Secrets of attraction may lie in immune system DNA

BY Rosemary Black
DAILY NEWS STAFF WRITER

Wednesday, February 17th 2010, 5:04 PM

Here’s some new information about the science of attraction: Your body odor may provide your mate with subconscious clues about the strength of your immune system.

Researchers from the University of Western Australia, reporting in the journal “Animal Behavior,” say that whether or not the object of your desire finds you irresistible may depend on how sweet your sweat smells, according to a report in the Daily Mail. A woman’s sweat holds genetic information that signals to a potential hubby whether their offspring would possess the best chance of fighting off illness.

The more varied a woman’s histocompatibility, or MHC, genes are, the more attractive she appears to the opposite sex.

The researchers studied the DNA of nearly 150 college students, who filled out questionnaires about their love lives. They looked at the students’ DNA to find variation in genes that are known to have an influence on the immune system, and found that the more diverse these genes were, the more disease-resistant a person was.

The researchers then matched the results of the genetic tests with the survey answers and learned that the women with the most varied histocompatibility (MHC) genes also had the greatest number of sexual partners.

Previous research has shown that the more different a person’s perspiration is to yours, the more pleasant you’re likely to find him or her. It’s theorized that this phenomenon came about so people wouldn’t accidentally marry their relatives or anyone else who’s genetically similar.

Another theory is that women with varied MHC genes could be more outgoing.

“It is possible that MHC-diverse women have more sexual partners because they actively seek more partners, rather than because males prefer diverse partners,” wrote the researchers.

Relationship expert Laurent Mackler says parents may affect how successful a woman is at finding a boyfriend – but not necessarily because of genetics.

“We are invariably attracted to people based on how familiar that person is to us from childhood,” says Mackler, author of “SoleMate: Master the Art of Aloneness & Transform Your Life.”

“As human beings, we are always seeking homeostasis, or balance, and looking for the parts of us that got lost as we grew up and had to adapt to the family system. So we’re attracted unconsciously to the people who embody these traits. We are looking for our other half and may not always find him.”

DNAWellnessinfo.com Resource:  http://www.nydailynews.com/lifestyle/health/2010/02/17/2010-02-17_secrets_of_attraction_may_lie_in_immune_system_dna_thats_sensed_through_sweat_sc.html

A new theory of how low doses of antibioitics create antibiotic resistance

Feb 11, 2010 – usatoday.com

E.coli bacteria is seen under a microscope.

CAPTION

By Centers for Disease Control

Exposure to low levels of antibiotics increases mutations in E. coli and Staphylococcus bacteria hundreds of time more than normal, making the creation of drug-resistance strains more likely, says a paper in today’s edition of the journal Molecular Cell.

This finding adds to concerns about antibiotic resistance brought on by poor prescriptions practices among doctors, patients who don’t take all their medicine and even low doses of antibiotics given to help animals grow faster.

The researchers found that while low levels of antibiotics may not be enough to kill off the bacteria, they still stress them. That stress causes them to produce free radicals, says James Collins, a biomedical engineer at Boston University and one of the paper’s authors.

Those free radicals are produced by oxidation, a process that’s known to damage cells. In the case of bacteria, the free radicals damage the bacteria’s DNA, causing some of the affected bugs to mutate.

Two and a half years ago Collins’ group began looking at how bacteria respond to antibiotics. It was then that they discovered that antibiotics can stimulate the pathways that create free radicals in bacteria.

A year ago they started considering what other implications their discovery might have.

“We wondered whether sub-lethal levels still produce free radicals. We know the cells wouldn’t die, but we know that free radicals can damage DNA, and that increases mutenigenesis,” he says.

And that’s exactly what they found. Basically, if the antibiotic dose isn’t high enough to kill every bacteria in sight, “you could be creating a zoo with a wide range of mutations,” he says.

The  finding is important “within the context of our understanding — or lack of understanding — of how bacteria become resistant to antibiotics,” says Deborah Hung, a molecular biologist at Massachusetts General Hospital, who wrote an accompanying Perspective piece on the article.

The  truth is that no one really knows exactly how bacteria become resistant to antibiotics, says Hung. So knowing that low levels of antibiotics might potentially increase the random chance that bacteria might mutate into resistant forms could have important implications for medicine.

