Stop Blocking Estrogen: Use Metformin Instead

0:10 Hey everybody, this is Hunter Williams. I hope you're doing amazing wherever you are at in the world. Today's video is called metformin versus estrogen. So I think I may be doing something that no one else is probably stupid enough to do, which is to make a video helping men understand that estrogen is not bad. And to take it a step further, I'm going to recommend that you use metformin to help quote unquote, manage your estrogen. I am not a big fan of quote, unquote saying, quote-unquote, manager estrogen, but what I have noticed through the years of doing this is that men with

0:50 higher amounts of body fat tend to aromatize more of their testosterone, whether that's exogenous or endogenous testosterone into estrogen. So what I have noticed is that first of all, before I started testosterone while I'm on testosterone I've never had a lot of visceral fat on my body. All of the high estrogen symptoms that men speak of I never experienced.

1:20 And I've even taken in as high as 750 milligrams of testosterone per week, and I have never really had high estrogen symptoms. Now I'm sure if I continue up into the 1000, 2000, 3000 milligrams a week of Testosterone, which, hey, maybe I'll do one day just to try it. I am sure at some point I would run into over quote unquote aromatization if push my levels up high enough, but maybe not. And my theory around this has been that the more visceral fat that someone has on their body, the they aromatize testosterone into estrogen,

1:56 thus exacerbating the balance between testosterone and estrogen that they would naturally have. In fact, in my case, I actually add in injectable estrogen because in, my experience, even on 200 milligrams of testosterone per week, My estrogen really is not that high. It usually sits around like 20 to 25. So I add an estrogen and it gets me into like the 40s and 50s range. And it feels really good. My sex drive is better. Or my cognition is. Better and my mood is, better and I like it. Now I'm sure I could bump up my testosterone, you know, to four or 500 milligrams per week to get the same level.

2:29 But do I really want to do that? Nah, I couldn't, but I don't know if I want too. So I just take 200 to 250 milligrams of testosterone per weak, add in one to three milligrams, of estrogen per weekend. I feel really good. And I promise this is all going to come back and I'll do a screen share, I could talk about this all day, and what I have noticed, like I said, is that the higher visceral fat a man has, the more propensity he has to aromatize his testosterone into estrogen.

3:00 And so today I'm going to make the argument that metformin could actually be a better aromatase inhibitor than your aromates inhibitors itself, because the way met formin works is it helps control insulin resistance. It helps get rid of insulin, resistance in the body, thereby reducing the amount of visceral fat that you have, there by reducing amount arometates enzyme that to express, their by controlling your estrogen to where you feel good. So like I said, whether you're just relying on your own natural production, Most of you probably listening to this are going to be using exogenous testosterone, so I'll focus more on that for the sake of this presentation.

3:33 But I think for people that think that they need an aromatase inhibitor to have testosterone could replace that aromates inhibitors with metformin and get the same effect. And not only would they not be damaging their health, they would be improving their heath in the long term. So that's what I'm going to talk about today. Again, I realize this is not for everyone. If you don't agree with this, that is totally cool. Leave a comment. It can be a mean comment to me. Just don' be mean to other people in comments. But understand that this is my unique perspective, this my theory around this.

4:07 I don't know if it's right scientifically, I did my best to show you in this presentation. What I'm going to do But understand, this is just one person's opinion. So if you are dogmatically adherent to using an aromatase inhibitor, I'm not trying to stop you, but I do think you should be informed about the dangers and about something that you could use in the case of an Aromatases inhibitors, which is metformin and actually improve your health for the long term rather than Sabotage so that's what I got for today as always check out pep talk cheat sheet down in the description below and then join foh Which is fully up

4:41 to myself the best part of community on the planet for these type of things so Without further ado let's get into it and today. Let's learn about that foreman versus estrogen All right, I am Hunter Williams and today is all about metformin versus estrogen. So let us get into it. Let's look at this idea of aromatase. Aromatases is the key enzyme that converts androgens to estrogents, testosterone to estradiol, and its activity in adipose or fat tissue plays a very crucial

5:12 role in systemic and localized estrogen production, which we're going to talk a lot about today. but especially in postmenopausal women and obese individuals. So in obesity, the fat tissue often becomes chronically inflamed, leading to elevated levels of cytokines and prostaglandin that up-regulate aromatase's expression via specific gene promoters. This results in increased local estrogen synthesis in fat deposits such as breast adipose and stomach adepose tissue, which has linked to various pathologies.

