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Tanya Borowski Nutrition & Functional Medicine, The Candlemakers, West Street, Lewes (2026)

26/02/2026

Back with another lessons in nutrition chemistry - this week focusing on increasing plant diversity (and fibre) in your diet and my way of increasing that boost seasonally!

Let me know if you’d give this a whirl!

25/02/2026

We know that microbial diversity & abundance is significantly reduced in people with depression compared to healthy controls. That gut microbes regulate cortisol rhythms & the HPA axis. That early-life microbial colonisation shapes brain development in ways we're only just beginning to understand. And that microbiome shifts can precede clinical flares in inflammatory conditions like Crohn's disease — meaning the gut is often signalling long before symptoms do.

So what can we actually do about it? Diet remains one of THE most powerful levers we have. Specific dietary components, fibre, resistant starch, polyphenols, phytochemicals including flavonoids & isoflavones, & yes, vitamin D, positively influence microbial composition & diversity & in doing so modulate immune & inflammatory pathways in profound ways. Mostly plant-based dietary patterns are consistently associated with greater microbial diversity & higher production of short chain fatty acids (SCFAs), the metabolites our gut lining (intestinal epithelium), immune system & metabolism all appear to “run’ on.

So here's the challenge - hitting 🔢 30g of fibre per day & 🌿 30 different plants per week. Why 30 plants? The landmark American Gut Project found that people eating 30+ different plant foods per week had significantly more diverse microbiomes than those eating 10 or fewer - regardless of whether they were vegan, vegetarian or omnivore. Diversity of plants = diversity of microbes.

What counts as a plant? Vegetables, fruits, wholegrains, legumes, nuts, seeds, herbs & spices all count - each different one ticks a new box. That means your morning sprinkle of cinnamon counts. So does a handful of mixed seeds on your lunch salad or soup🍲

What does 30g of fibre actually look like in a day? 👉 Swipe to see a full day of meals hitting the target, without feeling like a chore.

Download my plant diversity tracker you & fill in as you go through the week (or screenshot the template in stories). Tick off each new plant as you eat it: aim for 30 by next Wed.

Drop a 🌿 in the comments if you're in - tomorrow I'll be sharing some practical tips & quick meal ideas to help you hit your numbers.

https://f.mtr.cool/bythsvwmrg

24/02/2026

I'm a conference addict - always on the lookout for learning more & challenging what I thought I knew, or had nailed! Because that's the beauty of science, it changes… we have to keep an open mind & drive to learn 🤓

I obsessively follow the work of the European Society of Neurogastroenterology & Motility (ESNM) - who provide a dedicated arm called Gut Microbiota for Health (GMFH), focusing on the microbiome's role in health & disease. Their 2025 year in review of published research in this area is brilliant.

Some of the biggest gut microbiome science themes emerging:
❤️ microbiome & cardiovascular risk: A metabolite called imidazole propionate (produced by specific gut bacteria) has been identified as a driver of arterial plaque & a potential early biomarker of cardiometabolic disease. We may soon be able to detect cardiovascular vulnerability before standard markers even flag it. Meanwhile, new mechanistic research is showing how gut microbes directly regulate bile acid production & cholesterol balance

🧠 The gut-brain axis: research is showing that intestinal dendritic cells can physically migrate to the brain & influence behaviour, meaning early-life microbial colonisation may have long-term neurological consequences. New findings are showing the microbiome helps regulate cortisol rhythms & circadian-HPA axis balance…. Literally mind blowing!

🔥 IBD, IBS & precision medicine: Microbiome shifts appear to precede clinical flares in Crohn's disease, opening the door to predictive biomarkers & more personalised treatment. As for IBS? A trial found that many people who believe they react to gluten may actually be responding to FODMAP load / expectation - huge clinical implications!

🧓 Prebiotics for cognitive ageing: A trial for adults over 60 found that an inulin + FOS blend improved cognitive performance versus placebo. The microbiome-brain connection is getting very practical, very fast.

The microbiome is no longer just a digestive story, it's cardiovascular, neurological, immunological, & metabolic - all combined!

This week I'll share practical tools for feeding your microbiome well: fibre, phytochemicals & a challenge you can actually do. Stay tuned.

See the full research finding here: https://f.mtr.cool/qnzczayzxi

19/02/2026

A 2024 UBC study from J C Prior & colleagues refines decades of assumptions about dysmenorrhoea (painful periods) & ovulation – with significant implications for how we assess cycle health!

Since 1938 (!!!) medical teaching has stated that menstrual cramps only occur in ovulatory cycles. The mechanism seemed straightforward: falling progesterone at cycle end triggers prostaglandin release, causing uterine contractions & pain. No ovulation = no progesterone = no cramps. Logical, neat - job done... Apparently not!

