Caught My Eye…

Body Temperature Is Your Most Underrated Sleep Tool

Sleep researchers talk about body temperature far less than they talk about screens, supplements, and sleep schedules. They should probably swap those priorities.

Your core body temperature needs to drop by approximately 1–1.5°C from its daily peak to initiate and maintain deep, slow-wave sleep. This isn’t a small adjustment, it’s a significant physiological shift that the body actively manages through a process called distal vasodilation: blood is sent to the hands and feet, where heat can radiate away from the body, cooling the core. This is why warm hands and feet are associated with faster sleep onset. The heat is redistributing from the centre outward.

Several things interfere with this process in ways that most sleep content doesn’t address:

A warm bedroom. The optimal sleeping temperature for deep sleep is approximately 18–19°C (65–67°F) for most people. Research from the Sleep Foundation and multiple sleep labs found that room temperatures above 24°C significantly increase waking during the night and reduce slow-wave sleep time. Sleeping hot is one of the most common and least discussed causes of fragmented sleep.

The luteal phase of the menstrual cycle. As covered in the sleep deep dive: progesterone raises resting body temperature by 0.3–0.7°C in the two weeks before a period. When the baseline is already elevated, the body has less temperature range to drop through on the way to deep sleep. This is the primary mechanism behind the sleep fragmentation that most women notice in the premenstrual window.

Alcohol. Alcohol initially causes peripheral vasodilation, it feels relaxing because it redistributes heat but as it metabolises, it disrupts the temperature regulation required for sustained deep sleep and produces arousal in the second half of the night.

A warm bath or shower 60–90 minutes before bed works paradoxically: it heats the skin surface, accelerating peripheral vasodilation, which speeds up the cooling of the core. The bath doesn’t make sleep better because it relaxes you. It makes sleep better because it accelerates the physiological temperature drop that deep sleep requires.

Practical for right now: make your bedroom colder than you think you need to. Research suggests most people sleep at temperatures 3–5°C higher than is optimal. The discomfort of a cool room lasts about two minutes before you’re under a duvet and the sleep is measurably better.

The Stress-Skin Connection Is a Loop, Not a Line

Most content on stress and skin treats it as a one-way relationship: stress raises cortisol, cortisol disrupts your skin. That’s true, but it’s only half the picture. The full picture is a feedback loop and understanding the loop changes what you do about it.

Chronic stress raises cortisol. Cortisol degrades collagen, increases sebum production, disrupts the skin barrier, and suppresses the overnight repair processes that depend on deep sleep and growth hormone. This produces reactive, acne-prone, dull, or inflamed skin.

Here’s the other half: skin conditions themselves activate the stress response. Dermatology research has consistently found that inflammatory skin conditions like acne, eczema, rosacea, psoriasis, elevate psychological stress, which in turn elevates cortisol, which worsens the skin condition, which elevates stress further. The loop feeds itself from both directions.

This explains why people with stress-driven skin conditions often find that topical treatments produce improvement but not resolution. The topical intervention is addressing the skin end of the loop without addressing the nervous system end. The cortisol that’s driving the barrier disruption, the sebum overproduction, or the inflammatory flare is being re-generated continuously by the stress loop that the product can’t reach.

Research from 2025 examining psychodermatology interventions found that cognitive behavioural therapy and mindfulness-based stress reduction produced measurable improvements in inflammatory skin conditions, independent of any topical treatment. The mechanism is direct: reducing HPA axis activation reduces the cortisol signal to the skin. Less cortisol means less sebum production, less barrier disruption, better overnight repair, less inflammation.

The most powerful single intervention for this specific pattern is sleep. A single night of sleep deprivation measurably elevates cortisol and inflammatory markers. Chronic poor sleep maintains the cortisol elevation that keeps the skin loop running. No topical product can compensate for what consistently disrupted sleep is doing to the hormonal environment the skin has to function within.

This is the real sequence:

The entry point to this loop, for most people, is sleep. Not a new serum.

The Exercise Snack Research Is Genuinely Interesting

“Exercise snacking,” short bouts of physical activity (typically 2–10 minutes) spread across the day rather than consolidated into one workout, has accumulated a surprisingly strong evidence base over the past two years, and it matters specifically for people who struggle to maintain longer exercise sessions.

A 2025 systematic review found that exercise snacks specifically short bouts of vigorous stair climbing, brisk walking, or bodyweight exercises performed 2–3 times per day produced measurable improvements in cardiovascular fitness (VO2max), blood sugar regulation, and insulin sensitivity comparable to longer, continuous moderate exercise. The key finding: accumulated short bouts appear to produce similar or equivalent metabolic benefits to a single longer session of equivalent total duration.

For women specifically, there’s an additional angle: the blood sugar spike that follows meals can be meaningfully reduced by a 2–5 minute walk within 30 minutes of eating. Research published in Sports Medicine found that post-meal walking (even very short duration) significantly blunted post-meal glucose responses compared to sitting. The mechanism: muscle contraction uses glucose directly from the bloodstream as fuel, reducing the amount of work insulin has to do.

This matters practically because the meal-to-meal blood sugar swings that drive cravings, energy crashes, and the luteal phase blood sugar instability I’ve covered repeatedly in Simply Salvia are most effectively managed at the point of the meal and not through general lifestyle changes that work on a longer timescale.

The honest caveat: exercise snacking is not a replacement for progressive resistance training for body composition, bone density, and long-term metabolic health. The evidence supports it as an effective strategy for people with limited time or access, or as an addition to a broader movement practice and not as a complete substitute. Walking after meals and taking the stairs consistently are genuinely useful habits with evidence behind them. They are not a replacement for 2–3 weekly resistance sessions.

The Inflammation Biomarker Most Young Women Have Never Heard Of

CRP (C-reactive protein) is a blood marker of systemic inflammation. It’s produced by the liver in response to inflammatory signals from anywhere in the body; infection, injury, autoimmune activity, or chronic low-grade inflammation from lifestyle factors. It’s included in standard blood panels in some countries and omitted in others, and most women in their 20s and 30s have never had it discussed with them.

Here’s why it matters:

Low-grade chronic inflammation, reflected in mildly elevated CRP is one of the most consistent underlying mechanisms in the conditions that most affect young women:

• Depression and anxiety (elevated inflammatory cytokines are found in a significant subset of both),

• Acne and inflammatory skin conditions,

• Menstrual irregularity and painful periods (prostaglandin-driven pain is an inflammatory process), and

• Insulin resistance and metabolic dysfunction.

A 2025 analysis found that CRP levels in young adults are rising, driven by increasing rates of ultra-processed food consumption, sleep disruption, sedentary behaviour, and chronic psychological stress. This isn’t a condition with obvious symptoms. It’s a background state of heightened immune activation that quietly makes all of the above conditions harder to manage and more severe.

The factors with the strongest evidence for reducing CRP in healthy young women:

These are the same interventions that show up across every category of women’s health research, not because wellness content keeps repeating the same things, but because chronic systemic inflammation is genuinely at the root of a wide range of conditions and these interventions address it at the source.

The things with the strongest evidence for raising CRP:

• Ultra-processed food,

• Sleep deprivation,

• Physical inactivity,

• Abdominal obesity, and

• Smoking.

These, too, are the same factors that show up repeatedly in the risk literature across multiple conditions. The biological mechanism connecting them all is inflammation.

If your GP runs a full metabolic panel and CRP isn’t included: ask for it specifically. A high-sensitivity CRP (hs-CRP) below 1 mg/L is low risk. 1–3 mg/L is moderate. Above 3 mg/L is elevated and worth investigating. It won’t be discussed unless you ask, but it tells you more about your background inflammatory state than most of the other markers routinely measured.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research roundup from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings

The Role Temperature Plays in Sleep Quality

Changes in sleeping energy metabolism and thermoregulation during menstrual cycle

Psychodermatology: Bridging Dermatology and Psychiatry

Positive impact of a 10-min walk immediately after glucose intake on postprandial glucose levels

The effectiveness of exercise snacks as a time-efficient treatment for improving cardiometabolic health in adults: a systematic review and meta-analysis

C-Reactive Protein: Clinical Relevance and Interpretation

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

Caught My Eye…

Cortisol Peaks When You Wake Up. Your Phone Makes It Worse.

When you wake up, your body produces a surge of cortisol - your highest cortisol output of the entire day. This is called the Cortisol Awakening Response (CAR), and it’s intentional. Cortisol in the morning mobilises blood sugar, activates the immune system, sharpens focus, and prepares you physiologically for the demands of the day. It is the biological equivalent of your body booting up.

This morning cortisol peak is important and healthy. The problem is what happens when you immediately amplify it before your nervous system has had time to regulate it.

Checking your phone within the first few minutes of waking floods your brain with social comparison, unresolved notifications, stressful news, and dopamine-seeking behaviour before your prefrontal cortex (the part of the brain responsible for rational decision-making and emotional regulation) has fully come online. It typically takes 15–30 minutes after waking for the prefrontal cortex to reach full functional capacity. Stimulating the amygdala (the threat and reward detection centre) with a phone screen before that window closes means starting the day in a reactive, slightly elevated-stress state that carries forward.

A 2024 study on morning digital media use found that checking phones within 10 minutes of waking was associated with higher reported stress and more fragmented attention for the remainder of the morning. The mechanism isn’t complicated: cortisol is already at its peak, the nervous system is in a sensitised state, and the phone is an effective cortisol amplifier.

The 30-minute phone-free window after waking isn’t a productivity hack. It’s giving the nervous system the time it needs to land from sleep before being asked to process stimulation. Morning light exposure in that same window, ideally outdoor if possible, has the strongest evidence for anchoring the circadian rhythm, supporting serotonin synthesis, and improving mood and focus for the hours that follow.

The Breakfast Research Has Been Saying This For Years. Most People Are Still Not Doing It.

The most consistent finding in breakfast nutrition research for women is so simple it sounds like it can’t be right: eating 25–30g of protein at breakfast produces better blood sugar control, reduces hunger and cravings for hours, and has measurable effects on what you eat for the rest of the day.

A University of Missouri study found that when women consumed high-protein breakfasts, they maintained significantly better glucose and insulin control than they did with lower-protein or no-protein meals, and the benefit extended beyond breakfast, with improved blood sugar control even after lunch. Research on premenopausal women found that increasing protein at breakfast to 30g reduced daily caloric intake by an average of 441 calories over 12 weeks and produced significant weight loss without any instruction to eat less. Just more protein at breakfast.

The mechanism: protein at breakfast triggers GLP-1 and PYY; the satiety hormones that signal fullness to the brain. These hormones take 15–20 minutes to reach the brain after eating, which is why eating quickly defeats the system. Protein stimulates these hormones more powerfully than carbohydrates or fat. It also stabilises blood sugar in a way that carbohydrate-heavy breakfasts (cereal, toast, pastry, fruit juice) don’t. Setting up stable energy for the morning rather than the blood sugar spike-and-crash that drives the 10am hunger and the need for caffeine to push through it.

The typical British and American breakfast is optimised for the opposite of this: fast, convenient, carbohydrate-heavy, low protein. A bowl of cereal and orange juice starts the day with a blood sugar spike before 8am and a crash by 10am. The tiredness, the craving, the difficulty concentrating mid-morning all of these are very often blood sugar consequences of the first meal, not signs that you need more coffee.

Why You Should Wait 90 Minutes Before Your First Coffee

Caffeine works by blocking adenosine receptors. Adenosine is the compound that accumulates in your brain while you’re awake and produces sleepiness -it’s the biological pressure that builds throughout the day and makes you tired by evening. Caffeine doesn’t remove adenosine. It sits in adenosine’s receptor seats, blocking the signal. When the caffeine clears (after 5–7 hours) the adenosine that accumulated while you were drinking coffee floods back in all at once, often producing the afternoon crash that prompts another coffee.

Here’s the part most people don’t know: adenosine levels are actually at their lowest when you wake up, because sleep cleared most of the previous day’s accumulation. For the first 60–90 minutes after waking, your cortisol peak is handling the alertness that caffeine would normally provide. Drinking coffee in this window isn’t giving your brain something it needs, it’s adding caffeine to a system that’s already running on its own alertness mechanism.

