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36 PEDs cycle progression phase dependent compounds

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UNIVERSITY

PEDs
Cycle Progression: Phase
Dependent Compounds


Lesson Overview
PED deployment for situational drugs
Winstrol
Halotestin
Anadrol
Boldenone
Sample Contest Prep Cycle design


PED Deployment
Anabolic Androgenic Steroids

Ancillary Compounds

Testosterone Based
Testosterone
Boldenone**
Halotestin*
Dianabol*

Estrogen and Fertility Management
Anastrozole*
Extremestane*
Nolvadex*


Clomid*
HCG

Dihydrotestosterone Based
Primobolan
Masteron
Anavar
Proviron
Winstrol*
Anadrol*
Nandrolone (19-Nor) Based
Nandrolone
Trenbolone*

Peptide Hormones
Growth Hormone

Blood Glucose
Metformin
Slow and Fast Insulin*
Blood Pressure
ARBs PPAR y-agonist Telmisartan

Fat Loss Agents
Clenbuterol*
T3/T4*
Yohimbine HCl*
No asterisk = frequent use allowable; and have been or currently in human clinical use.
*Phase Dependent Drug to deploy conditionally due to necessity, goal and/or safety risk, have
been or currently in human clinical use.

**Not approved for Human Use, rare situation deployed


Winstrol (Stanozolol)
Clinical Application
Came to market in 1962
Application in osteoporosis, children with growth failure, anti-catabolic
during corticosteroid therapy and burns, later used in breast cancer,
angioedema (swelling subdermal tissue). Still approved drug, but no
longer in usage.
PED in horse racing
Originally dosing 6mg per day
Properties
Structure: DHT derivative with Pyrazol group in A-ring limiting 3α hydroxysteroid dehydrogenase (3α-HSD) activity in skeletal muscle,
improving anabolic property compared to DHT
Estrogen Interaction: Not effected by aromatase enzyme, limits any water
retention. “dry out effect” and increase in androgen to estrogen ratio.
Progesterone Interaction: Possible slight antagonism
5-alpha reductase interaction: Not subject to 5-alpha reductase, already 5
alpha reduced
Glucocorticoid interaction: slight antagonism “dry out effect”
SHBG: strong suppressor of SHBG
Cardiovascular: 6mg per day for 6 weeks: mean HDL reduction of 33% and
29% increase in LDL.
Liver:c17aa, liver toxic. Studies giving 12mg per day for 27 weeks showed
no change in LFTs. IM Winstrol still liver toxic.
Test suppression: 10mg for 14 days enough to suppress natural
testosterone for 14 days.
Tendon ruptures: increases collagen synthesis increase in muscle strength
likely effect of increase in tendon damage along with times implemented.



Winstrol (Stanozolol)

Bodybuilding Application
Offseason:
No application. Liver toxic, limited building properties compared to
other IM steroids.
Increased liver toxicity test suppression and lipid alterations compared
to Anavar mg for mg.
Contest Prep:
Implemented last 4-6 weeks of contest prep to offset androgen to
estrogen ratio allowing for less water retention.
Increased strength during later stages of dieting
Reduction on muscle catabolism
Dosing: 25-75mg per day


Halotestin (fluoxymesterone)
Clinical Application
Came to market in 1956
Used in both males and females
Osteoporosis, cachectic conditions, treating androgen deficiency,
breast cancer. Still FDA approved drug but rarely used today.
Prescribing guidelines of 5-20mg per day
Properties
Structure: Testosterone derivative w/ fluro group added to carbon 9
and hydroxyl group at carbon 11 enhances anabolic action.
Estrogen Interaction: Not effected by aromatase enzyme, limits any
water retention. “dry out effect” and increase in androgen to estrogen

ratio.
5-alpha reductase interaction: substrate for 5 alpha reductase
increasing androgenic action on non skeletal muscle targets. Likely the
“aggression” known from Halo.
Cardiovascular: Oral 17aa steroids will alter lipid profiles.
Liver:c17aa, liver toxic. 20mg a day is enough to elevate liver strain.
Test suppression: 10-30mg highly suppressive to endocrine
testosterone


Halotestin (fluoxymesterone)

