughes, Syed & Saleh. Telogen Effluvium — StatPearls, NIH, 2024 update

Shapiro Medical. Hair loss from stress and telogen effluvium — mechanism review, 2025–2026 research

Sobral et al. Efficacy and safety of oral vs topical minoxidil — meta-analysis of RCTs, International Journal of Dermatology, 2025

Akiska et al. Low-dose oral minoxidil initiation consensus statement — JAMA Dermatology, January 2025

Olsen et al. Summation and recommendations for topical and oral minoxidil — JAAD, August 2025

Löffler et al. Omega-3 fatty acid deficit in acne patients — PMC, 2024

Lau et al. Physiological differences in sebum composition in menstruating women — Journal of Dermatology, August 2025

Part 1 ended at the evidence hierarchy. Which is where most acne content either starts (with a product recommendation) or never gets to at all (because the actual research doesn’t make for exciting content).

Part 2 takes everything from Part 1 and builds it into a routine, a dietary approach, and a cycle-aware protocol that accounts for the weeks that are reliably harder. Not a product list. Not a ten-step routine. A framework based on the research, adapted for what’s actually practical.

4. The Ingredient Guide - What Each Thing Does and When to Use It

5. Diet and Acne - What the Research Actually Supports

6. How to Build a Routine That Actually Works

7. The Hormonal Acne Protocol - What to Do Differently in the Premenstrual Week

8. The Complete Practical Guide

9. Conclusion: The Guide Your Dermatologist Didn’t Have Time to Give You

Read more

Not the vague “hormones” explanation. Not “you need to drink more water.” The actual mechanism. The biology. The reason certain weeks are reliably worse than others. The reason the cleanser that’s supposed to “clear pores” sometimes makes things worse. The reason the expensive serum did nothing while the cheap tube from the pharmacy did something.

Nobody told me any of it. Not the GP. Not the dermatologist I waited four months to see. And definitely not the TikTok comments.

So this short dive is the explanation I didn’t get at 16. What acne actually is, why your hormones are involved in more ways than you probably realise, what the evidence hierarchy actually looks like for treatment, and the practical guide that puts all of it together.

Let’s start at the beginning.

1. What Acne Actually Is And Why Most People Are Fighting It Wrong

2. Why Your Hormones Are Running the Show — The Menstrual Cycle and Your Skin

3. The Evidence Hierarchy — What the Research Actually Ranks

Chapter 1: What Acne Actually Is And Why Most People Are Fighting It Wrong

The Four-Step Mechanism

Acne isn’t caused by dirty skin. It isn’t caused by not washing your face enough. And it definitely isn’t caused by touching your face. These ideas have been so thoroughly embedded in the way we talk about breakouts that they’ve produced an entire generation of people over-cleansing, over-exfoliating, and stripping their skin barrier in the name of treating acne, which, as I’ll get to, actively makes acne worse.

Here’s what’s actually happening.

Inside each of your pores is a hair follicle with an attached sebaceous gland; a tiny oil-producing structure. Your sebaceous glands produce sebum, which is the oil that keeps your skin lubricated and barrier-protected. This is not a bad thing. Sebum is a normal, necessary part of skin function.

Acne happens when four things go wrong in sequence inside these pores:

Step 1: Too much sebum. The sebaceous gland produces more oil than the follicle can handle. Androgens, specifically dihydrotestosterone (DHT), a form of testosterone, are the main driver of this. More androgen activity means the gland works harder and produces more sebum. This is why acne is so common in puberty (androgens surge), why it’s connected to the menstrual cycle (androgen levels fluctuate relative to estrogen), and why it’s often worse in the premenstrual week.

Step 2: The pore gets blocked. The skin cells that line the inside of the follicle normally shed naturally and exit through the pore. When they don’t, when they build up and stick together instead of exiting they form a plug. This blockage is called a comedo. A comedo that stays closed under the skin is a whitehead. One that opens at the surface and oxidises (turns dark on contact with air) is a blackhead. The dark colour is not dirt. It’s oxidised sebum and skin cells.

Step 3: Bacteria multiply. A bacterium called Cutibacterium acnes (C. acnes) lives on everyone’s skin all the time. It’s part of a healthy skin microbiome. The problem is that C. acnes loves the environment inside a blocked, sebum-filled follicle. It feeds on the sebum, multiplies rapidly, and in doing so breaks down the sebum into free fatty acids that are irritating to the follicle wall.

Step 4: Inflammation. Your immune system detects the bacterial activity and sends inflammatory signals to the area. This is what turns a blocked pore into a red, raised, painful spot. The inflammation can be mild (a small red papule), moderate (a pus-filled pustule), or severe (a deep, painful cyst or nodule that sits under the skin and never comes to a head).

This four-step process — excess sebum, blocked pore, bacterial growth, inflammation, is the foundation of all acne. Understanding it explains why specific treatments work: retinoids target the blocked pore step, benzoyl peroxide targets the bacterial step, anti-inflammatory ingredients and hormonal treatments target the sebum step upstream.

Why Washing Your Face More Makes It Worse

Here’s the part that matters practically: harsh cleansing, over-exfoliation, and stripping products — the instinctive response to oily, broken-out skin, all damage the skin barrier.

A damaged skin barrier makes acne worse in two ways. First, it triggers an inflammatory response that is the same pathway as the inflammatory acne response. Second, it signals the skin to produce more sebum as a compensatory repair mechanism. So stripping your skin makes it oilier and more inflamed which is the exact opposite of what you’re trying to achieve.

A December 2025 review in Molecules covering over 100 acne sources confirmed that maintaining the skin barrier is now considered a critical component of acne management and not just a nice-to-have alongside active treatments.

The correct cleansing approach for acne-prone skin: a gentle, non-foaming or low-foam cleanser, twice a day maximum, that removes surface excess without stripping. That’s it. The work of treating acne happens with the treatments applied after cleansing, not with the cleanser itself.

Chapter 2: Why Your Hormones Are Running the Show — The Menstrual Cycle and Your Skin

This is the chapter that most acne content skips entirely, or covers in one vague sentence about “hormonal acne.” The biology is more specific than that, more interesting than that, and more useful than that because once you understand which hormones do what in which week, the monthly breakout pattern that felt random starts to make complete sense.

The Phase-by-Phase Skin Picture

Your skin contains receptors for estrogen, progesterone, and androgens. Which means every hormonal shift across your cycle is being detected and responded to in your skin and not just in your mood or your sleep.

Week 1 — Menstrual phase: Both estrogen and progesterone are at their lowest. Skin is often in a post-breakout recovery phase. The barrier can be more reactive than usual because prostaglandins (which drive cramping) also affect the skin’s inflammatory state. Sebum production is lower in this phase.

Week 2 — Follicular phase: Estrogen is rising. Estrogen has a genuinely beneficial effect on skin: it supports the skin barrier, promotes collagen synthesis, and critically, reduces sebum production. As estrogen rises through the follicular phase, skin tends to clear and brighten. Many women notice their skin looks best in the week after their period ends. This is why.

Around ovulation: Estrogen peaks, and with it comes the clearest, most luminous skin of the month for many women. But this is also when a brief testosterone surge occurs alongside the LH spike that triggers egg release. For women with more androgen-sensitive sebaceous glands, this can trigger a small breakout right around ovulation even when the rest of the month is clear.

Weeks 3–4 — Luteal phase: This is where things get more complicated. After ovulation, progesterone rises and becomes the dominant hormone. Progesterone stimulates the sebaceous glands to produce more oil. At the same time, as estrogen falls in the late luteal phase, its sebum-suppressing effect disappears. And androgens, still present throughout the cycle become relatively more dominant as estrogen drops.

The result: sebum production peaks in the premenstrual week. The follicular environment is oilier, the conditions for bacterial growth are better, and the inflammatory threshold is lower because the late luteal phase is already a time of heightened systemic inflammation. A 2025 study published in The Journal of Dermatology found that sebum composition changes measurably across the menstrual cycle, with the luteal phase showing the most significant shifts in the lipid profile that drives C. acnes activity.

Approximately 65% of women report worse breakouts in the week before their period. The hormonal explanation is real, documented, and explains exactly why.

Where Hormonal Acne Shows Up and Why

The location of acne breakouts is not random. It’s connected to the density and sensitivity of sebaceous glands in specific areas, and to the hormonal pathways driving them.

Hormonal acne has a signature location: the lower third of the face. Jawline, chin, and the area around the mouth. These are the areas with the highest concentration of androgen-sensitive sebaceous glands aka the glands that respond most to DHT. When androgens drive excess sebum production, this is where it shows up first.

Forehead acne tends to be more connected to skin microbiome disruption, hair products, and barrier issues than to hormones. Cheek acne often has a bacterial, environmental, or friction component (phone screens, pillowcases). Jawline and chin acne that reliably worsens in the week before your period is almost always hormonally driven, which means treating it purely topically, while not addressing the hormonal environment driving it, is treating the symptom rather than the cause.

The Gut-Estrobolome-Jawline Connection

This is the link that’s gaining research attention and that almost no skincare content is discussing yet.

As covered in Between Saturdays, the estrobolome (the collection of gut bacteria responsible for metabolising estrogen) plays a direct role in how much estrogen circulates in the body. When gut microbiome diversity is low, estrogen clearance is impaired. Estrogen that should be processed and excreted stays in circulation longer. Elevated estrogen levels relative to progesterone create a hormonal environment that can worsen acne through several pathways, including by suppressing testosterone-binding proteins, which effectively raises free androgen activity in the skin.

A 2025 review in Dermatology Research and Practice confirmed that the gut-skin axis is now considered a significant factor in acne pathogenesis and that gut microbiome composition is measurably different in people with acne compared to those without it.

This is why for some women, persistent hormonal acne, especially the jawline cystic kind that doesn’t fully respond to topical treatment has a gut health component. The dietary pattern that most consistently supports the estrobolome and reduces the gut-skin inflammatory pathway: high-fibre eating from varied plant sources, fermented foods, reduced ultra-processed food. The same pattern that supports gut health generally.

Chapter 3: The Evidence Hierarchy — What the Research Actually Ranks

This is the chapter where I tell you that most of what wellness TikTok recommends for acne is not at the top of the evidence hierarchy and what actually is.

The American Academy of Dermatology’s 2024 Guidelines

The AAD published updated clinical guidelines for acne management in 2024. These are evidence-based recommendations from the largest body of dermatological research. 18 specific recommendations ranked by strength of evidence. Here’s what got strong recommendations:

Topical retinoids. Strongly recommended. Work at step 2 of the acne mechanism. They accelerate cell turnover so the dead skin cells that form the follicular plug shed properly rather than building up and blocking the pore. They also have anti-inflammatory effects. Tretinoin, adapalene, tazarotene, and trifarotene are all FDA-approved for acne, with no evidence that any one is significantly better than another. Adapalene 0.1% is available over the counter in most countries and is a genuinely effective starting point.

Benzoyl peroxide. Strongly recommended. Works at step 3 — it kills C. acnes bacteria. Notably, it’s one of the only acne treatments that doesn’t create bacterial resistance with extended use (unlike antibiotics). Available at any pharmacy at 2.5–10% concentration. Higher concentration doesn’t mean more effective, it mainly means more irritation. 2.5–5% is where to start.

Topical antibiotics (with BPO). Strongly recommended as part of a combination, never as monotherapy, because antibiotic resistance is a real concern with acne bacteria. Clindamycin combined with benzoyl peroxide has strong evidence. Used alone it’s less effective and risks creating resistant strains.

