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Priceless information from BTPB by L.Rea
CONTROLLED CATABOLISM
FOR MAX ANABOLISM
During any period in which calorie expenditure is greater than calorie absorption, a
catabolic (tissue wasting) state exists. (DUH!) Bet you did not know that such a state
also induces an anabolic environment? (HUH?)
That's right boys and girls! Catabolism creates the best environment for freak
status growth. This is due to the body's survival response during which all kinds of
enzymes, intermediates, hormones, and receptor-sites are up-regulated to store and
utilize every possible nutrient absorbed as, or within, metabolically active tissue
(protein based like, uh, muscle!).
Have you ever noticed what happens when a competing bodybuilder diets for
weeks and months to get body fat levels down to 3-4% or so, then face-slams
anything that doesn't eat him/her first about 2 seconds after final judging? What
happens? For about 14 days body weight increases at an incredible speed with little
fat gain.
The body reacts positively to most stimuli for 14-21 days before initiating
counter measures.
Remember: The body seeks homeostasis? It is also paramount to realize that we grow
(or not) as a result of what we "absorb", not due to what we eat. During this controlled
catabolic period (Frank whined at this point) we create the ability to absorb, transport,
and utilize amazing amounts of calories.
There are Always Choices
There were two best choice protocols possible for setting the perfect
environment for Frank. One was simply a matter of reducing calories (fats/carbs) to
about 50% (or less) normal and over-train for 14 days before beginning Phase I. The
other involved a little chemistry and 1 1 days. (Gee, which do you think Frank N.
Steroid chose? Ya, so let's get on with it.)
CONTROLLED CATABOLISM
(Training/Daily Calorie Decreases utilized)
DAY 1: CHEST- 6 triple drop sets/shoulders 3 triple drop-sets (Any pressing exercise),
super-set side laterals/ rear delt raises 3 sets/ cut 500 calories from diet.
DAY 2: BACK-3 triple drop-sets any rowing exercise/3 triple drop-sets any pull-down
exercise/2 down the rack sets of shrugs/ cut 250 more calories from diet.
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DAY 3: LEGS-Squats 3 sets of 20 reps/leg press 3 triple drop-sets/2 down the stack
sets of leg extensions/leg curls 3 triple drop sets/drop 250 calories diet
DAY 4: ARMS-Super set E.Z curls with skull crushers 4 sets/ Non stop super-set rope
push-downs with preacher curls 4 sets/1 set triple drop wide bar push-downs/ 1 set
down the rack DB curls. (Calories remain constant from this point through day #1 1)
DAY 5: 20-30 minute aerobic periods (Stair climber or bike) 90-120 minutes "Freaky
monkey type love" sex. (With partner)
DAY 6: Repeated day #1 training , 5mg DNP per kg of body weight daily .
DAY 7: Repeated day #2 training, 5mg DNP per kg/d, 3 table spoons PG oil
DAY 8: Repeated day #3 training, 5mg DNP per kg/d, 3 table spoons PG oil
DAY 9: Repeated day #4 training, 5mg DNP per kg/d, 3 table spoons PG oil
DAY 10: Repeated day #5 training, 5mg DNP per kg/d, 3 table spoons PG oil
REPEATED SEX OLYMPICS (Again with partner)
DAY 11: Slept
*During the 11 day controlled catabolic period it was paramount that Frank drank at
least one gallon of water daily. It takes a great deal of water to remove catabolic
waste. A good daily multi-vitamin/mineral was a must. 1 5-50 grams of glutamine
daily reduced protein loss (divided into 3-5 even dosages). Peptide glutamine is said
to be best (Though valid research is lacking), and 50-100 g/d was better. Alpha Lipoic
Acid (ALA) is a great anti-oxidant wisely added to Frank's periods of DNP employment.
PG OIL MIX: 2 parts flaxseed oil/1 part extra virgin olive oil/1 part evening
primrose oil. Divided dosages into 1 tablespoon 3 times daily. 25 ml of glycerine in
16 oz of water helped, too. PG oil was used as a supply of omega 3, omega 6, and
GLA fatty acids. Perfect for prostaglandin production. (Go read prostaglandins
"Chemical Muscle Enhancement")
Frank had done near non-stop AAS cycles for the past 56 months with few, if
any, off periods. At this point he was working out but small for obvious reasons on
both counts. However, he was ready to become a beast now. A dangerous chemical
called DNP helped burn off fat as well as clear out androgen (and other) receptor-
sites.
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By now, the body had up-regulated anabolic receptor-sites, storage enzymes
and hormones, as well as intermediates that focus upon lean protein based tissue
anabolism.
THE OFF SEASON GOALS INTENDED FOR FRANK SHOULD
SEEM OBVIOUS...
1. Keep liver enzymes within acceptable ranges.
2. Avoid excessive fat build up (12%-14% max body fat)
3. Induce as much lean mass growth as possible
4. Control excessive water retention and heart/ kidney trauma.
5. Maintain estrogen and prolactin levels within growth ranges (estrogen increases
IGF- production and glycogen storage) but low enough to avoid gyno, female
pattern fat deposits, and excessive water retention (continue to the next section
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ESTROGEN CONTROL
Estrogen "Control" was paramount for health and result potential reasons.
High/prolonged circulating estrogen levels could have negatively affected the heart
and other organs due to excess fat deposits and water retention. As you know, most
severe water retention during AAS phases is due to estrogen and the resulting
hormonal production increase of aldosterone.
Elevation of aldosterone affects the body's water table by altering electrolyte
balances favoring sodium retention. Since sodium regulates extracellular (outside the
cell) water and potassium regulates intracellular (inside the cell) water, an imbalance
favoring sodium results in extra water in the vascular system and under the skin. This
is the reason that some athletes look like "Bloat Boy" and have very high blood
pressure.
It is important to remember that electrolytes such as sodium and potassium
regulate the electric charges for flow of water molecules across cell membranes and
are an intricate part of the sodium-pump mechanism that allows goodies like
nutrients and creatine to actually enter the muscle cells.
Blood Pressure and Water Retention
Normal blood pressure readings for average individuals is around 120 over 80.
In fact, this is considered pretty healthy. However, bodybuilders and power lifters are
not average. (Certainly none of my monsters) They tend to be much larger and
heavier, carrying significantly more lean mass tissue. For this reason, they have larger
more powerful hearts to supply high volumes of blood to a greater amount of tissue.
The first number of a blood pressure reading indicates blood pressure after the
heart contracts, which raises vascular pressure, and blood is pumped through the
body. Obviously the second number indicates or measures blood pressure before the
heart contracts.
Since bodybuilders and power lifters have more powerful larger hearts, a first
number of 150, 160, or even 180 is relatively normal. (And as a lone factor was not
usually a reason to be concerned for Frank) However, if the second number was over
100, it was time to be very concerned! If the second number exceeded 100 during
an AAS phase, it was usually due to excessive water retention and that meant that
counter measures were immediately taken.
