When obesity and depression begin in childhood, the conditions tend to persist throughout life, often playing out in a painful cycle. For example, young people with depression may experience a bout of overeating to try to make themselves feel better, followed by weight gain, ongoing depressed feelings and then weight-related bullying that further worsens their depression.
Although previous brain-scan studies focused on either obesity or depression have revealed abnormalities in the brain’s reward centers, the new study is the first to document this link among both conditions in children.
“Independently, in obesity and depression, the same brain networks popped up, and that was curious to us,” said the study’s lead author, Manpreet Singh, M.D., assistant professor of psychiatry and behavioral sciences at Stanford University School of Medicine. “We thought maybe that was a link that would help us understand better why these symptoms coexist.”
For the study, the Stanford researchers analyzed the brain scans of 42 children and teenagers, aged 9 to 17. All had a body-mass index greater than the 85th percentile and also struggled with moderate-to-severe untreated depressive symptoms. All study participants were offered treatment referrals.
Prior to seeking treatment, they were assessed with standard clinical tests and questionnaires to gauge their levels of depression, their experience of pleasure and certain eating behaviors, such as uncontrolled eating and emotional eating. They also had their insulin resistance measured while fasting and after consuming a standard dose of glucose.
The findings show that participants with both depression and obesity had low volumes in two of the brain’s reward-processing areas: the hippocampus and anterior cingulate cortex. The participants’ brain abnormalities also were linked to their level of insulin resistance.
Insulin helps sugar move from the blood into the body’s cells, where it can be used as fuel. When a person is insulin-resistant, the hormone works less effectively than usual; insulin resistance is a marker of metabolic dysfunction that precedes Type 2 diabetes.
Compared with insulin-sensitive participants, participants with more insulin resistance experienced less pleasure from eating, had more eating disinhibition (meaning they were more likely to eat in an unrestrained manner) and also had more generalized anhedonia (difficulty experiencing pleasure).
“We want to help children and families understand that these conditions are brain-based phenomena,” said Singh, who is also a child and adolescent psychiatrist at Lucile Packard Children’s Hospital Stanford.
Children and teens who struggle with both depression and their weight often feel stigmatized and may hesitate to pursue treatment, he said. “We want to destigmatize these issues. Understanding that there’s a brain basis may help both children and parents be solution-focused.”
In previous studies, Stanford researchers had already noted how these same changes could be seen in adults with obesity and depression.
“With this new study, we are trying to understand the earliest age at which this vulnerability begins, and also the earliest time we will be able to intervene when we find the appropriate intervention,” said the study’s senior author, Natalie Rasgon, M.D., Ph.D., professor of psychiatry and behavioral sciences.
“Early intervention is important because, later in life, these are the same brain areas which will ultimately be vulnerable to neurodegenerative processes as well. It’s a double whammy.”
The characteristics of the childrenâ€™s hippocampus and anterior cingulate cortex were correlated to their levels of insulin resistance and also to their degree of depression, with lower volumes of the two brain regions in those who had more insulin resistance or severe depression, or both.
Higher levels of insulin resistance and depression were also linked to stronger connections between the two reward centers. The childrenâ€™s insulin levels during fasting versus after consuming glucose correlated to the exact location and nature of their brain abnormalities, with somewhat different brain features in those whose insulin was higher during fasting rather than after-glucose states.
Source: Stanford Medicine