Older adult psychiatric inpatients with non-cognitive disorders should be screened for vitamin B12 deficiency.

OBJECTIVE: Vitamin B12 (B12) deficiency is most prevalent among older adults. Practice guidelines recommend screening older adults with symptoms of cognitive disorder for B12 deficiency. However, guidelines for non-cognitive psychiatric disorders typically do not mention screening older adults for B12 deficiency. The purpose of this study was to determine whether routine screening of older adult psychiatric inpatients for B12 deficiency, regardless of cognitive symptoms, is clinically justified. DESIGN: We conducted a retrospective chart-review study of consecutive inpatient admissions. SETTING: Older Adult Acute Psychiatric Inpatient Unit at the University of Maryland Medical Center from 10/2007-4/2010. PARTICIPANTS: Acute psychiatric inpatients aged ≥50 years who met inclusion criteria (N=374). MEASUREMENTS: Mean (SD) B12 levels and percentages of probable (<180pg/mL) and possible (180-350pg/mL) B12 deficiency as well as characteristics of patients with probable and possible B12 deficiency compared to patients with optimal B12 levels. RESULTS: Mean (SD) B12 levels and percentages of probable and possible B12 deficiency, respectively, for cognitive disorder patients [468 (284) pg/mL, 7.8 % (n=5) and 29.7% (n=19)] and for non-cognitive disorder patients [481(268) pg/mL, 4.8 %(n=15) and 33.2%( n=103)] were not significantly different (t=0.339, df=372, P=0.735; χ2=1.084, df=2, P=0.582, respectively). CONCLUSION: Considering the potential benefits and low costs of screening and treatment, we conclude that it is justified to routinely screen older adult psychiatric inpatients for B12 deficiency whether or not cognitive disorder symptoms are present.

Mitochondrial detachment of hexokinase 1 in mood and psychotic disorders: implications for brain energy metabolism and neurotrophic signaling.

The pathophysiology of mood and psychotic disorders, including unipolar depression (UPD), bipolar disorder (BPD) and schizophrenia (SCHZ), is largely unknown. Numerous studies, from molecular to neuroimaging, indicate that some individuals with these disorders have impaired brain energy metabolism evidenced by abnormal glucose metabolism and mitochondrial dysfunction. However, underlying mechanisms are unclear. A critical feature of brain energy metabolism is attachment to the outer mitochondrial membrane (OMM) of hexokinase 1 (HK1), an initial and rate-limiting enzyme of glycolysis. HK1 attachment to the OMM greatly enhances HK1 enzyme activity and couples cytosolic glycolysis to mitochondrial oxidative phosphorylation, through which the cell produces most of its adenosine triphosphate (ATP). HK1 mitochondrial attachment is also important to the survival of neurons and other cells through prevention of apoptosis and oxidative damage. Here we show, for the first time, a decrease in HK1 attachment to the OMM in postmortem parietal cortex brain tissue of individuals with UPD, BPD and SCHZ compared to tissue from controls without psychiatric illness. Furthermore, we show that HK1 mitochondrial detachment is associated with increased activity of the polyol pathway, an alternative, anaerobic pathway of glucose metabolism. These findings were observed in samples from both medicated and medication-free individuals. We propose that HK1 mitochondrial detachment could be linked to these disorders through impaired energy metabolism, increased vulnerability to oxidative stress, and impaired brain growth and development.