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Андрей Васильевич
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Доброе утро господа спортсмены!!!
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Калимера
Андрей Васильевич
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Доброе утро Господа спортсмены!!!
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Как она, Котэ?издрасссьти
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Чё то меня оч сильно пугает тишина от Сашки...
Кот, чё он задумал, а???
Кот, чё он задумал, а???
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Ну и кому ты потом доказываешь, что не подыгрываешь мне? )))
Привет, друзья!
Поскольку мне пока лениво писать полноценную статью, выложу ее анонс с тезисами.
Разрушение мифов, ч.3.
1. ГСПГ (печень) не является регуляторным механизмом в отношении синтеза эндогенного Тестостерона, но влияющий на него. Т.е. ГСПГ (печень) не может регулировать Т.св. в нужных организму пределах, как снизу, так и сверху, это есть - функция гипоталамуса (ГнРГ).
After birth, testicular testosterone output is primarily regulated by the pulsatile pattern of pituitary LH secretion. This is driven by the episodic secretion of GnRH from hypothalamic neurons into the pituitary portal bloodstream providing a direct short circuit route to pituitary gonadotropes. Under this regular but intermittent GnRH stimulation, pituitary gonadotrophs secrete LH in high amplitude pulses at ~60-90 min intervals with minimal intervening LH secretion between pulses with the net effect that circulating LH levels are distinctly pulsatile. This pulsatile pattern of trophic hormone exposure maintains Leydig cell sensitivity to LH to maintain mature male patterns of testicular testosterone secretion (184).
_____________
Testosterone is a key element in the negative testicular feedback cycle through its inhibition of hypothalamic GnRH and, consequently, pituitary gonadotropin secretion. Such negative feedback involves both testosterone effects via androgen receptors as well as aromatization to estradiol within the hypothalamus (195-196). These culminate in reduction of GnRH pulse frequency in the hypothalamus together with reductions in amplitude of LH pulses due to both reduced GnRH quantal secretion as well as gonadotropin response to GnRH stimulation(184). By contrast, the small proportion of estradiol in the bloodstream that is directly secreted from the testes (~20%) means that cirulating estradiol is under minimal physiological regulation and unlikely to be a major influence on negative feedback regulation of physiological gonadotropin secretion in men.
_____________
Testosterone is a key element in the negative testicular feedback cycle through its inhibition of hypothalamic GnRH and, consequently, pituitary gonadotropin secretion. Such negative feedback involves both testosterone effects via androgen receptors as well as aromatization to estradiol within the hypothalamus (195-196). These culminate in reduction of GnRH pulse frequency in the hypothalamus together with reductions in amplitude of LH pulses due to both reduced GnRH quantal secretion as well as gonadotropin response to GnRH stimulation(184). By contrast, the small proportion of estradiol in the bloodstream that is directly secreted from the testes (~20%) means that cirulating estradiol is under minimal physiological regulation and unlikely to be a major influence on negative feedback regulation of physiological gonadotropin secretion in men.
2. Эндогенный Тестостерон не повышает ГСПГ, а понижает его, но очень незначительно.
The disease-related mechanisms that impede androgen action vary but the most frequent is increase in hepatic SHBG secretion due to the underlying disease and/or its drug treatments that impede androgen action by reducing testosterone transport from blood to tissues as part of its overall reduction in metabolic clearance rate of testosterone. For example, in hyperthyroidism, increased blood LH and testosterone concentrations with clinical features of androgen deficiency (263) are mediated by increased circulating SHBG due to thyroid hormone-induced hepatic SHBG secretion (264)
_____________
Circulating SHBG (and thereby total testosterone) concentrations are characteristically decreased (androgens, glucocorticoids) or increased (estrogens, thyroxine) by supraphysiologic hormone concentrations at the liver such as produced by oral administration (first pass effects) or by high-dose parenteral injections of androgens. In contrast, endogenous sex steroids and parenteral (non-oral) administration, which maintain predominantly physiologic circulating hormone concentrations (transdermal, depot implants), have minimal effects on blood SHBG levels (69-70) (71). Other modifiers of circulating SHBG levels include up-regulation by acute or chronic liver disease and androgen deficiency and down-regulation by obesity, protein-losing states (64) and, rarely, genetic SHBG deficiency(72-74). Under physiologic conditions, 60% to 70% of circulating testosterone is SHBG bound with the remainder bound to lower affinity, high-capacity binding sites (albumin, a1 acid glycoprotein, corticosteroid binding protein) and 1% to 2% remaining non-protein bound.
