Why do women become more prone to UTIs in perimenopause and menopause?

18 October 2022

Why do women become more prone to UTIs in perimenopause and menopause?

Why do women become more prone to UTIs in perimenopause and menopause?

Basically, there are 3 interconnected mechanisms that work in harmony to prevent UTIs and other infections:
1. Having strong defences - this is an epithelial mucosal barrier that lines the vaginal tract
2. Developing additional resilience to this defence barrier - a mucus lining; called glycogen
3. Increasing the artillery - a number of protective Lactobacillus “families” (termed community states - CST) dominate the healthy vaginal microbiota in most reproductive-age women to include the following CST states of lactobacillus: CST I L. crispatus CST II L. gasseri, CST III L. iners, and CSTV L. jensenii.

In our higher oestrogen life stages (pre-menopauase), oestrogen promotes the proliferation of our barriers - epithelial cells and the accumulation of glycogen. This gorgeous gloopy glycogen is broken down to lactic acid by Lactobacillus species creating a protective acidic environment (pH, 3.5–4.5) at the expense of other anaerobic bacterial species like e-coli, the no 1 bug responsible for UTIs.

So as our oestrogen levels decline following late stage perimenopause and graduation into menopause, we lose our barrier defences and in turn our Lactobacillus “communities”.

BUT there is much that can be done to improve barrier function and restore community status. Lactobacillus communities are a protective element to the vaginal microbiome. Let me introduce you to the 5 community states: 
CT I: Lactobacillus crispatus
CT II: Lactobacillus gasseri 
CT III: Lactobacillus iners 
CT V:Lactobacillus jensenii
CT IV: Has lower levels of Lactobacillus

Interestingly, of all the communities, L. iners lacks the ability to make a specific form of lactic acid; namely D-lactic acid, and it turns out D-lactic acid is more protective against vaginal dysbiosis than L-lactic acid.

D- Lactic acid levels are highest when L. crispatus is the dominant species in the vagina and lowest when L. iners, Gardnerella or Streptococcus predominate ; and this partly accounts for the higher protection against urogenital infections.

There  is LOTS than can be done knowing this information and when applying a functional approach:

  • We can test, to assess your community status type - with the Vaginal EcologiX from @invivohealthcare
  • Build a thriving community -  nurture optimal  dominance with targeted species and strain probiotiocs; Bio.Me Femme V is the only available vaginal probiotic containing Lactobacillus crispatus
  • Improve that barrier - with nutritional interventions such as sea buckthorn, vitamins A, D & E for epithelial & mucosal membrane support (speak with your practitioner for correct doses for your individual  situation)
  • Crowd out the bad - consuming a diet rich in polyphenols for their prebiotic actions in the gut  increases lactobacillus & bifidobacteria and restricts pathogen growth in the gut to prevent translocation to the vagina