Natural Treatment Of Gynecomastia Exercise
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Lose Moobs Naturally Summary
Contents: Online Course
Creator: Cliff Manchaster
Official Website: www.losemanboobs.com
This structural and numerical chromosomal condition presents as either a male with gynecomastia at puberty or with azoospermia (Schweikert et al., 1982). Typically, there are normal male external and internal genitalia. Hormone evaluation reveals elevated FSH and LH and low or normal testosterone. Testis biopsy demonstrates an absence of spermatogenesis with hyalinization, fibrosis and clumps of Leydig cells. The most obvious explanation for the disease is that SRY is translocated from the Y to the X chromosome so that testis differentiation is present. However, the AZF regions on the Y chromosome are not similarly translocated, resulting in azoospermia. This mechanism has been suggested because of the high degree of homology (98.7 ) that exists between the short arm of the X and Y chromosomes (van der Auwera et al., 1992).
This disorder is the most common genetic cause of azoospermia, accounting for 14 of cases. It is classically associated with a triad of findings small, firm testes, azoospermia and gynecomastia. Other features of the syndrome are increased height, decreased intelligence, varicosities, obesity, diabetes, leukemia, increased likelihood of extragonadal germ cell tumors and breast cancer (20 X higher than normal). Most affected individuals, however, do not exhibit the classic clinical phenotype. This is an abnormality of chromosomal number in which 90 of men carry an extra X chromosome (47 XXY) and 10 are mosaic with a combination of XXY XY chromosomes. It is thought that approximately half of XXY cases are paternally derived and recent evidence suggests that its occurrence may correlate with advanced paternal age (Lowe et al., 2001). Testis biopsies show sclerosis and hyalinization. Hormonal evaluation usually demonstrates a low testosterone and frankly elevated luteinizing hormone (LH)...
SBMA is an adult onset, slowly progressing MND that may be associated with signs of androgen insensitivity (gynecomastia, reduced fertility). This X-linked disease is caused by increased size of a polymorphic, tandem CAG repeat in the coding region of the AR gene (CAG coding for glutamine or Q ) (1) and thus belongs to the group of trinucleotide repeat diseases. The normal number of CAG repeats is 11-36, but extends up to 68 in AR with disease-associated mutations. Because other polyQ diseases, including Huntington's disease, are presented in detail in this volume, discussion of SBMA is brief.
The number of CAG repeats in this region to more than 50 generally results in clinically apparent disease (Kupker et al., 1999). The clinical infertility resembles that due to mild androgen insensitivity and may include gynecomastia in addition to testis atrophy. Interestingly, some affected patients may have only mild oligo-zoospermia and as such may be able to conceive naturally or with ICSI. Men, fertile at an early age, may actually experience a significant reduction in their sperm counts with advancing age and disease progression. Importantly, affected couples should be counseled about the phenomenon of genetic 'anticipation' that occurs with this disorder, in which offspring may inherent an even larger number of CAG-nucleotide repeats than that of the parent. Clinically, this translates into a more severe disease phenotype that is manifest earlier in life. Specialized laboratories offer exon 1 CAG-nucleotide repeat analysis of the AR gene.
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