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Can you bridge with Anavar?
- Thread starter Nighthawkk
- Start date
Suppression is a relative term. I am sure there is some suppression in some men. But since there is evidence in research that boys on oxandrolone where still producing LH even after 6 months there is no question that you can take it and not lose your testicular size. That would also mean that the HPTA is still signaling for natural test.
slat1
New member
What do you get when you cross a scientific mind and a whole whack of steroid misinformation?
Stumped?
Well, you get Karl Hoffmann (aka "Nandi" on the Internet), a science writer based in Salt Lake City whose articles are published regularly in Mind & Muscle Magazine. He is also the co-owner of a web-based Anabolic Fitness Forum.
Karl grew up in San Francisco and did his undergraduate studies at San Francisco State University, and his graduate work at The University of California, Berkeley. He has an MS in Physics, but confesses his true loves are Biochemistry & Physiology.
The topic of anabolic drugs and how they react within the body is a hot one. Anyone who's every used them knows something about the subject. However, the trouble is, what people know and what the truth actually says is often skewed.
I was fortunate enough to collaborate with a great authority in this field, and had the opportunity to listen in on some idle ramblings that are sure to stir the pot.
Wannabebig: 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?
Nandi: 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.
(11) Clin Endocrinol (Oxf). 2003 Jun;58(6):710-7
Diurnal rhythms of serum total, free and bioavailable testosterone and of SHBG in middle-aged men compared with those in young men.
Diver MJ, Imtiaz KE, Ahmad AM, Vora JP, Fraser WD
Stumped?
Well, you get Karl Hoffmann (aka "Nandi" on the Internet), a science writer based in Salt Lake City whose articles are published regularly in Mind & Muscle Magazine. He is also the co-owner of a web-based Anabolic Fitness Forum.
Karl grew up in San Francisco and did his undergraduate studies at San Francisco State University, and his graduate work at The University of California, Berkeley. He has an MS in Physics, but confesses his true loves are Biochemistry & Physiology.
The topic of anabolic drugs and how they react within the body is a hot one. Anyone who's every used them knows something about the subject. However, the trouble is, what people know and what the truth actually says is often skewed.
I was fortunate enough to collaborate with a great authority in this field, and had the opportunity to listen in on some idle ramblings that are sure to stir the pot.
Wannabebig: 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?
Nandi: 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.
(11) Clin Endocrinol (Oxf). 2003 Jun;58(6):710-7
Diurnal rhythms of serum total, free and bioavailable testosterone and of SHBG in middle-aged men compared with those in young men.
Diver MJ, Imtiaz KE, Ahmad AM, Vora JP, Fraser WD
slat1
New member
Oxandrolone had androgenic effects, suppressing mean serum LH concentrations from 1.7 +/- 0.3 to 1.1 +/- 0.2 U/I and serum testosterone concentrations from 1.9 +/- 0.6 to 0.8 +/- 0.1 nmol/l. SHBG concentrations were also reduced from 130.9 +/- 14.6 to 30.7 +/- 7.3 nmol/l.
Oxandrolone has an androgenic action as shown by changes in serum LH, testosterone and SHBG concentrations and by the lack of effect on FSH
Clin Endocrinol (Oxf). 1993 Apr - The effects of oxandrolone on the growth hormone and gonadal axes in boys with constitutional delay of growth and puberty.
Oxandrolone has an androgenic action as shown by changes in serum LH, testosterone and SHBG concentrations and by the lack of effect on FSH
Clin Endocrinol (Oxf). 1993 Apr - The effects of oxandrolone on the growth hormone and gonadal axes in boys with constitutional delay of growth and puberty.
slat1
New member
Quick overview:
Active Life: 8-12 hours
Drug Class: Anabolic/Androgenic Steroid (Oral)
Average Dose: Men 20-50 mg/day......Women 5-15 mg/day
Acne: Only in higher doses
Water Retention: Rare
High Blood Pressure: Rare
Liver Toxic: Yes, c17-alfa-alkylated steroid. Due to low doses, toxicity is low to medium
Aromatization: None
DHT Conversion: Low
Decrease HPTA function: Dose depandant
Anavar was the old U.S. brand name for the oral steroid oxandrolone, first produced in 1964 by the drug manufacturer Searle. It was designed as an extremely mild anabolic, one that could even be safely used as a growth stimulant in children. One immediately thinks of the standard worry, "steroids will stunt growth". But it is actually the excess estrogen produced by most steroids that is the culprit, just as it is the reason why women stop growing sooner and have a shorter average stature than men. Oxandrolone will not aromatize, and therefore the anabolic effect of the compound can actually promote linear growth. Women usually tolerate this drug well at low doses, and at one time it was prescribed for the treatment of osteoporosis. As the opinions surrounding steroids began to change in the 1980's, prescriptions for oxandrolone began to drop. Lagging sales probably led Searle to discontinue manufacture in 1989, and it had vanished from U.S. pharmacies until recently. Oxandrolone tablets are again available inside the U.S. by BTG, bearing the new brand name Oxandrin. BTG purchased rights to the drug from Searle and it is now manufactured for the new purpose of treating HIV/AIDS related wasting syndrome.
