[00:00:00] Jay Feldman: Welcome to episode 3 of the Bioenergetic View. In today's episode, we'll be joined by Georgi Dinkov, and Georgi is going to respond to some criticism of his view of estrogen from an article titled, Rebuttal to Mercola's article on hormone therapy. We'll also be going over the major point that Sim Land is missing when it comes to increasing NAD.

[00:00:19] We'll discuss why we think Dr. Berg is completely wrong on serotonin. We'll go over nutrition with Judy's suggestion that thyroid issues on a carnivore diet are not caused by the lack of carbohydrates and why we don't think this is the case. And lastly, we'll discuss Dave Asprey's recommendation to drink orange juice and whether we think this is for the right reasons.

[00:00:38] I did want to mention that we had some tech issues early on in the show, so the video quality is pretty poor, but it does get better after around an hour and a half. And with that, let's jump right in.

[00:00:48] Danny Roddy: Okay. Welcome to a bioenergetic view with Jay Feldman, Mike Fave, me, and our very special guest Georgie Dinkov.

[00:00:54] How are you, Georgie? I'm

[00:00:56] Georgi Dinkov: all right. The usual guest, right?

[00:00:58] Danny Roddy: So special.

[00:00:58] Georgi Dinkov: He's

[00:00:58] Danny Roddy: here every time. Now we have these other two people here, Georgie. Jay and Mike great to all be here some big minds here and we're going to talk about the news and so the first thing we wanted to get into is Georgia, you are on Mercola, you talked about estrogen and there was, we're not going to get into too fine of the details, we can save that for a later date, but there was a woman named Devaki Berkson, and she did bring up many different points about she was critical of your interview with Mercola.

[00:01:23] So again, this is not going to be a fine point by point tackle of everything she says. We'll save that for another time. But did you have any just basic I don't know thoughts about what

[00:01:32] Georgi Dinkov: she had written? The way I would try to focus on is to is to drive home the point that estrogen is a carcinogen.

[00:01:38] Once people understand that, and I think once they internalize that, it would be very difficult to argue that you need to be supplementing with, I don't know optimal doses of carcinogen that somehow, is going to give you benefits. It is a carcinogen, and it was declared as such in 2001, I think, by the CDC and the NIH.

[00:01:56] very much. And then she said that was reversed subsequently due to the re analysis of the Women's Health Initiative studies. I think that was her point. But in 2005, the World Health Organization also declared estrogen a known human carcinogen. Not probable, not possible. Known human carcinogen.

[00:02:12] And the WHO, the World Health Organization, made a decision independently of the CDC. And basically it did that based on data submitted by over a hundred different countries independently. Okay. And that to me, to my knowledge, the designation by the World Health Organization of estrogen is a known human carcinogen, in other words, proven, still stands, has not been retracted.

[00:02:33] And then I also, basically the way I was going to approach it, if I was arguing with her, is that I found maybe 30 additional studies of every cancer you can imagine out there. And basically in every single one of these cancers, most of which are thought to be non endocrine dependent, in other words, like glioblastoma, brain cancer or melanoma, brain skin cancer, deadly skin cancer, pancreatic cancer, gastric cancer, ovarian, uterine endometrial, cervical, all of these different cancers, there's like a ton of evidence out there that estrogen, at best at best promotes the growth of the cancer after it has already formed.

[00:03:09] And basically there's also evidence for every single one of these cancers, that estrogen can also cause it de novo. In other words, no cancer, you give it a sufficient amount of estrogen or for sufficiently long period, even if it's a low dose. And I confirm what Pete has been saying that it's probably, it's not a benign thing to have let's say even tiny sub physiological exogenous supplementation with estrogen.

[00:03:29] But if it's uninterrupted and continued for too long without having such as something such as progesterone or something else that would antagonize the estrogen at the receptor level. Then the effect over time will still be pretty much guaranteed carcinogenic. And I was going to probably tell her if like we ever got into an argument, we'll say, okay, come up with a cancer, any cancer you want, no matter how obscure it is, I will find you evidence that estrogen is involved there.

[00:03:53] And I challenged the audience to come up with a cancer and go to Google and type that cancer and estrogen, and just look at the flood of studies. And these are a lot of, most of these studies actually from independent groups that don't know about each other's works. When you have every single cancer out there known to man, and you have estrogen implicated in it, in its, formation or development.

[00:04:13] And you also have different groups that don't know about each other's work and those independently discovering these effects. I think it's hard to argue that estrogen is not a carcinogen. Now if once that is admitted, and if that is admitted, then it becomes splitting hairs of okay, maybe if we'll give a sub carcinogenic dose, we're not going to get these effects.

[00:04:32] That's not what the evidence is saying, and I included a study which showed that a non carcinogenic estrogen, which they've, I think 17 alpha 18 elastradiol was the specific one. It becomes very highly carcinogenic in a environment with high reactive oxygen species, which happens when you eat a lot of pufa, when you oxidize primarily fat, when cortisol is high, when the h HP axi is activated, when thyroid is low, and all of just the, just this benign, oh, I won't say benign, but like everyday thing that happens to all these, everybody, you can be taking this no carcinogenic estrogen, but if you are in the state, it very quickly turns into a potent carcinogen.

[00:05:08] So I think that to me is because when I talk to doctors, usually the argument is. After you, beat into their dumb heads, that estrogen is a carcinogen, then eventually the defense starts becoming, oh, okay, so the dose makes the poison. No, plenty of evidence that low dose uninterrupted estrogen is also carcinogenic.

[00:05:24] And then they say we have these marvelous new types of estrogens that are not carcinogenic. No, again, they become very quickly carcinogenic in the quote unquote right environment, which is what is being promoted right now. Eat polyunsaturated fat, right? Oxidized, mostly fat cut down on the glucose.

[00:05:39] Yeah, those would be the main, but the main points, I think it's important to I would focus on estrogen being consumption because in everybody's mind that cannot possibly be good. And if this gets accepted I think it will be easier to argue all the other factors.

[00:05:53] And I think some other, some of our arguments were that the reanalysis of the WHI studies show that in some subgroups, The estrogen was protective against cardiovascular disease I think Alzheimer's and whatnot. There are, again, tons of studies showing not in, unfortunately, not in animals sorry, not in humans.

[00:06:11] In the humans, there are mostly associative studies, in other words epidemiological. But in animals, I can find you basically, studies, multiple studies showing that the exogenous administration of any type of estrogen, synthetic or bioidentical, is capable of producing strokes, heart attacks, because no, estrogen is probably one of the most potent clotting factors that we have endogenously, serotonin is another one and basically it could cause Alzheimer's disease, many other things.

[00:06:36] Thank you. And if you think of Alzheimer's as, as diabetes of the brain, which is what they're now trying to reclassify it as, it's, I think it's a very accurate description. And if you, then you know that basically that diabetes of any kind is driven by excess, by hyperlipidemia and also excess oxidation of fatty acids and driving up glucose through the Randall cycle.

[00:06:56] Then it's basically it falls from there directly that estrogen is involved. It's the most potent in cancer of lipolysis and in cancer of fatty acid oxidation. And in fact, that was the reason why back in the day estrogen was promoted as for as a weight loss because they were saying you can't get rid of the fat unless you oxidize it.

[00:07:12] So yes, here's this great thing, this estrogen, and we want to put you on the HRT on the pill. And one of the side effects is that you'll be losing weight. Unfortunately, women started gaining weight. And that was back in the day when most of the contraceptives were estrogen only. Then they started adding.

[00:07:26] So if estrogen is so great, why did the pharmaceutical industry did 180 degrees and now it's very hard to find, if not impossible, to find a contraceptive pill on the market that is estrogen only. Every single one now includes a progestin. You know why pharma industry very quickly realized that estrogen by itself, number what?

[00:07:44] It's an abortion pill, not on the contraceptive field. So they thought they're gonna get in trouble with the religious establishment, especially the Catholic church. And number two. Basically, the results from the long term follow up studies were abysmal. And the new estrogen promotes, causes and promotes breast cancer.

[00:07:59] All three types, the estrogen receptor positive, the estrogen receptor negative, and the triple negative. The new estrogen promotes basically all the cancers of the female reproductive system. So they said, okay, it also causes clotting. So they said, okay, we need something to balance the estrogen. So the effects of progesterone, the tame, the taming effects of progesterone estrogen are very well known in the farm industry.

[00:08:20] That's precisely why they added the synthetic progestins. It just so happens, unfortunately, that most of the synthetic progestins are themselves estrogenic. But, it's hard to, convince these doctors, even though this is published data, to come up with a synthetic progestin, look, go Wikipedia and look at its pharmacology more often than not, you'll see that it's a, despite being a potent progestin, activating progesterone receptor alpha or beta, it's also a potent estrogen as well.

[00:08:44] Many of them are glucocorticoid agonist as well, so they act like cortisol. In fact, most of the synthetic progestins have a warning by the FDA that can cause Cushing's syndrome. But again, it's almost impossible to find a contraceptive, hormonal contraceptive for females on the market that is pure estrogen.

[00:09:01] Now they're all producing an estrogen precisely because Even Big Pharma admitted to itself that they were afraid they were going to get sued. So they said, now we need to do something preemptively and then they added the progestin to tame the progesterone. I did not see anything in her rant about progesterone, about estrogen needed to be tamed.

[00:09:17] She, it sounded like she, she thinks it's the greatest thing since sliced bread.

[00:09:22] Danny Roddy: Jay, Mike, did you want to comment on that? Yeah, I think

[00:09:27] Jay Feldman: go ahead, Jay, you got it. I don't have much to add. I think it was a good overview. And if maybe we can dig into Georgie, if you're interested the two different receptors that she discussed and the difference between estrone and estradiol and their effects there.

[00:09:42] She made it sound as though the problem with estro with estrone is that it doesn't signal the beta estrogen receptor beta. And because estradiol does, that makes it protective and non cancer causing. Maybe we can touch on that a little bit, but

[00:10:00] Georgi Dinkov: Yeah, the estrogen receptor beta is a negative regulated receptor.

[00:10:03] If you have something that's a pure estrogen receptor beta agonist, I think it may have a positive effect because it will actually have the effect of reducing estrogen synthesis. And basically some of the signaling that estradiol does to receptor alpha will also be taped down. The endogenous matrices that we do have in our body, they're all agonists on both receptors.

[00:10:23] And I don't think estradiol is a higher agonist on beta than it is on alpha. It is the most potent estrogen in the body. And I guess what she's trying to say is that estrone is more dangerous than estradiol, right? But, estrone is the, if you look at it, if you look at the data that's published out there, estrone is actually a biomarker, predictive biomarker, for both developing and dying.

[00:10:45] From breast cancer and prostate cancer, and specifically estrone sulfate, which is functions in the body similar to DHEA sulfate it's basically the long term storage of estrogen, and it's probably one of the reasons why Big Pharma and the medical industry has been trying, has been getting away with murder for so many years, literally murder, is that they measure estradiol in the blood of menopausal women, and estradiol is low because most of it is produced in the ovaries, and we know that they atrophy, right?

[00:11:10] But if you measure estrone or estrone sulfate, they don't decline. And in fact, our tests with several of the women actually who who sent me these this doctor's response, we actually found out they did blood tests. And some of them are premenopausal or menopausal, and the estrogen levels in the blood came back low.

[00:11:27] But when we tested in here, all three, estrone, estradiol, and estriol were high. It's hard to argue that this is a good combination. Every single one of these estrogens individually and combined, even worse, has been associated with many cancers, and it's a very good predictive biomarker. Estradiol, if she's arguing that estradiol is somehow less dangerous than estrone it's hard for me to accept that estradiol is the actual declared humer carcinogen in both the CDC and the WHO.

[00:11:54] Estrone is a precursor. If you have high amounts of estrone basically, because that's usually what you synthesize. Estradiol is the final step because it's the, with the two hydroxyl groups. But if you're synthesizing estrogen, usually the pathway is through DHEA, then androstenedione. And then you synthesize from that estrone, and that gets finally reduced to estradiol.

[00:12:13] So basically if you're synthesizing a lot of estrone, that's not a good sign. It means your aromatase activity is high. And even the aromatase activity and expression is actually one of the most one of the best predictors for any type of cancer death. And actually, survival in the ER room.

[00:12:30] One of the first studies that I posted on the forum the RAPI forum, back in 2014, was that the best predictor whether a critically ill person arriving in the ER will survive was their levels of estradiol at admission, and they were negatively correlated with survival. No, of course you can say, correlation doesn't equal causality, it's not just a study.

[00:12:48] I'm saying that everywhere you look, it does seem like estradiol is a stress hormone that rises, during times of stress and general lack of energy. And it's very hard for me to accept that just because it's an agonist on both the beta and the alpha. Somehow it's agonism on beta negates the effects that it has on alpha.

[00:13:07] Most of the studies with cancer and promoting the cancer are done with a trial. They're not done with a stroke. So if Estradiol has all of these gen genis, generating and promoting effects from cancer in all of these animal studies that we have I would say Estradiol is really, it's not any less of a culprit than Estro.

[00:13:24] And it is a much, much more potent estrogen than the receptor level. I think Estrone is only about 4 percent of the affinity of what Estradiol has for both of the receptors, but Estrone is produced in much larger amounts and it does serve as a, as the reservoir. So none of these estrogens really are good to have in high amounts.

[00:13:40] Even as Estriol, which is considered almost inactive there are a ton of studies that are showing that it's correlated with, a bunch of different cancers in a few months. And then there's also animal studies showing that administrating Estriol can actually exacerbate an already existing cancer.

[00:13:54] So yeah I think we're giving these people too much of a leeway. I think the way we should be approaching the argument is show me a cancer case. We're giving women estrogen or the people estrogen or the animals estrogen resulted in beneficial results. In other words improve the situation.

[00:14:08] If they can show that's a clear, it's indisputable evidence that it's estrogen is protective in cancer. But right now we have, maybe, maybe we have two sets of evidence that, some people argue it's, that it's good. I, we argue that it's bad, but the argument on the side of people that estrogen is good is not based on any intervention data.

[00:14:27] Okay. Then the only intervention data that we have in humans are the women's health initiative studies. And now they're trying to reanalyze them. What this really means is a euphemism. They're throwing out certain data that they don't like, and then they're coming up with specific subgroups that maybe, somehow benefited from estrogen therapy.

[00:14:41] But the cumulative results of the women's health initiative studies are indisputable. That's what led to dropping the HRT on a nationwide level back in like the early 2000s. And I know now it's been some attempts to reintroduce it, the estrogenic HRT. That's, that, that's unfortunate.

[00:14:58] And I do, recognize that estrogen can some, can initially, ameliorate some of the symptoms of menopause, but we've discussed this with Danny many times and with Ray. But this is because estrogen has a suppressive effect on the pituitary. And a lot of the symptoms of menopause, which are hot flashes and higher inflammation and mood changes, are due to these elevated levels of LH prolactin and whatnot.

[00:15:19] Not prolactin, and even TSH. And those are highly inflammatory. And if estrogen can suppress them temporarily, you may feel a relief. But over time, The evidence is overwhelming, and the evidence that we have interventional from animals is indisputable. There is not a single study, to my knowledge, with a cancer model in animals where they injected estrogen and the animals got better.

[00:15:42] It caused the cancer in high doses, and then in smaller doses, if the cancer is already there, it promoted it and killed the animals faster. Mike, any thoughts? Yeah. It's quite a, it's quite a bit of information. I think that I think overall the picture that the one thing that she does point out beneficial, at least is that the synthetic progestins are problematic, which you already mentioned Georgie.

[00:16:03] Mike Fave: So it's this it's, we understand that synthetic progestins are problematic. We're seeing that there's a recognition that progesterone is useful. But then there's this weird dichotomy where oral estrogens are problematic, but transdermal estrogens are not. And that's something that's borne out inside the article.

