How Not to Age (Part 1)

Today, we have the first in a two-part series – where I offer some of the highlights from my latest book, How Not to Age, taped in front of a live audience at the University of Pittsburgh. 

There may be no such thing as dying from old age. From a study of more than 42,000 consecutive autopsies, centenarians—those who live to be a hundred—were found to have succumbed to disease in 100% of the cases. Though most were perceived—even by their physicians—to have been healthy just prior to death, not one “died, of old age.” They died from disease––most commonly, heart disease.

If aging kills via diseases, why wasn’t my book How Not to Die all the longevity book anyone needs? In it, I ran through preventing, arresting, or reversing each of our top 15 killers—starting with heart disease, not only the #1 killer of centenarians, but of men and women across the board, and projected to remain that way in the decades to come. But is it really?

Because the single greatest risk factor for most of our killer diseases is how old you are, one could argue that the leading cause of death is actually aging. The rate of death increases exponentially for age-related diseases, such as heart disease, cancer, stroke, dementia. So yes, within the same age bracket, having a high cholesterol can increase your risk of heart disease up to 20-fold, but an 80-year-old may have five hundred times the risk of having a heart attack compared to a 20-year-old. Now, the reason we focus on things like cholesterol is because it’s a modifiable risk factor. But what if the rate of aging was modifiable too?

Instead of our current piecemeal approach of focusing on individual diseases, what about slowing down the aging process itself? When I was a nerdy little kid, I wanted to cure cancer when I grew up. But even if all forms of cancer were eliminated, the average life expectancy in the U.S. would only go up about three years. Why? Because dodging cancer would just mean delaying death from a heart attack or stroke. If one age-related ailment doesn’t get us, another will. So, rather than playing “whack-a-mole” by tackling each disease separately, slowing the rate of aging could potentially address all these issues simultaneously.

Imagine if there were an intervention that didn’t just reduce your risk of the leading killers, but also arthritis, osteoporosis, sensory impairments. Because risks tend to double every seven years—like if the average 65-year-old had the health of a 58-year-old? Slowing aging by even just seven years could cut everyone’s risk of death, frailty, and disability in half.

That’s why I wrote How Not to Age.

The problem is that the anti-aging field is said to be a “fertile ground for cons, scams, and get-rich-quick schemes.” As a former president of the Gerontological Society wrote, there have been “few subjects which have been more misleading to the uncritical and more profitable for the unscrupulous.” Not only does the popular literature on the subject harbor a “huge amount of misinformation,” but most age-researching scientists widely known to the public are said to be “unscrupulous purveyors of useless nostrums,” according to the editor-in-chief of a leading gerontology journal.

When it comes to something as life-and-death important as to what to feed ourselves and our families, we should rely not on anecdote, but on evidence. That’s why I cite everything to the teeth. How Not to Die had about 2,000 citations. How Not to Diet, 5,000 citations. How Not to Age ended up with 13,000 citations, all of which I have hyperlinked for you online to access all the original sources. So, you can download the studies and read them all yourself. My aim was to cover every possible angle for developing the optimal diet and lifestyle, for the longest, healthiest lifespan—based on the best available balance of evidence.

My inspiration for writing the book was a consensus document “Interventions to Slow Aging in Humans,” compiled by the top researchers in the anti-aging field (the likes of Drs. Longo, Sinclair, Fontana). They were brought together to identify the most promising strategies to combat aging. They identified a list of “essential pathways,” for example, drugs that can block the hormone IGF-1, or drugs to block the pro-aging enzyme TOR.

But I realized as I looked at this: Wait, every single one of these pathways could be regulated through diet. That became the first section of the book.

The term “anti-aging” has been much abused in popular culture, attached to all manner of unproven products and procedures, whereas the term should really be reserved for things that can delay or reverse aging by targeting one of the established aging mechanisms, the so-called hallmarks of aging, the common denominators of the aging process like, for example, the buildup of misfolded proteins that can be disposed of through “autophagy.”

See, at any given time, most of our cells are producing and assembling more than 10,000 distinct proteins, each of which can become misfolded or damaged at any time and require a cleanup, in aisle three. But during times of excess nutrition, our body figures why bother? We can just toss it in the corner and make another. Having evolved in a context of scarcity, our body expects to fall on hard times any day now, and can put off spring cleaning until then. But these days, these lean times hardly ever come; so, our cells just continually end up hoarding junk.