What got conditional recommendations (real but not the strongest evidence):

Salicylic acid. A beta-hydroxy acid that exfoliates inside the pore. Useful for non-inflammatory, comedonal acne (blackheads and whiteheads). Less effective for inflammatory spots. A good addition but not a first-line treatment for inflammatory acne.

Azelaic acid. Antibacterial and anti-inflammatory, and has the additional benefit of reducing post-inflammatory hyperpigmentation, the dark marks left after spots. Excellent for darker skin tones where PIH is a significant concern. Evidence is real but thinner than for retinoids or BPO.

Niacinamide. Not in the AAD guidelines as a primary acne treatment but has research support for reducing sebum production and skin inflammation. Works as a supporting ingredient rather than a primary treatment.

What Didn’t Make the Evidence Hierarchy

Tea tree oil. Some evidence for mild antibacterial effects, but not at a level that competes with the above. Useful for very mild, occasional breakouts. Not a treatment for inflammatory acne.

Hypochlorous acid. Trending at 132% YoY search growth in 2026. Genuinely useful as it kills C. acnes without creating resistance and is extremely well tolerated by sensitive and compromised skin barriers. But: the acne evidence is thinner than the eczema and wound-healing evidence, and the AAD guidelines don’t include it as a primary treatment. It belongs in a routine, but it’s not doing the heavy lifting.

Natural alternatives generally. Witch hazel, apple cider vinegar, lemon juice, none of these have evidence comparable to the treatments above. Apple cider vinegar and lemon juice can actively damage the skin barrier and should not be applied directly to the face.

Supplements marketed for skin. Zinc has the most interesting acne evidence, it has some anti-inflammatory and antibacterial properties and several studies have found it reduces inflammatory lesion count. But even zinc’s evidence is modest compared to topical retinoids. Supplements sit at the bottom of the evidence hierarchy for acne treatment, not the top.

Why the Evidence Hierarchy Matters

The reason most people cycle through product after product and don’t get consistent results is that they’re investing money and time in ingredients at the bottom of the evidence hierarchy (trendy, gentle, wellness-adjacent) while avoiding or misusing the ingredients at the top (retinoids, BPO) because they’re less aesthetically appealing, require a learning curve, or are just less well marketed.

Adapalene 0.1% costs less than most trendy serums. It has strong evidence behind it. It’s available without a prescription in most countries. The reason it’s not on TikTok every week is that you can’t make it in a pretty bottle with a compelling brand story — the patent expired decades ago.

That’s not a knock on the skincare industry. It’s useful information for where to put your attention and your money.

Part 1 ends here. Part 2 is the practical half. The ingredient guide, the routine, the diet chapter, the hormonal acne protocol, and the phase-by-phase skincare guide for the weeks where breakouts are reliably worse.

Now you know more about what’s actually happening in your skin than most skincare content will ever tell you. You know the four-step mechanism. You know how estrogen, progesterone, and androgens play out across the month and why the premenstrual week is reliably the hardest. You know that the gut microbiome is involved in hormonal acne in a specific way that most people aren’t talking about. And you know what the evidence hierarchy actually looks like, which treatments are strongly recommended, which are conditionally recommended, and which are mostly marketing.

Part 2 is where it becomes a system you can actually use.

Chapter 4 is the ingredient deep dive. How each of the evidence-backed ingredients works, which skin types they suit, and what concentration to start with. Including the honest assessment of hypochlorous acid, azelaic acid, and niacinamide and where they actually belong in a routine.

Chapter 5 is the diet chapter. What the research genuinely supports for acne and skin. The glycaemic index evidence is stronger than most people know. The dairy evidence is more nuanced than most people have been told. The omega-3 finding will probably surprise you.

Chapter 6 is how to build a routine that treats acne without destroying your barrier in the process, because the most common reason acne treatments don’t work is the over-treating that compromises the very barrier you need intact.

Chapter 7 is the hormonal acne protocol. Specific, phase-aware adjustments for the week before your period when the sebum-androgen-inflammation picture is at its most difficult.

Chapter 8 is the complete practical guide: a simple, evidence-based routine from cleanser to SPF, shopping suggestions at different price points, and the signs that mean your acne needs a GP or dermatologist rather than a product change.

Subscribe to read Part 2 →

Sources & Further Reading

Li & Jin. The Mechanism and Research Progress of Skin Microbiota in Pathogenesis of Acne — Dermatology Research and Practice, October 2025

Molecules. Rebalancing the Skin: The Microbiome, Acne Pathogenesis, and the Future of Natural and Synthetic Therapies — December 2025

MDPI Biomolecules. The Evolving Microbial Paradigm in Acne — March 2026

Lau et al. Physiological Differences in Sebum Composition in Regularly Menstruating Healthy Women — Journal of Dermatology, August 2025

Menstrual cycle phases and acne flares — ScienceDirect, September 2025

Healthline. Period acne guide — updated January 2026

AAD Guidelines of care for the management of acne vulgaris — JAAD, January 2024

Taha & Shakhshir. The mediterranean diet and acne vulgaris: systematic review and meta-analysis — Nutrition & Metabolism, November 2025

Systematic review: low glycaemic load diets and acne, 2025

Khanna et al. Effects of diet on acne and its response to treatment — American Journal of Clinical Dermatology

Löffler et al. Deficit of omega-3 fatty acids in acne patients — PMC, 2024

La Belle Vie. Acne treatment trends 2026 — hypochlorous acid and emerging ingredients

Skin Science Hub. Hypochlorous acid for skin — December 2025

Part 1 ended at hunger. Which is where most diet advice loses people, because it either ignores the hunger entirely and tells you to push through, or it tells you to eat more and somehow still be in a deficit, without explaining how.

Part 2 is the “how.”

The research gives us a clear enough picture of what actually works: not a single diet or exercise plan, but a set of principles with good evidence behind them that can be built into a real life. This part takes everything from Part 1 and makes it something you can use week by week, meal by meal, without tracking every calorie forever or living in a permanent state of deprivation.

Here’s what Part 2 covers:

Chapter 4 is the GPL framework in practice. What meals actually look like when you build them around blood sugar stability, protein, and fat, with specific numbers and food combinations.

Chapter 5 is the exercise guide. What the research says about training during a calorie deficit, how much is actually enough, and the cycle-aware adjustments that make it sustainable.

Chapter 6 is the invisible saboteurs; sleep, stress, and alcohol, and the hormonal reasons they undo fat loss even when everything else is right.

Chapter 7 is the sustainability chapter. What the research says about keeping the weight off, which is a completely different question from losing it.

Chapter 8 is the practical guide. The weekly food template, the tracking approach, and the cycle-phase adjustments.

Let’s go.

Read more

Weight loss is not complicated because people don’t know what to do. It’s complicated because the advice that exists was mostly built around men’s bodies and then handed to women without any adjustments. The calorie counts, the macros, the meal timing, the exercise prescriptions. Most of it comes from research conducted primarily on men and applied universally.

This matters because women’s bodies don’t work the same way. Not because they’re broken or more difficult. But because estrogen, progesterone, and the hormonal cycle create a completely different metabolic environment — one that affects how much you eat, how much you store, how hungry you are, and how quickly you lose. The research is only starting to catch up.

What this Short Dive is going to do is give you the honest, research-backed version of what weight loss actually involves for a woman’s body. Not the calorie-counting app version. Not the influencer version. The part that explains why you’ve done everything “right” and still felt like your body wasn’t cooperating and what to actually do about it.

Three chapters in Part 1. The rest in Part 2. Let’s go.

This Substack is reader-supported. To receive new posts and support my work, consider becoming a free or paid subscriber.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.

Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

Table of Contents:

1. What Weight Loss Actually Is And Why Your Body Pushes Back

2. The GPL Framework — Why What You Eat Matters as Much as How Much

3. Why Your Hunger Isn’t a Willpower Problem

Chapter 1: What Weight Loss Actually Is And Why Your Body Pushes Back

The Part That’s True

Yes, a calorie deficit is required for fat loss. This is one of the most well-established findings in nutrition science and it hasn’t changed. To lose fat, you need to consume less energy than your body is using. That’s it.

But the way that’s been communicated; “eat less, move more,” 500 calories less per day, one pound per week, clean and simple — misses so much of what actually happens in a body when you try to do that.

Here’s what the research shows actually happens when you reduce your food intake:

Your Hunger Hormones Change

Ghrelin (the hormone that tells your brain you’re hungry) rises when you’re in a calorie deficit. This isn’t a character flaw or a lack of willpower. It’s your body doing exactly what it was designed to do: fighting to bring you back to your previous weight. Research published in 2024 in the journal Current Opinion in Endocrinology confirmed that gut hormones including ghrelin, GLP-1, and PYY are the primary drivers of appetite regulation, and that in a deficit, ghrelin rises while the hormones that make you feel full (GLP-1 and PYY) become less effective.

Your Metabolism Adapts

Your body is remarkably good at adjusting to less food. When you eat less for long enough, your resting metabolic rate (the amount of energy your body burns just existing) can drop. This is sometimes called “metabolic adaptation.” It’s why the deficit that worked in week one stops working by week eight. It’s not that you’re doing it wrong. It’s that your body has literally become more efficient.

You Lose Muscle As Well As Fat

This is the part of calorie restriction that doesn’t get talked about enough. When you cut calories without doing resistance training, a significant portion of what you lose isn’t fat — it’s muscle. A January 2026 study from Tel Aviv University published in Frontiers in Endocrinology found that people who dieted without any exercise had the worst fat-to-muscle-loss ratio of any group tested. Aerobic exercise improved it. Resistance training improved it the most, to the point where the resistance training group actually lost a higher proportion of fat compared to lean muscle than any other group.

Why does losing muscle matter for weight loss? Because muscle burns more calories at rest than fat does. Every kilogram of muscle you lose makes your metabolism slightly slower. Which means the more times you’ve crash dieted and regained the weight, the harder your body works to hold onto fat and lose muscle next time — a documented phenomenon sometimes called “yo-yo dieting” that has real metabolic consequences.

Why Women’s Bodies Are Different

This is the conversation that most weight loss content skips entirely.

A 2025 study published in the Journal of the International Society of Sports Nutrition put 323 people (83% women) on an identical 30% calorie deficit with the same protein prescription and tracked how long it took to lose 5% of their body weight. Men and women lost weight at the same overall rate but the experience getting there was measurably different, and the research notes clearly that women’s hormonal profiles create a distinct metabolic environment.

Here’s what we know about why women’s bodies respond differently to calorie restriction:

Estrogen Promotes Fat Storage In Specific Places

Estrogen encourages fat to be stored around the hips and thighs (subcutaneous fat that sits under the skin). This fat is less metabolically active than visceral fat (the belly fat men tend to accumulate) and more resistant to being burned. This is not a design flaw. It’s an evolutionary adaptation related to reproductive function. But it does mean that hip and thigh fat is genuinely harder to shift than abdominal fat and that the comparison to a male friend or partner who’s “doing the same thing” and losing faster is not a fair comparison.

Women’s Metabolic Rate Drops Faster In A Large Deficit

Research found that when calorie intake is restricted too aggressively, women’s bodies slow their metabolism to preserve reproductive function — a protective mechanism that’s absent or much weaker in men. This is why aggressive 1200-calorie diets are counterproductive for most women: they produce the fastest initial loss and the most severe metabolic adaptation, making long-term maintenance nearly impossible.

