 Yeah, okay. All right. If you don't mind taking a seat, we will get started. A couple months ago I started following this woman on Twitter. I thought everything she wrote and tweeted was absolutely brilliant. Who is this woman? And now I have the pleasure of introducing her and knowing who she is. She is Kelly Brogan, MD. She is boarded in psychiatry and psychosomatic medicine and reproductive psychiatry and integrative holistic medicine and she practices functional medicine. She is one of the only physicians with perinatal psychiatric training who takes a holistic evidence-based approach to the care of patients. She is medical director also for fearless parent and I'm very happy to introduce her. Thank you. Okay. So I'd like to first talk a bit about how, it's my perception that psychiatry is sort of the blob that's consuming the American populace and with 11% of Americans on an antidepressant, one in four women of reproductive age taking one going into a potential pregnancy, there's something we have to look at as a collective. I also want to introduce you to what I believe will be an exciting paradigm shift that's predicated on this idea of evolutionary mismatch and also the role of concepts like epigenetics and nutrition in adult mental health. I think that this is often prizes the concept of our denatured, devitalized and demoralized foodstuffs as being an important place to start. But first we have to acknowledge the failure and really dangers of the current paradigm. So I'm sure most of you have some assumptions about the role of monoamines, the role of serotonin for example in depression and think about medications like Zoloft and Prozac as being integral to the treatment of these disorders or diseases. But there have been many, many oops in medical history. In 1949 the Nobel Prize was awarded for therapeutic lobotomy and in my opinion we're not so far off in missing the target with this theory either. And really psychiatry as a field is in crisis because of the fundamental failures of this most heavily promoted and sanctioned meme which is the serotonin hypothesis of depression and anxiety. So where did it come from? How did the pharmaceutical industry sort of get a foothold with this concept? And really the origins are very humble. So it was a hypothetical paper in the 1960s by Joseph Schildkraut and it was also the observations around treatment of tuberculosis patients with monoamine inhibiting medications. And this was really what gave birth to this hypothesis which it still is today. And this is called deductive reasoning, right? So it's not very different than as David Healy, a British psychiatrist, says then thinking about potentially viewing alcohol as an effective treatment for anxiety, social anxiety. So you think about somebody who's really nervous at a party and you think about giving them a couple glasses of wine and probably they're going to feel a little bit better. You can imagine doing a six-week placebo-controlled trial and probably having pretty good outcomes and making recommendations for long-term treatment. But what happens when this theory is applied to so many different disorders and encompasses an impossibly broad list of diagnoses is that we have to start looking at how and why we are making recommendations. What is the evidence base? And in this regard, we have to appreciate the role of expectation in mental health treatment and the role of the placebo. And the pioneering researcher in this regard is Irving Kirsch, a psychologist, and he's put forth two very notorious meta-analyses now at this point where he has demonstrated that the vast majority of the effect of antidepressants is attributable to what's called the active placebo effect. So what that is is that you have two arms, you have the patients getting placebo and you have the patients getting medication. But these medications have known side effects that actually patients are warned about. And so when they start to have a bit of a headache or some gastrointestinal distress, they know they're getting the treatment. And so something about the role of direct-to-consumer advertising, teaching patients that actually they're fixing a chemical imbalance and then they start to feel that actually probably something is going on and they're being fixed, that expectation plays the majority of the role in positive outcomes. But are we really seeing the whole story? And the most impressive paper is a now famous study from 2008 in the New England Journal that uncovered data from unpublished data. There were 12 antidepressants essentially approved based on 74 studies. And what Turner found was that of 38 positive studies with positive outcomes, 37 of them were published, right? That sort of makes sense. But of 37 negative outcomes, only three of them were published, 22 of them weren't, and actually 11 of them were published with a positive spin, which is often referred to as data dredging. So if we're making these recommendations to patients, we're putting one in four women on these medications based on questionable short-term efficacy data. What about long-term safety, right? Because as a psychiatrist I observe that most patients are started on medications that they really remain on for the rest of their lives for the most part. And in this realm we have Robert Whitaker, who's a pioneering investigative journalist, to thank for analyzing the