That’s where autophagy comes from, from the Greek words for “self-eating.” It’s a housekeeping process by which defective cellular components are broken down and scrapped for spare parts. This doubles as both salvage operation and quality control, clearing out some of the damaged debris implicated in the aging process, while renewing our cells in a sort of cellular reset. As one review put it, “The janitor is the undercover boss.”

Our ancient ancestors often went for several days without food; so, autophagy was constantly being switched on. But these days, our cells no longer need to clean out the corners for sustenance. And so, the tainted heaps just pile higher and higher, which isn’t good, because autophagy is essential for lifespan extension. It’s not only necessary, but sometimes sufficient, for increasing longevity.

Self-digestion for lifespan extension. Boosting autophagy alone can boost lifespan, at least in mice, by an average of 12 percent, and it also boosts healthspan.

Unfortunately, our bodies’ ability to take out the trash declines with age, leading to this vicious cycle. Garbage builds up, accelerating aging, which leads to more garbage buildup. No wonder the drug industry is so eager to pharmacologically modulate autophagy to combat aging—but we can do it naturally. One way is through fasting.

Unfortunately, autophagy doesn’t really maximally ramp up until after a day or two of fasting, which may be too long to do it unsupervised. Fasting more than 24 hours should probably only be done under medical supervision––ideally in a live-in clinic. In other words, don’t try this at home. This not just legalistic mumbo-jumbo. For example, normally, your kidneys dive into sodium conservation mode, but should this response break down, you could rapidly develop an electrolyte abnormality that might only manifest with non-specific symptoms like fatigue or dizziness, which could be easily dismissed, until it’s too late.

Thankfully, there’s another way to activate autophagy. You can fast or go fast. Exercise induces autophagy. As one of the researchers said, “I’ve always known exercise was good for you, but when we found that it increases autophagy, I finally got a treadmill.” You have to do enough, though. Autophagy is activated after 60 minutes of moderate intensity exercise, but only 20 minutes fails to move the needle.

What about diet? Any foods to avoid? In 2021, we found out acrylamide can inhibit autophagy––at least in cells in a petri dish. Acrylamide is a toxin concentrated in French fries and potato chips that’s formed during the frying process. The fact that high acrylamide exposure is associated with as much as double the risk of premature death would be consistent with an anti-autophagy effect, though diminished lifespans among eaters of fatty, salty snacks isn’t exactly a revelation. You can’t know if it’s cause and effect until you…put it to the test.

Before being asked to eat a bag of potato chips every day for a month, study subjects were given weeks of boiled potatoes mixed with the same amount of fat and salt as the chips. Compared with the fatty salty boiled potatoes, their C-reactive protein levels shot up 50 percent on the chips, suggesting “chronic ingestion of acrylamide-containing products induces a proinflammatory state.”

However, deep frying causes the formation of all manner of “undesired food-borne toxicants.” So, we can’t be sure it was the acrylamide. As one of the earliest geriatric medicine textbooks presciently concluded back in 1849, “frying…is an abomination.” (If you just must have your French fry fix, air-frying produces about 90 percent less acrylamide.)

Anything that can help? Starving yourself “generates discomfort,” but there is something that activates autophagy that many people find comforting: coffee. At a human-equivalent dose, both regular and decaf rapidly induce autophagy within hours—in mice, and coffee can extend the lifespans of some rats. But what about people?

In humans, we only have observational research, but to date, about 20 studies have followed more than 10 million people over time, and those drinking three cups (720 ml) of coffee a day had 13 percent lower risk of dying from all causes put together. And decaf appears to be just as protective; so, it’s not the caffeine. Coffee contains more than a thousand bioactive compounds. The polyphenol chlorogenic acid is the most abundant antioxidant in coffee; so, researchers started there, and indeed, it was found to enhance autophagy in human cells.

More than a hundred coffees have been tested, and chlorogenic acid levels vary by more than 30-fold. Interestingly, the major contributor to this wide range is Starbucks, with its extremely low chlorogenic acid content––thought to be because they roast their beans so dark that they destroy it.

Freeze-drying is okay, and brewed has more than espresso. Paper-filtered is the best, because it traps the cholesterol-raising compounds in coffee, perhaps explaining why those drinking filtered coffee had even lower mortality rates than those drinking unfiltered coffee.

Any food components that can activate autophagy? Spermidine, the longevity elixir, spermidine. Don’t be put off by the name. Spermidine and its by-product spermine are actually found throughout the body. When it was later independently discovered in the brain and the muscles, it was called  neuridine and musculamine, until they found out it was all the same compound. And so, naming rights defaulted to the less palatable original.

