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THE SEVEN PILLARS OF AGING

Okay, now you’ve decided not to let the Four Killers take you out. That means it’s time to shore up the Seven Pillars of Aging. When I was working to reverse my early aging as a young man, I learned that there are specific forms of cellular aging that drive all forms of aging and disease, even my premature symptoms of aging. Later, I gleaned more detail from longevity experts such as Aubrey de Grey, who is the chief science officer at the SENS (Strategies for Engineered Negligible Senescence) Research Foundation, which has the ambitious mission of curing aging by funding anti-aging research around the world. A lot of my elite anti-aging longevity friends (yes, I have weird and awesome friends) are focused on what SENS calls the “classes of cellular and molecular damage that constitute aging.” I call them the Seven Pillars of Aging.

THE SEVEN PILLARS OF AGING

It’s important to understand how the Seven Pillars of Aging affect your body on the cellular level. While some degeneration over time is a given, there’s a lot you can do to protect yourself from the worst of it. From simple and inexpensive lifestyle changes and nutritional modifications to high-end technologies that are rapidly becoming more affordable, I’ll outline multiple strategies to hack the aging process—most of which I’ve tried out myself.

Is this anti-aging science still nascent? Yes. Do we have ironclad evidence that these strategies work perfectly? No. But we do have some pretty compelling research that suggests they will help you spend more quality years on this planet. Plus, they’re not going to kill you—and aging definitely will. So why not give them a shot?

First, let’s take a closer look at each of the aging pathways and how they affect us.

PILLAR 1—SHRINKING TISSUES

When you are young, your body has a multitude of stem cells—undifferentiated cells that are capable of giving rise to many more cells of the same type. When cells die via apoptosis, your stem cells spring into action to replace them. As you age, however, a few things happen. Your stem cell reserves dwindle, your stem cells themselves age and thus become less efficient at replacing dead cells, and your mitochondria may not trigger apoptosis at the right times. Some cells die before they’re supposed to. Others aren’t quickly replaced. As a result, tissues throughout your body lose more and more cells and begin to atrophy, or break down.

Quick, picture a stereotypical “old person.” In your mind’s eye you probably see a frail person with loose skin, no muscle tone, shaky hands, and a foggy memory—right? The truth is that these things happen as we age and cells die and are not replaced. In fact, loss of muscle tissue is so common that it has its own name, sarcopenia, a condition that can lead to falls and broken bones and even impairs the body from fully recovering after those tumbles (or a surgery).¹ In most people, sarcopenia sets in as early as age thirty and gets worse with each passing decade.²

When neurons in the brain die and your body isn’t able to replace them, your brain literally shrinks. And yes, this typically happens as we age. This contributes to cognitive decline and dementia, as well as a decrease in fine motor skills. In particular, when that neuron loss takes place in the hippocampus—the part of the brain that controls emotion, memory, and the nervous system—you begin to look and sound a lot like that old person you just imagined. Since hippocampal atrophy is so common, the size of your hippocampus is considered a key marker of aging.³ But there is nothing normal about it—at least, there shouldn’t be.

So the big question becomes, What can you do to make sure those dead cells get replaced (or don’t die in the first place)?

It turns out that if you keep your mitochondria healthy, you can avoid a lot of unnecessary cell loss. The biggest game changer here is eating foods that boost the efficiency of your mitochondria so they can make more energy and your body has the raw goods it needs to manufacture all the proteins, hormones, and fatty acids they require to function. We’ll cover those foods in the next chapter.

It is possible to reverse atrophy by taking advantage of stem cell therapy—a medical treatment in which stem cells are injected into your body. I’ve had more stem cell treatments than probably anyone on Earth (more on this later), and it’s been a game changer for me. I went from having chemical-toxin-induced brain damage as a young man to having a hippocampal volume that’s in the 87th percentile for someone my age. But stem cell therapy does not come cheaply or easily, so it’s better to prevent atrophy in the first place!

The key to success with any of these interventions is to start them now, even if you don’t think you need them. After all, humans are good at avoiding things that hurt. You don’t step on nails or burn yourself because you feel the impact of those cuts immediately. But when it comes to aging, you’re the proverbial frog in a pot of slowly heating water. You keep taking the hits because you don’t feel the impact right away. But cutting down on just a few of those hits by making small changes in your environment can really ramp up what’s possible for you. Perfection not required.

