Tanya Borowski Nutrition & Functional Medicine

30/10/2025

Endometriosis is a chronic inflammatory condition- where endometrial “like”(it is NOT endometrial itself) tissue is found body wide, causing a variable range of manifestations & symptoms form pain to mood and everthing inbetween.

The pathogenesis of endometriosis still has many questionable aspects, but one we know to be occurring is a disrupted coordinated progesterone and oestrogen response. While historically viewed as primarily an oestrogen-driven disease—since oestrogen promotes endometrial lesion growth—research has revealed a more complex picture: the condition involves both oestrogen dominance and progesterone resistance in endometriotic tissues.

Local Oestrogen Dominance
Critically, "oestrogen(E2) dominance" in endometriosis is driven by local E2 synthesis within the lesions themselves, not systemic hormone imbalance. Local E2 levels are elevated due to:
➡️ Upregulation of aromatase (CYP19A1 gene), the key enzyme converting testosterone → estradiol and androstenedione → estrone( which via 17β-HSD1 can be converted into E2)
➡️ Reduction of 17β-HSD2, which normally inactivates E2 into weaker estrone

The Vicious Cycle 🔁 This creates a self-perpetuating inflammatory loop:
⬆️ Elevated E2 stimulates prostaglandin E2 (PGE2) production
➡️ PGE2 further stimulates aromatase activity → more E2
➡️ PGE2 and E2 suppress progesterone receptor (PR) expression → progesterone resistance
➡️ Loss of progesterone action allows even higher local E2 levels
➡️ PGE2 induces VEGF → angiogenesis → lesion survival and growth

This mechanism explains why endometriosis persists despite normal systemic hormone levels and why progestogen-based treatments may have limited efficacy in some.

Want to dive deep into this aspect and multiple other topics with me? The Beyond the Lesions: Unravelling the Endometriosis Puzzle Virtual Masterclass is Monday 3rd November and goes live at 10am …… tickets still available to join live online and of course receive the entire days lecture recordings.

Tanya x

29/10/2025

Shakespeare was onto something... Rosemary's reputation as a memory herb has solid biochemical backing particularly through its influence on acetylcholine pathways in the brain.

Acetylcholine (ACh) is one of the brain's most critical neurotransmitters for learning and memory formation. It facilitates communication between neurons, particularly in brain regions like the hippocampus and cerebral cortex where memories are encoded and stored. When acetylcholine levels decline—as they do naturally with aging or dramatically in conditions like Alzheimer's disease—memory and cognitive function suffer.

The key to maintaining healthy acetylcholine levels lies in controlling an enzyme called acetylcholinesterase (AChE), which breaks down acetylcholine after its release into Choline and acetate. If AChE activity becomes excessive, acetylcholine is degraded too quickly, and neural signalling weakens. This is where rosemary enters the picture; specifically- rosmarinic acid—rosemary's star compound.

This potent antioxidant acts as a natural inhibitor of acetylcholinesterase, effectively slowing the breakdown of acetylcholine in synaptic spaces.

The mechanism works like this: Rosmarinic acid binds to the active site of the AChE enzyme, reducing its ability to hydrolyze acetylcholine. With less enzymatic degradation, acetylcholine remains available longer in the synaptic cleft, allowing for sustained neurotransmission. The result is enhanced cholinergic signalling—the same principle behind pharmaceutical drugs used to treat Alzheimer's disease, such as donepezil and rivastigmine, but through a gentler, food-based approach.

Of course this does not in any way replace medical advice - just to highlight the nutritional powers of one of our locally grown herbs 🌿 😊

23/10/2025

Today wraps up our bone health series 🦴 The Nutrigenomic Osteoporosis Story

🧬 CASR GENE (Calcium-Sensing Receptor) is where the story STARTS! Blood calcium is tightly regulated by calcium-sensing receptors encoded by the CASR gene.

When calcium drops → CASRs trigger parathyroid hormone (PTH) → PTH activates Vit D to promote calcium absorption from the Gut → PTH reduces calcium excretion → PTH triggers calcium release from bone (resorption)

⚠️ The A986S SNP = a receptor that MORE readily stimulates PTH to raise blood calcium → Result: Increased bone resorption (breakdown) → Linked to OSTEOPOROSIS risk

🧬 The CYP2R1 gene encodes the enzyme responsible for the first step conversion of supplemental or food source Vit D > 25-hydroxyvitamin D. SNPs in CYP2R1 can reduce efficiency, meaning some need higher Vit D intake to achieve optimal 25(OH)D levels.

