Holly Warner, Fix What They Missed (The Patient Pod)

Depression Isn’t a Fibre Deficiency

First off, I adore Dr haver, this is not an attack. This is me having a bit of an issue with how this “study” was framed and the bad taste it leaves when you look at the fact that she sells… fibre supplements. Not that there is anything wrong with selling supplements, even ones you’ve white labelled to for your own brand. I spent years in R&D, in fact I’ve helped develop some of the brands in Dr’s offices and on store shelves. I know how it works, white labelling and the push to have your own line. I opted out for a number of reasons, one is that you don’t need to reinvent the already perfect wheel in many cases. Another is that it can be seen as (especially in cases like this) a conflict of interest. I don’t have to push fibre, I don’t sell it as a supplement. You could be saying that I promote HRT and that’s the same thing, except I don’t make money off of how much or how little is prescribed. I’m paid for my service either way. Back to the main reason for this article, the video circulating about fibre and depression, based off of an association based “study”. This isn’t an interventional study. It’s observational, specifically a cross sectional analysis of NHANES data. That means it can show associations, not causation. These are the types of studies that we get slammed for when we try to use them to support a claim. These studies don’t hold weight, they’re a great eye opener to do a REAL trial/study, to look deeper and discover if there is something to it all. This study in particular took existing NHANES survey data, looked at self reported fibre intake from dietary recalls, and compared it to depression scores using the PHQ 9 at a single point in time. No intervention, no randomization, no temporality. Now for the flaws (and sadly there are several). First, reverse causation This is the biggest problem I see with this study. People with depression often eat differently. Lower appetite, less meal planning, more ultra processed food, less total intake. So is low fibre causing depression, or is depression causing low fibre intake? This study doesn’t answer that. The authors acknowledge it (which is great!), then they proceeded anyway (not so great). Second, dietary recall bias NHANES uses 24 hour dietary recalls, which are notoriously unreliable. People misreport, underreport, forget, or guess. Fibre intake is especially vulnerable to this since it depends on food type, preparation, and portion estimation (it’s usually guesswork not true calculations). One or two recalls don’t properly or accurately represent habitual intake. Third, fibre is a proxy, not a mechanism. What I mean is that high fibre intake correlates with a whole bunch of behaviours. Higher socioeconomic status, better access to food, more home cooking, higher protein quality, more micronutrients, more daylight exposure, more physical activity, less metabolic disease. Fibre isn’t acting alone ladies, but this analysis sure does treat it as if it is. Fourth, residual confounding They do adjust for some variables, but NHANES can’t fully control for things like trauma history, chronic illness burden, sleep quality, hormone status, perimenopause, antidepressant use duration, or inflammatory disease. These are all tightly linked to both mood and diet. Fifth, depression measurement limitations PHQ 9 is a screening tool, not a diagnostic tool. It captures symptoms over the previous two weeks. That’s a very small snapshot in time, not a clinical diagnosis, and it’s highly sensitive to acute stress, illness, and life events. You’re correlating a short term mood score with a presumed long term dietary pattern. That’s weak data at best. Sixth, no dose response clarity They show an association when intake is divided into four equal groups from lowest to highest, but this doesn’t establish a biologically meaningful threshold. There’s no evidence here that increasing fibre intake in someone with depression improves symptoms. That’s a leap that’s commonly made online and isn’t supported by this data. Seventh, sex and hormone blindness This is a big one for me, for obvious reasons (and because Dr Haver is in this space, it should have been for her as well). NHANES includes women across all ages, but the analysis doesn’t account for perimenopause or menopause status. Estradiol status is a massive contributing factor for mood, gut function, and dietary tolerance. Ignoring this makes the conclusions especially shaky for midlife women. I’m not saying this isn’t a real paper, it is. It’s published in a real journal, using real data. But it’s hypothesis generating only. It doesn’t prove that fibre reduces depression, treats depression, or should be prescribed as a mental health intervention. Observational nutrition data like this is cheap, it’s everywhere in abundance, and it’s ridiculously easy to mine. NHANES is a massive, and publicly available dataset. Anyone who has statistical software can slice it and dice it a hundred different ways until something lights up. Fibre is especially attractive since it correlates to so many as a marker of health. Plus association sounds just scientific enough for the public to eat it up (pun intended). The correct conclusion shouldn’t be that people with higher fibre intake report fewer depressive symptoms when we can’t determine direction, causality, or mechanism. I know plenty who have gone carnivore or animal based (cutting out all fibre) and completely reversed depression. But I wouldn’t go around stating carnivore is a cure for depression. Sadly most people don’t understand the difference between association and causation. We read “Associated with lower depression” and we hear “fibre improves mental health”. Saying something “may be an important modifiable factor” doesn’t mean the data proved it is one. These kinds of studies keep getting weaponized online to sell fibre supplements, and many other fancy things, despite (as my mentor used to always say) being grade D evidence at best. This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit hollywarnerhealth.substack.com/subscribe [https://hollywarnerhealth.substack.com/subscribe?utm_medium=podcast&utm_campaign=CTA_2]

