The majority of us here want to return to normal. We are not striving for an LSD trip. The crackhead comment is quite telling to me and I mentioned in my previous post that your documentation of your experiences with this protocol are strikingly similar to those who articulate their illicit drug trips.
I see the intellect. I see the scientist. I see the logic. But I also see the addict.
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This is going to sound like a manifesto, and maybe it is.
What this self-experimentation is, is ART - not science.
Androgen Replacement Therapy, rather than Testosterone Replacement Therapy.
ART includes TRT and a whole lot more because it encompasses the entire field of androgens, doses, timings and routes of administration.
ART strives to accomplish the activation of under-activated androgen receptors in both body and brain using the most suitable and appropriate androgen(s), doses, timings and routes of administration that best fit each case.
ART and TRT are not mutually exclusive but one contains the other.
Because of genetic and circumstantial hormonal individuality in each man, personally acceptable route(s) of administration, economic factors and numerous other considerations, the field of options must be kept as wide open as possible to be able to treat so many cases that are simply left in the cold as of today’s offical medical practice.
ART is inclusive, not exclusive.
ART is not a fixed practice like TRT seems to have become. Instead it is always trying new options and alternatives because of both the complexity of each individual case and the new types of damages caused by modern technology itself - Xenoestrogens in particular. These chemicals can mangle a man’s Leydig cells before he is even born, leaving him with half or less of his full complement of cells. By the time he reaches the age of twenty-five or thirty-five, his circulating Testosterone can be half of normal or less.
ART - unlike so many physicians - recognizes that these victims are now often young men in their twenties and thirties and does not attempt to deny their suffering or assume that they are trying to obtain androgens for other purposes but rather, fully investigates and treats with seriousness their conditions using the full array of therapeutic options.
ART recognizes that these young victims, if exposed to the currently-standard Testosterone replacement therapy, will have their fertility compromised or destroyed. Unlike the older practice of TRT for aging men whose fertility is not so critical, it’s crucial that the younger victims of today be given more and better options to live a decent life while still being able to have children.
ART recognizes that these environmental casualties are increasing in both number and percent of the population each year as the planet and food supply become ever more polluted with a growing list of xenobiotic estrogenic molecules - some of which have already been found to kill Leydig cells in the womb. I have the studies.
ART also strives to have minimal negative impact on the patient’s own Testosterone production if he still has some, so it steps lightly on his system by using androgens, timings, doses and routes of administration that have the absolute minimum impact on his natural production in a best-effort attempt to function as a complement rather than a suppressor.
Recognizing the normal circadian release of Testosterone, ART tries to imitate it rather than suppress it as current medical HRT practice does by introducing androgens at inappropriate times. The current medical practices of weekly injections or patches that provide continuous-release dosing cause abnormally continuous androgen receptor activation thereby maximizing negative-feedback mediated suppression and causing other issues since the entire body is evolved to receive its androgen receptor activation in a circadian rhythm.
Using supplemental Testosterone - while contained within the definition of ART practice - is in some ways opposed to its fundamental tenets due to supplemental Testosterone’s strong suppression of endogenous production. Alternative androgens with less suppressive activity and often having other advantages over supplemental Testosterone - dbol being one among many - are often preferred by ART practitioners.
Nevertheless, since the ART field is inclusive and wide, TRT therapy is included within it as an option - one that is not always the best choice for many men but is always available alone or in combination with other therapeutic agents and modalities.
ART Therapy is a light at the end of the tunnel for the numerous men who are unable to receive Testosterone replacement therapy and others who failed on it or found that its negative effects were not to their liking.
ART Therapy is not perfect or ideal but strives to excel the current and limited therapeutic HRT options while also including them.
Finally, ART Therapy has no respect for and does not recognize the artificial and arbitrary limitations imposed on the treatments available to patients by the law, by corporate profits or by the medical Establishment so it can always perform at its best for the patient without denying options.
Buddy your a fucking wack job man… Nobody needs this kind of advice here!! Please go away and “fight” someone else… Seriously… Lol snort d Bol lol… WOW
I have no need to fight anyone and won’t do so. I am here to help those who were left behind by the medical establishment find their way to a cure.
The only fight I’m involved in is the fight for health and life.
If you don’t want to hear what I have to say then leave this thread and don’t come back. There’s plenty of room for you elsewhere and you have shown twice now that you have nothing to contribute to the discussion that would help those who have been left behind.
Find your passions and pursue them in your course of self-development rather than pushing others down with anger and hatred. If you think I’m wrong then test my ideas yourself, prove them wrong and report back. Of course you’d need to be low-T to do that.
I will not be replying to any more of your attacks - it isn’t worth my precious time. You are now on my ignore list so I won’t be reading any more of your posts anyway.
It’s now 10:03pm and today’s 7mg nasal dbol was right on the mark. My hands are warm but not sweaty and inside my core burns a metabolic fire at just the right temperature. Just like the titration of thyroid hormone is highly individual, so is the titration of androgen.
Tonight I realized that my HRT treatment protocol is more advanced than even Trimel Corporation’s nasal Testosterone patch because it’s less suppressive and does not involve placing weird foreign objects into the nose. Not to mention it’s about a hundred times cheaper and already available on the market for immediate relief of low-T cases.
The stars! THE STARS!
Tonight I went outside as I usually do each night to sit under a skyful of stars in my beautiful rural area with no streetlights or other light sources to ruin the view.
This time was shockingly different from each night for the last twenty years! For the first time in twenty years I could see every star sharp as perfection. Not all the nootropics, vitamins, minerals and dietary manipulations ever approached this.
I don’t know why the androgen replacement is working so well because I have no training in medicine - just a lot of experience in self-treatment for various conditions and lots of research under my belt. I was expelled from high school in grade 11 for pointing out to the computer lab teacher a security flaw in their network.
I never did graduate because the secondary program I was using to complete high school had its funding decimated by the government and at that point I was already moving far ahead of their old program, so I didn’t push to make the effort of completion. It was just a formality after all - I already knew enough at that time. Maybe it was a mistake to not obtain basic qualification but that’s history now.
I thought of a proper name for the ART program too: HEART!
Health Enhancing Androgen Replacement Therapy
It’s got to be full of love and life and consideration for the patient and the self too if it’s self-treatment.
The usual secondary metabolic flush of heat bringing wet sweat to the hands and a mild elevation of internal temperature manifested again tonight at about 11:00pm - about 14 hours after the 9:09am nasal dbol dose of 7mg. Both the pharmacodynamics and pharmacokinetics of dbol perfusion from the CNS into the rest of the body are consistently predictable yet strangely cyclical, along with its androgenic-estrogenic biphasicity when administered as a single small morning dose for HRT purposes.
My real expertise is in two narrow areas totally unrelated to hormones: nootropics and how light modulates the circadian rhythm. I’m typing this now under a monochrome red screen with only dim red lights in order to avoid shifting my circadian rhythm with green or blue light so I can get to sleep immediately upon falling into bed, for example.
My circadian background keeps telling me that the 14 hours between dosing and the secondary heat is very close to twelve hours and that part or all of this peculiar effect is somehow caused by circadian rhythmicity but I don’t have enough knowledge to understand why.
