SuperDrol On cycle

T H E O R E M

T H E O R E M

Member
Awards
1
  • Established
For superdrol, what would be a good precautionary supplement to have on hand to add in ON cycle if a flareup occurs? I have a SERM which some say you should just add that in if you choose to continue. Is there something less harsh or better option? ATD, AI?
 
SupremeSE

SupremeSE

Banned
Awards
1
  • Established
For superdrol, what would be a good precautionary supplement to have on hand to add in ON cycle if a flareup occurs? I have a SERM which some say you should just add that in if you choose to continue. Is there something less harsh or better option? ATD, AI?
Superdrol(REAL) does not aromatize and thus, and aromatase inhibitor or SERM is not required while ON cycle.

However, you may want STACK Superdrol with The AndroGenerator, which will minimize HPTA inhibition while simultaneously increasing GAINS while ON cycle. www.AndroGenerator.com
 
Ziquor

Ziquor

Well-known member
Awards
1
  • Established
Superdrol(REAL) does not aromatize and thus, and aromatase inhibitor or SERM is not required while ON cycle.

However, you may want STACK Superdrol with The AndroGenerator, which will minimize HPTA inhibition while simultaneously increasing GAINS while ON cycle. www.AndroGenerator.com
A low dose of any AI would be fine. Arimidex, formestane, 6-Oxo. Super's not SUPPOSED to aromatise however an extreme high amount of users got gyno, some on - some delayed, meaning in some way it does indeed aromatise - but not with everyone who takes it which's strange. I plan on having an AI on hand just in case since this has happened to so many. My theory on this is without any quality restrictions on supplements and since this only seems to happen to some people I believe it could be a quality of materials issue where the batches made aren't truely 100% pure methyl-drostanolone.
 
I

Interlocutor

New member
Awards
0
For superdrol, what would be a good precautionary supplement to have on hand to add in ON cycle if a flareup occurs? I have a SERM which some say you should just add that in if you choose to continue. Is there something less harsh or better option? ATD, AI?
cabergoline, if you already have a SERM. more often than not, descriptions of issues with superdrol (lactating etc.) seem more indicative of prolactin issues than estrogen issues.

however, another concern is contamination of the SD with oxymetholone, apparently an intermediate production step. oxymetholone has direct estrogenic activity, i.e. an AI will not help, but a SERM might.

the combo of SERM + cabergoline may be your best bet.

However, you may want STACK Superdrol with The AndroGenerator, which will minimize HPTA inhibition while simultaneously increasing GAINS while ON cycle. ANDROGENERATOR - The World's Most Powerful Natural Anabolic & Male Sexual Enchancement
can you please expound on the pathways through which this is supposedly achieved by your "penis enlarging" product (your words, not mine)? wasn't the AG mainly a LJ100/Trib based compound (correct me if i'm wrong)? i don't understand the real cost/benefit ratio of a mainly SHBG mod product in a very-low-test environment, well, and the discussion on the merits of trib... let's say was inconclusive so far, or not?

also, you claim
Not only does AndroGenerator drastically increase TOTAL AND FREE TESTOSTERONE, it also decreases CORTISOL, ESTROGEN. and PROLACTIN, the three primary enemies of HPTA recovery in a post-cycle environment! It is imperative to increase testosterone levels, decrease estrogen, prolactin, and cortisol, and to restore your hormonal balance as swiftly and effectively as possible. AndroGenerator features a unique combination of highly anabolic, pro-androgenic agents that drastically increase endogenous ANDROGEN concentrations while simultaneously reducing prolactin and balancing progesterone and Estrogen. You will NEVER use Clomid or Nolvadex again!
can you please expound by which mechanisms a mainly LJ100/Trib based product is supposed to replace SERMs? any independent bloodwork that verifies your claims?

also, wasn't there some concern that the GPA as contained in your product may raise homocysteine count?

Plasma Protein Aspartyl Damage Is Increased in Hemodialysis Patients: Studies on Causes and Consequences -- Perna et al. 15 (10): 2747 -- Journal of the American Society of Nephrology
Uremic toxins were also incubated with purified human albumin, and dose-response experiments with the two most toxic agents in terms of protein damage (guanidine and guanidinopropionic acid) were carried out.
T.I.
 
SupremeSE

SupremeSE

Banned
Awards
1
  • Established
cabergoline, if you already have a SERM. more often than not, descriptions of issues with superdrol (lactating etc.) seem more indicative of prolactin issues than estrogen issues.

however, another concern is contamination of the superdrol with oxymetholone, apparently an intermediate production step. oxymetholone has direct estrogenic activity, i.e. an AI will not help, but a SERM might.

the combo of SERM + cabergoline may be your best bet.



can you please expound on the pathways through which this is supposedly achieved by your "penis enlarging" product (your words, not mine)? wasn't the AG mainly a LJ100/Trib based compound (correct me if i'm wrong)? i don't understand the real cost/benefit ratio of a mainly SHBG mod product in a very-low-test environment, well, and the discussion on the merits of trib... let's say was inconclusive so far, or not?

also, you claim can you please expound by which mechanisms a mainly LJ100/Trib based product is supposed to replace SERMs? any independent bloodwork that verifies your claims?

also, wasn't there some concern that the GPA as contained in your product may raise homocysteine count?

Plasma Protein Aspartyl Damage Is Increased in Hemodialysis Patients: Studies on Causes and Consequences -- Perna et al. 15 (10): 2747 -- Journal of the American Society of Nephrology

T.I.

AndroGenerator will minimize HPTA inhibition and increase your gains on cycle. AndroGenerator will MINIMIZE HPTA INHIBITION, through several different mechanisms. During a steroid cycle, the testicles SHRINK. This is known as testicular atrophy. The testicles shrink as a result of being "SHUTDOWN". They are not functioning to produce testosterone, because the body has ceased all endogenous androgen production as a result of detecting exogenous hormones. AndroGenerator is so powerful and effective, it will actually PREVENT HPTA SHUTDOWN from ocurring while ON CYCLE! While on cycle, the body's natural production of testosterone(and LH) becomes suppressed. Just like HCG, AndroGenerator signals the Pituitary to secrete LH, which subsequently causes the testicles to produce more testosterone. This increase in LH and subsequently testosterone, maintains testicular mass and function while on anabolic steroids. AndroGenerator also decreases PROLACTIN, which is the primary sex hormone responsible for "HPTA sensitivity". Prolactin is a nasty hormone that will cause the HPTA to SHUTDOWN almost immediately, which is why steroids such as Deca and Tren are so suppressive to HPTA function. By decreasing prolactin, we can decrease HPTA sensitivity and further minimize total HPTA inhibition experienced while on cycle. Running AndroGenerator with a mild steroid such as Anavar, Dianabol, or Epistane, will result in virtually no HPTA inhibition at all. Including Androgenerator in your full cycle will result in much less HPTA inhibition and of course, much GREATER GAINS while on cycle, due to the pro-androgenic, muscle-building effect of AndroGenerator.

Scientific Studies: Supreme Sports - Contact Us
 
D

dice404

Member
Awards
0
AndroGenerator will minimize HPTA inhibition and increase your gains on cycle. AndroGenerator will MINIMIZE HPTA INHIBITION, through several different mechanisms. During a steroid cycle, the testicles SHRINK. This is known as testicular atrophy. The testicles shrink as a result of being "SHUTDOWN". They are not functioning to produce testosterone, because the body has ceased all endogenous androgen production as a result of detecting exogenous hormones. AndroGenerator is so powerful and effective, it will actually PREVENT HPTA SHUTDOWN from ocurring while ON CYCLE! While on cycle, the body's natural production of testosterone(and LH) becomes suppressed. Just like HCG, AndroGenerator signals the Pituitary to secrete LH, which subsequently causes the testicles to produce more testosterone. This increase in LH and subsequently testosterone, maintains testicular mass and function while on anabolic steroids. AndroGenerator also decreases PROLACTIN, which is the primary sex hormone responsible for "HPTA sensitivity". Prolactin is a nasty hormone that will cause the HPTA to SHUTDOWN almost immediately, which is why steroids such as Deca and Tren are so suppressive to HPTA function. By decreasing prolactin, we can decrease HPTA sensitivity and further minimize total HPTA inhibition experienced while on cycle. Running AndroGenerator with a mild steroid such as Anavar, Dianabol, or Epistane, will result in virtually no HPTA inhibition at all. Including Androgenerator in your full cycle will result in much less HPTA inhibition and of course, much GREATER GAINS while on cycle, due to the pro-androgenic, muscle-building effect of AndroGenerator.
Not to be blunt, but I would like to hear the MECHANISMS by which your product works, rather than marketing.

Just like HCG, AndroGenerator signals the Pituitary to secrete LH
And someone correct me if I'm wrong, but HCG is a synthetic gonadotropin and does not stimulate release of LH, rather HCG is HPTA suppressive. What HCG does stimultate is the leydigs cells of the testes to secrete testosterone, essentially replacing LH and thus increasing testicular size and function. But again does not stimulate the natural release of LH.
 
SupremeSE

SupremeSE

Banned
Awards
1
  • Established
THE ANABOLIC EFFECTS OF LJ100™
For a printable copy of this study, please click here.

Sareena Hanim Hamzah & Ashril Yusof
Department of Exercise Physiology, Sports Centre, University of Malaya, Kuala Lumpur

Introduction
Eurycoma longifolia (LJ100™) is a tall shrub tree of a Simaroubaceace family and is commonly found along the hilly jungle slopes of Malaysia. It has been used for years as a traditional medicine to treat fever, ulcer, malarial, swelling, reduce high blood pressure and fatigue. However, LJ100 is better known for its aphrodisiac properties. In a clinical study by Ismail (2002), he demonstrated that this herb enhanced sexual activities and increased free testosterone levels in men. Increases in testosterone levels is associated with an improvement in fat free mass, muscle size and muscle strength in men (Brodsky, 1996; Bhasin, 1997), which could be further amplified by strength training (Bhasin, 1996). In this study, the effect of LJ100 water-soluble extract on body composition and muscle size in men will be measured.