By Elizabeth Weise

DNAWellnessinfo.com Resource:  http://content.usatoday.com/communities/sciencefair/post/2010/02/a-new-theory-of-how-low-doses-of-antibioitics-create-antibiotic-resistance/1

Stem Cell Research Makes Another Advance

February 8, 2010 – health Day

MONDAY, Feb. 8 (HealthDay News) — Scientists say they’ve developed a new and easier way to create what’s known as pluripotent stem cells

— cells that can develop into one of many cell types for use in regenerative medicine.

Unlike many other methods, this new technique doesn’t use viruses to introduce genes into cells or permanently alter a cell’s genome. Instead, tiny circles of DNA are used to transform stem cells taken from human fat into induced pluripotent stem cells, which are the starting point for research into many human diseases.

This is the first time that adult (non-embryonic) stem cells have been reprogrammed this way and it could be an important advance toward the use of such cells in humans, according to the Stanford University School of Medicine researchers.

“This technique is not only safer, it’s relatively simple,” study co-author Dr. Michael Longaker, a professor of surgery and deputy director of Stanford’s Institute for Stem Cell Biology and Regenerative Medicine, said in a Stanford news release. “It will be a relatively straightforward process for labs around the world to begin using this technique. We are moving toward clinically applicable regenerative medicine.”

The researchers plan to create pluripotent stem cells to learn more about, and perhaps some day treat, human heart disease.

“Imagine doing a fat or skin biopsy from a member of a family with heart problems, reprogramming the cells to pluripotency and then making cardiac cells to study in a laboratory dish. This would be much easier and less invasive than taking cell samples from a patient’s heart,” study senior author Dr. Joseph Wu, an assistant professor of cardiology and radiology and a member of Stanford’s Cardiovascular Institute, said in the news release.

The study was published online Feb. 7 in the journal Nature Methods.

More information

The U.S. National Institutes of Health has more about stem cells.

DNAWellnessinfo.com Resource:  http://www.usnews.com/health/managing-your-healthcare/womens-health/articles/2010/02/08/stem-cell-research-makes-another-advance.html

Living fast? Scientists show lifespan is linked to DNA

Ian Sample, science correspondent
guardian.co.uk, Sunday 7 February 2010 19.55 GMT

Scientists have isolated a gene sequence that appears to determine how fast our bodies age, the first time a link between DNA and human lifespan has been found.

The discovery could have a profound impact on public health and raises the best hope yet for drugs that prevent the biological wear and tear behind common age-related conditions such as heart disease and certain cancers.

The work is expected to pave the way for screening programmes to spot people who are likely to age fast and be more susceptible to heart problems and other conditions early in life. People who test positive for the gene variant in their 20s could be put on cholesterol-lowering statin drugs and encouraged to exercise, eat healthily and avoid smoking.

The breakthrough is unlikely to lead to drugs that dramatically extend lifespan, but doctors say it may help prolong the lives of patients whose genes make them susceptible to dying young.

The research gives the kind of insight into the biology of ageing that has not emerged from work on other strategies that claim to extend lifespan, such as consuming vast quantities of antioxidants or pursuing a severely calorie-restricted diet.

“This may help us identify patients who are at a greater risk of developing common age-related diseases so we can focus more attention on them,” said Professor Nilesh Samani, a cardiologist at the University of Leicester, who led the research.

The research highlights the difference between chronological age and biological age, the latter of which is determined by our genetic makeup and lifestyle factors, such as diet and smoking. Two people of the same age can have biological ages that differ by more than 10 years.

A team led by Samani and Professor Tim Spector at King’s College, London found a common sequence of DNA was strongly linked to a person’s biological age. In a study of nearly 3,000 people, around 38% inherited one copy of the gene variant and were biologically three to four years older than those who did not carry the sequence.

A minority of 7% inherited two copies of the DNA sequence and were on average six to seven biological years older. The majority of the population, 55%, do not carry any copies of the variant.

The study, published in the journal Nature Genetics, was prompted by the huge variability in the age at which people develop medical problems that are often considered diseases of the elderly.

“I see patients in their 80s with high blood pressure who have healthy coronary arteries and I see people in their 40s who don’t seem to have any risk factors yet have advanced heart disease,” Samani said. “We think this kind of variability must have something to do with premature ageing.”

Most of the cells in our bodies contain long molecules of DNA called chromosomes that have protective caps at either end called telomeres. Every time a cell divides, the telomeres shorten, like plastic tips fraying on a shoelace. When the telomeres become very short, the cell starts to malfunction and show signs of ageing.

From blood samples, Samani and Spector found a particular gene sequence was more common in people who had unusually short telomeres for their age. The section of DNA was found on chromosome three, next to a gene called TERC, which makes an enzyme that repairs telomeres when they shorten.

People who carry one or two copies of the genetic sequence probably make less of the enzyme, called telomerase, when they are growing in the womb. This means they are born with shorter telomeres, and so are prone to ageing more quickly.

“The effect may be built in at a very early stage in life. If you’re born with shorter telomeres, there’s evidence you will be prone to heart disease and other age-related diseases,” Samani said.

Scientists are unlikely to reverse the ageing process by boosting telomerase in people’s bodies. Telomerase is almost completely deactivated after birth, but is switched back on in cancer cells so they can divide endlessly without dying. “Introducing telomerase might protect you from heart disease, but if you turn it on willy nilly you could cause cancer instead,” Samani said.

DNAWellnessinfo.com Resource:  http://www.guardian.co.uk/science/2010/feb/07/ageing-genetics

Missing DNA tied to obesity

Last Updated: Wednesday, February 3, 2010 | 6:02 PM ET
CBC News

Some severely obese people are missing a set of genes, a new study has found.

Researchers have found a small proportion of obese people are born without 30 or so of the estimated 30,000 genes in the human genome.

This deletion of genes was not found in any subjects of normal weight, the team from Imperial College London and their colleagues in Europe, the United States and Montreal reported in Wednesday’s issue of the journal Nature.

The missing genes may account for seven out of 1,000 cases of morbid obesity — people with a body mass index, or BMI, over 40, the study found. The body mass index is a tool used to determine the healthy weight range for a particular height. A BMI over 30 is considered obese and 25 to 29.9 is overweight.

The recent rise in obesity in the developed world has been attributed to an abundance of unhealthy food and too little exercise, but the way people respond to these environmental factors is often genetic, said Prof. Phillipe Froguel, lead author of the study at the School of Public Health at Imperial College London.

“It is becoming increasingly clear that for some morbidly obese people, their weight gain has an underlying genetic cause,” Froguel said in a news release.

“If we can identify these individuals through genetic testing, we can then offer them appropriate support and medical interventions, such as the option of weight-loss surgery, to improve their long-term health.”

Searched general population
In the first part of the study, researchers looked for the genes in obese teenagers and adults with learning difficulties or delayed development. They found 31 severely obese people with nearly identical deletions in one copy of their DNA.

The second part of the study looked at the genomes of 16,053 European people in the general population, reflecting a range of weights. Nineteen people in this group were missing the same set of genes, and all were morbidly obese.

Those lacking the genes tended to be normal weight as toddlers, overweight during childhood and severely obese as adults, the researchers said.

The study is the first to confirm that severe obesity in otherwise physically healthy individuals can be caused by a rare deletion of DNA, the authors said.

Until now, individual genes linked to weight gain have had a relatively modest effect of about two pounds.

“The genetic change identified in this study is much less common but leads to much more substantial changes in the body weight of the individuals that it affects,” study co-author Dr. Robert Sladek of McGill University in Montreal said in a release Wednesday.

Researchers have found a similar modest effect with genes influencing Type 2 diabetes. The approach the obesity researchers used — identifying the deletion in very obese people and then looking for the variant in a much broader population — could help to identify genetic influences on Type 2 diabetes and other diseases, the researchers said.

They now plan to study the function of the missing genes. Previous studies have suggested that deletions of these genes may be linked with delayed development, autism and schizophrenia.