[00:16:19] And then these, there's different receptor I'm not refuting the perspective that you're proposing there, Georgie, I'm seeing, it's like the argument has to get into these like really fine points on the different effects to start to make a case for the estrogens, right? So it's like transdermal and these receptors and this and that.

[00:16:40] And yeah, so it's it's almost obfuscating the points, it seems.

[00:16:43] Georgi Dinkov: But even at the high level, again, number one point. Why, first of all, who declared Christianity still there, not retracted? Why every single contraceptive on the market includes now a synthetic progestin? There's a very good reason.

[00:16:57] There are editorials published in BMJ, New England Journal of Medicine, decades ago, which said, guys, pure estrogen is bad. Okay. We need to do something about it because we're going to get, the crap shoot out of us. It may be even worse. So they made a conscious decision to start adding the progestins to tame the pro carcinogenic effects of estrogen.

[00:17:15] That is undisputable. I don't know if these doctors are still alive because it happened decades ago, but these editorials are still there. This is what they need to explain, okay? If estrogen is so great, why do we move away from pure estrogen therapy? If estrogen is so great, why is it still on the list of known humeric synergies?

[00:17:33] If estrogen is so great, why is a negative predictor of survival in critical illness, any kind of critical illness? So it's one of the best predictors of all cause mortality if you end up in the hospital. Doesn't matter if it's infection, doesn't matter if it's like you got a broken bone and you need surgery, doesn't matter if it's COVID, it does not matter.

[00:17:51] Basically you get a menopausal for whatever reason, your levels of estradiol determine if you'll survive or not. It is an association, but in combination with all of these other pieces of evidence that we have, I think it becomes very difficult to argue, and I may agree with her that the oral estrogen may be worse than the transdermal, because the oral estrogen will probably, a good portion of it will go through the liver, and there are very few things more toxic and more toxic to the liver than estrogen.

[00:18:15] Because the liver views estrogen as such a powerful toxin, It and because estrogen has a higher affinity for most of the cytochrome P450 enzymes that are responsible for metabolizing so called xenobiotics it will clog those enzymes and prevent the neutralization of other things, such as endotoxin.

[00:18:32] So if you get a hefty dosage of oral estrogen, you will be impeding your detoxification of endotoxin, and maybe that will lead to, lead to a, worse outcome. With transdermal estrogen, you will probably accumulate quite a bit of estrogen in your tissues. So you may spare your liver a little bit, but I don't think that will do the body any good.

[00:18:50] And I don't see what else can change from transdermal to oral because the estrogen, the estradiol itself, if you're administering estradiol, cannot really get metabolized by the skin into anything else. It's already an endpoint steroid. The only thing that can happen afterwards through transdermal route is two things, accumulation in tissues, or again, through second phase detox, goes back to the liver, gets glucuronidated or sulfated.

[00:19:15] And then basically becomes more easily excluded by the kidneys. So all of these arguments that I'm hearing for her are splitting hairs. Oh, I don't like this portion of the Women's Health Initiative study. We're going to reanalyze some of it and we're going to present only those results. The cumulative results of the WHI still stand.

[00:19:31] I have not, retracted. That study is still in PubMed, right? Yeah. So all contraceptives, estrogen and progestin. Why? Basically transdermal and oral, okay, maybe you're, because you're absorbing slower amount over longer periods of time, you don't get the immediate effects toxic effects of a bolus dose that you'll get through oral, especially because you're not in, in OB GYN, you liver as much, but again, back to Ray's point, and it's also published data, longer exposure to lower the concentrations of estrogen are just as carcinogenic as a, as a single high concentration dose.

[00:20:05] Okay. The effects are basically cumulative. So you can think of estrogen as radiation. They kept telling us that the radiation exposure risk is the threshold, right? So unless you, and the threshold, of course, they said is different for everybody. But we think that, you can probably have a hundred x rays per lifetime without significantly increasing your risk of cancer.

[00:20:24] Turned out that none of that is true. And in fact, The study that got, that I posted a couple of years ago showed that there was a collusion at the National Academy of Sciences to publish and to push the fraudulent threshold theory, even though the people there knew that it is an, that it is a cumulative effect.

[00:20:41] And the reason they pushed the threshold theory is to help GE, which was the largest manufacturer of radiation machines at the time, probably still is, together with Siemens or something. To help GE sell more machines worldwide and it published study on Springer. Unretracted directly says this was fraud.

[00:20:59] So like the Carla Rottenberg paper, which also says this is fraud. These people in the pharma industries, they knew that estrogen is dangerous. So we're not talking, I know the saying don't attribute to malice. What can be attributed to stupidity. I'm actually the older I get I feel it's the other way around because stupidity is self limiting.

[00:21:17] You can, you mess up and then usually after two or three times kind of life, kicks you out and you cannot do any more damage. But if it's consistent and goes over all of these long decades there's some evil mind behind it somewhere. Maybe more than one.

[00:21:31] Danny Roddy: Any final thoughts before we move on?

[00:21:34] Go ahead, Danny. There you go.

[00:21:37] Mike Fave: No, I was going to say, it's just. Putting this all in the context of everything that you mentioned, everything that you discussed in response. So I, it's interesting then because it's like you have contraceptive therapies out there now that can bind both oral estrogens and synthetic progestins.

[00:21:53] So it's even from both camps arguments, it's probably the worst possible things that you could be giving to women on a regular basis. So just interesting to bring that into a context. So it's like the most women or many women are running the contraceptive at this point. They run their contraceptives throughout their lifetime until they want to have children.

[00:22:11] If they can, if they don't have issues having children, then once menopause hits, then the idea now is to then go on a replacement therapy, right? So like some type of, Ideally, it wouldn't be oral estrogen from the arguments that are saying it's transdermal estrogen and transdermal progesterone. But the solutions in this case would be to not use transdermal estrogen and to use specifically progesterone because the case would be that some tissue estrogen levels are likely already high, and you may not see a high serum value of estradiol because ovarian function has failed, even though aromatase expression would still be higher inside the tissues, and then that's where you're seeing the higher estrone values, like estrone sulfate and whatnot, correct?

[00:22:53] Georgi Dinkov: Yes, and also because the inflammation activates aromatase specifically the prostaglandin is one of the most potent activators, and we know that the inflammatory biomarkers rise with age, invariably, in everybody, both men and humans. I'm sorry both males and females. So you can't have low estrogen in the context of high inflammation.

[00:23:10] It's just not possible. And the reason it can is because when inflammation causes damage, the role of estrogen is as a growth hormone, as a placement hormone, is to actually trigger cellular proliferation and repair whatever is there. That's what, that is its role. So it's, it should be high, in, in trauma, in, in some kind of a wounding situation in chronic inflammation, in autoimmune conditions.

[00:23:30] But unfortunately over time, it starts to contribute to the underlying pathology because estrogen itself. Also activates the, the coxin locks enzyme, so you're going to produce even more positive, so it forms positive feedback cycles with many of the, stress like response steroids, such as cortisol, aldosterone, it activates the synthesis of serotonin, estrogen is one of the most potent activators of tryptophan, hydroxylase.

[00:23:53] So over time, you get into this, in this bad situation where multiple pathological markers are elevated and it becomes very difficult to tease out, which is the original cause, but because they are actually, they form positive feedback cycles with each other, you can think of it as a fully connected graph, usually really like stomping down on one of them real hard tends to, break the vicious cycle.

[00:24:14] So yeah, so basically the and this is just an argument, but now we're seeing that inherent in, in, in nail analysis, there is no woman over 40 that presented with estrogen that was in the normal range. They all had at least one of the estrogens high and about 40 to 50 percent of them had all three of them high.

[00:24:33] You can if estrogen is high in the hair, you cannot argue that it's low in the body. There's nothing unique about the follicles. The, that results in the production of insane amount of it. And in fact, let's go up actually has some of the lowest amounts has lowest expressions of aroma days.

[00:24:49] And some of the lowest expressions of the estrogen receptors. So if estrogen is high there, or at least in the normal range for menopausal women, you can imagine what happens in the rest of the tissues. And another point we need to drive is that almost every cell in the body expresses aromatase. So almost every cell in the body is capable of synthesizing estrogen.

[00:25:06] So this idiotic idea, whoever came up with it, that you use the blood test to basically argue about systemic deficiency is absurd. In fact, if you talk to most endocrinologists but don't mention estrogen, just say, Hey, what is the blood level of a steroid usually representative of, without triggering them with, with a politically incorrect topic, they will readily admit that blood is just a transport mechanism and it's usually a reflection.

[00:25:30] Of the functioning of whatever organ is producing that steroid, right? So if you have low cortisol the blood means adrenal failure or low aldosterone, one of the, what I think is zona reticularis, the one that's producing aldosterone. So maybe it's atrophied, right? So if you have like low levels of testosterone, your gonads are not functioning well, but it's, it does not argue, it does not necessarily mean systemic deficiency.

[00:25:53] Now, estrogen is unique in the sense that every cell in the body, almost every cell can produce it. I think one of the reasons people accepted the blood results as a reflective of tissue levels. is that for the rest of the steroids, that's usually not the case. You are producing testosterone mostly in your gonads.

[00:26:10] There is some production going on in muscles if you train them well. There is some production in the brain, but usually about 80 percent of your circulating testosterone is of testicular origin. If there is low testosterone in the blood, chances are you will be systemically hypogonadal.

[00:26:23] Not just, low testosterone, but low in the blood, but also low in tissues. Because most of the tissues don't produce it. They don't have the machinery for it. They don't have the full steroidogenic enzyme cascade expressed there. That's not the case with estrogen. And it's unique in that respect.

[00:26:37] Which shows you how systemically, how systemic its effects are. And basically I think the only other steroid that is produced in more than one tissue exception is pregnenolone. So the brain produces a lot of pregnenolone. Your adrenal glands obviously produce a lot of pregnenolone. The liver and the gastrointestinal tract can also produce a lot of pregnenolone.

[00:26:57] There, there's some steroids that can be produced everywhere and estrogen is perhaps the best example. I think it's the one that really aromatase, I don't know of a cell type that does not express aromatase. And if we can show people this evidence, then we can say, okay. Unless, until you guys start doing tissue biopsies on a very large, sub population of menopausal women.

[00:27:18] And see what the estrogen levels are there. You cannot argue that the estrogen levels are low in menopause. And by the way, partial studies of this have already been done. Women with breast cancer. You are known to have drastically elevated estrogen levels in the breast tissue. But then the response of the doctors were like of course, they have cancer.

[00:27:34] And we know that this is driven by the estrogen. So it's only localized there. The estrogen is not high in other tissues. However, tests have been done. I forget what the reason was, but women present with certain cancer. And I think by mistake, they did a biopsy on a different tissue. And the estrogen was high there as well.

[00:27:49] So we do have indirect evidence. It's not, they don't consider statistically similar because those were mistakes. They didn't, get a population of women and test their, did the biopsy five or ten different tissues. These are women who went, let's say, for like breast biopsy, but got like a, I don't know, uterine biopsy instead.

[00:28:05] And the cells got tested for it and it was high there too, despite not having any cancer in that specific organ. So we have a lot of indirect evidence. Unfortunately, doing a study purely for informational purposes of what are the estrogen levels in menopausal women without cancer?

[00:28:21] It will probably not happen due to ethical reasons. They'll say it's an invasive procedure. And there is no good reason to do it. So they know how to cover the tracks. What can I say?

[00:28:31] Mike Fave: I also think it's interesting too, because when you look at, as another example of besides estrogen, you look at something like cortisol and people on low carbohydrate diets, you see the shift in 11 beta HS1 and 11 beta HSD2 metabolism of cortisol.

[00:28:45] So while serum levels may not be drastically elevated. The upregulation of activation of cortisol inside the tissues can be increased as well. So the serum levels are really and I think the confusion for a lot of people is because You look at serum levels and that can give you a sense of perhaps ovarian function and how much the hormone is being put out or what's being put out from the adrenal glands and whatnot.

[00:29:07] But then the question is more, what's going on at the target tissue for these different hormones? How is that being metabolized? Or another example is thyroid hormone, right? Your T4 levels can be fine. Your TSH can be suppressed, but if you're shifting more towards reverse T3, or there's a change in deiodinase enzymes at the tissues, then you may not have an active T3 or something like that.

[00:29:26] So all the hormones it's understanding, you have the gland that's producing it. You have signals from the brain. But then you, what you have, what's going on in terms of livers, conversion factor and metabolism of those things. And then what's going on at the target tissues. And unless you understand that full picture, you can get really wonky perspectives around what's actually going on with the different hormonal cascades.

[00:29:46] Georgi Dinkov: Yep. And it's surprisingly hasn't been done for hormones considered that they've done a pretty good job for iron. They basically now have stopped using serum iron as a, a universal test for anemia because you can have very low serum iron, but extremely high ferritin and iron saturation index, right?

[00:30:00] They call it anemia of coronary disease. In fact, it's an overload of iron, but they know this and basically, good doctors usually do the full iron panel and, gives you a good picture. Something like this should be happening for all of the hormones. Unfortunately, it isn't. But when you actually have blood tests showing that estrone sulfate, even if you want to go strictly by blood test, estrone and estrone sulfate do not decline in age, especially in menopausal women.

[00:30:24] And the arguments, the response that I've been hearing from doctors like, yeah, but they're inactive. Yeah, but they're almost just like DHEA sulfate. We've been told that DHEA sulfate is the long term inactive at the receptor level. It's the sulfated version, but it has a very long half life. And it's a measurement of your adrenal glands output of your production.

[00:30:43] And as needed, it gets passed through, I think it's called the sulfatase enzymes. So basically, that's converted into DHEA and it gets used for further conversion down into other steroids. So it's already accepted. A DHA sulfate is a very good indicator of adrenal production and of future DHA levels, which is the active hormone, right?

[00:31:03] The same thing is true of atrial sulfate. It is very well known that it easily metabolizes into gets, gets des sulfated and in tissues, gets easily metabolized into a str and actually with age, since you are in a reductive stress estro, which is the oxidized version. It's actually very easily converted to a stradiol because you have an excess of hydrogen ions.

[00:31:25] So it's served almost as a semiquinone, has one carbonyl group. And you will expect the basically with age, your synthesis, your tissue synthesis of estradiol will increase because you're in a much more reduced state than a younger person. And there are multiple studies actually with estrone to estradiol ratios showing basically like trying to tighten different pathologies.

[00:31:45] And I haven't looked that much into it, but the ratio is actually indicative. For the survival of several different types of cancer. In other words, if you have more estro than Ara, that's good. Okay. You may, you probably survive. But if the ratio astro to ara is low it's a very good predictor. I think for cervical cancer and for liver cancer, it was basically a very good predict predictor of future mortality.

[00:32:06] It, 'cause it's it's a redox indicator, right? So the same thing as the cortisone to cortisol ratio or the, I dunno, NADH to NAD plus to NADH. So we can do the same thing with the steroids. So if we have the evidence indisputed in the blood, estrone sulfate levels are high or the variance do not decline with age.

[00:32:24] It is absurd to speak of menopause as a condition of estrogen deficiency. The tissues will produce estrogen, estradiol actually specifically. And the more inflamed they are, the more estrogen actually will go there because inflamed tissues uptake hydrophilic steroids much more easily. Because Estrone and Estradiol are more hydrophilic than the other steroids.

[00:32:45] Basically, they have trouble getting into a cell that's It's membrane, if that thing even exists. If it's composed of mostly saturated fats, they don't have very good affinity for estrogen. So estrogen will have trouble getting in there. But in an inflamed tissue, basically the cell permeability increases in both directions and you get both leakage of debris into the bloodstream, which causes systemic inflammation, and also increased uptake of all kinds of literally crap from the bloodstream, including viruses.

