There are also some who complain of joint pain when using Winstrol. As a steroid that does not aromatize there will be no water retention but the “dry feeling” may not be what many think it is. Most who use the steroid will be physique athletes or gym rats during a cutting phase. They will also typically add it into a plan late in the diet once they’re already lean. Typically, when you become very lean, bodybuilding lean, this makes the joints a little uncomfortable. With or without Winstrol this discomfort could potentially exist. As for pro athletes who have nearly every last steroid at their disposal, remember, if Winstrol weren’t effective in competitive sports so many athletes wouldn’t make it a primary and favorite choice. In fact, the combo of Winstrol with low doses of Nandrolone is a very common stack among many athletes, and this stack will greatly eliminate any potential joint discomfort should it exist.
Can et al. (1998) studied the molecular genetics of a large isolated inbred Turkish kindred with male pseudohermaphroditism (PPSH; 264600 ) due to either 5-alpha-reductase-2 (SRD5A2) or 17-beta hydroxysteroid dehydrogenase-3 (HSD17B3; 605573 ) gene defects. Using SSCP analysis and DNA sequencing, a new mutation in exon 5 of the SRD5A2 gene was detected in some male pseudohermaphrodites from this kindred. This single base (adenine) deletion caused a frameshift at amino acid position 251, resulting in the addition of 23 amino acids at the C terminus of this 254-amino acid isozyme. Expression of the mutant isozyme in CV1 cells showed a complete loss of enzymatic activity in the conversion of [14C]testosterone to dihydrotestosterone, without a change in the mRNA level compared to that of the wildtype isozyme. Analysis of the HSD17B3 gene in other male pseudohermaphrodites from this kindred revealed a G-to-A transition at the boundary between intron 8 and exon 9, disrupting the splice acceptor site of exon 9 ( ). In addition to finding male pseudohermaphrodites with either a homozygous SRD5A2 or HSD17B3 gene defect in this kindred, other affected males were found to be genetically more complex, ., homozygous for the SRD5A2 defect and heterozygous for the HSD17B3 defect, or homozygous for the HSD17B3 defect and heterozygous for the SRD5A2 defect. Also, phenotypically normal carriers were identified with either one or both gene defects. Homozygous male pseudohermaphrodites with SRD5A2 or HSD17B3 gene defects were phenotypically distinguishable by the presence of mild gynecomastia in the latter. Hormone data were consistent with the particular homozygous gene defect. The authors concluded that 2 gene defects, one in SRD5A2 and the other in HSD17B3, can each cause male pseudohermaphroditism in a large isolated Turkish kindred, and that the 2 defects segregate independently and can be inherited from 2 different progenitors. They stated that the analysis of a new mutation in exon 5 of the SRD5A2 gene supported the functional importance of the C terminus of the SRD5A2 isozyme.
Individuals with steroid 5-alpha-reductase 2 deficiency are 46,XY with normal testosterone production but impaired virilization during embryogenesis, due to defective conversion of testosterone to dihydrotestosterone (DHT). The nature of the enzyme abnormality in this disorder was discovered when it was demonstrated that 5-alpha-reductase activity in cultured genital skin fibroblasts from affected subjects was reduced [ 8 ]. Cloning of the cDNAs that encode the enzymes revealed that there are two steroid 5-alpha-reductases, termed types 1 and 2 [ 9 ].