LoneTree said:
I will beg to differ.
It never happens with human grade. It has nothing to do with the enzymes. There are no pharmacological effects of test that may cause flu like symptoms.
It is because of contamination in UG test. The contaminants cause allergic type of reaction. The symptoms of allergic reactions are very similar to flu like symptoms.
Find a better source with better quality stuff. That is the best 'cure'.
you may beg to differ, but you are wrong.
there are a number of reported instances of flu-like symptoms associated with hrt pharm grade test--just search this board alone, but found this w/o much effort:
Pyrogenicity of etiocholanolone and interleukin-1 in New and Old World Monkeys.
Steinetz BG, Randolph C, Werner R, Mahoney CJ.
New York University Medical Center, Laboratory for Experimental Medicine and Surgery in Primates, Tuxedo 10987, USA.
[email protected]
Etiocholanolone (5beta-androstan-3alpha-ol-17-one; designated E) is one of the major products of metabolism of testosterone and androstenedione (androst-4-ene-3,17-dione) in many mammalian species, including humans. E and several other 5beta-reduced steroids have been found to induce fever in humans. The pyrogenic effect of these steroids has been shown to be due to the release of interleukin-1 (IL-1) from the leukocytes that are mobilized in response to the steroid injections. Old World Monkeys such as Rhesus monkeys (Macaca mu/atta), metabolize androgens similarly to humans, and E is a normal metabolite. However, New World Monkeys such as Squirrel monkeys (Saimiri sciureus), lack hepatic 5alpha- and 5beta-steroid reductases and excrete androgens primarily in an unaltered state; E is not produced. Therefore, we postulate that Squirrel monkeys likewise may have lost the ability to respond to 17-ketosteroids such as E. To test this hypothesis, adult male Rhesus and Squirrel monkeys were treated with E, and their rectal temperatures were recorded over a 24-hr period. Rhesus monkeys exhibited a rise of up to 3 degrees F following E injection. Squirrel monkeys, on the other hand, did not exhibit any increase in rectal temperature over the 24-hr period, even when doses up to 250 times the effective human dose were used. However, both species responded to injected IL-1alpha with a robust increase in rectal temperature. The data show that E is pyrogenic in Rhesus, but not Squirrel monkeys. The findings support the notion that injected E may induce release of IL-1 in Rhesus monkeys, but not in Squirrel monkeys
and from nandi2001 in an EF post a few years ago:
Etiocholanolone is a metabolite of testosterone that when injected directly causes fever and flu like symptoms. According to Goodman & Gilman's The Pharmacological Basis of Therapeutics, 5th ed p. 1465, temperature as high as 105 degreees have been recorded after IM etiocholanolone. This is assumed to be the cause of "steroid fever".
This is not a problem with therapeutic doses of test, but when frontloading "steroid fever" can definitely be a problem. Equipoise - boldenone undecylenate - causes it as well at high doses since testosterone, and hence etiocholanolone, are metabolites of Equipoise - boldenone undecylenate - .
and this from good old rio 2001 (MD) from a post a few years ago
Just for the record ....I found further evidence that links anabolic androgenic steroids and inflamatory response. One of the main metabolites of test, ethiocolanolone, has a direct impact on IL1 release, fever and inflamation. Since ethiocolanolone is quickly conjugated in the liver and only high levels of unconjugated Eth. can cause fever, I presume when high doses of a short esther are administered, the liver can´t handle all the substract for conjugation and consequently high concentrations of unconjugated ethiocolanolone will be responsible for an inflamatory response.
Although this can explain an inflamatory response from test, pathogenesis from others like trenbolone and win that have different metabolites but can cause flu like symptoms as well remain unclear, but I´m pretty sure by now that is either the molecule or some metabolite that, reaching high plasma concentrations, produce a pro inflamatory response.
The induction of interleukin-1 in humans and its metabolic effects.
Watters JM, Bessey PQ, Dinarello CA, Wolff SM, Wilmore DW.
