Written by Christopher Kelly
Feb. 17, 2015
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Julie: Hi, everyone, and welcome to the Paleo Baby Podcast. I'm Julie Kelly. And I'm very excited today to be joined by psychiatrist and medical doctor, Kelly Brogan. Kelly has an MA BS in Brain and Cognitive Science Systems Neuroscience from MIT, a Doctor of Medicine from Cornell University Medical College, board certified in Integrative Holistic Medicine and board certified in Psychosomatic Medicine -- I knew I was going to screw it up at some point -- Consultation Psychiatry. Welcome, Kelly. Thank you so much for being on the show.
Kelly: Happy to be here. Happy to be here.
Julie: As I was saying, before we started recording, there's a bazillion things that I want to ask you about and we could talk about that are completely and totally relevant to Paleo baby, Paleo moms and health and all of these avenues. I'm sure you can probably talk about all of these things in depth. But what I really wanted to focus on today was something that really interests me and you've talked a lot about. I just re-watched one of your presentations from AHS talking about depression and this inflammatory model of depression.
I wanted to jump right into that and if you could really give the audience a little bit of idea of what that means. What does depression look like and how is it manifesting itself in people that you see in your practice today?
Kelly: Absolutely. I'd be happy to talk about that. I was conventionally trained. I trained at Bellevue, which is considered one of the more preeminent residencies in psychiatry. So I really dived in the wall [Phonetic] in terms of my belief systems around what causes depression, for example. If you ask anyone on the street even what causes depression, odds are they're going to give you some hand waving explanation that relates to the notion of serotonin imbalance or some sort of chemical imbalance.
And the truth is that we learned that as a culture. We learned that from direct to consumer advertising from pharmaceutical companies from one or two countries in the entire world that permits that model of industry to consumer contact. And it has taken hold in a powerful way. It's not worth going into now but if you scratch the surface of this serotonin model or what's called the monoamine model of depression, you really can come up pretty sure in terms of science that actually supports a consistent mechanism in human beings for depression and the specific role of serotonin in generating depressive states.
I started to, I guess, disabuse myself from a lot of the assumptions that I had made and my mentors had handed down to me which is that you have to take an antidepressant because it's like insulin to a diabetic or putting glasses on if you're myopic. It's never going to get better and you have to take it for the rest of your life. And, in fact, the data in psychiatry is rife with contradictions to that, not only in establishment of short term efficacy of these medications but also long term safety.
And then, of course, we know and acknowledge in psychiatry, even conventional psychiatrists will acknowledge that only about a third of patients are helped by medications. And, of course, there's reason to believe that even that third is only helped because of something called the active placebo effect or at least a good portion of them. So that leaves us with our pants down. So what is going on and how do we possibly make sense out of the fact that one in four reproductive age women are taking a psychiatric medication?
Julie: It's just mindboggling.
Kelly: Yeah, it's ballooning. It's ballooning. A journalist who really, in many ways, changed my life, Robert Whitaker, he wrote a book called Anatomy of an Epidemic and he maintains a very active forum called madinamerica.com for disillusioned psychiatric patients. And he essentially went through the literature that suggests that if you buy in to this model and you engage in long term treatment, your outcomes are actually going to be worse than if you were never treated at all.
And he's saying we have more and more prescriptions being written but we also have more and more mental health disability in this country and it's slated to be the number one cause of disability in the world in the near future. So what's going on? If we have more treatment, shouldn't we have less disability? That makes sense, right? That's not what's going on. So we have to start to unpack the role of medication in actually inducing long term chronic illness around something that might otherwise have been just an episode.
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But then we still have to ask the question: Okay, if we're not going to reduce it to something as simple as a chemical imbalance, then what might be going on? And that's where this idea that a lot of us talk about, which is this idea of evolutionary mismatch. And it's very relevant to psychiatry because the chronic long term nature of a lot of psychiatric illness maybe furthered, exacerbated and perpetuated by medications but the manifestations of these illnesses is also something to consider because of how our environment, our diet, our exposure to industrial toxins, to things that we don't even see like electromagnetic fields, to pharmaceutical products like antibiotics and birth control and vaccines, our exposure to all of these things is not something that we have evolved to accommodate or recognize on an immune level.