Hunger And Appetite Change Across The Menstrual Cycle

Studies have consistently found that caloric intake increases by 100–500 calories per day in the luteal phase (the two weeks before your period). This is driven by progesterone raising metabolic rate and the body genuinely needing more fuel. Eating more in this phase is not a failure. It’s biology. But it does mean that week three and four of the month are reliably harder and any weight loss approach that doesn’t account for this will feel randomly inconsistent, because the calorie needs are genuinely different week to week.

Women Store More Fat After Eating

Research published in PMC found that after eating, women switch to fat-storage mode faster than men, and that the post-meal fat storage window lasts longer. Men burn more ingested fat after eating. Women store it more efficiently during non-exercising periods, even when eating the same foods in the same amounts. This is the biology behind the experience of feeling like you can’t eat the same things as the men around you without different results.

What This Means Before You Do Anything Else

The practical implications of all of this come down to three things:

Don’t Go Too Aggressive

A deficit of 300–500 calories per day is the range supported by research for sustainable fat loss with minimal metabolic adaptation. More than this produces faster initial results and faster metabolic slowdown; the trade-off isn’t worth it. The research points to 0.5–1kg per week as the rate at which you lose primarily fat rather than muscle.

Resistance Training Is Not Optional

This is the single most consistently supported finding in weight loss research for women. The Tel Aviv study found that resistance training produced the highest fat-to-muscle loss ratio of any group, meaning more of the weight you lose is actually fat. It also preserves the muscle that keeps your metabolism functioning. 2–3 sessions per week of resistance training is enough to produce this effect alongside a calorie deficit.

Expect Variation Across Your Cycle

If you track your intake or weight, understanding that the luteal phase reliably drives higher hunger and slightly higher water retention will prevent the last two weeks of every month from feeling like the process is breaking down. It isn’t. It’s your hormones.

Chapter 2: The GPL Framework — Why What You Eat Matters as Much as How Much

The GPL framework: Glucose, Protein, Lipids, is a way of thinking about macronutrients not as numbers to hit but as levers that directly affect hunger, hormones, and how your body decides what to store versus burn. It’s not a named clinical protocol with its own RCTs. But the individual components are among the best-supported areas of nutrition science for weight management.

This chapter is about the three levers and why each one matters.

G — Glucose: Why Blood Sugar Stability Isn’t Just a Wellness Buzzword

Blood sugar stability is one of those topics that wellness content has turned into a vague aesthetic — Glucose Goddess, green vegetables before carbs, dramatic CGM graphs. Some of it is overstated. But the underlying biology is genuinely relevant to weight loss, and here’s why.

When you eat carbohydrates especially refined ones with no fibre, protein, or fat to slow them down, your blood sugar rises quickly. Your body releases insulin to bring it back down. If the spike is large, the correction can be aggressive, bringing blood sugar below where it started. That drop is what your brain experiences as a craving: specifically, a craving for fast sugar that will bring it back up again quickly. This is not psychological. It’s a direct biochemical response to a blood sugar crash.

The cycle this creates; spike, crash, craving, spike again is one of the most common reasons calorie deficits are hard to maintain. It’s not that you have no discipline. It’s that your blood sugar has been signalling an emergency and demanding a rapid fix.

Research on cortisol and blood sugar confirms another layer of this: when blood sugar drops too low, your body releases cortisol to bring it back up. Cortisol raises blood sugar through the liver. It also, when chronically elevated, promotes fat storage particularly around the abdomen. Skipping meals, eating too few carbohydrates, or crash dieting can actually elevate cortisol enough to make fat loss harder, not easier. The body experiences severe restriction as a threat and responds hormonally accordingly.

What Blood Sugar Stability Actually Requires:

• Pairing carbohydrates with protein and fat to slow the digestion and reduce the glucose spike

• Prioritising fibre-rich, lower-GI carbohydrates (oats, sweet potato, legumes, wholegrain bread) over refined ones

• Not skipping meals as blood sugar drops are what drive the worst cravings and the cortisol response

• Eating protein at breakfast specifically, research shows that high-protein breakfasts reduce glucose spikes post-meal and improve satiety significantly compared to high-carbohydrate breakfasts

The practical result of better blood sugar stability: fewer cravings, more consistent energy, less of the cortisol-driven fat storage that defeats the calorie deficit from the hormonal side.

P — Protein: The Most Important Macro for Fat Loss

Protein is the one area where the research is the most consistent and the most clear. If you change one thing about the way you eat for fat loss, it should be your protein intake.

Here’s why:

Protein Keeps You Fuller For Longer Than Any Other Macronutrient

The mechanism: eating protein triggers the release of GLP-1 and PYY (satiety hormones that travel to your brain and signal that you’re full) while simultaneously reducing ghrelin, the hunger hormone. A 2025 study in Obesity Pillars examining high-protein versus high-fat snacks in women found that protein-based snacks produced stronger satiety hormone responses and greater appetite suppression than fat-based snacks. A review of the research on proteins and satiety hormones confirmed that protein is the most effective macronutrient for reducing food intake compared to both carbohydrates and fats.

GLP-1 is particularly relevant here because it’s the hormone that drugs like Ozempic mimic, the mechanism behind why those medications work so well for reducing appetite. Protein produces this same hormone naturally, though at lower intensity. Understanding this explains why a high-protein meal genuinely keeps hunger quieter than a high-carb or high-fat meal of the same calories.

Protein Has A Higher Thermic Effect

This means your body burns more energy digesting protein than it burns digesting carbohydrates or fat. Roughly 20–30% of protein’s calories are used in digestion itself, compared to 5–10% for carbs and 0–3% for fat. This isn’t a huge effect, but it does mean that a high-protein diet is slightly more energetically expensive to maintain than an equivalent-calorie lower-protein diet.

Protein Preserves Muscle

I’ve established that losing muscle alongside fat is one of the most common problems with calorie restriction. The most effective dietary strategy to prevent this is adequate protein intake. The research consensus for people in a calorie deficit doing resistance training is approximately 1.6g of protein per kilogram of body weight per day. For a 65kg woman, that’s approximately 104g of protein daily, significantly more than most women are consuming on a typical diet.

Practical Protein Sources

Chicken breast, eggs, Greek yoghurt, cottage cheese, salmon, tinned sardines, tofu, tempeh, lentils, chickpeas, edamame. The goal of 25–30g of protein per meal is achievable with these foods without supplementation, though a protein shake is a convenient way to close the gap.

L — Lipids (Fats): The Macro People Are Still Afraid Of

The fat-is-bad narrative from the 1980s and 90s is one of the most damaging pieces of dietary advice in modern history. It isn’t true, and the research has known it for decades. But it has been slow to filter into general consciousness.

Here’s what fats actually do and why they matter for weight loss:

Fat Slows Digestion And Extends Satiety

Including fat in a meal slows how quickly everything else in that meal is digested, which means the glucose spike is smaller, the satiety lasts longer, and you stay satisfied for more hours after eating. Research on how different macronutrients trigger satiety hormones confirmed that fat triggers the release of CCK (cholecystokinin), a hormone that signals fullness to the brain. Removing fat from meals in the name of reducing calories often makes meals less filling, which drives more eating later.

Fat Is Required For Hormone Production

Estrogen, progesterone, and cortisol are all synthesised from cholesterol. A diet too low in fat disrupts hormone balance. For women particularly, severely low-fat diets have been associated with irregular cycles, low estrogen, and hormonal disruption — the exact opposite of the conditions that support fat loss.

Not All Fats Are Equal

Unsaturated fats (olive oil, avocado, nuts, fatty fish) are anti-inflammatory and support metabolic health. Saturated fat in moderate amounts is not the health disaster it was presented as, but excessive intake of processed saturated fat from ultra-processed foods carries legitimate health risks. Trans fats remain clearly harmful. The framing of “fat is bad” ignored all of this nuance.

Practical Fat Intake For Weight Loss

The goal isn’t to eat as much fat as possible or to avoid it entirely. It’s to include enough fat in meals to slow digestion, support hormone production, and keep you full, while prioritising unsaturated sources. Around 25–35% of calories from fat is the well-supported range for most women.

Chapter 3: Why Your Hunger Isn’t a Willpower Problem

This chapter is short and it’s the one I most want you to actually hear.

The dominant narrative about weight loss — in media, in diet culture, in casual conversation, frames failure as a discipline problem. You ate the thing you weren’t supposed to eat. You didn’t stick to the plan. You need more willpower.

This framing ignores the physiology almost entirely.

Here’s what’s actually happening when you’re in a calorie deficit and struggling with hunger:

Ghrelin Rises And Stays Elevated

When you eat less than your body is used to, ghrelin (the hormone that tells your brain to eat) increases. This is not temporary. Research has found that ghrelin remains elevated even after significant weight loss, meaning the hunger you feel after losing 10kg is genuinely more intense than the hunger you felt before you started, driven by hormones rather than habit.

Satiety Hormones Become Less Effective

As you lose weight, the satiety signals; GLP-1, PYY, leptin, don’t work as efficiently at suppressing appetite. Your brain becomes more sensitive to food cues while the hormones that would dampen that sensitivity are less effective. This is a documented biological mechanism, not a weakness.

Your Brain Prioritises Food Seeking

Chronic mild calorie restriction activates the same reward-seeking pathways in the brain as other forms of deprivation. Research on sustained calorie restriction found that people in a deficit reported heightened focus on food, increased food-related thoughts, and reduced ability to maintain dietary restraint over time. Again: documented physiology, not lack of character.

What This Means Practically:

The goal of weight loss isn’t to fight these systems indefinitely. It’s to structure your eating in a way that works with them.

• High protein at every meal because protein is the most powerful natural stimulus for the satiety hormones that resist hunger

• Blood sugar stability because blood sugar crashes are hunger crises engineered by chemistry

• Not too large a deficit because the larger the deficit, the more forcefully the hunger hormones respond

• Resistance training because it preserves the muscle that keeps your metabolism from adapting as aggressively

• Consistency without perfection because the data shows that adherence over time matters far more than the precision of any single day

Hunger during a calorie deficit is real. It is hormonal. It is not your fault. And understanding what’s driving it is the difference between fighting it blindly and building an approach that actually accounts for it.

Part 1 ends here.

Now you know the actual biology behind why weight loss is harder than “eat less, move more” and why it’s specifically harder for women. You understand what a calorie deficit actually does to your hunger hormones, why muscle loss is the hidden problem with most diets, what blood sugar stability actually means and why it matters, what protein does that no other macro does, and why your hunger is not a personal failing.

Part 2 is where all of this becomes a practical system.

Chapter 4 goes deeper into the GPL framework in practice. What a day of eating actually looks like when you’re building meals around glucose stability, protein, and fats, with specific targets and food combinations that the research supports.

Chapter 5 is the exercise chapter. The research-backed breakdown of what kind of training produces the best body composition results during a calorie deficit, how much is enough, and the cycle-syncing dimension that determines which weeks to push and which to protect.

Chapter 6 covers the things that wreck a calorie deficit from the outside; sleep, stress, alcohol, and the hormonal mechanisms behind each one. These are the invisible factors that can undo everything else, and most diet advice ignores them entirely.

Chapter 7 is the sustainability chapter. The research on what actually determines whether weight loss is maintained long term, and the specific behaviours that separate people who keep the weight off from people who regain it.

Chapter 8 is the practical guide: the weekly template, the meal framework, the tracking approach that doesn’t become obsessive, and the phase-by-phase adjustments for different weeks of your cycle.