The most commonly used water retention counter measure was a low dose
diuretic such as 20 mg Lasix daily. I have found natural diuretics such as dandelion
root often resolved the problem. Regardless of diuretic form, liquids were always
replaced before bedtime. Sometimes counter measures required backing off on
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aromatizing androgenic dosages, but usually this could be resolved with estrogen
control.
Most AAS Aromatize to estrogen to some degree. The higher androgenic
steroids more so than the higher anabolics. In the first book "Chemical Muscle
Enhancement" under drug descriptions, it is easy to find "aromatization". This gives
an evaluation of each drug's reported aromatization characteristic.
We employed three types of estrogen control drugs with
Frank:
1. ANTAGONISTS: These are drugs that act as competitive inhibitors by simply
competing with the estrogen molecule for its receptor-site.
The antagonist is like a little brother that beats you to the bathroom. If he gets in
first, he only sits there doing nothing but keep you out so you can't do your thing. If
estrogen can't get in, nothing happens.
Contrary to what is often claimed, antagonists are not "great" at controlling water
retention, in my opinion. Since they simply block receptor-sites they do not decrease
the levels of circulatory estrogen. This means potential increased levels of
aldosterone. They do have "some" positive effects upon water retention, but they were
best utilized as a drug for prevention of gynecomastia (Gyno/ bitch tits) and female
pattern fat deposits. Nolvadex and Cyclofenil are examples of antagonist.
An advantage of utilizing the properties of specific estrogen antagonist (Faslodex,
Clomid or Cyclofenil) for Frank was IGF-1 production. When estrogen is deactivated by
the liver, IGF-1 secretion results. It is also interesting that under the right conditions,
estrogen can increase GH levels by positively influencing the pituitary gland.
So in short, antagonists inhibit estrogen at receptor-sites and some aid in GH/IGF-1
secretion.
2. AROMATASE INHIBITORS: Aromatase inhibitors are sometimes called
antagonist also (which is a pretty loose term). Aromatase inhibitors control
estrogen by limiting or preventing the activity of the aromatase enzyme.
Normally, the aromatase enzyme induces the conversion of some types of androgens
into estrogens. By utilizing an aromatase inhibitor this conversion is either limited or
prevented. In most cases the difference between limiting and preventing conversion is
dose dependant. Pretty simple, huh?
By inhibiting the aromatization of androgens to estrogen there is not a build-up of
estrogen in the system. This was a plus during contest prep for Frank since elevated
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estrogen levels inhibited fat loss and increased water retention. It also meant less of
an estrogen induced negative feed-back loop inhibiting HPTA function for Frank.
Post cycle lean mass tissue loss was a significant concern.
Most AAS suppress HPTA function and therefore inhibit endogenous androgen
production. Elevated estrogen levels further inhibit HPTA regeneration post-cycle.
By utilizing estrogen inhibitors that decrease aromatase enzyme activity during
AAS phases, there was a much lower build-up of estrogens post cycle to inhibit
HPTA regeneration.
So the lesson here was that "inhibition" was finally a good thing. Arimidex,
Teslac, 4-OH Testosterone, Formastane, Aromasin and Proviron are examples of
aromatase inhibitors. In short, aromatase inhibitors prevent the introduction (or
limit) of more estrogen into the system than is normally produced by biosynthesis.
Some also possess low antagonist qualities as well.
3. BIOSYNTHESIS INHIBITORS: These inhibitors control estrogen at its very
base, by preventing its endogenous biosynthesis. Normally the body begins the
synthesis of most hormones with the conversion of cholesterol into pregnenolone.
As usual, this is due to the activity of an enzyme. In this case it is the P-450
enzyme complex.
The hormone estrogen is several biochemical steps away from cholesterol...as you
know already. If the P-450 enzyme complex is inhibited then the chain or sequence of
biochemical steps are inhibited. Therefore so is the formation of estrogen and every
other endogenous P-450 enzyme dependant hormone.
Cytadren is a 2-step estrogen inhibitor. First Cytadren inhibits the P-450 enzyme
complex, and second it inhibits the aromatase enzyme. There are other biosynthesis
inhibitors such as Trilostane and Metyrapone. Normally all 3 drugs are utilized in
medicine as cortisol biosynthesis inhibitors.
That is entirely another issue. Since biosynthesis inhibitors control estrogen
beginning at the very base of hormone biosynthesis, obviously they are effective at
controlling water retention. Unfortunately, some negatively effect endogenous
androgen production as well.
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LIVER HEALTH (GROW FASTER/LIVE LONGER)
Changes in liver enzyme values can occur during AAS use. This is especially
true when oral c17-alkylated steroids or high dosage Tylenol are utilized. When a c17-
alkylated steroid is introduced into the system, the liver must work harder to
deactivate its molecule before excretion. Levels of Bilirubin, LDH (lactate
dehydrogenase), and alkaline phosphatase are all good indicators of liver health and
stress. I wrote a great deal more about this in "Chemical Muscle Enhancement". The
upper normal level for LDH is about 250 U/L.
However, during Frank's AAS phases employing oral c17-alkylated drugs, this
number may have risen to 400 U/L and above. "Usually" most doctors do not note
this as a major concern unless other indicators suggest excessive liver stress. If
alkaline phosphatase was above its upper limit of 1 50 IU/L as well, liver stress
became a factor. Often levels were reported to elevate for the first 2-3 weeks of a
cycle only to return to acceptable ranges a week later. For the most part brief
variations in liver enzymes were not harmful as this was potentially an adaptive
reaction. Another consideration was excessive alcohol use during AAS phases.
*You should see most people's blood work after a hard night of drinking and
partying. You would think Anadrol-50 was mild in comparison. This is not to say that
the abuse of any drug is a good idea.
BETTER HEALTH/BETTER BODY
I often find myself amazed at the great lengths some athletes will go to build
the ultimate living physical edifice with little regard for actual health. When reviewing
blood work-ups, it often becomes necessary to explain the most fundamental reality;
Destroy the inside and the outside will follow quickly. Sounds kind of silly to say, but
some individuals have invested as much as $50,000.00 a year into various
polypharmacological chemistries but not even $10.00 into health.
The body is an adaptive organism with Action/Reaction Factors both good and
bad. In the case of building the perfect beasts each factor had to be considered and
responded "to" or "with" the appropriate response for long term ultimate progress to
be achieved. In most cases, the beast's bodies reacted positively to chemical muscle
enhancement protocols of a brief intense nature. "Get in, grow harder, get out"
was the ideal intent. However, if any phase or protocol ran too long the body would
have begun counter measures that could have eventually resulted in failure and the
destruction of the organism.
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AAS and The Heart
Studies based upon valid research show prolonged high dose AAS use can have
negative effects upon the heart. Eventually non-stop high dosage AAS cycles will lead
to a decrease in high-density lipoprotein cholesterol (HDL). HDL protects against
cardio vascular disease by shuttling cholesterol out of the blood and back to the liver.