And so that really brings the realm of psychiatry into where the rest of functional medicine and the rest of integrative health is already which is that heart disease and diabetes and cancer and autoimmunity. These are all manifestations of dis-regulated inflammatory signaling and of an immune system that has been put on tilt. And so it's just applying that same model. And there's a long standing at this point literature, the first coining of the term the cytokine theory of depression was in the early '90s.
And so now there's just like -- It's really exciting literature to follow. The term for it is called psychoneuroimmunology. So that speaks to the relationship between our gut as the seat of our immune system, inflammatory signaling that traffics between the gut and the brain and from systemic bodily sources to the brain itself. And then what happens in the brain? So what happens when the brain actually gets that signal? The interesting thing is that we didn't even really know that there was any immune activity in the brain even ten years ago.
So this is all really emerging. But it turns out that there are little immune hubs in the brain and they're called microglia. And once this signal from the system, whether it's the gut or otherwise, is sent to the brain that there is stressor, stimulus, then the brain takes over. And it has a whole cascade of perpetuating those inflammatory signals. And we know that the end product is that there are compounds that have names like kynurenine, for example, a quinolinic acid and these compounds, you can even test for them.
They actually start to accumulate and cause excitatory firing in different areas of the brain, which, of course, can be adapted for short term. But it's a problem if it perpetuates long term because then your stress response system, which is really cortisol driven, stress hormone driven tries to interfere, to dampen it down and that is not a long term adaptation either. So you end up in this burnout phase over time still chronically inflamed.
Julie: Yeah. I was going to ask you about that. You took some of the words out of my mouth. Because, as practitioners, we run an organic acids test on almost everyone that comes on the door. And we are consistently seeing what you mentioned, these inflammatory markers, the kynurenate, the quinolinic acid.
Kelly: Yeah, I know. It's a crazy word.
Julie: [0:08:57] [Indiscernible] all together. They also come with a low turnover of serotonin and dopamine on organic acids test. What would that mean to you as a practitioner if you're seeing that over and over?
Kelly: Yes. So essentially, you can see that if patients are taking antidepressants. Antidepressants do a whole lot of things beyond just mess with serotonin trafficking. In fact, if I'm going to be fair and not cherry pick the literature, I should also say that antidepressants have been shown in a number of studies to have anti-inflammatory effects. Of course, it's my personal opinion that there's a better way to achieve that like adaptation, but the truth is there that maybe in a small subset of people for whom they are effective in a way that isn't driven by active placebo effect, maybe because of their anti-inflammatory effects.
So they do a whole lot of stuff. One of the things that they do, of course, is in their name. So it's serotonin reuptake inhibitor. So they're keeping more serotonin in the synapse. And so that is going to be influencing the turnover. So you might see that in even testing for amino acids.
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But what you'll see when somebody has inflammatory driven up-regulation of an enzyme called IDO, you'll see that they shift from using the amino acid tryptophan to make not only serotonin but maybe even more importantly melatonin, which has antioxidant property and also is important for circadian rhythm. So from producing that to producing these compounds that have different activity, what's called the NMDA receptor, so this excitatory activity.
And so you can end up spewing your use and breakdown, called metabolism, your breakdown of tryptophan to this other arm. Again, it's adaptive in a certain circumstance. The body really doesn't make mistakes. It's responding in a complex sophisticated way to a perceived stimulus. But it's in the chronic nature of these different triggers where the problem lies. In the literature, it's called the inflammatory response. In psychiatric manifestations, it's called sickness syndrome. And that is essentially characterized by withdrawal, by loss of appetite, by loss of libido, by slowing down where you feel less cognitively able perhaps, you withdraw socially, so potentially not to interact with others.
