Further Evidence Genetics Has Role in Determining Sexual Orientation in Men

Canadian scientists have uncovered new evidence which shows genetics has a role to play in determining whether an individual is homosexual or heterosexual.

The research was conducted by Dr. Sandra Witelson, a neuroscientist in the Michael G. DeGroote School of Medicine at McMaster University, and colleagues at Sunnybrook Health Sciences Centre in Toronto who studied the brains of healthy, right-handed, 18- to 35-year-old homosexual and heterosexual men using structural Magnetic Resonance Imaging (MRI).

About 10 years ago, Witelson and Dr. Cheryl McCormick, then a student of Witelson’s, demonstrated there is a higher proportion of left-handers in the homosexual population than in the general population – a result replicated in subsequent studies which is now accepted as fact.
Handedness is a sign of how the brain is organized to represent different aspects of intelligence. Language, for example, is usually on the left - music on the right.

In other research, Witelson and research associate Debra Kigar, had found that left-handers have a larger region of the posterior corpus callosum – the thick band of nerve fibers connecting the two hemispheres of the brain – than right handers.

This raised the hypothesis for the current study – whether the anatomy of the brain of the sub-group of right-handed homosexual men is similar to that of left-handers.

They found that the posterior part of the corpus callosum is larger in homosexual than heterosexual men.

The size of the corpus callosum is largely inherited suggesting a genetic factor in sexual orientation, says Witelson. “Our results do not mean that heredity is destiny but they do indicate that environment is not the only player in the field,” she says.

While this is not a litmus test for sexual orientation, Witelson said this finding could prove to be one additional valuable piece of information for physicians and individuals who are trying to determine their sexual orientation. “Sometimes people aren’t sure of their sexual orientation.”

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Gene Responsible for Common Hearing Loss Identified for 1st Time

A gene responsible for the single most common cause of hearing loss among white adults, otosclerosis, has been identified for the first time, a scientist told the annual conference of the European Society of Human Genetics in Nice, France. Melissa Thys, from the Department of Medical Genetics, University of Antwerp, Belgium, says that this finding may be a step towards new treatments for otosclerosis, which affects approximately 1 in 250 people.

Otosclerosis is a multifactorial disease, caused by an interaction of genetic and environmental factors. The outcome is a progressive hearing loss as the growing bone in the middle ear interrupts the sound waves passing to the inner ear. While the causative factors remain unknown, now one of the genetic components has been identified, Thys told the conference.

“The gene in which the variant is located points to a pathway that contributes to the disease. This may be a lead for better forms of treatment in the future; currently the best option is an operation. However, there is often an additional component of hearing loss which can’t be restored by surgery. As the gene involved is a growth factor, and the disease manifests itself by the abnormal growth of bone in the middle ear, it may have a large potential for therapy”, she said. Improved understanding may also lead to prevention strategies.

Thys and her team decided to study a gene called TGBF1 which they already knew had non-genetic indications of involvement in otosclerosis: it plays a role during embryonic development of the ear and is expressed in otosclerotic bone. They used SNP (single nucleotide polymorphism) analysis, or looking at DNA sequence variations occurring in a single nucleotide, A, T, C or G, to study a large patient and control population from Belgium and The Netherlands.

They found significant results for an amino acid changing SNP inTGBF1, and that this remained
significant after correcting for multiple testing. Analysis of a large French group showed the same association.

“Combining the data from both groups with a common odds ratio gave a very significant result, from which we were able to conclude that we were the first to identify a gene that influences the susceptibility for otosclerosis”, says Thys. “And, as further evidence, we were also able to show that a more active variant of this gene is protective against the disease.”

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Studies Identify DNA Regions Linked to Nicotine Dependence

Americans are bombarded with antismoking messages, yet at least 65 million continue to light up. Genetic factors play an important role in this continuing addiction to cigarettes, suggest scientists at Washington University School of Medicine in St. Louis.

In two studies in the January 2007 issue of Human Molecular Genetics, the scientists show that certain genetic variations can influence smoking behaviors and contribute to a person's risk for nicotine dependence.

The smoking-related genes identified normally facilitate communication between nerve cells in the brain. One gene in particular, the alpha-5 nicotinic cholinergic receptor (CHRNA5) gene, was a very strong indicator of risk for nicotine dependence. Individuals with a specific variation in the gene seemed to have a two-fold increase of developing nicotine dependence once exposed to cigarette smoking. CHRNA5 is from a class of receptors that plays a role in dopamine pathways in the brain, which are linked to a person's experience of pleasure.