Methods
Fourteen healthy adult males (age 25.64 ? 3.73 years) received either 100 mg/day LJ100 water-soluble extract (n = 7) or placebo (n = 7) for 8 weeks. Simultaneously, both groups performed an intensive strength-training program with initial load of 60% repetition maximum (RM), which was carried out on alternate days. A total of 10 exercises, which make up the circuit, were catered towards providing a total lower body and upper body workout. Each workout was done in two sets of 10 repetitions with 1-minute rest in between. The loads were gradually increased 10% per week. Body composition measurement using skin fold test was taken at two sites as recommended by McArdle (1993). A standard strength test that comprised of 1 RM test was administered on the subject to determine their strength. The upper limb strength was measured by determining their ability to resist maximum load using the shoulder press machine (Nautilus, USA) following the American College of Sports Medicine (ACSM, 2001) standard measurement procedure. The arm circumference measurement was taken using a measuring tape at proximal 1/3rd of the arm. Electromyography reading of the isometric contraction of bicep muscle was taken using the surface electrodes. Subjects were instructed to perform an isokinetic flexion of the elbow using free barbells with load of 10 kg for the durations of 5 seconds. The mean amplitude was analyzed using the MyoResearch Software (Noraxon, USA).
All the measurements were taken 1 day prior to supplementation (LJ100 and placebo) and training period, and 1 day after the completion of 8 weeks experiment. All data were analyzed using the Statistical Package for Social Science (SPSS) computer software version 10.0 (2000) for t-test, means and standard deviation. Statistical significance was established at p<0.05.

Results
The results for fat free mass, fat mass, 1 RM, arm circumference, and sEMG of both groups are shown in Table 1.

Table 1. Average fat free mass, fat mass, 1 RM test, arm circumference and sEMG of the group consuming LJ100 water soluble extract and placebo before and after the period of supplementation and training program


* Results of mean ± SD for pre and post experiment showed significant difference (p<0.05)

The fat free mass of the group supplemented with LJ100 water-soluble extract showed a significant increment of approximately 2.1 kg. There were no significant changes in fat free mass in placebo. Body fat percentages were significantly decreased in treatment and placebo. However, a greater decrement was shown in treatment compared to placebo i.e. 9.14% and 6.57%, respectively. The 1 RM test muscle strength test showed an increase in gross muscle power in both groups. The treatment group showed a greater increment in strength compared to placebo i.e. 6.78% and 2.77%, respectively. The mean arm circumference in treatment group increased significantly by 1.8 cm following the supplementation while no significant changes observed in placebo group. The mean sEMG reading of the treatment and placebo showed a significant decrement in values after going through the exercise program. However, the treatment group showed 2.92% higher reduction in electrical activity of the muscle measured at the end of the experiment period compared to placebo (25.70% and 22.78%, respectively). During and after the administration of LJ100, no adverse effects were noted within the treatment group.

Discussion/ Conclusion
In this study, although the testosterone level was not measured during the test period, an increased in fat free mass in treatment group may be linked to the rise in steroidal hormones in the body. The percentage of body fat appeared to decrease in both groups, this finding is in agreement with a study by Brodsky (1996). However, the further decrease in fat mass by the treatment group could be explained by the higher metabolic rate after consuming LJ100. The increment in muscle strength with strength training in both the treatment and placebo groups were consistent with the finding by Kraemer (1993), he suggested that the improvement in strength was caused by the increase in testosterone levels. Jones and Round (1996) proposed that increases in strength are greater than increases in muscle size during the first 6-8 weeks of strength training. Thus, an increase in arm circumference observed in treatment group could be explained by the testosterone enhancing effect of the extract. In conclusion, results obtained from this pilot study suggest that the administration of LJ100 improved fat free mass, reduce fat mass, increase muscle strength and size suggesting LJ100 might be used as an ergogenic aid. Further studies will be carried out to determine the mechanism of action at hormonal and molecular level.

Water-soluble extract of LJ100™ as a potential
natural energizer for healthy aging in men.
M.I.M.TAMBI1, S. OTHMAN2and J.M SAAD2

1Specialist Reproductive Research Center, National Population & Family Development Board, Ministry of Women & Family Development, Malaysia.
2Department of Biochemistry, Faculty of Medicine, University of Malaya, Malaysia.

Introduction
Malaysia has a rich source of rainforests that contain thousands of plants with potential medicinal values. One such plant is the tall shrub tree from the Simaroubaceace family, Eurycoma Longifolia (LJ100™ Tongkat Ali) which is commonly found along the hilly jungle slopes of Malaysia (Burkill and Hanif, 1930). The local name of the shrub is 'Tongkat Ali' or Ali's Walking Stick' which is rather suggestive of its traditional function of sexual support for aging males. Similar trees are also found in other Asian Rainforests; however, it is traditionally known that only two species of the shrub namely E.Longifolia and E.apiculata have medicinal properties (Burkill and Hanif, 1930). The medicinal elements are only found within the roots. The root of Eurycoma Longifolia was used as a decoction by the natives of old Malaya, especially the elderly for strength and energy (Burkill and Hanif,1930), this practice remains to this day.
Early experimental studies on animals were mainly focused on the aphrodisiac properties of LJ100. Mice treated LJ100 demonstrated higher frequency of mounting compared to the control group (Ali and Saad, 1993). Additionally, the serum testosterone of the dissected mice showed an increase of 480% compared to the placebo-controlled group (Ali and Saad, 1993). Further studies provided evidence that LJ100 produced a dose-dependent increase in mounting frequency in male rats, hence, acting as a potent stimulator of sexual arousal in the absence of feedback from genital sensation (Ang and Sim,1997). It was also shown that LJ100enhanced and maintained a high level of crossovers, mountings, intromissions, and ejaculations.

Other studies showed that when the extract of LJ100 was injected into male mice, they showed intense physical activities and copulatory behavior (Ang and Sim, 1998). Even frail mice were observed to be active and alert. In another study, LJ100 was exposed to penile muscular tissue of male mice; results demonstrated that the muscular tissue was found to relax. Analysis on the mitochondria homogenates of the liver and penile muscle of the mice showed that the extract could enhance the respiration of mitochondria, leading to 60% increase in ATP production through oxidative phosphorylation (Khamis and Saad, 1993).

Early clinical trials studied the effect of LJ100 on testicular tissues. The samples were incubated along with human testicular tissues taken from men who were orchidectomised as part of treatment of prostate cancer (Aminuddin et al, 1995). There was significant increase in the concentration of testosterone and its precursors. The results suggest that the LJ100 has the ability to increase the biosynthesis of androgens (Aminuddin et al, 1995).


Androgen is the generic term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of masculine characteristics in vertebrates. This includes the activity of the accessory male sex organs and development of male secondary sex characteristics. The primary, and most well known, androgen is testosterone.

In this study, we intend to investigate the effect of the LJ100 water-soluble extract on testosterone, dehydroepiandrosterone (DHEA) and sex hormone binding globulin (SHBG) levels in human subjects. Dehydroepiandrosterone (DHEA) is a natural steroid hormone produced from cholesterol by the adrenal glands. Dehydroepiandrosterone is structurally similar to testosterone and estrone and can be easily converted into those hormones (DHEA is a precursor for testosterone). Sex hormone binding globulins are carrier proteins that regulate the amount of unbound steroid in the blood. A decrease in SHBG is associated with an improvement in free testosterone index. Additional parameters that will be measured include Quality Of Life (QOL) via the PADAM score and Sexual Health Inventory Questionnaires (SHI-Q).

Methodology
In a Reproductive Research Center in Kuala Lumpur, Malaysia, 30 human volunteers were recruited in a randomized open trial. The volunteers were selected among married men whose age ranges between 31-52 years. There were no other specific criteria for the selection of volunteers. Dr. Johari M. Saad and co-workers from the Department of Biochemistry, University Malaya, Malaysia, produced LJ100 water-soluble extract of E.Longifolia root.
Upon registration, the volunteers were asked to fill out two questionnaires: (i) a validated Sexual Health Inventory Questionnaires (SHI-Q) and (ii) the PADAM Score Questionnaires. Peripheral venous blood sample was collected from each individual to evaluate his total testosterone hormone, dehydroepiandrosterone sulphate (DHEA) and sex hormone binding globulin (SHBG) levels. Following this, each volunteer was given a supply of the encapsulated LJ100. These were to be consumed regularly for three consecutive weeks, twice daily, and two capsules per day (100 mg/day). The volunteers were requested to come back for a follow-up after week one and week three. During the follow-up sessions, they were asked to again fill out two sets of questionnaires and provide blood samples for analysis of serum testosterone, SHBG and DHEA.

Results
Questionnaires Analysis
Analysis of the SHI-Questionnaire results have shown that 62% of the cases had either increased or a maximum score after consuming LJ100. Another 24% showed reduction while 14% of the cases showed no change in the score (Figure 1). This indicates that the majority of the volunteers demonstrated an increase in their sexual health satisfaction and performance. Breakdown of the SHI-Questionnaire showed subjects has an increase in sexual desire and the success at the attempts at sexual intercourse.


Figure 1: Effect of LJ100™ consumption on SHI-Q Score


PADAM Analysis
Analysis of the PADAM Score demonstrated that 82% of the cases showed a decrease in total score (decrease is positive effect). There is 91% improvement in the sexual PADAM score component, a 73% improvement in the physical component, and an 82% improvement of psychological component. The vasomotor score showed improvement in 50% of the subjects (Figure 2). The improvements in the first three components of the PADAM score reflects that consumption of LJ100 had resulted in an improvement of their quality of life with regards to their physical, sexual and psychological well being.

Figure 2: Percentage of Improvement or Reduction for Various Components of the PADAM Score


Serum Hormones analysis
Testosterone
Total testosterone levels were not significantly different between those raised (43%) and those declined (39%) in this study (Table 1). This gives an initial impression that LJ100 does not have any effect on steroidogenesis. Considering that almost all the volunteers have normal levels of total testosterone, the feedback system is activated to ensure the testosterone levels are within the individual needs range. In 6 volunteers whose serum total testosterone is low, there is an increase in total testosterone on first and third week as well as improvement in the Quality of Life Scores (SHI-Q and PADAM Score).





