![]() Notably, in mice, orally administered taurine at 5 milligrams per kilogram body weight per day was also associated with improvements in strength, coordination, and cognitive functions and slowed several key markers of aging, including cellular senescence, mitochondrial and DNA damage, and inflammageing. Reversal of this decline through taurine supplementation increased the median lifespan of worms and mice by 10 to 23% and 10 to 12%, respectively. Declining taurine levels were also observed in aging mice and the authors found that mice lacking the major taurine transporter had shorter adult lifespans. Similarly, taurine levels decreased by more than 80% over the human lifespan. ![]() They discovered that in 15-year-old monkeys, serum taurine concentrations were 85% lower than in 5-year-old monkeys. To better understand if and how taurine abundance influences a healthy lifespan, Parminder Singh and colleagues measured blood taurine concentrations at different ages in mice, monkeys, and humans. Small clinical trials of taurine supplementation have suggested benefits in metabolic and inflammatory diseases, but the influence of taurine concentrations on animal health and longevity remains poorly understood. Previous studies in several species have shown that taurine deficiency during early life causes functional impairments in skeletal muscle, eyes, and the nervous system, all in ways that are related to aging-associated disorders. Taurine, a semi-essential micronutrient, is one of the most abundant amino acids in animals. For those seeking to bypass the caffeine and other ingredients typically found in energy drinks, taurine supplements offer a straightforward way to obtain the nutrient. Taurine is a common ingredient in energy drinks, such as the brands Red Bull, Monster Energy, Rockstar, NOS, Full Throttle, and AMP. These findings warrant further human trials to examine taurine’s effect on healthy lifespan in humans and to understand the potential risks involved. According to the authors, reversing age-associated taurine loss through supplementation improved the healthy lifespan in worms, rodents, and non-human primates. This study evaluated the amino acid’s effect on health and longevity across several animal models. Taurine deficiency may be a driver for aging, according to a new study. ![]() However, further human trials are necessary to validate these potential anti-aging effects of taurine. In animal models, including mice and monkeys, restoration of taurine levels increased lifespan and slowed aging markers. Research indicates taurine deficiency may contribute to aging, and supplementation could improve longevity and health. Credit: Columbia University Irving Medical Center Taurine structure is depicted as a ball and stick model in the taurine shower. In the illustration an old man is seen walking through a taurine shower and coming out as rejuvenated healthy man. The present review tests this hypothesis by comparing the symptoms of MELAS and taurine deficiency.Taurine supplementation increases healthy life span. On the other hand, if the aminoacylation defect dominates, significant differences should exist between taurine deficiency and MELAS. Hence, the wobble hypothesis predicts that the symptoms of MELAS mimic those of taurine deficiency, provided that the dominant defect in MELAS is wobble modification deficiency. Taurine serves as a substrate in the formation of 5-taurinomethyluridine-tRNA(Leu(UUR)) therefore, taurine deficiency should mimic 5-taurinomethyluridine-tRNA(Leu(UUR)) deficiency. Because 12 out of the 13 mitochondria-encoded proteins are more dependent on UUA decoding than UUG decoding, the aminoacylation defect should have a more profound effect on protein synthesis than the wobble defect, which more specifically alters the expression of one mitochondria-encoded protein, ND6. Both changes result in reduced transcription of mitochondria-encoded proteins however, reduced aminoacylation affects the decoding of both UUG and UUA while the wobble defect specifically diminishes UUG decoding. These mutations reduce both the aminoacylation of tRNA(Leu(UUR)) and a posttranslational modification in the wobble position of tRNA(Leu(UUR)). MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) is a mitochondrial disease caused by one or more mutations of tRNA(Leu(UUR)).
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