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Raising Serum Androgens Using DHEA, Pregnenolone, And Vitamin K

Discussion in 'Scientific Studies' started by haidut, Nov 11, 2016.

  1. haidut

    haidut Member

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    Many people use supplements like DHEA, pregnenolone, and progesterone with the goal of raising their androgens and lowering estrogen. While this approach works for raising tissue levels of steroids, it takes anywhere in the range of 6-12 months for this increase to be reflected in blood levels, and in some people no change in serum levels is noted at all. And when it does work, it seems to mostly work in females whose baseline levels of androgens are lower. I have been researching for ways to increase blood levels of androgens in males more quickly (and reliably) and it seems that steroid precursors application to the scrotum (for males) may achieve that. I found a few studies using DHEA and pregnenolone applied directly to Leydig cells showing increases synthesis of androgens like testosterone as well as known male pheromones. The reason for this approach is that serum levels of androgens in males are primarily a symptom of gonadal activity, which is a sign of good health. Adrenal hyperactivity raises serum DHEA levels and can maintain androgenic tone in tissues but it is not a sign of good health. Gonadal activity correlates highly with thyroid activity, so optimizing gonadal output should have a systemic beneficial effect.
    Finally, scrotal application has been shown to dramatically increase bioavailability of the applied steroids. As the study with scrotal application of testosterone (T) below shows, bioavailability of scrotally applied T is 8-fold higher, so a much lower dose can be used to achieve the same results, which helps limit the risk of side effects. Furthermore, according to the same study, scrotal application of androgens like DHEA creates a positive feedback mechanism so that most of the applied steroids are converted into strong androgens like DHT and T.

    Marked decline in serum concentrations of adrenal C19 sex steroid precursors and conjugated androgen metabolites during aging. - PubMed - NCBI
    "...The present data show a dramatic decline in the circulating levels of DHEA, DHEA-sulfate (DHEA-S), androst-5-ene-3 beta,17 beta-diol (5-diol), 5-diol-sulfate, 5-diol-fatty acid esters, and androstenedione in both men and women between the ages of 20-80 yr. In the 50- to 60-yr-old group, serum DHEA decreased by 74% and 70% from its peak values in 20- to 30-yr-old men and women, respectively. The serum concentrations of the conjugated metabolites of dihydrotestosterone (DHT), namely androsterone (ADT)-G, androstane-3 alpha,17 beta-diol (3 alpha-diol-G), androstane-3 beta,17 beta-diol (3 beta-diol-G), and ADT-sulfate are the most reliable parameters of the total androgen pool in both men and women, whereas serum testosterone and DHT can be used as markers of testicular secretion in men and interstitial ovarian secretion in women. The serum concentration of these various conjugated androgen metabolites decreased by 40.8% to 72.8% between the 20- to 30-yr-old and 70- to 80-yr-old age groups in men and women, respectively, thus suggesting a parallel decrease in the total androgen pool with age. As estimated by measurement of the circulating levels of these conjugated metabolites of DHT, it is noteworthy that women produce approximately 66% of the total androgens found in men. In women, most of these androgens originate from the transformation of DHEA and DHEA-S into testosterone and DHT in peripheral intracrine tissues, whereas in men the testes and DHEA and DHEA-S provide approximately equal amounts of androgens at the age of 50-60 yr. An additional potentially highly significant observation is that the majority of the marked decline in circulating adrenal C19 steroids and their resulting androgen metabolites takes place between the age groups of 20- to 30-yr olds and 50- to 60-yr-olds, with smaller changes are observed after the age of 60 yr."

    Pharmacokinetics of testosterone cream applied to scrotal skin. - PubMed - NCBI
    "...The bioavailability of testosterone via the scrotal skin is striking higher than for abdominal skin. Using the same testosterone cream and steroid LC-MS assay measurements, in this study a Cmax (4.6 ng/mL, 16.0 nM) was achieved with the lowest dose (12.5 mg) applied to the scrotal skin whereas applying 100 mg testosterone cream to the abdominal skin produced a Cmax of 16.3 nmol/L (4.7 ng/mL). This suggests an about eightfold increase in testosterone bioavailability, using the scrotal compared with abdominal skin routes."

