Louise - when lying down for a length of time... as in sleeping... my concern is that ginger tea might activate stomach acid which is definitely not what one wants. The literature on taurine... which is not driven by brand names... says that taurine may elevate stomach acid and increase risk of causing ulcers... therefore taking with food is recommended. This comes from The Healing Nutrients Within by Eric Braverman, MD... who also says that if you take it alone, you can use magnesia... in this case, you could probably make the magnesium bicarbonate water (WW) and drink that with the taurine at bedtime...if you can't take it with meals.
But that said... taking supplements with ginger tea would probably only mean enhanced metabolism from whatever increased stomach acid happens to occur.
Jackie
Past posts on taurine's importance with arrhytymia...
Original post - What About Taurine?
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Also these:
Taurine, an anti-excitatory amino acid, serves as a central nervous system (CNS) sedative to help alleviate the hyperactivity associated with ADHD. It is most effective at 3,000 mg per day in divided doses between meals
Taurine is the most important and abundant free amino acid in the heart. It modulates the activity of cyclic AMP, which activates important enzymes that contribute to the heart’s contractibility. It also plays a role in calcium’s function of nerve transmission in the heart. Taurine plays a vital role in the adaptive response of the heart to stress. 5
5 Pfeiffer, Carl and Eric Braverman, The Healing Nutrients Within New Caanan Cn. Keats, 1987 pp. 121-124
Medical Hypothesis
Volume 63, Issue 3, Pages 426-433 (2004)
Sub-optimal taurine status may promote platelet hyperaggregability in vegetarians
Mark F McCarty
Received 20 September 2002; accepted 11 November 2002.
Abstract
Although vegan diets typically have a very favorable effect on a range of vascular risk factors, several independent groups have reported that the platelets of vegetarians are more sensitive to pro-aggregatory agonists than are those of omnivores. In light of clear and convincing evidence that platelet function has an important impact on risk for thromboembolic events, it is important to clarify the basis of platelet hyperaggregability in vegetarians. A dietary deficit of long-chain ω-3 fatty acids is not likely to explain this phenomenon, since most omnivore diets do not include enough of these fats to discernibly influence platelet function. A more plausible possibility is that relatively poor taurine status – a function of the facts that plants are devoid of taurine and the human capacity for taurine synthesis is limited – is responsible. Plasma taurine levels are lower, and urinary taurine excretion is substantially lower, in vegetarians than in omnivores. Platelets are rich in taurine, which functions physiologically to dampen the calcium influx evoked by aggregating agonists – thereby down-regulating platelet aggregation. Supplemental intakes of taurine as low as 400 mg daily have been reported to markedly decrease the sensitivity of platelets to aggregating agonists ex vivo. Although the average daily intake of taurine from omnivore diets may be only about 150 mg, it is credible to speculate that a supplemental intake of this magnitude could normalize the platelet function of vegetarians in the long term; in any case, this thesis is readily testable clinically. Taurine is just one of a number of nutrients found almost solely in animal products – “carninutrients” – which are rational candidates for supplementation in vegans.
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Amino Acids. 2000;19(3-4):509-26. Links
Taurine and neural cell damage.
Saransaari P, Oja SS.
Brain Research Center, Medical School, University of Tampere, Finland.
blpisa@uta.fi
The inhibitory amino acid taurine is an osmoregulator and neuromodulator, also exerting neuroprotective actions in neural tissue. We review now the involvement of taurine in neuron-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress, and the presence of free radicals, metabolic poisons and an excess of ammonia. The brain concentration of taurine is increased in several models of ischemic injury in vivo. Cell-damaging conditions which perturb the oxidative metabolism needed for active transport across cell membranes generally reduce taurine uptake in vitro, immature brain tissue being more tolerant to the lack of oxygen. In ischemia nonsaturable diffusion increases considerably. Both basal and K+-stimulated release of taurine in the hippocampus in vitro is markedly enhanced under cell-damaging conditions, ischemia, free radicals and metabolic poisons being the most potent. Hypoxia, hypoglycemia, ischemia, free radicals and oxidative stress also increase the initial basal release of taurine in cerebellar granule neurons, while the release is only moderately enhanced in hypoxia and ischemia in cerebral cortical astrocytes. The taurine release induced by ischemia is for the most part Ca2+-independent, a Ca2+-dependent mechanism being discernible only in hippocampal slices from developing mice. Moreover, a considerable portion of hippocampal taurine release in ischemia is mediated by the reversal of Na+-dependent transporters. The enhanced release in adults may comprise a swelling-induced component through Cl- channels, which is not discernible in developing mice. Excitotoxic concentrations of glutamate also potentiate taurine release in mouse hippocampal slices. The ability of ionotropic glutamate receptor agonists to evoke taurine release varies under different cell-damaging conditions, the N-methyl-D-aspartate-evoked release being clearly receptor-mediated in ischemia. Neurotoxic ammonia has been shown to provoke taurine release from different brain preparations, indicating that the ammonia-induced release may modify neuronal excitability in hyperammonic conditions.
Taurine released simultaneously with an excess of excitatory amino acids in the hippocampus under ischemic and other neuron-damaging conditions may constitute an important protective mechanism against excitotoxicity, counteracting the harmful effects which lead to neuronal death. The release of taurine may prevent excitation from reaching neurotoxic levels.