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Circa 2011 essentially cancer could help with evolution as it can challenge the immune system to be more strong. Essentially a symbiotic relationship to evolve with it and grow stronger with it then like it can be used as a good thing to make sure that evolution has stronger genetic code.


Evolutionary theories are critical for understanding cancer development at the level of species as well as at the level of cells and tissues, and for developing effective therapies. Animals have evolved potent tumor suppressive mechanisms to prevent cancer development. These mechanisms were initially necessary for the evolution of multi-cellular organisms, and became even more important as animals evolved large bodies and long lives. Indeed, the development and architecture of our tissues were evolutionarily constrained by the need to limit cancer. Cancer development within an individual is also an evolutionary process, which in many respects mirrors species evolution. Species evolve by mutation and selection acting on individuals in a population; tumors evolve by mutation and selection acting on cells in a tissue. The processes of mutation and selection are integral to the evolution of cancer at every step of multistage carcinogenesis, from tumor genesis to metastasis. Factors associated with cancer development, such as aging and carcinogens, have been shown to promote cancer evolution by impacting both mutation and selection processes. While there are therapies that can decimate a cancer cell population, unfortunately, cancers can also evolve resistance to these therapies, leading to the resurgence of treatment-refractory disease. Understanding cancer from an evolutionary perspective can allow us to appreciate better why cancers predominantly occur in the elderly, and why other conditions, from radiation exposure to smoking, are associated with increased cancers. Importantly, the application of evolutionary theory to cancer should engender new treatment strategies that could better control this dreaded disease.

We expect that the public generally views evolutionary biology as a science about the past, with stodgy old professors examining dusty fossils in poorly lit museum basements. Evolution must certainly be a field well-separated from modern medicine and biomedical research, right? If the public makes a connection between evolution and medicine, it is typically in the example of bacteria acquiring antibiotic resistance. But what does evolution have to do with afflictions like heart disease, obesity, and cancer? As it turns out, these diseases are intricately tied to our evolutionary histories, and understanding evolution is essential for preventing, managing and treating these diseases (1, 2). This review will focus on cancer: how evolutionary theories can be used to understand cancer development at the level of species as well as at the level of cells and tissues. We will also discuss the implications and benefits of an evolutionary perspective towards cancer prevention and therapies.

For almost all animals, old age is associated with a general decline in tissue structure and function. This decline is thought to reflect the lack of selective pressure to maintain tissues beyond an age when the animal would be likely to contribute genetically to future generations (3−5). Similarly, there is little selective pressure to limit cancer in old animals who are substantially beyond their reproductive years. For example, while mice can live 2–4 years in the lab, and tend to develop cancer in their second and third years, it is rare to find a mouse greater than 1 year old in the wild. Most wild mice will be dead from other causes, such as cold, hunger, disease or predators, well before the age when cancer would be a likely cause of their demise. Thus, evolution has favored a “breed early, breed often” strategy for mice.

A recent study has taken an in-depth look at the age-related changes that occur in the microbiome, particularly in regards to bacterial populations.

A detailed look at bacterial populations in the gut microbiome

The publication contains multiple graphs that track age-related changes to various bacterial populations in the gut. These graphs show a common trend: the abundance of these bacterial species increases with aging but then falls significantly in extreme old age. On these charts, Groups 1–5 contain various ages of children, Group 6 consists of 19- to 29-year-olds, and each following group is ten years older than the previous, with Group 14 containing 99- to 110-year-olds.

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MOTHERBOARD met up with Russian billionaire Dmitry Itskov at his Global Future 2045 Conference in New York City to talk about immortality, spirituality, and the coming age of cybernetic avatar-based living.

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In mouse studies, a “methylation clock” on the ELOVL2 gene ticks toward impaired vision, but when gene expression was boosted, age-related visual function improved.


A lengthy-named gene called Elongation of Very Long Chain Fatty Acids Protein 2 or ELOVL2 is an established biomarker of age. In a new paper, published online January 14, 2020 in the journal Aging Cell, researchers at University of California San Diego School of Medicine say the gene appears to play a key role in age-associated functional and anatomical aging in vivo in mouse retinas, a finding that has direct relevance to age-related eye diseases.

Specifically, the research team, led by senior author Dorota Skowronska-Krawczyk, PhD, assistant professor in the Viterbi Family Department of Ophthalmology at UC San Diego Shiley Eye Institute, found that an age-related decrease in ELOVL2 gene expression was associated with increased DNA methylation of its promoter. Methylation is a simple biochemical process in which groups of carbon and hydrogen atoms are transferred from one substance to another. In the case of DNA, methylation of regulatory regions negatively impacts expression of the gene.

When researchers reversed hypermethylation in vivo, they boosted ELOVL2 expression and rescued age-related decline in visual function in mice. “These findings indicate that ELOVL2 actively regulates aging in mouse retina, provides a molecular link between polyunsaturated fatty acids elongation and visual functions, and suggests novel therapeutic strategies for treatment of age-related eye diseases,” wrote the authors.

“A neuroscientist explains how our brains age and provides tips for aging with more vitality and happiness.”

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About 13 years ago, I watched my very vital mother die a slow death from Lewy-Body dementia. For me, it was a wakeup call. If there were anything I could do to stay healthy myself—to avoid the slow decline of an aging brain—I wanted to do it. But what really helps us stay sharp longer? And how can we separate fad ideas from solid, evidence-based advice around aging?

Enter Daniel Levitin’s new book, Successful Aging: A Neuroscientist Explores the Power and Potential of Our Lives.

Levitin is a neuroscientist, psychologist, professor emeritus at McGill University in Montreal, and faculty fellow at UC Berkeley. His highly researched book provides fascinating insights into how our early childhood experiences, personalities, social relationships, and lifestyles all drive our brain’s development, dispelling stubborn myths around the inevitability of cognitive decline. Arguing against ageism and highlighting the unique gifts of older people, Levitin shows us what we can all do to become sharper, happier, and wiser as we age.

After getting a considerable success in convincing scientists and investors, in the last decades, that undoing aging through a damage repair approach is possible and desirable, Aubrey de Grey is turning his advocacy efforts to politicians. In this video, he explains why.


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Aubrey de Grey delivers a keynote on the next steps for longevity for policy makers.

Dr Aubrey de Grey is a biomedical gerontologist based in Mountain View, California, USA, and is the Chief Science Officer of SENS Research Foundation, a California-based 501©(3) biomedical research charity that performs and funds laboratory research dedicated to combating the ageing process. He is also VP of New Technology Discovery at AgeX Therapeutics, a biotechnology start up developing new therapies in the field of biomedical gerontology. In addition, he is Editor-in-Chief of Rejuvenation Research, the world’s highest-impact peer-reviewed journal focused on intervention in ageing. He received his BA in computer science and Ph.D. in biology from the University of Cambridge. His research interests encompass the characterisation of all the types of self-inflicted cellular and molecular damage that constitute mammalian ageing and the design of interventions to repair and/or obviate that damage. Dr de Grey is a Fellow of both the Gerontological Society of America and the American Aging Association, and sits on the editorial and scientific advisory boards of numerous journals and organisations. He is a highly sought-after speaker who gives 40–50 invited talks per year at scientific conferences, universities, companies in areas ranging from pharma to life insurance, and to the public.