Power Up Your Brain (17 page)

Our lab had gained international recognition for its achievements in this new and exciting field and often attracted visiting professors from around the world. It was soon after a delegation of Spanish neurosurgeons had visited that I found myself accepting an invitation to continue my research at a prestigious hospital in Madrid, the Ramón y Cajal Center. Their microneurosurgery program was in its infancy, but their team was dedicated, and I felt honored to be assisting them in their groundwork efforts, especially in the work dealing with understanding the brain’s blood supply.

The Spanish hospital was named to honor Nobel Laureate Santiago Ramón y Cajal (1852–1934), a great pioneer of neuroscience. Images of Dr. Ramón y Cajal were numerous in the hospital, and there was clearly a deep sense of pride among my Spanish colleagues that they could claim such an influential scientist as one of their own.

During my visit to Madrid, I felt compelled to learn more about Dr. Ramón y Cajal and came to deeply respect his explorations of human brain anatomy and function. One of his major tenets held that brain neurons were unique compared to other cells of the body, not only because of their function but also because they lacked the ability to regenerate. Thus, the liver, for example, perpetually regenerates itself by growing new liver cells, and there is similar regeneration of cells in virtually all other tissues including skin, blood, bone, intestines, and so on. But not so with neurons in the brain—or so stated Dr. Ramón y Cajal.

I admit that I was pretty well sold on his theory at the time, but I did wonder why it wouldn’t make sense for the brain to retain the ability to regenerate itself, to have the ability grow new brain neurons. After all, researchers at the Massachusetts Institute of Technology had shown a decade before that neurogenesis, the growth of new brain neurons, occurred throughout the entire lifetime in rats.

Soon after I concluded my research in Spain, I was off to medical school at the University of Miami. And it was while learning histology, the microscopic study of tissues, that I realized how deeply entrenched in science was this notion that neurogenesis, while clearly defined in some animals, was not something that occurred in humans.

This teaching never sat well with me, especially when I thought back to my college years when the idea that “every beer you drink destroys 20,000 brain cells” was often kicked around late on a Friday night when surely more than that number had met their demise.

BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF)

A major component in this gift of neurogenesis—and it is a gift to be revered—is a protein called brain-derived neurotrophic factor (BDNF), which, as we read in previous chapters, plays a key role in creating new neurons. And it also protects existing neurons, helping to ensure their survivability while encouraging synapse formation—that is, the connection of one neuron to another— which is vital for thinking, learning, and higher levels of brain function. Studies have in fact demonstrated that BDNF levels are lower in Alzheimer’s patients, which is no surprise, given our current understanding of how BDNF works.

But we gain an even greater appreciation for the health benefits of BDNF when we consider its association with other neurological conditions, including epilepsy, anorexia nervosa, depression, schizophrenia, and obsessive-compulsive disorder.

BDNF Activation

We now have a very firm understanding of the factors that influence our DNA to produce BDNF. Fortunately, these factors are by and large under our direct control. Increasing your production of BDNF and thus increasing neurogenesis while adding protection to your existing brain neurons doesn’t require that you enroll in a research study to determine if some new laboratory-created compound will enhance BDNF production. The gene that turns on BDNF is activated by a variety of factors, including voluntary physical exercise—animals forced to exercise do not demonstrate this change—calorie reduction, intellectual stimulation, curcumin, and the omega-3 fat known as docosahexaenoic acid.

This is a powerful message because all of these factors are within our grasp; they represent choices we can make to turn on the gene for neurogenesis. So let’s explore them individually.

Physical Exercise:
Laboratory rats that exercise have been shown to produce far more BDNF than sedentary animals. But, interestingly, animals forced to exercise produce considerably less BDNF than those who voluntarily choose to spend time on the running wheel. Researchers have shown that there is a direct relationship between elevation of BDNF levels in the voluntarily exercising animals and their ability to learn.

With the understanding of the relationship of BDNF to exercise, researchers have examined the effect of physical exercise in humans, both apparently healthy individuals as well as persons at risk or already diagnosed with Alzheimer’s. The findings have been fairly remarkable. In a recent paper, Nicola Lautenschlager of the University of Western Australia found that elderly individuals who engaged in regular physical exercise for a 24-week period demonstrated an astounding improvement of 1,800 percent in memory, language ability, attention, and other important cognitive functions, compared with an age-matched group not involved in the exercise program. The exercise group spent about 142 minutes exercising each week—about 20 minutes a day.
³

In a similar study, Harvard researchers found a strong association between exercise and cognitive function in elderly women and concluded, “In this large, prospective study of older women, higher levels of long-term regular physical activity were strongly associated with higher levels of cognitive function and less cognitive decline. Specifically, the apparent cognitive benefits of greater physical activity were similar in extent to being about three years younger in age and were associated with a 20% lower risk of cognitive impairment.”
⁴

These and other studies clearly indicate that exercise enhances brain performance and is directly associated with increased production of BDNF. Simply by voluntarily engaging in regular physical exercise, even to a relatively moderate degree, you can actively take control of your mental destiny.

Calorie Reduction:
Another factor that turns on the gene for BDNF production is calorie reduction. Extensive studies have clearly demonstrated that when animals are fed a diet with reduced calories, typically by around 30 percent, their brain production of BDNF soars, along with a dramatic enhancement in memory and other cognitive functions.

