Think Smart: A Neuroscientist's Prescription for Improving Your Brain's Performance (3 page)

With the completion of adolescence the brain is fully functional and, barring disease or injury, will remain so until late in life. The transition from adolescence to adulthood involves:

The dominance of the frontal lobes over the limbic system.
As a result, the adult, in contrast to the adolescent, is no longer as dominated by impulses, moods, or emotions in general. This comes about because of several frontal-lobe-mediated changes that increase ability to put things in context; to plan and organize one’s life; to guard against distractions caused by thoughts, impulses, and fantasies; and to focus on the present while simultaneously envisioning how one can change current circumstances by judicious effort.

Specialization within the brain, thanks to the creation of millions of new circuits,
which vary from one person to another based on life experience. The most dramatic specialization takes place within the two hemispheres. The brain of a lawyer differs from that of an architect, for instance, thanks to enhancement of different circuits within the two hemispheres. The lawyer’s facility in the use of written and spoken language relies heavily on the circuitry of the left hemisphere, where language is primarily processed; the architect’s ability to envision structures in three-dimensional space results from the buildup of circuits within the right hemisphere. But such arrangements aren’t mutually exclusive. Thanks to the brain’s plasticity, circuitry within both sides of the brain can develop equally. (My brother is both an architect and a lawyer.)

Continuation of the brain’s plasticity.
Think of the brain as almost infinitely plastic throughout our lives. I’ve qualified my statement with
almost
because of the influence of genes on the brain’s structure and function. And although this brain plasticity diminishes with age, it never completely disappears. Until the day we die our brain remains capable of change, according to the challenges that we set for it.

The brain reaches its maximum size (measured by weight) in early adult life and decreases by about 10 percent over an average life span. And what a marvelous organ it is.

The adult human brain weighs about three pounds and contains about a hundred billion brain cells (neurons) with a million billion connections (synapses) linking those neurons to each other.

While it’s hard to grasp the scope of a number like one million billion, it’s easier if you approach it in stages. One million is easy to conceptualize: 1,000 x 1,000, about the population of a moderate-size city. A billion is one thousand times one million—a thousand small cities or a hundred very large cities. To put one million billion into perspective, there are about six billion people currently living on our planet—a small number compared with those hundred billion nerve cells and a truly paltry number compared with those million billion connections.

Although the number of synapses generally decreases as a person ages, most neuroscientists no longer believe that brain cell loss occurs at the frequently quoted figure of fifty thousand cells a day. Nor is the loss of neurons equally distributed throughout the brain. Rather, recent evidence points to a more selective loss of neurons with little or no significant neuron loss in many cortical regions used in normal cognition. Most striking is the variability in brain aging between one older person and another. This is undoubtedly secondary to genetic factors. As one neuroscientist humorously put it, “The best way to guarantee a normal brain in old age is to pick your parents carefully.”

Even more important than loss of neurons and the thinning of synaptic connections, especially in the frontal lobes, that occurs as we age, is the loss of cells from clusters of cells (nuclei) about the size of a pinhead located in the brain stem, which itself is only about the length of an adult forefinger. Dubbed “juice machines” by neuroscientist Paul Coleman, these clusters of cells send ascending fanlike projections to many parts of the cortex. The brain’s chemical messengers (neurotransmitters) travel along these projections. Reduction in the levels of neurotransmitters leads to many of the infirmities that increasingly afflict us as we get older: memory loss, depression, decrease in overall mental sharpness, inefficient information processing. Fortunately, these infirmities can be improved by drugs that rev up or supplement deficient neurotransmitters.

Finally, as we age, our brain accumulates chemical breakdown products resulting from the sum total of all of the metabolic processes that take place within our brain cells over our life span. Every older person’s brain contains a certain quantity of these products (but nowhere near the amount seen in people suffering from Alzheimer’s disease). Further, while some loss of neurons occurs normally with aging, the loss can be compensated by increases in the networking capacity of the remaining neurons. While the number of neurons decreases from birth onward, fewer but stronger and more enduring connections form among the remaining neurons. This capacity to compensate for the loss of its components makes the brain the only known structure in the universe that works more efficiently despite a loss of its components. To this extent the brain is unique among both biological and mechanical structures: over the years it doesn’t “wear out.”

Given all this change within the brain as we progress from infant to child to adolescent to young and, finally, aged adult, here is the key question: What can be done to preserve and enhance the brain’s powers? The next 230 pages suggest a practical program based on my own experience as doctor and author, and the suggestions of many of the world’s most prestigious neuroscientists. Let’s start with the most basic need of all: What does the brain like to eat?

PART TWO

Care and Feeding of the Brain: The Basics

It takes only a glance at the cover of self-improvement magazines to confirm our nation’s enduring interest in discovering the perfect diet. Curious readers can also choose from a steady stream of books making various dietary claims. Some suggest that one should eat, for instance, more carbohydrates, or fewer carbohydrates, or perhaps no carbohydrates at all. But despite their differences, all of the books conform to a common theme: If you follow
this diet,
you will be thinner, healthier, and sexier than you’ve ever been before. But whether the diets originate in South Beach or Beverly Hills—and however successful they may be for inducing general weight loss in individual dieters—they offer scant advice for people more interested in preventing mental rather than physical flab: tuning up their frontal lobes rather than their abs.

