The mechanism that makes dry fasting categorically different from water fasting is endogenous metabolic water production. When you deny the body exogenous water, it's forced to generate its own water by oxidizing fat at an accelerated rate. Every 100g of fat your body burns produces roughly 107g of metabolic water. This metabolic water is deuterium-depleted compared to tap water, spring water, or basically any exogenous water source you'd be drinking. Your mitochondria are literally manufacturing clean, light water from your own fat stores to keep you alive, and that water spins through the ATP synthase nanomotor without the kinetic drag that deuterium-enriched water creates.
This is why dry fasting burns fat at roughly 3x the rate of water fasting. Your body has no choice but to ramp up lipolysis dramatically because hydration depends on it. The fat loss isn't just a caloric deficit effect, it's a survival driven metabolic acceleration that water fasting simply cannot replicate because the body has no urgency to oxidize fat for water when you're handing it water exogenously.
At the cellular level, dry fasting also creates a more aggressive autophagic environment. Cells that are damaged, dysfunctional, or infected cannot compete for the limited intracellular water supply. Healthy cells with intact membranes and functioning aquaporins outcompete sick cells for available water, which means the weak and damaged cells dehydrate and get tagged for autophagy faster than they would under water fasting conditions. Every inflammatory process in the body requires water, and when you restrict water availability, inflammation gets choked out at the source because the inflammatory cascade literally cannot sustain itself without adequate hydration at the tissue level.
Good morning! Is there a way to tell if someone is a hyper responder to DHT esters, average responder or a low responder? Similar to how with Test esters there’s hyper, average and low/non responders. For example if someone took 125mg/week of Test Cyp and their serum Total Test was 1600ng/dL you could say that they’re a hyper responder.
I kept wondering the last couple weeks why in all the DHT articles that there isn’t serum DHT level recommendations, but instead just dose recommendations. But I just reread your DHT Esters: The Complete Guide download yesterday and found on pg 52 “why serum levels can be misleading”. So that’s because they don’t show androgenic activity in your tissues. So now I understand why the dose recommendations.
Basically why I’m also really wondering is I took 75mg DHTE(allegedly) weekly EOD dosing for 6 weeks and got a serum DHT trough level of 407ng/dL. Was wondering if there is anyway to tell if that’s an average or maybe higher response? coupled with maybe the positive benefits I’ve felt with it also? Is there enough data gathered within the DHT community that you’re in, to maybe say at least for serum levels that this is an average or above response to that dose? Or maybe not enough data yet or more info needed?
Thanks and sorry for the long question(s). I didn’t really know how else to word/ask this so I just kinda kept going haha.
Gmulungu and dont apologize for the long question because this is actually one of the better ones ive gotten and it touches on something the entire dht ester community needs to understand before anyone tries to build responder categories off bloodwork
short answer is no, we cant reliably categorize dht ester responders into hyper/average/low the way we do with testosterone, and the reasons go way deeper than "we dont have enough data yet." honestly we cant even categorize testosterone hyper responders in any meaningful way either unless your definition of hyperresponse is "most serum test per mg injected" which has absolutely nothing to do with the actual androgenic response happening in your tissues. thats just pharmacokinetic clearance rate, it tells you how fast your body processes the ester depot, not how much work the hormone is doing once it arrives at a receptor. the entire conceptual framework of using serum levels as a proxy for response quality is broken for testosterone and its catastrophically broken for dht because dht adds multiple additional layers of disconnection between what shows up on your blood draw and what your tissues are actually experiencing.
With testosterone people get away with the serum framework because testosterone is primarily endocrine, it circulates in meaningful concentrations, and serum measurement at least roughly correlates with tissue exposure even though that correlation is weaker than most guys realize. you can say 125mg test cyp producing 1600 ng/dL total T is a "hyper response" and everyone nods along because we have decades of pharmaceutical grade data from millions of men to build population distribution curves against, but even that guy with 1600 on 125mg could be getting less actual androgenic output than a guy sitting at 900 on the same dose if the first guy has long CAG repeats and garbage AR density while the second guy has short repeats and a fuckton of muscle tissue pulling hormone into productive use. we just collectively ignore that because for testosterone the serum number is at least in the right ballpark most of the time dht breaks that entire framework in ways that make the ballpark irrelevant. dht is predominantly paracrine meaning the majority of dht produced or delivered to target tissues gets metabolized to androstanediols, androsterone, and other neurosteroid metabolites before it ever reaches the bloodstream. your serum number captures the leftovers that escaped local metabolism rather than the total androgenic signal your tissues actually received.
