AI and brain fog, morning wood
- Thread starter trtthings
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bochinit
Active Member
Orals have the most noticiable effects on lipids among other steroids (excluding Trembolone). Masteron is not harsher as an oral. Similar to Primobolan, I could say. I never saw anyone getting out of range in the lipid painel by using them. I will incorporate it sooner on my protocol. Seems to be a good and relative safe drug.
It is mild on the liver. It’s effects on lipids are unrelated to liver toxicity.
madman
Super Moderator
The degree as to what impact an AAS will have on serum lipids (decreased HDL/increased LDL) comes down to the route of administration (oral vs injectable), type of steroid (aromatizable or nonaromatizable), dose, duration of use, and level of resistance to hepatic metabolism.
C-17 alpha alkylated orals such as oxandrolone (Anavar), stanozolol (Winstrol), methyltestosterone (Android), methandrostenolone (Dianabol), oxymetholone (Anadrol), and fluoxymesterone (Halotestin) will have the biggest impact on lipids (decreasing HDL/increasing LDL) and even the non-alkylated oral methenolone (Primobolan) can still have a negative impact on lipids when using higher doses due to lack of aromatization
Even the injectable esterified AAS is more prone to driving down HDL when used in high doses and even then it would be the non-aromatizing compounds such as trenbolone (Finajet), drostanolone (Masteron), stanozolol (Winstrol), methenolone (Primobolan) which would have a stronger impact due to lack of aromatization.
Healthy estradiol levels are lipid/cardioprotective.
Doubtful there will be any significant impact on driving down HDL/increasing LDL when using very low daily doses (2-5 mg) of oxandrolone and I would be much more concerned with where your e2 levels sit as driving it down too low is detrimental to overall health.
As you should very well know having healthy e2 levels are critical due to its beneficial effects on (cardiovascular health, brain health, libido, erectile function, bone health, tendon health, immune system, body composition).
As I stated above although methenolone is a non-alkylated oral and trenbolone is administered by injection (esterified) when used in high doses they can both have a negative impact on lipids/cardiovascular health due to being non-aromatizing compounds.
Primobolan (Methenolone)
Methenolone should have a stronger negative effect on the hepatic management of cholesterol than testosterone or nandrolone due to its non-aromatizable nature, but a much weaker impact than c-17 alpha-alkylated steroids. Due to the route of delivery, oral methenolone will have a slightly stronger negative effect on lipids compared to methenolone enanthate injections. Anabolic/androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation, and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction.
Trenabol (Trenbolone)
Due to its non-aromatizable nature and strong resistance to metabolism, trenbolone has a moderate to strong (negative) impact on lipid values and atherogenic risk.
C-17 alpha alkylated orals such as oxandrolone (Anavar), stanozolol (Winstrol), methyltestosterone (Android), methandrostenolone (Dianabol), oxymetholone (Anadrol), and fluoxymesterone (Halotestin) will have the biggest impact on lipids (decreasing HDL/increasing LDL) and even the non-alkylated oral methenolone (Primobolan) can still have a negative impact on lipids when using higher doses due to lack of aromatization
Even the injectable esterified AAS is more prone to driving down HDL when used in high doses and even then it would be the non-aromatizing compounds such as trenbolone (Finajet), drostanolone (Masteron), stanozolol (Winstrol), methenolone (Primobolan) which would have a stronger impact due to lack of aromatization.
Healthy estradiol levels are lipid/cardioprotective.
Doubtful there will be any significant impact on driving down HDL/increasing LDL when using very low daily doses (2-5 mg) of oxandrolone and I would be much more concerned with where your e2 levels sit as driving it down too low is detrimental to overall health.
As you should very well know having healthy e2 levels are critical due to its beneficial effects on (cardiovascular health, brain health, libido, erectile function, bone health, tendon health, immune system, body composition).
As I stated above although methenolone is a non-alkylated oral and trenbolone is administered by injection (esterified) when used in high doses they can both have a negative impact on lipids/cardiovascular health due to being non-aromatizing compounds.