Unlike the last three weeks of 7mg oral dbol and exactly like the last two nights of nasal dbol, tonight was also free of mental and physical tiredness due to the new nasal route of administration removing liver burden and thus preventing glucose-glycogen interconversion dysregulation.
Now that it’s been almost a month, I’d like to look back on the two major milestones in HRT treatment achieved thus far:
August 8th, 2013: The first successful, publicly-documented use of low-dose morning oral synthetic androgen dbol for the treatment of low Testosterone while complementing and supporting remaining internal production with correct circadian timing and careful dose control.
August 31st, 2013: The first successful, publicly-documented use of nasal administration to deliver a whole-body HRT therapeutic dose of synthetic androgen dbol while eliminating hepatic first-pass metabolism and most if not all subsequent hepatic exposure.
Admittedly, Trimel Corporation beat me to it by four years - but with a crappy patch and olde Testosterone. Their only advancement was the nasal route of administration. No correct circadian timing and nothing better than the highly-suppressive Testosterone.
Not much advancement for a large, rich corporation. The fact that I could do better with chump change and internet research speaks volumes about the HRT industry’s abysmal state today.
Some day in my hoped-for future these types of advanced treatments will be standard medical procedure. Until then, it is up to each low-T individual to find their way out of the hormone war matrix. And yes, my next exposition will be about the cause of all these low-T problems affecting the populations of advanced countries.
It’s a hormone war - a silent but very real and deadly war. A kind of Silent Spring with humans as the victims instead of birds and xenoestrogens substituting for pesticides. The guns are cans with their BPA and DEHP-saturated plastic liners leaching for months and years on store shelves and the bullets are the xenoestrogen molecules.
[quote]Batman00 wrote:
I see the intellect. I see the scientist. I see the logic. But I also see the addict. [/quote]
Agreed. While this is a very interesting thread that I will continue to observe, I can’t help but wonder what therapeutic needs this treatment program has met for you, and where it stands in comparison to past protocols you’ve tried (and why).
From your descriptions, the effects almost seem more akin to a recreational psychoactive than a treatment protocol. Has the 99% purity claimed been verified by an outside source? It’s not impossible that a mild psychoactive compound could be used as a cutting agent if not.
I would think it unwise to recommend that others, whose personal health history is unknown to you (who also claims to have no formal medical training), undertake a similar experimental procedure therapy with an illicit compound. If you must recommend this, you should make it clear that there is potentially a high degree of risk in choosing this therapy.
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I apologize for giving the impression that nasal administration is anything like a recreational psychoactive.
It is not.
I was just blown away by how well the racetam nootropics I’ve been taking started to work.
Increased visual color saturation and sharpness are caused by Oxiracetam which normally creates these visual effects - they just aren’t usually so strong for me because my brain androgen level wasn’t high enough since years ago for it to work properly.
Now that I’m seeing full and optimal nootropic effects from Oxiracetam - in fact this morning I have not even taken my morning ART dose and the colors and brightness of my screen are already noticeably higher than yesterday morning.
The therapeutic effects on the brain are retained far past each morning ART dose because of the long-term regeneration of organ function. I’ve seen this effect in other ways from racetam nootropics but never so fast and strongly.
I don’t expect those who are not also concurrently taking vision-enhancing racetams to notice such large improvements in visual function - though it’s likely they will notice some improvements.
As for the risks - Trimel Corporation has four studies validating the safety of nasal ROA for Testosterone - I wrote them up in a previous post on this thread. It’s true that dbol has two differences in its molecular structure, so I’m going out on a limb saying it’s safe.
The nasal ROA is beta for sure so I can’t recommend it to low-T sufferers unless they are willing to take a (small) risk. Each person has to decide for themselves the risk/benefit ratio.
What I can vouch for is the safety of low (<=10mg) single oral dbol within an hour of awakening for the treatment of low-T. It has not shown any serious or even concerning problems in my case for just shy of a month’s treatment.
Further evidence for the old oral route’s safety with dbol is the bodybuilders themselves who take much higher doses. I have not been able to find one forum poster on the whole net who complained of actual chemically-induced hepatitis from taking even their high dbol doses.
There are a couple reports here and there but I looked into them and some were infectious hepatitis and others were mistaken symptoms. A few might be legitimate but we’re looking at less than 0.1% of users or 1 in 1000. Common over-the-counter drugs such as Aspirin cause far more cases and they are freely available on drugstore shelves without a prescription for anyone to destroy their liver with.
Relative to the vicious and worsening symptoms of low-T which always become worse with aging - including a 33% increase in death risk - the tiny dbol risks after much research became a joke. Just this one effect of low-T is orders of magnitude stronger than all the medical and legal risks of independent hormone therapy. Never mind all the other consequences added onto it!
That’s why it’s so important to keep the risks in relative perspective and always look at the bigger picture. I don’t have time today to list all the consequences but I have the papers on file. Below are the first three studies I easily grabbed off Google this morning in only five minutes of searching:
Low Testosterone Could Kill You
“Low testosterone may lead to a greater risk of death, according to a study presented Tuesday at the annual meeting of the Endocrine Society in Toronto.”
“Men with low testosterone had a 33 percent greater death risk over their next 18 years of life compared with men who had higher testosterone, according to the study conducted by Dr. Elizabeth Barrett-Connor and colleagues at the University of California at San Diego.”
“It’s very exciting and potentially a groundbreaking study,” said Barrett-Connor. “But it needs to be confirmed.”
“The study tracked nearly 800 men, 50 to 91 years old, living in California. Their testosterone level was measured at the beginning of the study, and their health was then tracked over the next 20 years.”
Low Testosterone May Cause Depression
“Feb. 3, 2004 – Low testosterone levels may cause clinical depression in older men, a new study shows.”
“Age related decreases in the male sex hormone testosterone are common in older men; some 30% of men over age 55 have it. Low levels of the hormone can cause symptoms of fatigue, a decreased sex drive, and irritability. However, because some symptoms of this disorder are similar to symptoms of depression, the link between the two disorders has been unclear.”
“In this study, researchers analyzed medical records over a two-year period for 278 men – all age 45 and over – who had no diagnosis of depression before that time period. These were also men who had low or normal levels of testosterone test results. Doctors often order these tests when there are libido or other sexual function problems.”
“During the two-year period, the men with low testosterone were four times more likely to be diagnosed with clinical depression, reports researcher Molly M. Shores, MD, with the Veterans Affairs Puget Sound Health Care System and the University of Washington in Seattle.”
“Her study appears in the Archives of General Psychiatry.”
The following study is good reason to be sure that your androgen receptor activation is neither too low nor too high, another feature of HEART:
PubMed: Low testosterone levels may be associated with suicidal behavior in older men while high testosterone levels may be related to suicidal behavior in adolescents and young adults: a hypothesis.
"Abstract
Several lines of evidence suggest that there is an association between testosterone and suicidal behavior. A link between testosterone and the neurobiology of suicidal behavior may be related to: a) a direct effect of testosterone on suicidality via certain brain mechanisms; and/or b) a testosterone influence on aggression and, consequently, suicidality; and/or c) a testosterone effect on mood and, consequently, suicidality; and/or d) a testosterone effect on cognition and, consequently, suicidality. At least one study has demonstrated a relation between high levels of testosterone and suicide in young people. A significant number of studies suggest that high testosterone levels are associated with aggression in adolescents and adults. Multiple lines of evidence indicate that aggression is associated with suicidal behavior.
