Archive for the ‘Male Genetics’ Category

Introduction

There is a common belief among liberals that people are born either gay or straight. Conservatives tend to believe that sexual orientation is actually sexual preference, which is chosen by the individual. This page represents a review of the scientific literature on the basis for homosexual orientation.

Are people born gay or straight? Much of the current media sources assume the question is a solved scientific problem with all the evidence pointing toward a biological (probably genetic) basis for a homosexual orientation. Contrary to this perception, the question has been poorly studied (or studied poorly), although there is some evidence on both sides of question. In addition, many of the initial studies, which were highly touted by the media as "proof" for a biological basis for homosexuality, have been contradicted by later, more thorough studies. This evidence falls into four basic categories:

Until a few years ago, sexual orientation used to be called sexual preference. Obviously, the two terms denote significant differences in the the manner by which sexuality develops. A preference is something that is chosen, whereas orientation is merely something that defines us. The differences are potentially important regarding how the law applies to those who are gay. If homosexuality is not chosen, but actually is a biologically-determined characteristic over which we have no choice, then laws should not treat gays and straights differently, since homosexuality would be equivalent to one's race, over which we have no control.

Since sexual attraction begins in the brain, researchers first examined the question of sexual orientation by comparing the anatomy of brains from males and females. These studies showed that male and female brains showed sexual dimorphism in the pre-optic area of the hypothalamus, where males demonstrated a greater than two-fold difference in cell number and size compared to females.1 A second study found that two of four Interstitial Nuclei of the Anterior Hypothalamus (INAH) were at least twice as large in males as females.2 Since the INAH was involved in sexual dimorphism, it was hypothesized by Simon LeVay that there might be differences in this region in heterosexual vs. homosexual men. Postmortem examination of the brains of AIDS patients vs. control male subjects (presumed to be heterosexual) showed that the presumably heterosexual men exhibited INAH3 that were twice the size of both females and presumably homosexual men who had died of AIDS.3 The study has been criticized for its uncertainty of sexual orientation of the subjects, and potential complications caused by the AIDS virus (which does infect the human brain), and also by lowered testosterone levels found in AIDS patients. A popularized Newsweek cover story, "Is This Child Gay?"4 characterized LeVay as a "champion for the genetic side," even though the study involved no genetic data at all.

A subsequent study by Byne, et al. examined the question of INAH3 size on the basis of sex, sexual orientation, and HIV status.5 The study found large differences in INAH3 volume on the basis of sex (with the male INAH3 being larger than the female INAH3). However, the volume of IHAH3 was decreased in male heterosexual men who had contracted AIDS (0.108 mm3 compared with 0.123 mm3 in male controls). There was no statistically significant difference between IHAH3 sizes of male heterosexuals vs. male homosexuals who had contracted AIDS (0.108 mm3 and 0.096 mm3, respectively). The study also found that there were no differences in the number of neurons in the INAH3 based upon sexual orientation, although researchers found significant differences between males and females, as in other studies.5 It was obvious from this study that LeVay's study was fatally flawed due to the AIDS complication, and that there were no differences in the INAH3 based upon sexual orientation.

The role of the hypothalamus in sexual orientation was further studied by Swaab, et al. Other researchers had hypothesized that differentiation of the hypothalamus occurred before birth. However, Swaab's study showed that the sexually dimorphic nucleus (SDN) of more than 100 subjects decreased in volume and cell number in the females only 2-4 years postnatal. This finding complicated the findings of the brain studies, since not only chemical and hormonal factors, but also social factors, might have influenced this process.6

A study by Allen and Gorski examined the anterior commissure of the brain, finding that females and homosexual males exhibited a larger size than heterosexual males.7 However, later studies using larger sample sizes found no such differences.8

Complicating the issue of brain differences between homosexuals and heterosexuals is the problem that sexual experiences themselves can affect brain structure.9 So, the question will always be whether homosexual practice changes the brain or whether the brain results in homosexual practice.

Since sexual differentiation occurs within the womb, as a result of hormonal influences, it has been hypothesized that homosexuality may result from a differential hormone balance in the wombs of those who eventually exhibit a homosexual orientation. Since hormonal levels within the womb are not available, proxies for hormonal influences have been used to examine the question of how hormonal influences might impact sexual orientation. These proxies include differences in skeletal size and shape, including the ratio of the long bones of the arms and legs relative to arm span or stature and the hand bones of adults (the ratio of the length of the various phalanges).

Studies have shown that ratios of digit length are predictors of several hormones, including testosterone, luteinizing hormone and estrogen.10 In women, the index finger (2D, second digit) is almost the same length as the fourth digit (4D). However, in men, the index finger is usually shorter than the fourth. It has been shown that this greater 2D:4D ratio in females is established in two-year-olds. It has been hypothesized that the sex difference in the 2D:4D ratio reflects the prenatal influence of androgen on males. A study by Williams, et al. showed that the 2D:4D ratio of homosexual men was not significantly different from that of heterosexual men for either hand.11 However, homosexual women displayed significantly smaller 2D:4D ratios compared with heterosexual women (see figure to right). It has been hypothesized that women exposed to more androgens in the womb tend to express a homosexual orientation. However, since these hormone levels were never measured, one is left with the proxy of finger lengths as a substitute. Studies have found that the more older brothers a boy has, the more likely he is to develop a homosexual orientation.12 This study also found that homosexual men had a greater than expected proportion of brothers among their older siblings (229 brothers: 163 sisters) compared with the general population (106 males: 100 females). Males who had two or more older brothers were found to have lower 2D:4D ratios,11 suggesting that they had experienced increased androgens in the womb. Why increased androgens would predispose both males and females to be homosexual was not explained in the study.

Another study examined the length of long bones in the arms, legs and hands. Both homosexual males and heterosexual females had less long bone growth in the arms, legs and hands, than heterosexual males or homosexual females.13 Accordingly, the researchers hypothesized that male homosexuals had less androgen exposure during development than male heterosexuals, while female homosexuals had greater steroid exposure during development than their heterosexual counterparts. Of course, with regard to male homosexuality, this study directly contradicted the presumed results of the Williams study above, which "showed" that males with multiple older brothers (who tended to be homosexual) experienced increased androgen exposure.

A study of one homosexual vs. two heterosexual male triplets found that the homosexual triplets scored more on the female side of the Masculinity-Femininity scale of the Minnesota Multiphasic Personality Inventory,14 suggesting a possible hormonal influence (decreased androgens) involved in male homosexual orientation.

All of the studies reporting possible hormonal influence on homosexuality suffer from the lack of any real evidence that hormones actually play any role in sexual orientation. The fact that contradictory studies report increased11,15 vs. decreased13-14 androgens as a basis for homosexuality doesn't provoke confidence that the proxies are really true. Obviously, a study that documented real hormone levels, as opposed to proxies, would probably provide more definitive data.

