Blood Work & Spermatic Cytoanalysis after Oxandrolone Cycle at 63 mg ed (averaged)

[BJJ]

BLOOD, URINE, FAECES & SPERM ANALYSES:
__________________________________________________18__________36__________51__________56__________98 (4W PCT)_____122 (8W PCT)

BLOOD
ERYTHROCYTES: 5,18 mil/mmc [4 - 5,5]__________________________________________________ ___5,2_________5,34
LEUCOCYTES: 7,3 mila/mmc [4 - 9]__________________________________________________ _______8,6_________7,5
- NE: 4,1 / 55,8 % [2 - 6 / 37 - 80]__________________________________________________ __________________4,1 / 54,8
- LY: 2,4 / 33 % [0,6 - 36 / 10 - 50]__________________________________________________ _________________2,7 / 35,6
- MO: 0,6 / 8,6 % [0 - 0,9 / 0 - 12]__________________________________________________ __________________0,5 / 7,1
- EO: 0,2 / 2,1 % [0 - 7 / 0 - 7]__________________________________________________ _____________________0,1 / 1,8
- BA: 0 / 0,5 % [0 - 0,2 / 0 - 2,5]__________________________________________________ ____________________0,1 / 0,7
HEMOGLOBIN: 14,9 gr/dl [14 - 18]__________________________________________________ ________13,6________15,6
HEMATOCRIT: 45,3 % [42 - 52]__________________________________________________ __________44,1________45,5
MCV: 87,5 femtol [82 - 98]__________________________________________________ ______________84,8________85,2
MCH: 28,8 picogr. [27 - 31]__________________________________________________ _____________26,2________29,2
MCHC: 32,9 gr/dl [32 - 36]__________________________________________________ ______________30,8________34,3
RDW: 13,5 % [11,6 - 16]__________________________________________________ ___________________________14
GRAN-NEUTROPHILS: 55,8 % [37 -80]__________________________________________________ _____60,7________54,8
GRAN-EOSINOPHILS: 2,1 % [0,0 - 7]__________________________________________________ ______1,9_________1,8
GRAN-BASOPHILS: 0,5 % [0,0 - 2,5]__________________________________________________ ______0,7_________0,7
LYMPHOCYTES: 33,0 % [10 - 50]__________________________________________________ ________28,4________35,6
MONOCYTES: 8,6 % [0,0 - 12]__________________________________________________ ___________8,3_________7,1
PLATELETS: 163000 /mmc [150000 - 400000]________________________________________________336000_____164000
PCT: 0,12 % [0,1 - 1]__________________________________________________ ______________________________0,12
MPV: 7,3 fl [5 - 10]__________________________________________________ ________________________________7,2
PDW: 17,4 % [12 - 18]__________________________________________________ _____________________________18,5

HEART, KIDNEYS, LIVER, PANCREAS & PROSTATE
GLYCEMIA (basal): 90 mg/dl [70 - 110]__________________________________________________ ________________98

QUICK PROTHROMBIN TIME: 13,7 s_________________________________________________ ____________________13,1
PROTHROMBIN ACTIVITY: 69,6 % [70-130]__________________________________________________ ____________86
INR: 1,18__________________________________________________ ________________________________________1,09
APTT: 27,5 s_________________________________________________ ______________________________________27,8
FIBRINOGEN: 185 mg/dl [180 - 350]__________________________________________________ __________________184,7
HOMOCYSTEINE: 10 mcmoli/l [6 - 15]__________________________________________________ _________________9,5
MYOGLOBIN: 26 ng/ml [10 - 46]__________________________________________________ ______________________38

AZOTEMIA: 49 mg/dl [15-40]__________________________62__________57______________________56__________53______________52,8
CREATININE: 1,2 mg/dl [0,8 - 1,3]_____________________1,2__________1,2______________________1,3_________1,3
HYPERURICEMIA: 5,9 mg/dl [3,5 - 7,2]__________________________________________________ ________________5,5

CHOLESTEROL TTL: 168 mg/dl [140 - 220]______________179_________205______________________232________194
CHOLESTEROL VLDL: 33 mg/dl [20 - 40]__________________________________________________ _______________30
CHOLESTEROL LDL: 105 mg/dl [< 150]__________________157_________199_____________________202_________129_____________101
CHOLESTEROL HDL: 41 mg/dl [> 40]____________________13__________11_______________________13__________45
INDEX RISK HDL: 4,1 [till 5]___________________________13,76_______19,2_____________________17,8________4,3
APO A1: 185 mg/dl [115 - 220]__________________________________________________ ______________________190
APO B: 77 mg/dl [55 - 125]__________________________________________________ __________________________79
RATIO B/A1 APO: 0,41 [0,35 - 1]__________________________________________________ _____________________0,41
TRIGLYCERIDES: 95 mg/dl [< 150]__________________________________________________ ____________________104

GAMMA (YGT): 28 u/ltr [15 - 85]______________________29__________28_______________________26__________40
ALKALINE PHOSPHATASE: 71 u/ltr [50 - 136]__________________________________________________ ___________72
BILIRUBIN TTL: 1,98 mg/dl [0,2-1]_____________________0,83________0,78_________________________________0,93____________1,54
BILIRUBIN DIRECT: 0,22 mg/dl [0,05 - 0,3]______________0,1__________0,1__________________________________0,1_____________0,53
BILIRUBIN INDIRECT: 1,76 mg/dl [till 0,7]________________0,73________0,68_________________________________0,83____________1,01
TRANSAMINASE GOT/AST: 21 u/ltr [15 - 37]_____________55__________50_______________________46_________28______________58
TRANSAMINASE GPT/ALT: 41 u/ltr [30 - 65]_____________86__________66_______________________95__________71______________77
FERRITIN: 124,5 ng/ml [24 - 336]__________________________________________________ ____________________124

LIPASE: 236 u/ltr [114 - 284]__________________________________________________ ________________________298____________216
AMYLASE: 62 u/ltr [25 - 115]_________________________55__________63_______________________64__________75_____________76

LDH: 160 u/ltr [100 - 190]__________________________________________________ __________________________155
CPK MB: 200 u/ltr [35 - 232]__________________________________________________ ________________________230
CK NAK: 150 u/l [till 167]__________________________________________________ ___________________________165
PROTIDES TTL: 7,4 gr/dl [6,4 - 8,2]__________________________________________________ _______7,8_________7,7
ALBUMIN: 59,1 % [51 - 63,3]__________________________________________________ ____________60,3________63,1
ALFA 1: 2,9 % [2,2 - 4,3]__________________________________________________ _______________2,4_________2,3
ALFA 2: 10,1 % [9,5 - 14]__________________________________________________ ______________12,6________8,5
BETA: 9,6 % [10-14,5]__________________________________________________ _________________11,3________9,3
GAMMA: 18,3 % [12 - 20]__________________________________________________ _______________13,4________16,8
A/G RATIO: 1,44 [1,0 - 1,7]__________________________________________________ _____________1,52________1,71