_____________
Circulating SHBG (and thereby total testosterone) concentrations are characteristically decreased (androgens, glucocorticoids) or increased (estrogens, thyroxine) by supraphysiologic hormone concentrations at the liver such as produced by oral administration (first pass effects) or by high-dose parenteral injections of androgens. In contrast, endogenous sex steroids and parenteral (non-oral) administration, which maintain predominantly physiologic circulating hormone concentrations (transdermal, depot implants), have minimal effects on blood SHBG levels (69-70) (71). Other modifiers of circulating SHBG levels include up-regulation by acute or chronic liver disease and androgen deficiency and down-regulation by obesity, protein-losing states (64) and, rarely, genetic SHBG deficiency(72-74). Under physiologic conditions, 60% to 70% of circulating testosterone is SHBG bound with the remainder bound to lower affinity, high-capacity binding sites (albumin, a1 acid glycoprotein, corticosteroid binding protein) and 1% to 2% remaining non-protein bound.
3. Для оценки андрогенного статуса на интактной оси ГГЯ не достаточно сдавать только Тестостерон общий, в дополнение к нему крайне желательно сдавать ГСПГ и/или Тестостерон свободный.
Measuring blood testosterone concentration is an important part of the clinical evaluation of androgen status and for confirming a clinical and pathological diagnosis of androgen deficiency. The circulating testosterone concentration is a surrogate measure for whole body testosterone production rate and the inferred impact of androgens on tissues. However, the reliance on a spot measurement of blood testosterone concentration neglects changes in the whole body metabolic clearance rate as well as other factors influencing net androgen effects at tissue levels. These include the efficiency of blood testosterone transfer into adjacent tissues during capillary transit as well as pre-receptor, receptor and post-receptor factors influencing the testosterone activation, inactivation and action in that tissue.
4. Чувствительность к ААС у людей может сильно различаться, вплоть до патологической нечувствительности.
Among healthy people, where the glutamine repeat polymorphism has alleles of lengths between 5 and 35 (population mean ~21), the length of the glutamine repeat is inversely proportional to AR transcriptional efficiency so that this polymorphism dictates genetic differences between individuals in the androgen sensitivity of their target tissues (204). This genetic variation in in vivo tissue androgen sensitivity is proven experimentally (205) but, although modest in magnitude, influences physiological responses to endogenous testosterone in prostate size (206) and erythropoeisis (207) in carefully controlled studies.
_____________
Laboratory investigations of post-pubertal individuals show elevated blood LH, SHBG (at adult female levels) and testosterone (at adult male levels) prior to gonadectomy. The androgen sensitivity index, the product of LH and testosterone concentrations, is elevated (228). These features reflect high amplitude and frequency LH pulses due to the absence of effective negative androgenic feedback on the hypothalamus as well as the increased LH drive to maintain high-normal male levels of testicular testosterone secretion.
_____________
Laboratory investigations of post-pubertal individuals show elevated blood LH, SHBG (at adult female levels) and testosterone (at adult male levels) prior to gonadectomy. The androgen sensitivity index, the product of LH and testosterone concentrations, is elevated (228). These features reflect high amplitude and frequency LH pulses due to the absence of effective negative androgenic feedback on the hypothalamus as well as the increased LH drive to maintain high-normal male levels of testicular testosterone secretion.
