The Science of Aging Well

For civilization, there’s no better time to understand aging. With roughly 10,000 baby boomers turning 65 in the U.S. every day, the “silver tsunami” is predicted to raise the national health care bill to $4 trillion in 2030. Globally, the 65-plus demographic is estimated to triple from 524 million in 2010 to about 1.5 billion by 2050.

Most of us hope to live to a vigorous old age. And to help us do that, researchers are exploring ways to manage or overcome some of the most common and vexing age-related ailments. Here you’ll get a look at some of the most groundbreaking developments.

But there are plenty of self-anointed health and nutrition gurus out there, too, spouting advice about diets, supplements and exercise to a population eager to try almost anything. What sometimes gets lost in this life-extending frenzy is what science actually tells us about healthy aging. What dietary habits help you live longer? Do you have to lift weights or run marathons to keep your body in tiptop shape? Is there proof that brain training actually works? We’ve culled recent research to lend some scientific perspective and understand what works when it comes to healthy-aging claims.

A small but intriguing 2014 study is the first to suggest that memory loss from Alzheimer’s may be reversed through a 36-point therapeutic program that includes dietary changes, brain stimulation, exercise, improved sleep and other methods that affect brain chemistry. After undergoing the complex process, nine of the 10 participants, who suffered from cognitive impairment or memory loss associated with Alzheimer’s, displayed improvement in memory three to six months into the program — a joint venture between the Mary S. Easton Center for Alzheimer’s Disease Research at UCLA and the Buck Institute for Research on Aging. The biggest leap forward in Alzheimer’s research has been in the imaging of two prominent players that build up in the brain and are assumed to be behind the disease: plaques, the abnormal clumps of beta-amyloid protein pieces found between nerve cells, and tangles, twisted threads made up mainly of the protein tau that are found within the cells.

“It used to be that you could only see the plaques through an autopsy, but now we can image beta-amyloid in the living brain to see how it changes before somebody presents clinical symptoms,” says Laurie Ryan, chief of the Dementias of Aging Branch in the National Institute on Aging (NIA) Division of Neuroscience. Although tau imaging is still in its earliest stages, Ryan hopes that such imaging will accelerate drug development and that finding a blood-based biomarker for Alzheimer’s to reveal risk (much like cholesterol serves as a marker for cardiovascular risk) will change the field dramatically in terms of how doctors can diagnose the disease.

Stem cells may also unlock some of the doors that Alzheimer’s and other age-related diseases close. Pick a body part, and you can bet researchers are scrambling to figure out ways to reactivate, repair — and yes, even regrow — the cells within it. But stem cells aren’t being considered purely as a method to restore age-induced degradation, but as a means to prevent it. Using functioning human brain cells grown from stem cells, neuroscientists at Massachusetts General Hospital have most recently discovered how to create in a petri dish the same plaques and tangles associated with Alzheimer’s. According to lead researcher Rudolph Tanzi, this key model will help accelerate research on Alzheimer’s and other neurodegenerative diseases that will be both more thorough and less expensive.

Meanwhile, a protein commonly found in the blood of young mice (and humans) may hold the key to rejuvenating brain cells. According to a study published in Science, the protein, called growth differentiation factor 11 (GDF11), can reverse the decline in blood vessel volume seen in the brains of aging mice and enhance neurogenesis (the generation of new nerve cells). But how these findings may translate into potential therapies for the mind remains to be seen.

“Research has shown that there are steady declines in a number of different cognitive functions, such as memory and speed of processing, from young adulthood to older age,” says Molly Wagster, the chief of the Behavioral and Systems Neuroscience Branch in the NIA’s Division of Neuroscience. “However at the same time, there is an improvement in cognitive function as we age in some domains, including vocabulary and semantic understanding.”

Wagster says research over the past several decades has shed new light on what may cause age-related cognitive decline and what is no longer considered to be true. “It was once believed that we lose significant numbers of nerve cells as we age, particularly in the areas important for learning and memory,” she says. “But data now shows we lose less than previously thought, that in fact, our brains are capable of neurogenesis both in adulthood and even into older age.” — MM

Diets high in fructose (fruit sugar) and sucrose (table sugar) can induce metabolic changes associated with Type 2 diabetes. And having diabetes later in life jacks up your risk of Alzheimer’s disease by 40 to 50 percent, according to a meta-analysis of studies in the 2014 World Alzheimer Report.