PSA: 0,64 ng/ml [till 4]__________________________________________________ _________________0,39_________0,58
PSA FREE: 0,22__________________________________________________ ____________________________________0,24
PSA FREE/TTL: 0,40 [>0,15]__________________________________________________ _________________________0,41
PAP: 4,8 u/ltr [<= 4,7]__________________________________________________ ______________________________5,1

IGG: 1447 mg/dl [681 - 1648]__________________________________________________ ________________________1455
IGA: 304 mg/dl [87 - 474]__________________________________________________ ___________________________321
IGD: 50 u/ml [till 100]__________________________________________________ _______________________________57
IGM: 99 mg/dl [48 - 312]__________________________________________________ ____________________________97
IGE (prist): 37,47 iu/ml [1,31 - 165,3]__________________________________________________ _________________39,77

INFECTIVITY & ALLERGOLOGY
HIV-Ab (1+2): 0,16 non-react u/cutoff [<0,9]__________________________________________________ __________0,18 non-react
HCV-Ab: 0,13 non-react u/cutoff [<0,9]__________________________________________________ _______________0,12 non-react
HBS-Ag: 0,37 non-react u/cutoff [<0,9]__________________________________________________ _______________0,39 non-react
HAV-Ab (IgT): >85 react miu/ml [<35]__________________________________________________ _________________>85 react
HAV-Ab (IgM): 0,08 non-react u/cutoff [<0,9]__________________________________________________ __________0,07 non-react
TAS: 110 ui/ml [0 - 166]__________________________________________________ ____________________________111
VDRL: negative [negative]__________________________________________________ ___________________________negative
CRP: 2 mg/dl [till 5]__________________________________________________ _________________________________2,1
REUMA TEST: <20 iu/ml [<20]__________________________________________________ ________________________<20
ESR: 5 mm/h [till 15]__________________________________________________ ________________________________5
LYSOZYME: 7 picog/ml [4 - 13]__________________________________________________ _______________________7
ACE: 9 mcg/l [6 - 12]__________________________________________________ _______________________________8,5

RAST Egg: 0,1 [<0,3]
RAST Yolk: 0,1 [<0,3]
RAST Crayfish: 0,1 [<0,3]
RAST Yeast: 0,1 [<0,3]
RAST Pork: 0,1 [<0,3]
RAST Fish Mix: 0,1 [<0,3]
RAST Olea Europaea Pollen: 0,1 [<0,3]

VITAMINS & ELECTROLYTES
VITAMIN A: 779,2 mcg/l [300-650]__________________________________________________ ___________________692,1
VITAMIN E: 12,6 mg/ltr [5 - 20]__________________________________________________ ______________________100
VITAMIN C: 0,9 mg/ml [0,5-1,5]__________________________________________________ ______________________1,2
VITAMIN B12: 587 pg/ml [179 - 1162]__________________________________________________ _________________787
VITAMIN D3: 60 ng/ml [10-45]__________________________________________________ _______________________40
VITAMIN H: 82 ng/ml [70-100]__________________________________________________ _______________________90
VITAMIN K: 22 mcg/ml [15-30]__________________________________________________ _______________________26
VITAMIN PP: 0,7 mg/ml [0,5-0,8]__________________________________________________ _____________________0,7

SODIUM: 142 meq/l [136 - 145]__________________________________________________ ______________________139
POTASSIUM: 4,0 meq/l [3,5 - 5,1]__________________________________________________ ____________________4,4
CALCIUM: 9,0 mg/dl [8,5 - 10,1]__________________________________________________ ______________________9,1
MAGNESIUM: 2,0 mg/dl [1,8 - 2,4]__________________________________________________ ____________________2,2
PHOSPHORUS: 3,7 mg/dl [2,7 - 4,5]__________________________________________________ ___________________4,3
IRON: 148 mcg/dl [35 - 150]__________________________________________________ _________________________96
ZINC: 103 mcg/dl [80 - 125]__________________________________________________ _________________________132
CHLORINE: 103 meq/l [98 - 107]__________________________________________________ ______________________99
COPPER: 88 ku/l [76 - 153]__________________________________________________ __________________________88

HORMONAL
GASTRIN: 31 pg/ml [28-125]__________________________________________________ _________________________33
MELATONIN: 47 pg/ml [20 - 85]__________________________________________________ ______________________50
C-PEPTIDE: 1,2 ng/ml [0,78 – 1,89]__________________________________________________ ___________________1,25
INSULIN: 3,34 micru/ml [1,9 - 23]______________________3,6_________3,04_________________________________2,39
GLUCAGON: 55 pg/ml [40-130]__________________________________________________ _______________________55
ACTH: 20 pg/dl [till 50]__________________________________________________ _____________________________21
CORTISOL: 12,53 mg/dl [8,7 - 22,4]__________________________________________________ ______13,64_______18,7
FT3: 3,48 pg/ml [2,2 - 4,7]__________________________________________________ ______________4,82_______3,13
FT4: 1,26 ng/dl [0,8 - 2]__________________________________________________ ________________1,29_______1,16
MSH: 9,7 pmol/l [7,9 - 14,4]__________________________________________________ _________________________9,8
HTG: 7,65 ng/ml [0,0 - 35]__________________________________________________ __________________________6,61
TBG: 18 mcg/ml [15 - 32]__________________________________________________ ___________________________18,6
TSH: 2,92 micru/ml [0,34 - 5,6]__________________________________________________ __________3,88________3,92
FSH: 4,16 miu/ml [1,27 - 19,26]_______________________2,09________2,56_____________________1,42________3,9
LH: 3,80 miu/ml [1,24 - 8,62]_________________________2,19________2,58_____________________2,61________4,84
PREGNENOLONE: 155 ng/ml [10 - 230]__________________________________________________ ________________160
ANDROSTENEDIONE: 1,77 ng/ml [0,3 - 3,1]__________________________________________________ ____________1,79
ALDOSTERONE: 180 pg/ml [10 - 160]__________________________________________________ _________________184
DHEA: 7,3 ng/ml [2,5 - 9,5]__________________________________________________ _________________________6,2
DHEAS: 191 mcg/dl [106 - 464]_______________________209_________209,6________________________________221,6
DHT: 71 ng/ml [31 - 146]__________________________________________________ ___________________________70
TESTOSTERONE TTL: 3,86 ng/ml [1,75 - 7,81]___________0,72________0,61_________________________________6,29
TESTOSTERONE FREE: 11,7 pg/ml [8 - 47]______________5,2_________4,8_______________________9,6_________13,5
SHBG: 38 pg/ml [13 - 71]____________________________10__________<0,1_________________________________36
ESTRONE: 47 pg/ml [40 - 60]__________________________________________________ ________________________45
ESTRADIOL 17-BETA: 36 pg/ml [<20 - 47]__________________________________________________ __9__________30
ESTRIOL: 5,7 pg/ml [4,7 - 7,1]__________________________________________________ _______________________5,5
PROGESTERONE: 0,93 ng/ml [0,14 - 2,06]__________________________________________________ _____________0,87
PRL: 9,88 ng/ml [2,64 - 13,13]__________________________________________________ ___________12,78______13,05
IGF-1: 190 ng/ml [96 - 424]__________________________184_________163__________________________________392
HGH: 0,2 ng/ml [0,0 - 10]____________________________<0,1________<0,1_________________________________0,3

