Welcome to Running: A FEVER. Welcome back if you’re a frequent flyer. My name is Michael Davis. This is a podcast about fitness, diet, and medicine. The goal is to live a long, healthy, happy, active life right up to the very end. If that aligns with your philosophy, you’re in the right place. We’ll get there together.

Well, these are perhaps the most intense episodes I’ve ever done. There was a lot of technical info to sift through, and I hope I’ve made it more accessible to more people. It is exciting to learn about the work being done in genetics and what it all may mean for our future, including how long that future may be for each of us as individuals.

The goal of this episode is to summarize what we’ve been through and highlight some of the highlights so they stick with us. This is important, especially with regard to the things we can do now to extend our lives. So, let’s get into it.

Part 1 of the series was an introduction. I introduced questions I hope would be answered in the series, and some just for contemplation, such as: Why do I want a longer life? What would I do with all the extra time I would have? Will my current ailments be cured? What is the cost? Would I have to do backbreaking work for the rest of my life to pay for the privilege of that long life?

In Part 2, we discussed reclassifying aging as a disease. Research funding is based on a hierarchy of diseases mainly focused on mortality: how many deaths are attributed to a particular disease. If aging were on that list, it would be number one. In addition to research funding, this list also determines which drugs are developed and what is covered by medical insurance. If aging were classified as a disease, we could extend life more than would curing any of the current top diseases.

In part 3, we got a bit more technical, exploring an information theory of aging. Aging can be viewed as a loss of information in our epigenome. We looked at the science behind this theory. DNA contains all of the information about youth. It doesn’t change, but the epigenome does. Like a computer, it is binary, switching genes on and off. It is information being communicated to the DNA. When cells are damaged, the epigenome is overworked, and the information doesn’t get through. It’s too noisy to communicate. So DNA doesn’t work the way it should and we begin to lose things. This is the process of aging at the genetic level.

Part 4 was about the details of the important enzymes called sirtuins, their fuel NAD, and other substances in our bodies that can affect aging. We learned that sirtuins are part of the epigenome discussed in part 3. They are fueled by NAD, which begins to run out as we age chronologically. If we can boost NAD, we can keep the sirtuins doing their job accurately and tirelessly, keeping the epigenome focused on the youth that is still present in the DNA. We learned about mTOR, which also repairs DNA and regulates protein production, digesting the old and signaling the production of the new. Most importantly, the idea is that cellular stress in the right amount can activate these enzymes and extend life.

Part 5 was all about calorie restriction and fasting. This is a way of inducing the kind of cellular stress we just mentioned. Remember that Americans consume two-thirds more food than we need to survive. We’re just talking about eating less than we want. We found that a safe way to restrict is to use intermittent fasting. And found many examples in research and in real-life observations such as those by Dan Buettner, author of “The Blue Zone: Lessons for Living Longer From the People Who’ve Lived the Longest,” in places like Okinawa, where lifespans are considerably longer, and the diet has 20% fewer calories than the typical Japanese diet.

We knew exercise was healthy, but in part 6, we learned of its intense effect on longevity. Exercise, like calorie restriction, is another way to induce cellular stress. The most effective is high-intensity interval training, which you can see me doing in episode 101. Exercising only 15 minutes daily can reduce the risk of heart attack by 45%. But only 10% of people over 65 exercise. Even ten minutes a day can increase your lifespan by years. In this episode, I provided a formula for the right exercise intensity to cause cellular stress but not cellular damage. In short, exercise turns on the genes that drive bodily activities that normally would be reduced as we age.

Part 7 explored the effect of cold and heat exposure on longevity. There’s a kind of fat we need to increase in our bodies. It’s called brown fat. Exposure to cold triggers its production. Brown fat and cold exposure can limit the risk of diabetes, obesity, and Alzheimer’s disease. Some people do this by using cryotherapy, standing in a cryogenic chamber at extremely cold temperatures for a few minutes. But you can get the same effect by exercising in short sleeves on a cold day, or keeping your environment cold enough to be a little uncomfortable.

Part 8 was pretty amazing. We talked about some supplements and drugs available right now that can battle the effects of aging. And some future technology that might provide additional support in the battle. Rapamycin, which is a regulated drug with some dangerous side effects, was one. Metformin, also a regulated drug used to treat diabetes, has anti-aging effects. Resveratrol is the magic ingredient in red wine that can protect against cancer and other aging-related diseases. Lab experiments show that it can extend life to the equivalent of fifty years. And the NAD boosters NMN and NR. We’ve already mentioned the effect of increased NAD. These two molecules are currently available over the counter. And there are many more of these being researched right now.

The impact of a longer-lived population on our society was the focus of part 9. It seems inevitable that the human lifespan will increase, possibly dramatically, based on what we’ve discovered in this series. But we’re woefully unprepared for it. Much of the data is based on us living into our 80s and not beyond. We delved into the implications for social programs, medicine, the labor force, and all of the problems that could arise based strictly on an increase in population. Also, how would the advancement of technology impact not just lifespan but also healthspan? Because we all want to live a long and healthy life.

There are now thousands of scientists working on solutions to the aging problem. It is no longer a wild theory that aging can be treated and possibly reversed. And the World Health Organization has classified a condition known as “Old age.” Once that gets reported on enough death certificates, who knows what could happen? Aging may make it to the top 10 causes of death and get enough funding to make a big difference in the average lifespan of you, me, and everyone else.

I want to thank once again David A. Sinclair and Matthew D. LaPlante for writing the book that inspired this series, “Lifespan: Why We Age — and Why We Don’t Have To”

I hope you have enjoyed this series as much as I have. If you’re watching this on YouTube, give us a thumbs up and consider subscribing for the low, low price of one click. And if you have the fever, keep it burning, but if you don’t, catch the fever. And I’ll see you next time on Running: A FEVER.

References:
http://Runningafever.com/101
Sinclair, David A. and LaPlante, Matthew D. (2019). Lifespan: Why We Age — and Why We Don’t Have To. Atria Books.