Reversed Seasonal Affective Disorder

  Since we are just a little over a week past the summer solstice, which I personally really look forward, I thought reversed seasonal affective disorder would be a  timely topic.

 Most of you are familiar with SAD, with depression occurring more often in the winter months when the days are shorter and improving in the spring and summer when the days are filled with much more light. 

Well, reversed SAD is just the opposite.  I have seen this in just a few patients and accordingly, it comprises a very small minority indeed of around 1%!

Again this underlines the incredible individualistic variety of neuronal activity in humans.  In other words, we are all different!

Just because something makes most people feel better such as increased sunshine, it can have the opposite effect on a select few. Why this might happen is a complicated question.

First of all we must look at melatonin.  Melatonin is secreted by the pineal gland in the brain, which is dependent on the amount and duration of light picked up by the retina.

Serotonin is a precursor of melatonin.  Melatonin increases the production of progesterone, in women.

You may remember that progesterone is the “pregnancy” hormone responsibility for sleepiness and the mellowness or calming effect of first trimester women.

More light will decrease melatonin as it does in the spring and summer and there will be an increase of melatonin secretion in the fall and winter.

One wonders if in reversed SAD patients if decreased amounts of melatonin increases receptor site dysfunction or neuronal transmitters in ways we do not yet understand.

There has been a long-standing history of increased psychiatric admissions in the spring and fall for bipolar patients.

You can see more bipolar mania in the spring/summer and more depressive phases in the fall/winter.

Although SAD and bipolar disorder are two distinct and different disorders, one can nevertheless spot some overlapping similarities.

Primary of these is the instability of the neuron and then of course the seasonal aspects.  Bipolar patients are extremely sensitive to all sorts of stimuli.

This includes light, loud music, sleeplessness, over socialization at parties, caffeine and other stimulants.

Neurons in SAD seem to be only stimulated to variants of light induced levels of melatonin.  Perhaps melatonin plays a larger role in neuronal regulation that we know.

So I wonder if reversed SAD patients(those not pregnant) are more affected by lower progesterone levels since they have lower melatonin levels too?

I would say most women are affected by suddenly diminished progesterone levels as we see often in premenstrual syndrome and of course the baby blues postpartum.

Would the majority of all SAD patients be helped by the newer antidepressant, agomelatine that effects the serotonergic and melatonergic pathway?

One that is marketed in Europe, called Valdoxen is not available in the US, but treatment carries a risk of liver damage.

Not surprising that the majority of SAD patients are women. Once again this points to very complex interplay between the female hormones and their effects on neurons, which at least from a clinical viewpoint is quite obvious, if not completely understood!