And this is essentially depression. I mean, you go to the DSM and it looks something a lot like that. That's what researchers like Charles Raison and [0:11:45] [Indiscernible], they've done a lot of work elucidating how this was at one time an adaptive response for the body to heal in the face of inflammatory triggers. But that now with this onslaught of inflammatory triggers from all these myriad sources, it becomes like unremitting and that's where we get into trouble.
Julie: What about cortisol? I mean, you mentioned that a little bit. How does that come into play? I mean, people always talk about it as the bad guy. All we ever see is low cortisol on tests and pretty much everybody that comes in the door is their cortisol is in the toilet by the time that they get to us and they're looking for help. What does that mean to you?
Kelly: It's very complex. I think the notion of adrenal fatigue is very alluring because it makes sense to our minds to see somebody who's struggling with lethargy and brain fog and low mood and to say, "Okay, they're just burned out. Their endocrine glands is--"
Julie: It seems like a gross oversimplification when you know what's really going on.
Kelly: Yeah. So we just have to keep chipping away at it. Those of us who are trying to understand the role of inflammation in adrenal -- It's called HPA signaling -- have tried to focus on the role of the brain. So the brain is actually responsible for asking for cortisol and other endocrine outputs. It's actually in the brain where that signal originates. And so there are some thinking that -- The hippocampus, for example, is part of the brain. It's like a memory center. It has very rich density of cortisol receptors.
And so essentially, the body adapts to what it perceives we think, to what it perceives to be a prolonged cortisol exposure by becoming less sensitive. And so, you can have this high state of cortisol that exists without the feedback loop. And that's called glucocorticoid resistance. That is what has been best studied in literature and best correlated with depression is this high cortisol state actually. And so if you look at through the -- Even mainstream psychiatric literature, you'll find that a lot of it correlates with high cortisol.
But there is a little subset or sub-category of depression called atypical depression that is characterized by overeating, oversleeping, a lot of reactive sensitivity. Sometimes it's physical symptoms. They actually refer them as leaden limbs, so there's heaviness of your body. And that some category has actually been associated with suppressed cortisol level and output and also more associated with this out of control inflammatory response. This is also true of postpartum depression. Postpartum depression looks more like the atypical model. It looks more like a flat line cortisol.
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It looks more like once you throw out the placenta in the garbage, you're asking the mom's brain to come back online and start to cycle in this way, the HPA axis signaling around the relationship between the brain and the adrenals. And if and when that doesn't happen, then you end up in this hypocortisolemic state. And that allows for, as best we understand, it allows for uncontrolled inflammation because cortisol is not a bad guy. Part of its role is a natural anti-inflammatory. It's part of how we regulate our immune and inflammatory response.
And so in the absence of it, you can have more unregulated inflammatory response. And so that's one of the theories that ties together low cortisol states and inflammatory, chronic inflammatory disregulation. I do cortisol tests also on my patients as well, salivary test. But the truth is the amount of cortisol is such a small part of the picture because it doesn't tell us anything about that signaling and about the receptor sensitivity. It doesn't tell us what the origin of the problem is, if there is a problem, in terms of whether or not it's at the granular level which, I think, it rarely is. Or whether it's actually at the brain level.
And there are a lot of things that can induce. Even there are papers that implicate even sugar in hippocampal glucocorticoid resistance. So there may be a lot of things that can drive that aberrant response on the brain side of things. But I do think that's where we need to focus is more at regulating inflammation so that the brain can come back online and in normal way.
Julie: Yeah, definitely. I mean, I'm just curious. What are some of the ways that we can be regulating this? I mean, if people are trying to go more towards the direction of veering away from the psychiatric drugs and trying to manage these things in a more natural and more holistic way, I mean, I know you're big on some of the natural remedies for depression. But before that, I mean, what are some of the other things that are causing them that we need to take care of? One of the things we're always doing is we're trying to find these root causes.
And part of it sometimes, I think, even can come from doing stool analysis and trying to find out if there's any major bacterial infection or overgrowth and things like that. Is that of one the things that you're looking at as well?