[00:33:13] And also, more, the more hydrophilic steroids. So the inflamed tissue, you can, you should probably, there should be a study that looks at inflamed tissue in menopausal women. I will be extremely surprised if they don't find very high levels of estradiol, or at least one of its precursors.

[00:33:28] Mike Fave: Do you, Two things on that one, the first one, the question is, so the hydrophilic nature of those steroids is because of the increased number of double bonds. Correct. That makes them the two hydroxyl groups. The more hydroxyl groups you have, the more hydrophilic. Now there's still lipophilic molecules, but there's a degree of lipophilicity.

[00:33:45] Georgi Dinkov: Pregnenolone being ridiculously high. I posted a study on my blog. Not sure if you guys saw a couple of months ago, showed the affinity of cells uptake for different steroids. Pregnenolone and DHEA got uptaken in amounts. 30 to 100 times higher than what was in the blood. And that study was very good because it showed that the tissue concentrations, the cellular concentrations of estradiol were 10 to 20 times higher than what's in the blood.

[00:34:09] So that alone should already be proof that the blood is not reflective of what's inside of the cell. So maybe we should take the blood, because when they do the blood test for women in menopausal women for arao, they still detect the strato, but they say it's very low. We'll multiply that value, but 10 to 20 and we'll probably get, a good indication of what's in, in the cells.

[00:34:27] And I'll be surprised if that does not exceed the normal range. So yeah. And then, so basically the most highly lipophilic steroids get uptake the most followed by, things like in the middle of the road like testosterone and progesterone. They have a Carbon hill group. And the ones with two hydroxyl groups like estradiol, one hydroxyl groups, but still three double bonds, like estradiol and estradiol, they had the lowest cellular concentration as a ratio compared to the serum.

[00:34:53] So yeah,

[00:34:55] Mike Fave: and then the second piece is to jump into the next topic here. I think it bridges in well, it's talking about reductive stress. So you mentioned, we talked about the differences between like cortisone and cortisol and an estrogen and, or estradiol and estrone. But then inside the cell you have the ratios for NAD and then NADH.

[00:35:16] And basically, I don't know if you want to share the post here, Danny.

[00:35:20] Danny Roddy: Yeah, so okay, so this is Sim Lad, and he is a is he like a keto influencer? But he had a post and he said, NAD is considered a longevity molecule. It decreases with age and low levels of NAD accelerate the hallmarks of aging. But most people go about raising NAD levels in the wrong way.

[00:35:36] Here's a thread of blah, blah, blah. What's Jay, tell me where you want to stop, but what's the reason NAD levels decline with age primarily because degraded and destroyed by oxidative stress? The primary protein responsible for that is CD38 with age, you see an increase in CD38 and corresponding decrease in NAD levels.

[00:35:52] And then there's a salvage pathway that has a bottleneck called NAMPT. NAMPT is the rate limiting enzyme, the NAD salvage pathway, meaning that controls how much NAD gets recycled. Okay, before you, let's pause here, continue Danny.

[00:36:05] Mike Fave: The premise for this and the reason that I wanted to segue here, Is because there's, what we're talking about here is reductive stress and like an overproduction or a larger amount of NADH in ratio to NAD.

[00:36:17] And there's a lot of focus in the low carb and keto spheres. In terms of the salvage pathways, right? The idea we need to salvage NAD, but the idea that makes more sense. And this kind of goes with the aging. It's like, why is NAD decreasing and aging? Why is there increased reductive stress? And I think the biggest piece here is a, over an increased reliance on fatty acid oxidation, instead of reliance on carbohydrate oxidation, because of what happens inside the electron transport chain with the overreduction of coenzyme Q and the FADH and NADH ratio.

[00:36:49] Yep. So I don't know, I don't know if you want to talk a little bit about that. I think that's central instead of this, let's worry about all these ways we can work on the salvage pathway. It's or you can just oxidize carbohydrates better.

[00:37:00] Georgi Dinkov: In fact, if you look at the Randall page the Randall cycle page on Wikipedia, they have a quote there, which hopefully they're not going to delete it anytime soon, which says that one of the ways the fatty acids block the oxidation of glucose is because oxidizing primary fatty acids drops the NAD to the NADH ratio.

[00:37:16] And when that ratio is low, the first rate limited step of carbohydrate utilization, which is pyruvate dehydrogenase, crucially depends on NAD to the NADH ratio. And then also, of course, the, the over oxidation of fats consumes FAD, right? So step electrotransfer chain two will be basically taken over will be clogged.

[00:37:35] And you're going to start having buildup of H, of hydrogen ions. They're going to start leaking through the inner mitochondrial membrane. And then you're going to start combining with oxygen, creating a hydroxy radical. And basically that's how you get the reactive oxygen species. And in fact, if the buildup of electrons is too high, you get reverse electron flow.

[00:37:53] So basically you start getting the entire metabolic chain. All all the way, I think down to glycolysis, not including glycolysis, but everything with electron transport chain and Krebs cycle can actually start flowing in reverse if you have too many electrons.

[00:38:06] Mike Fave: You can ask, I think you can also ATPase or ATPase can also reverse flow and actually reuse ATP to then create ADP.

[00:38:16] And then you also see that the cell tries to create more NAD by converting NADH back into NAD at complex one. And in a lot of the problem at complex one, when you get all jammed up as the electrons from NADH at complex one can't move through appropriately. So then you start creating the RLS there as well.

[00:38:34] And then there's arguments here. It's Oh, this is a good thing. And this is why we have uncoupling. And it's no, the uncoupling is there to help. with the dysfunction at the electron transport chain and try to solve the excess production of ROS. You don't want to stimulate this dysfunction first to drive uncoupling.

[00:38:50] If you want, Jay, the whole thing that you tend to discuss is like having uncoupling after you have adequate ATP, correct?

[00:38:59] Jay Feldman: Yeah, there's a massive difference between stimulating, uncoupling in a high ATP, low reactive oxygen species, oxidative state, as opposed to a reduced state, which, whoa, we can get to it as we go through this, his post here, because Sim talks about the increase in AMP kinase as a way to stimulate NAMPT, but of course AMP kinase generally being a marker of low ATP levels.

[00:39:25] Okay. And so we'll get to that. But even just to zoom out for a moment here. So as we'll get through this post, there's no mention of oxy, redox state at all. There's no conception that NADH and NAD are related here. He's trying to just fully be. Look at biosynthesis pathways for NAD and and it's totally ignoring the actual cellular environment that, that conducts and determines whether we're going to be in a highly reduced or oxidized state and whether we're going to have NAD and the whole reason why NAD plus and a high NAD to NADH ratio is valuable as a marker of longevity and health Is because of this, is because of it being a marker of how well the cells producing energy, how well the mitochondria are functioning, not based on how well you can synthesize NAD from various precursors.

[00:40:13] I don't know, maybe we'll work through it and then Georgie can, provide some more context there on what's being missed.

[00:40:18] Georgi Dinkov: I have his I, it's good that he brought up CD38 because niacinamide is the only molecule of all the, all of the NAD plus precursors that inhibit CD38. CD38 is highly expressed in all types, every single type of cancer.

[00:40:33] It's not a coincidence. It's also highly expressed in many autoimmune conditions. And now I know the things like nicotinamide ribozyte and nicotinamide mononucleotide become very fashionable for raising NAD right? They do not inhibit CD38. And a number of studies, different studies show that as you grow older or sicker, The CD 38 and the PARP one fully it's a, both of them are A NAD consuming enzymes.

[00:40:58] They're responsible for the majority of, basically of the the consumption of NAD plus and degeneration of NADH. So if you can inhibit those two enzymes, and Niacinamide is the only precursor that does both. I think that will be a, a great step towards basically addressing 80 percent of the issue.

[00:41:15] The other 20 percent of the issue is the redox state if the metabolism is not working well. But they go hand in hand. If you're in a reduced state, this usually means there's going to be a tissue breakdown somewhere. And the PARP enzyme is a DNA repairing enzyme. And the CD38, I think, is basically a cellular differentiation enzyme.

[00:41:33] So they, the reason they're activated is because of the low redox state. And that's how it all starts. But then they start affecting each other again, unfortunately, in a positive feedback cycle. And I think niacinamide can break that cycle. I haven't seen his full post, my opinion is that a combination of niacinamide and something that can directly oxidize non enzymatically NADH back into NAD, such as methylene blue, vitamin K, Tetracyclines, things like that.

[00:41:58] That's probably the best way to, to to raise NAD and it can probably get away by using much lower dosages of each one when you combine them than if you use only one of them separately.

[00:42:08] Danny Roddy: Also,

[00:42:08] Mike Fave: Jordi, overall, the perspective here would be to oxidize carbohydrate effectively. Make sure that you have adequate NAD precursor, which is something that he does mention.

[00:42:18] And you're saying in the form of niacinamide instead of the more expensive nicotinamide mononucleotide or nicotinamide riboside. And then if you are having issues in terms of you have the, an over activation of the PARP enzyme or CD38, you can try to increase the oxidation of the NADH back into NAD using quinone molecules, which could be something like vitamin K, The tetracyclines methylene, methylene blue wouldn't be a quinone, but may, or even something like a moden or the anthroquinones or something along those lines.

[00:42:49] That, that would be a better perspective than just prime, than focusing on like, How do I fix this backup pathway, right? If

[00:42:56] Georgi Dinkov: you fix the metabolic pathway, which oxidizes NADH back into NAD naturally, the activity of PARP1 and CD38 declines naturally. They only get activated because you're already in a redox state, and they have stuff to repair.

[00:43:06] Because all of these floating electrons around and the reactive oxygen species they create, that's what's damaging the tissues and the DNA, and that's why upregulated. So all, everything falls back to metabolism and the proper oxidation of glucose and not fatty acids. Because if you do fatty acids and predominantly fatty acids, even if they're fully saturated, you will have low mitochondrial NAD plus to NADH.

[00:43:28] I think another thing we need to mention is that it's the mitochondrial ratio that matters because cancer cells have extremely high NAD plus to the NADH ratio, but in the cytosol. In the mitochondria, their net ratio is very low. So the reason they are very high in the cytosol is because they use the lactate hydrogenous enzyme to rapidly re oxidize NADH back into NAD in the process of creating lactate, right?

[00:43:50] That's, we don't want that. So it's the mitochondrial ratio that matters, and in order for that ratio to stay optimal, we need the oxidative phosphorylation, the oxidative metabolism of glucose. All the way down to APAs and creation of a TPI think we can we can do with mild uncoupling, I think mild uncoupled organisms.

[00:44:07] There are several studies showing that they tend to live longer. We don't need to have a hundred percent efficiency of a TP creation from every glu glucose molecule. About 20% are coupled. Seems to be optimal for longevity. But in highly pathological states, higher uncoupling seems to work better.

[00:44:22] They're now pushing there's a drug that works like dinitrophenol. I forgot its name, but it's been used in clinical research for a long time as an uncoupler. The abbreviation is CCCP. And basically now they're pushing using that drug for obesity, for diabetes, for cardiovascular disease, and it achieves about 40 percent uncoupling of ATP synthesis.

[00:44:42] And that seems to be good for short periods of time to repair the pathology. And after, after that, you go back to basically the about 20 percent on top. And the reason is, I think is good is because the ATP higher like complete efficiency of oxidation of glucose, the ATP levels actually have a negative feedback mechanism with pyruvate dehydrogenase.

[00:45:01] So you don't want too much ATP. About 20 percent loss of that ATP is heat. I think is is optimal for health, for long term health.

[00:45:09] Danny Roddy: What else, Jay?

[00:45:10] Mike Fave: Yeah think there's something interesting to point out here that you touched on in the beginning was this idea that these DNA repairing enzymes or another example would be like heat shock proteins that are all the rage in the hormetic spheres.

[00:45:23] People are inducing these things through these hormetic means like the heat exposure or creating a lot of oxidative stress inside the cell and then saying, look, we have these beneficial enzymes that are upregulating. It's the same thing with fish oil, right? It's we're going to provide you these peroxidized lipids.

[00:45:41] And then you're going to have this activation of NRF2 and all these antioxidant enzymes come in. And it's look, it's beneficial. It's an antioxidant. And it's yes, but in every single one of these states, you had to induce dysfunction first to get the cells to respond. And I think a question that is not usually asked, number one, Jay and I talk about this all the time in the podcast is like, This stuff is cumulative, just like when you're talking about estrogen or the radiation piece.

[00:46:04] But then the other thing is, at what point does the body's response to these things fail? At what point do you start to envision a general adaptation syndrome response curve to the hormetic stressors and say, okay, like we have this alarm stage and we're responding to these, this dysfunction, and then we have this resistance stage and now we're in fatigue.

[00:46:22] And when you start to look at like the different damaging processes, for example, When you look at things like diabetes, or you look at cancer, you look at some of these processes, you start to see, oh, wow, there's a lot of uncoupling going on inside diabetes or, and in these different disease states, or all these activations of PGC1 alpha inside diabetes, and it creates dysfunctional mitochondria, and a large, or like really large mitochondria that can't produce energy effectively.

[00:46:45] And so the question is like, where's that cutoff, right? Where do you determine that you've stimulated enough damage and tried to trigger this hormetic response? And why are you even going about that in the first place is like the initial question, when you could just, again, oxidize glucose effectively, instead of driving fatty acid oxidation in the RLS.

[00:47:02] I think zooming out and having that context is extremely important because you get into these niche biochemical pathways. And if you're only looking linearly in this pathway and you have no larger context, you're, you miss the whole, you miss the forest for the trees, essentially.

[00:47:17] Georgi Dinkov: I have a great example Dr.

[00:47:19] Mercola and I discussed ubiquinol and ubiquinol. And he got like some pushback from some other doctors saying in young people, the blood is predominantly ubiquinol. That's the one we need to be supplementing with. And then I found a study that if you maintain a ubiquinol to ubiquinol ratio below 0.

[00:47:35] 5, In other words, in favor of ubiquitin, or the reduced version, all that it takes is for this ratio to stay below 0. 5 for 24 hours, and then the cell starts physically disintegrating electron transport chain complexes 1 and 2. Just being in a reduced state. mitochondrial reduced state for 24 hours is all that it takes for physical structural damage to occur to the cellular mitochondrial apparatus.

[00:47:59] Now, the good news is reversing that ratio in favor of ubiquinone quickly restored, and the cell was able to resynthesize that complex, these two complexes back. The question is this always reversible, right? What if you stayed, uh, highly reduced state for a continuous period of time because cells have memory, as Ray mentioned many different times, and if this accumulates and the cells also have a quorum, right?

[00:48:21] So at some point, if it's sufficient amount, a number of cells, I don't know if there's like a threshold, there's probably cumulative, just like for radiation, there's going to be a point where basically that organ says, The heck with it, I'm going to start growing because, providing with the optimal environment.

[00:48:35] I have to do something with these electrons. I started, I, my initial emergency pathway was synthesizing fat, right? But you don't learn, you keep giving me more electrons, and now all I can do is grow another organ, but that differentiated, in other words, cancer.

[00:48:49] Danny Roddy: That would be a reason not to eat the desiccated liver because it's like the biggest source of ubiquinone, right?

[00:48:54] And then it shifts into the ubiquinol form. Yeah. Crazy. Okay, Jay, what,

[00:48:58] Georgi Dinkov: no, it's okay to take the ubiquinol. It's the not take to take the ubiquinol, which they're promoting now everywhere, is the preferred version of the body because, again, relied on blood tests. And said, Oh, in young people, it's mostly ubiquinol.

[00:49:11] So that must be good. Okay. Again, association, not causality. And now if you go to the store, actually, most of the products are ubiquinol and they're much more expensive than the ubiquinol there. In fact, they even have like statements on the ubiquinol bottle saying this is the more, the body preferred, more absorbable version.