5:44 You could say estrogen-dependent cancer. I'm not a big believer in that, especially for people that aren't fat, but also for obesity itself. So in men, obesity-driven aromatase elevation in adipose tissue contributes to higher estradiol and lower testosterone levels with metabolic and reproductive consequences. And when we can look at metformin today, it's a widely used insulin sensitizing agent is basically my opinion that it could be a modulator of aromatase

6:15 rather than a suppressor or an inhibitor of aroma taste that may counteract the pro aromatics environment of obesity. So we. Can also look. At AMPK and its role as a master regulator of energy homeostasis. And then also metformin's role in activating AMPK as a molecular link between obesity and some of the issues that come from over-aromatization in people. So in healthy people, fat tissue expresses aromatase at baseline levels regulated by tissue-specific promoters of enzyme to produce small amounts of estrogen.

6:49 In post-menopausal women, fat becomes a primary site of estrogen biosynthesis since ovarian function has ceased. And they also, because they're not using hormone therapy, a lot of times have very low testosterone levels, meaning they have no estrogen levels. Again, they don't have testosterone. Ovarians function had ceased, and because of that, their fat become much more inflamed, so they had much visceral fat on the body. So aromatase expression in adipose is tightly regulated by the hormonal and local factors in that tissue.

7:21 We can look at glutocorticoids and cytokines like interleukin-6 and TNF-alpha to stimulate aromatase transcription via the adepose-specific promoter I.4 while CAMP protein kinase A signaling trigger by factors such as PGE2 and catecholamines can activate promoter of 2.1.3 often associated with pathological or tumor related aromatase expression. And basically obesity, exacerbates this. So enlarged adipocytes and infiltrating macrophages in obese fat form crown-like structures and secrete pro-inflammatory mediators,

7:55 which in turn drive up aromatase expression in local stromal cells. Studies in rodents and humans have shown that inflamed adepose tissue from obese subjects exhibits elevated aromatase mRNA and protein levels, particularly in subcutaneous fat deposits. So when we have inflamed fat, that fat is going to automatically convert more of your testosterone and testosterone, which is interesting too,

8:25 because if you think about injecting subcutaneously into the body fat what's going happen to that testosterone that is getting injected sub-cutaniously? There's a higher amount of fat tissue and the fat tissues is gonna over-aromatize what it normally would even if it was just injected into muscle. So, men with subcutaneous adipose aromatase expression is increasing obesity and correlates with higher estradiol levels and insulin resistance contributing

8:55 to hypogonadism and metabolic issues. And visceral and subq fat are not merely energy stores, but also endocrine sites where aromatase can be dysregulated by metabolic disturbance. So let's look at metformin's effect on aromatase expression in adipose tissue. So, let us look what's going on here. Well, we can look in vitro where it's been studied. It was reported that metormin directly inhibits aromatase in human breast adepose tissues, stromal cells, and again, very fatty tissue there. It also significantly decreased aromatase mRNA in expression that has been induced by CAMP analog foreskin and formal ester without affecting basal levels

9:32 in the body. And notably metformin activated AMPK and upregulated its upstream kinase LKB1 in these cells, correlating with aromatase suppression. Metformine also prevented the nuclear localization of CRTC2, a co-activator that normally enhances arometase transcription in response to CAMPs signaling. And so basically, when we explain that in layman terms, metformin effectively reduce the ability of adipose tissue stromal cells to produce estrogen, suggesting a potential therapeutic strategy to lower local estrogen in obese men and women.