Neuroscientist Dr. Andrew Huberman’s popularisation of the “wait 90 minutes for coffee” protocol has research backing, even if the specific 90-minute number isn’t from a single definitive study. The evidence behind it: cortisol suppresses caffeine’s effectiveness (they both compete for similar arousal pathways), so caffeine consumed during the cortisol peak provides less benefit than caffeine consumed after it. Waiting until cortisol has begun its natural post-peak decline( typically 60–90 minutes after waking) means the caffeine is doing more useful work and the afternoon crash is less severe.

This doesn’t mean no coffee before 90 minutes will ever work. Caffeine still blocks adenosine receptors regardless of timing. But the effectiveness, the dependency curve, and the afternoon crash are all affected by when in the morning you drink it.

Skipping Breakfast Has Different Effects in Women Than Most Research Suggests

Intermittent fasting and time-restricted eating have strong evidence for metabolic health particularly in overweight and metabolically compromised populations. The 16:8 protocol (eating within an 8-hour window, fasting for 16 hours) has consistent research support for blood sugar regulation and weight management.

But there’s a sex-specific dimension that most of the content on intermittent fasting completely ignores. Most of the foundational IF research was conducted in men. Women’s hormonal systems, specifically the hypothalamic-pituitary-ovarian (HPO) axis that governs the menstrual cycle are more sensitive to caloric restriction and meal timing than men’s.

A 2025 review of time-restricted eating in overweight women found meaningful metabolic benefits but also flagged that aggressive fasting windows (over 16 hours) can activate the same stress responses in the HPO axis that underlie hypothalamic amenorrhoea (period loss in response to energy restriction). Cortisol rises with prolonged fasting. Elevated cortisol suppresses GnRH, the hormone that controls the reproductive cycle. In women who are already hormonally sensitive; those with irregular cycles, high stress levels, low body weight, or a history of disordered eating, extended fasting windows can disrupt the cycle.

Research on women specifically found that those who skip breakfast consistently show higher levels of cortisol and more menstrual irregularity than those who eat breakfast. The mechanism: overnight is already a prolonged fasting period, and extending it through skipping breakfast means the body is in a cortisol-driven fasting state well into the morning. For women whose hormonal health is stable and who aren’t showing any cycle disruption, moderate time-restricted eating (12–14 hour windows rather than 16+) appears metabolically beneficial with minimal hormonal risk. For women with irregular cycles, high stress, or hormonal sensitivity, skipping breakfast may not be the right intervention, regardless of its general evidence base.

This isn’t “intermittent fasting is bad for women.” It’s “the research was built on male participants and the female-specific data adds complexity that most fasting content doesn’t acknowledge.”

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research roundup from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings

Morning Light Exposure Affects Cortisol Levels and Stress Response

Protein-packed breakfast prevents body fat gain in overweight teens

Caffeine Science

Understanding Cortisol Hypothalamic Amenorrhea: The Science of Stress

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

Caught My Eye…

Berberine Is Not “Nature’s Ozempic”. A March 2026 Review Finally Said It Directly.

Berberine has had 100 million+ TikTok views as a natural alternative to Ozempic. The claim: it works on the same pathways, produces the same appetite suppression, and gives you the weight loss results of semaglutide without the prescription or the side effects.

A review published in the International Journal of Molecular Sciences in December 2025, summarised by Medical Xpress in March 2026, looked at this claim carefully and reached a clear conclusion: the comparison is an oversimplification that doesn’t reflect how berberine actually works, or how strong the evidence is.

Here’s the honest picture. Berberine is a plant compound that activates an enzyme called AMPK, which plays a role in regulating metabolism and improving insulin sensitivity. It does have genuine evidence for lowering blood sugar particularly in people with type 2 diabetes and some modest evidence for supporting weight loss over 8–12 weeks. These are real effects.

But Ozempic (semaglutide) is a GLP-1 receptor agonist. It directly mimics a gut hormone that tells your brain you’re full, dramatically suppresses appetite, slows gastric emptying, and produces an average weight loss of 15–20% of body weight in clinical trials. Berberine does not work through the GLP-1 pathway. It doesn’t suppress appetite in the same way. It doesn’t produce remotely comparable weight loss outcomes. The mechanisms are different, the effect sizes are different, and the evidence base is different.

What the March 2026 review specifically found: responses to berberine differ widely between individuals likely because its effects run through the gut microbiome, which varies enormously between people. One person’s berberine response is completely different from another’s in a way that doesn’t happen with semaglutide. The individualised, microbiome-dependent mechanism is interesting and worth more research. It is not the same mechanism as Ozempic.

What berberine does have evidence for: modest blood sugar reduction, some support for insulin sensitivity, potential gut microbiome benefits. What it doesn’t have evidence for: appetite suppression comparable to GLP-1 drugs, significant weight loss as a standalone intervention, long-term safety beyond 3–6 months.

If you’re taking it: the evidence doesn’t suggest it’s harmful at standard doses (500mg 2–3x daily) for most healthy adults. The evidence does suggest the “natural Ozempic” framing is marketing, not science. And there are specific groups who should avoid it entirely: pregnant or breastfeeding women, people on blood sugar or blood pressure medication, and people with clotting disorders.

Microplastics Are In Your Ovarian Follicular Fluid. Here’s What the Research Actually Says.

This is the one that wellness content gets very wrong in two opposite directions: either “microplastics are fine, the danger is overhyped” or “microplastics are destroying your hormones and fertility right now.” The actual research sits in a more specific and more unsettling place than either of those.

A systematic review published in Archives of Gynecology and Obstetrics in January 2025, covering 15 experimental studies, found that microplastic exposure significantly affects ovarian function, decreases fertility rates, and disrupts hormone levels in female subjects. A separate review in the International Journal of Gynecology & Obstetrics in October 2025 confirmed the pattern: microplastics and nanoplastics interfere with the hypothalamic-pituitary-ovarian axis (the hormonal control system that regulates the menstrual cycle) in ways that disrupt estrogen and progesterone production.

The most striking single finding: researchers detected microplastics inside human ovarian follicular fluid. The fluid that surrounds developing eggs. This means microplastics are reaching the immediate environment of egg development. The clinical implications of this aren’t fully established yet. But the fact that they’re present is not a small finding.

A meta-analysis published in August 2025 found that consuming food in plastic containers significantly increased microplastic contamination in pregnant women, and that microplastic content in the placenta correlated with worse pregnancy outcomes including intrauterine growth restriction.

The honest caveats: most of the reproductive health studies are in animals (mice, zebrafish, rats), not humans. Human studies exist but are fewer and typically smaller. The dose-response relationship (how much exposure is needed to produce harm) isn’t fully established. “Microplastics are present” is confirmed. “Microplastics are causing X level of harm in healthy women in their 20s” is still being quantified.

What this means practically - not catastrophically, but concretely:

These aren’t reasons for anxiety. They’re reasons for easy, low-effort swaps that reduce the highest-dose exposures while the research catches up.

The Vagus Nerve Trend Has Something Real To It. The Devices Being Sold Around It Have More Confidence Than Evidence.

Vagus nerve stimulation has gone from a clinical procedure for treatment-resistant epilepsy and depression to a TikTok wellness aesthetic involving ear seeds, special breathing devices, cold plunges, and $400 gadgets - in approximately 18 months.

The biology is real. The vagus nerve is the longest nerve in the body, running from the brainstem through the heart, lungs, and gut. It’s the primary conduit of the parasympathetic nervous system; the “rest and digest” counterpart to the “fight or flight” sympathetic system. Stimulating it activates anti-inflammatory pathways, slows heart rate, reduces cortisol output, and shifts the nervous system toward calm. A 2026 comprehensive review in Comprehensive Physiology confirmed that vagus nerve stimulation affects the brain’s arousal, emotion, and homeostatic networks through direct anatomical pathways.

The clinical evidence for implanted vagus nerve stimulators (for epilepsy, treatment-resistant depression, and PTSD) is solid. For non-invasive transcutaneous auricular VNS (taVNS), stimulating the vagus nerve through the ear, the evidence is growing and genuinely interesting. A 2025 placebo-controlled trial found significant reductions in stress, cognitive anxiety, and somatic anxiety with auricular VNS. A 2025 systematic review found non-invasive VNS significantly improved symptoms across gut disorders including IBS and inflammatory bowel disease. A 2022 trial found 50% improvement in self-reported sleep quality after one month.

The honest state of the evidence: non-invasive VNS shows real promise. Most studies are small. Effect sizes vary considerably between individuals. The consumer devices being sold, ranging from electrical ear clips to vibrating neck devices, are not the same as the devices used in clinical trials, and their efficacy hasn’t been independently validated. “The vagus nerve is real and stimulating it does things” is confirmed. “This £200 device will regulate your nervous system” is a different claim with much weaker evidence.

What does have good evidence for improving vagal tone without a device:

Sleepmaxxing: What the Trend Gets Right, and the One Thing It Gets Wrong

Sleepmaxxing - the Gen Z TikTok movement to optimise sleep through supplements, devices, and routines, has been described by the director of UC Berkeley’s sleep centre as Gen Z “reclaiming their right to a full night of sleep without embarrassment.” Which is genuinely good.

The things sleepmaxxing gets right:

The thing the trend gets wrong: the assumption that more optimisation tools equals better sleep. Mouth taping (covered in an earlier Between Saturdays; the 2025 PLOS One systematic review found it can be dangerous for people who mouth breathe due to obstruction, which is most people who mouth breathe). Sleep tracking devices creating anxiety about sleep scores - a documented phenomenon researchers now call “orthosomnia,” where sleep tracking itself causes sleep anxiety that worsens sleep quality. Stacking multiple supplements (magnesium + melatonin + L-theanine + ashwagandha + glycine) without understanding what each does and whether the combination makes sense. And taking magnesium, which does have good evidence for sleep quality, in the wrong form (magnesium oxide, the cheapest and most common, has the lowest bioavailability for neurological effects).

The sleepmaxxing principle is right. Sleep is the most foundational health intervention available and the most consistently undervalued. The one well-evidenced, accessible intervention that most people can add without any device or supplement: a consistent wake time, maintained even on weekends. Sleep research consistently finds that irregular sleep timing (varying by more than 60 minutes between weekdays and weekends) has measurable negative effects on metabolism, mood, and cognitive function - independent of total sleep hours. The sleep schedule is more powerful than the sleep gadget.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research roundup from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings

What to know about berberine, the so-called “nature’s Ozempic”

Impact of microplastics on female reproductive health: insights from animal and human experimental studies: a systematic review

A review of the impact of micro‐ and nanoplastics on female reproduction

A Review of Vagus Nerve Stimulation for Disease: Comprehensive Theory and Evidence for Mechanisms of Action

The Effects of Vagus Nerve Stimulation on Stress, Competitive Anxiety, and Depression in Elite Shooters

Caught My Eye…

Why Your 20s and 30s Are the Most Metabolically Important Decade of Your Life

This is not a scare story. It’s a reframe that the research supports and that almost no mainstream health content communicates properly.

Peak bone density is reached somewhere between the ages of 25 and 30. After that point, bone density can be maintained and protected, but it can’t be significantly increased. The bone density you build during your teens and twenties is what you’ll be drawing on for the rest of your life. Women who enter their 40s and 50s with higher bone density have a measurably lower risk of osteoporosis, fractures, and the cascade of health complications that follow, particularly after menopause, when estrogen decline accelerates bone loss.

Peak muscle mass follows a similar trajectory, peaking in the early 30s and declining gradually from around 35 onwards unless active resistance training maintains it. The Frontiers in Endocrinology January 2026 study I covered in the weight loss Short Dive confirmed that resistance training is the single most effective strategy for preserving lean muscle during a calorie deficit, but the same principle applies beyond dieting. Muscle built now is metabolic capital. It raises your resting metabolic rate, supports blood sugar regulation, protects joints, and is the most reliable predictor of independence and physical function in later life.