Studies involving a rare hormonal imbalance, congenital adrenal hyperplasia (CAH), caused by defective 21-hydroxylase enzyme, suggest that hormonal abnormalities can influence sexual orientation. CAH results in increased production of male hormones during development. In males, increased androgens has little effect. However, female fetuses that develop in this environment develop ambiguous external genitalia, which complicates subsequent development. In utero treatment with dexamethasone reduces the androgen imbalance, resulting in an individual who is genetically and phenotypically female. However, dexamethasone treatment also results in reduced homosexual orientation among treated females,16 suggesting that some homosexuality may result from hormonal influences during development. Homosexual rights groups have suggested that dexamethasone treatment not be given, because it reduces homosexual orientation in females affected by CAH.

The observation that familial factors influence the prevalence of homosexuality led to a the initiation of number of twin studies, which are a proxy for the presence of possible genetic factors. Most of these early studies suffered from methodological flaws. Kallmann sampled subjects from correctional and psychiatric institutionsnot exactly representative "normal" populations.17 Bailey et al. published a number of studies in the early 1990's, examining familial factors involved in both male and female homosexuality. These studies suffered from the manner in which subjects were recruited, since the investigators advertised in openly gay publications, resulting in skewed populations.18 Later studies by the same group did not suffer from this selection bias, and found the heritability of homosexuality in Australia was up to 50 and 60% in females but only 30% in males.19

A study by Kendler et al. in 2000 examined 1,588 twins selected by a random survey of 50,000 households in the United States.20 The study found 3% of the population consisted of non-heterosexuals (homosexuals and bisexuals) and a genetic concordance rate of 32%, somewhat lower than than found in the Australian studies. The study lost statistical significance when twins were broken down into male and female pairs, because of the low rate (3%) of non-heterosexuals in the general U.S. population.

A Finnish twin study reported the "potential for homosexual response," not just overt homosexual behavior, as having a genetic component.21

On a twist on homosexual twin studies, an Australian research group examined the question of whether homophobia was the result of nature or nurture.22 Surprisingly, both familial/environmental and genetic factors seemed to play a role as to whether or not a person was homophobic. Even more surprising, a separate research group in the U.S. confirmed these results (also adding that attitudes towards abortion were also partly genetic).23 Now, even homophobes can claim that they were born that way!

Twin studies suffer from the problem of trying to distinguish between environmental and genetic factors, since twins tend to live within the same family unit. A study examining the effect of birth order on homosexual preference concluded, "The lack of relationship between the strength of the effect and degree of homosexual feelings in the men and women suggests the influence of birth order on homosexual feelings was not due to a biological, but a social process in the subjects studied."12 So, although the twin studies suggest a possible genetic component for homosexual orientation, the results are certainly not definitive.

An examination of family pedigrees revealed that gay men had more homosexual male relatives through maternal than through paternal lineages, suggesting a linkage to the X chromosome. Dean Hamer24 found such an association at region Xq28. If male sexual orientation was influenced by a gene on Xq28, then gay brothers should share more than 50% of their alleles at this region, whereas their heterosexual brothers should share less than 50% of their alleles. In the absence of such an association, then both types of brothers should display 50% allele sharing. An analysis of 40 pairs of gay brothers and found that they shared 82% of their alleles in the Xq28 region, which was much greater than the 50% allele sharing that would be expected by chance.25 However, a follow-up study by the same research group, using 32 pairs of gay brothers and found only 67% allele sharing, which was much closer to the 50% expected by chance.26 Attempts by Rice et al. to repeat the Hamer study resulted in only 46% allele sharing, insignificantly different from chance, contradicting the Hamer results.27 At the same time, an unpublished study by Alan Sanders (University of Chicago) corroborated the Rice results.28 Ultimately, no gene or gene product from the Xq28 region was ever identified that affected sexual orientation. When Jonathan Marks (an evolutionary biologist) asked Hamer what percentage of homosexuality he thought his results explained, his answer was that he thought it explained 5% of male homosexuality. Marks' response was, "There is no science other than behavioral genetics in which you can leave 97.5% of a phenomenon unexplained and get headlines."29

A study of 13,000 New Zealand adults (age 16+) examined sexual orientation as a function of childhood history.30 The study found a 3-fold higher prevalence of childhood abuse for those who subsequently engaged in same sex sexual activity. However, childhood abuse was not a major factor in homosexuality, since only 15% of homosexuals had experienced abuse as children (compared with 5% among heterosexuals).30 So, it would appear from this population that only a small percentage of homosexuality (~10%) might be explained by early childhood abusive experiences.

If homosexual orientation were completely genetic, one would expect that it would not change over the course of one's life. For females, sexual preference does seem to change over time. A 5-year study of lesbians found that over a quarter of these women relinquished their lesbian/bisexual identities during this period: half reclaimed heterosexual identities and half gave up all identity labels.31 In a survey of young minority women (16-23 years of age), half of the participants changed their sexual identities more than once during the two-year survey period.32 In another study of subjects who were recruited from organizations that serve lesbian/gay/bisexual youths (ages 14 to 21 years) in New York City, the percentage that changed from a lesbian/gay/bisexual orientation to a heterosexual orientation was 5% over the period of just 12 months (the length of the survey).33 Other studies have confirmed that sexual orientation is not fixed in all individuals, but can change over time, especially in women.34 A recent example of an orientation change occurred with The Advocate's "Person of the Year" for 2005. Kerry Pacer was the youngest gay advocate, chosen for her initiation of a "gay-straight alliance" at White County High School in Cleveland, Georgia. However, four years later, she is raising her one year old daughter, along with the baby's father.35 Another former lesbian, British comedienne Jackie Clune, spent 12 years in lesbian relationships before marrying a man and producing 4 children.36 Michael Glatze came out at age 20 and went on to be a leader in the homosexual rights movement. At age 30, he came out in the opposite direction, saying, "In my experience, "coming out" from under the influence of the homosexual mindset was the most liberating, beautiful and astonishing thing I've ever experienced in my entire life."37 A 2011 study of Christian gays who wanted to change their sexual orientation found that 23% of the subjects reported a successful "conversion" to heterosexual orientation and functioning, while an additional 30% reported stable behavioral chastity with substantive dis-identification with homosexual orientation.38 However, 20% of the subjects reported giving up on the process and fully embraced a gay identity, while another 27% fell in between the two extremes.38 Obviously, for at least some individuals, being gay or straight is something they can choose.