10:03 Importantly, this inhibition appeared context-specific. So a follow-up study found metformin suppresses aromatase driven by tumor-related signals, but not by normal physiological stimuli. It also seems to suppress the aromatase or localized estrogen that would be deleterious to the body, not beneficial to body because a lot of estrogen is beneficial. Also, metformin was shown to markedly reduce aromatase transcripts from the cancer-associated promoters in breast adipose cells stimulated with foreskin

10:33 while having no significant effect on aromatase driven by the normal adepose promoter. So that means that metformin selectively targeted the bad aromatase expression and spared normal adipose aromatase expressions. So not only is it affecting aromas expression of fat tissue, it's expressing in the fat tissues, which is good. This selective inhibition hints that Metformins could act as a breast or fat specific arometase modulator in post-menopausal women but also in obese men

11:03 and women, dampening local estrogen production in at-risk tissues without completely shutting off systemic estrogen synthesis, which is what an aromatase inhibitor does. Now, yes, there are, I guess you could call them breast-specific aromatase-inhibitors. I would stay away from those. Let's keep looking at this. A study in postmenopausal breast cancer rat model demonstrated metformin's aromatase-lowering effects in vivo. Metformins is given to obese and lean rats after menopause, and it significantly suppressed mammary tumor growth compared to controls.

11:37 So mechanistic analysis of the mammary fat pads and tumors revealed that metformin did not alter aromatase levels within the tumor epithelial cells, but it caused a notable reduction in aromate expression in the stromal compartment surrounding the tumors. Specifically met form and treated animals had fewer aroma taste positive cells in tumor border area than control animals. It also selectively decreased the number of CD68 plus macrophages that were positive for aromatase in the tumor microenvironment. So this matters because obesity and weight gain are known to increase infiltration of M2 polarized macophages in adipose tissue and such macraphages exist

12:15 or express aromatase and contribute to local estrogen production in fat tissue. So metformin's ability to reduce these aromatase-producing immune cells suggests it targets the inflammatory component of aromatase dysregulation. So the outcome was lower local estrogen stimulation in the breast tissue, in this case, or the fat tissue. And tumors from metormin-treated rats showed reduced expression of progesterone receptor in ER-regulated gene, indicating decreased estrogen signaling within the tumor environment. Notably ER levels were unchanged, but their activation by estrogen was bunted consistent with diminished aromatase activity in estrogen synthesis in tissue.

12:53 And basically this all supports the fact that metformin in vivo can recapitulate the anti-aromatases effect seen in cells by reducing stromal aromatase and thereby lowering estrogen level in tissues specifically attenuating tumor growth, But also helping with over arometization of our testosterone. Let's look at ovary and lung tissue. So beyond fat tissue, metformin's aromatase modulating actions extend to other estrogen producing tissues, which is relevant for things like PCOS or pulmonary hypertension. In the ovaries, insulin resistance can cause hyperinsulinemia and influence steroidogenesis.

13:31 A notable study on human ovarian granulosa cells found that insulin can directly upregulate aromatase expression and activity in these cells, obviously metforming counter axis. Also, these cells treated with insulin showed increased aromatase. mRNA and estrogen production while metformin significantly blunted both basal and insulin stimulated aromatase expression and enzyme activity in these ovarian cells. So the mechanism was traced to an unexpected pathway and the met formin activated the MEK-ERK signaling cascade, which in turn suppressed transcription

14:09 of key aromates promoters in the granulosa cells, Also using an ERK pathway inhibitor reverse metformin suppression of aromatase confirming that met formins inhibition of aroma taste was mediated by ER K activation. So this is different from the AMPK mediating effects observed in adipose cells indicating tissue specific pathways. Where present and clinically, this may explain part of metformin's benefit in PCOS by lowering insulin and directly inhibiting ovarian aromatase metforming can reduce excess estradiol in the ovariant microenvironment and help normalize the hormone balance, which is going on a lot of times include testosterone,

14:45 progesterone, and estrdiol, in ovaerian environment. We can also, too, look at the lung tissue. Study found that metformin normalized aromatase expression in lung tissue. So in rats with pulmonary hypertension, lung aromatase levels and estrogen concentrations were pathologically elevated. Treating these rats met form and reversed the disease progression and brought lung aroma taste expression back down to normal levels. Metformin also reduces circulating estrogen and the expression of estrogen-related enzymes in the lungs.