The 2026 women’s health trends report from Mira noted that women aged 25–30 are now the most active health trackers, and cited a growing research consensus that the habits built in your 20s and 30s become your biological reserves for your 50s and 60s. Muscle mass, bone density, cardiovascular fitness, metabolic health, gut microbiome diversity — all of these peak and plateau in early adulthood, and the maintenance trajectory from there depends heavily on the habits already in place.

What the practical version looks like: resistance training started in your 20s or early 30s is not just fitness. It’s bone and muscle maintenance that will matter more in 20 years than it does now. Adequate calcium and vitamin D during this same window supports the bone mineralisation that peaks before 30 and can’t be fully recaptured afterwards. The baseline tests worth considering in your 20s to early 30s: AMH (ovarian reserve, if fertility planning is relevant), a DEXA scan if bone density is a concern (family history, history of hormonal disruption or very low body weight), full metabolic and hormone panel, and vitamin D levels.

None of this is about anxiety. It’s about using information. The research on longevity is consistent on one point: the time to build the reserves is before you need them, not after.

You’re Probably Not Applying Enough Sunscreen. The Research on How Much Is More Specific Than You Think.

Most people who wear SPF daily are wearing significantly less than the amount the SPF rating was tested at. This is not a minor discrepancy. It changes the protection level in a meaningful way.

SPF ratings are calculated at a standard application density of 2mg per square centimetre of skin. For the face alone, this translates to approximately a quarter teaspoon (roughly 1.25ml) of SPF product. Research has consistently found that most people apply somewhere between a quarter and half of this amount in their actual daily routine, which means an SPF 50 product is effectively delivering somewhere between SPF 10 and SPF 25 in real-world conditions.

The implication is simple: if you’re wearing SPF 30 and applying about half the recommended amount, you’re getting approximately SPF 9–12. If your concern is photoageing (UV-driven collagen breakdown, hyperpigmentation, uneven texture) or skin cancer prevention, the application amount matters as much as the SPF number.

The practical guidance from dermatology research: a shot-glass amount (approximately 30ml) for the whole body when in a swimsuit. For the face, a nickel-sized amount, more than most people use. Two finger lengths of product from two fingers placed together (the “two-finger rule”) is a commonly cited estimate for face and neck combined.

Reapplication also matters more than most SPF content acknowledges. SPF degrades with UV exposure, sweating, and time. The standard guidance is reapplication every two hours in direct sun, or after swimming or heavy sweating. A morning application of SPF for a day spent mostly inside doesn’t require reapplication. A morning application for a day that includes extended outdoor time, a lunch break in the sun, or outdoor exercise does.

The SPF type matters less than application consistency and amount. A well-applied SPF 30 beats a poorly applied SPF 50 every time. The more important variables are: physical (mineral) or chemical filter based on your skin type and preference, broad-spectrum coverage (both UVA and UVB), and a texture you’ll actually use every day.

Rest Is Not the Opposite of Progress. The Research on Recovery Makes This Concrete.

The fitness and productivity culture version of health has a rest problem. Rest is framed as a necessary evil. The minimum required recovery before you can train again, the time when nothing useful is happening. The research says something different.

Here’s what is actually happening during rest and sleep after exercise:

The muscle tissue that was stressed during training is being repaired and reinforced by satellite cells (muscle stem cells). This process requires growth hormone, which, as the UC Berkeley research covered above shows, is primarily released during deep non-REM sleep. Without adequate sleep after training, the repair signal is dampened and the adaptation is incomplete.

Cortisol, the stress hormone that rises during intense training, is cleared during sleep. When the next training session happens before cortisol from the previous one has fully cleared, because recovery time was too short or sleep was too disrupted, cortisol accumulates. Chronically elevated cortisol promotes muscle breakdown (catabolism) rather than muscle building (anabolism), drives fat storage, and reduces the training adaptation you were working for.

Glycogen (the stored form of carbohydrate that powers high-intensity exercise) is replenished during rest, primarily through dietary carbohydrates eaten after exercise. Without adequate carbohydrates post-training and adequate rest time, glycogen stores remain depleted. The next training session starts at a lower energy substrate than the previous one. Performance declines, fatigue compounds, and the body starts pulling energy from muscle protein rather than stored fat, the opposite of what most training programmes are designed to produce.

The research on overtraining syndrome (the documented condition that occurs when training volume exceeds recovery capacity) finds that its primary symptoms are declining performance, persistent fatigue, disrupted sleep, elevated resting heart rate, and increased injury risk. These are the same symptoms that, in women, are also associated with low energy availability (not eating enough to support training volume) a well-documented condition in female athletes that suppresses the hormonal cycle and, in its more severe form, leads to bone stress injuries.

The practical version: rest days are not days when nothing is happening. They are days when the adaptation you trained for is actually occurring. The minimum effective dose of training for health and body composition is 2–3 resistance sessions per week. Adding more sessions without proportionally increasing recovery; sleep, nutrition, rest days does not produce proportionally better results. It produces overtraining.

For women specifically: in the late luteal phase, when sleep is already more fragmented and the nervous system is already more reactive, recovery from the same training stimulus takes longer. Protecting sleep, reducing evening training intensity, and not interpreting reduced capacity in this window as weakness are all evidence-informed responses to a documented physiological reality.

The Stress-Skin Feedback Loop, And the One Thing That Breaks It

I’ve covered the cortisol face content in the Short Dives. This is a specific addition to that picture that came from more recent research and is worth its own paragraph.

The relationship between stress and skin isn’t one-directional. Stress worsens skin through the cortisol mechanism; barrier disruption, increased sebum, impaired overnight repair. But skin conditions themselves then produce stress, which produces more cortisol, which worsens the skin condition further. Research has documented this bidirectional feedback loop in acne, eczema, and rosacea specifically, conditions where flares both cause and are caused by psychological stress, creating a cycle that’s genuinely difficult to break purely through topical intervention.

The finding that matters: a 2025 study specifically examining skin-related quality of life and stress found that psychological interventions, specifically cognitive behavioural therapy and mindfulness-based stress reduction produced measurable improvements in inflammatory skin conditions independent of topical treatment. This isn’t “your skin problem is in your head.” It’s that the HPA axis (the stress response system) is a direct regulator of skin inflammation, and interventions that reduce HPA activation produce skin improvements through that pathway.

The practical implication for anyone dealing with stress-driven skin: topical treatment matters and is worth doing properly. But if your skin consistently flares during high-stress periods and doesn’t fully respond to topical approaches, the HPA axis is likely a maintaining factor. Sleep, which is the most powerful cortisol regulator with the most evidence, is the intervention with the clearest mechanism for this specific pattern. Even single-night sleep deprivation measurably elevates cortisol and inflammatory markers and multiple consecutive nights of poor sleep drives the chronic cortisol elevation that makes stress-driven skin conditions persistent rather than episodic.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research roundup from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings:

Resistance training as a key strategy for high-quality weight loss in men and women

Mira’s Women Heath Trends Report: 6 Trends Reshaping 2026 and Beyond

How Much Sunscreen Are We Really Getting?

Why Does Sunscreen Only Last 2 Hours?

Scale-Free and Multifractal Time Dynamics of fMRI Signals during Rest and Task

Cortisol rises during intense workouts. Is that really a bad thing?

What is psychodermatology?

The Skin–Brain–Exposome Axis in Stress-Sensitive Dermatoses: A Narrative Review

Microbiome-Skin Axis in 2026

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

Caught My Eye…

Ultra-Processed Food and Mental Health: The Evidence Has Reached a Different Level

The research on ultra-processed food and mental health has been building for several years. It has now reached a point where it is difficult to describe the findings as preliminary.

A longitudinal study of over 30,000 participants, published in 2025 and followed over an average of 12.6 years, found that those with high ultra-processed food intake had increased risk of mental disorders including depression and anxiety. A review published in Oxford Journal in August 2025 synthesised multiple large cohort studies and found a consistent dose-response relationship: the more ultra-processed food consumed, the higher the risk of depression and anxiety, across populations and across study designs. One earlier cohort study found that a 10% increase in ultra-processed food intake relative to daily calories was associated with a 21% higher risk of developing depression symptoms over a five-year follow-up period.

The Harvard Nurses’ Health Study II finding is probably the clearest single data point: women in the top fifth of ultra-processed food consumption had a 50% higher risk of developing depression than those in the bottom fifth. The link was particularly strong for artificially sweetened products.

The mechanism runs through several routes simultaneously. Ultra-processed foods are low in the dietary fibre that gut bacteria need to produce short-chain fatty acids, which means the gut microbiome becomes less diverse, inflammatory cytokines rise, and the gut-brain axis produces pro-inflammatory signals in the brain. Ultra-processed foods are also typically low in the micronutrients; magnesium, zinc, B vitamins, omega-3s, that serve as cofactors for neurotransmitter synthesis. Without them, serotonin and GABA production is impaired at the chemistry level.

A scoping review published in Frontiers in Nutrition in January 2026 made the lipid metabolism angle explicit: ultra-processed foods alter brain lipid composition over time in ways that affect the structure and function of neuronal membranes, particularly in regions involved in mood regulation. This is a structural change and not just a nutritional deficiency.

Two caveats worth knowing: most of the studies are observational, meaning they show a consistent association, not a confirmed causal direction. People with depression may also be more likely to reach for ultra-processed food, not only the other way around. A 2025 cross-sectional study in Iran explicitly noted that women may be more vulnerable than men to the mental health effects of ultra-processed food consumption, suggesting the association is sex-specific in ways that warrant further investigation.

What the evidence doesn’t support: the idea that eating one ultra-processed food item causes depression. What it does support: that a diet consistently high in ultra-processed food creates a biological environment, through the gut microbiome, through chronic inflammation, through micronutrient depletion, that makes depression and anxiety more likely over time. And that women, specifically, may be more sensitive to this effect.

The Scale Is the Worst Measure of Progress. Here’s What to Use Instead.

This one is short because it doesn’t need to be long. It needs to be said clearly.

The number on the scale is measuring your total mass — including bone, muscle, organs, water, and the contents of your digestive system at that moment. It is not measuring fat loss. It is not measuring health. It is not measuring body composition. It is not stable from day to day, from morning to evening, or from week one to week two of any given month.

The research on why scales mislead is particularly relevant for women because of water retention. Progesterone promotes fluid retention in the luteal phase, which can add 1–3kg of water weight in the two weeks before a period. This is not fat. It reverses within days of menstruation starting. A woman who has genuinely lost fat and built muscle through three weeks of training can step on a scale in the late luteal phase, see a number higher than when she started, and conclude that nothing is working. When the reality is the exact opposite.

The measures that tell you more:

• How your clothes fit: specifically how the waist and hip of the same clothing item sits over time, which is a body composition measure, not a weight measure

• Progress photos taken in consistent lighting and positions across weeks and months. Visual changes in body composition that the scale won’t show

• Performance measures: how much you lift, how far you walk without fatigue, how your resting heart rate changes over time

• Energy and sleep quality: if your energy is higher and your sleep is better, your metabolic health is improving regardless of the scale

• How you feel across your cycle: if PMS symptoms are reducing, if energy is more consistent across the month, the dietary and lifestyle changes are working

If you track weight at all, the most useful approach is to weigh in the same conditions daily (same time of day, same level of hydration) and look at the rolling 7-day average rather than the daily number. The 7-day average smooths out the hormonal water retention, the digestive fluctuations, and the noise of day-to-day variation. The trend over 4–8 weeks is the signal. The daily number is mostly noise.

The deeper point: the scale measures one thing (mass) and we use it to measure a completely different thing (progress). These are not the same measure. Replacing a bad measure with better ones is not giving up. It’s doing it properly.

Meal Timing: The Research That Doesn’t Get Enough Attention

The nutritional research has for years focused almost entirely on what to eat. More recently, it’s started asking when, and the findings are interesting enough to be worth knowing.

The short version: when you eat matters, and it matters more in certain windows of the day than others. Here’s the research that’s accumulated:

Breakfast protein reduces post-meal glucose spikes all day.