The liver degrades cholesterol into bile and only then can it be excreted from the
body. This is the only method the body has to get rid of excess cholesterol. It is not
like fat which can be burned or oxidized. A possible explanation for the significant
increases in low-density lip-protein (LDL) cholesterol during long AAS protocols is
simply a matter of biosynthesis.
Normally the body utilizes cholesterol to synthesize sex hormones
endogenously (produced inside the body). Testosterone, estrogen and others all
begin as cholesterol. When AAS are introduced exogenously, this process is inhibited.
This in turn allows cholesterol to build-up to dangerous levels until discontinuance of
the AAS. An interesting fact is that anything that stimulates HPTA (hypothalamus-
pituitary-testes-axis) function/activity also decreases bad cholesterol levels. It does so
by increasing hormone (like testosterone) production endogenously. Oral AAS have
the greatest negative effects upon HDL. Nandrolones have little or no negative effect.
In fact there are some studies that support the belief that nandrolones have a positive
effect upon HDL levels, though I have found this not to be true in all athletes.
AAS and Red Blood Cells
Another concern realized from AAS use is due to AAS induced increases in
production of red blood cells. AAS stimulate the kidneys synthesis of erythropoietin
(EPO) which in turn stimulates red blood cell production. Anadrol-50 was actually
medically prescribed for this purpose. An increase in red blood cell counts increases
oxygen transport, vascularity, muscle fullness/hardness and to a lesser extent body
weight. From Frank's point of view this was cool, to a point! Having too many red
blood cells for prolonged periods increases blood volume to a point of slowing
circulation. This increases the chances of blood clots and therefore also increases the
chance for strokes and heart attacks.
AAS and Aldosterone
AAS induce activation of the renin-angiotension system in the kidneys. This in
turn promotes the release of aldosterone from the adrenals which has a connection to
some types of high blood pressure or hypertension. Aldosterone is a hormone that
helps preserve blood volume via increased sodium retention and therefore water
retention. High water retention increases blood pressure and heart health risk if the
condition is over prolonged.
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So obviously AAS abuse is a bad idea. However, brief AAS protocols were
seldom reported to cause these negative effects simply due to their brief nature. Like
most things in life, it is not so much a matter of what we did, as how we did it.
ACTION/REACTION.
Diet Plays An Important Role In Heart Health
Diet plays an important role in heart and total physical health. A diet higher in
monounsaturated fats and Omega-3/Omega-6/GLA essential fatty acids aids in
preventing heart rhythm disturbances and raise protective HDL levels. They also
promote formation of good prostaglandins for growth. Any diet should not allow
more than 1 0% saturated fats by macronutrient ratio.
For elevated cholesterol there is a prescription drug called Mevacor that
contains Lovastatin which inhibits the liver from synthesizing cholesterol. It does so
by inhibiting a specific liver enzyme.
Red yeast rice contains Lovastatin naturally and is available over the counter. 2.5-3
grams daily has been shown to have similar effects as the drug Mevacor. Lovastatin
can cause muscle damage in higher dosages. So again more is not necessarily better.
Coenzyme Q-l 0 appears to prevent this effect.
Niacin (Flush-free) also aids in reducing negative cholesterol problems. 1-3 grams
daily has shown significant results in most individuals. Niacin should not be taken
before training unless the goal is carb depletion. B-complex vitamins can inhibit the
use of fat as an energy source and increase glycogen use during training. (B-vitamins
should be ingested after training)
Guqqal sterones also seem to aid in reducing negative cholesterol problems but I am
still researching this one. So far it looks very good.
Thyroid Drugs
Another issue we needed to look at was prolonged high dosage administration
of thyroid drugs. Much more will be discussed later on the metabolic thyroid hormone
factors, but for now I have a specific point.
Basically thyroid hormones reduce body fat stores by increasing the resting
metabolic rate. If more thyroid hormone is introduced exogenously, the body burns
more calories. To do so the dosage must be in excess of endogenous production. The
resulting effect is called hyper metabolic. When exogenous thyroid hormones are
introduced the result is a negative feed-back loop to the pituitary gland that shuts off
the release of thyroid stimulating hormone (TSH). This in turn shuts down thyroid
production/release of endogenous thyroid hormones. The higher and longer the
exogenous dosage, the worse or more powerful the negative feed-back loop. Several
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elite level athletes utilized thyroid hormone dosages daily that are 4-8 times over
natural production in the belief that this would cause an equivalent increase in protein
synthesis, protein-turn-over-rate (PTOR), and fat burning aspects. This was true to a
point.
When metabolic rate is increased, there is a resulting increase in calorie
expenditure. These calories come from amino acids, glucose/glycogen, and fatty
acids. Not only fat stores (Fatty acids).
Initially the body will burn more lean mass than fat. Can you say muscle loss? When
anabolic and anti-catabolic (Protein synthesis and protein sparing) chemistry was
stacked with thyroid hormones the focus turned to burning fat stores. The main
problem was that most athletes introduced more thyroid hormone than the counter
chemistry could react to. This resulted in decreased muscle strength of up to 40%,
soft tissue damage, and suppressed endogenous thyroid hormone production post-
cycle.
"More is not always better unless we are discussing breasts".
Post-cycle thyroid function was restored fairly quickly with 250 mg of guggal
sterone (or 25 mg pure extract) per 50 LBS of bodyweight daily in 4 divided dosages.
3-5 grams of the amino acid tyrosine daily and 1-2 grams of phosphates helps also.
This also worked well during the first week of GH use. More on that later.
So my point is that some athletes decided their muscle building chemistry
dosages based upon thyroid hormone dosages. It should have been the other way
around.
If the goal was to add mass or/and lose fat stores it was paramount to long
term potential (and health) that no dosage threshold be exceeded before a dosage
failed to provide acceptable results.
When excessive dosages of thyroid hormones were erroneously utilized this
necessitated the need for excessive counter chemistry. As a direct result GH and other
protein synthesis/protein sparing drug dosages would be quickly ramped up beyond
what was necessary. The result was a significant reduction in long term potential for
those whom chose this path.
The other issue should be the negative feed-back loop realized from exogenous
thyroid hormone use (or abuse). If normal TSH production was not restored post-
cycle, reported bodybuilding progress came to a stand still.
You will understand this better as we continue. I have never met anyone who
has abused thyroid drugs to a point of "permanent" TSH suppression, but have noted
31
many individuals who had over administered to a point of catabolism exceeding
anabolism. A few of these individuals thought so-called androgen-receptor-site burn-
out was the cause of their lack of progress.
They then proceeded to increases AAS dosages to the point where negative side
effects far out weighed the positive. It took some time and work, but they too began
to progress again.
"More is not always better. Enough is just right. Think of it like this: If
more were always better, why do you hate alimony payments, Frank?"
PSA
I will remind you of this several times, but PSA level test were important. The
normal reference range is 0.0-4.0 ng/ml. The lower the better. By the way, different
countries and labs will use slightly different reference ranges on any testing protocol.