How could a hard-core snacking habit damage your brain? As millions of cake and candy lovers can attest, frequent sugar binges tend to bring on weight gain. Fat cells grow larger when we gain weight, and the larger they get, the less sensitive they are to the hormone insulin, which cues the cells to take up glucose from the bloodstream. Decreased insulin sensitivity causes blood sugar levels to remain higher after a meal. If your average blood glucose levels climb high enough, you’ll be diagnosed as diabetic — and that’s bad news for your cognitive health.

Insulin is critical to cognitive health because it kicks off a biochemical cascade that protects brain cells, and when the cells become insulin-resistant, they may begin to falter. If the situation gets bad enough, neurons degenerate, and dementia sets in. For these reasons, “Alzheimer’s [is] considered the diabetes of the brain,” says neuroscientist Paula Moreira of Portugal’s University of Coimbra. That’s reason enough to watch your soda and churro intake. Even if you’ve got mental firepower to spare, is overdosing on sweets worth the risk of brain damage as you approach old age? — ES

New evidence suggests that brain training, the cognitive equivalent of jumping jacks, can help keep your mind sharp into old age. Johns Hopkins researchers followed more than 2,800 adults age 65 and older who attended 10 one-hour brain-training classes over the course of six weeks. Participants solved puzzles, memorized lists and did other mental exercises to hone their memory, reasoning and information-digesting skills. Five to 10 years later, most subjects maintained gains they’d made and outperformed untrained control subjects, the researchers reported in 2014. So don’t let yourself become a mental couch potato. Keep up your cognitive fitness by tackling Sudoku puzzles or committing your grocery list to memory. — ES

It may start slowly, as a blurred spot in your center of vision. Over time, it can grow to full-on dim or blank spots, making it difficult or impossible to perform daily activities like reading or driving. For people over 50, age-related macular degeneration (AMD) affects about 15 million Americans and remains the leading cause of vision loss in the entire Western world, according to Abdhish Bhavsar, director of clinical research at the Retina Center of Minnesota. As the name of the disease indicates, AMD occurs due to slow, progressive deterioration of the macula, a part of the eye necessary for clear, central vision. A common type of the disease, known as neovascular or “wet” AMD, is typified by abnormal blood vessels growing under the retina; these vessels can leak and cause damage to the macula. Treatment for this type of AMD has shifted away from standard laser treatments and photodynamic therapy, a combination of light-sensitive medication and laser light used to block the growth of abnormal blood vessels. At the moment, this treatment improves vision only in a small percentage of patients.

Instead, Bhavsar says doctors are moving toward multiple new medicines and cutting-edge technologies. One medication in particular is bevacizumab, a drug used to treat advanced cancers that slows the growth of new blood cells. “In spite of the drug not being FDA-approved for use in the eye, it’s probably the most common medicine used worldwide right now for treating age-related macular degeneration,” says Bhavsar.

There’s also the Argus II Retinal Prosthesis System, or, as Bhavsar and others in ophthalmology like to call it, the bionic eye. “It’s actually an artificial retina implanted into the weaker eye,” he says of the recently FDA-approved device. A pair of camera-equipped glasses worn by the patient receives light, which is converted to a wirelessly transmitted signal and sent to an antenna in the artificial retina. The artificial retina then converts the signal into electrical impulses, which bypass damaged photoreceptors and stimulate the retina’s remaining cells.

Another surgical innovation tackles presbyopia, the normal, age-related loss of near-focusing that causes many to rely on reading glasses in later years. “At about age 40, we begin to lose the accommodative ability to focus up close like we used to, and it’s an unavoidable change that gradually gets worse,” says Ivan Schwab, professor of ophthalmology at the University of California, Davis School of Medicine.

That’s where the KAMRA corneal inlay, the first device of its kind to win FDA approval, may help. Inserted into the eye, the removable implant acts like a camera aperture, adjusting the depth of field when needed. So far, more than 80 percent of implanted patients experienced 20/40 vision or better for a period of three years, making the easily reversible option a less permanent alternative to procedures such as LASIK. — MM

Doctors call it presbycusis, but you’ve heard it called another name: age-related hearing loss. Even though experts know the condition is primarily due to the loss of hair cells in the inner ear (among other factors), they remain no closer to figuring out how to prevent it.