    "...Disproportionate increases in serum DHT are reported after administration of all transdermal testosterone products with the higher DHT/T ratio attributable to the strong expression of 5-alpha reductase in skin structures which foster the conversion of testosterone to DHT during transdermal passage. Furthermore androgens induce greater expression of the 5a reductase enzyme whereby administration of an androgen directly onto the skin creates a feed-forward (positive feedback) mechanism (Russell & Wilson, 1994; McNamara et al., 2013)."

    TLDR
    : Serum androgen levels are indicative primarily of gonadal function. Elevated serum androgens benefit all tissues and raising them is often desirable for optimal health. Using steroids (pregnenolone, DHEA) and vitamin K2 (MK-4) dissolved in DMSO, and applying directly to the scrotum is likely to increase serum androgen (T, DHT, Androstenedione) levels significantly more than using the same chemicals orally or topically (not applied to the scrotum). This is due to optimal delivery of these chemicals directly to the Leydig cells in the gonad, which are responsible for androgen synthesis. Optimal doses for DHEA appear to be in the range 2mg - 3mg daily, pregnenolone can probably be used in doses of up to 10mg daily, and vitamin K2 (MK-4) dose would be either about 1mg or 3mg-5mg, depending on caffeine usage. A single application daily is probably enough and the effects from that single dose can last for up to 5 days.


    1. DHEA: The study below was in vitro but used actual Leydig cells found in the male gonads. Knowing how much each testicle weighs (on average 25g - 30g each) and the optimal concentrations used in the study (100μM), I was able to calculate that applying 2mg - 3mg DHEA dissolved in DMSO (the study did use DHEA in DMSO) directly in the scrotum should replicate the setting in the study and hopefully its results. As you can see, DHEA managed to raise both levels of T and also to inhibit aromatase. In addition, DHEA increased activity of the steroidogenic enzymes 3β-HSD and 17β-HSD, which are necessary for the synthesis of testosterone from any precursor, including cholesterol, pregnenolone, and even progesterone.
    So, this is one reason I often suggest males try scrotal application of Pansterone :) You get a lot more bang for the buck as DHEA not only raises serum T levels when used this way but also upregulates the actual steroidogenic activity inside the gonads so they keep producing androgens from other raw materials like cholesterol. Low serum androgen levels are indicative of hypogonadism, and should be treated by stimulating the gonads. But using hCG is not the way to go as it can lead to development of cancer. In fact, peeing on a pregnancy test is a reliable diagnostic method for testicular cancer in males (and likely other cancers as well). So, I'd stick to DHEA - it's much safer and combined with pregnenolone removes the need for hCG.

    The activity of 3 beta-hydroxysteroid dehydrogenase and delta 4-5 isomerase in human follicular tissue. - PubMed - NCBI
    Dehydroepiandrosterone ameliorates H2O2-induced Leydig cells oxidation damage and apoptosis through inhibition of ROS production and activation of ... - PubMed - NCBI
    https://www.karger.com/Article/FullText/430150

    "...The concentration of testosterone in primary Leydig cells under basal or stimulated conditions was determined using an RIA kit. After culturing for 24 h in DMEM-F12 medium at 37°C, cells were incubated with a dimethyl sulfoxide solution of DHEA (1μM, 50μM or 100μM) for 24 h (n = 6)"

    "...In the present study, we first determined the effect of DHEA on the cell viability of primary Leydig cells by MTT method. As shown in Fig. 1A, cells viability increased when primary Leydig cells were treated with 1-100μM DHEA for 24h (P<0.01). Testosterone content was not detected in the control group, while a marked increase in testosterone was observed in the DHEA-treated groups (P < 0.01) in a dose-dependent manner (Fig. 1B)."

    "...As shown in Fig. 2, the expression of 3β-HSD mRNA was significantly higher in with 50 μM (P < 0.05) and 100μM (P < 0.01) treatment groups compared to the control group (Fig. 2A). The 100μM DHEA-treated cells also had significantly higher levels of 17β-HSD mRNA expression compared to control group (P < 0.05) (Fig. 2B). Thus, we used the 100μM DHEA treatment to culture primary Leydig cells to study its effect on the protein expression of steroidogenic metabolic enzyme."

