Genetics

Human code

Once again our thought processes have gone down the line of least common denominator. We believe there is significance to the understanding there are just two single coded amino acids, methionine and tryptophan. Methionine (AUG) serves as an initiation site and can be considered a start codon for translation into a protein. We considered and asked ourselves why there are three “nonsense” codons for a stop of a chain in the universal code. Why aren’t the stop codons amino acids?

Mitochondrial code

Tryptophan is recognised as a stop codon in the mitochondrial code and coded as UGA for mammalian, invertebrates and yeast. Coincidence, perhaps but UGA is the codon for opal, a nonsense codon and a stop codon in the universal code.

Human/Mitochondrial code

It is becoming more widely recognised the importance of mitochondria within humans. Current understanding suggests that all mtDNA is inherited. The potential of SOL to produce mtDNA and the potential of genetic transfer would lead us to postulate that tryptophan is a stop codon in all mitochondria within the human body.

Essential amino acids

With the notion of SOL being genetically transferred through replication/reproduction leads to the question is methionine and tryptophan essential amino acids. Our hypothesis is no, but inherent in all life.

Gene transfer across BBB

Our considerations started with what molecules can and those that can’t cross the tightly packed endothelial cells of the blood-brain barrier. We believe many of the studies relating to gene transfer across the blood-brain barrier have not taken into consideration a vital factor.

CYP P450 – Alzheimer’s disease and other Dementia

In our research of CYP’s we have discovered many potentially contain SOL. We believe there is a significant factor which has not been taken into consideration for drug delivery.

We are currently working on relationships between what we believe are significant genes; TPH1, MOAO, DDC, SLC6A4, TH, HTR2A, TDO2, ASMT, CYP1A2, HTT, HTR2C, COMT, IDO1, AANAT, DRD4, VIP, YWHAZ and TPH2. As well as C-fos, CDC2, MAPK’s, JNK’s, MYC, GSK3B, MYLK and PAK2

Galantamine/Rivastigmine/Donepezil/Phenytoin/
Memantine/Dimebolin/Cilostazol

We believe all of these drugs used in the treatment of Alzheimer’s and other dementia contain SOL and as such can be delivered in a way to maximise their effectiveness.

Current work

We are currently working on relationships between what we consider significant genes; (current list plus SNCA, ALB, IL1B, IL2RA, IL2RB, IL6, IL8, LEP, KRIT1, VCAM and SNORD. All of these genes we believe are highly significant for metabolism, disease and repair.

We are also looking into other disorders working on the principal that, disease is the imbalance of homeostasis and ease is the balance. Our hypothesis being homeostasis is created by serotonin and melatonin equilibrium.

A major health problem in western society, and spreading, is that of obesity. There are many theories as to the cause, of which we have a few novel hypotheses. If genetic modification in the production of processed foods doesn’t take account for the balance of serotonin and melatonin, this could lead to an imbalance of homeostasis. We are also about to start research (if we had some funding) on a possible link between obesity and antidepressant drugs. Many antidepressant drugs are designed to stimulate the production of serotonin. This could upset the natural balance of homeostasis. It would be interesting to see the correlations between the exponential rise in obesity since 1979 and the rise in use of antidepressant drugs.