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

14/01/2026

New research from Aarhus University reveals what we have know for a while now; that as we enter late stage perimenopause > menopause when oestrogen declines, our brain cells lose their ability to efficiently use glucose for energy. But, the body is prepared for this metabolic plot twist - healthy brains can switch to using lipids instead. We call this “metabolic flexibility’.

This isn't just interesting biochemistry. It's a critical survival mechanism. But for the ~163 million people worldwide carrying two copies( homozygous) of the APOE4 gene variant, this metabolic flexibility is compromised.

The APOE4 variant blocks the receptor that nerve cells need to take up lipids- specifically saturated fats. When glucose metabolism declines (as it inevitably does with aging), and the backup fuel system can't engage, we see potential accelerated neurodegeneration.

Why this matters for women: We know oestrogen plays a crucial role in brain glucose metabolism. As estrogen declines through later stages of peri into menopause, we're seeing metabolic shifts that may unmask vulnerabilities—particularly in APOE4 carriers. This helps explain why 2/3 of Alzheimer's cases are women, and it's NOT just because we live longer.

Connecting to my food pyramid series last week: This research validates everything we've been discussing about dietary fats. The study specifically highlights polyunsaturated fatty acids (think omega-3-rich fish, algae, walnuts, flax) as potential protective factors. Your brain isn't just tolerating these fats - it's literally depending on them as alternative fuel as it can’t access the ketones as an alternative fuel from saturated fats.

This is personalised, preventative medicine in action: know your Nutrigenomics, understand your metabolic requirements, don’t fall for HRT cures all approach, and don't fear the fats your brain needs to thrive.

Look out for tomorrow’s lessons in nutritional chemistry where I walk you through where you find saturated fats and polyunsaturated fats in your foods.

Tx

08/01/2026

Yesterday we talked about appetite regulation - how incretins like GLP-1, PYY & CCK signal satiety when you prioritise protein & fibre.

But here's what happens after those nutrients are absorbed: your glyceamic & inflammatory responses determine metabolic health & flexibility or accelerating dysfunction & dis-ease

Consuming rapidly-absorbed carbs from refined grains & sugars (think colourless refined & processed “foods” aka CRAP) creates a sharp post meal glucose spike. This isn't benign.

High 🩸 glucose generates reactive oxygen species (ROS) >activating immune system> Forms AGEs (advanced glycation end products) > Damages blood vessel lining> Drives systemic inflammation🔥

We spend up to 18 hours per day in a post-fed state. That's multiple daily glucose spikes triggering inflammatory responses & oxidative damage. This chronic low-grade inflammation is THE underlying driver of metabolic syndrome, type 2 diabetes, cardiovascular disease & accelerated aging.

Back to rapidly-absorbed carbohydrates - not all carbs produce the same glycemic response, so lets not demonise an entire food group. Slowly-digested whole grains, legumes, & fibre-rich foods produce dramatically lower glucose excursions than refined flours & sugars found in CRAP “foods” 👉 Swipe

Why High-Fat meals complicate this? Fat delays gastric emptying, which can reduce glycemic response when combined with carbs. But high-fat meals—particularly those high in saturated & trans-fat - trigger their own inflammatory cascade.

So meals high in both refined carbohydrates & saturated fat? You're hitting both pathways simultaneously—glycemic-driven oxidative stress plus lipid-driven inflammation.

The Fasting Window: Metabolic Reset.
This is where time-restricted feeding (TRF) becomes mechanistically relevant—not as a weight-loss hack, but as a tool for glycemic control & inflammation reduction. TRF works through several pathways: 👉 Swipe

Next up, I'll bring all this together to show you how to meal sequence (the order to eat foods in) - to optimize all 3 axes simultaneously: satiety, glycemic response & oxidative/inflammatory load.

This is where the Mediterranean approach with TRF comes into play

07/01/2026

Welcome to my educational series; today we explain appetite; how it’s managed and what nutritional concepts best support this biochem.

Appetite regulation is far more sophisticated than just willpower.

It's a complex system orchestrated by three key players:
➡️ Neuronal - POMC/CART neurons suppress appetite (anorexigenic) ; NPY/AgRP neurons stimulate (orexigenic) it. Both located in the arcuate nucleus (ARC) of your hypothalamus.
➡️ Hormonal - Your gut produces ~100 bioactive peptide hormones called incretins. Yes, the gut is your largest endocrine organ + hormones like leptin from other tissues
➡️ External cues - sensory signals (sight, smell, taste), environmental factors (time of day, portion size, location), social context (we typically eat more alone than with others), and learned associations (think popcorn at the cinema).

What makes the ARC part of the 🧠 unique?
It lacks a complete blood-brain barrier, allowing circulating hormones - GLP-1, PYY, leptin, ghrelin—to directly access these appetite-regulating neurons.

