The Alzheimer’s Prevention & Treatment Diet by Richard S. Isaacson MD, Christopher N. Ochner PhD
Poor lifestyle habits, such as a lack of exercise, are also associated with a higher risk of AD.
Research has shown that the best way to prevent and treat Alzheimer’s is to use a multifaceted approach that includes specific nutritional supplements, physical exercise, stimulating intellectual and social activities, and stress-reduction techniques.
For example, scientists have noted that people with Alzheimer’s disease have a reduced capacity to metabolize (use) glucose, a form of sugar that is the brain’s primary source of fuel. This reduction in healthy glucose metabolism, known as glucose hypometabolism, is significant because when brain cells are deprived of their main fuel source, they have a hard time functioning properly and eventually become damaged.
If you’d like to try some examples of these kinds of tests, go to http://www.AlzU.org and sign up for a free account; samples are available on the Activities tab. (Also see the discussion of diagnostic tests on page 40.)
The symptoms of age-associated cognitive decline may include intermittent memory loss, word-finding difficulties, and a slower speed of thinking. When the cognitive changes are isolated to difficulties with memory, this condition is sometimes referred to as age-related memory loss.
In turn, this glucose hypometabolism may be caused by mitochondrial dysfunction, a problem in which the mitochondria (or “batteries” of the brain cells) have difficulty processing energy. For reasons that are not yet clear, mitochondrial dysfunction not only causes glucose hypometabolism, but may additionally contribute to a condition called oxidative stress. In oxidative stress, cells that are deprived of sufficient energy find it difficult to detoxify, potentially leading to cell damage and injury. As you’ll see in this book, some of the most powerful therapies that may improve mitochondrial function and reduce oxidative stress also happen to be among the simplest to implement. By making easy changes to your diet and lifestyle, you may be able to protect your brain.
After completing the initial questionnaire, patients complete an online course about AD prevention that our team created on Alzheimer’s Universe (www.AlzU.org), which is also free for the public to join.
Between 20 and 30 percent of all Americans will inherit one or more copies of APOE4; studies show that these people may have a greater risk of developing AD. Studies indicate that between 40 and 65 percent of all Alzheimer’s patients have at least one copy of the APOE4 gene. Conversely, the 10 to 20 percent of Americans who inherit one or more copies of APOE2 may have a reduced risk of developing AD.
For example, research shows that people with the APOE4 gene who engage in regular exercise can reduce amyloid deposits in the brain so that their levels are equivalent to the levels in people who don’t have the APOE4 gene. (See page 178 to learn more about exercise and AD.)
Based on their research, Dr. Sacco and his colleagues created a model, the Global Vascular Risk Score (GVRS). The GVRS considers the factors that contribute to vascular (blood vessel) damage in the brain—such as obesity, high blood pressure, and alcohol consumption—and is primarily seen as a way of evaluating how likely a person is to have a stroke. But because vascular damage is itself a major risk factor for brain shrinkage and cognitive decline, the GVRS can be a useful tool in helping doctors determine and modify cardiovascular risk that may also adversely affect the brain. To discover your GVRS, you can use the online GVRS calculator at http://neurology.med.miami.edu/gvr. As always, you should talk to your doctor about your results. Keep in mind, however, that your score doesn’t have an exact bearing on whether or not you will develop cognitive decline or AD.
For one thing, people who carry certain variants of the fat mass and obesity-associated (FTO) gene are more likely to develop Alzheimer’s, especially when they also carry the APOE4 gene. In addition, the FTO gene seems to be linked to reduced brain volume. That is, people who have the FTO gene tend to have certain regions of their brain atrophy, or shrink, much more significantly than do people without the gene. With less brain matter available, cognitive function is impaired.
Insulin is essential to a number of brain processes, playing a role in memory formation and regulating a neurotransmitter called acetylcholine, a special chemical that allows brain cells to communicate with one another. Insulin also helps maintain the blood vessels that feed the brain, supporting the circulation of oxygen and nutrients. With insulin resistance, these functions are undermined, potentially leading to cognitive decline and memory loss. Interestingly, different areas of the brain may become more insulin resistant than others—research suggests that the hippocampus, the brain’s memory center, may be particularly prone to insulin resistance. In addition, some studies indicate that insulin resistance is associated with a higher growth rate of beta-amyloid plaques, one of the hallmarks of AD. While more research still needs to be done to explain the exact connection between diabetes, insulin resistance, and AD, the evidence supporting those associations is strong.