Kelly: Absolutely. I'm super interested in the role of the gut microbiota in inflammatory signaling and specifically in influencing behavioral symptoms and brain function. We know that it's a bidirectional relationship that anxiety and psychological symptoms even on a thought level can signal to our gut. And that's no surprise. The last time you were really nervous about something you might have had diarrhea or butterflies in your stomach.
And that direction, I think, makes intuitive sense for people. But that it can also move in the other direction as something that we're just elucidating which is that dysbiosis or suboptimal ecology in the gut can actually signal to the brain that it needs to be on guard and that there's something going on. In the animal models of depression, they actually induce this state, like in rats, by injecting them with something called lipopolysaccharide. It's the component of gram negative bacteria and that's literally how they cause depression in animals.
It's compelling that it may just be that if this breeches the gut blood barrier that maybe sufficient to put the entire body on inflammatory alert and to manifest these symptoms. So that is a huge piece of it. It's like simplify maybe the top three things that you can regulate to promote better signaling around the hypothalamic pituitary access, I think related to that is certainly not going probably be a surprise to you or any of your listeners, but it's going to be the role of gluten specifically in promoting gut inflammation.
So like what we have observed, based on emerging literature around this, is that sometimes up to 80% plus of people don't have gastrointestinal symptoms despite having gluten intolerance. So despite mounting an inflammatory response, one of the places that can be a focal endpoint of this inflammatory response is the brain, of course.
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The skin is another but the brain. And we know that antibodies transglutaminase 6 is specific to the brain. We know that there's crossover and molecular mimicry with GAD. So components, different components of neurologic signaling in the brain. And we know that there's also an inflammatory response in almost everybody who eats gluten. And we really don't have a great understanding of why that is. Is it because of how it's been hybridized over time? Is it because it's [0:20:36] [Indiscernible]? Is it because it's processed with vegetable oil almost always?
We don't have a good understanding. But one of the theories is that actually we have become deficient in bacteria specifically bifido factor that play an important role in breaking gluten down. Because we are not capable of breaking it down natively. But it's possible that we might have outsourced that to bacteria over recent history. Recent history, meaning in the past 10,000 years. And now, in the setting of, let's say, rampant antibiotic use or chlorination of our water or any other elements, we become deficient in bacteria that were otherwise making us more capable of digesting it.
So I do think that that's a huge, huge focus for me. I tend to be very admittedly biased and absolutist about this where in my practice there is not a patient who I recommend, even reintroduction of gluten. It's just not a part of my practice model, period. I think that's one I think seemingly less sexy consideration in terms of the biochemistry is to be how do we promote and tone the parasympathetic nervous system.
So a lot of my patients and I am extremely type A and doers and we want to check things off our list. But the truth is that there is no equivalent to cultivating a practice that tones that part of your nervous system because the sympathetic and parasympathetic drive influence every single organ in your body, period. And there are folks out there from oncologist and beyond who look at the role of the nervous system in the cultivation of disease, whether it's heart disease or cancer or autoimmunity.
Specifically, it's this balance and tone between the fight or flight and the relaxation nervous system. The relaxation nervous system is also critical for digestion, for triggering enzymes and stomach acid release. So if you eat lunch like I do, which is in four minutes between patients, it's just not -- You might as well not bother really eating healthy food because you're not engaging this evolutionary process that is a dance. It's a complex dance.
I often recommend when there is adrenal dysregulation and most people would recommend this, I think, but my patients find one appeal -- On a long menu, one appealing option for starting with five minutes of breathing exercise. So it can be just counting your breaths. It can be using a mantra. It can be doing a six count in, six count out. It can be doing a four count in, eight count hold. There's so many different models and there are apps and there are websites with [0:23:47] [Audio Glitch] content.
I am a big Kundalini Yoga fan, so I really like the kriyas that are very specific exercises. You can even Google like what do the kriyas do for brain fog? And it's a five to seven minutes breathing exercise based on ancient principles and using yoga technology essentially to shift the state of your nervous system. And it's something as simple as alternate nostril breathing or left nostril breathing. I mean, you do that for five minutes and your entire energetic state is different from beginning to end. There's not just much out there like that.