A comprehensive review on dht physiology confirmed this directly, intracellular concentrations of androgens particularly in androgen sensitive tissues are essentially independent of circulating levels. nih two guys can have identical serum dht on the same dose while having completely different tissue level androgenic activity depending on how efficiently their tissues are pulling the hormone in and utilizing it
now heres where it gets really important and where i should have started in the first place
the relationship between serum androgen levels and actual androgenic response is modulated by androgen receptor sensitivity AND androgen receptor density, and both variables can make higher serum levels indicate worse tissue utilization rather than better. this is the insulin resistance analogy and it applies to every androgen including testosterone, its just that dht's paracrine nature makes the problem dramatically worse
AR CAG repeat length determines how hard each individual receptor fires when dht binds it. shorter CAG repeats mean higher transactivation activity per binding event, longer repeats mean the receptor binds the ligand but doesnt drive transcription as efficiently. the research on this is unambiguous across multiple large population studies. free testosterone increased progressively with CAG repeat length across over 2600 healthy men, and the variability in serum FT was underlain in part by differences in androgen sensitivity and feedback set point with a contributory role of AR polymorphism. PubMed men with longer CAG repeats had 10-14% higher circulating free testosterone than men with shorter repeats. testosterone and LH levels are higher in men with longer AR CAG, probably reflecting reduced negative feedback through a less sensitive receptor. PubMed
the mechanism is straightforward. a less sensitive AR means less efficient negative feedback at the hypothalamus and pituitary so the HPTA doesnt suppress as hard, endogenous production stays higher, and more hormone accumulates in circulation because tissues arent clearing it as aggressively through receptor mediated uptake. the clinical consequence is that men with normal testosterone concentrations who had longer AR CAG repeat lengths showed significantly higher risk of developing andropausal symptoms compared to those with shorter repeats. PubMed symptomatic androgen deficiency at perfectly normal serum levels because the receptor cant do its job efficiently. the serum number lies to you and it lies to every guy on bodybuilding misc who posts his bloodwork like a trophy without knowing his CAG genotype
applied to your question, a guy with short CAG repeats is pulling dht out of serum and into tissues efficiently, his receptors are grabbing the ligand translocating to the nucleus and cranking through transcription at a higher rate per molecule. his serum dht reads lower because the hormone is being utilized. meanwhile a guy with long CAG repeats has receptors that are less transcriptionally active per binding event so more dht stays circulating because the tissues arent clearing it as aggressively, AND reduced negative feedback means endogenous production stays higher on top of the exogenous dose. his serum dht looks impressive on paper while his tissues are extracting less functional androgenic output per nanogram. the guy who posts "407 ng/dL serum dht on 75mg, am i a hyper responder?" could be getting more or less actual tissue response than a guy posting 200 ng/dL on the same dose and there is literally no way to tell from bloodwork alone
AR expression density is the other half and it determines how many receptors exist to fire in the first place. CAG repeat length tells you how efficiently each receptor works, AR density tells you how many receptors are even there, and they interact multiplicatively not additively. a guy with short CAG repeats AND high AR density is extracting maximum androgenic signal per nanogram of circulating dht while a guy with long CAG repeats AND low AR expression is functionally deaf to androgens leaving more in serum with less of it doing anything useful at the genomic level. same blood draw, completely opposite biological realities
Three factors control AR expression density and all three are actionable
androgen exposure multiplied by time creates a virtuous cycle because AR expression is itself androgen regulated meaning sustained AR activation upregulates AR protein levels through translational autoinduction. the more consistently you maintain adequate androgen signaling the more receptors your tissues express to receive that signal. this is why men on stable TRT for years often report continued improvement even at the same dose, because AR density is climbing and each milligram hits more targets. its also why prolonged hypogonadism or years of crushed dht from finasteride creates a receptor deficit that takes months to fully reverse. a guy coming off years of adequate androgen exposure has a fundamentally different tissue response to 75mg DHTE than a guy whos been hypogonadal even if their serum dht comes back identical
muscle mass is almost comically underappreciated and this is where the looksmaxxing crowd needs to pay attention. skeletal muscle is the largest androgen responsive organ in the body by sheer mass. more muscle tissue means more total AR protein, more total binding capacity, and faster clearance of androgens from serum into tissues where the hormone actually does work. two guys on identical dht ester doses with identical CAG repeats but a 30lb difference in lean mass are running fundamentally different pharmacokinetic profiles because the guy with more muscle has a larger androgen sink pulling dht out of circulation. this compounds over time too, as you add lean mass from the dht protocol youre adding AR expressing tissue that increases your capacity to utilize the same dose which drives further improvements which adds more tissue.
