Researchers may have discovered a genetic equivalent  of the Fountain of Youth hidden in the DNA of centenarians.

Only 1 in 6,000 people reaches the century mark and just 1 in 7 million lives to be a supercentenarian (someone who is 110 or older). A new study, published online in Science, suggests that more people may have the right genetic stuff for extreme longevity.
This new study, looked at genetic markers called single nucleotide polymorphisms (SNP), in 1,055 centenarians and 1,267 younger people, all of European descent. The researchers found 150 genetic SNP variants which were linked to extreme longevity.

At first, the team identified only 33 SNPs found more often in people aged 90 to 114 years but not in a control group made up of people who will presumably live an average lifespan.  Thomas Perls, a geriatrician at Boston University School of Medicine who coauthored the new study, the researchers felt that they were still missing part of the story.

Biostatistician Paola Sebastiani of the Boston University School of Public Health devised a different statistical method to identify additional SNPs that would improve the team’s ability to predict longevity. The team tested their predictions on a separate group of centenarians and controls. With the 150 SNPs, the researchers could correctly predict who was a centenarian 77 percent of the time.

“77 percent is a very high accuracy for a genetic model, which means that the traits that we are looking at have a very strong genetic base,” Sebastiani says. On the other hand, the 150 SNPs can’t explain why the remaining 23 percent of centenarians in the study have reached such ripe old ages. It could mean that those people have other, rare genetic variants or lifestyles responsible for their longevity or some combination of the two, she says.

Extrapolating these results to try to predict how long the average person will live would be a mistake, says Nicholas Schork, a statistical geneticist at the Scripps Translational Science Institute and the Scripps Research Institute, both in La Jolla, Calif.  “They’ve identified markers for something, but what that something is remains a mystery,” Schork says. How the combination of genetic markers work together to extend health and life “is the zillion-dollar question.”

Don’t expect the genetic data to lead to a Methuselah pill, Perls says.  “I look at the complexity of this puzzle and feel very strongly that this will not lead to treatments that will get a lot of people to become centenarians,” he says. But the research could conceivably lead to treatments that delay diseases such as Alzheimer’s.

Supercentenarians (someone who is 110 or older) had nearly all of the longevity markers. But most of the over-100 crowd carried different combinations of SNPs that fell into one or more of 19 different genetic profiles. These results indicate that there are many different genetic combinations to longevity and that many different biological processes are involved, Sebastiani says.

The researchers had expected that centenarians would lack disease-associated variants, but that isn’t the case. Some of the genetic profiles correlated with extreme delays in the onset of diseases such as dementia, heart disease or cancer. Others seem to allow centenarians to withstand the effects of such diseases.

About 15 percent of people in the general population may actually have what it takes genetically to reach 100, says Perls. “If they’re not hit by a bus, if they’re not in a war, if they haven’t had some other accident happen, maybe they get to fulfill that,” he says. “Now, a bunch of those people may also need to not smoke and not be obese and a number of important lifestyle factors as well.”

Sebastiani says, “One can conjecture that genetically we’re built to live longer,” and longer life expectancies associated with improved public health measures seem to bear that out.

Other studies have shown that genetics account for only 20 percent to 30 percent of a person’s chances of living beyond age 85. Environmental factors, including lifestyle choices such as diet, smoking and exercise habits, are still the most important determinants of longevity.

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Muscle growth is governed by myostatin, a protein that determines whether an animal has compact muscles tuned for rapid sprints or a leaner body suited for endurance. There are three possible combination at this specific genetic marker. This test is not designed to identify how good a horse is likely to be, but rather what it will be good at.

According to Equinome, the three genetic combination that are possible are C:C, C:T and T:T. A C:C horse is likely to be a fast, early maturing horse that performs well as a two-year-old, while a C:T horse has a mixture of speed and stamina and is the most versatile in terms of distance, and a T:T horse is best suited to races greater than 1 mile that require stamina.

Horse Genome Project coordinator Ernest Bailey of the University of Kentucky, Lexington stated that breeders have adopted genetic tests for paternity, coat color, and diseases but that performance prediction is new ground.

