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Vol. LXVI, No. 20
September 26, 2014

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Eating Habits, Body Fat Related to Differences In Brain Chemistry

Coauthors Dr. Kevin Hall (l) and Dr. Juen Guo examine PET data.
Coauthors Dr. Kevin Hall (l) and Dr. Juen Guo examine PET data.

People who are obese may be more susceptible to environmental food cues than their lean counterparts due to differences in brain chemistry that make eating more habitual and less rewarding, according to an NIH study published in Molecular Psychiatry.

Researchers at the Clinical Center found that, when examining 43 men and women with varying amounts of body fat, obese participants tended to have greater dopamine activity in the habit-forming region of the brain than lean counterparts and less activity in the region controlling reward. Those differences could potentially make the obese people more drawn to overeat in response to food triggers while simultaneously making food less rewarding to them. A chemical messenger in the brain, dopamine influences reward, motivation and habit formation.

“While we cannot say whether obesity is a cause or an effect of these patterns of dopamine activity, eating based on unconscious habits rather than conscious choices could make it harder to achieve and maintain a healthy weight, especially when appetizing food cues are practically everywhere,” said Dr. Kevin Hall, lead author and a senior investigator at NIDDK. “This means that triggers such as the smell of popcorn at a movie theater or a commercial for a favorite food may have a stronger pull for an obese person—and a stronger reaction from their brain chemistry—than for a lean person exposed to the same trigger.”

Study participants followed the same eating, sleeping and activity schedule. Tendency to overeat in response to triggers in the environment was determined from a detailed questionnaire. Positron emission tomography (PET) scans evaluated the sites in the brain where dopamine was able to act.

“These findings point to the complexity of obesity and contribute to our understanding of how people with varying amounts of body fat process information about food,” said NIDDK director Dr. Griffin Rodgers. “Accounting for differences in brain activity and related behaviors has the potential to inform the design of effective weight-loss programs.”

Single Animal to Human Transmission Event Responsible for 2014 Ebola Outbreak

Scientists used advanced genomic sequencing technology to identify a single point of infection from an animal reservoir to a human in the current Ebola outbreak in West Africa. This research has also revealed the dynamics of how the Ebola virus has been transmitted from human to human, and traces how the genetic code of the virus is changing over time to adapt to human hosts. Dr. Pardis Sabeti, a 2009 NIH Director’s New Innovator awardee and her team carried out the research.

“Dr. Sabeti’s research shows the power of using genomic analysis to track emerging viral outbreaks,” said NIH director Dr. Francis Collins. “This ability produces valuable information that can help inform public health decisions and actions.”

The 2014 Ebola outbreak is now the largest outbreak in history, with 5,347 total cases and 2,630 total deaths [as of Sept. 14] since it began in late December 2013, according to the World Health Organization. This outbreak is also the first in West Africa and the first to affect urban areas.

Sabeti, senior associate member of the Broad Institute in Cambridge, Mass., led an extensive analysis of the genetic makeup of Ebola samples from patients living in affected regions. Joined by an international team of scientists, Sabeti used advanced technology to analyze the genetics of the Ebola samples extremely rapidly and with high levels of accuracy. Using this technology, the researchers pinpointed a single late 2013 introduction from an unspecified animal reservoir into humans. Their study showed that the strain responsible for the West African outbreak separated from a closely related strain found in Central Africa as early as 2004, indicating movement from Central to West Africa over the span of a decade. Studying RNA changes occurring over the span of the outbreak suggests that the first human infection of the outbreak was followed by exclusive human-to-human transmissions.

Schizophrenia Not a Single Disease but Multiple Genetically Distinct Disorders

New research funded by NIMH shows that schizophrenia isn’t a single disease but a group of 8 genetically distinct disorders, each with its own set of symptoms. The finding could be a first step toward improved diagnosis and treatment for the debilitating psychiatric illness.

The research, conducted at Washington University School of Medicine in St. Louis, was reported online Sept. 15 in the American Journal of Psychiatry.

About 80 percent of the risk for schizophrenia is known to be inherited, but scientists have struggled to identify specific genes for the condition. Now, in a novel approach analyzing genetic influences on more than 4,000 people with schizophrenia, the research team has identified distinct gene clusters that contribute to 8 different classes of schizophrenia.

“Genes don’t operate by themselves,” said Dr. C. Robert Cloninger, one of the study’s senior investigators. “They function in concert much like an orchestra, and to understand how they’re working, you have to know not just who the members of the orchestra are but how they interact.”

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