The authors of the study found:
➡️ They tracked 75 women (aged 19-35) through a single menstrual cycle, monitoring cramp presence, intensity & duration via daily diaries. They compared 35 anovulatory cycles with 40 ovulatory cycles.
➡️ The unexpected finding? Not only did anovulatory cycles produce cramps – they were worse. More painful, longer duration & higher overall cramp scores than ovulatory cycles.
➡️ Cycle lengths were identical between groups (fewer than 10% exceeded 35 days in either cohort), so this wasn't about prolonged cycles or heavy withdrawal bleeds.

This challenges fundamental assumptions we've relied on for nearly a century >>> swipe to read more

Of course we have to consider the context. Interestingly, nearly one-third of cycles in this study were anovulatory – likely reflecting pandemic-era stress (study was conducted in the pandemic) on the HPO axis. This aligns with what we know about stress, underfueling & ovulatory suppression.

A meta-analysis of 4 previous studies confirmed cramps occur in both cycle types, though they were twice as likely in ovulatory cycles (supporting conventional thinking but still contradicting the absolutist "only ovulatory cycles" claim).

The clinical implications for practitioners? It allows us to reframe our thinking, painful periods do not confirm ovulation. For women experiencing dysmenorrhoea: you may not be producing progesterone despite regular, crampy cycles.

For researchers? it's time to revisit first principles & understand what's actually happening at the endometrial level. Sometimes the most valuable research doesn't give us answers – it shows us we've been asking the wrong questions.

18/02/2026

In yesterday's post I highlighted the vital importance of ovulatory cycles to produce progesterone, and the two distinct patterns behind low progesterone; anovulation—when ovulation simply doesn't occur, meaning no corpus luteum forms and therefore no progesterone is produced at all. The second is a shortened luteal phase—you do ovulate and progesterone is produced, but the window is inadequate, and levels fail to reach the optimal concentrations needed for full physiological function.

“Diagnosing” menstrual cycle disturbances typically relies on blood tests or other laboratory investigations. However, blood tests have significant diagnostic limitations that we need to acknowledge.

Firstly, hormonal patterns are by nature substantial variabile—not only between different women, but also from cycle to cycle within the same individual.

Secondly, the pulsatile nature of oestrogen, progesterone, testosterone, LH and FSH secretion means that a single snapshot measurement can be profoundly misleading and fails to capture the dynamic hormonal picture. Finally, accurate diagnosis of a shortened luteal phase actually requires serial daily progesterone measurements throughout the luteal phase—something rarely feasible in clinical practice.

There are 3 ways , which you can combine, to assess ovulation and length of luteal phase >>> Swipe

17/02/2026

From menarche onwards, ovulation is the only way a cycling woman produces meaningful progesterone. This is why ovulatory cycles are considered a vital sign – not just for fertility, but for overall health and wellbeing.

Progesterone receptors exist throughout the entire body – from brain to bone, cardiovascular system to immune function. This isn't a reproductive hormone. It's a whole-body signal - like a hug!

We assume regular cycles (roughly monthly) means we're ovulating and therefore producing progesterone …. right? …. not necessarily.

Even in women with what is deemed to be “textbook” 28-day cycles, research shows approximately one-third of regular asymptomatic menstrual cycles have ovulatory disturbances when we actually measure progesterone.

"Ovulatory disturbance" - what’s this?

Ok, firstly, let’s define healthy menstrual cycle parameters: A cycle length of 21–36 days that a woman consistently maintains, with a luteal phase of at least 10 days. Disturbances to these parameters; is an umbrella term that covers:
➡️ Anovulatory cycles (no egg released), no egg = no progesterone
➡️ Short luteal phase (ovulation occurs but the luteal phase is

12/02/2026

Next concept to discuss in my mini series on testing: timing. And this is where s*x hormones really come into their own.

Today, let's talk about oestrogen.

Here's something that creates endless confusion—and I hear this constantly in clinical practice: A woman has an oestradiol level of 800 pmol/L. Is this "oestrogen dominance" (don't get me started), normal, or pathological?

The answer? It depends entirely on when you tested in her cycle and where she is in her lifecycle.
Mid-cycle? Perfectly normal - that's the pre-ovulatory surge. Early follicular phase (Day 2-5)? That's concerning and needs investigation.

Oestradiol fluctuates dramatically across the menstrual cycle - the same woman can range from 100 pmol/L to 1500 pmol/L depending on cycle day. Testing without considering cycle phase makes results uninterpretable.

The gold standard: Day 2-5 (early follicular phase)

At this phase, oestradiol should be low (50-150 pmol/L). Elevated early follicular oestradiol can indicate diminished ovarian reserve, functional cysts, or incorrect timing.