But it’s one thing to read research studies involving rats in an experimental laboratory and quite another to make recommendations to human patients based on animal research. Fortunately, studies that show the powerful effect of reducing caloric intake on brain function in humans are now appearing in some of the most well-respected medical journals.

In a 2009 study, German researchers imposed a 30 percent calorie reduction on the diets of elderly individuals and compared their memory function with a group of a similar age who ate whatever they wanted. At the conclusion of the three-month study, those who ate without restriction experienced a small but clearly defined
decline
in memory function, while memory function in the group who consumed the calorie-reduced diet actually
increased
profoundly. In recognition of the obvious limitations of current pharmaceutical approaches to brain health, the authors concluded, “The present findings may help to develop new
prevention
and treatment strategies for maintaining cognitive health into old age.”
⁵

What a concept. Preventive medicine for the brain. While the tenets of preventive medicine have seemingly taken hold in so many other areas of health care, from heart disease to breast cancer, for some reason the brain has always been left out. Gratefully, with these new research findings, that is changing.

Further evidence supporting the role of calorie reduction to strengthen the brain and provide more resistance to degenerative disease comes from Mark P. Mattson at the National Institute on Aging Gerontology Research Center, who reports, “Epidemiological data suggest that individuals with a low calorie intake may have a reduced risk of stroke and neurodegenerative disorders. There is a strong correlation between per capita food consumption and risk for Alzheimer’s disease and stroke. Data from populationbased case control studies showed that individuals with the lowest daily calorie intakes had the lowest risk of Alzheimer’s disease and Parkinson’s disease. In a population-based longitudinal prospective study of Nigerian families in which some members moved to the United States, it was shown that the incidence of Alzheimer’s disease among individuals living in the United States was increased compared to their relatives who remained in Nigeria.”
⁶

The Nigerians who moved to the United States were obviously genetically the same as their relatives who remained in Nigeria. Only their environment changed. And this research clearly focused on the detrimental effects on brain health as a consequence of the increase in calorie consumption.

While the prospect of reducing calorie intake by 30 percent may seem daunting, consider that Americans now consume an average of 523 more calories daily than in 1970. Current United Nations estimates show that the average American adult consumes 3,770 calories each day. In contrast, most health-care professionals consider normal calorie consumption (i.e., the amount of calories needed to maintain body weight) to be around 2,000 calories daily for women and 2,550 for men, obviously with higher or lower requirements depending on level of exercise. A 30 percent reduction of calories from an average of 3,770 per day provides 2,640 calories, still more than a normal minimum requirement.

Much of the calorie increase in Americans comes from our overwhelming increase in sugar consumption. The average American now eats and drinks an incredible 160 pounds of refined sugar each year, which represents a 25 percent increase in just the last three decades. This becomes particularly troubling in light of animal research done at UCLA showing a strong link between “the typical diet of most industrialized Western societies rich in saturated fat and refined sugar” and reduced BDNF levels and, as expected, correspondingly reduced memory function.

Lowering sugar intake alone might go a long way toward achieving a meaningful reduction in calorie consumption; weight loss would likely be a side benefit. Indeed, obesity, in and of itself, is associated with reduced levels of BDNF, as is elevated blood sugar, a common consequence of obesity. Furthermore, increasing BDNF provides the added benefit of actually reducing the appetite.

We hope that this data and the desire to help your brain turn on BDNF production will motivate you to follow a reduced-calorie diet. But, if you want to do more, you can implement a program of intermittent fasting, which we will describe in Chapter 14.

Intellectual Stimulation:
BDNF is described as a neuronal trophic factor, which means that it is a chemical that induces positive growth, health, and functionality in the target tissue—in this case, brain neurons. So it would only make sense to expect BDNF to increase when the brain is challenged. Just as muscles will gain strength and thus functionality when exercised, the brain also rises to the challenges of intellectually stimulating circumstances by becoming faster and more efficient as well as having a greater capacity for information storage.

These positive features are all facilitated by the increase in BDNF caused by stimulating activities. Inversely, it is likely that BDNF levels are low in individuals who spend several hours each day watching television, playing rote computer games, or otherwise engaged in mindless and passive activities.

An agile mind is also a good deterrent to help us avoid debilitating diseases associated with old age. Mark Mattson suggests that agility education and linguistics are two ways to keep an active, functional mind. He states, “In regards to aging and age-related neurodegenerative disorders, the available data suggest that those behaviors that enhance dendritic complexity and synaptic plasticity also promote successful aging and decrease risk of neurodegenerative disorders. For example, there is an inverse relationship between educational level and risk for Alzheimer’s disease; people with more education have a lower risk. Protection against Alzheimer’s disease, and perhaps other age-related neurodegenerative disorders, likely begins during the first several decades of life, as is suggested by studies showing that individuals with the best linguistic abilities as young adults have a reduced risk for Alzheimer’s disease. Data from animal studies suggest that increased activity in neural circuits that results from intellectual activity stimulates the expression of genes that play a role in its neuroprotective effects. Levels of several different neurotrophic factors, including BDNF, are increased in the brains of animals maintained in complex environments, compared to animals maintained under usual housing conditions.”
⁷