DNAWellnessinfo.com Resource: http://www.cbc.ca/health/story/2010/02/03/obesity-dna-deletion.html

HIV Researchers Solve Key Puzzle After 20 Years of Trying

ScienceDaily (Jan. 31, 2010) — Researchers have made a breakthrough in HIV research that had eluded scientists for over 20 years, potentially leading to better treatments for HIV, in a study published January 30 in the journal Nature.

The researchers, from Imperial College London and Harvard University, have grown a crystal that reveals the structure of an enzyme called integrase, which is found in retroviruses like HIV. When HIV infects someone, it uses integrase to paste a copy of its genetic information into their DNA.

Prior to the new study, which was funded by the Medical Research Council and the US National Institutes of Health, many researchers had tried and failed to work out the three-dimensional structure of integrase bound to viral DNA. New antiretroviral drugs for HIV work by blocking integrase, but scientists did not understand exactly how these drugs were working or how to improve them.

Researchers can only determine the structure of this kind of molecular machinery by obtaining high quality crystals. For the new study, researchers grew a crystal using a version of integrase borrowed from a little-known retrovirus called Prototype Foamy Virus (PFV). Based on their knowledge of PFV integrase and its function, they were confident that it was very similar to its HIV counterpart.

Over the course of four years, the researchers carried out over 40,000 trials, out of which they were able to grow just seven kinds of crystals. Only one of these was of sufficient quality to allow determination of the three-dimensional structure.

Dr Peter Cherepanov, the lead author of the study from the Department of Medicine at Imperial College London, said: “It is a truly amazing story. When we started out, we knew that the project was very difficult, and that many tricks had already been tried and given up by others long ago. Therefore, we went back to square one and started by looking for a better model of HIV integrase, which could be more amenable for crystallization. Despite initially painstakingly slow progress and very many failed attempts, we did not give up and our effort was finally rewarded.”

After growing the crystals in the lab, the researchers used the giant synchrotron machine at the Diamond Light Source in South Oxfordshire to collect X-ray diffraction data from these crystals, which enabled them to determine the long-sought structure. The researchers then soaked the crystals in solutions of the integrase inhibiting drugs Raltegravir (also known as Isentress) and Elvitegravir and observed for the first time how these antiretroviral drugs bind to and inactivate integrase.

The new study shows that retroviral integrase has quite a different structure to that which had been predicted based on earlier research. Availability of the integrase structure means that researchers can begin to fully understand how existing drugs that inhibit integrase are working, how they might be improved, and how to stop HIV developing resistance to them.

DNAWellnessinfo.com Resouce:  http://www.sciencedaily.com/releases/2010/01/100131142438.htm

A New Way to Look for Diseases’ Genetic Roots

The hunt for the genetic roots of common diseases has hit a blank wall.

The genetic variants found so far account in most cases for a small fraction of the genetic risk of the major killers. So where is the missing heritability and why has it not showed up?

A Duke geneticist now suggests that the standard method of gene hunting had a theoretical flaw and should proceed on a different basis. The purpose of the $3 billion project to decode the human genome, completed in 2003, was to discover the genetic roots of common diseases like diabetes, cancer and Alzheimer’s. The diseases are called complex, meaning that several mutated genes are probably implicated in each.

A principal theory has long been that these variant genes have become common in the population because the diseases strike late in life, after a person has had children. Bad genes would not be eliminated by natural selection at that age, as they would if the diseases struck before the child-bearing years.

So to find disease genes, the thinking went, do not decode the entire genome of every patient — just look at the few sites where genetic variations are common, defined as being present in at least 1 percent of the population.

These sites of common variation are called SNPs (pronounced “snips”), and biotech companies have developed ingenious devices to recognize up to 500,000 SNPs at a time. The SNP chips made possible genomewide association studies in which the genomes of many patients are compared with those of healthy people to see which SNPs are correlated with the disease.

The SNP chips worked well, the studies were well designed, though enormously expensive, and some 2,000 disease-associated SNPs have been identified by university consortiums in the United States and Europe.

But this mountainous labor produced something of a mouse.

In each disease, with few exceptions, the SNPs accounted for small percentage of the genetic risk. A second puzzling feature was that many of the disease-linked SNPs did not occur in the DNA that codes for genes, but rather in the so-called junk regions of the genome. Biologists speculated that these SNPs must play an as-yet-undefined role in deranging the regulation of nearby genes.

