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A Neuroendocrinology Researcher on the Front Lines
209 Plays1 year ago
Dr. Alexander Kauffman runs the Kauffman Lab at University of California, San Diego. As a professor and researcher, he studies neuroendocrinology mostly in animal models. He has served on the editorial boards for several peer reviewed research journals, run numerous studies, has prolifically published research and won several awards. Thank you to Dr. Kauffman for being on the show.
In this episode we talk about PCOS, how androgens affect the brain, epigenetics, and the neurons responsible for controlling ovulation.
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Transcript
Introduction to Dr. Alexander Kaufman
00:00:05
Speaker
As I've been researching for this podcast, a name kept popping up in my studies, Dr. Alexander Kaufman. I reached out to him and amazingly, he agreed to be on the show. Dr. Kaufman runs a neuroendocrinology lab out of the University of California, San Diego, and has a young but storied research career. He has won numerous awards, been published many times,
00:00:28
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and has been on the editorial boards for several peer-reviewed endocrinology and neuroendocrinology journals. I wanted to talk to him because he's on the front lines of this research, of how the brain controls ovulation.
Understanding GNRH Neurons and Hormone Release
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He'll tell us the ongoing study he's most excited about, how certain neurons behave differently in many cases of PCOS, and how chronic stress affects these reproductive neurons in the brain. I'm Stephanie Greenwood, and this is The Life Detox.
00:00:58
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you
00:01:09
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Before I get started with my interview with Dr. Kaufman, here's a quick primer on the neuroendocrinology of ovulation. In a small part of the brain called the hypothalamus, there's a type of neuron called GNRH neurons. GNRH stands for gonadotropin-releasing hormone.
00:01:29
Speaker
GnRH neurons secrete the synonymous hormone to the pituitary gland that lives next door. If the frequency of the GnRH hormone is released in slow pulses, the pituitary creates FSH, follicle-stimulating hormone, which travels through the blood to the ovaries and helps an egg or two mature. If the GnRH signaling to the pituitary is fast,
00:01:53
Speaker
The pituitary makes LH, luteinizing hormone, which matures an egg and helps it release. In other words, creates ovulation. In a normal, healthy menstrual cycle, the GnRH neurons respond to a small fluctuation of estrogen and create an LH surge that stimulates ovulation. But for many years, researchers didn't know how, as GnRH neurons have no estrogen receptors.
00:02:19
Speaker
So, how are they responding to a rise in estrogen? I'll let Dr. Kaufman answer that one. The thing that's interesting about GNRH neurons is that they respond to fluctuations of estrogen, yet have no estrogen receptors themselves. These seem to get by with a little help from their friends.
00:02:39
Speaker
True. Very well put, yes. And you know, that wasn't always known to be the case. In fact, you know, for decades, it was well known that estrogen and testosterone and progesterone, these kind of big famous hormones, could affect GNRH neurons and therefore affect the reproductive axis.
00:02:55
Speaker
And initially it was thought, hey, they just act on these, these hormones act on the gene or H neurons and tell them what to do. But as you mentioned, we ultimately learned that these gene or H neurons don't have the appropriate receptors to receive that hormone signal. So as you said, get by with a little help from your friends to quote the Beatles, you know, the hunt was on for, you know, 15, 20 years to find what are the other brain sites and brain cells that actually are responding to estrogen and testosterone and then
00:03:23
Speaker
convey that signal somehow some way to the GNRH neurons.
Role of Kisspeptin and Candy Neurons in Hormone Regulation
00:03:26
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And that was a big mystery for a long time. And it wasn't until the early 2000s that we really got a handle on what the best candidate is, at least right now. And that's the kiss-pepton neurons in the hypothalamus. Kiss-pepton neurons do have estrogen receptors, and they send out a peptide called kiss-pepton to the GNRH neurons, which then sending that signal to the pituitary that ultimately leads to LH or FSH.