existing data about naturalistic retrospective and prospective studies, which essentially all demonstrate without exception that long-term treatment with antidepressants, and actually he goes into the other categories of psychotropics as well, benzodiazepine stimulants and antipsychotics, that long-term treatment actually confers worse functional outcomes so that we're turning what might otherwise have been a one-episode illness with recovery within six to 12 months spontaneously, we're turning this into a chronic and disabling disease. So these are some of the mainstream concerns for those who are challenging the paradigm of psychiatry, but with my training I bring even a couple more concerns to the table. I'm concerned about the role of medications, the sort of unintended consequences, so mitochondrial damage, the effects on cortisol, receptor status, and also the role of in utero exposure in epigenetic expression, so methylation, and this was a paper on Prozac. So from this perspective we really need to sort of reinvent how we're thinking about depression and mental illness in general, and we need to start to think about it as the way we think about a fever, right, that it shows us that there's potential for multifocal etiology, there are many things that can contribute to this symptom, but in the same way, you know as I described to my patients in the same way that you can have, your toe can hurt for many different reasons, right, you can have a string tied around it, you can have a hammer dropped on it, or you can have an infection in your toenail, and the pain is actually just an indication that there's something out of balance, it doesn't actually tell us more than that. So through this lens we think about depression and anxiety as having these many contributors and we'll sort of tour through some of them now, so we think about concepts like oxidative damage, nutritional deficiency, endocrine disruption, and also the role of the microbiome, and this is really what has given birth to sophisticated terms like psychoneuroendocrinology and psychoneuroimmunology to demonstrate really the interconnectedness that as Nando said, it's not a head up phenomenon anymore, we're missing the mark, and really the thread that ties all of these concepts together is through my lens really that of inflammation. Okay, so this is going to be familiar to just about everyone here, but it's a schematic essentially depicting how inflammatory contributors and exposures have changed, right, so with highlights on the agricultural and industrial revolution, and in this way depression really joins the ranks of other chronic diseases, heart disease, autoimmunity, diabetes, and cancer, and the model is really from an evolutionary perspective is that of depression functioning as what has been dubbed sickness behavior, so with symptoms that were potentially, again as Nando was describing, potentially adaptive at a certain point in history when there was an inflammatory threat or infectious threat, so symptoms of lethargy, sleep disturbance, decreased social activity, mobility, libido, learning, anorexia, and anhedonia, this is depression, right, and in many ways evolutionarily this is probably an adaptive state for bodily repair, and we're looking at what was formerly adaptive now confronting the triggers of our modern environment, and there's a mismatch that we have to reckon with, so the literature on the cytokine model as it's called of depression is actually about two decades old now, and we have evidence for the predictive value of biomarkers like C reactive protein, so something you can measure just about any lab in America very easily, we have demonstrated that these biomarkers can be predictive and also linearly correlated so that the higher blood levels of cytokines like interleukin 6 and TNF alpha, the more sick a patient is, and that in fact when they recover symptomatically you can monitor those cytokines as tapering down, and my specialization is in perinatal psychiatry, so I think that the model of postpartum depression as an inflammatory condition is actually one of the most helpful to elucidate the potential for thinking about an inflammatory model of depression punctuated with anxiety, so these are some of the papers substantiating the role of inflammatory markers as being highly correlated and again predictive of incidents of postpartum depression. What's interesting to me is that you know again sort of in a long legacy of medical oopsies you know we didn't really know that the brain had any immune activity even 10 years ago, and now it's really sort of there's an explosion of literature substantiating the importance of brain-based immunity not only in healthy individuals but certainly in states of of neurological pathology and psychiatric pathology, so in this model we understand that inflammatory cytokines like the ones that I've mentioned, what they what they can potentially do is traffic this message from the body to the brain, stimulate an enzyme called IDO, and actually skew tryptophan catabolism so that there is production of these you know excitotoxic sort of you know otherwise problematic compounds the most the best studied one is called quinolinic acid, it's actually an NMDA agonist so it has highly stimulating effects and in different parts of the brain it has different levels of activity, so in postpartum depression