The question of nature vs. nurture can also be seen by examining children of homosexual vs. heterosexual parents. If homosexuality were purely biological, one would expect that parenting would not influence it. Paul Cameron published a study in 2006 that claimed that the children of homosexual parents expressed a homosexual orientation much more frequently than the general population.39 Although claims of bias were made against the study, another study by Walter Schuum in 2010 confirmed Cameron's results by statistically examining the results of 10 other studies that addressed the question.40 In total, 262 children raised by homosexual parents were included in the analysis. The results showed that 16-57% of such children adopted a homosexual lifestyle. The results were even more striking in daughters of lesbian mothers, 33% to 57% of whom became lesbians themselves. Since homosexuals makeup only ~5% of the population, it is clear that parenting does influence sexual orientation.

It always amazes me when people say that they were born gay. Looking back on my own experience, I would never say that I was "born straight." I really didn't have any interest in females until about the seventh grade. Before that time, they weren't really interesting, since they weren't interested in sports or riding bikes or anything else I liked to do.

I am not a huge fan of Neo Darwinian evolution. Nevertheless, there is some clear evidence that natural selection (and sexual selection) does act upon populations and has acted on our own species to produce racial differences.41 Natural selection postulates that those genetic mutations that favor survival and reproduction will be selected, whereas those that compromise survival and reproduction will be eliminated. Obviously, a gene or series of genes that produce non-reproducing individuals (i.e., those who express pure homosexual behavior) will be rapidly eliminated from any population. So, it would be expected that any "gay gene" would be efficiently removed from a population. However, it is possible that a gene favoring male homosexuality could "hide" within the human genome if it were located on the X-chromosome, where it could be carried by reproducing females, and not be subject to negative selection by non-reproducing males. In order to survive, the gene(s) would be expected to be associated with higher reproductive capacity in women who carry it (compensating for the generation of non-reproducing males). I can't imagine a genetic scenario in which female homosexuality would ever persist within a population.

Within the last decade, genetic analysis of heritable traits has taken a huge step forward with the advent of DNA microarray technology. Using this technology, it is possible to scan large lengths of the human genome (even an entire genome wide scanGWAS) for numerous individuals, at quite reasonable costs. This DNA microarray technology has led to the discovery of genes that are associated with complex diseases, such as Crohn's Disease, which is the topic of my research. If homosexuality truly has a genetic component, DNA microarray studies would not only definitively prove the point, but would identify specific gene(s) or loci that might be associated with those who express a homosexual orientation. The first attempt to do genome wide scans on homosexual males was done by Mustanski et al. in 2005.42 The results suggested possible linkage near microsatellite D7S798 on chromosome 7q36. However, an attempt to repeat the finding (along with ~6000 well-defined SNPs spread comparatively evenly across the human genome) failed to find any significant SNPs.43 However, a third study using Chinese subjects found a weak association at the SHH rs9333613 polymorphism of 7q36.44 A more general study, examining mate choice among different populations, found no genetic link, prompting the investigators to speculate that such choices were "culturally driven."45 The largest genome wide scan was conducted by 23andMe. 7887 unrelated men and 5570 unrelated women of European ancestry were analyzed by GWAS. Although unpublished, the data was presented at the American Society of Human Genetics annual meeting in San Francisco, showing that there were no loci associated with sexual orientation, including Xq28 on the X chromosome.46 So, the preliminary studies on possible genetic causes of homosexual orientation tends to rule out any dramatic genetic component to sexual orientation.

Why are people gay? The question of how homosexual orientation originates has been the subject of much press, with the general impression being promoted that homosexuality is largely a matter of genes, rather than environmental factors. However, if one examines the scientific literature, one finds that it's not quite as clear as the news bytes would suggest. The early studies that reported differences in the brains of homosexuals were complicated by HIV infection and were not substantiated by larger, better controlled studies. Numerous studies reported that possible hormonal differences affected homosexual orientation. However, these studies were often directly contradictory, and never actually measured any hormone levels, but just used proxies for hormonal influences, without direct evidence that the proxies were actually indicative of true hormone levels or imbalances. Twin studies showed that there likely are genetic influences for homosexuality, although similar studies have shown some genetic influences for homophobia and even opposition to abortion. Early childhood abuse has been associated with homosexuality, but, at most, only explains about 10% of those who express a homosexual orientation. The fact that sexual orientation is not constant for many individuals, but can change over time suggests that at least part of sexual orientation is actually sexual preference. Attempts to find a "gay gene" have never identified any gene or gene product that is actually associated with homosexual orientation, with studies failing to confirm early suggestions of linkage of homosexuality to region Xq28 on the X chromosome. The question of genetic influences on sexual orientation has been recently examined using DNA microarray technology, although, the results have largely failed to pinpoint any specific genes as a factor in sexual orientation.

La Gentica y la Homosexualidad: Nace la gente, homosexual?

http://www.godandscience.org/evolution/genetics_of_homosexuality.html Last updated November 25, 2013

Read the original here:
Are People Born Gay? Genetics and Homosexuality

Genetics

Background:

Homunculus in Sperm One question that has always intrigued us humans is Where did we come from? Long ago, Hippocrates and Aristotle proposed the idea of what they called pangenes, which they thought were tiny pieces of body parts. They thought that pangenes came together to make up the homunculus, a tiny pre-formed human that people thought grew into a baby. In the 1600s, the development of the microscope brought the discovery of eggs and sperm. Antonie van Leeuwenhoek, using a primitive microscope, thought he saw the homunculus curled up in a sperm cell. His followers believed that the homunculus was in the sperm, the father planted his seed, and the mother just incubated and nourished the homunculus so it grew into a baby. On the other hand, Regnier de Graaf and his followers thought that they saw the homunculus in the egg, and the presence of semen just somehow stimulated its growth. In the 1800s, a very novel, radical idea arose: both parents contribute to the new baby, but people (even Darwin, as he proposed his theory) still believed that these contributions were in the form of pangenes.

Modern genetics traces its beginnings to Gregor Mendel, an Austrian monk, who grew peas in a monastery garden. Mendel was unique among biologists of his time because he sought quantifiable data, and actually counted the results of his crosses. He published his findings in 1865, but at that time, people didnt know about mitosis and meiosis, so his conclusions seemed unbelievable, and his work was ignored until it was rediscovered in 1900 by a couple of botanists who were doing research on something else. Peas are an ideal organism for this type of research because they are easy to grow and it is easy to control mating.

We will be looking at the sorts of genetic crosses Mendel did, but first, it is necessary to introduce some terminology:

Monohybrid Cross and Probabilities:

A monohybrid cross is a genetic cross where only one gene/trait is being studied. P stands for the parental generation, while F1 and F2 stand for the first filial generation (the children) and second filial generation (the grandchildren). Each parent can give one chromosome of each pair, therefore one allele for each trait, to the offspring. Thus, when figuring out what kind(s) of gametes an individual can produce, it is necessary to choose one of the two alleles for each gene (which presents no problem if they are the same).