00:03:51
Speaker
100% correct. Exactly. Yeah. So, you know, in the early 2000s, KISpeptin, I want to say burst on the scene as this very new and important regulator of GNRH neurons. This was sort of a unique case in that it was first discovered in human patients who were, had mutations in the receptor for KISpeptin. And so that receptor didn't work. And those, those individuals had severe infertility issues and did not go through puberty normally.
00:04:18
Speaker
So it was a big red flag saying, hey, when you don't have that kiss-peptin receptor, reproduction doesn't work. That caused everyone in the field, like myself, who's a basic science researcher, meaning we don't study human populations. We use molecular studies or mouse models or sheep models or whatever it might be. Those of us studying animals to say, hey, what does kiss-peptin actually do? And a flurry of activity in the mid-2000s
00:04:42
Speaker
showed very, very nicely that Kispepton potently stimulates the GNRH neurons. So it was a situation where a clinical observation ultimately drove the experimental studies in mice and other species. And then the information that we learned in animal models was then brought back and reapplied in the clinic for human populations. So it's been this nice kind of back and forth from bed to bench side, back to bed, as we call it.
00:05:09
Speaker
And there are a couple other types of neurons, if I'm not mistaken, that work with the GNRH neurons, the KNDY neurons. So KNDY neurons, which are actually, most people pronounce that candy neuron as an acronym.
00:05:24
Speaker
And that's to be a little bit cheeky because we have the kiss neurons, like the Hershey kiss. And so now you have the candy neurons. So it turns out the candy neurons are actually kiss-peptin neurons. They are one in the same. The interconnectivity of these neurons, so they talk to each other. In addition to talking to gene RH, these candy neurons
00:05:43
Speaker
talk to each other and help form and regulate the pulsatile release of GNRH hormone from the brain, which then causes LH pulses, which will then regulate the ovaries. Yeah. I found you through a paper that you had published in Neuroendocrinology titled Emerging Insights into Hypothalamic Pituitary Gonadal Access Regulation and Interaction with Stress Signaling.
Impact of Stress on Fertility
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Can
00:06:07
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Can you tell us how chronic psychological stress, especially during developmental years, affects ovulatory function and development in females? Infertility is on the rise. One of the things that could affect infertility or cause subfertility is stress, certainly
00:06:24
Speaker
chronic stress. That's something that my lab has worked on a little bit in the past seven or eight years. We've studied how stress and stress hormones can affect the reproductive axis. Sure enough, it has a very strong inhibitory effect on female fertility. It can inhibit or impair normal cycles, so menstrual cycles in women or estrus
00:06:45
Speaker
cycles and rodents as we call them. It can diminish the ability to ovulate, it can impact the ability for the ovary to develop healthy follicles and eggs and it can certainly block ovulation. So we've shown this a number of different ways in mice. It's been shown in rats, sheep, monkeys, less studied in humans because as you know, it's really hard to study humans in a lot of these cases because you have to have a very properly controlled situation and that's not always easy to do for long-term studies.
00:07:14
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There's a little bit of evidence in humans, but in fact, I would actually argue that the evidence in humans is more kind of casual observations that when women are stressed, their cycles aren't very great, and they have trouble conceiving, and then suddenly they go to a nice, happy, less stressed situation, and suddenly she gets pregnant, right, or she ovulates. So it's more kind of casual observation in humans, but all the animal data strongly suggests that stress and stress hormones can inhibit reproductive function in women.
00:07:43
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Are these stress hormones affecting these cycles through GNRH neurons? Are they acting upon and throwing that signaling of kisspeptin and that functioning off? That's a good question. So we think that there is a component going through both kisspeptin and therefore ultimately GNRH.
