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:

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 ↓

Read more

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.

See you on the other side.

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Let’s get into it.

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

Sunscreen FAQs

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

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

Now for what you can do about it.

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

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

Let’s get into it.

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

Short Dive below ↓

Read more

This edition is a bit of a myth-bust. Four things that are all over your feeds right now — iron deficiency, cortisol face, seed cycling, and women’s sleep needs, and what the research actually says about each of them.

Let’s get into it.

Caught My Eye…

40% of Teenage Girls Are Iron Deficient. Routine Tests Are Missing Most of Them.

If you’ve ever been told your blood test came back normal and still feel exhausted, brain-fogged, and like you’re functioning at about 60%, this one is for you.

A 2023 study published in JAMA examined iron levels in over 5,000 American girls and women aged 12–21. The finding: nearly 40% had iron deficiency. Not anaemia — iron deficiency, which is the earlier and more common stage where your iron stores are depleted before it shows up in red blood cell counts.

The part that should frustrate you: routine screening missed 83.6% of these cases. The reason is that standard blood panels typically check haemoglobin; the protein that carries oxygen in red blood cells rather than ferritin, which is the protein that stores iron. You can have haemoglobin levels that look normal while your iron reserves are nearly empty. And the symptoms of non-anaemic iron deficiency — fatigue, difficulty concentrating, low mood, hair shedding, coldness in hands and feet, reduced exercise tolerance, are vague enough that they get attributed to stress, sleep, or just being a busy person.

The CDC currently recommends screening for anaemia in adolescent girls every 5 to 10 years. Not iron deficiency — anaemia, which is the more severe, later-stage condition. A 2024 study in Blood Advances found that in a cohort of over 13,000 people diagnosed with iron deficiency, 58% still had not achieved resolution three years later and of those who did, it took an average of almost two years.

Two years of low energy. Two years of brain fog. Often while being told your results look fine.

What to ask for: request a ferritin test specifically, not just a full blood count or haemoglobin check. A ferritin level below 30 µg/L is considered iron deficient by most haematologists, even if haemoglobin looks normal. If you menstruate heavily, or follow a plant-based diet, or have been feeling persistently tired in a way sleep doesn’t fix — this is worth checking.

Cortisol Face: What TikTok Got Right and What It Got Very Wrong

#cortisolface has tens of millions of views. The premise: chronic stress raises cortisol, which causes facial puffiness, weight redistribution to the face, and a rounded, swollen appearance that people are calling “cortisol face.”

The emotional hook: “you’re not ugly, you just have cortisol face,” has understandably resonated. It offers an explanation and reframes appearance in terms of physiology rather than personal failing. But dermatologists and endocrinologists have been consistent in their pushback, and it’s worth understanding why.

Chronic everyday stress is unlikely to raise cortisol enough to cause visible facial changes. The kind of cortisol-driven facial puffiness that looks like what people are calling “cortisol face,” the uniform rounding of the cheeks, the redistribution of fat to the face and back of the neck is clinically called moon facies, and it occurs primarily in people with Cushing’s syndrome (a rare condition causing pathologically elevated cortisol) or those taking corticosteroid medications at high doses over prolonged periods. Cushing’s syndrome affects approximately 2.2 people per 100,000 — not the substantial portion of TikTok users who have self-diagnosed.

That doesn’t mean stress has no effect on your face. Chronic stress disrupts the cortisol rhythm, damages the skin barrier, contributes to collagen breakdown, and, this is the important part — impacts your habits. Poor sleep causes under-eye puffiness and fluid retention. High-sodium stress eating causes facial bloating. The anxiety-driven 3am snacking does too. These are real cortisol-adjacent effects on appearance. They’re just not the same as cortisol directly redistribution fat to your face.

The nuanced version: stress affects your face, mostly through secondary effects — what it does to your sleep, your diet, your inflammation levels. If you’re puffy, tired-looking, and breaking out, stress is very likely involved. But the mechanism isn’t “cortisol accumulating in your cheeks.” The treatment isn’t supplements that claim to lower cortisol. It’s the less glamorous stuff: sleep consistency, less salt, more water, actual stress management.

If your facial puffiness is persistent, uniform, accompanied by worsening acne, weight gain concentrated around the abdomen, or increased facial hair growth. That is a reason to see a doctor and get cortisol levels actually tested, not to buy an adaptogen stack from an influencer.

Seed Cycling: The Honest Version of What We Know

Seed cycling is everywhere. The protocol; eating flaxseeds and pumpkin seeds in your follicular phase, switching to sunflower and sesame seeds in your luteal phase, claims to balance oestrogen and progesterone through the compounds in each seed, reducing PMS, supporting fertility, and improving hormonal symptoms across the cycle.

The appeal makes sense. It’s food-based, low-cost, low-risk, and framed around supporting your natural cycle rather than overriding it.

But here’s the honest research summary: there are currently no clinical trials on seed cycling as a practice. The evidence that exists is on individual seeds in isolation and not on the cycling protocol, and not in high-quality randomised controlled trials.

What that evidence does show is genuinely interesting. Flaxseeds contain lignans that interact with oestrogen receptors and have been associated with longer luteal phases and more consistent ovulation in a small study of 18 women. Pumpkin seeds are high in zinc, which plays a role in corpus luteum function and progesterone support. Sesame seeds contain lignans that may modulate oestrogen activity in the luteal phase. Sunflower seeds provide vitamin E and selenium, both involved in antioxidant protection and hormone metabolism.

The individual nutritional case for eating these seeds is real. The specific claim that eating them in phase-timed rotation creates a meaningful hormonal effect — that’s where the evidence runs out.

A 2025 review in Food and Humanity found preliminary evidence that seed cycling may improve some hormonal markers in PCOS, but concluded that “robust clinical trials are urgently needed to validate these claims scientifically.”

The realistic take: eating these seeds as part of a varied diet is nutritionally sensible and unlikely to cause any harm. Eating them in the specific protocol might work for you — the individual seed compounds have biological rationale. But if you’re managing PCOS, irregular cycles, severe PMS, or fertility concerns, seed cycling is not a substitute for medical assessment. It’s a food habit, not a treatment.

Women Sleep More Than Men — And Still Report Worse Sleep. Here’s Why.

The research on women’s sleep is one of those topics where the headlines and the reality don’t quite line up, and it’s worth separating the two.

What’s true: women sleep slightly longer than men on average, about 8 to 11 minutes more per night. Sleep lab studies consistently show women spend more time in deep non-REM sleep. Women also fall asleep faster than men, which is often interpreted as a sign of a greater biological sleep need.

What’s also true: women are 40% more likely than men to have insomnia, twice as likely to be diagnosed with anxiety and depression (both strongly associated with disrupted sleep), and consistently report lower sleep quality despite the objective measures looking comparable or better.

A 2024 review published in Sleep Medicine Reviews by researchers from Southampton, Stanford, and Harvard found that women’s circadian periods are approximately six minutes shorter than men’s — which sounds small but creates a meaningful misalignment between the internal body clock and external cues like light and darkness. Women’s melatonin is secreted earlier, core body temperature peaks earlier, and the result is a sleep-wake cycle that is more vulnerable to disruption from late nights, irregular schedules, and artificial light. The researchers found that circadian misalignment is approximately five times larger in women than in men.

The hormonal piece compounds everything. The follicular-to-luteal transition drops core body temperature and disrupts sleep architecture in ways that track across the cycle. Progesterone has mild sedative properties but also raises body temperature in the luteal phase, which fragments sleep. The premenstrual window; when oestrogen and progesterone both fall is associated with more awakenings and lighter sleep.

What this means practically: the generic “get 7–9 hours” advice treats sleep as if it’s identical across sexes and life stages. For women, sleep quality is more hormonally dependent, more disrupted by circadian misalignment, and more sensitive to irregular scheduling than the standard advice accounts for. A consistent sleep and wake time, even on weekends has outsized benefit for women specifically because of the circadian vulnerability. And the sleep deficit you accumulate across a poorly-timed week isn’t fully recovered by a long Saturday lie-in.

It’s not that you need more sleep. It’s that your sleep is harder to protect, and the disruptions cost more than you might think.

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.

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.

Detailed Readings

Prevalence of Iron Deficiency and Iron-Deficiency Anemia in US Females Aged 12-21 Years, 2003-2020

Over 38% of Young Women Iron Deficient, New Research Finds

Iron Deficiency Remains Unresolved Years After Diagnosis

Is ‘cortisol face’ a real thing?

What Is Cortisol Face?

Is Seed Cycling Legit for Hormone Balance?