In an article this week in the journal PLoS Biology, the Duke geneticist David B. Goldsteinph.d and his colleagues propose an explanation for both findings.

They argue that the common disease-common variant idea is largely incorrect: natural selection has in fact done far better than expected in eliminating disease-causing variants from the population. It follows that the major burden of disease is carried by a multitude of rare variants — ones too rare to have been programmed into the SNP chips.

So why have the genomewide association studies linked some SNPs to disease, if in fact it is the rare variants that cause it?

In Dr. Goldstein’s view, the SNPs could simply be acting as surrogate markers for the rare variants. Until now, geneticists have assumed a disease-linked SNP was either itself a cause or was a marker for a disease variant nearby. But Dr. Goldstein’s team calculated that the rare variants associated with a SNP can occur up to two million units of DNA away from it. This means that the disease-associated SNPs do not necessarily point to anything useful and that it is dangerous to assume the nearest gene is the cause of the disease.

If SNPs are indeed rather indirect markers of disease, that would explain why many have turned up in junk DNA.

But why do the SNPs get implicated in the genomewide association studies if in fact it is the rare variants that cause disease? Most of the SNPs are ancient, which is how they got to be common, whereas the disease-causing rare variants are mostly recent, because natural selection is always sweeping them away. After a SNP is created, some of the population has it and the rest continue to carry the standard DNA unit at that site in their genome.

When the rare disease-causing variants build up much later, Dr. Goldstein suggests, some will be on stretches of DNA containing the SNP and others on stretches of DNA with the standard unit. Since the allocation is random, more rare variants will be sometimes lie on the DNA with the SNP, and the SNP will appear as statistically associated with the disease even if it is not.

The association is not exactly spurious — Dr. Goldstein calls it “synthetic” — but it is indirect, so much so as to make many SNPs useless for identifying the genes that cause disease.

Geneticists have long been aware of this possibility, but Dr. Goldstein’s team has shown theoretically that this could happen more often than expected. He has also examined the question in reverse by doing a genomewide association study of sickle cell anemia.

Though the disease is known to be caused by a variant in a single gene, the Duke geneticists found a statistically significant association with 179 SNPs, spread across a stretch of DNA two and a half million units in length and containing dozens of genes. Most of these SNPs were clearly pointing at the wrong thing.

Genomewide association studies, conducted with hundreds of patients, can each cost in the range of $10 million or more. Though the studies may have led researchers up a blind alley in many cases, they were not a mistake, Dr. Goldstein believes.

“I think most people now view genomewide association studies as something we absolutely had to do and have now done,” he said. “It’s fair to say that for many common diseases nothing of very great importance was discovered, but those studies have told us what to do next.”

That next step, in his view, is to sequence, or decode, patients’ entire genomes and then to look for likely mutations in the genes themselves. The cost of sequencing a human genome has been plummeting in recent years, and it may now be possible to sequence large numbers of patients.

Finding even a few of the rare variants that cause disease could point to genes that make suitable targets for drug makers. The SNPs statistically linked to disease have mostly failed to identify the right genes, but the rare variants may, Dr. Goldstein said.

The Icelandic gene-hunting firm deCODE genetics, which emerged last week from bankruptcy, has long led in detecting SNPs associated with common disease. Dr. Kari Stefansson, the company’s founder and research director, agreed that whole genome sequencing would “give us a lot of extremely exciting data.” But he disputed Dr. Goldstein’s view that rare variants carried most of the missing heritability. Both deCODE genetics and scientists at the Broad Institute in Cambridge, Mass., have sequenced regions of the genome surrounding SNPs in search of rare variants, but have found very few, Dr. Stefansson said.

“We can speculate till we are blue in our faces,” he said, “but the fact of the matter is that there is no substitute for data.”