The effect of high testosterone levels on suicidality in adolescents and young adults may be mediated by testosterone-related elevated aggression. It is also possible that, in young people, high testosterone levels are directly linked to suicidality via certain brain mechanisms. In older men, decreased testosterone levels are associated with depressive symptoms and reduced cognitive function, whereas higher blood levels of testosterone are associated with better mood and cognitive functioning. Depression and reduced cognition are associated with suicidal behavior and may mediate the effect of decreased testosterone levels on suicidality. Therefore, it is reasonable to propose that suicidal behavior in adolescents and young adults is associated with high testosterone levels, whereas suicidality in older men is associated with decreased testosterone secretion."
I’m back from my first bike ride in town since switching to nasal dbol 7mg on Saturday - three days ago.
This is day four and I have new pharmacokinetic data!
First, I must apologize for misleading everyone by coming to the fast and incorrect conclusion that the metabolic ‘fire’ heat type effects generated by the insufflation route were correlated with anabolic activity in my body.
They were not.
I should have known better because since the second day after switching from oral 7mg dbol to nasal, I noticed two things which as of today have gotten far worse: first, I noticed a soreness in my leg muscles. It’s been getting stronger over the last three days. Second, I noticed that the nice padding of flesh that grew over the bony area between my knees after starting the oral program three weeks ago was thinning again with the bones pressing against each other again.
With cognition roaring like a jet engine I ignored these symptoms but not anymore as they are now stronger and totally obvious. The old low-T muscle fatigue was back with a vengeance today.
Now for the pharmacokinetic conclusions:
- Nasal administration of dbol up to 7mg results in the the majority of molecules staying within the brain - judging from my muscular pain and catabolism, I’d say 90% of it can’t get out - maybe 95%. The dbol molecule is Testosterone with an added, bulky methyl group (CH3). The blood-brain barrier’s pores are small and the size of a molecule is one of the crucial determining factors deciding how well it penetrates this obstacle.
Dbol’s greater size makes it a poor penetrator of the BBB. When taken orally, only a tiny bit has to get into the brain for some mental effects, but in the reverse situation - when taken into the brain first - it’s just too hard for enough to exit to provide anabolic body effects. BBB transport of the dbol molecule may also be asymmetric with import more efficient than export.
This has excellent advantages!
It means the brain acts as a separate dbol pool. This means even women can use 7mg/day nasally to enhance brain function without leakage into the body with accompanying androgenic and anabolic effects, and both sexes will have no worries about hepatic stress via the intranasal route.
- Poor BBB dbol export also means anyone can use nasal dbol up to 7mg/day with zero androgenic or anabolic body effects since it stays in the brain. This makes nasal dbol the most powerful nootropic in existence short of the highly potent Sunifiram, Unifiram and Noopept.
The bad news is that a low, ART oral dose of dbol - unlike injected Testosterone - will not produce sufficient repletion of brain androden receptor activation. That was why I was still gettting mentally sleepy - especially in the evening - on the oral dosing. My brain wasn’t getting the androgenic benefits but it was having to deal with the metabolic burden caused by liver glucose-glycogen interconversion dysregulation.
For a brief while over the last two days I have toyed with the idea of upping the nasal dose in a risky venture to try to force some useful amount to spill over past the BBB but now I realize that idea is foolish.
Dose-splitting between oral and nasal is the ideal, with the pefect ratio not yet known. That exciting and new experimental task will start tomorrow with 7mg nasal + 7mg oral to - for the first time in almost four weeks - produce full repletion of both the brain androgen pool and body androgen pool.
This pharmacologic data is also a world first - now we know much more about dbol’s blood-brain barrier conductance properties and how these properties apply to the ART application. We now have experimental data that for the dbol molecule, the brain is a separate pool from the rest of the body - accessible only by insufflation or direct injection into the brain itself - at least for ART therapeutic doses.
The bottom line for those interested in using dbol for ART: low 7mg oral doses won’t produce complete or necessarily even usable brain repletion so the nasal route of administration will be necessary to see full or even noticeable cognitive benefits.
Why don’t you spend you energy getting into doing biology, and doing a PHD into investigating this. I know you are in your late thirties, and I don’t know what you are doing with yourself now, but with these effects you should use your apparent increase in cognitive abilities to provide some scientific justification in what you are doing. If you really have hit something truly remarkable that can revolutionize HRT, then I don’t see what’s stopping you in using your newly found energy into investigating how this works.
You have everything gain ad nothing to lose. You may potentially help millions of people if you solidify your suspicions into scientific fact. People are not going to believe that snorting dbol is going to be good for you. It has never been done before, and people should be skeptical. Remove the skepticism from this by publishing studies on how and why it works the way it does (assuming the same effect occurs with other people/animals etc).
People on this forum, including, me are desperate for a solution. People’s emotions take over their rational mind when they are impaired. Saying these people need to try this is akin to a marketer appealing to a fat person about their latest fat loss shake or supplement, minus the financial incentive. I understand your good intentions, but not everyone is too open to shove things that don’t have a lot of research for it’s long term use and effectiveness. Yes, I know that experimentation comes before trials, but people what for the trials to insure that it will do what it’s said to do.
I appreciate your efforts here, but your statements are in vain without proper scientific backing, or thousands of anecdotal reports. From what we know, you are the only person in the world who has tried this. Who says it will work for everyone?
This is not a personal attack, but just constructive criticism in your approach to your experiences.
I know that once I am fully healed, I am going to use all my energy into something that will revolutionize has something is done, helping many people a long the way. I don’t know what industry this will be in, but when you have have suffered like all of us, I will feel obligated to help others with the same principle of pain, because I was helped a long the way for better health.
Oh what a trip it is.
I have been noticing something starting with the first day of switching from oral to nasal dbol. My specialty is nootropics and other psychoactives, but this is going way beyond what I ever expected.
First some background. Perhaps one of my few remaining sins is a small pipe of tobacco before bed while laying out under the dark starlit night sky late at night. In that silent darkness many a time since months ago - but not recently as my supply had ended and new material was unavailable - I would have a bit of the magical 5F-AKB48, a very potent full-agonist synthetic cannabinoid.
Having been dry for almost a month now and just using the pipe for smoking the night’s tobacco with nothing on top, these last four days something has been showing up that doesn’t belong in the experience… something which by all standards of science should be nearly impossible.
After having put about a month’s worth of nightly tobacco through the bowl and after several screen changes and plenty of old tarry junk scraped out so that since weeks ago it was rather clean… that first night after switching to nasal administration, I detected a distinct + on the Shulgin scale and the unmistakeable effects of 5F once again.
The impossiblity of a few microgram traces left causing this reaction were quickly dismissed three days ago. Not tonight.
After what happened tonight, I now realize that these effects were quietly increasing over the last three days. Tonight, from what should have been nothing at all, suddenly and without warning came something so radically amazing and beautiful that I’m having trouble fitting it into words.