it's very common to have a woman who presents with profound you know sort of self-reported depression but also punctuated often with intense anxiety and agitation and often intrusive images you know of her baby being knocked on the corner of the table or falling out of the window or you know knives and it's often very you know sort of intensely disturbing and so there's an understanding through this model of why the limbic system is differentially stimulated by quinolinic acid relative to the frontal lobe so she's actually not able to inhibit in a normative way inhibit these sorts of images and thoughts and I find that really satisfying to sort of have an explanation for what I'm seeing with my patients but how is it that inflammation can get out of control and I think that's where we need to recruit in the endocrinology we have to recruit in the role of our stress response system and appreciate that the brain is actually the master organ when it comes to managing our stress response and namely the role of cortisol feedback so we have this concept of allostatic load sort of how how full is your bucket before it overflows and we know that there are many factors that can contribute to when our buckets do overflow and a lot of that is perception but it's the ability to adapt that actually determines you know in our best understanding when symptoms do emerge and when they don't so this is sort of schematic of different patterns of adaptation some of which may be you know sort of beneficial in terms of suppression and some of which may actually lead to further inflammation so in the setting of pregnancy you know it's again a good model because we have this tremendous stress put on you know put on the system in terms of adaptation within 24 hours of delivery you have all of these tremendous you know plummeting hormones and in in pregnancy the placenta actually takes over the role of cortisol production and sort of quiets down the brain-based production and what happens we're you know we're the only mammals that don't consume our placenta and so when you eliminate that stimulatory organ the body is forced to adapt and obviously in the majority of cases about 90 of the time that actually happened successfully but this is thought to be one of the determining factors poor adaptation to cortisol regulation that can that can lead to a suppressed state of a suppressed cortisolemia and also this inflammatory incline right because it's cortisol that is our natural anti-inflammatory hormone and this mirrors sort of what we're seeing in the rest of psychiatry there's sort of probably a false dichotomy but at least there's two categories that we're looking at melancholic and atypical depression and it's a typical depression which has different features so sort of oversleeping overeating intense reactivity to the environment a lot of agitation and anxiety it's this pattern that has been more correlated symptomatically with the inflammatory model so it certainly fits that this pattern is also the one that demonstrates consistently low levels of cortisol so again what's happening postpartum as far as we understand is that there's this hypercortisolism of late pregnancy which leads to an adrenal suppression you throw out the placenta and the hypothalamus has to come back on board but sometimes it doesn't and this is actually being mirrored in some other syndromes like fibromyalgia and and Cushing's syndrome Cushing's disease so you know this is how we have to start to think about things from multiple different etiologic viewpoints so in this list you know there's consideration of many different potential causes of postpartum depression in any given woman it could be any of these right it could be dietary could be hormonal could be particularly thyroid autoimmunity and you know what we're focusing on now is the role of the hypothalamic pituitary adrenal axis and inflammatory mechanisms so we have this sort of complex web you know that I've woven up until this point and we know that inflammation is at least a driver but it's not the cause necessarily there's still something that has to trigger the inflammation and drive it so where do we enter you know where where does you know the clinician actually think of starting and so for this we actually have a large body of literature supporting the role of lipopolysaccharides so this compound gram negative bacteria in the gut that when it's exposed to the immune system through intestinal permeability actually has the potential to induce states of clinical depression and we this is actually how they cause quote unquote depression in an animal model whatever that means and this schematic is actually I think pretty helpful because if you follow the orange lines you'll see that it's actually with the gut microbiota that we need to begin that's probably where we should start to focus because it's actually the early seeding what's called self-completion of the microbiota in early infancy that the stress response is established so I need things to be sort of simple in my mind so for me this is very appealing to think about the fact that actually the gut microbes come first and they dictate the nature of a lifelong stress response system and dysregulated inflammation as a result and you know there's sort of papers to substantiate my opinion which which is that it's the gut microbiota that are the most important