October 28, 2011
by Andy Coghlan
How’s this for a brain teaser: gene patents scrapped last year on the grounds that they were based on natural molecules were last week reinstated on the grounds that the molecules are, after all, unnatural. The development is the latest twist in a dispute over patents on the BRCA1 and BRCA2 gene variants that raise the risk of breast cancer.
The result will likely be welcomed in the biotech industry, which has already patented 4000 human genes, but civil liberties groups are less than impressed.
In a ruling last March, the US District Court for the Southern District of New York declared the patents invalid because they describe genes found in nature, which cannot be patented as they are not inventions.
Last week, the Court of Appeals for the Federal Circuit reached the opposite conclusion. It decided that the BRCA genes patented by Myriad Genetics of Salt Lake City, Utah, differ from their natural counterparts by omitting non-coding “junk” regions that are present in the human body. “The molecules as claimed do not exist in nature,” says the judgment.
The American Civil Liberties Union and the Public Patent Foundation, which originally brought the case in 2009, may yet appeal. “Human DNA is not a manufactured invention, but a natural entity like air or water,” says Chris Hansen, a lawyer with the ACLU.
October 7, 2011
The Huffington Post
By: Emma Gray
It’s true. We all turn into our mothers (or fathers) as we age, and by that logic our kids will one day grow up to be … just like us? How much influence do parents really have on their children? Although it’s no secret that some kids are more easily swayed by their parents than others, a new study suggests that how much you affect your kids may actually boil down to genetics.
Published this week in Translational Psychiatry, researchers examined 1,900 kids between the ages of 9 and 15, reports HealthDay. Focusing on a version of the seratonin-transporter gene, the study found a significant link between this genetic variation and the degree to which a child is affected by his or her environment.
A 2003 study got a lot of people talking about this gene. The media nicknamed it the “depression gene” because research showed carriers were more likely to feel sad when faced with “life stressors.” These results were exacerbated when it came to individuals that had experienced childhood trauma. Subsequent research on the subject has consistently focused on backing up or refuting this claim.
Benjamin L. Hankin, lead author on the most recent study — and associate professor of clinical child and developmental cognitive neuroscience psychology at the University of Denver — said that he views the gene in a slightly different way. “In this research, we took the same gene … and said, maybe it doesn’t just put you at risk for negative outcomes,” Hankin told The Huffington Post. “It might mean that you’re more sensitive and responsive to environments [in general].” Instead of calling the shortened version of the 5-HTTLPR gene the “depression gene,” it might be more aptly referred to as the “sensitivity gene.”
Children who carried the long version of the 5-HTTLPR gene seemed to be able to maintain a positive attitude in the face of less-than-supportive parenting. Kids with the shorter variation were hit much harder. On the flip side, when their parents were more responsive and accommodating, these same kids’ feelings of happiness surpassed those of their long-gene counterparts. Hankin compared this phenomenon to the botanical difference between weeds and orchids:
Some individuals are orchids, some are weeds. Weeds will grow anywhere; they’ll be just fine. Those are the kids who carry the long version of this gene. The orchid, if [it has] a wonderful, flourishing environment, [will] grow up into a beautiful flower. If not, it’ll wither.
Clearly kids aren’t plants, but Hankin’s study is far from the first to tie our dispositions to factors beyond our control. In 2008, TIME reported University of Endinburgh researchers had found that happiness was determined by a set of innate personality traits. Other studies have linked happiness to age or socioeconomic status.
The ultimate takeaway from this recent research seems to be that providing a supportive environment for your kids to grow up in is more important than ever. If you’re thinking, “well, duh!” we understand — this “lesson” seems like little more than parenting common sense. However, Hankin was quick to point out a caveat to this PSA-sounding message.
While the researcher — who is a father himself — does not suggest getting your kid genotyped, he does suggest that parents pay extra attention to children with more “irritable temperaments,” as these kids are more likely to have the shortened gene. “[With these children], your input has a greater impact,” he says. “As your child grows up, the challenges are going to change, but you can put your kid on a trajectory for more adaptive, positive mental health.”