DHEA
Analysis of the DHEA showed gradual increase from 26% after 1 week to 47% after 3 weeks. This suggests that LJ100may influence the DHEA production, which subsequently would be aromatized to testosterone (Figure 3).

Figure 3: Percentage of Increment in DHEA level





SHBG Analysis
The results showed that SHBG levels were reduced in 36% of the cases after one week and improved to 66% after 3 weeks. This suggests that LJ100 could have an effect on the production of SHBG (Table 2).





Free Testosterone Index Analysis (FTI)
When the SHBG level declines, the Free Testosterone Index (FTI is calculated as a percentage of the total testosterone against SHBG) goes up. Results demonstrated that the FTI increased in 39% of the subjects after 1 week to 73% after 3 weeks (Table 3)




Conclusion
Increasing testosterone is the key factor in increasing sex drive. Testosterone is the most important of the male sex hormones, known as androgens, produced in the gonads. Testosterone plays a key role in the development and maturity of male sex organs. The hormone promotes secondary sex characteristics, including the appearance of facial hair, sexual desire, and sexual behavior. However, testosterone is not just a sex booster for men. Women also produce testosterone, about 5 to 10 percent the amount produced in men. In woman, this vital hormone also stimulates sex drive and produces heightened sensitivity of erogenous zones.

In this study, the aqueous LJ100 extract has a strong potential in providing sufficient free testosterone to the body as demonstrated by the increase in the free testosterone index between weeks one and three. The high score in the Physical and Sexual Domain of PADAM and the Desire and Sexual Attempts in the SHI-Q score suggests this extract can delivery sexual health effects for both men and women.

The results demonstrated that the circulating androgen concentration affects SHBG synthesis. The increase in DHEA levels (DHEA is a precursor to testosterone) between week 1 and week 3 resulted in elevated testosterone levels that caused a decrease in SHBG levels. It is important to note the any decrease in SHBG levels has an overall effect to increase free testosterone index as indicated in table 3. The results of this study suggest that LJ100 inhibits SHBG allowing more free testosterone to remain in the blood. This additional testosterone stems the aging process, improves energy and sexual function, and helps reduce body fat and reduces the risk factors associated with heart health.

Since this study is just an exploratory study to look into the marketing potential of LJ100, the volunteers were asked about personal feedbacks with regard to the extract. The following responses were received:
48% felt that they are feeling healthy, not easily tired, feeling active and energized.
40% felt easily aroused, increase sexual desire and maintained an erection longer.
16% felt their joints and backache are feeling better.
24% felt warm and easily sweat (sign of better circulation)
8% experience better sleep.
8% felt an improvement in their memory.
20% felt their appetite has improved and their bowel movements are better than before.

References
1.Burkill, IH and Hanif, M; (1930) Malay Village Medicine, The Garden Bulletin Strait Settlements.
2.Ali, JM and Saad, JM (1993); Biochemical effect of Eurycoma Longifolia Jack on the sexual behavior, fertility, sex hormone and glycolysis. Dissertation Paper for Bachelor of Science, Department of Biochemistry, University of Malaya
3.Ang, HH and Sim,MK (1997); Effect of Eurycoma Longifolia Jack on sexual behavior of male rats. Archives of Pharmacal Research (Seoul),20(5),656-58
4.Ang, HH and Sim,MK (1998)[1]; Eurycoma Longifolia Jack and orientation in sexually experiences male rats. Biol and Pharmaceutical Bulletin 21(2);153-55
5.Ang, HH and Sim,MK (1998)[2]; Eurycoma Longifolia Jack increases sexual motivation in sexually naive male rats. Archives of Pharmacal Research (Seoul),21(6),778-81
6.Khamis, ZM and Saad, JM (1993); Dissertation Paper for Bachelor of Science, Department of Biochemistry, University of Malaya.
7.Aminuddin, N; Saad, JM; Hadi, AH and Abdullah, R (1995); The effect of Eurycoma Longifolia extracts on androgen synthesis.


LJ100™ Saliva Testosterone Test

Saliva Testosterone Test of 9 Individuals 26-52 years of age
Dosage 2x2 (50mg/capsules) morning & evening for 10 days
Normal range for athlete 800 = 150ng/dl of blood



Volunteers 1-5 are athletes - data are an average of 3 different studies at different times
Volunteers 6-9 do not exercise on a regular basis

Conclusion
The results demonstrate that 100 mg per day of LJ100 caused an increase in bioavailability testosterone within 10 days. Furthermore, all subjects (athletes and non-athletes) showed a positive increase in testosterone suggesting that LJ100 causes an increase in the free testosterone index.
 
SupremeSE

SupremeSE

Banned
Awards
1
  • Established
Effect of LJ100 Tongkat Ali on Anabolic Balance During Endurance Exercise

Talbott S, Talbott J, Negrete J, Jones M, Nichols M, and Roza J. Effect of Eurycoma longifolia Extract on Anabolic Balance During Endurance Exercise. SupplementWatch, Inc. Draper, UT, 84020 USA and Source One Global Partners, Chicago, IL 60611 USA. [email protected]

Eurycoma longifolia, commonly known as “Tongkat Ali” or “Longjack,” is often touted as a testosterone “booster” and marketed to athletes as a training aid and performance enhancer. Rodent studies have shown oral delivery of Eurycoma extract to improve sexual performance and increase serum testosterone levels. Open-label human trials have suggested that Eurycoma extract may help prevent age-associated androgen deficiency, improve sexual function, and increase psychological parameters such as mood, energy, and sense of well-being. The purpose of this study was to determine the effects of Eurycoma longifolia on testosterone and cortisol levels during intense endurance exercise. We used a water-soluble extract of Eurycoma longifolia (E) standardized to 22% eurypeptides and 40% glycosaponins. Male subjects (N=30) were recruited from a 24-hour mountain biking event and asked to provide a saliva sample before and after each lap for measurement of cortisol and testosterone by enzyme immunoassay (Salimetrics, State College, PA). Subjects completed 4 laps (14.91 miles/lap) and provided 8 saliva samples over a 24h period. Subjects consumed 100mg of E or a look-alike placebo (P) approximately 30 minutes prior to endurance exercise. Cortisol levels were 32.3% lower in E compared to P (0.552+0.665 versus 0.816+0.775 ug/dL, P < 0.05). Testosterone levels were 16.4% higher in E compared to P (86.72+40.90 versus 72.47+33.77 pg/mL, P < 0.05). These results suggest that Eurycoma longifolia extract may help to maintain normal levels of cortisol (low) and testosterone (high) and thus promote an overall “anabolic” hormonal state (versus a “catabolic” state characterized by elevated cortisol and suppressed testosterone) during intense endurance exercise.




--------------------------------------------------------------------------------



TRIBESTAN EFFECT ON THE CONCENTRATION OF SOME HORMONES IN THE SERUM OF HEALTHY SUBJECTS
S. Milanov, A. Maleeva, M. Taskov

RIRR - Radioisotope and Radioimmunological Laboratory, Sofia

Chemical Pharmaceutical Research Institute,
Sofia, Bulgaria

SUMMARY

Tribestan effect has been studied on the serum concentration of hypophyseal hormones, of ACTH, STH, LH, FSH, adrenal hormone aldosterone and cortisol and sex hormones - testosterone and estradiol. The experiments have been carried out on 8 males and 8 females, aged 28 - 45 years of age. The product was perorally administered in a single dose of 250 mg, three times daily for 5 days. Serum samples were withdrawn at 8 a.m. and 12 a.m., prior to and post treatment. The product has been established not to change essentially the concentrations of adrenal hormones and of ACTH. The hypophyseal-gonadal axis however has significantly been affected in the females with predominantly increased concentration of FSH and estradiol and in the males - mainly of LH and the testosterone. The mechanism of that action is presumed to be complicated and realized both by direct effect on gonadal apparatus and by the tropic hormones.
The probable established changes in the concentration of the hormones studied do not get out of the frames of the physiological limits.

The lyophilized extract of Tribulus terrestris, introduced in veterinary practice as TB-68, has pronounced sex-stimulating function. The initial studies of this product showed that it stimulates the spermatogenesis of albino rats (Vankov S., et al., 1973) and enhanced the ovulation of female rats (Vankov S. et al. 1973). Zarkova S. (1976) has also established in rats an increased number of spermatogonia, spermatocytes as well as increase of neutral mucopolysaccharides in seminiferous tubules of the testes. Gendzhev Z. and S. Zarkova, in other experiments (1978) proved the increase of spermatic reserve in the epididymis of rats.

With the view to the need of human medicine of a product stimulating sexual function, Tribestan was formulated on the base of the indicated phytochemical product. It contains saponins of furostanol type (Tomova M. et al., 1978). The first studies of Tribestan confirmed its high sex-stimulating activity in experimental animals (Zarkova S., 1981). Later, the clinical studies established a similar stimulating effect in humans as well (Protich M. at al. 1981). The present study was carried out with a view to throwing light on some aspects of the mechanism of that action of Tribestan, aiming at attaining an effect from the product on the serum concentration of some hypophyseal, sexual and adrenal hormones.

MATERIALS AND METHODS

The experiments were performed on 16 subjects (8 females and 8 males), aged 28-45. All subjects were in good health, without any complaints and good capacity for work. The following schedule was used:
1. The basic levels of hypophysiotropic hormones (ACTH, STH, LH, FSH), of sexual hormones (testosterone and estradiol) and of adrenal hormones (aldosterone and cortisol) were determined. They were determined twice, at 8 a.m. and 12 p.m. - one day prior to Tribestan treatment.
2. The treatment with the product was initiated on the following day, which was periodically administered, 250 mg, three times daily for 5 days.
3. After the termination of Tribestan treatment (day sixth after the initiation of the experiment), blood was again withdrawn (at the same hour - 8:00 a.m. and 12 p.m.) for the determination of the concentration of the indicated hormones.

