Have you ever wondered if there’s a natural way to lower your high blood pressure, guard against Alzheimer's, lose weight, and feel better? Well as it turns out there is. Michael Greger, M.D. FACLM, founder of NutritionFacts.org, and author of the instant New York Times bestseller “How Not to Die” celebrates evidence-based nutrition to add years to our life and life to our years.

A Longer Life

Today we look at the best way to live healthier into old age.

This episode features audio from Why Do We Age?, Longer Life Within Walking Distance, and Brain-Healthy Foods to Fight Aging. Visit the video pages for all sources and doctor’s notes related to this podcast.


There is a lot of information out there about the best foods to help us lose weight, prevent cancer, fight inflammation – the list goes on. In fact, for everything about our health we try and improve, there’s someone out there with a new theory on how to do it. But what does the science say?

Welcome to the Nutrition Facts Podcast. I’m your host Dr. Michael Greger. Today, we look at ways to live a longer healthier life.  Well, we actually do that everyday on Nutrition Facts, but today we are going to emphasize the LONGER part of that equation. It turns out a bacteria discovered on Easter Island may hold the key to the proverbial fountain of youth by producing rapamycin, which inhibits the engine-of-aging enzyme TOR. Here’s the story.

It sounds like science fiction. A bacteria in a vial of dirt, taken from a mysterious island, creating a compound that prolongs life and, not in the traditional medical sense. Thanks to advances in modern medicine, we are living longer. But, we’re doing it by “lengthening the morbidity phase.” In other words, we live longer, but sicker, lives.

Traditional medicine increases the number of old people in bad health.” Ideally, though, we’d extend lifespan by slowing aging to delay the onset of deterioration.

And that’s what this appears to do. They called it rapamycin, named after Easter Island, known locally as Rapa Nui. It inhibits an enzyme they called TOR, which stands for “target of rapamycin,” which may be a “master determinant of lifespan and ageing.” The action of TOR has been described as the engine of a “speeding car without brakes.”

Rather than thinking of aging as slowly rusting, a better analogy may be “a speeding car that enters the low-speed zone of adulthood and damages itself because it does not and cannot slow down.” Why don’t living organisms have brakes? Because they’ve never needed them. “In the wild, animals don’t live long enough to experience aging.” Most die before they even reach adulthood. Just a few centuries ago, “life expectancy in London was less than 16 years old.”

“Therefore, living beings need to grow as fast as possible to start reproduction before they die from external causes. The best evolutionary strategy may be to run at full speed. But, once we pass the finish line, once we win the race to pass on our genes, we’re still careening forward at an unsustainable pace thanks to this enzyme TOR, which in our childhood is an engine of growth, but in adulthood can be thought of as the engine of aging. “Nature simply selects for the brightest flame, which in turn casts the darkest shadow.”

Sometimes, though, in our youth, even in our youth, our bodies need to turn down the heat. When we were evolving, there were no grocery stores; periodic famine was the norm. And so, sometimes even young people had to slow, or they might never even make it to reproductive age. So, we did evolve one braking mechanism. The way caloric restriction extends lifespan appears to be mainly through the inhibition of TOR.

When food is abundant, TOR activity goes up, prompting the cells in our body to divide. When TOR detects that food is scarce, it shifts the body into conservation mode, slowing down cell division, and kicks in a process called “autophagy” from the Greek auto, meaning self, phagy, meaning to eat; autophagy: eating one’s self. Our body realizes there isn’t much food around, and starts rummaging through our cells, looking for anything we don’t need. Defective proteins, malfunctioning mitochondria, stuff that isn’t working any more and our body cleans house. Clears out all the junk, and recycles it into fuel, or new building materials, renewing our cells.

