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Seasonal Affective Disorder as a lack of detox of Poison/"Vitamin A"

If Seasonal Affective Disorder aka SAD 🙁  is related to less sunlight during the winter months, what if it ISN'T necessarily from a LACK of Vitamin D production, but RATHER was from an EXCESS of Poison/"Vitamin A" not getting broken down from the sunlight/UVB missing from one's day?Lo and behold! Remember, retinoic acid and retinoids are terms for Poison/"Vitamin A":

The Neurobiology of Retinoic Acid in Affective Disorders

Several studies have shown that the molecular components required for retinoic acid signaling are expressed in the adult brain; the overlap of brain areas implicated in retinoic acid function and stress and depression suggest that retinoids could play a role in affective disorders. This report reviews the evidence in this area and describes several systems that may be targets of retinoic acid and which contribute to the pathophysiology of depression.

Retinoic Acid and Affective Disorders: The Evidence for an Association

It was found in this same study that photoperiod regulates RALDH in tanycytes as well as RAR/RXR’s in the hypothalamus, therefore showing changes in RA signaling driven by seasonal changes. Given that seasonal affective disorder is a form of depression driven by seasonality there is the potential for RA to influence this disorder.

One particular RA regulated gene in the hypothalamus that may provide a link between RA and depression is corticotrophin-releasing hormone (CRH), a key regulatory factor in the HPA axis which may contribute to HPA axis hyperactivity in depression.

This article isn't the place for me to get deep into what I call the dehydrogenase system, but the connection mentioned above between RALDH (retinaldehyde dehydrogenase, aka aldehyde dehydrogenase) is absolutely KEY.  Here is the paper they got it from:

Photoperiodic expression of two RALDH enzymes and the regulation of cell proliferation by retinoic acid in the rat hypothalamus.

Investigations of the dynamics of RALDH1 expression in the rat hypothalamus have shown that this enzyme is in tanycytes under photoperiodic control with highest levels during long versus short days.

So, there is more RALDH / ALDH being produced in long days (summer!) and less during short days (winter!).  SAD is a fall/winter problem during the shorter days.

The short story is, that if RALDH / ALDH is running more slowly, the Poison/"Vitamin A" detox system runs more slowly, more retinaldehyde and retinol back up in the system, and TOXICITY IS INCREASED.

SAD happens during the shorter days, when the RALDH / ALDH, quite possibly the most important enzyme system to all of Poison/"Vitamin A" Detox runs slower!

If Poison/"Vitamin A" is a major cause of humanity's epidemics of modern diseases, and photoperiod (length of day, aka "how much sun one can get") slows down a KEY enzyme in Poison/"Vitamin A" detox, we could expect to see major connections between photoperiod and all aspects of health, correct?

Photoperiodic Programming of the SCN and Its Role in Photoperiodic Output

More recently, seasonal factors have been linked to human health. While we have benefitted greatly from understanding the seasonal responses of the organisms on which we rely for survival, evidence is emerging that we are also photoperiodic organisms ourselves [6]. Over the last several years, much research has been done on the relationship among photoperiods, especially extreme photoperiods, and psychiatric health, sleep, and noncommunicable diseases [712].

In another post, I will get into the photoperiod connection to Poison/"Vitamin A" and how that connects the "flu season" to the winter months as well.  It is the same reasons as above.

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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