Could a father’s level of stress affect his unborn children? A new study suggests that there may be a relationship between a dad’s stress and his child’s risk of developing depression.

It has already been established in prior studies that the risk of developing depression is significantly increased by exposure to chronic stress, both from the the environment and from genetics.

While most studies to date have focused on maternal effects, the researchers in this case worked with male mice and found that those exposed to chronic stress pass along the stress behaviors to their offspring.

Both male and female offspring showed increased depression and anxiety-like behaviors, though the effects were stronger in males.

Additionally, these behavioral effects were only seen in offspring produced through natural reproduction, and not in those produced via in vitro fertilization. This suggests that most stress-related vulnerabilities are transmitted to children behaviorally.

These findings in mice raise the possibility that part of an individual’s risk for clinical depression or other stress-related disorders may be determined by his or her father’s life exposure to stress, a provocative suggestion that now requires direct study in humans,” said lead author Dr. Eric Nestler, from Mount Sinai School of Medicine in New York.

The study was published in the journal Biological Psychiatry.

Parents pass a number of traits onto their children such as height, temperament or eye color.  A new study suggests parents also may be passing on a risk of alcoholism.

Researchers have discovered a strong link between parental alcohol use disorders (AUDs) and the risk of their children developing an AUD.  In other words, a parent’s alcoholism is associated with a increased risk of alcoholism among their children.

Danish researcher Erik Lykke Mortensen, associate professor in medical psychology at the University of Copenhagen and author of the study, collected data from over 7,000 people regarding alcohol abuse and other psychatric disorders.  They also examined parental alcohol use, gender and social status.

The results showed that parental alcohol abuse corresponds to offspring alcohol disorders, independent of other predictors such as gender, social status and other psychiatric disorders.

Furthermore, Mortensen said, the association appeared to be stronger for female offspring than it was for males.

“The key message for the general public is that there is an increased risk associated with parental alcoholism,” said Mortensen, “but obviously many other factors determine whether an individual develops an AUD.”

The study will be published in Alcoholism: Clinical & Experimental Research.

Scientists have used stem cells to grow a rudimentary eye in the laboratory in a landmark study that raises the prospect of creating tissues to treat blindness and tease apart how diseases can destroy eyesight, The Guardian reported.

The team of Japanese scientists is the first to make significant progress in turning embryonic stem cells into an organ as complex as the eye.  They hope their work will help shed light on the progression of diseases that lead to blindness and screen for drugs that might slow or reverse the conditions.

Their success also may mean that someday we may have banks of healthy retina cells to transplant into patients whose vision has been damaged by illness or accidents.

The scientists grew the rudimentary eye by using embryonic stem cells from mice to grow an optic cup – the structure that forms the retina and contains the light-sensitive cells and neurons necessary for proper sight.

The eye and the different cells took shape spontaneously from a floating cluster of embryonic cells the scientists had cultured.  The eye measured 2mm across – approximately the size of an eye of a newborn mouse.

“This is a step I never thought I would see,” said Professor Robin Ali, a molecular geneticist at the UCL Institute of Ophthalmology in London in a interview with The Guardian. “This is the first time anyone has been able to make a complex structure from embryonic stem cells.”

Researchers are hopeful that they will be able to replicate the process with human cells within two years.

The study was published in the journal Nature.

Click here to read more from The Guardian.

Blame it on the alcohol – or the genes? Scientists believe they have identified a gene that plays a role in regulating how much alcohol people drink.

In a study of over 47,000 people, researchers observed a common genetic variation was associated with lower levels of alcohol consumption.

The gene, called autism susceptibility candidate 2, or AUTS2, is most active in the parts of the brain that deal with reward mechanisms, which may indicate that it plays a part in regulating the positive reinforcement people feel when they drink alcohol.

The AUTS2 gene has two variations, with one that expresses itself three times as much as the other. People with the less common version of the gene drink on average five percent less alcohol than people with the more common version.

AUTS2 has previously been linked to autism and attention deficit hyperactivity disorder, but its exact function is not known.

The study was conducted by an international consortium led by scientists at Imperial College London and King’s College London. The scientists collected DNA samples from all the participants and had them fill out a questionnaire about their alcohol consumption.

They hope their findings will lead to a better understanding of the mechanisms behind alcohol consumption and the development of individually targeted prevention and treatments for alcohol abuse and addiction.

Until now, only one other gene had been shown to have an effect on alcohol consumption – the gene encoding alcohol dehydrogenase, an enzyme that breaks down alcohol in the liver.

The study was published Proceedings of the National Academy of Sciences.

In the largest study of its kind, researchers have identified four new genes linked to late-onset Alzheimer’s disease, the most common form of dementia. An additional study has confirmed a previously identified gene and found a fifth, USA Today reported.

In the first study, researchers compiled and analyzed genetic data from 54,000 individuals – about a third whom had Alzheimer’s and the rest of whom did not – to identify the four new genes.

The study was conducted by scientists from 45 universities and research institutes in the United States.  Collectively, the group was called the Alzheimer’s disease Genetics Consortium.  The research was funded by the National Institutes of Health.

Later, the consortium also helped to identify a fifth gene, which was reported in the second study by scientists from the U.S., the United Kingdom, France and other European countries.

“I’ve been in Alzheimer’s genetics since 1985, and I would have to say this is the most exciting event that’s happened,” said lead author of the first study Gerard Schellenberg, professor in the Department of Pathology and Laboratory Medicine at the University of Pennsylvania School of Medicine, in Philadelphia.  “Up until this point, there have only been five known genes for Alzheimer’s risk, and so we’ve essentially doubled the genes people know about.”

Finding new genes is essential, according to Schellenberg, because each gene is a clue as to what causes the degenerative disease.  The researchers hope their findings will help scientists develop new drugs and identify high-risk individuals.

“The brain is like a black box. You can do some imaging when patients are alive, and poke around after someone dies, to try to figure out why someone has Alzheimer’s or not,” but the new findings may increase the ability to predict who will get it, Schellenberg said.

Currently, treatments for Alzheimer’s are limited, and there is no prevention or cure for the disease.

Many of the genetic researchers involved with these studies are planning an even larger, similar study in the future, called the International Genomics of Alzheimer’s Project.

Both studies were published in the journal Nature Genetics.

Click here to read more from USA Today.

According to scientists, a new method for detecting Down syndrome during pregnancy may eventually be available as a safer, less invasive alternative to amniocentesis, WebMD reported.

The experimental method screens for genetic markers of Down syndrome in blood samples from the mother taken between the 11th and 14th weeks of pregnancy.  Early testing of the method showed it had 100 percent accuracy in distinguishing between 14 fetuses with Down syndrome and 26 without.

The method works by screening for extra copies of a fetal chromosome in the mother’s blood.  In Down’s syndrome, the fetus has three copies of chromosome 21, called trisomy-21.  In healthy fetuses, there are only two copies.

Amniocentesis, the standard method for Down syndrome testing, involves taking samples of genetic material from the fetus and comes with a risk of miscarriage.  Other less invasive tests are not as accurate and can only estimate the risk of Down syndrome in the fetus.

The study was published in the journal Nature Medicine.

Click here to read more from WebMD.