Eliminating AR downregulators is the third leg and its the one most guys completely ignore while obsessing over dose optimization. chronic estrogen dominance downregulates AR expression. sustained supraphysiological glucocorticoids from chronic stress suppress AR transcription. chronic inflammation and elevated TNF-alpha reduce AR density in target tissues. insulin resistance impairs AR expression in muscle specifically. sleep deprivation. you can have great genetics with short CAG repeats and solid lean mass but if youre chronically stressed sleeping five hours drinking regularly and systemically inflamed your AR population is being actively suppressed and your tissue utilization of whatever you inject is degraded at the receptor level before it even gets to transcription
this is why we never shut up about foundation before pharmacology. circadian optimization, mineral status, gut integrity, body composition, stress management, all of that boring unsexy shit is literally building the receptor infrastructure that determines whether your dht ester protocol works well or works poorly. pinning exogenous androgens into a body with downregulated AR from lifestyle factors is like upgrading your internet plan while your router is broken
on top of all that the dht specific 5AR feedforward loop means your pharmacokinetics are a moving target across the entire duration of the protocol. if youve been running DHTE for six weeks your 5AR is already upregulating which means your endogenous testosterone to dht conversion is climbing in the background on top of your exogenous dose. your week six serum dht reflects both the exogenous ester AND whatever additional endogenous dht your upregulated 5AR is producing from your own testosterone. that moving target doesnt exist with exogenous testosterone because testosterone doesnt feedforward upregulate its own synthesis enzyme so a trough at week two and a trough at week six on the same dose are not comparable data points even within the same individual
And then theres UGL product variability which is extreme right now. You flagged "allegedly" and thats the right instinct. assay methodology matters too because masteron shows up as dht on immunoassay but not on LC-MS/MS so confirm which method your lab used. if that 407 came back on LC-MS/MS thats a strong product authenticity signal
so your 407 ng/dL serum dht at trough on 75mg DHTE weekly cannot be interpreted as good or bad response in isolation because serum dht and quality of androgenic response are potentially inversely correlated depending on your AR genetics and expression levels. that number could mean your tissues are efficiently saturated with overflow spilling into circulation, or it could mean your AR has longer CAG repeats with reduced transactivation capacity and lower expression density so your tissues arent pulling dht in as aggressively leaving more in serum while extracting less functional output per molecule. same number on the lab printout, two completely opposite biological realities, and standard bloodwork cannot distinguish between them.
Thank you so much for this very detailed and informative answer. You’ve answered all my questions and then some. Gonna see what method my lab used for my DHT level right away, that’s very interesting that Masteron shows up on the immunoassay method. I’ll never look at my Test and DHT levels the same again well using exogenous hormones haha
Not yet, I’m in Canada and unfortunately it’s not as simple as just calling up the lab and asking. There’s only 1-2 hospitals in the country that can preform the DHT blood test, whatever lab you get bloods pulled at has to send it to them. I have to get the original doctor that gave me the DHT blood requisition to call this hospital and ask. I can’t call them myself and docs are mad slow in this country. I’ll try to remember to post an update when I eventually find out
If DHT E upregulates 5ar. How long does it take for noticeable upregulation on lets say 125mg a week? Also if the DHT/Test ratio gets more favorable due to 5ar upregulation. Would this supress estrogen to the point that local DHT overpowers Estrogen in the growth plate chondrocyte. And would thus delay fusion or improve the growth environment?