One reason is that it’s impossible to tell the difference between age-related damage and damage due to prior noise exposure, says Frank Lin, associate professor of otolaryngology and epidemiology at Johns Hopkins University School of Medicine. “All we do know is that many cells within the inner ear are post-mitotic, which means once they’re destroyed, the body can’t regenerate them.”

There are no proven pharmacologic therapies for age-related hearing loss, but that may soon change. One area researchers are looking into is symptomatic therapies that could boost hearing on a daily basis. “Imagine a drug that could act like Viagra in the inner ear,” says Lin, who notes that clinical trials are already underway to study the effects of such disease-modifying drugs. One such drug — known as a Kv3 potassium channel modulator, in development by U.K.-based Autifony Therapeutics — may help improve neuron function in the part of the brain responsible for processing sounds.

“There’s also a push to develop neurorestorative therapies that can repair hair cells within the inner ear,” says Lin. One clinical trial involves the drug CGF166, a one-time gene therapy, which, if proven successful in humans, could regenerate new hair cells within the cochlea that can signal the part of the brain that processes sound. — MM

You know it’s important to get the requisite eight hours (or at least seven) per night, but what’s more surprising is why it’s so important. People who have trouble sleeping are two to three times more likely to be depressed, a condition that weakens late-life physical defenses and accelerates mortality. When cognitive behavioral therapy, a form of talk therapy, was designed to instill better sleep habits — like waking up at the same time every day and confining sleep to bedtime only — it helped vanquish stubborn insomnia, according to data from an ongoing study at Toronto’s Ryerson University. Fully 87 percent of patients whose insomnia vanished saw their depressive symptoms improve as well. — ES

Time can be unkind to all the muscles in your body, especially the heart. “As it ages, it gets bigger, thicker and stiffer due to hypertrophy, a process that causes its muscle cells to become larger,” says Michael Lauer, director of the division of cardiovascular sciences at the National Institutes of Health’s National Heart, Lung, and Blood Institute. “Although we understand heart hypertrophy increases the risk of premature death and other forms of heart disease, we still don’t fully understand how to reverse it, but we may be getting there.

In 2013, researchers reported that they were able to cure hypertrophy in mice by surgically merging the circulatory systems of an older mouse with a younger mouse. “The process, known as heterochronic parabiosis, managed to reverse hypertrophy in the older mouse after just four weeks,” says Lauer. But they’re not sure exactly what’s driving the changes.

The GDF11 protein commonly found in the blood of young mice (the same protein that enhanced neurogenesis in aged mice) and placed in individual older mice was thought to have the same reversal effect on hypertrophy; however, more recent research suggests another molecule besides GDF11 may be at work.

Aging research may be on the rise, but it does have its own set of unique limitations in terms of how quickly discoveries in the lab turn into human clinical trials. “There’s a lot of grumbling, both in the general public and the scientific community, about how often we cure diseases in mice that never translates when we try those cures in humans,” says Felipe Sierra, director of the Division of Aging Biology at the National Institute on Aging.

Part of the problem, he says, is that the incidence of many human chronic diseases rises with age, yet many researchers prefer using young mice because of the pressures of being published and getting funding. Since most grants are usually only for a four- to five-year period, using younger mice is not only less expensive, but it avoids the delay of waiting for an animal to age.

“The physiology is quite different, so it’s not surprising that a drug may show efficacy in a young, resilient animal that has the ability to fight off things, but that same cure may not work in an older animal,” says Sierra. One of his greatest goals is to convince people of the importance of using both younger and older animals in research that is meant to be translatable to aging humans. “It may cause delay in the early stages, but it will save money and lives in the long run,” he says. — MM 

Since the mid-20th century, researchers have noted that calorie-restricted lab animals live longer than their well-fed counterparts. Naturally, some self-proclaimed health gurus have seized on these studies as evidence that humans could reap the same benefits by slashing their food intake. That prospect has inspired calorie-restricted diets that feature arcane ingredients like brewer’s yeast and psyllium husk and may total less than 1,200 calories per day.

Despite these dieters’ herculean efforts — forgoing dessert in favor of processed whey protein is a pretty drastic move — there’s still no solid evidence that slashing calories will extend human lives.