Stay Tuned, part 2 drops next week

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding your health, weight, or nutrition.

Sources & Further Reading

Rodriguez Da Silva et al. Comparing weight loss rates between males and females — Journal of the International Society of Sports Nutrition, August 2025

Lahav, Yavetz & Gepner. Resistance training as a key strategy for high-quality weight loss in men and women — Frontiers in Endocrinology, January 2026

Systematic review and meta-analysis: resistance exercise during dietary weight loss — BMJ, 2025

Chen et al. Time-restricted eating in overweight and obese women — Frontiers in Nutrition, September 2025

Hong & Choi. Gut hormones and appetite regulation — Current Opinion in Endocrinology & Diabetes and Obesity, 2024

Al-Bayyari et al. Effects of high protein versus high fat snacks on satiety, gut hormones and insulin secretion in women — Obesity Pillars, September 2025

Proteins and Peptides with Effect on Satiety — PMC, October 2024

Sex Differences in Energy Metabolism — PMC

Caloric intake and the menstrual cycle — PMC

Cortisol and blood sugar — Superpower.com, March 2026

Part 1 did the work that cycle syncing content almost never does: it separated the evidence from the extrapolation.

You now know which biology is real. You know that the exercise research doesn’t support phase-specific training prescriptions for performance outcomes, but does validate the lived experience of feeling different across the month. You know that the programme as sold is built on a foundation of real science but extended several steps further than the data supports.

Part 2 takes that foundation and builds something you can actually use. Not a programme with day-numbered prescriptions. A framework that works with your real cycle, which may not be 28 days, may include anovulatory phases, and may be significantly altered if you’re on hormonal contraception and that adjusts to your individual pattern rather than an average.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.

Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

Read more

A girl I’d never heard of explained that if I ate seeds at the right time of month, exercised according to my hormonal phase, and structured my whole life around a four-phase framework, I would feel completely different. More energy. Less PMS. Better skin. Clearer thinking. Hormonal balance. I scrolled through the comments — thousands of women saying it changed their lives, asking how to start, tagging friends to try it with them.

And I thought: okay, but what actually is this?

So I did what I always do. I went looking for the research.

What I found was not a simple story. It was not “cycle syncing is a scam,” that’s the hot take making the rounds in the medical community, and it’s not the full picture. But it was also not “this programme will transform your hormones,” which is what the wellness industry is selling with aggressive confidence.

The actual answer is considerably more interesting than either of those.

#cyclesyncing has amassed tens of millions of views. A 2025 study published in Perspectives on Sexual and Reproductive Health analysed 100 cycle syncing TikTok videos and found that only 30% of creators provided any credentials, and a remarkable 4% cited scientific sources. Four percent. The content is viral, the messaging is confident, and almost none of it is connected to research in any verifiable way.

Meanwhile, the scientific literature on whether exercise or diet should be structured around the menstrual cycle is genuinely contested. The Strength and Conditioning Journal published a 2025 critical review concluding that “research does not support the idea that periodizing or programming strength or endurance training according to the menstrual cycle confers additional benefits over more traditional approaches.” A different 2020 meta-analysis found exercise performance is trivially reduced in the early follicular phase — just not enough to build a training programme around.

Both are true. The nuance between them is where cycle syncing either becomes genuinely useful or becomes another wellness framework that makes you feel guilty for not doing it right.

Here’s what I want to do: give you the evidence-based version of cycle syncing. The part where the biology is real and the practical applications make sense. The part where the wellness industry has overreached. And the most important part — which nobody in the TikTok ecosystem is explaining, which is the why behind the recommendations, because once you understand the biology you can make your own decisions rather than following a programme someone invented in 2014.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.
Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

Table of Contents:

1. What Cycle Syncing Actually Is And Where It Came From

2. What the Exercise Science Actually Says

3. Hormones and How They Actually Change Your Body Across the Month

4. What The Research Actually Supports For Nutrition

5. Cycle Awareness vs. Cycle Syncing — The More Useful Framing

6. The Evidence-Backed Nutrition Guide for Each Phase

7. The Workout Framework That Evidence Actually Supports

8. Cycle Awareness in Practice — How to Track and What to Do With It

9. The Phase Guide — Everything in One Place

10. The Point Is Awareness, Not Optimisation

Chapter 1: What Cycle Syncing Actually Is And Where It Came From

The Origin Story

Cycle syncing as a named practice was introduced by functional nutritionist Alisa Vitti in her 2014 book WomanCode. The core idea: the four phases of the menstrual cycle; menstrual, follicular, ovulatory, and luteal, create four distinct hormonal environments, and aligning your diet, exercise, and lifestyle with those environments will optimise how you feel across the month.

This is, broadly, a reasonable premise. The hormones are real. The four phases are real. The idea that different hormonal environments might require different inputs is biologically plausible. The problem is that the leap from “hormones change across the cycle” to “here is the exact programme you should follow” was made without the clinical trials that would justify it.

Cleveland Clinic’s Dr. Albers notes that the cycle syncing programme “hasn’t been researched in a clinical setting,” meaning there are no randomised controlled trials testing whether following a cycle-synced diet and exercise plan produces better outcomes than a standard healthy diet and exercise plan. What exists are studies on hormonal fluctuations and their biological effects. Cycle syncing takes those studies and builds a lifestyle programme on top of them. Whether that specific programme works is the untested part.

This is not unusual in wellness. Most of the practical advice that turns out to be useful was plausible before it was proven. The question is how to use the genuine biology without buying wholesale into the unprovable programme.

The Four Phases — The Real Biology

The four phases of your cycle aren’t a wellness invention. They’re real biology. Here’s what each one actually looks like — no jargon, just what’s going on.

Menstruation (Days 1–5) Both estrogen and progesterone are at their lowest. They dropped off at the end of last month’s cycle, and that drop is what triggered your period. Hormonally, this is the quietest and most depleted point of the whole month.

Follicular Phase (Days 6–13) Your period ends, and estrogen starts climbing. Progesterone stays low. There’s one hormone doing one thing, in one direction. No conflict, no competing effects. This is why most women feel noticeably better in this stretch, their hormonal environment is simple and rising.

Ovulation (Days 13–15) Estrogen hits its peak, which triggers the release of an egg. This window is short, usually 24 to 48 hours. After ovulation, progesterone starts to rise and takes over as the dominant hormone for the rest of the cycle.

Luteal Phase (Days 16–28) Progesterone is in charge now. Your body temperature goes up slightly. If pregnancy doesn’t happen, both hormones drop off toward the end of this phase and that drop is what kicks off the next period, starting the whole thing again.

One thing the TikTok version almost never mentions: this neat 28-day cycle with ovulation on day 14 is a textbook average, not a guarantee. Real cycles can be anywhere from 21 to 35 days. Ovulation timing shifts. Some cycles don’t produce an ovulation at all. And if you have PCOS, irregular periods, or you’re on hormonal contraception, your hormonal pattern may look completely different from this template.

This matters because most cycle syncing content is built around the idealised 28-day version. If your cycle doesn’t match that — which many women’s don’t. The day-specific prescriptions (”do HIIT on day 12, eat seeds on day 18”) may not apply to you at all. That’s the first reason to hold the specific programme loosely.

So Why Do So Many People Swear By It?

Because the underlying biology is real, even if the programme built on top of it isn’t fully proven.

Hormones genuinely affect your body in ways that are documented in research. Progesterone raises your body temperature and disrupts deep sleep in the second half of your cycle. Estrogen supports serotonin, which is why your mood tends to be more stable when estrogen is rising. In the week before your period, both hormones drop off quickly, and that drop removes two of your nervous system’s natural calming effects at once. Your body actually burns more calories at rest in the luteal phase; somewhere between 100 and 500 extra per day which is why you’re genuinely hungrier, not just emotionally reaching for food.

These things are real. Women who say their energy, mood, sleep, and capacity feel completely different week to week aren’t imagining it. They’re noticing something that research confirms.

The issue isn’t that cycle syncing is made up. It’s the jump from “your hormones change your body across the month” which is true to “therefore follow this exact food and exercise plan day by day” which has almost no clinical trials behind it. The biology is solid. The specific programme built on top of it is largely extrapolation.

That gap is what this Short Dive is here to close.

Chapter 2: What the Exercise Science Actually Says

This is the most contested territory in cycle syncing and the most important to get right, because exercise advice is where the most confident claims and the most contrary evidence collide.

The Claim

The cycle syncing exercise framework looks approximately like this: rest and gentle movement (walking, stretching, yoga) during menstruation; build with cardio and lighter resistance in the follicular phase; push with high-intensity training and peak performance around ovulation when estrogen is highest; then reduce intensity in the luteal phase, particularly in the late luteal window.

This framework is presented on TikTok with the confidence of established clinical guidance. Let’s see what the research actually supports.

What the Meta-Analyses Say

A systematic review and meta-analysis published in Sports Medicine (McNulty et al., 2020), the largest and most frequently cited review on this topic, covering 78 studies found something more modest than the cycle syncing content suggests: exercise performance was trivially reduced during the early follicular phase (days 1–5, i.e. menstruation) compared to all other phases. The effect size was 0.06 — which researchers classify as trivial. The quality of evidence was rated “low.”

The finding that survival-relevant: performance is mildly reduced at the start of your period, not in the luteal phase as most cycle syncing content implies. Every other phase of the cycle appeared roughly equivalent for exercise performance.

A 2025 review published in Frontiers in Sports and Active Living was even more direct, examining whether periodising resistance exercise training around the menstrual cycle produced better outcomes. Their conclusion: “current evidence shows no influence of women’s menstrual cycle phase on acute strength performance or adaptations to resistance exercise training.” Menstrual cycle phase had trivial effects on maximal voluntary contraction force, isokinetic peak torque, and explosive strength.

The 2025 Strength and Conditioning Journal critical review summarised the state of the evidence clearly:

This is the consensus among sports scientists who have looked at this literature carefully.

The Important Nuance

Here’s where it gets interesting and where the nuance matters more than either “cycle syncing is real” or “cycle syncing is debunked.”

The research is measuring performance outcomes — how much you lift, how far you run, your VO2 max scores. It is not measuring how hard training feels, how well you recover, or how much it disrupts your sleep and mood. These are different questions, and the evidence on the first question doesn’t fully answer the second.

The progesterone-driven temperature elevation of the luteal phase genuinely impairs sleep quality. Elevated body temperature, increased resting heart rate (3-5% higher), and more fragmented sleep in the luteal phase are documented. A demanding training session on top of already-fragmented sleep, in a phase where the nervous system is more reactive to cortisol, may be a different experience in your body than the same session in the follicular phase even if your measured performance is similar.

The Harvard Women’s Health Study analysed 22.85 million logged workouts across 461,163 cycle days and found that women actually exercise very similar amounts in both phases; 21 minutes per day in the follicular phase versus 20.9 in the luteal. People are listening to their bodies and self-adjusting without being told to. That’s the practical version of cycle syncing, and it turns out women are largely already doing it.

What This Means Practically

The sports science evidence says: your hormonal phase is unlikely to determine whether you perform better or worse at the gym. What it may affect is how hard training feels and how well you recover from it.

The cycle syncing advice to “push hard around ovulation” and “back off in the luteal phase” is not well-supported for performance outcomes. But the advice to “listen to your body across the month and adjust intensity based on how you actually feel” is not only well-supported, it’s what the Harvard data shows women are already doing intuitively.

