A new epidemiological study published in The BMJ explores the association between eating red meat and the risk of death, specifically how risk of death can be lessened through dietary change—decreasing red meat consumption while increasing intake of healthier animal and plant-based foods. This correlates with OFAS research in rodents demonstrating that a sulfur amino acid-restricted (SAAR) diet can increase lifespan and delay onset of age-related diseases. In general, meat and other animal-based food sources have high SAA while plant-based food sources such as vegetables, legumes, whole grains, and fruits have low SAA.
The study looked to produce evidence backing previous studies showing “that higher red meat consumption, especially processed red meat, is associated with an increased risk of type 2 diabetes, cardiovascular disease, certain types of cancer, including colorectal cancer, and mortality.” Analyzing data from a cohort of 81,469 US health professionals (male and female) from a 16-year period, this study found 1) increases in red meat consumption, especially processed meat, are associated with a higher risk of death and 2) decreases in red meat consumption and simultaneous increases in healthy alternative food choices over time are associated with a lower mortality risk, further supporting the health benefits of replacing red and processed meat with healthy protein sources, whole grains, or vegetables.
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Zheng Yan, Li Yanping, Satija Ambika, Pan An, Sotos Prieto Mercedes, Rimm Eric et al. Association of changes in red meat consumption with total and cause specific mortality among US women and men: two prospective cohort studiesBMJ 2019; 365 :l2110
Human health, diet, and environmental sustainability are prevailing concerns that share many common uncertainties. Fulfilling the nutritional needs of a growing population while limiting environmental degradation is a critical challenge that requires global collaboration and commitment. Current food systems, in addition to supporting unhealthy diets and practices, greatly impact the environment, leading to climate change, biodiversity loss, freshwater misuse, interference with the global nitrogen and phosphorus cycles, and land-system change. Current global food systems are simply unable to provide the population of ~7.7 billion with healthy diets while also achieving environmental sustainability.
The EAT-Lancet Commission brings together scientists and experts from the diverse fields of human health, agriculture, political sciences, and environmental sustainability in an effort to establish global targets for healthy diets and sustainable food production. Using the best scientific evidence available, the Commission seeks a global transformation of food systemsthat will help to achieve the goals set forth in the UN Sustainable Development Goals (SDGs) and the Paris Agreement. The SDGs are global goals reduce hunger and improve nutrition. The Paris Agreement sets a budget on greenhouse gas emissions to keep the global mean temperature increase to less than 2°C.
The EAT-Lancet Commission has quantitatively characterized a universal healthy reference diet that will positively impact both human health and the environment. This healthy reference diet consists predominantly of vegetables, fruits, whole grains, legumes, and unsaturated oils; includes a low to moderate amount of seafood and poultry; and includes no or little red meat, processed meat, added sugar, refined grains, and starchy vegetables. The commission has also rendered scientific boundaries that will aid in the reduction of environmental degradation caused by food production at all scales.
At OFAS, we have spent over 25 years studying how a low-methionine diet improves lifespan and healthspan. This diet consists primarily of vegetables, fruits, whole grains, and legumes and contains limited quantities of meats, seafood, and poultry—much like the the EAT-Lancet Commission’s healthy reference diet. Thus, a low methionine diet not only provides benefit to an individual’s health but also promotes a sustainable environment.
The EAT-Lancet Commission proposes five strategies to achieve the “Great Food Transformation”.
1. Seek international and national commitment to shift towards healthy diets
2. Reorient agricultural priorities from producing large quantities of food to producing healthy food
3. Sustainably intensify food production, generating high-quality output
4. Strong and coordinated governance of land and oceans
5. At least halve food loss and waste, in line with global SDGs
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Willett, W., Rockström, J., Loken, B., Springmann, M., et.al. 2019. Food in the Anthropocene: the EAT–Lancet Commission on healthy diets from sustainable food systems. EAT-Lancet EAT–Lancet Commission on healthy diets from sustainable food systems DOI: 10.1016/S0140-6736(18)31788-4
Ables, G.P., and Johnson, J.E. (2017). Pleiotropic responses to methionine restriction. Exp Gerontol 94, 83-88.
The hallmarks of aging in skeletal muscle include endothelial cell dysfunction, impaired microcapillary formation, and a progressive decline in exercise capacity, yet the underlying causes of these symptoms are poorly understood. In a recent paper, researchers identify the mechanism behind vascular aging in mice and its effects on muscle health, and show the means by which they successfully reversed the process in animals.
The vascular aging process causes us to suffer from disorders such as cardiac and neurologic conditions, muscle loss, impaired wound healing, and overall frailty. As we age, our tiniest blood vessels wither and die, causing reduced blood flow and compromised oxygenation of organs and tissues. Endothelial cells are essential for the health and growth of the blood vessels that they line. Unfortunately, as these endothelial cells age, blood vessels deteriorate, new blood vessels fail to form, and blood flow to most parts of the body gradually diminishes. This process heavily affects the muscles, which are vascularized and rely on a robust blood supply to function. Exercise can slow the process, but over time, it becomes less effective.
The research team found that reduced blood flow develops as endothelial cells start to lose a critical protein known as SIRT1, which has been known to delay aging and extend life in yeast and mice. SIRT1 loss is precipitated by the loss of NAD+, a key regulator of protein interactions and DNA repair. Through a series of experiments, researchers found that NAD+ and SIRT1 provide a signaling network between endothelial cells in the walls of blood vessels and muscle cells, thus generating new capillaries to supply oxygen and nutrients to tissues and organs. By using an NAD+ precursor treatment in aging mice, the scientists saw a boost in the number of blood capillaries and capillary density, increasing the blood flow to muscles. These findings have implications for improving blood flow, increasing human performance, and reestablishing a cycle of mobility in the elderly, paving the way for therapies to address diseases that arise from vascular aging.
Over the past ten years, understanding of the physiological changes that occur as people age has greatly improved. Common mechanisms seem to support several age-related diseases, including diabetes, Parkinson’s disease and Alzheimer’s. A review of more than 400 studies of people and animal models indicates that similar processes are the basis of DNA damage, cellular senescence, or inflammation and autophagy. Over the years, studies have shown that one age-related disease can accelerate the onset of others. Until now, aging research has focused mainly on single diseases or on delaying death, meaning that the fundamental mechanisms of aging are being missed as targets for the treatment or prevention of several age-related conditions. What’s more, patients multiple diseases are being exposed to many drugs at once, often with adverse effects.
A class of drugs called geroprotectors might be able to delay the onset of concurrent age-related diseases (multimorbidity) and boost resilience. In various animal models, these drugs can ward off problems of the heart, muscles, immune system and more. However, there are various factors, such as agreeance on definitions and desired metrics, preventing these drugs from reaching the clinic. With an ever-increasing aging population and the social and health-care systems of many nations close to a crisis point, we must take a different approach. Proof-of-concept clinical studies could demonstrate the value of geroprotectors as boosters of resilience in frail patients within the next decade. If successful, such studies could catalyze efforts to advance definitions, animal models, and the characterization of measurable outcomes against which to test the drugs.
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