    "...To find out whether increased testosterone affected the protein levels of steroidogenic enzymes, the Leydig cellular steroidogenic enzymes protein expression levels were assayed. As shown in Fig. 3, with the extension of culture time, the protein levels of 3β-HSD, 17β-HSD and aromatase were not changed relative to the control group. The 3β-HSD and 17β-HSD protein levels showed an enhancement trend with treatment with DHEA; the 3β-HSD protein level was significantly increased from 12-48 h (P < 0.05; Fig. 3A), and the 17β-HSD protein level significantly increased from 24-48 h (P < 0.05; Fig. 3B). However, the aromatase protein level was significantly decreased at 48h (P < 0.05; Fig. 3C) with DHEA-treated primary Leydig cells."

    "...Compared to the control group at the same time, 3β-HSD and 17β-HSD protein levels increased (P < 0.05; Fig. 3A and B) while the level of aromatase protein decreased (P < 0.05; Fig. 3C) when subjected to DHEA incubation for 24-48h in primary Leydig cells."

    "...Present results showed that cells viability was significant increase after 1-100μM DHEA treatment in primary Leydig cells, and this indicated that there no any cytotoxic effect of DHEA on Leydig cells. Also, a rapid increase in testosterone content was seen as the concentration increased from 1 to 100μM, and maximum testosterone content accumulation was observed in the 100 μM DHEA-treated group. These data are consistent with our previous study showing that DHEA can lead to high serum levels of testosterone in male rats [18] and higher concentrations of testosterone in TM-3 cells (a Leydig cell line) in a doseand time-dependent fashion [30]. Leblanc et al. [31] also reported that the administration of DHEA to cynomolgus monkeys significantly increased the serum concentrations of androstenedione and testosterone. DHEA can be converted into androstenedione by 3β-HSD in peripheral target tissues. It can then undergo further conversion to testosterone and estrone by 17β-HSD and aromatase, respectively [10]. The expression of 3β-HSD mRNA was significantly increased by treatment with 50 and 100μM DHEA. Cells treated with 100μM DHEA also had markedly higher 17β-HSD mRNA expression when compared to the control group."

    "...Our results suggest that exogenous DHEA could preferentially convert to testosterone rather than estradiol due to the un-regulation of 3β-HSD and 17β-HSD protein levels and the down-regulation of aromatase protein expression levels in primary Leydig cells. Several studies suggest that the MEK/ERK signaling pathway can play a critical role in steroidogenesis [23, 24]

    2. Pregnenolone: I have experienced first hand the powerful effects of pregnenolone when used topically and combined with DHEA. The studies on using pregnenolone for androgen synthesis are not many but they do exists. There are several relevant studies that I was able to find. One of them found that Leydig cells converted 20% - 30% of the provided pregnenolone to testosterone. In addition, the next most significant metabolites were androstenedione (2.3%) and DHT (~2%). This is not a small yield! Perhaps even more importantly, the increased androgen synthesis continued for at least 5 days and adding hCG did not enhance the steroid synthesis further. This suggests that hCG is not needed to stimulate steroid synthesis, which I have mentioned before on the forum. And given the correlation of hCG with a number of cancers, it is probably best to stick just to pregnenolone as it is all the Leydig cells need to produce T, A, and DHT.
    Another study found that about 20% of the supplied pregnenolone was converted to the potent pheromones androsta-5,16-diene-3-beta-ol and androsta-4,16-diene-3-one. There was only a small yield of progesterone and DHEA. The combination of these results suggests that when pregnenolone is used as a precursor and supplied directly to the Leydig cells, the results are predominantly androgenic steroids like testosterone. In addition, given that pregnenolone did not yield much DHEA (in agreement with the human studies using only pregnenolone) combining pregnenolone and DHEA will likely be synergistic for purposes of enticing Leydig cells to synthesize androgens and inhibit aromatase. Finally, as you can see from one of the studies cholesterol was also effective as a precursor, but the HDL portion was much less effective than the LDL one. So much for the "good" HDL, which as I mentioned in another post, is much more of an unhealthiness biomarker than your doctor would have you believe.

