C15:0 is a recently discovered essential fatty acid that plays a critical role in physically strengthening cell membranes and protecting cells against lipid peroxidation. As part of a cell stability hypothesis, it is proposed that adequate concentrations of C15:0 in cell membranes are required to prevent ferroptosis, a recently discovere…
C15:0 is a recently discovered essential fatty acid that plays a critical role in physically strengthening cell membranes and protecting cells against lipid peroxidation. As part of a cell stability hypothesis, it is proposed that adequate concentrations of C15:0 in cell membranes are required to prevent ferroptosis, a recently discovered method of cell death that involves lipid peroxidation of cell membrane fatty acids and intracellular iron, which has also been linked to type 2 diabetes, cardiovascular disease, and NAFLD.
Based on numerous studies provided in this review, a definition of C15:0 nutritional deficiency (circulating C15:0 ≤ 0.2% of total fatty acids) is offered. A description of the pathophysiology behind this C15:0 nutritional deficiency syndrome (cell fragility syndrome) is provided, explaining how low C15:0 can accelerate the progression of diseases associated with aging, including overload syndrome. of dysmetabolic iron, type 2 diabetes, cardiovascular disease and NAFLD.
In addition to correcting nutritional deficiencies, there is evidence that optimal concentrations of circulating C15:0 (>0.4% to 0.64% total fatty acids) may support cardiovascular health and long-term longevity. Continued studies, including clinical trials, will help to further test the cellular stability hypothesis and the proposed definition of C15:0 nutritional deficiencies. Given the global decreases in dietary C15:0 intake, further studies are needed to better understand the depth and breadth of the cellular fragility syndrome driven by C15:0 deficiency in different human populations and how this syndrome may be contributing to the increase in diseases associated with aging, especially among younger people.
C15:0 is a recently discovered essential fatty acid that plays a critical role in physically strengthening cell membranes and protecting cells against lipid peroxidation. As part of a cell stability hypothesis, it is proposed that adequate concentrations of C15:0 in cell membranes are required to prevent ferroptosis, a recently discovered method of cell death that involves lipid peroxidation of cell membrane fatty acids and intracellular iron, which has also been linked to type 2 diabetes, cardiovascular disease, and NAFLD.
Based on numerous studies provided in this review, a definition of C15:0 nutritional deficiency (circulating C15:0 ≤ 0.2% of total fatty acids) is offered. A description of the pathophysiology behind this C15:0 nutritional deficiency syndrome (cell fragility syndrome) is provided, explaining how low C15:0 can accelerate the progression of diseases associated with aging, including overload syndrome. of dysmetabolic iron, type 2 diabetes, cardiovascular disease and NAFLD.
In addition to correcting nutritional deficiencies, there is evidence that optimal concentrations of circulating C15:0 (>0.4% to 0.64% total fatty acids) may support cardiovascular health and long-term longevity. Continued studies, including clinical trials, will help to further test the cellular stability hypothesis and the proposed definition of C15:0 nutritional deficiencies. Given the global decreases in dietary C15:0 intake, further studies are needed to better understand the depth and breadth of the cellular fragility syndrome driven by C15:0 deficiency in different human populations and how this syndrome may be contributing to the increase in diseases associated with aging, especially among younger people.
https://www.mdpi.com/2218-1989/14/7/355 (2024).--