What came from the blue was a +++ on the Shulgin scale from what could only be a few dozen micrograms of 5F left somewhere from a month ago, but I just can’t figure out how. After so much experience with this material over half a year I know that it could not be possible, yet it happened.
Not only that, but this +++ experience was so perfectly clean that never in my life have I ever experienced such a state. It was so much more than that though. Because as the peak washed over me in the darkness and silence of the vast, empty fields and forests of this natural place, I began to hear the silent yet completely overpowering sound of the universal chorus once again.
The song of a trillion eternities in holiness. As I lay in stillness and silence wave after wave of the most complex insights and understandings unfolded to the full completion of understanding within a depth of living emotionality that had dried up so many decades ago.
If there were enough words to describe it they would certainly overflow all the time and space left to write them. The best way I could put it was that the silent voice of the spirit itself which had so many decades ago spoken in its eternal voices of purity, the eternal umbilical that connects each living soul to the heart of what I can only imagine is the core of this universe’s will of existence started flowing again.
If I had a religion then I would say that God sang me a song but I don’t so I won’t. All I can say is that something which used to fill me with endless silent understanding and knowledge in a perfect balance of understanding and feeling came calling with absolutely no foreknowledge or prompting on my part. It just happened.
Now that I’ve gotten that out of the way I will explain how it relates to ART. A Testosterone deficiency implies a deficiency in estrogenic activity as well. It implies that the Yin force within both the mind and body is also deficient. I chose to correct my body’s Yang deficiency with a molecule that at least partly converts as its natural father does to the Yin: Estradiol. The missing female component that is absolutely required to allow a mind to function correctly at its full potential.
The brain is filled with TRT, E1, E2 and E3 receptors. They are part of its core functionality not just a sexual accessory. Without proper activation the mind cannot fulfill its function and cannot connect with its destiny which is to fully actualize both its evolutionary and transcendental purposes simultaneously. And it is capable of that. I was informed of that so long ago but lost the connection and the understandings as the functionality losses piled up.
In a moment all these understandings washed over me even as the most intense peak experience was occurring. The understandings were absolutely integral to the entire process yet even in their sophistication they did not detract from, contradict or in any way feel discordant with that most amazing chorus.
Over the course of the next twenty minutes the river of new understandings became airy and began to fade as the chorus of song quietly began its journey back home again, leaving a most perfect peaceful fulfilment and joy. Something which has not occurred in so many years that memory can’t recall. To have the spirit appear like that is so rare that I consider it the most valuable gift a living being can experience. And rare it is. I can count on the fingers of one hand perhaps, the times over the course of thirty-five years - and none in recent memory.
A mark of the sad state of my health these last two decades. The first thing to be lost when a being becomes sick is its connection to the spirit. With that loss the eyes and ears of the higher self close shut and personal development slows to a crawl, stops and begins to regress.
Despite its problems and failings, the old yet always new again molecule Dianabol has some special abilities. Unlike its non-aromatizing brethren, its capacity to express both halves of the spirit still exists. Therefore, with this single molecule, repletion of both chemical biofunctionality and spiritual capacity can be achieved. However, I have now found that oral administration - at least at the 7mg per day dose - does not, thanks to its stunted ability to pass the blood-brain barrier - provide sufficient activation of both the Yin and Yang receptors of the human mind when it exists in a state of deficiency.
Thanks to the new route of administration started only four days ago, the ongoing repletion has both refunctionalized these receptor systems and - judging by the increasingly powerful effects of tinier and tinier traces of remaining CB1/CB2 agonist in that silly pipe - it has also massively potentiated the CB system’s functionality as well.
Potentiated to the point that I am now very, very nervous about what’s coming in the mail in four more days. I am going to have to be exquisitely careful with what’s coming. What used to be a comfortable dose of 5F is going to be something else entirely. It looks like only a few grains are going to do what hundreds did before - and with exponentially greater cleanliness. Potentiation yields dose reduction which yields an increase in the Q factor for most every psychoactive.
The quality factor of any psychoactive experience including those mediated by CB agonists decreases as dose increases due to secondary effects - what we call side effects - becoming more intense relative to desired effects. However, the same dynamic in reverse also holds true. As sensitivity increases, dose is reduced to compensate and side effects decrease relative to desired effects. Having much experience with these agents, I can now be sure that profound increases in cognitive functionality over the last four days have radically changed the expected dynamics.
It was so beautiful to have found out by unexpected chance that not only is cognitive capacity recovering, but it seems something else is too. Something transcendent, something totally necessary to the fulfillment of a life. A living connection to the center of all existences and times, perhaps what could only be correctly described as divinity.
The hormone war is far more than a medical problem. It’s not merely an economically less-costly alternative to food-safe non-corroding metal cans or plastic containers. It is something whose results end in far worse because it’s not just the material side of human existences which are being affected.
It is their ability to both function as creators and conductors of the spirit itself. Without that capacity people are mere slaves to lower instincts and desires and I can now see how both that state and the lack of drive to overthrow tyrannies are potent reasons the powers that be have allowed the biochemical destruction of humanity to continue accelerating via many mechanisms - one of the most vicious and powerful being loss of hormonal integrity induced by xenoestrogen exposure.
8:45a: 7mg IN
9:00a: 7mg Oral
First test of both together.
Woke up clear and sharp this morning after four hours sleep and a single vivid dream of startling clarity - a new one too - outside the usual repeat-cycle. A very pleasant R-rated dream to boot - such are extremely rare in my sleeps, usually about twice a year.
The coincidence with the new ROA and its accompanying slew of procognitive effects is rather obvious.
Apologies for not listing all the other nutrients loaded in each morning, and the three each evening:
Morning:
Ascorbate: 8000mg (80% sodium salt, 20% acid)
Ca: 1g (Citrate)
Mg: 1g (Citrate/Oxide)
B-Complex 100mg
Zn: 50mg (Citrate)
Cr: 500mcg (Picolinate)
KI: 7-12mg
Evening:
Vitamin A: 10,000IU (preformed Retinol, not procarcinogenic beta-carotene)
Vitamin D: 10,000IU (preformed Cholecalciferol [D3], not the more toxic D2)
Fish Oil: 16g from 213g of pacific wild caught salmon
It should be noted that D3 is an excellent potentiator of Testosterone activity.
Also note that fish oil decreases SHBG and increases LH.
For those that don’t care about circadian timing, the transdermal ROA works well with most steroids including dbol:
From: METHANDROSTENOLONE - National Library of Medicine HSDB Database
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?dbs+hsdb:@term+@DOCNO+3360
“LOCAL EFFECTS: Effects from the transdermal system include pruritus (itching) at the application site (37%) and burn-like blisters (12%). Rarely, erythema, vesicles, allergic contact dermatitis, burning, and induration at the application site of the transdermal system may occur.”
A bit of DMSO and transdermal is guaranteed with molecules whose molecular mass is less than 1000. Dbol’s is 300.
Patent WO2009055859 A1: Transdermal delivery system for hormones and steroids
http://www.google.com/patents/WO2009055859A1
Includes Methandrostenolone in the listed steroids of Section 11.
I did a self-check yesterday and determined the best two spots for transdermal patches - just under the ear on the neck. No hair and no clothes or other items touch it. The negative curvature of that area in general makes accidental contact with others unlikely.