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Scientist say that more research is needed before the therapy can be tested in patients, but the discovery in human colon cancer cell lines and mice with established human tumors suggests that the addition of a small molecule to the cancer drug Temozolomide disrupts repair mechanisms in a type of tumor cells that is highly resistant to treatment.

Satya Narayan professor of anatomy and cell biology at the college of Medicine and a member of the University of Florida Shands Cancer Center said that, “This is very important because aside from aggressive surgery with possibly chemotherapy, there are no specific treatments for colon cancer. The recurrence rate for this type of cancer after surgery is very high, about 30 to 50 percent, and there is an urgent need to develop new approaches to manage this deadly disease.”

The National Cancer Institute estimates there will be about 106,000 new cases of colon cancer in the United States in by the end of 2009. It is the second most common cause of cancer-related death in both men and women in the Western hemisphere.

Colon cancer forms in the large intestine and survival rates vary according to how soon the cancer is diagnosed and the treatment is started. The challenge of treating patients is that colon cancer is not a single disease but an array of disorders with distinct molecular mechanisms, with one type being quite proficient at repairing the DNA damage inflicted by the drugs currently used to treat the disease.

Narayan’s research team evaluated more than 140,000 small molecules, finally arriving at a tiny molecule that precisely blocks the ability of cancer cells to recognize and repair the DNA damage inflicted by Temozolomide, or TMZ. Narayan said, “Our idea was if you induce DNA damage (with TMZ), and at the same time block cell repair, you can synergize toxic effects to the cancer cells. We hope that with this combination treatment we can reduce the tumors drastically and expand the lifetime of patients much longer than is currently possible.”

TMZ is commonly used against certain types of brain cancer. It works by damaging the DNA of the cancer. By combining TMZ with the small molecule, Narayan’s team was able to disable the colon cancer’s ability to manufacture repair enzymes.

The UF researchers effectively used an amount of TMZ that is about 10 times lower than recommended in its studies of mice with human colon cancer tumors. According to Narayan, if only about one-tenth as much TMZ is needed to kill cancer cells, it will be possible to use lower doses of a drug that creates a great deal of adverse side effects, a partial listing of which includes anxiety, back pain, breast pain, constipation, cough, diarrhea, dizziness, drowsiness, dry skin, hair loss, headache, joint pain, loss of appetite, mouth sores, muscle aches and nausea.

“By using these strategies we can predict that disruption of DNA repair by small molecules can bypass drug resistance factors and dramatically reduce side effects caused by toxic doses of TMZ,” Narayan said.

More study is needed before the combination can be tested in patients, but Narayan believes that TMZ can be combined with the small molecule in a single dose in pill or capsule form.

Sankar Mitra, Ph.D., a professor in the department of biochemistry and molecular biology at the University of Texas Medical Branch in Galveston, who did not participate in the study, said that, the research demonstrates that it is possible to sensitize colon cancer cells to TMZ more broadly than is now possible — a benefit of particular importance to patients with cancers that are as varied as colon cancer. “This could be the start of other small molecule inhibitors”

Sankar Mitra also noted that the therapeutic molecules were selected through sophisticated analysis of the structure of tens of thousands of potential small molecules from the National Cancer Institute database. The computer-based process, which can suggest likely cancer therapeutics within hours, replacing manual analysis which would normally have taken weeks or months.

Robert W. Sobol, Ph.D., an assistant professor of pharmacology and chemical biology, and human genetics, at the University of Pittsburgh Cancer Institute said that, “There have been a multitude of studies suggesting that inhibition of DNA polymerase beta would enhance chemotherapeutic response. However, potential inhibitors have been challenging to identify and most have proven to be non-specific and/or non-selective. The compound identified by Dr. Narayan appears to be the first in what I expect to be a growing list of DNA polymerase beta inhibitors that have clinical potential.”

The research was supported by grants from the National Cancer Institute of the National Institutes of Health.

