I've been depressed for 4 years now. My depression started at the beginning of high school and coincidentally, at the beginning of my puberty. It has only gotten worse over the past 4 years. Now my motivation has disappeared and I have severe anhedonia. I only partially-enjoy doing a very limited number of things. My libido is non-existent and I have severe attention problems. I suspect I have low dopamine levels. I took 150 mg of Wellbutrin XL starting in October of 2011, but discontinued it after reading many negative studies about it; I read it can cause hypersensitivity and reduce white blood cell count, it can cause parkinsonism and it can reduce tyrosine hydroxylase expression. It's also anticholingeric. I was taking piracetam and choline bitartrate at the time, but it didn't help me with the short-term memory loss that was induced by Wellbutrin.
Wellbutrin helped me tremendously. It increased my libido, motivation, mood and allowed me to genuinely laugh at funny things for the first time in my life.
Did I overact when I decided to stop Wellbutrin? I remember reading a study that suggested antidepressants increased BDNF levels and therefore, antidepressants are neuroprotective.
Here's the study that suggested depression may cause neurotoxcicity:
A number of studies indicate that prolonged, major depression is associated with a selective loss of hippocampal volume that persists long after the depression has resolved. This review is prompted by two ideas. The first is that overt neuron loss may be a contributing factor to the decrease in hippocampal volume. As such, the first half of this article reviews current knowledge about how hippocampal neurons die during insults, focusing on issues related to the trafficking of glutamate and calcium, glutamate receptor subtypes, oxygen radical generation, programmed cell death, and neuronal defenses. This is meant to orient the reader toward the biology that is likely to underlie any such instances of neuron loss in major depression. The second idea is that glucocorticoids, the adrenal steroids secreted during stress, may play a contributing role to any such neuron loss. The subtypes of depression associated with the hippocampal atrophy typically involve significant hypersecretion of glucocorticoids, and the steroid has a variety of adverse effects in the hippocampus, including causing overt neuron loss. The second half of this article reviews the steps in this cascade of hippocampal neuron death that are regulated by glucocorticoids.
What should I do?