The researchers also identified genes related to gamma aminobutyric acid (GABA) receptors, another set of proteins vital to nerve cell function. Both GABA and nicotinic receptors had been suspected of involvement in nicotine addiction, but these findings strengthen those suspicions.

The studies also identified a gene not previously known to be involved with nicotine dependence. Called the Neurexin 1 (NRXN1) gene, it helps regulate the balance between excitatory mechanisms — those that increase communication between nerve cells — and inhibitory mechanisms — those that slow firing between nerve cells.

"An imbalance between excitatory and inhibitory activity in the brain may predispose people to addiction, such as alcoholism, drug dependence or nicotine dependence," says Laura Jean Bierut, M.D., associate professor of psychiatry and principal investigator of both studies. "The Neurexin gene we've identified is really a key factor in the balance between inhibition and excitatory activity in neurons."

Bierut suspects a large number of genes are involved in nicotine dependence, and she says understanding how they work may make it possible to develop new treatments for smoking cessation.

The research team analyzed data from almost 2,000 participants in two ongoing studies. One, called the Collaborative Genetic Study of Nicotine Dependence, is a U.S.-based sample that includes both addicted smokers and "social" smokers from St. Louis, Minneapolis and Detroit. The other is an Australian study of smokers of European ancestry called the Nicotine Addiction Genetics study.

The scientists combined two approaches for analyzing genetic information. One approach scanned the entire human genome for suspicious areas of DNA while the second approach closely examined specific target genes.

"The combination of these two approaches represents the most powerful and extensive study on nicotine dependence to date and is an important step in a large-scale, genetic examination of nicotine dependence," says Elias A. Zerhouni, M.D., the director of the National Institutes of Health, which funded the studies. "As more genomic variations are discovered that are associated with substance abuse, we can better understand addictive disorders."

The researchers identified an area of DNA variation that seems to alter the function of a nicotinic receptor protein. That small variation makes a big difference in risk for nicotine dependence.

Current drug treatments for nicotine dependence continue to be only marginally successful, and Bierut believes using information about genetic traits to tailor medications to individuals could make them significantly more effective. "The type of variant you have at this particular receptor — the alpha-5 nicotinic receptor — may actually predict whether or not you will do well on nicotine replacement therapy," she says.

<---Anyone who's been or is a smoker, knows how hard it is to quit cigarettes. Even after we hear again and agian the risk of lung cancer for some reason we pick up a cigarette, ignoring the cancer statistics. Smokefree seems far away. But eventually, there is a point when quitting smoking makes the most sense.The effect of smoking takes too much of a toll.--->

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Researchers 1st To Map Gene That Regulates Adult Stem Cell Growth

A new discovery in stem cell research may mean big things for cancer patients in the future. Gary Van Zant, Ph.D., and a research team at the University of Kentucky published their findings in Nature Genetics, an international scientific journal.

The researchers genetically mapped a stem cell gene and its protein product, Laxetin, and building on that effort, carried the investigation all the way through to the identification of the gene itself. This is the first time such a complete study on a stem cell gene has been carried out. This particular gene is important because it helps regulate the number of adult stem cells in the body, particularly in bone marrow. Now that it has been identified, researchers hope the gene, along with its protein product Latexin, can be used clinically, such as for ramping up the stem cell count in cancer patients undergoing chemotherapy and bone marrow transplantation.

The researchers agreed that this very process is not only interesting, but important because of its usefulness in a wide variety of future genetics studies.

"We're thinking about cancer in a big way," Van Zant says. "This is a great example of translational research – from the most basic type of genetic research all the way to possible treatments for patients."

One big obstacle chemotherapy patients face is stem cell loss after treatments. This limits the dosage amount and types of chemotherapy that can be given. But if Latexin were used to increase the stem cell count, patients would be able to receive increased doses of chemotherapy and be able to recover more quickly. Increased stem cell counts also would be valuable during bone marrow transplants, where the greatest number of stem cells are desired to help a patient recover from cancer.

Another possible use for Latexin would be to help increase the number of stem cells available in umbilical cord blood, which also is used to transplant healthy stem cells in blood marrow transplants. Currently, stem cell transplants with cord blood can only be used in children because cord blood does not contain enough stem cells for an amount needed to be transplanted into an adult.