15:20 And this highlights that metformins' aromatase-lowering effect is not limited to fat. It can occur in any tissue where aromatase is abnormally elevated due to metabolic or inflammatory dysregulation, and that the core correction of arometase overexpression is part of how metormin exerts its beneficial effects. So this is pretty cool because what metformin is doing is it is helping to lower the expression of aromatase, again, in the fat tissue, but then other tissue where it could overexpress and then cause a hormonal imbalance, basically.

15:51 So we see it in ovaries and we also see in lungs, which is very interesting. Now, let's look at some of the molecular mechanisms linking met formin to aromatase modulation. I talked about AMPK, everyone loves to activate AMP, because it means we're going to burn fat. So metformin is known as an activator of AMP activated protein kinase, otherwise known is AMPk, a cellular energy sensor. Activated AMP can directly influence gene expression and inflammatory pathways in adipose tissue. And research has shown that AMP in concert with upstream kinases, LKB1, like I mentioned before, can inhibit aromatase expression in the adepose stromal cells,

16:28 providing a link between energy metabolism and estrogen synthesis. And then a breast adipose cells metformin induced AMPK activation was correlated with lower aromatase levels. So how does AMP K signaling translate to aromatase repression? One route is through interference with CMP mediated transcription. Aromatases transcription requires the CREB transcription factor and its co-activators. Fossilation of CRTC2 by AMPk retains it in the cytoplasm, thereby blunting CReB driven arometase expression.

16:58 Also, AMPK activation can antagonize mTOR signaling and other growth pathways, potentially reducing the expression of aromatase up-regulators. So the net effect of all this is metformin's AMPk activation shifts adipose tissue towards an anti-estrogenic state by down- regulating the transcription of arromatases. So metformin, let me say that again, met formin by activating AMPK shifts the fat tissue in your body towards an anti-estrogenic state by down-regulating the transcription of aromatase in that fat issue.

17:29 To me, if I wanted to quote unquote manage my estrogen, I would want to do that before I cut off all the estrogen in my body, good or bad. Let's look at the reduction of insulin because this is very important. So metformin's primary clinical action obviously is to improve insulin sensitivity and lower circulating insulin in the body. Chronic hyperinsulinemia is associated with upregulation of rheumatase and estrogen production in various contexts. So high insulin and IGF-1 can enhance rheuma test activity in ovarian granulosa cells and possibly in adipose thromal cells.

18:01 Hyperinsulinemia also contributes to high androgen, low sex hormone binding globulin balance that can increase estrogenic stimulation of tissues. By lowering circulating insulin in the body, Metformin removes a proliferative and pro-aromatase stimulus. So when we have high circulating insulin chronically, that is going to be pro aromatases. Meaning that even if you're not fat, but you are in a state that creates a high insulin environment in the body, you potentially are going aromatize more

18:32 of your testosterone into estrogen. Reducing insulin levels is thought to beneficial in breast cancer prevention and hyperinsulinemia has been linked to higher risk and worse prognosis in that type of cancer. Insulin alone clearly stimulated aromatase expression and metformin negated that effect by activating an alternate pathway to shut down aromatase promoters. So an adipose tissue of insulin resistant individuals, we can extrapolate the met formin by improving insulin sensitivity would reduce insulin-driven signaling cascades that might otherwise enhance arometase gene expression.