[00:49:28] So you should be buying this 40 bucks for a bottle of ubiquinol and 15 for the same milligram base, basically per, but how much total amount of ubiquinone you're getting. So ubiquinone is pushed to the side, even though when you look into the tissues, that's the one you need.

[00:49:42] Yeah. Because if it's ubiquinol, then the ETC2 doesn't work. Did I must've misspoke. You want

[00:49:47] Danny Roddy: the oxidized version, not

[00:49:48] Georgi Dinkov: the reduced and drying. Exactly. So another marker of redox status is ubiquinol to ubiquinol ratio. And that study showed that. It's shift in favor of reduction is all that it takes for 24 hours, maintain the state, and you start getting structural changes just because of functional interference.

[00:50:04] Got it. Jay, what

[00:50:05] Danny Roddy: else about this SimLad post?

[00:50:08] Jay Feldman: Maybe we could just go through. Yeah this we'll just read through this slide. Got it.

[00:50:13] Danny Roddy: Here's the hierarchy of raising NAD levels and maintaining them during aging. Minimize NAD loss by inhibiting inflammation and CD 38. Maintain circadian rhythm alignment.

[00:50:21] To keep N-A-M-P-T online activate A MPK. That stimulates A NMA, , N-A-M-P-T with exercise dietary precursors to NAD.

[00:50:32] Georgi Dinkov: Have a. Go ahead. I have a great story to share about AMPK. Another thing that's considered great turns out to be terrible.

[00:50:40] Jay Feldman: Yeah, totally. And this is what happens when you land on something you land on something that's correct, which is NAD plus is a marker of health and you want to hire NAD plus to NADH ratio, but completely miss the entire context of what that means in the cellular environment.

[00:50:55] I wouldn't be surprised if number five here was produce as much lactate as possible, like just stimulate lactate dehydrogenase as much as possible. So that's the best way to get your NAD. You're just completely missing what's going on in the cellular environment. And the ironic part, as you were saying, Mike, is if you do things that increase MPK, exercise like excessive exercise or any form of starvation, carb diet, fasting, things like that. The first thing you do is deplete NAD. That's the first thing that happens and that is why so A, that causes low ATP production which will trigger AMP kinase. Then the other thing that'll happen is because of the low NAD, you want to trigger N-A-M-P-T.

[00:51:34] That's the whole point. You're just creating, we talk about this with autophagy, right? Autophagy is a cleanup process, so we need to make a mess and destroy everything just to increase auto to save it. Yeah, totally. Like you're completely missing the point here. And that was, I think, the most important thing.

[00:51:49] And yeah, missing the larger context of the way, the actual way to increase the NAD to N 80 H ratio and increase N 80 plus. It's to fix your mitochondrial function to make sure you're oxidizing glucose efficiently and not favoring fat oxidation and not overstressing, not increasing AMP kinase. Yeah, let's hear that story, Georgie, about AMP kinase.

[00:52:07] Georgi Dinkov: Oh, so that was related to a post with Dr. Mercola because he was giving a speech on aspirin and I said in my study that aspirin basically mimics the effects of fasting without fasting. And reduced a lot of inflammatory biomarkers, it raised NAD to the NEH, et cetera. And then I found a study, he said what about a AMP, AMPK?

[00:52:27] So then I found just one, and even the Wikipedia page is actually a pretty good source. It says, there's a section there that says potential pathological effects. AMPK is upregulated in every type of cancer. In fact, it's what protects the cancer cells from basically committing apoptosis. If you bombard the cell with, with the reactive oxygen species, which is what happens when you do chemotherapy and radiation.

[00:52:48] The cell uses things like NAC, N acetylcysteine and basically the upgraded AMPK in order to basically protect, prevent itself from committing apoptosis. So now they have drugs on the market that have already been developed and they're clinical trials, stage 2 clinical trials with AMPK inhibitors to actually treat cancer, very advanced forms of cancer.

[00:53:11] Jay Feldman: And I just saw as well, NAMPT inhibitors for cancer is what they're looking at.

[00:53:15] Mike Fave: They're also trying to target NRF2 for cancer as well. It is called NRF2,

[00:53:20] Georgi Dinkov: it's the other antioxidant, master antioxidant that the cancer cell uses to protect itself from basically, because if the cancer, if the cell is dysfunctional, it has a mechanism and that depends on pH.

[00:53:30] So all that it takes for a dysfunctional cell to commit apoptosis, which is the good way to go, right? Instead of killing you or growing and dividing, is for pH to drop into the acidic range. And that happens when you have high production of carbon dioxide, right? It's a lewis acid. When you don't have that, basically, and because the cell exports lactate very vigorously throws it into the bloodstream.

[00:53:50] I think one of the risks is because if too much lactate stays into the cell, you will also commit apoptosis. But the cell expels the lactate and in the process becomes alkaline. So basically if you want to, for cancer to commit apoptosis, you just have to drop the pH or get rid of its antioxidants.

[00:54:06] So things that deplete NAC NAC cysteine dietary cysteine depletion has been tried for cancer treatment. Unfortunately, you have a lot of cysteine in your muscle cells and if you're in an advanced state of cancer, you're going to have a lot of breakdown of tissue, so that's not very, reasonable.

[00:54:21] But things that inhibit Nrf2 are also now being tried for cancer as well. So the cancer industry knows that a reduced state is not good for the health of the organism. They're just refusing to admit that a reduced state can cause a de novo. They're saying, okay, once you are in a cancer state, Yes, we want oxidation.

[00:54:37] We want oxygen there. They even they've tried hyperbaric oxygen therapy to push moisture into the cell, but it's not being used. But they do understand that it's the fact that it's not, there's no consumption of oxygen and there's no oxidative phosphorylation that, that it is a problem.

[00:54:50] They just refuse to take the first step, which is. To get to the cancerous state, all you need to do is do these things for X number of, I don't know, days, months, et cetera. It's probably unique for each person. And, AMPK, which if you do it chronically, I think there are several epidemiological studies now showing that basically chronic fasting does increase your risk of cancer, and I have an anecdotal example.

[00:55:13] Steve Jobs was a notorious faster and a fruitarian. And basically, even though the doctors never said that his pancreatic cancer was caused by this regimen, Aston Kutcher, when he did the Steve Jobs biopic, went on the exact same diet, ended up in the hospital not once, but twice with acute pancreatitis, which is a precursor condition to pancreatic cancer.

[00:55:33] And basically, the doctors told him, I don't know what you're eating, but you better stop right now because you're gonna end up like Steve Jobs. This chronic upregulation of AMPK is not good. Even if you look at from evolutionary perspective, we're not supposed to be fasting all the time.

[00:55:46] So I think that's why some of the smarter members of the fasting community started advocating things like the warrior diet, which is okay. We're going to fast a little, I don't know, 18 hours, but for the next six hours, we gorge, right? All of these, they have little support in archeology or in history.

[00:56:03] I think that we're going to do a full back circle back and eventually going to come back to, you have to eat and you have to oxidize primarily glucose, right? And at rest you oxidize fats, which means maintain good muscle mass because that's what, that's the, that, that's the tissue that prefers to oxidize fat at rest.

[00:56:19] When you in act, when you act, if you better be oxidizing glucose or she'll will break loose. And the same thing happens when you fast chronically.

[00:56:26] Mike Fave: I think something interesting here to this picture too, and this is something that's, I don't think it's talked about so often, inside these alternative spheres, there's this idea that cancer is also actually running on glucose.

[00:56:38] But there's some interesting papers out there that's discussing that the mitochondria inside of a variety of cancer cells is actually running on fatty acid oxidation and using like a futile fatty acid shuttle. So they're super over reduced. And then they're using lactate as a way to recycle NAD for a variety of different processes.

[00:56:58] And then there's also the idea of the Warburg effect where the cell's mitochondria is damaged and then the cancer cell's mitochondria is damaged and it's relying on lactate or lactic acid fermentation process. But what they're also starting to show too is that some cancer cells, particularly the ones that are running on things like the fatty acid oxidation, are actually exporting the ROS to other cells.

[00:57:21] And then those other cells are producing lactate. So it's like this whole environment where the cells are, some of them are damaged and they're running on they're running on lactic acid fermentation and a large portion of them are actually oxidizing fatty acids. So you're seeing the same picture play out, where you have this over reduced state going on.

[00:57:37] inside the cancer cells. And then the, this reliance on these backup pathways to generate NAD through lactate. And I think that ties in directly and this, I think this is also explaining why you're seeing upregulation of things like NRF2 inside cancer cells and why it's known that things like AMPK are driving fatty acid oxidation in states of starvation.

[00:57:56] So you're watching these people run these four medic approaches and they're literally driving the stress and this dysfunction. And you can say, Hey, Diabetes is characterized by fatty acid oxidation. Hey, cancer is looking like it's characterized to a large extent by fatty acid oxidation or issues inside the electron transport chain or elevations in AMPK and all this type of stuff.

[00:58:18] I'm like, Oh no, these things have to be good. These things have to be good. And it's you're literally pushing towards these problematic things, even if you're up regulating these protective pathways in the short term. And that picture is completely missed.

[00:58:29] Georgi Dinkov: There is actually, they even came out with a specific molecule that mimics glucose, but it's non metabolized.

[00:58:33] It's called 2 deoxyglucose. To do a sort of, so called bait and switch therapy for cancer. Because they said, Oh, cancer cells rely on glucose fuels cancer. So if we give it a fake glucose, cancer will go away. Not only did not, but basically became ridiculously more aggressive. So you should not be depriving the cancer cell of glucose because it needs it.

[00:58:52] And if you don't give it, or if you restrict it or give it the fake glucose. That is going to increase the tissue breakdown to provide even more glucose. And I think the whole thing about the hormetic stuff, if you look at its history, it actually came out of the Catholic church. So it was the idea of that periodically you need to torture yourself, otherwise you're not a good Christian and basically, we all heard the story of no pain, no gain, but this has been taken to the extreme in medicine where basically they believe that no pain, no gain, but if more pain It means more gain.

[00:59:21] So maybe there is some truth to the first one, but not chronically. I think chronic suffering is universally bad, but there's definitely no truth to more pain equals more gain. Unfortunately, that's how the entire oncology industry is based on that. The most the most advanced treatments is a euphemism for the most aggressive ones and usually the ones with the highest mortality rate.

[00:59:41] But people, hear that and say, Oh, I'm going to get the most advanced treatment and they assume this is the best, medicine can offer. And maybe it is, but it's really nothing, it's not going to do you any good. Yeah. So speaking of the fatty acid oxidation. It's already recognized as a factor in diabetes.

[00:59:56] So if fatty acid oxidation, I know the public relations facing portion of the medical industry still claims it's glucose. But if you talk to an endocrinologist, they know that it's a, type 2 diabetes is invariably caused by lipids because you cannot find a type 2 diabetic person who is not obese.

[01:00:12] It's just not possible. Type 1 maybe, but not type 2. And even for type 1, it was found out that It's basically it usually happens in your early childhood years, like up to the age of 12 after a very, we've experienced something extremely stressful and which, again, when you're very stressful, you're going to have very high lipolysis and number of studies demonstrated that the polyunsaturated fats and the prostaglandins are lethal to the beta cells of the pancreas.

[01:00:37] So you can give yourself diabetes with extreme exertion. And also extreme fasting back in, I think it was 2015, there was a study that I posted on bears, show that bears, basically they gorge themselves on food and they become, really bulky, right? And they carry a lot of fat because they have a feeding season and they're going to hibernation.

[01:00:59] But remarkably, while they're gorging themselves on all of this yummy stuff that they're eating, they're actually very healthy and insulin sensitive. When they're going to hibernation, which is a period of very extended fasting, they burn predominantly the fat that they've stored, and they become fully diabetic.

[01:01:14] And they remain diabetic until they emerge from hibernation and start, guess, guess guess what's the first thing that they try to eat? Honey, because it's got sugar and the sugar will lower the free fatty acids, and then they reverse back to normal state. So there's I would say controvertible evidence from animal studies that diabetes is a fat driven disease.

[01:01:32] And if diabetes is a precursor state to many cancers, which not even mainstream medicine admits, I just don't see how the cancer can suddenly switch and do 180 and say, Oh yeah, you got me to this point by loving fat, but now I'm going to switch over to glucose. Plenty of evidence that glucose is not pathological in cancer.

[01:01:48] The 2 deoxyglucose molecule that they specifically came up with failed every single clinical trial. And quite a few for many different types of cancer, but that's stuff you don't hear on the popular press because it's not politically correct. You have to demonize the sugar.

[01:02:03] Mike Fave: No matter what, even if you completely eliminated sugar, as you mentioned, it would just break down amino acids. Exactly. And the cancer cells will use the amino acids regardless. And the other thing that I think to keep in mind, it's just something interesting when you start looking in the cancer papers is that, The cancer cells can actually make as much ATP as a normal cell from glucose.

[01:02:21] Exactly. But they have to use way more glucose because they're just wasting it through glycolysis. Precisely, yeah. But you only generate two, what is it, two ATP atoms per molecule? And so they have to probably get a lot but they generate a lot of lactate in the process because that process of glycolysis consumes the NAD into NADH, in order for the cell to stay alive, I need to go back to NAD and if I'm not using oxygen, then I need an emergency oxidant, and that's basically pyruvate.

[01:02:48] Georgi Dinkov: So there have been proposals, by the way, of using quinones as a treatment for cancer. And there's some very promising study in animals, specific with vitamin K. In fact, there's some studies showing complete regression of the cancer. But the only study that I know so far with vitamin K in humans is for liver cancer.

[01:03:05] And it's about to get approved by the FDA. Completed all three stages of the clinical trials. So now we're going to have, unfortunately, MK4, metatetranone declared as a drug very soon for both prevention and treatment as a monotherapy for liver cancer. And if it works for that cancer, if we believe in the systemic nature of cancer in the metabolic nature of cancer, there is no reason why it shouldn't work for all the others because the mechanism of action really is predominantly that.

[01:03:30] It has some other effects such as converts estradiol back into estrone, so makes it a weaker estrogen. It's also a mild aromatase inhibitor. My group in Bulgaria, the lab, we did some studies with yeast and also some some enzyme binding studies. So it's a mild aromatase inhibitor, but I think the it's quinoa nature, it's redox modulating nature is what is most responsible for the for the therapeutic effect on cancer, incidentally also known to be therapeutic in diabetes.

[01:03:55] The strongest inverse correlation between a nutrient and a disease known so far that has been discovered is between vitamin K and diabetes. And now that we know that it's vitamin K and cancer is also, so they're largely the same condition. And if one is driven by fat, so is the other. And the evidence is there.

[01:04:11] It's just not synthesized and not popular to talk about that metabolism alone can cause cancer. They're still very much into the whole genetic theory. Did you see the argument? Not only, but there's a thread on Reddit, couple, maybe 2018 or 2019 there was a paper of a very famous oncologist, I think from Anderson Cancer Center in Texas, who basically said, for a hundred years, we've been, saying that first we have the cancerous mutations and then the metabolic derangements happen.

[01:04:38] Based on our studies and everything we've reviewed so far, apparently we've been wrong. It's the exact opposite. Something that we has been saying as well. So functional, functional dysfunction precedes structural damage which we already have evidence from the ubiquitin and ubiquitin study as well.

[01:04:53] So the evidence is there. It's just these obscure individual studies. And unfortunately when you combine them and try to present a unified argument, because they're so disjointed and these groups don't cite each other's work. Most people, most doctors are not willing to accept that argument.

[01:05:08] They're saying. If it was that obvious, we would've found it by now.

[01:05:12] Danny Roddy: So speaking of Tor torpor and lipolysis and cancer and estrogen and all the redox balance Jay, do you wanna set this video up of Dr. Berg talking about serotonin?

[01:05:22] Jay Feldman: I think you set it up perfectly. Let's let's hear about serotonin as the happy hormone and got it.

