A new blood test for depression?

Dr. Weeks’ Comment:  Depression can be hard to accurately diagnosis and all too frequently is determined either by “intuition” (“clinical judgment) or simply on the patients’ say so:  the self-assessment or declaration.  However, there are physiologic parameters which must be considered in addition to the patient’s account of neuro-vegative signs (appetite, sleep, mood, energy, feelings of helplessness, hopelessness, worthlessness). While all this information is fairly moot/academic since primary care doctors dispense most of the antidepressant medications in the USA,  nonetheless plasma aldosterone levels, if normal, might argue against a diagnosis of depression. 

(thanks to Dr. Pilar for bringing this to our attention!)

 

Increased Plasma Aldosterone in Patients with Clinical Depression
Enzo Emanuele, Diego Geroldi, Piercarlo Minoretti, Enrico Coen, Pierluigi Politi
March 29th  2005.

Background
Clinical depression has been increasingly recognized as an independent risk factor for adverse cardiovascular events, but the biological mechanisms of this association remain unclear. Recent evidence for renin system dysregulation in patients with depression led us to hypothesize that aldosterone””a well-recognized contributor to vascular injury””could be increased in depressed patients. The present study was designed, therefore, to be a cross-sectional investigation of plasma renin and aldosterone levels in depressed patients as compared with healthy controls with no history of psychiatric illness.

Methods
A total of 65 depressed patients and 65 age- and gender-matched control subjects were enrolled. Following a fixed sodium and potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the influence of circadian rhythms.

Results
Although there were no significant differences in plasma level of renin among subjects with depression and controls (7.9 ± 5.8 vs. 6.4 ± 4.3 pg/mL, respectively; p=0.10), depressed subjects exhibited greater mean aldosterone levels as compared with control subjects (157.2 ± 67.5 vs. 125.7 ± 38.1 pg/mL, respectively; p=0.0014). After adjusting for potential confounders, multivariate logistic regression analysis showed that subjects with depression had 2.77 times higher odds of elevated aldosterone levels compared with healthy control subjects (95% confidence interval, 1.30-5.92, p=0.008).

Conclusions
Our present findings support the hypothesis that hyperaldosteronism could be a common feature among depressed patients, thereby suggesting that increased aldosterone levels may act as a mediator in the pathway linking depression to unfavorable vascular events.

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