The nasal route is so superior that I won’t bother wasting more time investigating transdermal. Also, transdermal does not deliver the entire dose and cannot provide such a guarantee, while intranasal always delivers the full dose unless one blows the nose or spits less than an hour after administration. Any tiny bit that doesn’t absorb goes down the throat and into the GI.
ISO -
PLEASE… your ingestion of methandrostenalone in the manner you describe has put you into a hypomanic episode. Please try and objectively evaluate what you have written and UNDERSTAND that you meet ALL of the criteria listed below:
A hypomanic episode is characterized by a distinct period of persistently elevated, expansive, or irritable mood, lasting throughout at least 4 days and present for most of the day nearly every day. This hypomanic mood is clearly different from the person’s usual mood.
During the period of mood disturbance, 3 or more of the following symptoms have persisted (4 if the mood is only irritable) and have been present to a significant degree:
Inflated self-esteem or grandiosity
Decreased need for sleep (e.g., feels rested after only 3 hours of sleep)
More talkative than usual or pressure to keep talking
Flight of ideas or subjective experience that thoughts are racing
Distractibility (e.g., attention too easily drawn to unimportant or irrelevant external stimuli)
Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation
Excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., the person engages in unrestrained buying sprees, sexual indiscretions, or foolish business investments)
This is for your own help, and hopefully recovery.
I have met a few genius whom inherit the bipolar mental disorder. Their brainpower is truly superhuman. Its amazing.
I take it you haven’t had the pleasure of seeing the other side of them have you?
No I’m speaking from a strictly intellectual standpoint. Not the reality nor the subject matter at hand.
Now for the most frighteningly powerful papers every man and pregnant woman should read.
The papers below indicate the sources and results of this deadly serious emergency - no, plague - afflicting men all over the first world. If trends continue as the final paper indicates then there is no future for humanity. None at all.
Exhibit 1: Inhibition of Testicular Steroidogenesis by the Xenoestrogen Bisphenol A Is Associated with Reduced Pituitary Luteinizing Hormone Secretion and Decreased Steroidogenic Enzyme Gene Expression in Rat Leydig Cells
Abstract: Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells - PubMed
Full PDF: http://endo.endojournals.org/content/145/2/592.full.pdf
ABSTRACT
“Exposure of humans to bisphenol A (BPA), a monomer in polycarbonate plastics and a constituent of resins used in food packaging and dentistry, is significant. In this report exposure of rats to 2.4 microg/kg.d (a dose that approximates BPA levels in the environment) from postnatal d 21-35 suppressed serum LH (0.21 +/- 0.05 ng/ml; vs. control, 0.52 +/- 0.04; P < 0.01) and testosterone (T) levels (1.62 +/- 0.16 ng/ml; vs. control, 2.52 +/- 0.21; P < 0.05), in association with decreased LHbeta and increased estrogen receptor beta pituitary mRNA levels as measured by RT-PCR. Treatment of adult Leydig cells with 0.01 nm BPA decreased T biosynthesis by 25% as a result of decreased expression of the steroidogenic enzyme 17alpha-hydroxylase/17-20 lyase. BPA decreased serum 17beta-estradiol levels from 0.31 +/- 0.02 ng/ml (control) to 0.22 +/- 0.02, 0.19 +/- 0.02, and 0.23 +/- 0.03 ng/ml in rats exposed to 2.4 microg, 10 microg, or 100 mg/kg.d BPA, respectively, from 21-35 d of age (P < 0.05) due to its ability to inhibit Leydig cell aromatase activity. Exposures of pregnant and nursing dams, i.e. from gestation d 12 to postnatal d 21, decreased T levels in the testicular interstitial fluid from 420 +/- 34 (control) to 261 +/- 22 (P < 0.05) ng/ml in adulthood, implying that the perinatal period is a sensitive window of exposure to BPA. As BPA has been measured in several human populations, further studies are warranted to assess the effects of BPA on male fertility.”
A 25% drop in Testosterone biosynthesis from only 0.01 nanomolars of BPA. That’s because BPA metabolizes within both the rat and human bodies into MBP [Wikipedia:MBP 4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene - Wikipedia ], a xenoestrogen with a HUNDRED to a THOUSAND (yes you read that right) times more potency than BPA’s ability to agonize estrogen receptors. Worse - as another paper shows - the male fetus is permanently damaged for life by apoptosis - cellular suicide - of Leydig cells in the womb due to exposure. This explains the population-wide Testosterone decreases seen in men during the last fifty years as they are born with less-than-necessary complements of Leydig cells. The normal decline in Testosterone biosynthesis with aging starts at a much lower level to begin due to in-utero cell suicides and drops faster than normal due to further later life exposure to these xenoestrogens.
Not only do men born these days come out of the womb already deficient and damaged but they suffer vastly accelerated drops in Testosterone synthesis and thus circulation - with a particularly nasty cliff reached when the negative-feedback HPTA system reaches its maximum level of retrocompensation and can no longer increase Testosterone production by sending more LH to the testicles. After that point - when the remaining living Leydig cells are churning out their absolute maximum Testosterone production - the system has run out of compensatory capacity for further production decreases. It can no longer compensate for either age-caused or Leydig-loss-caused declines in Testosterone production ability. After that point production drops like a stone over the cliff.
MBP - BPA’s in-vivo metabolite whose estrogenic power is 100x to 1000x stronger than BPA itself - fits quite nicely into both Estrogen Receptor alpha and beta:
Exhibit 2: 3D Models of MBP, a Biologically Active Metabolite of Bisphenol A, in Human Estrogen Receptor Alpha and Estrogen Receptor Beta
Abstract: 3D Models of MBP, a Biologically Active Metabolite of Bisphenol A, in Human Estrogen Receptor α and Estrogen Receptor β
Full PDF: http://www.plosone.org/article/fetchObject.action;jsessionid=6FF4C5E32EB997BBDBB003135A75AB16?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0046078&representation=PDF
To read a more accessible summary of this paper:
BPA’s Real Threat May Be After It Has Metabolized
ABSTRACT
"Bisphenol A [BPA] is a widely dispersed environmental chemical that is of much concern because the BPA monomer is a weak transcriptional activator of human estrogen receptor Alpha [ER Alpha] and ER Beta in cell culture. A BPA metabolite, 4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene[MBP], has transcriptional activity at nM concentrations, which is 1000-fold lower than the concentration for estrogenic activity of BPA, suggesting that MBP may be an environmental estrogen. To investigate the structural basis for the activity of MBP at nM concentrations and the lower activity of BPA for human ER Alpha and ER Beta, we constructed 3D models of human ER Alpha and ER Beta with MBP and BPA for comparison with estradiol in these ERs.
These 3D models suggest that MBP, but not BPA, has key contacts with amino acids in human ER Alpha and ER Beta that are important in binding of estradiol by these receptors. Metabolism of BPA to MBP increases the spacing between two phenolic rings, resulting in contacts between MBP and ER Alpha and ER Beta that mimic those of estradiol with these ERs. Mutagenesis of residues on these ERs that contact the phenolic hydroxyls will provide a test for our 3D models. Other environmental chemicals containing two appropriately spaced phenolic rings and an aliphatic spacer instead of an estrogenic B and C ring also may bind to ER Alpha or ER Beta and interfere with normal estrogen physiology. This analysis also may be useful in designing novel chemicals for regulating the actions of human ER Alpha and ER Beta."