Ну и на закуску, самый скандальный тезис:
5. На курсах ААС для исключения Тестостеронового дефицита не обязательно использовать экзогенный Тестостерон, его функцию могут исполнить другие ААС, такие как Прима, Маст, Наны + Метан с грамотным администрированием.
Androgen therapy can be classified as physiologic replacement or pharmacologic therapy according to the dose, type of androgen and objectives of treatment. Androgen replacement therapy aims to restore tissue androgen exposure in androgen-deficient men due to pathological hypogonadism (disorders of the reproductive system) to levels comparable with those of eugonadal men. Using the natural androgen testosterone and a dose limited to one that maintains blood testosterone levels within the eugonadal range, androgen replacement therapy aims to restore the full spectrum of androgen effects while replicating the efficacy and safety experience of eugonadal men of similar age. Androgen replacement therapy is unlikely to prolong life because androgen deficiency, whether due to castration (274-278) or biological disorder (279) has minimal effect in shortening life expectancy (280). As an alternative, pharmacologic androgen therapy uses androgens without restriction on androgen type or dose but aims to produce androgen effects on muscle, bone, brain, or other tissues. In such pharmacological treatment, regardless of androgen status, an androgen is used therapeutically to exploit the anabolic or other effects of androgens on muscle, bone, and other tissues as hormonal drugs in various non-reproductive disorders. Such pharmacological androgen therapy is neither constrained to using the natural androgen, testosterone, nor it is limited to physiological replacement doses or their equivalent. Rather, it is judged on its efficacy, safety, and relative cost-effectiveness for that specific indication just as any other hormonal or xenobiotic non-hormonal therapeutic drug. Many older uses of pharmacologic androgen therapy are now considered second-line therapies as more specific treatments are developed (281). For example, erythropoietin has largely supplanted androgen therapy for anemia due to marrow or renal failure and improved first-line drug treatments for endometriosis, osteoporosis and advanced breast cancer have similarly relegated androgen therapy to a last resort while newer mechanism-based agents in development for hereditary angioedema may displace 17a-alkylated androgens (282-283). Nevertheless in many clinical situations, pharmacological androgen therapy remains a cost-effective option with a long-established efficacy and safety profile.
__________________
The principal goal of androgen (testosterone) replacement therapy is to restore a physiologic pattern of net tissue androgen exposure in androgen deficient men whose damaged reproductive systems are unable to secrete adequate testosterone to levels comparable with those of eugonadal men. This treatment uses only the natural androgen, testosterone, aimed at restoring a physiologic pattern of androgen exposure using a dose limited to that which maintains blood testosterone levels within the eugonadal range. Such treatment aims to restore the full spectrum of androgen effects when endogenous testosterone production fails due to pathological disorders of the reproductive system (testicular-hypthalamic-pituitary axis). This requires restricting replacement therapy to the major natural androgen, testosterone, which aims to not only replicate physiological circulating testosterone levels but also to provide testosterone’s two bioactive metabolites, DHT and estradiol, so that all 3 bioactive sex steroids are available to androgen target tissues. Synthetic androgens are unsuitable because they are incapable of metabolism to the more potent 5α reduced metabolites or aromatized to estrogens. The overall goal of such replacement therapy is to replicate the efficacy and safety experience of eugonadal men of similar age by recreating the full spectrum of endogenous natural androgen effects on tissues so as to recapitulate the natural history of efficacy and safety of endogenous testosterone.
