Answer: It seems very unlikely that much of the gains realized from this type of cycle

would be retained post-cycle. (There are always a couple of exceptions somewhere

to the rule) This is mostly due to the fact that testosterone (Sustanon-250 is a 4
testosterone ester blend) and methandrostenolone (AKA D-bol or Dianabol) are
highly susceptible to the aromatase enzyme that converts many AAS into estrogens.
(As many are aware, body fat is a prime site for aromatase enzyme production and
therefore plays a significant role in the amount of a given AAS that will be converted
into estrogens) In fact, the aromatase conversion product of methandrostenolone is
a particularly powerful super-girl-like estrogen that has given more guys a shot at
winning wet T-shirt contests than any other AAS.
Raisin Nuts Syndrome
Estrogen has a inhibiting effect upon the male's HPTA (hypothalamus-pituitarytestes-axis) that results in shut down of natural androgen production. When the
HPTA has been shut down for a prolonged period due to high aromatizing AAS use,
the result is no natural testosterone production for several weeks after the drugs
have been discontinued. This means an athlete's body has no androgens post-cycle
to support the new muscle tissue and the gains soon fall to fat due to a high estrogen
environment in the body.
Better Choices = Bigger Boys (Yes, Those too)
Shorter AAS protocols decrease the degree of HPTA shut-down as does the use of
non-aromatizing AAS such as oxandrolone during the cycle exit. Of course some
anti-aromatase drugs during periods of high estrogen during the cycle and HPTA
Regeneration chemistry post-cycle is a real plus also when the goal is to keep some
of those hard earned gains.
Day

Example Protocol

1. Sustanon-250 250mg/Methandrostenolone 40mg

2. Methandrostenolone 40mg
3. Sustanon-250 250mg/Methandrostenolone 40mg
4. Methandrostenolone 40mg
5. Sustanon-250 250mg/Methandrostenolone 40mg
6. Methandrostenolone 30mg
7. Sustanon-250 250mg/Methandrostenolone 30mg
8. Methandrostenolone 30mg
9. Sustanon-250 250mg/Methandrostenolone 30mg
10. Methandrostenolone 30mg
11. Sustanon-250 250mg/Methandrostenolone 20mg
12. Methandrostenolone 20mg
13. Sustanon-250 250mg/Methandrostenolone 20mg
14. Methandrostenolone 20mg
15. Sustanon-250 250mg/Methandrostenolone 20mg16.
17. Sustanon-250 250mg
18.
19. Sustanon-250 250mg

20.
21. Sustanon-250 250mg
22.
23. Sustanon-250 250mg
24.
25. Sustanon-250 250mg
26.
27. Sustanon-250 250mg
28.
29. Sustanon-250 250mg
30.
31. Oxandrolone 25mg
32. Oxandrolone 25mg
33. Oxandrolone 25mg
34. Oxandrolone 25mg
35. Oxandrolone 25mg
36. Oxandrolone 25mg
37. Oxandrolone 25mg
38. Oxandrolone 25mg
39. Oxandrolone 25mg
40. Oxandrolone 25mg
41. Oxandrolone 25mg
42. Oxandrolone 25mg
Day 1-42 Arimidex 1mg
Day 39-58 HCG 500iu
Day 46-50 Clomid 100mg and 50mg day 51-60
Question: In my attempt to look into the possibility of using steroids, I was
recommended by a friend who has one of the best looking bodies (dense and
ripped) at the gym to use Winstrol. After numerous readings from the net, I
come to realize that being a DHT-derivative, Winstrol is potentially harsh on
hair. I have already exhibited a mild case of male pattern baldness at crown,
would Winstrol aggravate the condition? Since MPB rather than liver problem
is more a concern to me, is there any steroids out there would impart a lesser
damage that suit DHT sensitive guys like us? Thanks.
Answer: An informed decision is always the better option, Lad. So perhaps I can be
of help and shed some useful light upon the subject. First off, you must realize that
each anabolic substance can have a slightly different response on different
individuals. So your friend may do well when using a somewhat mild AAS like
stanozolol (Winstrol), or he may be employing very high dosages and spending a
small fortune to do so. Then again, he could be one of the rare true genetic freaks
we all love and hate.
Testosterone Is Still El-Rey (The King)
One error that exists in choosing a single AAS is the assumption that one cannot
alter its characteristics in favor of personal needs. As example, consider
testosterone. As a whole testosterone has been responsible for more tons of new

