COLUMBUS , Ohio – New research suggests that depression mayhasten the progression of heart disease by increasing the levels of akey protein that causes inflammation.
In a study of 32 peoplewith heart failure, the 14 patients who felt the most depressed hadnearly twice the levels of this protein in their blood.
Theprotein, tumor necrosis factor alpha (TNF-alpha), is one member of alarge family of proteins called cytokines, chemical messengers that aremobilized when the body is injured or has an infection. These cytokinesoften cause inflammation in their effort to repair an injured orinfected area of the body. In the case of heart failure, thisinflammation makes it even more difficult for the heart to pump blood.(Heart failure is a disease in which the heart loses the ability topump blood with normal efficiency.)
“People with heart failuretypically have much higher TNF-alpha levels than people without thedisease,” said Amy Ferketich, the study's lead author and an assistantprofessor of public health at Ohio State .
“But depression seems to make levels of this cytokine even higher, which is bad for patients.”
Thestudy's results appear in a recent issue of the American Heart Journal.Ferketich worked with Ohio State colleagues Jeanette PohorenceFerguson, a graduate student in pathology, and Philip Binkley, aprofessor of internal medicine.
They recruited 32 patients fromthe heart failure clinic at Ohio State . The participants answered the21-question Beck Depression Inventory, a tool that physicians andscientists use to measure symptoms of depression. Answers to eachquestion are given a value of zero (no symptoms at all) to 3 (severesymptoms). A score of 10 or more suggests that a patient has at leastmild symptoms of depression.
The researchers drew blood samplesfrom each patient. From these samples they evaluated levels of threecytokines: TNF-alpha, interleukin-6 (IL-6) and interleukin-1beta(IL-1beta). Previous research by other scientists has shown that thethree cytokines, which all cause inflammation, are elevated in patientswith heart failure.
Indeed, all of the patients in the study hadhigher-than-normal levels of each cytokine. However, TNF-alpha wasstill markedly higher in patients who reported feeling depressed on aregular basis.
“We were surprised to find that this wasn't thecase for the other two cytokines,” Ferketich said. “That suggests thatsomething about depression may trigger the production of TNF-alpha.”
Theresearchers measured cytokine levels in picograms, or trillionths of agram. Patients with scores of 10 or higher on the BDI had levels ofTNF-alpha nearly twice that of patients with a score less than 10 (4.9pg/ml vs. 2.7 pg/ml.)
Levels of the other two cytokines weresimilar for depressed and non-depressed patients: 5.9 pg/ml vs. 5.1pg/ml for IL-6 and 4.4 pg/ml and 3.6 pg/ml for IL-1beta, respectively.
Other researchers estimate that anywhere from 24 to 42 percent of heart failure patients also suffer from depression.
“Depressionclearly raises the levels of one cytokine, which plays a role inincreasing inflammation,” Ferketich said. “What we don't know for sureis if depression causes the inflammation which may lead to heartfailure or if heart failure causes depression which acceleratesinflammation.”
A study at Duke University found that patientswith major depression are twice as likely to die or to be re-admittedto the hospital a second time within 12 months.
“Patients withheart disease are prone to developing depression,” Ferketich said.“Physicians need to pay more attention to this. But research stillneeds to be done to find out if treating patients with anti-depressantswould help to actually slow the progression of heart disease.”
The study was supported by the National Institutes of Health's National Heart, Lung and Blood Institute.
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