97 replies to this topic

[Isochroma]

It's now 4:45pm and for the last hour and most noticeably in the last half-hour the whole-body dbol effects are becoming stronger, weird.

The usual 7mg which I have gotten used to over the last three weeks of oral use is just too much, my body is saying it's just too much via intranasal. Overdose.

Leg muscles feel just a bit tense and electrically charged and a bit in the arm muscles too - like the first few days on dbol when I had no 'tolerance'. The mouse is a mess of sweat, I've got to wipe it every ten minutes.

I guess due to lack of body load movement feels like the body is light as a feather. It's so very different from usual. My hands are trembling a bit too - another effect which disappeared in the first few days three weeks ago due to what I assume is tolerance to the usual 7mg. It's just so overcranked.

There is one new effect which I never noticed before in the last three weeks of dbol oral dosing or at any point in my past: my heart is trying to skip a beat each time it beats, or it feels a bit like that. It isn't too disturbing but it's subtle and has been ongoing for the last couple hours. The effect seems to parallel the intensity of heat and sweat. I assume it's due to overdose.

My palms are sweating bucketloads like the first day and my whole body is cooking like an oven. I have not had such strong and blatant effects from the usual 7mg since weeks ago, I guess due to my body becoming accustomed to it via the oral route. I measured this morning's dose with extra special care to ensure that it would precisely match the dose I've been taking these last three weeks so as to be able to compare only the differences produced by intranasal administration.

The nasal route appears to be ridiculously efficient at delivering dbol to both the brain and entire body. The mental clarity and energy at this time - 5:00pm - is superb and blows oral dosing out of the water. Both the body and brain effect profiles are so different that it can't be denied that the majority went in via nasal mucosal absorption and likely perfusion through brain and other unusual regions as the pubmed study showed.

Suprisingly, intranasal did not simply deliver a fast spike after that single morning dose of 7mg at 9:41am but a very high and long effect plateau which is still too strong for my liking at 4:48pm.

Overall, despite the strange brain and body effects I am pleased enough to switch to intranasal for my low HRT dose. Luckily I purchased what I'm hoping is a more accurate 1mg digital scale on eBay two days ago: the PRO-20A 0.001g / 20g.

Edited by Isochroma-Reborn, 01 September 2013 - 12:17 AM.

[Isochroma]

It's 9:09pm and the dizziness is 70% gone.

But for the last hour I notice that my palms are hot and sweaty again and body's hot with metabolic fire like it normally has been up until about 4:00pm these last three weeks of oral dosing the same 7mg dbol.

The metabolic fire type body effects are continuing. It's just crazy. The duration is insanely extended though the intensity has faded to the point where the hot flashes in hands and forehead and heat inside main body area are much lower so it isn't unpleasant. My hands are still half-slick with sweat even in the coolness of the night with the window wide open. This has never happened before even on the first day of dbol.

The additional muscle tension's about 70% gone too but I can still feel a bit of it just barely. The electricality's gone. These things were also unpresent in the last week due to tolerance/accustomment but were noticeable a bit when beginning but even then only in the first four hours after oral dosing.

The half-life after insufflation is not 3-4 hours like oral or injection. It is about 8 hours in the brain and a long high plateau for the body effects with unpredictable releases near the end that must be the result of some weird diffusion dynamic. It's very nonlinear too - the heat effects faded for a few hours late this afternoon and then fired back up again in the evening!

The problem is that the brain and body effects didn't increase in proportion. Body effects increased by about 50% for the same dose in mg but brain effects increased by about 3x-4x! That is going to restrict the dosing to small amounts.

I have not been taken for a ride like this since my careless days of youthful experimentation with psychoactives. At its strongest it felt like my brain had been hit by a Mack truck or perhaps a freight train. It's still running slow and I'm having trouble typing without making mistakes.

[Isochroma]

It's now 11:42pm and the stimulation in both mind and body won't stop. Every time I think it's done - twenty minutes later more heat comes again.

It's precisely like being on some future super-stimulant mentally and physically with no body load or side effects and an energized yet neutral body.

I'm not restless at all physically or mentally but no trace of sleepiness or tiredness either.

Unlike every single day since three weeks ago on the same dose orally there was no estrogenic effect during the latter half of the day either. I had become used to having the morning dbol dose aromatize into estrogens later in the day resulting in a biphasic effect with relaxation starting about 5:00pm and then shading into mental sleepiness and body fatigue so strong that I would just slide into bed and instantly fall asleep all night long without a single awakening.

My whole body is light as a feather when walking and moving just like it usually is during the morning peak - but it's midnight.

There is zero body load and endless energy.

Today has been totally the opposite of every single day since three weeks ago when I started the dbol. Every single day has been a carbon-copy duplicate of the same biphasic effect of strong morning and early afternoon stimulation follows by the estrogenic flop. Not anymore.

The aromatization just didn't happen much or at all today. There wasn't a trace of the sleepiness, body load or tiredness. Right now at 11:48pm - 14 hours - yes fourteen hours later - the strong stimulation effects in both mind and body won't stop. The mental clarity and visual sharpness are unreal. Under the cold night air the stars were obviously sharper tonight.

I could run twenty miles right now but I need to sleep and it's going to be a long wait in bed for sleep to come.

I just cannot believe that 53 years of dbol and nobody tried this or they didn't publish it online. I've been searching for the last week trying to get background on what to expect but I can't find a single forum or blog report - and only the one study on pubmed in the literature.

If anyone can find any report please post the link. All I can find is endless forum threads where the first poster proposes the idea and then long strings of ridicule in reply.

It seems the joke is on the jokers now - times ten squared.
And please, somebody else try this. Just one other person to verify that I'm not insane.

If it's consistent tomorrow too then this is revolutionary and opens up whole new fields.

There's no need to bother anymore with methylated steroids because intranasal absorbs them all just dandy with 50% more peak power and 2x-3x longer duration of both body and mind effects.

Even olde Test goes thru quite nicely according to the pubmed study and I don't doubt it for a second now.

My hands are still slick with heat and sweat as I type and it's two minutes to midnight.
The big problem is trying to cut the dose down to some couple milligrams to prevent overdose.

God I hope the new scale can measure less then 7mg.

My ten grams of dbol powder which should have been a 3.9 year supply just turned into something like an 8 year supply overnight.