Research uncovers differences between sexes in sleep, circadian rhythm and metabolism

Do Women Need More Sleep Than Men?

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

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

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

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

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

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

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

What’s covered:

Let’s get into it.

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

Short Dive below ↓

Table of Contents:

1. What Is Cortisol, Actually?

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

3. What Cortisol Actually Does to Your Skin

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

5. What Your Diet Is Doing to Your Cortisol Levels

6. Sleep, Exercise, and the HPA Axis

7. Supplements and Adaptogens — Honest Rankings

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

9. Your Cortisol Action Plan

10. What to Take Away From This

CHAPTER 1: What Is Cortisol, Actually?

The hormone everyone talks about, explained properly

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

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

What Cortisol Does (It’s Not Just Stress)

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

Its roles are extensive. Cortisol:

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

• Controls blood pressure and supports cardiovascular function

• Modulates the immune system, suppressing excessive inflammation

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

• Regulates metabolism; how the body converts food to energy

• Is involved in memory consolidation and cognitive function

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

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

The HPA Axis: How Cortisol Is Made

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

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

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

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

The Cortisol Rhythm: Why Timing Matters

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

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

• Cell turnover,

• Collagen synthesis,

• Immune regulation

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

Acute vs. Chronic Cortisol: The Critical Difference

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

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

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

Read more

Let’s get into it.

Caught My Eye…

Your Pre-Workout Is Probably Ruining Your Sleep. Here’s the Research.

If you take a pre-workout supplement before evening training or anytime after about 3pm, there’s a good chance it’s affecting your sleep more than you realise.

A study published in Sleep Epidemiology in December 2025 from researchers at the University of Toronto analysed data from 912 participants aged 16 to 30. The finding: people who had used pre-workout supplements in the past year were more than twice as likely to report sleeping five hours or less per night compared to those who hadn’t. That’s not a marginal difference, five hours or less is well below the 7-9 hours recommended for this age group and sits in a range that sleep researchers consistently describe as a clinically significant risk to mental health, immune function, and long-term cardiovascular health.

The mechanism isn’t mysterious. Pre-workout formulas typically contain between 90 and 350mg of caffeine per serving. For reference: a cup of coffee contains roughly 100mg, a can of Coke roughly 35mg. Some of the most popular pre-workouts — Bang!, C4, Jack3d, sit toward the higher end. Caffeine has a half-life of approximately 5-7 hours, which means a 200mg serving taken at 6pm still has 100mg active in your system at midnight.

The researchers were careful not to frame this as “stop exercising,” the point isn’t that the training is the problem. It’s that the supplement being used to fuel it may be quietly dismantling the recovery that makes the training worthwhile in the first place.

If you use pre-workout: take it at least 12-14 hours before you need to sleep, check the caffeine content specifically (it varies dramatically between products), and consider whether a lower-stimulant or stimulant-free version achieves the same outcome for afternoon or evening sessions.

Over Half of Women in Their 30s Are Already Experiencing Perimenopause Symptoms. Most Don’t Know It.

This one sat with me for a while after I read it.

A study published in npj Women’s Health in February 2025, led by researchers at UVA Health and the University of Virginia, surveyed more than 4,400 American women aged 30 and older about perimenopausal symptoms. What they found challenged the assumption that perimenopause is something that happens in your late 40s or 50s.

Among women aged 30-35, 55.4% reported symptoms that met the criteria for “moderate” or “severe” on the Menopause Rating Scale, a validated clinical tool used to measure perimenopause symptom burden. That figure rose to 64.3% in women aged 36-40.

Here’s the part that matters most for a younger audience: the symptoms that arrive first are not the ones we associate with menopause. Hot flashes and night sweats, the classic markers most women expect peak at ages 51-55 and were lowest in the 30-35 group. What appears early, years or even decades before those physical symptoms, are psychological symptoms: anxiety, irritability, and depression. These peaked in women aged 41-45 in the study but were already measurable in women in their 30s.

Which means: the anxiety that feels out of proportion. The irritability that doesn’t quite have an explanation. The mood cycling that doesn’t map neatly onto your menstrual calendar. For some women, these are being attributed to stress, workload, or mental health conditions. When they are actually early markers of a hormonal transition that nobody told them could start this early.

The researchers called the gap in awareness and medical education “alarming.” Over 90% of women in the study who experienced symptoms eventually sought medical care but the median age at which women first see a doctor about these symptoms is 56. Decades after the symptoms can start.

If you’re in your 30s and experiencing unexplained mood instability, irregular cycles, changes in sleep, or brain fog that doesn’t track with your obvious life stressors — it is worth raising hormones specifically with your GP. Ask about oestrogen and progesterone levels, and ask whether perimenopause should be on the differential.

If you are suspecting perimenopause maybe this can help:

Mouth Taping: What the Systematic Review Actually Found

Mouth taping for sleep is everywhere. The premise: tape your mouth shut at night to force nasal breathing, improving sleep quality, reducing snoring, and fixing a range of respiratory and cognitive issues. This has accumulated tens of millions of views and spawned an entire product category.

The nasal breathing rationale is scientifically sound. Nasal breathing filters, warms, and humidifies air, produces nitric oxide that improves oxygen uptake, and during sleep, upper airway resistance is significantly lower through the nasal route than the oral one, which means nasal breathing is genuinely better for sleep architecture and reduces the risk of airway obstruction.

The question is whether taping your mouth shut is a safe and effective way to achieve that.

A 2025 systematic review published in PLOS One, conducted by researchers at London Health Sciences Centre in Canada, reviewed 10 studies on oral occlusion during sleep. Their conclusions were more cautious than the TikTok content suggests.

For people with mild obstructive sleep apnea who are already primarily nasal breathers, some studies showed minor improvements in apnea-hypopnea index and snoring index. But for people who breathe through their mouth because their nasal passages are obstructed, due to allergies, a deviated septum, enlarged adenoids, chronic congestion, mouth taping doesn’t solve the problem. It removes the compensatory mechanism the body is using to get enough air. The researchers identified potential for serious harm in this group, including asphyxiation risk. The evidence for clinical benefit outside of mild apnea was minimal and not statistically significant.

The honest version: if you breathe through your mouth at night and your nose is clear and unobstructed, mouth taping is probably low-risk and may offer mild benefit for snoring. If you wake with a dry mouth, snore, feel unrefreshed after sleep, or have known nasal obstruction from allergies or structural causes, get assessed for sleep-disordered breathing before taping your mouth shut based on a TikTok recommendation. The correct intervention for nasal obstruction is addressing the obstruction, not overriding the compensatory mouth breathing.

The Largest Women’s Health Study in US History Just Lost Its Funding. Here’s Why It Matters.

This one isn’t a myth-bust or a new discovery. It’s a news item but it’s one that matters specifically for what it means for women’s health research going forward.

The Women’s Health Initiative (WHI) — a landmark longitudinal study that has followed more than 161,000 women since the early 1990s, was informed in April 2025 that the Department of Health and Human Services would terminate its regional centre contracts as part of the broader NIH budget cuts. After significant public and congressional pushback, some of those contracts were reportedly reversed but the situation remains uncertain, and the study’s coordinating centre has been operating without confirmed funding clarity.

Why does this matter for women aged 15 to 35?

The WHI has been the single most influential source of evidence on women’s cardiovascular health, bone density, cancer risk, and hormone therapy safety. It’s the study that transformed HRT prescribing globally, preventing an estimated 126,000 breast cancer cases and 76,000 cardiovascular disease cases over a decade. The participants are now 78-108 years old, providing data on ageing that doesn’t exist anywhere else.

Defunding the WHI doesn’t affect women who are young now in an immediate, visible way. But it does affect the evidence base that will exist when they’re older. Women’s health research has historically been underfunded, under-represented in clinical trials, and routinely dismissed as a lower priority. The WHI was one of the few studies designed from the outset specifically around women’s health outcomes. Cutting it removes decades of longitudinal data collection that can’t be retroactively replaced.

This is the context behind something Melinda French Gates said at the start of this year: that 2026 needs to be the year we “finally stop tolerating women’s suffering.” The research infrastructure to understand that suffering is currently being dismantled.

Worth knowing about. Worth caring about.

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.

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.

