Big Fat Bastards and Insulin
Ask any of the bodybuilding elite who has become truly massive beasts which
anabolic substance has had the most profound effect upon their
physique and the answer from the largest mammals will unanimously be
insulin. Though HGH has brought to the forefront of competitive stages
the well retained lean muscle mass tissue displayed beneath an onion
skin exterior of today, it is the symbiotic relationship insulin has
with all other physical enhancement chemistry that has made beasts
what they are in the new millenium.
Insulin is predominantly a storage hormone in that it initiates a
cascade of cellular events that result in up-regulation of cellular
nutrient content. It obviously goes without saying then that
supraphysiological plasma levels of insulin result in
supraphysiological cellular levels of nutrients. This in itself
allows for a highly anabolic effect known as an osmotic response. A
cellular osmotic response is nothing more than an increase in water
and growth potentiating nutrients intracellularly that has a effect
similar to increasing the amount of air in a balloon. More air in the
balloon means a larger balloon. More water and proportionate growth
nutrients means a larger cell. Interesting enough is the fact that
this also triggers another survival mechanism that tells the
stretched cell wall to increase in thickness to accommodate the
osmotic response. This is due to an up-regulation in localized IGF-1
and MGF production and the synergistic response initialize. Oh ya.
That is anabolism in the form of hypertrophy. Unfortunately, insulin
is quite anabolic to fat cells too.
Since insulin is the body�s main "storage" hormone it
should come as no surprise to the reader that many diabetics and
would-be beasts alike have become horribly fat as a result of
improper insulin use and misguided dietary habits. Many bodybuilders
have employed the 10-15 grams of carbohydrates per IU of insulin
administered protocol with a great deal of success in spite of the
inherent dangers of non-medical insulin use. However many, who have
either become insulin resistant/insensitive or are genetically
predisposed to inordinate adipose (fat) tissue accumulation, have
endured a greater anabolism of adipose tissue than muscle. Some have
foolishly put on more covering clothing and simply accepted this as a
necessary side effect endured for the greater eventual goal. Others
have added the additional potential negative side effects of heart
arrhythmia/tachycardia, diabetes, and other not so fun stuff as well.
As I have pointed out many times before, adipose tissue is a major
site for aromatase enzyme activity which in itself compounds the Big
Fat Bastard problem. Many AAS (anabolic/androgenic steroids) are
susceptible to the effects of aromatase enzyme conversion to
estrogens as is endogenously produced (made inside the body)
androgens such as testosterone. Obviously the greater the volume and
activity of this enzyme that exists in the body, the greater the
chance and degree of aromatization that occurs. Estrogen is directly
anabolic to a minor degree to muscle tissue. Both fortunately and
unfortunately it is highly anabolic to adipose tissue. Since estrogen
is the hormone that induces female pattern fat deposits it is
fortunate because a nice rack is a thing of beauty. Unfortunately I
have as of yet not noted a single male bodybuilder who looked good or
happy with boobs or any other fatty female attributes. So a greater
degree of adipose tissue accumulation from insulin administration
results in a compounded adipose tissue storage effect from aromatase
enzyme susceptible AAS employment.
In some instances the result of this vicious cycle is bodybuilders
who fail to ingest adequate calories during AAS protocols as a means
of decreasing adipose tissue accumulation. Unless you are from
another planet you realize this also limits muscular growth potential
Before we discuss all of the interesting facts concerning the means
of becoming a big fat bastard, it is necessary to have a fundamental
understanding of the macronutrient product glucose.
Glucose is the body�s preferred energy substrate. Though the
brain�s nutrient make-up is nearly 1/3 omega-3 fatty acids it is
glucose that is without fail mandatory for continued sentience. So
carb up a little and read closely as we learn a few things about the
body we have been entrusted to play nice with.
When we ingest food stuffs in the form of the three macronutrients
protein, carbohydrates, and fats the GI track introduces a series of
chemical Action/Reaction Factors that result in the break-down of
these nutrients to metabolic substrates.