Edited by Isochroma-Reborn, 01 September 2013 - 07:36 AM.

[Isochroma]

Whatever this nasal ROA does, for sure it delivers some incredible dose of dbol to the brain rather directly - achieving concentrations that no oral dosing or IM/IV injection could ever approach.

The text and icons on my screen - like the last three days - are ridiculously bright, insanely color-saturated and sharp. There was only a hint of this effect - maybe 5% - during the last three weeks of orally dosing the same 7mg dbol.

Those are even more additional improvements to the exact visual effects of my daily Oxiracetam dosing protocol which already cranks up visual color saturation and sharpness to a higher level than any other racetam.

This is unreal. It's only been five more minutes but colour saturation in particular and visual sharpness also are increasing far past the highest level yesterday morning, which itself was higher than the first morning of nasal ROA.

It's becoming distracting.

I just can't believe the visual effects are so good and strong, and zero of the first day's dizzines or other sides.

Body heat effects are going strong too and about equal to yesterday's - so far.

Having extensive experience with nootropics - brain-function enhancing drugs such as the racetams (Piracetam, Aniracetam, Oxiracetam, Pramiracetam, etc.) and their visual effects... I'm blown away.

Nasal dbol has a ridiculously powerful - and cumulative - nootropic effect on the visual cortex at the least, and judging by my improved daily intellectual output other areas as well.

---------------------------

Note: Sorry for all the fast posting - I'm copy-pasting them from the T-Nation thread I created:

TESTOSTERONE NATION: Insufflation (Snorting) Dbol: Trip Report

This forum auto-merges the posts when I post them, perhaps due to speed, so I am using horizontal lines of hyphens [ --------------------------- ] to divide up what are chronologically-separate posts on the original T-Nation thread.

The post above and those below are all from my writings this morning on that thread.

---------------------------

Just returned from a walk in foresty nature.

The visual sharpness, colour saturation and 3D processing are off the charts.

Admittedly, I am on the following nootropics as well:

Sunifiram: 25mg every 3 hours (6x per day)
Oxiracetam: 500mg every 3 hours (6x per day)
Pramiracetam: 275mg every 3 hours (6x per day)

But still, I've been on this program for months and never, never, never, never ever ever ever ever, EVER did visual effects come close to this point. Hell, not even the olde days of highdosing Oxiracetam at up to 2g/3hr. come close.

The dbol is multiplying the power - NO, squaring or perhaps cubing the power of visual effects I normally get from the racetams I'm taking. Likely the Oxiracetam is responsible for such intense coloration.

This completely validates my experiences with the declining power of racetams since Summer 2008 as my natural Testosterone level continued to drop in parallel with the low-T symptoms. I was forced to switch from Piracetam to Aniracetam, then to Oxiracetam, Pramiracetam and finally Sunifiram to maintain effects and prevent daytime tiredness and sleepiness.

The initial visual colour and sharpness increases produced by these racetam nootropics also faded in lock-step synchrony with the worsening low-T symptoms.

The racetams require normal androgenic receptor activation within the brain to function correctly and providing that activation makes them roar like jet engines.

I noticed the 3D depth effect yesterday but today it's become stronger. I mean that objects even far away stand out like paper cut-outs - I can see the depth effect easily between two trees hundreds of feet away.

Chromed sufaces like faucets, etc. are shining so intensely that the only comparison is to LSD or shrooms but without any visual distortions. Just pure 100% clean enhancement with zero sides.

Over the course of a mere twenty minutes at the one-hour mark my entire visual field became saturated by intense colour and sharpness with no edge-ring or other artifacting. The images on my monitor have turned into a splendid palette of brilliantly colorful hues.

It feels exactly like my visual cortex was upgraded from Model-T to 747. Same as yesterday but stronger. Same as the day before that but stronger still again. I'm starting to wonder when it will stop increasing.

Hell, even a lower dose like 2-3mg would likely work wonders since the effect is cumulative and building each day. At such a low dose dbol would work as an almost pure nootropic by the nasal route with so little spillover into the rest of the body that both anabolic and androgenic effects would be minimal to nonexistent, making it suitable for wide use as a nootropic.

Truthfully, it feels like I just opened the door into a carnivalesque world of undiscovered countries. It's so overwhelming that all I can do is stare in quiet awe.

Intranasal travels amazingly well into the brain and starts fixing things superfast. Things that I had forgotten I'd lost over the years.

---------------------------

Somebody else - especially someone with low T - has got to try this. Preferably stacked with some Oxiracetam. It feels like I won some billion-dollar lottery.

The mind enhancements are so strong that I'm forgetting my original reason for taking dbol. The anabolic effects are nice but they're a sideshow.

A sideshow compared to this.

I'm having difficulty holding back tears.

Edited by Isochroma-Reborn, 02 September 2013 - 07:57 PM.

[Isochroma]

It is possible to optimize the ratio of brain to body repletion effects by splitting the morning dbol HRT dose between oral and nasal for each individual's needs.

In my case, the same 7mg taken orally produced sufficient anabolic effects to reverse the physical fatigue and other body symptoms of low-T, but it had only minor therapeutic effects on cognition. Raising the dose was not an option.

Due to either poor blood-brain-barrier permeability, brain androgen receptor insensitivity, abnormally low brain androgen receptor count or any combination of the three, the correct body dose of HRT dbol could not achieve anywhere near optimal mind results.

Now that the direct-to-brain nasal route of administration is available it is easily possible to adjust the ratio to achieve complete optimality of effect on both organ systems. The brain - being behind the blood-brain-barrier - is almost an entirely separate system from the rest of the body that oral dbol does not penetrate so well due to the majority latching onto body androgen receptors. Raising the oral dose to compensate can cause increases in side effects and liver stress rather than achieve desireable results.

It's my goal and fervent hope to move HRT practice from the 19th century to the 20th and maybe - Lord willing - to the 21st.

Considering the high percentage of men posting on this forum and others that they can't achieve good results on the single medically-approved HRT therapy of TRT, I think that critics should reserve their words until after they have some personal experience using alternative androgens and/or alternative routes of administration for HRT.

Official HRT practice has remained stagnant for decades and has failed to make use of the vast array of options available to create good results for patients - the huge list of androgens and the new methods of administration and timing. Instead it continues to blunder about like a bull in a china shop, achieving successes only by luck and leaving a long trail of disappointed patients.

