Nutritional Influences on Illness: Anxiety; Dietary Influences

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Nutritional Influences on Illness: Anxiety; Dietary Influences

Anxious patients often report that physical exertion can elicit or increase their anxiety and its physical manifestations and we have known for about half a century that, during exercise, people who suffer from panic attacks develop excessive lactic acid levels in their blood. Proof that excessive blood lactate could cause an attack of intense anxiety in susceptible people came in 1967, when Pitts and McClure published an article in the New England Journal of Medicine which reported that a lactate infusion yielding concentrations equivalent to those produced during strenuous exercise would elicit anxiety symptoms in patients with anxiety neurosis but not in normals.( 1)

To understand the metabolic role of lactic acid, we first need to review the important process of glycolysis. Glycolysis (the degradation of glucose) is a key biochemical pathway for the release of energy. When oxygen is present, and the cell contains mitochondria, pyruvate is the end product of glycolysis and it enters the citric acid cycle where it is eventually metabolized to carbon dioxide and water.

Because of the vital importance of glycolysis for cellular energy, we have an alternative pathway to utilize when the conditions for aerobic glycolysis are not met; this pathway serves as an emergency backup energy-producing system. Anaerobic glycolysis can still release energy, but the amount is smaller. Its end product, instead of pyruvate, is lactate. The more this pathway is utilized, the higher the ratio is of lactate to pyruvate.

It has been theorized that, in susceptible people, elevation of this lactate/pyruvate ratio may be a cause of anxiety.( 2) While this model of anxiety is far from perfect, you will find that it helps to explain some of the observed relationships between anxiety and nutritional factors.

Many anxious patients find sugar elimination to be effective in reducing their anxiety levels. One explanation may be the finding that, in anxiety-prone patients, a glucose load increases lactate while decreasing pyruvate, thus elevating the lactate/pyruvate ratio.( 2) Also, the elevation in blood glucose following sucrose ingestion stimulates insulin release, and may thus cause a reactive decrease in blood glucose. In susceptible people, a relatively low blood sugar level may be associated with enough of a reduction in brain sugar to be associated with anxiety.( 2)

Caffeine is another substance that increases the lactate/pyruvate ratio.( 3) Results of controlled studies have shown that people with elevated levels of anxiety, especially if they are prone to panic attacks, are unusually sensitive to the anxiogenic effects of caffeine. In addition, withdrawal from regular caffeine intake may temporarily exacerbate anxiety.

Alcohol causes a sharp rise in the hepatic ratio of niacinamide adenine dinucleotide (NAD) to NADH. This inhibits gluconeogenesis (the formation of glucose) from lactate, raising the lactate/pyruvate ratio.( 3) While people often drink alcoholic beverages to relieve anxiety, under placebo-controlled conditions, its ingestion may actually increase anxiety.( 4) Like other brain depressants, tolerance develops with continued use, eventually resulting in withdrawal phenomena.

Alcohol may also contribute to anxiety by fostering reactive hypoglycemia. While this effect could be explained by the high sugar content of many alcoholic beverages, alcohol itself increases the production of hydrochloric acid which may cause the excessive release of gut secretagogues. These substances augment beta-cell responsiveness to fluctuations in blood sugar levels, resulting in excessive insulin release and, consequently, hypoglycaemia.( 5)

Anxiety is well-known to be part of acute alcohol withdrawal syndromes, but there is also a subacute withdrawal syndrome that consists of anxiety, hyperventilation and alcohol craving.( 6) Therefore, if you have an anxious, hyperventilating patient with a history of alcoholism, ask how long it has been since that last drink!

Doctor Werbach cautions that the nutritional treatment of illness should be supervised by physicians or practitioners whose training prepares them to recognize serious illness and to integrate nutritional interventions safely into the treatment plan.

References
(1.) Pitts FN Jr. McClure JN Jr. Lactate metabolism in anxiety neurosis. N Engl J Med 277(25): 1329-36, 1967.

(2.) Wendell OW, Beebe WE. Glycolytic activity in schizophrenia, in D Hawkins & L Pauling, Eds. Orthomolecular Psychiatry: Treatment of Schizophrenia. San Francisco, W. H. Freeman, 1973

(3.) Alberti KG, Nattrass M. Lactic Acidosis. Lancet ii: 25-9, 1977.

(4.) Monteiro MG et al. Subjective feelings of anxiety in young men after ethanol and diazepam infusions. J Clin Psychiatry 51(1): 12-16, 1990.

(5.) Freinkel N, Getzger BE. Oral glucose tolerance curve and hypoglycemias in the fed state. N Engl J Med 280: 820-8, 1969.

(6.) Roelofs SM. Hyperventilation, anxiety, craving for alcohol; a subacute alcohol withdrawal syndrome. Alcohol 2(3): 501-05, 1985.

Reprinted with permission from the International Journal of Alternative and Complementary Medicine, Green Library, 9 Rickett St., Fulham, London SW6 1RU, United Kingdom.

Townsend Letter for Doctors & Patients.

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By Melvyn R. Werbach

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