September 28th, 2011
The Huffington Post
By: Michael Sigman
I once dated a woman who was happy. She slept well, ate when she was hungry and exercised when her body needed it. I had insomnia, ate gallons of chocolate chip ice cream and ran eight miles a day. She felt good when something good happened and bad when something bad happened. I felt anxious no matter what happened. She shared her dreams of verdant meadows and flowing rivers. After a time, I stopped sharing my naked/unprepared for the final exam reruns.
We both had plenty to be thankful for, and she experienced more real-world tragedy than I. I didn’t want her to be neurotic, but it seemed unfair that she got to be so much happier.
A new study by UCLA life scientists found that the oxytocin receptor gene (OXTR) is a strong predictor of optimism and self-esteem. Apparently, if you’re missing certain nucleotides at a specific location on that gene, you’re much more likely to see the glass as half full. If you have ‘em, the researchers say, you’re likely to have “substantially lower levels of optimism, self-esteem and mastery, and significantly higher levels of depressive symptoms” than your more fortunate brethren.
This survey has been hailed as a breakthrough, but its basic message — that humans are born with a tendency toward a “happiness quotient” — comes as no great surprise. Google the phrase “happy gene” and you’ll get various older citations pointing to the conclusion that about half of our sense of well-being is inherited. Other scientists claim that a different gene (5-HTTLPR) regulates the neurotransmitter serotonin, aka the “happy hormone.”
And then there’s the “happy hour gene,” which may explain why some of your friends can drink you under the table and still wake up on the right side of the bed the next morning.
Some reacted to the UCLA findings by connecting the news with the desire — presumably among the happy-gene deprived — to achieve better living through chemistry. One blogger led with, “Happy Gene Discovered by UCLA Researchers (And It’s Not Called Cocaine).” And there was a spirited Facebook thread which confused oxytocin with OxyContin, a powerful narcotic that makes people so happy that if it weren’t also highly addictive, we could just put it in the water supply and forget the whole discussion.
I’m convinced, of course, that I possess the glass-half-empty gene — a certainty that may be evidence I’m right. But the survey results also brought a sense of relief that my default state of mind isn’t some kind of weakness.
In fact, scientists behind the UCLA survey emphasize that the effects of the happy gene are far from determinative. If you have the gene for green eyes, you will have green eyes. But the happiness gene appears to be more malleable. Myriad factors — a mother’s nurturing, good sex, close friendships, therapy, exercise and meditation practice — can improve your oxytocin levels and facilitate optimism and self-esteem.
I mentioned this to a Type-A friend whose basic feeling-state is a cocktail of dread mixed with self-laceration. He was too busy multi-tasking to give a considered reply, but managed to blurt, “No time for sex, meditation or exercise! Perhaps I can do all three at once.”
It does no good to fret about our genes. Besides, happiness is in the eye of the beholder. As one of my favorite Genes — Pitney — observes in song, “To you it may seem like misery but, for me, this is happy.” Self-pity may be counterproductive, but I would have been unhappy growing up in a town without Pitney.
After reading about the UCLA study, I resolved to find out more about how the other half lives. So I visited the Facebook page, Happy Gene. This did not make me happier because I ran head-on into the message, “Happy only shares some information with everyone. If you know Happy, add her as a friend or send her a message.”
If you’re lucky enough to have the happiness gene, no need to ruminate about the whys and wherefores. You’re probably not reading this anyhow. You’re having too good a time white-water rafting, marveling at a sunrise or just basking in the wonderfulness of your own company.
July 21st, 2011
By: Ja’nel Johnson
Should you drink five or six cups of coffee a day to try to prevent cancer? Millions of people are asking themselves this question following research suggesting coffee lowers the risk of breast and prostate cancer.