The more useful reframe: cycle syncing is less about following a prescribed exercise programme and more about giving yourself permission to train differently in different weeks without thinking something is wrong with you. The permission-giving is the valuable part. The specific programme is the oversimplified part.

Chapter 3: Hormones and How They Actually Change Your Body Across the Month

The Menstrual Phase: What’s Happening and What It Costs

When estrogen and progesterone drop sharply, several things happen simultaneously:

Why you can’t sleep the week before your period and why you feel wired and exhausted at the same time. During the second half of your cycle, progesterone produces a mild calming effect in your brain. It works through the same pathway that anti-anxiety medications and sleep aids target. That’s why many women feel genuinely sleepier in the weeks after ovulation — your body is producing its own mild sedative.

Then, right before your period, progesterone drops off sharply.

And that calming effect disappears with it.

Your nervous system, which had that chemical support, suddenly doesn’t. The result is a kind of rebound, heightened anxiety, difficulty falling asleep, a restless, on-edge feeling that doesn’t have an obvious cause. The “wired but exhausted” state that so many women describe in the week before their period isn’t a mood or a mindset. It’s your brain chemistry changing underneath you.

Iron loss. Menstruation involves blood loss, and blood contains iron-rich haemoglobin. Average menstrual blood loss depletes approximately 0.5–1mg of iron per day of bleeding in a typical period, significantly more with heavy periods. For a population that already has an iron deficiency rate of 40% among teenage girls (with 83.6% of cases missed by routine screening), this monthly loss is clinically relevant.

Why your period actually hurts. Your uterus doesn’t shed its lining passively. It contracts to push it out and those contractions are driven by chemicals called prostaglandins. The higher your prostaglandin levels, the stronger the contractions, and the worse the cramping.

But prostaglandins don’t stay neatly in the uterus. They also trigger inflammation, nausea, diarrhoea, headaches, and general flu-like misery. If your periods leave you feeling genuinely unwell and not just uncomfortable, but actually sick, prostaglandins are almost certainly why. This is not a low pain threshold. It’s a real physiological process with measurable effects on the body.

Reduced memory consolidation. Research by Genzel et al. found that women’s memory consolidation during sleep is poorest in the early follicular/menstrual phase. When both estrogen (which enhances sleep spindle activity) and progesterone (which also drives spindle activity) are low.

The Follicular Phase: Your Best Week

This is the good week. And there’s a reason for it.

As estrogen rises, your brain starts producing more serotonin, which is why your mood lifts, things feel more manageable, and you generally feel more like yourself. Your memory is sharper. Your energy is more consistent. Your sleep is deeper and more restorative. Your body temperature is lower, which sounds random but actually matters a lot for how well you sleep.

Appetite drops a little too. Research has found women naturally eat slightly less in the lead-up to ovulation, partly because estrogen quietly suppresses hunger. That’s not a bad thing. It’s just your body doing its thing.

In short: this is the phase where everything feels easier. Because hormonally, it is.

Ovulation: The 48-Hour Window

Ovulation itself is a brief moment, usually 24 to 48 hours. Estrogen is at its absolute peak, and energy and motivation tend to match it.

One thing worth knowing if you work out: research has found that joint laxity (how loose your ligaments are) is highest around ovulation. Estrogen triggers a hormonal chain reaction that softens connective tissue slightly, including in the knee. This is part of why women tear their ACL at 2 to 8 times the rate of men in the same sports. It’s not a reason to avoid training, but it is a reason to warm up properly and pay extra attention to form when you’re doing anything with jumping, heavy squats, or sharp directional changes.

The Luteal Phase: Why You Feel Two Things at Once

This is the phase where cycle syncing content gets the most interest and where the biology is most complex and most misrepresented.

Here's the thing that confuses people: in the luteal phase, you feel sleepier and sleep worse. You feel more tired and actually need more food. You're doing less and your body is working harder. These are not contradictions. They're all happening at once, and there's a reason for each of them.

Why you feel sleepy:

After ovulation, progesterone rises and produces a mild sedative effect in the brain. The same chemical pathway that sleep medications target. So the sleepiness is real.

Why sleep is still rubbish:

At the same time, progesterone raises your body temperature by about half a degree. That doesn’t sound like much but it matters as your body needs to cool down significantly to get into deep, restorative sleep. When your baseline temperature is already elevated, it can’t cool down as far, and you end up in lighter, more broken sleep. Tired enough to fall asleep, but not sleeping deeply enough to actually feel rested. Research from Harvard found that the faster progesterone rises after ovulation, the more women wake up in the middle of the night. Not because of stress or your phone but because of hormones.

Why you’re hungrier and that’s fine:

Your resting metabolic rate actually increases in the luteal phase. Your body is burning roughly 100–500 more calories per day just existing. The hunger is your body asking for more fuel because it genuinely needs more fuel. Eating more in this phase is not a willpower problem. It’s biology.

Why the week before your period is the worst:

As your period approaches, both estrogen and progesterone drop off sharply. That drop removes the sedative progesterone effect and lowers serotonin at the same time so your nervous system loses two of its calming supports within the same few days. The result is the heightened anxiety, broken sleep, and “everything feels harder” experience that most women just call PMS, without realising it has a very specific neurochemical explanation.

It’s not in your head. It’s your hormones withdrawing.

Now you know more about your cycle than most of the people making content about it.

You know that the four phases are real biology, not a wellness framework someone invented. You know that the exercise research doesn’t actually support the phase-specific training prescriptions but does explain why some weeks feel genuinely harder than others. And you know what’s happening hormonally in each phase: why the follicular phase feels like a reset, why the luteal phase makes you sleepy and wrecks your sleep, and why the week before your period feels like the floor has dropped out.

That’s the why. Part 2 is the what to do about it.

Because here’s the thing: understanding your cycle is only half the equation. The more useful half is knowing which nutritional interventions the research actually supports — not the made-up ones, but the ones with real clinical evidence behind them. Knowing how to train in a way that works with your hormonal environment rather than against it. Knowing how to track your own pattern rather than following a generic programme that was built for someone else’s cycle. And having a phase-by-phase guide you can actually use.

Part 2 covers all of it.

Chapter 4 is the nutrition chapter. What the research genuinely supports eating in each phase, and what’s marketing dressed up as science. The difference is bigger than you’d think, and the evidence-backed version is simpler and more useful than the programme.

Chapter 5 reframes the whole conversation, from cycle syncing as a rigid protocol to cycle awareness as a way of understanding your body. This is the shift that makes everything else actually work.

Chapters 6–9 are the practical half: the workout framework, the tracking guide, and the phase-by-phase summary you can save and actually refer back to month by month.

Part 2 is for paid subscribers. If you’re not one yet, you can upgrade below.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding your health.

Sources & Further Reading

Pfender, Wanzer et al. Sync or Swim: Navigating the Tides of Menstrual Cycle Messaging on TikTok — Perspectives on Sexual and Reproductive Health, 2025

Pfender, Kuijpers et al. Cycle Syncing and TikTok’s Digital Landscape: A Reasoned Action Elicitation — Qualitative Health Research, 2025

McNulty et al. The Effects of Menstrual Cycle Phase on Exercise Performance in Eumenorrheic Women: A Systematic Review and Meta-Analysis — Sports Medicine, 2020

Colenso-Semple et al. Current evidence shows no influence of women’s menstrual cycle phase on acute strength performance or adaptations to resistance exercise training — Frontiers in Sports and Active Living, 2023

Wen, Gao et al. Exercise performance at different phases of the menstrual cycle: a narrative review — Frontiers in Endocrinology, December 2025

Harvard Apple Women’s Health Study: Exploring Exercise Habits by Menstrual Cycle Phase, 2025

Evidence for Periodizing Strength and/or Endurance Training According to the Menstrual Cycle — Strength & Conditioning Journal, December 2025

Weyand et al. Iron Deficiency in Girls and Women — JAMA, 2023

Shiff et al. Objective Sleep Interruption and Reproductive Hormone Dynamics in the Menstrual Cycle — PMC, Harvard, 2014

Baker et al. Tracking Sleep, Temperature, Heart Rate, and Daily Symptoms Across the Menstrual Cycle with the Oura Ring — PMC, 2022

Facchinetti et al. Magnesium prophylaxis of menstrual migraine — Headache, 1991; Magnesium and PMS

Moghadamnia et al. Effect of fish oil on dysmenorrhea — Iranian Journal of Nursing and Midwifery Research, 2010

Nutrition and the Menstrual Cycle — Clue Health Platform, evidence review

Worldhealth.net: Cycle Syncing — Separating Social Media Hype From Real Hormone Health, 2025

Part 1 ended with something a lot of cortisol content never gives you: an actual map of the mechanism.

You now know that “cortisol face” is three different things. That the skin has its own cortisol-producing system. That the barrier proteins holding your skin together decline measurably under chronic stress, and that the collagen your skin relies on for firmness is being downregulated while you’re in that relentless stretch of bad weeks.

Now for what you can do about it.

Part 2 starts with diet, because what you eat is one of the most direct inputs into how reactive your HPA axis is. Not in a “clean eating will save you” way. In a specific, mechanism-based way that actually explains why certain dietary patterns keep your system in a higher state of alert than necessary.

From there: sleep and exercise, where the research is genuinely unambiguous. Supplements, ranked with actual evidence behind the rankings, not trending. A skincare protocol specifically designed for the stressed, cortisol-compromised barrier. And a full action plan with a clear sequence.

Let’s get into it.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.
Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

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Maybe it’s the breakout that showed up two weeks after the most stressful month of your life — right when you thought you’d gotten through it. Maybe it’s the puffiness that’s taken up permanent residence under your eyes no matter how much sleep you get. The dullness that settles in during exam season and lifts, mysteriously, when you’re on holiday. The skin that used to tolerate everything and now stings when you put anything on it.

Or maybe you’ve seen the TikToks. The ones about cortisol face; the rounder jaw, the puffier cheeks, the idea that your stress hormones are physically redistributing fat in your face. And you’ve looked in the mirror and wondered: is that what’s happening to me?

The honest answer is: maybe. But probably not in the way the algorithm is describing it.

In early 2024, the comedian Amy Schumer posted on Instagram that she’d been diagnosed with Cushing’s syndrome after people online made comments about her face looking different. It was a genuine diagnosis — a rare hormonal condition in which the body produces so much cortisol that it causes clinically measurable physical changes, including facial fat redistribution. The internet took this moment, stripped out the “rare hormonal condition” part, and turned it into a content category.

Now “cortisol face” is everywhere. Along with cortisol supplements, cortisol-lowering routines, cortisol morning protocols, and a general cultural anxiety about a hormone that, ironically, spikes in response to anxiety.

Here’s what I found when I actually went looking at the research: the relationship between cortisol and your skin is real, well-documented, and genuinely significant. But it’s not what most of the content describes. It’s more interesting than that and more actionable.

This Short Dive separates the three things that all get called “cortisol face.” It explains what cortisol actually does to your skin at the cellular level, because it’s more than just “stress causes breakouts.” It covers how to tell if stress is driving your skin symptoms, what diet and lifestyle changes the research supports, which supplements have real clinical evidence behind them, and how to build a routine that works with your cortisol rather than against it.

What’s covered:

Let’s get into it.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.
Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

Table of Contents:

1. What Is Cortisol, Actually?

2. The Three Things People Call "Cortisol Face" (They Are Not the Same)

3. What Cortisol Actually Does to Your Skin

4. How Do You Know If Cortisol Is Affecting Your Skin?

5. What Your Diet Is Doing to Your Cortisol Levels

6. Sleep, Exercise, and the HPA Axis

7. Supplements and Adaptogens — Honest Rankings

8. The Skincare Side: Building a Routine That Works With Your Cortisol, Not Against It

9. Your Cortisol Action Plan

10. What to Take Away From This

CHAPTER 1: What Is Cortisol, Actually?