Our body can make it from scratch, but we can also boost levels by eating spermidine-rich foods, which is good news, because our spermidine levels tend to decline with age, dropping more than half by the time we reach our 50s. This decline is seen across the biological spectrum with one remarkable exception: naked mole rats, also known by  their more cuddly nickname “sand puppy,” considered to be a “non-aging mammal” without any visible signs of aging, and almost no decline in physiological function over decades, or typical signs of aging like loss of muscle mass or fertility. Perhaps in part because they are able to maintain their high levels of spermidine, something you also see in human centenarians.

To prove cause and effect, extra spermidine was fed to animals and “Induction of Autophagy by Spermidine Promotes Longevity,” increasing the lifespans of mice, for example, by as much as 25 percent. In a database of more than a thousand life-extending compounds, among the small subset with the fewest side effects, spermidine has the largest documented lifespan extension.

Longevity can be improved even when started late in life, kind of the human equivalent of changing your diet when you’re already in your fifties. Anti-aging effects were found in the heart and kidneys, rejuvenating immune function, delaying brain aging, and improving cognitive function. Yeah, but this was in animals like fruit flies and mice. I mean, who cares if spermidine cures flies of senior moments. What about in people?

Hundreds of men and women in their 40s through 80s were followed for 20 years, and after looking at 146 different components of their diets, the single most predictive of longevity was spermidine. How much spermidine? Higher spermidine intake is linked to lower mortality. Those who consumed the most spermidine had a reduced risk of death from all major causes, which is what we’d expect from an anti-aging compound. Critically, this survival advantage persisted even after controlling for dietary excellence, meaning that it wasn’t just because they were eating healthier foods in general, but rather spermidine-rich foods in particular.

How big of an effect are we talking? The reduction in mortality risk between getting more than 12 mg of spermidine a day compared to getting less than nine was as if those eating more spermidine were 5.7 years younger. It’s as if by eating more of certain foods, they were effectively able to turn back the clock nearly six years. The findings were so extraordinary, the researchers sought to replicate their results in a whole new set of individuals and, indeed, arrived at the same conclusion.

This led some to propose that spermidine may be an anti-aging vitamin. When we’re younger, we seem to be able to make enough, but as we get older, we may need to start ensuring we’re getting enough in our diet to maintain autophagy into old age. Well, if spermidine is going to be considered an anti-aging vitamin, where is that vitamin found?

Beans are said to have the highest natural amounts, but I compiled a list of the top spermidine sources, and pig pancreas beat out bean burritos for the bronze.

As a certified dark green leafy snob, I was begrudgingly impressed to see lettuce score so high, though lettuce is so light, a 100-gram serving would be about three cups. But even the spermidine in little side salads could really add up. In the book, I spend a lot of time going through the entire list, but the single most concentrated source is wheat germ, with two-and-a-half milligrams of spermidine in just the seven grams in a tablespoon. It’s also the cheapest source, costing as little as two cents per milligram. You can’t get a lot of pancreas for two cents.

Does wheat germ actually do anything? Let’s randomize people to some dinner rolls, and find out. A randomized, double-blind pilot in which older individuals were secretly slipped some spermidine in the form of wheat germ baked into bread rolls, versus placebo rolls with wheat bran instead.

And, those with mild dementia improved way beyond all available antidementia drug treatments so far. Admittedly, that’s not saying much, but what’s the harm of sprinkling a little wheat germ on your food?

The latest Alzheimer’s drugs don’t appear to work at all. All you get for your $56,000 is a dramatically increased risk of swelling or bleeding into your brain. When the FDA approved it anyway, the head of the American Geriatrics Society replied, “My head just exploded.” (Maybe they just got slipped a dose of the drug.)

Anyway, lots of other clinical spermidine studies, but just to wrap up this section, autophagy is considered the “primary system for cleaning the body” from the inside out. And, we can boost autophagy with aerobic exercise, skipping fries and chips, drinking coffee, and eating specific foods to reach a target of 20 mg of spermidine a day.

I offer similar diet and lifestyle takeaways for each of the other ten anti-aging pathways, but don’t have time to touch on them, because there are still three other major sections to the book. Part Two focuses on the diets and lifestyles of the healthiest and longest-lived populations around the world.

The odds of living to a hundred have risen from approximately 1 in 20 million to as high as 1 in 50. Why do some make it and others not? It’s not just a matter of picking better parents. Studies following identical twins suggest that only about 25 percent of the variation in lifespan is explained by genetics. So, what can we do for the majority over which we may have some control? The media loves stories of hard-living centenarians who attribute their longevity to some combination of lard, vodka, and favorite brand of cigarette, but how do the oldest and healthiest really eat and live?

