More Action Reaction For More Action

The clinical term for excessive release of prolactin is hyperprolactinemia. It is actually a relatively common disorder in humans. There are many causes that initiate the condition including prolactin-secreting tumors and therapy with certain drugs.

Interesting is that the use of progestin-like AAS such as nandrolone and trenbolone will usually result in an increase in prolactin secretion. The employment of drugs such as cabergoline (0.25-0.5mg 2xW) bromocriptine (2.5-5.0mg/d) or mirtazapine for 2-4 weeks post use normally brings prolactin levels back to normal or below. This results in increased HPTA function, improved determent from accumulative female pattern fat and significantly heightened libido.

Males that experience hyperprolactinemia commonly develop hypogonadism (the shut down of the HPTA) with decreased sperm production, decreased sex drive and impotence. Those affected normally show breast enlargement (gynecomastia), but very rarely actually lactate. The gyno can initially manifest itself as an increase in fatty tissue under the lower pectorals and a puffy appearance to the areola and nipple.

A simple blood test for serum prolactin levels is commonly employed to evaluate the degree of potential feminization a male can or is experiencing. The lab results are quite simple to read, though a trained professional should interpret the results.

Normal Levels:

A. Adult: <20 ng/ml (including males)

B. Newborn: 100 to 300 (falls below 20 after 6 weeks)

C. Pregnancy

1. First Trimester: <80 ng/ml

2. Second trimester: <160 ng/ml

3. Third Trimester: <400 ng/ml

*References: Bakerman (1984) ABCs of Lab Data, p. 342

BIOSYNTHESIS INHIBITORS and THYROID FUNCTION

Another Action/Reaction factor that was considered during protocols utilizing biosynthesis inhibitors was possible inadequate thyroid hormone levels/activity. In some cases (Usually due to prolonged high dosage use) biosynthesis inhibitors have decreased thyroid hormone levels due to another negative feed-back loop.

As the reader knows already, or will soon learn, inadequate T-4/T-3 levels will severely decrease muscle protein synthesis due to poor nutrient turn-over and a sluggish metabolism.

Again the solution was simple. Frank used protocols such as Cortisol/Estrogen Suppression Phases for 30 days or under, and followed a 2 day on-2 day off schedule for those that included these drugs.

The one time his post-cycle thyroid function was low we utilized Guggulsterones and another TSH stimulator listed in "Chemical Muscle Enhancement", to normalize thyroid function. This was not necessary in most cases when phases were cycled as explained later in this discussion of Frank's story.

LOW DOSE AAS PHASE?

The idea behind a low dose AAS Phase was to maintain or even add some high quality muscle tissue, allow vascular and nerve tissue growth to catch up with the mega growth from serious weight/mass gain cycles (and site injection protocols) while not inhibiting HPTA function significantly.

This meant using high anabolics such as Primobolan Depot, 4-OH Testosterone, 4-OH Nandrolone, Equipoise, Oxandrolone and/or Nandrolone in an off set androgen alternating protocol with HPTA function chemistry. Total AAS dosages equaled about 1 mg per pound of bodyweight per week, and always pivoted upon very clean chemistry. This is often considered bridging by many.

After reviewing several blood test results, I had come to the realization that when done properly, low dose AAS phases could run 4-12 weeks with little decrease in HPTA function and few variances in liver enzyme profiles. To be effective, these phases included Action/Reaction time periods.

Simply stated, the body began to adapt and react to most chemistry or stimuli in 2-3 weeks. So each androgen /HPTA function period could not exceed 2 weeks.

Most high anabolic injectable AAS did not cause significant decreases in HPTA function and were very liver friendly. Nandrolone and Boldenone did cause some HPTA suppression even at 1 mg per pound of body weight weekly when utilized for more than 2 weeks consecutively. So mixing or alternating the three AAS was possible and was employed dependant upon the beast.

Few orals, except Primobolan tabs, could have been utilized since all others were cl7alkylated structures that could negatively affect liver function. Oxandrolone is a cl7alkylated AAS oral but at reasonable dosages failed to induce significant liver enzyme alterations.

Of course, just Primobolan Depot, oxandrolone or Equipoise had been utilized on numerous occasions. Fast acting Testosterone suspension was a useful androgen choice (if at all) since it cleared the system in a few days. This approach kept Frank easily within the 2 week alternating time frame.

LOW DOSE AAS PHASE EXAMPLE (250

LB Man)

DAY

DRUGS

DAY

DRUGS

1.

200 mg. Primo D/50 mg. Test. Sus.

23.

200 mg. Primo D/50 mg. Test. Sus.

2.

24.

3.

25.

4.

26.

5.

27.

6.

28.

7.

29.

8.

200 mg. Primo D/50 mg. Test. Sus.

30.

200 mg. Primo D/50 mg. Test. Sus.

9.

HCC 500iu

31.

HCG 500iu

10.

HCG 500iu

32.

HCC 500iu

11.

HCG 500iu

33.

HCG 500iu

12.

HCC 500iu

34.

HCG 500iu

13.

HCG 500iu

35.

HCC 500iu

14.

HCC 500iu

36.

HCG 500iu

15.

HCG 500iu

37.

HCC 500iu

16.

HCG 500iu

38.

HCG 500iu

17.

HCC 500iu

39.

HCG 500iu

18.

HCG 500iu

40.

HCG 500iu

19.

HCG 500iu

41.

HCG 500iu

20.

HCC 500iu

42.

HCC 500iu

21.

HCG 500iu

43.

HCG 500iu

22.

HCC 500iu

44.

HCG 500iu

• Frank continued in same manner or mixed AAS from this point on for up to 12 weeks. Cycle /Phase always ended with an HPTA function period.

• Low dose AAS phases had also been utilized as part of a site injection protocol by creating a dosage equivalent Max Mix for maintenance periods.

• The addition of Clomid 50-1 00 mg/d during the last 1 4 days of a low dose protocol was very beneficial.

• Bromocriptine 2.5mg/d on listed HCG days resulted in an increase in HPTA activity due to inhibition of prolactin. (And an increase in libido is always nice)

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