PILLAR 2—MITOCHONDRIAL MUTATIONS

Mitochondrial mutations—aka damaged mitochondria—are the second pillar of aging. The importance of this aging pathway cannot be overstated. When the power plants of your cells—the very things that create the energy that keeps you alive—start mutating, is it any wonder everything goes haywire?

Unfortunately, this is a cause of aging that is often overlooked. Even those on the forefront of biotechnology have been so focused over the past several decades on mapping the human genome that they have paid little attention to mutations in mitochondrial DNA. Don’t get me wrong—the sequencing of the human genome changed the world, and I’m grateful for the scientists who accomplished this monumental task. But unless you have a significant genetic disorder, it turns out that the human genome is not usually of great value in predicting how you’ll age compared to your mitochondrial DNA status.

You can think of your genetic code as the building plans for your body—but who wants a body that doesn’t have any energy? (Hint: That’s called death.) Remember, your mitochondrial genome is separate from your human genome—mitochondria evolved from bacteria and have their own genetic code. But your mitochondrial DNA serves a very important function—it controls how your body makes energy. Unfortunately, your mitochondrial DNA is a lot more susceptible to mutations than your human DNA because mitochondrial DNA has a limited ability to repair itself when it is damaged. So you’re going to want to take fewer hits to your mitochondria.

Think of it like this: Your DNA provides a picture of how a building (your body) will look—how many rooms, how many windows, what kind of roof, how tall, etc. Your mitochondrial DNA describes what kind of wiring, heating, lighting, and air conditioning will be in the building. The building itself is going to be there for a while, but if the wiring goes bad, the air conditioner breaks, and the bulbs burn out, it’s not going to be a building you want to live in. Mitochondrial DNA breaks and mutates easily, which is why it’s so important.

When it comes to aging, it’s helpful to look at epigenetics, the science of how the environment in and around our bodies influences genetic expression, and how these changes are passed down from generation to generation. A 2018 review from leading stem cell researchers found that mitochondrial epigenetic mechanisms influence cell fate, cell division, cell cycle, physiological homeostasis, and even pathologies.⁴ In other words, your ancestors’ environment controls the mitochondria in your cells. And of course problems with those important cell functions can lead to every one of the Four Killers.

As you read in chapter 1, mitochondrial DNA can become damaged when excess free radicals are present. Damage to mitochondrial DNA from free radicals causes deletions in the mitochondria’s genetic code. The damaged mitochondria produce energy inefficiently, generating huge amounts of additional free radicals and less of the energy that you would rather put toward your Super Human efforts. And as we know, damaged mitochondria generate inflammation and accelerate aging throughout the body.

Remember, this cycle all started with an excess of free radicals, which are created by … dysfunctional mitochondria! So the more efficient your mitochondria, the less likely you are to suffer damage to your mitochondrial DNA, regardless of the genetic code you inherited from your parents. This is one of many reasons my anti-aging protocol focuses so heavily on making sure my mitochondria are running like rock stars for the long term.

PILLAR 3—ZOMBIE CELLS

Death-resistant cells, aka senescent cells, are cells that won’t die when they’re worn out, and they are a major focus of anti-aging research today. These cells no longer divide or function properly. These cells literally become dead weight. They do not function, yet they persist and secrete inflammatory proteins, causing all the problems that stem from chronic inflammation,⁵ including an increased risk of the Four Killers. Even worse, the mitochondria in senescent cells become dysfunctional and release huge amounts of reactive oxygen species. This is called senescence-associated mitochondrial dysfunction (SAMD), and it will age your body very quickly.⁶

Over time, you gain more and more senescent cells, and the accumulation of the damage they create is a major cause of aging and disease. For one thing, when you have too many zombie cells in your tissues, your body becomes less efficient at responding to the hormone insulin. This is the definition of insulin resistance, which as we discussed earlier is a precursor to type 2 diabetes. Zombie cells also lead to an increase in visceral body fat, the type of fat that is stored around important organs in the abdominal cavity and is associated with an increased risk of many diseases, particularly type 2 diabetes.