Rats do live about 40 percent longer on a calorie-restricted regimen, and roundworms live up to 50 percent longer. But evidence is mixed in monkeys, whose responses presumably mimic ours. In a University of Wisconsin study published in 2014, older rhesus monkeys that ate spartan diets for years were less likely to die, while scientists at the National Institute on Aging (NIA) reported in 2012 that calorie-restricted rhesus monkeys lived about as long as those on a normal diet.

Calorie restriction does seem to forestall aging, at least somewhat, on the cellular level. University of Washington researchers have found that a calorie-restricted diet reduces the activity of a cell-signaling protein called TOR-1 that may speed up cell aging. And scientists at Harvard Medical School, the NIA and elsewhere have shown that caloric restriction drives expression of proteins called sirtuins, which help promote cell survival.

Such research may help scientists understand the mechanisms that underlie aging and identify promising drug candidates that mimic the health-promoting effects of caloric restriction, says NIA’s Felipe Sierra.

Right now, though, “people are subjecting themselves to these very harsh regimes, [but] I don’t suggest anyone follow any of the leads that we have,” Sierra says. Essentially, caloric restriction involves a lot of pain for no sure gain. — ES

Maintaining a strong social network may foster good health in part because support from sympathetic friends and family helps cushion the impact of life’s blows. When you lead a less anxious life, you’re less prone to certain chronic conditions, such as cardiovascular disease.

George Vaillant, a psychiatrist who directed a study that has monitored a group of former Harvard students since 1939, writes, “It is social aptitude, not intellectual brilliance or parental social class, that leads to a well-adapted old age.”

Barring a major drinking binge, being the life of the party is good for you. In fact, highly social people have a 50 percent better chance of survival than loners over a period of several years, according to Brigham Young University psychologist Julianne Holt-Lunstad. She analyzed over 100 studies on the long-term relationship between social activity and health.

The studies followed subjects for an average of seven and a half years. A misanthropic lifestyle, she reported in PLOS Medicine, could be as unhealthy as skipping exercise or smoking over a dozen cigarettes a day. — ES

The more you do for others as you age, the more you do for yourself. Volunteering eases stress, which, in turn, lowers the risk of disease and mortality, particularly in those with cardiovascular disease. People older than 70 who volunteer for more than 100 hours a year report better health than senior non-volunteers, University of Minnesota researchers reported in 2005. Other studies show that committed volunteers have less chronic pain. Volunteering also gives participants a sense that they are valued and needed, which may ward off thoughts of being worn out or useless, says psychologist Benjamin Gottlieb of the University of Guelph in Ontario. — ES

When it comes to your physique, it’s known that with age, hormone production changes, our bodies begin storing more fat, and you lose between 3 and 8 percent of lean tissue mass per decade starting at around age 30.

“Many people that have maintained the same weight throughout their lives are not fully aware how their body composition has changed — until it unfortunately becomes unavoidably evident,” says Luigi Ferrucci, scientific director of the National Institute on Aging and former director of the Baltimore Longitudinal Study of Aging, America’s longest-running scientific study of human aging.

Some of that process can be reversed through exercise and hormone therapy, but your bones are another matter. “You can only build your bone mineral density up until around age 25 to 30,” says Elizabeth Matzkin, surgical director for women’s musculoskeletal health at Brigham and Women’s Hospital in Boston. “After that, what you have is what you have, and anything you do from that point forward (including exercise) may maintain it — but you can’t build them to be any stronger.”

Current research is looking at why inhibiting certain molecules, such as mouse protein Stat3, promote muscle regeneration in mice and how to engineer orthopedic implants from stem cells to replace damaged cartilage and bone, but the results of that effort aren’t expected to be necessarily aimed at the old. As with other parts of the body, such as the ears or the lungs, it can be difficult in orthopedics to separate the effects of pure aging from the effects of long-term wear and tear, Matzkin notes. She adds that a lot of what’s emerging in orthopedics is for the moment being targeted to treat those with muscle-wasting diseases, as well as a younger population with injuries due to athleticism.

If you’re waiting for science to concoct a magical elixir to extend life span, you may end up wasting the rest of your life in vain — for now.

“There are a lot of disparate theories about what could have a profound impact on aging and age-related processes, but at this point, we simply do not have evidence-based strategies to significantly change our life expectancy that come in the form of a pill,” says Ronald DePinho, professor of cancer biology and president of the University of Texas MD Anderson Cancer Center. However, science has proven that a few specific tactics can dramatically increase your life expectancy and reduce age-associated diseases.