    Lack of Metabolism of Progesterone, Testosterone and Pregnenolone to 5α-Products in Monkey and Human estes Compared with Rodent Testes1 | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic
    "...The formation of testosterone was greater from pregnenolone than from progesterone. However, no 5a-reduced metabolites of A4 -3-ketosteroids were formed (less than 0.2% of each) from progesterone and pregnenolone in any of these human testes of different ages used (Tables 5 and 6)."

    Steroid metabolism by purified adult rat Leydig cells in primary culture. - PubMed - NCBI
    "...Testosterone production was, however, not maintained. Because this decline in testosterone production may have been due to the lack of a suitable substrate after several days in culture, cells were cultured initially in the presence of exogenous pregnenolone and low-density lipoproteins (LDL). Both substances were found to enhance basal and LH-stimulated testosterone production and to extend responsiveness of the cells until at least day 4, but by day 7 response was lost. Cells were then cultured in the presence of rat and human LDL and HDL and in both cases LDL was found to enhance consistently testosterone production, but HDL was much less effective. Scanning and transmission electron micrographs showed that changes in cell shape occurred during culture, but indicated that the cells were not depleted of lipid droplets by the end of culture or after LH stimulation."

    16-Ene-steroids in the human testis. - PubMed - NCBI
    "...Incubation of human testicular homogenates with [4-14C]pregnenolone gave substantial amounts of an unknown metabolite within 1 min, reaching plateau values of 17-23% of total radioactivity added within 5 min. Mass spectrometry of the metabolite showed it to be identical to the boar sex pheromone precursor androsta-5, 16-diene-3 beta-ol (ADL). In cell cultures the major source of ADL and its dehydrogenated metabolite androsta-4, 16-diene-3-one (ADN) was the Leydig cell. In rat and monkey testicular homogenates 16-ene-synthetase activity, a prerequisite for the synthesis of ADL and ADN, was completely lacking, limiting the presence of 16-androstenes to boars and men. In contrast to boars, however, in the human testis no 5 alpha-reductase activity was found and consequently no 5 alpha-reduced-16-androstenes, e.g. androstenol (AL, musk like) and androstenone (AN, urine like), known sex pheromones in pigs."

    Steroid metabolism by purified adult rat Leydig cells in primary culture. - PubMed - NCBI
    "...The major steroid metabolite of purified Leydig cells at 0, 3 or 5d of culture was testosterone. This steroid accounted for approximately 22, 32 and 23% of the H-pregnenolone converted (Figure 1). This corresponds to 7.10 + 0.45, 10.64 + 0.31 and 7.55 + 0.46 ng of (3H)pregnenolone converted to testosterone (Table 1) on days 0, 3 and 5 of culture, respectively. The relative percent conversion of (3H)pregnenolone to testosterone was significantly greater (p<0.05) at 3d than on days 0 or 5 of culture. Androstenedione and dihydrotestosterone were the next most significant metabolites isolated from 0 and 3d cultures. Significant accumulation of progesterone (4.9 t 0.8% conversion) was identified in 5d cultures - whereas at 0 and 3d, the isolated progesterone represented less than 1% of the (3H)pregnenolone converted."

    "...The ability of purified Leydig cells to convert (3H)pregnenolone to testosterone was maintained for at least 5d days in primary culture. The percent conversion to testosterone was slightly greater by 3d cultures but there was no marked reduction in conversion of (3H)pregnenolone to testosterone in 5d cultures relative to freshly isolated (Od) cells."


    Effect of cadmium and other metal cations on in vitro Leydig cell testosterone production. - PubMed - NCBI
    "...For testosterone production 1 ml of dissociated testicular cells was incubated in triplicate in 12 X 75-mm test tubes in the presence or absence of maximally stimulating amounts of hCG, 100 mIU; db-CAMP, 1 mM; HCHOL, 7 PM; or PREG (5-pregnene-3beta-ol, 20-one), 2 uM. In the study with Cd’+, maximally stimulating concentrations of progesterone (4-pregnene 3, 20-dione), 2 PM; 17a-hydroxyprogesterone (Cpregnene 17a, 20&diol-3-one), 2 PM; or androstenedione (Candrostene 3, 17.dione). 2 PM also were evaluated to further characterize the Cd2+ effects."