Studies show that a high-protein breakfast (25g+ of protein) reduces the glucose response not just to that meal but to subsequent meals throughout the day. The mechanism: early morning protein intake primes the insulin response and sets a metabolic tone that carries through. A high-carbohydrate breakfast (cereal, toast, fruit juice) does the opposite. It starts the blood sugar rollercoaster early and the instability compounds.

Insulin sensitivity is highest in the morning, lowest in the evening.

This is a circadian rhythm finding with direct dietary implications. Your body handles carbohydrates more efficiently in the first half of the day than the second. A large, carbohydrate-heavy meal at 9pm produces a larger and more prolonged glucose response than the same meal eaten at 12pm. This is why shifting calorie-dense, carbohydrate-rich eating earlier in the day and making dinner lighter on carbohydrates and heavier on protein and vegetables, supports better metabolic health and body composition without necessarily reducing total calories.

Eating too fast removes the satiety signal.

Satiety hormones (GLP-1, PYY) take approximately 15–20 minutes to reach the brain after eating begins. A meal eaten in 7–10 minutes finishes before the fullness signal arrives. A cohort study of 59,000 people found that self-reported fast eaters had significantly higher rates of metabolic syndrome, independent of total calorie intake. Eating slowly is not a wellness affectation. It’s working with the timing of your own hormones.

Not eating after 8–9pm supports overnight cortisol rhythm and sleep quality.

Late-night eating elevates blood sugar during the overnight period, which can trigger cortisol releases to regulate it (particularly if glucose drops low), which fragments sleep. The same mechanism covered in the Between Saturdays sleep edition: the 3am waking that many women experience in the luteal phase is partly a blood sugar event.

None of this requires a rigid meal schedule. It requires broadly aligning eating with the body’s daily rhythms: protein earlier, carbohydrates earlier, dinner lighter and earlier when possible, and meals eaten slowly enough for the satiety system to do its job.

Why You’re Hungrier in the Second Half of Your Cycle, And Why That’s Not a Flaw

This one is a direct follow-up to the weight loss Short Dive and worth saying again in plain language because it gets misunderstood so consistently.

In the two weeks after ovulation — the luteal phase, your resting metabolic rate increases. Your body is burning approximately 100–500 more calories per day at rest compared to the first half of the cycle. This is driven by progesterone and by the body’s preparation for a potential pregnancy, which requires additional energy reserves. The hunger that goes with this is the body accurately signalling a real increase in energy demand.

Research has confirmed that caloric intake increases by this amount in the luteal phase in studies tracking food intake across the cycle. Women are not imagining the increased appetite. They are not losing their discipline. Their body is asking for more fuel because it is genuinely using more fuel.

The problem is not the hunger. The problem is what tends to satisfy it: high-GI carbohydrates and sugar, because the blood sugar instability of the luteal phase (progesterone promotes mild insulin resistance) drives cravings for fast glucose. Eating more refined carbohydrates in this phase produces bigger blood sugar spikes and crashes, which produce more cravings, which produce more eating. A cycle that has nothing to do with willpower and everything to do with blood sugar chemistry.

The answer is not to resist the hunger. It is to satisfy it with foods that don’t restart the blood sugar loop: protein-dense meals, complex carbohydrates with fibre, fat sources that slow digestion. Eating more in the luteal phase is appropriate. Eating more chocolate and crisps specifically because the blood sugar crash is signalling an emergency is the version that’s worth redirecting.

If you track your intake and see a consistent increase in the luteal phase every month, that’s not failure. That’s the data confirming what the research says. The goal is to meet the increased energy demand in a way that doesn’t compound the blood sugar instability that’s already making this phase harder.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research roundup from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings

The Impact of Ultra-Processed Foods on Depression and Anxiety: A Literature Review

Ultra-Processed Foods and Mental Health: What the Research Actually Says

Ultra-processed foods may increase risk of depression

Neurobiological insights into the effects of ultra-processed food on lipid metabolism and associated mental health conditions: a scoping review

The Association between Ultra-Processed Foods and Depression, Anxiety and Sleep in Adults: A Cross-Sectional Study in Iran

Dietary energy intake across the menstrual cycle: a narrative review

Caught My Eye…

The Brain Circuit That Builds Your Muscle While You Sleep — UC Berkeley Just Mapped It

Most people know sleep is important. Fewer people know exactly why, in the specific, biological, this-is-the-mechanism sense. A study published in the journal Cell in September 2025 and summarised by ScienceDaily in March 2026 is one of the clearest answers yet, and it matters for anyone who exercises, anyone trying to change their body composition, and anyone who’s ever wondered why bad sleep makes everything harder.

Researchers at UC Berkeley mapped the neural circuits in the hypothalamus (the brain region that controls hunger, temperature, and hormone release) that control the release of growth hormone during sleep. What they found is that deep, non-REM sleep (the early, restorative phase of sleep that happens in the first few hours of the night) is the primary trigger for growth hormone surges. Not the only trigger, but the main one. And growth hormone is not just about growing taller as a teenager. In adults, it builds and repairs muscle tissue, strengthens bones, regulates fat distribution, supports blood sugar management, and plays a central role in metabolic health. Low levels are linked to muscle loss, belly fat accumulation, insulin resistance, and faster biological ageing.

The study also uncovered a feedback mechanism: as growth hormone builds up during sleep, it signals the brain region that controls alertness, which eventually pushes the body toward waking up. This explains why both too little sleep and disrupted sleep (the kind where you fall asleep but don’t get sustained deep sleep) both reduce growth hormone output: the feedback loop needs uninterrupted time to run its full cycle.

As the researchers put it, sleep is not passive downtime between the real business of being awake. It is active, essential biology — the period where the body runs its repair and maintenance programme, and growth hormone is the main tool it uses.

What this means practically: if you train and you’re not sleeping, you are working against yourself in a way that no supplement, no protein intake, and no training programme can fully compensate for. The muscle repair that happens in the gym requires growth hormone. Growth hormone requires deep sleep. That’s the chain. Cutting sleep to make time for more training is one of the more common and counterproductive trade-offs in fitness culture.

The finding is also relevant specifically for women in the luteal phase of the menstrual cycle (the two weeks before a period) where progesterone raises body temperature and fragments deep sleep specifically. During this phase, growth hormone output is lower not because of anything you’re doing wrong, but because the hormonal environment is making it harder to reach and sustain deep non-REM sleep. More sleep time in this phase, cooler sleeping environment, and avoiding alcohol and intense late-evening exercise are the most direct ways to protect the deep sleep that’s being most disrupted.

Your Gut Microbiome Is Showing Up On Your Face. The Mechanism Is More Direct Than You Think.

The gut-skin axis (the idea that gut health affects skin health) has been circulating in wellness content for several years. Like most wellness topics that go viral, it’s been both overstated (every skincare problem has a gut cause, take this probiotic) and undersold (the actual mechanism is more interesting than the vague content suggests).

A systematic review published in Microorganisms in December 2025 pulled together the current state of the evidence, covering atopic dermatitis, psoriasis, acne vulgaris, rosacea, chronic urticaria, and melasma, and found that for all of them, there are consistent associations with gut microbiome composition.

The mechanism isn’t a mystery. It runs through several overlapping pathways:

When gut microbiome diversity is low (driven by low-fibre diets, antibiotic use, chronic stress, or poor sleep) the gut produces fewer short-chain fatty acids (SCFAs). SCFAs are the compounds that gut bacteria make when they ferment dietary fibre, and they serve as a primary fuel source and anti-inflammatory signal throughout the body, including in the skin. When SCFA production drops, systemic inflammation rises. Systemically elevated inflammation makes skin more reactive, impairs the skin barrier, and makes inflammatory skin conditions more likely to flare.

The second pathway is direct: the same inflammatory cytokines that circulate when gut dysbiosis is present show up in skin tissue and activate inflammatory cascades there. For acne specifically, research has found that people with acne have measurably different gut microbiome compositions than people without it, and that restoring gut diversity reduces inflammatory acne in a subset of cases.

The third pathway is relevant specifically for hormonal skin issues: the estrobolome (the collection of gut bacteria that metabolise estrogen) regulates how much estrogen is cleared from the body. When gut diversity is low, estrogen clearance is impaired, circulating estrogen rises, and the hormonal acne driven by estrogen dominance worsens. This is the direct route from gut health to jawline and chin breakouts in women.

The practical implication is not that every skincare problem has a gut solution. It’s that for inflammatory skin conditions that aren’t fully responding to topical treatment (persistent acne, rosacea, eczema, reactive or red skin) the gut environment is worth looking at as a contributing factor. The dietary pattern that most consistently supports gut microbiome diversity: high-fibre eating from varied plant sources, fermented foods (kefir, kimchi, yoghurt, sauerkraut), reduced ultra-processed food, consistent sleep, and stress management. None of these are dramatic interventions. Together, they create the conditions in which a diverse gut microbiome can do its job, including the job of keeping your skin less inflamed.

Exercise for Depression and Anxiety Just Got Its Strongest Evidence Yet. The Finding About Type Matters.

There is now more research supporting exercise as a treatment for depression and anxiety than there is for many approved medications. That statement is not an exaggeration.

A systematic umbrella review published in the British Journal of Sports Medicine in February 2026, the most comprehensive analysis of this evidence to date, synthesised 57 pooled data analyses covering 800 individual studies and 57,930 participants. The pooled effect size for exercise on depression was large (standardised mean difference of −0.97). For anxiety, it was medium to large (SMD −0.66). The authors concluded that exercise may be “one of the most powerful treatments” for both conditions, and recommended it as a first-line intervention alongside therapy and medication, not after them.

What this means is worth sitting with: a 2026 review of 800 studies, involving nearly 58,000 people, found that exercise has a large effect on depression. Not a small supportive effect. A large clinical effect comparable to, and in some analyses exceeding — psychological therapy alone.

The finding about type of exercise is the part that matters most for the Simply Salvia audience:

Aerobic exercise, resistance training, and mind-body practices (yoga, tai chi) all showed significant benefits for depression. A separate meta-analysis published in early 2026 found that meaningful clinical improvement in depression and anxiety was observed at exercise volumes well below the WHO weekly guidelines — meaning two short sessions a week produced real effects, and pushing to five sessions a week didn’t add proportionate benefit. The best exercise for mental health is the one you actually keep doing.

There’s also a finding specifically for women: a 2025 study in the Journal of Clinical Medicine found that a resistance training programme significantly reduced depressive symptoms in women, independent of aerobic exercise. The mechanism: resistance training reduces inflammatory cytokines (specifically IL-6 and TNF-alpha), raises BDNF (brain-derived neurotrophic factor, a compound that supports brain plasticity and mood), and produces consistent hormonal changes that support mood regulation. The effect was significant with just two to three sessions per week.

For anyone who’s been in a low period and felt too depleted to exercise: the evidence suggests that starting at a low volume; two sessions per week, moderate intensity produces real and measurable mood effects. The hurdle to get there is real. The effect on the other side of it is also real.

Magnesium: Why Women Are More Deficient, and What the Research Now Says About It

Magnesium is one of the more well-evidenced supplements in the research and one of the most overlooked in general nutrition conversation. A narrative review published in PMC in July 2025, specifically examining sex-based differences in magnesium metabolism found something important: women have lower dietary magnesium intake than men across most populations, and the hormonal fluctuations of the menstrual cycle create additional demand for magnesium that isn’t reflected in the standard recommended daily intake.

Why does this matter? Because magnesium is involved in over 300 enzymatic reactions in the body. The ones most relevant for women specifically:

GABA receptor activation. Magnesium activates the GABA-A receptor system, the same system that progesterone’s metabolite activates, and the same system that targeted by anxiety medications. When magnesium is low, GABA support is lower, the nervous system is more excitable, and anxiety, restlessness, and difficulty sleeping all increase. When magnesium falls (as it does in the late luteal phase, when progesterone drops), the GABA gap widens. Supplementing magnesium in the late luteal phase partially fills this gap.

PMS symptom reduction. Research has consistently found that 300mg of magnesium daily reduces PMS symptoms, specifically bloating, mood changes, and anxiety. A 2026 guide from Mito Health noted that combining 300mg magnesium with 30mg B6 reduces PMS symptoms by approximately 60%, because B6 amplifies magnesium’s absorption at the cellular level and independently supports serotonin and GABA synthesis.