_______________
Although these traditional indications for androgen therapy are often superseded by more specific, effective but costly treatments, androgens usually persist as second-line, empirical therapies for which the lower cost and/or equivalent or synergistic efficacy may still favor androgen therapy in some settings. For historical reasons, pharmacologic androgen therapy has often involved synthetic, orally active 17a-alkylated androgens despite their hepatotoxicity including cholestasis, hepatitis, adenoma and peliosis (311-312). Other than in treating angioedema, in which direct hepatic effects of 17a-alkyl androgens (rather than androgen action per se) may be crucial to increasing circulating C1 esterase inhibitor levels to prevent attacks (313-315), safer (nonhepatotoxic) testosterone preparations should generally be favored for long-term clinical use, although the risk-benefit balance may vary according to prognosis. For hereditary angioedema, newer mechanism-based, more specific and costly therapies such as purified or recombinant C1 inhibitor and bradykinin or kallekrein antagonists may overtake the traditional role of 17a-alkylated androgens such as danazol for long-term prophylaxis of hereditary angioedema (282-283, 316) or endometriosis. In most clinical applications, pharmacological androgen therapy remains a cost-effective option relative to newer, more costly therapies.
___________________
The goal of androgen replacement therapy is to replicate the physiologic actions of endogenous testosterone, usually for the remainder of life as the pathological basis of hypogonadism is usually irreversible disorders of the hypothalamus, pituitary or testis. This requires rectifying the deficit and maintaining androgenic/anabolic effects on bone (141, 538), muscle (320), blood-forming marrow (323, 539), sexual function (70, 540), and other androgen-responsive tissues. The ideal product for long-term androgen replacement therapy should be a safe, effective, convenient, and inexpensive form of testosterone with long-acting depot properties providing steady-state blood testosterone levels due to reproducible, zero-order release kinetics. Androgen replacement therapy usually employs testosterone rather than synthetic androgens for reasons of safety and ease of monitoring. The aim is to maintain physiologic testosterone levels and resulting tissue androgen effects. Synthetic steroidal and non-steroidal androgens are likely to lack the full spectrum of testosterone tissue effects due to local amplification by 5a reductase to DHT and/or diversification to act on ERa by aromatization to estradiol. The practical goal of androgen replacement therapy is therefore to maintain stable, physiologic testosterone levels for prolonged periods using convenient depot testosterone formulations that facilitate compliance and avoid either supranormal or excessive fluctuation of androgen levels. The adequacy of testosterone replacement therapy is important for optimal outcomes (541) as suboptimal testosterone regimens, whether due to inadequate dosage or poor compliance, produce suboptimal bone density (542-544) compared with maintenance of age-specific norms achieved with adequate testosterone regimens (541, 545). Differences in testosterone-induced bone density according to type of hypogonadism (546) may be attributable to delay in onset and/or suboptimal testosterone dose in early onset androgen deficiency (547-548) leading to reduced peak bone mass achieved in early manhood. Similarly, the severity of the androgen deficiency also predicts the magnitude of the restorative effect of testosterone replacement with greatest effects early in treatment of severe androgen deficiency (538, 541) whereas only minimal effects are evident for testosterone treatment of mild androgen deficiency (304-305)
________________
The identification of a single gene and protein for the androgen receptor in 1988 (553-555) explains the physiologic observation that, at equivalent doses, all androgens have essentially similar effects (556). The term “anabolic steroid” was invented during the post-WWII golden age of steroid pharmacology to define an idealized androgen lacking virilizing features but maintaining myotrophic properties so that it could be used safely in chidren and women. Although this quest proved illusory and was abandoned after all industry efforts failed to identify such a hypothetical synthetic androgen, the obsolete term “anabolic steroid” persists mainly as a lurid descriptor in popular media despite continuing to make a false distinction where there is no difference. Better understanding of the metabolic activation of androgens via 5a-reduction and aromatization in target tissues and the tissue-specific partial agonist/antagonist properties of some synthetic androgens may lead to more physiological concepts of tissue-specific androgen action (“specific androgen receptor modulator”) governed by the physiological processes of pre-receptor androgen activation as well as post-receptor interaction with co-regulator proteins analogous to the development of synthetic estrogen partial agonists with tissue specificity (“specific estrogen receptor modulator”) (557). The potential for new clinical therapeutic indications of novel tissue-selective androgens in clinical development remain to be fully evaluated (558).