A PSA level test indicates the risks of prostate cancer among other bad things. If the
level is high, DHT (Dehydrotestosterone) and estrogen together can trigger growth.
Recent studies have often sited the 5-LO enzyme as the mediator for BPH and prostate
cancer.
An interesting study relating to testosterone and its effects divided 61 men
ranging from 18-35 years of age into different dosage test groups utilizing
testosterone enanthate. The group divisions were: 25, 50, 125, 300, or 600 mg. One
of the tests monitored was PSA. Interestingly enough after 20 weeks there was no
significant difference in PSA levels between the lower and highest testosterone
dosage. Bhasin, s., et al. (2001) Testosterone dose response relationships in
healthy young men. Am J Physiol. 281 (6):E11 72-81
"There will be lots of sites and research quotes at the end of this text.
Sometimes they are just too interesting to wait.
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EFFECTIVE DOSAGE FACTORS
If any chemical muscle enhancement substance introduced was to have an
effect, it had to first establish a plasma level above normal for that individual. As
example, normal endogenous testosterone production for a male is "about" 50 mg
weekly. This is a 50 mg weekly plasma circulating level. Not 50 mg per day, but 50
mg per week, which amounts to about 7 mg per day.
For simplification, let's say that the 50 mg weekly production represented the
normal plasma threshold for Frank, and that plasma level refers to the circulating
plasma level per week. In order for an injection of (or oral dosage) exogenous
testosterone to have an effect, it had to be at a dosage which entered the circulatory
system at a rate and dosage that exceeded the normal plasma level and therefore the
normal plasma threshold. This threshold had to be maintained or elevated to remain
effective. This means that if the example AAS utilized suppressed HPTA function
(natural endogenous testosterone production is suppressed) then this too had to be
compensated for with exogenous dosages (longer low dosage cycles only).
Active-Life and Half-Life?
Each AAS and chemical enhancement compound has a theoretical active-life of
its own. An active-life is the period of time that a chemical remains active. Also each
has their own half-life. A half-life is the period necessary for half of the dosage to
migrate from the injection site into the vascular system and clear. So a 200 mg
injection of testosterone enanthate would theoretically release 100 mg of
testosterone by its half-life of 4 days, but remain effectively active for its active-life
for 8 days. Naturally there is a continued clearing of each half-life after this time
frame, but not to any real significance in our discussion.
So if testosterone enanthate was injected on day #1 and then released half of
its 200 mg dose (100 mg) by day #4, then this would have exceed the normal plasma
level/threshold and establish a new one. Thus caused an effect superior to normal
plasma levels. This is what is meant by the term supraphysiological by the way.
When I wrote "CME", a few critics complained about the fact that I listed drug
active-life ranges (in some examples) rather than a firm single period for each. After
years of monitoring blood tests it became obvious a drug could have different active
and half -lives in different people, under different conditions. I created a series of
charts which included multiple dosage thresholds during those years and utilized the
information to establish actual ranges. Obviously a "firm" number was not possible.
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Dosage Thresholds
There also were lowest and highest thresholds for most drugs with multiple
thresholds in between. The lowest threshold was the dosage required to cause an
effect, where as the highest was the maximum dosage: The point where any higher
dosages failed to cause better or more results (the latter is not listed in Chemical
Muscle Enhancement). There were notable multiple thresholds in between as well.
Simply stated, some drugs caused positive results at 100 mg but did not improve
results until 400 mg dosages were utilized.
To express another example of thresholds, 10 mg of oral Dianabol daily was
about equal in "activity" to normal male endogenous androgen activity. Yet it took 20
mg, usually, to exceed this threshold. The highest threshold, usually, was equal to 5
mg per 25 LBS of body weight daily for Dianabol (methandrostenolone).
Chemical and training history also greatly influenced dosage factors. A novice
who had a few years of training experience only required 1 mg per LB of bodyweight
of nandrolone decanoate (Deca) weekly to make excellent progress on a 28 day cycle.
My experience has been that athletes were foolish to exceed any threshold level
of a drug until it failed to deliver acceptable results. This was one of the greatest
long-term mistakes I saw and it significantly reduced long-term growth potential. If all
of this was not enough to deal with when structuring a cycle for Frank, consider this:
Different AAS have different affinities for receptor-sites and each has different activity.
Some are more potent androgenics or anabolics than others and would
therefore require lower dosages for equal response or goal. Some have longer or
shorter circulatory half-lives. Some even have different anabolic/anti-catabolic ratios
to consider. Therefore each drug is individualistic in action and reaction and these
factors had to be accounted for in order to make the best possible progress.
Please Read...and Think
I write to encourage thought. Controversy is great if it forces individuals to be
individuals who think! Well, are you frustrated yet? For some readers, much of that
information is simplistic, but in truth most individuals just play gun-slingers shooting
combinations in any order and for any period of time and hope for the best. Then
they wonder why they lost most of their gains post-cycle or failed to respond
significantly. In our perfect imaginary bodybuilding country, I started by making all of
this information clear to Frank.
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In the following sections, several of Frank's and other beast's protocols are
explained. Each of these took into consideration effective dosage factors and some
are out lined in multiple levels, as they were utilized by Frank N. Steroid and other
beasts. More is not always better and synergy is a key to success.
Remember, once a dosage established a threshold, concurrent dosages of other
AAS elevated the plasma level, and properly timed consecutive dosages of other AAS
would have maintained it. Does that make sense? If not, it will soon. A fact I must
make clear about half- and active-life periods is that some drugs with longer active-
lives, required a longer period to reach their effective potential. An example is Deca.
Deca has an active-life of about 14-16 days. However even after migrating from the
injection site a day passed before the drug became initially effective.
PROTOCOLS
The goal of any growth inducing protocol was to gain as much lean mass as
possible. To do this with a plan meant to gain, not merely maintain or regain losses
from prior cycles.
The Body Has Action/Reaction Periods and Factors
The body has Action/Reaction periods and factors. Basically the body begins to
adapt significantly to most attempts at altering homeostasis after 2-3 weeks. This
sucked since the best results from a cycle usually came during days #10-30. But we
also profited from this information and used it to Frank's advantage by utilizing brief
phases and cycles of 21-30 days, (this is the point where cycles provided serious
results) then got out before side effects out weighed benefits.
"To be successful it is necessary to create maximum growth thresholds and stop
before the body is able to achieve its own counter measure thresholds."
Action/Reaction
Let me explain. My experience has been that a cycle of 8 weeks providing a
continuous plasma level weekly of 400-800 mg testosterone begins to fail to provide
results about week #6 in most cases. This is because the level of endogenous
catabolic hormones becomes elevated as a reaction to the exogenous testosterone
administration and cellular signaling proteins begin to become overwhelmed, which is
due to the action of increase androgens. So anabolism and catabolism are again
about equal. Remember to create a growth environment one or both sides of the
anabolic/catabolic ratio must be altered in favor of either more tissue building or less
tissue wasting.