Purple Pea Flower White Pea Flower For example, a true-breeding purple-flowered plant (the dominant allele for this gene) would have the genotype PP, and be able to make gametes with either P or P alleles. A true-breeding white-flowered plant (the recessive allele for this gene) would have the genotype pp, and be able to make gametes with either p or p alleles. Note that both of these parent plants would be homozygous. If one gamete from each of these parents got together to form a new plant, that plant would receive a P allele from one parent and a p allele from the other parent, thus all of the F1 generation will be genotype Pp, they will be heterozygous, and since purple is dominant, they will look purple. What if two individuals from the F1 generation are crossed with each other (PpPp)? Since gametes contain one allele for each gene under consideration, each of these individuals could contribute either a P or a p in his/her gametes. Each of these gametes from each parent could pair with each from the other, thus yielding a number of possible combinations for the offspring. We need a way, then, to predict what the possible offspring might be. Actually, there are two ways of doing this. The first is to do a Punnett square (named after Reginald Crandall Punnett). The possible eggs from the female are listed down the left side, and there is one row for each possible egg. The possible sperm from the male are listed across the top, and there is one column for each possible sperm. The boxes at the intersections of these rows and columns show the possible offspring resulting from that sperm fertilizing that egg. The Punnett square from this cross would look like this:

Note that the chance of having a gamete with a P allele is and the chance of a gamete with a p allele is , so the chance of an egg with P and a sperm with P getting together to form an offspring that is PP is =, just like the probabilities involved tossing coins. Thus, the possible offspring include: PP, ( Pp + pP, which are the same (Pp), since P is dominant over p), so = Pp, and pp.

Another way to calculate this is to use a branching, tree diagram:

Here is the original post:
Genetics - biology

Male-pattern hair loss, also known as androgenic alopecia and male pattern baldness (MPB), is hair loss that occurs due to an underlying susceptibility of hair follicles to androgenic miniaturization. It is the most common cause of hair loss and will affect up to 70% of men and 40% of women at some point in their lifetimes. Men typically present with hairline recession at the temples and vertex balding, while women normally thin diffusely over the top of their scalps.[1][2][3] Both genetic and environmental factors play a role, and many etiologies remain unknown.

Classic androgenic hair loss in males begins above the temples and vertex, or calvaria, of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a 'Hippocratic wreath', and rarely progresses to complete baldness.[4] The Hamilton-Norwood scale has been developed to grade androgenic alopecia in males.

Female androgenic alopecia is known colloquially as "female pattern baldness", although its characteristics can also occur in males. It more often causes diffuse thinning without hairline recession; and, like its male counterpart, rarely leads to total hair loss.[5] The Ludwig scale grades severity of androgenic alopecia in females.

Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[6]chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss.[7][8]

Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction".[9] However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.[10]

Research indicates that the initial programming of pilosebaceous units begins in utero.[11] The physiology is primarily androgenic, with dihydrotestosterone (DHT) the major contributor at the dermal papillae. Below-normal values of sex hormone-binding globulin, follicle-stimulating hormone, testosterone, and epitestosterone are present in men with premature androgenic alopecia compared to normal controls.[12] Although follicles were previously thought permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitors from which the follicles arose.[13]

Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor at the dermal papillae, which is affected by DHT.[14]Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age,[15] androgens stimulate hair growth on the face, but suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[16]

These observations have led to study at the level of the mesenchymal dermal papillae.[17][18]Types 1 and 2 5 reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[19] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[16] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but stimulate TGF 1, TGF 2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[16] Hair follicles in anaphase express four different caspases. Tumor necrosis factor inhibits elongation of hair follicles in vitro with abnormal morphology and cell death in the bulb matrix.[20]

Studies of serum levels of IGF-1 show it to be increased with vertex balding.[21][22] Earlier work looking at in vitro administration of IGF had no effect on hair follicles when insulin was present, but when absent, caused follicle growth. The effects on hair of IGF-I were found to be greater than IGF-II.[23] Later work also showed IGF-1 signalling controls the hair growth cycle and differentiation of hair shafts,[14] possibly having an anti-apoptotic effect during the catagen phase.[24]In situ hybridization in adult human skin has shown morphogenic and mitogenic actions of IGF-1.[25] Mutations of the gene encoding IGF-1 result in shortened and morphologically bizarre hair growth and alopecia.[26] IGF-1 is modulated by IGF binding protein, which is produced in the dermal papilla.[27]

DHT inhibits IGF-1 at the dermal papillae.[28] Extracellular histones inhibit hair shaft elongation and promote regression of hair follicles by decreasing IGF and alkaline phosphatase in transgenic mice.[29] Silencing P-cadherin, a hair follicle protein at adherens junctions, decreases IGF-1, and increases TGF beta 2, although neutralizing TGF decreased catagenesis caused by loss of cadherin, suggesting additional molecular targets for therapy. P-cadherin mutants have short, sparse hair.[30]

See more here:
Male-pattern hair loss - Wikipedia, the free encyclopedia

Although there are a number of hair loss conditions that can affect men, the most common is Male Pattern Baldness (MPB). Other names for this condition are androgenetic alopecia and genetic hair loss. This page will concentrate primarily on this condition but will also make reference to the less widespread hair loss conditions that could be affecting you, with links to more informative pages.

Male Pattern Baldness is a genetic condition that can be passed down from either side of the family tree. So if your Father has a perfectly thick head of hair, dont think you are definitely safe (although you could be!). It is a condition caused by a bi-product of testosterone named Dihydrotestosterone, or DHT. DHT attaches to the hair follicles and causes them to shrink over time, which causes the hair to become thinner and thinner until some men become totally bald on the top of the head.

This is a very good question, and although the answer might seem obvious, many men do not identify their hair loss until it has become fairly advanced, which could be too late to achieve a full recovery. The reasons men do not identify their own hair loss are usually down to simple denial, or because the process is very slow and it is something that they simply might not notice. At the opposite end of the scale, many men worry about hair loss when they have no reason to worry.

The best ways to know if you are losing your hair are:

MPB is in fact easy to identify even for somebody with no clinical experience as it only affects hair on the top of the scalp and not the sides, causing a horseshoe-shaped pattern of hair loss. There are a number of different common patterns of hair loss a receding hairline, a thinning crown, or general thinning spread over the top area of the head. You can read more about these below. MPB never affects the sides or back of the hair.

There are a number of options available for treating Male Pattern Baldness, including clinically proven medications, laser devices and hair restoration surgery. There are also numerous products out there that have no clinical efficacy, so it is easy to waste time and money whilst your hair continues to shed. It is therefore very important that you carry out the necessary research before deciding how you are going to treat your hair loss. The good news is that unless you have lost all or most of your hair, there is a solution out there for you, whether it be a medical solution, a surgical one, or a combination of the two.