The Billion-Dollar Menopause Drug That Doesn’t Replace Estrogen

In this episode, we break down the billion-dollar hype behind Elinzanetant and Fezolinetant, the so-called non-hormonal menopause drugs. Learn how NK3 blockers reduce hot flashes without replacing estrogen, and why real HRT still wins for bone, brain, and heart protection. This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit hollywarnerhealth.substack.com/subscribe [https://hollywarnerhealth.substack.com/subscribe?utm_medium=podcast&utm_campaign=CTA_2]

Stop the Panic: A Lump Isn’t a Diagnosis.

A breast lump is not cancer until it’s confirmed to be cancer. Yet some clinicians still advise women to stop ALL hormone therapy the moment a lump is found, before any imaging, biopsy, or investigative work is done. That’s not evidence-based medicine, it’s panic medicine. When used properly, estradiol is preventative medicine. It lowers risk factors for cardiovascular disease, dementia, bone loss, and even certain cancers. Automatically stopping estradiol without context is reckless. I understand the knee-jerk reaction from practitioners who lack hormone training, but saying “stop the estrogens” without nuance does more harm than good. And for clarity, estrogen and estradiol are not interchangeable terms. If caution feels warranted, fine…pause, assess, and refer back to the hormone specialist managing that patient’s care. That specialist knows the dosing, the receptor status, and the clinical context. They’re the ones who can determine whether something should be titrated, reduced, or continued. As for progesterone and testosterone, stopping those is flat-out wrong. Vaginal estradiol is also fine to continue, it’s NOT systemic folks. Many benign reasons exist for a breast lump, it could be cysts, fibrocystic changes, lipomas, and even if a biopsy confirms cancer, we must consider receptor type before making sweeping changes. Progesterone receptor–positive (PR+) and estrogen receptor–positive (ER+) cancers don’t automatically exclude bioidentical hormone therapy. In fact, studies show that natural progesterone (not progestins) induces apoptosis (programmed cell death) in abnormal breast cells and helps regulate estrogen’s proliferative effects. Real progesterone is protective. Progestins are not. Testosterone is also protective and, in many cases, therapeutic. Telling a woman to stop progesterone or testosterone “just in case” is outdated and dangerous. Properly used, these hormones improve outcomes, not worsen them. The responsible path isn’t to strip a woman of her protective hormones but to investigate properly, confirm pathology, and collaborate with the hormone specialist overseeing her therapy. A lump warrants investigation, not a hormone shutdown. Evidence-based care starts with facts, not fear. If you want to read more I have more articles specific to breast cancer that you might enjoy (or want to share with friends) This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit hollywarnerhealth.substack.com/subscribe [https://hollywarnerhealth.substack.com/subscribe?utm_medium=podcast&utm_campaign=CTA_2]

Why training, nuance and clinical expertise matter.

This episode takes on misinformation from a pharmacist giving advice on hormone therapy. While pharmacists know medications, that does not automatically mean they understand how those medications are applied in clinical practice. Hormone therapy is not simply about knowing what a drug is, it’s s about understanding dosing, timing, symptom tracking, lab interpretation, patient history, and how those factors interact in real life. Training matters. Credentials alone do not make someone qualified to advise on hormone therapy. Without advanced, hands-on training and clinical experience, it is easy to misinterpret research, oversimplify treatment, or make recommendations that do not work in practice. In this episode, I break down why the information in his video was incorrect and provide accurate, evidence-based corrections. If we want women to receive safe and effective care, the people speaking in this space must have both the knowledge and the clinical expertise to apply it. This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit hollywarnerhealth.substack.com/subscribe [https://hollywarnerhealth.substack.com/subscribe?utm_medium=podcast&utm_campaign=CTA_2]