So, caloric restriction has been heralded as a fountain of youth. The potential health and longevity benefits of such a dietary regimen may be numerous, but symptoms may include dropping our blood pressure too low, “loss of libido, menstrual irregularities, infertility, loss of bone, cold sensitivity, loss of strength, slower wound healing, and psychological conditions such as depression, emotional deadening, and irritability.” And, you walk around starving all the time. There’s got to be a better way, which I’ll cover in my next video.

In our next story we look at how researchers find exercise often works just as well as drugs for the treatment of heart disease and stroke, and the prevention of diabetes. Exercise is medicine.

 “Physical inactivity has been called the biggest public health problem of the 21st century.” Of course, just because someone calls it that doesn’t mean it’s true. In fact, physical inactivity ranks down at #5 in terms of risk factors for death, and #6 in terms of risk factors for disability. Diet is by far our greatest killer, followed by smoking.

But still, “there is irrefutable evidence of the effectiveness of regular physical activity in the prevention of several chronic diseases (cardiovascular disease, diabetes, cancer, hypertension, obesity, depression and osteoporosis) as well as premature death, adding an additional one or two years onto our lifespan helping to “add years to our life”, and, above all, “life to our years.” It truly may be survival of the fittest.

How much do we need to exercise? In general, the answer is the more the better. “Currently, most health and fitness organizations advocate a minimum of” a thousand calories burned of exercise a week, which is like walking an hour a day, five days a week. But, seven days a week may be even better in terms of extending one’s lifespan. Moderate intensity can be practically defined by the “Talk but Not Sing Test,” where you can still “carry on a conversation but would feel breathless if trying to sing.”

Exercise is so important that not walking an hour a day is considered a “high-risk” behavior, alongside smoking, excess drinking, and being obese. Having any one of these effectively ages us three to five years in terms of risk of dying prematurely though, interestingly, those that ate green vegetables on a daily basis did not appear to have that same bump in risk. But, even if broccoli-eating couch potatoes do live as long as walkers, there are a multitude of ancillary health benefits to physical activity so much so, that doctors are encouraged to prescribe it, “to signal to the patient that exercise is medicine.” In fact, powerful medicine.

Researchers at the London School, Harvard, and Stanford compared exercise to drug interventions, and found that exercise often worked just as well as drugs for the treatment of heart disease and stroke, and the prevention of diabetes. Of course, there’s not a lot of money to fund exercise studies, so one option would be to require drug companies to compare any new drug to exercise. “In cases where drug options provide only modest benefit, patients deserve to understand the relative impact that physical activity might have on their condition.” We could throw diet into the mix, too. Yes, the FDA could tell drug companies, your new drug beats out placebo, but, does it work as well as kale?

What is the best source of lutein, the primary carotenoid antioxidant in the brain? Let’s find out.

There’s an “extensive scientific literature describing the positive impact of dietary plant compounds on overall health and longevity.” “However, it is only now becoming clear that the consumption of diets rich in plant foods can influence neuro-inflammation brain inflammation leading to the expression of cytoprotective cell protective and restorative proteins.” Just “over the last decade, remarkable progress has been made to realize that oxidative stress and chronic, low-grade inflammation are major risk factors underlying brain aging.” So, no wonder antioxidant and anti-inflammatory foods may help.

“The brain is especially vulnerable to free radical attack oxidative stress due to its high fat content and its cauldron of high metabolic activity.” You don’t want your brains to go rancid. So, you’d think one of the major fat-soluble dietary antioxidants like beta-carotene would step in, but the major carotenoid concentrated in the brain is actually lutein; the brain just preferentially sucks it up.

For example, if you look at the “oldest old,” like in the Georgia centenarian study. Recognizing that oxidation” is involved in age-related cognitive decline,” they figured dietary antioxidants “may play a role” in its prevention or delay, so they looked at eight different ones: vitamin A, vitamin E, on down the list, and “only lutein was significantly related to better cognition.” Now in this study, they looked at brain tissue on autopsy, but by then, it’s a little too late. So, how could you study the effects of diet on the brain while you’re still alive? If only there was a way we could physically look into the living brain with our own two eyes. There is! With our own two eyes.