That’s what we have the blue zones for––areas of exceptional longevity around the world, where there may be ten times the rate of those reaching those triple digits (named for a color a demographer used in a global “heat map” of mortality around the world). What lessons can we learn?

The Blue Zones organization distilled findings from more than 150 dietary surveys from the world’s longest-living people to create a set of ten food guidelines. The foundation of the Blue Zones Food Guidelines is making your diet at least 95 percent plant-based, avoiding highly processed foods, emphasizing beans as the healthiest source of protein, water as the best beverage, and nuts as the healthiest snack. That’s the foundation.

The final five guidelines are “Go easy on fish,” “Eliminate eggs, “Slash sugar,” “Reduce dairy,” and “Retreat from meat,” noting that blue zones centenarians only eat about two ounces (57 g) of meat, or less, about five times a month.

Historically, there’ve been five recognized blue zones. But only one survives and thrives to this day; the red, white, and blue zone––the Seventh-Day Adventists in Loma Linda, California, with perhaps the longest life expectancy of any formally-studied population in history.

There are a number of shared Blue Zone lifestyle characteristics: family coherence, avoiding smoking, daily exercise, social engagement. But plant-based nutrition appears to be the principal component, alone accounting for about half the difference in lifespan. No surprise, since the number one risk factor for death in the United States is the American diet. So, unsafe sex? Bad. Sedentary lifestyle? Bad. Alcohol and drugs—especially tobacco––bad. But cigarettes only kill about a half million Americans every year, whereas our diet kills many more.

We are what we eat. Which is good news, because it means we have the power. Changing from a more typical diet to a more optimized diet, starting at age 2, would be expected to increase the lifespan of women by about 11 years and men by 13 years. The largest life expectancy gain would be made by eating more legumes—in other words, more beans, split peas, chickpeas, and lentils. So, if there was one thing we could do: Legumes for longevity. Hummus for health! Then, comes whole grains and nuts, and eating less meat.

Now, for the few of you who aren’t 20 anymore, not to worry. Starting to eat healthier at age 60 could still mean adding eight or nine more years to your lifespan. Even starting as late as age 80 could add years.

Changing your health destiny can start tomorrow morning at breakfast.

And it doesn’t take much. The NIH-AARP study is the largest forward-looking study on diet and health in history. Based on its six million person-years of observation, replacing just three percent of daily caloric intake from animal protein with plant protein was associated with a 10 percent decreased risk of overall mortality in both men and women. Just swapping three percent!

Of all the animal protein sources, eggs were found to be the worst. Swapping in three percent of plant protein for egg protein was associated with twice the benefit: 20 percent lower mortality for swapping in a few British beans for breakfast instead.

Harvard researchers found that when it comes to premature death, processed meat was the worst, followed by eggs. In essence, they found that tuna salad may be better than egg salad or a BLT. But a bean burrito beat out the bunch. When it came to death from all causes put together, plant protein beat out every type of animal protein—including dairy, fish, and chicken. A three percent swap from chicken to chickpeas, or fish to falafel, was linked to a six percent decreased risk of premature death.

But does eating healthy actually slow down aging? Randomize hundreds of women to a diet centered around healthy plant foods, or exercise, or neither, and though the physical activity failed, those in the plant-based dietary intervention group had a significant slowing of biological aging.

Of course, it isn’t just about adding years to your life, but life to your years. An unhealthy aging index was devised to measure functional impairments, vitality, mental health, physical health. Substituting even just one percent of calories from plant protein for animal protein appeared to lead to significantly less deficit accumulation. And substituting five percent may reduce the risk of dying from the greatest deficit: dementia. That may help explain why those who don’t eat any meat at all may be up to three times less likely to become demented. But again, it’s not all-or-nothing.

In fact, the worst thing about humanity’s diet is neither animal nor vegetable but mineral: sodium.

Here are the top five fatal flaws of our diet. Millions of deaths may be attributed every year to not getting enough whole grains, not eating enough fruit, not enough nuts and seeds, not enough vegetables. But the single deadliest ingredient in humanity’s diet is something we get too much of, and that’s salt, our number one dietary risk factor for death.

A recent whopping study, for example, of more than a half million people found that those who salted their food at age 50 appeared to have about a two-year lower life expectancy compared to those that didn’t. So, just swapping out the salt shaker for some salt-free seasoning or salt substitutes could potentially add years to your life.