HRT needs a breath of fresh air and new minds with new ideas and solutions.

Quote of the day: "First they ignore you, then they laugh at you, then they fight you, then you win."

Edited by Isochroma-Reborn, 02 September 2013 - 11:33 PM.

[Isochroma]

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.

Edited by Isochroma-Reborn, 03 September 2013 - 01:38 AM.

[Isochroma]

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.

Edited by Isochroma-Reborn, 03 September 2013 - 02:45 AM.

[Adaptogen]

Interesting, i hope all goes well. what is your weight change looking like as of recently?

[Isochroma]

I'm stable at 138lbs, height 6'2".

Yes, my BMI is horrendously low - I have always been a lean ectomorph with fast metabolism and am a regular mid-range cyclist.

The conservative, low 7mg morning dose of dbol is enough to hold on the muscle mass I need - I don't get tired anymore or feel 'wasted' inside despite my low weight and BMI.

The best part is even now my hands and feet are warm when before during my entire life history I always had metabolic problems that worsened each year after puberty. Bad enough that the doctors repeatedly drew my blood to test me for hypothyroid but always found normal TSH, T3 and Y4 levels.

Never once did they even think to test my Testosterone. It was me that had to demand the test on July 16th of this summer and I was proven horribly correct in my guess of the cause. With a total Testosterone count of 340 ng/dl, I am placed in the 85-100 year old 'normal' category by a survey of healthy Boston men in 1996. My category, the 35-40 year age group - I'm 35 - had levels averaging 650 ng/dl - twice mine.

After testing myself with purchased Clomid last year at 50mg/day for a week it was unable to raise my production which self-diagnosed me as primary hypogonadal.

Edited by Isochroma-Reborn, 03 September 2013 - 05:02 AM.

[Isochroma]

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.

Edited by Isochroma-Reborn, 03 September 2013 - 08:06 AM.

[Isochroma]

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:

1. 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.

2. 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.

Edited by Isochroma-Reborn, 03 September 2013 - 10:19 PM.

[Isochroma]

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.

Edited by Isochroma-Reborn, 04 September 2013 - 10:06 AM.

[Isochroma]

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.
Reference for these.

Edited by Isochroma-Reborn, 04 September 2013 - 05:01 PM.

[Isochroma]

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.ni...erm @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.co.../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.

Edited by Isochroma-Reborn, 04 September 2013 - 06:38 PM.

[Isochroma]

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: http://www.ncbi.nlm....pubmed/14605012
Full PDF: http://endo.endojour.../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 synthesis from only 0.01 nanomolars of BPA. That's because BPA metabolizes within both the rat and human bodies into MBP [Wikipedia:MBP http://en.wikipedia....4-hydroxyphenyl)pent-1-ene ], 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: http://www.plosone.o...al.pone.0046078
Full PDF: http://www.plosone.o...resentation=PDF

To read a more accessible summary of this paper:

BPA's Real Threat May Be After It Has Metabolized
http://ucsdnews.ucsd...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 ? [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: http://www.ncbi.nlm....les/PMC3223004/
Full PDF: http://www.ncbi.nlm....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: http://environmental...pa-canned-foods
Full PDF: http://environmental...eport final.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 [ http://en.wikipedia....is(2-ethylhexyl)_phthalate ]:

"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.biolrepro...ontent/48/3/454
Full PDF: http://www.biolrepro.../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 atapproximately 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: http://articles.merc...a-does-not.aspx

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.oxford.../27/5/1451.full
Full PDF: http://humrep.oxford...1.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 [ http://en.wikipedia....abolic_Syndrome ]

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: http://www.scienceda...80904151629.htm

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: http://www.ncbi.nlm....pubmed/16093964
Full PDF: http://www.med.unc.e...ic syndrome.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.diabetes...27/5/1036.short
Full PDF: http://care.diabetes...6.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.

------------------------------------------------------

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 11: A Population-Level Decline in Serum Testosterone Levels in American Men
Abstract: http://jcem.endojour.../1/196.abstract
Full PDF: http://jcem.endojour...6.full.pdf html

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 a very fast 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.

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: http://www.ncbi.nlm....pubmed/14605012
Full PDF: http://endo.endojour.../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 synthesis from only 0.01 nanomolars of BPA. That's because BPA metabolizes within both the rat and human bodies into MBP [Wikipedia:MBP http://en.wikipedia....4-hydroxyphenyl)pent-1-ene ], 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: http://www.plosone.o...al.pone.0046078
Full PDF: http://www.plosone.o...resentation=PDF

To read a more accessible summary of this paper:
BPA's Real Threat May Be After It Has Metabolized
http://ucsdnews.ucsd...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 ? [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: http://www.ncbi.nlm....les/PMC3223004/
Full PDF: http://www.ncbi.nlm....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:

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Exhibit 4: No Silver Lining: An Investigation Into BPA Canned Foods
Abstract: http://environmental...pa-canned-foods
Full PDF: http://environmental...eport final.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 [ http://en.wikipedia....is(2-ethylhexyl)_phthalate ]:

"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.biolrepro...ontent/48/3/454
Full PDF: http://www.biolrepro.../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 atapproximately 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: http://articles.merc...a-does-not.aspx

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.oxford.../27/5/1451.full
Full PDF: http://humrep.oxford...1.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 [ http://en.wikipedia....abolic_Syndrome ]

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: http://www.scienceda...80904151629.htm

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: http://www.ncbi.nlm....pubmed/16093964
Full PDF: http://www.med.unc.e...ic syndrome.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.diabetes...27/5/1036.short
Full PDF: http://care.diabetes...6.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.
------------------------------------------------------
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 11: A Population-Level Decline in Serum Testosterone Levels in American Men
Abstract: http://jcem.endojour.../1/196.abstract
Full PDF: http://jcem.endojour...6.full.pdf html

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 a very fast 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.

Edited by Isochroma-Reborn, 05 September 2013 - 04:54 AM.

[Isochroma]

Wow! Today marks the 30th day of my Dianabol ART program - dosing began on on August 7th, 2013 - the very day my ten grams of 99% pure Dianabol arrived by Express mail directly from the Chinese chemical company that manufactured it. After a month I can report results whose accuracy is far better than after only a few weeks.

It also marks the first week of using dual-mode administration: daily doses of 7mg orally and 7mg intranasally taken about a half-hour after awakening.