Zombie cells also contribute to many symptoms of aging that won’t kill you but will make your later years a lot less comfortable. For instance, doctors have known for years that patients who need knee transplants have excess senescent cells in their knee cartilage. In fact, injecting just a few senescent cells into your knees can actually cause arthritis.⁷ Did senescent cells in my joints cause my arthritis when I was fourteen? Possibly.

Some senescent cells are easy enough to kill off. Others persist like a Netflix binge of The Walking Dead. Perhaps the most damaging types of zombie cells are immune cells. Remember, when you get a cut or an infection, your immune cells proliferate to promote rapid healing. Once you have healed, those extra immune cells are supposed to die off. When they don’t die, they inhibit your immune system’s ability to respond to new infections or injuries. This is one reason the immune system usually becomes weaker as we age. Talk about not dying—pneumonia and the flu together are the eighth leading cause of death in the United States and are both much more common and deadly in people over sixty-five. This is in part because of senescent cells weakening the immune system.

The good news is that there are many things you can do to prevent damage from zombie cells. One of the most important is to keep your cell membranes strong so the cells can function well for as long as possible. I take a supplement comprising calcium, magnesium, and potassium salts of amino ethanol phosphate (AEP)—which helps to support healthy cell membrane function.

The common diabetes drug metformin is also believed to kill senescent cells. In studies, metformin has been shown to alleviate a range of age-related disorders in animals and humans, including metabolic dysfunction, cardiovascular disease, cancer development, and cognitive dysfunction.⁸ In elderly humans, it has been shown to increase life-span by an additional five years.⁹ Studies on mice show that these effects stem from reduced cellular senescence and fewer free radicals.¹⁰

Another exciting zombie killer is rapamycin. This drug inhibits a growth pathway called mammalian target of rapamycin (mTOR), which is responsible for regulating critical cellular functions such as cell growth, cell death, cell proliferation, and autophagy. Inhibiting mTOR appears to prevent the growth of senescent cells. In mice, rapamycin increases life-span, improves immune response, delays tissue loss, alleviates frailty with age, and decreases risk of heart failure, cancer, and cognitive impairment.¹¹ Not bad. Some doctors have quietly been using it as an anti-senescence drug since 2015.

I’m currently planning to experiment with taking rapamycin intermittently. It is not without risk—as we’ve discussed, any time you take a drug that accelerates cell turnover, there is a risk of accelerating cancer cell growth. In a couple more years, we’ll know more about the risk-reward ratio, and it will be a lot more affordable. I’m always happy to be a guinea pig, and cutting-edge anti-aging people are using it today. However, unless you’re in desperate straits, this is one hack you might want to hold off on for a little while as new research comes in.

And besides, there are other more affordable and more accessible natural compounds for fighting zombie cells. My favorite is fisetin, a polyphenol found in seaweed and strawberries. One study showed that high doses of fisetin could kill up to 50 percent of senescent cells in a particular organ.¹² While research on how to use fisetin to most effectively destroy zombie cells isn’t complete, research indicates that it is a cognitive enhancer.¹³ This is likely thanks to its direct antioxidant activity and ability to increase levels of other antioxidants in your cells. More antioxidants equals less oxidative stress and more energy throughout the body, including your brain!

It’s not uncommon for researchers to discover that traditional herbs and plant compounds that have been used for thousands of years have anti-aging properties. A prime example is the Japanese herb ashitaba, which is available as a tea or powder and helps prevent zombie cells. It is traditionally used to treat high blood pressure, hay fever, gout, and digestive issues, but researchers recently discovered a compound in the plant called dimethoxychalcone (DMC—no relation to the famous rappers), which slows senescence. In worms and fruit flies, DMC increases life-span by 20 percent.¹⁴ We don’t know yet if it will have the same impact on humans, but it may be worth trying this tea to help with one of the Seven Pillars of Aging. I do.

