Researchers at Oxford University and the Swiss agricultural research institute, Agroscope, have created the most comprehensive database on the environmental impacts of nearly 40,000 farms and 1,600 processors, packaging types, and retailers. This allows them to assess how different production practices and geographies lead to different environmental impacts for 40 major foods. According to this new study, there are environmental costs in what humanity chooses to eat and drink and shows how these choices make a difference.
Environmental scientist Joseph Poore of the University of Oxford says that the agricultural data shows wide differences in environmental impacts — from greenhouse gas emissions to water used — even between producers of the same product. The amount of climate-warming gases released in the making of a pint of beer, for example, can more than double under high-impact production scenarios. For dairy and beef cattle combined, high-impact providers released about 12 times as many greenhouse gases as low-impact producers. Those disparities mean that there is room for high-impact producers to tread more lightly, Poore says. If consumers could track such differences, he argues, purchasing power could push for change.
Poore and colleague Thomas Nemecek report in their study that protein from beef releases an increased amount of greenhouse gas emissions in comparison to protein from cheese, poultry, and tofu. “Food production creates immense environmental burdens, but these are not a necessary consequence of our needs. They can be significantly reduced by changing how we produce and what we consume” says Poore. Replacing meat and dairy foods from producers with above-average environmental effects with plant-based products could make a notable difference in greenhouse gas emissions.
For producers, the researchers present evidence in favor of using new technology. This technology often works on mobile devices, taking information on inputs, outputs, climate, and soil, to quantify environmental impacts. The technology then provides recommendations on how to reduce these impacts and increase productivity. However, producers have limits on how far they can reduce their impacts. Specifically, the researchers found that the variability in the food system fails to translate into animal products with lower impacts than vegetable equivalents. Diet change, therefore, delivers greater environmental benefits than purchasing sustainable meat or dairy. Further, without major changes in technology that disproportionately target animal products, the researchers show that animal product-free diets are likely to deliver greater environmental benefits than changing production practices both today and in the future.
Producing food overall accounts for 26 percent of global climate-warming emissions, and takes up about 43 percent of the land that’s not desert or covered in ice, the researchers found. Out of the total carbon footprint from food, 57 percent comes from field agriculture, livestock and farmed fish. Clearing land for agriculture accounts for 24 percent and transporting food accounts for another 6 percent. “We need to find ways to slightly change the conditions so it’s better for producers and consumers to act in favor of the environment,” says Poore. “Environmental labels and financial incentives would support more sustainable consumption, while creating a positive loop: Farmers would need to monitor their impacts, encouraging better decision making; and communicate their impacts to suppliers, encouraging better sourcing.”
For years, Orentreich Foundation for the Advancement of Science has researched biomedical interventions to prevent, halt, or reverse those disorders that decrease the quality or length of life. Our groundbreaking research on dietary methionine restriction has shown its dramatic ability to increase longevity while improving healthspan, lowering body weight, and reducing the incidence of age-related diseases.
In addition to our dedication to discovery, we are also committed to promoting the exchange of knowledge and strengthening of relationships within the scientific community. We host a biennial symposium on healthy aging, support meetings in the field, and, each year, our scientists represent us at conferences and seminars around the globe.
This year, OFAS will host a pre-meeting session at the AGE 47th Annual Meeting in Philadelphia. The theme of the conference is “Improving Resiliency to Delay Aging”, and the OFAS-sponsored session is focused on Nutrition and Longevity. The panel of speakers includes: Dr. Sebastian Brandhorst from University of Southern California; Dr. John Newman from the Buck Institute and UCSF; Dr. John P. Richie from Penn State University; and Dr. Brian Kennedy from the Yong Loo Lin School of Medicine at the National University of Singapore.
The Orentreich Foundation for the Advancement of Science is excited to announce that we will be leading our first Jane’s Walk in New York City this year. For those who do not know, Jane’s Walk is an event inspired by Jane Jacobs, an activist who greatly influenced urban renewal and city planning. These walks are an active memorial to Jane’s work and usually revolve around topics that identify with her ideals.
Our walk will be focused on addressing the quality of sidewalks in Central Harlem, which has some of the widest sidewalks in all of Manhattan, and discussing what attributes make a sidewalk more walkable than others. Medical research shows that walking can improve health outcomes in everything from heart disease and diabetes to improved mental and cognitive functions. Improving walkability can encourage residents to walk more in their neighborhoods.
Our Deputy Director, Bernardita Calinao, will be leading the walk along with our GIS Specialist, Marie Rusin. The walk will start in front of Red Rooster restaurant and you will find them holding a Jane’s Walk Flag that will also have our OFAS logo on it. Click here if you want to attend. The title of our walk is “The Quality of Central Harlem Sidewalks.” We look forward to seeing you there!
In our minds, old age is often associated with negative outcomes, such as a decline in physical health, but research consistently finds that older adults tend to experience more positive emotion than their younger counterparts. In this study, older adults reported greater awareness of being in the present moment, also known as mindfulness, than younger adults. Furthermore, this mindfulness helped to explain why older adults reported more positive emotion than younger adults do, suggesting that mindfulness facilitates healthy aging.
The researchers asked participants about their mood, mindfulness, and perspective on the future to see how these factors might be related. The participants reported their current positive and negative emotions, such as enthusiasm, fear, interest, and hostility. They reflected on how much they were mindfully aware in the moment, rather than living in the past or anticipating the future. And participants considered whether they felt concerned about the limited time left in their life or positive about the opportunities awaiting them.
The older adults tended to recognize that they had fewer remaining years on earth than the younger participants, but they also felt greater positive emotion. And according to the researchers’ analysis, it was their focus on the here and now—their greater mindfulness compared to young people—that explained their good moods. The higher their mindfulness, the better they felt. Since being mindful could help us regulate our emotions and relieve stress, it could be useful for humans to naturally grow in mindfulness as we get older. This is significant because positive emotions can also lead to better physical health. However, implications of these findings for health and well-being in younger and older adults are still being discussed.
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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