🧬 CYP27B1 gene encodes the enzyme (1-alpha-hydroxylase) that converts 25-hydroxyvitamin D → to ACTIVE 1,25-dihydroxyvitamin D (calcitriol). SNPs can impair this conversion, potentially affecting bone health even when storage (& tested) levels as 25(OH) Vit D appear adequate.

🧬 VDR (Vit D Receptor) gene: Perhaps the most studied! rs1544410 & rs731236 SNPs affect how well your cells respond to active Vit D. Even with perfect activation, receptor SNPs can reduce cellular response, impacting bone density & calcium absorption.

🧬 GC (Vit D Binding Protein) gene: Encodes the protein that transports Vit D through the bloodstream. SNPs here affect how much Vit D reaches tissues & can influence circulating Vit D levels.

Genetic variations mean Vit D requirements are highly individual. Two people with identical sun exposure & diet may have different Vit D status due to SNPs affecting:
Conversion efficiency (CYP2R1, CYP27B1)
Transport (GC)
Cellular response (VDR)

This is why nutrigenomic testing is valuable for personalising Vit D supplementation, esp for those with low levels despite adequate intake or persistent bone health issues. 🥰 I always use - in particular their Nutrient core & Metals & Mineral panels 

Remember - Nutrigenomic variants aren’t your destiny, but they ARE your instruction manual

23/10/2025

Today wraps up our bone health series 🦴 The Nutrigenomic Osteoporosis Story

🧬 CASR GENE (Calcium-Sensing Receptor) is where the story STARTS! Blood calcium is tightly regulated by calcium-sensing receptors encoded by the CASR gene.

When calcium drops → CASRs trigger parathyroid hormone (PTH) → PTH activates Vit D to promote calcium absorption from the Gut → PTH reduces calcium excretion → PTH triggers calcium release from bone (resorption)

⚠️ The A986S SNP = a receptor that MORE readily stimulates PTH to raise blood calcium → Result: Increased bone resorption (breakdown) → Linked to OSTEOPOROSIS risk

🧬 The CYP2R1 gene encodes the enzyme responsible for the first step conversion of supplemental or food source Vit D > 25-hydroxyvitamin D. SNPs in CYP2R1 can reduce efficiency, meaning some need higher Vit D intake to achieve optimal 25(OH)D levels.

🧬 CYP27B1 gene encodes the enzyme (1-alpha-hydroxylase) that converts 25-hydroxyvitamin D → to ACTIVE 1,25-dihydroxyvitamin D (calcitriol). SNPs can impair this conversion, potentially affecting bone health even when storage (& tested) levels as 25(OH) Vit D appear adequate.

🧬 VDR (Vit D Receptor) gene: Perhaps the most studied! rs1544410 & rs731236 SNPs affect how well your cells respond to active Vit D. Even with perfect activation, receptor SNPs can reduce cellular response, impacting bone density & calcium absorption.

🧬 GC (Vit D Binding Protein) gene: Encodes the protein that transports Vit D through the bloodstream. SNPs here affect how much Vit D reaches tissues & can influence circulating Vit D levels.

Genetic variations mean Vit D requirements are highly individual. Two people with identical sun exposure & diet may have different Vit D status due to SNPs affecting:
Conversion efficiency (CYP2R1, CYP27B1)
Transport (GC)
Cellular response (VDR)

This is why nutrigenomic testing is valuable for personalising Vit D supplementation, esp for those with low levels despite adequate intake or persistent bone health issues. 🥰 I always use - in particular their Nutrient core & Metals & Mineral panels

Remember - Nutrigenomic variants aren't your destiny, but they ARE your instruction manual

22/10/2025

Continuing our bone health theme this week – let’s talk about vitamin D. Yesterday I mentioned calcitriol as the “active” form. But what does that actually mean? And come to think of it, have you ever wondered why (most) vitamin D supplements stipulate “not the active form”? 🤔

Vitamin D requires two conversion steps to become active before the body can actually use it. Here’s how:

Step 1: The Liver 🫀 Vitamin D (from sunlight exposure on skin or dietary sources like oily fish, eggs, or supplements) → travels to liver → Converts via hydroxylation process to 25-hydroxyvitamin D (calcidiol or 25(OH)D) 

* This is the storage form of vitamin D
* What’s measured 🩸tests to check vit D status

Step 2 :THE KIDNEYS 💚 25-hydroxyvitamin D → travels to kidneys → Converts to 1,25-dihydroxyvitamin D (calcitriol or 1,25(OH)₂D)

This is the ACTIVE form that:
Promotes calcium absorption via gut
Regulates bone health
Do all the important other vitamin D tasks( and that’s for another post!)