Importantly, physical activity has also been shown to directly reduce amyloid levels in the brain, and may also stimulate the growth of brain cells and the development of
Evidence suggests that head injuries involving loss of consciousness (such as a concussion) can increase the risk of AD, especially when the trauma is severe, suffered later in life, or occurs in people who carry the APOE4 gene. Scientists believe that serious brain injuries
Some scientists have explored the possibility that heavy metals might also cause Alzheimer’s disease.
There is some evidence that overexposure to copper (usually through food and water) may accelerate the progression from mild cognitive impairment (MCI) to dementia due to Alzheimer’s disease. It is believed that higher blood concentrations of free copper (copper that is not bound to proteins) may lead to either an increase in the accumulation of beta-amyloid protein or a decrease in the ability to process and clear those plaques. High free copper may also contribute to brain inflammation, which is a risk factor for AD.
In patients with AD, melatonin production is even further reduced. It remains unclear whether melatonin
At other times, food stimulates the release of certain chemicals that influence brain function—specifically, hormones and neurotransmitters, the chemicals that enable your brain cells to communicate. As one example, chocolate (especially dark chocolate) contains small amounts of both the neurotransmitter serotonin and its “building block” L-tryptophan, a substance that allows your brain to make more serotonin. Serotonin is a chemical responsible for happiness; it’s the target of certain antidepressants, as higher levels of this neuro-transmitter can make you feel better. By eating chocolate, you boost your brain’s serotonin levels, and thus also boost your mood.
Research shows that those who have a higher BMI and waist-to hip ratio tend to see both lower total brain volume and greater shrinkage of the hippocampus (the brain’s memory center) later in life. With fewer brain cells available, cognitive functioning suffers. A number of studies have reported an inverse relationship between body weight—particularly body fat—and memory function. In other words, having more body fat is associated with poorer memory. Higher “central adiposity”—basically, larger accumulations of subcutaneous and/or visceral fat in the abdominal area, or having a “beer belly”—is also associated with a greater risk of cognitive impairment.
For one thing, high levels of insulin may contribute to the accumulation of beta-amyloid proteins, one of the hallmarks of AD (see page 10). Research indicates that insulin and beta-amyloid protein are both degraded (broken down) by the same enzyme, insulin-degrading enzyme (IDE). When the bloodstream is flooded with insulin, more IDE is needed to clear that insulin from your system. This may mean that there’s less IDE available to break down and remove beta-amyloid proteins in the brain. Some researchers feel this leads to greater plaque growth and cognitive decline.
a few studies have found that people who lacked the APOE4 gene have experienced cognitive benefits from supplementing their diet with certain omega-3 fatty acids and caprylic triglyceride. However, people who had the APOE4 gene did not experience this benefit. In the PREDIMED-NAVARRA study—a long-term study that examined the effect of the Mediterranean diet on cardiovascular disease risk—researchers found that people who had certain genes saw greater benefits from adopting a Mediterranean-style food plan. Specifically, individuals who had the “genetically favorable” profile of genes called CR1, CLU, and PICALM saw their cognitive performance improve much more significantly on the Mediterranean diet than did people with the same genetic profiles who were assigned a low-fat diet.
To find carbohydrate counts, we generally visit the USDA Supertracker website. To find glycemic index and glycemic load, we use the Mendosa.com Table of Glycemic Index and Glycemic Load. (See page 231 of the Resources list for more information on these websites.)
Using brain imaging studies, investigators found that people with low blood DHA benefited considerably from the multidomain intervention plus DHA (800 mg per day), showing significant improvements in brain metabolism. This was especially true in people who tested positive for the APOE4 gene, and in those who already had deposits of beta-amyloid protein—one of the hallmarks of AD—in their brain. The researchers demonstrated that the multimodal approach plus DHA supplementation slows cognitive decline in older adults. Although further study of
suggest choosing a brand that has at least 200 to 500 mg of DHA, and 100 to 300 mg of EPA in each capsule. While individual recommendations can