How do we know it’s cause and effect? Five kitchens at a veterans’ retirement home were randomized into two groups for a few years, offering meals salted either with regular salt or, unbeknownst to them, a 50/50 blend of regular salt, sodium chloride, with a salt substitute like these, potassium chloride. The kind of salt was the only difference between the meals, and cardiovascular disease death rates plummeted by 40 percent in the folks getting the reduced sodium blend.

The new difference in life expectancy between the two groups at age 70 was equivalent to that which would have occurred naturally in 14 years––meaning simply switching to even half potassium salt—for which you wouldn’t even be able to taste the difference of––appeared to effectively make people more than a decade younger when it came to the risk of premature death.

What do the likes of the Salt Institute have to say about public health recommendations to reduce sodium intake? In testimony before a Congressional committee, the presumption that healthier diets would cut healthcare costs was challenged. “Indeed,” one processed food defender testified, “healthcare expenditures increase if the lifespan is prolonged.” If people eat healthier and live longer, it could be more expensive, noting that if tobacco were banned, the increase in expected lifespan would “increase the cost of care of old people.”

Think how expensive it would be if people started taking care of themselves and didn’t, conveniently, die on time.

Ultra-processed foods, often packed with added salt, sugar, and fat, consistently account for more than 50 percent of our dietary caloric intake. More than half of our diet is junk. Not surprisingly, those foods are associated with significantly increased risk of dying prematurely. So, just cutting back on animal foods isn’t enough. Healthy plant-based diets are associated with significantly lower risk of dying, but unhealthy plant-based diets are not.

In the Harvard cohorts, the more you minimize meat, eggs, and dairy, the lower your risk of death falls. But that’s only if you’re eating healthy plant foods. If you, instead, just pile on the junk, like chips and soda, you can increase your risk of death overall—even if animal product consumption remains low. Same in the Million Veteran Program study; healthy plant foods reduced their risk of death. But if your idea of a plant-based diet is fries and a Coke, you’re not doing your body any favors.

Same with the risk of cognitive impairment. Only healthy plant foods reduce risk. The same with dementia and depression. The same with frailty. Healthy plant foods good; plant-based junk bad. That’s why Cornell Professor Emeritus of Biochemistry T. Colin Campbell coined the term whole food, plant-based diet. As a physician, terms like vegetarian or vegan just tell me what you don’t eat. I mean, do you actually eat vegetables?

Professor Campbell’s physician son and daughter-in-law tried putting a group of vegetarians and vegans on a whole food, plant-based diet. In eight weeks, they lost ten pounds, dropped their LDL cholesterol 15 points. In other words, vegans may benefit from eating a little more plant-based, too.

Now, meat is a problem. In terms of lifespan, eating a burger may cut one’s life as short as smoking two cigarettes. So, if it wouldn’t even occur to us to light up before and after lunch, maybe we should choose the bean burrito instead.

There are certainly ways to make meat safer, though. For example, one of the ways whole food, plant-based diets can help is by reducing the load of gerontotoxins, age-accelerating toxins, such as advanced glycation end-products, also known as glycotoxins, or AGEs, an acronym intentionally chosen to emphasize their toxic role in age-related disease.

AGEs occur naturally in animals, but dry cooking methods can generate 10 to 100 times more. When muscle cells rupture under dry heat, highly reactive compounds combine with blood and body sugars to form AGEs within the meat. So, even without cutting down on meat, you can significantly cut down on glycotoxin intake, just by switching up cooking methods. The safest ways of cooking meat are moist methods, such as boiling, poaching, steaming, stewing.

When people are randomized to a meal of fried or broiled chicken breast and veggies—or the same meal with the same ingredients—including the oil, but with steamed or boiled chicken breast instead, that single high-AGE meal with the fried or broiled breast induced a profound impairment of artery function within hours. The steamed chicken still impaired artery function, but not as much as the fried or broiled.

So, we can eat an “age less” diet by switching to moist methods, for example. But dietary approaches are said to have “zero commercial value” and hey, stewed chicken may not be as tasty. So, why not just take a drug to block AGE absorption every time we eat? It does lower your blood levels of AGEs. It’s just activated charcoal, like when people are poisoned or for drug overdoses.

I’m sure our AGEs would also go down if we chased our chicken with a little ipecac, too.

What about fish? Unfortunately, our oceans have essentially become humanity’s sewer. Everything eventually flows into the sea. So, the consumption of contaminated seafood has become the main route of human exposure to chemical pollutants.