CONTROLLED CATABOLISM
FOR MAX ANABOLISM
During any period in which calorie expenditure is greater than calorie absorption, a
catabolic (tissue wasting) state exists. (DUH!) Bet you did not know that such a state
also induces an anabolic environment? (HUH?)
That's right boys and girls! Catabolism creates the best environment for freak
status growth. This is due to the body's survival response during which all kinds of
enzymes, intermediates, hormones, and receptor-sites are up-regulated to store and
utilize every possible nutrient absorbed as, or within, metabolically active tissue
(protein based like, uh, muscle!).
Have you ever noticed what happens when a competing bodybuilder diets for
weeks and months to get body fat levels down to 3-4% or so, then face-slams
anything that doesn't eat him/her first about 2 seconds after final judging? What
happens? For about 14 days body weight increases at an incredible speed with little
fat gain.
The body reacts positively to most stimuli for 14-21 days before initiating
counter measures.
Remember: The body seeks homeostasis? It is also paramount to realize that we grow
(or not) as a result of what we "absorb", not due to what we eat. During this controlled
catabolic period (Frank whined at this point) we create the ability to absorb, transport,
and utilize amazing amounts of calories.
There are Always Choices
There were two best choice protocols possible for setting the perfect
environment for Frank. One was simply a matter of reducing calories (fats/carbs) to
about 50% (or less) normal and over-train for 14 days before beginning Phase I. The
other involved a little chemistry and 1 1 days. (Gee, which do you think Frank N.
Steroid chose? Ya, so let's get on with it.)
CONTROLLED CATABOLISM
(Training/Daily Calorie Decreases utilized)
DAY 1: CHEST- 6 triple drop sets/shoulders 3 triple drop-sets (Any pressing exercise),
super-set side laterals/ rear delt raises 3 sets/ cut 500 calories from diet.
DAY 2: BACK-3 triple drop-sets any rowing exercise/3 triple drop-sets any pull-down
exercise/2 down the rack sets of shrugs/ cut 250 more calories from diet.
22
DAY 3: LEGS-Squats 3 sets of 20 reps/leg press 3 triple drop-sets/2 down the stack
sets of leg extensions/leg curls 3 triple drop sets/drop 250 calories diet
DAY 4: ARMS-Super set E.Z curls with skull crushers 4 sets/ Non stop super-set rope
push-downs with preacher curls 4 sets/1 set triple drop wide bar push-downs/ 1 set
down the rack DB curls. (Calories remain constant from this point through day #1 1)
DAY 5: 20-30 minute aerobic periods (Stair climber or bike) 90-120 minutes "Freaky
monkey type love" sex. (With partner)
DAY 6: Repeated day #1 training , 5mg DNP per kg of body weight daily .
DAY 7: Repeated day #2 training, 5mg DNP per kg/d, 3 table spoons PG oil
DAY 8: Repeated day #3 training, 5mg DNP per kg/d, 3 table spoons PG oil
DAY 9: Repeated day #4 training, 5mg DNP per kg/d, 3 table spoons PG oil
DAY 10: Repeated day #5 training, 5mg DNP per kg/d, 3 table spoons PG oil
REPEATED SEX OLYMPICS (Again with partner)
DAY 11: Slept
*During the 11 day controlled catabolic period it was paramount that Frank drank at
least one gallon of water daily. It takes a great deal of water to remove catabolic
waste. A good daily multi-vitamin/mineral was a must. 1 5-50 grams of glutamine
daily reduced protein loss (divided into 3-5 even dosages). Peptide glutamine is said
to be best (Though valid research is lacking), and 50-100 g/d was better. Alpha Lipoic
Acid (ALA) is a great anti-oxidant wisely added to Frank's periods of DNP employment.
PG OIL MIX: 2 parts flaxseed oil/1 part extra virgin olive oil/1 part evening
primrose oil. Divided dosages into 1 tablespoon 3 times daily. 25 ml of glycerine in
16 oz of water helped, too. PG oil was used as a supply of omega 3, omega 6, and
GLA fatty acids. Perfect for prostaglandin production. (Go read prostaglandins
"Chemical Muscle Enhancement")
Frank had done near non-stop AAS cycles for the past 56 months with few, if
any, off periods. At this point he was working out but small for obvious reasons on
both counts. However, he was ready to become a beast now. A dangerous chemical
called DNP helped burn off fat as well as clear out androgen (and other) receptor-
sites.
23
By now, the body had up-regulated anabolic receptor-sites, storage enzymes
and hormones, as well as intermediates that focus upon lean protein based tissue
anabolism.
THE OFF SEASON GOALS INTENDED FOR FRANK SHOULD
SEEM OBVIOUS...
1. Keep liver enzymes within acceptable ranges.
2. Avoid excessive fat build up (12%-14% max body fat)
3. Induce as much lean mass growth as possible
4. Control excessive water retention and heart/ kidney trauma.
5. Maintain estrogen and prolactin levels within growth ranges (estrogen increases
IGF- production and glycogen storage) but low enough to avoid gyno, female
pattern fat deposits, and excessive water retention (continue to the next section
24
ESTROGEN CONTROL
Estrogen "Control" was paramount for health and result potential reasons.
High/prolonged circulating estrogen levels could have negatively affected the heart
and other organs due to excess fat deposits and water retention. As you know, most
severe water retention during AAS phases is due to estrogen and the resulting
hormonal production increase of aldosterone.
Elevation of aldosterone affects the body's water table by altering electrolyte
balances favoring sodium retention. Since sodium regulates extracellular (outside the
cell) water and potassium regulates intracellular (inside the cell) water, an imbalance
favoring sodium results in extra water in the vascular system and under the skin. This
is the reason that some athletes look like "Bloat Boy" and have very high blood
pressure.
It is important to remember that electrolytes such as sodium and potassium
regulate the electric charges for flow of water molecules across cell membranes and
are an intricate part of the sodium-pump mechanism that allows goodies like
nutrients and creatine to actually enter the muscle cells.
Blood Pressure and Water Retention
Normal blood pressure readings for average individuals is around 120 over 80.
In fact, this is considered pretty healthy. However, bodybuilders and power lifters are
not average. (Certainly none of my monsters) They tend to be much larger and
heavier, carrying significantly more lean mass tissue. For this reason, they have larger
more powerful hearts to supply high volumes of blood to a greater amount of tissue.
The first number of a blood pressure reading indicates blood pressure after the
heart contracts, which raises vascular pressure, and blood is pumped through the
body. Obviously the second number indicates or measures blood pressure before the
heart contracts.
Since bodybuilders and power lifters have more powerful larger hearts, a first
number of 150, 160, or even 180 is relatively normal. (And as a lone factor was not
usually a reason to be concerned for Frank) However, if the second number was over
100, it was time to be very concerned! If the second number exceeded 100 during
an AAS phase, it was usually due to excessive water retention and that meant that
counter measures were immediately taken.
