Depression predisposes to panoply of infectious, autoimmune, cardiovascular and neurodegenerative disorders, and to cancer. Relatively recent additions include diabetes mellitus, Parkinson’s, Alzheimer’s and Huntington’s diseases, seizure disorders, chronic obstructive lung disease, congestive heart failure, and cancer. The intensity of depression appears to correlate with the severity, morbidity, and mortality of the disorders to which it predisposes. It is no longer a question of which disorders depression predisposes to, but to which it does not.
Increased synthesis of prostaglandins by brain enzymes above a critical threshold is responsible for depression on the one hand, and for defective immunity, autoimmunity, cancer, cardiovascular, and neurodegenerative disorders on the other. Antidepressants are often effective in preventing, alleviating or reversing these disorders. They inhibit the enzymes that synthesize prostaglandins, and stimulate the enzyme that degrades them. These mechanisms illuminate the cause of these disorders, but not their variations. Why does one person suffer from depression and heart disease, another from depression and recurrent infections, a third from depression and various autoimmune disorders? To what may one ascribe the variation among cancers?
The answers must reside within the arachidonic acid cascade, in the regulation by prostaglandins of the synthesis, inhibition and expression of genes, or both. In 1977 researchers showed that prostaglandins regulate nucleic acids. Later, others showed that prostaglandins regulate the synthesis, inhibition and expression of genes.
When the human genome was found to contain fewer genes than could account for human diversity, geneticists came up with “epigenetics” to search for factors that control our genes, while ignoring these studies. The logical conclusion is that excessive synthesis of prostaglandins converts the genes of physiology to those of pathology, the variations determined by the genes. Antidepressants are like a clutch, disengaging the brain in overdrive from genes, thus restoring physiological activity.
Why would excessive production of prostaglandins in the brain account for both defective immune, and autoimmunity? A provisional explanation, is that prostaglandins are inherently paradoxical. Why do antidepressants both alleviate disorders of defective immunity and autoimmunity?
A provisional explanation is that antidepressants have paradoxical actions on prostaglandins. More than forty years ago reports began to enter the literature on medical uses of antidepressants, their impact diluted by the apparent lack of credible pathological and pharmacological explanatory mechanisms. A cadre of researchers knew of the role of prostaglandins in these disorders, but few knew of the inhibitory actions of lithium and antidepressants on prostaglandins.
Medical Uses of Antidepressants:
High blood pressure (hypertension)
Ischemic heart disease
Preventing heart attacks
Recurrent heart attacks
Congestive heart failure
Allergic rhinitis (hay fever)
Ciguatera fish poisoning
Peptic ulcer disease
Irritable bower syndrome
Recurrent canker sores
Recurrent cold sores
Prevention, treatment, and recovery from strokes
Multiple sclerosis *
* Response is variable, but may be substantial. Tolerance may occur, but long term remission is possible. Clinical observation and epidemiological studies will tell the tale.
Low back pain
Tic doloroux (trigeminal neuralgia).
Peripheral neuritis of diabetes
Recurrent spontaneous first trimester miscarriages
Recurrent vaginal monilia (yeast) infections.
Numerous bacterial, viral, fungal and parasitic disorders.
Lithium tends to be effective, for acute or recurrent viral and bacterial infections, antidepressants for chronic viral, bacterial, parasitic, and fungal infections.
Often effective for arthritis, variably for multiple sclerosis, questionably for lupus erythematosus and amyotrophic lateral sclerosis. Tachyphyaxis and paradoxical exacerbation
are problems. Lithium not known to be effective, and may induce or worsen autoimmunity.
Hyperhidrosis (excessive sweating)
Alcohol, opiates, amphetamines, euphorohallucinogens, nicotine. Ironically, psilocybin, ketamime, ecstasy, and L.S.D are under investigation, not by the D.E.A, but by distinguished medical researchers, attempting to find a solution for the thirty percent of depressed people not responding to conventional antidepressants.
Veterinary, Marine and Space Medicine
These benefits apply in equal measure to veterinary, marine, and space medicine.
The ornithologist John Gould drew Charles Darwin’s attention to the variations between the beaks of finches. In studying sea barnacles, Darwin found that no two specimens were identical. Although Darwin is best known for his theory of natural selection, variation is the mechanism on which natural selection acts. Prostaglandins (as variation) determine the combinations and permutations of the actions of the brain on mood and immune function.
I believe when variation is extreme, it becomes paradoxical. One wonders how many “genetic” disorders might respond to antidepressants in dislocating nucleic acids from the impact of excessive prostaglandin production. The surprising effectiveness of antidepressants in such disorders as Huntington’s, autism and Down’s Syndrome suggests that they may be equally effective in muscular dystrophy, among others.
This information is for educational purposes only. All treatment decisions must be made in consultation with a physician.
For naysayers, Pubmed is loaded with evidence. This list is provisional andopen to modification, but it is a roadmap and blueprint, of where we should soon be headed.
I have no conflicts of interest.