Proteins = amino acids
Carbohydrates = glucose
Fats = fatty acids
It appears simple on the surface but in fact glucose can be converted
to triglycerides and adipose tissue or lean tissue glycogen stores
and toilet tinkle. Like wise fatty acids can be stored as fat or
utilized as an energy substrate by the body�s tissues but it cannot
be converted to glucose. This is interesting when one considers the
fact that carbohydrates can become glucose or fat, but fat cannot
become glucose (though the cellular mitochondria can use fatty acids
as an energy substrate as a keto response). Protein is ultimately
destined to become amino acids employed for cellular repair and
growth or intimate moments with the bathroom. But certain amino acids
called gluconeogenic amino acids can be converted to glucose too.
This can be disastrous for a bodybuilder who hopes to be a beast one
day since lean muscle mass is predominantly made up of protein in the
form of amino acids and a complete spectrum is necessary. We will get
to this later. For now simply accept that glucose is necessary for
life and bodybuilding progress alike.
The average circulatory value for glucose allows for about only 4
grams of glucose. It is actually uncommon for blood glucose levels to
rise beyond an additional 1.5-2.0 grams or to drop below the 4 gram
mark. A healthy individual who ingests a meal containing 50-150g of
mixed carbohydrates will realize the normal increase in circulatory
glucose for only about an hour. Interesting thing here is that
endogenous (made by the body) insulin secretion will remain elevated
for an additional 2 hours after glucose clearing. When the same
individual ingests 300g of carbs (Fat Bastard) at one time the
resulting insulin secretion levels will be 300% above normal for an
additional 7 hours after blood glucose clearing. This is clearly a
highly anabolic environment, but after tissue glycogen stores reach
maximum levels a grotesque amount of the excess glucose finds its way
to adipose tissue. And don�t worry. If all of the existing fat
cells are full, the body is way to happy to make new ones to secrete
lots of aromatase enzyme. And herein awaits the key to greater lean
mass tissue and a decrease in adipose tissue.
Gluconeogenesis is the biosynthesis of new glucose. This means that
glucose is synthesized from other substrates than carbohydrates or
glycogen stores. Obviously since the only source of fuel for the
brain, testes, kidneys, and erythrocytes is glucose the body in its
amazing adaptive manner can manufacture glucose from other materials.
Those who are up on keto diets are aware of the fact that the body
can derive energy from ketone bodies (which are converted into
acetyl-CoA). But that is an entire different topic for now. In short
the body utilizes the carbon structures within substrates to create
energy in the eventual form of ATP (adenosine triphosphate). ATP is
cellular energy that, as readers are aware, is the body�s only
energy currency. In the case of gluconeogenesis the carbon structures
can come from other sources.
Triglycerides are structures consisting of three fatty acids adjoined
by a glycerol molecule. By cleaving the fatty acids away from the
glycerol molecule the body can utilize the freed glycerol molecule to
make glucose through a series of conversions and subsequent carbon
With the exception of lysine and leucine all 20 (or 22 if you are of
that school of thought) amino acids can be turned into TCA cycle
intermediates which in turn allows for the carbon skeletons of the
amino acids to be converted to pyruvate. The newly formed pyruvate
can then be utilized by the gluconeogenic pathway to create glucose
by way of another series of metabolic pathways. Let me explain that a
little better. When glycogen stores in the liver and muscle are
depleted the working/recovering muscles, brain and organs need
another energy source. Catabolism of muscle tissue proteins to amino
acids becomes the main source of carbon skeletons for the maintenance
of mandatory blood glucose. As you will recall the body can clear 50
�150 grams of carbohydrates in only a few hours.
So how much muscle do you think the gluconeogenic adaptive process
can munch in the same period of inadequate nutrient supply from diet?
By the way, the amino acid Alanine is the favorite gluconeogenic
snack with Arginine and Glutamine coming in as close seconds.
THINK ABOUT IT
In the presence of circulatory insulin elevation gluconeogenesis in
the liver and muscle tissue decreases. During periods of circulating
supraphysiological levels of amino acid muscle catabolism decreases.
In the presence of both protein synthesis occurs.