These incretins can also signal via the vagal nerve, creating a direct gut-brain communication pathway.
When this system is balanced, energy intake matches expenditure. When dysregulated? Weight gain follows.

Let’s look at these incretins individually; what nutrients trigger their release and what impact they have on appetite - anorexigenic vs orexigenic 👉 Swipe

So what type of food do we need to be eating and in what order?

1️⃣ High fibre foods (vegetables & wholegrains) fermented by gut microbiota to produce SCFA’s which stimulate the release of the satiety hormones

2️⃣ Protein rich foods (animal meat , dairy, legumes, eggs, soya) provides the most satiety per calorie. Then wholegrain carbohydrates. Fat last.

So what does this actually mean for your meals?

Start with water-rich foods - soups, vegetables, salads. These create mechanical satiety through gastric distension. Your stomach physically registers fullness. Then bring in your protein. This is when you get that powerful incretin response - GLP-1, PYY - telling your brain 'okay, we're satisfied. And then - only then - your wholegrain carbs & fats

06/01/2026

6 days into January, and social feeds are already flooded with promises of a healthier you. Carnivore diets, keto shakes, endless "new you" fitness programmes, and of course the newly launched M&S & others to follow I’m sure range of “GLP-1 friendly ready meals”.

Don't misunderstand—I'm all for evolution in health science. But I fear the field and art of nutritional “therapy” advise has been overshadowed by quick hacks, social media hype, over obsession of wearable tracking devices and endless longevity-touting and menopause weight-gain "solving" supplements.

By now, you know me well enough to know I WON'T be jumping on here extolling the virtues of the next best diet promising the optimal weight management plan, Instead, this week I'm running a series of educational posts myth-busting and uncovering the truths around diet models and concepts that have come and gone over the years.

👉 Swipe through to see the rogue's gallery of diets we've been asked to try over the last century 👉

From Lucky Strike ci******es marketed as appetite suppressants in the 1920s to today's GLP-1 pharmaceutical revolution - we've been through it all.

I'll draw out the best salient features from each era and pull it all together with a model that incorporates the most researched, evidence-based combinations to deliver the three most important nutritional tennants for optimal health;

〰 ️Regulated Insulin response
😋 Appetite Regulation
🔥 Reduced inflammation—which is, of course, THE major contributor to weight gain, metabolic syndrome, type 2 diabetes, and cardiovascular disease.

I'll walk you through what actually works and why, arriving at a way of living that's therapeutic without sacrificing pleasure.After all, food serves as a powerful focal point for human connection as well as our health.

Tomorrow we’ll start with appetite regulation ….. No Lucky Strikes, I promise😉 !

30/12/2025

If like me you’ve been travelling over the festive season - then now is the perfect time to catch up on some podcasts…

After five seasons of expert interviews, the 2025 Best of Health podcast season incorporated more voices directly from the women sitting across from you in clinics every day. I felt that it was only right to give these women a voice and share their perspective on the challenges that come with women’s health diagnosis, treatment and the journey towards their optimal health.

I was honoured to spend time speaking to a stellar lineup on the Best of Health podcast season 6 including:
It’s hard to pick one as a standout episode as there are plenty of moments of insight in each - some of the topics we covered included:

🔍 - What happens when hormones are prescribed without proper investigation, and the practitioner-patient journey back to health

🦴 Sarah Magree + - a fabulous journey from diagnosis, management and road to recovery

♀️A truly inspirational conversation with sharing her lived experience of endometriosis- as you’ll hear it took 20 years for her to receive a formal diagnosis!

🌿 perspective on the conversations we need to be having about women's health beyond 2025.
🤼 A double trouble 3 way interview with two of my besties where we opened up the mic for a truly open and frank conversation!

🩺 - who brilliantly articulated why "society has normalized women feeling terrible" and shared her integrated approach combining TCM, Naturopathy, and Functional Medicine. Her wisdom on why we can't afford the "cheap fix" in healthcare really resonated.

💡 - cutting through the menopause noise after interviewing 150+ experts. Her message was crystal clear: "Your body is exquisite - it's an ecosystem. When you mess with one thing, there's a chain reaction." She reminded us not to outsource our health decisions but to learn enough to know what WE'RE doing.

Catch up on your podcast platform - search Tanya Borowski & watch out for season 7 coming in 2026!

27/12/2025

I love this time of year - it gives us the gift of time… to stop & reflect on the year: the ups and the downs. We all have achievements throughout the year, big & small, personal & professional - and they are ALL worth celebrating.

Combining hosting events with education brings me so much joy - esp when I get to connect with delegates and hear directly those moments of inspiration that you’ve taken away to implement in your own practice. Thank you for continuing to support the events I have hosted this year, and also those who have found me via education in 2025.