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In a study published on September 2nd in HealthDay News the question of why some people are more likely to become addicted to opioid painkillers (like morphine, codeine or oxycodone) has now been partially unraveled by the Geisinger Health System in Pennsylvania.

For the study, Geisinger Health System researchers interviewed and analyzed DNA from 705 patients with back pain who were prescribed some kind of opioid painkillers for more than 90 days.

Geisinger Health System researchers found that the group most vulnerable to addiction has four main risk factors in common: age (being younger than 65); a history of depression; prior drug abuse; and using psychiatric medications. Painkiller addiction rates among patients with these factors are as high as 26 percent.

The researchers also looked at a gene located at chromosome 15 that had been linked with alcohol, cocaine and nicotine addiction. This study indicates that genetic mutations on a gene cluster on chromosome 15 may also be associated with opioid addiction.

According to Joseph Boscarino, an epidemiologist and a senior investigator at Geising’s Center for Health Research, “these findings suggest that patients with pre-existing risk factors are more likely to become addicted to painkillers, providing the foundation for further clinical evaluation.”  He Added, “by assessing patients in chronic pain for these risk factors before prescribing painkillers, doctors will be better able to treat their patients’ pain without the potential for future drug addiction.”

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I just came across an article distributed by the Slate discussing the above topic. This brought my thinking to the use of DNA and the idea of anonymity in general.

DNA testing makes them easy to trace
By Rachel Lehmann-Haupt Last Updated Monday, March 1, 2010, at 9:36 AM ET

When Donor 3066 signed up with the California Cryobank, he offered some basic information about himself on a piece of paper: that he had a BA in theater; that his mother was a nurse and his father was in the Baseball Hall of Fame; that his birthday was Sept. 18, 1968. He made it clear that he didn’t want to be found by signing a waiver of anonymity…

Donor 3066 was being sought out by Michelle Jorgenson, a 39-year-old waitress from Sacramento, Calif., whose daughter, Cheyenne, was born in 1998.  When her daughter turned 5, Jorgenson joined the Donor Sibling Registry and began searching for other mothers and donor offspring who used Donor 3066. She was concerned because her daughter was sensitive to sounds and walked on her toes, and she wanted to know if other half-siblings were displaying similar behavior. Through the registry, she met a number of other mothers and half-siblings. She discovered that two had autism and two others showed similar signs of sensory disorder…

Jorgenson began her search by approaching a mother in her group with a son named Joshua and suggested he do a cheek swab so she could explore his paternal roots through a Y chromosome test. The mother agreed. Through the test, Michelle learned about some of Joshua’s genetic markers. A few weeks of searching on the Family Tree DNA Web site using these markers led to two families with matching DNA. Through one of the families, she met a woman who mentioned that she found the obit of a relative who was a former baseball manager, and three children were listed. Michelle suspected that this might be her donor’s father, so she looked up the phone number of his listed son. When Michelle called the number, the deceased man’s son answered the phone. She began to ask him questions: Was your father in the Baseball Hall of Fame? Were you born in Illinois? Did you ever donate sperm? When the man said yes, she asked him if his birthday was Sept. 18, 1968. When he answered yes, she burst into tears. “You’re the biological father of my daughter,” she said. He was shocked but agreed to talk to Cheyenne on the phone—and eventually allowed the two to come visit him in Los Angeles.

Although in this case there appears to be a happy out come for all parties this is not always the case.  What about the request for privacy that Donor’s sign up for when they choose to remain anonymous?  Is that even something that clinic should offer since there is no guarantee that the donor can’t be found?  What are the options for men who do become donors?  There are many questions that are raised in this article and very few answers, partly because technology is growing at such a fast rate and party because it appears in the article many clinics are ignoring this issue of privacy.  Let us know what you think about this issue.

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The blood test uses the mother’s plasma to extract Genetic information about their unborn baby. The test can be used to determine if the unborn baby carries specific genetic abnormalities, such as muscular dystrophy, this test can be conducted shortly after conception.

Currently, testing for genetic abnormalities and gender cannot be carried out until at least 9 weeks and as late as 24 weeks. The current methods of testing are either through a Chorionic Villus Sampling (CVS) or an Amniocentesis.