The work proceeded in the following way: after centrifugation of 6 - 8 ml blood, the serum obtained was frozen at 20°C till the day of the determination of hormonal concentration. The determination was performed by radioimmune tests. LH and FSH were determined by the modified method of Midgley A.R., (1967), making use of some kits of Biodata company, Italy and ACTH and STH - according to the method of Berson S.A. and R. S. Yalow (1963). Testosterone was evaluated by the method of William R. H. (1968), and of estradiol by Orezyk G.P. et al. (1974), making use of kits of Sorin Company, Belgium for both hormones. The adrenal hormones cortisol and aldosterone were also determined by kits of that company, making use of Vescei P. (1974) and of William G and R. Hunderwood (1974).

The obtained results were statistically processed by variation analysis, by Student - t test.

RESULTS AND DISCUSSION

As could be seen from Table 1, LH level in the males was elevated with a high significance after the treatment (p < 0.001). The changes affected both samples to the same rate (at 8 a.m. and 12 p.m.). FSH concentration was not affected under the same conditions. The other two hypophyseal hormones, ACTH and STH were not changed.

An insignificant tendency to elevation was observed in STH level (mean values - 2.9 prior to and 3.2 mg/ml post treatment) in some of the cases. The level of sex hormones was strongly affected. Thus testosterone concentration was three-fold (2) increased and that of estradiol - about 1.5 times (Table 1).

Table 1
Hormone Prior to Tribestan
Post Tribestan

8 a.m.
12 p.m.
8 a.m.
12 p.m.

LH, mIU/ml X 13.0 14.38(1) 37.25 24.75
SX 0.64 0.73 1.01 0.79
Pt 0.001 0.001
FSH, mIU/ml X 13.38 13.50 13.38 11.38
SX 0.35 0.28 0.35 0.36
Pt >0.5 >0.5
Testosterone, ng % X 628 610 882 845
SX 48 46 35 32
Pt <0.001 <0.001
Estradiol pg/ml X 79 76 133 137.5
SX 3.46 2.24 6.72 5.86
Pt <0.001 <0.001

LH concentration was also increased in females under Tribestan effect. What impressed was that the significance was lower than the first sample. The greatest discrepancy, as compared with the results of the males, was the sharp stimulation of FSH. A strong effect was observed there, which could be explained by blood withdrawal during the early phase of the menstrual cycle, the so-called follicular phase. Estradiol was also strongly affected (Pt < 0.001), whereas testosterone in the females during the early hours of the day was less affected (Table 2).

Table 2
Hormone
Prior to Tribestan
Post Tribestan

8 a.m.
12 p.m.
8 a.m.
12 p.m.

LH, mIU/ml X 15.25 13.50 17.13 16.88
SX 0.64 0.87 0.73 0.35
Pt 0.02 0.001
FSH, mIU/ml X 11.00 11.88 17.75 15.25
SX 0.13 0.09 0.71 0.38
Pt 0.001 0.001
Estradiol mIU/ml X 72.13 59.38 77.13 87.50
SX 6.02 5.73 5.47 3.24
Pt 0.5 0.001

The level of adrenal hormone was identically affected both in males and females (Table 3). A significant increase of the concentration was also established though that effect had a relatively low significance (p < 0.05). At the same time, cortisol level was no changed (Table 3).

Table 3
Aldosterone Cortisol
Prior to Post Prior to Post
X 11.59 13.77 8.63 8.63
S 2.52 3.48 2.20 1.92
SX 0.63 0.87 0.55 0.48
Pt 0.05 0.05

The results obtained provided grounds to admit that Tribestan had a pronounced stimulating effect on the secretion of some hormones. The effect on the hormones along the hypophyseal-gonadal axis was particularly well manifested. The effect was manifested both at hypophyseal and gonadal level. Some sexual discrepancies were also established. Thus, FSH was mainly affected in the females. The presence of that hormone is exceptionally important during the follicular phase for the development of the follicle. When its development is stimulated, its secretory ability is also intensified and hence - estradiol level is elevated. Lutenizing hormone is more strongly influenced in the male, which on its part stimulates the secretion of testosterone.

ACTH and cortisol were not changed suggesting that they were not significantly involved in the realization of Tribestan effects. The tendency of stimulation of STH and aldosterone explained the activation of the anabolic processes in the body and general stimulating action of the product. The absence of effect on the level of cortisol showed however that the general tonic action was very strongly manifested.

It should be stressed that the level of the hormones studied did not go out beyond the physiological frames i.e. it did not disturb the physiological mechanisms of hormonal regulation.

References

Vankov S., S. Zarkova, Z. Gendzhev, M. Tomova - Effect of TB-68 on the spermatogenesis in albino rats. Proceeding of the Third National Conference of Pharmacology and Clinics of New Bulgarian Drugs, Sofia, November 14-16, 1973, v.2, 161-163.
Vankov S., S. Zarkova, M. Tomova - TB-68 effect on ovulation of albino rats. Proceedings of Third National Conference of Pharmacology and Clinics of New Bulgarian Drugs, Sofia, November 14-16, 1973, v.2, 165-167.
Gendzhev Z., S. Zarkova - Effect of the phyto-pharmaceutical TB-68 on the number of spermatozoa in epididymis of rat. Med. Archive, 1978, N I, 113-118.
Dimova P., M. Taskov - Comparative enzyme-histological studies of some phyto-products. MBI (at the printer's), 1981.
Zarkova S. - Morphological and histological changes in testes of rat under the effect of TB-68, Med. Archive, 1976, N 4, 49-53.
Protich M., D. Zvetanov, V. Nalbanski, R.Stanislavov, M.Kazarova - Clinical trial of Tribestan on infertile males, MBI (at the printer's).
Tomova M., V. Gyulemetova, S. Zarkova - Author's certificate N 77584 A 61 K 35/1978.
Berson S.A., R. S. Yalow - Immunoassay of protein hormones, The Hormones, Vol. V, Acad. Press., New York, 1963.
Midgley A.R. - Radioimmunoassay for Human, J. Clin. Endocr., 1967, 27, 295.
Orezyk, Gaylo P., Burton v. Caldwell, Harold H. Behrmaan - Methods of Hormone Radioimmunoassay - Ed. B. Jaffe, H. Berhmaan, A6. Press, NJ, London, 1974, 333-343.
Vescei P. - Glicocorticoids: Cortisol Corticosterone - Methods of Hormone Radioimmunoassay; Ed. B. Jaffe and H. Behrmaan, Ac. Press, NJ, London 393-412.
William R.H. - Textbook of Endocrinology 4th Edit. Saunder, Philadelphia, 1968.
Williams Gordon H., Richard H. Hunderwood - Methods of Hormon Radioimmunoassay; Ed. B. Jaffe and H. Behrmaan, Ac. Press, NJ, London, 1974, 371-390.
 
SupremeSE

SupremeSE

Banned
Awards
1
  • Established
Aphrodisiac properties of Tribulus Terrestris extract (Protodioscin) in normal and castrated rats.Gauthaman K, Adaikan PG, Prasad RN.

Department of Obstetrics and Gynaecology, National University Hospital, National University of Singapore, Singapore 119704, Singapore.

Tribulus terrestris (TT) has long been used in the traditional Chinese and Indian systems of medicine for the treatment of various ailments and is popularly claimed to improve sexual functions in man. Sexual behaviour and intracavernous pressure (ICP) were studied in both normal and castrated rats to further understand the role of TT containing protodioscin (PTN) as an aphrodisiac. Adult Sprague-Dawley rats were divided into five groups of 8 each that included distilled water treated (normal and castrated), testosterone treated (normal and castrated, 10 mg/kg body weight, subcutaneously, bi-weekly) and TT treated (castrated, 5 mg/kg body weight, orally once daily). Decreases in body weight, prostate weight and ICP were observed among the castrated groups of rats compared to the intact group. There was an overall reduction in the sexual behaviour parameters in the castrated groups of rats as reflected by decrease in mount and intromission frequencies (MF and IF) and increase in mount, intromission, ejaculation latencies (ML, IL, EL) as well as post-ejaculatory interval (PEI). Compared to the castrated control, treatment of castrated rats (with either testosterone or TT extract) showed increase in prostate weight and ICP that were statistically significant. There was also a mild to moderate improvement of the sexual behaviour parameters as evidenced by increase in MF and IF; decrease in ML, IL and PEI. These results were statistically significant. It is concluded that TT extract appears to possess aphrodisiac activity probably due to androgen increasing property of TT (observed in our earlier study on primates).

The hormonal effects of Tribulus terrestris and its role in the management of male erectile dysfunction - an evaluation using primates, rabbit and rat.

Gauthaman K, Ganesan AP.
Department of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, 5 Lower Kent Ridge Road, 119074 Singapore.

Hormonal effects of Tribulus terrestris (TT) were evaluated in primates, rabbit and rat to identify its usefulness in the management of erectile dysfunction (ED). TT extract was administered intravenously, as a bolus dose of 7.5, 15 and 30mg/kg, in primates for acute study. Rabbits and normal rats were treated with 2.5, 5 and 10mg/kg of TT extract orally for 8 weeks, for chronic study. In addition, castrated rats were treated either with testosterone cypionate (10mg/kg, subcutaneously; biweekly for 8 weeks) or TT orally (5mg/kg daily for 8 weeks). Blood samples were analyzed for testosterone (T), dihydrotestosterone (DHT) and dehydroepiandrosterone sulphate (DHEAS) levels using radioimmunoassay. In primates, the increases in T (52%), DHT (31%) and DHEAS (29%) at 7.5mg/kg were statistically significant. In rabbits, both T and DHT were increased compared to control, however, only the increases in DHT (by 30% and 32% at 5 and 10mg/kg) were statistically significant. In castrated rats, increases in T levels by 51% and 25% were observed with T and TT extract respectively that were statistically significant. TT increases some of the sex hormones, possibly due to the presence of protodioscin in the extract. TT may be useful in mild to moderate cases of ED.