players so what am I talking about when I when I'm speaking about the microbiome it's probably one of the hottest buzzwords right now I think and for good reason because what we're discovering is that you know with completion of the human genome project we needed to figure out where it was that we were outsourcing all of our bodily functions and it turns out that you know 90 percent of of the cells that we walk around with every day are actually microbial in origin so non-human and in fact you know our 23,000 genes are dwarfed by as many estimates but at least the three million genes that are brought to the table by primarily bacteria but other commensals and you know the functions that are performed by this ecosystem are vast you know including inhibition of pathogen adherence enterocyte you know sort of gut cell protection and also management of inflammatory signaling through through IGA so through this signaling molecule and in many ways this has been you know this is what leads us to to think about of ourselves as a super organism and and in many ways blurs the boundaries between us and our environment and in particularly the microbial world and so some of the sort of relevant functions of gut bacteria to psychiatry and neurology are in production of short chain fatty acids so specifically butyrate which has been demonstrated to have brain-based anti-inflammatory effects specifically in microglia also nutrient production and metabolism of toxins but really this is part of a bigger picture of epigenetic communication and and really rendering largely secondary sort of you know what our genes are dictating because of the role of mRNA of transcription factors and trans genes in in helping to determine our gene expression and helping us to appreciate that environment and lifestyle are in many ways where it's at so how do we build this microbiome how has it been done for several million years and how is it that we've we've come so far off course well we used to think that the the uterus was and and and sort of the womb was a sterile place right and should be no bacteria in there and of course we've we've learned that we were wrong once again and that actually you know maternal provisioning of bacteria is actually universal in the animal kingdom and we're no exception that that maternal gut bacteria is actually passed to the baby in utero the placenta itself actually harbors a specific unique microbiome and this is also news to us and exciting news I think at that and then beyond the in utero experiences of course the the birth experience so I think it's now largely undisputed that that the role of vaginal birth is is is paramount in establishment of the microbiome or this self-completion notion and in a recent study actually I thought was very interesting looked at the role of birth location right so it took women who birthed vaginally in the hospital versus those who birthed at home and found that they had that those babies had very different microbiota and actually had different propensities towards allergy and asthma food allergy and asthma later in life at around age seven and they think that one of the mediating factors was colonization with clostridium difficile which is considered by all accounts to be a pathogen and that maybe the role of the hospital microbiome so this microbiome that's cultivated you know with excessive use of purell and and sanitization and sort of you know this this kill the bugs mentality as opposed to cohabitate with the bugs mentality might be responsible for altering the microbiome of even vaginally born babies when of course we now have a good understanding that surgically born babies are often colonized with with the skin flora of of non-maternal organisms so that's also interesting and then there's the role of breastfeeding so there's this this sort of continued tailoring of the individual infant microbiome through these the myriad factors in this like incredibly sophisticated dynamic food that transfer that transfers you know multiple immune factors and specifically over 200 oligosaccharides which are essentially prebiotics specifically designed for the promotion of beneficial bacterial growth and interestingly you know even the potential epigenetic communication of these immune related mRNAs and you know it just sort of floors me because the last time I checked you know enfamil or your standard formula it doesn't have these in the ingredient list so I think that it's an important thing to sort of appreciate the significance of when we are considering the the potential benefits of breastfeeding but what's interesting to me is that you can actually according to at least this one study you can undo so many of those benefits with the weaning diet so with weaning your infant to a standard American low fat diet in this study the potential protective effects around obesity and inflammation were actually largely undone and so that's maybe how we are messing things up so that might be one of the many ways that we've influenced and evolved our microbiome that now we are handing down transgenerationally this was a I thought a very important study that came out this past year that looked at comparative fecal analysis of one of the the last hunter-gatherer tribes in Africa to comparing them to urban dwelling Italians and found that there was almost no overlap in their microbiota and interestingly