Muscle relaxation and cramping. Magnesium relaxes smooth muscle including uterine smooth muscle. This is the mechanism behind its effect on menstrual cramping. It also explains why magnesium deficiency is associated with more severe cramping: the muscle is less able to relax between contractions.

Blood sugar regulation. Magnesium is required for insulin receptor function. Low magnesium is associated with insulin resistance which creates worse blood sugar instability, which drives the energy crashes and carbohydrate cravings of the luteal phase. Correcting magnesium deficiency supports insulin sensitivity and smooths the blood sugar rollercoaster that makes the premenstrual week harder.

Sleep quality. Magnesium activates GABA, which is why it promotes the nervous system calm that supports sleep initiation. Magnesium glycinate specifically (the form with highest bioavailability for neurological effects) has the most consistent evidence for improving sleep quality and reducing sleep onset time.

The standard blood test for magnesium (serum magnesium) only measures about 1% of the body’s total magnesium stores and is notoriously unreliable for detecting true deficiency. This means you can test as “normal” and still be functionally deficient. Symptoms of low magnesium; fatigue, irritability, muscle cramps, poor sleep, PMS, are also the symptoms most commonly attributed to stress or “just being a woman.” They are worth taking seriously.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research roundup from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings

What’s striking, once you look at the research side by side, is not just that stress affects everything. It’s that it does so through predictable pathways. And those pathways explain why stress feels the way it does and why it accumulates in ways that are easy to dismiss until they’re not.

Caught My Eye…

Stress and the Heart: The Risk That Builds Without Symptoms

There’s a version of cardiovascular risk that doesn’t feel like risk.

A large pooled analysis of nearly 200,000 individuals looked at what happens when people live under sustained job strain; high demand, low control. Over time, those individuals had a 23% higher risk of developing coronary heart disease.

Not dramatically higher. But consistently higher. And importantly, higher even after accounting for the usual explanations like smoking, weight, socioeconomic factors.

The mechanism is not a single trigger. It’s repetition.

Chronic stress keeps the body in a state of low-grade activation:

• Cortisol remains elevated longer than it should

• Blood pressure resets slightly higher

• Inflammatory signaling becomes more persistent

• The autonomic nervous system leans sympathetic instead of balanced

None of these changes are extreme enough to notice day-to-day. But over years, they alter the baseline the heart operates within.

The important shift here is conceptual: stress is not just an emotional experience. It becomes a physical environment the cardiovascular system has to function inside.

The Immune System: Why Stress Can Help — Until It Doesn’t

Stress is not inherently harmful.

A meta-analysis spanning over 300 studies shows that acute stress, the short-lived kind, actually enhances certain immune functions. It mobilizes immune cells, increases inflammatory readiness, and prepares the body for potential injury or infection.

This is the stress response working exactly as designed.

But the system is built on a cycle: activation, then recovery.

When stress becomes chronic, the recovery phase disappears. And the immune system shifts in a different direction entirely.

Instead of heightened readiness, you see:

• Suppressed cellular immunity

• Reduced antibody responses

• Impaired ability to regulate inflammation

The system doesn’t stay “on.” It becomes dysregulated.

This explains something people often notice but don’t connect: why periods of prolonged stress are often followed by getting sick, slower recovery, or persistent low-level fatigue. The immune system hasn’t failed — it’s been operating without reset.

Stress and Sleep: When the Body Refuses to Power Down

Sleep is where stress becomes visible.

In a large longitudinal analysis designed to approximate a trial, researchers tracked how changes in job strain influenced sleep over time. When stress increased, the likelihood of developing new insomnia symptoms rose significantly. When stress decreased, those symptoms were less likely to persist.

What this shows is direction.

Sleep disruption isn’t random, and it isn’t purely behavioural. It is often a direct reflection of physiological arousal that hasn’t resolved.

Under chronic stress, the body struggles to transition into the state sleep requires:

• Cortisol remains elevated later into the evening

• Sympathetic nervous system activity stays higher

• The usual “drop” in arousal that initiates sleep is blunted

The result is familiar: difficulty falling asleep, fragmented sleep, waking without feeling restored.

The key detail here is that when stress changes, sleep follows. The system is still responsive, it’s just responding to the signal it’s being given.

Stress and Depression: A System That Feeds Itself

One of the most persistent misconceptions about stress and mental health is that the relationship runs in one direction.

A longitudinal study in young adults showed something more complex. Perceived stress predicted increases in depressive symptoms over time but depressive symptoms also predicted increases in perceived stress.

This creates a feedback loop.

• Stress lowers mood by altering neurotransmitter balance, sleep, and energy regulation.

• Lower mood reduces resilience and increases cognitive load.

• Reduced resilience makes the same external demands feel more overwhelming.

The environment hasn’t changed. The internal response has.

This is why stress-related mental health patterns often feel difficult to break. They are not a straight line from cause to effect. They are a system reinforcing itself from both directions.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research round-up from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings:

Work stress can raise risk of heart attack by 23%, study finds

Immunology of Stress: A Review Article

Change in Job Strain as a Predictor of Change in Insomnia Symptoms

Depressive Symptoms, Perceived Stress, Self-Compassion and Nonsuicidal Self-Injury Among Emerging Adults

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

Caught My Eye…

The Premenstrual Energy Crash Has a Name, a Mechanism, and It’s Not “Just PMS”

Most women are familiar with the pattern: two weeks before your period, something shifts. Energy drops. Motivation drops. Cognitive tasks that felt easy feel effortful. Sleep doesn’t seem to restore the way it usually does. The body feels heavier. This window, roughly days 22 through 28, is usually labelled “PMS” and attributed, with a kind of vague handwave, to hormones.

What the research has been establishing, piece by piece, is a much more specific biological picture that deserves a more specific name and a more specific response.

The mechanism runs through several simultaneous pathways:

The GABA withdrawal pathway. Progesterone’s metabolite allopregnanolone activates GABA-A receptors, the same receptors that benzodiazepines act on. In the late luteal phase, as progesterone falls sharply, allopregnanolone levels fall with it. For women whose nervous systems have upregulated sensitivity to progesterone during the luteal phase, the withdrawal produces a rebound arousal state that looks and feels like anxiety, insomnia, and an inability to wind down. This is the neurochemical reality behind what women describe as “everything feels too loud” or “I’m wired but exhausted.”

The serotonin connection. Oestrogen supports serotonin synthesis. As oestrogen drops in the late luteal phase, the serotonergic buffer on mood and anxiety reduces. The brain is simultaneously losing its primary inhibitory support (GABA via progesterone) and its primary mood-stabilising support (serotonin via oestrogen) in the same 5–7 day window.

The sleep fragmentation. As covered in Deep Dive: Why You’re Always Tired — Even When You Sleep Enough: late luteal sleep is objectively more fragmented, with reduced slow-wave sleep and more nocturnal arousals. The fatigue that compounds through this window isn’t imagined. You’re sleeping lighter and waking more, on a cycle that’s driven by the hormonal withdrawal, not by behaviour.

The blood sugar instability. Progesterone promotes insulin resistance in its dominant phase. As it withdraws rapidly in the late luteal phase, blood sugar regulation can become temporarily unstable. Research has found that women in the late luteal phase have different glucose responses to the same meal than in their follicular phase, and that the 3am waking that’s common in this window is partly driven by nocturnal blood glucose management.

Understanding this combination explains why the typical advice “take ibuprofen for the cramps, it’ll pass,” doesn’t address most of what’s happening. The fatigue, anxiety, insomnia, and cognitive difficulty of the late luteal phase are driven by four specific biological mechanisms that respond to four different interventions:

For the GABA withdrawal: magnesium glycinate in the evening, which activates GABA-A receptors and partially fills the gap left by falling allopregnanolone. Reducing alcohol completely as alcohol compounds GABA withdrawal rather than relieving it.

For the serotonin drop: regular moderate exercise during this phase, which upregulates serotonin synthesis independent of oestrogen. Morning light exposure for its serotonergic effects.

For the sleep fragmentation: earlier bedtime, cooler environment, no high-intensity training in the evening, no alcohol.

For the blood sugar: a protein-and-fat-inclusive dinner, no high-GI snacking in the late evening, consistency in meal timing.

None of this eliminates the late luteal window as a harder stretch. What it does is reduce how much harder it is and shift it from an experience you’re just waiting to survive into one you have a biological map for.

Eating Speed and Metabolic Health: The Research Most People Haven’t Heard

This one is simple, well-established in the research, and almost completely absent from mainstream nutrition conversation.

Eating speed — specifically, eating fast is independently associated with higher rates of metabolic syndrome, obesity, insulin resistance, and type 2 diabetes. Not because fast eaters eat more (though they often do, more on that). But because of a hormonal mechanism that operates on a slower timescale than most people’s meals.

The mechanism: satiety hormones primarily GLP-1, PYY, and leptin are released by the gut in response to food, but they take approximately 15–20 minutes from the start of eating to reach the brain at levels that register as fullness. If a meal is eaten in 7–10 minutes, the satiety signal arrives after the meal is already finished. The brain doesn’t receive the “we’re full” signal until the stomach is already past comfortable capacity.

A landmark Japanese cohort study of more than 59,000 people found that self-reported fast eaters had significantly higher rates of obesity and metabolic syndrome than slow or normal-speed eaters, independent of total calorie intake and after adjustment for confounders. Multiple meta-analyses have since confirmed the association.

For women specifically, there’s a cycle-linked dimension: appetite and eating speed both change across the menstrual cycle. Studies have found that total caloric intake increases in the luteal phase by 100–500 calories per day on average, driven by progesterone and by the body’s increased metabolic demands in the second half of the cycle. Eating speed may also increase in this phase, when cravings are more pronounced and the impulse to eat quickly is higher.

The practical intervention requires no calorie counting, no food elimination, and no expensive supplements. It is simply: slow down. Put the fork or spoon down between bites. Chew fully before swallowing. Aim for a meal that takes at least 15–20 minutes. This gives the satiety signalling system time to do the job it was designed for.

Research on mindful eating specifically has found that slowing eating speed reduces total calorie intake at a meal, improves post-meal satiety ratings, and in longer-term studies reduces BMI and metabolic risk markers. The mechanism is purely physiological, not psychological. The brain needs time to receive the message the gut is sending.

In a food environment designed to encourage fast consumption; grab-and-go packaging, working lunches, screen eating, this is a more subversive intervention than it sounds.

Your Kidneys Affect Your Skin. The Connection Nobody Talks About.

This one surprises people. The skin and the kidneys don’t seem obviously related. But the kidney-skin connection is well-documented in dermatology.

The kidneys’ primary role is filtration: removing waste products, excess fluid, and toxins from the blood. When kidney function is impaired, even subclinically, at levels below what shows up in routine blood tests, waste products accumulate in the bloodstream at levels that have direct effects on skin.

The two most relevant waste products for skin appearance:

Urea. Normally excreted in urine, urea builds up in the blood when kidney filtration is compromised. At elevated blood levels, urea deposits in skin tissue and contributes to dryness, itching (pruritus), and a dull, pallid complexion. Topical urea in low concentrations (2–10%) is actually used as a moisturiser because it’s a natural humectant but systemic urea at elevated blood levels has the opposite effect, disrupting skin barrier function.

Advanced Glycation End-products (AGEs). These are compounds formed when sugars react with proteins, exactly what happens when blood glucose is repeatedly elevated. Kidneys filter AGEs; when kidney function declines, AGE accumulation increases. AGEs directly cross-link with collagen and elastin in skin, making them rigid, reducing their structural function, and accelerating visible ageing. Skin affected by AGE accumulation tends to appear duller, less elastic, and more wrinkled for its biological age.

For a young, healthy person this isn’t about kidney disease. It’s about the factors that affect kidney function subclinically: chronic dehydration (which concentrates waste products), consistently high blood glucose (which accelerates AGE formation and burdens kidney filtration), and high sodium intake (which increases the filtration load). All three are common in typical diets and all three have measurable effects on skin appearance through the kidney pathway.