Our comprehensive hair loss treatment guide walks you through all the most effective options available for treating hair loss and also gives you an in-depth look at the products that may not be worth using.

hair loss treatment guide

This depends on a number of factors. Firstly, the condition causing your hair loss if you have a temporary hair loss condition (which is unusual in men) then the answer may be no. Please refer to our list of other hair loss conditions below if your problem doesnt appear to be MPB.

Assuming your condition is Male Pattern Baldness, the extent of your eventual hair loss really depends. Those men who have a very early or aggressive onset of MPB are more likely to lose their hair more extensively or at a faster rate, which could result in baldness at an early age. We see men who begin to lose their hair at 18 years old (or sometimes earlier). These men will of course be the ones most likely to reach eventual baldness, sometimes at a fairly early age (mid-twenties). Whereas some men only begin to see signs of thinning in their mid-to-late twenties, or even later. These men are much less likely to experience eventual baldness and may just have thin hair by the time they reach old age.

Read more here:
Male Hair Loss All You Need To Know - The Belgravia Centre

Your Expert in Male Fertility & Sexual Health

High technology approaches to fertility, including ICSI, are really a two edged sword: they allow us to treat severe male infertility, but they may alter natural selection in that decisions regarding sperm and eggs are made in the laboratory and not by nature.

Dr. Paul Turek

Among the 15% of couples who experience infertility, about 40% of the time the infertility is due to male factors. About half of male infertility cases are due to defined reasons, including varicocele, infection, hormone imbalances, exposures such as drugs or medications, x-rays, tobacco use and hot tubs, blockage of the reproductive tract ducts, and previous surgery that has left scarring. Another cause of male infertility that has been underestimated in the past, but is now gaining in importance is genetic infertility. The reason for its increased importance is that our knowledge about genetics is growing so quickly. Men who may have had unexplained infertility in the past may now be diagnosed with genetic causes of infertility through recently available testing. In fact, this field is progressing so quickly that genetic infertility has already become one of the most commonly diagnosed reasons for male infertility.

Developed in the early 1990s, assisted reproduction in the form of IVF and ICSI (intracytoplasmic sperm injection) is a revolutionary laboratory technique in which a single sperm is placed directly inside an egg for fertilization. This technique has opened the door to fertility for men who formerly had few available treatment options, as it allows men who were previously considered severely infertile or sterile the possibility of fatherhood. However, with ICSI sperm are chosen by laboratory technicians and not by nature and because of this, it is not clear what barriers to natural selection are altered. Thus, along with this technology comes the possibility of passing on to a child certain genetic issues that may have caused the fathers infertility, or even more severe conditions. Another reason to know whether male

Infertility is genetic or not is because classic treatments such as varicocele repair or medications given to improve male infertility. In fact, Dr Turek was one of the first to publish on this issue, showing that varicocele repair was not effective in improving fertility in men with genetic infertility. Because he recognized these issues early on, Dr. Turek, while at UCSF in 1997, founded the first formal genetic counseling and testing program for infertility in the U.S. Called the Program in the Genetics of Infertility (PROGENI), Dr. Tureks program has helped over 2000 patients at risk for genetic infertility to navigate the decision-making waters that surround this condition.

Men with infertility should be seen by a urologist for a thorough medical history, physical examination, and appropriate medical testing. If genetic infertility is a possibility, then a genetic counselor can help couples understand the possible reasons, offer appropriate genetic testing, and discuss the complex emotional and medical implications of the test results. The approach taken early on by Dr. Turek is outlined in Figure 1. Just like the medical diagnosis from a urologist or fertility specialist, information about family history plays a critical role in genetic risk assessment. This approach to genetic evaluation, termed non-prescriptive, has been the corner- stone of Dr. Tureks critically acclaimed clinical program that now has over a dozen publications contributing to our current knowledge in the field. It is important to note that a lack of family history of infertility or other medical problems does not eliminate or reduce the risk of genetic infertility. In fact, a family history review will often be unremarkable. However, family history can provide crucial supporting in- formation toward making a genetic diagnosis (such as a family history of recurrent miscarriages or babies born with problems). Dr. Turek has published that having a genetic counselor obtain family history information is much more accurate than simply giving patients a written questionnaire to fill out and bring to their visit. A genetic counselor can also discuss appropriate genetic testing options and review the test results in patients in a meaningful way.

When speaking to Dr. Tureks genetic counselor about genetic testing, keep in mind that he or she will not tell you what to do. Genetic counselors are trained to provide information, address questions and concerns, and support you in the decision making process. A genetic counselor does not assume which decisions are most appropriate for you.

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The Genetics of Male Infertility - The Turek Clinic

Genetic Components of Sex and Gender

Humans are born with 46 chromosomes in 23 pairs. The X and Y chromosomes determine a persons sex. Most women are 46XX and most men are 46XY. Research suggests, however, that in a few births per thousand some individuals will be born with a single sex chromosome (45X or 45Y) (sex monosomies) and some with three or more sex chromosomes (47XXX, 47XYY or 47XXY, etc.) (sex polysomies). In addition, some males are born 46XX due to the translocation of a tiny section of the sex determining region of the Y chromosome. Similarly some females are also born 46XY due to mutations in the Y chromosome. Clearly, there are not only females who are XX and males who are XY, but rather, there is a range of chromosome complements, hormone balances, and phenotypic variations that determine sex.

The biological differences between men and women result from two processes: sex determination and differentiation.(3) The biological process of sex determination controls whether the male or female sexual differentiation pathway will be followed. The process of biological sex differentiation (development of a given sex) involves many genetically regulated, hierarchical developmental steps. More than 95% of the Y chromosome is male-specific (4) and a single copy of the Y chromosome is able to induce testicular differentiation of the embryonic gonad. The Y chromosome acts as a dominant inducer of male phenotype and individuals having four X chromosomes and one Y chromosome (49XXXXY) are phenotypically male. (5) When a Y chromosome is present, early embryonic testes develop around the 10th week of pregnancy. In the absence of both a Y chromosome and the influence of a testis-determining factor (TDF), ovaries develop.

Gender, typically described in terms of masculinity and femininity, is a social construction that varies across different cultures and over time. (6) There are a number of cultures, for example, in which greater gender diversity exists and sex and gender are not always neatly divided along binary lines such as male and female or homosexual and heterosexual. The Berdache in North America, the faafafine (Samoan for the way of a woman) in the Pacific, and the kathoey in Thailand are all examples of different gender categories that differ from the traditional Western division of people into males and females. Further, among certain North American native communities, gender is seen more in terms of a continuum than categories, with special acknowledgement of two-spirited people who encompass both masculine and feminine qualities and characteristics. It is apparent, then, that different cultures have taken different approaches to creating gender distinctions, with more or less recognition of fluidity and complexity of gender.