So it would seem that the two choices a wanna-be beast faces is 300
grams of carbohydrates to induce a sufficient prolonged insulin spike
and a Big Fat Bastard pose down or non-stop keto diets and
declarations of "Hey, I may look like a weenie but I am really
cut" for life.
The obvious solution is an elevation in both circulatory insulin and
a corrected amino acid pool rendered highly efficient by design and
not by chance.
Insulin administration is nothing new to the larger beasts of the
bodybuilding world. Unfortunately neither is Big Fat Bastard status
in the brief off-season. So it should come as no surprise to those
who have entered the realm of the chemically enhance athlete to learn
that insulin can make even the best genetically predisposed
individual fat. It has been my experience that this is simply not
Insulin forces excessive amounts of amino acids into muscle cells
when an adequate supply exists at the time of insulin exposure.
Insulin also triggers increased muscle cell glycogen synthesis by way
of positively effecting the rate limiting enzyme glycogen synthase.
We also know the positive effects correct application of
supraphysiological insulin levels has had upon the most catabolic
pathway there is that affects muscle mass from reading my two prior
books. Add to this the fact that insulin is synergistic to and with
all other chemicals of muscular enhancement and realize the
In relationship to goals it would seem evident that a protocol
employing the attributes of insulin would necessitate the symbiotic
relationship the hormone has with macronutrients as it applies to
lean muscle mass tissue.
Muscle is more than 80% protein by dry weight.
ATP is the energy currency of muscular contractions, repair, and
Glucose is the prime source substrate for ATP synthesis and mandatory
for proper brain and organ function (yes, that one also).
Excess blood glucose will result in excess adipose tissue
When this protocol was created its intent was rapid accumulation of
lean mass tissue without an increase in adipose tissue deposits.
Since the foundation of the diet was structured for efficient
gluconeogenic dependant upon a correct ratio and amount of amino
acids, a great deal of protein was consumed daily. The most effective
protein intake minimum was the equivalent of 3 grams of protein per
pound of bodyweight daily divided into at least 6 meals. Using a 200
pound individual as an example it was possible to reduce this
slightly by simply eating 4 whole food meals daily providing 50 grams
of whole protein each and sipping on whey protein drinks in water
throughout the day
providing the remaining 400 grams of protein. I preferred whey
protein simply because it is one of the only two drinkable products I
am aware of that allows for actual hyperaminoacid response in the
circulatory system. Casein, egg, and (some people still use it) soy
proteins fail to clear the GI track at a rate significant enough to
induce the necessary supraphysiological amino acid concentrations for
the protocol. The fact that whey protein is easily oxidized by the
liver should be the first clue to the reason why results are
superior. By the way, the other is Human Profile by Hazardous
Materials (it is nearly 100% absorbed)
So here is the kicker. Though fat intake could be quite high, total
daily carbohydrate intake could not exceed 0.5 grams per 25 pounds of
bodyweight daily. The reason is simple: The goal was to force the
body to employ the gluconeogenic pathway as a means of energy
production. Any degree of actual glycogen regeneration resulted in
the body returning to the glycosis pathway which allows for adipose
tissue accumulation. The reason this worked so well was simplistic in
nature. The making of ATP through amino acid gluconeogenesis is very
inefficient thus allowing for a huge calorie expenditure similar to
what occurs during DNP utilization. During calorie expenditure the
body does not store fat but it does undergo protein anabolism. When
enough protein was ingested the result was always a net increase in
lean body mass of 5-8 pounds by the end of a two week protocol. Not
bad for an experienced beasts, huh?
Since exogenous insulin was utilized during this protocol and, as
mentioned prior, the gluconeogenic energy pathway loves certain amino
acids it is easy to realize that the normal ratio of amino acids
derived from whey protein and whole foods was not likely adequate. A
mixture of 4 parts Alanine, 2 parts Glutamine, 2 parts Arginine and 1
part Taurine was created and capsulated. The dosage ingested was 1
gram of the supplemental mix per I.U. of insulin administered daily
divided into 2 post administration dosages.