The practical implications: adequate hydration matters for skin in part because of this mechanism and not because water directly “plumps” skin, which it doesn’t, but because adequate hydration supports kidney filtration efficiency and reduces waste product accumulation. Blood glucose stability matters for skin in part because of AGE formation and not just because of direct collagen glycation, which is the usually-cited mechanism, but because kidneys clearing AGEs adds a secondary buffering system when glucose is controlled.

This is why the skin of people with well-controlled type 1 diabetes and those with poorly-controlled type 1 diabetes looks different, decades before either group develops clinical kidney disease. The metabolic-skin-kidney connection operates at subclinical levels throughout a lifetime.

Women Are More Likely to Attribute Their Own Symptoms to Stress. Research Suggests This Is Medically Dangerous.

This one came out of a finding I kept encountering in different literatures — sleep, cardiovascular health, hormones and it deserves to be named directly.

Research consistently finds that women are more likely than men to attribute their own physical symptoms to psychological causes; stress, anxiety, “overdoing it” and that healthcare providers are more likely to do the same when seeing female patients. This pattern has been documented in cardiovascular medicine (women presenting with heart attacks are more often initially diagnosed with anxiety), in gastroenterology (women with serious GI conditions are more often referred to psychotherapy before organic causes are investigated), and as this newsletter has covered extensively; in sleep medicine, where female OSA, restless legs, and cycle-linked insomnia are routinely attributed to stress or anxiety before a diagnostic workup.

The consequence isn’t just delayed diagnosis. It’s that women learn to interpret their own symptoms through this lens. Persistent fatigue becomes “I need to slow down.” Breathlessness on exertion becomes “I’m out of shape.” Morning headaches become “I’m stressed.” Restless legs become “I’m anxious at night.”

The medical recommendation that emerges from this data, and I want to be direct about it — is: do not accept “it’s probably stress” as the conclusion of an investigation unless investigations have actually been done. Stress is a real and common contributor to many symptoms. It is also a default explanation that, in female patients, has been documented to delay the diagnosis of conditions including autoimmune disease, cardiac conditions, sleep disorders, and hormonal pathologies by years and sometimes decades.

When a symptom is persistent, patterned, and not responding to the stress management interventions that should address it, that is a reason to push for investigation rather than accept the framing. The following is worth knowing: you can ask for specific tests rather than simply describing symptoms. “I’d like my ferritin tested specifically, not just haemoglobin” is a specific request. “I’d like to discuss whether a sleep study is appropriate given these symptoms” is a specific request. Specificity gets results that vagueness doesn’t.

The most important version of this note: heart disease is the leading cause of death in women worldwide. Women are 50% more likely to be misdiagnosed following a heart attack than men, and are more likely to die from a first heart attack. The female presentation of cardiac symptoms; fatigue, jaw pain, nausea, shoulder pain, breathlessness is routinely attributed to anxiety. This is the extreme end of a pattern that operates at all levels of female healthcare.

Know the symptoms. Don’t explain them away before a doctor has investigated them.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research round-up from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings:

The link between your menstrual cycle and glucose

Self-reported eating rate and metabolic syndrome in Japanese people: cross-sectional study

Dietary energy intake across the menstrual cycle: a narrative review

Mindful Eating: The Art of Presence While You Eat

Urea in Dermatology: A Review of its Emollient, Moisturizing, Keratolytic, Skin Barrier Enhancing and Antimicrobial Properties

Women and Stress

Women are 50% more likely than men to be given incorrect diagnosis following a heart attack

You’ve been told to sleep 7–9 hours. You’ve fixed your routine. You’ve put your phone down. And you still wake up tired. This isn’t a discipline problem. It’s a data problem. The data just wasn’t collected on you.

This is Part 1 of a two-part Deep Dive. It covers the foundational research, the hormonal architecture of female sleep, how your sleep changes across the menstrual cycle, and what happens when you’re on the pill. Part 2 covers why you’re still tired, the sleep disorders being missed in women, what actually works, and your full action plan.

There’s a specific kind of tired that doesn’t have a name.

Not the tired that comes from a late night out. Not the tired that a weekend of good sleep fixes. Not the tired that lifts after a holiday when you finally stop setting an alarm and let your body find its own schedule.

This kind is different. It’s the tired that’s just there when you wake up — before the day has asked anything of you, before the first obligation, before coffee. A baseline heaviness that’s been present since your mid-teens and has never really gone away. Some weeks it’s manageable. Some weeks it’s not. Some months your sleep feels genuinely good and you think you’ve finally cracked it, and then it falls apart again, on a schedule you can’t quite identify.

You’ve done the things. You know about sleep hygiene. You’ve heard about blue light and consistent bedtimes and the importance of winding down and not being on your phone after 10pm. Some of you have read the books. Some of you have downloaded the apps. Some of you have made actual spreadsheets.

And you still wake up tired on half the mornings of your life, for no clear reason, doing everything right.

At some point, this stops feeling like a habit problem. At some point, it starts feeling like something is actually wrong with you. Like your body has a fundamental incapacity for good sleep that other people seem to have figured out. Like you’re broken in a way that’s not dramatic enough to be a condition but persistent enough to quietly undermine your life.

Here’s what I want to tell you before anything else: you’re not broken. But the advice you’ve been given is incomplete, in a very specific way, about a very specific thing, that has a very specific explanation.

The 7–9 hours recommendation has been given to you since you first complained about being tired in school. It comes from the CDC, the NIH, the National Sleep Foundation. It’s backed by decades of research.

It also comes, largely, from research conducted on men.

And a 2024 landmark review published in Sleep Medicine Reviews by researchers from Stanford University, Harvard Medical School, and the University of Southampton found that females are

and that the gap between the biology the science was built on and the biology it’s being applied to has real, measurable consequences. The same study found that women’s intrinsic circadian periods are shorter than men’s by around six minutes, and that the resulting misalignment between biological and social sleep timing is approximately five times larger in women than in men.

Five times.

The sleep advice that’s been failing you was built on a body that works differently from yours. The question that actually needs answering isn’t:

It’s:

This Deep Dive is the answer to that question. Both parts, across 11 chapters, cover what the science actually says — not the simplified version that ends up in sleep hygiene articles, but the research on female sleep architecture, on how hormones interact with sleep, on how your sleep changes across the month in ways most people never have a framework for.

Part 1 covers:

• Why the standard sleep model has a significant blind spot, and whose biology it was built on

• The paradox: why women sleep better in the lab and feel worse in real life

• The full hormonal architecture of female sleep — estrogen, progesterone, cortisol, melatonin — and what each one does while you’re supposed to be resting

• How your sleep changes across the menstrual cycle, phase by phase

• What happens to your sleep architecture on the pill — and coming off it

The tiredness you’ve been carrying isn’t a character flaw. It’s a biological experience that hasn’t been named properly yet.

Let’s name 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.

Deep Dive below ↓

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Caught My Eye…

The FDA Just Removed the HRT Black Box Warning. Here’s What That Means and Why It Was There in the First Place.

In late 2025, the FDA removed the black box warning (the most serious warning a drug can carry) from menopause hormone therapy products. The warning had been in place for 22 years. FDA Commissioner Marty Makary stated publicly that:

This is a significant moment in women’s health. To understand why, you need to understand what put the warning there in the first place.

In 2002, the Women’s Health Initiative, the landmark study of 161,000 women (I’ve discussed in a previous Between Saturdays) published findings from a large trial of combined oestrogen and progestin therapy (the specific formulation was conjugated equine oestrogen plus medroxyprogesterone acetate, which is synthetic progestin). The trial was stopped early after observing higher rates of breast cancer, heart disease, stroke, and blood clots in the hormone therapy group compared to placebo.

The findings were widely reported, widely misunderstood, and dramatically changed prescribing. HRT use plummeted globally. Women who had been on it for years stopped. Women approaching menopause were advised against starting.

What subsequent analysis found: the initial findings were specific to the particular formulation tested (synthetic progestin, not bioidentical progesterone), the age group studied (the average participant was 63, significantly older than the women typically starting HRT for menopausal symptoms), and the duration and dose. Further research found that for women who start hormone therapy in the early menopause transition, within 10 years of menopause and before age 60, the risk profile is substantially different. The cardiovascular risk didn’t replicate. The benefits; relief of vasomotor symptoms, improved sleep, bone protection, and emerging evidence for cognitive protection were real and significant.

The Society for Women’s Health Research documented the consequences of the original interpretation: millions of women undertreated for severely disruptive menopausal symptoms; women aged into significant bone density loss, cardiovascular events, and cognitive changes that earlier intervention might have mitigated.

What this means practically: the black box removal doesn’t mean HRT is risk-free or that it’s appropriate for every woman. Individual medical history, family history, and risk factors all remain relevant. But for women in the early menopausal transition who are experiencing significant symptoms like sleep disruption, hot flashes, mood changes, the conversation with their doctor about hormone therapy is no longer framed by a 22-year-old warning based on a study population that doesn’t represent them.

If you’re in your 20s reading this: this matters to you eventually, and it matters to your mother now. The treatment is evidence-based, the previous caution was based on a misread of a single study, and the reversal is significant.

Menopause Linked to Grey Matter Loss in the Brain. The Implication for Young Women Is About Timing.

A major study published in February 2026 and summarised by ScienceDaily found that menopause is linked to changes in brain structure, mental health, and sleep. Brain scans revealed grey matter loss in areas tied to memory and emotional regulation in menopausal women.

This is part of a larger picture that’s been assembling in the research over the past five years. Oestrogen has neuroprotective properties — it supports neuronal survival, reduces inflammation in brain tissue, and appears to have a role in maintaining the grey matter of specific brain regions. When oestrogen declines during the menopausal transition, those protective effects decline.

The research specifically implicates the hippocampus (memory formation) and regions involved in emotional regulation. Women commonly report “brain fog,” memory lapses, and mood changes during perimenopause and the structural data is beginning to suggest these are not entirely subjective. They may reflect real, measurable changes in brain tissue that occur during the hormonal transition.

The implication for young women is this: the “timing hypothesis” in HRT research suggests that the neuroprotective benefits of oestrogen therapy are greatest when hormone therapy is initiated early in the menopausal transition before significant neurological changes have accumulated. Starting HRT at 65, after a decade of low oestrogen, may not offer the same cognitive protection as starting at 51 when the transition begins.

This doesn’t mean every woman should be on HRT. It means that the conversation about hormone therapy, which previous research had deferred to late life is increasingly being framed as a decision with earlier windows that matter. The oestrogen window for brain protection may be narrower than the window for symptom relief.

It’s also, again, a reminder that perimenopause in women in their 30s is more common than most people know. If you or someone you know is in that age bracket and experiencing unexplained cognitive changes, mood instability, or disrupted sleep, hormones are worth checking.

The Gut Microbiome and Ovarian Ageing: A New Mouse Study That Matters

This is a research finding that’s early-stage and needs the appropriate caveats — it’s in mice, not humans. But the mechanism is so compelling and the implications so significant that it belongs in this edition.

A study published in Nature Aging in March 2026 found that ovarian ageing in female mice is directly linked to gut microbial profiles and that transferring gut microbiota from young mice to older mice produced measurable changes in the ovarian transcriptome, reduced inflammation-related gene expression, and induced transcriptional features the researchers described as consistent with “ovarian rejuvenation.”

In plain language: changing the gut microbiome of older female mice changed what their ovaries were doing, at the gene expression level, in ways that looked more like younger ovaries.

The mechanism the researchers identified involved NAD metabolism and inflammatory pathways in the ovarian tissue. The gut microbiome appears to regulate ovarian function through at least two routes: direct influence on circulating oestrogen levels (through the estrobolome, the set of gut bacteria that metabolise oestrogen), and systemic inflammation pathways that affect ovarian tissue ageing.

Earlier menopause is linked to shorter lifespan and higher risk of cardiovascular disease, osteoporosis, and dementia. If the gut microbiome influences the timing and pace of ovarian ageing and this study provides the most direct evidence yet that it does, then gut health is a fertility and longevity issue, not just a digestive one.