And then there's a whole compelling literature out of the Herbert Benson Institute, four decades of literature that show that we can promote inflammatory signaling with 20 minutes of some stupid meditation that somebody listens to an iPad. This is not complex stuff. It doesn't have to be religion. But it's very powerful. I think that's another. And then I think the final one, a big one in my practice is the role of sugar. Again, that's not going to be any surprise to anyone probably but sugar because of its inflammatory signaling.
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And what I mentioned even about its interference with hippocampal signaling but also because of what it does to your endocrine system to have this rollercoaster effect of blood sugar in the setting particularly of a low fat diet, which a lot of my patients come to me. I work in Manhattan. As much as there's a huge subculture of people interested in more progressive diets, there are still as many women who will still believe that a low fat diet is an important [0:25:35] [Audio Glitch] to their lifestyle. That was a long answer, but I think those are three I would consider.
Julie: I think those were huge and I agree with you wholeheartedly. Yeah, you're right. That's not surprising to us. I think it would be awesome if we could spend the rest of the time -- I would love to transition to how does this differ, how does everything that we've talked about -- Maybe it doesn't differ that much, but with postpartum depression? You talked a little bit about the placenta and I think that was great because we have this event where we have this endocrine organ that all of a sudden it just disappears.
And if you're in the late stages of pregnancy, it's been pumping out all of this cortisol and then all of a sudden it's gone. And we have this dramatic plummet of these crucial hormones. How does all of this come to play in terms of figuring out who gets postpartum depression and who doesn't. I mean, is it a lot to do with some of the things that you've just been talking about in terms of inflammation? Is it a completely different system? What's the difference between the [0:26:40] [Indiscernible] model?
Kelly: We don't know. We know that there are epidemiologic risk factors like history of sexual abuse, personal and family history of depression. That's a no-brainer if you're already somebody who responds to stress in this way whether it's physiological or psychological. It's going to probably be something that crops up in the postpartum window. We haven't been able to really pin it to motive of delivery, meaning caesarian or vaginal. And people had been, researchers had been digging and digging like [0:27:16] [Indiscernible] had done a lot of work around looking for serotonin genes.
And nothing has come up. Nobody has been able to really identify anything. So there isn't literature that I find really compelling that I've been following that says we can actually predict postpartum depression onset in the month before delivery with elevation of these inflammatory cytokines, some specific ones like interleukin one before for delivery. And we can actually protect who might then to develop it.
And again, it probably is, for reasons related to abnormal signaling around that HPA access and the adrenal brain relationship in the mom postpartum that facilitates this inflammatory response in a state where she is not able to regulate it appropriately once the placenta is taken out the picture. It is undoubtedly more complex than just that. But that's at least a framework.
There is also literature, for example, that suggests that hypothyroidism and even thyroid antibodies can predict postpartum depression and are correlated at least in one, I think, pretty interesting study with postpartum psychosis. And so that would suggest and, again, corroborate that there's a role for the immune system and dysfunctional immune signaling -- Again, I call it dysfunctional. It's really not dysfunctional. It's the immune system responding appropriately to an inappropriate exposure so that, again, we're looking at what put somebody at risk for autoimmune disease.
So the senses, so far, [0:29:06] [Indiscernible] has done, for example, is that it's some genetics. But then it's an environmental trigger and it's intestinal permeability. It may be something similar that you have, let's say, a woman with a gene variant like a snip in her glucocorticoid receptor. So that's going to make it harder for her to regulate under stress and then the trigger of delivery. And by the way, nine months of nutrition depletion essentially because we don't go into pregnancy as you well know, we don't go into pregnancy nutrient repleted.
We go into it with our tanks half empty taking birth control for 12 years which is sucking all of our antioxidants and B vitamins out with it. And then we wing a pregnancy and then we wonder why we're struggling to get back on our feet.