to me there were gender disparities you know between the men and women in this tribe that they suspected were related to consumption of tubers so like root vegetables by the women specifically and also that what one of our most prized beneficial bacteria which is bifidobacter you know if you buy any probiotic on the market it's going to have bifidobacter in it was actually totally absent from the from the microbiome of these hunter-gathers so sort of you know we have more questions than we have answers at this point but we do know that we are manipulating us you know somewhat strategically and somewhat recklessly our immune systems through these various exposures unfortunately you know research into most of these agents is thoroughly insufficient to justify safety if we're looking through the lens of the relevance of the microbiome you know this concept is really totally novel to the allopathic researcher or even clinician and so when we when I find a study like this it's sort of impressive to me that anyone's really looking at it so this is Cyprexa this is the best-selling anti-psychotic on the market that's used for myriad indications not just for schizophrenia and you know this particular study found that it's actually altered the microbiota in rodents we don't know how that's happening but you know at least that it's demonstrated it is just gives us some indication that we probably should be paying attention to the relevance of this organ you know when we're looking at safety profiles of medications so how is it that we can actually potentially influence epigenetic gene expression and optimize our microbiota it's always going to be in my sort of clinical practice it's always going to be first through dietary change so the type of dietary approach that I take with my patients is one that primarily looks at controlling for the role of blood sugar instability which I believe strongly can masquerade as many different psychiatric symptoms from panic to generalized anxiety to even obsessive compulsive disorder which is the sort of like up and down roller coaster ride that your blood sugar can take if you are eating a carb-based diet particularly refined flowers but also looking at the role of agricultural foods and certainly post-industrial foods in triggering inflammation so getting back to that initial etiology I referenced in the beginning and so the template that I find most helpful clinically is one's very similar to Paul Gemini's perfect health diet maybe save for the dairy component which I often do experiment with with patients based on literature and psychiatry implicating casein in all sort of different categories of mental illness from bipolar to schizophrenia to depression but it's actually you know sort of a moderate carb high-fat profile so I focus a lot on saturated fats with the women that I treat and actually push them to go out of their way to include things like egg yolks and ghee and coconut oil and animal products and I find that it's within you know two to three weeks we can shift them into a more keto adapted state and then we can start to introduce non-grain carbs after about a month and this method has you know afforded me very you know robust clinical results I haven't started a patient on medication in several years now for that reason I think and so again just the focus on fat sort of orienting patients to what that actually means because I think a lot of patients when they think of fat they think of olive oil and they stop there right so I also try to you know sort of introduce my patients to an appreciation of again this like hyper sophisticated mechanism of many sort of culinary herbs and and spices I'm very interested in in the power of turmeric and specifically curcumin there are about five randomized trials at this point demonstrating its efficacy for treatment of course a single agent a single pill is never going to be you know the cure even if it's a natural one probably but it requires a more holistic lens but I do think this is pretty engaging and it's probably because cumin does about you know at least these this many things if not more all at once so I have in my practice I focus a lot on sort of food tricks as I call them sort of using foods therapeutically so so gelatin for its glycine content which is the calming amino acid and coconut oil for its medium chandelier glycerides liver fur just about everything it offers if you're not willing to eat it as an actual food there's many ways to cheat on that and and also the role of fermented foods and this concept of using what's now being dubbed psychobiotics so using beneficial probiotics and of course I also tend to recommend them in in nutraceutical products but using them as treatment and there's actually a randomized double blind placebo control trial using a 30-day probiotic regimen for anxiety that demonstrated statistically significant efficacy I mean I think that's pretty remarkable and and begs us to sort of look at this through through a remarkably different lens so this is sort of what I hope early intervention will begin to look like rather than toddlers on stimulants and teens on antipsychotics so it's an appreciation of of food as information food that influences the microbiome the inflammatory and stress response feedback loops and really in many ways establishes resilience for for future mental health so that's it 