--------------------------------------------------------------------------------


Treatment of cyclical mastalgia with a solution containing a Vitex agnus castus extract: results of a placebo- controlled double-blind study.
M Halaska , P Beles , C Gorkow , C Sieder

In a placebo-controlled, randomized, double-blind study the efficacy of a Vitex agnus castus extract-containing solution* (VACS) was investigated in patients suffering from cyclical mastalgia. Patients had mastalgia on at least 5 days in the pre-treatment cycle. During this cycle and during treatment (3 cycles; 2 x 30 drops/day), the intensity of mastalgia was recorded once per cycle using a visual analogue scale (VAS).After one/two treatment cycles, the mean decrease in pain intensity (mm, VAS) was 21.4 mm /33.7 mm in women taking VACS (n= 48) and 10.6 mm/20.3 mm with placebo (n=49). The differences of the VAS-values for VACS were significantly greater than those with placebo (p= 0.018;p= 0.006). After three cycles, the mean VAS-score reduction for women taking VACS was 34.3 mm, a reduction of 'borderline significance' (p= 0.064) on statistical testing compared with placebo (25.7 mm). There was no difference in the frequency of adverse events between both groups (VACS:n = 5; placebo: n= 4). VACS appears effective and was well tolerated and further evaluation of this agent in the treatment of cyclical mastalgia is warranted.


[Effectiveness of Vitex agnus-castus preparations]
C Gorkow , W Wuttke , R W März

The prolactin-inhibiting effect of ACF-preparations, which is due to dopaminergic activities, has been shown in humans too and gives a pharmacological rationale for the clinical effects observed in the different indications (2, 11, 25, 26, 35, 41). Confirmation of efficacy in the treatment of mastalgia has been best endorsed by two recently published double-blind studies conducted according to the principles of GCP (14, 41). One double-blind study, several open and postmarketing surveillance studies have shown that the premenstrual syndrome, or individual symptoms, can be influenced positively (3, 6, 7, 9, 19, 21, 37). Design shortcomings in a second double-blind study should be eliminated in future studies in this indication to improve the body of evidence (18). Hither to there has been one controlled double-blind study of cycle disorders in the case of corpus luteum insufficiency with significant results and a number of non-controlled open studies (1, 4, 15, 16, 20, 24, 26, 27, 32, 35, 36). The high success rates in the open studies indicate therapeutic effects, and it should be possible to reproduce these results under double-blind conditions. The success rates on fertility disorders should be confirmed in controlled double- blind studies (10, 33, 34).


The effects of a special Agnus castus extract (BP1095E1) on prolactin secretion in healthy male subjects.
P G Merz , C Gorkow , A Schrödter , S Rietbrock , C Sieder , D Loew , J S Dericks-Tan , H D Taubert

The effects of three doses of a special Agnus castus extract (BP1095E1)--extracts from 120 mg, 240 mg and 480 mg of drug per day--were examined within the framework of a placebo-controlled clinical study of tolerance and prolactin secretion in 20 healthy male subjects during a period of 14 days. There was good tolerance during the study as regards the following: adverse effects, the effects on blood pressure and heart rate, blood count, Quick's test, clinical chemistry as well as testosterone, FSH and LH values. During each study phase the 24-hour prolactin secretion profile was measured from the penultimate to the final day, and the amount of prolactin release was monitored an hour after TRH stimulation on the last day. A significant increase in the 24-hour profile was registered with the lowest dose in comparison to placebo, the opposite being the case with the higher doses, i.e. a slight reduction. In contrast to the administration of placebo, the 1-hour AUC after TRH stimulation resulted in a significant increase with the lowest dose and a significant reduction with the highest dose. The results suggest effects of the special Agnus castus extract which are dependent on the dose administered and the initial level of prolactin concentration.


English Title: Evidence for estrogen receptor β-selective activity of Vitex agnus-castus and isolated flavones.

Personal Authors: Jarry, H., Spengler, B., Porzel, A., Schmidt, J., Wuttke, W., Christoffel, V.
Author Affiliation: Abteilung für Klinische und Experimentelle Endokrinologie, Universitätsfrauenklinik Göttingen, Robert Koch-Strasse 40, 37075 Göttingen, Germany.
Editors: No editors
Document Title: Planta Medica, 2003 (Vol. 69) (No. 10) 945-947

Abstract:
Recent cell culture experiments indicated that extracts of V. agnus-castus (VAC) may contain yet unidentified phytoestrogens. Estrogenic actions are mediated via oestrogen receptors (ER). To investigate whether VAC compounds bind to the currently known isoforms ERα or ERβ, ligand-binding assays (LBA) were performed. Subtype specific ER-LBA revealed a binding of VAC to ERβ only. To isolate the ERβ-selective compounds, the extract was fractionated by bio-guidance. The flavonoid apigenin was isolated and identified as the most active ERβ-selective phytoestrogen in VAC. Other isolated compounds were vitexin and penduletin. These data demonstrate that the phytoestrogens in VAC are ERβ-selective.


Vitex agnus castus L., - traditional drug and actual indications

Karl Peter Odenthal *
Pharmacology, Experimental Research, Madaus AG, Ostmerheimerstraße 198, D-51101 Köln, Germany
*Correspondence to Karl Peter Odenthal, Pharmacology, Experimental Research, Madaus AG, Ostmerheimerstraße 198, D-51101 Köln, Germany

Abstract
There is a long tradition for the use of different preparations of drugs of Vitex agnus castus in complementary medicine in Europe. The indications in disorders of the female sexual cycle have been confirmed by experimental and clinical results. The activity of hitherto unidentified constituents of the ethanol seed extract could be localized within the pituitary-gonadal axis. Research in pituitary cell assays further elucidated a dopaminergic inhibition of prolactin synthesis and/or release. The effective administration of ethanol seed extracts against mastodynia and symptoms related to female cycle disorders with concomitant hyperprolactinaemia has been documented and awaits further establishment. © 1998 John Wiley & Sons, Ltd.

Vitex and Dopaminergic Activity

Prolactin secretion from the anterior pituitary is under the dual control of a yet unknown hypothalamic factor which stimulates prolactin release and the catecholamine dopamine which acts as a prolactin inhibiting factor. Several intrinsic (e.g. sleep) and exogenous (e.g. stress) stimuli enhance prolactin release. The prolactin-producing cells of the pituitary, the lactotropes, express the D2 subtype of the dopamine-receptor which is coupled to adenylate cyclase. Activation of the D2 receptor by either dopamine or compounds related in their molecular structure to dopamine reduces the synthesis of cAMP resulting in an inhibition of prolactin secretion. Prolactin has numerous targets in the body, among them the mammary glands and the corpus luteum. While a hyposecretion of prolactin appears to be without pathophysiological consequences, an excessive release of prolactin causes fertility disorders like corpus luteum insufficiency. Premenstrual symptoms (PMS) like breast tenderness might be associated with the s o-called "latent" hypersecretion of prolactin, i.e. in response to a stimulus, the lactotropes release supraphysiological amounts of prolactin. As a consequence the mammary gland tissue is stimulated subchronically which causes the symptom of mastalgia (breast pain). Recent research attention has focussed on the dopaminergic activity of Vitex agnus castus (chaste tree) in an attempt to explain its action in PMS and its general activity in regulating female hormonal function. One German research team reviewed at Munich their work to date in this area. [1] Both clinical and in vitro studies demonstrated a prolactin-inhibiting activity in Vitex, in particular on stimulated prolactin release. In vitro the dopamine-antagonist haloperidol counteracted this effect which confirms the assumption that Vitex contains constituents which inhibit prolactin release via interaction with the D2-subtype of the dopamine receptor. During the bioguided fractionation of Vitex using prolactin release in pituitary cell cultures and binding of test compounds to isolated D2 receptors, it became evident that Vitex contains at least two different types of dopaminergic compounds: hydrophilic, thermolabile dopamine agonists but also lipophilic, more thermostable endocrine active compounds. The latter type of substances could be identified as bicyclic diterpenes. These diterpenes inhibit cAMP-production and thereby prolactin release with a virtually equimolar potency to dopamine. The purification of the hydrophilic dopaminergic principle in Vitex is currently in progress. The same team then went on to describe their assessment of the dopaminergic activity of Vitex products on the German market. [2] Commercially available preparations of Vitex are prepared from the fruits using water/ethanol mixtures as the excipient. The percentage of ethanol in the marketed formulation ranges from 0 to 60%. Therefore, it is very likely that formulations which contain high, low or even no ethanol will also contain different amounts of the prolactin lowering activity. To test this assumption three different lots of nine liquid Vitex preparations commercially available in Germany were bought at a public pharmacy and were examined for their dopaminergic potency in the D2-receptor binding assay (DRBA). The highest ethanol content (v/v) in the formulations was 70%, the lowest 0%. The dopaminergic potency was determined as a [micro]M concentration of dopamine which causes the same displacement in the binding assay as the test product. There was about a 100-fold difference in the dopaminergic potenc y between formulations tested. Since the two most active preparations contained additives, these ingredients were also examined for displacement capacity in the DRBA. None of these additives exerted a significant activity in this assay system. Although it has not been conclusively proven that dopaminergic activity is essential for clinical success with Vitex preparations, these large discrepancies in activity are certainly cause for concern.

References
(1.) Jarry H, Spengler B, Wuttke W at al. Phytotherapy in gynecology; pharmacological rationale for the use of dopaminergic principles. Paper presented at the 3rd International Congress on Phytomedicine, Munich, October 11 to 13,2000 (SL-6a).
(2.) Jarry H, Metten M, Wuttke W. Comparison of the dopaminergic potency of various commercially available Agnus-castus preparations: the need for biological standardization. Paper presented at the 3rd International Congress on Phytomedicine, Munich, October 11 to 13,2000 (SL-6b).
 
T H E O R E M

T H E O R E M

Member
Awards
1
  • Established
cabergoline, if you already have a SERM. more often than not, descriptions of issues with superdrol (lactating etc.) seem more indicative of prolactin issues than estrogen issues.

however, another concern is contamination of the superdrol with oxymetholone, apparently an intermediate production step. oxymetholone has direct estrogenic activity, i.e. an AI will not help, but a SERM might.

the combo of SERM + cabergoline may be your best bet.

T.I.
I would only get this from a prescription source?:blink: or is it obtainable by the same means of my research chem?

also would that whole b6 or (p-5-p) dosing protocol be fairly ineffective in comparison to cabergoline? id like to have these items prior to cycle not before.

thanks
repped
 
I

Interlocutor

New member
Awards
0
1. as has been mentioned: HCG does NOT signal the pituitary to release LH. AG does not work as does HCG.