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But the truth is, it's about ten to 10% to 15% of women who do develop true diagnostic like syndromal postpartum depression because, of course, in psychiatry, we have no actual means of diagnosing anything. It's just an impression. So it's not everyone. And probably people who have the same dietary exposures and have traumatic birth and had a sex abuse history, there are folks who don't want to develop it. But there also seems to be reciprocal relationship with breast feeding that is probably very complex, part physiologic and part psychological, where breast feeding onset can protect against -- Successful breast feeding onset can protect against depression but then depression can also impede successful breast feeding. So it can be like that.
Julie: Yeah. It's maddening how many catch 22s there are with all that.
Kelly: Yes. Absolutely. It is. And for me or anyone else to pretend like we cracked the code, I would never pretend that. I am so interested in where my logic is breaking down because I'm trying to connect the dots on this and I do think that it is thoroughly and completely insufficient to project on to the postpartum experience, which is rife with known and identified changes in physiology let alone psychology. And to just project this generic model of chemical imbalance that we projected on the entire population of the world who is depressed, just project on to these new moms, I think is totally irresponsible.
I think even I prescribe antidepressants to patients for many, many years of my career. And that was my specialty. My fellowship was essentially prescribing medication to pregnant and breast feeding moms. And there are two randomized trials in postpartum depression around efficacy of antidepressants. So it's just like all assumptions. There's a pile of assumptions. And my concern is, and where my colleagues really get their panties in a bunch if I ever say anything like this, my concern is that these medications have a demonstrated documented history of inducing suicidality, violence and homicide.
And you can go to websites that document all of these cases and in the setting of news making infanticide in postpartum, the worst possible outcome, all of those women were treated. All of them were treated with medication. So I do believe that not only can we be missing the mark but we could be making it worse. And while telling ourselves, "Oh, they just don't take a high enough dose. They just needed more treatment." And this is what we do all the time. We do it with vaccines too. And not to open that can of worms.
Julie: It's nice to have you back on to open that can of worms.
Kelly: Happily. But we say, "Okay, it's not working. Let's just add on another." Six boosters of pertussis before we can admit the thing doesn't work. It's a similar psychology. We're so married to the idea that these pharmaceuticals whole promise. It's very hard for us to admit when they may actually be dangerous.
Julie: That's definitely difficult for people to take that step back. Just to even have the conversation. I mean, not even saying, "Okay, you're right. It doesn't work." We're just saying, "Maybe it doesn't work." Or, "Are we sure it works?"
Kelly: That's a question. Let's look at it with curiosity.
Julie: Right. I mean, do you find that you find working in your practice with women who are trying to get pregnant and trying to take more of a proactive approach? I've got this mission to encourage women to take more of a proactive role in their health before they venture down the path and decide to wing a pregnancy. I feel like it's possible. I feel like at least since a lot of women are waiting longer to have kids, why not use that time appropriately and get really, really healthy before you do decide to have kids? So that when you get there, it's not a devastatingly difficult struggle.
One of my favorite questions to ask is: How do you do that? How do you prepare for a pregnancy? How do you get out ahead of it? What are some of the things that you will recommend women can do?
Kelly: Julie, you just cut out. Just say the last sentence.
Julie: I was going to say what do you recommend women do to get out ahead of a pregnancy and work on getting themselves really, really healthy so that maybe that can stave off some of the things that we've been talking about like depression and postpartum depression?
Kelly: Absolutely. So I have the pleasure really of working with women who are motivated in advanced. And often it's because they're on psychiatric meds that they want to come off of before pregnancy.
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Sometimes we even have a year or two to optimize things before pregnancy. And the beauty of what I do now versus what I used to do is that I used to have to help women make sort of a Sophie's Choice around their own medication treatment versus their pregnancy in some cases. We would comb the literature and see what there was in the literature to support the use of medication and the triggers that the literature is not as scary as you might think it is.
So there is reason to believe that it could be in the best interest of a pregnancy and the woman's care to continue taking Zoloft, for example. It's my opinion that the literature is not asking the right questions. It's been asking these old school questions like: Are babies born with ten fingers and ten toes? It's not asking: Are babies born with mitochondrial disorders or autoimmunity or propensity toward that or neurodevelopmental issues?