The preparation for this protocol required a liver glycogen depletion
period of 24 hours prior to initial insulin administration. This was
done to initiate the gluconeogenic pathway prior to protocol onset
thus preventing any loss of lean tissue growth potential.
Though only a total idiot would ever assume that non-medical
exogenous insulin use was safe, the utilization of a fast acting
insulin was the better choice for this protocol. The first reason of
course being that short acting chemistry also means shorter periods
of potential exposure to negative side effects like a coma. Second is
the fact that it was necessary due to the relevance in liver capacity
for glucose manufacture by way of gluconeogenesis. Running out of
adequate glucose reserves would introduce a series of potential
negative side effects that would have required the ingestion of
dextrose to inhibit.
EXAMPLES OF INSULIN
Name of Insulin Start Activity Highest Activity Ends Activity Low BS
Very short-acting (Humalog) 10 minutes 1.5 hours 3 hours 2-4 hours
Short-acting (Regular/-R) 20 minutes 3-4 hours 8 hours 3-7 hours
Intermediate acting (Nor L) 1.5-2 hours 4-15 hours 22-24 hours 6-13
Long-acting (Ultra Lente) 4 hours 10-24 hours 36 hours 12-28 hours
Combination: 70% N/30% R 0-1 hour 3-13 hours 12-20 hours 3-12 hours
Combination: 50% N/50% R 0-1 hour 3-12 hours 12-20 hours 3-12 hours
Humalog was administered about 15 minutes before an appropriate meal
Regular Type-R was administered 30 minutes before an appropriate meal
Low BS = Low blood sugar (Glucose).
As the reader can see when viewing the examples of insulin above, the
employment of Humalog allowed for a total of 4 daily administrations
of 10-15iu each and Humulin-R (Short-acting) only allowed for 3 daily
administrations. This is not to say some have not increased the
dosage or chose different insulin analogs, but it is to say that
under these circumstances it was not necessary or more effective.
When looking at the following example consider these facts:
Testosterone suspension has an active-life of about 24 hours tough
plasma androgen levels remain elevated for about an additional 24
Sex hormones such as testosterone and estrogens are inactive when
bound by SHBG (sex hormone binding globulin) and free or active when
Insulin is a powerful SHBG inhibitor.
Insulin increases muscle glucose transporters and androgen receptors
NOTE: This is for advanced users only.
Always start out at a much lesser dosage. IE: 2iu's maybe post
workout and work your way up from there. basskiller
1. Testosterone Sus. 150mg
2. Humalog 10iu 4xd
3. Testosterone Sus. 150mg
4. Humalog 10iu 4xd
5. Testosterone Sus. 150mg
6. Humalog 10iu 4xd
7. Testosterone Sus. 150mg
8. Humalog 10iu 4xd
9. Testosterone Sus. 150mg
10. Humalog 10iu 4xd
11. Testosterone Sus. 150mg
12. Humalog 10iu 4xd
13. Testosterone Sus. 150mg
14. Humalog 10iu 4xd
15. Testosterone Sus. 150mg
16. Humalog 10iu 4xd
17. Testosterone Sus. 150mg
18. Humalog 10iu 4xd
19. Testosterone Sus. 150mg
20. Humalog 10iu 4xd
21. Testosterone Sus. 150mg
22. Humalog 10iu 4xd
23. Testosterone Sus. 150mg
24. Humalog 10iu 4xd
25. Testosterone Sus. 150mg
26. Humalog 10iu 4xd
27. Testosterone Sus. 150mg
28. Humalog 10iu 4xd
Testosterone Sus. = testosterone suspension
150mg of testosterone suspension created a great deal of estrogen
since it originates as a non-esterfied AAS. Estrogen up-regulated the
muscle cells glucose transporters called GLUT-4 and increased
androgen receptor sensitivity. This also meant that the administered
testosterone was free or unbound from its inactivating protein SHBG.
A great deal of the hormone entering the circulatory system was
quickly bound, though not before a serious degree of anabolism
occurred. But there is a portion left bound and in reserve.
by Author L. Rea (author of Chemical Muscle
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