IS THE SKIN CIRCADIAN SENSITIVE?

If you look at the latest data from mice as cite one does below,  it appears this is true.  Mice are noctural mammals so their results will not be identical to ours but they useful in working out how proteins of the circadian mechanism work with sunlight.  Skin, like all organs, has a distinctive night-day cycle. Skin cells divide and proliferate more at night, performing essential repairs. During this time, skin is more acidic, less hydrated and even has a slightly higher temperature than during the day.  Acidic environment have lower pH and a lower pH is associated with a smaller exclusion zone of water.  Given the last blog on aquaphotomics you might see why this study has some deep relevance to the the idea of a "quantum batter".  A lowered pH would offer less control of entanglement and make things in cells and mitochondria more subject to pertubation. This would also lower the number of "wits" present with tissues and would lead to lower energy generation in tissues.  This is the perfect set up for an autoimmune or infectious process to manifest.  A lowered pH = acidic environment = lowered EZ = lowered DC electric current = lowere regeneration = Alterations in ANT1 and ANT 2 in mitochondria = inflammation = mitochondrial disease generation.  

The inflammation of psoriasis follows a similar pattern, with higher levels of immune cells late at night and thus more proliferation of unneeded skin cells. Eczema also appears to worsen significantly at night, disrupting the sleep of many people who suffer from the condition. This is a big quantum clue for the mitochondriac. 

A new study (cite 1) may have identified the genes that cause this discomfort within the skin.  It also maybe key in understanding why the solar callus is not built up in many mammals who's skin has undergone a circadian mismatch.  It turns out the highly conserved clock genes in mammals, such as the CLOCK and PER2, are intricately and critically involved in regulating and maintaining the circadian rhythm of the skin, appear to also be part of the cause of many common skin maladies. Mice who have mutations in the CLOCK gene have a lower severity of skin diseases like psoriasis. Psoriasis is a pre-cancerous autoimmune condition.  Their skin does not react as strongly to the autoimmune activity that normally causes psoriasis flares. Mice who had a mutation in the PER2 gene, on the other hand, developed psoriasis even when they lacked other autoimmune symptoms usually associated with the skin disorder.  The CLOCK and PER2 genes appear to be a coupled thermodynamic gene pair.  If one goes awry it leads to loss of control of the local circadian timing mechanism in the skin.  I would tell you to refer back to the many blog where I talk about what happens to each side of a coupled system once one is altered exogenously..........it leads to extinction of both cycles and leads to disease.  Artificial blue light exposure at night is a strong skin stimulus for this uncoupling event.    

Could Chronotherapy Offer Relief from Skin Disorders?

The symptoms of skin diseases such as eczema and psoriasis appear to be intricately linked with the circadian rhythm. Previous published studies have found that topical medications are better absorbed in the evening when sunlight is absent, so this is might be an ideal time to use them. In addition, taking medications for night-dominant disorders before bedtime may alleviate some of the more severe symptoms seen at night. Last, stopping damage to cells at the time when it is most likely to occur will likely reduce symptoms even during the day.

Chronotherapy may allow many people suffering from these and other skin diseases to get the healthy skin and good night of sleep that they need. However, this is not the only area where study of the circadian rhythm can allow us to achieve better health. Understanding the circadian rhythm of different parts of our bodies is often the first step to developing more effective treatments for mitochondrial diseases.  I believe today,most modern diseases are related to increases in mtDNA heteroplasmy rates. 

CITES:

 1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4653315/

2. https://www.ncbi.nlm.nih.gov/pubmed/26549635