IF1 Protein Controls Aging Rate

Published on Apr 15
An improved version of the preprint (IF1 Protein Controls Aging rate) is presently undergoing peer review at a journal. ASSUMING this will be published - perhaps unwisely counting chickens... - I've written the following to disseminate cometh the time. Thought worth sharing here first, ahead of time.
Why Do Some Species Live Longer?
A New Study Points to a Single Protein
One of the biggest mysteries in science is: Why do different species have such different maximum lifespans? For example, why does a mouse maximally live 4 years, whereas a bowhead whale can live for more than two centuries? How can a dog be chronologically younger - but biologically older - than its human owner? A paper published today in the peer-reviewed journal TO BE SEEN suggests that it is simply because of a single protein. IF1 protein. Species with more IF1 protein age slower and live longer.
The author of this paper is Cambridge University graduate Dr. Michael Forrest. Before collecting data, Dr. Forrest hypothesized that IF1 protein is the Master Switch of aging rate. He subsequently discovered a statistically significant correlation between maximum lifespan and IF1 protein activity across species. Moreover, before collecting data, Dr. Forrest hypothesized that this IF1 protein activity is the lynchpin in a cascade of other physiological variables, which were also each subsequently observed to (statistically significantly) correlate with maximum lifespan across species. What is the chance that all these hypothesized - and then observed - correlations are due to chance? Improbably low. Critically, this multi-pronged hypothesis was not from the data. It preceded obtaining the data. So, this data tests and validates the hypothesis. A confirmatory (hypothesis before data, which tests the hypothesis) rather than an exploratory (hypothesis from data) study: a pivotal distinction. Moreover, a mathematical technique that can infer causality, called instrumental variable analysis, reports causality. Corroborated, especially in aggregate, by dozens of other varied and powerful mathematical methods, such as a Bayesian Structural Equation Model (BSEM) whose Bayes Factor, upon a well-known calibration scale, greatly exceeds the threshold for "decisive" evidence. Furthermore, conferring interventional evidence, increasing the IF1 protein amount reduces aging in mice.
Dr. Forrest says: "Aging is typically considered intractable. But since different species can have strikingly different lifespans, nature might have a dial to control the aging rate, which I think - in IF1 protein - has been discovered."
Dr. Forrest has filed patents for using IF1 protein and derivatives thereof, including cell-permeable variants, to modulate the aging rate. Moreover, he has invented (and patented) small-molecule drugs that work like IF1 protein, which have - as he hypothesized - potent anticancer activity. Demonstrated in independent testing by the National Cancer Institute in the USA. Dr. Forrest has founded a company in Delaware, Biophysical Therapeutics, to commercialize this and other research. Commercialization gets drugs to people. The company boasts one of the biggest names in biotech, Professor George Church of Harvard Medical School, as an advisor.
Dr. Forrest closes by saying: "Aging is causal to the many and varied maladies and diseases of aging, such as Alzheimer's disease, and so a single drug against aging could be efficacious for them all. Plus, it would likely have cosmetic applications."