Deuteration of nutrients above their natural 2H abundance, including supplements, metabolites, intermediates, drugs (1), fatty acids, glucose (2), etc.. is a bad idea in my biochemist view. This is because our enzyme reactions constantly discriminate (fractionate) protons from deuterons via all water proton exchange reactions, either as the reaction solvent and/or the proton/deuteron donor/acceptor during literally all metabolic reactions that occur in living cells (3). The continuous proton/deuteron fractionation processes via glycolysis, among many other reactions, form the (human) deutenome, which has similar importance as the proteome, metabolome, genome, transcriptome, etc…
Indeed, deuterons and deuterated amino acids, for example, are critically important to make structural elements stronger and resistant to peroxidation. Sequestrating deuterium from naturally enriched metabolites and water, for example, (hydroxy)proline of collagen in mammals can accumulate over two times higher, likely more, deuterium concentrations under challenging environments (seals hunted by sharks) (4). The fully detailed mechanisms are still under search but, apparently, there is no need to supply extra deuterium externally to produce highly deuterated products with specific (structural) roles. Our cells are readily able to deuterate, or deuplete intermediary metabolites and products based on physiological demands. These, of course, may include polyunsaturated fatty acids when and where there is a need, like for mitochondrial or cellular membranes and other structural components to prevent peroxidation.
The danger of deuterating fatty acids, supplements, drugs, nutrients, drinks, etc… above their natural enrichment is that if/when they happen to get oxidized in mitochondria and/or peroxisomes, instead of being rapidly deposited into structural elements to prevent peroxidation, they produce deuterium enriched metabolic water protons that break mitochondrial nanomotors. This causes metabolite crowding, which is the priming metabolic condition to induce cancer, diabetes, cellular degenerative diseases, diabetes, etc... (the list is long). Our cells fractionate, distribute and allocate sufficient (~two, three times higher) deuterium for structural elements from relatively low natural abundance in fatty acids obtained via a grass-fed ketone and protein rich animal sources. Our cells seem to know how to distribute and regulate deuterium (5) based on many environmental factors that I am not going to detail here further. To this regard it is important to consider that site specific deuteration of the common (intra)cellular membrane phospholipid DOPC chain causes a reduction in the lamellar repeat spacing and bilayer thickness, while deuterated headgroups cause an increase (6). For saturated membrane lipids, such as DSPC, DPPC, DMPC, DOPC in excess water, the gel-fluid phase transition temperature is significantly lower by ~4.3 ± 0.1 °C with deuterated chains compared to protiated ones.
Yes, we do need deuterium in chemical covalent bonds in a few key locations for strength, durability, stability, flexibility and protection from peroxidation, for example, based on deuterium’s hard to remove, exchange or replace chemical bonding structures known as kinetic isotope effects. On the other hand, we do not need to supplement deuterium above natural abundance via chemical and industrial processes. Sufficient deuterium is available in grass feed meat sources, in my opinion, to humans and many other carnivore species, primarily.
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