• Exercise turns hours into years: Engaging in physical activity for 2.5 hours at a moderate intensity (or 75 minutes at a vigorous intensity) each week can increase your life expectancy by 3.4 years. Choose to do only half that amount, and you’ll still add 1.8 years to your life.

• Manage your stress: One common thread among all long-lived animals appears to be that their cells — and in some cases, the animals themselves — are more resistant to a variety of stresses. “Chronic unrelenting stress is an accelerant for the aging process,” says DePinho. So whether it’s trying a new hobby, getting more sleep, talking to a therapist or stopping to take a deep breath once in a while, whatever helps reduce your stress will increase your time on Earth.

• Watch your body mass index (BMI): “Obesity creates a chronic inflammatory state that drives free radicals, fast-tracks aging and increases your risk of developing many age-related diseases,” says DePinho. The solution: maintaining an ideal body weight through a simple, balanced diet and minimizing processed foods in favor of fruits, vegetables and other healthier foods. Ideally, your BMI (determined by dividing your weight in pounds by height in inches squared, then multiplying by a conversion factor of 703) should fall between 18.5 and 24.9 (Example: [150 pounds / (68 inches)2] x 703 = 22.8 BMI). —MM

While exercise is no panacea, it does confer plenty of benefits as we age. When Cardiff University epidemiologist Peter Elwood tracked the health outcomes of more than 1,600 people older than 45, he identified regular exercise as a key habit that reduced people’s risk of chronic conditions, such as diabetes and vascular disease in old age.

“Exercise is one of the more important healthy behaviors and one of the things we can modify,” Elwood says. Regular exercisers enjoy a mental payoff as well as a physical one. Aerobic workouts not only stop brain shrinkage, but they also can help the hippocampus grow, according to University of Illinois research. And perhaps as a result, adults who routinely exercise are less likely to develop dementia, according to a 2014 study from the University of Cambridge.

But just walking around the block once in a while is not enough. You should strive to exercise five days a week for at least half an hour each day.

To stick to this kind of regimen, “try to translate half an hour [of exercise] into your normal activities. Walk up the stairs rather than taking the elevator,” Elwood says. — ES 

Red wine contains substances that may delay aging. These include a plant-produced chemical called resveratrol, which spurs cells to increase production of sirtuins, the proteins that promote cell survival. A University of Connecticut study suggests that resveratrol helps stave off heart disease, and another study suggests that antioxidants like those found in red wine protect blood vessels from premature damage. But drinking too much worsens conditions like diabetes and high blood pressure, and may cause cancer and liver damage. National Institutes of Health experts advise that women consume no more than three drinks in a day and seven per week; men should not surpass four in a day and 14 per week. — ES

From his work on the Baltimore Longitudinal Study on Aging (BLSA), Luigi Ferrucci has witnessed firsthand that, for everything we currently know, the process of aging remains as enigmatic as it is inevitable. And what knowledge we have gained over the years can sometimes be easily overturned.

“For example, we used to believe people became grumpy as they got older. But an analysis of long-term data from the BLSA discovered that an adult’s personality generally doesn’t change much after age 30,” says Ferrucci. “In fact, people who are happy when they’re younger are likelier to be the same when they’re much older.”

It turns out “grumpy old men” — or women, for that matter — may be gruff not because of age, but because they’re set in a personality shaped by their youth during times when war, poverty and other harsh experiences were more common. “It also suggests that significant changes in personality may not be due to aging,” says Ferrucci, “but could be a sign of disease or dementia instead.”

The BLSA has been connecting the dots on the physical and cognitive changes that take place as we age since 1958. In that time, the study has been the basis for more than 800 scientific papers on aging, papers that have expanded our understanding of the relationship between aging and cardiovascular health, metabolism, psychology and cognition.

It also remains hard at work on a project called IDEAL — Insights into the Determinants of Exceptional Aging and Longevity — that hopes to understand “exceptional agers,” individuals 80 and older who are healthy and disease-free. If successful, it could be yet another tool to find solutions to age-related health issues, as well as unravel the mystery of what causes us to age in the first place.

While many researchers are seeking new ways to combat age-related issues one at a time, some experts in the field of geroscience — the study of how aging causes disease — are uniting to develop preventive and therapeutic approaches to fight multiple diseases.