Chorionic Villus Sampling (CVS) is a medical procedure conducted by an OBGYN that is typically performed between 9 – 13 weeks gestational age, which is often mistakenly referred to Chronic Villus (or Villi) Sampling. CVS is a vaginal procedure that removes a very small portion of the placenta.

Amniocentesis is a medical procedure conducted by an OBGYN that is typically performed between 14 – 24 weeks gestational age. The amniocentesis procedure involves insertion of a needle into the womb and drawing out approximately 10cc’s of amniotic fluid, which surrounds the unborn baby.

Professor Michael Chapman, head of women’s and children’s health at the University of NSW, said that this new testing method was the “holy grail” of research. “Scientists have been chasing this for about 25 years,” he said. “The biggest advantage of this in a wanted pregnancy is there is no risk of miscarriage during testing.”

The research team from the University Medical Center, in The Netherlands, used the test on 200 women. Only in 10 cases could the gender not be determined. The procedure works by taking a sample from the mother’s blood plasma and extracting fetal DNA, which circulates in the mother’s blood. Looking for a specific gene sequence, doctors can then determine if the baby is a boy or a girl and is a carrier of specific disorders. In most cases, the test will be performed on a seven-week-old fetus.

But Australian obstetricians warn the medical breakthrough is unlikely to be used in Australia because it could be used for gender selection and due to “ethical and moral” dilemmas.

The test did not address the fact that fetal DNA that is found in a mother’s blood can be from previous pregnancies even years later. The research have not address how to determine if the DNA is from the current fetus. While their are some DNA testing companies that have offered to use “simple” blood test to determine paternity for several years. These test can often be unreliable. While this new test promise great answer at no risk there are still some very big questions that haven’t been answered.

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For years, pregnant and nursing women have been warned to limit the amount of fish they eat.  This is because many marine species may contain high levels of mercury, which endangers development in newborns and fetuses. Recently, National Healthy Mothers, Healthy Babies Coalition, a children’s health group challenged the this conventional wisdom.  National Healthy Mothers, Healthy Babies Coalition are advising pregnant women and nursing mothers to eat more fish so as to ensure optimal brain development in their babies.

Due to the fear or mercury contamination, many pregnant women avoid seafood altogether. That may actually harm newborns, according to some scientists. (John McConnico for The New York Times) What’s going on here? Currently, the Food and Drug Administration advises pregnant women to limit their weekly seafood consumption to no more than 12 ounces, or about two servings, per week. In addition they recommend staying away from fish that are meat eating (shark, tuna, etc.) as they tend to have higher levels of mercury. Notice they do not say not to eat fish just to watch what type and how much you consume.

The newest recommendation from the National Healthy Mothers, Healthy Babies Coalition, a nonprofit group that focuses on childhood health issues. That group’s scientific advisers say that pregnant women and nursing mothers should eat at least 12 ounces of fish per week. Although both recommendations acknowledge that pregnant women can safely eat about two servings a week, fears of mercury contamination in seafood have prompted many pregnant women to forgo fish entirely neither organization recommends that.

And here is the issue that pregnant women face: an increasing number of studies indicate that omega-3 fatty acids, (found mostly in fish) are essential to brain development in fetuses and newborns. A report in The Lancet medical journal, concluded that women who had eaten more than 12 ounces of fish per week during pregnancy produced better developed, more intelligent children. “Advice that limits seafood consumption might reduce the intake of nutrients necessary for optimum neurological development,” wrote scientists from the National Institutes of Health and the University of Illinois at Chicago.

“The real problem here are the women who are just eliminating fish from their diet,” said Judy Meehan, executive director of the National Healthy Mothers, Healthy Babies Coalition. “Eating 12 ounces is a very safe, smart move, and nobody is disputing that.’’ While none of the research cited in the coalition’s recommendations has been funded by the fish industry, the coalition is using a grant from the National Fisheries Institute, a seafood industry group, to fund its educational campaign, according to Ms. Meehan.

