Mental Health and Environment

Elise Miller, MEd
Director

According to the National Institute of Mental Health, one in five children under the age of 18 have or have had a serious debilitating mental illness—that is even more than the proportion of children under 18 who have been diagnosed with a learning, developmental or behavioral disorder (which the CDC indicates in one in six). In this light, I was gratified to attend a meeting of the Northern California Association of Child and Adolescent Psychiatrists last month that focused on not only social stressors, but on toxic chemicals. In fact, this may have been the first time chemical contaminants appeared on the primary agenda at any meeting of a psychiatric association across the country. Given the scientific literature associating a number of chemicals—including pesticides, bisphenol A, flame retardants, lead and mercury found in products used or ingested every day—with learning and developmental disabilities, it would make sense that at least some of these chemicals could also play a role in mental illness (see: Scientific and policy statements on environmental agents associated with neurodevelopmental disorders by Steven G. Gilbert, et al). After all, if a chemical can disrupt the neurological system, the result could range from ADHD to depression depending on a number of other factors for that individual.

But why should a psychiatrist or psychotherapist care about possible chemical exposures? Well, if these health professionals understand that certain contaminants might hinder a person’s mental health, then it may be that a patient’s suffering could be alleviated by reducing their exposures to certain chemicals. No amount of prescriptions for psychopharmaceuticals nor talk therapy is going to ultimately help if the environment in which a person lives, works, studies or plays is contaminated and thereby contributes to a mental health diagnosis.

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You Are What Your Great-Grandmother Ate? Transmission of Obesity Across Generations

Sarah Howard
Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group

Two important studies have been published this month on chemical exposures that cause obesity in subsequent generations of rodents, long after the exposure ends. Until now, no prior studies on transgenerational obesogen exposures had been published. The results are alarming.

In the first study, pregnant mice (F0 generation) were exposed to low doses of the known obesogen tributyltin (TBT) and bred for 3 generations (up to the F3 generation). Thus, the F0 generation was exposed directly, the F1 generation exposed in the womb, the F2 generationsl could have been primordially exposed as germ cells in the developing fetus, and the F3 generation was not exposed directly (changes in the F3 generation are considered truly transgenerational). The TBT exposure had obesity-promoting effects on fat deposition on the F1 through the F3 generation, including increasing the number of fat cells, fat cell size, fatty tissue weights, and fatty livers (similar to non-alcoholic fatty liver disease (NAFLD) in humans). Interestingly, TBT exposure reprogrammed stem cells to develop into fat cells instead of bone cells.

The study, entitled “Transgenerational inheritance of increased fat depot size, stem cell reprogramming, and hepatic steatosis elicited by prenatal obesogen tributyltin in mice”, was written by Raquel Chamorro-García, Margaret Sahu, Rachelle J. Abbey, Jhyme Laude, Nhieu Pham, and Bruce Blumberg, of the University of California, Irvine.

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