URINE
COLOUR: straw-coloured____________________________straw-coloured____________________________________straw-coloured
APPEARANCE: lightly opalescent [limpid]_______________lightly opalescent__________________________________limpid
PH REACTION: 5,5 [5 - 6,5]___________________________6________________________________________________5,5
SPECIFIC WEIGHT: 1020 [1015 - 1028]_________________1016_____________________________________________1018
PROTEINS: none mg/dl [0,0 - 10]______________________none_____________________________________________none
HEMOGLOBIN: none [none]___________________________present +_________________________________________none
GLUCOSE: none gr/litre [0,0 - 0,2]_____________________none_____________________________________________none
KETONE BODIES: none [none]_________________________none_____________________________________________none
UROBILINOGEN: none mg/dl [0,0 - 0,2]_________________none_____________________________________________none
BILIARY PIGMENTS: none [none]______________________none_____________________________________________none
NITRITE: none [none]_______________________________none_____________________________________________none

FAECES
SHAPE: solid [homogeneous]__________________________________________________ ________________________caprina
CONSISTENCY: compost [poltacea]__________________________________________________ __________________solid
COLOUR: brown [brown]__________________________________________________ ____________________________brown
ODOUR: sui generis [sui generis]__________________________________________________ _____________________sui generis
MUCUS: absent [absent]__________________________________________________ ___________________________absent
BLOOD: absent [absent]__________________________________________________ ____________________________absent
PH REACTION: 7__________________________________________________ ___________________________________7,4
PARASITOLOGICAL: negative [negative]__________________________________________________ _______________negative
SALMONELLA: negative [negative]__________________________________________________ ___________________negative
HELICOBACTER PYLORI: negative [negative]__________________________________________________ ___________negative
GIARDIASIS: negative [negative]__________________________________________________ ____________________negative

SPERM
VOLUME: 2,8 ml [>= 2]__________________________________________________ ______2,5____________________________________2,6
PH: 8,1 [7,2-8]__________________________________________________ ____________7,2_____________________________________7,3
APPEARANCE: own__________________________________________________ _________own____________________________________own
VISCOSITY: increased + [within limits]__________________________________________within limits_____________________________within limits
FLUIDIFICATION 45': finely irregular [physiologic]_________________________________physiologic______________________________physiologic
SPERMATOZOON CONCENTRATION: 89.000.000 /ml [>= 20.000.000]__________________42.000.000______________________________85.000.000
EJACULATE SPERMATOZOON COUNT: 249.200.000 [>= 40.000.000]__________________105.000.000_____________________________228.000.000
2ND HOUR MOTILITY: 60 % [>= 50 %]___________________________________________45______________________________________57
TYPICAL MORPHOLOGIC SPERMATOZOON: 30 % [>= 35 %]__________________________28______________________________________35
ATYPICAL MORPHOLOGIC SPERMATOZOON: 70 %__________________________________72______________________________________71
LEUCOCYTE: 300.000 /ml [<= 1.000.000]________________________________________500.000_________________________________335.000
ERYTHROCYTE: absent [absent/rare]____________________________________________absent__________________________________absent
GERMINAL CELLS: rare [absent/rare]____________________________________________present_________________________________absent
EPITHELIAL CELLS: rare [absent/rare]___________________________________________absent__________________________________absent
SPERMAGGLUTINATION ZONES: rare [absent/rare]_________________________________absent__________________________________absent

[Necrosaro]

Wow nice to see some blood work

[Hard.On]

is this good?

[BJJ]

is this good?

To me is quite obvious.
What is your concern?

[FranciscoG]

who old where you when you first started this cycle, biological age? 27?

Was this your first cycle, inclusive of any prohormone usage?

Anavar only, I believe correct? Can you elaborate on your pct protocal?

I did look through some of your old threads... Just wondering a few things.

[BJJ]

1. who old where you when you first started this cycle, biological age? 27?

2. Was this your first cycle, inclusive of any prohormone usage?

3. Anavar only, I believe correct? Can you elaborate on your pct protocal?

I did look through some of your old threads... Just wondering a few things.

1. I was 36 yo, last September. My biological age was 27 as you correctly stated.

2. Yes it was and I never used any prohormone.

3. Oxandrolone + Mesterolone (proviron).
My pct had to be only 2/3 weeks of Tamoxifen citrate since my LH and FSH were never below the normal range values throughout the cycle. Though, my levels of testosterone prior the beginning of the cycle were low; so I decided to add clomid to raise them and have them higher after the end of pct. GSH was used to clean up my system, mostly.

[FranciscoG]

It looks good.

How long do plan on staying off, as in when do you plan on starting again, taking into account you last dosage of aas as the first day off?

[BJJ]

I will probably start a new cycle by the end of February or in the middle of it.

[FranciscoG]

That is what i would do also.

Although, your fsh/lh/globins/over all liver/ over all kidney and so on are all good, the only up coming issue I see is

CORTISOL: 12,53 mg/dl [8,7 - 22,4]__________________________________________________ ______13,64_______18,7


The rebounding effect of cortisol is a delayed reaction in some cases.

I frankly do not fully understand the rebound/negative feedback with respect to cortisol fully,

I do understand that post last dosage of aas the cortisol production is inhibited to a certain degree. I also understand usage of hcg/clomid and other bridges such as dbol keep cortisol in check. However, months post last dosage administration cortisol levels have been known to climb.

Hence the visiual affects. Softness of the muscle tissue. Low levels of energy. Metabolic decline.

such is your case you have a 50% rise. Very on point though. 18.7 is high for biological age 27. 50% rise in a show period of time is also high.

Once you get back on it will be inhibited once again.

[BJJ]

Well, also my GPT/GOT are a little higher...

Anyway, thanks for the info of cortisol.
I am curious to see the values of ACTH which is stricly related to cortisol. I might have a better view then.

PS
How did you get the 27yo biological age?... since I got rid of that information?

[FranciscoG]

I read it a few weeks back, when you had your anavar thread up.