The most commonly used water retention counter measure was a low dose
diuretic such as 20 mg Lasix daily. I have found natural diuretics such as dandelion
root often resolved the problem. Regardless of diuretic form, liquids were always
replaced before bedtime. Sometimes counter measures required backing off on
25
aromatizing androgenic dosages, but usually this could be resolved with estrogen
control.
Most AAS Aromatize to estrogen to some degree. The higher androgenic
steroids more so than the higher anabolics. In the first book "Chemical Muscle
Enhancement" under drug descriptions, it is easy to find "aromatization". This gives
an evaluation of each drug's reported aromatization characteristic.
We employed three types of estrogen control drugs with
Frank:
1. ANTAGONISTS: These are drugs that act as competitive inhibitors by simply
competing with the estrogen molecule for its receptor-site.
The antagonist is like a little brother that beats you to the bathroom. If he gets in
first, he only sits there doing nothing but keep you out so you can't do your thing. If
estrogen can't get in, nothing happens.
Contrary to what is often claimed, antagonists are not "great" at controlling water
retention, in my opinion. Since they simply block receptor-sites they do not decrease
the levels of circulatory estrogen. This means potential increased levels of
aldosterone. They do have "some" positive effects upon water retention, but they were
best utilized as a drug for prevention of gynecomastia (Gyno/ bitch tits) and female
pattern fat deposits. Nolvadex and Cyclofenil are examples of antagonist.
An advantage of utilizing the properties of specific estrogen antagonist (Faslodex,
Clomid or Cyclofenil) for Frank was IGF-1 production. When estrogen is deactivated by
the liver, IGF-1 secretion results. It is also interesting that under the right conditions,
estrogen can increase GH levels by positively influencing the pituitary gland.
So in short, antagonists inhibit estrogen at receptor-sites and some aid in GH/IGF-1
secretion.
2. AROMATASE INHIBITORS: Aromatase inhibitors are sometimes called
antagonist also (which is a pretty loose term). Aromatase inhibitors control
estrogen by limiting or preventing the activity of the aromatase enzyme.
Normally, the aromatase enzyme induces the conversion of some types of androgens
into estrogens. By utilizing an aromatase inhibitor this conversion is either limited or
prevented. In most cases the difference between limiting and preventing conversion is
dose dependant. Pretty simple, huh?
By inhibiting the aromatization of androgens to estrogen there is not a build-up of
estrogen in the system. This was a plus during contest prep for Frank since elevated
26
estrogen levels inhibited fat loss and increased water retention. It also meant less of
an estrogen induced negative feed-back loop inhibiting HPTA function for Frank.
Post cycle lean mass tissue loss was a significant concern.
Most AAS suppress HPTA function and therefore inhibit endogenous androgen
production. Elevated estrogen levels further inhibit HPTA regeneration post-cycle.
By utilizing estrogen inhibitors that decrease aromatase enzyme activity during
AAS phases, there was a much lower build-up of estrogens post cycle to inhibit
HPTA regeneration.
So the lesson here was that "inhibition" was finally a good thing. Arimidex,
Teslac, 4-OH Testosterone, Formastane, Aromasin and Proviron are examples of
aromatase inhibitors. In short, aromatase inhibitors prevent the introduction (or
limit) of more estrogen into the system than is normally produced by biosynthesis.
Some also possess low antagonist qualities as well.
3. BIOSYNTHESIS INHIBITORS: These inhibitors control estrogen at its very
base, by preventing its endogenous biosynthesis. Normally the body begins the
synthesis of most hormones with the conversion of cholesterol into pregnenolone.
As usual, this is due to the activity of an enzyme. In this case it is the P-450
enzyme complex.
The hormone estrogen is several biochemical steps away from cholesterol...as you
know already. If the P-450 enzyme complex is inhibited then the chain or sequence of
biochemical steps are inhibited. Therefore so is the formation of estrogen and every
other endogenous P-450 enzyme dependant hormone.
Cytadren is a 2-step estrogen inhibitor. First Cytadren inhibits the P-450 enzyme
complex, and second it inhibits the aromatase enzyme. There are other biosynthesis
inhibitors such as Trilostane and Metyrapone. Normally all 3 drugs are utilized in
medicine as cortisol biosynthesis inhibitors.
That is entirely another issue. Since biosynthesis inhibitors control estrogen
beginning at the very base of hormone biosynthesis, obviously they are effective at
controlling water retention. Unfortunately, some negatively effect endogenous
androgen production as well.
27
LIVER HEALTH (GROW FASTER/LIVE LONGER)
Changes in liver enzyme values can occur during AAS use. This is especially
true when oral c17-alkylated steroids or high dosage Tylenol are utilized. When a c17-
alkylated steroid is introduced into the system, the liver must work harder to
deactivate its molecule before excretion. Levels of Bilirubin, LDH (lactate
dehydrogenase), and alkaline phosphatase are all good indicators of liver health and
stress. I wrote a great deal more about this in "Chemical Muscle Enhancement". The
upper normal level for LDH is about 250 U/L.
However, during Frank's AAS phases employing oral c17-alkylated drugs, this
number may have risen to 400 U/L and above. "Usually" most doctors do not note
this as a major concern unless other indicators suggest excessive liver stress. If
alkaline phosphatase was above its upper limit of 1 50 IU/L as well, liver stress
became a factor. Often levels were reported to elevate for the first 2-3 weeks of a
cycle only to return to acceptable ranges a week later. For the most part brief
variations in liver enzymes were not harmful as this was potentially an adaptive
reaction. Another consideration was excessive alcohol use during AAS phases.
*You should see most people's blood work after a hard night of drinking and
partying. You would think Anadrol-50 was mild in comparison. This is not to say that
the abuse of any drug is a good idea.
BETTER HEALTH/BETTER BODY
I often find myself amazed at the great lengths some athletes will go to build
the ultimate living physical edifice with little regard for actual health. When reviewing
blood work-ups, it often becomes necessary to explain the most fundamental reality;
Destroy the inside and the outside will follow quickly. Sounds kind of silly to say, but
some individuals have invested as much as $50,000.00 a year into various
polypharmacological chemistries but not even $10.00 into health.
The body is an adaptive organism with Action/Reaction Factors both good and
bad. In the case of building the perfect beasts each factor had to be considered and
responded "to" or "with" the appropriate response for long term ultimate progress to
be achieved. In most cases, the beast's bodies reacted positively to chemical muscle
enhancement protocols of a brief intense nature. "Get in, grow harder, get out"
was the ideal intent. However, if any phase or protocol ran too long the body would
have begun counter measures that could have eventually resulted in failure and the
destruction of the organism.
28
AAS and The Heart
Studies based upon valid research show prolonged high dose AAS use can have
negative effects upon the heart. Eventually non-stop high dosage AAS cycles will lead
to a decrease in high-density lipoprotein cholesterol (HDL). HDL protects against
cardio vascular disease by shuttling cholesterol out of the blood and back to the liver.
