19 Jun 2018 --- Adolescent rats who consume a diet high in saturated fats are at an increased risk of psychopathology in adulthood, a study published in the journal Brain, Behavior, and Immunity has found. Moreover, the researchers from Loma Linda University in California found that the areas of the brain that handle the fear/stress response were altered to the point that subjects began exhibiting behaviors that mirror post-traumatic stress disorder (PTSD). The findings could help researchers to target mental health illness in the coming generations and express the lasting, and potentially irreversible, effects of a poor diet.
“The teen years are a very critical time for brain maturation, including how well (or not) we'll cope with stress as adults,” says Dr. Johnny Figueroa, Assistant Professor, Division of Physiology, Department of Basic Sciences and Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine. “The findings of our research support that the lifestyle decisions made during adolescence - even those as simple as your diet - can make a big difference in our ability to overcome everyday challenges.”
“Although more research is needed to clarify our findings, the anatomical and behavioral patterns observed in the obese rats suggest that consumption of an obesogenic high-saturated fat diet during the critical brain maturational period of adolescence increases the risk of psychopathology and conduct disorders.”
Startle reflexes, which are studied in humans and lab animals, have a prominent role in anxiety and PTSD research. In this study, consumption of an obesogenic diet during adolescence reduced the extinction of fear memories - a major impairment observed in people suffering from PTSD. In addition to not properly learning fear associations, the rats on the high-saturated fat diet incorrectly assessed the level of threat. This suggests that obesity and associated metabolic alterations may predispose individuals to PTSD-related psychopathology.
“Normally, in rodents, exposure to threatening environments alters fear conditioning, resulting in enhanced acquisition and reduced extinction of fear. Surprisingly, we found that the rats that were exposed to the obesogenic diets exhibited atypical fear conditioning, resembling externalizing psychopathology. The rats that consumed the obesogenic diet during adolescence showed impaired fear conditioning and poor discrimination between conditioning and non-conditioning cues. This pattern of altered fear conditioning has been associated with PTSD and proposed as a mechanism of increased risk factor for psychopathology in maltreated children,” Figueroa tells NutritionInsight.
Study findings demonstrate that the consumption of an obesogenic diet during adolescence has a profound effect on phasic and sustained components of fear in the adult rat. Notably, the rats that consumed the high-saturated fat diet exhibited more anxiety, problems with associative and non-associative learning processes and an impaired fear-startle response.
Understanding the neural networks that predispose obese adolescents to develop anxiety and stress-related disorders may help target metabolic measures to alleviate the burden of mental illness in this growing population.
“The findings of the study have implications for stress management and general mental health not only for obese individuals but for individuals that were obese and overweight early in life. The findings of poor threat–safety discrimination in our model might reflect either enhanced fear generalization or a more global deficit in associative learning. Disruptions in fear conditioning (and its brain circuits) might represent a mechanism underlying the development of stress-related psychopathology in obese individuals. Our study supports that lifestyle choices during adolescence, including diet, have a long-term impact on mental health. Considering that childhood and adolescent obesity is linked to stress-related psychopathology, a scenario thus emerges in which a dramatic increase to the levels of mental and conduct disorders could emerge in the next few years,” Fidueroa adds.
Figueroa says the study leaves other questions open for further investigation, such as replicability in human subjects and if the alterations seen in the brain structures are permanent or whether the effects can be reversed. Study limitations include lack of clarity on how the high-saturated fat diet impacts the adult brain, and whether the effects of the obesogenic diet on the fear response are related to deficits in fear memory consolidation, retrieval, and expression.
“There is an unmet need to identify molecular mechanisms connecting nutrition, stress, and mental health. Very little is know about the interplay between these factors, particularly in the adolescent brain. If we are to effectively combat the obesity epidemic, we must improve our mechanistic understanding of the consequences of early-life obesity in the brain. Another important area that warrants research is the identification of targetable processes to improve cognitive function in overweight/obese populations at risk. Our research is now focused to identify interventions that show promise to ‘rewire’ the brain of obese individuals,” he adds.
By Laxmi Haigh
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