1 question per Q&A guys! It depends on a lot of factors. mostly DHT to E2 ratios. We don't advise running DHT esters for 5AR upregulation purposes because even though they work well, if you're not getting constant blood panels and don't have exogenous e2 and adrenal support on hand to be deployed instantly, you can run into a ton of undesirable issues. get truly lean (12% deep 6 pack abs) and strong (3 plate bench, 4 plate squat, 5 plate deadlift) before you even think about epigenetically hacking your 5AR. chances are if you just get lean and strength train, you'll have high AF DHT, naturally, the right way, in superior form, without sides.
We really don't advise using DHTE without medical supervision bro. Ebook came out because there are UGLs selling it and we don't want people to get more hurt than they're already going to. But it's not an endorsement. dutasteride's half life is long, yes. but it's not like that makes a difference to whether or not you could use dht e. it might make it less effective since it actually does block AR
Grok says Testosterone cream on scrotum increases DHT significantly is this true? Trying to avoid pinning DHT & adding Teat cream. Now already on 100mg/wk TestC resulting in 760 Total T; 186 Free T; 40 DHT
Im an organic beef and small crop farmer. Recently got into freeze drying and trying to make replacements for majority of my mineral and vitamin, supps. Im doing beef thymus, heart, and liver caps and a variety of heavily mineralized young plants like nettle, dandelion, clover, and purslane. I use grok to try to figure out concentration approximations. Guess my question is do you think i need less absolute mg of plant mineralization since uptake is probably higher? For example can i get by with 300mg of magnesium in plant powder forms over say 500 mg of magnesium glycinate?
Sure thing! days in the life are HORRIBLE rn and goes against everything we believe in, but we're grinding hard on releasing a bunch of stuff for you guys.
What is your go to protocol at the very first signs of illness if the goal is to do everything realistically worth doing to either stop it early or get over it as fast as possible?
always have thymosin alpha 1 on hand. we take a big dose right when we realize we're getting sick. spend all the time we can in sun, and chroma trinity if supplemental is needed. will specifically also get oysters for antiviral properties and to increase thymic function. this is also when you make sure you're magnesium sufficient and patch up any other nutrient deficiencies with supplements as necessary. we spam tablespoons of blackseed oil 2-3x a day too. bone broth for glycine/collagen. liposomal vit C supp. NAC before bed if really starting to get sick. and tons of rest. cancel activities and make sure to keep stress LOW.
Idk what you mean TRT plus levels? what's your baseline? if you are going from guevedoce levels to 200ng/dl then you should notice something impressive. but of course it gets insane and tren-like when you go much higher than that. you just can't really run that for more than a month or 2 without serious side effects and damage to your health
I meant HRT plus in the same sense you use it in your guide to exogenous Dht esters so low dose androgen replacement therapy eg DHT enanthate 5 to 50 mg per week.
Best supplements to take while bulking,is there anything good to take(maybe berberine for insulin sens) ,i went from 10% to 14%,want to bulk up more because i always wanted to set some PR on couple of lifts
Haha, probably time to cut. uh supplements isn't going to change too much. perfect scenario is you eat at maintenance with high protein, keep sets at 5 reps to failure, increase 5 lbs every session, and your lifts will go up while you lean out and stay the same weight :)
Would love a post about fasting and how to optimize it, both dry and wet fasts. How to prep, how long for max benefit, how to break, etc.
If you have time, you can just answer those about 3 questions for a dry fast.
Thank you!
The mechanism that makes dry fasting categorically different from water fasting is endogenous metabolic water production. When you deny the body exogenous water, it's forced to generate its own water by oxidizing fat at an accelerated rate. Every 100g of fat your body burns produces roughly 107g of metabolic water. This metabolic water is deuterium-depleted compared to tap water, spring water, or basically any exogenous water source you'd be drinking. Your mitochondria are literally manufacturing clean, light water from your own fat stores to keep you alive, and that water spins through the ATP synthase nanomotor without the kinetic drag that deuterium-enriched water creates.
