How Old Can Humans Get?

A Longer Healthier Life is Within Reach!

Greenland Sharks May Live Over 500 years

That is the title of an article in Scientific American from the end of July this year and there is a growing body of evidence that we can stay healthy and fully functional much longer. Here is a quote from the article:

“João Pedro de Magalhães, a professor of molecular biogerontology at the Institute of Inflammation and Ageing at the University of Birmingham in England, thinks humans could live for 1,000 years. He has scrutinized the genomes of very long-lived animals such as the bowhead whale (which can reach 200 years) and the naked mole rat. His surprising conclusion: if we eliminated aging at the cellular level, humans could live for a millennium—and potentially as long as 20,000 years.”

Of course, that seems crazy. Really crazy. But we are learning a great deal about the core biology of the aging process. The naked mole rat lives 30 years and that is ten times as long as the rats that we usually think about. Greenland sharks live from 270 over 500 years. Tiger sharks live about 30 years. They are both very large sharks, but one lives many times longer than the other. And remember this. A shark must be fully functional to stay alive. It must be able to find food and catch it. There are no nursing homes for sharks. That leads to a very important question. Why would two animals that are so similar have high functioning life spans that are so dramatically different? The new science of aging and chronic disease is providing some surprisingly detailed answers.

At this point it is important to say this. No one wants a longer life where we are frail and must depend on others for everything. But what if we could function at 60 like we did at 30. New science suggests that is possible. Aging and chronic diseases are related, and they are governed by genetics, epigenetics, and molecular biology. That is why the Greenland shark lives ten times as long as a tiger shark. Here is a clue. A Greenland shark only grows about fifteen hundredths of an inch a year or 2.3 inches in 16 years. They aren’t sexually mature until they are 150 years old. Tiger sharks may grow up to 90 centimeters in a year. That is 35 inches a year. Both sharks can be over 20 feet long. Tiger sharks just get there a lot faster.

Based on what we know already, this link between growth rate and longevity is almost certainly critical. Obviously, if two sharks of about the same size experience vastly different longevity, the old idea that we just wear out cannot be right. Our genes function like a computer code and longevity is determined by the genetics, gene regulation (epigenetics), and the molecular biology that they control. Here is the link between growth rate and longevity. In sharks, mole rats, and humans, growth rate and longevity are regulated by a master metabolic genetic switch named the mechanistic target of rapamycin (mTOR). As the name suggests, mTOR is inhibited by rapamycin which is an antibiotic found in nature that is already used in humans. Rapamycin leaks out slowly in heart artery stents to inhibit the growth of scar tissue that would block the stent. Those stents last much longer. It is also used to slow the growth of cancer and to suppress immunity. Switching off mTOR slows growth. Switching on mTOR speeds up growth.

In the human fetus and child mTOR coordinates growth with food availability and you can already see the effects of that. American men today are two and a half inches taller than they were a hundred years ago. Over the last 40 years, sixty year-old American men are 33 pounds heavier. You can really see the difference in football players. The biggest players are more than 50 pounds heavier than they were a few decades ago. That is because very high calorie food is available for many people all day long. It is not just us either. Bears who live in cities and eat what we eat are 30% bigger and they don’t hibernate.

Some animals never stop growing, but humans do at about age eighteen. After that switching on mTOR with too much food is no longer beneficial and it accelerates the aging process and causes chronic diseases. Slender, healthy young adults on a good diet who are not smoking have the lowest mTOR activity.

Once we have stopped growing, food still switches on mTOR and mTOR still promotes growth but it is making fat stores larger, the arteries thicker, and the heart bigger. Too much food is making us older and sicker faster. There is another way to switch on mTOR. Extra abdominal fat makes hormones that produce oxidants that activate growth factors that also switch on mTOR. The oxidants in tobacco smoke do the same thing. Too much food all day long, extra abdominal fat, and smoking all act in the same way to switch on mTOR and accelerate aging and chronic disease development. mTOR is essential in the young to support normal growth and development. In the young it is the growth switch. That is its key function. In the old it is the death switch.

mTOR is paired with another master metabolic genetic switch called AMPK. When mTOR is switched off, AMPK is switched on. When there is no food, mTOR is inactivated and AMPK is activated to promote survival until there is food again. AMPK is the survival switch and that is its function as long as we live. The death switch leads to faster aging and more chronic illness earlier. The survival switch keeps us healthier and more functional longer.

There have already been significant strides in this area for humans. Patients with type 2 diabetes and chronic kidney disease on optimal medical therapy (OMT) lived 8 years longer free of heart attack and stroke compared with patients who receive usual care--the treatment that most of us receive. Their longer, healthier life was documented over 21 years of follow-up of patients who used a protocol based on our knowledge in 1995. OMT is the best practice combination of lifestyle and medical treatments to slow aging and delay chronic illness. They used diet and exercise, metformin for diabetes, a statin for cholesterol, losartan or lisinopril for hypertension, along with aspirin treatment and encouragement to stop smoking.

Our current protocols are even more powerful. Now we know that eating fewer calories, intermittent fasting, and exercise all switch off mTOR and switch on AMPK. Rapamycin, metformin, and drugs like Jardiance do the same thing. They directly switch off mTOR and switch off AMPK to protect cells and organs regardless of factor status. Jardiance was developed to treat diabetes, but it lowers hospitalizations for heart failure whether the patient is diabetic or not. Lisinopril, losartan, spironolactone, and eplerenone for high blood pressure and statins for cholesterol do the same thing by reducing oxidant production, growth factor activation, and mTOR activation with AMPK deactivation. We also know that beginning earlier in diabetes and related conditions before complications like kidney disease is more effective. This latest understanding should prolong healthier life by more than eight years.

We understand these pathways now in some considerable detail. Researchers have extended lifespan in some lab animals tenfold already as the link above demonstrates. The signaling pathways are very well worked out. These benefits are not only for the very wealthy and well connected. They can be available for everyone. The medicines are almost all generic and inexpensive. We have decades of experience with them. They are safe and proven to work. Healthier, longer lives are within our reach now. That matters to all of us. Let’s make it happen!