Would you knowingly feed your children an ingredient derived from coal tar? That's exactly what you may be doing, if you let them eat any orange or yellow artificially-colored products including sodas, cheese-flavored products, flavored chips, pickles or a myriad of other foods and beverages. The industrial waste-derived coloring chemical tartrazine is a common ingredient in all these foods, underscoring the need to read food labels religiously. (Why would anyone put artificial colors into pickles? Read the labels, and you'll see!)

Tartrazine, also known as E102 or Yellow #5, was one of the colorings linked to childhood hyperactivity in a landmark 2007 study conducted by the United Kingdom's Food Standards Agency. As a consequence, products containing it must carry a warning label anywhere in the European Union.

Not surprisingly, the United States has no such law -- even though the coloring has been linked to asthma, migraines and cancer. But since when the FDA ever bother warning the public about dangerous chemicals in their food anyway? After all, aspartame, MSG and sodium nitrite are all legal -- so why not add a little food coloring poison to the cocktail and call it "nutrition?"

Scientists at the U.S. Department of Energy's (DOE) Brookhaven National Laboratory, Cold Spring Harbor Laboratory, and the University of California, San Diego School of Medicine, have identified hyperactive cells in a tiny brain structure that may play an important role in depression. The study, conducted in rats and appearing in the February 24, 2011, issue of Nature, is helping to reveal a cellular mechanism for depressive disorders that could lead to new, effective treatments.

The research provides evidence that inhibition of this particular brain region -- the lateral habenula -- using implanted electrodes can reverse certain behaviors associated with depression, and also provides a mechanism to explain this effect. These findings lend support to the use of deep brain stimulation as a clinical treatment for people with long-standing, treatment-resistant depression.

"This research identifies a new anatomical circuit in the brain that mediates depression, and shows how it interacts with the brain's reward system to trigger a constant disappointment signal -- which certainly would be depressing," said Fritz Henn, a neurobiologist and psychiatrist at Brookhaven and Cold Spring Harbor laboratories and a co-investigator on the research. "But," he added, optimistically, "identifying this circuit and how it works may open new doors to reversing these effects."

For example, said co-investigator Roberto Malinow, a professor of neurosciences at the UCSD School of Medicine, "it's possible that the genes specifically expressed in these neurons could be targeted genetically or pharmacologically in order to manipulate them and reduce depression."

Scientists have known that cells in the lateral habenula are activated by negative or unpleasant events, including punishment and disappointment, such as when you don't get an expected reward. It may seem intuitive that such negative stimuli can lead to depression, but not everyone who experiences disappointment collapses into a state of helplessness. To explore this connection, the scientists wanted to take a closer look at the brain circuits.

They examined the sensitivity of lateral habenula brain cells -- particularly those that connect and send signals to the brain's reward centers -- in two animal models of "learned helplessness," a form of depression, as well as in control animals that weren't helpless.

Overall, the scientists found that these lateral habenula nerve cells were hyperactive in the depressed animals but not in the controls. Furthermore, the degree of hyperactivity coincided with the degree of helplessness.

"The activation of the lateral habenula is known to influence the release of serotonin and norepinepherine, two targets of current antidepressant medications," said Henn. "The current study looked at the role of the lateral habenula in terms of the dopamine system, the system involved in reward signaling. We found that hyperactivity in the lateral habenula due to stress-induced helplessness shuts off the brain's reward system."

To explore whether electrical stimulation could potentially reverse this reward-dampening effect, the researchers placed a stimulating electrode in the lateral habenula and measured the effects on the brain cells leading to the reward center. This was a study of rat brain cells that simulated the effects of deep brain stimulation, a technique that is currently being explored as a treatment for clinical depression, which has shown promising results. The scientists found that electrical stimulation of hyperactive habenula brain cells markedly decreased excitatory activity leading to the reward center.

Next the scientists tested to see if deep brain stimulation in living rats that exhibited helplessness would affect their behavior. The result was a marked reduction in helpless behavior that was dependent on both placement of the electrode in the lateral habenula (not adjacent brain regions), and the intensity of the stimulation.

"Our results clearly show that suppression of synaptic transmission at the lateral habenula through deep brain stimulation can acutely reverse helpless behavior in rats," said Henn. "It's very likely that this beneficial effect was mediated by a suppression of excitatory nerve cells leading to the brain's reward system, as we observed in the cellular studies."

"Our study provides a cellular mechanism that may explain the hyperactivity of lateral habenula nerve cells observed in depressed humans and animal models of depression, as well as why 'silencing' these circuits, whether surgically or pharmacologically, can reduce depression-like symptoms in animals," Henn said.

Identifying these specific brain circuits and their dysfunction in depression may open the door to new effective treatments, including, potentially, lateral-habenula-targeted deep brain stimulation.

A new study concluded that children with ADHD can sometimes have more difficulties on math and reading tests compared to their peers.

Researchers used identical and fraternal twins to look at the genetic and environmental influences underlying ADHD behaviors, reading, and math skills in children in an attempt to understand the relationship among them.

Sara Hart, of the Florida State University, said by focusing on twins specifically, psychological scientists were able to tease out the difference between nature and nurture.

To do this, scientists compared identical twins, who have nearly the same DNA, with fraternal twins, who generally only share about half of their DNA.

The researchers found that ADHD behaviors, reading achievement, and math achievement were all influenced by the same genetic influences; this doesn't prove anything about what causes what, but some psychological scientists think that all three might be linked through the working memory system.

Although common genetic influences are a typical result from twin studies, the exciting aspect of this work was that that ADHD behaviors, reading achievement, and math achievement are also associated by common environmental influences.

Although it is not known what the actual environmental influences are, Hart and her colleagues suggest that it could be related to aspects of the classroom and homework environment.

The study is published in Psychological Science, a journal of the Association for Psychological Science.

Research to be presented at an international conference (Asia Pacific Conference on Tobacco or Health) in Sydney today (8 Oct) shows that children exposed to second-hand smoke have significantly higher rates of attention deficit hyperactivity disorder (ADHD), headaches and stuttering than those who are not exposed.

The US study asked about exposure to cigarette smoke at home among children aged four to 11 and adolescents aged 12 to 15, and also measured the cotinine levels in their blood (a measure of exposure to tobacco smoke). After controlling for socioeconomic factors and prenatal exposure, the study found children exposed to second-hand smoke had double the rate of ADHD (10.6% compared to 4.6%), almost double the rate of stuttering (6.3%% compared to 3.5%) and an increased rate of headaches (14.2% compared to 10.0%). Adolescents also had significantly higher rates of headaches (26.5% compared to 20.0%).

Researcher Wendy Max, Professor of Health Economics at the University of California San Francisco, said the results showed children's exposure to second-hand tobacco smoke could have a negative impact on their learning and education, as well as their health and overall wellbeing.

"Our research shows children who are exposed to tobacco smoke are impacted in three different areas of their development. These physical and mental problems are a disadvantage to a child's cognitive and social development," Professor Max said. "Children in countries with high smoking prevalence are at greatest risk. As smoking rates in developed countries continue to fall, the burden of childhood exposure to second-hand smoke will be disproportionately borne by countries that already face economic disadvantages."

Cancer Council Australia CEO, Professor Ian Olver, said the research added to evidence that smoking not only harms active smokers but also those around them, with children often at highest risk. "The right to a smoke-free childhood is a basic human right," Professor Olver said. "Governments need to work together to educate communities everywhere about what smoking is - an addiction that kills more than half of those addicted and harms others as well, particularly where smoking is unregulated."