Parkinson's raises risk of depression in family

Parkinson's raises risk of depression in family

First-degree relatives - parents, siblings and children - of people with Parkinson's disease are about 50 percent more likely than relatives of healthy people to suffer depression or anxiety, a new study reports.

That relatives of people with Parkinson's have a higher risk of neurological disorders is well known, but their risk for psychiatric disorders has been unclear.

Researchers studied 1,000 first-degree relatives of 162 people with Parkinson's and 850 first-degree relatives of 147 healthy people. The team found a 45 percent increased risk for depressive disorders and a 55 percent increased risk for anxiety disorders among the Parkinson's relatives.

The study, published in the December issue of The Archives of General Psychiatry, also found that the earlier the onset of Parkinson's, the more likely a relative was to suffer depression.

ANOREXIA AND HORMONES Anorexia is 10 times as common in women as in men, and a new study suggests that female sex hormones in the womb may play a part.

Researchers used the Swedish twin registry to study 4,226 pairs of female twins, 3,451 pairs of male twins and 4,478 pairs of opposite-sex twins, all born from 1935 to 1958. They found 51 cases of anorexia among the female twins, 3 among the male twins and 36 among the opposite-sex pairs. The study was published in the December issue of The Archives of General Psychiatry.

As expected, the risk of anorexia in female twins was higher than in male twins. But in the opposite-sex twins, 16 anorexia cases, almost half, were in males. In other words, the male member of a male-female twin pair had a risk for anorexia statistically no different from the risk among females.

Studies have shown that shared family environment has little effect on the development of anorexia. Instead, the researchers theorize, the shared intrauterine environment of male-female twin pairs is what leads to the increased risk for the males. Female sex hormones may influence neurodevelopment and later risk for anorexia, they suggest, and males in that uterine environment would be similarly affected.

TAME A CHILD'S COUGH WITH HONEY A spoonful of honey might quiet a child's cough more effectively and safely than the most common over-the-counter cough medicine.

Researchers tested 105 children 2 to 18 with coughs from upper-respiratory infections, dividing them randomly into three groups. One received no treatment. The other received a remedy: one or two teaspoons of buckwheat honey, depending on age, or an age-appropriate dose of honey-flavored dextromethorphan. The study was supported by a grant from the National Honey Board, an industry-backed agency of the U.S. Department of Agriculture.

Using questionnaires filled out by the parents, the scientists measured cough frequency and severity, and the effect on the children's and parents' sleep. By all measures, honey provided the greatest relief.

Honey, the authors wrote in the December issue of The Archives of Pediatric and Adolescent Medicine, has well-established antioxidant and anti-microbial effects, and it might be that sweet substances of any kind help dissolve mucus in the airways and soothe the back of the throat.

In October, a U.S. Food and Drug Administration advisory panel recommended a ban on over-the-counter cold medicine intended for children under age 6.

Ian Paul, the lead author and an associate professor of pediatrics at Penn State, said parents should consider honey "as an alternative to cough medicine for children over age 1." In rare cases, honey can cause infantile botulism in children under 1.

Now an international group of researchers has found at least one reason why. BRCA1 inactivates a tumor suppressor gene known as PTEN.

Mutations occur spontaneously, but most organisms have mechanisms that can prevent the damage they might cause. PTEN has instructions to produce a protein that stops the uncontrolled cell growth of cancer.

BRCA1, the scientists reported online Sunday in Nature Genetics, prevents PTEN from doing its work.

The researchers found that inactivating the PTEN gene in mice led to the formation of the malignant tumor associated with BRCA1 mutations. Then they examined PTEN in nonhereditary breast tumors from 297 patients and tumors from 34 women who had inherited the BRCA1 mutation. In most cases, the protein that PTEN produces was undetectable in tumor cells, but clearly present in nearby normal cells.

PTEN might be a target for chemotherapy. "I am cautiously optimistic," said Ramon Parsons, the lead researcher and a professor of pathology at Columbia, "that within the next five years we'll be using drugs that are effective on the PTEN pathway."