[01:05:27] Dr Berg: You

[01:05:27] Jay Feldman: goodness, you tell me when you want to stop and all the things that we can do to increase it. Got it.

[01:05:31] Dr Berg: Serotonin, the happy hormone. What is serotonin and what does it do? It's a hormone. A hormone is a communication that travels through the body. And serotonin is made by your brain, it's made by your gut, and it contributes to feelings of happiness.

[01:05:41] It helps raise your mood, it helps make you calm, it decreases cravings for carbs, it helps you focus, and it reduces anxiety. Now, if you're deficient in serotonin, your mood might be suppressed, okay? You may have depression, you may have anxiety, you may be irritable, you may even have a worsened self esteem, sleeping problems, and even memory loss.

[01:05:58] So what can you do?

[01:05:59] Danny Roddy: Okay. First the symptoms, what What do you guys think?

[01:06:02] Georgi Dinkov: Every single anti serotonin drug, there's at least 40 of them. I've looked at them, all the serotonin antagonists. Some of them very specific. Every single one of them has demonstrated effectiveness as an anti depressant in animal models.

[01:06:18] Some of them in humans as well. The drug myansirine, which is now approved for treatment of clinical treatment resistant depression. It's actually very structurally similar to cyproheptadine and is a pure serotonin antagonist. It has no agonism effect on any of the serotonin receptors. It's, I think it even has some partial dopamine agonism as well.

[01:06:39] The studies with tryptophan depletion acute tryptophan depletion, they do that by either feeding people protein that's deficient in tryptophan. Or they give them something that I mentioned many years ago on the forum and the show, you can do a combination of branching amino acids and phenyl alanine or tyrosine because they will out compete tryptophan for entry into the brain.

[01:06:58] So you're going to have a low tryptophan state in the brain, which translates for low serotonin. So they thought that acute tryptophan depletion will cause depression, but every single study done so far with humans as well has not found that. The only thing they found is that people become very tolerant to bullshit.

[01:07:15] I think several of the studies actually had situations where some of these patients lashed out at doctors and beat them up. Because the doctors treated them poorly. So if you're in a high serotonin state, you're going to be very survival, very docile, and you're going to respect hierarchy. I did a post study on that, that the way they train courses, the way they break courses is actually by raising the serotonin levels through torture or like whatever it is that they do, they got to show, put the horse in a learn, help us the state.

[01:07:41] And only after that, it follows commands and learns. If it's a wild horse in a state of low serotonin, it does not tolerate that. It'll kick the crap out of you. So basically as far as serotonin there's also states of high serotonin that have been observed. Naturally in people with carcinoid tumor, these people are anything but happy.

[01:07:58] In fact, they suffer from psychosis, extreme aggression, homicidal sometimes memory loss. Everything that he mentioned that serotonin prevents, he's actually seen as a symptom in people with extremely high serotonin levels, such as those that basically have a carcinoid tumor. People with serotonin syndrome also basically a state of usually briefly elevated serotonin.

[01:08:19] First of all, it's lethal, 40 percent lethality if untreated. Okay. Even with treatment, it has about 10 percent lethality. So not exactly a happy hormone, it can kill you 40 percent of the time if you raise your kind up, right? But even in physiological amounts, serotonin is now known to drive fatty liver disease.

[01:08:35] So things like 5 HT3 antagonists, like ondansetron, which was developed for nausea, now has a number of clinical trials in humans for treating fatty liver disease, including also nono NASH, nonalcoholic steatohepatitis, and even cirrhosis. And that's not surprising because serotonin is a, the known, probably the major driver of fibrosis in any tissue or organ.

[01:08:57] And one of the best, indications that the doctors are lying to us is that the company Pfizer bought the rights, the commercial rights to a serotonin antagonist called turgoride, which is an ergot derivative, a basically very potent antagonist specifically on 5 HT2B, which is the fibrosis receptor.

[01:09:14] And while Pfizer sells you SSRI antidepressants, behind the scenes, they're running clinical trials with an anti serotonin drug to reverse all of these things that elevated serotonin they actually admit that it causes. And, I just don't understand how this can be out there and published.

[01:09:28] And these people can go with a straight face on TV and say, Oh, serotonin is the happy formula. Yeah, you'll fibrosis, I don't know, you'll cause fibrosis in every organ that we know of. And it will destroy your brain, but we have a pill for that. At the very least admit as a start that it's not, that it's it's not good for us.

[01:09:43] And also studies that have been done on serial killers and people who committed suicide demonstrated extremely high levels of serotonin in their cerebrospinal fluid and also very high levels of serotonin metabolite, 5 hydroxyindoleacetic acid. So we know that people, with very bad mental states have very high levels of serotonin in the brain.

[01:10:03] And even when it's peripherally elevated now there are multiple endocrine groups around the world that say that peripheral serotonin is bad, they still maintain that central is good. But the peripheral serotonin BAD is actually gaining momentum. In fact, there are multiple clinical trials with tryptophan hydroxylase inhibitors specifically developed to not cross the blood brain barrier.

[01:10:21] So the only inhibit peripheral sense of serotonin is a prevention and treatment of obesity, diabetes, cardiovascular disease, osteoporosis, infertility, all of these things. So the the way medicine has been getting away with this by saying serotonin doesn't cross the blood brain barrier.

[01:10:37] Complete and utter crap. The same lie is the one they were told about GABA. Oral GABA doesn't work because it doesn't cross the blood brain barrier. It does. Both of them do. And that's why people with carcinoid syndrome, which is usually, it's not in the brain, somewhere in the gastrointestinal tract, that's why they have these psychotic states, is because the high serotonin, extremely high serotonin they produce peripherally, it does get into the brain and causes these these mood changes there.

[01:11:00] And how does it cause these mood changes there? The recent debunking of the SSRIs, I don't know if you saw it, was a lady out of Cambridge or Oxford. He made the news and then of course they, started to try to shoot her down saying that she's a fraud or whatnot. But she's a very famous psychiatrist out of the UK and basically said the serotonin hypothesis of depression is dead.

[01:11:18] There's no evidence for it. In that study, she says, how can serotonin be a happy hormone if it's one of the most potent negative metabolic regulators in the brain? It drops oxidative phosphorylation in the brain like nothing else, almost nothing else that we know. So it cannot possibly be good for the mood.

[01:11:34] We know that drop of ATP in the brain causes actually aggression of at least souring up of the mood, but if it drops below 40 percent below baseline, you're getting into basically people lashing out and doing crazy things, almost like a temporary insanity. So if serotonin does that, how can we tell people, how can we argue that serotonin actually is an upper?

[01:11:54] And there was another study published in 2019, I think it's called serotonin, an upper or downer. I think Danny has seen it. Made the exact same argument. And in fact, that study said every patient with clinical depression that we tested. We tested whole blood serotonin, not serum serotonin.

[01:12:08] Every single of these people had either upper limit of the normal range or above. So we cannot argue that serotonin is low in depression, and that's why they use the brain barrier, the blood brain barrier argument saying maybe it's high in the blood peripherally, it's not in the brain.

[01:12:22] It does affect the brain. The patient with carcinoid syndrome proved this conclusively. So it's hard to say it's, I don't know what, I don't know what serotonin does that's good for us. I think it's role really is this in times of trouble. It turns off your higher cognitive function. It numbs basically your response to negative stimuli.

[01:12:39] It also numbs the response to positive stimuli as well. And it makes you go by on, much fewer calories than before. So it's the misery hormone. It's the suffering hormone. It just makes you get by and get through. On, much lower, much smaller amount of calories and without really paying attention much what's going on around you.

[01:12:56] That doesn't sound like a model for a good, maybe it is these days. Maybe that's what they want, but it doesn't sound like a healthy person, right? It's basically a zombie and coincidentally or not, most people describe the most common side effects of going on an SSRI is basically numbing of the senses, numbing of things down there.

[01:13:15] So basically these people cannot experience orgasms and above all emotional numbing to everything that's going on around them. So the term serotonin zombie is actually a term that is widely used in the SSI support forums. They're saying, Hey, once you get to that stage, that the drug is working.

[01:13:30] So you're no longer at risk of suicide. But it's a very widely acknowledged thing that it turns you into a, emotional and mental cognitive zombie, and those are things that are not disputed by psychiatry. They just say that you are feeling sad. So we basically lobotomized you and now you no longer feel sad.

[01:13:45] Oh, great. Yeah, but I can feel happy either. So they just like the hormetic thing, they destroy you in order to prevent you from feeling bad.

[01:13:52] Mike Fave: The other thing too that I find difficult with the serotonin hypothesis is like the research is really clear on the peripheral serotonin issue, right?

[01:14:01] And it being associated with all these types of diseases, even in cancers, they're showing as a negative effect on immune function. And I was actually looking at the studies before we talked, before this call about the tryptophan hydroxylase 1 inhibitors, treating all of these different diseases that are producing the drugs now.

[01:14:17] But the problem is if you're going to make this argument that serotonin is good. And then you look at. They're saying now that first it was 90, I think they're saying more than 95 percent of serotonin is produced in the gut. It's so it's okay in the brain, but it's not, but if it's peripheral, it's everywhere else outside of the central nervous system.

[01:14:35] We just need to, we just need to increase serotonin inside the central nervous system only. It's like, How are you going to do that by these other mechanisms? You can't do that by taking tryptophan. Yeah, that'll increase serotonin everywhere as well. And most of the anti serotonin drug or most of the SSRI drugs address serotonin across the whole body.

[01:14:54] They're not just a brain effect as well. So it's even if you were to make an argument and say, Oh, we're going to get it in the brain. It's yes, but you will also get it peripherally. And if you look at the side effects of a large portion of these drugs, depending on which receptors they interact on, some people are gaining massive amount of weights.

[01:15:09] Taking these SSRIs, and then you're also seeing, the increased risk of suicide, and you're seeing a variety of these other symptoms that come with the different receptor profiles. Some of them also affect dopamine and other neurotransmitters as well, which is problematic, but overall, you're looking at that, and it's like, there's no way that, that you can't have the, these two things can't exist, right?

[01:15:28] You can't have peripheral serotonin's problematic, central's fine, but all the serotonin's produced in the gut, and these drugs address serotonin across the whole body. There's no way that argument can exist. There's no way that you can have that. That's there and situate and say Oh, these drugs are a good thing to use long term.

[01:15:43] Georgi Dinkov: And we have evidence from humans that central depletion of serotonin does not cause depression, right? They could acute tryptophan depletion studies and high peripheral serotonin equals high central as well because the carcinoid tumor people, and then there's, they're anything but happy, right?

[01:16:01] Depression is a very common symptom. They usually explain that way as well, of course, they've been diagnosed with cancer, so it's normal to be depressed, so it's not the serotonin causing it. Yeah, but all of these other things that are known, actually, the psychosis, the changes in consciousness, the impaired cognitive function, fatigue, and all these things, they're classic signs of serotonin excess, and they exist as well in people with proven elevation of central serotonin.

[01:16:26] In fact, There's something called the central fatigue hypothesis. I don't know if you've seen it. So they looked at athletes and basically they said, okay, so these competitive athletes, the one that are highly trained, when they get to the end of the, whatever the running, rowing or whatnot and they start feeling fatigued.

[01:16:41] And then at some point they break and it's okay, I'm done. But then they looked at the levels of ATP and the ATP to the ADP ratio. They looked at lactate and all these other biomarkers, and they said physiologically, these people should not be tired. Something else is driving their fatigue. And they said, it's the, they came up with a central fatigue hypothesis.

[01:16:59] It's legit. It's out there. You can read about it. So they're saying that the reason these people get tired is because their levels, brain levels of serotonin rise. And in fact, that group and a bunch of others are saying if we inhibit serotonin, if we block the receptor level or inhibit tryptophan uptake into the brain.

[01:17:15] We actually can extend, we can have an ergogenic effect that almost like a doping drug. That does sound like a good thing, right? But it's the exact opposite of what they're claiming that serotonin will do. So this group is trying to lower serotonin to increase your athletic and cognitive performance.

[01:17:30] Whilst the medical industry still claims that serotonin is a happy hormone. I don't know how you get this information. I think the fact that we're combining so many different pieces of information from such a diverse group of researchers is what makes the medical industry highly suspicious.

[01:17:46] First of all, it probably scares them. But also suspicious because they're saying you can't, it sounds too disjointed in order to be right as a coherent theory, but every piece of evidence that we have so far demonstrated serotonin is pathological. It was widely accepted in the 40s and 50s.

[01:18:02] And that's at a time when I think it was a canceller that called it theramin, but I think it was it was accepted name around the time of the general of serotonin was called theramin and everybody knew that if you had high serotonin, you're going to have a gastrointestinal issues. I think the therapy with charcoal, which helps reduce a serotonin and of course, endotoxin as well eating soluble fiber, all of these things grew out of research.

[01:18:24] Basically with serotonin. At the time they didn't know what the exact name of it was. For a while they confused it with histamine if you look at some of the earlier studies. But they knew very well that it's something produced in the gastrointestinal tract. Mostly there. And it's elevation is not good.

[01:18:40] And it causes, really bad gastrointestinal symptoms. Including the fibrosis and the cancer as well. In fact, people with carcinoid tumor, they don't die from the tumor, they die from the massive disseminated fibrosis that this these highly elevated levels of peripheral serotonin do. And if you give these people cyprohepatidib, or another nonspecific serotonin antagonist, they continue to live, even though the tumor may not necessarily disappear.

[01:19:03] It's just as long as you break the, as long as you block sufficiently the effects of this highly produced serotonin, then these people can live a normal life. Incidentally, when you're given the cyproheptadine, the psychosis, the bad mood, and all these other things also disappear. So we have multiple indisputable, from different pathways, evidence that serotonin is not good.

[01:19:22] You want it low or the way it is blocked by something so that, doesn't put you into a low metabolic state. Because that's really its underlying basic mechanism is that it's a negative metabolic regulator. And, being on a mean, it's also a reductive and also it just inhibits the, I think that it has an inhibitory effect on some of the two of the enzymes in the Krebs cycle.

[01:19:43] And I saw a study showing that if you administer animals with exogenous serotonin the activity of cytochrome C oxidase declines, but they didn't explain the mechanism. So it is definitely a negative metabolic regulator, and in a, being that, being such an agent cannot be possibly positive or beneficial in the metabolic, from the metabolic theory point of view.

[01:20:05] Mike Fave: Yeah, another thing I think that goes to the central element coming from the gut with serotonin is when you look at people who have IBD, so ulcerative colitis and Crohn's, they're characterized by really high serotonin levels. And then also their gut microbiota is producing large amounts of serotonin in general.

[01:20:21] And there's a lot of research talking about mental disorders and psychiatric dysfunction in patients who have irritable bowel diseases or inflammatory bowel diseases. And you could make a case that it's the inflammatory mediators, but I think anybody who's ever had a really irritated gut, they've eaten something that's irritated, you will tend to see the mood change as well.

[01:20:42] And I think it's likely driven by the serotonergic response.

[01:20:47] Georgi Dinkov: Doctors now admit that, actually, this point is a very well established fact, that people with clinical depression always, almost always have IBS and the other way around. So they know that the two feed off of each other. If one of them is in a state of high serotonin and it's undisputed, In fact, IBS, you can have both the diarrhea, for a while they thought that only the IBS type D, which is a diarrhea one, only that one is associated with serotonin because they, they think serotonin causes diarrhea, but it's, it has a bio, it's a dual effect.

[01:21:16] It increases motility in the small intestine, but inhibits it in the large. They found out that administering anti serotonin drugs helped the IBS both the D and the C type. So you, both of these are driven by serotonin. And if people with IBS and IBD almost always have depression and the other way around, if that condition is high serotonin, the other one cannot be low.