Detailed Readings

Use of pre-workout dietary supplements is associated with lower sleep duration among adolescents and young adult

Perimenopause symptoms, severity, and healthcare seeking in women in US

Effect of nasal or oral breathing route on upper airway resistance during sleep

Breaking social media fads and uncovering the safety and efficacy of mouth taping in patients with mouth breathing, sleep disordered breathing, or obstructive sleep apnea: A systematic review

WHI Funding Announcement

HHS Cuts Funding for NIH-Based Women’s Health Initiative Threatening Decades-Long Study

That’s the part that struck me most when I pulled the research for this week’s post. Not that it’s alarming, though some of it is but that it’s invisible. The plastic particles are too small to feel. The bacteria shaping your mood are doing it through pathways you never think about. The supplement that’s been studied for decades for men’s athletic performance is only just being investigated in women’s brains. The thing that’s burning out your nervous system looks, from the outside, like a completely ordinary Tuesday.

This week I wanted to look at four things that are happening inside people’s bodies right now, whether they know it or not and what, if anything, the research actually tells us to do about it.

Caught My Eye…

The Plastic Particles Inside Human Ovaries

In February 2025, a team of Italian researchers published what they described as a first: evidence of microplastic particles in human ovarian follicular fluid; the liquid that surrounds a developing egg before ovulation. It was the first time anyone had confirmed their presence there.

The study was small with a total of 18 women undergoing IVF treatment at a clinic in Salerno, but the findings were striking. Microplastic particles smaller than 10 micrometers were detected in 14 of the 18 follicular fluid samples, with an average concentration of 2,191 particles per millilitre. These are particles small enough to cross cellular membranes. They entered through the bloodstream and reached the granulosa cells surrounding the egg.

The researchers also found something that deserves more attention than it has received: a significant correlation between microplastic concentration in the follicular fluid and levels of Follicle-Stimulating Hormone (FSH). Elevated FSH can indicate reduced ovarian reserve. One of the key markers used to assess a woman’s fertility potential. The study didn’t establish causation, and the researchers were careful to note that no direct correlation was found with fertilisation outcomes or live birth rates. But the signal is there, and it’s the first time anyone has looked.

This finding doesn’t exist in isolation. A 2024 scoping review published in the Journal of Global Health found that microplastics have now been detected in 8 out of 12 human organ systems, including the cardiovascular, digestive, endocrine, reproductive, and urinary systems. They have been found in breast milk, in the placenta, in the lungs, the liver, the kidneys, the colon, and, as a study published in Nature Medicine in early 2025 confirmed, in human brain tissue — at concentrations roughly 50% higher in 2024 samples than in samples from 2016. Researchers found that brain tissue samples from cognitively normal individuals averaged 4,800 micrograms per gram, the equivalent of an entire plastic spoon by weight.

We are at the beginning of understanding what this means. The mechanisms are not fully mapped, and researchers are cautious about drawing firm conclusions from what is still an emerging field. What is clear is that microplastics primarily enter the body through ingestion, inhalation, and skin contact, with traces now found across a broad range of human tissues and biological fluids. The exposure is ongoing. It is not avoidable, but it is reducible: glass or stainless steel water bottles over plastic, not microwaving food in plastic containers, swapping synthetic clothing for natural fibres where possible. These are not solutions. But they matter at the margins, and the margins are where individual exposure can be reduced while the larger regulatory and industrial questions are fought out.

Your Gut Is Producing Your Mood And You’re Probably Feeding It Wrong

You have likely heard that gut health matters. What the research is now showing is how specifically and mechanistically it matters, in ways that go well beyond digestion.

The gut-brain axis is a bidirectional communication network between your gastrointestinal system and your central nervous system, mediated by the vagus nerve, the immune system, and the hormones your gut produces. Disruptions in gut microbiota composition may trigger or exacerbate symptoms of anxiety and depression by interfering with these communication pathways, including neural signalling through the vagus nerve, hormone regulation through the HPA axis, immune responses involving pro-inflammatory cytokines, and metabolic processes related to short-chain fatty acids.

Here is the part that most people don’t know: gut microbiota produce and regulate serotonin, dopamine, and GABA aka the key neurotransmitters involved in mood, emotional regulation, and anxiety. Around 90% of the body’s serotonin is produced in the gut, not the brain. The bacteria you’re hosting are not just processing food. They are producing the chemical environment of your emotional life.

A large-scale genome-wide association study published in Nature Communications, involving over 1,000 participants from the Rotterdam Study cohort and nearly 1,600 from a separate validation cohort, identified thirteen microbial taxa associated with depressive symptoms, including bacteria known to be involved in the synthesis of glutamate, butyrate, serotonin, and GABA. This wasn’t a correlation with lifestyle or diet in the conventional sense. It was a specific mapping of which bacterial species track with depression and which are absent in people who have it.

One of the most compelling pieces of evidence for causality came from a study by neurobiologist John Cryan at University College Cork. His team took microbiome samples from people with depression and transplanted them into healthy rats. The rats developed depression-like behaviours; anhedonia, anxiety, and altered tryptophan metabolism, suggesting the microbial community itself was driving the mood changes, not merely reflecting them.

The practical implications are still being worked out. Probiotics show promise but the research is not yet at the point of specific prescriptions. What is better established: a diet high in diverse plant foods, fibre, fermented foods, and omega-3 fatty acids supports microbial diversity, and microbial diversity is consistently associated with better mental health outcomes. Ultra-processed food, chronic stress, sleep deprivation, and antibiotics all deplete it. The gut is not separate from mental health. It is, increasingly, part of the same system.

Creatine: The Supplement Nobody Told Women About

If you follow fitness content, you’ve heard of creatine. You probably also absorbed, somewhere along the way, the idea that it’s a bodybuilder’s supplement — something for men trying to build muscle, not particularly relevant to you.

That assumption is being quietly dismantled by a growing body of research that has almost nothing to do with muscle.

Creatine is a naturally occurring compound that your body synthesises from amino acids, and that you get in small amounts from red meat and fish. Its primary role is in the phosphocreatine energy system, a fast-access energy pathway used heavily by muscles during intense exercise. But the same system operates in the brain. Your neurons use phosphocreatine to regenerate ATP during periods of high cognitive demand, and when brain creatine stores are depleted — by sleep deprivation, mental fatigue, stress, or simply the natural variation in creatine synthesis, cognitive performance drops.

There is emerging interest in the potential beneficial effects of creatine supplementation on brain health and function. Creatine supplementation can increase brain creatine stores, which may help explain some of the positive effects on measures of cognition and memory, especially in ageing adults or during times of metabolic stress such as sleep deprivation.

A 2024 meta-analysis published in Frontiers in Nutrition, reviewing randomised controlled trials spanning three decades, found that creatine supplementation showed meaningful cognitive benefits particularly under conditions of metabolic stress — sleep deprivation, mental fatigue, hypoxia. For women specifically, the picture is more complicated and less studied: whether any sex or age-related differences exist in regard to creatine and brain health is relatively unknown, because most of the trials have enrolled predominantly male participants.

What we do know is that women have naturally lower creatine stores than men, synthesise less of it endogenously, and experience significant fluctuations tied to the menstrual cycle particularly during the luteal phase, when energy demands increase and cognitive performance often dips. A 2025 clinical trial specifically enrolling perimenopausal and menopausal women found promising early results for creatine’s effects on brain creatine levels and cognitive resilience, though the authors noted that larger trials are needed before firm conclusions can be drawn.

The honest nuance: a key uncertainty is whether supplemented creatine crosses the blood-brain barrier in sufficient amounts to affect neuronal metabolism, and assertions of cognitive enhancement based solely on supplementation risk overstating available data. This is a field that is moving fast, but has not yet arrived at clinical consensus. Creatine is safe and well-studied for physical performance. Its brain effects are real but not yet fully quantified. If you’re already taking it for training, there is a reasonable case that your brain may also benefit, particularly on difficult cognitive days. If you’re not, it’s not yet evidence-based enough to recommend as a cognitive supplement for women specifically but the research is getting there, and getting there quickly.

Your Nervous System Is Exhausted And It’s Not the Same Thing as Being Tired

The last one doesn’t have a single landmark study. It has hundreds. And it’s the one your body is probably the most familiar with, even if you’ve never had language for it.

Nervous system dysregulation — sometimes called chronic sympathetic dominance, or persistent activation of the fight or flight response, is a state in which the autonomic nervous system gets stuck in high alert. Not because there is an emergency. But because the modern environment, for a lot of people, never stops signalling that there might be.

When the sympathetic nervous system remains chronically activated, such as in cases of ongoing stress or trauma, it can lead to cardiovascular problems, digestive disorders, immune system dysfunction, anxiety, and depression. Chronic sympathetic arousal can also impair the body’s ability to heal and repair itself as in a state of constant vigilance, resources are diverted away from maintenance and restoration towards immediate survival needs.

