Thread: Long term side effects.
04-09-2004, 10:17 AM #1
Long term side effects.
I was thinking last night and I know one day I want to settle down and start a family. my Question is does anybody know of or has heard of birth defects related to steroids . Alot of you guys probobly have kids, was this a concern?
Im 24 and i know nows not the right time for me to have kids but when im in my 30s i will most likly have done about 10-15 cycles.I just dont want to have kids with square heads lol.
04-09-2004, 10:28 AM #2
I had my last kid at your age so I am not familiar with the 30's. However I have a friend that is having a problem getting his wife pregnant and he is only 28. So the possibilites are definetly there. As far as the square head...nah...but I can say this. I had only quit for 2 months before my wife concieved and my son turned out a gnetic freak. What I mean is that yes if you are taking deca or long acting test then your baby could recieve a little dose of it. I have a picture of my son at age 2 standing in a little pool and he is ripped with muscles. I will tell you that I am not proud of this. If he has problems down the road I will never forgive myself. Now as for right now for his age ....no one...and I mean no one can keep up with him in anything that he does. He is faster, stronger, and thicker than most kids his age. I pray every day that he does not get any sides later in his life. Peace
04-09-2004, 10:29 AM #3
My mOm *& DAaad didd juuuce, and nufin evo happppend two mea, cereweusly.
04-09-2004, 11:07 AM #4Associate Member
Originally Posted by jbigdog69
- Join Date
- Feb 2004
I had to re-read this post one trillion times before deducing you were joking.
04-09-2004, 11:10 AM #5
Wtf!!!Originally Posted by BuffGuy
04-09-2004, 11:52 AM #6
04-09-2004, 12:25 PM #7
Ok explain this...BroOriginally Posted by Mr. Death
Many synthetic chemicals can bind to the estrogen receptor and thereby affect specific gene expression and cellular function (19). These compounds are now referred to as xenoestrogens (9, 20, 21). The persistence of these compounds and their metabolites in the environment poses risks for both the human and animal population (22), and studies are necessary to estimate this risk. Although some reports have described endocrine-disruptive effects of these chemicals, there is a great deal of controversy on these findings (23). Additionally, the endocrine disruptive activity of DES and other estrogens has been described less conclusively in the male than in the female. Furthermore, studies are needed to determine whether environmental estrogenic chemicals induce developmental malformation at the dosage that is comparable to the human consumption level (9-13, 21). In this study we chose to determine the effect of three such environmental chemicals, namely, BPA, aroclor, and DES. All of these chemicals have estrogen-like activity (12, 21, 22) and are consumed by the human population (9-13). Using a dosage that is comparable to the human consumption level (11, 13), we evaluated the prenatal effect of these chemicals on male sexual differentiation in the mouse. We report that these chemicals permanently affected male sexual differentiation by increasing anogenital distance, inducing prostate growth and its AR binding activity, and reducing epididymal weight. At high dosage, on the other hand, DES produced an opposite effect, inducing hypospadius and inhibiting prostate growth and AR binding activity. Some of the results obtained with BPA and DES are consistent with previous findings (8, 24), suggesting a teratogenic role of these chemicals on the developing organism at the dosage that is accepted by the FDA. This study, in addition, evaluated the effects of prenatal exposure to estrogenic chemicals in a more detailed fashion. Thus, it examined the prenatal effect of a number of chemicals with low estrogenic activity and studied their effects at all developmental phases. The results demonstrated that all of these chemicals acted very similarly and altered development of certain reproductive organs and functions at all phases of development.
The result of the in vitro studies is the other strength of this research. To our knowledge, this is the first demonstration that estrogenic chemicals induce reproductive malformation in vitro, suggesting that the chemicals have a direct effect on prostate development. Both prostatic enlargement and increased AR binding activity were demonstrated in the developing prostate, grown in vitro in the presence of all of the estrogenic chemicals. Thus, the in vivo and in vitro effects are comparable and therefore, the in vitro setup can be used in further elucidation of the mechanism of estrogen action.
It is interesting to note that estrogenic chemicals induced abnormal male reproductive functions in the presence of large concentrations of maternal circulating estrogen, estradiol, estrone, and estriol. One explanation for this observation could be that the fetal estrogen level is very low in spite of maternal high levels of estrogen (25). During the gestational phase, the fetus is protected from the maternal high-estrogen level by placental conversion of the maternal estrogen into biologically inactive estrogen. Estrogens are inactivated either by converting into conjugated estrogen, forming inactive estrogen metabolite, or binding with plasma protein (26). Thus, even a small change in the estrogen level during this fetal period may have a significant effect, and our findings, especially the in vitro findings, support this possibility.
The mechanism by which these chemicals induce male reproductive malformations is not known. The relatively low estrogenic potencies of suspected endocrine disrupters suggest that estrogenic activity of these chemicals alone is unlikely to produce adverse effects during fetal development. Some suspected endocrine disrupters have been shown to interact not only with the estrogen receptor (ER) but also with the androgen receptor (AR) or to interfere with steroid hormone synthesis or metabolism (27). At this time it is not known whether estrogenic activity is directly involved in the malformation induced by the chemicals. Additionally, there are two ER subtypes, Era and Erb, in the prostate (28). The xenoestrogens were shown to have higher binding affinity for the ER-▀ protein (29). The role of these two ER subtypes in relation to the action of these chemicals remains to be determined. The estrogenic potency of compounds is another issue. Although the chemicals are weak estrogens, the potency is dependent on a number of factors, such as differential effects on the transactivation functionalities of the receptor, the particular coactivator recruited and cell and target gene promoter context (30, 31). The apparently lower transcriptional activity of ER-▀ compared with ER- has been reported in transient transfection experiments using different cell lines (32). In contrast, in human osteosarcoma or human endometrial cells, the transcriptional activity of ER-▀ was higher than that of ER- (32). The reason for these differences in transcriptional activity of ER subtypes is unknown, but it might reflect differential expression of transcriptional coactivators or differential stability of the receptor proteins. At the present, it is not known whether any of the ER-mediated activities are involved directly or whether these chemicals alter recruitment of ER activators causing malformation of the prostate gland.
The results described here demonstrate that AR binding activity is permanently altered by these chemicals. There are several possibilities of how this effect is mediated. First, it is possible that the estrogenic chemicals enhance synthesis of the AR protein resulting in enhanced activity. Second, the estrogenic chemicals may enhance recruitment of AR coactivators, resulting in enhanced AR binding. Finally, since these xenoestrogen-exposed offspring have enlarged prostate growth, it is also possible that AR-mediated transcriptional activity has been enhanced in these animals. This possibility is supported by the observations that estrogenic chemicals enhance EGF and IGF-1 synthesis in the adult uterus (33) and that EGF and IGF-1 enhance AR-mediated transcriptional activity (34,35). At this time it is not known whether these chemicals induce EGF/IGF-1 synthesis in the prostate gland mediating AR-mediated transcriptional activity and prostate growth. Further experiments are needed to examine these possibilities.
04-09-2004, 12:39 PM #8Anabolic Member
Originally Posted by TheSevnthWarrior
- Join Date
- Jan 2003
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