Anavar is a mild anabolic with low androgenic activity. Its reduced androgenic activity is due to the fact that it is a derivative of dihydrotestosterone (DHT). Although one might think that this would make it a more androgenic steroid, it in fact creates a steroid that is less androgenic because it is already "5-alpha reduced". In other words, it lacks the capacity to interact with the 5-alpha reductase enzyme and convert to a more potent "dihydro° form. It is a simple matter of where a steroid is capable of being potentiated in the body, and with oxandrolone we do not have the same potential as testosterone, which is several times more active in androgen responsive tissues compared to muscle tissue due to its conversion to DHT. It essence oxandrolone has a balanced level of potency in both muscle and androgenic target tissues such as the scalp, skin and prostate. This is a similar situation as is noted with Primobolan and Winstrol, which are also derived from dihydrotestosterone yet not known to be very androgenic substances.
This steroid works well for the promotion of strength and duality muscle mass gains, although it's mild nature makes it less than ideal for bulking purposes. Among bodybuilders it is most commonly used during cutting phases of training when water retention is a concern. The standard dosage for men is in the range of 20-50mg per day, a level that should produce noticeable results. It can be further combined with anabolics like Primobolan and Winstrol to elicit a harder, more defined look without added water retention. Such combinations are very popular and can dramatically enhance the show physique. One can also add strong non-aromatizing androgens like Halotestin, Proviron or trenbolone. In this case the androgen really helps to harden up the muscles, while at the same time making conditions more favorable for fat reduction. Some athletes do choose to incorporate oxandrolone into bulking stacks, but usually with standard bulking drugs like testosterone or Dianabol. The usual goal in this instance is an additional gain of strength, as well as more quality look to the androgen bulk. Women who fear the masculinizing effects of many steroids would be quite comfortable using this drug, as this is very rarely seen with low doses. Here a daily dosage of 5mg should illicit considerable growth without the noticeable androgenic side effects of other drugs. Eager females may wish to addition mild anabolics like Winstrol, Primobolan or Durabolin. When combined with such anabolics, the user should notice faster, more pronounced muscle-building effects, but may also increase the likelihood of androgenic buildup.
Studies using low dosages of this compound note minimal interferences with natural testosterone production. Likewise when it is used alone in small amounts there is typically no need for ancillary drugs like Clomid/Nolvadex or HCG. This has a lot to do with the fact that it does not convert to estrogen, which we know has an extremely profound effect on endogenous hormone production. Without estrogen to trigger negative feedback, we seem to note a higher threshold before inhibition is noted. But at higher dosages of course, a suppression of natural testosterone levels will still occur with this drug as with any anabolic/androgenic steroid and therefore require post cycle therapy to restore the HPTA.
Anavar is also a 17alpha alkylated oral steroid, carrying an alteration that will put stress on the liver. It is important to point out however that dispite this alteration oxandrolone is generally very well tolerated. While liver enzyme tests will occasionally show elevated values, actual damage due to this steroid is not usually a problem. Bio-Technology General states that oxandrolone is not as extensively metabolized by the liver as other l7aa orals are; evidenced by the fact that nearly a third of the compound is still intact when excreted in the urine. This may have to do with the understood milder nature of this agent (compared to other l7aa orals) in terms of hepatotoxicity. One study comparing the effects of oxandrolone to other agents including as methyltestosterone, norethandrolone, fluoxymesterone and methAndriol clearly supports this notion. Here it was demonstrated that oxandrolone causes the lowest sulfobromophthalein (BSP; a marker of liver stress) retention among all the alkylated orals tested. 20mg of oxandrolone in fact produced 72% less BSP retention than an equal dosage of fluoxyrnesterone, which is a considerable difference being that they possess the same liver-toxic alteration. With such findings, combined with the fact that athletes rarely report trouble with this drug, most feel comfortable believing it to be much safer to use during longer cycles than most of other orals with this distinction. Although this may very well be true, the chance of liver damage still cannot be excluded, especially with hogher dosages.
