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In this paper, we explore the potential role of certain amyloidogenic proteins, including amylin, amyloid beta, the prion protein, huntingtin, and -synuclein, in disease processes that result in the accumulation of deposits of protein fibrils, along with lipid membrane components of damaged mitochondria, which we argue may be a mechanism to sequester deuterium in order to reduce the deuterium burden in the tissues

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Considering that insulin resistance is regarded a hallmark of NAFLD progression closely linked to inflammation, oxidative stress, and disease progression [54-56], an additional benefit of a LCD in NAFLD is reasonable from a pathophysiological perspective

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