If I had thought that the first oral-only regime was solving problems - which it was - I was as wrong as the Sun rising in the East.

Combined administration has produced results for both mind and body which have far exceeded any results obtained in those first three weeks. In the last week both physical and mental productivity are through the roof - the washroom cupboards are now cleaned as of this morning, a chore waiting since April to be done. Lights are changed to a whole new system, etc.

Confidence is through the roof and I'm planning new projects at a dizzying pace and implementing them with a dedication and level of organization which I have not seen since before Summer 2008 when I started on Piracetam.

Now for the differences between my customized Dianabol program compared to Testosterone shots or patches in point form:

Positive: The benefits compared to Testosterone

1. I have kept about 80% of my natural production because - even if Dianabol were as suppressive as Testosterone molecule-for-molecule, both its anabolic and its cognition-restoring effects are many times more potent on a milligram basis. I've heard numbers as high as 8x relative to Testosterone. The dose of Testosterone required to provide equal anabolic and I presume cognitive effects would be many times higher and thus far more suppressive of my natural production. Having kept such a high level of my own Testosterone production also means I keep my sperm production in case I want to have a kid. Kids are not for me but for many other guys - especially the ever-younger men falling prey to toxin-induced low-Testosterone - fertility is important.

2. I don't have painful memories and scars from weekly Testosterone injections.

3. Androgen is loaded during the correct phase of my circadian rhythm so it functions optimally. Males are genetically evolved to have a large spike of Testosterone release in the early morning - not to have a high level throughout the day as a depot injection or patch would produce. If the only option was a needle then injections would have to be daily and taken early each morning.

4. My hair is still as it always was with not a trace of recession or increased fallout.

5. Chest is of course still flat as a board - I can't imagine why filling unoccupied androgen receptors with just enough Dianabol to make up for my Testosterone deficiency would do anything else. What little I take is just barely enough to fill them with almost nothing left over in circulation to aromatize to methyl-Estradiol, which even though it has higher affinity for activating a man's breast-cells is still so low that there won't ever be a problem. My body is naturally thin to begin with and I've always been dangerously underweight with my current weight at 138lbs on a 6'2" frame - a BMI of 17.7 (underweight). At such a low BMI I have precious few fat cells - they are much more efficient converters of both Testosterone and Dianabol into their corresponding Estradiolic sister molecules.

6. Muscles are no longer constanty painful from the slightest exercise or even heavy exercise so it's become a plesure to use them fully each day for more than I would have dared a month ago or five years ago. They've bulked up a bit too and at the low 7mg dose with virtually no aromatization to methyl-Estradiol the new growth is tight. I feel the tightness every time I walk because as a lifetime cyclist my main muscle development has always been the in the legs. It's great feeling that was unexpected - they want to be stretched and exercised. It's strange, like they have minds of their own.

7. Cognition. The place where as much benefit accrued as the rest of my body combined. Intellectual output has shot through the roof and increases daily without significant symptoms of excess such as restlessness, anger, tension, etc. Rather, mood is consistently upbeat and incredibly positive every day with a trend of daily improvement that has not stopped since starting the intranasal component a week ago with minor improvements seen since the beginning of oral use on August 7th.

Neutral: The effects which would likely be the same with equivalent Testosterone supplementation:

1. Appetite. Before starting the program I had poor appetite and stomach stayed 'full' for a long time with no new hunger for the entire day until dinner from a single light breakfast - exercise or not. Now I can't eat enough - exercise or not. A couple hours after a massive breakfast my stomach is literally hurting - ravenously hungry for more food. My shelves are emptying of food at a frightening pace and I've had to increase my food budget for next month.

2. Weight. My DNA programs my body to BURN BABY BURN - literally. I wish I was kidding. Every last calorie that I can absorb is burned away faster than I can eat more. It's always been this way whether I sit still or cycle miles on hilly roads. Now it's even 'worse' if that could be imagined. The new Dianbol-induced hot metabolic fire which roars from morning until late afternoon is burning away those last fat cells even faster along with every single calorie I can dump in. It's vicious and unforgiving and I feel like I'm running a race against Death itself to inject enough calories. Yet despite this vastly accelerated metabolism the Dianabol's anabolic function is just powerful enough to hold my existing muscle mass steady. Just barely.

Negative: Now for what I likely would have experienced if the doctor had been 'nice' enough to give me the Testosterone shots I foolishly asked him for:

1. Shutdown of natural Testosterone and sperm production to a high degree - many times more than the current program and possibly complete. By today - a month after beginning - the Testosterone would have devastated my natural production of both.

2. Hair recession. The higher Testosterone dose required to produce equivalent anabolic and cognitive benfits would convert to vastly more DHT which would activate whatever hair-loss genes undoubtedly exist in my DNA.

3. Painful weekly injection experiences and the memories of them in mind and muscle.

4. Total dependency on the medicos for weekly injections - the $200/month patch is not convered and was never a financial option. Due to shutdown production I would be highly dependent on the doctors whose carelessness and frank lack of expertise have already pushed their reputation into the toilet in my eyes.

5. Incorrect circadian timing. The weekly injections would produce a continuous Testosterone release or a single once-a-week spike - not only totally abnormal but maximally suppressive of my own production due to the haywire timing.

6. Excessive androgenicity. Dianabol has an Anabolic:Androgenic ratio of at least 2:1 while Testosterone has a 1:1 ratio. I don't want more facial hair, deeper voice or prostate growth. It doesn't suit my personality. This is a personal choice that varies by individual. I do want the anabolic and cognitive benefits which Dianabol provides quite nicely as testing has shown. I have seen some increase in androgenicity of personality and other cognitive functions but little to none in other body systems. The increases so far are at the limit of what I will tolerate but in absolute level would be nearly unnoticeable to more typical men. I'm OK with the changes but no more please.

Overall, after a month it's been a blazing success. Sex functions work as always if not even better and outputs in quantity and quality have not changed since before starting the program. Careful weekly testing has confirmed this.

The only disadvantage to my Dianabol program is that the Dianabol molecule itself with its bulky added Methyl group - CH3: lightweight at just over 15 Atomic Mass Units compared to Dianabol's total of 300.441 - prevents enough from passing to the brain from general circulation to treat more than about 10% of the cognitive dysfunctions induced by low Testosterone. A human has a very selective blood-brain-barrier which does not allow most molecules to pass through - including charged species and large species. The charged and the large. Though more complex than the size of its holes - let's just say that it has small pores. Small enough that Dianabol molecules mostly bounce off of it rather than passing through.

