QUANTUM ENGINEERING #19: AUTISM/FOLATE & TERRESTRIAL SUNLIGHT

It has been estimated that approximately 30% of all cancer cases are attributable to diet and lifestyle.  This "belief" is tied to a misunderstanding of how our genome is affected by hypermethylation.  The process of methylation is one of the software programmed by sunlight that is a key epigenetic controller of DNA expression.   Folate is a natural water-soluble B vitamin.  That water comes from mitochondrial metabolism.  Solar exposure creates that water.  If you do not get sun you do not create water and your folate levels will suffer. 

Folate helps reduce depressive symptoms in the brain. Natural folate is needed in the brain for the synthesis of norepinephrine, serotonin, and dopamine. Sunlight also increases melatonin production at the same time.  Melatonin is made from tryptophan.  All of them are substrates that have seasonal variations.  

Folate is the naturally occurring form of vitamin B9. Before entering your bloodstream, your digestive system converts it to the biologically active form of vitamin B9 ⁠— 5-MTHF.

Folate's synthetic form is folic acid.  

Folic acid is a synthetic form of vitamin B9 that’s also known as pteroylmonoglutamic acid.

It’s used in supplements and added to processed food products, such as flour and breakfast cereals.

Unlike folate, not all of the folic acid you consume is converted into the active form of vitamin B9 — 5-MTHF — in your digestive system. Instead, it needs to be converted in your liver or other tissues.

Yet, this process is slow and inefficient in some people. After taking a folic acid supplement, it takes time for your body to convert all of it to 5-MTHF.  Folate doesn't equal folic acid. Folic acid doesn't operate on DNA like folate does.

Folate functions as a donor of one-carbon units and it has been implicated in the regulation of DNA methylation as well as DNA synthesis.  Folate is affected by UVB light you experience or do not experience.  It is destroyed by excessive amounts of UVB.  This makes it a very responsive "photoelectronic switch" to control the genome by changes that begin in the mitochondrial matrix.   

Epidemiological studies suggest that suboptimal levels of folate and other B vitamins may affect DNA methylation rates and thereby influence genomic stability and cancer risk, although the exact underlying mechanisms have not been clarified.  Almost every study that used these two B vitamins (B12/folate) in cancer cases has failed to produce the effect the belief that dietary sources of these vitamins might prevent cancer has failed.

The Black Swan Mitochondriac perspective is quite different from these vitamins.  The proper amount of B12 and folate are built by the sun in the latitude you live and impacted by your skin color and your skin filters for sunlight by your SNP's.

UV radiation may destroy blood folates in test tubes, but clinical data are scarce if it happens in life. Folate deficiency may increase the risk of cardiovascular diseases, colorectal carcinoma, megaloblastic anemia, pregnancy and birth complications, depression, and dementia.

Melanin pigments are important regulators for color and photochemistry of the evolution of essential functions of human skin. Melanin is the main 'quencher' of superoxide created at cytochrome one of the mitochondria to limit photoreceptor damage in cytochromes.  I believe this effect is critical in protection from diseases like Alzheimer's & Parkinson's disease.  See where melanin comes from:  aromatic amino acids with action spectra in the UV range. 

The concentration of melanin, as well as its depth distribution, is strongly affected by ultraviolet radiation and its absorption.  You must have your skin and eye in the game to activate melanin, and if you are in blue light you must realize this destroys melanin.  Hence, why I said diabetes and PD are both blue light diseases.

In un-tanned skin, melanin pigments are found only in the basal layer of the epidermis, while in tanned skin it is distributed throughout the epidermis. In the eye is it found in the RPE.   So far, mainly the amount of melanin, and not its distribution, has been considered in view of skin photobiology. With an advanced radiative transfer model, investigations have shown how the depth distribution of melanin influences the amount of ultraviolet radiation that reaches living cells in the epidermis and thus can affect folate and B12 levels positively or negatively and affect repair or damage the DNA in the cells. 

The radiative skin simulations have been performed for average pigmented skins (type III-IV). Researchers got surprised yet again because they are solar light ignorant.  This is why dementia continues to perplex researchers in Big Pharma.  Pills cannot build neural networks but the refinement of solar light can. Folate is created by photosynthesis and is found in food webs.  This is how light is refined to become folate.  

They reported "a surprisingly large factor", up to 12, is found between the ultraviolet protection of skin with melanin distributed throughout the epidermis, and skin with melanin only in the basal layer of the epidermis. This is how the skin can vary its own optical penetration to meet the mitochondrial redox needs of the tissue below.  Our system is very dynamic with respect to incident light coming through our skin.  These researchers do not realize how adaptative we are to terrestrial sunlight. 

The clue was in their own work they showed that the synthesis of pre-vitamin D3, in the skin, can vary by more than 100% if the depth distribution of melanin is changed, while the degradation of folate in dermal blood is almost unaffected by variations in the melanin depth distribution.  This has huge implications for Black Swan's understanding of how mitochondrial diseases manifest as heteroplasmy increases.

