Perimenopause and post-menopause affect the gut ecosystem, the barrier, inflammation, motility and visceral sensitivity. According to Dr Christian Boyer and Dr Amin Gasmi, sex hormones act on the digestive tract and the microbiota, and the microbiota acts back on the hormones in turn. This loop sheds light on a large part of women's digestive disorders, from irritable bowel syndrome to endometriosis.
How hormones modulate the gut
Oestrogen
It contributes to the integrity of the gut barrier, reduces permeability and inflammation of the mucosa, increases the secretion of antimicrobial peptides and the activity of intestinal alkaline phosphatase (which neutralises the effect of LPS), and enriches bacterial diversity, particularly butyrate-producing bacteria. Conversely, an oestrogen imbalance can heighten visceral hypersensitivity and mast cell activation.
Progesterone
It protects gut integrity, relaxes smooth muscle, slows motility, reduces visceral hypersensitivity and mast cell activation, lessens the pro-inflammatory effect of LPS and modulates Lactobacillus and Bifidobacterium. It therefore plays a key role in luteal phase symptoms and certain patterns of constipation.
Testosterone
In women too, it influences motility, visceral hypersensitivity, mast cell activity, LPS-related inflammation and the composition of the microbiota. A deficit is associated with slower motility and more pronounced digestive symptoms.
Why digestive disorders change across the cycle
During menstruation, the drop in oestrogen and progesterone, combined with a rise in prostaglandins (PGE2), promotes diarrhoea, bloating, abdominal sensitivity and hyperpermeability. In the luteal phase, a relative progesterone deficit often leads to bloating, gas, fermentation, cramps, sometimes constipation, and greater mast cell activation. This is also a period when histamine plays a bigger role, especially if DAO activity falls.
Mast cells, histamine and pain
Mast cells are central to digestive and pelvic pain. Once activated, they release histamine, tryptase, serotonin, prostaglandins, cytokines and leukotrienes, which sustains pain, visceral hypersensitivity and inflammation, and contributes to certain premenstrual syndrome symptoms. Progesterone and testosterone reduce this activation, while oestrogen can increase it depending on the context.
The microbiota, the estrobolome and menopause
The estrobolome refers to the gut bacteria capable of metabolising oestrogen through beta-glucuronidase activity: they deconjugate oestrogen and promote its enterohepatic reabsorption. Before menopause, an overactive estrobolome promotes oestrogen excess, premenstrual syndrome, fibroids, breast tenderness and endometriosis. After menopause, an underactive estrobolome worsens the oestrogen deficit (hot flushes, vaginal dryness, mood disturbances, bone loss). The microbiota becomes less diverse overall and moves closer to the male profile.
Endometriosis: hormonal, immune and intestinal
Endometriosis is not simply a gynaecological disease. It combines a genetic terrain, excess oestrogen exposure, progesterone resistance, inflammation, mast cell activation, dysbiosis, intestinal hyperpermeability and neuro-inflammation. Dysbiosis deconjugates more oestrogen, sustains this exposure and amplifies pain and inflammation. A low-histamine diet is not always enough: care combines mast cell stabilisation with an overall strategy targeting inflammation, the microbiota and hormonal exposure.
Excess oestrogen exposure: four parameters
This depends not only on oestrogen levels, but also on metabolites (protective 2-OH pathways versus the more aggressive 4-OH and 16-OH pathways), receptor sensitivity and the effect of progesterone. Hepatic methylation is involved in neutralising the most aggressive metabolites.
Micronutritional levers discussed
Depending on the focus, several levers were mentioned, to be individualised:
- Inflammation and prostaglandins: omega 3 (lowering PGE2, raising resolvins), turmeric, quercetin, EGCG, resveratrol.
- Menstrual phase: activated charcoal, clay, glutamine, Saccharomyces boulardii, soluble fibre and cooked vegetables.
- Luteal phase and hypersensitivity: PEA and luteolin, quercetin, resveratrol, black cumin, Lactobacillus rhamnosus GG, DAO.
- Constipation: magnesium, triphala, hydrolysed guar gum.
- Gut barrier: zinc carnosine, vitamin D, polyphenols, glutamine depending on the case.
- Hormonal support and post-menopause: DHEA, zinc, vitamin D, soya isoflavones, targeted probiotic strains.
Vitamin D plays a role in gut immunomodulation, and butyrate improves the sensitivity of its receptor. On hormone therapy, the data still need to be qualified (methodological limitations) and personalisation is paramount; the transdermal route for oestrogen is often preferred to the oral route in this context.
Care built on several pillars
According to the speakers, a coherent strategy combines: rebalancing hormones (progesterone, testosterone, assessment of hormone therapy when it is under discussion); supporting the microbiota (fibre, polyphenols, targeted probiotics, modulation of the estrobolome); protecting the barrier (zinc carnosine, vitamin D, butyrate, glutamine); modulating inflammation (omega 3, turmeric, quercetin); stabilising mast cells (PEA, luteolin, histamine management); and addressing stress (magnesium, adaptogenic plants, support for the neuro-hormonal terrain).
Putting this into practice with Simplycure
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