The biological age is a meter but not an over-all effective measure of the individual organ systems. An alcoholic that is 22 may have a liver system that is 50.

Your over-all endocrine system also is based on that simple principle.

There is no point of waisting your funds getting your ACTH tested. It will be higher. As you pointed to and understand the relationship with respect to that biological cycle, it is impossible IMHO for your ACTH to be low.

Have you reviewed the set point theory that was introduced in the 1980s?

Although I understand staying off for over 8 weeks due to the advice given on most boards. I humbly disagree. No disrespect to those who wrote the PCT base protocals, but it seams it is written by males in thier early to mid 20 for males in thier 20s.

The basis for the arguments made for pct these days do not account the average user of anabolics that is in his 30s.

[BJJ]

I read it a few weeks back, when you had your anavar thread up.

The biological age is a meter but not an over-all effective measure of the individual organ systems. An alcoholic that is 22 may have a liver system that is 50. agree

Your over-all endocrine system also is based on that simple principle.

There is no point of waisting your funds getting your ACTH tested. It will be higher. As you pointed to and understand the relationship with respect to that biological cycle, it is impossible IMHO for your ACTH to be low. probably you are correct but I am a fussy person

Have you reviewed the set point theory that was introduced in the 1980s? ???

Although I understand staying off for over 8 weeks due to the advice given on most boards. I humbly disagree. No disrespect to those who wrote the PCT base protocals, but it seams it is written by males in thier early to mid 20 for males in thier 20s. agree

The basis for the arguments made for pct these days do not account the average user of anabolics that is in his 30s. I guess so too

bold

[FranciscoG]

http://docs.google.com/viewer?a=v&q=...-nbuv1BRZD8FWw

There is the MIT link.

[FranciscoG]

If you apply to the 30 something year-old male and think in prospective it will shine a new light.

Assume you are 39 (35, 36) You body is used to being on or about 220 pounds (Ñ100KG) for the last 10 years. You introduce anadrogens to your body.

You loss fat weight and gain muscle in a relatively fast time period.

¿12 weeks later your cortisol levels are spiking, why?

[BJJ]

If you apply to the 30 something year-old male and think in prospective it will shine a new light.

Assume you are 39 (35, 36) You body is used to being on or about 220 pounds (Ñ100KG) for the last 10 years. You introduce anadrogens to your body.

You loss fat weight and gain muscle in a relatively fast time period.

¿12 weeks later your cortisol levels are spiking, why?

You tell me!
Furthermore, do you think that theory is correct?
Any scientific proofs?

[FranciscoG]

yes ans yes, give me a few hours, I am going to go dive...

[jasperhup]

i'm 32 and about to start my second cycle in a few weeks.

pharma doc what you are speaking to is very interesting to me. Do you have any resources, links, articles, or just any more thoughts on the topic?

thanks much

[BJJ]

yes ans yes, give me a few hours, I am going to go dive...

OK, I'll be awaiting...

[FranciscoG]

Let me state before writting anything about this that The Set Point Theory is not my theory. Me me go on to say that it was developed by researchers at MIT amoung other institutions. I am not due any credit here what so ever.

Having said that lets look at the basic premis of the theory, the research that back it up, and practical applications.

Basic theory: I am gonna write a novel here so let me apoligize prior for that:::

According to the set-point theory, there is a control system built into every person dictating how
much fat he or she should carry – a kind of thermostat for body fat. Some individuals have a
high setting, others have a low one. According to this theory, body fat percentage and body
weight are matters of internal controls that are set differently in different people.

Here again let us keep in mind it was 1982, this theory is developed for a person that was not on anabolics, keep in mind we´ll get to anabolics later. Let us call this state H, for homeostatis. So what have we learned in the last almost 30 years. We have seen in the human body that fat cell are a constant number. The human body does not make or destroy fat cell. The fat cells simply shrink or increase in size with weight loss and weight gain. We have also seen that in homeostasis the human body does not make new muscles or muscle groups. In practical applications you will not grow an extra bicep groups on your butt no matter how hard you lift. (maybe another face but no new bicept group)... We have come to understand the tyroid much better in the last 30 years also. We have seen the human tyroid increase in out put during periods of stress and decrease oput put when one is starving. So in practical application when one crash diets one´s body temp drops.

Christ, I don´t want to get into each and every hormone, but lets look at a few more. One of the more interesting hormones is ACTH. Much like tyroid function times of stress and starvation affect ACTH.

Keep in mind how simular these hormones work during starvation, for example, even though the actual application in your body is much different.

If one examines the endrocrine system one will find that in periods of stree and starvation hormones that are completely unrelated act much the same.


The set-point theory was originally developed in 1982 by Bennett and Gurin to explain why
repeated dieting is unsuccessful in producing long-term change in body weight or shape. Going
on a weight-loss diet is an attempt to overpower the set point, and the set point is a seemingly
tireless opponent to the dieter.

Cycling (I will get into actual changes with respect to hGH and pgf2-a and what have you at the end, if I dont remind me and I´ll cover it) while dieting is still covering an attemp to change the set point. This is regardless of the bulk or cut diets (IMHO the use of different aas is subjective to proper diet to see the wanted results)

Lets look at practical application. Let use BJJ as an example:

Sex: M
Age: 30+

Increased his protein and valoric intake and used anabolics, intake of anabolics were approx. 400% higher than what his body produces.

Set point hold that this increase in body weight (decrease in fat%/ increase in LBM%) is an altered state for his body. This sudden increase his body will fight. So by set point in his over-all increase in weight was 15LB then his body will have negative feedbacks to counter that. (certain people do not suffer any negative sides and thier HPTA are not effected, but that is not the norm)

So what happens.

The individual stops use of anabolics. The body tried to restore H. Negative feedbacks included increase in estrogen, combated with nolv. A period of low bio-active testosterna, combated with clomid. Increase in ACTH.

But why, Why is it when people bust thier ass lossing weight or gaining weight, that increase or reduction is fought by the body, why is it that when you gain 10LB LBM you body just wont leave you alone and allow you to keep any of it. Well simple acccording to the theory the body tries o stay in H. And, the body fight each and every way. On cycle with every proper measure taken your body increases myostatin activity 56 days into the cycle. A vast number of other hormones and negative feedback, and christ I don´t want to explain or get into every one but: dht, estrogen, progestrone, prolactin, acth, aromatiz: and others are produced to maintain H.


The ideal approach to weight control would be a safe method that lowers or raises the set point
rather than simply resisting it. So far no one knows for sure how to change the set point, but
some theories exist. Of these, regular exercise is the most promising: a sustained increase in
physical activity seems to lower the setting (Wilmore et al. 1999).

In theory that is all that is all you are trying to do. Go from 200lb to 220 and keep the 220. You are employing exercise and diet to aid. You are trying to restore H faster by PCT. In thoery anyways.

