DNA methylation of genes which code for proteins in protein pathways that have fallen into disuse

Could there be epigenetics changes to genes when protein pathways become non-fuctional? Say there is decreased activity in a rate limting enzyme in a protein pathway. Do other genes coding for proteins is the pathway keep producing proteins in the pathway even though those proteins now no longer serve any purpose?’

The Central Dogma of Biology according to James Watson – DNA makes RNA makes protein.

The Central Dogma of biology is at the same time a non-sequitur, strictly false and though simple is simpler than possible. What genes are transcribed matters a very great deal and what genes are transcribed is due to epigenetic changes on those genes so the Central Dogma is a non-sequitur is terms of activites of protein pathways and behaviors of organisms. The Central Dogma is strictly false as RNA viruses can change DNA. The Central Dogma is also simpler than possible. Very many genes code for proteins that are splice variants. The production of splice variants of genes is regulated by a system of trans-acting proteins that bind to cis-acting sites on primary transcripts.

Why bring up the the Central Dogma? The Central Dogma of biology is so 1960’s. The genetic determinism of the Central Dogma of biology is still an undercurrent that gets in the way of appreciating the epigenetic basis of many chronic illnesses.

If transcription of genes for proteins in protein pathways in specific organs can fall together this could give rise to unique illnesses where the basis of such illnesses would be due to epigenetic changes, which at first could be isolated to specific organs but which could spread over time worsening such illnesses in relatively predictable ways. With epigenetics, protein pathways falling into disuse can affect only specific organs though over time there could be a spreading effect which fits with how chronic diseases develop.

Another implication of genes becoming hypermethylated when proteins that those genes code for become unused is that optimum nutrition could result in increased numbers of healthy years lived. I would say that as of now there is very, very litttle useful information on what opimum nutrition is in terms of increasing number of healthy years lived. Preventive medicine in terms of nutrition has been one mistep after another. Huge errors have been made. For example, increasing free antioxidants by taking vitamin E, vitamin C and beta-carotene in more than RDA amounts has been a terrible disaster. The only path in terms discovering what optimum nutrition is would be to work back from nutrional strategies than cure diseases rather than are speculations on diet as to how to prevent diseases developing decades and decades later. Pilot studies are very, very frequently misleading. Supplements are now a minefield.

Epigenetics changes everything

Each cell has the same DNA.  As this is the case there must be ways for cells to differentiate from other cells while all cells have the same DNA. In different cell types different genes are translated which is achieved by genes in different cell types having different epigenetic marks.  Epigenetic marks on genes can increase or decrease transcription of genes. DNA methylation and histone methylation are two ways genes can be epigenetically marked and thereby transcription of genes affected. There are various other ways that genes can be epigenetically marked. Environment can affect what epigenetic marks are on genes.

With genetic diseases there is systematic evidence of  genetic anomalies. Take any cell from the body and genes in that cell will show the genetic anomaly.  For example, blood tests can be used to detect genetic anomalies   With epigenetic diseases, however, there is no genetic evidence of the disease and dysregulations do not have to be systematic whereby bloods tests might not be revealing.

Vitamin D is now suspected to play a part in lots of illnesses and I think this is correct  but with epigenetic anomalies there need not be any genetic anomalies though there is still disease.  The last step in the formation of calcitriol, which is active vitamin D, by CYP27B1 requires an iron-sulfur protein called adrenodoxin. Due to difficulties in forming iron-sulfur clusters there will be low levels of adrenodoxin  whereby there are low levels of calcitriol. Giving calcitriol alone, however, is not sufficient to treat many illnesses where there is evidence of calcitriol deficiencies.  With iron-sulfur proteins dysregulated a lot of processes besides the formation of calcitriol will also be adversely affected.

There not being diseases associated with aberrant epigenetic marks is basically impossible given the large part that epigenetics plays in regulations of cells.   I think schizophrenia is  an illness associated with epigenetic dysgulations, an illness in which there are deficiencies of vitamin D but which is basically non-responsive to calcitriol.