Posted on 11/28/2001 7:45:29 AM PST by patent
Some species (for example, bees) have evolved such that some members of the species pass along their genes, not by breeding, but by assisting the breeding of a close relative. But human beings are not bees; we have evolved to pass along our genes by breeding directly. As such, it is a logical impossibility to inherit infertility. Even if an infertile human "gets lucky" and reproduces once, it is a trait that is doomed to be rapidly weeded out.
We therefore must conclude that all human infertility is acquired (through mutation, injury or environmental interference) and not inherited. Because such an acquired trait interferes with the sole (epistemological) function of the human organism, it must necessarily be called a disfunction by any standard.
Right. And my carefully cultivated garden next to my bedroom window is the same as the hodge-podge of stuff growing in the empty lot across the street.
Mark W.
(My personal opinion is that genetic diversity is good, and that manipulation of the human genome will lead to greater diversity. While your garden may be less genetically diverse than the lot across the street, horticulture overall has added to the genetic diversity of flowers, by preserving and promoting entire sequences of rare mutations that would have been extremely unlikely in the wild.)
The difference between the garden and the empty lot is that the one is the way you want it to be. The useful and beautiful plants are cultivated to thrive, and the harmful are plucked out. Would you not like to see cystic fibrosis or muscular dystrophy eradicated? Those things kill people. If such genes could be replaced by properly functioning genes, would that not be a good thing?
But look, all this and more I discussed at length in the thread I linked above. We could go on this way, but I'd probably just be doing a lot of cutting-and-pasting from there.
You should be ashamed of yourself for the way you conduct yourself when people try to "discuss" something with you. In that Creation Science thread where you and I interacted, I got disgusted and said I would post any more to you there. Now I see that you engage in the same obnoxious behavior everywhere. This will be my last post to you any where
Specifically, I accuse you of dropping/rearranging contexts to suit yourself, and ignoring the obvious meaning & context of stuff posted to you.
I used the illustration of a garden compared to an empty lot in the context of rebutting your absurd notion that changes caused by genetic engineering were the same as changes caused by "random" mutation. Obviously that's goofy. Changes caused by genetic engineering, like a garden, are specifically directed changed unlike random changes affecting an empty lot. And, just as directed changes make a garden look VASTLY different than the random changes make an empty lot look, so too will DIRECTED changes caused by genetic engineering have VASTLY larger differences than random mutations.
And I never brought up the issue of "genetic diversity." What a red herring! Genetic engineering is about a heck of a lot more than that. Genetic engineering routinely involves taking genes from one species and implanting them in another. In specific ways for specific purposes, not randomly. And the observed consequences of this practice _seems_ to include difficult to predict interactions with viruses & bacteria that never bothered the initial, "unmodified" gene set (i.e., diseases and such "jump species").
Now I'm done with you.
Mark W.
Hold that thought --
Inheritance of Infertility - Dangers for Generations Downstream?
A. Trounson, D. Cram, B. Song, R. McLachlan,
D. De Kretser and E. Yong*
Institute of Reproduction and Development Monash University, Clayton, Victoria, Australia * Department of Obstetrics and Gynaecology, National University of Singapore, Singapore
Summary
It is apparent that male infertility is associated with mild to moderate expansion of the CAG trinucleotide repeat in the transactivation domain of the androgen receptor gene. Because this expansion may increase in succeeding generations, risking the spinal bulbar atrophy disease known as Kennedy’s disease, further research is warranted to determine the stability of this expansion in infertile men and their offspring conceived by IVF and ICSI.
Introduction
Human infertility can occur as a consequence of historical mutations where the cause of infertility may be an accumulation of defects that finally manifest under the appropriate conditions or be denovo mutations that appear in the genome of the individual without an inheritance from the parental somatic genotype. These latter mutations may occur in the germ cells of parents without being expressed in the remainder of their cells and tissues. Inherited infertility can be either male or female related. Congenital absence of the vas is closely related to cystic fibrosis and may be due to the same mutation. Polycystic ovarian disease also has a genetic component that is inheritable (1) and the deletions in the AZF regions of the Y chromosome are transmitted from father to son (2). Of some interest are the mutations found in the androgen receptor gene that is a nuclear transcription factor that when activated will induce androgen-regulated genes required for spermatogenesis and sexual differentiation. Mutations will cause androgen insensitivity syndrome and partial syndromes involving female phenotypes and ambiguous genitalia. There are also more subtle effects where no obvious phenotype exists except for reduced fertility that may also involve mutations in the androgen receptor (3).
Point mutations in the ligand binding domain of the androgen receptor can cause a functional defect in the transactivation property of the gene that is expressed in reduced semen quality and infertility (4). Men with severe infertility will usually not transmit gene mutations because they are unlikely to have children by natural methods of conception. The introduction of IVF and particularly intracytoplasmic sperm injection (ICSI) may enable many more mutations associated with infertility to be transmitted to succeeding generations and increase the likelihood of the need to provide assistance to these families for conception in the future. The concern may be increased if these mutations are associated with other pathologies and if the severity of these conditions increases. This may be the case for the trinucleotide (CAG) repeat that codes for a polyglutamine tract in the transactivation domain of the androgen receptor (5).