Finally, there’s piperlongumine (PPL), a pepper root extract that’s commonly used in Ayurvedic medicine. It looks promising for reducing senescence, but this knowledge is so new that researchers don’t yet understand the mechanism of action.¹⁵ PPL may also have cancer-fighting properties, too, although research hasn’t yet confirmed that benefit.¹⁶ It is likely safe to use, but taking it all the time or taking high doses could put a load on the liver. If you do decide to use PPL consistently, your body might have a reduced capacity for detoxing¹⁷—so it’s a good idea to take it for a limited period (one to two months) in conjunction with a liver-supporting supplement like glutathione.

It boils down to this: If you don’t want to die, you must make sure your cells do die when they’re supposed to and stay alive when they’re supposed to.

PILLAR 4—CELLULAR STRAITJACKETS

The space in between your cells contains a network of proteins called the extracellular matrix, which protects your tissues from stress, trauma, and even gravity while allowing them to do their jobs. Visualize a perfect wobbling bowl of Jell-O. Without the matrix, you’d just have weird red liquid. Now imagine that same bowl of Jell-O, but so hardened that it won’t wobble and you can’t even spoon it. That’s what anti-aging scientists call extracellular matrix stiffening.

Not only does the matrix literally hold your cells together, but it also gives your tissues their elasticity. This is incredibly important, especially when it comes to certain tissues such as those that make up the arteries. When these tissues lose their elasticity, they become stiff, and your body has to work harder to push blood throughout your circulatory system. This can of course lead to high blood pressure and heart disease.

So why does the matrix become so stiff? When sugar in your blood circulates throughout your system, it permanently binds with proteins, creating inflammatory advanced glycation end products, or AGEs. Glycation is the process of sugar bonding to protein. AGEs are aptly named, as these end products accelerate the aging process and create oxidative stress in the body.¹⁸

Think about it this way. When you eat something that contains sugar, glucose molecules travel through your body and look for proteins to bind with. Once stuck together, the glucose actually browns the proteins. This is the exact same chemical reaction that takes place when you brown onions in a pan and the sugar and onions become caramelized. When you have high blood sugar, it is at least partially because you made decisions that literally caramelized your insides. Yum. Not really.

There are multiple classes of AGEs. The most abundant in collagen is called glucosepane, and it contributes to diseases of aging from diabetes to vascular dysfunction. Thankfully, researchers are beginning to look for ways to break down AGEs and prevent them from stiffening the extracellular matrix. In 2018, the journal Diabetes reported that scientists had identified four enzymes that are able to break glucosepane cross-links.¹⁹ They are still looking at the exact mechanism of action and whether or not the process of degrading AGEs creates other harmful metabolites, but this is a very promising area of research if you have type 2 diabetes or heart disease or just want to avoid this pillar of aging.

Even if, as I predict, glucosepane-degrading enzymes do prove to be safe and effective, it’s better to just avoid extracellular matrix stiffening in the first place. To do that, you must reduce your blood sugar levels, particularly the spike in blood sugar you experience after meals. A study looking at glucosepane levels showed that this harmful AGE pretty much universally increases with age. In a nondiabetic control group, continuous high blood sugar more than doubled levels of this aging substance. Reducing blood sugar is not optional if you want to become Super Human. Fortunately, it’s not as hard as you might think. You’ll learn more about how to do this in chapter 3.

Chronic inflammation of any type is also associated with an increase in cross-linked proteins. This makes sense, since you already know that high blood sugar causes inflammation and high blood sugar causes these cross-links. In addition to managing your blood sugar levels, you should avoid eating foods that make you inflamed. When you are sensitive to a certain food, your body initiates an immune response that triggers inflammation. If this happens consistently, you end up with chronic inflammation and excess AGEs. There are good at-home tests that can help you pinpoint which foods you are sensitive to. I recommend Viome, which you’ll read more about later, and EverlyWell. (Disclosure: While I use both services, I’m an investor in and advisor to Viome, and EverlyWell has advertised on Bulletproof Radio.)

PILLAR 5—EXTRACELLULAR JUNK

As you age, waste products called extracellular aggregates build up both inside and outside your cells. Of the waste products that accumulate outside your cells, the main culprits are dysfunctional, misshapen proteins usually called amyloids. When amyloids start to accumulate, they stick together and form plaques that cause aging and disease by “gumming up the works” and getting in the way of healthy cellular interaction.

