Chapter 5
It’s in Your Genes? — 2
It can occur through two very different paths: by preventing or delaying age-related diseases or by slowing the aging process. The former is building on where we are now and for which we’ll be making considerable headway in the near term. The latter, changing aging per se, is a more formidable challenge. Mrs. L. R. escaped the major chronic diseases, which only 19 percent of over four hundred centenarians (aged 97–119 years) managed to do in the New England Centenarian Study. The majority in that study, 81 percent, developed comorbidities, and were classified as either “survivors,” having a diagnosis of age-related illness before age eighty years, or “delayers,” diagnosed at age eighty and beyond. Preventing or markedly delaying age-related diseases, thereby extending health span, is what this book is (nearly all) about.
A Historic Convergence of Breakthroughs
The recognition of the immune system as a common mechanistic underpinning for chronic diseases, whether it be related to why they occur or to the untoward sequelae that they induce, is a historic turning point (fig. 2.1). These diseases—heart, cancer, neurodegenerative—take two or more decades to develop, giving us a longtime window of opportunity to prevent them. Atherosclerosis, which leads to heart attacks and strokes, endures, despite progress, as the number one cause of death and disability globally. It is due to inflammation in blood vessel walls, and all inflammation is generated by our immune system. Cancer isn’t usually a killer unless it spreads, and our immune system can stop that from happening. If there weren’t inflammation in the brain, it would be difficult for conditions like Alzheimer’s or Parkinson’s to take hold. When our immune system engages in self-directed attack on our body tissue, be it the nervous system in multiple sclerosis, or joints in rheumatoid arthritis, it becomes the foundation for autoimmune conditions. Dysfunctionality in our immune response is a principal driver of accelerated aging. Only in recent years have we begun to develop tools to handle the delicate modulating of our immune and inflammatory response. It’s like a Goldilocks story whereby too little is not good and too much is bad, so we must get it just right—and target the precise tissue in the specific patient under care. Happily, the science of fine-tuning this pathway is rapidly advancing.
Figure 2.1. The common thread underlying major diseases and accelerating aging
There are other pathways. Transplanting feces between people started to be pursued as a treatment in the 1950s, but only in recent years has there been unequivocal proof of its lifesaving capacity, leading to its FDA approval in 2023 to prevent recurrent Clostridium difficile infection, which can result from antibiotics changing the balance of bacterial species on the gastrointestinal tract. Fecal microbial transplant has a “yuck factor,” obviously. It hasn’t been easy either. But now “crapsule” pills have been produced and are in clinical trials, not only to make it easier but also to extend its use for managing various conditions such as cancer, gastrointestinal diseases, and diabetes. The idea of “CRISPR-ing” or editing the gut microbiome is being explored too.