This is why dry fasting burns fat at roughly 3x the rate of water fasting. Your body has no choice but to ramp up lipolysis dramatically because hydration depends on it. The fat loss isn't just a caloric deficit effect, it's a survival driven metabolic acceleration that water fasting simply cannot replicate because the body has no urgency to oxidize fat for water when you're handing it water exogenously.
At the cellular level, dry fasting also creates a more aggressive autophagic environment. Cells that are damaged, dysfunctional, or infected cannot compete for the limited intracellular water supply. Healthy cells with intact membranes and functioning aquaporins outcompete sick cells for available water, which means the weak and damaged cells dehydrate and get tagged for autophagy faster than they would under water fasting conditions. Every inflammatory process in the body requires water, and when you restrict water availability, inflammation gets choked out at the source because the inflammatory cascade literally cannot sustain itself without adequate hydration at the tissue level.
Good morning! Is there a way to tell if someone is a hyper responder to DHT esters, average responder or a low responder? Similar to how with Test esters there’s hyper, average and low/non responders. For example if someone took 125mg/week of Test Cyp and their serum Total Test was 1600ng/dL you could say that they’re a hyper responder.
I kept wondering the last couple weeks why in all the DHT articles that there isn’t serum DHT level recommendations, but instead just dose recommendations. But I just reread your DHT Esters: The Complete Guide download yesterday and found on pg 52 “why serum levels can be misleading”. So that’s because they don’t show androgenic activity in your tissues. So now I understand why the dose recommendations.
Basically why I’m also really wondering is I took 75mg DHTE(allegedly) weekly EOD dosing for 6 weeks and got a serum DHT trough level of 407ng/dL. Was wondering if there is anyway to tell if that’s an average or maybe higher response? coupled with maybe the positive benefits I’ve felt with it also? Is there enough data gathered within the DHT community that you’re in, to maybe say at least for serum levels that this is an average or above response to that dose? Or maybe not enough data yet or more info needed?
Thanks and sorry for the long question(s). I didn’t really know how else to word/ask this so I just kinda kept going haha.
Gmulungu and dont apologize for the long question because this is actually one of the better ones ive gotten and it touches on something the entire dht ester community needs to understand before anyone tries to build responder categories off bloodwork
short answer is no, we cant reliably categorize dht ester responders into hyper/average/low the way we do with testosterone, and the reasons go way deeper than "we dont have enough data yet." honestly we cant even categorize testosterone hyper responders in any meaningful way either unless your definition of hyperresponse is "most serum test per mg injected" which has absolutely nothing to do with the actual androgenic response happening in your tissues. thats just pharmacokinetic clearance rate, it tells you how fast your body processes the ester depot, not how much work the hormone is doing once it arrives at a receptor. the entire conceptual framework of using serum levels as a proxy for response quality is broken for testosterone and its catastrophically broken for dht because dht adds multiple additional layers of disconnection between what shows up on your blood draw and what your tissues are actually experiencing.
With testosterone people get away with the serum framework because testosterone is primarily endocrine, it circulates in meaningful concentrations, and serum measurement at least roughly correlates with tissue exposure even though that correlation is weaker than most guys realize. you can say 125mg test cyp producing 1600 ng/dL total T is a "hyper response" and everyone nods along because we have decades of pharmaceutical grade data from millions of men to build population distribution curves against, but even that guy with 1600 on 125mg could be getting less actual androgenic output than a guy sitting at 900 on the same dose if the first guy has long CAG repeats and garbage AR density while the second guy has short repeats and a fuckton of muscle tissue pulling hormone into productive use. we just collectively ignore that because for testosterone the serum number is at least in the right ballpark most of the time dht breaks that entire framework in ways that make the ballpark irrelevant. dht is predominantly paracrine meaning the majority of dht produced or delivered to target tissues gets metabolized to androstanediols, androsterone, and other neurosteroid metabolites before it ever reaches the bloodstream. your serum number captures the leftovers that escaped local metabolism rather than the total androgenic signal your tissues actually received.