The vagus nerve is at the centre of the emerging science on how to regulate this. It is the longest cranial nerve in the body, running from the brainstem to the abdomen and connecting most of the major organs along the way. It is the primary nerve of the parasympathetic system aka the rest and digest counterpart to fight or flight. Decades of research have established a critical role for vagus nerve signalling in emotional regulation, cognitive performance, inflammation response, and physical recovery.

Crucially, vagal tone — the baseline activity of the vagus nerve is not fixed. It can be trained. Cross-sectional studies in healthy adults repeatedly show that higher vagal tone, measured by heart rate variability, tracks with superior executive performance, sustained attention, and working memory. And the practices that increase vagal tone are unglamorous but real: slow diaphragmatic breathing, cold water exposure to the face and neck, humming, singing, exercise, social connection, and adequate sleep. These are not wellness trends. They are physiologically grounded inputs into a system that a significant number of people are running on depleted.

A 2024 pilot study published in Frontiers in Neurology found that transcutaneous vagus nerve stimulation, a non-invasive form applied through the ear improved symptoms in a female cohort with Long COVID, a condition characterised in part by autonomic nervous system dysfunction. The study was small and preliminary. But it points toward the same conclusion that the broader research base is converging on: the nervous system is not a fixed background condition. It is responsive, trainable, and more central to overall health than most people are taught to think.

The question worth sitting with is not whether you are stressed. Most people reading this know they are. The question is whether your nervous system has had enough consistent input, enough moments of genuine, physiological safety to come back down between the stressors. For most people living with overfull schedules, screens, poor sleep, and chronic low-level anxiety, the honest answer is probably no. That’s not a personal failing. It is a mismatch between the nervous system’s evolutionary design and the environment it is currently trying to survive.

Source: Tyler, Frontiers in Psychology, 2025. Zheng et al., Frontiers in Neurology, 2024. MDPI Neuroimmune Review, December 2025.

In Summary

Four things happening in your body right now that most people don’t know about:

→ Microplastic particles have been found in human ovarian follicular fluid for the first time, at an average of 2,191 particles per millilitre. They’ve also been found in brain tissue, the placenta, lungs, liver, and blood. The science is still early. The exposure is real and ongoing. Reducing plastic in food and drink contact is the most practical lever available.

→ Your gut microbiome is producing serotonin, dopamine, and GABA — the neurotransmitters that shape your mood. Specific bacterial species are now linked to depression and anxiety at a mechanistic level. Microbial diversity, supported by a varied plant-rich diet, is increasingly understood as a component of mental health, not just digestion.

→ Creatine has cognitive benefits that most women don’t know about, particularly under conditions of sleep deprivation and mental fatigue. Women have lower natural creatine stores than men, and the research into sex-specific cognitive effects is only just beginning. Promising, but not yet at clinical recommendation stage for women specifically.

→ Nervous system exhaustion is not the same thing as being tired. Chronic activation of the fight-or-flight response has measurable effects on immunity, digestion, cognition, and emotional regulation. Vagal tone is trainable. Slow breathing, exercise, sleep, and genuine rest are physiological inputs — not indulgences.

The information in this post is for educational purposes only and does not constitute medical advice. If you have concerns about any of the topics covered here, please consult a qualified healthcare professional.

Detailed Readings

Microplastics in Human Ovarian Follicular Fluid — Montano et al., Ecotoxicology and Environmental Safety, 2025

Detection of Microplastics in Human Tissues and Organs: A Scoping Review — Journal of Global Health, 2024

Gut Microbiome-Wide Association Study of Depressive Symptoms — Nature Communications, 2022

Why Nurturing the Gut Microbiota Could Resolve Depression and Anxiety — Nature, 2025

Heads Up for Creatine Supplementation and Brain Health — PMC

The Vagus Nerve: A Cornerstone for Mental Health and Performance — Frontiers in Psychology, 2025

Transcutaneous Vagus Nerve Stimulation Improves Long COVID Symptoms in a Female Cohort — Frontiers in Neurology, 2024

Part 1 was a lot.

And if you’re here, something probably landed. Maybe it was the 73% statistic — the proportion of young adults with hypertension who have no idea. Maybe it was the realisation that your blood pressure has been rising since your early 20s and nobody mentioned it. Maybe it was just the uncomfortable truth that a condition with no symptoms requires active looking to find, and most people never look.

Either way: you’re back. Which means you want the rest of it.

Part 1 was the biology — how blood pressure works, what the numbers mean, why the body drives it up and keeps it there. This is the part where it gets specific to you. To your hormones, your medication, your diet, your stress physiology, your future pregnancies or your history of them. The part where “cut salt and exercise more” gets replaced by information you can actually use.

Section 2 opens with the question most women never think to ask: is something else causing this? Because in about 1 in 10 cases, high blood pressure isn’t the problem — it’s the symptom of one. The pill. A thyroid condition. A kidney issue. A hormonal imbalance producing too much aldosterone that a standard blood panel won’t catch unless someone orders the right test. This section covers all of it, including what changes at menopause and why the decade before it is the one that matters most for getting ahead of this.

Section 3 is where the evidence on lifestyle actually gets specific enough to be useful. Which diet changes move the needle and by how much. What the research says about the natural remedies that have clinical trial data behind them, and which are mostly expensive noise. A full week of meals built around blood pressure management, and a 5-minute breathing practice that has been shown in multiple studies to produce real reductions in resting blood pressure.

Section 4 is the one I’d send to anyone who is pregnant, planning to be, or has ever had a complicated pregnancy. It covers the blood pressure numbers that require same-day medical attention with no exceptions, what every class of medication actually does and why it was chosen, and the long-term cardiovascular implications of gestational hypertension and preeclampsia that most women leave the hospital never having been told.

The 24-year-old’s readings came down. Not overnight, and not from one thing but from understanding the system well enough to work with it rather than around it.

That’s what the rest of this is for.

Read more

The nurse took her blood pressure at the start of the appointment and paused.

Took it again. Paused again.

Her reading was 158/102.

Stage 2 hypertension. In a 24-year-old who exercised, didn’t smoke, didn’t feel unwell, and had no family history she knew of. Who would have gone home that day without the reading ever being taken, continued feeling fine, and had no idea that the pressure inside her arteries was high enough to be quietly damaging her heart, her kidneys, and her brain.

This is the thing about high blood pressure. It doesn’t feel like anything. It is the most common cardiovascular condition in the world, and it gives you almost no warning that it’s there.

I know what you’re thinking. Blood pressure is an old person’s problem. I’m 20. I eat reasonably, I’m not particularly unwell. Why does this apply to me?

Here’s why.

1 in 5 women aged 18 to 39 in the US currently has hypertension. Not 1 in 5 people in their 60s. Women. Our age. Right now. And 73% of young adults who have it have no idea — because it produces no symptoms, nobody checks at this age, and everyone assumes it’s a problem for later.

The American Heart Association published a scientific statement in early 2026 with a projection that stopped me when I read it: by 2050, nearly 1 in 3 women aged 22 to 44 are expected to have some form of cardiovascular disease. High blood pressure is the primary driver of that number. The women accumulating that risk aren’t in their 50s. They’re accumulating it now — in their 20s and 30s — while being told not to worry about it yet.

The problem with “worry about it later” is what happens in the gap.

High blood pressure doesn’t announce itself and then cause damage. It is the damage — building silently in the walls of your arteries, the muscle of your heart, the microvasculature of your brain and kidneys, for years before anything becomes visible or symptomatic. By the time a reading catches up with you, the question isn’t whether to prevent it. It’s how much has already accumulated.

Here’s what else I didn’t know until I went looking: women’s blood pressure starts rising faster than men’s from around age 20 onwards. Not from menopause. From now. The cardiovascular protection that oestrogen provides is real — but it doesn’t mean your blood pressure is staying flat while you coast through your 20s. The trajectory starts earlier than most women are ever told.

And it’s not just genetics or fate. Chronic stress activates the same hormonal pathways that raise blood pressure. Sleep deprivation disrupts the overnight drop in BP that healthy arteries depend on. Ultra-processed food erodes the sodium-potassium balance that keeps vascular tone in check. The oral contraceptive pill raises blood pressure in some women — and the ones most at risk often don’t know to ask. Every one of these things is more characteristic of being 22 than 62. The risk factors are not abstract. They are Tuesday.

I went down this rabbit hole because a close friend had a reading she couldn’t explain, and I realised neither of us knew anything real about what blood pressure actually was — how it worked, what drove it, and what a person our age could actually do about it. The standard advice felt hollow: cut salt, exercise more, relax. We’d heard it. It didn’t tell us anything we could use.

So I went to the research instead. What I found is that this is a topic that deserves to be understood at the systems level — not just as a number to keep below a threshold, but as a reflection of how your nervous system, hormones, kidneys, and vascular health are functioning together. And when you understand it that way, the interventions that actually work start to make a lot more sense.

