Young age at first drink can turn under-15s into alcoholics

September 19, 2009 By Leave a Comment

Washington, Sept 19 (ANI): Drinking at young age may affect genes linked to alcoholism and make youngsters vulnerable to severe problems, says a new study.

The study led by Dr Arpana Agrawal, from Washington University School of Medicine in St. Louis, revealed that the younger an individual was at first drink, the greater the risk for alcohol dependence and the more prominent the role played by genetic factors.

“There seemed to be a greater genetic influence in those who took their first full drink at a younger age,” said Agrawal.

“That’s very consistent with what has been predicted in the literature and in the classification of types of alcohol dependence, but we present a unique test of the hypothesis,” she added.

During the study, the researchers studied 6,257 adult twins from Australia and measured the extent to which age at first drink changed the role of heritable influences on symptoms of alcohol dependence.

The study showed that when twins started drinking early, genetic factors contributed greatly to risk for alcohol dependence, at rates as high as 90 percent in the youngest drinkers.

The team also found that those who were 15 or younger when they started drinking tended to have a greater genetic risk for alcohol dependence.

However, some who were 16 or older before they took their first drink later became alcohol dependent, but their dependence was related more to environmental factors.

“Something about starting to drink at an early age puts young people at risk for later problems associated with drinking,” Agrawal says.

“We continue to investigate the mechanisms, but encouraging youth to delay their drinking debut may help.

“Some early-onset drinkers do not develop alcohol problems and some late-onset drinkers do – we are working on why that is the case, but it is important to note that this is one risk factor among many and does not determine whether a person will, or will not, develop alcohol dependence.

“But age at first drink is a well-known risk factor, and there have been two main hypotheses about why:

One has been that common genetic and environmental factors contribute both to the risk for alcohol dependence and to the likelihood a person will be younger when consuming their first drink,” she added.

The study will be published Alcoholism: Clinical and Experimental Research. (ANI)

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Genetic link between dental disease, heart attack identified

May 26, 2009 By Leave a Comment

Washington, May 25 (ANI): Scientists from University of Kiel, Germany have identified a genetic link between dental disease periodontitis and coronary heart disease (CHD).

Dr. Arne Schaefer, of the Institute for Clinical Molecular Biology, University of Kiel, Germany, said that they have discovered a genetic variant situated on chromosome 9, which was shared between the two diseases.

“We studied a genetic locus on chromosome 9p21.3 that had previously been identified to be associated with myocardial infarction, in a group of 151 patients suffering from the most aggressive, early-onset forms of periodontitis, and a group of 1097 CHD patients who had already had a heart attack,” he said.

“The genetic variation associated with the clinical pictures of both diseases was identical,” he added.

The further analysis of 1100 CHD patients and 180 periodontitis patients showed that the genetic risk variant is located in a genetic region that codes for an antisense DNA called ANRIL and that it is identical for both diseases.

Both CHD and periodontitis are propagated by the same risk factors – most importantly smoking, diabetes and obesity – and there is also a gender relationship, with men possibly more liable to these diseases than women.

“These factors already indicated a possible mutual genetic basis underlying the two diseases”, said Schaefer.

“Now we know for sure that there is a strong genetic link, patients with periodontitis should try to reduce their risk factors and take preventive measures at an early stage.

“We hope that our findings will make it easier to diagnose the disease at an early stage, and that in future a greater insight into the specific pathophsyiology might open the way to effective treatment before the disease can take hold,” he added.

The study was presented at the annual conference of the European Society of Human Genetics. (ANI)

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Negative mood-related drinking may lead to major depression, alcohol dependence

May 13, 2009 By Leave a Comment

Washington, May 13 (ANI): A study has shown that negative mood-related drinking can make people vulnerable to developing both Major depression (MD) and alcohol dependence (AD).

“Although the frequent co-occurrence of AD and MD is widely recognized, the association between the disorders works differently for different people. There are likely multiple mechanisms that result in the disorders co-occurring, for example, having MD increases the risk to develop AD, having AD increases the risk to develop MD; and causal factors – such as genetic risk or social circumstances – also contribute to developing both disorders,” said Kelly Young-Wolff, whose master’s thesis provided the stimulus for the study.

Victor Hesselbrock, professor of psychiatry at the University of Connecticut School of Medicine, said that the link could also differ by gender.

“Studies of both clinical and community samples have found that primary depression – depression occurs first, followed by alcoholism – is more typical in females while primary alcoholism – alcoholism followed by depression – is more common among males.

Furthermore, while most persons affected with alcoholism do report a lifetime history of significant depressive symptoms, the reverse is not true. Most people with depression do not report long periods of heavy drinking nor do they report significant numbers of lifetime AD symptoms,” Hesselbrock said.

Young-Wolff added: “Previous research had shown that individuals with higher than average scores on mood-related drinking scales are at increased risk to develop heavy drinking and AD. There is also evidence for familial risk factors, such as shared social and environmental or genetic factors, that contribute to overlapping risk for MD and AD, and for AD and mood-related drinking motives. Yet no study had examined whether mood-related drinking motives explain the overlapping familial risk for MD and AD.”