2. Longjack works, as any SHBG mod by freeing up bound test. no one doubts that. most SHBG mod results i've seen so far indicate a raise in free, and a possible slight dip in total test. However, during a cycle, and in the beginning of PCT, we have low to zero test, and, if i'm not mistaken, low SHBG as well. little to nothing is there, little to nothing is bound, and little to nothing can be freed up. what benefit should thus be derived from a SHBG mod on cycle and in early PCT? what's there to unbind? the only/main benefit i see is in late PCT, especially if SHBG levels may rise due to SERM activity.

3. no one doubts that trib may improve libido. but about the LH let's talk on monday, i'm running out of time today.

4. i do not see other functions/properties of SERMs, AIs or SERM/Ai combos addressed. what about lipids, selective antagonizing of estradiol-beta receptor, what about serum level estrogen?

5. that some items (like Vitex extract) may provide some benefit as you mentioned in clinical studies or other products does not inherently imply that it does so in the extract and dosage in your product. furthermore, you surely do not wish to compare the effect of Vitex with that of Cabergoline on a quantitative level?

do you have independent blood work or clinical studies for your specific product that show that it works as claimed beyond inference from certain studies, some of which (see SHBG mods) may not be applicable at all to the situation at hand?

your product is available since when? mid 2006? why have i not seen any positive logs/reviews from established members with good rep here or on bb.com for example?

T.I.
 
SupremeSE

SupremeSE

Banned
Awards
1
  • Established
1. as has been mentioned: HCG does NOT signal the pituitary to release LH. AG does not work as does HCG.

2. Longjack works, as any SHBG mod by freeing up bound test. no one doubts that. most SHBG mod results i've seen so far indicate a raise in free, and a possible slight dip in total test. However, during a cycle, and in the beginning of post cycle therapy, we have low to zero test, and, if i'm not mistaken, low SHBG as well. little to nothing is there, little to nothing is bound, and little to nothing can be freed up. what benefit should thus be derived from a SHBG mod on cycle and in early post cycle therapy? what's there to unbind? the only/main benefit i see is in late PCT, especially if SHBG levels may rise due to SERM activity.

3. no one doubts that trib may improve libido. but about the LH let's talk on monday, i'm running out of time today.

4. i do not see other functions/properties of SERMs, AIs or SERM/Ai combos addressed. what about lipids, selective antagonizing of estradiol-beta receptor, what about serum level estrogen?

5. that some items (like Vitex extract) may provide some benefit as you mentioned in clinical studies or other products does not inherently imply that it does so in the extract and dosage in your product. furthermore, you surely do not wish to compare the effect of Vitex with that of Cabergoline on a quantitative level?

do you have independent blood work or clinical studies for your specific product that show that it works as claimed beyond inference from certain studies, some of which (see SHBG mods) may not be applicable at all to the situation at hand?

your product is available since when? mid 2006? why have i not seen any positive logs/reviews from established members with good rep here or on bb.com for example?

T.I.
LJ100 is PATENTED and scientifically proven to increase TOTAL and FREE Testosterone, while lowering cortisol and increasing HGH and IGF-1! Tribulus(20% Protodioscin) further increases total testosterone, while Vitex increases LH output, decreases estrogen, and reduces prolactin.

AndroGenerator has been available for 1 year exactly, it was released last March. Since that time, it has only received OUTSTANDING reviews.

Actually, Supreme Sports Enhancements began advertising EXCLUSIVELY to the steroid community, where we only sponsored a few small anabolic discussion forums. OUR VERY OWN forum of 5,000 members, now consists mostly "seasoned" bodybuilders:Supreme Sports Fitness :: Index

Supreme Sports Enhancemens designs products with the steroid user in mind. AndroGenerator has become the PREMIERE natural testosterone booster for PCT in the anabolic community.
 
I

Interlocutor

New member
Awards
0
LJ100 is PATENTED and scientifically proven to increase TOTAL and FREE Testosterone, while lowering cortisol and increasing HGH and IGF-1! Tribulus(20% Protodioscin) further increases total testosterone, while Vitex increases LH output, decreases estrogen, and reduces prolactin.
this may or may not be the case for individual compounds in studies wholly unrelated to your product. have you shown this also for your actual product?

AndroGenerator has been available for 1 year exactly, it was released last March. Since that time, it has only received OUTSTANDING reviews.
where? i don't mean mags where you put ads, or boards that you sponsor.

Actually, Supreme Sports Enhancements began advertising EXCLUSIVELY to the steroid community, where we only sponsored a few small anabolic discussion forums. OUR VERY OWN forum of 5,000 members, now consists mostly "seasoned" bodybuilders:Supreme Sports Fitness :: Index
then it should be no problem

1. to provide bloodwork from independent sources that show those claimed effects

2. to procure a handful of those that also frequent some of the major boards here

3. to quantify your claims for your specific product as relative to the products you match it up against, mainly SERMs and AIs and e.g. Cabergoline.

Supreme Sports Enhancemens designs products with the steroid user in mind. AndroGenerator has become the PREMIERE natural testosterone booster for PCT in the anabolic community.
if you say so. my impression was that this would be the Dermacrine, maybe followed by the PCS, but that is pretty new so far.

T.I.
 
SupremeSE

SupremeSE

Banned
Awards
1
  • Established
this may or may not be the case for individual compounds in studies wholly unrelated to your product. have you shown this also for your actual product?



where? i don't mean mags where you put ads, or boards that you sponsor.



then it should be no problem

1. to provide bloodwork from independent sources that show those claimed effects

2. to procure a handful of those that also frequent some of the major boards here

3. to quantify your claims for your specific product as relative to the products you match it up against, mainly SERMs and AIs and e.g. Cabergoline.



if you say so. my impression was that this would be the Dermacrine, maybe followed by the PCS, but that is pretty new so far.

T.I.

Google them BOTH. :)

We will continue to give away free samples so that logs HERE at AnabolicMinds can be completed. I appreciate the skepticism my friend, and the scientific fervor.
 
G

Goat

Member
Awards
0
Lol @ "hilly jungle slopes of Malaysia".

To be stacked with green tomato and wild yam extract for Xxtreme gains. 2 x's because its twice as extreme!
 
Ziquor

Ziquor

Well-known member
Awards
1
  • Established
Valvular heart disease
In two studies published in the New England Journal of Medicine on January 4, 2007, cabergoline was implicated along with pergolide in causing valvular heart disease.[2][3] Both drugs are ergot-derived dopamine agonists, although their molecular skeletons are different. As a result of this, the FDA removed pergolide from the U.S. market on March 29, 2007.[4] Since cabergoline is not approved in the U.S. for Parkinson's Disease, but for hyperprolactinemia, the drug remains on the market. Treatment for hyperprolactinemia requires lower doses than that for Parkinson's Disease, diminishing the risk of valvular heart disease.

I thought of using cabergoline until I read up on the cardio related effects. 1/3rd of the people who take it experience heart related side effects. Otherwise it's a good Dopamine agonist but I'd prefer to stick to Powerfull, much safer IMO.
 
Ziquor

Ziquor

Well-known member
Awards
1
  • Established
T.I. I been reading your posts & seem to be quite knowledgable. What's your overall take on Superdrol related gyno? 80-90% of the cases I seen happened 2-3 months after PCT. This leads me to believe its related to a wicked estro rebound. Prolactin can be an issue with almost any PH/PS ON cycle but it wouldn't cause gyno months later.
 
T H E O R E M

T H E O R E M

Member
Awards
1
  • Established
i used to seem him on BB.com alot in the past...im guessing by his sig he may have resigned from cryBaBy.com
 
Ziquor

Ziquor

Well-known member
Awards
1
  • Established
After much research & reading I came to the following conclusion. It's been really bothering me as to why so many people contracted delayed gyno after Super more so than any other PH. Masteron/Methylmasteron (Super) has this in its chemical profile:

"As well as it's anabolic/androgenic steroid activities, Masteron actually exhibits strong anti-estrogenic activity as well in the body, competing with other substrates for binding to aromatase."
This gives Super/clones strong similarities to AI's themselves as well as its steroidal properties. So an anabolic hormone which also acts as a strong AI in the body? I found a lot of info about the use of AI's (Rebound, Inhibit E) during Super-post cycle therapy being the culprit of this delayed gyno & now it's starting to make more & more sense. I researched from a lot of guys in the UK because it seems as if the delayed gyno incidence is more there than it is anywhere. I found that a majority of the people I contacted who got gyno used ATD during their PCT. In fact a huge majority used no SERM - only ATD along with other support supps. This makes a lot of sense now - due to different laws in the UK it's extremely hard for them to get certain prescription meds such as serms, making otc-inexpensive ATD's like Rebound & Inhibit-E very attractive to users there. Therefore I found a very large portion of Superdrol users in the UK used ATD. With ATD being a suicidal (irreversable) AI, it basically shuts down estro all together as some feel it's actually too strong of an AI. I stumbled upon a few cases of long term use of ATD alone causing delayed gyno. It makes sense as if estrogen levels are suppressed too much & for too long it will create a wicked hormone rebound which could easily lead to delayed gyno. By taking Superdrol/Masteron, seeing that it does bind/compete for aromatise receptors like an AI, then afterwards supressing aromatise even further by taking an AI during PCT - it's no wonder people got gyno in these cases. I'd conclude that the use of any AI will greatly increase the chances of Super delayed gyno but especially suicidal AI's such as ATD & exemestane. Stick to a standard serm like Toremifene & Tamoxifen.
 
jonny21

jonny21

Registered User
Awards
1
  • Established
For superdrol, what would be a good precautionary supplement to have on hand to add in ON cycle if a flareup occurs? I have a SERM which some say you should just add that in if you choose to continue. Is there something less harsh or better option? ATD, AI?
By "flare-up" are you are referring to symptoms of gyno e.g itchy swollen nipples, development of small bb size lump? If so then Nolvadex @ 60mg/day and Letrozole @ 1.25mg/EOD until resolves; then taper the Nolva out by 50% every 5 days and continue Letro for management until cycle finished.
 