Association of Trinucleotide Repeat Expansion in the Androgen Receptor Gene with Male Infertility
The androgen modulated DNA binding protein (androgen receptor) is encoded by a single copy gene on the X chromosome (Xq11-12). Hence men are affected by a mutation in the gene and women can be carriers. Besides its well documented role in male sexual differentiation, testicular descent and spermatogenesis, expansion of the CAG repeat in the transactivation causes the spinal and bulbar muscular atrophy disease known as Kennedy’s disease. Normally there are around 20 CAG repeats and expansion to 40 or more will be associated with Kennedy’s disease. Reduced numbers of CAG repeats have been associated with prostate cancer. Interestingly, moderate expansion of the CAG repeat sequence is associated with increasing severity of male infertility.
In a study (5) examining CAG repeat length in infertile and fertile men, where point mutations in the androgen receptor and Y chromosome DAZ and RBM deletions and other explanations for infertility were excluded, showed that men with spermatogenic failure had significantly higher CAG repeat lengths than the fertile controls (mean ± SE; 23.2 ± 0.7 vs 20.5 ± 0.3). Additional data has confirmed this significant difference between infertile and fertile men and also shows that increasing severity of infertility is correlated with increasing CAG repeat length.
Increasing CAG repeat length with increasing severity of male infertility raises the concern that further expansion might increase the possibility of more severe infertility or even Kennedy’s disease in succeeding generations. The continued expansion in trinucleotide repeat length in succeeding generations is characteristic of the trinucleotide repeat diseases and results in earlier and more severe onset of neurological and muscular disorders. This is known as anticipation. The possibility that CAG repeat expansion may occur in children conceived by ICSI because their fathers had moderate expansion needs to be examined. The androgen receptor will be passed to daughters of men treated by ICSI. Examination of the stability of inheritance of these moderate expansions could provide assurance of the safety of ICSI or give warning for the necessity to screen for CAG repeat length in men being treated for infertility by IVF and ICSI.
It is possible that sperm may vary in their CAG repeat length in men with moderate to severe expansion (>40). If this is the case, it would be possible to analyse CAG repeat length in embryos by preimplantation genetic diagnosis (PGD). This strategy could be used to reduce the likelihood of anticipation occurring for families at risk for trinucleotide repeat disorders such as Kennedy’s disease.
References
(1) GHARANI O, WATERWORTH DM, BATTY S, WHILE D, GILLING-SMITH C, CONWAY GS, MCCARTHY M, FRANKS S, WILLIAMSON R. Association of the steroid synthesis gene CYPIIa with polycystic ovary syndrome and hyperandrogenism. Hum Mol Genetics 6: 397-402, 1997.
(2) DE KRETSER DM, MALLIDIS C, MA K, BHASIN. Y chromosome deletions and male infertility. Reprod Med Review 6: 37-53, 1997.
(3) YONG EL, WANG Q, TUT TG, GHADESSY FJ, NG SG. Male infertility and the androgen receptor: molecular, clinical and theraputic aspects. Reprod Med Review 6: 113-131, 1997.
(4) WANG Q, GHADESSY FJ, TROUNSON A, DE KRETSER D, MCLACHLAN R, NG SC, YONG EL. Azoospermia associated with mutation in the ligand-binding domain of the androgen receptor with normal ligand binding, but defective transactivation. J Clin Endocrin Metab 83: 4303-4309, 1998.
(5) DOWSING AT, YONG EL, CLARK M, MCLACHLAN R, DE KRETSER DM, TROUNSON AO. Linkage between male infertility and trinucleotide repeat expansion in the androgen receptor gene. Lancet (in press).
Approximately one in five American couples are infertile. A large proportion of the medical conditions responsible for that infertility, such as ovarian cysts or vas deferens "disfunction," is strongly associated with genetic inheritance factors from one or both parents. Replicative studies have confirmed this over and over. And even as individual infertile family lines become extinct, these mutations and the infertility traits associated with them keep arising in the population quite independently. Far from being a "logical impossibility," inherited infertility appears to be one of nature's most persistent features.
Careful! Aposiopetic is going to jump down your throat. ;-)
is strongly associated with genetic inheritance factors from one or both parents. Replicative studies have confirmed this over and over.
You're right, of course; I misspoke. (I actually caught it as I clicked the post button; what is it about the irrevocable act of clicking that makes me so observant?) The point is that the genetic disfunctions--that word again!--that lead to infertility are transitory in the gene pool, and cannot be considered an integral part of the function of the human organism.
They are like wounds in the body; wounds are inflicted, they heal, and more are inflicted again, but they can in no sense be counted among the functions of the body.
Bottom line: it is the epistemological function of genes and organisms to replicate. Infertility, insofar as it interferes with that, is a disfunction.
But look on the bright side: you were right and I was wrong.
Rather surprising too. When organ transplants were the new thing, I saw a column in The Jewish Advocate cautioning that many orthodox rabbis considered it forbidden under the prohibition against looting the dead.
The "Boys from Brazil" meet Adolph Hitler.
.....my mistake...they are already well aquanted.
Oh, well, you could always storm off in a petulant huff; I've seen that done. <g>
If that's the case, then I'm afraid you're wrong again. If the infertility is due to anything but lack of viable eggs or lack of viable sperm, an infertile individual can pass along his traits by artificial insemination (in vivo implantation) or by in vitro fertilization. Depending on the cause of the infertility, that infertile individual can also pass along his traits by other means, such as drugs or surgery. This would apply to both infertile males and infertile females.
With enough re-writes, I'm sure you'll eventually get this right.
You're a lawyer, ain't ya?
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