What Controls This Process?
The kidneys tightly regulate the conversion to active vitamin D based on your body’s needs, particularly:
Parathyroid hormone (PTH) levels
Blood calcium levels
Blood phosphate levels

THE TAKEAWAY: You need healthy liver AND kidney function for optimal vitamin D activation. This is why liver or kidney issues can impact bone health even with adequate vitamin D intake >>> swipe to see visually in action.

Tomorrow: I’m doing to discuss how genetic variations- SNPs on genes that encode some of these enzymes responsible for this Vit D conversion, calcium regulation and receptor sensitivity meaning that vitamin D and mineral needs for bone health are HIGHLY individual 🧬…. Stay tuned xx

22/10/2025

Continuing our bone health theme this week – let's talk about vitamin D. Yesterday I mentioned calcitriol as the "active" form. But what does that actually mean? And come to think of it, have you ever wondered why (most) vitamin D supplements stipulate "not the active form"? 🤔

Vitamin D requires two conversion steps to become active before the body can actually use it. Here's how:

Step 1: The Liver 🫀 Vitamin D (from sunlight exposure on skin or dietary sources like oily fish, eggs, or supplements) → travels to liver → Converts via hydroxylation process to 25-hydroxyvitamin D (calcidiol or 25(OH)D)

* This is the storage form of vitamin D
* What's measured 🩸tests to check vit D status

Step 2 :THE KIDNEYS 💚 25-hydroxyvitamin D → travels to kidneys → Converts to 1,25-dihydroxyvitamin D (calcitriol or 1,25(OH)₂D)

This is the ACTIVE form that:
Promotes calcium absorption via gut
Regulates bone health
Do all the important other vitamin D tasks( and that’s for another post!)

What Controls This Process?
The kidneys tightly regulate the conversion to active vitamin D based on your body's needs, particularly:
Parathyroid hormone (PTH) levels
Blood calcium levels
Blood phosphate levels

THE TAKEAWAY: You need healthy liver AND kidney function for optimal vitamin D activation. This is why liver or kidney issues can impact bone health even with adequate vitamin D intake >>> swipe to see visually in action.

Tomorrow: I’m doing to discuss how genetic variations- SNPs on genes that encode some of these enzymes responsible for this Vit D conversion, calcium regulation and receptor sensitivity meaning that vitamin D and mineral needs for bone health are HIGHLY individual 🧬…. Stay tuned xx

16/10/2025

16/10/2025

Just over 6 weeks left of my Women’s Health Mastery affiliate mentoring programme in 2025 - every year the end creeps up on us so suddenly & leaves me feeling mixed emotions as I prepare to say goodbye to one cohort and get ready for the next.

If you've been curious about what it's actually like to be part of this mentoring journey, Thursday 23rd October at 7pm on Zoom is your chance to find out directly from the practitioners who are living it and of course chat to me directly!

Some of this year’s affiliates will be joining me to share their real experience of the year - the education, the clinical breakthroughs, the community, and the transformation that happens when you're part of a group genuinely committed to paradigm-shifting women's health care.

I know for many, this mentoring has changed their practices, completely overhauled their confidence, and their ability to support the most complex cases presented at their clinics. This affiliate mentoring programme is intense but brings with it, access to a community of practitioners who understand the nuances of women's health, and I’m so proud to not only lead the education but also bring in colleagues from across the world who can share their expertise too.

Choosing a mentoring programme is a commitment, so holding this discovery call gives you a chance to find out exactly what is involved and the shared experience of someone coming fresh out of the programme this year.

Save the date & hit the link in my bio to register for the discovery call. PLUS spaces on the mentoring programme are limited each year - by pre-registering or signing up for the discovery call it will mean you’ll get the details before I open up for general release. So don't miss this opportunity to connect with past and current affiliates, hear their stories, and decide if this is the right fit for you.

Ready to step into 2026 with a completely different level of education and support?

Join the call next week: https://www.tanyaborowski.com/affiliate-mentoring-2026-discovery

Tanya x

15/10/2025

Oestrogen usually steals the spotlight when discussing female s*x hormones, but progesterone is equally crucial, and I'd stick my neck out, saying it’s more important when we are discussing mental health. However, as with all hormones, individual genetic predispositions create nuances that make progesterone's effects complex—acting as both ally and adversary in women's mental health.

Progesterone is primarily produced by the ovaries during the second half of the menstrual cycle and is metabolized into several compounds, most notably allopregnanolone, which acts on GABA receptors in the brain.