Primobolan (Methenolone)
Methenolone should have a stronger negative effect on the hepatic management of cholesterol than testosterone or nandrolone due to its non-aromatizable nature, but a much weaker impact than c-17 alpha-alkylated steroids. Due to the route of delivery, oral methenolone will have a slightly stronger negative effect on lipids compared to methenolone enanthate injections. Anabolic/androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation, and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction.
Trenabol (Trenbolone)
Due to its non-aromatizable nature and strong resistance to metabolism, trenbolone has a moderate to strong (negative) impact on lipid values and atherogenic risk.
Interesting. So it doesn’t lower HDL due to liver toxicity, but due to another mechanism in the liver? Or Oxandrolone lowers HDL via mechanisms completely unrelated to the liver?
Actually madman pretty much answered this question I think. But just to clarify, does Oxandrolone effect HDL negatively because it’s an oral that the liver has to process and breakdown?
Interesting. Sad if this is true with E2 seeing as I seem to tolerate it horribly. I get highly emotional and it kills my libido / erections.
If I recall the normal range for E2 is somewhere from maybe 20 pg/ml to 40 pg/ml. But perhaps the T:E ratio matters most.
However while I don't have any other way to control the sides I have to stick to controlling the E2.
madman
Super Moderator
This is one study of many and as I stated in numerous threads previously that it is should not be used long-term.
Most sensible people whether adding oxandrolone or stanozolol for SHBG/e2 issues would be using lower doses short-term (6-8 weeks) or slightly longer.
If this approach is taken highly doubtful low dose oxandrolone 2-5mg/day (as I stated above) would have any significant impact on driving down HDL/increasing LDL let alone any liver/cardiovascular issues in healthy individuals.
Even though many tend to use doses in the 15-25 mg/day range for enhanced fat loss/muscle gain when adding to a trt protocol although the chances of driving down HDL/increasing LDL may be greater as long as one is sensible with the duration of use (6-8 weeks) and blood work is monitored (which is critical) than I see no major concern.
Mind you personally I would not want to be cycling on and off of a C17 alpha-alkylated oral long-term.
There are other ways to attack SHBG/e2 issues without having to resort to the use of a c17 alpha-alkylated oral.
History: Oxandrolone was first described in 1962.403 It was developed into a medicine several years later by pharmaceutical giant G.D. Searle & Co. (now Pfizer), which sold it in the United States and the Netherlands under the Anavar trade name. Searle also sold/licensed the drug under different trade names including Lonavar (Argentina, Australia), Lipidex (Brazil), Antitriol (Spain), Anatrophill (France), and Protivar. Oxandrolone was designed to be an extremely mild oral anabolic, one that could even be used safely by women and children. In this regard, Searle seems to have succeeded, as Anavar has shown a high degree of therapeutic success and tolerability in men, women, and children alike. During its early years, Anavar had been offered for a number of therapeutic applications, including the promotion of lean tissue growth during catabolic illness, the promotion of lean tissue growth following surgery, trauma, infection, or prolonged corticosteroid administration, or the support of bone density in patients with osteoporosis.
By the 1980s, the FDA had slightly refined the approved applications of oxandrolone to include the promotion of weight gain following surgery, chronic infection, trauma, or weight loss without definite pathophysiologic reason. In spite of its ongoing track record of safety, Searle decided to voluntarily discontinue the sale of Anavar on July 1, 1989. Lagging sales and growing public concern about the athletic use of anabolic steroids appeared to be at the root of this decision. With the Anavar brand off the market, oxandrolone had completely vanished from U.S. pharmacies. Soon after, oxandrolone products in international markets (often sold by or under license from Searle) began to disappear as well, as the leading global manufacturer of the drug continued its withdrawal from the anabolic steroid business. For several years during the early 1990s, it looked as if Anavar might be on its way out of commerce for good.