I

Interlocutor

New member
Awards
0
After much research & reading I came to the following conclusion. It's been really bothering me as to why so many people contracted delayed gyno after Super more so than any other PH. Masteron/Methylmasteron (Super) has this in its chemical profile:

This gives Super/clones strong similarities to AI's themselves as well as its steroidal properties. So an anabolic hormone which also acts as a strong AI in the body? I found a lot of info about the use of AI's (Rebound, Inhibit E) during Super-post cycle therapy being the culprit of this delayed gyno & now it's starting to make more & more sense. I researched from a lot of guys in the UK because it seems as if the delayed gyno incidence is more there than it is anywhere. I found that a majority of the people I contacted who got gyno used ATD during their post cycle therapy. In fact a huge majority used no SERM - only ATD along with other support supps. This makes a lot of sense now - due to different laws in the UK it's extremely hard for them to get certain prescription meds such as serms, making otc-inexpensive ATD's like Rebound & Inhibit-E very attractive to users there. Therefore I found a very large portion of Superdrol users in the UK used ATD. With ATD being a suicidal (irreversable) AI, it basically shuts down estro all together as some feel it's actually too strong of an AI. I stumbled upon a few cases of long term use of ATD alone causing delayed gyno. It makes sense as if estrogen levels are suppressed too much & for too long it will create a wicked hormone rebound which could easily lead to delayed gyno. By taking Superdrol/Masteron, seeing that it does bind/compete for aromatise receptors like an AI, then afterwards supressing aromatise even further by taking an AI during PCT - it's no wonder people got gyno in these cases. I'd conclude that the use of any AI will greatly increase the chances of Super delayed gyno but especially suicidal AI's such as ATD & exemestane. Stick to a standard serm like Toremifene & Tamoxifen.
this seems to an extremely complex issue with many appraches and viewpoints. basically, early 2006 (IIRC) there was already a lot of (inconclusive?) discussion about this.

there area few points to take into consideration:

1. Dana Houser from Leanbulk seems to imply that he believes that there does not even exist such a pathology as delayed gyno.

2. If it were related to the PCT alone, and not the compound as well, you should also get this with other compounds with similar properties. i do not seem to have noticed this, SD seems to be perceived as the main actor here.

3. it is very difficult to judge anything if the data base does not include information on tapering, ramping or steady-stade, on duration and dosing, on cycle used, on other compounds used (especially such which could raise/lower prolactin!), etc.

4. if ATD seems to be implied more often than other AIs, is it not possible that this is simply becaise it's used more?

5. the fact that ATD is suicidal/irreversible does not automatically imply that it is extremely strong. there are competitive/reversible/non-suicidal AIs which are MUCH more powerful than ATD, e.g. Letro. "strength" of an AI is determined by binding affinity of the compound, half-life, etc. (e.g. KI and IC50 values). check 6-bromo, 6-oxo, etc. in fact, if you look at certain studies, ATD does not lower serum estradiol by that much (as e.g. compared to adex), but is extremely active in the brain (i think ~80% reduction is the number most frequently quoted). so, if used at moderate dose, ATD does not (cannot?) "shut down"/"eliminate" estrogen totally, as is often believed. i'd guess ATD could overall be classified as moderate/strong AI, depending on dose. but not in a league at all with e.g. Letro.

what is specific to ATD and a few others (ATD metabolites) that - at least in animal studies - ATD also apparently inhibits Aromatase resynthesis. with other AIs this apparently tends to be increased.

6. the issue here is timing. if you look at the half-lifes of the compounds involved, we see that tamo (and metabolites), for comparison, has a half-life of about 9 days. this means in the average PCT there is quite some build up, with a long inbuilt taper over a few weeks until the stuff is finally gone. if you look at ATD, the half-life seems rather short (i've seen numbers ranging from 3.7 minutes to roughly 9 hours) - it should have pretty much cleared the system in a few days. it seems a little bit difficult to understand how a compound like this may have an effect 2 months later? that seems wayyyy off for a rebnound effect, especially if aromatase activity and possibly estrogen receptors are maybe upgraded straight after the cycle, and may dampen down during the tapering of the AI. i have seen, tough, some concern expressed that one of the ATD metabolites may have similar characteristics to ATD, but a very long half-life (several days/weeks?). if anything, THAT would be the culprit you'd be looking after. however, the data here seems pretty thin. if there's an estrogen rebound, why does it take THAT long???

7. my conclusion would be: if there is any specific concern about the use of ATD, simply use another OTC AI (if you can't/won't get stuff like adex):

6-bromo single isomer (e.g. Rebound Reloaded)
6-bromo isomer mix (e.g. AX aPCT)
6-OXO and clones
Formestan
etc. - but almost every compound has it's own issues.

there are a few things i would NOT rely on, mainly mATD and ADED - i have not seen any specific values/parameters for their actual AI capabilities, and simply describing sometiung as an AI does not make it such. which does not say that mATD or ADED may not be great AIs, it simply means i haven't seen anything confirming their AI properties. i also wouldn't use Havoc/clones in PCT, the AI properties as related to dose are to unclear IMHO as compared to suppressivness.

8. my current understanding would be more likely that people got issues not because they used ATD (or any other AI), but because they did NOT use a SERM.

9. for discussion let's just postulate that, whatever you do, for some reason (prolactin or estrogen rebound rebound, whatever) you get problems several weeks after an SD (but not/rarely other compounds) cycle. had you used a long half-life SERM (torm/nolva/clomid, but not Ralo) you may still have had some limited protection. now, the AIs typically used are long gone by then. ATD is simply identified most often as the culprit because it's used more often. the implication of this train of thought would be to extend mid/low dosed AI after SD cycle (IMHO always with prolactin blocker) for much longer than currently the norm, e.g. 8 weeks or more, i.e. a much longer taper down period.

10. don't use SD (that's my solution)

11. always consider that not only your SD may contain contamination which may alter/influence it's properties, but also that the ATD may not be of the quality you may think it is.

12. can anyone say for sure, based on available blood work, what the exact effect concerning prolactin SD has?

T.I.

P.S.: @Ross - a google search re "androgenerator bloodwork" comes up pretty empty, now does it not?
 
Ziquor

Ziquor

Well-known member
Awards
1
  • Established
Thanks for your input - excellent info as always TI. It is seemingly impossible to fully know what this is related to unless many clinical tests were to be done in a controlled environment but unless the FDA approves Super as a med it won't be happening. Abstinence is definitely the safest bet, I just never have been able to convince myself of abstinence... :think:
 
I

Interlocutor

New member
Awards
0
Thanks for your input - excellent info as always TI. It is seemingly impossible to fully know what this is related to unless many clinical tests were to be done in a controlled environment but unless the FDA approves Super as a med it won't be happening. Abstinence is definitely the safest bet, I just never have been able to convince myself of abstinence... :think:
well.. there is abstinence and abstinence. if abstinence simply means drinking singe malt instead of moonshine, i've got not problem with that. it is simply very difficult for me to understand the fascination there seems to be with SD. sure, it probably provides the best gains of all legal orals, but at a dose which seems to be laden with sides for many of the users.

i've just seen to many horror stories (and received desperate PMs) from guys that got problems (mainly lactating, gyno, ED) after some failed SD cycle that i've simply decided to never touch this stuff. i'd personally probably rather use low-dosed M1T than SD (no joke)!

if we have no or little scientific backing behind those compounds and their exact mechanics, my choice is then to go with those that have better anecdotal feedback.

sure, i may have gotten 2-4lbs more out of a SD cycle than a Havoc or similar cycle, but why worry about all those possible issues? do i intend to step on a pro stage? no. i simply want to maximize the effectivity of the time i spend in the gym. i guess it is the same for most. the additional gains as compared to safer compounds associated with SD simply do not seem worth the possible risks and negative feedback.

also, let me add one more speculative cause to your delayed gyno fears (lol): imagine that SD would act directly on the prolactin receptor. i don't say that it is, i honestly don't know. but all those "i'm lactating" feedback may seem to indicate such. now, you may THINK you have high prolactin. in reality, you have very low prolactin at the end of the cycle, it being suppressed by negative feedback loop and replaced through the SD. now, after your cycle, you may experience prolactin rebound, which may be a slower process than estrogen rebound = delayed gyno. throw in some SHBG perturbations, and voila...

T.I. How does this sound for a safe superdrol cycle post cycle therapy?
to be honest, i do not really believe there is such a thing.

Run your prolactin inhibitor throughout PCT then taper the dose back down for 1 month AFTER PCT.
i always use cabergoline (0.5mg every 3-4 days) in PCT and for about 4 weeks after. cheap (if you use cabaser or sogilen, that is) and effective. however, due to the related possible sides (see heart issue link above), it should not be taken at high dose and/or long term (i.e. it is good for prolactin control, but possibly risky as dopamin therapy, which uses much higher doses). P5P may be an effective and safe alternative, though personally i prefer pharmaceuticals... i've not seen comparisons on effectivity of P5P vs. cabergoline, for example.

there is IMHO no need in tapering it down, it has a pretty long half life, and at 0.5mg twice/week, one is at the lowest range of dosing anyway. if you'd use it like 2mg/day (as for dopamin therapy) for a few yeras, you'd probably have to taper it down to avoid prolactin rebound effects (recommended on the notes coming with pharma grade cabergoline).