According to the set-point theory, the set point itself keeps weight fairly constant, presumably
because it has more accurate information about the body’s fat stores than the conscious mind can
obtain. At the same time, this system pressures the conscious mind to change behavior,
producing feelings of hunger or satiety. Studies show that a person’s weight at the set point is
optimal for efficient activity and a stable, optimistic mood. When the set point is driven too low,
depression and lethargy may set in as a way of slowing the person down and reducing the
number of calories expended.
• The set point, it would appear, is very good at supervising fat storage, but it cannot tell the
difference between dieting and starvation. The dieter who begins a diet with a high set point
experiences constant hunger, presumably as part of her body’s attempt to restore the status quo.
Even dedicated dieters often find that they cannot lose as much weight as they would like. After
an initial, relatively quick loss, dieters often become stuck at a plateau and then lose weight at a
much slower rate, although they remain as hungry as ever.

That part of it is prety much explained.

Dieting research demonstrates that the body has more than one way to defend its fat stores.
Long-term caloric deprivation, in a way that is not clear, acts as a signal for the body to turn
down its metabolic rate. Calories are burned more slowly, so that even a meager diet almost
suffices to maintain weight. The body reacts to stringent dieting as thought famine has set in.
Within a day or two after semi-starvation begins, the metabolic machinery shifts to a cautious
regimen designed to conserve the calories it already has on board. Because of this innate
biological response, dieting becomes progressively less effective, and (as generations of dieters
have observed) a plateau is reached at which further weight loss seems all but impossible.

After all that lets look at the average aas user.

30 something
male
using aas as a means to increase LBM (never heard of anyone trying to distroy muscle)

We basically know what cycles are and we know what proper diets are.
So causes and effects:

One uses anabolics and alters diet to during the given cycle.

You have your consistants. Call those ç. Your fat tissue, Muscle tissue, boner density And, many more but lets look at the major ones.

One alters the state of H. The result in 10LB of gain (just for this example)

S lets assume that the set point might be a correct theory. Let us also assume the bio mechanics of the 30+ male. Let us assume that exactly on day 56 myostatin uptake did occur and the 30+ male stopped the cycle.

What possible chemical reactions will happen.

HPTA is completely out of H
Rebound of Estrogen, ACTH, DHL occur.

Sp this 30+ male takes the regular advice give. Time on + PCT = Time off

Lets look at (I know i am forgetting something here but I cant think of it right now) a regular example of a PCT for the purposes of this example let us not consider dosages or times of adminstration.

4 weeks of nolv
4 weeks of HCG

let us factor in post nolv and hcg increase in ACTH. So you ran a 8 week cycle. You did 4 weeks of pct. 8+4=12

There is your time off.

So whats happening post hcg and nolv. Simple that damn set point is here to rob you of what you busted your ass for. We you are in your 30 so you can kiss the possibility of 800 test out the window (the normal guy on a scale of 240-840) say more like maybe 500ish. Wait lets factor in you just used aas and just got done with pct, not gonna be whole just yet, say 400 something. And you stopped all other suppliments. here comes some ACTH.

So all in all its gonna be a long motherfvcking 12 weeks to bubba.

That is were my question comes in: If I am old and I will not recover to a rate of a 22 year-old should I stay off for that long? While all this is happening I have normal body and that body is fighting the LBM increase (assuming SP theory is true)

When I use my (my current pct) HCG, HMG, propecia, nolv, should I use of anabolics to help me while my body resets myostatin? Such as slin, hGH.

Is it praticle to follow the PCT advice given with respect to usage of pct drugs and time off?

[FranciscoG]

of course I forgot other factors such as you have been at your set point for years and many other things...

[M302_Imola]

great stuff pharmdoc...I enjoy reading your threads. Very informative!

[BJJ]

Let me state before writting anything about this that The Set Point Theory is not my theory. Me me go on to say that it was developed by researchers at MIT amoung other institutions. I am not due any credit here what so ever.

Having said that lets look at the basic premis of the theory, the research that back it up, and practical applications.

Basic theory: I am gonna write a novel here so let me apoligize prior for that:::

According to the set-point theory, there is a control system built into every person dictating how
much fat he or she should carry – a kind of thermostat for body fat. Some individuals have a
high setting, others have a low one. According to this theory, body fat percentage and body
weight are matters of internal controls that are set differently in different people.

Here again let us keep in mind it was 1982, this theory is developed for a person that was not on anabolics, keep in mind we´ll get to anabolics later. Let us call this state H, for homeostatis. So what have we learned in the last almost 30 years. We have seen in the human body that fat cell are a constant number. The human body does not make or destroy fat cell. The fat cells simply shrink or increase in size with weight loss and weight gain. We have also seen that in homeostasis the human body does not make new muscles or muscle groups. In practical applications you will not grow an extra bicep groups on your butt no matter how hard you lift. (maybe another face but no new bicept group)... We have come to understand the tyroid much better in the last 30 years also. We have seen the human tyroid increase in out put during periods of stress and decrease oput put when one is starving. So in practical application when one crash diets one´s body temp drops.

Christ, I don´t want to get into each and every hormone, but lets look at a few more. One of the more interesting hormones is ACTH. Much like tyroid function times of stress and starvation affect ACTH.

Keep in mind how simular these hormones work during starvation, for example, even though the actual application in your body is much different.

If one examines the endrocrine system one will find that in periods of stree and starvation hormones that are completely unrelated act much the same.


The set-point theory was originally developed in 1982 by Bennett and Gurin to explain why
repeated dieting is unsuccessful in producing long-term change in body weight or shape. Going
on a weight-loss diet is an attempt to overpower the set point, and the set point is a seemingly
tireless opponent to the dieter.

Cycling (I will get into actual changes with respect to hGH and pgf2-a and what have you at the end, if I dont remind me and I´ll cover it) while dieting is still covering an attemp to change the set point. This is regardless of the bulk or cut diets (IMHO the use of different aas is subjective to proper diet to see the wanted results)

Lets look at practical application. Let use BJJ as an example:

Sex: M
Age: 30+

Increased his protein and valoric intake and used anabolics, intake of anabolics were approx. 400% higher than what his body produces.

Set point hold that this increase in body weight (decrease in fat%/ increase in LBM%) is an altered state for his body. This sudden increase his body will fight. So by set point in his over-all increase in weight was 15LB then his body will have negative feedbacks to counter that. (certain people do not suffer any negative sides and thier HPTA are not effected, but that is not the norm)

So what happens.

The individual stops use of anabolics. The body tried to restore H. Negative feedbacks included increase in estrogen, combated with nolv. A period of low bio-active testosterna, combated with clomid. Increase in ACTH.