In the past, reports that coffee lead to insomnia, nervousness, restlessness, irritability, digestive problems and muscle tremors gave the beverage a bad rap. But new studies in recent years have shown that coffee can actually provide health benefits.
The latest research suggests that coffee can help prevent prostate cancer and breast cancer, the sceond most common cancers in men and women, respectively.
Researchers at the Karolinska Institute in Stockholm found that drinking coffee reduces the risk of antiestrogen-resistant estrogen- receptor (ER)- negative breast cancer among postmenopausal women. The study was published in May in the journal Breast Cancer Research.
“Women who drank five cups of coffee a day had a 57 percent lower risk for ER-negative cancer than those who drank less than one cup a day,” said Jingmei Li, author of the study.
She said ER-positive and ER-negative cancers are generally considered biologically distinct diseases and have been associated with remarkably different gene expression profiles.
Researchers tested 5,929 women between the ages of 50 and 74. Questionnaires were used to assess behavioral and health characteristics including coffee consumption, smoking and drinking patterns, physical activity routines, family history of breast cancer, hormone therapy protocols, nutritional intake, body mass index and education level, according to Li.
Lizette White,43, of Evanston, isn’t a regular coffee drinker, but when she does have a taste for the beverage, she usually goes to Kafein located in downtown Evanston. She said she found the research to be interesting, but not a reason to drink more coffee.
“If there were actual proof that there was a big difference, I might boost my coffee consumption a little bit, but I don’t think I would ever be the person drinking five cups a day,” White said.
Li said the study didn’t collect specific information on what kind of coffee was consumed and that the research doesn’t prove a cause-and-effect relationship.
“Before I go tell my neighbors to start drinking more coffee than they already do, I would like to know what is the biological mechanism at work here?,” Li said.
Researchers at the Harvard School of Public Health found in another study, that the biologically active compounds in coffee may lower the risk of lethal prostate cancer. The research was published in the Journal of the National Cancer Institute last month.
Men, who drank six or more cups of coffee a day, had an 18 percent lower risk of prostate cancer compared with men who did not drink coffee. Caffeine wasn’t found to be a factor in the study because those who drank decaf had the same protection as those who drank regular coffee.
Dr. Gerald Chodak, a former University of Chicago urologist who now consults and educates people about prostate cancer, said doctors can’t recommend patients to drink more coffee based on the study.
“It doesn’t prove cause and effect,” he said.
Researchers tested 47,911 men between the ages of 40 and 74 from 1986 to 2006. As in the breast cancer study, participants were given questionnaires to assess their coffee intake and food habits. Starting in 1986, participants reported their intake of regular and decaffeinated coffee every four years. The study was adjusted for smoking, obesity and other variables.
Chodak, author of the new book “Winning the Battle Against Prostate Cancer,” said researchers did a good job and that the information is recent, but it’s not enough to tell people to change their behavior.
“You tell people if they’re going to change their behavior it should be based on a study that has a clear result and this study design does not do that,” he said. “It might be true, but it might not be. And you don’t know the adverse effects of drinking six cups of coffee.”
Howard Soule, chief science officer at the Prostate Cancer Foundation in Santa Monica, Calif., said the research is an interesting observation. He said although it’s an important finding that should be tested, it’s not likely researchers are going to do an experiment.
“This is an observational study that generated the finding that six cups of coffee result in less prostate cancer,” he said. “It’s not a prospective clinical trial.”
Soule said that researchers believe the antioxidants associated with coffee beans protect tissues from environmental insults that cause cancer. He said people should consult with their doctors before making any changes.
“If they’re going to start drinking six cups of coffee a day, they need to talk to their doctor first and hopefully their doctor is well informed,” he said.
Paul Olczak, 26, of Evanston, found the research interesting since his father has late-stage prostate cancer, but doesn’t think the findings affect his life. He said he drinks four or five cups of coffee a day because he likes it. He said as an engineer, drinking coffee is the thing to do.
