Low levels of fat hormone may increase PTSD risk

New York: People who have low levels of a fat hormone might be more prone to developing post-traumatic stress disorder (PTSD) symptoms if they are exposed to a traumatic event, new research suggests.

Individuals with PTSD relive past traumas again and again, bound in a virtual prison of their memories.

The findings could lead to new treatment for PTSD as injecting this hormone – called adiponectin, which is secreted by fat cells called adipocytes – was found to decrease fear in mouse model of PTSD.

These mice were trained to associate a setting, such as a box, with a mild unpleasant stimulus. As expected, they showed a fear response when re-exposed to the setting.

Mice deficient for adiponectin and its receptor formed fearful memories just like healthy mice, but when placed again in the same setting minus the unpleasant stimulus, were slower to let go of the fear.

Injecting adiponectin prior to this training prompted faster learning to overcome fear, the measurements showed.

“Once the threat is no longer there, the fear should go away, but in PTSD it keeps flashing back,” said study senior author Xin-Yun Lu, professor at School of Medicine, The University of Texas Health Science Centre in the US.

“In the PTSD animal model, the circulating adiponectin is low, data suggest. If the genes encoding adiponectin and its receptor are disrupted, the mice extinguish fear responses much slower. If adiponectin levels are elevated in the brain, the mice get extinction faster,” Lu noted.

Adiponectin impairment is implicated in metabolic diseases such as obesity and Type-2 diabetes.

The new research, published in the journal Molecular Psychiatry, showed the hormone has a role beyond its metabolic control, Lu said.

“It is interesting that this hormone promotes fear extinction,” Lu said.

“Increasing adiponectin levels or activating its specific receptors might facilitate extinction-based exposure treatments for PTSD and other trauma- and stress-related disorders,” she noted.
IANS