    "...In control cultures, T production was increased over unstimulated values 3.9-fold with hCG stimulation to 5.1-fold with PREG stimulation."



    3. Vitamin K2 (MK-4): There are several animal studies that show oral administration of vitamin Ke2 (MK-4) raises serum levels of testosterone. The mechanism of action was stimulation of Leydig cells to produce testosterone from cholesterol. Now, given that the mechanism of action of vitamin K2 was localized (at least according to that study) - i.e. stimulation of Leydig cells - using oral administration of vitamin K2 (MK-4) appears wasteful as it would require quite a high dose to reach high enough concentrations in the gonads. The HED of the oral administration was about 1mg/kg, which makes it very expensive as an androgen raising approach. However, the goal is to get the vitamin K2 into the gonads. So, achieving the effective concentration of vitamin K in the gonads is actually quite easy and achievable with a much lower dose when you use vitamin K2 (MK-4) dissolved in DMSO and applied directly to the gonads. In that case you can get away with less than 5mg per dose, which both cheaper and likely more effective as the vitamin gets delivered directly to the tissue without any downstream metabolism occurring before reaching the gonads.
    The takeaways fro the vitamin K2 (MK-4) study are several. First, vitamin K1 had no effect so it is necessary to use vitamin K2 (MK-4). Second, with concurrent cAMP stimulation the optimal concentration of vitamin K2 (MK-4) for stimulating testosterone synthesis was 30μM. In the absence of such stimulation, the optimal concentration was the same as for DHEA in the study above - i.e. 100μM. This means, if you are using vitamin K2 (and DHEA/pregnenolone) without any cAMP stimulation then using a dose of 3mg - 5mg is needed. The dose in milligrams for vitamin K2 (MK-4) is higher than DHEA since the molar mass of MK-4 is much higher than the one for DHEA. So, consequently more mass is needed to achieve the same molar concentration. However, if you are using caffeine on a regular basis, which potently raises cAMP, then the optimal dose of vitamin K2 (MK-4) would be about 1mg per serving, as in the presence of increased cAMP using 30μM of vitamin K2 (MK-4) worked better than 100μM.

    Menaquinone-4 enhances testosterone production in rats and testis-derived tumor cells. - PubMed - NCBI
    "...In addition, treatment of I-10 cells with MK-4 in the presence of db-cAMP was found to significantly enhance testosterone secretion into the culture medium, and the maximum enhancement of secretion was observed when 30 μM MK-4 was present in the medium. Leydig cells secrete testosterone in a diffusive manner [15]; therefore, MK-4 directly enhances testosterone synthesis in the cells rather than only affecting release of testosterone from the cells. Because MK-4 induces apoptosis in several types of tumor cells [16] and osteoclast cells [17] and inhibits growth of hepatocarcinoma cells [18,19], we evaluated the effect of MK-4 on I-10 cell growth and viability. Our results showed that MK-4 did not promote cell growth but rather inhibited I-10 cell growth in a dose-dependent manner (Figure (Figure2B).2B). Therefore, enhanced testosterone secretion stimulated by MK-4 treatment was not due to an increase of the number of cells present. In addition, MK-4 stimulated testosterone secretion into the culture medium in a dose- and time-dependent manner in the absence of db-cAMP (Figures (Figures3A3A and and3B),3B), although intracellular levels of testosterone were not changed (data not shown). Previous studies have shown that rat testis-derived R2C tumor cells synthesize and secrete testosterone in a cAMP-independent manner [20]; similarly, we observed that MK-4 stimulates testosterone production in R2C cells without addition of db-cAMP (Figure (Figure3C).3C). Together, these results indicate that MK-4 directly enhances testosterone production in Leydig-like tumor cells independently of intracellular cAMP levels."