You can think of amyloids like the gunk clogging a sink. When you’re young, you won’t notice the impact—a single hair slips easily down a drain. But eventually, as more and more gunk accumulates in the pipes, water dissipates more and more slowly. It’s that gradual process that slowly wears you down as you age.

You’ve probably heard that patients with Alzheimer’s disease have a type of plaque (in this case called beta-amyloids, a type of protein aggregate) in their brains. But long before you develop Alzheimer’s, these same plaques can impair cognitive function. In the case of type 2 diabetes, one type of protein aggregate called islet amyloid inhibits insulin secretion. Protein aggregates also cause stiffening in the heart. This is called senile cardiac amyloidosis and is a major cause of heart failure.

So what causes proteins to stick together in the first place? The problem with amyloids is that they build up in different tissues for different reasons, and we don’t know all the reasons yet. We do know that autoimmunity, when the immune system attacks its own healthy cells, makes it worse, and at least 30 percent of people have some form of autoimmune disease. And recent research on mice links low insulin levels to the formation of amyloids in your brain.²⁰ This is one reason you don’t want to be on an unending low-carb diet that keeps you in ketosis without pause. You’ll live longer if you sometimes eat low carbs, sometimes eat moderate carbs, and always avoid sugar and bad fats. Low insulin is worse than high insulin in this case, but neither will keep you running at your peak.

Even if you don’t have full-blown autoimmunity, inflammation stemming from food sensitivities or even unending emotional stress can lead to amyloid buildup (in addition to AGEs). It appears that amyloids form during long periods of chronic inflammation from any cause. The smart strategy is to reduce your inflammation levels by avoiding foods you are sensitive to and learning how to chill out. If you’re eating food that’s not compatible with your biology, you’re going to end up inflamed, and that will age you in multiple ways. Same deal if you spend a lot of time in a state of stress.

The good news is there are simple strategies you can use to partially break down or reduce the formation of these proteins that age you prematurely. One of the best things you can do is to boost autophagy, your body’s recycling program, by consuming more of the foods you will read about in the next chapter. This will help break down these proteins so they don’t end up forming harmful plaques. So will fasting.

Gordon Lithgow, PhD, a professor at the Buck Institute for Research on Aging, has also found that vitamin D helps prevent proteins from losing their shape and sticking together. With vitamin D deficiency so widespread,²¹ this raises the question of whether Alzheimer’s rates are increasing in part because people do not have enough vitamin D to slow amyloid plaque formation.

There is also a clear connection between toxic heavy metals and amyloids. A study from the Society for Neuroscience found that excess copper prevented the body from clearing protein aggregates on its own.²² You need copper for many functions in the body, but too much of it is toxic. Medical research shows that the blood vessels and brains of patients with Alzheimer’s disease contain excess copper. Cadmium, another heavy metal, increases the formation of protein aggregates in the brain and appears in greater amounts in brain tissues of patients with Alzheimer’s disease than in healthy brains.²³ You’ll learn how to avoid and detox from these metals and others later in this book.

In his lab, Lithgow has demonstrated that chelators, small molecules that bind with heavy metals and help you detox, protect mice from developing protein aggregates. You won’t be surprised to hear that chelating from heavy metals has been a priority of mine for years. You’ll read all about how to do this later. Heavy metal exposure has been on the rise for decades, and no matter where you live or how clean you eat, chances are that you still have higher than ideal levels of metals like lead and mercury. Approximately 6 million pounds of mercury is released into the environment each year, and lead, arsenic, and cadmium are present in detectable levels in our air, water, food, medicine, and industrial products. Even organic kale is high in one heavy metal.

In addition to contributing to the buildup of amyloids, heavy metals also cause mitochondrial dysfunction.²⁴ A small amount of exposure to lead, mercury, nickel, uranium, arsenic, or cadmium for a short amount of time can impair mitochondrial energy production and increase mitochondrial death.²⁵ Even if you don’t realize it, the heavy metals already in your body are likely aging you right now. You’ll learn about how to detox them later.