[01:21:35] It's just not possible. And the whole argument the last defense that I've been hearing from doctors that serotonin can go across the blood brain barrier, multiple studies out there showing that it can and in fact, you can administer serotonin as a sodium salt or a potassium salt, and you get central effects.

[01:21:50] Danny Roddy: Okay, so here is a video of Judy Cho on the carnivore diet and stress, and then we'll have Georgie Jay and Mike disseminate this information and talk about it. So here we go.

[01:22:01] Judy Cho: Over time, as my carnivore patients or clients aren't moving the needle enough with their thyroid markers, it's usually not the diet.

[01:22:09] I. I know that so many people want to think it's just the carbohydrates or not, but if it was that simple, people on a paleo diet would be killing because they don't eat the bad carbs in a sense. I think a lot of times it could be environment, it could be stressors, it could be lots of other things that maybe I need to tweak things a little bit more or dig a little bit deeper.

[01:22:29] But it's usually not the diet or a need for carbs or no carbs or fruit or honey or reducing SHBG or something else. You could have low testosterone as a male because your DHEA is getting wonky.

[01:22:44] Danny Roddy: Okay, Georgie, I want you to talk about that video and especially the last part. You could have low testosterone because your DHEA is wonky.

[01:22:52] So what is

[01:22:53] Georgi Dinkov: that last argument, what is wonky? I

[01:22:56] Danny Roddy: don't know, you're just gonna have to interpret it like interpretive dance type of thing, you're just gonna have to figure it out.

[01:23:01] Georgi Dinkov: So DHA is not a reliable precursor to testosterone in males, it DHT if you use it in low enough amounts. If you abuse it, it very likely raises estro specifically.

[01:23:12] and ultimately estradiol as well. And multiple studies with males have demonstrated that taking more than the physiological dose, which I think a daily production is about at most 15 milligrams, one five reliably raises all of your estrogen and biomarkers. But it does not raise the serum testosterone in males, which means that the DHEA is not a reliable precursor to testosterone because most of the most of the testosterone is produced into the gonads.

[01:23:38] So if DHEA does not raise serum testosterone it means the gonads are not using it to produce testosterone. So if you take DHEA and the testosterone in males does not go up, it is a very reliable precursor to testosterone in females, interestingly. So taking oral DHEA or topical DHEA for females does raise serum testosterone.

[01:23:56] And it's less estrogenic seems to be than it is in males. In males, if you use DHEA, it should be, if it's used orally, no more than five milligrams per dose and no more than 50 milligrams total daily. I prefer the transdermal route because the skin has one of the lower expressions of the aromatase enzyme compared to other organs.

[01:24:15] But it does contain the full machinery for converting DHA downstream, and it does have high expression of 5 alpha reductase. So you're going to get more of the potent androgen dihydrotestosterone, but also some testosterone as well. It's just not going to get reflected into into serum levels.

[01:24:31] However, a study looked at the downstream metabolites of DHEA and found that topical DHEA in males raised the levels of urinary excretion of metabolites of dihydrotestosterone, such as 3 alpha androstenediol. 3 beta understained diol, androsterone, and androsterone sulfate. And the study title was tissue levels of DHA supplementation are not reflected in the blood if you're doing serum tests.

[01:24:59] So you should be doing something else. I don't know, tissue, like maybe hair or nail. But, so DHA, if DHA is wonky and you're a male I don't think it will have much of an effect on your testosterone levels because they mostly come from the gonads and the gonads don't seem to prefer DHA as a precursor.

[01:25:15] There have been some studies and I some experimentation going on by people on the forum as well that actually putting pregnenolone on the scrotum may raise serum testosterone levels. Several people did that and did blood tests before and after and they did get higher testosterone. All of them got higher testosterone levels, but of course it's a small group, non controlled.

[01:25:34] It, we don't know if it's statistically significant as, but in every single one of them, testosterone levels rose. There was no change in estrogen levels. In fact, in some of them, estradiol declined by doing topical prenatal on the scrotum. As far as the carnivore diet basically, first of all, if it's fresh meat, it's a misnomer to call it a low carb diet.

[01:25:53] Glycogen in most animals, including humans, is stored mostly in the liver and the muscles. So if you're eating fresh meat. You're actually consuming quite a bit of glycogen with that meat. Ray spoke about this several times. However, the more the meat ages and unfortunately, its price rises. So aged steak is one of the most expensive things you can buy.

[01:26:13] But if the more it's aged, the more glycogen gets fermented by bacteria, MBM bacteria, into lactic acid. And also, it's levels of endotoxin increase because of course the bacteria can process protein. It's the same bacteria that is in our gut. And you're basically eating rotten meat full of endotoxin.

[01:26:30] And almost no glycogen eat there, but fresh meat. If you're fully carbo diet and you eat a lot of fresh meat, you are consuming probably about equal percentages in terms of calories of carbohydrates and protein. So it's one to one. It's not, so it's not a low carb diet. It's not optimal, but it's not what they load to.

[01:26:49] It's not, it does not equate pal the carnivore diet to the paleo diet. The bad thing about, of course, the old meat, that is, that you're not consuming any fiber and you're consuming a lot of the inflammatory amino acid in the meat. And there's also the calcium to phosphorus ratio in meat is very low.

[01:27:02] And that has a cumulative pro aging effect. Tryptophan, of course, is a high balance in the muscle meats as well. So if you're going to be eating a carnivore diet, I think the, I would go with the tougher cuts of meat, such as skirt steak. It has a lot of collagen in it. And basically maybe even supplement some additional collagen as well and make sure the meat is fresh so you get sufficient amount of carbs.

[01:27:22] And then as far as her thyroid biomarkers, the conversion of T4 into T3, which happens mostly in the liver, is crucially dependent on glucose availability. You can eat all the meat you want but if you don't consume a sufficient amount of carbohydrates you will become eventually hypothyroid.

[01:27:39] Not to mention the fact that cysteine, methionine, and tryptophan, which are high in meats, have direct inhibitory effect on the thyroid gland producing T4. Multiple things going against eating just meat. It is a, it's a healthy component of diet as long as, you take into account its potential negative effects and you balance them by, eating more calcium or adding gelatin, in fact, I think we discussed it on one of the podcasts, they became known as the Bulgarian burger of adding gelatin and calcium carbonate to, to basically to ground meat and, creating these patties that you then eat.

[01:28:12] I've tried it. Actually, the effects are really good. You get like this metabolic kick, your core temperature rises, heart rate rises, that I don't get this with just the pure muscle meats. In fact, I get cold after eating a lot of meat, which is usually an indication that insulin when up.

[01:28:27] Blood pressure, blood sugar went down and I got into this hypoglycemic state and activated the stress system. Almost always happens if I eat a lot of meat without, supporting carbohydrates. And if you're eating only that, and if the meat is aged, you'll be eating low carb diet. But if you're eating fresh meat you will, that's probably why some people do really well, especially in the, these indigenous cultures.

[01:28:47] The meat that they eat is almost invariably fresh. They killed it a few hours ago so they consume a decent amount of carbohydrates with it. What other points did you have about the thyroid? I think Cheryl said that sometimes the thyroid markers will go down in her carnivore patients and she doesn't think it's the diet.

[01:29:01] It's definitely the diet. Not sufficient amount of carbs, too much phosphorus in regards in, in relation to calcium, the, and also the inflammatory and the antithyroid amino acids that are present in meat.

[01:29:14] Danny Roddy: Yeah,

[01:29:14] Georgi Dinkov: that

[01:29:14] Mike Fave: yeah, it's funny too. We spent all this time talking about glucose oxidation being so central and reductive stress and oxidative stress.

[01:29:21] And then she's saying it's just it can't be something as simple as not having enough carbohydrate and it's no, it really is that simple that your hormonal functions dependent on carbohydrate. I think the other thing that's even worse is if you, if the carnivore diet is super heavy in protein, then you have to start up regulating gluconeogenesis and then production of ammonia, which will also drive the gluco, the glucocorticoids like cortisol to support those processes as well as glucagon and whatnot.

[01:29:46] And you're also pushing fatty acid oxidation, not to mention that you have the iron overload piece. I can't say how many. Carnivore people I've worked with who come to me and then they have iron overload, where ferritin is high, iron saturation is high, and that's even, talking about oxidative stress and polyunsaturated fatty acids, while PUFA may be low on a carnivore diet, depending on how it's set up, if you then have a large amount of iron stored in the body, and you're under reductive stress, and you have PUFA, that's like the recipe for disaster.

[01:30:13] Georgi Dinkov: Exactly. Yeah.

[01:30:15] Mike Fave: Yeah. So I think the combination of those things are, There's a multiple reasons why the carnivore diet is not ideal. There's definitely reasons why it's probably better than a standard American diet. But it's also, there's, these are like serious issues that long term don't make sense. And yeah, as far as the hormonal stuff, I think the idea that it's just other external stress, or it's this, these like other environmental factors.

[01:30:41] That are causing these effects on people's hormonal profile. That is like a massive obfuscation of what's going on. It's like this complexity argument. Like it's, oh, it's also as complex as these other things. It's no, it's really simple. Or at least at the minimum fix the carbohydrate piece first and then see if you still have a problem after, instead of trying to search for all these external things, when we know that there, we know the mechanisms, we know how these things work, we know what happens with low carb diets and thyroid function.

[01:31:07] Yeah, that's the DHA and testosterone piece is funny. It's like the DHA is just DHA may be wonky on your carnivore diet because you're constantly driving cortisol and then you may have a lowered cortisol to DHEA DHAS ratio. You

[01:31:21] Georgi Dinkov: mean higher? Yeah, higher. Higher

[01:31:22] Mike Fave: cortisol to DHE ratio because you're constantly driving this stress pathway and burning out that this portion of the adrenal gland and then testosterone's gonna be whatever it's gonna be.

[01:31:32] Separate from that and likely lower given the state or I've actually seen some people on a carnivore diet have higher testosterone levels and part of going back to some of the arguments that we talked about this may be a reflection of tissue metabolism of some of the hormones in some of these states because some people that are on these low carb diets or the carnivore diets and whatnot, they'll come and I've worked with them.

[01:31:52] And they're like, they're, they have hypogonadal symptoms, but testosterone is high and an SHP, SHPG, sex, hormone binding, lobulin is also massively high. And they're like, why testosterone is great. It's a thousand nanograms per deciliter. I should be feeling amazing. And it's

[01:32:05] Danny Roddy: didn't you hear Judy? She said it's not from the SHBG, Mike.

[01:32:09] Mike Fave: That's true. That's true. Did you, I don't

[01:32:11] Danny Roddy: know what you call me, Danny. Yeah,

[01:32:13] Mike Fave: it's just, it's clear. I think in this, in her feel that she doesn't understand things in any holistic perspective. And her whole thing is just carnivore diet as a solution. Yeah. And if it's not working or these things aren't correct.

[01:32:30] Then it's because of these other external things and not because there's actually problems with the intervention of the carnivore diet. That's not to say that carnivore diet may not improve some things for some people, especially if they're coming from a carnivore diet or severe gut issues and they're lowering residue or something like that, but it's definitely not a long term solution and there are multiple problems with it that need to be recognized long term.

[01:32:49] And I think everybody here is speaking to the choir.

[01:32:53] Georgi Dinkov: A lot of the, some kind of a shift occurred in the medical paradigm. They basically stopped treating thyroid, like basically the metabolic rate control laboratory is a very important thing. In fact, because of the rate of living theory, they'd be trying to lower it for all these decades, right?

[01:33:07] They're trying to lower it, and now whenever it doesn't even cross their mind that basically that, that be having a low tire could be an issue. They're not making the connection, and if not, if they don't think thyroid is a problem, then they're not going to think carbs are a problem, low carbs are a problem, because back in the day, when we were going through medical school, I've talked to older doctors, they all knew that you eat a high carbohydrate diet when you're hypothyroid, and you want to raise your thyroid function.

[01:33:29] So you eat high carb, moderate protein, low fat. That was established and it was actually a treatment for, people that came with obesity or any kind of other endocrine problem related to low metabolic rate. However, this, I think things started to change around the 60s and 70s where they said, okay, high metabolic rate, not good.

[01:33:45] You're going to live less because you're producing a lot of ROS, which by the way is not true. 97. 2 percent of the ROS are produced in reverse electron flow, which only happens when you're over oxidizing fat, not when you're oxidizing glucose. So yeah, so whatever we would, I guess we're arguing, trying to like respond or debunk the statements of these people.

[01:34:06] A lot of the that, that state, a lot of these states would come from the fact that they don't think that thyroid is important and consequently the metabolic rate is not that important. It's basically, it's good to have a lower metabolic rate. Okay. Thanks. And in fact, basically the, taking, doing things that can lower it is fine.

[01:34:22] And I've had discussions with doctors who are saying that, yeah, I know cysteine suppresses thyroid function. What's wrong with that? You're going to lower your heart rate, and my heart rate is in the 30s, and that means I have an extremely well working, powerful heart. And if cysteine does that, I'll take it.

[01:34:36] If methionine does that, I'll take it. If Tryptophan does that, I'll take that as well. So I think if these people were raised in a different time and, studied according to the old medical books, a lot of these fat, dietary fats would not exist because thyroid was recognized initially up until I think probably the middle of the 20th century was recognized as a very important regulator of health.

[01:34:58] And in fact, the only weight loss drug to be used up until the 1950s was dinitrophenol. People did not diet. I'm sorry, they did not fast in order to lose weight. They did not drastically change their, their macronutrient ratios. If they wanted to lose weight, they knew that they need to raise their metabolic rate.

[01:35:14] If you look at the older studies, the two accepted methods for that were intravenous T3, Or dinitrophenol, none of that carnivore, just eating, only protein or only meat or, reducing your calories or chronic or intermittent fasting, none of that was practiced back in the day. And it tremendous results.

[01:35:30] They had the lowest rates of obesity, going, all the way back to whatever recorded history we have, at least in the United States, I think the good records start from the early 1800s up until the mid 1950s, people who were like lean and tall. All these other problems started happening afterwards when it became fashionable to lower the metabolic rate.

[01:35:49] And now they're wondering and, what is causing all this obesity, even though they're, at the same time, they're also saying lowering the metabolic rate is good. But they go hand in hand. How does nobody recognize this disconnection? It's not only obvious, it's officially taught in the, in medical school that low metabolic rate equals obesity.

[01:36:05] You can have, sometimes you have a, you have a hyper thyroid person also have a a bit carry a bit extra weight, but almost always low metabolic rate equals obesity and and the other way around. I don't know if this knowledge was somehow lost, even most doctors, when you talk to them, they don't recognize it, even though they were ready to admit that if you have basically, if you're eating, if you're, if you obese means too many calories in and not sufficient amount of calories out, but for some reason for them, the calories out piece is always related to exercise.

[01:36:32] So it's never about erasing, uncoupling the oxidative phosphorylation or raising the metabolic rate in general by taking T3. It's either exercise to increase the calories out or fasting to increase the calorie seed. It's never about non stressful, non stress related raising of the calories out portion.

[01:36:51] That, that thing has been somehow lost as knowledge. At least I don't know of any doctor that can offer anything in terms of increasing calories out except exercise. Or some kind of a hormetic exercise, like the, what's this guy, Jack Cruz that does the ice baths. Is that the one? You might think it's a lot of people.

[01:37:07] You're thinking of Wim Hof.

[01:37:07] Mike Fave: Aspirin does the ice baths.

[01:37:09] Danny Roddy: Wim Hof, I think you're thinking of, yeah, probably.

[01:37:11] Mike Fave: It's also funny too, right? Cause these are the same doctors who will say Oh, BMR is, it counts for the largest percentage of caloric burn. And then it's like exercise does, five to five to 15 percent or five to 10%, but you need to focus heavily on exercise.