_________________
Most oral androgens are hepatotoxic 17a-alkylated androgens (methyltestosterone, fluoxymesterone, oxymetholone, oxandrolone, ethylestrenol, stanozolol, danazol, methandrostenolone, norethandrolone) making them unacceptable for long-term androgen replacement therapy. The 1-methyl androgen mesterolone is an orally active DHT analog that undergoes neither amplification by 5a reduction nor aromatization but it is free of hepatotoxicity. Mesterolone is not used for long-term androgen replacement due to the need for multiple daily dosing, its poorly defined pharmacology (651) and suboptimal efficacy at standard dose (539, 546). For historical reasons, the other marketed 1-methyl androgen methenolone is used almost exclusively in anemia due to marrow failure (652-653) although it has no specific pharmacological advantage over testosterone or other androgens.
___________________
Preparations of testosterone or its esters are favored over synthetic androgens for all androgen replacement therapy applications by virtue of their long record of safety and efficacy, ease of dose titration and of monitoring of blood levels as well as the possibility that synthetic androgens lack the full spectrum of testosterone effects through pre-receptor tissue activational mechanisms (5a reduction, aromatization). The hepatotoxicity of synthetic 17a-alkylated androgens (311-312) makes them unsuitable for long-term androgen replacement therapy.
____________________
It is possible, but unproven, that the risks are dose-dependent although relatively few cases are reported among women using low dose methyl-testosterone (708-709) while clinical management of children using the alkylated androgen oxandolone often omits liver function tests. However, even if the risks are dose-dependent, the therapeutic margin is narrow.
____________________
Prolonged use of 17a-alkylated androgens, if unavoidable, requires regular clinical examination together with biochemical monitoring of hepatic function, the latter not required for non-alkylated androgens.
____________________
Because equally effective and safer alternatives exist, the hepatotoxic 17a-alkylated androgens should not be used for long-term androgen replacement therapy. By contrast, pharmacological androgen therapy often uses 17a alkylated androgens for historical reasons rather than the non-hepatotoxic alternatives.
__________________
The principal goal of androgen (testosterone) replacement therapy is to restore a physiologic pattern of net tissue androgen exposure in androgen deficient men whose damaged reproductive systems are unable to secrete adequate testosterone to levels comparable with those of eugonadal men. This treatment uses only the natural androgen, testosterone, aimed at restoring a physiologic pattern of androgen exposure using a dose limited to that which maintains blood testosterone levels within the eugonadal range. Such treatment aims to restore the full spectrum of androgen effects when endogenous testosterone production fails due to pathological disorders of the reproductive system (testicular-hypthalamic-pituitary axis). This requires restricting replacement therapy to the major natural androgen, testosterone, which aims to not only replicate physiological circulating testosterone levels but also to provide testosterone’s two bioactive metabolites, DHT and estradiol, so that all 3 bioactive sex steroids are available to androgen target tissues. Synthetic androgens are unsuitable because they are incapable of metabolism to the more potent 5α reduced metabolites or aromatized to estrogens. The overall goal of such replacement therapy is to replicate the efficacy and safety experience of eugonadal men of similar age by recreating the full spectrum of endogenous natural androgen effects on tissues so as to recapitulate the natural history of efficacy and safety of endogenous testosterone.