PILLAR 6—JUNK BUILDUP INSIDE CELLS

Okay, so waste products can build up outside of your cells, but the good news is that nearly all the cells in your body have their own built-in waste disposal system called a lysosome. Your lysosomes incinerate unwanted materials of all kinds, keeping your cells free of junk and able to function optimally.

You knew there was a but coming, right? When the lysosome can’t break down certain materials to incinerate them, the waste products end up just sitting there, clogging up the cell until it can no longer function. The name for this is intracellular aggregation. If this happens to too many of your cells, you end up with Pillar 1—loss of cells and tissue atrophy.

There are two reasons this might happen. The first is if the lysosome itself is damaged and can’t function properly. Lysosomes rely on over sixty types of enzymes to break down waste products, and mutations in the genes for these enzymes can prevent the lysosome from doing its job. These organelles can also be damaged by an excess of reactive oxygen species—free radicals—which happens when your mitochondria aren’t working efficiently.

But the more likely reason your cells fill up with junk is that you eat too many foods that your lysosomes are incapable of incinerating even if they are functioning perfectly. These are advanced glycation end products (AGEs) that you eat rather than the ones that are made by sugar inside your body. Remember when I said that when sugar and proteins link up inside your body, it is the same as caramelizing onions? Yeah, it also happens when you eat caramelized protein: aka charred meat (from grilling over an open flame, broiling, or cooking protein with sugars). The AGEs you consume get stuck inside your cells, and your lysosomes can’t clear them out.

Over time, these materials build up, making more and more of your cells dysfunctional, and this affects your ability to control blood sugar levels²⁶ and increases your risk of cancer²⁷ and heart disease.²⁸ When it happens to neurons, it can contribute to Alzheimer’s.²⁹

Fried, blackened, and charred meat all contain tons of AGEs that can overload your cellular waste system and leave your cells literally full of garbage. And this dramatically raises your risk of developing one or more of the Four Killers. A 2019 study published in BMJ looked at the dietary habits of over one hundred thousand women between the ages of fifty to seventy-nine over the course of several years. After taking into account potentially influential factors such as lifestyle, overall diet quality, education level, and income, the researchers found that regularly eating fried foods (which also contain AGEs, since frying produces a similar chemical process as charring meat) was associated with a heightened risk of death from any cause and, specifically, heart-related death. Those who ate just one or more servings of fried food a day had an 8 percent higher risk of death from heart disease than those who did not eat fried food. One or more servings of fried chicken a day specifically was linked to a 13 percent higher risk of death from any cause and a 12 percent higher risk of heart-related death than someone who ate no fried food.³⁰

This one hurts, I understand. When I was in my twenties, I was the master of the grill. I loved charring meat over an open flame, but now I love my clean, highly efficient cells even more. It’s worth ordering grass-fed steak with no char.

PILLAR 7—TELOMERE SHORTENING

Take a moment to picture the plastic tips on the ends of shoelaces that protect them from fraying. Your telomeres serve a very similar function—they are the endcaps of your DNA that protect your chromosomes from fraying with wear and tear (aka age). An enzyme called telomerase is responsible for maintaining telomeres, but these caps naturally deteriorate over time because each time a cell copies itself, the telomeres shorten. As you age, they get shorter and shorter until they can no longer protect the cell. The cell then either stops growing or submits to apoptosis. In fact, there is a term for the number of times a cell can divide before it is no longer protected by telomeres and dies—it’s called the Hayflick limit.³¹

Shortened telomeres are linked to a weakened immune system and chronic and degenerative diseases like heart disease and heart failure,³² cancer,³³ diabetes,³⁴ and osteoporosis.³⁵ The rate at which your telomeres shorten plays a huge role in determining the rate at which you age. Scientists view telomere length as a reliable marker of your biological age (as opposed to your chronological age). People with shorter than average telomere length for their age have a higher risk for serious disease and early death³⁶ than their peers with longer telomeres. In one study, people over the age of sixty with shorter than average telomeres had three times the risk of dying from heart disease and eight times the risk of dying from an infectious disease³⁷ as someone with average-sized telomeres for their age.