00:08:01
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But there's still a lot of unknowns, to be honest. I can think of dozens of studies that show that stress or stress hormones can negatively impact kiss-peptine neurons in the brain. That would turn off reproductive access. They can negatively affect GNRH secretion or LH secretion. But there's also some studies that show that stress can affect
00:08:21
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the pituitary gland. So it can bypass GNRH in the brain and have direct effects on the pituitary. There's a number of studies in sheep models showing that. And certainly stress hormones can act also in the gonads themselves, the ovaries, to have potentially negative effects on varying functions. So the way I personally view stress is it's hitting at three levels. It's hitting at the ovaries. It can hit at the pituitary and it can hit at the level of kiss-peptin neurons or GNRH neurons in the brain.
00:08:48
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which makes it, of course, hard to overcome sometimes, right? Because you can fix one level, but you still have stress or stress hormones possibly having adverse effects at the other levels. Have you seen microglial cells and astrocytes having an effect on GNRH signaling and functioning?
Glial Cells and Reproductive Neuron Function
00:09:04
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That's a really good question. The short answer is yes, glia have a very important role in GNRH and kisspeptin possibly function.
00:09:13
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Now before I play the rest of his answer, let me talk for a second about microglial cells. These cells are responsible for cleaning up dead brain cells, pathogens, and other material in the brain that needs to be removed. Research in the last 15 or so years has found that when we experience trauma,
00:09:33
Speaker
Microglial cells can start going haywire and actually attacking healthy brain cells. They're kind of like the immune system of the brain, and just like an autoimmune disorder, these cells can start attacking the brain. To learn more about this topic, I definitely recommend any of Donna Jackson Nakazawa's books. Okay, so back to how glial cells can affect GNRH neurons.
00:09:56
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Importantly enough, it hasn't been that well studied compared to studying neurons. Despite being more abundant in the brain, glia have been understudied compared to neurons in terms of reproductive control. There was a lot of very interesting work coming out of some labs in France in the 2000s showing that
00:10:13
Speaker
certain types of glia can affect how the GnRH neurons secrete and how those neurons function. It was studied for a while and then kind of died off a little bit, didn't really gain a lot of momentum, although I personally believe the data is strong. More recently, I would say just in the last three to five years, there's been a resurgence of looking at glia in the control of both GnRH neurons directly and also in the control of kisspeptin functioning.
00:10:38
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That data is all emerging, but long story short, it looks like if you impaired glial function, that could negatively impact how kiss-peptin neurons work or how GNRH neurons work. Again, it's kind of re-emerging now. Labs are starting to jump on this. We're starting to see more people get funding for this, which is great, but I still think we're a little ways away from really understanding the complexity of
PCOS: A Brain-Related Reproductive Disorder
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it.
00:11:00
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We have polycystic ovarian syndrome. We know from what I've read that GNRH neurons are almost kind of hyperactive in their signaling, in that they're not giving a smooth wave to provoke an LH surge. They're always just kind of throwing it out there. Do we know the underlying dysfunction or why the neurons are acting that way? That's a million dollar question, right?
00:11:27
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And I personally think we're getting a lot closer with the discovery of kisspeptin and now kind of considering kisspeptin and candy neurons, their relationship to GNRH, I think we're really moving forward at rapid pace now. I would first back up and say that for many decades PCOS was
00:11:46
Speaker
inappropriately viewed by most clinicians as an ovarian disorder, an ovarian syndrome exclusively. Because probably, in my own opinion, the name polycystic ovarian syndrome, ovaries right in the name, I actually think that limited us in terms of understanding the syndrome. Yes, there are pyramids at the level of the ovary, hypertrophied ovaries, cystic ovaries, and the inability to ovulate properly amongst other things. However,
00:12:12
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As a neuroendocrinologist, I know that a lot of how the ovary function is dictated upstream by hormones coming from the pituitary, and of course those pituitary hormones are driven by GNRH neurons coming from the brain. In the last couple decades, maybe even less, those of us who are reproductive neuroendocrinologists have taken a good look at PCOS,
00:12:32
Speaker
and really view it not just as an ovary disease or syndrome, but as a reproductive syndrome that has a very strong neuroendocrine component, a brain component. And in fact, I would argue that many of the PCOS cases, actually, the etiology is probably at the level of the brain.