The hormone everyone talks about, explained properly

Cortisol has a branding problem. It’s been positioned as the enemy. The stress hormone, the thing making you fat and anxious and spotty. The wellness industry has built an entire supplement category around “lowering” it, implying that less cortisol is always better and that you want your levels as low as possible.

Neither of those things is true. And understanding what cortisol actually does, and why you genuinely need it is the foundation for understanding what happens when it goes wrong.

What Cortisol Does (It’s Not Just Stress)

Cortisol is a steroid hormone produced by the adrenal glands, which sit just above your kidneys. It belongs to a class of hormones called glucocorticoids aka the hormones that regulate glucose metabolism, immune function, and inflammation throughout the body.

Its roles are extensive. Cortisol:

• Regulates blood sugar by prompting the liver to release glucose into the bloodstream

• Controls blood pressure and supports cardiovascular function

• Modulates the immune system, suppressing excessive inflammation

• Helps the body respond to infection, injury, and physical stress

• Regulates metabolism; how the body converts food to energy

• Is involved in memory consolidation and cognitive function

• Influences mood, motivation, and the sleep-wake cycle

Without cortisol, the body cannot regulate inflammation or blood pressure effectively, deficiency is life-threatening. The goal is never “as low as possible.” The goal is a well-functioning cortisol rhythm: the right amount at the right times.

The HPA Axis: How Cortisol Is Made

Cortisol production is controlled by a three-part communication system called the HPA axis — hypothalamus, pituitary, adrenal glands.

Here’s how it works: a stressor (physical, emotional, or perceived) activates the hypothalamus, which releases corticotropin-releasing hormone (CRH). CRH travels to the pituitary gland and signals it to release adrenocorticotropic hormone (ACTH). ACTH travels through the bloodstream to the adrenal glands and tells them to produce cortisol.

Once cortisol levels in the blood reach a certain point, the hypothalamus and pituitary detect this and reduce their signals — a negative feedback loop that normally keeps the system in balance. Chronic stress can disrupt this feedback sensitivity, leading to prolonged cortisol elevation and eventually reduced HPA axis responsiveness.

There’s also a separate system worth knowing about: the skin has its own peripheral HPA-like axis. Keratinocytes; the cells that make up your skin’s outer layer contain the components to produce cortisol locally. The skin doesn’t just respond to cortisol from the adrenal glands. It can produce it directly in response to local stressors like UV radiation, injury, and inflammation. This is why skin conditions can worsen with local stress even when systemic cortisol looks normal.

The Cortisol Rhythm: Why Timing Matters

Cortisol is not supposed to be a steady flatline. It follows a diurnal rhythm: levels spike sharply in the 30 minutes after waking; a phenomenon called the cortisol awakening response (CAR), and then gradually decline throughout the day, reaching their lowest point around midnight.

This rhythm is essential. The morning cortisol surge mobilises energy, increases alertness, and primes the immune system for the day ahead. The evening drop allows the body to shift into repair and recovery mode, supports sleep onset, and permits the overnight processes that healthy skin depends on:

• Cell turnover,

• Collagen synthesis,

• Immune regulation

When the rhythm is disrupted, by irregular sleep schedules, chronic stress, artificial light exposure at night, or extreme training, the consequences ripple through every system that cortisol touches. Including your skin.

Acute vs. Chronic Cortisol: The Critical Difference

Acute cortisol responses are healthy. You have a difficult conversation; cortisol spikes, helps you manage the stress, then returns to baseline. This is normal physiology working as intended.

The problem is chronic elevation, when the system never fully returns to baseline. When the stress is persistent enough, or the HPA axis becomes dysregulated enough, cortisol stays elevated not in spikes but as a sustained background hum. This chronic moderate elevation is what the research consistently links to impaired skin barrier function, collagen breakdown, delayed wound healing, and increased sebum production.

And here’s the important point: you don’t have to feel dramatically stressed for this to be happening. Chronic low-level stress; the kind that comes from a relentless schedule, financial pressure, sleep deprivation, or just the baseline anxiety of being young and alive right now, can be enough to sustain mildly elevated cortisol long-term, with cumulative consequences for the skin.

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You started reading Part 1 because you had questions.

Maybe you finished it with a few answers — and a whole new set of questions.

That’s exactly where I was too.

Because knowing what retinol does is one thing. Knowing how to use it without your skin staging a full revolt in week two is something else entirely.

Part 1 was the why. This is the how.

Chapters 7 through 12 are where things get practical and honestly, where most guides either go too vague or get too complicated. I’ve tried to do neither.

I’am talking about your actual routine. The ingredients that work with retinol and the ones that quietly work against it. What to do when your skin is sensitive, darker, pregnant, or just easily irritated. How to know if what you’re experiencing is normal adjustment or a sign to stop. And what long-term use actually looks like because retinol isn’t a 30-day fix. It’s closer to a relationship.

If Part 1 convinced you retinol is worth trying, Part 2 is what keeps you from quitting at week three.

Let’s get into it.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.
Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

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Dermatologists use it on their own faces.
It’s retinol.
And most people our age are either too scared to start or starting completely wrong.
I get it. I was one of them.
Every time I opened TikTok, someone was talking about it. Every time I scrolled Instagram, there was a new retinoid launch. Celebs swore by it. Dermatologists swore by it. Influencers were documenting their “retinol journeys.”

And I started wondering… is it actually that good? Or is this just another overhyped, over-marketed skincare phase?
Because right when you start thinking about trying it, the scary questions kick in.

And then it gets worse.

If I do start…
Do I use retinol?
Retinal?
Adapalene?
What’s the difference?
Serum or cream?
What percentage?
How often?

I genuinely felt like I was losing my mind.

I went down the rabbit hole — video after video, influencer after influencer. Watching their transformations and wondering… is that real skin or a filter? One TikTok creator said retinol destroyed her skin for months. Another said it changed her life.

Here’s what made me stop spiralling and actually start: the research isn’t ambiguous. Clinical trials show visible improvement in skin texture and tone beginning at week 4 and not after years.

A major 12-week study found that even a low 0.1% concentration significantly improved crow’s feet, dark spots, and uneven tone. And here’s the part nobody tells you when you’re 22 and Googling this at midnight: retinol works fastest on younger skin, because younger skin has more collagen left to protect.

Meanwhile, the industry has quietly solved most of what scared us. The products going viral right now — the ones people are calling “Botox in a tube” aren’t the harsh, stripping formulas from ten years ago.

Next-generation retinols use micro-encapsulation and barrier-supporting actives to deliver results with almost none of the irritation. You can get an effective starter retinol for under £10. Sensitive skin is no longer a reason to wait.
So back to the real question:

After three weeks of going through actual studies, dermatologist interviews, and ingredient breakdowns — not just social media — I finally know. And there’s one mistake almost every beginner makes in the first week that sets them back by months.
This is for you if you’re stuck in the same spiral. Keep reading.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.
Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

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Part 1 was a lot.

And if you’re coming back for Part 2, something probably landed. Maybe it was the moment you recognised your own routine in the list of things that damage the barrier — the glycolic acid toner, the retinol three nights in a row, the double exfoliation. Maybe it was the realisation that “sensitive skin” isn’t always a skin type. Sometimes it’s a skin condition. One that you caused without knowing, by doing exactly what the internet told you to do.

Either way: welcome back. Because Part 1 was the diagnosis. This is the treatment plan.

Chapters 4 through 9 are where it gets practical and this is the part where most barrier content either gets annoyingly vague (”moisturise! stay hydrated! reduce stress!”) or spirals into a 47-step protocol that makes you feel like you need a chemistry degree to wash your face. I’ve tried to do neither.

What’s actually in here: the specific nutrients that help your skin rebuild ceramides and collagen from within. The daily habits that most people don’t realise are quietly eroding their barrier, and the small ones that make a real difference. Which supplements have clinical evidence behind them, and which are mostly expensive speculation. What a real repair routine looks like — not the aesthetic version, the functional one, including what to stop, what to add, and in what order.

The 19-year-old with the ten-step routine who came up in Part 1 cut down to three products and healed in four weeks. Not because she found something better. Because she stopped getting in the way.

That’s the theme of everything that follows.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.
Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

Short Dive below ↓

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Nothing dramatic — just normal, unremarkable skin that she never thought about much. Then she turned 19, discovered skincare, and decided to actually take care of it.

She did everything she’d been taught to do on the internet. Double cleansed. Used a vitamin C serum in the morning. Introduced a glycolic acid toner. Added retinol at night because everyone said she should start young. Exfoliated twice a week. She had a ten-step routine and an entire shelf of products she’d carefully researched.

And her skin got worse.

Not a little worse. Noticeably, confusingly worse. She was doing more than she’d ever done for it, spending more money than she ever had, paying more attention than she ever had and her skin was redder, more reactive, breaking out in places it never had before, and stinging when she applied her moisturiser.

She went to a dermatologist. The verdict: her skin barrier was damaged. Not by neglect. By too much. By the very routine she’d built to help.

This is happening to a generation of women.

A 2024 survey by the International Dermal Institute found that 68% of dermatologists had treated patients in the last year for adverse reactions — contact dermatitis, severe purging, or barrier damage, linked to products or techniques popularised online. Not from using bad products. From using the right products in the wrong quantities, at the wrong time, in the wrong combinations, based on advice from people whose skin is different from theirs, who are paid to recommend things, and who are not dermatologists.

For years, the dominant logic of skincare was “more is better” — acids, peels, exfoliating toners, and masks layered together in pursuit of brighter, smoother skin. While these products delivered short-term results, the long-term impact was compromised skin barriers, chronic sensitivity, breakouts, and inflammation.

If you have skin that’s suddenly become reactive, that stings when you apply things it used to tolerate, that’s dry and oily at the same time, that breaks out more than it did when you were doing nothing — this might be why. And the fix is almost certainly the opposite of what the algorithm will tell you to try next.

Here’s what nobody explains clearly enough: your skin barrier is not just a cosmetic concern. It is a physical structure, a carefully maintained layer of cells and lipids and microbes that your body has been building and maintaining your entire life. It keeps water inside your skin and keeps pathogens, allergens, and irritants out. Your skin functions as an active immune organ that blocks pathogens and initiates immune responses. Keratinocytes — the cells that form your skin’s outer layer, act as biological alarm systems. When they detect danger, they release antimicrobial peptides and signalling molecules that alert your immune system.

When that barrier is intact, your skin is comfortable, hydrated, and resilient. When it’s damaged, everything you put on it goes where it’s not supposed to go. Actives that were designed to sit on the surface penetrate too deeply. Moisture evaporates faster than it can be replaced. Irritants get in. Your immune system activates in response to things it would normally ignore. Skin that used to be “normal” becomes “sensitive” not because your skin type changed, but because the structural layer that was protecting it has been thinned, stripped, and disrupted.

And it is very easy to damage it, because the tools that damage it are being marketed to you specifically as skincare.

I started looking into this properly because I noticed a pattern. So many women I know, and so many in the comments of the skin content I watch, describe the same trajectory: started taking skincare seriously, built a routine, saw initial improvement, then hit a wall where nothing seemed to work and everything seemed to make things worse. The assumption is usually that their skin needs something stronger. A new acid. A higher concentration retinol. A different routine.