Bodybuilding Application
Offseason:
No application. Liver toxic, limited building properties compared to
other IM steroids.
Increased liver toxicity test suppression and lipid alterations
Contest Prep:
Implemented last 3 weeks of contest prep to offset androgen to
estrogen ratio allowing for less water retention.
Increased strength during later stages of dieting
Reduction on muscle catabolism
Steroid is expensive and faked, effect can be mimic with Winstrol
Dosing: 20-30mg per day


Anadrol (Oxymetholone)
Clinical Application
Came to market in 1960s
HIV wasting, COPD

Red blood cell deficient Anemia (high increased in RBC production);
1-2mg/kg of body weight to treat anemia
Properties
Structure: unique DHT derivative; 2-hydroxymethylene group inhibits
3-hydroxy steroid dehydrogenase. Closer behavior to that of
nandrolone than a DHT.
Estrogen Interaction: Highly estrogenic with potential to bind the
estrogen receptor but not subject to the aromatase enzyme, high
amount of water retention.
5-alpha reductase interaction: Not a substrate for 5 alpha reductase
however the 2-hydroxymethylene group can be removed, reducing
anadrol to mestanolone, a potent androgen.
Cardiovascular: 50mg or 100mg daily given to 31 elderly men for 12
weeks caused a 19 and 23 point drop in HDL, respectively.
Liver:c17aa, liver toxic. 50mg or 100mg daily given to 31 elderly men
for 12 weeks increase LFTs significantly only in the 100mg group. 50mg
daily of one year increased GGT 17% and patient incurring a liver
tumor. Well known for decreasing appetite.


Anadrol (Oxymetholone)
*Overall Not Recommended
Bodybuilding Application
Offseason:
Limited application. Liver toxic, high RBC promotion, high water
retention, high blood pressure.
Not ideal for long term safe usage model
Strength and mass increase, however, may compromise appetite and
defeat that point of offseason and pushing food up.
Some use as a “plateau breakthrough”, but I see this is not needed

when we have injectables like Testosterone and Nandrolone.
Dosing: 50mg 4-6 weeks
Contest Prep:
Poor application in contest prep
Anadrol ”loading” has been done as a peaking strategy, however the
fullness from water retention is typically seen extracellular as well.


Dianabol (methandienone)
Clinical Application
1958 released to market
Post menopausal osteoporosis, pituitary deficient dwarfism
1980s withdrawn from market
5mg per day clinical dosing
Properties
Structure: testosterone derivative; double bond added b/w carbon 1
and 2 reduces androgenicity compared to testosterone
Estrogen Interaction: subject to aromatase enzyme into 17alphamethylestradiol, high water retention with this compound
5-alpha reductase interaction: limited interaction with 5-alpha
reductase.
Cardiovascular: being that it is c17aa oral it will alter lipid levels
significantly.
Liver:c17aa, liver toxic. Dosages over 10mg per day have shown liver
stress altered.
Testosterone suppression: 15mg per day for 8 weeks caused a 59%
reduction in endocrine test levels.


Dianabol (Methandienone)
*Overall Not Recommended

Bodybuilding Application
Offseason:
Poor application. Liver toxic,, high water retention, high blood
pressure.
Not ideal for long term safe usage model
Most gains will be water retention, subject to appetite decrease like
Anadrol
I see no place for this compound

Contest Prep:
No application here


Equipose (boldenone)
Clinical Application
Patented in 1940s
Brief history of human usage in 60s, clinical trials for osteoporosis (not
used as “better” steroids existed)
1970s brought to veterinary market for horses (lean bodyweight,
appetite) owned by Pfizer
Not human approved

Properties
Structure: testosterone derivative; double bond b/w 1 and 2 carbon,
reducing estrogenicity. Identical structure to Dianabol, different
behavior. Anabolic, low androgenic.
Estrogen Interaction: Subject to aromatase enzyme but far less than
testosterone.
5-alpha reductase interaction: limited interaction with 5-alpha
reductase. Will convert to Dihydroboldenone but limited.

Cardiovascular: No research in humans but subject to same effects of
HDL lowering as other IM steroids.
Liver: Not c-17 aa and limited hepatotoxic, but also limited human
data.
Erythrocytosis: all steroids increase EPO, potentially more renal toxic,
increased blood pressure.