The liver degrades cholesterol into bile and only then can it be excreted from the
body. This is the only method the body has to get rid of excess cholesterol. It is not
like fat which can be burned or oxidized. A possible explanation for the significant
increases in low-density lip-protein (LDL) cholesterol during long AAS protocols is
simply a matter of biosynthesis.
Normally the body utilizes cholesterol to synthesize sex hormones
endogenously (produced inside the body). Testosterone, estrogen and others all
begin as cholesterol. When AAS are introduced exogenously, this process is inhibited.
This in turn allows cholesterol to build-up to dangerous levels until discontinuance of
the AAS. An interesting fact is that anything that stimulates HPTA (hypothalamus-
pituitary-testes-axis) function/activity also decreases bad cholesterol levels. It does so
by increasing hormone (like testosterone) production endogenously. Oral AAS have
the greatest negative effects upon HDL. Nandrolones have little or no negative effect.
In fact there are some studies that support the belief that nandrolones have a positive
effect upon HDL levels, though I have found this not to be true in all athletes.
AAS and Red Blood Cells
Another concern realized from AAS use is due to AAS induced increases in
production of red blood cells. AAS stimulate the kidneys synthesis of erythropoietin
(EPO) which in turn stimulates red blood cell production. Anadrol-50 was actually
medically prescribed for this purpose. An increase in red blood cell counts increases
oxygen transport, vascularity, muscle fullness/hardness and to a lesser extent body
weight. From Frank's point of view this was cool, to a point! Having too many red
blood cells for prolonged periods increases blood volume to a point of slowing
circulation. This increases the chances of blood clots and therefore also increases the
chance for strokes and heart attacks.
AAS and Aldosterone
AAS induce activation of the renin-angiotension system in the kidneys. This in
turn promotes the release of aldosterone from the adrenals which has a connection to
some types of high blood pressure or hypertension. Aldosterone is a hormone that
helps preserve blood volume via increased sodium retention and therefore water
retention. High water retention increases blood pressure and heart health risk if the
condition is over prolonged.
29
So obviously AAS abuse is a bad idea. However, brief AAS protocols were
seldom reported to cause these negative effects simply due to their brief nature. Like
most things in life, it is not so much a matter of what we did, as how we did it.
ACTION/REACTION.
Diet Plays An Important Role In Heart Health
Diet plays an important role in heart and total physical health. A diet higher in
monounsaturated fats and Omega-3/Omega-6/GLA essential fatty acids aids in
preventing heart rhythm disturbances and raise protective HDL levels. They also
promote formation of good prostaglandins for growth. Any diet should not allow
more than 1 0% saturated fats by macronutrient ratio.
For elevated cholesterol there is a prescription drug called Mevacor that
contains Lovastatin which inhibits the liver from synthesizing cholesterol. It does so
by inhibiting a specific liver enzyme.
Red yeast rice contains Lovastatin naturally and is available over the counter. 2.5-3
grams daily has been shown to have similar effects as the drug Mevacor. Lovastatin
can cause muscle damage in higher dosages. So again more is not necessarily better.
Coenzyme Q-l 0 appears to prevent this effect.
Niacin (Flush-free) also aids in reducing negative cholesterol problems. 1-3 grams
daily has shown significant results in most individuals. Niacin should not be taken
before training unless the goal is carb depletion. B-complex vitamins can inhibit the
use of fat as an energy source and increase glycogen use during training. (B-vitamins
should be ingested after training)
Guqqal sterones also seem to aid in reducing negative cholesterol problems but I am
still researching this one. So far it looks very good.
Thyroid Drugs
Another issue we needed to look at was prolonged high dosage administration
of thyroid drugs. Much more will be discussed later on the metabolic thyroid hormone
factors, but for now I have a specific point.
Basically thyroid hormones reduce body fat stores by increasing the resting
metabolic rate. If more thyroid hormone is introduced exogenously, the body burns
more calories. To do so the dosage must be in excess of endogenous production. The
resulting effect is called hyper metabolic. When exogenous thyroid hormones are
introduced the result is a negative feed-back loop to the pituitary gland that shuts off
the release of thyroid stimulating hormone (TSH). This in turn shuts down thyroid
production/release of endogenous thyroid hormones. The higher and longer the
exogenous dosage, the worse or more powerful the negative feed-back loop. Several
30
elite level athletes utilized thyroid hormone dosages daily that are 4-8 times over
natural production in the belief that this would cause an equivalent increase in protein
synthesis, protein-turn-over-rate (PTOR), and fat burning aspects. This was true to a
point.
When metabolic rate is increased, there is a resulting increase in calorie
expenditure. These calories come from amino acids, glucose/glycogen, and fatty
acids. Not only fat stores (Fatty acids).
Initially the body will burn more lean mass than fat. Can you say muscle loss? When
anabolic and anti-catabolic (Protein synthesis and protein sparing) chemistry was
stacked with thyroid hormones the focus turned to burning fat stores. The main
problem was that most athletes introduced more thyroid hormone than the counter
chemistry could react to. This resulted in decreased muscle strength of up to 40%,
soft tissue damage, and suppressed endogenous thyroid hormone production post-
cycle.
"More is not always better unless we are discussing breasts".
Post-cycle thyroid function was restored fairly quickly with 250 mg of guggal
sterone (or 25 mg pure extract) per 50 LBS of bodyweight daily in 4 divided dosages.
3-5 grams of the amino acid tyrosine daily and 1-2 grams of phosphates helps also.
This also worked well during the first week of GH use. More on that later.
So my point is that some athletes decided their muscle building chemistry
dosages based upon thyroid hormone dosages. It should have been the other way
around.
If the goal was to add mass or/and lose fat stores it was paramount to long
term potential (and health) that no dosage threshold be exceeded before a dosage
failed to provide acceptable results.
When excessive dosages of thyroid hormones were erroneously utilized this
necessitated the need for excessive counter chemistry. As a direct result GH and other
protein synthesis/protein sparing drug dosages would be quickly ramped up beyond
what was necessary. The result was a significant reduction in long term potential for
those whom chose this path.
The other issue should be the negative feed-back loop realized from exogenous
thyroid hormone use (or abuse). If normal TSH production was not restored post-
cycle, reported bodybuilding progress came to a stand still.
You will understand this better as we continue. I have never met anyone who
has abused thyroid drugs to a point of "permanent" TSH suppression, but have noted
31
many individuals who had over administered to a point of catabolism exceeding
anabolism. A few of these individuals thought so-called androgen-receptor-site burn-
out was the cause of their lack of progress.
They then proceeded to increases AAS dosages to the point where negative side
effects far out weighed the positive. It took some time and work, but they too began
to progress again.
"More is not always better. Enough is just right. Think of it like this: If
more were always better, why do you hate alimony payments, Frank?"
PSA
I will remind you of this several times, but PSA level test were important. The
normal reference range is 0.0-4.0 ng/ml. The lower the better. By the way, different
countries and labs will use slightly different reference ranges on any testing protocol.
