We’re all familiar with terms such as "comfort food” and
"stress eating,” but is there really a scientific basis for the link between
obesity-related metabolic disease and stress-related psychological disorders?
Two College of Medicine faculty members say the answer is clearly yes, based on
current literature and their own collaborative investigations.
Yvonne Ulrich-Lai, PhD, an assistant professor in the UC Department
of Psychiatry and Behavioral Neuroscience, and Karen Ryan, PhD, an assistant
professor in the UC Department of Internal Medicine, Division of Endocrinology,
Diabetes and Metabolism, collaborate at UC’s Reading Campus, focusing on
interactions among diet, obesity and stress. Both receive research support from
the National Institutes of Health.
In a recent perspective paper for the journal Cell Metabolism, they gave an overview
of those interactions, including a review of current literature, discussion of
the role of reward-driven food intake and consideration of important
implications in the development of therapies for metabolism- or stress-related
"I’m by training primarily a stress researcher and I have
interest in how a person’s metabolic status affects the ability to cope with
stress,” says Ulrich-Lai. "Karen is primarily more of a metabolism/obesity
researcher, and she has interest in how that interacts with stress. So
together, we have complementary expertise in both topics.”
Put more simply: They can offer sophisticated insight into
why you might find yourself reaching for that fifth Girl Scout cookie when you
hear the boss’s footsteps approaching.
For example, in a 2010 study published in PNAS, the official
journal of the National Academy of Sciences, Ulrich-Lai and colleagues showed
that pleasurable activity—including food—reduces stress by inhibiting anxiety
responses in the brain. The research also indicated that the reduced-stress
effects continued for at least seven days, suggesting a long-term benefit.
In the Cell Metabolism
paper, "Neuroendocrine Circuits
Governing Energy Balance and Stress Regulation: Functional Overlap and
Therapeutic Implications,” Ulrich-Lai and Ryan cited separate studies showing
that obesity during the baseline period increased the risk of developing
depression and that depression increased the odds for developing obesity over time.
"Such associations likely arise … because neural circuits
governing energy balance and stress reactivity are substantially intertwined,
providing stress regulatory systems priority to redistribute fuels in response
to acute threats (or perceived threats) to an individual’s well-being,”
Ulrich-Lai and Ryan wrote.
The authors point out that these interrelationships have
important therapeutic implications, "underscoring the importance of assessing
the stress regulatory effects of metabolic therapies, as well as the metabolic
consequences of potential therapies for stress-related disorders.”
As Ulrich-Lai puts it: "Available research suggests that as
you develop a new therapy for one set of disorders, you should be considering potential
effects on the other systems.”
Ryan notes that the endocannabinoid receptor (CB1)
antagonist rimonabant, prescribed for the treatment of obesity, was withdrawn
from the European market in 2009 and was not approved in the United States
because its use was associated with significant increase in symptoms of
depression, anxiety and suicidal thoughts.
"There’s some interest in asking whether or not you can
avoid the brain side effects by targeting the appropriate receptors in
peripheral tissues,” she says. "The question becomes, can that approach
contribute to weight loss, and if you can create an effective compound that
doesn’t get into the brain could that potentially have a better side-effect
"But I think we would argue that the energy balance is so
tightly regulated by the brain that even if you’re targeting a peripheral
tissue, eventually you’re going to elicit changes in metabolic signals that may
act in the brain.”