    "...We also examined whether vitamin K analogues other than MK-4 stimulate testosterone production and found that vitamin K1 does not enhance testosterone production in I-10 cells (Figure (Figure5A).5A). Because vitamin K1 may not be incorporated into the cells, we determined the cellular concentration of vitamin K by fluorescence-HPLC after treating the cells with vitamin K1 for 3 h; vitamin K1 was incorporated into the cells at one-fifth the concentration of MK-4 present (Figure (Figure5B).5B). These results demonstrate that MK-4 is well-incorporated into I-10 cells and may stimulate testosterone production in steroidogenic tumor cells, whereas vitamin K1 is incorporated in I-10 cells less than MK-4 and likely has no stimulatory effect on testosterone production in these cells."

    "...CYP11A is the rate-limiting enzyme for testosterone synthesis in Leydig cells. We determined the expression levels of CYP11A and StAR proteins in I-10 cells treated with MK-4. CYP11A levels were significantly higher in cells at 1 h and 3 h post-MK-4 treatment compared to levels in control cells (Figure (Figure6A),6A), and tended to be higher at 9 h post-treatment; no difference of CYP11A levels was found at 24 h post-treatment (data not shown). The StAR expression levels in the cells were unchanged after MK-4 treatment (Figure (Figure6A).6A). Furthermore, CYP11A expression levels in the testis from rats fed a MK-4-supplemented diet for 5 weeks tended to be higher than those of the control rats (Figure (Figure6B).6B). These results indicate that MK-4 may enhance testosterone production via upregulation of CYP11A. It is well known that expression and activity of CYP11A is regulated by protein kinase A (PKA). Vitamin K stimulates the activities of PKA in various cultured cell types although the detailed mechanism of this activity has not been elucidated [22-24]. Thus, we examined whether MK-4 enhances testosterone production via activation of PKA. Phosphorylation levels of the catalytic subunit of PKA (p-PKA) in I-10 cells were significantly increased by MK-4 treatment at the 2 h and 3 h time points (Figures (Figures7A7A and and7B),7B), while total PKA levels were not changed (data not shown). In addition, phosphorylation levels of CREB (p-CREB), a typical substrate of PKA, were significantly increased by treatment with MK-4 after 3 h (Figure (Figure7B).7B). Both p-PKA and p-CREB levels were higher in I-10 cells at 9 h post-treatment (data not shown). Conversely, enhanced testosterone production induced by MK-4 was abolished by treatment with H89, a specific inhibitor of PKA (Figure (Figure8).8). Together, these results indicate that MK-4 increases testosterone production in I-10 cells by upregulating CYP11A expression through the activation of PKA."

    4. Thyroid (T3): While most endocrinologists will probably give you a blank stare if you told them that thyroid can trigger steroidogenesis, it is in fact probably the primary signal for the Leydig cells, and is much more important then hCG or LH/FSH. Here is a brief discussion of the effects of thyroid on steroidogenesis by the Leydig cells. As you can see in hyperthyroid animals given T3, testosterone synthesis was two times higher than in euthyroid animals.
    Topical T3 Testicular Application - Estrogen!

    Extrapolating from the in vivo study in that other thread, a dose of 0.5mcg - 1mcg per testicle is needed. This means 1mcg - 2mcg per dose, on its own, or combined with the Pansterone and vitamin K should be able to stimulate androgen synthesis even more, while also keeping estrogen at bay. Not many people know this, but T3 is an actual aromatase inhibitor.
     

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  2. tca300

    tca300 Member

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    I have done this off and on ( with Pansterone specifically ) for some time now. I find it very effective. Libido shoots through the roof within 1 hour of application. A later result after several hours is extra muscle hardness, and more vascularity. Thanks for the post!!
     
  3. raypeatclips

    raypeatclips Member

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    Time to wash those weighing scales?

    Thanks for this post, very interesting!
     
  4. Blossom

    Blossom Moderator

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    Do you have any idea if this could be helpful for females if used on the labia majora? I've read in other threads here that vaginal dhea is supposed to be helpful for dryness and prolapse but the dmso seems like it would be too irritating for direct vaginal application IMO. I think it is difficult to get dhea to dissolve in oil. Speculating only here but *If applying it in the general vicinity is good enough I think pansterone might be a possible option for females concerned with preserving or restoring vaginal health.* It could be a worthwhile experiment.
     