Equipose (boldenone)
*Overall Not Recommended
Bodybuilding Application
Offseason:
Poor application
Boldenone brings more anabolism to a cycle with some estrogen, we
have better drugs to do this (testosterone + primobolan or masteron).
Boldenone is potentially more renal toxic than comparable
compounds as well.
Not ideal for long term safe usage model

Contest Prep:
No application here for same reasons above.


Sample Cycle Progression Contest Prep
intermediate/advanced
16 weeks out
Test cypionate 300mg/wk
Primobolan 400mg /wk
GH 2IU pre workout and pre
bedtime

12 weeks out
Test cypionate 300mg/wk
Primobolan 400mg/wk
Masteron 400mg/wk
GH 2IU pre workout and pre
bedtime
8 weeks out
Test cypionate 300mg/wk
Trenbolone 200mg/wk
Masteron 400mg/wk
GH 2IU pre workout and pre
bedtime

5 weeks out
Test cypionate 300mg/wk
Trenbolone 200mg/wk
Masteron 200mg/wk
Winstrol 50mg/day
GH 2IU pre workout and pre
bedtime

3 weeks out
Test cypionate 300mg/wk *drop test
2 weeks out if needed for water
retention
Trenbolone 200mg/wk
Masteron 200mg/wk
Winistrol 50mg/day
Halotestin 20mg/day
GH 2IU pre workout and pre

bedtime *drop GH 2 weeks out


Summary
Testosterone is our established base growth anchor
A DHT derivative like Proviron, Anavar, Primobolan and/or Masteron are
secondary compounds to deploy.

Our next deployed drug will be a nandrolone derivative. Nandrolone for
offseason usage and Trenbolone reserved in contest prep.
Growth hormone and insulin will be implemented into the intermediate
level to maximize synergies.
Phase dependent steroids will be implemented such as Winstrol and
Halotestin during contest prep.
I see no place for need of Dianabol, Anadrol, or boldenone is safer use
PED protocols.
Compounds to mention: DHB, Superdrol, Turinabol, Trestalone, SARMS
By this point further advancing of cycle likely will need aromatase
inhibitors and Selective Estrogen Receptor Modulators. Combating effects
of estrogen and prolactin will be next.


References
Ferreira IM, Verreschi IT, Nery LE, Goldstein RS, Zamel N, Brooks D, Jardim JR. The influence
of 6 months of oral anabolic steroids on body mass and respiratory muscles in
undernourished COPD patients. Chest. 1998 Jul;114(1):19-28. doi: 10.1378/chest.114.1.19.
PMID: 9674442.
Thompson PD, Cullinane EM, Sady SP, Chenevert C, Saritelli AL, Sady MA, Herbert PN.
Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA. 1989
Feb 24;261(8):1165-8. PMID: 2915439.

Small M, Beastall GH, Semple CG, Cowan RA, Forbes CD. Alteration of hormone levels in
normal males given the anabolic steroid stanozolol. Clin Endocrinol (Oxf). 1984 Jul;21(1):4955. doi: 10.1111/j.1365-2265.1984.tb00135.x. PMID: 6430603.
Schroeder ET, Singh A, Bhasin S, Storer TW, Azen C, Davidson T, Martinez C, Sinha-Hikim I,
Jaque SV, Terk M, Sattler FR. Effects of an oral androgen on muscle and metabolism in older,
community-dwelling men. Am J Physiol Endocrinol Metab. 2003 Jan;284(1):E120-8. doi:
10.1152/ajpendo.00363.2002. Epub 2002 Sep 24. PMID: 12388137.
Shabir N et al. Effect of Nandrolone Decanoate, Boldenone Undecylenate on Renal Status of
Rabbits (Oryctolagus cuniculus. Global Veterinaria 14 (3): 432-438, 2015
DOI: 10.5829/idosi.gv.2015.14.03.92201

Kantarci UH, Punduk Z, Senarslan O, Dirik A. Evaluation of anabolic steroid induced renal
damage with sonography in bodybuilders. J Sports Med Phys Fitness. 2018 Nov;58(11):16811687. doi: 10.23736/S0022-4707.17.06763-9. Epub 2017 Nov 17. PMID: 29148625.

Books:
Llewellyn W. Anabolics. Jupiter, FL: Molecular Nutrition LLC; 2017.
Bond P. Book on Steroids: A complete evidence based reference. PeterBond.org; 2020.



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