Sex Chromosome Abnormalities Turner syndrome XXX Females Klinefelter Syndrome XYY Males

Typical sexual development is the result of numerous genes, and mutation in any of these genes can result in partial or complete failure of sex differentiation. These include mutations or structural anomalies of the SRY region on the Y chromosome resulting in XY gonadal dysgenesis, XX males, or XY females; defects of androgen biosynthesis or androgen receptors, and others.

Hermaphroditism Congenital Adrenal Hyperplasia Androgen Insensitivity Syndrome

The issues of gender assignment, gender verification testing, and legal definitions of gender are especially pertinent to a discussion on the ELSI of gender and genetics. These practices, however, are misnomers as they actually refer to biological sex and not gender. Such a discrepancy is highlighted by the existence of intersex individuals whose psychosexual development and gender sometimes do not match the biological sex assigned to them as infants. In this report the term sex will be used where the practice refers to biological sex and not the more social construct of gender.

Gender Assignment of Intersex Infants and Children Legal Definitions of Gender

Chromosomes are the structures that carry genes which in turn transmit hereditary characteristics from parents to offspring. Humans have 23 pairs of chromosomes, one half of each pair inherited from each parent. The Y chromosome is small, carries few genes, and has abundant repetitive sequence, while the X chromosome is more autosome-like in form and content. (14)Despite being relatively gene-poor overall due to reduced recombination, the X and Y sex chromosomes are enriched for genes that relate to sexual development. (15)

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WHO | Gender and Genetics

A male () organism is the physiological sex that produces sperm. Each spermatozoon can fuse with a larger female gamete, or ovum, in the process of fertilization. A male cannot reproduce sexually without access to at least one ovum from a female, but some organisms can reproduce both sexually and asexually. Most male mammals, including male humans, have a Y chromosome, which codes for the production of larger amounts of testosterone to develop male reproductive organs.

Not all species share a common sex-determination system. In most animals, including humans, sex is determined genetically, but in some species it can be determined due to social, environmental or other factors. For example, Cymothoa exigua changes sex depending on the number of females present in the vicinity. [1]

The existence of two sexes seems to have been selected independently across different evolutionary lineages (see Convergent Evolution). The repeated pattern is sexual reproduction in isogamous species with two or more mating types with gametes of identical form and behavior (but different at the molecular level) to anisogamous species with gametes of male and female types to oogamous species in which the female gamete is very much larger than the male and has no ability to move. There is a good argument that this pattern was driven by the physical constraints on the mechanisms by which two gametes get together as required for sexual reproduction.[2]

Accordingly, sex is defined operationally across species by the type of gametes produced (i.e.: spermatozoa vs. ova) and differences between males and females in one lineage are not always predictive of differences in another.

Male/female dimorphism between organisms or reproductive organs of different sexes is not limited to animals; male gametes are produced by chytrids, diatoms and land plants, among others. In land plants, female and male designate not only the female and male gamete-producing organisms and structures but also the structures of the sporophytes that give rise to male and female plants.

A common symbol used to represent the male sex is the Mars symbol, (Unicode: U+2642 Alt codes: Alt+11)a circle with an arrow pointing northeast. The symbol is identical to the planetary symbol of Mars. It was first used to denote sex by Carolus Linnaeus in 1751. The symbol is often called a stylized representation of the Roman god Mars' shield and spear. According to Stearn, however, all the historical evidence favours that it is derived from , the contraction of the Greek name for the planet, Thouros.[3]

The sex of a particular organism may be determined by a number of factors. These may be genetic or environmental, or may naturally change during the course of an organism's life. Although most species with male and female sexes have individuals that are either male or female, hermaphroditic animals, such as worms, have both male and female reproductive organs.

Most mammals, including humans, are genetically determined as such by the XY sex-determination system where males have an XY (as opposed to XX) sex chromosome. It is also possible in a variety of species, including human beings, to be XXY or have other intersex/hermaphroditic qualities. These qualities are widely reported to be as common as redheadedness (about 2% of the population).[4] During reproduction, a male can give either an X sperm or a Y sperm, while a female can only give an X egg. A Y sperm and an X egg produce a male, while an X sperm and an X egg produce a female.

The part of the Y-chromosome which is responsible for maleness is the sex-determining region of the Y-chromosome, the SRY. The SRY activates Sox9, which forms feedforward loops with FGF9 and PGD2 in the gonads, allowing the levels of these genes to stay high enough in order to cause male development;[5] for example, Fgf9 is responsible for development of the spermatic cords and the multiplication of Sertoli cells, both of which are crucial to male sexual development.[6]

The ZW sex-determination system, where males have a ZZ (as opposed to ZW) sex chromosome may be found in birds and some insects (mostly butterflies and moths) and other organisms. Members of the insect order Hymenoptera, such as ants and bees, are often determined by haplodiploidy, where most males are haploid and females and some sterile males are diploid.[citation needed]

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Male - Wikipedia, the free encyclopedia

-A curious adult from California

August 6, 2004

What a fun question! This sort of thing has been bothering me too lately. The usual statistic is that all people are 99.9% the same. But is that true for men and women?

And what about our similarity to other animals? We are really only about 80% the same as a mouse at the genetic level so men and women are clearly more similar to each other than to mice. But what about chimpanzees? If people really are 98.7% the same as a chimpanzee, are male chimpanzees closer genetically to men than men are to women?

As you know, men have an X and a Y chromosome and women have two X chromosomes. So besides the usual 0.1% (or 3.2 million base pair) difference between people, men and women differ by the presence of the Y chromosome.

The Y chromosome is a tiny thing; it is about 59 million base pairs long and has only 78 genes. If we look at base pairs, the difference between men and women would be 59 million divided by 3.2 billion or about 1.8%. This translates to men and women being 98.2% the same.

Men and women are actually a bit more similar as the Y chromosome has about 5% of its DNA sequences in common with the X chromosome. This would change the number to 98.4% the same.

If the 98.7% number for chimp-human similarity is right, then by this measure, men and women are less alike than are female chimps and women. (More recent data suggests that chimps may be 95% instead of 98.7% the same, but this is still up in the air.)

Now if we look at the gene level instead of at the base pair level, men and women become much more similar. If we assume 30,000 total genes, then men and women are about 99.7% the same instead of 98.4%. (I haven't been able to find a good number for how many genes chimpanzees and humans share.)

So is the bottom line that men and male chimps have more in common than men and women? Of course not. If we take a closer look, we see some of the dangers of looking at raw percentages instead of individual changes.