“It’s like a social norm,” he said. “If you don’t drink black coffee, you’re less of an engineer.”
Joseph DeRupo, director of external member relations and communications at the National Coffee Association, said 58 percent of all Americans drink coffee every day and the average number of cups per day is 3.4 per coffee drinker.
He said all of the research is welcomed by coffee drinkers who want to know that drinking coffee is good for them.
“Instead of having them drink more, it will stop them from feeling a need to drink less because there are no longer those old negative myths,” he said. “They have all been debunked.”
DeRupo said the science behind the healing powers of coffee makes sense.
“There are health benefits that come from this natural product,” he said. “It’s a bean that’s grown naturally and like any natural plant, it has many properties.”
Martin Zeff, 24, of Evanston, is also a regular customer at Kafein. He said although studies report coffee being good for those who consume it, he doesn’t plan to increase his coffee intake.
“I feel like if I drink six cups of coffee a day, maybe I wouldn’t have prostate cancer, but I’d be too twitchy to live in a normal environment,” he said. “That is way too much caffeine for one person to ever drink in a day.”
October 19th, 2010
By: Michelle Roberts
Experts say they have found a “tipsy” gene that explains why some people feel alcohol’s effects quicker than others.
The US researchers believe 10% to 20% of people have a version of the gene that may offer some protection against alcoholism.
That is because people who react strongly to alcohol are less likely to become addicted, studies show.
The University of North Carolina said the study aims to help fight addiction, not pave the way for a cheap night out.
Ultimately, people could be given CYP2E1-like drugs to make them more sensitive to alcohol – not to get them drunk more quickly, but to put them off drinking to inebriation, the Alcoholism: Clinical and Experimental Research journal reported.
Straight to the head
Lead researcher Professor Kirk Wilhelmsen said: “Obviously we are a long way off having a treatment, but the gene we have found tells us a lot about how alcohol affects the brain.”
Most of the alcohol people consume is broken down in the liver, but some is metabolised in the brain by an enzyme which the CYP2E1 gene provides coded instructions for.
People who have the “tipsy” version of CYP2E1 break down alcohol more readily, which explains why they feel the effects of alcohol much quicker than others.
The researchers made their discovery by studying more than 200 pairs of students who were siblings and who had one alcohol-dependent parent but who did not have a drink problem themselves.
They gave the students a mixture of grain alcohol and soda that was equivalent to about three average alcoholic drinks. At regular intervals the students were then asked whether they felt drunk, sober, sleepy or awake.
The researchers then compared the findings with gene test results from the students.
This revealed that CYP2E1 on chromosome 10 appears to dictate whether a person can hold their drink better than others.
Professor Wilhelmsen says more research is now needed to see if the findings could be used to make new treatments to tackle alcohol addiction.
“Alcoholism is a very complex disease, and there are lots of complicated reasons why people drink. This may be just one of the reasons,” he added.
Don Shenker, of the charity Alcohol Concern, said that, in most cases, alcohol abuse stemmed from social problems, with alcohol used as a prop.
Professor Colin Drummond, an expert in addiction at London’s Institute of Psychiatry, said it was likely to be combination of genes and environment.
“It is well recognised that alcohol dependence runs in families,” he said.
He said research suggests having an alcoholic parent quadruples a person’s risk of developing a drinking problem.
October 18th, 2010
By: Catherine Donaldson-Evans
Researchers at Yale University say they’ve identified a new gene that seems to trigger depression.
The scientists say the gene, MKP-1, might be a key contributor in the development of clinical depression.
“This could be a primary cause, or at least a major contributing factor, to the signaling abnormalities that lead to depression,” study lead author Ronald S. Duman, a professor of psychiatry and pharmacology at Yale, said in a statement.
Duman and his colleagues did genome scans of the brain tissue of 21 deceased people who had been diagnosed with depression and compared them to the genes of 18 people who hadn’t been diagnosed with the condition.