The research says the opposite. The skincare industry is now seeing a clear shift away from the “more is better” mindset. Over-exfoliation, compromised skin barriers, and sensitised complexions have pushed both brands and consumers to reassess what healthy skin actually looks like. The answer is moderation and precision — fewer products, better ones, applied in ways that respect the skin’s natural biology.

This Short Dive is about what the skin barrier actually is, why it’s breaking down in women our age in particular, and what the evidence says about repairing it — from both the outside and the inside.

Here’s what this Short Dive covers:

• What the skin barrier actually is — the science, in plain language

• How to tell if yours is damaged

• The most common ways it gets damaged — and the skincare habits most likely to be the culprit

• Different types of barrier disruption and why they need different approaches

• What to eat, how to sleep, and how to manage stress to rebuild from within

• The ingredients that actually repair it — and what to avoid while it heals

• A gentle 7-day reset routine to get you started

The 19-year-old with the ten-step routine has simpler skin now than she did when she started. Not because she found better products. Because she stopped using most of them.

Let’s get into it.

1. What Is the Skin Barrier?

2. Why Skin Barrier Damage Happens

3. Dry, Reactive, or Breaking Out? How to Diagnose Your Barrier Type

4. Feed Your Barrier: The Nutrients That Rebuild Your Skin From the Inside Out

5. The Daily Habits That Either Protect or Destroy Your Skin Barrier (Most People Get These Wrong)

6. Which Supplements Actually Help Your Skin Barrier — And the Doses That Make a Difference

7. The Kitchen Remedies and Herbal Teas That Calm, Repair, and Rebuild Your Barrier

8. The Barrier Rescue Routine: Exactly What to Use, In What Order, And What to Stop Immediately

9. What to Take Away from This

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Chapter 1: What Is the Skin Barrier?

If your skin keeps reacting no matter what you try — new products, gentle routines, more water. The problem probably isn’t your products. It’s the barrier underneath them. Before we fix it, let’s understand it. The skin is composed of multiple layers, but the “skin barrier” mainly refers to the outermost layer of the epidermis called the stratum corneum. This layer is extremely thin (think cellophane thickness) but tough. As mentioned, you can visualize it as bricks and mortar. The bricks are dead, flattened skin cells (corneocytes) that are rich in keratin and natural moisturizing factors. The mortar between them is a lipid matrix made up of fatty substances; ceramides (about 50%), cholesterol (about 25%), and fatty acids (about 25%). These lipids form structured layers around the cells, creating a water-resistant seal.

Together, this structure has two main jobs:

1. Keep bad stuff out (irritants, bacteria, allergens, pollutants)

2. Keep good stuff in (moisture especially)

When healthy, the barrier is selectively permeable. It lets in small beneficial molecules (like water and certain skincare ingredients) but blocks large or harmful ones. It’s amazingly effective: an intact barrier prevents most microbes and chemicals from penetrating, while holding onto natural hydration so our skin doesn’t constantly lose water.

Not only that, the barrier layer helps maintain skin’s immune balance. The surface is slightly acidic (pH around 5) which inhibits harmful bacteria and supports the skin microbiome. The collection of friendly microbes living on us. (Yes, we have good bacteria on our skin that act as microscopic bodyguards!) A healthy microbiome further crowds out pathogens and even “talks” to our skin’s immune cells to keep inflammation in check. In essence, your skin barrier isn’t just passive wall – it’s an active defense system, complete with its own ecosystem and alarm signals when breached.

Key barrier functions include:

Moisture Retention

The lipid “mortar” is hydrophobic, meaning it repels water. This prevents transepidermal water loss (TEWL) water evaporating from deeper skin. A strong barrier keeps your skin hydrated and plump. When the barrier is leaky, you get dryness and that annoying tight feeling. In fact, ceramides and cholesterol in the barrier are crucial to preventing moisture from evaporating.

Protection Against Outsiders

A healthy barrier is like a shield. It blocks toxins, pollutants, and germs from penetrating your skin. Those tightly packed bricks and lipids are very selective. For example, ceramides fill the gaps so well that they inhibit the penetration of foreign pathogens or allergens. This protects you from infections and irritation.

Immune Regulation

The barrier also contains specialized cells and signals (like antimicrobial peptides, cytokines) that trigger immune responses when needed. If something breaches the barrier, alarm chemicals signal deeper skin to react (sometimes seen as redness or inflammation). Also, the acidic pH and friendly bacteria on the surface are part of immune defense, they create an environment that deters harmful bugs and educates your immune system not to overreact to every little thing. When the barrier is intact, it helps calm the skin’s immune responses; when broken, the immune system can go into overdrive leading to conditions like eczema, where a broken barrier and inflammation feed each other.

Signs of a Damaged Barrier

How do you know if your skin’s barrier is compromised? Your skin will tell you. Common signs include:

You might see redness or feel itching, burning or stinging when you apply products whereas healthy skin wouldn’t react so strongly. Breakouts or rashes can occur because irritants and bacteria sneak in through the “cracks,” leading to pimples or irritant dermatitis. In fact, a damaged barrier often underlies adult acne or “sensitive” skin complaints as your skin becomes reactive because its shield is down. You may notice your skin is less plump and more dull, since it’s losing water and struggling to reflect light well. In summary, compromised barrier skin tends to be dry, reactive, red, and prone to breakouts or infections. If this sounds familiar, don’t worry – it’s fixable, and you’re in the right place to learn how.

Chapter 2: Why Skin Barrier Damage Happens

Now let’s explore what causes the barrier to break down. It usually isn’t just one thing rather its often a combination of factors slowly (or sometimes suddenly) wears away at that protective layer. Lets look at external triggers from skincare routines, and internal or environmental factors that weaken the barrier.

Skincare Triggers: Doing “Too Much”

Ironically, many barrier problems are self-inflicted by our well-intentioned skincare habits. In the quest for perfect skin, it’s easy to overdo it and strip or irritate the barrier. Some common culprits:

• Over-cleansing: Washing your face too often or with harsh cleansers can deplete the natural oils and disturb the acidic pH of your skin. Foaming cleansers with sulfates or alcohol-based astringents are especially guilty. They give that “squeaky clean” feeling which is actually your barrier being stripped. Over-cleansing (more than twice a day) or using strong soaps can weaken the mortar between skin cells.

• Harsh toners and alcohol: That bracing tingle from an alcohol-heavy toner might feel effective, but it often means your barrier is getting degreased. Denatured alcohol and witch hazel-based toners can overly dry out the stratum corneum, leading to microscopic cracks and water loss. If your skin feels tight or “shiny-dry” after toning, it’s a red flag. Opt for hydrating, alcohol-free toners instead.

• Excessive exfoliation: This is a big one. Exfoliants are useful in moderation to remove dead cells, but many of us have taken exfoliating to extremes with daily acids, peels, scrubs, and microdermabrasion. Alpha-hydroxy acids (AHAs), beta-hydroxy acids (BHAs), and scrubs can thin the stratum corneum if overused, eroding that protective brick wall. The result? Skin that’s smooth at first, then chronically irritated and prone to stinging and redness. Over-exfoliation basically sands away your mortar. Dermatologists often see patients with red, shiny, sensitive skin from using multiple exfoliating products at once. If your skin is inflamed, dial it way back on these.

• Strong actives without support: Potent ingredients like retinoids (retinol, tretinoin), benzoyl peroxide, high-percentage vitamin C or glycolic acid can transform skin but they also can cause barrier damage if used too aggressively. Retinoids in particular speed up cell turnover, which can cause peeling and microscopic barrier gaps (sometimes called the “retinol uglies” or “purge” at the start). Using these actives without moisturizing adequately or introducing them too fast is a recipe for a compromised barrier.

  Fragrance and preservatives in products can also trigger irritation in some people, further inflaming the skin. It’s not that these actives are “bad” it’s about how you use them. More on this in the routine chapter.

In short, the modern 10-step routine can backfire. When we bombard our skin with too many products – cleansers, peels, toners, serums, spot treatments, etc. we risk damaging the very barrier we’re trying to beautify. Simpler and gentler is often better for barrier health.

Internal & Environmental Factors: The Less Obvious Causes

It’s not only about skincare products. Lifestyle and environment play a huge role in skin barrier integrity:

• Poor nutrition or deficiencies: Your skin barrier needs certain nutrients as building blocks. For example, essential fatty acids (EFAs) like omega-6 and omega-3 are needed to produce the lipids (ceramides, etc.) in the stratum corneum. A diet very low in healthy fats can lead to dry, scaly skin and in extreme cases, an EFA deficiency causes eczema-like dermatitis with increased water loss.

  Vitamin C and Vitamin A are crucial for skin renewal; a lack of vitamin C impairs collagen formation and antioxidant defense, potentially leaving skin dehydrated and less resilient.

  Zinc is vital for wound healing and controlling inflammation, so low zinc can manifest as rough, easily irritated skin. In fact, a zinc deficiency is known to cause dermatitis and flaky rash in severe cases.

  Biotin (vitamin B7) and niacin (B3) are also important and deficiencies can cause dry, rashy skin. The bottom line: if your body is missing key nutrients, your skin barrier may weaken from the inside out. (I’ll dive deeper into diet in Chapter 4.)

  

• Dehydration: Not drinking enough fluids or losing too much (think intense exercise without rehydrating, or just living in a dry climate and forgetting to hydrate) can leave your skin poorly hydrated. When your body is dehydrated, skin cells don’t have the water content they need, and the barrier becomes more brittle. In fact, chronic dehydration is associated with reduced skin elasticity and a compromised barrier, essentially accelerating skin aging and fine lines. If you notice your skin looking dull and “crêpey,” ask if you’ve been drinking enough water.

  Tip: also check if you’re overdoing the caffeine or alcohol, which can dehydrate.

• Lack of sleep & disrupted circadian rhythm: Beauty sleep is a real thing. During deep sleep, your skin goes into repair mode – blood flow increases, and the barrier undergoes renewal and barrier lipids get replenished. If you’re chronically short on sleep, those repair processes may lag. Studies have shown sleep deprivation delays skin barrier recovery after irritation, basically, skin heals slower. Ever notice how a bad night’s sleep can leave your face looking dull or more inflamed? Over time, poor sleep correlates with more signs of skin aging and unevenness. Strive for a consistent 7–8 hours; your skin uses that time wisely!

• Chronic stress & high cortisol: Stress isn’t just in your head, it shows up on your skin. When you’re under psychological stress, your body releases cortisol (the stress hormone), which can impair skin’s barrier function. High cortisol can increase transepidermal water loss and delay barrier recovery. In one study, stressed individuals had significantly higher TEWL (water loss) and a weaker skin barrier compared to relaxed individuals. Have you ever gotten an eczema flare or breakout during a stressful week? That’s no coincidence, stress-induced barrier disruption plus inflammation is likely at play. Managing stress (through breathing, meditation, exercise, etc.) can actually improve your skin’s resilience. Think of stress as acid rain on your skin’s brick wall; over time it erodes the structure unless neutralized.

• Sun exposure (UV radiation): Excess unprotected sun is a major barrier saboteur. UV rays generate free radicals in the skin that damage cells and lipids. A sunburn is an acute example of barrier destruction. The red, peeling skin is essentially a compromised barrier that has to rebuild itself. Even low-level daily UV exposure depletes ceramides and causes inflammation. Always protect your skin with sunscreen, hats, etc. to minimize this. UV also ages the skin by breaking down collagen, another reason to shield yourself.