The clinical reality: Most random oestradiol tests in cycling women are essentially worthless because timing wasn't considered. We're measuring the tide without knowing if it's high or low.

And in perimenopause? Hormone testing becomes even less useful - cycles are irregular, ovulation is sporadic, and levels fluctuate wildly. Determining if you have entered perimenopause is primarily clinical, not biochemical( ie no test).

This is the 2nd example in our testing series where understanding physiology reveals why accurate measurement isn't enough - you need to know WHEN and WHAT you're actually assessing.

Swipe through to understand when oestradiol testing is useful - and when it's just noise.

Next in this series: Progesterone - the only hormone where timing is absolutely non-negotiable

10/02/2026

I wanted to run a series of posts on testing - which nutrients and hormones we can actually assess, when we should test (hormones), and what medium - blood (serum), urine or hair.
Today, starting with calcium - the most abundant mineral in the human body.

Ok, here's what many don't realise: the very mechanism that keeps serum calcium normal( and there’s less than 1% in blodd btw) is the very same one that masks deficiency. In other words, blood work can look perfect while their bones are being depleted.

This matters because we're making clinical decisions based on tests that simply don't measure what we think they're measuring.

In this series, we'll cover:
🧪 Why tight physiological regulation makes some serum tests useless for status assessment
⏰ When timing transforms a test from meaningless to essential (hello, hormones)
💇‍♀️ Why some testing modalities have no place in clinical practice (I'm looking at you, Hair Mineral Analysis )
✅ Understanding test validity isn't pedantic - it's the difference between effective clinical reasoning and guesswork with a veneer of data.

Starting with calcium because it's the perfect example of elegant homeostasis creating a clinical blind spot.

Swipe through to understand why normal serum calcium tells you almost nothing about calcium status - and what to assess instead.

What test confuses you most in practice? Drop it in the comments - it might be next in this series🤓

04/02/2026

I’m I tad obsessed with Olive Oil at the minute, and so I wanted to have a little chat with you all about why not all olive oils are created equal.

The polyphenol content in your olive oil determines whether it's actually therapeutic or just……. oil. And most supermarket brands? They're barely scraping the minimum.

I've been using Foods delicious OO lately and the difference is immediately obvious - that peppery finish that hits the back of your throat (That's the polyphenols doing their job) 👊

Swipe through to learn what to look for and why these plant compounds are so powerful for inflammation, cardiovascular health, and longevity ➡️

This isn't just about "healthy fats" - it's about the polyphenol payload that makes olive oil medicinal.

What's your go-to olive oil? 👇

29/01/2026

This myopic view isn't just short-sighted, it's a massive failing in our healthcare system. What are we waiting for – until a woman actually fractures before we assess her bones? Surely prevention is a better approach?

It seems to me that many in GP settings don't realise that by the time bone density drops enough to show osteoporosis on a DEXA scan, you've already lost 30% of your bone mass. We're catching it far too late.

And we're relying on assessment tools that only tell part of the story. DEXA measures bone mineral density – how much mineral is present – but nothing about bone quality, architecture, or active remodelling. It’s entirely possible to have "normal" density and still have fragile bones.

We need tools that catch deterioration earlier and tell us more than just mineral density so we can work from a standpoint of prevention, rather than chasing a “cure”. Here's what we should be measuring to truly understand bone health and fracture risk: 👉

The bottom line? Bone density alone doesn't tell you enough. We need to assess both remodelling markers (CTX and P1NP) to understand what's happening metabolically, and imaging that evaluates bone quality and architecture (REMS) to truly understand fracture risk.

Waiting for a fracture – or even osteoporosis on a DEXA – means we've missed years of opportunity for intervention.

Prevention requires better assessment. Period.

$Piers Morgan made headlines last week after a fall resulted in a fractured femur, requiring hip replacement surgery. At ...$

27/01/2026

Piers Morgan made headlines last week after a fall resulted in a fractured femur, requiring hip replacement surgery. At just 60 years old (and yes, younger followers – this IS 😉 young for a fracture), this incident highlights an issue we don't talk about enough: bone health and fracture risk.

Here's what rarely gets discussed or explained in routine wellness checks: : bone is living tissue, constantly remodelling through a dynamic process of breakdown and rebuilding. This remodelling requires far more than just calcium – it's a complex orchestra of nutrients, hormones, and lifestyle factors that determine whether our bones remain resilient or become fragile.

The oversimplified "calcium and vitamin D" narrative does a disservice to bone health. True fracture prevention requires attention to the full spectrum of bone-supportive nutrients and mechanisms.

Swipe to learn more about what really supports skeletal integrity ➡️

Tanya Borowski Nutrition & Functional Medicine

26/02/2026

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24/02/2026

19/02/2026

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Monday	10am - 4pm
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