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David A. Barton, FRANZP; Murray D. Esler, MBBS, PhD; Gavin W. Lambert, PhD

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Dr Anderson's critique rests heavily on his a priori assumption that the variability in serotonin turnover that we describe is inconsistent with the underlying physiological process examined. Such a view is not consistent with the observations that brain serotonin is involved in an array of physiological processes and may be influenced by, among other things, season,^1-3 bright light,^3-4 and adiposity.⁵ Otte and colleagues⁶ recently documented an association between carriage of the s allele of the serotonin transporter, depression, perceived stress, elevated urinary norepinephrine levels, and, by inference, sympathetic nervous activation. Using direct cardiac catheterization techniques coupled with state-of-the-art norepinephrine isotope dilution methods, we have recently demonstrated that sympathetic activity in unmedicated patients with depression follows a bimodal distribution, with values in some patients being extraordinarily high and others being marginally lower than those found in . . . [Full Text of this Article]

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