Paper 1- Dietary Causes of the Neurological Mechanisms Behind Multiple Sclerosis

It is known that the proximate cause of multiple sclerosis is the deterioration of the mielin sheath insulating neurons in the nervous system, termed “demyelination”. However, research is still being done to find the ultimate, underlying cause of demyelination. Increasing epidemiological evidence has recently pointed to food antigens as a suspect worthy of research. If food were to be incorporated into the widely accepted “infectious-agent model” of the cause of MS, the new model would be the following:

1) An individual is infected with a common virus (HHP-4 or HHP-6) during childhood. During infection, antibodies are produced that, by “molecular mimickry”, may target the central nervous system. However, the attack is not long enough to begin demyelination.

2) There is an increase of gut permeability arising from an environmental factor such as steroidal, anti-inflammatory drugs, or ingestion of cereal grains, legumes, and other lectin-producing foods (as found by Loren Cordain in 1999).

3) Increasing gut permeability leads to leakage of food antigens on an almost daily basis. “Molecular mimickry” among the food and individual’s own cells then triggers a T-cell attack by the body’s immune system, paving the way to such auto-immune disorders like multiple sclerosis.

 

Paper 2- Epigenetics: Looking Beyond the DNA Code

As people grow older we notice that some individuals “age well,” while others tend to lose hair at 20, develop wrinkles at 35, and die of heart disease at 40.

Although the scientific community often approaches disease and aging by looking for the DNA in our genomes that “code” for susceptibility to ailments and “modern disease”, perhaps we should explore beyond the effects that are dictated by raw genetic code. At this point, we will enter the area of epigentics. Instances during which factors outside of our DNA that nevertheless affect its expression can be found in the following:

1) The specialization of omnipotent stem cells,
2) the carcigenetic environment increasing changes of cancer, and even
3) cellular apoptosis in certain strains of fungi.

Number 3, in particular, draws attention to the possibility of epigentic interaction between mitochondria and muclear DNA within an individual fungus. Given the individuals with the same mitochondrial DNA, but different nuclear DNA, one of the specimens will live, while the other may fail to develop and promptly die, presumably from inter-conflict of the two sets of DNA within the individual. These two, although bearing the same genes, experience stark differences in their genetic expression.