Yes, a variety of foods are affected, but the number one source of DDT? Fish. The number one source of PCBs? Fish. Salmon is the worst when it comes to PCBs, followed by canned tuna.

Salmon also has the highest levels of dioxin-like compounds. So, on the one hand, fish has long been viewed as a healthy dietary component because of those long-chain-omega-3s. But on the other hand, we’re so polluting our world that we’re now seeing heavy metals, pesticides, flame retardants in fish––forever chemicals, which may explain why, despite their omega 3s, there’s been a failure to consistently observe beneficial effects of fish consumption.

So, if we had a time machine to go back before the industrial revolution, that would be one thing, but now, we have studies like this, where mice fed commercially available farmed salmon filets with common levels of persistent organic pollutants were found to develop insulin resistance, glucose intolerance, abdominal obesity, fatty liver, chronic low-grade inflammation. So, even just background levels of pollutants that might be presumed to be safe could completely counteract the potential benefits of omega 3s, in particular, leading to metabolic issues.

For mercury, it’s more about brain health. Hundreds of thousands of babies born with brain damage every year, seemingly as a consequence of their mothers consuming mercury-contaminated fish during pregnancy, with the resulting loss of intelligence estimated to cause billions of dollars of lost productivity every year.

In the aging literature, there are cases like this: a man with progressive memory loss tentatively diagnosed with Alzheimer’s dementia. His friends and family assumed he was nearing the end of his life. But a detailed history revealed that he had consumed swordfish once or twice a week. When the fish was removed from his diet, his mercury levels fell, and his memory bounced back. No more dementia. So, it seemed he didn’t have Alzheimer’s after all, but rather mercury poisoning from a handful of monthly meals of contaminated fish.

You can see the same remarkable reversals with hair loss. Here’s a common story: a perimenopausal woman seeks help for hair loss. Blood tests indicate elevated mercury levels. And no wonder, because she had a diet high in tuna. But within two months of stopping fish, her hair started growing back, and eventually her hair regrew completely.

So, doctors should consider screening for mercury toxicity when they see hair loss, since there’s something we can do about it. Instructing patients to reduce fish intake could offer relief of symptoms and uncover dietary habits that may be a source of heavy-metal-induced hair loss. (Though, admittedly, sometimes heavy metal can lead to too much hair.)

What about alcohol? That’s from plants! Sorry to be Dr. Buzzkill, but alcohol appears to be humanity’s seventh leading cause of death and disability. The safest level of drinking is none. But wait a second; what about the famous J curve, where light to moderate drinkers appear to have lower mortality rates than the teetotalers at zero drinks a day?

This may just be an artifact of the systemic misclassification of former drinkers as lifelong abstainers. This leads to the so-called “sick-quitter” effect, where the reason a person may be a nondrinker is because drinking made them sick, thereby making current drinkers look good in comparison. It’s the same reason studies can find higher mortality among those who quit smoking, compared to those who continue to smoke. It’s not that abstention led to poor health, but poor health. rather, led to abstention.

When researchers went back and controlled for the error of misclassifying former drinkers, the J curve disappeared. No more apparent benefit to moderate drinking. In other words, compared to true abstainers, the more alcohol, the more disease, with no apparent protection at low levels of consumption.

Even red wine? Unfortunately, interventional trials show that wine can cause inflammation within hours of consumption, both red and white—significantly more than just like drinking sugar water. And, you get a surge of fat in your bloodstream that you don’t get drinking “dealcoholized red wine” (the same wine with the alcohol taken out).

What about just taking supplements of the red wine compound resveratrol? Oh, you mean the supplement found to nearly triple the loss of brain tissue compared to placebo? No, thank you.

The healthiest beverages are probably water and tea. Increasing tea consumption three cups (720 ml) a day may decrease the risk of premature death from all causes by 24 percent. This applied to both green and black tea, though green may have a slight advantage. Part of this protection may be a lower risk of pneumonia. There have been five randomized, controlled trials showing those randomized to green tea are about a third less likely to come down with the flu, for example.

Within just one hour of drinking a single cup (200 ml) of green tea, we can significantly cut down on the rate of DNA damage in our cells, because green tea significantly boosts the activity of a DNA repair enzyme in our body that can fix DNA damage. And within a month, drinking two small daily cups (400 ml) of green tea can improve DNA resistance to free radical damage in the first place, indicating that green tea has significant genoprotective effects, or DNA-protecting effects.

Stay tuned next week for Part 2 of this “How Not to Age” presentation.