  5. OP
    haidut

    haidut Member

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    Absolutely, yes. If a person is able to tolerate the application on the labia majora then by all means. In fact, the female studies for vaginal dryness and atrophy due to menopause used intravaginal application of DHEA dissolved in ethanol and propylene glycol, which was probably even more irritating then applying DMSO to the labia majora. And it can probably be done once every few days, which should reduce the risk of irritation even more.
     
  6. Blossom

    Blossom Moderator

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  7. Constatine

    Constatine Member

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    Great post, will start immediately and report results in a few weeks.
     
  8. BobbyDukes

    BobbyDukes Member

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    Thanks for this post Haidut. I have a lot of pansterone, and might give this a go.
     
  9. schultz

    schultz Member

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    I had my wife try an application of 2 drops twice per day on the labia. She was breastfeeding at the time and had been doing so for about 4 or 5 months. She has no hair on her legs when she's pregnant and breastfeeding (for whatever reason) and taking the DHEA caused her leg hair to come back and also gave her her period (which she doesn't seem to get while breastfeeding... at least for a while.) Anyway, she got annoyed with me and stopped taking it and her period didn't come back and her leg hair went away again, so it seemed obvious to me that it was the DHEA. That is a pretty strong effect from 4 drops a day! I was hoping it would increase libido but we never got that far into the experiment (haha men... :cool)
     
  10. Blossom

    Blossom Moderator

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    Thanks for sharing a female experience @schultz.
     
  11. OP
    haidut

    haidut Member

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    Bump. I updated the post with a lot of additional info on pregnenolone and vitamin K2 (MK-4) as other stimulators of gonadal androgen synthesis.
     
  12. Evan

    Evan Member

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    If you only have the oily version of K2, would it still be effective if applying that one first, and then apply the pansterone which would then help absorb the K2 just recently applied?
     
  13. OP
    haidut

    haidut Member

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    Pansterone and oily solutions do not mix well. So, I would not mix Pansterone with that vitamin K but rather use them a few hours apart. Also, I don't know how much of that vitamin K will absorb in the testicles so it is difficult to estimate what dose would be needed.
     
  14. Regina

    Regina Member

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    Blossom,
    Do you think the re-appearance of a period is a sign of vitality or something going wrong?
    I thought I finally had my last one maybe 6 or 7 months ago. I've been Peating steadily during this time. A few days ago, I got my period. Just like ole times: light cramps, feeling thick and followed by regular flow for 3-4 days and feeling leaner. I recently turned 55.
    Good? Bad? Normal? Thx!
     
  15. Evan

    Evan Member

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    I was thinking applying the K2, letting it dry off a little, and then adding the pansterone after.
     
  16. Belsazar

    Belsazar Member

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    What a pity :(
    Anyway im in again with 1 drop of Pansterone. I guess i dont want to waste Thornes K2 topically. Any comments/experience with the immunosuppresive action of testosterone? My experience is that after 4-7 days on NoFap, i get flu like symptoms. I cant imagine that this is a "withdrawal symptom". But probably my Aromatase activity is too high, and 5ar too low.
     
  17. OP
    haidut

    haidut Member

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    I don't think T suppresses immunity, quite the opposite actually. T often lowers cortisol and since cortisol is proven to be immunosuppressive the "flu" symptoms may be ramped up immunity (or endotoxin).
     
  18. chispas

    chispas Member

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    Dec 4, 2014
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    I've had a bit more luck applying Pansterone to the inguinal canals (basically on left and right sides of abdomen) than directly on scrotum.
     
  19. Belsazar

    Belsazar Member

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    May 16, 2016
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    At least thats what i heard at university from anthropologists. (Handicap principle - Wikipedia).

    Anyway, never thought about it that way, but it makes much more sense. So basically the immunsystem is able again to fight latent infections, and maybe the bacterial "die off" releases endotoxin, what causes symptoms. I always was sure there is somehow a connection to the immunsystem, as in steroid forums they regularly discuss what they call testo-flu.
     
  20. Constatine

    Constatine Member

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    What dose do you use for this?
     
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