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Understanding Genetics

Member Type: Silver Member Age: 39 Location: Mexico City Juarez, Mexico Orientation: Straight (Genetic Male ) Listed As: Girl (M2F) Looking For: Friends, Genetic Female (GG), Girls (MtoF) Last Active: May 20th, 2015 Joined: Jul 18th, 2007 About Me

Hello everyone!

It is proven that having too much information in your profile is not an effective way to meet people LOL.

So I think that now I would rather say: "Please ask if you want to know".

I consider myself a big fan of everything feminine, and in a certain way I feel empathic towards anyone who shares this passion with me.

I'm not into kinky stuff such as having cybersex, sex-cams, phone, etc. Of course I prefer to talk with people that have complete profiles but I do understand why some people needs to remain anonymous.

Please check out my Facebook profile. I will add you if you happen to have a complete profile too 😉

http://www.facebook.com/profile.php?id=1317181520

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Lynda

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URNotAlone Profile for Lynda Flores, Genetic Male Straight ...

Androgenic alopecia (also known as androgenetic alopecia, alopecia androgenetica, or male pattern baldness) is hair loss that occurs due to an underlying susceptibility of hair follicles to androgenic miniaturization. It is the most common cause of hair loss and will affect up to 70% of men and 40% of women at some point in their lifetimes. Men typically present with hairline recession at the temples and vertex balding, while women normally thin diffusely over the top of their scalps.[1][2][3] Both genetic and environmental factors play a role, and many etiologies remain unknown.

Classic androgenic hair loss in males begins above the temples and vertex, or calvaria, of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a 'Hippocratic wreath', and rarely progresses to complete baldness.[4] The Hamilton-Norwood scale has been developed to grade androgenic alopecia in males.

Female androgenic alopecia is known colloquially as "female pattern baldness", although its characteristics can also occur in males. It more often causes diffuse thinning without hairline recession; and, like its male counterpart, rarely leads to total hair loss.[5] The Ludwig scale grades severity of androgenic alopecia in females.

Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[6]chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss.[7][8]

Research indicates that the initial programming of pilosebaceous units begins in utero.[9] The physiology is primarily androgenic, with dihydrotestosterone (DHT) the major contributor at the dermal papillae. Below-normal values of sex hormone-binding globulin , follicle-stimulating hormone , testosterone, and epitestosterone are present in men with premature androgenic alopecia compared to normal controls.[10] Although follicles were previously thought permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitors from which the follicles arose.[11]

Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor at the dermal papillae, which is affected by DHT.[12]Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age,[13] androgens stimulate hair growth on the face, but suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[14]

These observations have led to study at the level of the mesenchymal dermal papillae.[15][16]Types 1 and 2 5 reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[17] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[14] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but stimulate TGF 1, TGF 2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[14] Hair follicles in anaphase express four different caspases. Tumor necrosis factor inhibits elongation of hair follicles in vitro with abnormal morphology and cell death in the bulb matrix.[18]

Studies of serum levels of IGF-1 show it to be increased with vertex balding.[19][20] Earlier work looking at in vitro administration of IGF had no effect on hair follicles when insulin was present, but when absent, caused follicle growth. The effects on hair of IGF-I were found to be greater than IGF-II.[21] Later work also showed IGF-1 signalling controls the hair growth cycle and differentiation of hair shafts,[12] possibly having an anti-apoptotic effect during the catagen phase.[22]In situ hybridization in adult human skin has shown morphogenic and mitogenic actions of IGF-1.[23] Mutations of the gene encoding IGF-1 result in shortened and morphologically bizarre hair growth and alopecia.[24] IGF-1 is modulated by IGF binding protein, which is produced in the dermal papilla.[25]

DHT inhibits IGF-1 at the dermal papillae.[26] Extracellular histones inhibit hair shaft elongation and promote regression of hair follicles by decreasing IGF and alkaline phosphatase in transgenic mice.[27] Silencing P-cadherin, a hair follicle protein at adherens junctions, decreases IGF-1, and increases TGF beta 2, although neutralizing TGF decreased catagenesis caused by loss of cadherin, suggesting additional molecular targets for therapy. P-cadherin mutants have short, sparse hair.[28]

At the occipital scalp, androgens enhance inducible nitric oxide synthase (iNOS), which catalyzes production of nitric oxide from L-arginine.[14] The induction of iNOS usually occurs in an oxidative environment, where the high levels of nitric oxide produced interact with superoxide, leading to peroxynitrite formation and cell toxicity. iNOS has been suggested to play a role in host immunity by participating in antimicrobial and antitumor activities as part of the oxidative burst[29] of macrophages.[30] The gene coding for nitric oxide synthase is on human chromosome 17.[31]

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Androgenic alopecia - Wikipedia, the free encyclopedia

Sex-Linked Traits in Bird Genetics

Understanding the ZZ/ZW sex chromosome system is important for people who breed birds, whether the interest is in chicken genetics, parrot genetics, or some other type of bird. The way sex-linked traits are inherited is opposite to the way they are inherited by humans and other mammals.

For example, in cockatiels, budgerigars (parakeets), lovebirds, and other small parrots, the lutino color mutation is a sex-linked recessive trait. Lutino birds lack the dark pigment melanin, which is responsible for black, gray, and blue coloration in birds. As a result, lutino birds appear to have significant yellow coloration, which would ordinarily be covered up by melanin.

The lutino gene is located on the Z chromosome. Since lutino females have only one Z chromosome, they will pass this chromosome down to all their sons (remember male birds are ZZ), but not to their daughters (female birds are ZW and get the Z chromosome from their fathers).

A male bird will be lutino only if his father has the gene and his mother has the mutation as well. With a non-lutino mother, a male that inherits lutino from his father will be a heterozygous carrier, but will not have a lutino phenotype. A lutino-colored male must be homozygous, since the trait is recessive. In this situation all his daughters will be lutino-colored and all his sons will be carriers.

For a non-lutino carrier male (heterozygous), each daughter has a 50% chance of being lutino, and each son has a 50% chance of being a carrier.

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Difference Between Male and Female BirdsGenetics and ...

The development of in vitro fertilitzation (IVF) has allowed many couples to have the families they might otherwise have been unable to create independently. At the same time, this technology has allowed researchers to study the genetic make-up of the earliest stages of embryos. These advances are providing insights into the link between genetics and infertility and how defects (mutations) in specific genes may result in male or female infertility.It is possible that many cases of unexplained infertility will one day be found to have a clear genetic basis.

What has been learned in the last two decades of assisted reproduction is that some cases of severe male factor infertility are clearly related to gene deletions, mutations or chromosomal abnormalities.