The new findings are based on an examination of 5,181 individuals aged 30 and older (2,928 males and 2253 females), drawn from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, a longitudinal study of psychopathology in two samples of adult twins.

The researchers have revealed that the subjects completed a clinical interview which assessed lifetime MD, AD, and mood-related drinking motives.

“Our study suggests that the familial factors that underlie mood-related drinking motives are the same factors that contribute to the overlapping familial risk for MD and AD. The results are consistent with an indirect role for mood-related drinking motives in risk for depression and AD, and suggest that individuals with strong mood-related drinking motives may be vulnerable to developing both MD and AD,” said Young-Wolff.

Hesselbrock added: “In short, the findings indicate that the drinking motives for both males and females who are well into the period of risk for both AD and for major depressive disorder are similar.

However, it should be noted that the findings do not address motives regarding the initiation of drinking behaviour in adolescence; the findings apply only to the subjects’ current drinking behaviour. Since this was not a longitudinal study that began in adolescence, it cannot be assumed that these subjects’ motives for beginning to drink when they were teenagers were to cope with feelings of depression.”

Carol A. Prescott, professor of psychology at the University of Southern California, as well as corresponding author for the study, said: “We might remember that there are many people with high mood-related drinking motives who do not have a history of MD or AD. We would argue that the occasional use of alcohol to relax or unwind is not necessarily a bad idea.

What should be avoided is heavy drinking as a regular coping strategy, since this can lead to other problems and is often a means of avoiding dealing with the issues that are contributing to the negative emotions.”

The researchers are of the opinion that their findings may help doctors identify individuals at risk for both MD and AD, with a focus on examining motives for drinking, as well as finding alternative strategies for coping with negative mood states.

Hesselbrock said: “I think it is important that family members understand that there is a real link between drinking and depression. While the family member who is drinking may believe that they are doing so to cope with and relieve their symptoms of depression -and there is some pharmacological basis for this – they probably do not realize that their drinking will only prolong and exacerbate the negative feelings.

For the person without AD, reducing/stopping drinking will help reduce the negative effect/depression. For the person with MD, stopping drinking will help reduce depression symptoms but not totally relieve the depression. It is a complex picture.”

The study, to be published in the August issue of Alcoholism: Clinical and Experimental Research, is currently available at Early View. (ANI)

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Genetic risk for anxiety, depression not predestined: Study

May 2, 2009 By Leave a Comment

Washington, April 30 (ANI): Previous studies have provided a strong basis of support for hypothesis that individuals with particular genotypes are predestined to negative life outcomes such as depression, anxiety disorders. But now, a new study has challenged this view.

Researchers studied infant monkeys from four different rearing conditions to examine how social context and different forms of early adversity interact with genotype to influence behaviour.

Animals reared in small social groups were more likely to be aggressive and anxious, particularly among those with a low activity MAOA genotype.

However, no genotype effects were evident in monkeys reared in larger social cages.

There are some circumstances in a child’s development – such as abusive parenting – that everyone would agree constitutes “adversity.”

However, this study suggests that other, subtler features of the broader social environment influence development, and that genes that affect our behavioral responses are sensitive to these influences.

So even though an infant may be reared with its nurturing mother, the relative absence of other social partners, for both the mother and the infant, can result in the infant developing an anxious style of responding to challenges, particularly if it possesses a “risky” genotype.

Of particular significance, said senior author John Capitanio, Ph.D., is “that animals that were raised in rich, complex settings with mothers, other kin, and peers, were completely protected from the potentially deleterious effects of having the ‘risky’ form of the MAOA gene.”

The study is published in the May 1st issue of Biological Psychiatry. (ANI)

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Depression ups heart disease risk more than genetics

March 5, 2009 By Leave a Comment

Washington, March 5 (ANI): A new study suggests that depression increases the risk of heart disease more than genetics.

Led by researchers at Washington University School of Medicine in St. Louis and the VA, the study was presented at the annual meeting of the American Psychosomatic Society this week in Chicago this week.

Describing the study, the researchers revealed that they analysed data gathered from more than 1,200 male twins, who had served in the U.S. military during the Vietnam War.

The researchers said that the men were surveyed on a variety of health issues in 1992, including depression, and were assessed again in 2005.

During the course of study, the researchers focused on the onset of heart disease in depressed study participants between 1993 and 2005.

According to them, men with depression in 1992 were twice as likely to develop heart disease in the ensuing years, compared to those without history of depression.

“Based on our findings, we can say that after adjusting for other risk factors, depression remains a significant predictor of heart disease,” says first author Dr. Jeffrey F. Scherrer, research assistant professor of psychiatry at Washington University School of Medicine and the St. Louis Veterans Affairs Medical Center.

“In this study, we have demonstrated that exposure to depression is contributing to heart disease only in twins who have high genetic risk and who actually develop clinical depression. In twins with high genetic risk common to depression and heart disease, but who never develop depression itself, there was no increased risk for heart disease. The findings strongly suggest that depression itself independently contributes to risk for heart disease,” he added.