00:12:50
Speaker
And when I say brain, of course, I mean, you know, the reproductive neurons that control reproductive hormone secretion and perhaps even specifically kisspeptin neurons or those candy neurons that I alluded to earlier. So why do I say this? As you already mentioned, sort of one of the hallmarks of PCOS is this very abnormally high level of LH secretion. And as you probably know and have talked about,
00:13:14
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elsewhere on the podcast, LH is normally secreted in pulses, right? So it goes up, comes down very quickly, and then maybe 60 minutes later, it comes up again and then goes down. And that always goes on in this kind of very predictable, frequent pulsatile cycle. In PCOS women, not all of them, but in a majority, LH pulses are very rapid and they're higher concentration. So their basal levels are higher, their peak concentration per pulse is higher. So
00:13:40
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The pituitary gland is spitting out really high levels of LH and it's doing so very frequently. Now, anytime you see a change in the frequency of LH pulses, that tells you there's
00:13:53
Speaker
a change of the level of the brain because the timing of LH pulses, the frequency is 100% controlled by GNRH neurons and kisspeptin neurons. It's a brain controlled phenomenon. We now call this the GNRH pulse generator, which is sort of this elusive vague term that means some neural or brain processes coming together to help form GNRH pulsatile secretion, which will then cause
00:14:18
Speaker
downstream LH pulsatile secretion. So in PCOS women, we can't measure GNRH in the blood, but we can measure LH. And many, many studies, as you mentioned, have shown very high rapid LH pulses. That suggests that the GNRH pulses are abnormally rapid and have high amplitude as well. So about 10 years ago, the thought kind of was proposed that the GNRH pulses themselves are being controlled and driven by
00:14:45
Speaker
the kiss-peptin neurons, specifically the candy neuron population. And a lot of great work from multiple labs and multiple species has recently provided very strong, compelling evidence that these kiss-peptin neurons are controlling and dictating the pulse of gene marriage secretion, the pulse frequency of gene marriage secretion.
00:15:04
Speaker
So, if PCOS women have abnormally rapid LH pulses, one could hypothesize, as we did, that's caused by abnormally rapid kiss-pepton pulses coming from the brain. Kiss-pepton neuron firing must be abnormally rapid, and that's causing all the downstream hyperactivity, as you said.
00:15:21
Speaker
you can fix that, if you can slow down those kisspeptin neurons or diminish how active they are, you might be able to fix the rapid LH pulsatility and bring that down into a more normal healthy range. If by doing that you're going to have a more healthy normal levels of LH coming into the ovary and that's going to reduce the the buildup of testosterone and other androgen
00:15:46
Speaker
secretion at the level of the ovaries. Very excitingly, there's some new studies coming out in human clinical trials with PCOS women showing that if you can somehow pharmacologically slow down the kisspeptin neurons, you can reduce this abnormally high LH, and you can lower the testosterone levels in those women. There's promise.
00:16:07
Speaker
Do you think that these kisspepton neurons that are hyperactive, do you think there is an epigenetic factor going on with gene methylation that could be underlying this dysfunction?
00:16:23
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I don't think we have enough information at this point yet to say for sure there's an epigenetic component. The thinking that there might be an epigenetic component is partially due to, well, one, the fact that we know that kiss-pepton neurons and the kiss-pepton gene itself is under epigenetic regulation. So, you know, under normal healthy conditions, so it's possible.
00:16:42
Speaker
But in PCOS women, it's shown that PCOS women who are more likely to have PCOS daughters. So there's some genetic component that's being passed from generation to generation. So is this a genetic component or is this epigenetic component? We don't know. Some of the animal models are really interesting in that if you induce a PCOS-like condition in one generation of females, that condition persists through their daughters.