At one time oxandrolone was also looked at as a possible drug for those suffering from disorders of high cholesterol or triglycerides. Early studies showed it to be capable of lowering total cholesterol and triglyceride values in certain types of hyperlipidemic patients, which initially this was thought to signify potential for this drug as a hypo-lipid (lipid lowering) agent. With further investigation we find however that while use of this drug can be linked to a lowering of total cholesterol values, it is such that a redistribution in the ratio of good (HDL) to bad (LDL) cholesterol occurs, usually moving values in an unfavorable direction. This would of course negate any positive effect that the drug might have on triglycerides or total cholesterol, and in fact make it a danger in terms of cardiac risk when taken for prolonged periods of time. Today we understand that as a group anabolic/androgenic steroids produce very unfavorable changes in lipid profiles, and are really not useful in disorders of lipid metabolism. As an oral c17 alpha alkylated steroid, oxandrolone is probably even more risky to use than an injectable esterified injectable such as a testosterone or nandrolone in this regard.
Active Life: 8-12 hours
Drug Class: Anabolic/Androgenic Steroid (Oral)
Average Dose: Men 20-50 mg/day......Women 5-15 mg/day
Acne: Only in higher doses
Water Retention: Rare
High Blood Pressure: Rare
Liver Toxic: Yes, c17-alfa-alkylated steroid. Due to low doses, toxicity is low to medium
Aromatization: None
DHT Conversion: Low
Decrease HPTA function: Dose depandant
Anavar was the old U.S. brand name for the oral steroid oxandrolone, first produced in 1964 by the drug manufacturer Searle. It was designed as an extremely mild anabolic, one that could even be safely used as a growth stimulant in children. One immediately thinks of the standard worry, "steroids will stunt growth". But it is actually the excess estrogen produced by most steroids that is the culprit, just as it is the reason why women stop growing sooner and have a shorter average stature than men. Oxandrolone will not aromatize, and therefore the anabolic effect of the compound can actually promote linear growth. Women usually tolerate this drug well at low doses, and at one time it was prescribed for the treatment of osteoporosis. As the opinions surrounding steroids began to change in the 1980's, prescriptions for oxandrolone began to drop. Lagging sales probably led Searle to discontinue manufacture in 1989, and it had vanished from U.S. pharmacies until recently. Oxandrolone tablets are again available inside the U.S. by BTG, bearing the new brand name Oxandrin. BTG purchased rights to the drug from Searle and it is now manufactured for the new purpose of treating HIV/AIDS related wasting syndrome.
Anavar is a mild anabolic with low androgenic activity. Its reduced androgenic activity is due to the fact that it is a derivative of dihydrotestosterone (DHT). Although one might think that this would make it a more androgenic steroid, it in fact creates a steroid that is less androgenic because it is already "5-alpha reduced". In other words, it lacks the capacity to interact with the 5-alpha reductase enzyme and convert to a more potent "dihydro° form. It is a simple matter of where a steroid is capable of being potentiated in the body, and with oxandrolone we do not have the same potential as testosterone, which is several times more active in androgen responsive tissues compared to muscle tissue due to its conversion to DHT. It essence oxandrolone has a balanced level of potency in both muscle and androgenic target tissues such as the scalp, skin and prostate. This is a similar situation as is noted with Primobolan and Winstrol, which are also derived from dihydrotestosterone yet not known to be very androgenic substances.
This steroid works well for the promotion of strength and duality muscle mass gains, although it's mild nature makes it less than ideal for bulking purposes. Among bodybuilders it is most commonly used during cutting phases of training when water retention is a concern. The standard dosage for men is in the range of 20-50mg per day, a level that should produce noticeable results. It can be further combined with anabolics like Primobolan and Winstrol to elicit a harder, more defined look without added water retention. Such combinations are very popular and can dramatically enhance the show physique. One can also add strong non-aromatizing androgens like Halotestin, Proviron or trenbolone. In this case the androgen really helps to harden up the muscles, while at the same time making conditions more favorable for fat reduction. Some athletes do choose to incorporate oxandrolone into bulking stacks, but usually with standard bulking drugs like testosterone or Dianabol. The usual goal in this instance is an additional gain of strength, as well as more quality look to the androgen bulk. Women who fear the masculinizing effects of many steroids would be quite comfortable using this drug, as this is very rarely seen with low doses. Here a daily dosage of 5mg should illicit considerable growth without the noticeable androgenic side effects of other drugs. Eager females may wish to addition mild anabolics like Winstrol, Primobolan or Durabolin. When combined with such anabolics, the user should notice faster, more pronounced muscle-building effects, but may also increase the likelihood of androgenic buildup.