But why, Why is it when people bust thier ass lossing weight or gaining weight, that increase or reduction is fought by the body, why is it that when you gain 10LB LBM you body just wont leave you alone and allow you to keep any of it. Well simple acccording to the theory the body tries o stay in H. And, the body fight each and every way. On cycle with every proper measure taken your body increases myostatin activity 56 days into the cycle. A vast number of other hormones and negative feedback, and christ I don´t want to explain or get into every one but: dht, estrogen, progestrone, prolactin, acth, aromatiz: and others are produced to maintain H.


The ideal approach to weight control would be a safe method that lowers or raises the set point
rather than simply resisting it. So far no one knows for sure how to change the set point, but
some theories exist. Of these, regular exercise is the most promising: a sustained increase in
physical activity seems to lower the setting (Wilmore et al. 1999).

In theory that is all that is all you are trying to do. Go from 200lb to 220 and keep the 220. You are employing exercise and diet to aid. You are trying to restore H faster by PCT. In thoery anyways.

According to the set-point theory, the set point itself keeps weight fairly constant, presumably
because it has more accurate information about the body’s fat stores than the conscious mind can
obtain. At the same time, this system pressures the conscious mind to change behavior,
producing feelings of hunger or satiety. Studies show that a person’s weight at the set point is
optimal for efficient activity and a stable, optimistic mood. When the set point is driven too low,
depression and lethargy may set in as a way of slowing the person down and reducing the
number of calories expended.
• The set point, it would appear, is very good at supervising fat storage, but it cannot tell the
difference between dieting and starvation. The dieter who begins a diet with a high set point
experiences constant hunger, presumably as part of her body’s attempt to restore the status quo.
Even dedicated dieters often find that they cannot lose as much weight as they would like. After
an initial, relatively quick loss, dieters often become stuck at a plateau and then lose weight at a
much slower rate, although they remain as hungry as ever.

That part of it is prety much explained.

Dieting research demonstrates that the body has more than one way to defend its fat stores.
Long-term caloric deprivation, in a way that is not clear, acts as a signal for the body to turn
down its metabolic rate. Calories are burned more slowly, so that even a meager diet almost
suffices to maintain weight. The body reacts to stringent dieting as thought famine has set in.
Within a day or two after semi-starvation begins, the metabolic machinery shifts to a cautious
regimen designed to conserve the calories it already has on board. Because of this innate
biological response, dieting becomes progressively less effective, and (as generations of dieters
have observed) a plateau is reached at which further weight loss seems all but impossible.

After all that lets look at the average aas user.

30 something
male
using aas as a means to increase LBM (never heard of anyone trying to distroy muscle)

We basically know what cycles are and we know what proper diets are.
So causes and effects:

One uses anabolics and alters diet to during the given cycle.

You have your consistants. Call those ç. Your fat tissue, Muscle tissue, boner density And, many more but lets look at the major ones.

One alters the state of H. The result in 10LB of gain (just for this example)

S lets assume that the set point might be a correct theory. Let us also assume the bio mechanics of the 30+ male. Let us assume that exactly on day 56 myostatin uptake did occur and the 30+ male stopped the cycle.

What possible chemical reactions will happen.

HPTA is completely out of H
Rebound of Estrogen, ACTH, DHL occur.

Sp this 30+ male takes the regular advice give. Time on + PCT = Time off

Lets look at (I know i am forgetting something here but I cant think of it right now) a regular example of a PCT for the purposes of this example let us not consider dosages or times of adminstration.

4 weeks of nolv
4 weeks of HCG

let us factor in post nolv and hcg increase in ACTH. So you ran a 8 week cycle. You did 4 weeks of pct. 8+4=12

There is your time off.

So whats happening post hcg and nolv. Simple that damn set point is here to rob you of what you busted your ass for. We you are in your 30 so you can kiss the possibility of 800 test out the window (the normal guy on a scale of 240-840) say more like maybe 500ish. Wait lets factor in you just used aas and just got done with pct, not gonna be whole just yet, say 400 something. And you stopped all other suppliments. here comes some ACTH.

So all in all its gonna be a long motherfvcking 12 weeks to bubba.

That is were my question comes in: If I am old and I will not recover to a rate of a 22 year-old should I stay off for that long? While all this is happening I have normal body and that body is fighting the LBM increase (assuming SP theory is true)

When I use my (my current pct) HCG, HMG, propecia, nolv, should I use of anabolics to help me while my body resets myostatin? Such as slin, hGH.

Is it praticle to follow the PCT advice given with respect to usage of pct drugs and time off?

I now know what you meant before with your ACTH consideration.
Very complex subject to go through and the misfortune aas are banned in almost all the industrialized countries, does not help at all.

In any case, how do you know myostatin is uptaking after 8 weeks?
Also, HGH is the only compound able to create hyperplasia. Testosterone and derived can only lead to hypertrophy.

[FranciscoG]

I now know what you meant before with your ACTH consideration.
Very complex subject to go through and the misfortune aas are banned in almost all the industrialized countries, does not help at all.

In any case, how do you know myostatin is uptaking after 8 weeks?
Also, HGH is the only compound able to create hyperplasia. Testosterone and derived can only lead to hypertrophy.

Myostatin study:

Measurement of myostatin concentrations in human serum: Circulating concentrations in young and older men and effects of testosterone administration.

Lakshman KM, Bhasin S, Corcoran C, Collins-Racie LA, Tchistiakova L, Forlow SB, St Ledger K, Burczynski ME, Dorner AJ, Lavallie ER.

Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine, Boston Medical Center, 670 Albany Street, Boston, MA 02118, United States.

Methodological problems, including binding of myostatin to plasma proteins and cross-reactivity of assay reagents with other proteins, have confounded myostatin measurements. Here we describe development of an accurate assay for measuring myostatin concentrations in humans. Monoclonal antibodies that bind to distinct regions of myostatin served as capture and detector antibodies in a sandwich ELISA that used acid treatment to dissociate myostatin from binding proteins. Serum from myostatin-deficient Belgian Blue cattle was used as matrix and recombinant human myostatin as standard. The quantitative range was 0.15-37.50 ng/mL. Intra- and inter-assay CVs in low, mid, and high range were 4.1%, 4.7%, and 7.2%, and 3.9%, 1.6%, and 5.2%, respectively. Myostatin protein was undetectable in sera of Belgian Blue cattle and myostatin knockout mice. Recovery in spiked sera approximated 100%. ActRIIB-Fc or anti-myostatin antibody MYO-029 had no effect on myostatin measurements when assayed at pH 2.5. Myostatin levels were higher in young than older men (mean+/-S.E.M. 8.0+/-0.3 ng/mL vs. 7.0+/-0.4 ng/mL, P=0.03). In men treated with graded doses of testosterone, myostatin levels were significantly higher on day 56 than baseline in both young and older men; changes in myostatin levels were significantly correlated with changes in total and free testosterone in young men. Myostatin levels were not significantly associated with lean body mass in either young or older men. CONCLUSION: Myostatin ELISA has the characteristics of a valid assay: nearly 100% recovery, excellent precision, accuracy, and sufficient sensitivity to enable measurement of myostatin concentrations in men and women.
PMID: 19356623 [PubMed - in process]


The body will begin to build a tolerance. Myostatin, SHBG and other factors (not understood) are to blame.