00:17:09
Speaker
and also through their granddaughters. This is a very exciting study coming out of several different labs. These are hard experiments to do because you have to go out many generations and it takes a long time. There's at least several studies that I know of that suggest that once you induce a PCOS-like condition, at least in a female rodent,
00:17:26
Speaker
for what that's worth, it may be able to persist through the germline to not only their daughters, but their daughter's daughters. So that could suggest certainly an epigenetic component that's been altered. But I do think it's a little too early to know for sure. Right now you are part of a study looking at the timing of food intake
00:17:45
Speaker
and how it affects our reproductive health.
Influence of Meal Timing on Fertility
00:17:48
Speaker
This study is still in progress but are there any trends you've observed or hypotheses that you can share with us or anything about this study that you'd like to tell us? This is a new study and in fact it's just begun. I'd say we're
00:18:02
Speaker
We're literally six weeks into it out of a five-year proposal. We don't have a whole lot of data yet. And this is with a collaboration with Dr. Matthew Butler, who is at Oregon Health Sciences. Dr. Butler, his sort of expertise is circadian rhythms and how the circadian system impacts or
00:18:19
Speaker
first of all, can regulate the reproductive access, but how alterations in the circadian system might have negative consequences for fertility. And there's a whole literature of that, sort of probably a whole podcast in and of itself. What Dr. Butler's intriguing hypothesis is now for this new project is that the timing of when individuals eat, so the timing of food presentation, or for example, if you had your meal at one time of the day versus another, the timing of when that feeding occurs can affect
00:18:46
Speaker
clocks in our body, it may be our central clock in the brain, the SCN, the circadian clock, but it could also be other clocks. There's clocks in the liver, there's clocks in gene or H neurons, there's clocks in kispeptin neurons, they're sort of everywhere. And so by restricting the time of day that females intake food and energy and calories, that can affect these internal clocks in a negative way if the timing of feeding is restricted.
00:19:11
Speaker
And that can have consequences for reproductive outcomes and fertility. And so we have some initial data suggesting that's true in mouse models. We're really just getting off the ground with this new project to figure out the details of that. And also, again, where is this happening? Is it the level of kiss-peptin neurons? Is that the pituitary? Is it the ovaries? Is it all three? And what are the mechanisms? It's sort of a brand new hypothesis. We don't have a whole lot of exciting new outcomes yet. But get back to me in a couple of years.
00:19:39
Speaker
I also have to hear about another study that you are working on part of neurosecretory gene expression in the hypothalamus. What is the study looking
Gene Regulation in Reproductive Neuron Development
00:19:49
Speaker
at? It's actually looking at quite a number of different things. If I can simplify it, it
00:19:54
Speaker
And this is in collaboration with Pamela Mellon at UC San Diego. This is looking at how reproductive neurons in the brain develop and become normal adulthood functional status and connectivity and how specific genes in those neurons are regulated. And I know that sounds pretty vague, but of course, we're looking at GNRH neurons, how they develop and how that might be impaired in certain diseases, how the kiss-peptin neurons develop,
00:20:22
Speaker
And also how the circadian clock neurons are involved in all this like dr butler study looking at the circadian control of reproductive function that's also a component of dr melons collaboration that we're working on and the idea here is that the circadian clock in the brain which is in the suprachiasmatic nucleus or the scn.
00:20:42
Speaker
Those circadian clock neurons, their development and function can be affected by certain genes, and then that can affect downstream kiss-peptin neurons and also downstream gene generation neurons. So it's all tightly interconnected, and a problem at any given spot can lead to sub-fertility and infertility. So that's what we're looking at, again, in mouse models. Dr. Mellon's group has identified several very interesting genes that may be important for circadian clock
00:21:09
Speaker
function and when those are perturbed, we get problems with the timing of ovulation in women or their menstrual cyclicity. What's your favorite study that you're working on right now that
Testosterone's Effects on Female Reproductive Health
00:21:20
Speaker
you're amped about? We just got a very promising score on a new five-year project looking at the
00:21:27
Speaker
actions of testosterone in females. And so this is something that my lab has become very excited about in the last couple years. Of course, PCOS women, as we've already talked about, have many of them, not all, but the majority have high levels of androgens of testosterone.