One reason for this absence of a “brain diet,” I’ve discovered from consulting experts on the brain and nutrition, is that the specific class of foods we eat may be less important to the health of our brain than the number of calories we consume. At least that is the message conveyed by researchers on brain health in animals. Sixty-five years of animal research confirms that in every animal in which it has been tried so far, caloric restriction slows the onset of degenerative diseases such as dementia, cancer, diabetes, and other illnesses associated with loss of brain function. Caloric restriction (defined as a balanced reduction of the protein, carbohydrate, and fat content of food without reduction of the nutrient content) also increases the life span. As a rough rule of thumb, an animal of whatever species that eats 35 percent fewer calories will live 35 percent longer.

If we consider animal research, should we adopt caloric restriction diets? We should if we want to lessen our chances of getting Alzheimer’s disease, according to research on mice fed a diet containing 30 percent fewer calories than mice allowed to eat as much food as they chose. Examination of the brains of the mice on the calorie-restricted diet showed a reduction of amyloid, the brain-clogging protein implicated in Alzheimer’s disease. Moreover, these mice outperformed their counterparts on an unrestricted caloric diet.

According to researchers at Oregon Health and Science University and the National Institute on Aging (NIA), caloric restriction, combined with periodic fasting, reduced the impairment of “Alzheimer’s” mice. Specifically, these mice, with a progressive illness similar to many aspects of Alzheimer’s disease, performed better on learning and memory tests and explored their surroundings with renewed vigor.

While I’m impressed with the amyloid-reducing properties of caloric restriction in mice, and even more impressed by the mice’s enhanced mental performance, neither of these findings is likely to exert much of an influence on my planning for this evening’s meal. Sure, I’ll readily concede that I’m eating a tad more than I need; nonetheless, since I’m not a mouse, I’d like to base my decision about caloric restriction on research involving animals higher on the food chain. But such research isn’t likely to be available anytime soon, because of life-span differences among species. Two or three generations in the mouse world doesn’t come anywhere close, time-wise, to the more than two hundred years corresponding to three human generations.

But this extended time line hasn’t stopped some people from intentionally going hungry in order to improve brain function and live longer. In one study sponsored by the National Institute on Aging, forty-eight men and women were randomly assigned to one of two diets. The first was sufficient to maintain current weight, while the second diet reduced caloric intake by 25 percent. After six months, those on the restricted diet had lower body temperatures and levels of insulin whenever they ate—two key characteristics of long-lived people and animals. In essence, the body’s energy requirements decrease to meet the reduced number of calories in the diet—the explanation why people on caloric-restricted diets don’t starve to death. The body simply readjusts to less food. All of which leaves unsettled whether a severely calorie-restricted diet makes sense.

The important concept—and this is drawn from both human and animal research—is that in order to tune up your brain and reduce your likelihood of Alzheimer’s disease, you may not have to cut back drastically on your caloric intake but simply keep your caloric intake low enough to prevent obesity.

Nearly two-thirds of adults in the United States are overweight, with 30.5 percent considered obese. While everyone is aware of the general medical consequences of obesity (heart disease, hypertension, and diabetes), the effect of obesity on brain function has only recently been uncovered.

Mice placed on diets high in saturated fat and “empty calories” significantly underperform in tests of memory when compared with mice on a normal mouse diet. Accompanying this performance failure are all of the bad things associated with such a diet: higher levels of plasma triglycerides, total cholesterol, and both high- and low-density lipoprotein cholesterol. Tests involving reinforcing rewards are also affected, i.e., the obese mice require more time to learn to press a lever in order to obtain a squirt of milk or fruit juice.

“Our findings show that fast-food diets impair memory in mice and make their brains more vulnerable to toxins,” says Veerendra K. Madala Halaggappa, of the National Institute on Aging. “If such diets have similar effects in humans, then reducing the amount of fat and empty calories may improve one’s memory and increase resistance to age- and stress-related cognitive impairment.”

Dr. Halaggappa’s comment suggests that reducing the dietary fat and empty calories in our diets will improve our memory and brain function in general. Think about the potential benefits of that insight for the mental functioning of a nation with a penchant for fast foods. In addition, research over the past year points to elevated cholesterol and obesity as risk factors for the development of Alzheimer’s disease.

In short, measures to control obesity are worthwhile, whatever effort may be required, since, as tests of cognitive performance in humans indicate, obesity is more often associated with cognitive impairment than with age, gender, education, or IQ. Particularly affected are the functions carried out primarily by those all-important frontal lobes. As mentioned earlier, these most developed brain areas are known to be associated with setting and keeping to goals, controlling impulses, and monitoring one’s own behavior—three special problem areas for the chronically obese.

After deciding to reduce caloric intake, what other dietary measures are most likely to protect and enhance our mental functioning?

To begin with, follow the oldest dictum in public health:
Primum non nocere
(First do no harm). Start by identifying and eliminating from your diet those foods that can be proven to cause harm. The chief villains here are processed fats. Especially harmful are the so-called trans fats, formed when liquid oils are transformed into solid fats by adding hydrogen to vegetable oil.

About twenty years ago food manufacturers started adding trans fat to their processed foods to prolong shelf life and stabilize flavor. Thanks to trans fat, crackers, cookies, and snack foods will stay fresh for years. Once ingested, however, these hydrogenated fats clog arteries in the brain and heart, leading to cognitive decline (memory is especially affected) and heart attacks. The stiffer and harder the fat—which varies directly with the degree of hydrogenation—the greater the artery-clogging effect. Trans fats exert the same occluding effect on arteries as bacon grease exerts on the drain in the kitchen sink. In order to avoid all this, follow the following guidelines: