General Toxicity to Neurons and Other Cells

Writing from the viewpoint of the pharmacologist, rather than the psychiatrist, Peach (1975) observed  

The accumulation of lithium in the intracellular environment could be envisioned to perturb any event that is modulated by monovalent cations, e.g., sodium or potassium. These possible interactions signify the 

Lithium disrupts almost every measurable cellular activity pertaining to nerve transmission as well as many other vital functions. In addition, its distribution is fairly uniform throughout the central nervous system, with no known areas of specific concentration. It produces what Wilson et al. (1975) called a nonselective diminution in neuronal activity. The neurophysiology of lithium, even without supporting clinical data, renders absurd the notion of a specific biochemical treatment for a specific disease and confirms the brain-disabling effect. 

Lithium also impairs the function of the peripheral nervous system, reducing motor nerve conduction velocity (Faravelli et al., 1999). It causes many metabolic adverse effects, resulting in hypothyroidism, hyperthyroidism (rare), hyperparathyroidism, and diabetes insipidus (Livingston et al., 2006). 

Psychiatry has gone from denying that lithium causes kidney damage to trying to ignore it. The threat is very real. Lepkifker et al. (2004) reviewed the files of 140 patients exposed to lithium for at least 4 years and found that 20% developed creeping creatinine (a laboratory test for kidney malfunction) and renal insufficiency. Overall, lithium is very toxic to cells (Yao et al., 1999). 

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