A comprehensive review on dht physiology confirmed this directly, intracellular concentrations of androgens particularly in androgen sensitive tissues are essentially independent of circulating levels. nih two guys can have identical serum dht on the same dose while having completely different tissue level androgenic activity depending on how efficiently their tissues are pulling the hormone in and utilizing it
now heres where it gets really important and where i should have started in the first place
the relationship between serum androgen levels and actual androgenic response is modulated by androgen receptor sensitivity AND androgen receptor density, and both variables can make higher serum levels indicate worse tissue utilization rather than better. this is the insulin resistance analogy and it applies to every androgen including testosterone, its just that dht's paracrine nature makes the problem dramatically worse
AR CAG repeat length determines how hard each individual receptor fires when dht binds it. shorter CAG repeats mean higher transactivation activity per binding event, longer repeats mean the receptor binds the ligand but doesnt drive transcription as efficiently. the research on this is unambiguous across multiple large population studies. free testosterone increased progressively with CAG repeat length across over 2600 healthy men, and the variability in serum FT was underlain in part by differences in androgen sensitivity and feedback set point with a contributory role of AR polymorphism. PubMed men with longer CAG repeats had 10-14% higher circulating free testosterone than men with shorter repeats. testosterone and LH levels are higher in men with longer AR CAG, probably reflecting reduced negative feedback through a less sensitive receptor. PubMed
the mechanism is straightforward. a less sensitive AR means less efficient negative feedback at the hypothalamus and pituitary so the HPTA doesnt suppress as hard, endogenous production stays higher, and more hormone accumulates in circulation because tissues arent clearing it as aggressively through receptor mediated uptake. the clinical consequence is that men with normal testosterone concentrations who had longer AR CAG repeat lengths showed significantly higher risk of developing andropausal symptoms compared to those with shorter repeats. PubMed symptomatic androgen deficiency at perfectly normal serum levels because the receptor cant do its job efficiently. the serum number lies to you and it lies to every guy on bodybuilding misc who posts his bloodwork like a trophy without knowing his CAG genotype
applied to your question, a guy with short CAG repeats is pulling dht out of serum and into tissues efficiently, his receptors are grabbing the ligand translocating to the nucleus and cranking through transcription at a higher rate per molecule. his serum dht reads lower because the hormone is being utilized. meanwhile a guy with long CAG repeats has receptors that are less transcriptionally active per binding event so more dht stays circulating because the tissues arent clearing it as aggressively, AND reduced negative feedback means endogenous production stays higher on top of the exogenous dose. his serum dht looks impressive on paper while his tissues are extracting less functional androgenic output per nanogram. the guy who posts "407 ng/dL serum dht on 75mg, am i a hyper responder?" could be getting more or less actual tissue response than a guy posting 200 ng/dL on the same dose and there is literally no way to tell from bloodwork alone
AR expression density is the other half and it determines how many receptors exist to fire in the first place. CAG repeat length tells you how efficiently each receptor works, AR density tells you how many receptors are even there, and they interact multiplicatively not additively. a guy with short CAG repeats AND high AR density is extracting maximum androgenic signal per nanogram of circulating dht while a guy with long CAG repeats AND low AR expression is functionally deaf to androgens leaving more in serum with less of it doing anything useful at the genomic level. same blood draw, completely opposite biological realities
Three factors control AR expression density and all three are actionable
androgen exposure multiplied by time creates a virtuous cycle because AR expression is itself androgen regulated meaning sustained AR activation upregulates AR protein levels through translational autoinduction. the more consistently you maintain adequate androgen signaling the more receptors your tissues express to receive that signal. this is why men on stable TRT for years often report continued improvement even at the same dose, because AR density is climbing and each milligram hits more targets. its also why prolonged hypogonadism or years of crushed dht from finasteride creates a receptor deficit that takes months to fully reverse. a guy coming off years of adequate androgen exposure has a fundamentally different tissue response to 75mg DHTE than a guy whos been hypogonadal even if their serum dht comes back identical
muscle mass is almost comically underappreciated and this is where the looksmaxxing crowd needs to pay attention. skeletal muscle is the largest androgen responsive organ in the body by sheer mass. more muscle tissue means more total AR protein, more total binding capacity, and faster clearance of androgens from serum into tissues where the hormone actually does work. two guys on identical dht ester doses with identical CAG repeats but a 30lb difference in lean mass are running fundamentally different pharmacokinetic profiles because the guy with more muscle has a larger androgen sink pulling dht out of circulation. this compounds over time too, as you add lean mass from the dht protocol youre adding AR expressing tissue that increases your capacity to utilize the same dose which drives further improvements which adds more tissue.