To investigate the metabolic effects of interleukin-1 and its role as a mediator of host responses to trauma and sepsis, we injected seven healthy male subjects with etiocholanolone, an inflammatory agent that stimulates systemic responses thought to be mediated by interleukin-1. The subjects were fed a constant diet during each 4-day study and received three daily intramuscular injections of etiocholanolone, 0.10 mg/kg. Etiocholanolone injection resulted in inflammation, fever, leukocytosis, increased serum C-reactive protein, hypoferremia, and increased plasma activity of interleukin-1/lymphocyte-activating factor. Plasma concentrations of the counterregulatory hormones were normal. Protein metabolism, as reflected in nitrogen balance, 15N turnover, and forearm flux of alanine and glutamine, was unaltered. Serum glucose and insulin levels and tissue responsiveness to insulin were normal. This dissociation of acute-phase and catabolic responses may reflect the magnitude of the stimulus; higher levels of interleukin-1 may initiate catabolic responses. Alternatively, other mediators such as the counterregulatory hormones may direct the catabolic responses that occur after injury and sepsis.
anabolic androgenic steroids have immunomodulatory effects. Androgens are know to enhance inflammatory activity by increasing levels of cytokines , interleukines, TNF and interferon; and up regulate immunity by increasing lymphocyte activity.They also COUNTERACT immunosupressive effects of glucocorticoids. Remember that anabolic androgenic steroids are used on wasting diseases, and in those morbiditys frequently immune system is severily debilitated ( cancer, HIV...), and of course if anabolic androgenic steroids where to decrease immune response dramatically they would not be consider to treat such diseases.
I bumped into an interesting study that conclude that supraphysiological doses of anabolic androgenic steroids ASSOCIATED WITH HIGH INTENSITY TRAINING caused significant decrease in immune response, but a control group taking the SAME AAS DOSAGE and running an ENDURANCE TRAINING had no effect whatsoever on immunity ( study on rats), leading to believe that the problem was the intensity of training rather then AAS use.Intense bouts of training reduce significantly macrophage activity and lymphocyte expression, that´s a long known fact.
There is one classic study by Calabrese et al that is very enlightening, they compared the immune response on 13 competitive bodybuilders self-administering anabolic-androgenic steroids and ten competitive bodybuilders not administering these drugs. There were no significant differences in T-cell subsets among steroid users and non-users, but lymphocyte transformation studies revealed that the anabolic-androgenic steroid-using group had ENHANCED proliferative ability to the B-cell mitogen in comparison to non-bodybuilding controls. Natural Killer T( cell mediated immunity) activity was significantly augmented in the anabolic-androgenic steroid users but not in the non-using bodybuilders.
So, I think most of the so called " flus" in the beginning of cycles are in fact asseptic ( no microorganisms involved) inflammatory responses, and in some cases coincidental with an already existent , " would cause a flu anyway" virus .
Another thing to consider is how a higher intensity of training can decrease your immune response, and some times infections because of that would be wrongfully atributted to anabolic androgenic steroids,remeber that intensity goes much higher when "ON"...
Last, but not least, attention at the end of a cycle, when Test is low, glucocorticoid receptors are cleared and immune system can go down again.
Refs -
1) Ferrandez MD, de la Fuente M, Fernandez E, Manso R
Anabolic steroids and lymphocyte function in sedentary and exercise-trained rats.
J Steroid Biochem Mol Biol. 1996 Oct;59(2):225-32.
2)Padgett DA, Loria RM.
Endocrine regulation of murine macrophage function: effects of dehydroepiandrosterone, androstenediol, and androstenetriol.
J Neuroimmunol. 1998 Apr 1;84(1):61-8.
3)Hughes TK Jr, Rady PL, Smith EM.
Potential for the effects of anabolic steroid abuse in the immune and neuroendocrine axis.
J Neuroimmunol. 1998 Mar 15;83(1-2):162-7.
4) Hernandez-Pando R, De La Luz Streber M, Orozco H, Arriaga K, Pavon L, Al-Nakhli SA, Rook GA.
The effects of androstenediol and dehydroepiandrosterone on the course and cytokine profile of tuberculosis in BALB/c mice.
Immunology. 1998 Oct;95(2):234-41.
5) Padgett DA, Sheridan JF.
Androstenediol (AED) prevents neuroendocrine-mediated suppression of the immune response to an influenza viral infection.
J Neuroimmunol. 1999 Aug 3;98(2):121-9.
6)Loria RM.
Immune up-regulation and tumor apoptosis by androstene steroids.
Steroids. 2002 Nov;67(12):953-66.
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