19:04 So overall metformin's correction of insulin resistance leads to hormonal environment less favorable for excessive rheumatase activity. We also have its anti-inflammatory effects. So met formin is very well documented to have anti inflammatory properties, specifically in metabolic tissues. does this by inhibiting NF kappa B signaling, reducing macrophage infiltration into adipose tissue, and shifting macophage polarization away from the pro-inflammatory M1 state. So this matters because proinflammatories cytokines and factors like PGE2 are potent upregulators of aromatase in adepose stromal cells.

19:39 So TNF-alpha and interleukin-6 activate the distal promoter 1.4 of the aromatase gene, leading to an increased mRNA transcription in adipose fibroblasts, while PGE2 strongly reduces or induces the proximal-promoter 2. So by attenuating inflammation in the body, metformin indirectly suppresses these aromatase drivers. For example, Metformins treatment in obese rhodom models is shown to lower Tnf-Alpha- and Interleucin 6 levels and reduce the number of infiltrating macrophages into the fat.

20:12 Metformin's ability to reduce aromatase-positive M2 macrophages in the tumor setting shows that dampening inflammation curtails aromatase, and on a molecular level, metformins can inhibit NF-kB via AMPK-dependent mechanisms, thereby reducing cytokine gene expression. It also lowers circulating levels of C-reactive protein and other inflammatory markers. And so by breaking the obesity, inflammation, arometase feedback loop, Metforin dramatically lowers aromas expression and inflamed adipose tissue.

20:42 Now let's talk about the reduction of visceral fat masks. I think this is probably the biggest point in this presentation. Metformin often produces modest weight loss and a preferential reduction in visceral adiposity or visceral fat. So numerous clinical studies and animal experiments have shown that metformins decreases viscera fat stores and adepose tissue mass, likely through adapose-tissue improvement, insulin sensitivity, enhanced fatty acid oxidation, and mild appetite suppression.

21:12 Because total aromatase output from adopose is proportional to the mass of adposed tissue, a reduction of viscereal mass means fewer aromatase-expressing cells overall. Let me explain what that means. For men that over-aromatize testosterone, it's not that you have a genetic predisposition to over aromatized testosterone. It is that, you too much visceral fat. If we modulate the upstream effect of why you're converting too of your testosterone into estrogen to a point we can control how much we aromatize.

21:47 But if you have a lot of visceral fat, if your drinking alcohol, If you're doing things that increase the amount of inflammation expressing in your body, you are going to over aromatize So metformin's visceral fat reduction is accompanied by changes in adipokines. It tends to lower leptin and increase adeponectin. And adaponextin itself may inhibit aroma taste expression or oppose some effects of TNF alpha. In any case, by shrinking the inflamed fat depots, Metformin creates a leaner, metabolic profile, less conducive to aromatase overexpression.

22:18 For example, in children and adolescents, six months of metformin significantly reduced visceral fat and improved insulin sensitivity. Also in rodent models, metforming increased genes for adaptive thermogenesis, showing that reduces visceral fat through adaptive thermal genesis. Thus, beyond its cellular effects, Metformins' whole body effect of fat reduction translates to lower overall aromatase activity and lower estrogen synthesis from adipose tissue. And I will mention the crosstalk with estrogen receptors.

22:48 So while not as directly evidenced as those, metformin may also influence the estrogenic axis by modulating estrogen receptor activity and co-regulator expression. System studies have found that metforming can downregulate ER alpha expression in cancer cells or modulate the ER coactivator co repressor balance, which might indirectly reduce aromatase. Metformins reduction of circulating insulin and IGF-1 also diminishes the cross talk that can amplify ER signaling and aromatase expression, It also might upregulate tumor suppressors like BRCA1 in adipose stromal cells.

23:21 And so basically metformin simultaneously attacks the root cause of aromatase up-regulation, like I just talked about, which is energy surplus, hyperlensinemia, and inflammation. By doing so, it creates a metabolic state where aromatase expression in that post-tissue and other tissues recouples to normal regulatory signals rather than aberrant signals present in obesity or other insulin resistant states. Now, let's look at the consequences of altered aromatase activity. So let us look estrogen production and circulating levels.