10 minutes early that's probably not a good sign hi and thank you I had a question about you mentioned that you can undo a lot of the benefits of breastfeeding by weaning to a standard American diet is there any researchers if possible to do the opposite if your formula fed if you lean to a high fat high nutrient diet can you fix some of the problems from not breastfeeding so the the epigenetic window appears to be most relevant in the first three years so I would I would assume the answer would be yes I mean I also think that you know I encourage my my patients who are formula feeding to use what we got you know to use probiotics to to introduce as many sort of like you know whether it's it's vitamin D you know or other augmentation fats coconut oil to use these things to supplement this is really in my opinion not a formula on the market that's acceptable and so I I do think you could sort of augment and I certainly believe that there is malleability to to microbiome I mean it's what I treat adults who've been you know trashing their bodies for decades and I get outcomes within two months so it's it's certainly possible and I think that's absolutely it's a great question but it's probably also in the chronicity of exposure right so you know these these patients these babies were weaned to a low fat you know to to one percent milk or skim milk and they ate it for you know decades you know in this case seven years in that study but probably went on to eat it for decades so I mean again you know diet is is obviously only one piece of the puzzle so stress response movement you know it's not exposure there are many things that come into play here but of course it's the one I think I use as as leverage great question yeah she said are there any protective effects for the mother in terms of mood or maybe risk of postpartum depression with breastfeeding yes exactly so it seems to be sort of a two-way street just a couple papers that and I've written about this very subject that suggests that actually breastfeeding is protective for the first three months but also that depression itself if it's in the third trimester anti-natally is interfering with breastfeeding initiation so it's a bit of a two-way street and you know there are many reasons why that could be right it could be sort of like self-satisfaction or sort of bonding or maybe it is hormonal and certainly oxytocin is something is a hormone that that I use clinically in practice and one that's been implicated and and sort of one of the potential ideologies of postpartum. So the Westinay Price has written a lot about the quality of breast milk impacted by the mother's diet which makes a lot of sense of course they also talked about mothers that have a diet low and animal products are better off feeding their children homemade formula what are your thoughts about the breast milk quality and that whole kind of controversy. That's a great question I would probably disagree with that mostly because of you know the slides that I showed on those you know on exosomes and micro RNAs I mean there's just so much going on in breast milk we don't have the we're looking through a key hole you know we and so to think I certainly would recommend a homemade formula over a store bot but to think that we've captured all of the essential information it's not only about fats right it's it is about fats but it's also about immune factors maybe more importantly so I would probably disagree although I'm a big Westin price fan. Okay so my question is about breast milk banks do you recommend breast milk banks to your clients or what are the things that you're doing to promote breast milk banking for its growth. Yes I do support it there's very few I'm in New York and there's very few options there's a prominent one in New Jersey I think that you know it's it's again a trade-off right because they're probably elements immune factors that are passed on that we can assess for you know screening for HIV I mean that's just the sort of the drop in the bucket in terms of identifying the integrity of the breast milk so certainly I do think they're probably unknown risks but I I just have so many concerns about the insufficiencies of formula that I think it's certainly a better option probably even a better option for the same reason than then homemade formula. Yeah a couple quick questions what's the source of the bacteria in the placenta and do you know what type please. So that's a great question so most of the bacteria whether it's in the placenta or entero memory so it's a breastfeeding past bacteria or in the uterus is of gut origin some maternal gut so sequel specifically bacteria and of course it can be you know of dependent varieties depending on on the mom's health. How is it seeded then. We don't really know there are a couple of theories about like dendritic cells taking up bacteria from the mom's gut and shuttling them around you know systemically but they're they're mostly theories at this point I don't think anybody's like tagged bacteria and monitored its its motility but yeah so it's an it's an immune transfer yes yes and that's really what's debunked the myth of the sterile womb we thought you know that that there wasn't much that actually any pathogen in there was going to be cause of preterm labor or something like that and in fact you know it's it's not only that immune tolerance is