This may be an avenue for significantly reducing much of the morbidity in ME associated with dehydration, tachycardia, OI, etc. We need more doctors willing to investigate this avenue of treatment for a subset of our symptoms. Personally, it is my impression that a primary reason for the failure to go down this road is fear (patients, advocacy groups and doctors); fear of admitting that this disease is as serious as it really is (we're talking indirect evidence of brain damage - direct evidence is accumulating), fear of a maligned medication, fear of deviating from the "standard of care," and doctors who are unfamiliar with pituitary and hypothalamus function and as a result fear going into areas where they have no experience. Desmopressin acutely decreases tachycardia and improves symptoms in the postural tachycardia syndrome. Coffin ST, Black BK, Biaggioni I, Paranjape SY, Orozco C, Black PW, Dupont WD, Robertson D, Raj SR. Autonomic Dysfunction Center, Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University, Nashville, Tennessee. Heart Rhythm. 2012 May 3. [Epub ahead of print] BACKGROUND: Postural tachycardia syndrome (POTS) induces disabling chronic orthostatic intolerance with an excessive increase in heart rate on standing, and many patients with POTS have low blood volume. Increasing blood volume is a promising approach to this problem. OBJECTIVE: To test the hypothesis that desmopressin (DDAVP) will attenuate the tachycardia and improve symptom burden in patients with POTS. METHODS: In this protocol, patients with POTS (n = 30) underwent acute drug trials with DDAVP 0.2 mg orally and placebo, on separate mornings, in a randomized crossover design. Blood pressure, heart rate, and symptoms were assessed while seated and after standing for up to 10 minutes prior to and hourly for 4 hours following study drug. RESULTS: The standing heart rate was significantly lower following DDAVP than placebo (101.9 ± 14.5 beats/min vs 109.2 ± 17.4 beats/min; P <.001). Standing blood pressure was not affected (P = .28). The symptom burden improved with DDAVP (from a score of 18 ± 18 arbitrary units [AU] to 13 ± 15 AU at 2 hours) compared with placebo (from 18 ± 17 AU to 19 ± 16 AU; P = .010). CONCLUSIONS: Oral DDAVP significantly attenuated tachycardia and improved symptoms in POTS. The safety profile of this approach would need to be examined before it can be recommended for routine treatment of these patients.