[01:37:25] That's the thing. The other thing that I think is interesting is you have people like these health gurus now, what's his name, Brian Johnson, who's bragging about his body temperature, like 95 degrees, 95 degrees Fahrenheit, and then he's taking exogenous thyroid. It's it ain't working, my friend, that pulse and that temperature, 95, he should be hibernating

[01:37:44] Danny Roddy: with this temperature.

[01:37:44] Wasn't it lower? Wasn't it like 93? Alright. Did I just make that up?

[01:37:49] Mike Fave: No, it was excessively low with the heart rate.

[01:37:51] Danny Roddy: Oh,

[01:37:51] Mike Fave: got it.

[01:37:51] Danny Roddy: It was really

[01:37:52] Georgi Dinkov: low below 95. I think it's considerably consider officially considered hypothermia. And below 93. I think it's considered dangerous. You need to be wrapped into these blankets and, they start Yeah.

[01:38:02] Fair huggers in the hospital. Pituitary damage or something. Yeah. Damn.

[01:38:05] Jay Feldman: Yeah. One and that rate of living theory, has been long refuted at this point, obviously not acknowledged. As we were talking about with serotonin is a situation where marketing obviously takes over what's actually going on physiologically and circling back here we have this either denial as you're saying Georgia is either you either take one of two stances either you take the stance that you decrease thyroid hormone activity during carnivore diet but that must be a good thing or you have to take the stance of just denial that it happens despite the clear evidence that the presence of carbohydrates in the diet is essential for the conversion of T4 to T3 and keeping stress hormones down and keeping cortisol down and therefore also allowing for proper thyroid hormone production in the first place.

[01:38:49] Yeah, you have to completely flip your view of physiology in order to, we talk mental gymnastics, you have to have a mentally gymnastic view here in order to make an argument that carnivore is not the cause of your hypothyroid state.

[01:39:02] Georgi Dinkov: Also the, for the exercise to, the, it, it's known to actually lower your basal metabolic rate.

[01:39:07] So it's raised by you exercising, but if you chronically overseas it, it's known to lower the heart rate. And they're saying that's a great thing, but they don't refuse to discuss the fact that your risk, the metabolic rate as a competitive athlete declines if you are like an endurance athlete, like a runner or something.

[01:39:20] And actually if you look at those people, like the ones that are very, that are, that we used to be elite athletes in endurance exercises. They have a much higher rate of lung fibrosis and even lung cancer, even though most of these people never smoke. They have much higher rates of these cancers of the respiratory system.

[01:39:37] And also they have much higher rates of cancer in general, and their rates of cardiovascular disease are not lower than the general population, they're about the same. So the whole argument that exercise basically is helpful is not supported by literature. And the part that it, they even say, okay, oh, and by the way, some doctors have wisen up and saying, okay, yes, exercise, it only burns about 10 percent of the calories of your total metabolic, of your total daily consumption, right?

[01:40:02] It's the, really the resting metabolic rate that matters, right? We know that. But what exercise does, it increases your insulin sensitivity because you're burning the fat. But that has also been debunked. Every time you exercise, especially on an empty stomach, you increase lipolysis, you actually make yourself insulin resistant.

[01:40:16] That study with the hibernating bears is basically a perfect example. Even though they didn't exercise, they fasted, and the lipolysis is basically also elevated with them. And not even that, but chronic fasting especially combined with exhaustive exercise several studies show that actually increases your production of the 11 beta HSD1 enzymes.

[01:40:34] It doesn't simply put you into a reduced state, but it also increases your ability to produce cortisol. And one of the studies demonstrated that if you do this for for the animals, I think it was rats, for two months, The effects were so long lasting that eventually they had to start giving, and the animals after they stopped exercising, they gained such a tremendous amount of weight, they had to put them on a cortisol blocker in order to get them back to health.

[01:40:55] They kept gaining weight on a normal diet, which is what Ray said as well, like for chronic fasters and exercises, just like the Biggest Loser Study, right? Then after you stop your chronic exercise regimen, you start gaining weight on half the calories that you were eating before. So that means you butchered your basal metabolic rate.

[01:41:14] So exercise doesn't even help with insulin sensitivity. It destroys your metabolic rate, right? And the only good things that I think it has is that in younger people, because you're exerting yourself you have basically a burst production of DHEA as a countermeasure to decreased cortisol. But with aging, that does not happen.

[01:41:32] In fact, it's not a coincidence that older people have intolerance to exercise simply because their DHEA levels decline naturally, if you assume it's natural, but the cortisol levels don't. So your cortisol to DHEA ratio is chronically rising with age, so you're in a chronically catabolic state. So in, in such state, you have muscle weakness, you have joint problems, right?

[01:41:51] So it's not at all surprising that these people don't want to exercise and in fact feel worse when they're put on an exercise regimen. There's I hate that the show and the movie in general, but the Sex and the City, like the last episode, this guy Big, who was one of the big characters, he died after doing a session on the treadmill.

[01:42:07] And instead of the movie acknowledging, I thought it was funny they did this scene, but then they said it's because, if he had done more of it. This would have happened, but it's exactly the stressful event at his age of I don't know, I don't know how old we'll see in the movie, like 65 or something.

[01:42:21] That's exactly what killed him. At this age, you're, even if you're not doing anything, your cortisol to DHA ratio is already in the highly catabolic state. And cortisol is, we know it's destructive to the heart. You can go into a cardiac arrest if somebody injects you with a sufficiently high amount of cortisol.

[01:42:36] So this person got to that stage by being in a catabolic state and then raising that catabolic state even more by running on a treadmill for for half an hour. If exercise is ever considered, I think it should be mostly concentric and then basically if it's, if you do any endurance exercise, it better be glycogen bound.

[01:42:52] You shouldn't be getting to the point where you're burning fatty acids, right? And also, you should probably be taking measures to protect yourself from the increased lipolysis because most of that fat that's coming into your bloodstream from the tissues will be PUFA because PUFA is preferentially stored.

[01:43:06] Into the fatty tissues maybe a vitamin E or something, or a little bit of aspirin. Both of them have anti lipolytic effects. Vitamin U also protects from the peroxidation of the PUFA as well. And, really, you should not be overexerting yourself. This whole paradigm of that you need to torture yourself to help, that needs to end.

[01:43:22] Most people intuitively know it, but they're just too afraid to call their doctors, crappy advice and say, you know what, if you're lying to me about that, something so fundamentally simple as exercise. Can I really trust your advice on any other medical matter? And most people are not willing to take that step.

[01:43:37] There is a play by Oscar Wilde which basically, and apparently this was something he knew. What is it? A hundred years ago? He basically says that largely says the doctor is incompetent. The truth about the doctor is so terrible. And because doctors are so fundamental to the function of our society that nobody dares to think about it.

[01:43:54] So it's you can be lynched for speaking against doctors, basically, not physically, you can get canceled simply because it's terrifying for people to think that those, the profession that they should probably trust the most is actually one of the most vile ones around.

[01:44:09] And until that changes. I don't think we're going to see much progress but the good news is I'm seeing less and less people do their, go to the doctor or the specialist and do these annual checkups, which were found to be completely useless, by the way. So people who go for the annual checkup have a higher mortality rate than people who don't go for the annual checkup, but go to the doctor when they, have some troubling symptoms.

[01:44:29] So yeah, that's, that, that's the current state we're in. Something I want to highlight that you said is so important is this idea that exercise doesn't actually increase your metabolic rate. Yeah. This is being recognized now in what's called the constrained model of energy expenditure, but essentially our bodies adapt to the amount of energy they're expending because they only have so much energy to use for all their organ functions and whatnot.

[01:44:54] Jay Feldman: And so if you exercise and waste a ton of energy, on this, on movement, then there's less energy going to all of your other functions and leads to issues, leads to degeneration, leads to massive stress. And as you're getting at the, that is not actually increasing your basal metabolic rate or increasing your metabolic rate.

[01:45:12] That's going to be coming from increasing thyroid activity, increasing pro metabolic hormone activity, reproductive hormone activity. Yeah, we can't stress ourselves, whether it's through cold thermogenesis, cold baths, or exercise to a better metabolic rate, it directly lowers the metabolic rate.

[01:45:28] Georgi Dinkov: And the cold thermogenesis, they're promoting now because they're saying it browns your white fatty tissue, and they're saying the brown fatty tissue is much more metabolically active, so it's going to burn a lot more fat.

[01:45:39] Multiple studies already came out and said that one of the key processes that basically signifies the conversion. The turning of a specific tissue area into a malignant one, in other words, cancer. is basically the conversion of white fatty tissue in the area into brown fat. And because the activity of that fatty tissue is driven by adrenaline, right?

[01:45:58] Adrenaline is a known promoter of cancer, mostly through lipolysis. That connection should be obvious. When you're doing the brown, the cold thermogenesis and browning your fat, you're directly mimicking the early stages of cancer. And I think there was a long term study with there's like a, some cultures that do the cold exposure, like the Russians and the Finns but after they go into a sauna, and they actually do the exact opposite.

[01:46:20] So they do both brief exposure to cold, followed by much longer exposure to very high temperature, and they do okay. But then certain groups that used to live there moved to other countries, and they only practiced the cold exposure. These people had a much higher mortality rate than their genetic related peers that stayed back into the country and did both the cold and warm exposure.

[01:46:40] Mike Fave: Another thing that ties in with this specifically, the cold exposure, and I do want to make a note on the exercise piece. Is our friend who was talking about the estrogen study was also talking about the benefits of estrogen for weight loss by promoting the production of brown fat. So that was one of the mechanisms that she was discussing is like the anti obesity effect of estrogen specifically.

[01:47:01] And it just through the idea that brown fat obviously burns more fat than white fat, it's more metabolically active and whatnot. The other piece I wanted to just drop in here quickly that goes with the perspective that you guys are talking about. So Jay, you're mentioning the constrained energy model.

[01:47:14] And then George, you were talking about the damaging effect of exercise and then the overshoot in weight gain once you stop. There's actually a model as well talking about the fat overshoot. So essentially, when you exercise and you lose a bunch of body weight, if it's done incorrectly, you also lose a bunch of lean mass.

[01:47:31] And so what winds up happening is a body tries to get back to that lean mass, but since metabolism is so destroyed, what it will start to do is it will start to just keep, your appetite will drastically increase. And you'll put up a whole bunch of body fat on and your body won't stop putting that on until you resume breach that level of lean mass again.

[01:47:49] And the reason you're putting on so much body fat after you've lost this weight and dieted all the way down and whatnot, is because you're in this metabolic hole. Thyroid function is not working, cortisol is not working there's problems with the entire leptin cascade, there's problems with the androgenic hormones.

[01:48:03] Everything is out of whack and basically you have to like, you have to fix all that, build the lean tissue. And so it's not just a simple, oh, I'm just going to start eating again. It's like a really serious issue because the whole basal metabolic rate has dropped and the hormonal profile is destroyed.

[01:48:18] Georgi Dinkov: So there's a, there's studies with people that are survivors of concentration camps.

[01:48:22] Ray mentioned a couple of times, when they got liberated and they started eating again, there's something called refeeding syndrome. If you've been starving for a long time, you can actually die if you go back on a normal calorie diet. But the ones that didn't die, so I don't know what percentage, but some people, some of those people died because, just because of, they started eating normally again.

[01:48:41] It was just too much calories probably. The the others basically developed, a lot of them developed extremely high levels of prolactin. And also gain a tremendous amount of weight, mostly in the form of fat. So after a stress period is, so often the being lean through exercise is simply basically an indication that you're under stress.

[01:48:58] And when you stop that stress, you recompensate by building back up the weight. And the reason basically they're saying the the, there's something called the obesity paradox. There's a theory now gaining more momentum saying that obesity is an adaptive mechanism to raise your metabolic rate. In a suboptimal fashion if the other factors are not there, because an obese person will have, on average, higher metabolic rate than a lean person if they're of the same height.

[01:49:21] So obesity is like the, like a lesser evil, and it's, these people have a higher survival rate in cancer in, in diabetes, in cardiovascular disease, if you look it up on Google, even in infectious disease, actually. So it's it's best to be mildly obese. I think they said BMI, the best survival.

[01:49:38] The longest survival curves are for people with a BMI between 31 and 33. The ones that are lower or higher had lower survival ratings. As far as the muscle to fat loss when you're exercising or fasting, it's three to one in favor of muscle. You're losing three times more muscle weight wise, basically in a gram per gram relationship.

[01:49:57] When you're fasting or doing exercise, then you're losing fat. The process of lipolysis, probably because fat is much more energetically rich, it has nine calories per gram versus the four for protein, that may be why the body will prefer, and I think also the process of gluconeogenesis happens faster as well.

[01:50:13] So it makes sense that when you need an emergency access to resources, the body will break down more protein versus more fat. Fat is really meant for long term flow consumption, such as a hibernating bear. But if you're exercising and fasting, You will be losing mostly muscle mass, which is a really terrible result.

[01:50:30] And that's what happened to the contestants in the biggest in the biggest loser show, they all regained the weight after they stopped the show on lower calorie diets than before. So the base of metabolic weight was destroyed. And finally, probably the most incontrovertible proof. That estrogen is actually an obesogen.

[01:50:48] Estrogen is the most widely used weighing gain mechanism steroid in the livestock industry. Estrogen is officially and recognizably used to fatten up animals that are raised for slaughter. In cattle, where they want both muscle and a little bit of fat, they use a combination of estrogen and an androgen, or an androgenic anabolic steroid, such as Trembolone, which is what it was developed for.

[01:51:11] So cattle usually get an injection of Trembolone, acetate, and ethinyl estradiol so they bulk up and develop both muscle and fat. Pigs will get mostly basically a supplemental estrogen, and that's what makes them fat. Talk to any person who raises animals for their meat, and that person will invariably tell you that, yeah, if we want to fatten up the animal, we give it only estrogen.

[01:51:34] I don't see, I don't know how, why this has not been more widely acknowledged in the medical industry that, if it works as a fattening agent, every animal that we know, the old mammals, But it does work actually, no, it works in birds too. So it's a fattening agent in broilers. It's a fattening agent in rabbits, fattening agent in sheep in, in swine and even in cattle.

[01:51:53] And even in monkeys actually, but there's some studies about that too. How can not be a fattening agent in, in, in humans? It's just beyond me.

[01:52:00] Mike Fave: That's a very good question. The other thing too, is we were, when we were talking before about the About the trends for obesity, you're saying that there wasn't obesity before the early 1950s or so, or there wasn't high levels of it.

[01:52:11] That's talking about agents that are fattening animals or the heavy grain based diets and polyunsaturated fats. That's when the introduction of polyunsaturated fats heavily hit the market. And the other thing that's interesting with that is, so you see a lot of times they talk about trends and heart disease and whatnot, and you say, Oh, the After 1950s, the heart disease trend starts to actually decrease and people start to end, but we increase polyunsaturated fatty acids like, yeah, the 1950s was also 1950s and 60s were also the campaigns where they stop people from smoking.

[01:52:41] So you see this trend where smoking increases from the early 1900s. Peaks around the 1950s, 1960s. Then you have the campaigns to decrease it. And that's also in polyunsaturated fatty acids start to increase. And you see the heart disease trends increase increase, start to fall off as polyunsaturated fats start to increase.

[01:53:00] And now the heart disease trends are reversing. With the obesity and diabetes trends. And then I think the cancer trends, I'm not sure. I don't want to speak of cancer

[01:53:08] Georgi Dinkov: has always been rising. And in fact, cancer is now set to overtake. I think it's already the number one killer, the number one cause of that in the United States.

[01:53:16] It's slated to become the number one cause of that worldwide in the next five years. So if cancer rates are rising, whatever we're doing is not working, which goes back to the point that if estrogen is now everywhere, we have even synthetic estrogens and even the non steroidal ones, such as the bisphenols the from plastics.