What to do with this: the honest answer is that the specific interventions to translate this into human reproductive health practice don’t exist yet. This is a mechanistic finding in an animal model. But it adds weight to the growing evidence that the gut microbiome is a central regulator of female hormonal health and that the dietary and lifestyle choices that support gut microbiome diversity (high-fibre eating, fermented foods, reduced ultra-processed food, consistent sleep, stress management) are not just gut health choices. They may be, in a meaningful sense, choices about hormonal health, fertility, and the pace of biological ageing.

Sunlight, Vitamin D, and the Nuance the Dermatology Conversation Has Been Missing

For years the public health message on sunlight has been clear and almost one-dimensional: sun exposure causes skin cancer, wear SPF every day, minimise unprotected exposure. This is sound advice as far as it goes. But a growing body of research is adding significant nuance that isn’t reaching most people.

The finding that matters most: vitamin D insufficiency affects approximately 1 billion people globally, with estimates of deficiency particularly high in northern latitudes, among darker-skinned populations (who require more sunlight to produce equivalent vitamin D), and among people who consistently avoid all sun exposure. In the UK, Public Health England estimates that approximately 1 in 5 people have low vitamin D levels.

The health consequences of vitamin D insufficiency are not limited to bone density. Vitamin D receptors are present in almost every cell in the body. Emerging research links insufficiency to higher rates of depression, impaired immune function, increased susceptibility to autoimmune conditions, and disrupted menstrual cycle regularity and higher rates of PCOS symptoms. A 2024 meta-analysis found that vitamin D insufficiency is associated with worse PMS symptoms and more dysmenorrhea, with supplementation producing measurable improvements in both.

The nuance this adds to the SPF conversation: daily SPF on the face is still appropriate and sensible for preventing photoageing and reducing skin cancer risk. But blocking all skin sun exposure entirely, particularly in populations where diet and supplementation don’t fill the gap may be creating a different problem. Brief unprotected sun exposure on the arms or legs (10–15 minutes at midday, 2–3 times per week, outside peak UV months in northern climates) is generally considered sufficient for vitamin D synthesis in lighter-skinned individuals without the cumulative skin damage of prolonged exposure.

If you wear full-coverage SPF daily and eat a typical Western diet with limited fatty fish, eggs, and fortified foods: get your vitamin D levels tested. The target serum level is approximately 50–75 nmol/L; below 30 nmol/L is considered deficient. Winter supplementation of 1,000–2,000 IU daily is widely considered safe and appropriate for populations with limited winter sun.

The evidence suggests the optimal approach is not maximum sun exposure or zero sun exposure. It’s calibrated sun exposure with SPF where it counts (face, décolletage, any chronically sun-exposed area) and adequate vitamin D from some combination of diet, moderate sun, and supplementation.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research round-up from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings:

Looking Back, Moving Forward: Women’s Health Research in 2025 and the Road Ahead

Menopause is linked to reductions in grey matter volume in key brain regions as well as increased levels of anxiety and depression and difficulties with sleep, according to new research from the University of Cambridge.

Estropausal gut microbiota transplant improves measures of ovarian function in adult mice

Time for more vitamin D

Guidance for vulnerable groups offered vitamin D

Effect of vitamin D and E supplementation on pain relief and premenstrual symptoms in primary dysmenorrhea: a randomized controlled trial

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 ↓

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If you’ve been reading Between Saturdays every week — thank you. Genuinely. It means a lot that you show up.

I wanted to reach out personally because I’m running a limited promotion on paid subscriptions, and I wanted you to hear about it first.

For a short time, you can get full access to Simply Salvia for under $5.99 a month.

Here’s what that unlocks:

SHORT DIVES

Research-based guides on the topics all over your feed — retinol, cortisol face, cycle syncing, dark circles, jawline acne, skin barrier, collagen. The version that actually goes through the studies, separates what’s real from what’s marketing, and tells you what to do with it. Currently available: 10+ Short Dives, with new ones dropping regularly.

DEEP DIVES

The long-form, 80–120 page research investigations into the topics that deserve more than a TikTok. The women’s sleep deep dive alone is over 22,000 words covering the biology, the disorders that get missed, and the phase-by-phase guide to actually fixing it. These take weeks to write. They read in a few hours and stay useful for years.

Between Saturdays: the weekly research roundup you already read — stays free. Always.

The paid subscription is for the people who want to go deeper. Who are tired of wellness content that’s confident and sourceless. Who want to actually understand what’s happening in their body, not just be told what to buy.

If that’s you — this is the moment.

Get Full Access

This offer won’t be around forever. But more importantly: the next Short Dive and the next Deep Dive are already in progress, and paid subscribers get them the moment they land.

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Caught My Eye…

Creatine Isn’t Just for the Gym. The Brain Research Is Starting to Land.

If creatine is in your awareness at all, it’s probably as a bodybuilding supplement aka the thing that makes muscles bigger, associated with guys at the gym. The marketing has been so effective at positioning it that most women don’t consider it, and most people don’t know what it actually does.

Here’s what it actually does: creatine is a naturally occurring compound that serves as an energy buffer in cells with high energy demands. In muscle cells, it replenishes ATP (the currency of cellular energy) during high-intensity bursts of effort. In brain cells, it does the same thing, and the brain has extremely high energy demands.

The research on creatine and mental health has been accumulating for several years. What arrived this month is a more complete picture.

A systematic review published in the Canadian Journal of Psychiatry in January 2026, covering five RCTs totalling 238 participants, found that creatine monohydrate as an adjunct treatment for major depressive disorder outperformed placebo in several trials. In the most compelling single study; a 2012 trial by Lyoo et al. testing creatine as an add-on to SSRI treatment in 52 women with major depressive disorder, creatine produced significantly greater improvements in depression scores compared to SSRI plus placebo, with effects visible by week two. The effect size was Cohen’s d = 1.13 at eight weeks, which in psychiatric research terms is substantial.

A 2025 trial published in European Neuropsychopharmacology found that adding creatine to cognitive behavioural therapy significantly improved depression scores compared to CBT plus placebo. And neuroimaging research has found that depression is associated with lower brain phosphocreatine levels, meaning creatine supplementation may be working by restoring something that’s genuinely depleted.

There’s also an important reason this is specifically relevant for women. A 2025 review in Frontiers in Nutrition noted that women naturally produce less creatine than men, and that hormonal changes across the menstrual cycle and through perimenopause further reduce creatine synthesis. Women in the late luteal phase — when mood is typically lower may have a particularly elevated creatine deficit relative to their needs.

What the evidence is not saying: creatine is not an antidepressant, and a November 2025 meta-analysis in the British Journal of Nutrition found the overall effect on depressive symptoms to be below the clinical relevance threshold across studies meaning the average effect is real but modest. It’s not replacing therapy or medication. It’s an adjunct with a plausible mechanism and an accumulating evidence base, in a population (women) that has been almost entirely absent from the research until very recently.

The dose in clinical trials: 3–5g of creatine monohydrate per day. Same form sold in any sports supplement store. Extremely safe. No evidence of harm at standard doses across decades of research.

The practical note: if you’re a woman who trains, takes your mental health seriously, or just wants to hedge against the brain energy deficit that appears to track with low mood and hormonal fluctuation, the case for creatine is no longer just about muscle.

Your Menstrual Cycle Affects Your ACL Risk. Sports Medicine Has Known This for Years and Done Almost Nothing About It.

This one frustrated me the more I read it.

Female athletes tear their ACL at two to eight times the rate of male athletes in equivalent sports. This disparity has been documented since the 1970s. For most of that time, it was attributed to anatomical differences, women’s hips, women’s knees, the Q angle. Biomechanics. Structure.

The hormonal dimension has been understood for years and is only now beginning to enter sports medicine in any meaningful way.

The mechanism: estrogen peaks in the late follicular phase, around ovulation, and this rise increases the expression of relaxin receptors throughout the body. Relaxin is a peptide hormone that activates enzymes called matrix metalloproteinases (MMPs), the same enzymes that break down collagen. In ligament tissue, this means that at the point in the cycle when estrogen and relaxin are highest, collagen synthesis in the ACL is suppressed and collagen degradation is accelerated. The ligament becomes measurably more lax. Joint stability is reduced.

A systematic review published in Healthcare in May 2025 examined injury risk and well-being across the menstrual cycle in young elite female athletes, finding that injury patterns did track with cycle phase. Multiple earlier studies found higher ACL injury incidence around ovulation, when estrogen and relaxin are at their peak.

The important caveat: the research is not conclusive. There are conflicting studies with some finding higher injury risk at ovulation, others in the early follicular phase, others in the late luteal phase. The methodology across studies is inconsistent; most relied on self-reported cycle phase rather than hormonal confirmation. A 2025 commentary in Sports Health called for much better study design to actually resolve the question.

What is clear: the ACL contains hormone receptors. Male ACLs largely don’t. The ligament is hormonally responsive tissue and it changes across the cycle. The research on exactly when risk peaks is not settled — but the fact that risk varies with cycle phase is better established than most athletes or coaches know.

What this means practically is modest but real: if you play sports with high change-of-direction demands like football, basketball, tennis, climbing, skiing being aware that your joint laxity and neuromuscular control fluctuate across the month is useful information. More deliberate warm-up during high-risk phases. Neuromuscular training (specific landing and cutting technique drills) has the best evidence base for ACL prevention in female athletes and is effective regardless of cycle phase. And if you’ve had ACL issues before, this is a conversation worth having with a physio who’s familiar with the hormonal dimension.

What it also means is that the 2-to-8-fold higher ACL injury rate in women has probably been undertreated with structural interventions, better boot design, better landing mechanics while a hormonal dimension that’s been documented for decades has received almost no clinical attention.

Half of Young Adults Are Lonely. And the Research on Why Social Connection Matters Has Reached a Different Level.

In June 2025, the WHO Commission on Social Connection released its global report. The headline: 1 in 6 people worldwide is currently affected by loneliness. New estimates suggest loneliness contributes to approximately 871,000 deaths annually, around 100 deaths every hour.

The statistics on young people were the ones that stopped me. Between 2014 and 2023, the highest rates of loneliness were in adolescents (20.9% of 13-17 year olds) and young adults (17.4% of 18-29 year olds), not older adults, despite the widespread assumption that elderly people are most at risk. The more technologically connected a generation is, the lonelier it appears to be.

A March 2026 study from Washington University in St. Louis surveying 3,000+ young adults across eight countries found that nearly half reported loneliness, and confirmed the cross-national nature of the association with depression and anxiety. This isn’t a US problem or a post-pandemic anomaly. It’s a pattern in the demographic that spends the most time online.

The health evidence on what loneliness does to the body is now at a level where it should probably reshape how we think about public health. Meta-analyses have found that social isolation increases mortality risk by 29%, loneliness by 26%, and living alone by 32%, effects of a similar magnitude to smoking 15 cigarettes per day, as the US Surgeon General’s Advisory noted. Loneliness elevates inflammatory markers, disrupts cortisol rhythm, impairs sleep quality, and increases the risk of cardiovascular disease and type 2 diabetes through multiple pathways.

The mechanism relevant for this audience: loneliness activates the HPA axis. It is a chronic low-level stressor on the stress response system — elevating cortisol, maintaining hyperarousal, fragmenting sleep. The body treats social isolation as a threat to survival (which, evolutionarily, it was). The consequences; anxiety, low mood, poor sleep, increased inflammation, these are not psychological reactions to feeling lonely. They’re physiological responses to a detected threat.

A 2025 Cigna survey of 7,500 US adults found 57% reported loneliness. Younger generations were lonelier than older ones. Gen Z workers reporting loneliness at 72%. Online connection is not substituting for in-person connection in any way that registers in the body’s social signalling systems.

This isn’t a lecture about phones. It’s a data point: in-person social connection is a physiological need with measurable health consequences when unmet. The research has moved past the point where it can be treated as a soft outcome.

Your Gut Microbiome and Your Hormones Are Having a Conversation. The Mental Health Implications Are Significant.

This is the emerging story that hasn’t broken into mainstream wellness content properly yet, and it should have.