Is Estriol Better Than Estradiol for the Brain? Not So Fast…

You may have seen this video circulating social media. It’s a claim estriol, the “pregnancy estrogen,” is better for your brain than estradiol. The idea mostly stems from research in women with MS and a few animal studies, often tied to Dr. Rhonda Voskuhl’s work. But is this actually true for the average woman navigating menopause or trying to protect her long-term brain health? Here’s the clinical reality: no human study has ever directly compared estriol to estradiol for cognitive function or brain preservation. It’s a bold claim based on inference, not evidence. Estriol in MS: Exciting, but Niche Dr. Voskuhl’s NIH-funded studies explored estriol as an add-on treatment in relapsing-remitting multiple sclerosis (MS). In her 2016 Phase II trial, women taking 8 mg of oral estriol alongside glatiramer acetate had fewer relapses, less grey matter loss, and improved cognitive test scores. Sounds great! But estradiol wasn’t even in the trial. The improvements seen with estriol happened in a specific population: younger women with autoimmune inflammation affecting their brain. It doesn’t mean estriol would outperform estradiol in a healthy, aging postmenopausal brain. That’s a leap, and it’s never been tested. Estradiol is STILL the gold standard for Brain Health Don’t get me wrong, estriol is still considered investigational, more data is always a good thing. But remember, estradiol has decades of data behind it. * It prevents grey matter loss when started within the critical window postmenopause. * It’s been shown to preserve verbal memory and executive function in well designed trials like ELITE and KEEPS Cognitive. * It increases BDNF, enhances glucose metabolism in the brain, supports mitochondrial health, and protects synaptic density—especially in the hippocampus and prefrontal cortex. These aren’t mouse models. These are human trials. That whole ERβ spin is selective, not superior. The theory that estriol is better for the brain because it “selectively activates ERβ” oversimplifies the biology. Yes, ERβ is involved in neuroprotection. But: * Estradiol activates both ERα and ERβ, and both receptors play critical roles in brain structure and function. * Some regions of the brain, like the hippocampus, require ERα activation for optimal cognitive function and synaptic signalling. * Estriol is a weaker estrogen. Its effects may be dampened in the absence of high receptor expression (like we see during pregnancy). In simpler terms, selectivity isn’t always better, it’s simply different. If you’re choosing hormone therapy for long-term brain health, especially after menopause, the current evidence still points to oral estradiol, NOT estriol, as the most validated option. Until we have a head-to-head clinical trial comparing the two in average, healthy postmenopausal women (not just those with MS), we can’t say one is better than the other. Estradiol is the one with decades of proven cognitive and structural brain benefits. Estriol is still in the theoretical and experimental category. Claiming estriol is “better” for the brain than estradiol is extremely premature. It’s also misleading, especially in an already confusing hormone space. It’s a great hypothesis, and it may eventually carve out a niche role in neuroinflammatory diseases, and I’m 100% on board if it does. But in terms of evidence-based support for women’s brains as they age, Estradiol wins hands down Let the science evolve. But don’t let marketing leap ahead of the data. When a researcher or institution holds patents related to a compound or delivery method being studied, that introduces potential financial conflicts of interest, and it’s essential to talk about it openly, especially when the science is being used to make broad clinical claim. It’s red flags all over the place. Follow the Patent (you know, the one being boasted about in the video attached to this) Let’s talk about what doesn’t get mentioned often enough in posts, interviews, or social media claims: UCLA owns patents on estriol-based therapies, and Dr. Voskuhl is listed as an inventor. One of those patents covers the use of estriol for neuroprotection, including in menopause, cognitive decline, and MS. This means if estriol gets FDA-approved, licensed, or widely adopted, UCLA (and potentially the inventors) may benefit financially. There’s a financial stake in proving that estriol is effective, and perhaps even “superior” to other forms of estrogen like estradiol. And while patents don’t discredit the research, they absolutely create an incentive to promote one compound over another. Conflict of interest doesn’t mean the science is invalid. Voskuhl’s team has published legitimate, peer-reviewed research. The concern is how that research is interpreted, promoted, and monetized. This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit hollywarnerhealth.substack.com/subscribe [https://hollywarnerhealth.substack.com/subscribe?utm_medium=podcast&utm_campaign=CTA_2]