For women who want the health benefits but worry about mercury and other toxins, the wisest course is to choose fish with the lowest levels of mercury. A recent report in The Journal of the American Medical Association concluded that the health benefits are likely greatest from such oily fish as salmon, herring and sardines — which are all generally low in mercury anyway. Among the fish to avoid are shark, swordfish, king mackerel and tilefish, all of which may contain high levels of mercury and seem to be lower in omega 3.

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UCLA Scientists link genetic variant to autism risk. This discovery may explain the gap in autism cases between boys and girls. Dr. Stanley Nelson, professor of human genetics at the David Geffen School of Medicine at UCLA and his team narrowed their research on a region of chromosome 17 that previous studies have tied to autism. In that region they discovered a variant of a gene (a gene that is essentially the same as another, but has mutational differences) called CACNA1G. Dr. Stanley Nelson and his team looked at the DNA of 1,046 members of families with at least two sons affected by autism for common gene variants.

According to Dr. Stanley Nelson, “We wanted to identify what was happening in this region of chromosome 17 that boosts autism risk. When the same genetic markers kept cropping up in a single region of the DNA, we knew we had uncovered a big clue.”

The researcher team traced the genetic markers to CACNA1G. CACNA1G helps move calcium between cells. They discovered a common variant that appears in the DNA of nearly 40 percent of the population studied.

“This alternate form of CACNA1G consistently increased the correlation to autism spectrum disorders, suggesting that inheriting the gene may heighten a child’s risk of developing autism,” Nelson said, but he emphasized that it cannot be considered a risk factor on its own. “This variant is a single piece of the puzzle,” he said. “We need a larger sample size to identify all of the genes involved in autism and to solve the whole puzzle of this disease.”

This study was funded by the National Institute of Mental Health and Cure Autism Now. The DNA samples were provided by the Los Angeles–based Autism Genetic Resource Exchange (AGRE).

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Scientist are now saying that, Humans may have originally caught malaria from gorillas.  This is based on research that examined malaria parasites in great ape feces.  It was originally thought that the human malaria parasite split off from a chimpanzee parasite when humans and chimpanzees last had a common ancestor.

Scientists have found that the DNA of malaria from western gorilla was the most similar to human malaria parasites.  Scientists had assumed that when the evolutionary tree of humans split off from that of chimpanzees – around five to seven million years ago the malaria parasite had already jumped species.  But new evidence suggests human malaria is much newer.

Malaria disease that is caused by a parasite called Plasmodium, this parasite is carried by mosquitoes and is contracted when a person is bit by a mosquito.  Over 800,000 people die from malaria each year in Africa.

To study the DNA of malaria in wild apes, you cannot use blood samples. So researchers collected 2,700 samples of faecal material from both western and eastern gorillas as well as from chimpanzees and bonobos.

They sequenced Plasmodium DNA from the faeces with techniques that use a large sample, and drew a genetic family tree to see which parasites were related.  ”When we did conventional sequencing, the tree didn’t make any sense, because each sample contained a mixture of parasites,” Said Dr Beatrice Hahn of the University of Birmingham, Alabama.

Researches diluted the DNA so to isolate one parasite’s genome which represented in a single sample  From there they amplified the DNA, meaning that they were able to separate the DNA from different species of the parasite much more effectively.

Comparing both methods they found that looking a the larger sampling tree method made much more sense.

They found that the human Plasmodium was not very closely related to chimpanzee Plasmodium,but that the human strain was very closely related to one out of three species of gorilla Plasmodium.  Specifically the strain from western gorillas in Central and West Africa.

Researchers discovered that there was more genetic variety in the gorilla parasites than in human parasites.

The study which was published in Nature, and while it provides a lot of answer researchers are going to investigate further.  They want to see exactly how different the gorilla and human parasites are and to determine if cross-infection between humans and gorillas may be going on currently.

Members of the research team are hunters and loggers in Cameroon, who spend a lot of time in the forests to determine whether these workers carry malaria parasites from the gorillas, which would suggest that new infections from other species can still happen.

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