23:52 In conditions of aromatase overexpression, like obesity or PCOS, metformin's dampening of aroma taste can lead to measurable declines in estrogen levels, clinical studies have noted that metforme therapy reduces circulating estrogen in certain groups. For instance, a study of postmenopausal women on 1,500 milligrams a day of metiformin observed a 38% reduction in serum estradiol levels over a few months. Another trial found that three grams a day of metformin, which is a good amount, in diopedic postmenopausal women significantly lowered estradiol compared

24:23 to baseline, along with improving metabolic markers. So less aromatase activity means less conversion of adrenal and ovarian androgens into estrogenes. In premenopausal women with PCOS, metformin primarily lowers insulin and ovary and androgen, but by aiding weight loss, it also reduces peripheral aromatization to estrone, which is often elevated in overweight PCO patients. And then in men, Metformins weight and insulin effects can reduce excess arometization of testosterone to estradiol in adipose tissue, potentially improving the testosterone-estrogen ratio.

24:54 Indeed obese men have high estrdiol often have high estradiol that contributes to hypogonadism, weight loss, or metformin therapy can alleviate this by decreasing aromatase in fat. It's also important to note that, because this is important for me because I want healthy estrogen levels, it's important that met formin will not cause abnormally low estrogen. Its effect is normalizing rather than absolute suppression. So, for example, in the pulmonary hypertension study that I was talking about earlier, metformin brought elevated lung and plasma estrogen back to control

25:26 levels but did not drive estrogen below normal. So this is beneficial because patients retain sufficient estrogen for physiological needs while avoiding pathological excess amounts of estrogen. can look at the reproductive and endocrine effects. So in PCOS, where there is an imbalance of sex hormones, metformin's effect on aromatase can have a couple of different implications. On one hand, reducing excessive peripheral aromatization of androgens to estrogen may alleviate the continuous unopposed estrogen exposure of the endometria and potentially reducing the risk of endometric or hyperplasia.

25:59 in women with PCOS. On the other hand, a certain level of estradiol is needed for follicular development and metformin's main benefit for women's PCOs is fertility. However, It restores a normal pattern of aromatase activity in the ovaries by removing the inhibitory effect of high insulin and andrins. So the ovarian granulosa cell findings might initially seem contradictory. Why would one want to inhibit ovariant aromatase? But in PCOS, the issue is not a lack of aroma taste, rather an arrest of follicle development.

26:33 Metformin likely reduces intra-ovarian androgen excess, allowing the follicles to become responsive to FSH and aromatize androgens properly at the right time, which is what we want. We don't want to cut off estrogen. And so by lowering aromatase in the periphery, metformin could reduce estrone, while the cyclic estradiol can normalize. Also, for metabolic outcomes, this is very, very important. So aromatase activity itself might feed into metabolic regulation. There's evidence that higher aromates and adipose can improve insulin sensitivity as estrogen acts locally to curtail inflammation.

27:10 Wait a second. For instance, one study found that increasing adepose arometase in male mice reduced inflammation and improved insulin's sensitivity. So, what does this suggest? That too much aromatase is bad, but too little can also be metabolically unfavorable. So metformin's role here is to balance. It reduces the pathological overshoot of aromatase without eliminating normal estrogen production. In doing so, it likely maintains the beneficial metabolic effects of estrogen, such as fat loss, because met formin, or excuse me, met forma does, estrogen does help with fat-loss.

27:41 When I've crashed my estrogen it is way harder to lose fat, while preventing the deleterious effects So clinical data indicates that metformin's net effect is positive by cutting down aromatase in the context of obesity. It aids weight loss, reduces inflammation, and improves insulin action. And also, lower estrogen from fat may help break the cycle of adipose tissue expansion because estrogen can promote adepogenesis under some conditions. And so in men, reducing aromatase can elevate testosterone, which supports lean mass and insulin sensitivity.