[MuscleScience]

I now know what you meant before with your ACTH consideration.
Very complex subject to go through and the misfortune aas are banned in almost all the industrialized countries, does not help at all.

In any case, how do you know myostatin is uptaking after 8 weeks?
Also, HGH is the only compound able to create hyperplasia. Testosterone and derived can only lead to hypertrophy.

Muscle cells are terminally differentiated cells. They under virtually no circumstance de-differentiate (anaplasia) back to a more primordial cell type and undergo mitosis. Hyperplasia and Metaplasia are often times mistaken as the same thing. Metaplasia adds to the nuclear count of a muscle fiber, but is a one for one addition. Satellite cells are progenitor cells that when called upon first differentiate into a myoblastic cell before final terminal differentiation. This is a one for one process. To date in the literature Metaplasia is not considered a major contributor to muscle growth. Hyperplasia if it does occur in humans (cant say with certainty that it doesnt) should and could be very easily identified with simple muscle biopsy and nuclear staining techniques, when the process of mitosis initiates.

It is true that in some research it has shown that with certain cocktails of growth factors and or viral exposure that some anaplastic effect can be demonstrated in vitro. However this process has not been seen in vivo. Additionally under viral exposure and cancerous conditions, in vivo muscle cells can again be forced back into a state of mitotic reproduction. This is of course different and is termed neoplasia or sometimes called desmoplasia because it does not form normal myogenic tissue.

[BJJ]

Myostatin study:

Measurement of myostatin concentrations in human serum: Circulating concentrations in young and older men and effects of testosterone administration.

Lakshman KM, Bhasin S, Corcoran C, Collins-Racie LA, Tchistiakova L, Forlow SB, St Ledger K, Burczynski ME, Dorner AJ, Lavallie ER.

Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine, Boston Medical Center, 670 Albany Street, Boston, MA 02118, United States.

Methodological problems, including binding of myostatin to plasma proteins and cross-reactivity of assay reagents with other proteins, have confounded myostatin measurements. Here we describe development of an accurate assay for measuring myostatin concentrations in humans. Monoclonal antibodies that bind to distinct regions of myostatin served as capture and detector antibodies in a sandwich ELISA that used acid treatment to dissociate myostatin from binding proteins. Serum from myostatin-deficient Belgian Blue cattle was used as matrix and recombinant human myostatin as standard. The quantitative range was 0.15-37.50 ng/mL. Intra- and inter-assay CVs in low, mid, and high range were 4.1%, 4.7%, and 7.2%, and 3.9%, 1.6%, and 5.2%, respectively. Myostatin protein was undetectable in sera of Belgian Blue cattle and myostatin knockout mice. Recovery in spiked sera approximated 100%. ActRIIB-Fc or anti-myostatin antibody MYO-029 had no effect on myostatin measurements when assayed at pH 2.5. Myostatin levels were higher in young than older men (mean+/-S.E.M. 8.0+/-0.3 ng/mL vs. 7.0+/-0.4 ng/mL, P=0.03). In men treated with graded doses of testosterone, myostatin levels were significantly higher on day 56 than baseline in both young and older men; changes in myostatin levels were significantly correlated with changes in total and free testosterone in young men. Myostatin levels were not significantly associated with lean body mass in either young or older men. CONCLUSION: Myostatin ELISA has the characteristics of a valid assay: nearly 100% recovery, excellent precision, accuracy, and sufficient sensitivity to enable measurement of myostatin concentrations in men and women.
PMID: 19356623 [PubMed - in process]


The body will begin to build a tolerance. Myostatin, SHBG and other factors (not understood) are to blame.

Increase doses, add other compounds, change training volume/intensity and reduce SHBG is my advice.

Thanks for sharing.
Do you account any news in the science field regarding the ability to reduce the effect of myostatin?
Basically, is there any path to follow in order to mutate the gene which codifies the myostatine?

[FranciscoG]

I was going to touch on hGH, Igf-1, Pgf2-ª

All three as you pointed out will act out of the norm.

Pgf2-ª has been sited for distroying fat cells.

GH and IGF-1 are used to create hyperplasia.

There are many other peptides as well that can benifit.



God does not play dice with the universe. ~ Albert Einstein
Einstein went on to say the universe is created with order and in a logical order.

Here is a factors for the mathematical equation:

H-Homeostatis
ç- Constant factors that represent the feed back mechanisms that increase exponentially once you have distance from H
S- factors to aid in distance from H, D will become less effective with time

ç will exponentially increase for a set period of time, call this the time to stabolization period for the set point to reset.

H will never be achieved at advanced age

S- will be effective for 56 days and less effective from there on

S- will become effective after 56 days of none use

If Ç will never fully be combated what is the best course of action?

[FranciscoG]

Muscle cells are terminally differentiated cells. They under virtually no circumstance de-differentiate (anaplasia) back to a more primordial cell type and undergo mitosis. Hyperplasia and Metaplasia are often times mistaken as the same thing. Metaplasia adds to the nuclear count of a muscle fiber, but is a one for one addition. Satellite cells are progenitor cells that when called upon first differentiate into a myoblastic cell before final terminal differentiation. This is a one for one process. To date in the literature Metaplasia is not considered a major contributor to muscle growth. Hyperplasia if it does occur in humans (cant say with certainty that it doesnt) should and could be very easily identified with simple muscle biopsy and nuclear staining techniques, when the process of mitosis initiates.

It is true that in some research it has shown that with certain cocktails of growth factors and or viral exposure that some anaplastic effect can be demonstrated in vitro. However this process has not been seen in vivo. Additionally under viral exposure and cancerous conditions, in vivo muscle cells can again be forced back into state of mitotic reproduction. This is of course different and is termed neoplasia or sometimes called desmoplasia because it does not form normal myogenic tissue.

Good addition.

Use of peptides has not been known to upregulate myostatin production. As a contributing factor to retention the different cocktales can benefitual. Perhaps enough time can be passed and H can reset.

[FranciscoG]

Thanks for sharing.
Do you account any news in the science field regarding the ability to reduce the effect of myostatin?
Basically, is there any path to follow in order to mutate the gene which codifies the myostatine?

MYO-029 was in trials for years but it failed.

In humans no. In animal trials there a few mRNA meds used. Humans are 5-10 years away.