Eliminating AR downregulators is the third leg and its the one most guys completely ignore while obsessing over dose optimization. chronic estrogen dominance downregulates AR expression. sustained supraphysiological glucocorticoids from chronic stress suppress AR transcription. chronic inflammation and elevated TNF-alpha reduce AR density in target tissues. insulin resistance impairs AR expression in muscle specifically. sleep deprivation. you can have great genetics with short CAG repeats and solid lean mass but if youre chronically stressed sleeping five hours drinking regularly and systemically inflamed your AR population is being actively suppressed and your tissue utilization of whatever you inject is degraded at the receptor level before it even gets to transcription
this is why we never shut up about foundation before pharmacology. circadian optimization, mineral status, gut integrity, body composition, stress management, all of that boring unsexy shit is literally building the receptor infrastructure that determines whether your dht ester protocol works well or works poorly. pinning exogenous androgens into a body with downregulated AR from lifestyle factors is like upgrading your internet plan while your router is broken
on top of all that the dht specific 5AR feedforward loop means your pharmacokinetics are a moving target across the entire duration of the protocol. if youve been running DHTE for six weeks your 5AR is already upregulating which means your endogenous testosterone to dht conversion is climbing in the background on top of your exogenous dose. your week six serum dht reflects both the exogenous ester AND whatever additional endogenous dht your upregulated 5AR is producing from your own testosterone. that moving target doesnt exist with exogenous testosterone because testosterone doesnt feedforward upregulate its own synthesis enzyme so a trough at week two and a trough at week six on the same dose are not comparable data points even within the same individual
And then theres UGL product variability which is extreme right now. You flagged "allegedly" and thats the right instinct. assay methodology matters too because masteron shows up as dht on immunoassay but not on LC-MS/MS so confirm which method your lab used. if that 407 came back on LC-MS/MS thats a strong product authenticity signal
so your 407 ng/dL serum dht at trough on 75mg DHTE weekly cannot be interpreted as good or bad response in isolation because serum dht and quality of androgenic response are potentially inversely correlated depending on your AR genetics and expression levels. that number could mean your tissues are efficiently saturated with overflow spilling into circulation, or it could mean your AR has longer CAG repeats with reduced transactivation capacity and lower expression density so your tissues arent pulling dht in as aggressively leaving more in serum while extracting less functional output per molecule. same number on the lab printout, two completely opposite biological realities, and standard bloodwork cannot distinguish between them.
Thank you so much for this very detailed and informative answer. You’ve answered all my questions and then some. Gonna see what method my lab used for my DHT level right away, that’s very interesting that Masteron shows up on the immunoassay method. I’ll never look at my Test and DHT levels the same again well using exogenous hormones haha
Did you figure out which method it was?
Not yet, I’m in Canada and unfortunately it’s not as simple as just calling up the lab and asking. There’s only 1-2 hospitals in the country that can preform the DHT blood test, whatever lab you get bloods pulled at has to send it to them. I have to get the original doctor that gave me the DHT blood requisition to call this hospital and ask. I can’t call them myself and docs are mad slow in this country. I’ll try to remember to post an update when I eventually find out
Most labs are doing LC/MS , but in some countries they really mess up on DHT
If DHT E upregulates 5ar. How long does it take for noticeable upregulation on lets say 125mg a week? Also if the DHT/Test ratio gets more favorable due to 5ar upregulation. Would this supress estrogen to the point that local DHT overpowers Estrogen in the growth plate chondrocyte. And would thus delay fusion or improve the growth environment?