I mean, there are a handful of very small studies that go about seven years. But that being said, a lot of these patients are coming within mind that there is a preparatory phase. And, of course, all of these traditional cultures get that fact. They get that preconception couples should be eating nutrient dense foods. In fact, in some cultures, they even reserve food especially for preconception women. And this notion that you have to actually prepare not only physiologically but psycho-spiritually for engaging in this space of your life is just totally foreign to us.
I mean, I took birth control for 12 years. I decided I want to get pregnant. I stopped taking birth control and I was pregnant the next month. It makes me nauseous to think about that. And I haven't [0:36:52] [Indiscernible]. That's how we do it. And it's unfortunately coming round the roost because we have the sickest children ever walked the face of the earth, in my children's generation cohort. I love when people are motivated because the truth is, whatever it's going to be optimal for you and your health mission is going to be optimal for your pregnancy epigenetically.
So that's where the idea of using diet. So using diet to resolve autoimmune symptoms or resolve psychiatric symptoms. It's going to be the same diet that is going to support and promote a healthy gestational experience and birth. So it's really a win-win. I am relatively conservative with supplements in pregnancy, not for any real reason. I took plenty. But mostly because I'm trained in that model like where's the data, where's the data, where's the data.
And when it comes to propensity, we just don't have it. And what seem like good idea taking 200 milligrams of thiamine, we just don't totally know if we're spewing something. So if I do supplement with anything in pregnancy, I'm going to do a more broad spectrum. So if I use a fatty acid like omega three, which I actually rarely do, but if I do, I'll also have been taking primrose oil, acetylcholine, make sure they're getting saturated fat for the diet, obviously. So it's like the whole picture. Same with B vitamins you want them in the concert with other B vitamins, not alone. Same with amino acids.
So it's rarely necessary when people are eating ancestrally. One of the best, just an unsolicited shout out, I think one of the best books on this is Cate Shanahan's book Deep Nutrition. It really influenced me in my thinking about how we have deviated, like how we're devolving as a species physiologically, the spacing between our eyeballs and myopia, our teeth and our jaws and the need to extract wisdom teeth. All of these metrics of how we are not -- We can birth babies and we're struggling with that actually too.
But the actual morphology of this human is changing before our eyes because of not only what we're eating but then nutrient deficiency and the setting of chemical toxic and exposure. So it's like a two hit. You expose these nutrient-depleted women to a range of toxicants from pesticides to endocrine disruptors in their plastic water bottles, from that to their receipts. And then you prescribe them couple of antibiotics and they get a bunch of ultrasounds and they get their flu shot and Tdap vaccines and then they go into birth with an--
[0:40:02]
You could see how it's a cascade that we're probably overstepping our evolutionary balance in terms of what we can expect our genome to adapt to.
Julie: Right. Even to tolerate, I think, from --
Kelly: Yeah.
Julie: It's just a lot to absorb.
Kelly: Absolutely.
Julie: Well, this has been fascinating. And we're definitely going to have you back on because this could go directly into talking about post birth outcomes and breast feeding and diets for breast feeding women and we don't have time for that. So definitely have you back on, hopefully soon to talk about some of those things. We have to get my husband on to talk to you as well. That will be great. Where can people find out more about you and keep up with all the wonderful things that you are doing?
Kelly: Cool. It's been a total pleasure. Obviously, I can ramble lots. The next time, you have to interrupt me more because I could [0:41:01] [Audio Glitch]. I love it. This is just my favorite topic. I have a blog. I'm on social media. My website is just my name. It's kellybroganmd.com. I do this little called snippets where it's super short digestion of the most current literature. I probably read upwards of 70 papers a week and I try to just take from the new emerging science what might be of interest to people to support lifestyle based medicine essentially.
Julie: That's awesome. I appreciate all of that hard work that you're doing. It's not easy to keep up with all of it.
Kelly: It's compulsive. It's totally compulsive.
Julie: Great. Well, I can't wait to talk to you again. Thank you so much for joining us today.
Kelly: My pleasure. My pleasure.
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