By an order of magnitude the greatest BPA, DEHP and other xenoestrogen exposure for the wealthy populations of First World countries is canned foods. Unlike home plastic food containers which store food - often in the cold of a refrigerator which limits the leach-rate - for a week or two at a time, metal cans spend months or years in warehouses, months on store shelves and often weeks or months in home cupboards before use.
During these months or years the can liners are leaching testicle-cell-destroying, Testosterone-declining xenoestrogens into their contents.
By the time your average food can is opened for consumption the food it contains is saturated with these chemicals.
Exhibit 3: Food Packaging and Bisphenol A and Bis(2-Ethyhexyl) Phthalate Exposure: Findings from a Dietary Intervention
Abstract: Food Packaging and Bisphenol A and Bis(2-Ethyhexyl) Phthalate Exposure: Findings from a Dietary Intervention - PMC
Full PDF: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3223004/pdf/ehp.1003170.pdf
ABSTRACT
Background: Bisphenol A (BPA) and bis(2-ethylhexyl) phthalate (DEHP) are high-production-volume chemicals used in plastics and resins for food packaging. They have been associated with endocrine disruption in animals and in some human studies. Human exposure sources have been estimated, but the relative contribution of dietary exposure to total intake has not been studied empirically.
Objectives: To evaluate the contribution of food packaging to exposure, we measured urinary BPA and phthalate metabolites before, during, and after a fresh foods dietary intervention.
Methods: We selected 20 participants in five families based on self-reported use of canned and packaged foods. Participants ate their usual diet, followed by 3 days of fresh foods that were not canned or packaged in plastic, and then returned to their usual diet. We collected evening urine samples over 8 days in January 2010 and composited them into preintervention, during intervention, and postintervention samples. We used mixed-effects models for repeated measures and Wilcoxon signed-rank tests to assess change in urinary levels across time.
Results: Urine levels of BPA and DEHP metabolites decreased significantly during the fresh foods intervention [e.g., BPA geometric mean (GM), 3.7 ng/mL preintervention vs. 1.2 ng/mL during intervention; mono-(2-ethyl-5-hydroxy hexyl) phthalate GM, 57 ng/mL vs. 25 ng/mL]. The intervention reduced GM concentrations of BPA by 66% and DEHP metabolites by 53-56%. Maxima were reduced by 76% for BPA and 93-96% for DEHP metabolites.
Conclusions: BPA and DEHP exposures were substantially reduced when participants’ diets were restricted to food with limited packaging.
If anyone thinks they can easily avoid these vile toxin-leaching cans, think again: tests of canned foods found that 92% of cans leach BPA:
Exhibit 4: No Silver Lining: An Investigation Into BPA Canned Foods
Abstract: Home - Environmental Defence
Full PDF: http://environmentaldefence.ca/sites/default/files/report_files/No%20Silver%20Lining%20BPA%20Report%20final.pdf
Selected excerpts from the Executive Summary
“BPA was detected in 46 of 50, or 92%, of the canned food samples.”
“Our study details potential exposure to BPA from not just one can, but from meals prepared with canned food and drink that an ordinary North American person might consume over the course of a day. It shows that meals involving one or more cans of food can cause a pregnant woman to ingest levels of BPA that have been shown to cause health effects in developing fetuses in laboratory animal studies.”
Those fetal health effects include Sertoli cell suicide - apoptosis - induced by DEHP exposure. The next and most important paper of this entire exposition finds this effect. DEHP - the other most-commonly used plasticizer besides BPA you’ve never heard of - is a killer of these cells. From Wikipedia:DEHP [ Bis(2-ethylhexyl) phthalate - Wikipedia ]:
“This compound is the most common of the class of phthalate plasticizers, accounting for an almost 54% market share in 2010.”
THIS TESTICULAR TOXICANT HAS ACHIEVED ALMOST 54% OF MARKET SHARE.
MUST HAVE STOLEN SOME FROM YER OLD PAL BPA, EH?
A REAL WINNER IN THE RACE TO END MANHOOD.
Exhibit 5: Effects of Mono (2-Ethylhexyl) Phthalate [DEHP], a Testicular Toxicant, on Follicle-Stimulating Hormone Binding to Membranes from Cultured Rat Sertoli Cells
Abstract: http://www.biolreprod.org/content/48/3/454
Full PDF: http://www.biolreprod.org/content/48/3/454.full.pdf
ABSTRACT
The widely used plasticizer di(2-ethylhexyl) phthalate (DEHP) is a male reproductive toxicant. Its toxicity has been shown to be due primarily to the action of its metabolite mono(2-ethylhexyl) phthalate (MEHP) on Sertoli cells. We have previously shown that at least one of the sites of action of MEHP on the Sertoli cell is the cAMP second messenger system. MEHP inhibits the ability of FSH but not isoproterenol, forskolin, or cholera toxin to stimulate cAMP accumulation in cultured Sertoli cells in a dose- and time-dependent manner. To further characterize this effect of MEHP, we prepared a light membrane fraction from control and MEHP-treated Sertoli cells cultured from 18-day-old Fischer 344 rats and measured FSH binding in a radioligand receptor assay using 25I-labeled human FSH (25I-hFSH). MEHP inhibited FSH binding when preincubated with Sertoli cells in culture but not when added simultaneously with 25I-hFSH to the purified membrane preparation. Attenuation of FSH binding was evident after a 3-h preincubation with 100uM MEHP (18%) and was maximal after 15-24h of preincubation (70-90%).
Preincubation of Sertoli cells for 24h with 100uM DEHP had no effect on FSH binding. Half-maximal inhibition occurred at approximately 0.1uM MEHP. Scatchard analysis indicated a four-fold decrease in FSH affinity with no change in receptor concentration. Exposure of Sertoli cells to MEHP amplified the attenuating effect of guanosine triphosphate (GTP) on FSH binding, suggesting that the action of MEHP may be at the level of the GTP-binding protein that couples the FSH receptor to the adenylate cyclase catalytic subunit. This effect of MEHP is age-independent over the range of 18-45 days. The active metabolites of the other phthalates toxic in vivo, i.e., monobutyl phthalate and monopentyl phthalate, also reduced FSH binding to Sertoli cell membranes but only from the older animals. Monomethyl phthalate, which is not a testicular toxicant in vivo, had no effect on FSH binding from animals at any age tested. We conclude that the ability of certain phthalate esters to reduce FSH binding to Sertoli cell membranes is likely to be at least a part of the mechanism responsible for their testicular toxicity.
Exhibit 6: DEHP: One of the Top 6 Chemical Threats to Humans (2011)
Article: Dr. Mercola's Censored Library (Private Membership) | Dr. Joseph Mercola | Substack
Selected Quotes
“Chemical manufacturers say they will seek approval from the European Union to continue use of di(2-ethylhexyl)phthalate (DEHP), a plastic-softening phthalate that the EU is banning.”