a factor so you know you and I could both be colonized by a parasite for me I could have no inflammatory response and it can be a commensal and for you it can be you know the cause of a tremendous amount of inflammation so that's why this is going to be a tough thing you know one of the things I highlighted in the slide is you know is it too late to establish what a healthy microbiome actually looks like you know all of us are sort of far down this road right of deleterious sort of effects so I think that's one of the biggest questions is sort of how how can we establish what a healthy human is anymore yeah all right you um represented breast milk as the best guest that you use for the template for the for the template for macronutrient ratios for adults and what's your comment on I've read some research which suggests that maybe fallacious for adults in as much as the relatively high sugar content of breast milk bearing in mind that the infant is in mild ketosis is really there to to help the infant rapidly put on fat so it can survive the the winter so to speak and since adults don't really want to be rapidly putting on fat maybe it it the template would need to be tweaked for post-weaned individuals what's your comment yes really I arrived at that template clinically I think it's an interesting idea I think it's just an idea at this point you know the perfect health diet goes through a lot of the science supporting their claims and I think it's a wonderful starting point but what I found with adult women who were glucose metabolism adapted for the better part of 30 years was that when I would move them into a ketogenic diet they might feel better after the first 10 days for you know about two to three weeks and then they would start to have symptoms of essentially subclinical hypothyroidism so they would start to get dry skin hair loss cloudiness this actually was my personal experience as well on a ketogenic diet and so I do think that there's gender disparities that's why I found the Hasda research really compelling because it echoed what I observed which is that many women feel better on a moderate carb sort of root vegetable sort of carb sourced model now the therapeutic effects of a ketogenic diet are pretty well established I think at this point in psychiatry is a growing literature but there is suggestion that in bipolar mania and schizophrenia that there may be a therapeutic role for ketogenic diet so I do think that you know it's there's not one for everyone but I also think that's the beauty of using coconut oil therapeutically it's like even in a glucose adapted person you can provide immediate source of ketones even if they aren't producing them themselves okay I had a couple but for I'll ask both of them so the one is placenta so if somebody's encapsulating their placenta is that going to have the same clinical effect as eating your placenta right after birth and then second with the bacteria so there's this big push to if you're gbs positive right at week 36 you should take antibiotics once you go into labor and what's that effect that's having that's that's a very powerful question I've actually written recently about that if you want more information on it's on my website but um because I do think I'll just answer that answer that one first I do think that's one of the most powerful influences of the this sort of devolution of our microbiota as women is actually the administration of antibiotics intra uh intrapartum and you know that the according to the Cochran database which is you know the gold standard of evaluation of available medical research um it's it's not an effective intervention in terms of preventing infant mortality so what are we doing you know and and the effects and the consequences are so profound that you know if if there's not established benefit we need to re-examine that but I actually find you know if you scratch the surface no offense to any obese in the audience but if you scratch the surface of obstetrical practice you'll find that you know less than according you know to available data less than 30 percent of conventional obstetrical care is actually rooted in the literature you know that it's just like the wild west what they're doing it's and it's and it's you know as I've argued there's never a more important time to to protect you know epigenetic expression and and microbiota inflammatory responses it's during those nine months and and delivery so I have grave concerns about that and I encourage women to opt out you're allowed it's your body um and then in terms of encapsulation I get that question a lot I I think that there is uh you know I encourage women to actually like if they're going to consume their placenta to do it immediately raw right away pretty much because I've actually had a couple patients with negative clinical outcomes consuming it over weeks and I I've thought about again right because I talked about the placenta producing cortisol like I thought about the mismatch there in terms of like the temporal rehabilitation of that rhythm I was talking about so I think it's probably not dangerous for the most part it's certainly not an evident evidence-based practice in terms of depression treatment or prevention um but I think if you are going to do it it's probably best to find somebody help you do it the way it might be done you know by other mammals cool