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Since then, a growing body of evidence has emerged to support the role of mitochondria dysfunction, characterized by altered ATP production, loss of mitochondrial membrane potential ( mito ), and fragmented mitochondrial ultrastructure [Figure 3], as a contributor to AF in a diverse range of model systems and clinical samples [90]

Beyond calorie restriction: aging as a biological target for nutrient therapies

Clinical studies indicate that the combination maintains physiological GH pulsatility and IGF-1 elevation, which may reduce side effects compared with direct HGH therapy

Additionally, the potential cytotoxicity at high doses requires careful optimization of dosing regimens

The authors like to thank Dr

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