It would be approximately six years before oxandrolone tablets would be back on the U.S. market. The product returned to pharmacy shelves in December 1995, this time under the Oxandrin name by Bio-Technology General Corp. (BTG). BTG would continue selling it for the FDA approved uses involving lean mass preservation, but had also been granted orphan-drug status for the treatment of AIDS wasting, alcoholic hepatitis, Turner's syndrome in girls, and constitutional delay of growth and puberty in boys. Orphan drug status gave BTG a 7-year monopoly on the drug for these new uses, allowing them to protect a very high selling price. Many patients were outraged to learn that the drug would cost them (at wholesale price) between $3.75 and $30 per day, which was many times more costly than Anavar had been just several years back. The release of a 10 mg tablet from BTG several years later did little to reduce the relative cost of the drug.
Anavar (Oxandrolone)
Side Effects (Cardiovascular): Oxandrolone has a strong effect on the hepatic management of cholesterol due to its structural resistance to liver breakdown, non-aromatizable nature, and route of administration. In the previously cited study in HIV+ males, 20 mg of oxandrolone daily for 12 weeks caused a mean serum HDL reduction of 30%. HDL values were suppressed 33% in the 40 mg group, and 50% in the 80 mg group. This was accompanied by a statistically significant increase in LDL values (approximately 30-33%) in the 40 mg and 80 mg groups, further increasing atherogenic risk. Anabolic/androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation, and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction.
Side Effects (Hepatotoxicity): Oxandrolone is a c17-alpha alkylated compound. This alteration protects the drug from deactivation by the liver, allowing a very high percentage of the drug entry into the bloodstream following oral administration. C17 alpha-alkylated anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure may result in liver damage. In rare instances, life-threatening dysfunction may develop. It is advisable to visit a physician periodically during each cycle to monitor liver function and overall health. Intake of c17 alpha-alkylated steroids is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Oxandrolone appears to offer less hepatic stress than other c17 alpha-alkylated steroids. The manufacturer identifies oxandrolone as a steroid that is not extensively metabolized by the liver like other 17-alpha alkylated orals, which may be a factor in its reduced hepatotoxicity. This is evidenced by the fact that more than a third of the compound is still intact when excreted in the urine.405 Another study comparing the effects of oxandrolone to other alkylated agents including methyltestosterone, norethandrolone, fluoxymesterone, and methandriol demonstrated that oxandrolone causes the lowest sulfobromophthalein (BSP; a marker of liver stress) retention of the agents tested.406 20 mg of oxandrolone produced 72% less BSP retention than an equal dosage of fluoxymesterone, which is a considerable difference being that they are both 17-alpha alkylated.
A more recent study looked at escalating doses (20 mg, 40 mg, and 80 mg) of oxandrolone in 262 HIV+ men. The drug was administered for a period of 12 weeks. The group taking 20 mg of oxandrolone per day showed no statistically significant trends of hepatotoxicity in liver enzyme (AST/ALT; aminotransferase and alanine aminotransferase) values. Those men taking 40 mg noticed a mean increase of approximately 30-50% in liver enzyme values, while the group of men taking 80 mg noticed an approximate 50-100% increase. Approximately 10-11% of the patients in the 40 mg group noticed World Health Organization grade III and IV toxicity according to AST and ALT values. This figure jumped to 15% in the 80 mg group. While serious hepatotoxicity cannot be excluded with oxandrolone, these studies do suggest that it is measurably safer than other alkylated agents.
If using Oxandrolone in a TRT setting to control estrogen and/or lower SHBG, then one can infer the intent is less ephemeral than short-term use. As a long-term solution, oral anabolic do not make the cut if health and longevity are a priority.
Studies consistently demonstrate a statistically significant reduction in HDL in a dose-dependent manner. The single study I posted is evidence that even at low doses (~5-10 mg daily), Oxandrolone will cause sharp decreases in HDL. Whether the reduction is 40% or whether its lower will depend on genetics and lifestyle factors. However, the most important thing to note, which we are both in agreement on, is that Oxandrolone isn't a viable solution in TRT because it cannot be confidently used long-term, which is the primary reason someone in a TRT setting would use the drug (e.g. lowering SHBG or aiding in estrogen management).
If you lowered your E2 to 20 pg/mL by lowering your TRT dosage then you would not be at risk for suboptimal lipids. However, if you lower your E2 by 50% with the use of DHT-derivatives or AIs, then yes you would be at risk for a negative impact on your lipids.
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