The researchers said that they were searching for evidence of what they call incident heart disease, an event like a heart attack, heart surgery, stent placement or medical treatment for angina.

Those who had evidence of heart disease prior to the original survey in 1992 were excluded from this study, they added.

Given that twins were studied, the researchers said that it was possible to divided the participants into risk groups: twins with high genetic and environmental risk for depression, those with moderate risk and those with a low risk.

The risk groups then were compared for incident heart disease adjusting for other influences on heart disease, such as smoking, obesity, hypertension and diabetes.

“By separating the twins into these groups based on their genetic and environmental risks, we are able differentiate the genetic risks common to depression and heart disease and the risks for heart disease from exposure to depression,” says co-investigator Dr. Hong Xian, associate professor of mathematics in medicine at Washington University and health science specialist at the VA.

Twins automatically are matched by age, normally grow up in the same family environment, and in the case of identical twins, they share identical DNA.

“If one twin has depression, but his twin brother does not, both twins will share genetic vulnerability for depression, but it turns out the twin who was not depressed has less risk for heart disease. In sum, depression itself remains a significant contributor to incident heart disease after controlling for genes, environment and mental and physical risk factors,” says Scherrer.

The researchers are planning to follow these twins as they age, and to study the effects of successful depression treatment on heart disease risk. (ANI)

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Healthy diet can offset ‘obesity gene’ in kids

March 5, 2009 By Leave a Comment

Washington, Mar 4 (ANI): Eating a low energy density diet can offset the influence of a gene strongly associated with obesity in children, according to new research from University College London (UCL) and the University of Bristol.

Based on data from a sample of 2275 children from the Bristol-based ALSPAC study (Children of the 90s), the current study suggested that people might be able to avoid becoming obese if they adopted a healthier diet with a low energy density.

The researchers said that such a healthy diet could even benefit those who carry the FTO gene, identified as being a high-risk gene for obesity.

Dietary energy density (DED) refers to the amount of energy consumed per unit weight of food, or number of calories per bite.

A low dietary energy density can be achieved by eating lots of water-rich foods like fruits and vegetables, and by limiting foods high in fat and sugar like chocolate and biscuits.

The study focused on how DED affected the build up of fat in the body over a period of three years in children aged between 10 and 13 years old.

And the researchers found that children with a more energy dense diet (more calories per bite) tended to have more fat mass three years later, and also confirmed that those carrying the high risk gene had greater fat mass overall.

After looking at whether children with the FTO gene had a stronger reaction to an energy dense diet than children with a lower genetic risk, the researchers found that they did not.

The results indicate that if a child with a high genetic risk eats a diet with fewer calories per bite, they may be able to offset the effect of the gene on weight gain and so stay a healthy weight.

“This is an important finding because it provides evidence that it’s easier to eat too much energy and gain weight when your diet is packed tight with calories, so adopting a diet with more bulk and less energy per bite could help people avoid becoming obese regardless of their genetic risk. Obesity is not inevitable if your genes give you a higher risk because if you change the types of foods you eat this will help curb excessive weight gain,” said lead author Dr Laura Johnson, UCL Epidemiology and Public Health.

The study has been published in the latest issue of PLoS ONE. (ANI)

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Genetic variations behind brain aneurysms uncovered

November 13, 2008 By Leave a Comment

Genetic variations behind brain aneurysms uncoveredLondon, November 10 : Yale University researchers have moved a step closer to unravelling the mystery behind the oft-fatal rupturing of blood vessels in the brain, scientifically known as aneurysms, on the back of an international study.

Lead researchers Professor Murat Gunel and Sterling Professor Richard Lifton joined forces with a Howard Hughes Medical Institute investigator to scan the genomes of over 2,000 individuals suffering from intracranial aneurysms along with 8,000 healthy subjects.

The researchers found three chromosome segments, or loci, where common genetic variations could create significant risk for ruptured aneurysms, which in turn cause strokes.

Even though the subjects had come from hospitals in Finland, the Netherlands and Japan, the results were similar in all groups, suggesting that that such variations increase risk among diverse human populations.

The researchers believe that their findings may pave the way for new screening tests to identify hundreds of thousands of people at risk for strokes caused by bleeding, and point to new therapies that might be able to strengthen blood vessels in the brain before they burst.

“Even though we have made significant strides in treating unruptured aneurysms, until now we have not had an effective means of identifying the majority of individuals at risk of developing this deadly problem. These genetic findings provide a starting point for changing that equation,” Nature magazine quoted Gunel as saying.

The Yale research team said that the risk of aneurysm increased with the number of risk variants, or alleles.

According to them, people with the highest number of risk alleles tripled their risk of an aneurysm.

“These findings provide fundamental insights into the genetic and biochemical changes that cause this devastating brain disease, providing hope that we may also be able to provide preventive therapy before rupture occurs,” Lifton said.

The researchers revealed that their results implicated variations in the gene SOX17, which is known to play a crucial role in the early development and repair of endothelial cells that make up the arterial walls of blood vessels.

“These variations may interfere with the ability to produce cells that repair damage to the blood vessels, suggesting a path forward for developing new approaches to prevention,” Gunel said. (ANI)

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