_______________
Although these traditional indications for androgen therapy are often superseded by more specific, effective but costly treatments, androgens usually persist as second-line, empirical therapies for which the lower cost and/or equivalent or synergistic efficacy may still favor androgen therapy in some settings. For historical reasons, pharmacologic androgen therapy has often involved synthetic, orally active 17a-alkylated androgens despite their hepatotoxicity including cholestasis, hepatitis, adenoma and peliosis (311-312). Other than in treating angioedema, in which direct hepatic effects of 17a-alkyl androgens (rather than androgen action per se) may be crucial to increasing circulating C1 esterase inhibitor levels to prevent attacks (313-315), safer (nonhepatotoxic) testosterone preparations should generally be favored for long-term clinical use, although the risk-benefit balance may vary according to prognosis. For hereditary angioedema, newer mechanism-based, more specific and costly therapies such as purified or recombinant C1 inhibitor and bradykinin or kallekrein antagonists may overtake the traditional role of 17a-alkylated androgens such as danazol for long-term prophylaxis of hereditary angioedema (282-283, 316) or endometriosis. In most clinical applications, pharmacological androgen therapy remains a cost-effective option relative to newer, more costly therapies.
___________________
The goal of androgen replacement therapy is to replicate the physiologic actions of endogenous testosterone, usually for the remainder of life as the pathological basis of hypogonadism is usually irreversible disorders of the hypothalamus, pituitary or testis. This requires rectifying the deficit and maintaining androgenic/anabolic effects on bone (141, 538), muscle (320), blood-forming marrow (323, 539), sexual function (70, 540), and other androgen-responsive tissues. The ideal product for long-term androgen replacement therapy should be a safe, effective, convenient, and inexpensive form of testosterone with long-acting depot properties providing steady-state blood testosterone levels due to reproducible, zero-order release kinetics. Androgen replacement therapy usually employs testosterone rather than synthetic androgens for reasons of safety and ease of monitoring. The aim is to maintain physiologic testosterone levels and resulting tissue androgen effects. Synthetic steroidal and non-steroidal androgens are likely to lack the full spectrum of testosterone tissue effects due to local amplification by 5a reductase to DHT and/or diversification to act on ERa by aromatization to estradiol. The practical goal of androgen replacement therapy is therefore to maintain stable, physiologic testosterone levels for prolonged periods using convenient depot testosterone formulations that facilitate compliance and avoid either supranormal or excessive fluctuation of androgen levels. The adequacy of testosterone replacement therapy is important for optimal outcomes (541) as suboptimal testosterone regimens, whether due to inadequate dosage or poor compliance, produce suboptimal bone density (542-544) compared with maintenance of age-specific norms achieved with adequate testosterone regimens (541, 545). Differences in testosterone-induced bone density according to type of hypogonadism (546) may be attributable to delay in onset and/or suboptimal testosterone dose in early onset androgen deficiency (547-548) leading to reduced peak bone mass achieved in early manhood. Similarly, the severity of the androgen deficiency also predicts the magnitude of the restorative effect of testosterone replacement with greatest effects early in treatment of severe androgen deficiency (538, 541) whereas only minimal effects are evident for testosterone treatment of mild androgen deficiency (304-305)
________________
The identification of a single gene and protein for the androgen receptor in 1988 (553-555) explains the physiologic observation that, at equivalent doses, all androgens have essentially similar effects (556). The term “anabolic steroid” was invented during the post-WWII golden age of steroid pharmacology to define an idealized androgen lacking virilizing features but maintaining myotrophic properties so that it could be used safely in chidren and women. Although this quest proved illusory and was abandoned after all industry efforts failed to identify such a hypothetical synthetic androgen, the obsolete term “anabolic steroid” persists mainly as a lurid descriptor in popular media despite continuing to make a false distinction where there is no difference. Better understanding of the metabolic activation of androgens via 5a-reduction and aromatization in target tissues and the tissue-specific partial agonist/antagonist properties of some synthetic androgens may lead to more physiological concepts of tissue-specific androgen action (“specific androgen receptor modulator”) governed by the physiological processes of pre-receptor androgen activation as well as post-receptor interaction with co-regulator proteins analogous to the development of synthetic estrogen partial agonists with tissue specificity (“specific estrogen receptor modulator”) (557). The potential for new clinical therapeutic indications of novel tissue-selective androgens in clinical development remain to be fully evaluated (558).