This is the guide I wish existed before I started looking into this properly.

Here’s what this Deep Dive covers:

Section 1: The Silent Killer You Don’t Feel — Until It’s Too Late

1. What Is Blood Pressure and What Does “High” Actually Mean?

2. Why Your Body Pushes Blood Pressure Higher — And Keeps It There

3. The Minerals Your Diet Is Missing That Are Quietly Raising Your Blood Pressure

4. You Can Feel Completely Fine and Still Have Dangerously High Blood Pressure

5. What Happens at the Doctor and What Those Numbers Actually Mean

6. Normal, Elevated, Stage 1, Stage 2: Where Do Your Numbers Actually Fall

1. What Is Blood Pressure and What Does “High” Actually Mean?

Blood pressure is a measure of the force your blood exerts against artery walls as your heart pumps. High blood pressure (or hypertension) is a condition where the force of blood against the artery walls is consistently too high. It’s expressed in two numbers:

• Systolic (pressure when the heart contracts) and

• Diastolic (pressure when the heart rests between beats).

For example, a normal reading like 118/76 mmHg means a systolic of 118 and a diastolic of 76. Hypertension according to ACC/AHA guidelines, the categories break down like this:

• Under 120/80: Normal — maintain healthy habits

• 120–129/under 80: Elevated — not yet hypertension, but worth acting on

• 130–139/80–89: Stage 1 hypertension — lifestyle changes and possibly medication depending on risk

• 140/90 or above: Stage 2 hypertension — medication likely recommended alongside lifestyle changes

• 180/120 or above: Hypertensive crisis — requires immediate medical attention

It’s often called the “silent killer” because most people feel no symptoms even when blood pressure is dangerously high. This silent nature makes hypertension a silent epidemic, millions have it unknowingly. The WHO’s 2025 global hypertension report estimates that 1.4 billion adults worldwide currently live with hypertension — yet fewer than one in five have it adequately controlled. Over time, uncontrolled high blood pressure quietly damages blood vessels and vital organs. This is why hypertension is so dangerous without symptoms: by the time headaches, dizziness, or other signs occur, serious damage may have already taken place. Early detection through routine blood pressure checks is crucial. Simply put: hypertension is common, often invisible, but very serious if untreated.

2. Why Your Body Pushes Blood Pressure Higher — And Keeps It There

Primary (essential) hypertension accounts for about 90–95% of cases and has no single identifiable cause. It develops from a mix of genetic factors and lifelong habits. As we age, our arteries naturally stiffen and may narrow due to cholesterol plaque leading to increased pressure. The renin–angiotensin–aldosterone system (RAAS) plays a key role: it’s the body’s hormone system for regulating blood volume and vessel tone. When blood pressure falls, the kidneys release renin, which triggers production of angiotensin II, a hormone that constricts blood vessels and stimulates aldosterone release. Aldosterone causes the kidneys to retain sodium (and thus water), increasing blood volume.

In hypertension, RAAS can become overactive causing chronic vasoconstriction and fluid retention that drive blood pressure up. The sympathetic nervous system (the “fight or flight” response) may also be in overdrive, keeping heart rate and vessel tone higher than normal. Even the kidneys themselves influence pressure set-points by controlling how much sodium and water the body holds onto. In some people, the kidneys require a higher pressure to excrete salt, effectively “resetting” blood pressure to a high level.

Meanwhile, secondary hypertension (5–10% cases) results from an underlying condition. Common causes include kidney diseases; like chronic kidney disease or renal artery narrowing, endocrine disorders, and others (I’ll explore these in Section 8). In any case, hypertension usually arises from a combination of factors: the blood vessels may constrict or harden thus raising resistance, the heart may pump harder or faster, the kidneys may retain too much fluid, and the nervous/hormonal systems may overstimulate pressure. Think of blood pressure like water in a hose: narrowing the nozzle (vasoconstriction) or turning up the faucet (blood volume) will increase the pressure. Hypertension often involves both; tighter vessels and higher fluid volume.

The renin-angiotensin system exemplifies this dual effect. Angiotensin II tightens arteries and also leads to more fluid retention via aldosterone. Over time, these mechanisms become maladaptive. The result is chronically elevated pressure that makes the heart and vessels work overtime. Primary hypertension tends to develop gradually over years, influenced by lifestyle (diet, exercise, stress) and genetic predispositions. It is complex, but understanding these basics, vessel tone and fluid volume gives insight into why treating hypertension often requires a multifaceted approach e.g. medications that relax vessels or help the body shed water.

3. The Minerals Your Diet Is Missing That Are Quietly Raising Your Blood Pressure

Modern diets can leave us deficient in key minerals and nutrients that help regulate blood pressure. One common example is magnesium.

Magnesium: The Mineral That Helps Your Vessels Relax

Magnesium is nature’s calcium channel blocker, it helps blood vessels relax. A lack of magnesium is linked to higher blood pressure, and increasing magnesium intake (through diet or supplements) can produce modest reductions in BP. Magnesium supports the production of nitric oxide (NO), a molecule that signals arteries to dilate (widen). Low magnesium, therefore, may impair this vasodilation pathway. It’s estimated that 500–1000 mg of magnesium daily could lower blood pressure by up to 5.6/2.8 mmHg in some people though results vary. Diets rich in green leafy vegetables, nuts, seeds, and whole grains provide magnesium that many processed-food diets lack.

Potassium: The Quiet Counterbalance to Sodium

Potassium works hand in hand with magnesium. Potassium helps the body excrete sodium and relax blood vessel walls. Diets low in potassium and high in sodium are a recipe for hypertension. Conversely, increasing potassium while reducing excess sodium is strongly proven to lower blood pressure. High potassium foods include fruits (like bananas, oranges), vegetables (potatoes, avocados, spinach), beans, and dairy. Sodium, of course, is a major culprit as high salt intake causes water retention and raises blood volume, increasing pressure. Many people consume far above the recommended <2.3 grams of sodium per day. Balancing sodium and potassium is critical: potassium helps offset sodium’s pressure raising effect.

Calcium & Vessel Tension: The Mineral You’re Probably Undereating

Calcium is another player. While the evidence is mixed, some studies suggest that inadequate calcium intake may contribute to high blood pressure. Calcium is involved in blood vessel contraction and dilation. Low calcium might trigger the body to retain more sodium or cause arterial constriction. Diets following the DASH plan (rich in low-fat dairy) have shown blood pressure improvements, hinting that sufficient calcium (along with magnesium and potassium) is beneficial.

Vitamin D: The Hormone-Like Nutrient Your Arteries Depend On

Vitamin D deficiency has been linked to hypertension as well. Vitamin D isn’t just for bones. It also interacts with blood vessels and the immune system. Low vitamin D levels are associated with arterial stiffness and endothelial dysfunction. One reason is that vitamin D helps stimulate nitric oxide production for vessel relaxation. In lab studies, adding vitamin D increased nitric oxide (the vessel-widening compound) and reduced inflammatory substances that damage vessels. Insufficient vitamin D may therefore reduce nitric oxide availability, contributing to higher vascular tone. Observational research shows people with deficient vitamin D tend to have higher rates of hypertension and are at greater risk of stroke. Getting safe sun exposure or supplements to reach adequate vitamin D levels (and thus support healthy blood vessels) may be helpful if one is deficient.

Omega-3s: The Anti-Inflammatory Fat Your Heart Loves

Lastly, a deficiency in omega-3 fatty acids (the heart healthy fats found in fish, flaxseed, etc.) may remove a natural protection against high blood pressure. Omega-3s (like EPA and DHA) have anti-inflammatory effects and help the endothelium (vessel lining) function well. Studies show that consuming about 2–3 grams per day of omega-3s can modestly reduce blood pressure. One analysis found around 4.5 mmHg drop in systolic BP for people with hypertension taking 3g of omega-3 daily. If someone’s diet is very low in omega-3 (and high in pro-inflammatory fats), they might miss out on these blood pressure lowering benefits. Omega-3s help vessels stay flexible and may stimulate nitric oxide, so a deficiency could tilt the body toward higher pressure. Eating fatty fish (like salmon, tuna) or plant sources of omega-3 (chia seeds, walnuts) regularly is a natural way to support healthy blood pressure.

In summary, nutrient imbalances can contribute to hypertension. Modern diets high in processed foods often lack magnesium and potassium while overloading sodium creating a perfect storm for raising blood pressure. Ensuring adequate magnesium, potassium, calcium, vitamin D, and omega-3s through a balanced diet or supplements (if needed) can improve vascular health and complement blood pressure management. Later, I’ll discuss specific foods and supplements to boost these nutrients naturally.

