Boost Your Brain (33 page)

By now you know the likely end result of such brain structure changes: lowered cognitive performance and an increased risk of dementia.

Certainly, many studies have tied excess weight to an increased risk of dementia. One tracked 6,583 Northern California Kaiser Permanente patients between 1964 and 2006 and found central obesity was associated with a higher risk of dementia. Those who were overweight or obese but didn’t have central obesity had an 80 percent increased risk of developing dementia thirty years later, compared to non-overweight people. Those who had central obesity, however, were 3.6 times more likely than non-overweight peers to develop dementia—that’s a 360 percent increased risk. Even being merely overweight was associated with a 234 percent increased risk if the person had belly fat.
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Of course, this doesn’t mean that every overweight person will become demented or that every obese person is less smart than every thin person. Remember, we all have varying cognitive abilities to begin with, and there are other factors at play. If you’re an obese college professor who plays the violin, exercises, and belongs to a bird-watching club, you may be better off than a couch potato who weighs less but never exercises or explores his world. Still, it does mean that the brains of overweight people aren’t in the best possible shape and are more susceptible to decline later in life.

Perhaps an even bigger brain shrinker than obesity is diabetes, which has been tied to a smaller hippocampus
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and greater risk of stroke. One study found that having diabetes doubled the risk of stroke in the elderly and that young people with diabetes increased their risk of developing stroke by nearly six times.
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And while many of the worst effects of diabetes make their biggest mark as we age, they are by no means limited to the elderly. Just ask researchers at the New York University School of Medicine, who studied obese adolescents with type 2 diabetes and found that they had lower scores on tests of intellectual functioning, verbal memory, and psychomotor efficiency.
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The study, published in 2010, compared obese teens with type 2 diabetes to teens who were obese but didn’t have the disease, which points to diabetes having a greater effect on the brain than mere obesity.

In 2011, the team followed up on those findings with a report that obese adolescents with type 2 diabetes had measurably smaller hippocampi and frontal lobes than obese teens without diabetes.
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Those results were rather shocking. At a time when their brains are supposed to be developing, diabetic teens are actually experiencing brain
shrinkage
. And the number of such teens is on the rise. Imagine their future. If left untreated, their diabetes will continue to damage their brains for decades to come. Looking sixty years down the road, it’s not hard to imagine that they’ll suffer the consequences, with a higher risk of cognitive decline and Alzheimer’s disease.

As a neurologist, I see many different manifestations of diabetes, from the neuropathy that results in a loss of sensation in the toes, to the nephropathy that causes kidney failure, to the retinopathy that robs diabetic patients of their sight. And, of course, I often see the effects of diabetes on the brain. We don’t call it “brainopathy,” but perhaps we should. The impact is as life altering—if not more so—as any damages below the neck.

How High Cholesterol Factors In

High blood cholesterol is a vascular risk factor that often goes hand in hand with excess weight. And since it’s one of the conditions that slows blood flow to the brain, blood cholesterol bears mentioning in any discussion of brain shrinkers.

If you’re a bit rusty on your cholesterol facts, here’s a quick refresher. High-density lipoprotein (HDL) is often referred to as “good cholesterol” because it helps to remove excess cholesterol from your blood. Low-density lipoprotein (LDL), on the other hand, is considered “bad cholesterol” because it can build up on the walls of your arteries. Triglycerides, a type of fat, are also part of the overall picture, which we call your “cholesterol profile.” Ideally, I like to see my patients keep their HDL above 60 mg/dL and their LDL and triglycerides each below 100 mg/dL.

An unhealthy cholesterol profile can lead to atherosclerosis, a buildup of cholesterol plaques in the blood vessels, including those in the brain, which sixty years ago was referred to as “hardening of the arteries.” The name is fitting: if you were to touch the blood vessels affected by atherosclerosis, you’d actually find them to feel crunchy under your fingertips.

High cholesterol doesn’t directly produce symptoms, so it can go undetected. If unchecked, the plaques associated with high cholesterol trigger inflammation, which causes further growth of atherosclerotic plaques. The resulting high blood pressure (you’ll read more about this in
chapter 12
) adds to the damage by putting continuous pressure on the artery walls, weakening them, and increasing the likelihood of plaque buildup. Over time the interior channel of the blood vessel—called the lumen—narrows, slowing the flow of blood. Eventually the blood vessel can be blocked entirely, cutting off blood supply.

Atherosclerosis can affect blood vessels in any part of the body. When it occurs in blood vessels leading to the heart, it can cause a heart attack. When it occurs in the brain or in the arteries leading to the brain, the result is a stroke. Whether they’re large strokes, small strokes, or even micro strokes, such “brain attacks,” as you’ll read in chapter 12, starve the brain of nutrients and kill neurons. The result can be a serious loss of function—physical, cognitive, and emotional.

