OBJECTIVE: The incidence of posttraumatic stress disorder (PTSD) and obesity are on the rise, and evidence continues to support the observation that individuals who have symptoms of PTSD are more likely to develop obesity in their lifetime. The incidence of obesity in individuals with PTSD, including war veterans, women, and children exposed to trauma, is not solely attributable to psychotropic medications, but actual pathophysiologic mechanisms have not been fully delineated. Additionally, there are no studies to date demonstrating that obese individuals are predisposed to developing PTSD compared to the general population. This review explores the pathogenic pathways common to both PTSD and obesity, which include inflammation, the renin-angiotensin-aldosterone system, cellular structures, and neuroendocrine activation. DATA SOURCES AND SYNTHESIS: A PubMed search for the years 2000-2015 with the keywords PTSD and obesity was performed. There were no language restrictions. RESULTS: More research is needed in human subjects to understand the pathogenic pathways common to both PTSD and obesity and to further clarify the direction of identified associations. Ideally, in the future, clinical interventions targeting these pathways may be able to modify the course of PTSD and obesity. The outcome of studies investigating the utility of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in the treatment of PTSD symptoms will be relevant to control both PTSD and obesity. Importantly, outcomes assessing inflammation, obesity, and cardiac function in the same subjects also should be determined. CONCLUSION: Research is needed to reveal the multidimensional and intricate relationship between PTSD and obesity. The implications of this research would be essential for treatment, prevention, and potential public health reforms.
OBJECTIVE: The incidence of posttraumatic stress disorder (PTSD) and obesity are on the rise, and evidence continues to support the observation that individuals who have symptoms of PTSD are more likely to develop obesity in their lifetime. The incidence of obesity in individuals with PTSD, including war veterans, women, and children exposed to trauma, is not solely attributable to psychotropic medications, but actual pathophysiologic mechanisms have not been fully delineated. Additionally, there are no studies to date demonstrating that obese individuals are predisposed to developing PTSD compared to the general population. This review explores the pathogenic pathways common to both PTSD and obesity, which include inflammation, the renin-angiotensin-aldosterone system, cellular structures, and neuroendocrine activation. DATA SOURCES AND SYNTHESIS: A PubMed search for the years 2000-2015 with the keywords PTSD and obesity was performed. There were no language restrictions. RESULTS: More research is needed in human subjects to understand the pathogenic pathways common to both PTSD and obesity and to further clarify the direction of identified associations. Ideally, in the future, clinical interventions targeting these pathways may be able to modify the course of PTSD and obesity. The outcome of studies investigating the utility of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in the treatment of PTSD symptoms will be relevant to control both PTSD and obesity. Importantly, outcomes assessing inflammation, obesity, and cardiac function in the same subjects also should be determined. CONCLUSION: Research is needed to reveal the multidimensional and intricate relationship between PTSD and obesity. The implications of this research would be essential for treatment, prevention, and potential public health reforms.
Authors: Dorcas J Dobie; Daniel R Kivlahan; Charles Maynard; Kristen R Bush; Tania M Davis; Katharine A Bradley Journal: Arch Intern Med Date: 2004-02-23
Authors: Karl-Heinz Ladwig; Anne Catharina Brockhaus; Jens Baumert; Karoline Lukaschek; Rebecca T Emeny; Johannes Kruse; Veryan Codd; Sibylle Häfner; Eva Albrecht; Thomas Illig; Nilesh J Samani; H Erich Wichmann; Christian Gieger; Annette Peters Journal: PLoS One Date: 2013-07-03 Impact factor: 3.240
Authors: Jose M Santiago Santana; Julio D Vega-Torres; Perla Ontiveros-Angel; Jeong Bin Lee; Yaria Arroyo Torres; Alondra Y Cruz Gonzalez; Esther Aponte Boria; Deisha Zabala Ortiz; Carolina Alvarez Carmona; Johnny D Figueroa Journal: Behav Brain Res Date: 2020-12-07 Impact factor: 3.332
Authors: Carolina Muniz Carvalho; Frank R Wendt; Gita A Pathak; Adam X Maihofer; Dan J Stein; Jennifer A Sumner; Sian M J Hemmings; Caroline M Nievergelt; Karestan C Koenen; Joel Gelernter; Sintia I Belangero; Renato Polimanti Journal: Neurobiol Stress Date: 2021-09-17
Authors: Thomas P Chacko; J Tory Toole; Spencer Richman; Garry L Spink; Matthew J Reinhard; Ryan C Brewster; Michelle E Costanzo; Gordon Broderick Journal: Front Psychol Date: 2022-07-26
Authors: Julio D Vega-Torres; Matine Azadian; Raul A Rios-Orsini; Arsenio L Reyes-Rivera; Perla Ontiveros-Angel; Johnny D Figueroa Journal: Front Neurosci Date: 2020-06-30 Impact factor: 4.677