4. You Can Feel Completely Fine and Still Have Dangerously High Blood Pressure

One of the most important things to understand about hypertension: it is almost entirely asymptomatic. You can feel perfectly fine while high blood pressure is quietly damaging your body. That’s why routine screening is so important. In most people, hypertension is asymptomatic (“silent”) hence the nickname “silent killer.” In fact, many patients only discover it during a doctor’s visit or through home monitoring, not because they felt anything wrong.

That said, extremely high blood pressure (or a sudden spike) can sometimes produce symptoms. Possible warning signs include:

However, these symptoms are not reliable indicators as they typically occur only in severe cases or hypertensive crises. For example, a hypertensive crisis (BP >180/120) may present with a severe headache, anxiety, nosebleed, and shortness of breath, and is a medical emergency. But someone with moderate hypertension (say 160/100) might have no clue.

It’s a common myth that high blood pressure always causes noticeable symptoms like frequent headaches or nosebleeds. In reality, if such symptoms occur, it’s usually because blood pressure has reached dangerously high levels over time. For instance, nosebleeds and headaches can happen, but by then BP may be crisis-level and organ damage could be underway. As one doctor put it: when symptoms do occur, high blood pressure may have already reached life-threatening levels.

Therefore, do not wait for symptoms to gauge your blood pressure status. The absence of symptoms is not a sign that all is well. Millions of people walking around with 140/90 or 160/100 feel normal. The first symptom of hypertension could tragically be a heart attack or stroke. That’s why hypertension is often discovered when patients present with complications rather than complaints of blood pressure itself.

This is especially relevant for the 15–35 age group, where there’s a cultural assumption that high blood pressure is an older person’s condition. The statistics don’t support that anymore.

In summary, often no symptoms – which means the only way to know your blood pressure is to measure it. Home blood pressure monitors and periodic checks at the clinic are invaluable. Be aware of subtle clues too: some hypertensive individuals report occasional flushed face, pounding in the ears or chest, or slight visual disturbances when BP is high. But these are inconsistent. Treat any severe acute symptoms (like intense headache + high BP reading, chest pain, neurological changes) as an emergency. Otherwise, assume hypertension is silent and stay vigilant with monitoring.

5. What Happens at the Doctor and What Those Numbers Actually Mean

Diagnosing hypertension is straightforward: it’s based on blood pressure measurements. Typically, if your BP is high on at least two separate days/visits, you may be diagnosed with hypertension. Doctors measure with a cuff and stethoscope or digital monitor. It’s important that the reading is done under standardized conditions; sitting quietly for 5 minutes, arm at heart level, no caffeine or smoking 30 minutes prior, to get an accurate baseline reading.

Understanding the two numbers is key: systolic (top number) is the pressure when the heart contracts, and diastolic (bottom number) is the pressure when the heart relaxes. Both are measured in mmHg (millimeters of mercury). A reading consistently ≥130/80 (per current American guidelines) or ≥140/90 (per older and global standards) indicates hypertension.

Sometimes, blood pressure readings in a medical office are higher than normal due to anxiety this is known as “white coat hypertension.” The nerves of being in a doctor’s office can spike the pressure temporarily. White coat hypertension is not benign: it occurs in an estimated 10–30% of patients and can be a precursor to sustained hypertension. To sort this out, doctors may use home monitoring or 24-hour ambulatory blood pressure monitoring (ABPM). With ABPM, you wear a portable device that takes BP readings throughout your normal day and night. This provides a true picture of your typical blood pressure. If your office readings are high but home/ABPM readings are normal, you likely have white coat hypertension. Current guidelines don’t recommend drug treatment for isolated white coat hypertension if ambulatory readings are normal, but such patients should be monitored closely as many will develop true hypertension over time.

Conversely, some people have “masked hypertension,” where readings are normal at the doctor’s but high at home perhaps due to stress or lifestyle factors outside the clinic. Up to 1 in 3 adults with apparently normal office BPs may have masked hypertension identified by home monitoring. That’s why home blood pressure cuffs are so useful they can reveal if your pressure creeps up during daily life.

Ambulatory monitoring is especially helpful to confirm a diagnosis and check for patterns: for example, whether your BP dips at night (it should normally drop about 10-15% during sleep; if not, that can signal higher risk). It also can capture morning surges or episodes of very high BP that might be missed in single office checks.

In practice, a diagnosis is made after repeated measurements. A doctor might ask you to record your BP at home twice a day for a week. If the average of those readings is elevated, that clinches the diagnosis. They may also do basic tests (blood tests for kidney function, etc.) to see if there’s any secondary cause or damage.

It’s worth noting that on any given day, blood pressure fluctuates. Stress, exercise, even talking can raise it transiently. That’s why a single high reading isn’t enough to diagnose hypertension, it must be persistent. “Persistent” is usually defined as two or more properly measured readings ≥130/80 or ≥140/90 on different days. The threshold might differ slightly by organization, but the process is similar.

In summary, hypertension is diagnosed by measuring it – no fancy scans or symptoms needed, just a blood pressure cuff. Ensure readings are accurate and representative of your usual levels. If you suspect white coat effect, discuss home or ambulatory monitoring with your provider.

6. Normal, Elevated, Stage 1, Stage 2: Where Do Your Numbers Actually Fall?

Health professionals classify blood pressure into categories to better guide treatment. According to the American College of Cardiology/American Heart Association (ACC/AHA) 2017 guidelines (widely used in the U.S.), the stages are:

These categories highlight that both numbers matter. For instance, 135/95 is stage 2 because the diastolic of 95 is in stage 2 range, even though systolic is 135. On the flip side, 145/78 is stage 2 (systolic in stage 2) despite a normal diastolic.

It’s also notable that the ACC/AHA thresholds are a bit more aggressive than older schemes. Organizations like WHO or the International Society of Hypertension often consider 140/90 as the cutoff for hypertension. The ACC/AHA introduced the 130/80 definition to encourage earlier intervention, as evidence showed cardiovascular risk begins rising at those slightly lower levels. Under these guidelines, an “Elevated” BP (120-129/<80) is essentially pre-hypertension, a critical window for lifestyle changes to prevent progression.

To put it simply:

• <120/80: great, maintain healthy habits.

• 120-129/less than 80: not yet hypertension, but higher than ideal so take action (diet, exercise) to prevent further rise.

• 130-139/80-89: Stage 1 – officially high BP. Depending on your risk factors, lifestyle changes and maybe medication might be recommended.

• ≥140/90: Stage 2 – clearly high, likely requiring medication in addition to lifestyle changes.

• Less than 180/120: Crisis – requires immediate medical attention, especially if symptomatic (e.g. severe headache, vision changes, shortness of breath, etc.).

Understanding your category helps in gauging urgency. For instance, someone with 128/78 (elevated) should take steps to bring it down, even though it’s not “hypertension” yet. Meanwhile, someone at 145/95 (stage 2) should work closely with a doctor on a treatment plan to avoid serious complications. These stages provide a roadmap for both patients and providers to stratify risk and act accordingly.

Section 1 was the foundation.

You now know what the numbers mean, why your body drives blood pressure up and keeps it there, which nutritional gaps are quietly making it worse, and maybe most importantly — why you can feel completely fine while something serious is accumulating. That last part tends to stay with people.

But here’s where it gets more complicated. And more specific to you.

Because the story of blood pressure in women isn’t the same as the general story. The pill can raise it and most women on hormonal contraception are never told to monitor theirs. Your thyroid, your kidneys, a hormonal imbalance you might not know about yet — any of these can be the actual driver, which means the standard lifestyle advice will never be enough on its own. The oestrogen that’s been quietly protecting your cardiovascular system since puberty doesn’t stay forever. And then there’s pregnancy, where elevated blood pressure isn’t just a symptom to manage, but a warning signal with implications that follow you for decades.

Part 2 is where the research gets women-specific. And where the practical part starts.

In Part 2:

Section 2 covers what’s actually behind high blood pressure in women; the pill, the thyroid, the kidneys, the hormonal conditions that often go undiagnosed for years and what happens when oestrogen stops protecting you at menopause.

Section 3 is the evidence on what actually lowers blood pressure. Not the “cut salt and relax” version. The DASH diet versus Mediterranean eating, what the research says about hibiscus tea and magnesium and garlic, a full week of meals that are designed around blood pressure and actually look good, and the specific breathing practice that clinical studies show produces measurable reductions in just five minutes a day.