“DEHP is highly lipophilic (fat soluble). When used in PVC plastic, DEHP is loosely chemically bonded to the plastic and readily leaches into blood or other lipid-containing solutions in contact with the plastic.”
“This leaching of DEHP into humans via the solution with which it is in contact increases the risk of certain adverse health outcomes. Animal studies show that exposure to DEHP can damage the liver, kidneys, lungs, and reproductive system, particularly the developing testes of prenatal and neonatal males.”
Our loving chemical manufacturers want to keep dosing us with DEHP until there are neither Testosterone nor men left.
They have a special - perhaps pedophilic - attraction to dosing prenatal and neonatal males to achieve maximum destructive effect.
But what of humans? None of the studies above have checked men’s testicles for Leydig or Sertoli death and repression, or decreased Testosterone production.
Men aren’t rats yet so maybe they won’t be affected. Sorry guys:
Exhibit 7: Human testis steroidogenesis is inhibited by phthalates
Abstract: http://humrep.oxfordjournals.org/content/27/5/1451.full
Full PDF: http://humrep.oxfordjournals.org/content/27/5/1451.full.pdf+html
Background: Phthalic acid esters are widely used in the manufacture of plastics. Numerous studies have shown that these phthalates impair testicular testosterone production in the rat. However, the scarce and contradictory data concerning humans have cast doubt over whether these compounds are also anti-androgenic in man. We therefore investigated the direct effects of di-(2-ethylhexyl) phthalate (DEHP) and mono-(2-ethylhexyl) phthalate (MEHP) on organo-cultured adult human testis and a human cell line.
Methods: Adult human testis explants or NCI-H295R adrenocortical human cells were cultured with DEHP or MEHP. The effects of ketoconazole, used as a reference molecule, were also assessed.
Results: In both models, DEHP and MEHP significantly inhibited testosterone production. The effects of both phthalates appeared to be specific for steroidogenesis, as INSL3 production by Leydig cells was not altered. Furthermore, the phthalates of interest had no effect on inhibin B production by Sertoli cells or on germ cell apoptosis. As only a small fraction of the phthalates added was found in the testis explants, and as these compounds were found to be metabolized, we estimate that the anti-androgenic effects observed occurred at concentrations of phthalates that are of the same order of magnitude as exposures reported in the literature for men.
Conclusions: We provide the first evidence that DEHP and MEHP can inhibit testosterone production in the adult human testis. This is consistent with recent epidemiological findings of an inverse correlation between exposure to MEHP and testosterone concentrations.
Next we turn to the predictable results of this hormone war, starting with the beerbelly and heart-attack inducing Metabolic Syndrome:
Wikipedia: Metabolic Syndrome [ Metabolic syndrome - Wikipedia ]
The perverse Metabolic Syndrome comes regardless of how much exercise one undertakes - so long as circulating Testosterone is insufficient no amount will help.
Despite the cause being well-known by now, at this time the Wikipedia article contains not a mention of Testosterone.
Exhibit 8: Toxic Plastics: Bisphenol A Linked To Metabolic Syndrome In Human Tissue
Full Article: Toxic Plastics: Bisphenol A Linked To Metabolic Syndrome In Human Tissue -- ScienceDaily
Choice Quote: “They found that exposing human tissues to BPA levels within the range of common human exposure resulted in suppression of a hormone that protects people from metabolic syndrome.”
That unnamed hormone which protects against metabolic syndrome - which 25% of Americans now have - is in fact Testosterone:
Exhibit 9: Hypogonadism and metabolic syndrome- implications for testosterone therapy
Abstract: Hypogonadism and metabolic syndrome: implications for testosterone therapy - PubMed
Full PDF: http://www.med.unc.edu/~mcoward/urology/hypogonadism%20and%20metabolic%20syndrome.pdf
ABSTRACT
Purpose: Metabolic syndrome, characterized by central obesity, insulin resistance, dyslipidemia and hypertension, is highly prevalent in the United States. When left untreated, it significantly increases the risk of diabetes mellitus and cardiovascular disease. It has been suggested that hypogonadism may be an additional component of metabolic syndrome. This has potential implications for the treatment of metabolic syndrome with testosterone. We reviewed the available literature on metabolic syndrome and hypogonadism with a particular focus on testosterone therapy.
Materials and Methods: A comprehensive MEDLINE review of the world literature from 1988 to 2004 on hypogonadism, testosterone and metabolic syndrome was performed.
Results: Observational data suggest that metabolic syndrome is strongly associated with hypogonadism in men. Multiple interventional studies have shown that exogenous testosterone has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure, which are the parameters most often disturbed in metabolic syndrome.
Conclusions: Hypogonadism is likely a fundamental component of metabolic syndrome. Testosterone therapy may not only treat hypogonadism, but may also have tremendous potential to slow or halt the progression from metabolic syndrome to overt diabetes or cardiovascular disease via beneficial effects on insulin regulation, lipid profile and blood pressure. Furthermore, the use of testosterone to treat metabolic syndrome may also lead to the prevention of urological complications commonly associated with these chronic disease states, such as neurogenic bladder and erectile dysfunction. Physicians must be mindful to evaluate hypogonadism in all men diagnosed with metabolic syndrome as well as metabolic syndrome in all men diagnosed with hypogonadism. Future research in the form of randomized clinical trials should focus on further defining the role of testosterone for metabolic syndrome.
Exhibit 10: Testosterone and Sex Hormone Binding Globulin Predict the Metabolic Syndrome and Diabetes in Middle-Aged Men
Abstract: http://care.diabetesjournals.org/content/27/5/1036.short
Full PDF: http://care.diabetesjournals.org/content/27/5/1036.full.pdf+html
ABSTRACT
OBJECTIVE: In men, hypoandrogenism is associated with features of the metabolic syndrome, but the role of sex hormones in the pathogenesis of the metabolic syndrome and diabetes is not well understood. We assessed the association of low levels of testosterone and sex hormone binding globulin (SHBG) with the development of the metabolic syndrome and diabetes in men.
RESEARCH DESIGN AND METHODS: Concentrations of SHBG and total and calculated free testosterone and factors related to insulin resistance were determined at baseline in 702 middle-aged Finnish men participating in a population-based cohort study. These men had neither diabetes nor the metabolic syndrome.
RESULTS: After 11 years of follow-up, 147 men had developed the metabolic syndrome (National Cholesterol Education Program criteria) and 57 men diabetes. Men with total testosterone, calculated free testosterone, and SHBG levels in the lower fourth had a severalfold increased risk of developing the metabolic syndrome (odds ratio [OR] 2.3, 95% CI 1.5-3.4; 1.7, 1.2-2.5; and 2.8, 1.9-4.1, respectively) and diabetes (2.3, 1.3-4.1; 1.7, 0.9-3.0; and 4.3, 2.4-7.7, respectively) after adjustment for age. Adjustment for potential confounders such as cardiovascular disease, smoking, alcohol intake, and socioeconomic status did not alter the associations. Factors related to insulin resistance attenuated the associations, but they remained significant, except for free testosterone.
CONCLUSIONS: Low total testosterone and SHBG levels independently predict development of the metabolic syndrome and diabetes in middle-aged men. Thus, hypoandrogenism is an early marker for disturbances in insulin and glucose metabolism that may progress to the metabolic syndrome or frank diabetes and may contribute to their pathogenesis.