SUMMARY

An early review of potential problems with mass folic acid supplementation of the food supply was undertaken by Lucock and Yates. Here, they noted that a drastic increase in folates could lead to a selection for the previously rare MTHFR genetic substitution of T for C at area 677 (MTHFR C677T), and that if folic acid is supplemented at doses above 400 mcg that unmetabolized folic acid will circulate in the blood supply at a level largely consistent with the excess dose. In 2005, Lucock and Yates noted that high levels of folic acid in the blood does not generally occur as a result of ingesting natural folates and that “no work has been done so far to evaluate the biological and genetic consequences of excess long term exposure” to these circulating folic acids. After that review, there were two separate findings of unexpected increases in asthma and breathing problems associated with folic acid use.

It now appears clear that excessive methyl donor transfer has epigenetic effects in humans.  This work dovetailed with another review questioning the wisdom of mass folic acid supplementation published in 1996. Smith et al. pointed out that by supplementing the food supply; several hundred thousands of persons are exposed to greatly increased levels of folic acid.

These authors noted that prior research had shown that expectant mothers with low vitamin B-12 (vegans/vegetarians) AND high levels of folic acid were associated with offspring having an unexpected increased risk for insulin resistance and diseases associated with this condition.  Folate

Troen et al. found that some women past childbearing age subjected to high folic acid supplementation may be at risk for reduced immune system functioning causing inflammatory autoimmune conditions to spike.  I believe this link is big for disease risk like autism.  

Decreased terrestrial sunlight also lowers serotonin levels. Given that the relationship between sunshine and serotonin is probably a multimediated phenomenon, one contributory facet may be the role of sunshine on human skin. Human skin has an inherent serotonergic system that appears capable of generating serotonin.

In addition to other body sites (e.g., brain, gut, platelets), serotonin is present in human cutaneous tissue. This conclusion is founded upon the discovery that the machinery of the serotonergic system is present in the skin. For example, tryptophan hydroxylase, the initial enzyme in the synthesis of serotonin, is found in human skin.  Likewise, serotonin and serotonin transporters have been detected in human keratinocytes, the predominant cell type (90%) in the epidermis. This leads to the deduction that mammalian skin can actually produce serotonin.  Stated in scientific prose, Slominski et al. posit that human skin expresses intrinsic serotonin biosynthetic pathways. Slominski et al also point out the common embryological ectodermal origin of the brain and the epidermis, which supports the presence in both of similar biological elements. These researchers even suggest that the cutaneous serotonergic system may be the evolutionary remnant of an ancestral system that operated primarily in the periphery.

In addition, terrestrial solar light has been reported to influence the binding of serotonin at the serotonin 1A receptor site, with lower light levels associated with lower binding levels in the cortical and subcortical limbic regions of the brain affecting psychiatric diseases.

SUNLIGHT reduces all these risks and it appears nature is trying to tell us that the sun lowers folate in foods in the summertime for a deep reason.  That reason is epigenetic hypermethylation which can lead to sleep apnea and cancer formations later in life.  It also alters how RBC can work within their circadian cycles with the innate immune system and TOLL receptors.

Folate is destroyed by strong sunlight with both UVA and UVC light.  Dark skin protects the stores we have, but there is now proof that folate levels are designed to be low when the solar radiation is strong in the local environment.  These days most people are eating food humans have engineered or altered in some way.  This throws off the normal variation of the natural folate cycle during seasons.  Today, people in developed countries are getting MASSIVE amounts of folates in the form of folic acid. Folates are now being ingested in three ways: as natural folates from food, as synthetic folic acid added to processed grains and synthetic vitamin supplements.

As a result of the supplementation, the circulating level of unmetabolized folic acid, as well as total folates, has greatly increased over the past generation, probably to levels largely unprecedented in human history.

Folic acid has been shown to be able to epigenetically alter the functioning of the genome and to have long term effects on gene expression as I mentioned above.

The Centers for Disease Control Vaccine Safety Datalink data set compared children with autism to control children on several variables. Many people who think the link of vaccines to autism might be shocked to find out that folic acid supplementation during gestation is associated with a serious increased risk for autism. This effect remains even when health-seeking behaviors and other variables are controlled.  This is information parents of kids with AUTISM need to know.  Autism, asthma, allergy, ectopy, eczema, diabetes T1D, T2D, and MODY,  auto-immunity, and spinal abnormalities have their lowest incidence is lowest in equatorial environments and it appears now we know why this is the case.

CITES

https://www.eurekalert.org/news-releases/678258

Slominski A, Wortsman J, Tobin DJ. The cutaneous serotoninergic/melatoninergic system: securing a place under the sun. FASEB J. 2005;19:176–194.

Spindelegger C, Stein P, Wadsak W, et al. Light-dependent alteration of serotonin-1A receptor binding in the cortical and subcortical limbic regions in the human brain. World J Biol Psychiatry. 2012;13:413–422.

Lambert GW, Reid C, Kaye DM, et al. Effect of sunlight and season on serotonin turnover in the brain. Lancet. 2002;360:1840–1842.

Cheng YS, Chen KC, Yang YK, et al. No seasonal variation in human midbrain serotonin transporter availability in Taiwan. Psychiatry Res. 2011;194:396–399.

Praschak-Rieder N, Willeit M, Wilson AA, et al. Seasonal variation in human brain serotonin transporter binding. Arch Gen Psychiatry. 2008;65:1072–1078.