That risk can be even higher depending on the race and gender of the person who had the stroke.

The study looked at the risk of stroke for 807 siblings of 181 people who had strokes in Nueces County, Texas. All of the strokes were either an ischemic stroke in which a vessel supplying blood to the brain is blocked, or a transient ischemic attack, often referred to as a "warning stroke" that resolves itself. Nearly 60 percent of those with strokes were Mexican American. The rest were non-Hispanic whites. All were between the ages of 45 and 65.

According to the study, siblings of people who had a stroke face roughly double the risk of the average American of also having a stroke. The risk to Mexican American siblings was even greater. "The findings show there may be a genetic link to ischemic strokes in this ethnic group," said study author Lynda D. Lisabeth, PhD, with the Stroke Program and Department of Epidemiology at the University of Michigan in Ann Arbor. "Other possible explanations could include shared environmental factors such as diet, physical activity and smoking habits. Medical conditions like high blood pressure and diabetes which cluster in families may also play a role."

The study, a part of BASIC (Brain Attack Surveillance in Corpus Christi Project), also found a higher prevalence of strokes in siblings of Mexican American men than Mexican American women. Among the non-Hispanic whites, only siblings of women who have had strokes were at an increased risk. Lisabeth says more research is needed to explain the possible gender and ethnic differences in risk factors among siblings. "People of all ethnicities should be aware that strokes tend to cluster in families," said Lisabeth. "They need to know the warning signs, since treatment must be given within three hours of when the symptoms begin."

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Their current findings pinpoint STAMP2 as a critical factor to prevent overt inflammatory responses during everyday nutrient fluctuations or conditions of nutrient excess. In fat cells, a lack of STAMP2 led to aberrant inflammatory responses to both nutrients and acute inflammatory stimuli, they reported.

Similarly, they showed that the visceral fat surrounding the internal organs of STAMP2-deficient mice became inflamed, and the animals developed spontaneous metabolic disease on a regular diet, manifesting insulin resistance, glucose intolerance, high blood sugar and lipid levels, and fatty liver disease. They also showed that the loss of STAMP2 exacerbated the metabolic symptoms of mice with a genetic predisposition to obesity due to other factors.

When food enters the system, STAMP2 normally keeps the immunity response "button" from getting pushed, Hotamisligil said.

"We suggest that, over time, the accumulation of small cellular stresses due to daily changes and fluctuations in nutrients in STAMP2-deficient mice may lead to the activation of inflammatory pathways and inhibition of insulin action, resulting in systemic metabolic deterioration over the long term," he continued.

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