00:21:42
Speaker
well above a normal range in healthy women. That hyperandrogenemia is definitely a component of PCOS. Having said that, there's other scenarios in females in which the female can be exposed to high levels of testosterone or androgens that isn't PCOS. And so I've become very interested in that. And one of one, not the only one, but one of those scenarios is transgender men. So transgender men, for those who aren't fully familiar,
00:22:09
Speaker
are individuals who at birth are assigned female. They might have ovaries, two XX chromosomes. By the kind of the classical definition at birth, they are assigned female or they're termed female. But at some point in their life, they identify as being male. And so at some point, either now in the teenage years or in adulthood,
00:22:28
Speaker
they say, okay, I'm not female, I'm male. And so what these individuals can do is they can take testosterone treatment every couple weeks or every week, there's different ways to do it. And that testosterone will masculinize a lot of their external features, you can get facial hair growth and more muscle tone, etc, to be more
00:22:48
Speaker
quote, male-like. But one of the other things that that testosterone does, we think, is it shuts off the menstrual cycles, or actually we know it shuts off the menstrual cycles. And that's actually desirable because these individuals don't identify as female, so they don't want to have menstrual cycles.
00:23:05
Speaker
One of the outcomes of this testosterone therapy is it inhibits the cycles, the menstrual cycles. Sort of the million dollar question here is, how is that actually working? What is testosterone doing mechanistically to shut off a female cycle? Is it acting on the ovaries? Is it acting on the pituitary or the the G and H neurons in the brain? Is it acting on the kisspeptin neurons? Of course, my favorite.
00:23:25
Speaker
So we have a grant now, which I'm very excited about, to study sort of the molecular and physiological mechanisms by which testosterone at high levels is acting in the female's brain and pituitary to possibly turn off the reproductive systems there. One thing I will point out, which makes this complex but also interesting, I think, is that the concentration of testosterone or the dose of testosterone in these individuals is quite different from PCOS.
00:23:53
Speaker
PCOS women have androgen levels or testosterone levels in their blood that is two to three fold higher than a normal non PCOS women. So it's definitely high. Whereas transgender men have testosterone levels that can be eight to ten fold higher than a normal woman. So the androgen levels circulating in transgender men
00:24:12
Speaker
are much, much higher than the androgen levels in PCOS women. That might, and I stress, might be important down the line once we learn the mechanisms for what testosterone is actually doing. It may turn out that there's a dose component to what it does. We're not sure yet, but there's a hint there that there might be that. Ultimately, in this current new project, we are studying females who are taking
00:24:34
Speaker
very high doses of testosterone because they identify as male. And these testosterone levels are in the normal male range, the normal healthy adult human male, whatever his levels would be. That's the levels that we're giving to transgender men.
00:24:51
Speaker
These are much higher than PCOS levels. What are those high levels of testosterone doing? Yes, they're giving hair growth and muscle mass things that these individuals desire, but they could also have negative consequences. There's receptors for androgens all throughout the brain in many different spots. What is that testosterone doing in those different glia or neural cells? That's an exciting road that we're going down right now.
00:25:13
Speaker
It almost seems like there's a testosterone danger zone. Yes. And if it's too low for men or if it's too high for women and it's in this danger zone, that's when you start to see these metabolic changes, the insulin resistance and inflammation. And actually,
00:25:32
Speaker
your point about the metabolic and inflammation changes, that makes it even harder to figure out what's going on from a clinical or research component because, of course, it's well known that metabolism, metabolic status, energy balance, inflammation levels, those can all themselves affect the reproductive axis and they can impair reproduction if they're not in a healthy level.
