I was diagnosed as bipolar with psychotic features at age 41. I had several psychotic episodes over a period of several years before I discovered that adding a large quantity of salt to my diet could halt my illness. I was never diagnosed as being hyponatremic while in the hospital so I’m guessing that my low sodium level was an intermittent problem. After purchasing a commercial salt concentration meter, I discovered that my urinary salt level rose substantially during the evening. The level was normal during the daytime and while I was asleep. This is an indication that my body actively got rid of salt during the evening and my sodium blood level dropped at this time. I believe that low testosterone may be the culprit because of its circadian rhythm and effect on sodium reabsorption in the kidneys. I have yet to determine how low sodium levels effected my brain, but for the past three years I’ve had no psychotic episodes. All of my other mental and some physical symptoms have been eliminated as I’ve optimized the salt level. Currently I’m consuming about 14 grams of salt and a total of 1.9 liters of water for my body weight of 85 kg. Fortunately my blood pressure has not increased. Before my illness struck I had only been consuming a couple grams of salt a day. From my reading, I’ve found that about 10.5% of psychiatric patients are diagnosed as also being hyponatremic upon admission to a hospital. This is more than ten times the number of all other hospital admissions. My guess is that many more are hyponatremic the evening before admission. Currently hyponatremia is thought of as a symptom of polydipsia, an additional mental illness. From my experience, I believe it should be looked at as possible cause of bipolar disorder and possibly several other mental illnesses.
This post was submitted by Mr. Marlow .
Firstly, I should make it very clear that I cannot comment on an individual\’s case in this blog. However, a few general comments may be in order. Sodium is vital for health and abnormal levels are associated with a number of illnesses. The first objective should be to exclude frank endocrine disorders and a consultation with a suitably qualified physician should be arranged. I would not advise anyone to treat symptoms of bipolar disorder by consuming excess salt but rather establish the cause of any putative hyponatraemia. Sodium does have a possible role in the pathophysiology of severe affective disorder and this may be related to hormones (e.g., aldosterone) or membrane mechanisms (the sodium pump) but there are no treatments based on this at present.
Research into electrolytes has a long history in bipolar disorder, focussing mainly on the sodium pump. It perhaps commenced with Naylor’s observations in the 1970s that erythrocyte membrane Na,K-ATPase activity was altered in manic patients. El-Mallakh’s group in the USA found that the Na,K-ATPase-inhibiting compound, ouabain, increases the intracellular sodium concentration and induces manic activity in animals. These effects can be normalized by lithium (Huang et al, 2007). They also reported that ouabain increased the expression of the glial-specific alpha2 isoform of the sodium pump in the basal ganglia and the alpha3 isoform in the frontal cortex. These findings, in association with human post mortem studies finding that alpha2 is underexpressed in the temporal cortex of bipolar subjects, suggest that Na pump isoform expression may be of particular interest in the pathophysiology of mania (Hamid et al, 2009). By contrast, there is less recent research on alterations in serum sodium in bipolar disorder. In a separate field, it has long been known that about 5% of people of African origin with hypertension respond to amiloride. The T594M polymorphism of the epithelial sodium channel, which is found in approximately 5% of people of African origin, is significantly associated with high blood pressure. Baker et al (2002) reported that amiloride is effective in controlling blood pressure in those hypertensive individuals of African origin with this polymorphism. It is to be hoped that greater understanding of electrolyte pathophysiology will lead to innovative treatments in affective disorder. Like Prof Young, I can neither comment on an individual case nor recommend treatment by excessive salt intake, which is a recognised cause of hypertension. Baker et al Amiloride, a specific drug for hypertension in black people with T594M variant? Hypertension, 2002, Jul;40(1):13-7. Hamid et al. Effect of ouabain on sodium pump alpha-isoform expression in an animal model of mania. Prog Neuropsychopharmacol. Biol Psychiatry, 2009, Oct1;33: 1103-1106. Huang et al. Lithium normalizes intracellular sodium. Bipolar Disorders, 2007; 9: 298-300.