Why Menopause Might Be Behind Your Recurrent UTIs

Figure 2: This image shows the before and after of vaginal atrophy³

Your Vaginal Microbiome Changes

Hormonal changes during menopause don’t just affect your mood or period, they reshape the very environment of your body. Fluctuating oestrogen and other sex hormones alter the structure and function of various tissues and fluids, which in turn changes the habitat for your body’s microbial communities.

Menopause influences the microbiomes of multiple systems, including the oral cavity, gut (GI tract), and the urogenital system which covers the vaginal and urinary tracts. Even more fascinating? Your body’s natural bacteria (microbes) don’t just respond to hormones like oestrogen, they can actually break them down and even change them. This means the microbes and hormones are connected in a cycle: hormones affect your microbes, and your microbes can affect your hormone levels in return. This back-and-forth relationship can influence things like mood, metabolism, and overall health⁴.

In reproductive years, Lactobacillus species dominate the vaginal microbiome, keeping it acidic (pH ~3.8–4.5) and hostile to pathogens. Oestrogen helps them thrive.

With menopause:

• Lactobacilli decline
• Vaginal pH rises
• E. coli, Gardnerella, and Candida are able to flourish
  

The same bacteria that cause UTIs and other infections can now colonize the area more easily⁵.

 

Figure 3: This illustration shows how menopausal shifts trigger histological and physiological changes that impact microbial environments across different systems, particularly the gastrointestinal tract (GIT) and urogenital system (UGS). These microbial niches are reshaped by declining oestrogen and progesterone levels, influencing the composition and behaviour of local microbial communities.

The right side of the figure highlights how resident microbes metabolize key sex hormones estradiol (E2), estrone (E1), and progesterone (P4) by breaking down their conjugated forms into active free hormones. Microbial species such as Lactobacillus, Bacteroides, and Clostridium play crucial roles in this bioconversion, affecting hormone availability and, in turn, host health.

Source: Nature.com⁶

 

This feedback loop may contribute to increased susceptibility to infections, inflammation, and microbiome imbalances in postmenopausal women.

 

Bladder Function Declines with Age

Menopause also affects the bladder and pelvic floor:

• Bladder muscles weaken
• Less effective emptying  which then can lead to  urine retention
• Residual urine creates a breeding ground for bacteria⁷

As oestrogen levels drop during menopause, the bladder lining thins, becomes more fragile, and loses some of its protective mucus layer. At the same time, the pelvic floor muscles and urethral sphincter (which help you “hold it in”) weaken, increasing the risk of pelvic organ prolapse, where the bladder or uterus may shift downward, pressing against the vaginal wall and further compromising urinary function.

These changes not only cause symptoms like leaks, urgency, nocturia, and prolapse-related discomfort but also set the stage for more urinary tract infections (UTIs). Why? Because a thinner bladder wall, weaker urethral defences, and prolapse-related anatomical shifts make it easier for bacteria, especially ones like E. coli to climb up and cause infection. On top of that, incomplete bladder emptying becomes more common, leaving urine behind and giving microbes a warm, wet place to multiply.

And therefore you know now that it's not just "pee problems", it's a real shift in your urogenital defence system⁸.

Figure 4: A representation of how your bladder weakens as you age¹.

Sex Can Get Riskier

Due to vaginal dryness and thinning, sex during menopause may:

• Cause micro abrasions 
• Disrupt vaginal flora
• Introduce bacteria into the urethra more easily⁹

During menopause, lower oestrogen levels cause the vaginal walls to thin (vaginal atrophy) and lose their natural lubrication. This makes the tissue more fragile and less elastic, so what used to feel normal during sex can now lead to increased friction and microtrauma.

Without sufficient lubrication, penetrative sex can cause micro abrasions which are tiny, often invisible tears in the vaginal and vulvar tissue. These small injuries not only cause discomfort but act as entry points for bacteria, including E. coli, which is the most common cause of urinary tract infections.

Additionally, menopause alters the vaginal microbiome, reducing protective Lactobacillus species and increasing vaginal pH, which allows pathogens to flourish. When friction from sex pushes these bacteria toward the urethra, especially if there’s tissue trauma—they can quickly ascend and cause a UTI.

 

You are not alone

If you’ve entered menopause only to be greeted by a wave of recurrent UTIs, know this: you are not alone, and it’s not your fault. The changes happening in your body which can include hormonal shifts, weakened tissues, microbiome disruption, and yes, even painful sex are real, biological responses to a natural life transition.

Understanding these connections gives you the power to advocate for your health. Whether that means exploring topical oestrogen, probiotic support, better intimate care products, or simply having more open conversations with your doctor, you deserve care that evolves with you.

 

References

1. https://flytetherapy.com/blogs/news/the-menopause-incontinence-link-myth-or-fact
2. https://pubmed.ncbi.nlm.nih.gov/19493638/
3. https://bjgp.org/content/71/713/538
4. https://www.nature.com/articles/s44294-024-00050-y#:~:text=There%20is%20a%20pathology%20called,of%20infections%20in%20menopausal%20women
5. https://www.researchgate.net/publication/256763545_Vaginal_microbiota_and_viral_sexually_transmitted_diseases#read
6. https://www.nature.com/articles/s44294-024-00050-y#:~:text=There%20is%20a%20pathology%20called,of%20infections%20in%20menopausal%20women
7. https://www.geriatric.theclinics.com/article/S0749-0690(09)00029-9/abstract
8. https://pubmed.ncbi.nlm.nih.gov/27451320/
9. https://pubmed.ncbi.nlm.nih.gov/8350884/