Some men with very severe male factor infertility will be found, upon testing their blood chromosomes (known as a karyotype) to have an extra X chromosome. That is, instead of having a 46 XY karyotype, they have a 47 XXY karyotype. This condition is known as Klinefelter Syndrome and can result in failure to achieve puberty or even when puberty is achieved, these men often have male infertility. Some men with Klinefelter Syndrome can father pregnancies through the use of in vitro fertilitzation (IVF) with Intra-Cytoplasmic Sperm injection (ICSI).So far, we are not seeing an increased risk of Klinefelter Syndrome or other chromosome abnormalities in the offspring achieved in these cases.

Also discovered in recent years is that some men with very severe low sperm counts will be found to have deletions in a certain part of their Y chromosome, known as the DAZ gene. Their karyotype is normal (46 XY) but close inspection of the Y chromosome shows there are sections of the chromosome that are missing. A portion of these men will have no recoverable sperm in the ejaculate or on testicular surgery and donor sperm is the only option. With other deletions in the DAZ gene, there is a small amount of sperm present and conception with IVF-ICSI is possible. In these cases, the male offspring which will always inherit their fathers Y chromosome, will also have this deletion, and will themselves be infertile.

A single gene mutation in the gene for Cystic Fibrosis (CF) is associated with absence of the part of the tube (the vas deferens) that leads from the testicle to the urethra in the penis. These men are usually carriers for the CF gene mutation and do not themselves have the disease of Cystic Fibrosis. Sperm can be recovered from the testicles in these men to be used for IVF with ICSI but it is imperative that their wife (or egg provider) be fully tested for CF mutations as well, otherwise there is significant risk of having a child with Cystic Fibrosis.

For men with sperm counts routinely in the less than 5 million total motile sperm range, testing for genetic conditions is warranted so that these men or couples can be made aware of the genetic issues and how these issues might affect their offspring.

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Male Infertility | Genetic Abnormalities or Male ...

Male infertility refers to a male's inability to cause pregnancy in a fertile female. In humans it accounts for 40-50% of infertility.[1][2][3] It affects approximately 7% of all men.[4] Male infertility is commonly due to deficiencies in the semen, and semen quality is used as a surrogate measure of male fecundity.[5]

Factors relating to male infertility include:[6]

Pre-testicular factors refer to conditions that impede adequate support of the testes and include situations of poor hormonal support and poor general health including:

Male smokers also have approximately 30% higher odds of infertility.[9][not in citation given] There is increasing evidence that the harmful products of tobacco smoking kill sperm cells.[10][11] Therefore, some governments require manufacturers to put warnings on packets. Smoking tobacco increases intake of cadmium, because the tobacco plant absorbs the metal. Cadmium, being chemically similar to zinc, may replace zinc in the DNA polymerase, which plays a critical role in sperm production. Zinc replaced by cadmium in DNA polymerase can be particularly damaging to the testes.[12]

Common inherited variants in genes that encode enzymes employed in DNA mismatch repair are associated with increased risk of sperm DNA damage and male infertility.[13] As men age there is a consistent decline in semen quality, and this decline appears to be due to DNA damage.[14] (Silva et al., 2012). These findings suggest that DNA damage is an important factor in male infertility.

Testicular factors refer to conditions where the testes produce semen of low quantity and/or poor quality despite adequate hormonal support and include:

Radiation therapy to a testis decreases its function, but infertility can efficiently be avoided by avoiding radiation to both testes.[20]

Post-testicular factors decrease male fertility due to conditions that affect the male genital system after testicular sperm production and include defects of the genital tract as well as problems in ejaculation:

The diagnosis of infertility begins with a medical history and physical exam by a physician or nurse practitioner. Typically two separate semen analyses will be required. The provider may order blood tests to look for hormone imbalances, medical conditions, or genetic issues.

The history should include prior testicular or penile insults (torsion, cryptorchidism, trauma), infections (mumps orchitis, epididymitis), environmental factors, excessive heat, radiation, medications, and drug use (anabolic steroids, alcohol, smoking).

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Male infertility - Wikipedia, the free encyclopedia

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Size Genetics - Male Enhancement Reviews

This article is merely an attempt to find the scientific reasoning behind the origins of the ancient Gotra System and in no way endorses its imposition in the modern Hindu society to decide marriages or other things. In all probabilities, the modern Gotra system is no more relevant, and the best method to verify the genetic feasibility of a marriage, if at all required, would be to avoid cousin marriages (which have been proved to increase the risk of genetic disorders in the off springs) or to do a genetic test of the bride and grooms DNA for any possible genetic disorders in their off springs.

The Gotra is a system which associates a person with his most ancient or root ancestor in an unbroken male lineage. For instance if a person says that he belongs to the Bharadwaja Gotra then it means that he traces back his male ancestry to the ancient Rishi (Saint or Seer) Bharadwaja. So Gotra refers to the Root Person in a persons male lineage.

The Gotra system is practiced amongst most Hindus. See here for a List of Hindu Gotras practiced by different sections of the Hindu Society

Brahmins identify their male lineage by considering themselves to be the descendants of the 8 great Rishis ie Saptarshis (The Seven Sacred Saints) + Bharadwaja Rishi. So the list of root Brahmin Gotras is as follows

These 8 Rishis are called Gotrakarin meaning roots of Gotras. All other Brahmin Gotras evolved from one of the above Gotras. What this means is that the descendants of these Rishis over time started their own Gotras. The total number of established Gotras today is 49. However each of them finally trace back to one of the root Gotrakarin Rishi.

The word Gotra is formed from the two Sanskrit words Gau (meaning Cow) and Trahi (meaning Shed). Note that the English word Cow is a derived word of the Sanskrit word Gau with the same meaning Gau.

So Gotra means Cowshed, where in the context is that Gotra is like the Cowshed protecting a particular male lineage. Cows are extremely important sacred animals to Hindus and there were a large number of best breeds of Cows that ancient Hindus reared and worshipped, and hence the name Gotra referring to the system of maintaining individual male lineages seems more appropriate.

This Gotra system helps one identify his male lineage and is passed down automatically from Father to Son. But the Gotra system does not get automatically passed down from Father to Daughter. Suppose a person with Gotra Angirasa has a Son. Now suppose the Son gets married to a girl whose father belongs to Gotra Kashyapa. The Gotra of the girl automatically is said to become Angirasa after her marriage even though her father belonged to Gotra Kashyapa.

So the rule of the Gotra system is that the Gotra of men remains the same, while the Gotra of the woman becomes the Gotra of their husband after marriage. Now suppose a person has only daughters and no sons. In that case his Gotra will end with him in that lineage because his daughters will belong to the Gotras of their husbands after their marriage!

This was probably the reason why in the ancient vedic or hindu societies it was preferred to have atleast one Son along with any number of daughters, so that the Gotra of the father could continue.

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HitXP Science of Genetics behind the Hindu Gotra System ...