The vast global DNA library resulting from mass genomic profiling is helping us understand how we could extend “longevity”, that is living younger and healthier for longer. It also means the search for the elixir of youth may no longer be the preserve of billionaires but be accessible to billions.
As the new year begins, we approach one of the most awaited life extension events of 2019: the Undoing Aging conference.
Starting off with a success
The Undoing Aging conference series started off in 2018, with the first being held in Berlin, Germany, in mid-March. Especially when you consider that UA2018 was the inaugural event of the series, it was extremely successful; the three-day conference organized by SENS Research Foundation (SRF) and Forever Healthy Foundation (FHF) brought together many of the most illustrious experts in the fields of aging research, biotechnology, regenerative medicine, AI for drug discovery, advocacy and policy, and business and investment.
LEAF writer Nicola Bagalà considers whether living past 40 is fundamentally different from living past 80.
Imagine this scene: you, a life extension supporter, are with a group of people talking about this and that, and, at one point, the opportunity to mention life extension presents itself. You expect people to react to it with “Yay! Longer life in good health! No more aging!” but reality doesn’t quite match up to your expectations; rather, all you get is the frustration of looking at how everyone nods approvingly when somebody puts on a great philosopher’s hat and asks rhetorically: “Would it really make us happier if we could live to 150?” Boy, is that ever irritating.
Actually, it isn’t really the specific question per se that is irritating—basically, whether living much longer than the current average would bring us more happiness—but rather that nobody ever asks whether living to 80 years old, for example, would make you any happier than you would be if you lived to only 40. If the first question is legitimate, the second one should be as well, and, by induction, you could work your way down to zero and ask whether being born makes you any happier than not being born. (Arguably, it doesn’t—babies inside the womb are generally quite peaceful and blessed looking, which is more than can be said of their mood once they pop out, but few people would agree that this is a good reason to abort each and every fetus.)
Maybe it is somehow established that living to 80 is sure to bring more joy than checking out at 40? Maybe it is equally well proved that living to 150 doesn’t make you any happier than hopping off the life train at 80? (Hardly—I don’t know of any 150-year-olds complaining about it, and neither do you.)
Scientists at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have discovered that squamous cell skin cancers do not require increased glucose to power their development and growth, contrary to a long-held belief about cancer metabolism.
The findings could bring about a better understanding of many cancers’ metabolic needs and lead to the development of more effective therapies for squamous cell skin cancer and other forms of epithelial cancer.
The research, led by senior authors Heather Christofk and Bill Lowry, was published in the journal Nature Communications.
A drug to fight ageing may finally be on the horizon after the first trial in humans showed ‘impressive’ results.
For many years scientists have known that an accumulation of senescent cells in the body is linked to ageing symptoms such as frailty and arthritis, as well as diseases such as Alzheimer’s and Parkinson’s.
Senescent cells — also known as zombie cells — are not completely dead so are not cleared out by the body, but are too damaged to repair tissue or carry out normal functions. Unable to repair itself or clear out the waste, the body gradually deteriorates.
A new study published in Nature Metabolism finally reveals the answer to how NMN enters the cell in order to become NAD+ and that it does not need to convert into NR to do so.
In the last few years, there has been considerable interest in restoring levels of the nicotinamide adenine dinclueotide (NAD+) coenzyme to combat age-related diseases. Evidence suggests that NAD+ systemically declines with age in a variety of organisms, including rodents and humans, which contributes to the development of many age-related diseases and metabolic conditions.
What is NAD+?
Nicotinamide adenine dinucleotide (NAD) is a coenzyme found in all living cells. It is a dinucleotide, which means that it consists of two nucleotides joined through their phosphate groups. One nucleotide contains an adenine base, and the other contains nicotinamide.
Is an American syndicated talk show airing daily on television in the U.S., Canada, Mexico, Australia, Ireland, Sweden and Finland. It debuted on September 8, 2008. The hour-long daytime program is produced by Phil McGraw and his son Jay McGraw and is distributed domestically and globally by CBS Television Distribution. The series is a spin-off of Dr. Phil and is the first talk show to be a third generation talk show spin-off, as Dr. Phil itself spun off The Oprah Winfrey Show.
Rejuvenation is a medical discipline focused on the practical reversal of the aging process.
Rejuvenation is distinct from life extension. Life extension strategies often study the causes of aging and try to oppose those causes in order to slow aging. Rejuvenation is the reversal of aging and thus requires a different strategy, namely repair of the damage that is associated with aging or replacement of damaged tissue with new tissue. Rejuvenation can be a means of life extension, but most life extension strategies do not involve rejuvenation.
Facebook: https://www.facebook.com/agingreversed
We take a somewhat humorous look at the messaging and the comfort stories people tell themselves to distract themselves from seeing why age-related diseases and dying from them is a problem that needs solving.
Here’s what might be considered a paradox: right now, the Facebook page of Death Cafe—a place where you go to talk about death—is a rather lively place, whereas pages about life extension are comparatively rather dead places. This screenshot shows the activity of a Death Cafe post:
There is no doubt that the subscribers of the Death Cafe page are quite engaged, but if the average message that the page aims at conveying is the same as in the text snippet above, then there is no paradox at all. The core of that message is “don’t worry, death is nothing to fear” (which, incidentally, implies you don’t have to engage in any extra effort to prevent death), whereas the core message of a life extension page is, “death is a problem, but hey—with some effort, we can beat it. Maybe.” That’s a bit like a kiosk giving candy away for free right next to another kiosk that first serves you overcooked broccoli and then says that you might get a nice present decades from now, assuming that you work hard enough for it—where do you think most people would flock to? Exactly.
In a small and preliminary clinical trial, Johns Hopkins researchers and their collaborators have shown that an experimental gene therapy that uses viruses to introduce a therapeutic gene into the eye is safe and that it may be effective in preserving the vision of people with wet age-related macular degeneration (AMD). AMD is a leading cause of vision loss in the U.S., affecting an estimated 1.6 million Americans. The disease is marked by growth of abnormal blood vessels that leak fluid into the central portion of the retina called the macula, which we use for reading, driving and recognizing faces.
The study published on May 16 in The Lancet, reports an exciting new approach in which a virus, similar to the common cold, but altered in the lab so that it is unable to cause disease, is used as a carrier for a gene and is injected into the eye. The virus penetrates retinal cells and deposits a gene, which turns the cells into factories for productions of a therapeutic protein, called sFLT01.
The abnormal blood vessels that cause wet AMD grow because patients have increased production of vascular endothelial growth factor (VEGF) in their retinas. Current treatments require injections of proteins directly into the eye that bind and inactivate VEGF, reducing fluid in the macula and improving vision. However, the therapeutic proteins exit the eye over the course of a month, so patients with wet AMD usually need to return to the clinic for more injections every six to eight weeks in order to stave off vision loss. Eye specialists say the burden and discomfort of the regimen is responsible for many patients not getting injections as frequently as they need, causing vision loss.
The results from a human pilot study that focused on treating idiopathic pulmonary fibrosis with senescent cell-clearing drugs has been published. The drugs target aged and damaged cells, which are thought to be a reason we age and get sick, and remove them from the body.
Senescent cells and aging
As we age, increasing numbers of our cells become dysfunctional, entering into a state known as senescence. Senescent cells no longer divide or support the tissues and organs of which they are part; instead, they secrete a range of harmful inflammatory chemical signals, which are collectively known as the senescence-associated secretory phenotype (SASP).