It’s clearly critical to keep your telomeres long. There are some studies showing ways to lengthen telomeres, but not enough evidence yet to say that we know for sure how to do it in every case. But we do know some things about what make telomeres shorter and how to protect them from shortening. Interestingly, there seems to be a direct connection between telomere shortening and stress. In one study, women with the highest levels of perceived stress had telomeres that were shorter by the equivalent of one full decade than women who said they experienced less stress.³⁸ This is an important finding because it offers evidence that how you experience psychological stress has as much of a physiological impact as environmental stress. And this makes sense, since both psychological and physiological stresses are associated with increased oxidative stress in the body.

Exercise is another important way of preventing early telomere shortening. Researchers in Germany looked at telomere length in four groups of people: those who were young and sedentary, those who were young and active, those who were middle-aged and sedentary, and those who were middle-aged and active. There wasn’t much of a difference between the two groups of young people, but when the participants were middle-aged, the change in telomere lengths was striking. The sedentary middle-aged folks had telomeres that were 40 percent shorter than the young people, while the active middle-aged folks had telomeres that were only 10 percent shorter than the young people. In other words, the active group reduced their telomere shortening by 75 percent.³⁹ Exercise significantly reduces perceived stress levels and inflammation,⁴⁰ which may help to explain these results.

There are two promising lines of research about lengthening telomeres. One is a synthetic peptide called Epitalon that is modeled after a peptide your pineal gland produces (epithalamin). The research on Epitalon goes back to 2003, but no one has commercialized it. When researchers injected Epitalon into mice, it was shown to increase their life-span by up to 13.3 percent by activating telomerase⁴¹ while turning on apoptosis and slowing down tumor growth.⁴²

Someone with identical biology to me (ahem) has been injecting Epitalon for ten days every few months for the past several years despite the fact that it is not yet approved for human use and may never be, even though it seems to work. In fact, anti-aging substances like Epitalon often exist in a strange limbo. The pharmaceutical companies don’t develop them because they’re not patentable, which means they won’t pay for the huge studies the FDA requires before approving them. The result is that you can find Epitalon affordably online, but it’s hard to know that you’re getting it from a reputable source. To me, the risk-reward ratio is worth it, but this may not be the case for you.

Another supplement called TA-65, the name brand of cycloastragenol, also activates telomerase.⁴³ It is incredibly concentrated extract of an Ayurvedic herb called astragalus. By law, the makers of TA-65 can’t call it an “anti-aging” drug because it hasn’t been proved to extend life-span. But studies on this molecule show that in humans, it improves biological markers associated with health span through the lengthening of telomeres and rescuing of old cells. The downside here is that it is quite expensive. If you’ve experienced a lot of stress and/or feel that you are aging more quickly than you’d like and it’s in your budget, this might be worth considering. There are generic versions available, too.

Until we know more about how to maintain telomere length, avoiding excessive environmental stress and taking measures to reduce your psychological stress is a good start, along with getting good quality sleep to recover from stress that is truly unavoidable.

You’ve probably noticed that these simple interventions—good food, the right environment, moderate exercise, stress control, and quality sleep—are the best and most effective ways of avoiding all Four Killers and even slowing down or reversing many of the Seven Pillars of Aging. And you’re right! The vast majority of the hits to your mitochondria that cause aging come from your food, your environment, and your lack of quality sleep. So, before we move on to aging backward, let’s take a closer look at the most important ways to avoid dying. After all, what’s the point of being a Super Human if you’re dead?

Bottom Line

Want to not die? Do these things right now:

• Kill off death-resistant cells with natural or pharmaceutical compounds such as AEP, fisetin, and piperlongumine.

• Consider getting anti-aging drugs like rapamycin or metformin from your doctor.

• Stop eating fried, grilled, or charred meat. It’s just not worth it if you want to live a long, high quality life.

• Manage stress—meditate, practice yoga, get good quality sleep, and/or delegate tasks that are draining you. This is not indulgent or selfish—it will literally help you live a longer and fuller life.

• Consider supplementing with vitamin D to help your body avoid forming dangerous misshapen proteins.

• Do what it takes to find out which foods are not compatible with your biology, either through an elimination diet or a food sensitivity panel, and stop eating those foods.