A
Anthony Roberts
Guest
When I first started out in this world, I was a mod on Triedia with Nandi (Karl Hoffman). I bought into the Dbol for PCT bullshit, and he set me straight. Later I was a mod with him on SynergyMuscle, and he offered me a spot on a couple of his sites, and we corresponded regularly. Then he passed away tragically...and I dedicated my first book to him (and duchaine). He, dispite their claims, thought that the AnaFit boys were full of it, and he hated this theory that they always claimed was true. Anyway, because I can not do it better than he did, here is his explanation of why the AM Dbol theory is total bullshit:
Question: The D-Bol bridge theory claims that at the suggested dose of 10 mg each morning the HTPA will not be suppressed. Is there any truth to this?
Karl Hoffman: None whatsoever that I have ever seen. I would say to the people making this claim that the burden is on them to present some evidence that bridging does NOT suppress the HPTA. There is ample evidence that very low doses of Dianabol and Anavar, two drugs often cited as being good for bridging, significantly suppress the HPTA. Advocates of bridging counter this fact with the claim that while that may be true, the studies where the HPTA was suppressed do not specify at which time of the day the drugs were taken. The claim made by bridging advocates is that LH and testosterone levels are highest in the morning, and if one were to take say 10 mg of dbol so that plasma dbol levels peaked at the same time plasma test levels peaked, the body would somehow fail to notice the extra plasma androgen and hence there would be no suppression. There is just no evidence the body works this way.
There are other points to consider as well. The observation that testosterone peaks in the AM is true in the majority of young people, but not in all. And as we age, this AM peak is blunted and the pattern becomes one of a series of rather uniform peaks throughout the 24-hour period. (In fairness to bridging advocates some very recently published data are at odds with this previously widespread reported loss in the diurnal fluctuations in testosterone with aging [11].) There is tremendous individual variation in in the timing of these peaks and troughs. We also talked above about how androgens can act directly on the hypothalamus to block LH and testosterone production. Not enough is know about the temporal relationship between hypothalamic GnRH pulses, LH production, and test secretion to conclude that taking dbol when test peaks will have no effect on the GnRH signal(s) responsible for that peak. Moreover, some research has shown that 5 and 10 mg of dbol administered daily can reduce endogenous testosterone by 66 and 73% respectively, WITHOUT depressing LH, leaving open the possibility that the dbol is having a direct effect on testicular testosterone production without any hypothalamic or pituitary action. So we may not even fully understand all the mechanisms by which dbol (and other AAS) affects testosterone production (12). Lacking a complete knowledge of androgen actions, how can re reasonably conclude bridging does not suppress endogenous testosterone production?
If someone wants to stay "on" all the time and call it bridging, that is fine and is his or her choice. I just don't think they should try to justify the practice by claiming it is not suppressive of the HPTA or of endogenous testosterone production. I'm not making a value judgement here. There may not even be any serious health consequences to taking low doses of something like dbol between cycles, but on the other hand there in fact may be health implications. We saw above, for example, how very low doses of certain oral AAS can have dramatic effects on HDL. Steroids have traditionally been cycled to help avoid any long-term detrimental health effects associated with their use. Now we have certain individuals essentially advocating being "on" all the time, and using what are potentially the most dangerous steroids, 17 alpha alkylated orals, for this purpose. Am I overstating potential risks? Perhaps, but since there is little research to guide us, I'd rather err on the side of caution. If an individual wants to bridge, that is their business, but I don't think they should jump on the soapbox encouraging others to do so
Question: The D-Bol bridge theory claims that at the suggested dose of 10 mg each morning the HTPA will not be suppressed. Is there any truth to this?
Karl Hoffman: None whatsoever that I have ever seen. I would say to the people making this claim that the burden is on them to present some evidence that bridging does NOT suppress the HPTA. There is ample evidence that very low doses of Dianabol and Anavar, two drugs often cited as being good for bridging, significantly suppress the HPTA. Advocates of bridging counter this fact with the claim that while that may be true, the studies where the HPTA was suppressed do not specify at which time of the day the drugs were taken. The claim made by bridging advocates is that LH and testosterone levels are highest in the morning, and if one were to take say 10 mg of dbol so that plasma dbol levels peaked at the same time plasma test levels peaked, the body would somehow fail to notice the extra plasma androgen and hence there would be no suppression. There is just no evidence the body works this way.
There are other points to consider as well. The observation that testosterone peaks in the AM is true in the majority of young people, but not in all. And as we age, this AM peak is blunted and the pattern becomes one of a series of rather uniform peaks throughout the 24-hour period. (In fairness to bridging advocates some very recently published data are at odds with this previously widespread reported loss in the diurnal fluctuations in testosterone with aging [11].) There is tremendous individual variation in in the timing of these peaks and troughs. We also talked above about how androgens can act directly on the hypothalamus to block LH and testosterone production. Not enough is know about the temporal relationship between hypothalamic GnRH pulses, LH production, and test secretion to conclude that taking dbol when test peaks will have no effect on the GnRH signal(s) responsible for that peak. Moreover, some research has shown that 5 and 10 mg of dbol administered daily can reduce endogenous testosterone by 66 and 73% respectively, WITHOUT depressing LH, leaving open the possibility that the dbol is having a direct effect on testicular testosterone production without any hypothalamic or pituitary action. So we may not even fully understand all the mechanisms by which dbol (and other AAS) affects testosterone production (12). Lacking a complete knowledge of androgen actions, how can re reasonably conclude bridging does not suppress endogenous testosterone production?
If someone wants to stay "on" all the time and call it bridging, that is fine and is his or her choice. I just don't think they should try to justify the practice by claiming it is not suppressive of the HPTA or of endogenous testosterone production. I'm not making a value judgement here. There may not even be any serious health consequences to taking low doses of something like dbol between cycles, but on the other hand there in fact may be health implications. We saw above, for example, how very low doses of certain oral AAS can have dramatic effects on HDL. Steroids have traditionally been cycled to help avoid any long-term detrimental health effects associated with their use. Now we have certain individuals essentially advocating being "on" all the time, and using what are potentially the most dangerous steroids, 17 alpha alkylated orals, for this purpose. Am I overstating potential risks? Perhaps, but since there is little research to guide us, I'd rather err on the side of caution. If an individual wants to bridge, that is their business, but I don't think they should jump on the soapbox encouraging others to do so

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