Section 4 covers the numbers that mean see a doctor right now, how every class of blood pressure medication actually works and why your doctor chose it, and, the section most women never get access to — what gestational hypertension and preeclampsia actually are, why a history of either doubles your long-term cardiovascular risk, and what to do with that information after pregnancy ends.

The 24-year-old from the beginning of this post? She came back for Part 2.

Upgrade to read Part 2 →

Not to see if they need a file. Not to check your polish. Look at them the way a doctor would — the colour, the shape, the texture, the lines. Because your nails aren’t just keratin. They’re a slow-moving record of everything your body has been through over the past six months: the illness, the stress, the deficiencies, the things your blood work might not have caught yet.

In this edition of Between Saturdays, I’am going through four things your nails might be telling you right now, including one that gets misdiagnosed for an average of ten years, and one that most of the internet has completely wrong.

Let’s get into it.

Caught My Eye…

The Dark Streak That Gets Ignored For Years

Most people, if they noticed a dark vertical streak running down one of their nails, would assume it was a bruise. They’d wait for it to grow out. They’d forget about it.

That assumption has cost lives.

A dark longitudinal band under the nail — a line running from the base to the tip, brown or black in colour is the most common presenting sign of subungual melanoma: a rare but serious cancer that develops under the nail.

Unlike other melanomas, it has no connection to UV exposure. It doesn’t come from sunbathing or tanning beds. It can develop on anyone, at any age, regardless of skin tone. In fact, among people with darkly pigmented skin, subungual melanoma accounts for up to 30% of all melanoma diagnoses — making it disproportionately common in Black, Asian, and Hispanic populations.

The reason outcomes are often so poor is not because the cancer is inherently untreatable. It’s because it is almost universally diagnosed late. A 2019 study found that the average time from the appearance of a pigmented nail lesion to biopsy was more than ten years. Ten years of being told it was a bruise, a fungal infection, a harmless pigmentation. In most cases by the time a histologic diagnosis is made, the lesion is already deep. The 5-year survival rate when caught early sits around 97%. When caught late, it drops to between 15–20%.

This is a cancer where the difference between early and late diagnosis is the difference between a minor procedure, losing a digit or worse.

The warning signs to know: a dark band wider than 3mm, a band that is triangular in shape (wider at the base than at the tip), irregular or blurred edges, pigment that spreads onto the surrounding skin at the base of the nail, or a band that appeared recently and is growing. Dermatologists use an ABCDEF rule for subungual melanoma specifically:

• Age,

• Band characteristics,

• Change in the nail,

• Digit involved,

• Extension of pigment, and

• Family history.

Any band that you can’t explain with a specific remembered injury, or that is changing, is worth having assessed by a dermatologist promptly.

Take your nail polish off before your next skin check. Ask your GP or dermatologist to look.

Your Nails Recorded Your Illness — Even If You Didn’t Know You’d Had One

If you ever had COVID-19, or a serious fever, or a period of extreme physical stress, there is a chance your nails quietly recorded it — weeks or months after the fact.

Beau’s lines are horizontal grooves that run across the width of the nail. They form when the nail matrix aka the tissue at the base of the nail responsible for producing new growth temporarily slows down or stops completely. The nail keeps growing, but there’s a gap where it paused: a transverse dent in the plate that moves outward as the nail grows, like a ring on a tree.

A 2024 systematic review published in Pathogens found significant evidence linking Beau’s lines to COVID-19 infection, particularly severe cases requiring hospitalisation. The lines typically appear two to three weeks after the systemic insult, and their distance from the nail fold can be used to estimate roughly when the illness occurred — fingernails grow at approximately 2–3mm per month, so a groove sitting 6mm from the proximal fold means the event happened around two months ago.

But COVID-19 is just one trigger. Beau’s lines can follow any significant physiological disruption: severe febrile illness, chemotherapy cycles, extreme malnutrition, Kawasaki disease, major surgery, or acute emotional trauma — a death, a breakdown, a prolonged period of severe stress. Essentially, when the body reaches a triage situation, it stops building nails and redirects resources. The groove that appears weeks later is the physical receipt.

As one Cleveland Clinic dermatologist put it: your body was preoccupied, and growing nails is much lower on the priority list when you’re extremely sick.

The lines are harmless and will grow out. But if you notice a horizontal groove across multiple nails that you can’t explain by local trauma, it’s worth thinking back over the past two to three months and considering whether your body went through something significant, even something you thought you recovered from.

White Spots: The Myth That Won’t Die

If you’ve ever had white spots on your nails, you were almost certainly told one of these things: you’re low in calcium, you’re low in zinc, or you’re not absorbing vitamins properly.

You were almost certainly wrong — and so was whoever told you.

A study published in the Journal of Human Nutrition and Dietetics set out specifically to test this belief. Researchers surveyed 82 university students, measured their calcium and zinc intake scores using a validated food frequency questionnaire, and counted the white spots on their nails. The result: there was no statistically significant association between white spots and calcium intake, zinc intake, age, gender, hand dominance, or multivitamin use. The only factor that correlated with white spots was one variable: how frequently participants engaged in activities that knocked their hands.

Punctate leukonychia — the small white spots most people get is, in the overwhelming majority of cases, minor trauma to the nail matrix. The matrix sits beneath the skin at the base of your nail, and it doesn’t take much to disrupt it: an aggressive manicure, bumping your hand, pressing on your cuticles, wearing tight rings. The disruption happens, you don’t notice it, and two to six weeks later the spot emerges as the nail grows out. By the time you see it, the event that caused it is long forgotten.

The zinc-deficiency myth, in particular, has taken on a life of its own — spread by wellness influencers, supplement brands, and the kind of content that tells you every physical complaint is a nutritional deficiency you need to buy your way out of. According to the PMC review Leukonychia: What Can White Nails Tell Us?, punctate leukonychia

That said, nuance matters. If your white spots are persistent, spreading, involve the entire nail, or are accompanied by nail thickening, brittleness, changes in skin or hair, or other symptoms, they can occasionally point to fungal infections, psoriasis, or in rarer cases, systemic conditions. Zinc deficiency can cause leukonychia, but typically in severe, chronic deficiency and not the garden-variety kind your supplement brand is marketing to you.

The rule of thumb: isolated, small white spots that move as your nail grows are almost always old trauma, not a deficiency. Recurring spots across multiple nails with other symptoms are worth getting checked.

Spoon-Shaped Nails: When Your Body Has Run Out of Iron

The last one is quieter and more common than most people realise, especially in women.

Koilonychia is the medical term for nails that have lost their normal curve and become flat, then concave — literally scooped out, like the bowl of a spoon. In early stages, nails may just seem unusually flat or brittle, prone to splitting at the tips. As it progresses, the nail plate becomes visibly depressed in the centre and raised at the edges, sometimes enough that a water droplet placed on the nail will hold its shape rather than rolling off.

The most common cause is chronic iron deficiency anaemia. Iron deficiency is the commonest nutritional cause of anaemia worldwide, and it is considerably more prevalent in women of reproductive age — a combination of menstrual blood loss, dietary patterns, and the fact that iron deficiency frequently goes unrecognised and untreated for years before it reaches the point of anaemia. The nail changes aren’t caused by the anaemia itself but by iron depletion at a cellular level. Reduced iron in the iron-containing enzymes of epithelial cells weakens the connective tissue beneath the nail plate, causing it to deform under mechanical pressure.

A case report published in The American Journal of Medicine documented a patient whose spoon nails resolved entirely after 16 weeks of oral iron supplementation, demonstrating that the deformity is reversible when the underlying deficiency is addressed.

The reason this matters for our age group specifically: iron deficiency is common, it’s underdiagnosed, and its symptoms are often attributed to burnout, poor sleep, or stress. Fatigue, cold hands and feet, brain fog, brittle nails, hair thinning, pale inner eyelids — these are all signs that can be easy to explain away. Koilonychia is a physical sign that the deficiency has been going on long enough to change the structure of your nails.

If your nails are flattening or beginning to look concave, it’s worth asking your GP for a full iron panel and not just haemoglobin, but ferritin and transferrin saturation. You can be functionally iron deficient with a haemoglobin level that looks normal.

In Summary

Four things your nails might be recording right now:

→ A dark vertical streak is not automatically a bruise. It could be subungual melanoma, a cancer with a 97% survival rate when caught early, and a 15–20% rate when caught late. Average time to diagnosis: ten years. Take your polish off and look.

→ Horizontal grooves (Beau’s lines) are your body’s receipt for a stressful event: an illness, a fever, chemotherapy, extreme stress. They appear 2–3 weeks after the event and can be used to date roughly when it occurred.