I’ve hugely grateful for the support of fabulous colleagues who have enriched my events by providing another dynamic and perspective in 2025: .randell

We are incredibly lucky that there are also so many commercial businesses in this field who are just as passionate about women’s health and education too - your commitment and support is unwavering

I’m also grateful to .lifestyle.medicine and for letting me take the stage (and inevitably run over time 🤣) to delve into the biochemistry and arising research on women’s health, perimenopause and bone health.

If you’re in a bit of limbo before New Year, don’t forget, if you’ve joined an event this year you can re-watch recordings (some event recordings are available on demand now) check out the slide decks, or catch up on some of my Lessons In Nutritional Chemistry right here including:
𐬺 Minerals: Electrolytes
🦴Bone Building Breakfast
🥦 Sulfurophane activation in Broccoli
❌Cholesterol in food myths
🧠The neuroscience of alcohol
🫒A dive into the mediterranean diet & olive oil

As always happens when I have a little downtime, the creative ideas start sparking so I’m already planning the next masterclass and events for 2026 - including some new topics I’ve not explored yet! And your feedback always matters - so if you have a topic you’d like me to discuss, please drop a comment & I’ll add it to the list!

18/12/2025

There are 2 main categories of contraceptive pills
1️⃣ Combined Pills contain mainly synthetic oestrogen (as ethinylestradiol) plus a synthetic progestin.
2️⃣ Progestin-Only Pills (Mini-Pill) Contain only a progestin, preferred for women who cannot take oestrogen, such as those with certain health conditions, breastfeeding, or with endometriosis

It's primarily the progestin that prevents pregnancy by:
• Suppressing ovulation
• Inhibiting secretion of stretchy, fertile cervical mucus
• Thickening cervical mucus to prevent s***m pe*******on
• Thinning the endometrial lining

Progestins are synthetic hormones created in labs. Most are derived from testosterone, some from progesterone (but don’t behave like natural progesterone) & one is derived from spironolactone

The chemical structure of progestins differs from natural progesterone, meaning they can bind to multiple receptor types, which explains their varying side effect profiles:

➡️ Progesterone receptors: Primary target for contraceptive effect

➡️ Androgen receptors:
• can cause acne, oily skin, hirsutism, weight gain
• Anti-androgenic activity can improve acne, hirsutism & seborrhoea

➡️ Mineralocorticoid receptors can affect salt & water balance

➡️ Anti-mineralocorticoid activity may reduce bloating & water retention

➡️ Glucocorticoid receptors: Can cause bloating, weight gain & May affect carbohydrate metabolism

For women with:
With acne, hirsutism, or PCOS: Consider pills with anti-androgenic progestins (drospirenone, cyproterone, dienogest)
With water retention/bloating: Consider drospirenone (anti-mineralocorticoid activity)
With endometriosis: Dienogest-containing pills or progestin-only pills may be beneficial
Concerned about VTE risk: Second-generation progestins (levonorgestrel) have the lowest documented VTE risk among combined pills
Who cannot take oestrogen: Progestin-only pills are the appropriate choice

Understanding which receptors a particular progestin binds to helps predict its side effect profile & therapeutic benefits, allowing for more personalised contraceptive selection based on individual needs & health considerations.

Swipe >>> for a guide table with brand examples.

17/12/2025

There are distinct differences as to why women “deal” with alcohol so differently than men: hormones, enzyme activity & body composition + the contraceptive pill adds another layer of complexity.

The hormonal component is where it gets really interesting (I think), so first let’s view through the lens of how the cyclical nature of a menstrual cycle effects alcohol metabolism.

Mid Follicular Phase (rising oestrogen): Oestrogen can enhance alcohol's effects & slow metabolism. Some women report feeling effects more intensely mid-cycle when oestrogen is at its peak.

Luteal Phase (progesterone dominant): Progesterone via its GABAergic properties naturally calms the nervous system. When progesterone drops before menstruation > loss of GABAergic support, some women unconsciously reach for alcohol because it mimics what progesterone was doing - enhancing GABA activity & providing calm.

This also plays into why in perimenopuase - when progesterone is dropping dramatically & oestrogen is higher than in reproductive years women tend to crave/ reach for that glass of wine!

What’s the Contraceptive Pill link? Synthetic progestins suppress ovulation but don't produce allopregnanolone - the GABAergic metabolite that provides progesterone's calming effects. Without ovulation, there's no natural progesterone production all month. The result? Pill users often feel more anxious and stressed, potentially driving them to seek external GABA modulation through alcohol, food, or other substances.

These synthetic hormones also significantly slow alcohol Metabolism >>> Swipe

This matters because hormonal fluctuations affect neurotransmitter sensitivity throughout the cycle - & synthetic hormones fundamentally alter this landscape.