28:11 And indeed, metformin is reported to moderately raise testosterone in obese, insulin-resistant men likely via this mechanism. Well, so much for met formin shutting down your testosterone production because there are studies to show that in fat men it actually increases testosterone reduction, because of the reason we just mentioned. Just to sum up, metformin modulates, again it doesn't suppress, it modulate aromatase expression in adipose tissue to correct abnormal estrogen production, which a lot of men and women suffer from now because they are too fat.

28:42 Metformine influences the estrogen axis, leading to reduced estrogen levels in hyperestrogenic states. Metformin also improves insulin resistance and dampens inflammatory signaling, promoting endoquine equilibrium. And there is research to suggest that the use of metformine in targeting rheumatase offers metabolic benefits to make us healthier. So that is it for the slides. That is the ultimate paddle of Met formin versus estrogen. Obviously you can see the very tight dance or tight rope that we have to walk with estrogen as men and as women too.

29:21 A lot of men unfortunately still think that you need to suppress estrogen into some certain confined constricted range, which oftentimes is too low. And to that, I would say rather than doing that why not control the upstream effects that lead to the appropriate amount of downstream estrogen in the body. The way we do that is we get rid of inflammation. We get grid of visceral fat on the body. The more inflammation you have, the more you're going to turn testosterone into estrogen.

29:55 and you're injecting testosterone, 200 milligrams a week of testosterone and your drink alcohol and are above 15% body fat, you will have high estrogen symptoms because you have a lot of visceral fat inflammatory fat on your body that is taking that testosterone. And it is converting way more of it into estrogen than you need to. You do not need block the estrogen. you do need fix the problem which is that you too much viseral fat and too inflammation in the body. Most men under 10% body fat that are healthy, because you can be too low body, fat, most men that run to 10%, body that never have to worry about estrogen

30:32 on testosterone. And that's for instance, why someone like me can take up to 750 milligrams of testosterone per week. You're not really worried about what I'm converting into estrogen because I don't have visceral fat on my body. So my is not in a state that it over-expresses aromatase that causes a lot of that testosterone to be converted into estrogens. That's kind of the hill that I die on in this video, I guess, is that the more fat you have on your body, the worse it's going to be for you if you're supplementing with testosterone. And if your injecting sub-Q into the fat tissue, it is going be even that much worse because if have a lot of inflammatory fat that you are inject to subcutaneously,

31:09 then you going have the problem that we just talked about today. I'd love to hear you guys' thoughts and feedback on this one. I have been going around saying that if anyone gets off their enrollment test inhibitor and starts using Metformin, please let me know. Or if you did, leave them in the comments below so other people can see, because this is one of those things, you know, it would be easier if I had more

31:39 backup to say this, cause it's kind of a theory that I have. And I think if more guys switched over from the aromatase inhibitor to metformin, they would get the same desired effect without the negative consequences of the rheomatases inhibitors. In a lot of cases too, your inhibiting estrogen in your brain, and that's why a lotta guys appear to have roid rage. It's because they're actually inhibitting estrogen. the brain that makes them kind of crazy. And then they respond to comments, they responded to crazy comments and like get up in arms about it. Whereas when you have a lot of estrogen or not a Things don't really bother you and you're in a good mood almost all the time,

32:12 like I am. So anyway, I appreciate you guys so much. Again, leave your thoughts, comments. This one was kind of like a swing in the dark to see if it would be something that people enjoy listening to and watching. I appreciated your feedback on this one. Or if you just say, Hunter, go back to only doing videos about peptides. Probably won't do that, but I still got to throw some of these hormone videos in there. Cause it's so important. So, uh, again, I thank you guys so much. I appreciate you. You guys, so I have so gratitude in my heart for everyone that supports the channel. Love all of you out there to listen to this.

32:43 And again any way that you can support the. Like comment, subscribe, sign up for the email list, buy the products, all that stuff. Appreciate it so. Much more than you'll ever know. Thank you so, much and I'll see you in the next one. Peace.