Siegfried Hekimi is a professor of biology at McGill University and head of The Hekimi Lab where he and his team specialize in the study of aging. Hekimi delivers an informative overview of the complex, and often unknown, processes that produce aging, and the work his lab is involved with to try to uncover the mechanisms that accelerate, and retard aging, and why they do.

Hekimi studied biology at the University of Geneva. After Geneva, Hekimi began work at the celebrated Laboratory of Molecular Biology (LMB) of the Medical Research Council in Cambridge, UK, where he developed his method for using ‘the worm’ for translational studies on the biology of aging. While at Cambridge Hekimi identified the first mutants that supported the theory that aging could be manipulated genetically and that the process of inducing mild mitochondrial dysfunction can slow down the aging process of animals. Hekimi has worked and taught at McGill University for many years and is intensely focused on the important work his team is doing in the lab.

Hekimi discusses their laboratory work in genetics and the study of aging, as well as the process of drug development to combat aging. By using mutants of the microscopic worm Caenorhabditis elegans as well as the mouse to study aging, Hekimi hopes to develop new methods for medical intervention on the aging process. The Hekimi Lab focuses on gene activities that have a direct effect on mitochondrial function, and they are particularly interested in the biosynthesis and function of ubiquinone (UQ, Coenzyme Q, CoQ), the obligate, diffusible relay in the complete mitochondrial electron transport chain. The lab’s mission is to develop drugs that can alleviate diseases linked to ubiquinone deficiency.

Hekimi discusses some of the surprising outcomes of his research, one major point being that free radical increase actually fights aging and prolongs lifespan, contrary to past scientific thought. He talks about his correlation between this study and research to mitochondrial damage, etc. He explains that free radicals are only potentially toxic because they are produced by various processes, and there are mechanisms within the cells that defend against this potential damage. As Hekimi explains, free radicals are in fact signaling messengers, which ultimately help cells stay in homeostasis by talking between compartments, etc.

Hekimi states that the consumption of antioxidants has actually been shown to have no beneficial effects, contrary to widely accepted public opinion. He discusses his research with calorie restriction and metabolism, and the effects of mitochondria functioning at a slower rate. Some studies suggest that increased lifespan may actually be achieved by decreasing energy expenditure. By producing ATP (adenosine triphosphate), the primary energy carrier in all living organisms, more slowly, lifespan may possibly be increased. He talks about naked mole rats that live incredibly long lives, and yet their base level of free radical damage is exceedingly higher than mice or some other animals, which is further demonstrable evidence that the nature of free radicals is greatly misunderstood in the public consciousness. He explains that the same amount of damage happens in the mutant species but it happens over a greater span of time. Why this is happening in some and not others is one of the many questions that brilliant minds like Hekimi pose in their extensive laboratory research.

The molecular biology expert explains the complexity of their research and how there are still very many unknowns in the general understanding of why aging occurs, why cellular damage happens and cannot be repaired, etc. He details some of their methods utilizing CRISPR and other work on drug development for mitochondrial diseases. Asking questions and searching for answers is precisely what Hekimi and his team focus on daily, and they hope to find causative links to explain why we age and how to slow the process in regard to disease and overall longevity.

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