Run your AI inversely to your SERM and ramp the dose of the AI up each week as you taper the SERM dose down.
i know that this is one of the current recommendations, but i do not really follow this. IMHO this dosing does not take the respective half-life of the compounds into account. see also: http://anabolicminds.com/forum/post-cycle-therapy/73609-complete-ai-list.html#post1212970 and leaves you with the highest amount of AI (= estrogen suppression) when the SERM is strongest, and extending suppression of estrogen into a phase where the SERM already may lose effect. if you use a SERM in PCT, PCT IMHO should be designed around its capabilities and properties (especially half-life), with the following priorities:

1. prevention of long-term sides (gyno, ED, etc.)
2. maintenance of gains

think carefuly of which compound does what in PCT, exactly. where you start, endocrine-wise (test, estradiol, prolactin, cortisol, etc.), and where you want to end (stable pre-cycle equilibrium), and how best to get there.

this is one of the main problems with using a compound such as SD: it seems pretty risky to use at all, and then you get at least 5 different opinions on the best way to handle PCT, which will always leave you with the feeling to maybe not having done the best you could.

other compounds, such as Havoc (for example) seem to be much more forgiving concerning variations in PCT protocol in comparison.

i am thus extremely reluctant to give advice on SD PCT, as i've never used it, nor do i intend to.

my current state of mind on general PCT protocol would be like:

SERM (and if I can get it, anyone can): dosed moderately such as to provide an intrinsic ramp-up equivalent to the haf-life of the compound at double standard dose, then standard dose for 2 weeks (3 weeks for more suppressive stacks/compounds/dosings or to feel safer. Better IMHO to add one week - even at lower dose - than stop to early).

tamo (HL = 9 days) = 40 (9) / 20 (5) / 20 / 20
torm (HL = 5 days) = 120 (5) / 60 (2) / 60 / 60 / 30
ralo (HL = 27-32 hours) = 120 (1) / 60 (6) / 60 / 60 / 30
clomid (HL = 5-7 days) = 100 (6) / 50 (1) / 50 / 50 / 25

i'd maybe give ralo one more week than the others, as due to the shorter half life (~30 hours instead of 5-9 days) it does not have the slow in-built taper down as the others.

furthermore, as you see, i don't think tapering down to 10mg is necessary with tamo, due to the extremely long half-life of the compound. depending on bodyweight, severity of compound used, perceived shutdown, previous experience, and especially if it's combined with an AI, i'd probably go lower on the dosing: to high a dose of SERM may negatively impact IGF-1 (among other things, such as SHBG raise, possible libido issues, etc.), which in turn may make it more difficult to hang unto things (other sides notwithstanding).

with those compounds, more is definitely NOT better. the best dosing scheme is: as little as you can, as much as you must. but not more. certain studies seem to indicate that increasing the dose will not increasing benefits, but may increase (the often overblown IMHO) risk of sides/toxicity.

if you use a research liquid, and not pharma tabs, individual dosing is simpler, and if you're fairly below 200lbs and use an AI on top, you may well be advised to use the tamoxifen citrate (for example) in the amounts given above for tamo (which leads to slightly lower actual tamo dosing).

see also: http://anabolicminds.com/forum/supplement-articles/78343-torem-more-liver-2.html#post1218734

AI: here is where it gets tricky.

1. IMHO avoid any AI that you do not feel comfortable about. psychology is a huge element in cortisol control, motivation and recovery, and if you worry all the time about your PCT and if ATD may give you gyno, then this is not good at all. i've seen enough cases where people got so nervous about the compound they used that they broke of PCT at the slightest itch of a nipple (instead of simply adding some P5P - for those that don't like cabergoline or bromocriptine) - with a high risk of failed PCT.

use the compound you feel the most comfortable with (based on science and/or feedback), even if it may be a tad more expensive (e.g. 6-OXO vs. ATD). my experience with ATD so far was pretty positive (despite libido issues), so i still recommend it, but many do not feel safe with it.

2. avoid overdosing. if we look at our typical situation: 4 week cycle of non-aromatizing oral (methylated or not). we're already low on test, low on estrogen, and possibly high on cortisol. prolactin is in a more often than not unknown state. aromatase activity and estrogen receptor activity may be upgraded (really not sure here after 4 weeks).

it's IMHO thus not necessary to have a lot of AI to suppress estrogen: we want a slow build up of estrogen to allow body levels to normalize. we may want SOME AI, especially during the build-up of SERM serum levels, to maximize available test, to hep maintain gains in early PCT. IMHO a lot of dosing which is fine for 1. a standalone cycle, or 2. an AI-solo PCT, may be to high for a combined AI/SERM PCT (as is often the case with SERM dosing schedules derived for highly suppressive 12 week aromatizing cycles but applied to mild oral 4-weekers).

3. continue low-dosed/tapered down. IMHO taper down such that you are already running on moderate low levels of the AI while the SERM is still in effect (week 3-5). if a compound is used with a high concern of delayed gyno, extend low-dosed AI OR SERM (3-9 month courses of SERMs have been run for male gynecomastia treatment studies) until you feel safe.

examples would be:

ATD: 50/50/25/25/25/25/25EOD/25EOD
6-OXO: 400/400/300/300/200/200/100/100
etc. (which i know goes against the grain a little bit)

preferentially simply don't run compounds with high anecdotal gyno risk if you're concerned about it. a decent dosed Havoc/Propadrol or Havoc/PP stack may be a viable alternative to SD, with similar gains at possibly lower risk (just speculating, have not used that combo myself).

Continue to run the AI for 4 weeks AFTER PCT and taper the dose back down so that no estrogen rebound occurs. Would 4 weeks suffice, or would you go with 8 weeks after PCT? You mentioned 8 weeks, but I wasn't sure if that included the 4 weks during PCT or not. This is my plan for an upcoming phera-plex/superdrol bridge cycle. If you think 8 weeks AFTER PCT would be better, i'll have to get 1 more bottle of my AI. Thanks in advance!
personally, i would not extend the AI overlong, due to possible sides, especially if we see the cycle itself also as being a low-estrogen period. i'd guess (and that's just speculation) that 4 weeks low-dosed AI after PCT (8 weeks overall) would allow for estrogen recovery without rebound. especially for ATD, which may inhibit aromatase synthesis, IMHO tapering is extremely important.

in fact, if i were very afraid of getting delayed gyno, i'd probably rather - instead of an AI - run low dosed ralo (for example) for a few (4-6) more weeks, in conjunction with some prolactin control. i personally prefer ralo for such extended SERM protocols, despite it apparently being somewhat less effective than torm, because of the lower half-life of ralo and possibly toxic metabolites than other SERMs. this seems to make ralo (for me, at least) about as side-free and "easy" as possible with those compounds. IMHO the best protection against gyno is a compound which has been shown(!) in clinical studies to be effective against it. a SERM also is IMHO more beneficial on longer duration protocols on lipids etc. and to normalize endocrine levels than an AI.

the main risk with ralo apparently seems blood clots immediately after starting a ralo based protocol, due to the estrogenic effect in the liver. it thus may be advisable to combine ralo (and other serms) with blood-thinning supports, especially fish oil (which one should IMHO take anyway).

please also understand that what i write is merely my point of view, and the way i would personally run things for myself, given my current level of understanding. also, i've not looked to deeply into SD, as i don't intend to ever run it myself.

thusly, do not consider this the best possible advice. there are propably much better thought-out setups out there, from people knowing a lot more. check out what the sinner, dana houser or john crisler have to say on the subject (for example, there are several others). where i am in conflict with their opinions (which i surely am on some items) there is a very high likelihood that they are correct and that i am wrong. also, first and foremost, try to do your own research and find an understanding on what those compounds do, exactly (well, as exact as is known), and how they do it.

T.I.
 
Ziquor

Ziquor

Well-known member
Awards
1
  • Established
Geez you're like an encyclopedia on steroids (no pun intended) :rofl:. I understand & respect your opinions on Super/clones & agree but I also feel if it's run low & short (time) you may be able to still get solid results & decrease negatives greatly. And the excellent points you made about sides/toxicity leads me to Halo. I could never understand why Halo/clones are looked down upon on here by so many people. Sure it's not as potent as Super or Phera but I know so many people who have made excellent gains (5-10#) and the side effects are extremely low - no sides for many people. With your point of not truely knowing much about the compounds which some of us consume 'like vitamins' I think Halo compunds should get more respect so newbs will actually want to use them. It seems so many newbs wanna pack on muscle and disregard Halo because of all the polls and all the ppl who say it's nothing compared to Super etc. Of course I'm not even regarding the whole diet, age, etc. subjects because many newbs, no matter what you tell them, are going to run a cycle anyhow. But enough rambling back to cabergoline, I was really considering using this in December but after reading about the cardio issues it pushed me away. Most sides/issues don't bother me but the ones relating to cardio I don't take lightly considering most of us on here will go that way at some point. I did notice it has a half life of nearly 3 days (63-69 hrs) plus with the lower dose I may just get it after all. Plus all the cardio related effects were found in tests only when using it at 2-6 mg ED. So I assume you would keep a pretty steady blood level just by taking it once (0.5) every 3 days?
 
I

Interlocutor

New member
Awards
0
But enough rambling back to cabergoline, I was really considering using this in December but after reading about the cardio issues it pushed me away. Most sides/issues don't bother me but the ones relating to cardio I don't take lightly considering most of us on here will go that way at some point. I did notice it has a half life of nearly 3 days (63-69 hrs) plus with the lower dose I may just get it after all. Plus all the cardio related effects were found in tests only when using it at 2-6 mg ED. So I assume you would keep a pretty steady blood level just by taking it once (0.5) every 3 days?
it is commonly used at 0.5 mg twice/week as prolactin inhibitor (usually for treatment of prolactinoma, a type of prolactin-reactive tumor). there have been studies showing only slightly increased effect on prolactin at 0.75 and 1.0 mg twice/week, with slightly higher risk of sides (nausea, dizziness, fatigue, etc.) - i.e. it usually doesn't seem to make sense to increase the dose. doses up to 3.0mg per week were apparently used safely in those studies.

even if you'd wish to go over 0.5mg twice/week (and i don't see why anyone would want to do that), you'd start at that dose (0.5mg twice/week) and increase slowly over time.

the heart issues reported for cabergoline (and IIRC ALL ergot alkaloid class substances, including bromocriptine) are if used as parkinson therapy, which is at much higher doses (2-6mg/day = 14-42mg/week vs. 1mg/week for prolactin control), and for prolonged duration (vs. 4-8 weeks in post cycle therapy).

that's also the reason that cabergoline as active in parkinson meds (sogilen, cabaser) is much less expensive than the same active in prolactin meds (dostinex). few would be willing/able to pay the price for dostinex if you need 42mg/week.

T.I.
 

Similar threads


Top