[QUOTE=chaos]Is it true a drug like Prozac can be used to help treat adrenal fatigue? how?[/QUOTE]
You have to first define the term “Adrenal Fatigue”. When you look at James Wilson ND’s book “Adrenal Fatigue – the 21st Century Stress Syndrome”, you will find that Adrenal Fatigue is his term for any Non-Addison’s Disease form of low adrenal function which is primarily caused by stress.
This term is primarily descriptive. It doesn’t define the actual physiologic changes that lead to lower adrenal function. It includes a very broad array of conditions and illnesses that includes most mental illlnesses such as depression, anxiety, posttraumatic stress disorder. If anything, posstraumatic stress disorder is the best example of adrenal fatigue. However, stresses can also include infections, surgeries, and other non-psychological stresses.
Note that the primary contributing factor to the development of adrenal fatigue is “stress”.
Prozac and the Serotonin Reuptake Inhibitors (SSRIs) work by increasing the signal duration of serotonin. Serotonin reduces the perception of stress and reduces norepinephrine, the primary signal for stress, in the nervous system. There are other secondary events once these primary actions of serotonin are accomplished, such as reducing pro-inflammatory cytokine signaling. Thus, Prozac and the other SSRIs, can help reduce adrenal fatigue.
In depression, there are hypothalamic-pituitary-adrenal axis (HPA Axis) changes. In the early development of depression, adrenal function as measured by cortisol can be high. But under chronic stress, this ends up being low. This is referred to by Hans Selye (the father of stress research) as the adrenal exhaustion phase of the stress response. When one includes trauma such as child abuse to the mix in the development of depression, the development of low adrenal function is common.
Prozac and the other SSRIs have a 4-6 week delayed effect in reducing depressive symptoms. I believe one important reason is that it takes time to recover HPA axis function as a component of depression. The effect on stress signaling is nearly immediate – since increased serotonin signaling occcurs within 20 minutes of ingestion. But the recovery of HPA axis function takes a longer time.
Dosing is important. If serotonin signaling is increased excessively, dopamine signaling is inhibited excessively. Since dopamine is another control signal on norepinephrine, norepinephrine can increase despite the increase in serotonin. This condition of lower dopamine, higher norepinephrine can be expressed as akathisia (motor agitation), increased anxiety, insomnia. It can lead to worsening rather than improvement of one’s mental function. At worse, it leads to suicides associated with the SSRIs.
Note that depression is a highly complex, multisystemic illness – affecting nervous system, endocrine system, immune system function and metabolism. The reason that Prozac and other antidepressants often only partially work or not at all is that they address only part of the pathophysiology of depression.
Additionally, when it comes to stress, serotonin is only one control signal. Addressing other signal abnormalities that lead to excessive stress is important to help a person improve if the initial treatment of increasing serotonin signaling does not work well or completely. This may include addressing norepinephrine directly via other medications, or addressing it indirectly via other routes such as GABA, dopamine, CRH, cortisol, etc.