My Five Big Takeaways From The World Congress on Menopause in Rio de Janeiro
What is the World Congress on Menopause?
Bom Dia! The World Congress on Menopause is the premier global scientific meeting focused on midlife and menopausal women's health. Hosted by the International Menopause Society (IMS), it brings together top clinicians, scientists, researchers, and healthcare professionals from around the world. It occurs every other year, and this year it took place in Rio de Janeiro, Brazil.
The numbers:
4000 attendees, only 99 from the US
131 scientific sessions
1,375 abstracts received
565 posters on display - 1 of these was mine!
Live-translated into 60+ languages
And, for those who needs CME hours - it was 69.25 AMA category 1 credits!
Lesson 1: Not everything is related to estrogen deficiency.
Yup. You heard that right. In a time where social media is blowing up with everything being related to the chaotic decline of estrogen during perimenopause and therefore the solution is to sprinkle some hormones on it, there was much research presented that showed this is not the full picture. One of the most humbling plenaries I attended was one titled: “Vasomotor Symptoms & Health: Rethinking a classic symptom” by Drs. Pauline Maki and Rebecca Thurston, both of the US. They presented data from their studies: MenoBrain, MsBrain, and the SWAN study showing that it’s not just the loss of estradiol that causes cognitive decline or cardiovascular events - it’s the symptoms themselves. I know, read that again. The sleep disturbances, mood changes, and vasomotor symptoms themselves lead to brain changes (ie brain fog, trouble with verbal recall), and cardiovascular events (stroke, heart attacks), regardless of estrogen or not. It’s one place in medicine where we are beginning to understand - forget the “root cause”, actually treat the SYMPTOMS to potentially prevent disease. This latter part of the statement is still under investigation. If we prevent or fix the symptoms (with or without hormonal therapies) do we actually lead to disease reduction? To be determined.
From Drs. Anderson (Scotland), Vincent (Australia), and Nappi (Italy), there was also conversations around the estrogen deficient state of premature ovarian insufficiency (POI) that it is not just an estrogen deficient syndrome. There are many more conditions that can arise secondary to early loss of ovarian function, and the personalized approach relies on the etiology behind POI (if we know it), and again, symptom amelioration. Treating POI with estrogen is the standard of care, but it should not stop there.
Lesson 2: Be flexible in your prescribing
I attended a debate: Transdermal HRT for All? between Dr. Janice Rymer of the UK (affirmative) and Dr. Steven Goldstein of the US (opposed). While I am not afraid of oral estrogen therapies, and prescribe them quite often in my practice, I was kean to hear the evidence on both sides of this debate. Dr. Rymer shared data that oral estrogens are thrombogenic, and Dr. Goldstein shared data that oral conjugated equine estrogen leads to a reduction in breast cancer. Furthermore, conjugated equine estrogen is only systemically available as an oral formulation and not transdermal. The point of the debate was not that transdermal should be considered first line, but that Dr. Rymer was arguing that oral estrogen therapies should never be considered. My biggest take away is - individualize and personalize her therapy. Each hormonal preparation based on hormone type and route of administration has it’s own set of risks and benefits, and it must be taken in context with the woman in front of you. This is why I do not follow protocols, but follow guidelines and match them with my clinical experience and patient preference - the definition of evidenced based practice.
Lesson 3: Gut health is pivotal
This is an area of medicine that I have been slowly dipping my toes into over the last couple of years, as I learn about the estrobolome. The estrobolome is not a single organism. It is multiple organisms AND their genes. The estroblome encodes beta-glucuronidase, and this enzyme is important for regulating estradiol metabolism and circulation. The estroblome is dominated by the phyla of bacterium Firmicuates and Bacteroides (again, not a single organism). The issue clinically is that we do not have testing and protocols that are quite ready for prime time. While we do know that the gut microbiome plays a pivotal role in hormone metabolism, we do not quite fully understand the utility of gut microbiome testing. Additionally, probiotics are not routinely recommended to “fix” the issue. In a session titled: “Microbiome Hormone Interaction in Menopause-Emergning Evidence and Therapeutic Opportunities” by Drs. Naheed (Pakistan) and Deeba (Bangledesh) I took away the following:
Menopause leads to a decline in bifidobacterium, decline in microbial gut diversity and thus decline in short chain fatty acid production (SCFA).