→ White spots are almost always old trauma from knocking your nail matrix. The zinc and calcium deficiency myth has no solid research behind it. Isolated small spots that move as the nail grows are harmless. Persistent, spreading spots with other symptoms are worth checking.

→ Concave, spoon-shaped nails (koilonychia) are a physical sign of chronic iron deficiency — common in women of reproductive age, often missed because the symptoms look like burnout. Reversible with treatment. Ask for a ferritin test, not just haemoglobin.

The information in this post is for educational purposes only and does not constitute medical advice. If you notice any concerning nail changes, please consult a qualified healthcare professional or dermatologist. Do not self-diagnose based on nail appearance alone.

Detailed Readings

Subungual Melanoma — StatPearls, NCBI Bookshelf

Beau’s Lines and COVID-19: A Systematic Review — Pathogens, 2024

Leukonychia on Finger Nails as a Marker of Calcium/Zinc Deficiency — Journal of Human Nutrition and Dietetics, 2011

Koilonychia in Iron Deficiency Anaemia — American Journal of Medicine, 2022

This edition of Between Saturdays is about the things we’re doing right now, tonight, without realising they’re costing us. The collagen we’re buying. The sleep we’re cutting short. The loneliness we’re numbing with our phones. And the thing that works better than medication for depression that most of us still aren’t taking seriously as an actual treatment.

The research this week isn’t gentle. But it is hopeful. And it’s all pointing to the same place: the habits that feel harmless or even self-caring aren’t always what they seem.

Let’s get into it.

Caught My Eye…

The Collagen Supplement Reckoning

If you’ve ever added collagen to your coffee, stirred it into your smoothie, or paid £30 for a bottle of marine collagen capsules, this one is for you.

A landmark meta-analysis published in The American Journal of Medicine in 2025 looked at 23 randomised controlled trials involving 1,474 participants and set out to do something no previous review had properly done: separate the studies funded by pharmaceutical companies from the ones that weren’t.

The finding? When you strip out the industry-funded research, the independent, high-quality trials show no significant benefit from oral collagen supplements for skin hydration, elasticity, or wrinkles. The studies showing improvements were predominantly low-quality and funded by the very companies selling the supplements. The researchers concluded there is “currently no clinical evidence to support the use of collagen supplements to prevent or treat skin aging.”

This doesn’t mean the science is settled — the collagen industry has pushed back, and some researchers have pointed to methodological issues in how the studies were categorised. A Tufts University dermatologist noted that oral collagen “can be considered” alongside other interventions, but is not currently recommended as a standalone treatment. The debate is ongoing.

What it does mean: the confident, unqualified marketing behind most collagen supplements is running well ahead of the independent evidence.

The irony? The thing most reliably destroying your body’s own collagen production is something the next story will get into. Spoiler: it’s free, and you’re probably not getting enough of it.

Your Body Repairs Itself at Night — But Only if You Let It

Here is something most skincare marketing never tells you: your skin has its own internal clock.

A 2025 review published in the journal Dermatology confirmed what researchers have been building toward for years — the skin is not just a passive barrier. It is an active, circadian-regulated organ with its own peripheral clock system that operates in sync with the body’s master circadian rhythm. During daylight hours, skin cells focus on protection: maintaining thickness, managing sebum, keeping the barrier intact against UV and pollution. At night, the skin shifts into repair mode. Collagen production increases. Cell turnover accelerates. DNA damage accumulated during the day gets corrected.

The catch? This whole system depends on sleep being regular and timed with natural light-dark cycles. Disrupted sleep, whether from late nights, inconsistent schedules, or the blue light flooding our screens after dark — throws the skin’s clock out of sync. When that happens, collagen production drops. The skin barrier weakens. Inflammation rises. Cellular repair slows.

A separate study from 2025 found that sleep deprivation specifically disrupts the circadian rhythm of estradiol in women, impairing both skin barrier function and dermal collagen synthesis. In other words: poor sleep doesn’t just make you look tired. It is, over time, structurally aging your skin at a cellular level.

This is the connection most people miss when they’re spending money on supplements. You can buy collagen in a powder or a pill, but if your sleep is disrupted, your skin’s own collagen-producing machinery is already running at reduced capacity. The most effective overnight skincare routine might simply be getting to bed earlier and putting your phone away.

Exercise Works. Better Than We Thought. For Depression and Anxiety.

In February 2026, a research team published what may be the most comprehensive analysis of exercise and mental health ever conducted. The umbrella review, published in the British Journal of Sports Medicine, pooled data from 57 meta-analyses covering 800 individual studies and nearly 58,000 participants aged 10 to 90.

The conclusion: exercise reduces symptoms of depression and anxiety comparably to and in some cases better than psychological therapy. When compared directly to antidepressant medication, exercise showed similar benefits, though the evidence for that comparison was less certain and the researchers were careful to note the limitations. This isn’t a case of overselling it: exercise works, meaningfully, across all age groups, exercise types, intensities, and formats.

What made the findings particularly striking for our age group: the benefits were most pronounced for emerging adults aged 18–30 and for postnatal women. Young adulthood — the exact period when many mental health conditions first emerge is also the moment when exercise has the most to offer.

The social dimension matters too. Group exercise and supervised formats showed the largest benefits overall, suggesting that the mental health gains from movement aren’t just physiological. Being in a room with other people, moving together, is doing something that medication and solo workouts can’t fully replicate.

A note of nuance: experts have rightly pointed out that exercise is not a replacement for medication or therapy in all cases, particularly for severe depression. But for mild to moderate symptoms, the evidence now supports treating exercise with the same seriousness we give to clinical interventions. As the study’s authors put it:

That line hit me. We’re not talking about going for a walk to clear your head. We’re talking about structured movement as a clinical tool, with evidence strong enough to belong in the same conversation as an antidepressant prescription.

We Are the Loneliest Generation. Despite Being the Most Connected.

In 2025, the data on loneliness among young people stopped being surprising and started being undeniable.

The Cigna Group’s Loneliness in America 2025 survey, drawn from over 7,500 adults, found that 57% of Americans are lonely and that younger generations, specifically Gen Z and Millennials, report significantly higher rates than older adults. Gen Z came in at 67% classified as lonely. Millennials at 65%. The generations who have grown up with the most digital connectivity in human history are, by every measure, the least socially connected in terms of felt belonging.

A separate Gallup analysis found that young people aged 15–34 in the US reported feeling lonelier than their counterparts across 38 other higher-income countries. And a December 2025 AARP study confirmed that loneliness is not, as many assumed, primarily a problem of old age — its sharpest edges are felt earlier in life than almost any other period.

The physical consequences are not abstract. The former US Surgeon General, in a formal advisory, compared the mortality impact of chronic loneliness to smoking 15 cigarettes a day, and linked it to elevated risk of cardiovascular disease, dementia, stroke, depression, anxiety, and premature death.

What makes this particularly hard to sit with is the paradox at its centre. We have more tools for connection than any generation before us. We can reach anyone, anywhere, at any time. And yet the data consistently shows that digital connection is not substituting for the felt sense of belonging that human health requires. Social media creates what researchers have called “connected isolation,” the experience of being surrounded by activity and interaction while feeling profoundly alone.

There’s no clean resolution here. The research doesn’t prescribe a fix. But it does keep pointing in the same direction: the depth of a few relationships matters more than the breadth of many. Showing up in person, however imperfectly, seems to be doing something that no amount of scrolling can replicate.

Sources: Cigna Loneliness in America 2025; AARP Loneliness Study, December 2025; Gallup World Poll 2025

In Summary

Four things your body is doing quietly, right now, that most of us aren’t thinking about:

→ The collagen supplement industry is running ahead of the independent science. The studies showing benefits are predominantly funded by the companies selling the products.

→ Your skin repairs itself at night — collagen builds, cells renew, damage corrects but only if your sleep is regular and your circadian rhythm is intact. Disrupted sleep structurally ages skin over time.

→ Exercise is a genuinely powerful treatment for depression and anxiety, with effects comparable to therapy and medication, especially for young adults. The evidence now supports prescribing it with the same confidence.

→ Gen Z and Millennials are the loneliest generations on record, despite being the most digitally connected. The health consequences are serious and well-documented. Digital connection is not an adequate substitute for felt belonging.

The information in this post is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional for personal health decisions.

Detailed Readings

Effects of Collagen Supplements on Skin Aging — American Journal of Medicine, 2025

The Sleep–Skin Axis — Dermatology, 2025

Exercise and Depression/Anxiety: Systematic Umbrella Review — British Journal of Sports Medicine, 2026

Loneliness in America 2025 — Cigna / Evernorth Research Institute