• Pollution and environmental toxins: City dwellers, take note – air pollution like particulate matter, smoke, smog can cling to skin and generate oxidative stress, which inflames and weakens the barrier. Pollutants can disrupt the skin microbiome balance as well. It’s been observed that people in high-pollution areas have higher rates of eczema and irritation. While you can’t avoid air quality entirely, gentle cleansing at night to remove pollutant particles and using antioxidants can help counter this.

• Climate: cold, wind, and low humidity: Dry climates or winter weather are notorious for causing “winter itch” or dry, flaky skin. That’s because low humidity air draws moisture out from the skin. Cold temperatures also reduce skin’s natural oil production. The result is a dried-out mortar between your skin cells. Indoor heating in winter compounds this by creating desert-like air in homes. Likewise, strong wind can physically abrade and strip the skin’s oils (ever had windburn on your face?). To combat this, you need to add extra moisture and occlusion like heavier creams, in such conditions and use humidifiers indoors.

• Age and genetics: Our barrier naturally changes with age. After age 40, skin produces fewer lipids. Studies show ceramide levels in the stratum corneum drop by over 30% as we hit middle age. Less mortar means more dryness and slower barrier repair. This is why mature skin often leans dry and sensitive. Additionally, some people inherit a tendency for weaker barrier. For example, individuals with eczema (atopic dermatitis) often have a genetic mutation in the filaggrin gene (FLG). Filaggrin is a protein crucial for forming the skin barrier; if it’s deficient, the barrier is “leaky.” A loss-of-function mutation in FLG leads to reduced filaggrin and a skin barrier defect, contributing to the chronic dryness and inflammation seen in eczema. Psoriasis is another condition where the barrier is disrupted as part of the disease process. Even without a diagnosed disorder, some people are simply born with more delicate skin that needs extra care, if you know your skin is reactive from childhood, you might be one of them.

It’s often a combination of these factors that lead to barrier woes. For instance, you might be using a harsh foaming cleanser (skincare trigger) and living in a low-humidity environment and not getting enough omega-3s. A perfect storm for a damaged barrier. The empowering part is that many of these factors are modifiable. By adjusting your routine and habits, you can remove the causes and let your skin rebuild.

Before we jump to solutions, let’s identify what kind of barrier damage you might have, since that can guide the approach.

Chapter 3: Dry, Reactive, or Breaking Out? How to
Diagnose Your Barrier Type

Not all barrier problems are identical. Your skin could be lipid-depleted (lacking oils), microbiome-disrupted, inflamed, or a mix of all. Identifying the primary type of barrier impairment can help you target the fix. Here are a few types and their clues:

Lipid Barrier Disruption

This is when the “mortar” between your skin cells is deficient or damaged.

Essentially, without enough lipids, your skin can’t hold water. It literally loses moisture to the air and becomes rough. If your face ever feels paper-thin and crinkly, that’s it. This type often comes with increased sensitivity too, because cracks in the mortar let irritants in easily. Restoring lost ceramides and oils is key here. In fact, studies show that a drop in ceramide levels directly causes dry, barrier-disrupted skin. Think of this type as “desert skin” parched and in need of moisture and fats.

Microbiome Imbalance (Dysbiosis)

Sometimes the issue isn’t lack of lipids, but rather an imbalance in the skin’s microbial flora. We co-exist with millions of bacteria on our skin. If the “good” bacteria get wiped out say by harsh antiseptics, overuse of antibiotics or certain preservatives or the environment changes (pH rises, barrier lipids change), bad microbes can overgrow.

Clues: This often shows up as inflammation – redness, little bumps or pimples, and even breakouts. You might not be dry; in fact, areas could be oily or have clogged pores since some bacteria like C. acnes flourish and trigger acne. Or you might experience unexplained rashes or itching. Dysbiosis can also exacerbate conditions like eczema or rosacea.

Typical scenario: you over-cleansed with harsh soap, stripping your acid mantle and killing many commensal (good) bacteria, now your skin is red, broken out, and anything you apply stings. People often misattribute it to an allergic reaction, but it can be a microbiome issue. Research shows an imbalanced microbiome can lead to redness, itchiness or dryness as common symptoms. To fix this type, you focus on gentle products that support the microbiome (proper pH, possibly probiotic skincare) and avoid antibacterial overkill. Skin might also benefit from fermented ingredients or lactic acid, which lower pH to a healthy range for good flora.

Inflammatory Barrier Damage

In some cases, the barrier is acutely inflamed due to a trigger that caused irritation for example, you had an allergic reaction to a fragrance, or you did a too-strong chemical peel. Here the issue isn’t just lack of oils or microbes, but that the skin is angry.

Clues: Burning, redness, heat, and swelling are obvious signs of inflammation. The skin may be less dry and more irritated e.g. it turns red and stings when you apply even simple products like sunscreen. There could be a rashy texture.

This type often overlaps with the others for instance, once lipids are stripped, inflammation follows. But it’s characterized by that irritation sensation; a feeling that your skin is “hot” or prickly. If you have rosacea or allergic eczema, you know this feeling well. In acute cases, you might recall a specific event:

Immune cells are in overdrive and the barrier integrity is compromised, leading to nerve exposure (ouch). The focus here is on soothing and calming the inflammation first, then restoring moisture. Think cool compresses, anti-inflammatory botanicals (like colloidal oatmeal or aloe). Once the redness subsides, you’ll likely notice dryness and can address barrier lipids.

Combination Types

Often, these conditions overlap. For example, someone with eczema has a genetic lipid barrier weakness and often dysbiosis and inflammation. Acne-prone individuals might have a disturbed barrier, sometimes from harsh acne treatments, plus microbial imbalance with C. acnes bacteria plus inflammation. If you’ve ever used too many actives, you might get the trifecta: dry flakes, breakouts, and redness altogether. Don’t be overwhelmed though as the approach in such cases is a holistic one: gently restore moisture, rebalance the flora, and calm the skin. Luckily, many remedies like proper moisturizers and probiotics address multiple issues at once.

How can you differentiate?

Here are a few self-check tips:

In practice, the strategies to fix these overlap a lot because the goal is to restore balance in all aspects. But identifying the dominant issue helps. For instance, if you conclude “I’ve just over-exfoliated, my skin is parched but not super red,” you’ll lean heavily into replenishing oils and humectants. If instead “My face is on fire after a reaction,” you’ll first use calming soaks and balms to bring the inflammation down. So take a moment to assess your own skin: is it crying out mainly from dryness, or from irritation, or both? Keep that in mind as we move into solutions.

Now you know what your barrier is, what’s been breaking it down, and which type of damage you’re dealing with. That’s already more than most skincare content will ever tell you. But knowing the problem is only half the journey. In Part 2, I go deep on the fix: what to eat to rebuild your barrier from the inside, the supplements worth taking (and the ones that aren’t), the herbal teas and DIY remedies that actually work, a complete daily routine, and the hormonal connection that explains why your skin behaves completely differently depending on where you are in your cycle. Part 2 is available to paid subscribers. If this post resonated, that’s your sign

Not dramatically. Not visibly. Just quietly, consistently, compounding — the same way interest builds in a savings account, except in reverse.

Collagen is the main structural protein in your skin — it makes up 75 to 80% of your dermis, the deep layer that gives skin its firmness, bounce, and thickness. Think of it as the scaffolding underneath everything you can see. When it’s abundant, skin looks plump, resilient, and smooth. When it starts to go, fine lines appear where there weren’t any. Skin loses its snap. The jawline softens. Nothing looks wrong exactly — things just start looking slightly less right.

By your mid-20s, the decline has already started.

That means it applies to you. Now. Not in twenty years.

And most women our age have no idea, because collagen is marketed as a problem for women in their 40s and 50s, which means the advice, the products, and the preventative habits are all aimed at people who are already playing catch-up. Nobody talks about the decade before the visible damage. Nobody explains that the choices you’re making right now — what you eat, how you sleep, how much sun you get, how much stress you carry, whether you’re using the right things or unknowingly dismantling your own collagen supply, are what your skin will look like at 35.

And then there’s the TikTok version of this.

Which tells you to buy collagen supplements. Add collagen powder to your coffee. Use a collagen mask. Take a collagen shot. Build your entire routine around a single word without ever explaining what the word means, how collagen actually works, or whether any of those products do what the caption claims.

I started wondering: is collagen banking actually real? Do the supplements work? Why does everyone’s “routine for younger skin” look identical — retinol, vitamin C, SPF, collagen supplements, twenty-seven serums, and yet the science seems more complicated than anyone is saying?

So the questions started.

I went down the rabbit hole — the actual research, not the brand-funded content. Studies of skin biopsies across age groups show that collagen synthesis begins measurably declining in your 20s. Chronic UV exposure triggers a specific class of enzymes called MMPs that actively break collagen down — not over decades, but after every single unprotected sun exposure. Chronic stress raises cortisol, which directly accelerates collagen degradation. A diet high in sugar triggers a process called glycation that stiffens and damages collagen fibres. None of this is reversible. But all of it is slowable, if you understand what’s actually happening.

Here’s what made me stop spiralling and start actually doing something: the research on prevention is genuinely more compelling than the research on reversal. Studies show that higher antioxidant and vitamin C intake in younger years correlates with measurably fewer wrinkles later in life. The women with the best skin in their 40s aren’t the ones who panicked at 42 and started treatments. They’re the ones who started protecting at 22 — before there was anything to fix.

The dermatologists call it collagen banking. Building the account while it’s still full, rather than scrambling to replenish it once it’s been drawn down.

The best time to start was five years ago. The second best time is now.

So: not should I care about collagen in my 20s, but what do I actually need to know and do — based on research, not TikTok?

After going through the studies, I finally have an answer. And there’s one habit almost everyone our age has that is quietly undermining their collagen faster than anything else. You’ll probably recognise yourself in it.

This is for you if you’re somewhere between vaguely aware that collagen matters and genuinely confused about what to do about it. Keep reading.

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Part 1 left you with a question.

Specifically: okay, I know my type — now what?

Because knowing you have vascular dark circles, or pigmented ones, or a structural shadow that’s more about your tear trough than anything you ate this week, is only useful if you know what that means for how you treat it. Part 1 was the identification. This is the action plan.

And this is where it gets specific in a way that most eye cream marketing never does. Not “use caffeine,” but why caffeine works for one type and does almost nothing for another. Not “eat better and sleep more,” but which nutrients actually show up in the dermatology research for under-eye circles, and what sleep position does to overnight fluid drainage in a way that most people have never been told.

Chapters 4 through 9 cover the daily triggers you can actually control, the lifestyle and nutrition changes with real research behind them, the natural remedies worth your time versus the ones that are mostly vibes, and — the chapter nobody includes; when to stop treating this as a skincare problem and get proper eyes on it.

The cold spoon in the freezer was never going to fix it. But for a lot of people, the right combination of the right things, matched to the right type makes a visible difference within weeks.

Let’s finish what Part 1 started.

PS: We also have a subscriber-only group chat where members discuss the deep dives, share their sleep journeys, and ask me questions directly. See you there.
Disclaimer: The information and opinions expressed above are current as of the date of this post and are subject to change without notice. Materials referenced above are provided for educational and informational purposes only. None of the above constitutes medical advice, a diagnosis, a treatment recommendation, or a substitute for consultation with a qualified healthcare professional. Always seek the guidance of your doctor or another qualified health provider with any questions you may have regarding a medical condition or sleep disorder.

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