1 question per Q&A guys! It depends on a lot of factors. mostly DHT to E2 ratios. We don't advise running DHT esters for 5AR upregulation purposes because even though they work well, if you're not getting constant blood panels and don't have exogenous e2 and adrenal support on hand to be deployed instantly, you can run into a ton of undesirable issues. get truly lean (12% deep 6 pack abs) and strong (3 plate bench, 4 plate squat, 5 plate deadlift) before you even think about epigenetically hacking your 5AR. chances are if you just get lean and strength train, you'll have high AF DHT, naturally, the right way, in superior form, without sides.
If you take dutasteride how long after you come off can you start using DHTE
We really don't advise using DHTE without medical supervision bro. Ebook came out because there are UGLs selling it and we don't want people to get more hurt than they're already going to. But it's not an endorsement. dutasteride's half life is long, yes. but it's not like that makes a difference to whether or not you could use dht e. it might make it less effective since it actually does block AR
Bloodwork came back showing very high levels of the Covid spike protein. Anything I can do to fix this? Planning on doing one or two rounds of TPE.
Did you see the answer to this on last Q&A
My bad! I’m on it
I seek to improve my lab rat's size. How would my lab rat PCT off of a solo DHT:E2V cycle that was sub-200 mg DHT/week?
Grok says Testosterone cream on scrotum increases DHT significantly is this true? Trying to avoid pinning DHT & adding Teat cream. Now already on 100mg/wk TestC resulting in 760 Total T; 186 Free T; 40 DHT
Im an organic beef and small crop farmer. Recently got into freeze drying and trying to make replacements for majority of my mineral and vitamin, supps. Im doing beef thymus, heart, and liver caps and a variety of heavily mineralized young plants like nettle, dandelion, clover, and purslane. I use grok to try to figure out concentration approximations. Guess my question is do you think i need less absolute mg of plant mineralization since uptake is probably higher? For example can i get by with 300mg of magnesium in plant powder forms over say 500 mg of magnesium glycinate?
I just signed up-how can I get a access to the DHT esters E book
When is the best time to use HGH - before bed or in morning fasted?
morning before fasted if you want more fat loss
fasted cardio
Could the same be for Tesa?
What do you recommend if someone has parasites
Dry fasting regularly, Black Seed Oil, redacted seeds or ivermectin, doctor...
Best way to prevent graying of hair?
honestly bro, same exact stuff as preventing hair loss! stress, nutrition, circadian, light
Can we get another Day in the Life? Maybe targeted at getting back into a routine of light/nutrition maxxing?
Sure thing! days in the life are HORRIBLE rn and goes against everything we believe in, but we're grinding hard on releasing a bunch of stuff for you guys.
What is your go to protocol at the very first signs of illness if the goal is to do everything realistically worth doing to either stop it early or get over it as fast as possible?
always have thymosin alpha 1 on hand. we take a big dose right when we realize we're getting sick. spend all the time we can in sun, and chroma trinity if supplemental is needed. will specifically also get oysters for antiviral properties and to increase thymic function. this is also when you make sure you're magnesium sufficient and patch up any other nutrient deficiencies with supplements as necessary. we spam tablespoons of blackseed oil 2-3x a day too. bone broth for glycine/collagen. liposomal vit C supp. NAC before bed if really starting to get sick. and tons of rest. cancel activities and make sure to keep stress LOW.
At what level of DHT supplementation do the lipolytic effects become evident? At TRT plus levels or only at supraphysiological levels.
Idk what you mean TRT plus levels? what's your baseline? if you are going from guevedoce levels to 200ng/dl then you should notice something impressive. but of course it gets insane and tren-like when you go much higher than that. you just can't really run that for more than a month or 2 without serious side effects and damage to your health
I meant HRT plus in the same sense you use it in your guide to exogenous Dht esters so low dose androgen replacement therapy eg DHT enanthate 5 to 50 mg per week.
Best supplements to take while bulking,is there anything good to take(maybe berberine for insulin sens) ,i went from 10% to 14%,want to bulk up more because i always wanted to set some PR on couple of lifts
Haha, probably time to cut. uh supplements isn't going to change too much. perfect scenario is you eat at maintenance with high protein, keep sets at 5 reps to failure, increase 5 lbs every session, and your lifts will go up while you lean out and stay the same weight :)