A systematic review and meta-analysis published in Healthcare in November 2025 examined the evidence from 28 randomised controlled trials on gut microbiome-targeted interventions like probiotics, prebiotics, synbiotics and their effects on mental health symptoms in women during key hormonal transitions: the premenstrual period, pregnancy, and menopause.

The findings were clinically relevant. Across multiple trials, gut microbiome interventions significantly improved depression and anxiety symptoms in premenstrual women, pregnant women, and women going through menopause. The effect was consistent enough across studies that the authors concluded the gut microbiome is “a promising target for advancing women’s mental health.”

Why this makes sense: the gut microbiome produces approximately 90-95% of the body’s serotonin. It produces GABA. It produces short-chain fatty acids that directly influence brain function and inflammation. The gut-brain axis — the bidirectional communication network between the gut and the central nervous system, means that gut composition directly affects neurotransmitter availability and inflammatory signalling in the brain.

What makes this specifically a women’s health story rather than a general one: female hormones and the gut microbiome have a two-way relationship. Estrogen is metabolised partly in the gut by a set of bacteria collectively called the “estrobolome.” When gut diversity is low, estrogen metabolism is impaired, and circulating estrogen levels become more erratic. This worsens premenstrual symptoms, disrupts the hormonal balance of the cycle, and the research is now suggesting that it directly affects mood and anxiety through gut-brain pathways.

The practical takeaway is not a specific probiotic brand. The dietary pattern that most consistently supports a diverse and healthy gut microbiome — high fibre from varied plants, fermented foods, reduced ultra-processed food is associated with better hormonal regulation and lower rates of depression and anxiety in women. The effect isn’t dramatic and it isn’t immediate. It’s a background intervention that takes weeks to months to manifest. But it’s one of the few dietary changes with a plausible mechanism connecting it directly to both hormonal balance and mental health.

The one specific strain with growing evidence for women specifically: Lactobacillus gasseri CP2305, which in a study of women with premenstrual symptoms improved mood, reduced stress and anxiety, improved sleep, and in one study improved skin appearance. This is an area to watch rather than a recommendation. The research is preliminary and probiotic research has a history of not replicating but the direction of the evidence is interesting.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research roundup from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe.

Detailed Readings:

The Effect of Creatine Monohydrate on Mental Disorders: A Systematic Review of Randomized Controlled Trials

Creatine for Mental Health: What the Research Shows

Creatine in women’s health: bridging the gap from menstruation through pregnancy to menopause

Menstrual Cycle Hormone Relaxin and ACL Injuries in Female Athletes: A Systematic Review

Injury Risk and Overall Well-Being During the Menstrual Cycle in Elite Adolescent Team Sports Athletes

Social connection linked to improved health and reduced risk of early death

Nearly half of young adults report loneliness in eight-country study

Loneliness and social isolation as risk factors for mortality: a meta-analytic review

Efficacy of Gut Microbiome-Targeted Interventions on Mental Health Symptoms in Women Across Key Hormonal Life Stages

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

In that time I’ve written about cortisol and skin, about the iron deficiency that routine blood tests miss, about why your moisturiser isn’t the problem when your barrier is. I’ve broken down PMS and PMDD through the lens of hormonal physiology, traced the connection between pre-workout caffeine and the sleep you’re losing to recover, and tried to explain why cold plunge research doesn’t replicate in women the way it does in men.

The goal has always been the same: to give you a framework for understanding what your body is doing and why rather than a list of things to try.

I think the content is getting better. But I’m making decisions based on assumptions about what’s useful to you, what topics matter, and what’s missing. I’d rather make those decisions based on what you actually tell me.

Six questions. Click the options that feel right. Takes about two minutes.

Click to answer

The information exists. It’s just not reaching people. That’s what this is for.

Caught My Eye…

Ultra-Processed Food and Your Mental Health: The Research Has Reached a Tipping Point

This story has been building for years. It arrived somewhere significant this month.

A 2026 cross-sectional study in female adolescents aged 15–18 found that girls in the highest ultra-processed food consumption group had 3.69 times higher odds of depression, 2.84 times higher odds of stress, and nearly twice the odds of anxiety compared to those in the lowest consumption group. That’s not a small association. In a population that is already experiencing a mental health crisis by most measures, it’s a significant one.

This study sits within a broader body of evidence that has been accumulating since 2022. A major umbrella review published in the BMJ in 2024, which analysed 45 pooled meta-analyses covering 9.9 million people found highly suggestive evidence linking ultra-processed food consumption to depression and common mental disorders, alongside diabetes, obesity, and cardiovascular disease. The Lancet published a major three-part series on UPFs in November 2025 confirming that the dietary pattern is globally displacing whole foods and that the evidence for harm, including mental harm, has reached a threshold that can no longer be dismissed.

The mechanism is increasingly understood: UPFs disrupt the gut microbiome (which directly affects serotonin and dopamine signalling), drive systemic low-grade inflammation (strongly associated with depression), and alter the dopaminergic reward pathways involved in mood regulation through their hyperpalatable combination of fat, sugar, salt, and food additives.

The important caveat: most of the evidence is observational, which means causation hasn’t been definitively proven. People who eat more ultra-processed food may also experience more stress, sleep less, exercise less, and have fewer resources, all of which independently affect mental health. Randomised controlled trials are needed to establish direct causality. But the consistency of the association across populations, age groups, and countries has moved beyond coincidence.

What counts as ultra-processed: packaged snacks, flavoured crisps, soft drinks, fast food, instant noodles, mass-produced bread with long ingredient lists, flavoured yogurts, packaged cereals with added sugar, processed meat products. Not all convenience food, but most of what lines the centre aisles of a supermarket.

The message isn’t “you caused your depression by eating badly.” It’s that the food environment most of us navigate daily may be compounding mental health vulnerability in ways that are only now being quantified.

Cold Plunging for Women: The Study That Changed What I Think About This

The cold plunge trend has been everywhere for two years. Most of the research cited to support it was conducted predominantly in men. That turns out to matter — significantly.

A systematic review and meta-analysis published in PLOS One in January 2025 by researchers at the University of South Australia analysed 11 randomised trials involving 3,177 participants. The headline findings: cold-water immersion reduced stress levels and was associated with improved quality of life and fewer sick days. Sounds compelling.

But the detail buried in the analysis stopped me: men, but not women, reported sleeping better after cold-water immersion. The sleep benefit, which is one of the most frequently cited reasons young women adopt cold plunging, did not replicate in female participants.

There’s a biological reason for this. Women’s core body temperature regulation operates differently across the menstrual cycle — progesterone raises core temperature in the luteal phase, and the relationship between body temperature and sleep onset is more hormonally dependent in women than in men. Cold immersion before bed may interfere with the natural thermoregulatory process that helps women fall asleep rather than supporting it.

The other finding worth knowing: cold-water immersion increased inflammation immediately after and one hour post-exposure in all participants. The initial spike is the stress response that drives longer-term adaptation. But for women who are already dealing with elevated systemic inflammation from other causes — poor sleep, chronic stress, hormonal fluctuation, this initial inflammatory hit is worth thinking about.

What the evidence does support for women: cold exposure at moderate temperatures (around 14–15°C, not ice-cold) for stress reduction, mood, and metabolic benefits. Dr. Stacy Sims, a researcher who specialises specifically in female physiology and exercise, has been consistent in her guidance that women don’t need to go as cold as men to get the same adaptive benefits and that extremely cold water (4–6°C) may drive a cortisol response that is counterproductive for women specifically.

If you’re doing it and enjoying it: keep going. But “colder is better” is male-derived advice. For women, the evidence points to smarter rather than colder.

Ozempic and Your Bones: The Risk Nobody Is Discussing With Young Women

This is the story that broke properly in early March 2026 and deserves more attention than it’s getting in mainstream wellness content.

Research presented at the American Academy of Orthopaedic Surgeons’ annual meeting on March 8, 2026, drawn from nearly 150,000 patient health records over five years found that people taking GLP-1 medications (Ozempic, Wegovy, Mounjaro, Zepbound) faced a nearly 30% higher risk of osteoporosis, a 12% higher risk of gout, and a more than 150% higher risk of osteomalacia (softening of the bones from low mineral density) compared to those not on these drugs.

The researchers were careful to say this doesn’t outweigh the substantial benefits these medications offer for people with obesity and Type 2 diabetes. But the findings raise questions that are specifically relevant to younger women taking these drugs for weight loss rather than metabolic disease — where the risk-benefit calculation looks different.

Here’s the mechanism: rapid weight loss reduces the mechanical load on the skeleton, slowing bone formation. GLP-1 drugs also suppress appetite, which can lead to reduced intake of calcium, vitamin D, and protein. The three nutrients bone remodelling most depends on. Research from UC Davis found that roughly 15–25% of weight lost on GLP-1 drugs is lean mass, including muscle, and that bone acts as a single structural unit with muscle and tendon, so muscle loss and bone loss tend to move together.

For young women specifically: the years between 15 and 30 are when peak bone mass is still being built. Bone density peaks around age 25–30. Interventions that reduce bone density during this window don’t just affect you now, they affect your baseline for the rest of your life. The absolute risks in the study are still relatively low (about 4% of GLP-1 users developed osteoporosis versus 3% of non-users over five years). But that study population was predominantly older adults with metabolic disease. In younger, otherwise healthy women using these drugs off-label for weight loss, the picture may look different.

If you’re taking a GLP-1 medication: resistance training is the most evidence-backed way to preserve both bone and muscle during weight loss. Adequate protein (at least 1.2g per kg of body weight), calcium, and vitamin D intake matter. And it’s worth discussing bone density monitoring with your doctor especially before starting, if you have any risk factors.

You’re Probably Getting a Fraction of Your SPF’s Protection. Here’s Why.

This one is simple, annoying, and almost universally true.

Studies consistently find that most people apply between 0.5mg/cm² and 1mg/cm² of sunscreen, but the SPF on the label is tested at 2mg/cm². At half the application density, you don’t get half the protection. Because of the logarithmic relationship between SPF and UV protection, applying SPF 50 at half the recommended dose gives you an effective SPF of approximately 7 to 8.

Not 25. Not 15. Seven.

This has been documented in dermatology research for decades and still hasn’t reached most people who use sunscreen daily. The practical consequences: a significant proportion of people who believe they’re adequately protected from UV-induced collagen breakdown, hyperpigmentation, and skin cancer risk are not.

The 2mg/cm² standard translates to: for the face alone, approximately half a teaspoon of sunscreen per application (about 1/4 teaspoon if you’re using a separate neck application). Most people apply a fraction of that and pat it in until it’s invisible, which reduces coverage further.

What this means practically: use more than you think you need, apply it before sun exposure (not on the way out the door), and reapply every two hours when you’re outside, because SPF protection degrades with UV exposure, sweat, and physical contact even before the two-hour mark. Mineral sunscreens (zinc oxide, titanium dioxide) sit on the skin’s surface and tend to provide more consistent coverage than chemical ones, which require even distribution to work properly.

The SPF number on the bottle is a ceiling, not a guarantee. How much you apply is what determines what you actually get.

The information in this post is for educational and informational purposes only. None of the above constitutes medical advice. Always consult a qualified healthcare professional for personal health concerns.

Between Saturdays is a weekly research round-up from Simply Salvia. Four things from science and wellness worth knowing about. If someone sent this to you, you can subscribe here.

Detailed Readings:

Ultra-processed food exposure and adverse health outcomes: umbrella review of epidemiological meta-analyses

Ultra-processed foods and human health: the main thesis and the evidence

Ultra-Processed Foods and Mental Health: What the Research Actually Says

FACT CHECK: Do ultra-processed foods cause a decline in mental health?

Effects of cold-water immersion on health and wellbeing: A systematic review and meta-analysis

The health benefits (and risks) of cold plunges

Cold Plunging for Women: Why Colder Isn’t Always Better

UC Davis Health examines systemic impact of GLP-1–based therapies

GLP-1 drugs like Ozempic can raise bone and tendon injury risk, study suggests

Measuring U.S. consumer sunscreen application at home and online: optimizing our methods to determine sunscreen application thickness for improved environmental emissions estimates

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