muscle than any other two AAS combined in the history of anabolics. Why? Well, first
off it is relatively cheap, and second because it is equally anabolic and androgenic.
This means a significant increase in muscle protein synthesis occurs in conjunction
with a comparable increase in strength in the form of weight and work-load capacity.
More strength means more tissue is worked, and greater protein synthesis means a
greater amount of super-compensation results in the form of more muscle for the
effort. One fuels the other.
But Testosterone Is For Chrome Domes
Many assume that an increase in circulating testosterone means a swollen prostate,
chrome dome syndrome (due to DHT conversion) and gynecomastia (bitch tits, due
to estrogen conversion). Oddly enough few seem to consider the use of synergistic
drugs to control these negative side effects while potentiating the effects of
testosterone itself for personal goals. (Huh?)
DHT Control
The reason that some of the circulating testosterone in converted into DHT
(dihydrotestosterone) is due to an enzyme called 5-alpha-reductase. There are
several drugs on the market that either inhibit the enzyme or block the DHT receptor
sites. A prime and common example is finasteride (Proscar and Propecia).
Finasteride acts to inhibit the 5-alpha-reductase enzyme from reducing testosterone
(and other AAS) into DHT and has "some" capacity to block DHT receptor-sites. This
means the prior characteristic prevents DHT formation and the latter keeps the DHT
out of its receptors.
Those it is often said that 1mg daily of finasteride allows for adequate DHT control I
have found that for most 2.5 -5mg daily was needed when dosages of testosterone
reach or exceed 600mg weekly. Interesting when one considers that this also affords
a valuable control effect upon prostate growth (Benign Prostate Hyperplasia AKA:
BPH) and a reduction in prostate cancer risks.
Purchasing finasteride in 1mg tabs under the product name Propecia is nearly twice
as expensive as buying the 5mg tabs under the product name Proscar and cutting
them in half. (Yup!) Both are prescription drugs not all that difficult to acquire as the
mere existence of BPH in anyone's family history is cause enough for most
physicians.
Controlling Those Feminine Urges
It appears that few are aware of the fact that increased estrogens have been heavily
implicated as a primary cause of both hair loss and BPH. In fact it appears that the
accumulation of DHT combined with increased estrogens is the actual chrome dome
combo of all time. It also appears that males who experience a significant elevation
in estrogen tend to become more emotional. (Just what we need: A 300 pound freak
upset about his training gear color coordination. Geez!)
Aromatase Control

There are two three types of estrogen control drugs:

1. Estrogen receptor-site antagonist: These merely block the entrance of more
powerful estrogens from their own receptors. The result is less estrogenic
activity.
2. Biosynthesis Inhibitors: These drugs stop the synthesis of estrogens by
inhibiting the biosynthesis of the first step in all sex hormone synthesis
(namely the production of pregnenolone from cholesterol)
3. Anti-aromatase: This is a group of drugs that inhibit either the production or
activity of the aromatase enzyme that is responsible for the conversion of
testosterone into estrogens.
Which One?
Of these the most effective for the control of estrogen production from testosterone
are the anti-aromatase. Arimidex, Aromasin and Formestane are the best known.
(There is another soon to be available that is more effective, HPTA stimulating and
anabolic as welland it will be over the counterfor awhile). For most who suffer
hair loss from AAS use 1-2mg daily of Arimidex, 25-50mg daily of Aromasin, or
250mg of parental (injection) Formestane weekly will keep estrogen levels in
reasonable reference ranges.
More Testosterone?
A point to consider hear is that although DHT and estrogen both possess their
positive value in the muscle growth process one cannot discount the fact that if less
testosterone is converted to DHT and estrogen then there is more actual
testosterone left to do its job (Uh, like build muscle)

Read more from this MESO-Rx article at:

http://www.mesomorphosis.com/articles/rea/030704.htm#ixzz1J1qPvwrU