This means direct dosing to the brain in addition to systemic dosing is needed. Within the realm of reasonable things that can be done to accomplish this process - I decided based on the need to emulate my natural morning Testosterone spike that the only method which could deliver the needed dose in both amount and speed was intranasal administration. For some strange reason molecules cross into the brain very efficiently using this route of administration. I don't know why but I know it works like nothing else with its own unique pharmacokinetics and pharmacodynamics.

The consequence of nasal administration is the need for pure Dianabol powder because crushing up pills would mean insufflation of large amounts of cutters, fillers, binders, etc. which would induce too much nasal drip reaction which would result in too little absorption and too much drip into the throat and from there the GI tract - sabotaging the purity and function of separate mind/body dosing.
A nasal patch similar to Trimel Corpration's would likely work too but might have another problem: blood vessels inside the lower nose are more likely to move molecules into systemic circulation than those higher up in the nasal and sinus cavities - negating the original reason for intranasal administration which is fast, direct and exclusive brain delivery.

I intend this entire thread to be a guide for the coming wave of low-Testosterone victims. If my experiences with the disease process - it's both a process of degeneration and a state of being - are any guide then they will be very glad to hear the good news and know that at least one safe, effective alternative treatment is available. This alternative to the official, standard Testosterone injection/patch works even better and is far cheaper, far more under the patient's control and best yet is not subject to the yes-or-no of others - the medicos - who so often have no understanding or empathy for those who suffer by my experience.

That's the only thing really hurting my heart right now and I think about it every day. I think about all the low-Testosterone victims that don't have any relief. And I think about the others who have all-too-often partial, failed or otherwise dysoptimal relief using the standard medically-approved Testosterone replacement protocol of injections or patches.

Over the last hour today clouds which totally covered the sky in grey completely vanished, leaving a brilliant Sun shining in the vast, wide blue sky of my rural valley. Exactly like my life over the last month - not a trace of the darkness and grey remain.

It all burned away under the hot brilliance of a Dianabol star.

[Isochroma]

This might be difficult for readers to believe and it has been for me as well, which is why despite these unusal effects starting within the first week of my Dianabol morning therapy program I have not written about them yet. Before I get into details, a brief summary of the relevant details from my history.

I'm primary hypogonadal with natural production at half what it should be. Today my age is 35 years, and since about 15 years ago I have not noticed the normal morning Testosterone release pulse's symptoms: the metabolic fire of body warmth which brings both heat to the insides and also warmth and obviously enhanced skin circulation resulting in hands and feet being warm and flushed.

Accompanying these metabolic-energetic effects, for me the sex-specific effects of morning Testosterone release were also evident 15 years ago and earlier: regular morning 'wood' and stronger desire than the rest of the day except sometimes in the late evening or early night.

There is normally also a secondary, smaller Testosterone release spike in the evening or night, depending on how shifted the man's circadian rhythms are. I also lost the feeling of it at least 15 years ago.

During the first week-and-a-half of oral-only dosing (7mg) within an hour of getting up, I noticed a slight but increasingly strong effect occurring every other day - skip days when I took no Dianabol at all.

This strange effect was a significant body warmth and energy in the morning at the exact same time - about 1.5 hours after waking - that on dosing days the effects of taking 7mg Dianabol would begin: about one hour after dosing and 1.5 hours after waking.

Dianabol has a half-life of 4.5 hours - and for me on dosing days the metabolic heat effects are now subtle and completely done by 4:00p after dosing at 9:00a - that's 7 hours.

Now, any supplemental androgen including Dianabol should do two things:

1. Cut natural Testosterone prodction by causing downregulation of the HPTA axis.

2. Squish down the two peaks of natural Testosterone release - the first within an hour of awakening and the second about 12-14 hours later - for me anyway.

The problem is that since the end of the first week, I've noticed that the impossible is happening. I did not write about this in any of my previous reports because the effect was initially weak enough to be categorizable as 'placebo' and I did not want to embarrrass myself or mislead others by reporting effects that either did not exist or were not caused by the treatment program.

Trouble is, I did not change a single thing about my life including diet, vitamins, minerals or other drugs except for the Dianabol 7mg morning therapy program.

Furthermore, for the last 5-7 years, after orgasm not only did physical strength and all other mental/physical symptoms increase by a great extent for the next 2-3 days but recovery of ball-size and penis-turgidity was taking increasingly long periods of time - recently as long as 4 days and then still having a flaccid member all day.

I have been noticing that - opposite of expectations - during each night long after the Dianabol's gone at about 11:30p, a pulse of heat coupled with strong erections and desire. When I've made use of these things as I did two days ago, I found very strong results which have not appeared for at least the last 5 years.

At the usual 11:30p when the second pulse is appearing - on both on-days and off-days for the first 1.5 weeks, and each day for the following 3 weeks of every-morning 7mg oral dosing, I am noticing this pulse is becoming stronger. It's about 14 hours after the 9:00a morning Dianabol dose on dosing days, or the morning ghost-flush on off-days.

It is especially strong in both morning and night on dose-skip days. What brings me to write this report is that due to awful timing I went to bed way too late for the last two nights and woke up very late this morning: 11:45a.

It was too late to take the usual morning Dianabol dose so I skipped it today.

It's unusual since I've been dosing daily for the last three weeks. Again, in the morning about 1.5 hours after waking came the hot hands and lightness of body when walking along with high physical and cognitive energy along with spontaneous erections.

When I say hot hands I'm not being metaphorical or speaking within the ballpark of placebo-effect. I mean red hot hands dripping with sweat exactly like the first week of Dianabol when those heat effects were strongest. Slick with sweat and heat this morning along with some strong erection of the member.

Only three days after the last orgasm my member is now quite rigid during the morning and evening pulses and balls are unusally large for what I usually expect on day 3 after an expenditure. These things are totally abnormal for me since at least the last 10 years.

After 5 weeks of very careful self-observation on both the alternating day-on / day-off Dianabol program and the newer daily one, I can say with 100% confidence that these unexpected results are consistent both morning and night.