Muscular dystrophy would affectively disappear when an effective solution is found.

For now we got androgens and peptides.

[MuscleScience]

Good addition.

Use of peptides has not been known to upregulate myostatin production. As a contributing factor to retention the different cocktales can benefitual. Perhaps enough time can be passed and H can reset.

I am sure in future research they will figure out a compound that will render myostatins effect on muscle development to almost nothing. There is to much potential in muscle wasting diseases for this research to stall or not receive proper funding. Its just simple a matter of time.

[MuscleScience]

MYO-029 was in trials for years but it failed.

In humans no. In animal trials there a few mRNA meds used. Humans are 5-10 years away.

Muscular dystrophy would affectively disappear when an effective solution is found.

For now we got androgens and peptides.

Some types anyway.

[FranciscoG]

I used to think of MS as the ultimate off cycle period. The human body´s war upon itself.

Use of aas/peptides/experimental meds have not solved the waisting. Death from complications is almost certain in many cases.

[BJJ]

I used to think of MS as the ultimate off cycle period. The human body´s war upon itself.

Use of aas/peptides/experimental meds have not solved the waisting. Death from complications is almost certain in many cases.

What is your experience with aas?
How many cycles?
What type of drugs?

[BJJ]

I used to think of MS as the ultimate off cycle period. The human body´s war upon itself.

Use of aas/peptides/experimental meds have not solved the waisting. Death from complications is almost certain in many cases.

Because we do not know what the hell we are doing so deeply!

[FranciscoG]

What is your experience with aas?
How many cycles?
What type of drugs?

I started my first cycle 21 years ago in May of this year.

I have used most androgens, slin, GH, IGF-1 Pgf2-ª, All the Pct meds, Most Serms, Many of the AIs

The new peptides I have no experience with.

I am but a student.

[BJJ]

Muscle cells are terminally differentiated cells. They under virtually no circumstance de-differentiate (anaplasia) back to a more primordial cell type and undergo mitosis. Hyperplasia and Metaplasia are often times mistaken as the same thing. Metaplasia adds to the nuclear count of a muscle fiber, but is a one for one addition. Satellite cells are progenitor cells that when called upon first differentiate into a myoblastic cell before final terminal differentiation. This is a one for one process. To date in the literature Metaplasia is not considered a major contributor to muscle growth. Hyperplasia if it does occur in humans (cant say with certainty that it doesnt) should and could be very easily identified with simple muscle biopsy and nuclear staining techniques, when the process of mitosis initiates.

It is true that in some research it has shown that with certain cocktails of growth factors and or viral exposure that some anaplastic effect can be demonstrated in vitro. However this process has not been seen in vivo. Additionally under viral exposure and cancerous conditions, in vivo muscle cells can again be forced back into a state of mitotic reproduction. This is of course different and is termed neoplasia or sometimes called desmoplasia because it does not form normal myogenic tissue.

Sorry, I missed this.

I do not often mistake either of them since they are two different things and I wanted to mean what I just wrote, hyperplasia.

It can be hepatic, muscular and endometrial. In this specific case, HGH goaded, I was obviously speaking about the muscular one.

[BJJ]

I started my first cycle 21 years ago in May of this year.

I have used most androgens, slin, GH, IGF-1 Pgf2-ª, All the Pct meds, Most Serms, Many of the AIs

The new peptides I have no experience with.

I am but a student. we all are till death, who knows after that!

Why did you write you account HCG on your pct?
Should not it be run during cycle or just before of it?

[MuscleScience]

Sorry, I missed this.

I do not often mistake either of them since they are two different things and I wanted to mean what I just wrote, hyperplasia.

It can be hepatic, muscular and endometrial. In this specific case, HGH goaded, I was obviously speaking about the muscular one.

That sentence was more aimed at the causal reader that wouldnt really understand the difference in the two. I also meant hyperplasia in the context of muscle cells. Many other types of tissues can undergo hyperplasia, its just not currently believed that hyperplasia in humans is a major source of increase nuclear count or mass to muscles.

[BJJ]

That sentence was more aimed at the causal reader that wouldnt really understand the difference in the two. I also meant hyperplasia in the context of muscle cells. Many other types of tissues can undergo hyperplasia, its just not currently believed that hyperplasia in humans is a major source of increase nuclear count or mass to muscles.

Ok then.
Regarding the bold, you are totally correct.

[FranciscoG]

My personal experience is that the body adapts and desensitizes.

In 2001 or 2003 I purchased 100,000 IUs of pregnyl.

I ran it during cycle. I also used it off cycle. My expereince was that it was far less effective.


Today many are recommending use of HCG on cycle to address atrophy on cycle when using 100s of mg of aas. I simply do not agree with the science.

During use of aas can cause testicular atrophyis a result of reducing the amount of luteinizing hormone amoung other hormones.

Although use of HCG during cycle will certainly cause LH production, it does not address the cause, it impotently address the symptom, the atrophy itself.

The cause is administration of aas for a period of most generally months.

The human body restricts the production of fsh/gn/lh and so on to address the feed back. Administration of HCG during cycles will not stop this effect. It may make the subject feel better mentally cause his testicals are larger, but it will not address again the cause. Many argue that consistant administration of hcg aids post cycle. However, this flies in the face of science which dicates the feed backs for simple reasons of homeostasis. Again most pct advice given on the boards feels like it has been written by 20 something year-olds for 20 something year-olds.

Once aas are absent and the body needs to produce GN/LH/FSH hcg can aid in the process.

This PCT I am also using HMG and it feel much better than hcg alone.

[BJJ]

My personal experience is that the body adapts and desensitizes.

In 2001 or 2003 I purchased 100,000 IUs of pregnyl.

I ran it during cycle. I also used it off cycle. My expereince was that it was far less effective.


Today many are recommending use of HCG on cycle to address atrophy on cycle when using 100s of mg of aas. I simply do not agree with the science.

During use of aas can cause testicular atrophyis a result of reducing the amount of luteinizing hormone amoung other hormones.

Although use of HCG during cycle will certainly cause LH production, it does not address the cause, it impotently address the symptom, the atrophy itself.

The cause is administration of aas for a period of most generally months.

The human body restricts the production of fsh/gn/lh and so on to address the feed back. Administration of HCG during cycles will not stop this effect. It may make the subject feel better mentally cause his testicals are larger, but it will not address again the cause. Many argue that consistant administration of hcg aids post cycle. However, this flies in the face of science which dicates the feed backs for simple reasons of homeostasis. Again most pct advice given on the boards feels like it has been written by 20 something year-olds for 20 something year-olds.

Once aas are absent and the body needs to produce GN/LH/FSH hcg can aid in the process.

This PCT I am also using HMG and it feel much better than hcg alone.

That should be a sufficient reason to use it, or not?