“We’ve known that aging is a major risk factor for most chronic diseases for some time, but recently, we’ve gained a better understanding of the aging process’s basic underpinnings, which has allowed us to extend both life span and health — in animals at least,” says Felipe Sierra, director of the Division of Aging Biology at the National Institute on Aging. “There’s only so much we can gain in terms of disease-free longevity by curing individual diseases like cancer and Alzheimer’s one at a time, but if we can address the issue of aging, then we could potentially delay and diminish them all at once.”

That led Sierra in 2011 to form the Trans-NIH GeroScience Interest Group, which at a recent summit had leading scientists identify seven highly intertwined processes that promote aging: 

Deciphering these defined pillars of aging is what experts like Sierra believe affect age-related diseases and could help design the genetic, behavioral and pharmacological means to decelerate aging.

Among the seven pillars, one that has inspired much excitement is metabolism, where researchers have been trying to understand why calorie restriction seems to extend the life span in mice and other animals. Is it because metabolizing fewer calories results in less oxidative damage? Could the absence of nutrients trigger certain defense mechanisms that protect the body? According to Sierra, researchers have managed to identify several molecular pathways that, if modified through medicine, could one day mimic the life-expanding effects of calorie restriction in humans, without requiring anyone to eat less.

Another pillar being thoroughly explored is the fallout from long-term chronic inflammation. Ferrucci says centenarians and others who have lived longer, healthier lives often have less inflammation. We know that many age-related diseases involve inflammation, but we don’t yet know why. Nonetheless, interventions targeted to reduce chronic inflammation are also being examined closely.

We can’t shut down inflammation completely, says Ferrucci. Our bodies need the short-term adaptive form, which quickly turns on and off to fight bacteria and remove debris after injuries and infections. “We need to better understand the process on a molecular level to see if we can develop a drug that only targets what’s not working while leaving everything else functional,” he says. “But right now, we are shooting inflammation with a nuclear bomb — and we need to shoot inflammation with a rifle.”

Developing drugs to modify these processes is one area science is investigating, but it gets complex fast. Some anti-inflammatory drugs have been found to extend life in mice, but these drugs can have multiple effects, and it’s not yet clear why they work. The fact that they tackle chronic inflammation could just be one piece of the puzzle, not the whole solution.

The most promising drug so far has been rapamycin, an immunosuppressant often used in organ transplants that’s been shown to extend the life span of mice. “Rapamycin is already used in humans for unrelated things,” says Steven Austad, scientific director of the American Federation for Aging Research and chair of the University of Alabama at Birmingham biology department. “But in mice, it has an unbelievably wide range of effects that you’d never think a single drug could possibly have, ranging from preventing Alzheimer’s and cardiovascular disease to reducing cancer.”

Austad says other medications have shown similar effects on extending mouse life span, including acarbose (a common drug prescribed for Type 2 diabetes), and anti-inflammatory drugs such as masoprocol and basic aspirin. While the research has a long way to go before anything translates to humans, science may finally be on the right path to understanding aging at its core.

“For the first time in history, we have theories, and the technology to measure those phenomena in living humans longitudinally over time,” Austad says. “And I’m certain that in the next 20 years, science will reveal where we need to go.”— MM 

The grade-school Pollyanna who always turned in her homework may have had the right idea from a healthy-living standpoint.

In a University of California, Riverside meta-analysis of 20 published studies, conscientious people were more likely to live longer, which makes sense: If you’re good at keeping promises and showing up on time, you’ll probably be good at sticking to healthy diet and lifestyle habits.

An easygoing temperament may also confer a survival advantage. Studies of centenarians have found they’re more laid back than the general population and show more optimism about the future. On the other hand, people with pessimistic tendencies are more susceptible to conditions like high blood pressure and depression.

But if you’re a worrier or a dyed-in-the-wool pessimist, take heart. You can teach yourself to observe habitual negative thoughts and reframe them in a way that’s more positive but still realistic, says Stanford psychologist Carol Dweck. For instance, if you’re convinced you’ll die young from cancer because it runs in your family, you can instead opt to focus on how you’re minimizing your risk by adopting healthy lifestyle habits and having regular checkups. Changing the way you look at the world can shift your temperament, which, in turn, may improve your mental and physical health later in life. — ES

[This article originally appeared in print as "Age & Enlightenment."]