I still cannot believe it, but I am forced to conclude that the tiny early-morning dose of 7mg Dianabol has re-primed my pump, metaphorically-speaking. It may or may not have cut my total Testosterone production, but I can say with 100% confidence that the pulsatile application of that low dose early each morning has - just like the pulse of light upon awaking restores circadianicity to the Suprachiasmatic Nucleus (the SCN, our master pacemaker) - has restored my natural production's circadian rhythmicity at the very least.

In my field of expertise which is circadian phototransduction of light we call this entrainment. The circadian rhythm is both given its peakishness and also scheduled by the morning's first exposure to blue or green light. Blue light is 100% effective, green light is 50% as effective as blue light and red light has no effect.

Perhaps sustained, long-term and severe hypogonadism with circulating Testosterone only half of normal has caused such a level of HPTA dysfunction that it can't even produce the normal, tall spikes of circadian-rhythmic Testosterone release at morning and night. Being dry of both Testosterone and its product Estradiol for decades has had very nasty effects on so many of my body's systems that it seems logical the HPTA axis would be included in the victim-list.

It's the only explanation for the nightly pulse which is becoming stronger each night, and it is the only explanation for the morning pulse which is occuring absolutely 100% every day I skip my morning Dianabol dose. It's impossible to notice on dosing days because the strong Dianabol effects cover it up - but not at night because the Dianabol is long gone by then.

Thus on the daily program I only notice the night-pulse but if I choose to skip a morning's Dianabol dose I notice the morning pulse too.

This entire effect was so completely unexpected - I didn't even know - that I can completely discount placebo-effect. The pulses are so strong and undeniably obvious that it can also not be a result of slow Dianabol metabolism or excretion because that would only result in a slowly-decreasing effect from the morning dose into the night.

The consistent, circadian-timed, biphasic and most importantly - strongly-peaked - symptoms are shouting out a message to my logical mind loud and clear. I just can't keep ignoring it.

Edited by Isochroma-Reborn, 12 September 2013 - 04:16 AM.

[Werper]

Interesting read Isochroma-reborn , glad to hear it's having such profound and positive effects on you! I have to say that I am intrigued.
Isochroma-Reborn

[Isochroma]

Thanks for the feedback!

It's been about 42 days since the start of my protocol and 8 days since switching to Dianabol 7mg oral + 7mg Intranasal to provide both body and cognitive relief of low Testosterone symptoms.

The program continues to be a blazing success with incremental improvements noted daily and no negative effects appearing other than the long-standing loose stool which I get from many different compounds due to a sensitive GI tract - including moderate Oxiracetam doses and more than about four tablespoons of sugar per day to name the worst two culprits.

[Werper]

Would you mind PM'ing me the details of your supplier in china. I have never ordered directly from a chinese supplier. Many thanks.

[Isochroma]

I actually have a list of 13 companies that replied from my RFQ with quotes and that passed my careful auditing to be sure that not only were they not scammers, but that they had success shipping product by EMS to my country.

It's a small web page using the Racetam Prices template except with only one section.

I have not yet decided if or how to send copies to others due to security.

Edited by Isochroma-Reborn, 20 September 2013 - 02:27 PM.

[robosapiens]

Concerning circadian patterns - How can I encourage you to take some (decent) Tongkat Ali in the morning, just as an adjunct to this protocol?

[Isochroma]

If you'd taken the time to read my posts in detail you would know that I'm primary hypogondal.

That means none of the herbs, etc. that stimulate LH production work for me and neither does clomid. Primaries are really screwed and have very few options compared to secondaries.

My Leydigs are already working flat-out to produce everything they can. Too bad most of them are long dead.

Herbs, etc. work for those with secondary hypogonadism by stimulating LH production directly or indirectly.

Unfortunately, my last and only choice is direct hormone replacement therapy along with potentiating what Testosterone production I have left with Vitamin D, for example. I'm on 10KIU of that per day.

Furthermore, the coming wave of low-Testosterone Xenoestrogen victims are also primaries due to their Leydig cells being killed off in the womb. Read my report on Xenoestrogens to learn more.

Edited by Isochroma-Reborn, 20 September 2013 - 07:03 PM.

[robosapiens]

I have read everything in this thread, and come to different nuanced conclusions based on the admittedly limited amount of information that I have in this instance.

Because of my own personal heuristic models regarding health and healing, I would not have concluded full stop that my ledig cells were utterly non responsive based merely on a clomid run, even though this is a reasonable assumption.

Unless I was a complete casterati, I would have continued to optimize what ledig activity is still had and found ways of regenerating them, even if only a little, whilst still opting for your ART regimen, cyclicaly, for some reasonable relief,

a hybrid course of action.

e.g. http://link.springer...00215521#page-1

[Isochroma]

I read that study yesterday.

Even as you're criticizing me for using a proven safe 50+ year-old androgen, you're suggesting I take a known Leydig-cytotoxic molecule that is proven to kill them all off - Ethane Dimethanesulphonate.

Theory and affordable, safe reality are universes apart.

I will stick with my Dianabol therapy. It has the secondary - and unique - benefit among the anabolics that it induces increased Dopamine synthesis, providing a nice sunny mood that lasts all day. I have the study and yes, it does work nicely

[robosapiens]

AH, I see it now.. "criticizing me for using a proven safe 50"

I'm not criticizing you, I'm speculating upon how I would handle this myself (I have been on HRT)

I don't think anyone should take Ethane Dimethanesulphonate, the article points to the fact that Ledigs regenerate.

Why? Tongkat is so intense that it can actually increase the size of genitalia

Edited by robosapiens, 21 September 2013 - 05:58 PM.

[Isochroma]

Regarding Tongkat Ali, I'm not referring to its 'intensity', I am referring to its mechanism of action.

It is a stimulator of LH and FSH secretion but it cannot make up for lost Leydig cells any more than Clomid can:

How Eurycoma longifolia boosts testosterone levels

"A dose of 25 mg per kg bodyweight of the active Eurycoma longifolia extract caused a considerable rise in rats' testosterone levels over a period of 52 days. This increase was accompanied by a rise in LH and FSH levels."

Further validation of this mechanism of action comes from many forum reports of TA doing nothing - those men are primary hypogonadal like myself.

Worse, yesterday I found a number of forum reports detailing how TA stopped working after 2-3 days. Androgenic agents that stop working after a few days and thus require constant cycling are useless for a lifetime HRT/ART program:

T-Nation Forum:

"Just updating.