A PSA level test indicates the risks of prostate cancer among other bad things. If the
level is high, DHT (Dehydrotestosterone) and estrogen together can trigger growth.
Recent studies have often sited the 5-LO enzyme as the mediator for BPH and prostate
cancer.
An interesting study relating to testosterone and its effects divided 61 men
ranging from 18-35 years of age into different dosage test groups utilizing
testosterone enanthate. The group divisions were: 25, 50, 125, 300, or 600 mg. One
of the tests monitored was PSA. Interestingly enough after 20 weeks there was no
significant difference in PSA levels between the lower and highest testosterone
dosage. Bhasin, s., et al. (2001) Testosterone dose response relationships in
healthy young men. Am J Physiol. 281 (6):E11 72-81
"There will be lots of sites and research quotes at the end of this text.
Sometimes they are just too interesting to wait.
32
EFFECTIVE DOSAGE FACTORS
If any chemical muscle enhancement substance introduced was to have an
effect, it had to first establish a plasma level above normal for that individual. As
example, normal endogenous testosterone production for a male is "about" 50 mg
weekly. This is a 50 mg weekly plasma circulating level. Not 50 mg per day, but 50
mg per week, which amounts to about 7 mg per day.
For simplification, let's say that the 50 mg weekly production represented the
normal plasma threshold for Frank, and that plasma level refers to the circulating
plasma level per week. In order for an injection of (or oral dosage) exogenous
testosterone to have an effect, it had to be at a dosage which entered the circulatory
system at a rate and dosage that exceeded the normal plasma level and therefore the
normal plasma threshold. This threshold had to be maintained or elevated to remain
effective. This means that if the example AAS utilized suppressed HPTA function
(natural endogenous testosterone production is suppressed) then this too had to be
compensated for with exogenous dosages (longer low dosage cycles only).
Active-Life and Half-Life?
Each AAS and chemical enhancement compound has a theoretical active-life of
its own. An active-life is the period of time that a chemical remains active. Also each
has their own half-life. A half-life is the period necessary for half of the dosage to
migrate from the injection site into the vascular system and clear. So a 200 mg
injection of testosterone enanthate would theoretically release 100 mg of
testosterone by its half-life of 4 days, but remain effectively active for its active-life
for 8 days. Naturally there is a continued clearing of each half-life after this time
frame, but not to any real significance in our discussion.
So if testosterone enanthate was injected on day #1 and then released half of
its 200 mg dose (100 mg) by day #4, then this would have exceed the normal plasma
level/threshold and establish a new one. Thus caused an effect superior to normal
plasma levels. This is what is meant by the term supraphysiological by the way.
When I wrote "CME", a few critics complained about the fact that I listed drug
active-life ranges (in some examples) rather than a firm single period for each. After
years of monitoring blood tests it became obvious a drug could have different active
and half -lives in different people, under different conditions. I created a series of
charts which included multiple dosage thresholds during those years and utilized the
information to establish actual ranges. Obviously a "firm" number was not possible.
33
Dosage Thresholds
There also were lowest and highest thresholds for most drugs with multiple
thresholds in between. The lowest threshold was the dosage required to cause an
effect, where as the highest was the maximum dosage: The point where any higher
dosages failed to cause better or more results (the latter is not listed in Chemical
Muscle Enhancement). There were notable multiple thresholds in between as well.
Simply stated, some drugs caused positive results at 100 mg but did not improve
results until 400 mg dosages were utilized.
To express another example of thresholds, 10 mg of oral Dianabol daily was
about equal in "activity" to normal male endogenous androgen activity. Yet it took 20
mg, usually, to exceed this threshold. The highest threshold, usually, was equal to 5
mg per 25 LBS of body weight daily for Dianabol (methandrostenolone).
Chemical and training history also greatly influenced dosage factors. A novice
who had a few years of training experience only required 1 mg per LB of bodyweight
of nandrolone decanoate (Deca) weekly to make excellent progress on a 28 day cycle.
My experience has been that athletes were foolish to exceed any threshold level
of a drug until it failed to deliver acceptable results. This was one of the greatest
long-term mistakes I saw and it significantly reduced long-term growth potential. If all
of this was not enough to deal with when structuring a cycle for Frank, consider this:
Different AAS have different affinities for receptor-sites and each has different activity.
Some are more potent androgenics or anabolics than others and would
therefore require lower dosages for equal response or goal. Some have longer or
shorter circulatory half-lives. Some even have different anabolic/anti-catabolic ratios
to consider. Therefore each drug is individualistic in action and reaction and these
factors had to be accounted for in order to make the best possible progress.
Please Read...and Think
I write to encourage thought. Controversy is great if it forces individuals to be
individuals who think! Well, are you frustrated yet? For some readers, much of that
information is simplistic, but in truth most individuals just play gun-slingers shooting
combinations in any order and for any period of time and hope for the best. Then
they wonder why they lost most of their gains post-cycle or failed to respond
significantly. In our perfect imaginary bodybuilding country, I started by making all of
this information clear to Frank.
34
In the following sections, several of Frank's and other beast's protocols are
explained. Each of these took into consideration effective dosage factors and some
are out lined in multiple levels, as they were utilized by Frank N. Steroid and other
beasts. More is not always better and synergy is a key to success.
Remember, once a dosage established a threshold, concurrent dosages of other
AAS elevated the plasma level, and properly timed consecutive dosages of other AAS
would have maintained it. Does that make sense? If not, it will soon. A fact I must
make clear about half- and active-life periods is that some drugs with longer active-
lives, required a longer period to reach their effective potential. An example is Deca.
Deca has an active-life of about 14-16 days. However even after migrating from the
injection site a day passed before the drug became initially effective.
PROTOCOLS
The goal of any growth inducing protocol was to gain as much lean mass as
possible. To do this with a plan meant to gain, not merely maintain or regain losses
from prior cycles.
The Body Has Action/Reaction Periods and Factors
The body has Action/Reaction periods and factors. Basically the body begins to
adapt significantly to most attempts at altering homeostasis after 2-3 weeks. This
sucked since the best results from a cycle usually came during days #10-30. But we
also profited from this information and used it to Frank's advantage by utilizing brief
phases and cycles of 21-30 days, (this is the point where cycles provided serious
results) then got out before side effects out weighed benefits.
"To be successful it is necessary to create maximum growth thresholds and stop
before the body is able to achieve its own counter measure thresholds."
Action/Reaction
Let me explain. My experience has been that a cycle of 8 weeks providing a
continuous plasma level weekly of 400-800 mg testosterone begins to fail to provide
results about week #6 in most cases. This is because the level of endogenous
catabolic hormones becomes elevated as a reaction to the exogenous testosterone
administration and cellular signaling proteins begin to become overwhelmed, which is
due to the action of increase androgens. So anabolism and catabolism are again
about equal. Remember to create a growth environment one or both sides of the
anabolic/catabolic ratio must be altered in favor of either more tissue building or less
tissue wasting.