Diets don’t help everyone, which is why soy products don’t always work. Patients have to be able to convert soy daidzein into equol to get the benefits from soy. This is the job of the microbiome.
There’s one axis (gut microbiome) and 3 components - gut, vagina, bladder. However, microbiome restoration alone does not predict symptom resolution; there needs to be layered in hormonal treatment as well.
Bones! I had no idea that certain probiotics can improve bone density (SCFA regulate osteoclast activity) - Lactobacillus paracasei LPC 100 + Lactobacillus plantarum LP 140 (work in synergistic effect, not on their own).
It’s not what species is in the probiotic product but what strain. This is why I typically only use Microbiome Labs products because they specify the strain of probiotic in their products.
Lesson 4: Vulvar care should be a staple in clinics caring for women
As someone who worked in gynecologic oncology for the first 3 years of my career, I have seen the vulvar lesions that go unchecked for so long wondering - how did someone not pick up on this sooner? Now my gut instinct whenever someone has a vulvar complaint is to bring them in for an exam. I attended the jointly organized lecture with International Menopause Society and International Society for the Study of Vulvovaginal Disease (ISSVD) titled “The Vulva and the Menopause: Clinical insights and care” by Drs. Bornstein (Israel), Baptista (Portugual), and Gunter (Canada).
We heard from the scientists who are evaluating the mast cell activation role in hyperinnervation of the vulva leading to neuroproliferative vestibulodynia (will talk about this in a blog post in a couple of weeks), and the current clinical trials looking at using ketotifen as a topical treatment.
I had a perspective change in that not everything is genitourinary syndrome of menopause, and how we overuse these diagnoses which causes us to miss other diagnoses such as lichen sclerosus. Dr. Baptista shared practical tips for us clinicians on how to pick up on the differences during the exam. While I have had many lectures and hands-on training on diagnosing vulvar conditions, I’ve never had someone compare GSM and LS side by side. This was extraordinarily helpful.
I learned some very helpful vulvar care tips from Dr. Gunter.
I tell women, the skin of your vulva is the same as the rest of the skin on your body. Problems can arise. Despite us spacing out cervical cancer screenings, and now with the introduction of self-screening, it’s still important that annually someone is assessing the skin of the vulva.
Lesson 5: Premature ovarian insufficiency is significantly underdiagnosed.
Over the last year, I have had an increasing clinical and research interest in premature ovarian insufficiency (POI). There were many lectures on this topic during the World Congress on Menopause, and they also introduced the Special Interest Group for POI, for which I joined. POI used to be thought to affect 1% of the population, but due to underdiagnoses it actually affects 3-4% of the population. The time to diagnosis is about 4 years. The consequences are vast! Those with POI are more at risk for shortened life expectancy, osteoporosis, cardiovascular disease, and depression. We reviewed the latest ESHRE guidelines, which I admittedly was unaware of - but this is why we go to conferences. To stay up to date!
We, myself included, typically say that the etiology of POI is idiopathic, or unknown. I was very humbled to learn that actually about 30% of cases of POI had a diagnosis when assessed with genetic testing (specifically next gen sequencing) whereas previously they were diagnosed with POI of idiopathic origin based on a normal karyotype and negative FMR1. Interestingly, whole genome sequencing will actually miss the diagnosis. The implications of accurate diagnosis is that these genetic abnormalities can help inform on additional disease states and prevention including cancer. Furthermore, we can then stratify patients based on their POI type (mind blown - who knew there was a POI type!). We can also personalize their treatments. For example, one of the genetic mutations is on the TACR3 locus, which is the NK3 pathway. Does this ring a bell? NK3 pathway is the target of the newest class of menopausal medications, neurokinin receptor antagonists such as fezolinetant (Veoza) and elinzanetant (Lynkuet).
I will have more to say about POI in a future blog post.
For now, I will continue to work hard for accurate POI diagnoses and personalized treatment of my patients.
Lastly, I will leave you with this - after a hike up a very tall mountain called Twin Brothers Peak, where you could see all of Rio, I came across this marker. Translated from Portuguese it says “Happiness doesn't wait for your crises.”