_________________
Most oral androgens are hepatotoxic 17a-alkylated androgens (methyltestosterone, fluoxymesterone, oxymetholone, oxandrolone, ethylestrenol, stanozolol, danazol, methandrostenolone, norethandrolone) making them unacceptable for long-term androgen replacement therapy. The 1-methyl androgen mesterolone is an orally active DHT analog that undergoes neither amplification by 5a reduction nor aromatization but it is free of hepatotoxicity. Mesterolone is not used for long-term androgen replacement due to the need for multiple daily dosing, its poorly defined pharmacology (651) and suboptimal efficacy at standard dose (539, 546). For historical reasons, the other marketed 1-methyl androgen methenolone is used almost exclusively in anemia due to marrow failure (652-653) although it has no specific pharmacological advantage over testosterone or other androgens.
___________________
Preparations of testosterone or its esters are favored over synthetic androgens for all androgen replacement therapy applications by virtue of their long record of safety and efficacy, ease of dose titration and of monitoring of blood levels as well as the possibility that synthetic androgens lack the full spectrum of testosterone effects through pre-receptor tissue activational mechanisms (5a reduction, aromatization). The hepatotoxicity of synthetic 17a-alkylated androgens (311-312) makes them unsuitable for long-term androgen replacement therapy.
____________________
It is possible, but unproven, that the risks are dose-dependent although relatively few cases are reported among women using low dose methyl-testosterone (708-709) while clinical management of children using the alkylated androgen oxandolone often omits liver function tests. However, even if the risks are dose-dependent, the therapeutic margin is narrow.
____________________
Prolonged use of 17a-alkylated androgens, if unavoidable, requires regular clinical examination together with biochemical monitoring of hepatic function, the latter not required for non-alkylated androgens.
____________________
Because equally effective and safer alternatives exist, the hepatotoxic 17a-alkylated androgens should not be used for long-term androgen replacement therapy. By contrast, pharmacological androgen therapy often uses 17a alkylated androgens for historical reasons rather than the non-hepatotoxic alternatives.
Цитаты в спойлерах из относительно свежей книжки с ПабМеда: Androgen Physiology, Pharmacology and Abuse - Endotext - NCBI Bookshelf
Последнее редактирование:
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Дед пихто!!, хто?
Жизнь, говорю, как твоя старая котейская??))
Вася
Хммм... Пока не читал, но чувствую что ОПЯТЬ тебе задницу надеру!!
Может сразу деньги дашь, а Саш??
Ну неужели ты не устал от ударов в челюсть?! (это метафора если что)
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Во, сюда ещё можно период действия пришпандорить. От той же энки у одного через 2 недели 2 рефа, а у другого уже через 5 дней почти нижний реф.. И вот первый говорит энка шикарная, а второй что полупустая
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"Пришпандорить" то конечно было бы неплохо, только к андрогенной чувствительности это не имеет отношения. Это скорее вопрос к Цитохрому P450, т.е. системе отделения гормона от масла (основы для инъекций) и эфира препарата.Во, сюда ещё можно период действия пришпандорить. От той же энки у одного через 2 недели 2 рефа, а у другого уже через 5 дней почти нижний реф.. И вот первый говорит энка шикарная, а второй что полупустая
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Mondular, ну я имею ввиду ещё один пунктик, близкий к этому.. но это как бы не совсем миф\заблуждение, а просто такой вот факт, которого многие не знают, а кто и отрицает мол "примерно одинаково на всех должно работать"
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Странно, но я не ощутил ни одного "удара в челюсть", только танцы перед собой и невозможность нормально дышать из-за горы шапок с Дочи. А еще это было похоже на Капоэйру со стороны оппонентов. )))
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Такие факты имеют место быть, подтверждаю, я даже как-то недавно описывал множество причин, которые могли повлиять на такие разные результаты.