I'm particularly concerned about those uni years where social drinking pressure coincides with pill use. Without the natural anxiolytic effects of progesterone, young women may unconsciously reach for more alcohol to compensate.

Understanding this neurochemistry helps us make better informed choices about both hormone support and alcohol consumption- and at the very least should be explain to young women when prescribed - what do you think?

10/12/2025

Following on from my last post about the mevalonate pathway & protein prenylation, let's talk about HOW bisphosphonates a) actually works and b) what the down stream effects of blocking prenylation are as a result.

The commonly prescribed Nitrogen-containing bisphosphonates (alendronate, risedronate, ibandronate, zoledronic acid) actually work by inhibiting farnesyl pyrophosphate synthase (FPPS) - another key enzyme in the mevalonate pathway, subsequently blocking the production of:
➡️ FPP (farnesyl pyrophosphate)
➡️ GGPP (geranylgeranyl pyrophosphate)

See diagram ☝️remember these are the lipid anchors needed for protein prenylation.

So…. the intended mechanism in bone to how Bisphosphonates work;
1️⃣ Bisphosphonates bind tightly to bone mineral (hydroxyapatite)
2️⃣ When osteoclasts attempt to resorb bone, they internalise ( the bisphosphonate
3️⃣ Inside the osteoclast, the drug blocks FPPS
4️⃣ Without FPP/GGPP, osteoclasts can't prenylate their Rho, Rac, and Rab proteins
5️⃣ Without prenylated proteins, osteoclasts can't:
🦴 Form the ruffled border needed to attach to bone
🦴 Traffic bone-resorbing enzymes properly
🦴 Maintain their cytoskeleton

Result: osteoclast dysfunction and eventual apoptosis.

This is brilliant for stopping excessive bone resorption. But here's what we need to consider:
Whilst bisphosphonates accumulate primarily in bone, their effects on the mevalonate pathway help explain common side effects >>> swipe

And through a FUNCTIONAL LENS understand that bone health isn't about suppressing a process - it's about supporting healthy, BALANCED remodelling & understanding the mevalonate pathway and the importance of prenylation now helps us:
✅ Provide more targeted nutritional & lifestyle support &
✅ Make informed decisions about type treatment plan

>>> Swipe to understand more

Finally, consider the cumulative effects of multiple medications affecting the same pathway - basically one drug or approach isn’t going to be the lifelong approach - it needs to evolve.

09/12/2025

When we think about the mevalonate pathway, most think "cholesterol". But this biochemical assembly line produces far more than cholesterol, which is essential (yes!) for making cell membranes, producing hormones like oestrogen & progesterone, creating vitamin D & making bile acids for digestion.

Beyond cholesterol the mevalonate pathway generates:
✅ Coenzyme Q10 (vital for production energy (ATP) in mitochondria, acts as a powerful antioxidant protecting cells from damage & supports overall cell growth & maintenance, particularly in organs with high energy needs like the heart & brain)
✅ Farnesyl pyrophosphate (FPP) & geranylgeranyl pyrophosphate (GGPP) - lipid “anchors” used for protein prenylation.
PREN-A-WHAT? Bear with me… this is super interesting!

Prenylation is the process of attaching these lipid "anchors" to specific proteins, allowing them to embed into cell membranes where they can do their job. Rather like giving proteins a key to access cell membranes & without this anchor, these proteins can't access the cellular locations where they regulate critical processes in every body system >>> swipe

Understanding prenylation & the mevalonate pathway is crucial when we consider how commonly prescribed medications affect this system. Statins prescribed for cardiovascular “protection” - block HMG-CoA Reductase" resulting in;
✅ ⬇️ Cholesterol (intended)
❌ ⬇️ CoQ10 (fatigue, muscle issues)
❌ ⬇️ FPP/GGPP (impaired prenylation)

When prenylation is disrupted we see the potential negative effects & why some people on statins experience:
😖 Muscle aches & weakness
😴 Fatigue (reduced CoQ10 & energy production)

STATINS AREN'T THE ONLY MEDICATIONS AFFECTING THIS PATHWAY. Bisphosphonates (prescribed for osteoporosis) also work by disrupting the mevalonate pathway - just at a different point.

Tomorrow, I'll break down how bisphosphonates inhibit this pathway, why this IS in fact their primary mechanism of action (not a side effect) & what this means if on both medications simultaneously. Understanding this changes how we support clients, monitor for adverse effects & make informed decisions about treatment duration / alternatives.

💾 SAVE & 👀 watch for Pt2

Tanya Borowski Nutrition & Functional Medicine

14/01/2026

08/01/2026

07/01/2026

06/01/2026

30/12/2025

27/12/2025

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