00:25:54
Speaker
So teasing apart testosterone's effects in metabolism and energy balance versus testosterone's effects directly on reproductive neurons and reproductive hormone secreting cells is challenging to do. It's likely that testosterone is having an effect in both of those. And so one of the things that my project is doing is trying to tease that out. And so we have
00:26:16
Speaker
what i think are quite innovative ways to selectively study testosterone's actions in just specific cells or just specific neurons and ignore the effects or not have there be effects in other neurons and so this will be an exciting way to pinpoint where testosterone is having its effects.
00:26:35
Speaker
And ultimately, I think it's going to be affecting the metabolic cells in our body and also the reproductive cells. But we're going to separate those two in our studies and try to really focus in on the reproductive cell effects. Very interesting. I'll be excited to read that one.
00:26:51
Speaker
Yeah, yeah, right. Give us five. We'll have some data certainly in the next couple of years. We already have some exciting data coming out of the kitchen right now. To your point about the danger zone of testosterone, that's sort of been known for a while based on sports athletes who dope. And by dope, I mean taking anabolic steroids, you know, to try and get massive muscles. So anabolic steroids, you know, we heard about that
00:27:13
Speaker
big in the news with Barry Bonds and Jose Conseco back in the day. But, you know, it was used a lot with wrestlers and bodybuilders trying to get that extra edge in the Olympics. So a lot of those drugs that both men and women were taking in those scenarios are basically androgens, versions of androgens.
00:27:28
Speaker
And these individuals were taking these androgens at very high levels. They were either in the male range, the healthy male range, which is high for a female, or even higher, what we call super physiological. So in the case of a lot of males, a male athlete, a bodybuilder trying to get that extra muscle, he might be doping himself with extremely high levels of androgens that are way above what his body would normally make.
00:27:50
Speaker
Now, we've known for decades that when you do that, females who are doing that, their menstrual cycles get totally messed up and often they become acyclic. In men, you see that with lower activation of the reproductive axis and one of the telltale signs of that is that the gonads, the testes shrink because they no longer have the reproductive hormones coming in to tell them to grow and to be at a healthy size. And so, same with women, their cycles stop and they have problems,
00:28:17
Speaker
So, even now, that still happens. There's hundreds of thousands of individuals in the US every year who take anabolic steroids. What is that doing to their brain? That's sort of been overlooked. Is there anything else that you just want to share with our listeners? People value the importance of the research going into this to try and understand PCOS and also just how testosterone or androgens can have
00:28:43
Speaker
negative effects on females.
Treating Neuroendocrine Aspects of PCOS
00:28:45
Speaker
There's a lot we don't know, but I'm optimistic that we're getting there. And as I said, just in the last five, 10 years, I think personally, I think we've made really more rapid progress in understanding the brain's component of this and also now therefore being able to treat some of the PCOS symptoms. There's been a couple
00:29:04
Speaker
really exciting clinical studies that just came out in the last couple years showing that we can improve the hormonal levels in PCOS women and bring them down to a healthy level with some of these new pharmacological treatments that are targeting the brain, basically. And so a lot more work to be done, but I personally believe we're making much more rapid progress now than we were, you know, 15, 20 years ago. So that's the good news.
00:29:29
Speaker
Thank you again to Dr. Kaufman for taking time out of his very busy schedule to talk to me and let me nerd out about neuroendocrinology. I love this science and I'm excited to see new research as it emerges. The hypothalamus controls our stress response, our body temperature, our thyroid, and our hormones. It does so much for us and is susceptible to physical and emotional stress.
00:29:56
Speaker
So if you're struggling with your hormones or metabolism, take a close look at your life because you might need a life detox.
00:30:14
Speaker
The Life Detox is produced by me, Stephanie Greenwood, and brought to you by Bubble and Be Organic. The views and opinions expressed are the speakers' own and do not necessarily represent those of myself or my company. Material and information presented here is for general information purposes only and is not medical advice. Being a guest on this show does not imply endorsement of Greenplay LLC or any of its projects. Stay well, friends.