They found that one gene, MKP-1, increased more than twofold in the brains of people who were depressed. That gene blocks a molecular pathway neurons need to survive and function properly, which, when rendered inactive, has been linked to depression and other disorders.
The team also discovered that when MKP-1 is impaired in mice, the mice become resistant to stress, but when it’s activated, they show signs of depression.
University of Pennsylvania psychiatrist Dr. Christos Ballas said the study is flawed.
“You can’t say this is a gene for depression because it’s a gene for only one kind of depression,” he told AOL Health. “It’s a gene for a specific description of depression.”
Ballas said there is evidence that depression is in part genetic, but there are other factors involved in the illness.
“Certainly, there’s probably a common genetic component that makes us susceptible to depression,” he said. “But the problem is the effect of that gene is probably overwhelmed by the effect of everything else that happens in our life, including other genes.”
The findings were published October 17 in the journal Nature Medicine. Researchers say they may inspire a new class of antidepressants.
Doctors and scientists have had trouble pinpointing the causes of depression, which costs the United States $100 billion a year and affects nearly 16 percent of Americans.
Numerous physiological factors are believed to contribute to major depressive disorder, whose symptoms can vary from person to person. Patients given prescription antidepressants often respond differently to the drugs, and up to 40 percent don’t respond at all.
Ballas said that while the Yale research and other studies on depression genes are helpful, such findings aren’t revolutionary or applicable to all those who suffer from the condition.
“It is in no way generalizable to everybody,” Ballas said. “It’s much more useful to give a drug to treat the symptom than finding a gene for this one tiny aspect of depression. The more of these little genetic findings we get that don’t have any immediate usefulness, the more we minimize the environmental impact.”
August 30, 2010
Gene detectives on Sunday announced they had found the first inherited link to common types of migraine, a finding that boosts hopes for new drugs to curb this painful and costly disorder.
Scientists from 40 medical centres pored over the genetic profiles of more than 50,000 people, comparing those who suffered badly from migraines with others who were otherwise healthy.
What came up in the net was a tiny but telltale variant of DNA that boosts the risk of getting migraines by around fifth.
“This is the first time we have been able to peer into the genomes of many thousands of people and find genetic clues to understand common migraine,” said Aarno Palotie, head of the International Headache Genetics Consortium at Britain’s Wellcome Trust Sanger Institute, which led the study.
Previous research has found links for some extreme, but mercifully rare, forms of migraine, but this is the first to pinpoint an association for common types of the disease.
The tiny genetic variant, or allele, is called rs1835740.
Lying on Chromosome 8 between two genes, PGCP and MTDH/AEG-1, it allows a messenger chemical called glutamate to accumulate in junctions between brain cells, and this unleashes the migraine, the scientists believe.
If so, drug engineers have a tempting target in preventing glutamate buildup, they hope.
The paper, published online in the journal Nature Genetics, cited figures that migraine affects 17 percent of European women and eight percent of men.
The UN’s World Health Organisation (WHO) ranks migraine in the top 20 diseases in terms of “years lived with disability,” a benchmark of handicap. A US estimate put migraine’s economic cost on a par with diabetes.
The study first compared the genome of more than 3,000 migraine sufferers in Finland, Germany and the Netherlands against that of some 10,000 non-sufferers.
These results were then compared in a second phase with the genomes of a second batch, comprising 3,000 migraine patients and more than 40,000 otherwise healthy people.
The study found rs1835740 to be one of several connecting genetic cogs in regulating glutamate levels.
The allele alters the MTDH/AEG-1 gene, which in turn affects a gene called EAA2.
The EAAT2 gene controls a protein that is responsible for clearing glutamate from the brain synapses. This protein has previously been linked with epilepsy, schizophrenia and various mood and anxiety disorders.
The authors say further work is needed to confirm the findings and see whether other genetic culprits abound.