[01:53:32] So in another argument for the carcinogenic, carcinogenicity of estrogen and the fact that we should not be, definitely not be exogenously supplemented with it.

[01:53:43] Jay Feldman: Yup. Of course.

[01:53:46] Georgi Dinkov: Yeah if people don't believe it, just go to Google and type estrogen fattening livestock and you will get just, a wall, massive wall, like a waterfall of studies that explains the dosages, which estrogen version is the most fattening.

[01:53:59] Usually the more potent activity has estrogen receptor alpha, the better. What combination between an estrogen and an androgen you need to use for the proper, partitioning between muscle and fat. But invariably, all of these studies say basically that estrogen is the hormone that's used to increase the fatty tissue of an animal.

[01:54:16] So in swine, where they really prefer the fat. Basically they use mostly exogenous estrogen. In cattle, they use an anabolic steroid, which is, it's invariably androgenic, and an estrogen as well. And they tried actually, they tried several times using only Tremblone in the cattle.

[01:54:32] It was basically, it had no fat, it was extremely lean. And if you can see those we have seen those pictures of the, this extremely ripped bull, bull, and they thought it was the myth is, the myth propagated on the internet is that bull was given a myostatin inhibitor, but if you look at the picture and you find a study that's behind it, He did not have a mastitis inhibitor because at the time those inhibitors were not known.

[01:54:54] It was injected purely and only with high dose trimbolone acetate. But the meat was very poor quality in the sense that it was very tough, and people did not like it. It had no fat. It was very difficult to cook. So that's when they decided that they would give the cattle More tremolo, but a little bit of a strategy was also so the cattle get fat as well.

[01:55:12] Danny Roddy: Okay, one Georgie we'll just jump into this really quickly. And I'm not so interested in the endotoxin orange juice connection, but more so in the meaning of this clip. What does this mean for where the health world is going?

[01:55:27] Dave Asprey: So let's play this clip really quickly. In terms of fruit juice, if you have food poisoning, or you have really severe hypoglycemia, orange juice surprisingly works really well.

[01:55:36] What? Orange juice for food poisoning? It's because when you have bad bacteria in your gut making something called lipopolysaccharides, this is the bacterial toxin, an endotoxin. When they get orange juice, they stop making toxins because they like the sugar. So you could take activated charcoal and orange juice and you'd do better off.

[01:55:51] But otherwise, why would you juice a fruit when you could just eat it?

[01:55:53] Danny Roddy: I've heard those things in many different places and just for context Dave is a very pro keto for a long period of time. And then now when these health influencers are talking about orange juice and lipopolysaccharide and and charcoal, it where do you see the wind blowing?

[01:56:09] What does this mean to you? He's

[01:56:10] Georgi Dinkov: wrong in the claim that it's the sugar that's basically that's causing the reduction of the endotoxin. Because if you drink apple juice, which is pure and it has the almost very similar sugar composition to orange juice. But it doesn't have the other ingredients, which I think are responsible for the effects of orange juice.

[01:56:24] Apple juice does not reduce endotoxin levels, but orange juice does. So there's something in the orange juice which is containing the orange color, probably, because the rest is just the sugary water, which is what apple juice is. And those things are naringin and apigenin that are present, mostly naringin in it.

[01:56:39] And those things, first of all, they have some antibiotic effect, but most of the oranges will probably not make it to the colon to affect the bacteria. But what it does do is that both of the naringin and apigenin are endotoxin receptor antagonists. They block specifically TLR4. But also a bit, a little bit TLR, TLR 9 and 1.

[01:56:58] So you're going to get an endotoxin blocking effect. And I think that they're also the the flavonoids themselves are also inhibitors of the serotonin pathway. And that's, they've, another reason, another proof probably that serotonin is not a happy hormone is that they have an antiserotonergic effect and have displayed an antidepressant effect in both humans and animals.

[01:57:17] So I think the, some of the beneficial effects of the orange juice is not necessarily through the endotoxin but limiting the effects of endotoxin. Which is most, and most of that effect is increasing the production of serotonin by the enter chromin cells and also the production of NI nitric oxide. Both of these flavonoids as well as all of the other related ones, such as quercetin and gertin are also inhibitors of the inducible nitric oxide syntase enzyme.

[01:57:43] So if you're drinking orange juice, you're gonna get a mostly systemic effect that acts in a way opposite to endotoxin, some direct blocking of the endotoxin and the receptor level. And if a sufficient amount of the flavonoids makes it to the colon where most of the bacteria is, you're gonna get some direct antibacteria effect as well.

[01:58:00] And also, finally, the most of the flavonoids are actually electron accepting agents as well. So they work similarly to quinones, and I think the naringin and apigenin specifically, they can accept up to three electrons. So they're probably even more efficient, more effective than than even like the two electron acceptors, such as methylene blue and and vitamin K in the tetracyclines.

[01:58:20] So you're going to get a prometabolic effect directly and shifting the redox status towards oxidation, which by the way, endotoxin and serotonin specifically, both of them shift towards reduction.

[01:58:30] Jay Feldman: Yeah, and as you said, it's not the sugar feeding the bacteria. In the study that I'm assuming he's referencing because it's been referenced in the peat sphere for, what, a decade now, That, Dave is trying to get hip to they compared it with glucose and the orange juice was effective in lowering the inflammatory effect, but the glucose wasn't like a glucose sweet beverages beverage or whatever it was.

[01:58:54] And yeah, they point to the polyphenols and they don't mention the fructose, although I'm sure the fructose had a protective effect as well. The other important point being that if you're consuming orange juice and it's feeding bacteria, that's a problem because you should be absorbing that sugar way higher up in the small intestine than you're seeing any bacteria.

[01:59:10] Yeah, I think what you were getting at, Danny, is just, the swing in this, in the general alternative health sphere toward. Slowly to dipping into the idea that things like endotoxin cause disease and inflammation and things like orange juice can be protective and it's only a matter of time until, a high carb diet that involves a lot of food and things like orange juices.

[01:59:32] Is it going to be next, but yeah, obviously there's a bit of a I don't know, botching here of that transition. By

[01:59:38] Georgi Dinkov: the way, if the bacteria is consuming the sugar, they will produce even more endotoxin because it increases bacterial turnover. So anything that feeds the bacteria will by definition, increase the endotoxin.

[01:59:47] So it cannot definitely be that, that just on that claim alone, I think this is the direct debunking there.

[01:59:53] Mike Fave: I think it's like the, as you were saying, Jay, it's like a one step, right? It's just Oh, orange, just as good in this particular context. And then we're going to slowly expand these contexts as we go forward.

[02:00:04] Or the other thing could be is like some of these health gurus will start to rationalize why you're seeing beneficial effects of some of these different components, like orange juice, which are directly counter to the narrative that they've been putting out for so long. You see this even inside the research circles, right?

[02:00:19] So it's like at first genetics. We're going to synthesize the human genome, we're going to solve all these problems. And then they did, they like, synthesized the human genome and no problems were solved. So I was like, oh there's this thing called epigenetics. So it's like keto starts or the keto or carnivore stuff.

[02:00:33] It's oh, low carbs are terrible. You need to stay away from them. And then it's these certain carbs are like evolutionarily consistent. And then it's carbs are evolutionarily consistent, but grains and these other things. So it's, it starts to, it's like walking things one step forward to change the narrative slowly in, without really fully again, without fully understanding the context, like to just say, Oh, it's because sugar feeds bacteria.

[02:00:56] As you guys mentioned it, it doesn't even make sense of any, the other thing that you see in this study too. And if it's the same orange juice study that I'm thinking about is the blood glucose regulation in that study. If you look at the graphs actually improved in the orange juice group. So they had more carbohydrate intake.

[02:01:12] They had a less insulin response and they had a lower blood glucose curve inside that study. The inflammatory markers were lower and so were the immune markers. in this high fat, high carbohydrate meal. So it's there's much more going on, even though the endotoxin markers were lower other things were improved, and it could partly be from the endotoxin, but it could be partly be from other mechanisms, including the fact that the carbohydrates were having a beneficial effect as well as the polyphenolic compounds.

[02:01:38] Danny Roddy: Low carb is the ending scene in the second Matrix movie. Where the whole scene like starts shifting towards carbohydrate and then the matrix like starts over again going back to low carb and it just does that like literally infinitely because even in 2011, I went to the Ancestral Health Symposium, I've probably told this story a thousand times.

[02:02:00] But like I went to the Ancestral Health Symposium and I remember the orientation of people there were like, we are so over carb restriction tell us anything other than carb restriction. And then it got like real popular again, going back to keto, like it always reverts back because the foundation has nothing more to say other than restricting carbs like 99 percent of the time.

[02:02:22] Georgi Dinkov: Because the things are so interconnected, if they finally admit that oxidizing fat is bad. Then basically it's very, it's a very small step between that and saying PUFA is terrible, right? Because I say, okay, if simply oxidizing them in the normal oxidative pathway, which is the beta oxidation, if that is bad, then what about all these other bad effects that that PUFA are having?

[02:02:42] And if PUFA has all of these effects, so its oxidation is bad, It's peroxidation is bad, it's enzymatic transformation into prostaglandins is bad, even non metabolized, it's actually now, there's a study that I posted recently, it actually acts directly like estrogen at the receptor level, right? So all of these things go together.

[02:03:00] So if, basically, if PUFA is bad, it's also an estrogen, then estrogen is also bad, right? So the whole house of cards is so interconnected to these, a few central themes, which I think is. Carbohydrates is bad, fat good, right? Polysaturated fat is good, saturated fat is bad. If any of these collapses, everything else will collapse as well.

[02:03:19] And that's why they're so desperate at keeping the narrative about the very basic things under control. I, when I, if you pick something more remote, such as, I don't know more specific, more, more differentiated, like if you're talking about a very specific disease, I found that doctors are basically a lot less hostile.

[02:03:35] Then if you start to attack in the very fundamental such as high carb may be actually good for diabetes and not the cause of it. If you say something like that, it's like a, almost like a visceral reaction is that, what the fuck is this little thing talking about, right? Who is he to teach me?

[02:03:49] But if you talk about something, even if it's their specialty, right? If it's like a very specific disease, they're much more willing to listen. But if you say something absurd, or at least I don't know, existentially threatening to them, which is something very key, like cancer is not genetic, it's metabolic, and it's definitely environmental.

[02:04:05] It threatens the entire profession because what any of these pillars collapses, everything collapses and also implicates them directly into causing a lot of the issues too, right? So it's if you're a dietitian or your doctor, your primary care has been telling you to eat high fat diet, low carb and over, over exercise, and every single one of these things turns out to be independent contributor to disease.

[02:04:26] Not only are you not going to go to that doctor, you may sue or may even attack him or her physically. So they, I think they sensed that, and that's why These debates about central things like serotonin, I'm sorry, serotonin, estrogen, like that lady. Is she like a endocrine professional? Is she a gynecologist?

[02:04:40] In order for her to react like that, to feel threatened by a layman like me, I suspect estrogen is a very core part of her profession or her daily activities. Otherwise, why would she even bother responding to me? She has a lot more to lose than I do.

[02:04:54] Danny Roddy: Yeah, that's true.

[02:04:55] Mike Fave: Plus you're

[02:04:55] Danny Roddy: a man.

[02:04:55] Mike Fave: I think she's a clinician who works with people.

[02:04:58] In providing estrogen or hormone replacement therapy that includes estrogen. And so basically if the perspective that you're saying is correct. Then you basically blow out a large portion of her therapy, right? Not only that, she's basically

[02:05:12] Georgi Dinkov: culpable. She's culpable. This isn't simply what you call negligence.

[02:05:16] This is malpractice, right? So it's if somebody's saying this is terrible, right? It directly threatens not just her, the entire profession, but her specifically, because I'm sure women have probably emailed her. The only reason for her to do that is that maybe she got 10 emails from clients, patients, and saying, are you actually killing me?

[02:05:31] And then you have to say something, in a response, otherwise they're gonna, who knows, maybe these people are influential and they're like, listen, I know where you live.

[02:05:39] Danny Roddy: You just have to read the comments on the bottom of that post, but I know this is a tired quote, but it is difficult to get a man to understand something when his salary depends on him not understanding it.

[02:05:48] And again, we could, same thing could be Not

[02:05:50] Georgi Dinkov: just salary, freedom and potentially even life. I'm telling you, if this You saw what happened with COVID. After it became clear to most people that first of all, it's not that serious disease. Number two, now there's like a lot of evidence coming out about the vaccines.

[02:06:03] Even from official journals, right? I know quite a few doctors that quit the profession altogether and even moved out of the country. I think some of them are expecting a very massive backlash or at the very least such a decline in the rate of like people using their services that you might as well start looking for another job because you're not going to have that many clients anymore.

[02:06:20] Danny Roddy: Don't worry. The EMP will go off and none of this will matter anymore. Okay. We can wrap it up here. Georgie, why don't you tell everybody about Idealabs real quick?

[02:06:28] Georgi Dinkov: It's this unicorn. Nobody's ever seen it. No, it's my boutique company, as you usually mention for cosmetics and R& D chemicals.

[02:06:35] And basically all of them are based on, either erased writings or, things that I've researched myself. But they're all pro metabolic basically, the underlying theme is just increasing metabolic rate. Some of them are very fundamental, such as natural desiccated thyroid directly increases your intake of thyroid.

[02:06:53] Others are attacking some of these, unhealthy biomarkers that we discussed, the mediators of the sickness field like estrogen, serotonin, prolactin, right? Others are, increasing your the levels of the youthful hormones, pregnenolone, progesterone, DHEA androsterone even, which is a saturated version of DHEA.

[02:07:11] Others are just vitamins, which we've been told are only vitamins and nothing else. Let's say vitamin E, but there's all the research saying it's, it's acting in a way opposite to estrogen. It's actually a direct estrogen receptor blocker. It does basically it lowers prolactin prevents the most of the negative effects from the peroxidation of the polyunsaturated fats.

[02:07:31] It has some effects potentially on stimulating dopamine synthesis. It's really things that, that we've been told are ineffective they're just vitamins. You cannot possibly do any good unless you're really deficient on them. If you dig down, dig in into the literature, you'll see that they have much more diverse effects ultimately having to do with improving oxidative phosphorylation, specifically the production of energy from glucose.

[02:07:53] That's really the underlying theme. Everything else flows from that. If you inhibit that through whatever means, stress, poor diet I don't know, bad environment radiation, including non ionizing one. Anything that inhibits the flow of electrons ultimately leads to disease, which is a quote from the Nobel laureate, Otto von Warburg.

[02:08:11] So we develop products that do the opposite, stimulate the flow of electrons through various pathways. So that's the company.

[02:08:17] Danny Roddy: Got it. Got it. Let me just flash these. Okay. We got idealabsdc. com. You can go to check out Georgie's supplements. You can go to hateit. me. This is Georgie's blog.

[02:08:26] And then you can also follow Georgie on twitter. com slash hateit. And those are all the best ways to find him. And

[02:08:33] Georgi Dinkov: whatever I post on the blog goes on Twitter as well. So that's, that's probably the easiest way to follow because the, I don't think the forum has there's an RSS

[02:08:40] Danny Roddy: feed.

[02:08:40] Twitter is better. Hey dude, really appreciate it. Before I let you go, Mike real fist let everybody know where they can find you.

[02:08:46] Mike Fave: You guys can find me at mikefabe. com or you can find me in the energy balance podcast with Jay

[02:08:51] Jay Feldman: and Jay. Yep. My, my website is jfeldmanwellness. com and yeah, Mike and I do a podcast called the energy balance podcast.

[02:09:00] Danny Roddy: Cool. Hey, Georgie infinite. Thank you so much. Even through this tech problem, which seems to happen almost every time I do a podcast these days. Thank you so much to give a huge amount of your time. Really appreciate