DNAWellnessinfo.com Resource:  http://www.nytimes.com/2010/01/26/science/26gene.html

Gene discovery may help guide breast cancer care

DNA Mapping Used To Track MRSA Transmission

Submitted by Barinder Khatra on Sat, 01/23/2010 – 18:50

In path breaking research, scientists from Britain’s Bath, Oxford and London and Portugal, Thailand and the United States came together at the University of Cambridge to discover a revolutionary method for precisely tracking the spread of MRSA from country to country, patient to patient. The technique involves the usage of DNA mapping technology in studying the genome of the bacteria.

HUMAN-DNA-MAPING

This study would now help scientists and medical practitioners to better understand the spread and of the super bug, whether the bacteria is being transmitted as a result of inner hospital infections or its coming in from the outside.

By comparing samples of patients from various parts of the world, the team appeared to have reached the conclusion that MRSA originated in Europe in the early 1960s as a result of the first large scale usage of anti-biotic.

According to Dr. Shannon Peacock of Cambridge University, “Our research should inform global surveillance strategies to track the spread of MRSA. The implications for public health are clear: this technology represents the potential to trace transmission pathways of MRSA more definitively so that interventions or treatments can be targeted with precision and according to need”.

DNAWellnessinfo.com Resource:  http://topnews.co.uk/22109-dna-mapping-used-track-mrsa-transmission

Omega-3 Fatty Acids Are Linked to Longevity

1/20/10

By THOMAS M. BURTON

Omega-3 fatty acids, from fish like salmon and other sources, have for years been shown to help lower levels of heart disease and cardiac death.

New research suggests the fatty acids may possess an even more fundamental benefit: Heart patients with high omega-3 intake had relatively longer “telomeres,” which are stretches of DNA whose length correlates with longevity.

Cardiologists from the University of California, San Francisco, and other hospitals measured telomere length over five years in 608 patients who had coronary-artery blockage and previous heart attacks. Researchers found that people with high levels of omega-3 fatty acids in their white blood cells experienced significantly less shortening of telomeres over five years, as compared with patients with lower omega-3 levels.

“What we’re demonstrating is a potentially new link between omega-3 fatty acids and the aging process,” said Ramin Farzaneh-Far, a clinical cardiologist and assistant medical professor at UCSF and San Francisco General Hospital who is the lead author of the research.

Published in this week’s Journal of the American Medical Association, the study focused only on “marine” omega-3 found in fish, not the type found in vegetable sources like flaxseed, walnuts, canola oil or soybean oil.

The study didn’t distinguish between meals of fatty fish and fish-oil supplements—leaving open the question of whether it’s better for people to eat more fish, to eat plants such as flaxseed or just to take omega-3 supplements.

The American Heart Association, in a 2002 scientific statement in the journal Circulation, concluded that consuming omega-3 fatty acids in fish or supplements “significantly reduces subsequent cardiac and all-cause mortality.” The fish most often cited are salmon, herring and sardines.

John LaPuma, a Santa Barbara, Calif., physician and nutrition expert, says, “The best data are in fish rather than supplements, but the data for supplements are better than they were five years ago.”

There is “very little good evidence for the omega-3s from flax and walnuts,” said Dr. LaPuma, author of “ChefMD’s Big Book of Culinary Medicine.” But these foods have other benefits, he said. For instance, “flax meal, by itself, is an important part of lowering LDL,” or bad cholesterol, Dr. LaPuma said.

Researchers in the new study said they observed “baseline levels of marine omega-3 fatty acids were associated with decelerated telomere attrition over 5 years.”

Additionally, Dr. Farzaneh-Far said, “in multiple studies, short telomere length [in white blood cells] has been shown to predict death and cardiovascular events and heart failure.” He cautioned that “it’s an open question as to whether telomere length is causal or just a marker” of cell death. But he referred to telomere shortening as “a key part of cellular aging.”

“To definitively address the question of whether omega-3 fatty acids inhibit cellular aging, a double-blind, randomized, placebo-controlled trial would be necessary,” the authors wrote. Dr. Farzaneh-Far suggested that such research should be done in healthy adults because the evidence already is powerful on behalf of advantages of these fatty acids in heart patients.

Write to Thomas M. Burton at tom.burton@wsj.com

DNAWellnessinfo.com Resource:  http://online.wsj.com/article/SB10001424052748703837004575013393566949312.html?mod=rss_Today%27s_Most_Popular