High levels of LDL, and low levels of HDL, have also been tied to cognitive decline, independent of obvious signs of stroke. One study, led by my friend and colleague University of California professor Dr. Kristine Yaffe, whom I consider a star in the field of brain health research, found that older women with the highest levels of LDL were more likely than those with low LDL to have mild cognitive impairment.
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High LDL cholesterol, and even borderline high LDL cholesterol, especially in combination with high blood pressure, also increases the risk of developing Alzheimer’s disease later in life, as one study of nearly 1,500 people in Finland found.
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Even more compelling, perhaps, is evidence that ties low HDL to poor memory—even in midlife.
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Researchers made that link by combing through data on 3,763 participants of a long-term study of more than 10,000 British civil servants. Study participants with low HDL (less than 40 mg/dL) were 27 percent more likely to show memory deficits by age fifty-five than those with high HDL (60 mg/dL or more). That number rose to 53 percent by the age of sixty. Knowing this often helps people get motivated to improve their cholesterol profile.

More research needs to be done to determine just how high HDL affects brain function, but it’s important to know that both HDL and LDL matter when considering brain health. Even more important, such effects can begin to take a toll—robbing you of brain reserve—long before you reach old age.

Obesity, smoking, poor diet, lack of exercise, diabetes, and other factors can all boost your risk of developing high cholesterol. Heredity can also play a role.

By now you’re probably ready for some good news. Fortunately, the brain-draining effects of high LDL seem to be reversible. In the University of California study by Dr. Yaffe and her colleagues, for example, women who lowered their levels of LDL over a four-year period had better cognitive function than those whose LDL levels remained high.

The study also noted a positive correlation between statin use and better cognitive function, independent of whether or not study subjects taking them actually lowered their LDL levels. Statins are cholesterol-lowering medications that are highly effective in reducing the risk of heart attack.

Why might statins offer neuroprotective benefits? Some experts suggest that in addition to their LDL-lowering properties, statins may act as an anti-inflammatory agent.

Other studies have shown a reduced occurrence of dementia in people who take statins, although they don’t yet prove that taking statins reduces a person’s risk of dementia. (We don’t know, for example, whether people who take statins happen to also do other things that result in them being less likely to develop dementia.) And there’s no proof that statins can slow the progression of Alzheimer’s disease.
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Interestingly, although some people have complained of cognitive problems after they started taking statins, studies show this is actually a rare occurrence and that the benefits of statins far outweigh the small risk of minor cognitive problems.
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How Your Brain Affects Your Weight

In the winter of 2012, a fifty-year-old man named Randall walked into my office. Or rather, he wheeled in. At 450 pounds Randall could walk, but just barely. Instead, he spent most of his day in a motorized wheelchair.

Randall hadn’t always been obese, but marital strife a decade earlier had sent Randall into a tailspin of overeating. “I was so stressed and sad that I just ate uncontrollably,” Randall told me on his first office visit. Over the years, Randall’s weight had ballooned from 200 pounds to 290. By then his knees had begun to ache. Eventually, as he passed the 300-pound mark and kept going, his knee pain would essentially cripple him.

Randall was a smart software engineer in New York, making a nice living creating computer networks for business clients. He was skilled in his field, but as Randall’s health went downhill, something else happened: Randall’s business began to suffer. By the time he came to see me—worried that he might be developing Alzheimer’s disease—Randall had had two major projects fail, had stopped working, and had started collecting disability payments. Once vibrant and gregarious, Randall was now flat-out miserable.

After my usual complete evaluation, I told Randall that he didn’t have Alzheimer’s disease and that there was plenty we could do to help him regain his memory, clarity, and creativity. But Randall would have to change his body. And to do that, he’d have to change his brain.

To understand why, you first need to know the role the brain plays in the development of excess weight and obesity. While there are many complex psychological underpinnings to obesity, there’s also some very clear neuroscience involved. That science starts below the neck with three hormones—insulin, leptin, and cholecystokinin (CCK)—that are released every time we eat. These hormones act as a negative feedback system, similar to a thermostat, helping you to stop eating when your glucose levels are high (insulin), your fat levels accumulate (leptin), or when your stomach is full (CCK). Unfortunately, this thermostat stops working when a patient becomes obese.

Of course, there are parallel pathways involved as well. Researchers in Finland, for example, presented evidence in 2012 that the brain’s reward system in response to food is more active in obese people.
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In that study, obese people shown pictures of food had increased activity in the brain’s reward area and decreased activity in the prefrontal cortex, the main part of the brain’s braking system, which helps prevent overeating.

It’s a terrible combination of factors. And it may explain (along with the faulty “thermostat”) why many people find it so hard to stop overeating. As you gain weight, changes in your brain’s reward system may make you crave certain foods. At the same time, your brain’s braking system is asleep at the wheel, failing to help you control your impulse to seek out the short-term reward. This is why I sometimes refer to obesity as a prefrontal cortex problem more than a food problem. It’s the brain that’s driving the choices you make, after all, telling you to choose french fries when you really should order a side salad.

Treatment: Barreling Back from the Brink

When I told an ecstatic Randall that many of his memory and cognitive problems could be reversed, I wasn’t exaggerating. As severe as his weight problems were, there’s ample evidence that weight loss and the treatment of diabetes have a dramatic effect on brain health.

One study of bariatric surgery patients, for example, found that those who’d lost weight after surgery were able to improve their cognitive testing scores and reverse damage to their brains’ highways in just twelve weeks. For that study, researchers tracked the progress of 109 bariatric surgery patients enrolled in the Longitudinal Assessment of Bariatric Surgery project, plus 41 obese control subjects who hadn’t had bariatric surgery.
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Study subjects were given a cognitive evaluation at the start of the study and again twelve weeks later.