The definitive proof that metabolic syndrome is not just associated with low Testosterone and xenoestrogen exposure but is actually caused by it can be found in Exhibit 11:
Exhibit 11: Effect of 12 months of testosterone replacement therapy on metabolic syndrome components in hypogonadal men: data from the Testim Registry in the US (TRiUS)
Abstract: Effect of 12 months of testosterone replacement therapy on metabolic syndrome components in hypogonadal men: data from the Testim Registry in the US (TRiUS) | BMC Endocrine Disorders | Full Text
Full PDF: http://www.biomedcentral.com/content/pdf/1472-6823-11-18.pdf
ABSTRACT
Background
Recent evidence suggests that there may be a bidirectional, physiological link between hypogonadism and metabolic syndrome (MetS), and testosterone replacement therapy (TRT) has been shown to improve some symptoms of MetS in small patient populations. We examined the effect of 12 months of TRT on MetS components in a large cohort of hypogonadal men.
Methods
Data were obtained from TRiUS (Testim Registry in the United States), a 12-month, multicenter, prospective observational registry (N = 849) of hypogonadal men prescribed Testim 1% testosterone gel (5-10 g/day). Data analyzed included age, total testosterone (TT), free testosterone (FT), sex hormone-binding globulin (SHBG), and MetS components: waist circumference, blood pressure, fasting blood glucose, plasma triglycerides, and HDL cholesterol.
Results
Of evaluable patients (581/849) at baseline, 37% were MetS+ (n = 213) and 63% were MetS- (n = 368). MetS+ patients had significantly lower TT (p < 0.0001) and SHBG (p = 0.01) levels. Patients with the lowest quartile TT levels (<206 ng/dL [<7.1 nmol/L]) had a significantly increased risk of MetS+ classification vs those with highest quartile TT levels (=>331 ng/dL [=>11.5 nmol/L]) (odds ratio 2.66; 95% CI, 1.60 to 4.43). After 12 months of TRT, TT levels significantly increased in all patients (p < 0.005). Despite having similar TT levels after TRT, only MetS+ patients demonstrated significant decreases in waist circumference, fasting blood glucose levels, and blood pressure; lowest TT quartile patients demonstrated significant decreases in waist circumference and fasting blood glucose. Neither HDL cholesterol nor triglyceride levels changed significantly in either patient population.
Conclusion
Hypogonadal MetS+ patients were more likely than their MetS- counterparts to have lower baseline TT levels and present with more comorbid conditions. MetS+ patients and those in the lowest TT quartile showed improvement in some metabolic syndrome components after 12 months of TRT. While it is currently unclear if further cardiometabolic benefit can be seen with longer TRT use in this population, testing for low testosterone may be warranted in MetS+ men with hypogonadal symptoms.
And finally, the most devastating result of this war on hormonal integrity: a multigenerational decline in American men’s circulating Testosterone that continues to worsen every year.
This decline is not limited to American men but extends to all men who are exposed to the main cause: xenoestrogens leaching from cans and secondarily from other sources.
This decline is already devastating their health and will soon bankrupt the entire medical establishment along with the funding governments - which could in fact be an excellent thing since it’s headed there anyway for many other but similar reasons:
Exhibit 12: A Population-Level Decline in Serum Testosterone Levels in American Men
Abstract: http://jcem.endojournals.org/content/92/1/196.abstract
Full PDF: http://jcem.endojournals.org/content/92/1/196.full.pdf+html
Figure 1: http://i41.tinypic.com/2pmqo.jpg
ABSTRACT
Context: Age-specific estimates of mean testosterone (T) concentrations appear to vary by year of observation and by birth cohort, and estimates of longitudinal declines in T typically outstrip cross-sectional decreases. These observations motivate a hypothesis of a population-level decrease in T over calendar time, independent of chronological aging.
Objective: The goal of this study was to establish the magnitude of population-level changes in serum T concentrations and the degree to which they are explained by secular changes in relative weight and other factors.
Design: We describe a prospective cohort study of health and endocrine functioning in randomly selected men of age 45-79 yr. We provide three data collection waves: baseline (T1: 1987-1999) and two follow-ups (T2: 1995-1997, T3: 2002-2004).
Setting: This was an observational study of randomly selected men residing in greater Boston, Massachusetts.
Participants: Data obtained from 1374, 906, and 489 men at T1, T2, and T3, respectively, totaling 2769 observations taken on 1532 men.
Main Outcome Measures: The main outcome measures were serum total T and calculated bioavailable T.
Results: We observe a substantial age-independent decline in T that does not appear to be attributable to observed changes in explanatory factors, including health and lifestyle characteristics such as smoking and obesity. The estimated population-level declines are greater in magnitude than the cross-sectional declines in T typically associated with age.
Conclusions: These results indicate that recent years have seen a substantial, and as yet unrecognized, age-independent population-level decrease in T in American men, potentially attributable to birth cohort differences or to health or environmental effects not captured in observed data.
Observing Figure 1, note that generation T3 born in the years 2002-2004 shows not only a lower starting Testosterone than previous generations T1 and T2, but that it also shows an abnormally rapid decline with age. This is consistent with men who are both born with a substandard or inadequate complement of Leydig cells and also exposed to high levels of xenoestrogens during later life.
All this writing has made me hungry. There’s some delicious canned Ravioli in my closet just waiting to be eaten.
Dear reader, you must be hungry too. I’m sure you can find something to quell that appetite in your cupboard though it might require a can opener.
Over and out.
Finally, done! It feels great to get all that causative research off my chest - I’ve had those files sitting on my drive for way too long. The heaviness of knowing about the hormone war situation and having the data but not having it organized or having the energy to put it all together in a coherent form is now lifted like a teraton weight.
That entire post was constructed from scratch today on only four hours of sleep last night - I went to bed at 3:30a and woke up naturally well-rested at 7:30a this morning. I don’t have an alarm or morning responsibilities so I sleep until my body is done regenerating each night. Therefore, my sleep hours are purely reflective of actual regenerative needs rather than artificial constraints.
It’s now 8:22p and for not a second all day have I felt a trace of the usual sleepiness or tiredness. I take zero caffeine and no other stimulants either.
And no, there is no hypomania - how that would be logically possible on a bare androgen replacement dose I do not know. I’m calm, totally relaxed and sleep each night like a baby including last night. It helps that I’m on three very powerful nootropics - one of which passed directly from experimental research to public sale in North America without even FDA oversight 
Yes, I am into many more experimental therapeutics. There’s always risks being so close to the cutting edge and I am intimately familiar with these risks.
No Phase I/II/III: straight from rats to humans. Sunifiram for the win. Likely the most powerful NMDA receptor sensitizer in existence according to my tests and stacked with two top racetams. The stack itself just barely kept me awake before fixing the under-activated TRT receptor problem. It now roars like a jet engine.
Now that I’m done I will enter a laziness period of not really posting much except minor status updates for a while - days, weeks or months.
[quote]
Now that I’m done I will enter a laziness period of not really posting much except minor status updates for a while - days, weeks or months.[/quote]
Sounds like your coming off of your hypomania, I’m glad to hear that.