key: cord-0008636-dd4ek5zd
authors: Majumdar, K. Pradyumna; Gangula, Shravan K.; Chelakari, Sravanth Karteek; Mannem, Santhosh Reddy; Gupta, Vishal; Majumdar, Pramod Krishna
title: The future of disease prevention
date: 2009-05-28
journal: Med Hypotheses
DOI: 10.1016/j.mehy.2009.04.038
sha: ba011da927cb4dea4c98df65170b36626c39f1c8
doc_id: 8636
cord_uid: dd4ek5zd

nan

and furnish intestinal microflora; however, they simultaneously reduce the relative intake of tryptophan. Non-fat, 1% and 2% skim milk, at 5.8%, 5.0% and 5.3% Try/LNAA%, respectively, are only 23%, 6% and 12% above the benchmark sorghum (4.7%) and yogurt is below it (À50%), as previously noted. Whole milk, with a Try/LNAA% of 11.3%, has about twice the tryptophan of the lower-fat milks. Dieticians need to consider the relative tryptophan levels to prevent developmental delays and also to ensure that apparently normal children develop to their full potential. The future of disease prevention

After the Severe Acute Respiratory Syndrome (SARS) and Avian Flu pandemics we see another in the making; Swine Flu. As we take to fighting them with new weaponry we should also be in control of those that are already established.

In the near future of immunology, a one-cure-all panacea might evolve. In the cutting edge we foresee memory type lymphocyte transfusion. Mature memory type lymphocytes are known to directly induce and guide the developments of the hematopoietic cells [1] . We propose that these cells be taken from elder individuals, whose immunity has seen them through many a battle with diseases over time, and be transfused in small quantities, sufficient to direct the development of other lymphocytes, into young infants. This, of course, is only after testing for blood group and other compatibilities.

These cells can now direct the production of antibodies and other necessary arsenal to combat infectious agents the body was never exposed to. Pooling from various donors with similar compatibility profiles would be the order of the day. Vaccines currently in vogue would become redundant.

Mammal trials in this arena would do much justice to the current state of health affairs. Can adenosine substitute for SAM-e as an adjunct in the treatment of depression?

The antidepressant effects of S-adenosylmethionine (SAM-e) have been known for many years, and researchers generally regard SAM-e as being effective as an adjunctive or even standalone treatment for major depression [2] . The assumption has generally been that SAM-e produces antidepressant effects by serving as a cofactor for methyltransferase enzymes [2] , but the true mechanisms underlying the antidepressant effects of SAM-e are still unknown. Renshaw et al. [15] proposed that increases in adenosine (Ado), a major metabolite of SAM-e, or its nucleotides, may mediate the antidepressant effects of SAM-e [15] . Ado monophosphate (AMP), Ado diphosphate (ADP), and Ado triphosphate (ATP) comprise the ''adenylate pool," meaning AMP + ADP + ATP. Researchers have found that Ado can produce antidepressant effects in animal models of depression, and those effects seem to be mediated by changes in a variety of neurotransmitter systems [6] [7] [8] [9] [10] .

In various types of cultured cells or tissues, exogenous SAM-e has been shown to increase the overall, tissue adenylate pool [4, 16] or the concentrations of intracellular adenosine [4, 14, 18] , ATP [4, 13, 14] , or cAMP [17] . SAM-e increases Ado formation by serving as a cofactor for numerous methyltransferase enzymes [2] , and the S-adenosylhomocysteine (SAH) formed as a product of those transmethylations can then be hydrolyzed, by SAH hydrolase (SAHH), to Ado and homocysteine [2] . The increases in the intracellular concentrations of Ado or its nucleotides would then be expected to equilibrate with and buffer or increase the pools of extracellular Ado or its nucleotides, leading to the activation of Ado receptors [14] .

In many cases, researchers have noted that these elevations in Ado or its nucleotides are at least partially responsible for the protective effects of SAM-e against ischemia-induced damage to tissues or for other cellular effects of SAM-e [4, 17, 19] . Researchers have also frequently found that the effects of SAM-e can be mimicked by Ado [16, 18] or blocked by Ado receptor antagonists [3, 14, [17] [18] [19] .

The use of oral AMP or ATP disodium as an alternative to the use of SAM-e might be advantageous, given that the bioavailability of oral SAM-e has been shown to be extremely low [20] . Yang et al.

[20] found that the relative bioavailability of a 1000-mg dose of oral SAM-e, expressed as AUC(oral)/AUC(intravenous) over 24 h,

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