The Impact of Impaired Glycemic Control on Bipolar Disorder


As the intricate relationship between impaired glycemic control and bipolar disorder begins to unravel, possible directions for treatment options for the mood disorder continue to expand.

The risk of metabolic side effects has long been a prominent concern when determining optimal treatment for a variety of psychiatric disorders. This is perhaps most significant for patients with disorders of mood instability and psychosis since the second generation antipsychotics (SGA) have proven to be extremely effective. These medications present varying risks for causing or contributing to metabolic syndrome.

Many of the discussions at APA 2015 highlighted the significance of poor blood glucose control on psychiatric morbidity and mortality. They emphasize our roles as physicians to look at the whole picture: body, brain, and mind. As the field begins to unravel the intricate relationship between impaired glycemic control and bipolar disorder, the possible directions for treatment options continue to expand.

In some of the studies discussed, it was found that up to 53% of bipolar disorder patients have pre-diabetes or diabetes. More alarming yet is that up to 75% of these patients did not know they had impaired glycemic control. The gravity of these numbers really hits home when we keep in mind that the leading cause of death among patients with bipolar spectrum disorders is cardiovascular disease. It is often easier to remember to screen for suicidal risk factors, such as access to firearms that threaten the well-being of our patients here and now. However, the long-term poorly-controlled blood sugars of many patients will end up claiming more lives.

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From this point forward, I for one will look at poor glycemic control among this patient population as a loaded gun (pun intended).

While the neurotoxic effects of hyperglycemia are well known, a prominent theme heard at the APA is the direct effect of insulin on neuronal function. I learned that insulin is believed to serve as a neurotropic factor, similar in some respects to brain-derived neurotropic factor (BDNF). Insulin may play a role in inhibiting neuronal apoptosis, regulating beta amyloid plaque deposition and tau protein function, broadening the scope of patients to those with neurocognitive disorders for whom this is of particular importance.

It is not hard to imagine that compromised insulin function could detrimentally affect neuronal health and function, leading to prominent neurocognitive symptoms. Studies discussed showed reduced hippocampal size and poorer cognitive performance among bipolar patients with type 2 diabetes mellitus compared with patients who had bipolar disorder alone. Conversely, bipolar patients with optimal glycemic control showed increased grey matter volume compared with their less optimally glycemic controlled peers.

We also heard how insulin resistance was shown to reduce patient response to lithium for treatment of bipolar disorder. There does appear to be a relationship between insulin resistance and bipolar disorder but its nature is unclear. More than likely, the mechanism will be complex, involving numerous other variables.

Might there be a common etiology underlying both insulin resistance and bipolar disorder (or at least a subset)? A few of the clues that connect the two include a relationship with the hypothalamic-pituitary axis, increased noradrenergic tone, and elevated markers for neuro-inflammation. Etiological considerations for a number of psychiatric illnesses including major depression, bipolar disorder, and schizophrenia have begun to look more closely at the role of the latter.

Given the plethora of anti-inflammatory tools already being used by many of our medical peers, optimism for continued improvement in the treatment of our patient population grows each day.


Dr Prabhu is Chief Resident in the Department of Psychiatry and Neuroscience at Detroit Medical Center/Wayne State University.

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