Here is a mainstream view of the growth in interest in aging research, a focus on discovery of how exactly aging progresses in fine detail and how that progression is influenced by environment and genes, and no mention of doing more than slightly altering the pace of aging. Growth in the field is ultimately a good thing, however, as at some point in the near future the disruptive approach of damage repair typified by the SENS programs, aiming for rejuvenation treatments that can reverse the progression of age-related degeneration, will produce practical results that are indisputably far better and far cheaper than those emerging from drug development to modestly slow aging. The more researchers available to move over to that line of work once persuaded, the better off we all are.
Aging is at the center of many of the world's most prevalent and deadly diseases, including cancer and heart disease. Over the last 20 years we have seen amazing advances in our understating of the mechanisms behind aging-related processes at the level of genes, cells and whole organisms. Many countries are now facing a growing aging society, with a high prevalence of fatal age-related diseases, such as cancer, cardiovascular, and pulmonary disease.
Exciting new lines of research have shown that aging involves a complex interplay between the genome, epigenome, microbiome, and the environment. Recent work on epigenetic modifications, the chemical signatures branded on our genome that affect gene expression, has revealed surprising links to the aging process and established a connection with environmental factors. Important epigenetic marks such as the methylation of regulatory DNA sequences, covalent modifications of histone proteins, and the expression of regulatory non-coding RNAs are affected during aging. The effect of the environment on this epigenetic landscape is clearly shown by studies using identical twins. As they age, these twins are no longer identical in their epigenome, showing differences in gene expression and ultimately, lifespan. Changes to the epigenetic landscape may affect gene expression and ultimately the aging process, especially through the modification of metabolism.
Food scarcity is one of the most important environmental factors affecting epigenetic modification; it is therefore not surprising that many molecules and signaling pathways that have been implicated in aging, such as mammalian target of rapamycin, sirtuins, and insulin-like growth factor/insulin signaling pathways, are related to metabolism. Thus, how our genes modify our metabolic status, depending on the food intake and consumption, is a central issue of aging science. Another new and exciting area in aging research involves the tiny microbes living in our bodies. Our gut, for example, hosts microorganisms that amount for 10 times as many cells than found in our body and 150 times as many genes as there are in our genome. Understanding the fundamental mechanisms of aging may lead to the development of new treatments that could be applicable to a wide variety of age-related diseases.