After 3 days off, I started another 5 day cycle.

This time I felt NOTHING! Just my regular self.

I mentioned this to the guy who recommended it; he said that he had the same results. (He has functioning testicles).

We decided that maybe we need longer time off than 3 days."

pherotruth.com Forum: Eurycoma Longifolia Jack (aka Longjack aka tongkat ali) as a pheromone

"Also I've noticed that it's significantly more effective taken orally if I take a long break between uses. Your body builds up a tolerance to it very quickly. After taking some two days in a row I barely get any effects on the third day."

Anabolic Minds Forum: Best Tongkat Ali

"I just want the best Tongkat Ali Available. I bought the source naturals version of LJ100, and it increased libido for a few hours and then stopped working. I've taken it for 4 days straight now and nothing."

All Things Male Forum: Tongkat Ali reverses hypogonadism

"Looks like i spoke to soon lol its been a few days and its not working anymore =/ hopefully taking a break will make it work again."

There are too many reports to add them all here: both of total failures and success for 3-4 days followed by no effects.

Edited by Isochroma-Reborn, 21 September 2013 - 06:58 PM.

[Isochroma]

Today I realized that with numerous TRT failures reporting their sad stories on the T-Nation forum and others - and considering my next Dianabol shipment of 20g pure powder should arrive soon - the next course of action is obvious.

I will direct the world's first documented Phase I trial of Dianabol for hormone replacement therapy in a single man. To accomplish this task I will post a request for a volunteer on various forums including this one.

The successful applicant will receive a free 14-day supply of premeasured 7mg Dianbol doses printed onto edible paper using a cheap off-the-shelf bubblejet printer with edible ink purchased cheaply from a local grocery store and edible 8.5" x 11" rice paper.

There are three primary reasons to use the new process of bubblejet printing for dosing:

1. Bubblejets create very precise and repeatable deposits of ink with a precision of less than 19 microliters per micronozzle.

2. Printed paper is easily mailable in standard envelopes. Legally, US Lettermail cannot be opened without a warrant:

Can Postal Inspectors open mail if they feel it may contain something illegal?

"First-Class letters and parcels are protected against search and seizure under the Fourth Amendment to the Constitution, and, as such, cannot be opened without a search warrant. If there is probable cause to believe the contents of a First-Class letter or parcel violate federal law, Postal Inspectors can obtain a search warrant to open the mailpiece. Other classes of mail do not contain private correspondence, and therefore may be opened without a warrant."

3. Printing is very fast and convenient, allowing a single person to reliably and repeatably produce thousands or tens of thousands of dose units per day with little labor.

Unlike capsules or tablets, sheets of paper cannot be felt as something of interest from outside the envelope and even if opened it is hard to tell what the item really is.

The PrintDrug process works as follows:

0. All handling of the paper from start to finish is done with rubber-gloved hands to avoid leaving either prints or DNA.

1. A cheap used bubblejet printer - likely a Canon - will be purchased.

2. Refillable, sponge-free chipped cartridges will be purchased from eBay. Here's an example for only U$13.00: Non-OEM Refillable Ink Cartridge For EPSON R200 R220 R300 R320 R330 R340. These cartridges are indefinitely refillable due to the special chip they contain which always reports them as 'full' to the driver software. Furthermore, they have handy rubber-capped refill holes for easy refilling.

3. All cartridges will be left empty except black and yellow. The black is used to print the empty guide-outlines for each dose-square. The yellow cartridge is used to print the drug-infused ink. Why did I choose the yellow cartridge? There's a special reason. Assuming the use of a CMYK cartridgeset, the yellow and only the yellow cartridge offers perfect RGB -> CMYK software colorspace conversion. Even 'black' is sometimes made synthetically by combining colors. Yellow is 100% red plus 100% green - a direct conversion from RGB to CMYK colorspaces. It never contains any cyan or magenta. This is required to ensure that the full dynamic range of color-to-ink translation is available and also required to insure that no other cartridges' output is used by the printer. Cyan is a non-integral mix of various colors and so is magenta. Software colorspace conversion varies by driver and printer and is too difficult to reverse-engineer and will not be consistent between driver softwares and printer hardwares.

4. The black cartridge is filled with normal or edible black ink.

5. The yellow cartridge is filled with 99% or 70% Isopropyl Alcohol - whichever works best - and about two grams of pure Dianabol powder. The fat-soluble powder will dissolve after a few shakes in the alcohol. A few drops of edible black or blue ink is added so the dose-squares can be seen. This extra ink will leave a microgram residue per square, slightly off-calibrating the final weighed dose but by less than 1%.

6. All cartridges are loaded into the bubblejet printer.

7. A sheet of edible rice 8.5" x 11" paper is loaded into the bubblejet's tray. A pack of 25 sheets of this size costs only $18.50 or $0.74 each. Each sheet can hold a month of daily doses.

8. The first of two losslessly-compressed PNG image is created on my computer. An image of 5 x 6 black-outlined squares. I use Microsoft Word's AutoShapes to make them quick and easy. The preview image below is linked to a free copy of the fullsize DOC file:

Image 1: 6 x 5 Array of Black Outline Squares

9. Image 1 is printed onto the sheet of rice paper.

10. The sheet with only Image 1 is allowed to dry completely.

11. The sheet with only Image 1 is weighed using my 1mg-accurate digiscale and the weight recorded.

12. The sheet with only Image 1 is reloaded into the printer's input tray.

13. Image 2 - a PNG image of solid yellow squares - is printed onto the sheet. The image is of yellow squares but the yellow cartridge contains only the drug, solvent and a few drops of black or blue edible ink so that the dose-squares are observable on the final printed paper. The preview image below is linked to a free copy of the fullsize DOC file:

Image 2: 6 x 5 Array of Yellow Squares

14. After printing, the sheet containing both Image 1 and Image 2 is allowed to dry. Due to the solvent used in the yellow tank it dries quickly - fifteen minutes max. I leave it for an hour to make dead sure all the solvent is evaporated. The final sheet of paper looks like this:

Final Sheet of Paper as Seen After Printing

10. The sheet of paper with both Image 1 and Image 2 printed onto it is re-weighed on my 1mg-accurate digiscale.

11. The weight of the sheet before it had Image 2 printed onto it is subtracted from the weight of the paper after it has both images printed onto it. All solvents must be fully evaporated before this is done.