Patients in the study were recruited mainly from specialist headache clinics, which means they are likely to represent only the more extreme end of those who suffer from common migraines, said Gisela Terwindt of Leiden University Medical Centre, the Netherlands.
“In the future, we should look at associations across the general population, including also people who are less severely affected,” she said.
Migraine is believed to occur when inflammatory chemicals are released around the nerves and blood vessels in the head, inducing pain that can be excruciating. It is sometimes accompanied by nausea and hyper-sensitivity to light and sound.
Common migraines fall into two categories — those with an “aura,” or shimmering circle seen by the sufferer, and those without.
Sufferers tend to be aged 35-45, although the frequency and duration of the attacks can very widely.
August 12, 2010
British scientists have found a new gene that allows any bacteria to become a superbug, and are warning that it is widespread in India and could soon appear worldwide.
The gene, which can be swapped between different bacteria to make them resistant to most drugs, has so far been identified in 37 people who returned to the U.K. after undergoing surgery in India or Pakistan.
The resistant gene has also been detected in Australia, Canada, the U.S., the Netherlands and Sweden. The researchers say since many Americans and Europeans travel to India and Pakistan for elective procedures like cosmetic surgery, it was likely the superbug gene would spread worldwide.
In an article published online Wednesday in the journal Lancet Infectious Diseases, doctors reported finding a new gene, called NDM-1. The gene alters bacteria, making them resistant to nearly all known antibiotics. It has been seen largely in E. coli bacteria, the most common cause of urinary tract infections, and on DNA structures that can be easily copied and passed onto other types of bacteria.
The researchers said the superbug gene appeared to be already circulating widely in India, where the health system is much less likely to identify its presence or have adequate antibiotics to treat patients.
“The potential of NDM-1 to be a worldwide public health problem is great, and coordinated international surveillance is needed,” the authors wrote.
Still, the numbers of people who have been identified with the superbug gene remains very small.
“We are potentially at the beginning of another wave of antibiotic resistance, though we still have the power to stop it,” said Christopher Thomas, a professor of molecular genetics at the University of Birmingham who was not linked to the study. Thomas said better surveillance and infection control procedures might halt the gene’s spread.
Thomas said while people checking into British hospitals were unlikely to encounter the superbug gene, they should remain vigilant about standard hygiene measures like properly washing their hands.
“The spread of these multi-resistant bacteria merits very close monitoring,” wrote Johann Pitout of the division of microbiology at the University of Calgary, Canada, in an accompanying Lancet commentary.
Pitout called for international surveillance of the bacteria, particularly in countries that actively promote medical tourism.
“The consequences will be serious if family doctors have to treat infections caused by these multi-resistant bacteria on a daily basis,” he wrote.
July 14, 2010
By Rebecca Smith
Broccoli has been hailed as a ‘superfood’ after several studies suggested it had anti-cancer properties.
Now scientists have identified a chemical in the vegetable which interact with genes involved in cancer development.
The chemical called sulforaphane seems to counteract a fault with the gene called PTEN which is involved in prostate cancer.
The gene normally stops cancer from developing but in certain cells it is missing and this is when the disease can begin. However sulforaphane seems to dampen the effect of these cells that are missing PTEN and prevent them from triggering cancer growth.
The study was conducted by a team at the Institute of Food Research at the Norwich Research Park, using prostate tissue from men and cancerous cells from mice.
The discovery could lead to new treatments for the disease which affects 36,000 men a year.
June 24, 2010
By Alastair Jamieson
Genetic information will be available to most people in the developed world within 10 years, allowing better treatment and safer prescription of drugs.
Francis Collins, director of the US National Institutes of Health, believes mass genome sequencing of individuals would soon be possible at a cost of less than $1,000 per person (£670).
In an interview with The Times to mark the 10th anniversary of the sequencing of the human genome, he said bespoke genetic health care would identify those with a higher inherited risk of conditions such as heart disease, diabetes or cancer and reduce the diseases though drug treatment, early screening or diet and exercise.