The retina, the back of our eyeball, is actually “an extension of” our central nervous system, an outpouching of the brain during development and right in the middle there’s a spot. This is what the doctor sees when they look into your eye with that bright light. That spot, called the macula, is our HD camera, where you get the highest resolution vision, and it’s packed with lutein.

And indeed, levels in the retina correspond to levels in the rest of your brain, so your eyes can be a window into your brain. So, now, we can finally do studies on live people, to see if diet can affect lutein levels in the eyes, which reflects lutein levels in the brain, and see if that correlates with improvements in cognitive function. And indeed, significant correlations exist between the amount of macular pigment, these plant pigments like lutein in your eye and cognitive test scores. You can demonstrate this on functional MRI scans, suggesting lutein and a related plant pigment called zeaxanthin, “promote cognitive functioning in old age by enhancing neural efficiency”, the efficiency by which our nerves communicate.

So, do Alzheimer’s patients have less of this macular pigment? Significantly less lutein in their eyes, significantly less lutein in their blood, and a higher occurrence of macular degeneration, where this pigment layer gets destroyed. The thickness of this plant pigment layer in your eyes can be measured, and may be a potential marker for the beginnings of Alzheimer’s. Let’s not wait that long, though. We know macular pigment density is related to cognitive function in older people; what about during middle age?

“One apparent consequence of aging appears to be loss of some aspects of cognitive control,” which starts out early, in ‘mid-adulthood,’ but not in everybody suggesting maybe something like diet could be driving some of these differences. Younger, on average, do better than older adults. But, older adults who have high macular pigment, lots of lutein in the back of their eyes, do significantly better. These results suggest that the “protective role of carotenoids like lutein within the brain may be evident during early and middle adulthood, decades prior to the onset of” more apparent cognitive decline later in life.

You can take 20-year-olds and show superior auditory function in those with more macular pigment in their eyes. Look: “The auditory system, our hearing, like the rest of the central nervous system, is ultimately constructed and maintained by diet, and it is therefore, not surprisingly, sensitive to dietary intake throughout life” all the way back to childhood.

Higher macular pigment is associated with higher academic achievement among schoolchildren. You can look into a kid’s eyes and get some sense of how well they may do in subjects like math and writing. “This finding is important because macular lutein is modifiable and can be manipulated by dietary intake.” Okay, okay, so where is lutein found? The avocado and egg industries like to boast about how much of these macular pigments they have in their products, but the real superstars are dark green leafy vegetables. A half-cup of kale has 50 times more than an egg, a spinach salad, or a 50-egg omelet.

And the earlier the better. Pregnant and breastfeeding women should definitely be checking off my Daily Dozen greens servings. But it’s also apparently never too late. While some age-related cognitive decline is to be expected, these effects may be less pronounced among those eating more green and leafy.

We would love it if you could share with us your stories about reinventing your health through evidence-based nutrition. Go to NutritionFacts.org/testimonials. We may share it on our social media to help inspire others. To see any graphs charts, graphics, images or studies mentioned here, please go to the Nutrition Facts Podcast landing page. There you’ll find all the detailed information you need plus links to all the sources we cite for each of these topics.

For recipes, check out my “How Not to Die Cookbook.” It’s beautifully designed, with more than 100 recipes for delicious and nutritious meals. And all proceeds I receive from the sales of all my books goes to charity.

NutritionFacts.org is a nonprofit, science-based public service, where you can sign up for free daily updates on the latest in nutrition research via bite-sized videos and articles. Everything on the website is free. There’s no ads, no corporate sponsorship. It’s strictly non-commercial. I’m not selling anything. I just put it up as a public service, as a labor of love, as a tribute to my grandmother – whose own life was saved with evidence-based nutrition. Thanks for listening to Nutrition Facts. I’m your host, Dr. Michael Greger.

Pin It on Pinterest

Share This