The "Friend" Side: When Progesterone Helps 😇
Progesterone plays vital roles in:
• Preparing the uterus for implantation
• Maintaining pregnancy and preventing preterm birth
• Through allopregnanolone and the GABA receptor affinity (in most women) elicit calm & anti-anxiety effects - so much so, that the drug Brexanolone (synthetic allopregnanolone), is now FDA-approved for treating postpartum depression!

The "Foe" Side: When Progesterone Causes Problems 👿
For 2-5% of women, progesterone fluctuations during the menstrual cycle trigger severe mood symptoms including depression, irritability, mood swings, and anxiety. Paradoxically:
• Women with PMDD have normal progesterone levels
• They appear to have increased sensitivity to progesterone fluctuations
• Symptoms worsen during progesterone withdrawal (late luteal phase), not at peak levels

Swipe >>> for a deep dive into understanding PMDD's complex relationship with progesterone

Putting it all together - Imagine a woman with PMDD's brain as a three-legged stool

Leg 1️⃣ Progesterone sensitivity
Normal levels, but abnormal response to fluctuations
Rapid tolerance development
Severe withdrawal symptoms

Leg 2️⃣ GABA dysfunction
Paradoxical response to luteal phase changes
Altered receptor plasticity

Leg 3️⃣ Serotonin dysregulation
Secondary to hormonal fluctuations
Affects emotional regulation

When progesterone fluctuates, all three legs become unstable, and the stool collapses into severe mood symptoms. Supporting all 3 components through an integrative approach can significantly help provide better equilibrium ⚖️

09/10/2025

Yesterday we talk about the incredible journey of the female follicles, from utero to ovulation through the process - Folliculogenesis

Multiple factors are involved, some within our control other not so much, that can disrupt primordial follicle activation including:
💨 Environmental factors (like pollutants and chemical exposure )
🧬Genetic factors
🔥 Autoimmune disorders
🧪 Liatrogenic causes (such as chemotherapy and radiation)
⚡️Stress and sleep deprivation can also lead to premature activation by stimulating adrenal hyperactivity

Disruptions can also stem from imbalances in the intricate molecular pathways controlling follicle dormancy, such as those involving PTEN, FoxO3a, and mTORC1 signalling…. Yes the body is beautifully complex!

But let’s focus today on these "environmental factors". Enter the term endocrine-disrupting chemicals (EDCs) -compounds like BPA (found in hard plastics and can linings), phthalates (in flexible plastics) and parabens (common in beauty and skincare products). Research shows these chemicals target the ovaries and interfere with follicular development, potentially leading to infertility and menstrual irregularities. Abnormal follicular development is also a hallmark of polycystic ovarian syndrome (PCOS).

Take a look at the image and see how you can start removing some of this EDC burden in your environment - just start small , look at the make up and skin care products you use …. Swap for brands that don’t list words like methylparaben, propylparaben, and butylparaben( all parabens), that act as preservatives in cosmetics.

08/10/2025

We talk endlessly about periods & ovulation but what rarely gets the spotlight: the developmental journey of the follicles, the microscopic structures that house developing eggs (oocyte).

This journey (folliculogenesis) begins in utero long before the first period & can be influenced by factors dating back 3 generations.

The basics: Females are born with approx 2M primordial follicles - tiny, immature egg capsules. Throughout childhood, the number naturally declines through a process called atresia, so by puberty approx 400k-500k remain. From menarche onward, approximately 1k are lost each month, forming her ovarian reserve for her reproductive years.

Mind-blowingly: it takes 365 days (an entire year) for a single follicle to mature from primordial state into a pre-ovulatory follicle ready for release >>> Swipe

Maturation process is no simple feat. As follicles develop, they're given different names based on their stage & progression depends on a complex interplay of factors: genetic blueprint, inflammatory status, nutritional adequacy, growth factors & hormonal signals (particularly FSH +LH).

But this delicate choreography can be disrupted - here's where my Russian Doll analogy becomes profound. This journey spans 3 generations.

When your grandmother was pregnant with your mother, she was also nurturing the follicles that would one day become you. Your grandmother's nutrition, hormonal balance, trauma & chemical exposures didn't just affect your mother - they shaped the very follicle that became you. Her undernourishment or stress, thyroid function, even environmental exposures, rippled through time, influencing your follicular health before you were conceived.

What's more remarkable? Each follicle embarks on its own unique journey. Every menstrual cycle is singular - shaped by that follicle's development, the hormones it produces & cellular signals it sends. While the differences between cycles may be subtle, each is distinct as the follicle itself. No cycles are identical, just as no cells are truly the same.

Your menstrual health isn't just yours - it echoes across generations, yet every cycle you experience is uniquely, irreplaceably yours 🥰