12. The weight difference is the number of milligrams of drug deposited plus the micrograms of the couple drops of edible black or blue tracer ink added to the yellow tank to allow the dose-squares to be visible. It's not necessary to add tracer-ink and in such a case the dose-squares themselves are invisible with only the black outlines giving a clue as to where the doses are located on the sheet. The tracer ink's weight is less than 1% of the drug's weight and can be disregarded.

13. The weight difference in milligrams is divided by the number of squares - 30 in this case. This tells me how many milligrams of drug is in each square.

14. The page is run through the bubblejet one final time with the number itself - minus any other giveaway indicators such as 'mg' that would make the paper's contents obvious - printed in edible or inedible black ink onto the top of the sheet or above/below each square. This final printing rather than hand-writing the number is chosen to prevent both DNA contamination and the possibility of handwriting recognition if the paper is inspected by governments in-transit.

15. The paper can be quickly sliced row-by-row and column-by-column using a cheap paper-cutter: eBay: A4 TO B7 Size Paper Photo Cutter Guillotine Metal Trimmer Base 12 Sheets W Grid for $35.99. This tool produces paper squares with incomparable speed and efficiency: massloads of paper-square doses can be cut at once since these guillotine cutters can slice 5-10 sheets at a time. Alternatively, the paper can simply be folded and placed into the envelope.

16. The PrintDrug technique is suitable for use with any drug that dissolves in either water or alcohol and is potent enough to fit on the squares: I guess the usable dose-range per square as 1mcg - 10mg. Dianabol doses of 7mg will fit nicely into decently-small squares. So will LSD or many other powerful psychochemicals including Sunifiram and Unifiram.

17. The dose of the drug deposited on each square can easily be varied by adjusting the color saturation of the PNG image's yellow squares.

18. Using a RGB -> CMYK math routine, the other color ink tanks can also be used for other drugs, allowing multiple different drugs to be deposited in varying ratios on each individual square. A month's hormone replacement for a woman with each square containing a slightly different ratio of two or more different drugs.

19. With differently-colored edible tracer inks in each tank, the ratios of all the drugs can be observed on the final printed page by the colour of each square. For example, orally bioavailable Ethinyl Estradiol could be loaded into Tank 2 with a tracer of red ink while the orally-bioavailable androgen Dianabol could be loaded into Tank 3 with blue ink. The colour of the squares in the PNG image could be varied between red to blue, transiting some nice shades of purples in-between. Those nice shades will be the Female/Male hormone ratio.

20. The recipient receives a letter without return address or even name - just destination address. He opens it, takes out a square of edible rice-paper infused with drug, and either eats it or puts it under his tongue for sublingual administration. It's easy to hold the rice-paper square under the tongue and the rice starch dissolves slowly to provide steady absorption by the sublingual bed of blood-vessels.

21. Using a special additive to the drug-containing yellow tank that turn sticky when the solvent evaporates, the squares can be made sticky. The tank also contains added DMSO to allow the drug to penetrate human skin. The squares are cut out by the recipient and stuck on his skin where they adhere and deliver the drug as transdermal patches.

The total cost for my implementation of the PrintDrug system is less than $100 for everything excluding the drug itself - provided a working used bubblejet printer can be purchased for $25 - $45. There's tons of them in every used store because the chip-sabotaged cartridges run out and cannot be refilled, the printer itself isn't worth using because it's cheaper to buy an entirely new printer with fresh cartridges. Razor-and-blades sales model.

Edited by Isochroma-Reborn, 22 September 2013 - 03:44 AM.

[Isochroma]

Due to irresponsibility I went to bed at 3:00a last night. Way too late compared to my usual 1:00a - 2:00a. I slept in and knew it would be too late to take my usual ART dose. And just before I woke up at 9:30a - around 9:15a while still lightly dreaming some intense dreams I was assaulted by the most intense morning woods I've had in years - excepting my last dose-skip day about 1.2 weeks ago. I always take my morning Dianabol ART dose at 8:00a and the main effects kick in at around 9:30a.

It's not just a coincidence because if you read my reports you'll notice I document the 'ghost surges' both at the usual morning time with no dosing and at a late time in the night when the secondary natural Testosterone spike occurs.

It's great verification that my circadian Testosterone release is working dandily and also verification that suppression is minimal if not unexistent from the single tiny morning Dianabol dose. It's also good to have a single break-day once a week to let my HPTA axis recalibrate.

Edited by Isochroma-Reborn, 22 September 2013 - 05:11 PM.

[Isochroma]

A more detailed report of today's Ghost Drive due to skipping my morning Dianabol ART dose:

Today was a rare once-a-week break day with no Dianabol and boy was it fun! This break was due to my bedtime irresponsibility last night: 3:00a instead of 1:00a or 2:00a. It was just too late by the time I awoke to take the dose due to circadian timing. It's nice to take a day off once or twice a week anyway - to enjoy the Ghost Drive!

You see I have once again rediscovered something amazing about the Dianabol molecule. At 7mg taken within the first hour after waking in those who are already badly low on Testosterone - it restarts the natural Testosterone circadian cycle!

Yet again today - just like every day when I skipped my morning Dbol dose - came the Ghost Drive. Yes, this morning I woke up with intense wood which I could feel even before waking and then at the exact time when my Dbol dose would be kicking in - 9:30a - came my new, natural Testosterone spike! A surge and push of heat and energy that increased my body temperature by a degree - enough to flush my skin with heat and drive me in the most euphoric way with amazing continuous spine tingles from head to lower back peaking at 2:30p!

So much physical and mental energy that I just powered through a ridiculous amount of work - so fast I even shattered a mug on our granite countertop Absolutely none of this has been happening for at least the last 15 years. Dbol has a 4-hour half-life. It's been six half-lives since I took the dose yesterday morning - it's all gone! That's 24 hours since the last dose. No effects are present for that long.

It was pure clean natural Testosterone drive from my restored natural production

Dbol taken by those who need it in that tiny precise dose once early each morning creates not only a spike of androgen receptor activation but also a spike of another very unusual molecule - 17α-methyl-Estradiol. One or both of these is repriming my HPTA axis - the endocrine system whose job it is to manage Testosterone production and create both the big early-morning spike and the smaller late-night spike.