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Anxiety and the Effects of Sodium Lactate Assessed Clinically and Physiologically

Published online by Cambridge University Press:  29 January 2018

Desmond Kelly ,
Nita Mitchell-Heggs  and
Daniel Sherman
Desmond Kelly
Affiliation:
St. George's Hospital Medical School, Atkinson Morley's Hospital, 31 Copse Hill, London, S.W.20 (Department of Psychological Medicine, St. Thomas' Hospital)
Nita Mitchell-Heggs
Affiliation:
St. Thomas' Hospital, London, S.E.1
Daniel Sherman
Affiliation:
The Johns Hopkins Hospital, Baltimore, Maryland, U.S.A.
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Extract

Anxiety neurosis has been the subject of intensive study during the past ten years. Renewed interest in this syndrome has arisen both from the stimulus of new methods of treatment and from attempts to classify anxiety more accurately. Recently Pitts and McClure (1967) reported that anxiety symptoms and anxiety attacks could be produced by a specific biochemical stimulus: sodium lactate. This work was prompted by the finding that 'standard exercise’ tends to produce an excess amount of lactic acid in patients with anxiety neurosis (Cohen and White, 1950; Jones and Mellersh, 1946; Linko, 1950; Holmgren and Strom, 1959). Pitts and McClure found that an intravenous infusion of 10 ml. of half-Molar sodium (DL) lactate per kilogram of body weight, given over a twenty minute period, produced an anxiety attack in patients suffering from anxiety neurosis. The symptoms began a minute or two after the infusion was started and developed rapidly, and some patients reported ‘exacerbations of their characteristic symptom profiles for two to five days after the sodium lactate infusion’. In their double-blind study, many fewer symptoms were produced when calcium ion was added to the lactate infusion, and almost no symptoms were produced by an infusion of glucose in saline of similar osmolarity. Many fewer and less severe symptoms were produced in normal controls than in the patient group, both in response to sodium lactate and to lactate with added calcium, and almost no symptoms during the glucose and saline infusion. Pitts and McClure postulated that anxiety symptoms may have a common determining biochemical end-mechanism, involving the complexing of ionized calcium at the surface of excitable membranes by lactate ion with resulting interference ‘with the normal functioning of calcium in transmitting nerve impulses' (Pitts, 1969). They concluded that ‘there may be something highly specific about lactate ion in producing the naturally occurring hypocalcaemic anxiety symptoms in human beings'.

Type
Research Article
Information
The British Journal of Psychiatry , Volume 119 , Issue 549 , August 1971 , pp. 129 - 141
Copyright
Copyright © The Royal College of Psychiatrists, 1971 

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