The only stem cell population that has been examined for effects of Latexin to date is in bone marrow. Van Zant says it is possible, even probable, that other stem cell populations in tissues such as the liver, skin, pancreas or brain may be similarly affected by Latexin. This could open up new therapeutic strategies such as using stem cells for the treatment of other diseases and conditions such as liver disease, diabetes and central nervous system damage as a result of trauma or stroke.

The researchers also are looking into the possible role the gene plays in transforming healthy stem cells into cancerous ones, such as in leukemia and lymphomas. If the gene does in fact play such a role, it is possible that it also could provide the keys to new therapies.

Van Zant describes his discovery as an elation. He worked on the project for six years with Ying Liang, a former graduate student who is now a postdoctoral fellow at UK. Van Zant says this research and publication of the journal article is the culmination of a difficult but rewarding scientific journey.

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Newsweek: Genome Sequencing Begins To Payoff

Three years after scientists announced they had sequenced the human genome, new knowledge about how our genesaffect our health is transforming the way diseases are understood, diagnosed, treated-and even predicted, reports Newsweek senior writer Claudia Kalbin.

Newsweek's latest installment of its ongoing "Health for Life" series,"What's Next in Medicine" is in the December 11 issue, on newsstands Monday, December 4.

Today gene tests are available for more than 1,300 diseases, including cystic fibrosis and hemophilia. And now, as genetic screening gets cheaper and faster, researchers are hunting down the biological underpinnings of more-complex disorders that involve multiple genes-big,rampaging illnesses that strike millions of Americans every year. On the list: type 2 diabetes, Alzheimer's, heart disease and depression.

If the scientists are right, genetic tests for some of these diseases could beavailable by 2010. "We are on the leading edge of a genuine revolution,"says Dr. Francis Collins, head of the National Human Genome Research Institute.

The gene tests currently offered for certain diseases, like breast andcolon cancer, affect only a small percentage of total cases. But the impacton a single life can be huge. The key: being able to do something to ward off disease. "Genetic testing offers us profound insight," says Dr. Stephen Gruber, of the University of Michigan. "But it has to be balanced with ourability to care for these patients."

For example, the risk of breast and ovarian cancers in people with BRCA mutations can be reduced by frequent screening and radical surgery. Having healthy breasts or ovaries removed isn't easy, but the payoff--an end to constant anxiety and a pre-emptivestrike at disease--can be well worth it.

"Most women I've met who've had prophylactic surgery are glad they made the choice even if they're unhappy they were put in that position," says Sue Friedman, a breast-cancer survivor and head of FORCE, an advocacy and support group focused on hereditary cancers. "It's a double- edged sword."

The value of testing becomes especially murky -- and ethically complicated -- when there is no way to prevent or treat disease, as in the case of early-onset Alzheimer's, which often strikes before the age of 50,or Huntington's, Kalb reports.

Today, only about 5 percent of people whoare at risk for Huntington's, a devastating neurological disorder, take the test. Many are worried that genetic testing will put their health insurance or job security in jeopardy. Some people, however, can't live with uncertainty.

Stephanie Vogt knew Huntington's ran in her family -- her paternal grandfather and his three brothers all died from complications ofthe disease-and she wanted to find out where she stood. "As soon as I foundout there was a test, I just had to do it," she says.

In August 2000, after comprehensive genetic counseling, Stephanie, her sister, Victoria and their mother, Gayle Smith, learned her results: positive. "It was like a scene out of the Matrix, where everything freezes and starts again," says Stephanie.

On good days Stephanie feels empowered; on bad days she's frightened. "But most of the time," she says, "I'm comfortable with the fact that I have the knowledge."

Testing is just one piece of the genomic revolution. A major goal is to create new sophisticated therapies that home in on a disease's biological glitch, then fix the problem. Already, genes are helping to predict a patient's response to existing medications. A prime example in this field of pharmacogenetics, says Dr. Wylie Burke of the University of Washington, is a variant of the gene called TPMT, which can lead to life-threatening reactions to certain doses of chemotherapy. Knowing a patient's genotype,or genetic profile, may also help researchers uncover new preventative therapies for intractable diseases.

At Johns Hopkins University School of Medicine, Dr. Christopher Ross has tested several compounds shown to slow the progression of Huntington's in mice. Now he wants to test them in people who are positive for the Huntington's mutation but have not yetdeveloped symptoms--a novel approach to clinical drug trials, which almost always involve sick people seeking cures. "We're using genetics to move from treating the disease after it happens," he says, "to preventing the worst symptoms of the disease before it happens."