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A new study has demonstrated that increasing the expression of a single gene was enough to reverse age-related visual decline in the eyes of old mice.

Introducing ELOVL2

Elongation of Very Long Chain Fatty Acids Protein 2 (ELOVL2) is both a bit of a tongue twister and a known aging biomarker. The results of a new study from researchers at the University of California San Diego School of Medicine suggest that the ELOVL2 gene plays a pivotal role in both the functional and anatomical aging of the retinas of mice and may also have relevance to human age-related eye conditions.

Genomics and BioPharma Pioneer!! — On this ideaXme (http://radioideaxme.com/) episode, I had the honor of being joined by Dr. William Haseltine — biologist, entrepreneur and philanthropist, known for his groundbreaking work on HIV/AIDS and the human genome, now focusing on the issues of healthcare costs, dementia care, and aging — #Ideaxme #Genomics #RegenerativeMedicine #BillHaseltine #Dementia #Biotechnology #Harvard #JamesWatson #WalterGilbert #DavidBaltimore #MIT #CraigVenter #Health #Wellness #Regeneration #Longevity #Aging #IraPastor #Bioquark #Regenerage


Ira Pastor, ideaXme exponential health ambassador, interviews Dr. William Haseltine, American biologist, entrepreneur and philanthropist, known for his groundbreaking work on HIV/AIDS and the human genome.

Ira Pastor Comments:

On today’s show we have a thought leader who sits amongst a rare group of people who have been responsible for creating many aspects of the modern biopharma / genomics / regenerative medicine system as we know it today.

Dr. William Haseltine

Routinely listed in major media sources as one of the world’s most influential business people and most influential leaders in biotechnology, Dr. William Haseltine is an American biologist, entrepreneur and philanthropist, known for his groundbreaking work on HIV/AIDS and the human genome.

Dr. Haseltine earned a PhD in Biophysics at Harvard University, where he worked under the direction of Dr. James Watson, co-discoverer of the structure of DNA, and Dr. Walter Gilbert, Nobel prize winner for developing DNA sequencing techniques.

For the past 10 years, Yale Professors David Spiegel and Jason Crawford have been working on tools to enable the development of glucosepane-cleaving drugs. Kizoo Technology Capital investors say now is the time to advance this groundbreaking research toward the clinic and are leading funding of a new company, Revel Pharmaceuticals Inc., founded by Drs. David Spiegel, Jason Crawford, and Aaron Cravens.

Kizoo leads the seed financing round at Revel, with Oculus co-founder Michael Antonov participating. SENS Research Foundation provided funding to the YaleGlycoSENS group for several years.

The long-lived collagen proteins that give structure to our arteries, skin, and other tissues are continuously exposed to blood sugar and other highly reactive molecules necessary for life. Occasionally, these sugar molecules will bind to collagen and form toxic crosslinks that alter the physical properties of tissues and cause inflammation. As a result, tissues slowly stiffen with aging, leading to rising systolic blood pressure, skin aging, kidney damage, and increased risk of stroke and other damage to the brain.

A method and apparatus for ameliorating the aging process and the effects of aging and maintaining the integrity of health is provided. The method includes subjecting biological systems to alternating and steady magnetic fields having flux densities ranging from 10-6 gauss to 10-20 gauss and frequencies from 0 Hertz to 1014 Hertz. The calculation is made with reference to the equation mc2 =Bvlq, where m=mass; c=speed of light; B=magnetic flux density; v=inertial velocity of the mass contained in l; l=length of the conductive body; q=unity. The process begins by targeting the larger targets first and then diminishing the field magnitude slowly and incrementally according to the targets. The frequency when AC is indicated is calculated with the cyclotron resonance formula, fc =qB/(2πm). The apparatus includes a specially constructed pool or tub for generating the specific magnetic flux necessary for treatment. Orientation of the patient with reference to North, South, East and West is varied. The earth’s position in relation to the sun is taken into account. The patient may be in an upright, prone or swimming position depending on the specific treatment scheme.

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.”

https://greatergood.berkeley.edu/topic[/li

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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.