Studies using low dosages of this compound note minimal interferences with natural testosterone production. Likewise when it is used alone in small amounts there is typically no need for ancillary drugs like Clomid/Nolvadex or HCG. This has a lot to do with the fact that it does not convert to estrogen, which we know has an extremely profound effect on endogenous hormone production. Without estrogen to trigger negative feedback, we seem to note a higher threshold before inhibition is noted. But at higher dosages of course, a suppression of natural testosterone levels will still occur with this drug as with any anabolic/androgenic steroid and therefore require post cycle therapy to restore the HPTA.
Anavar is also a 17alpha alkylated oral steroid, carrying an alteration that will put stress on the liver. It is important to point out however that dispite this alteration oxandrolone is generally very well tolerated. While liver enzyme tests will occasionally show elevated values, actual damage due to this steroid is not usually a problem. Bio-Technology General states that oxandrolone is not as extensively metabolized by the liver as other l7aa orals are; evidenced by the fact that nearly a third of the compound is still intact when excreted in the urine. This may have to do with the understood milder nature of this agent (compared to other l7aa orals) in terms of hepatotoxicity. One study comparing the effects of oxandrolone to other agents including as methyltestosterone, norethandrolone, fluoxymesterone and methAndriol clearly supports this notion. Here it was demonstrated that oxandrolone causes the lowest sulfobromophthalein (BSP; a marker of liver stress) retention among all the alkylated orals tested. 20mg of oxandrolone in fact produced 72% less BSP retention than an equal dosage of fluoxyrnesterone, which is a considerable difference being that they possess the same liver-toxic alteration. With such findings, combined with the fact that athletes rarely report trouble with this drug, most feel comfortable believing it to be much safer to use during longer cycles than most of other orals with this distinction. Although this may very well be true, the chance of liver damage still cannot be excluded, especially with hogher dosages.
At one time oxandrolone was also looked at as a possible drug for those suffering from disorders of high cholesterol or triglycerides. Early studies showed it to be capable of lowering total cholesterol and triglyceride values in certain types of hyperlipidemic patients, which initially this was thought to signify potential for this drug as a hypo-lipid (lipid lowering) agent. With further investigation we find however that while use of this drug can be linked to a lowering of total cholesterol values, it is such that a redistribution in the ratio of good (HDL) to bad (LDL) cholesterol occurs, usually moving values in an unfavorable direction. This would of course negate any positive effect that the drug might have on triglycerides or total cholesterol, and in fact make it a danger in terms of cardiac risk when taken for prolonged periods of time. Today we understand that as a group anabolic/androgenic steroids produce very unfavorable changes in lipid profiles, and are really not useful in disorders of lipid metabolism. As an oral c17 alpha alkylated steroid, oxandrolone is probably even more risky to use than an injectable esterified injectable such as a testosterone or nandrolone in this regard.
slat1
New member
If you spend enough time searching the internet for an answer you can find the one you want. The above should show that.
What you do comes down to your own value that is put on safety.
You are either "on" or you are "off". We are adults and make our own decisions. We also have to live with the consequences of them.
The decision is yours and yours only!
What you do comes down to your own value that is put on safety.
You are either "on" or you are "off". We are adults and make our own decisions. We also have to live with the consequences of them.
The decision is yours and yours only!
Unfortunately Nandi was wrong as often as he was right. He had his theories trounced on this board, by much more informed people, several times over the last 6 years. He's been corrected by Animal, Macro, and myself on a variety of topics. So excuse me if I don't take his word as Gospel. There is just as much research showing that LH was only surpressed by a third under the same conditions as studies that show it was suppressed by two thirds.
The point I made is actually not disputed by what you posted. If the LH is present, as it was in what you quoted, then the HPTA is up and running. There would be NO LH if it wasn't. So for the purposes of a bridge you're getting exactly what is intended. You're starting the HPTA back up again and allowing LH to be produced in the testes.
Those of us who have used this technique and had blood tests done know it to be effective.
The point I made is actually not disputed by what you posted. If the LH is present, as it was in what you quoted, then the HPTA is up and running. There would be NO LH if it wasn't. So for the purposes of a bridge you're getting exactly what is intended. You're starting the HPTA back up again and allowing LH to be produced in the testes.
Those of us who have used this technique and had blood tests done know it to be effective.
In regards to your second post, and some of the first, NONE of these studies are acceptable by the medical community as clinical proof. Any study done with less than 60 participants isn't considered proof. I think the one Nandi quotes had 10 boys and most the others have 3-14. So there is evidence both ways but there is nothing either way that proves the point clinically.
