By Sharon Palmer, RD Today’s Dietitian Vol. 11 No. 7 P. 24
Open your mind to the emerging field of research that suggests diet may have a powerful impact on brain health and function.
My Aunt Prussia, with her cat-eyed glasses, bright red lipstick, and neat black updo, used to cook up the meanest batch of scrambled eggs and bacon for breakfast in her country kitchen in Yakima, Wash. Over breakfast, she spun tales of her childhood growing up in the South, with her young nieces and nephews lined up to listen.
But then she started forgetting her stories, even though her body was as strong as ever. She paid her bills twice, lost her favorite jewelry, and couldn’t find her home in her own neighborhood. Aunt Prussia eventually ended up in a long-term care facility, along with hundreds of other patients with Alzheimer’s disease (AD), where she would not even recognize her friends and family who came to visit.
Most families have been touched by a similar story of the devastating effects of age-related neurodegenerative diseases such as AD. Watching the essence of a loved one’s life slip away, day by day, is a heart-wrenching experience—and it’s a costly one, too. The economic impact of a projected 8 million people with AD in the United States by 2030 will be roughly $500 billion.
A neurodegenerative disease is a disorder caused by the deterioration of neurons. Changes in these cells cause them to function abnormally, eventually bringing about their death. The neurodegenerative diseases AD, Parkinson’s disease (PD), Creutzfeldt-Jakob disease, and multiple sclerosis occur due to neuronal degeneration in the central nervous system. Current treatments for neurodegenerative diseases have proven inadequate thus far.
AD is the most common cause of dementia among older people. Scientists have much to learn about the cause of AD, an irreversible, progressive brain disease that slowly attacks memory and thinking skills, eventually leading to the affected individual’s inability to perform simple activities of everyday life. AD is marked by changes in the brain that include neurofibrillary tangles in the entorhinal cortex, amyloid plaques, and the loss of connections between neurons in the brain. These lead to widespread damage in the brain tissue.
However, there is new hope on the horizon for neurodegenerative diseases in the form of lifestyle modification. David Perlmutter, MD, FACN, a board-certified neurologist, a fellow of the American College of Nutrition, author of The Better Brain Book, and the director of the Perlmutter Health Center in Naples, Fla., is an internationally recognized expert in the field of nutrition and neurological disorders. Perlmutter, who presented at the Fifth Annual Nutrition and Health Conference: State of the Science and Clinical Applications in April 2008, believes that AD is preventable. He reports that in recent years, there has been growing scientific support for the roles of both inflammation and free radical activity in brain functional decline across the spectrum of neurodegenerative diseases. Though the cause of neurodegeneration appears to be multifactorial, lifestyle choices may play a big role in reducing inflammation and free radical-induced neuronal damage as part of preventive medicine in brain health.
Perlmutter puts his theories into practice at the Perlmutter Health Center, where complementary health approaches, including nutritional therapy, are combined to create an integrated treatment plan designed for the individual. While Perlmutter treats a number of chronic diseases at the center, his skills are particularly valuable for patients who visit the center with neurological problems such as headaches, epilepsy, stroke, PD, dementia (including AD), myasthenia gravis, multiple sclerosis, amyotrophic lateral sclerosis, dystonia, other movement disorders, and neuropathy.
This Is the Brain on Inflammation Slow, smoldering inflammation in the brain appears to play a big part in neurodegenerative diseases. Inflammation is characteristic of all neurodegenerative conditions and paves the way for free radical activation, explains Perlmutter. Recent findings indicate that the activation of microglia (tissue macrophages in the central nervous system) in response to injury, illness, aging, or other causes begins a cascade of events that can be characterized as an inflammatory process, according to a 2006 article in The American Journal of Clinical Nutrition. This cascade is mediated at first by the proinflammatory cytokine interleukin-1, which is overexpressed by the activated microglia. Through various pathways, interleukin-1 causes neuronal death, which activates more microglia, which in turn releases more interleukin-1. Over time, this ongoing inflammation in the brain destroys enough neurons to cause the clinical signs of AD.
According to an article published in a 2005 issue of The International Journal of Biochemistry & Cell Biology, inflammatory components related to AD neuroinflammation include not only microglia but also astrocytes (star-shaped glial cells of the central nervous system), the classic and alternate pathways of the complement system, the pentraxin acute-phase proteins, neuronal-type nicotinic acetylcholine receptors, peroxisome proliferator-activated receptors, and cytokines and chemokines. Both the microglia and astrocytes have been shown to generate beta-amyloid protein, one of the main pathologic features of AD.
Excess tumor necrosis factor-alpha (TNF-alpha) is also involved in the development of AD. Not only does it have pro-inflammatory functions, but TNF-alpha has also been recognized recently as a gliotransmitter that regulates synaptic function in neural networks and mediates the disruption in synaptic memory mechanisms caused by beta-amyloid. Scientists tested the perispinal administration of etanercept, a biologic antagonist of TNF-alpha, in a patient with late-onset AD and found rapid cognitive improvement beginning within minutes. The case report was published in the Journal of Neuroinflammation in 2008. “This is very exciting news,” says Perlmutter. “It’s been described as suddenly waking up from Alzheimer’s disease.”
The neuroinflammation connection may be glimpsed through studies linking anti-inflammatory drug use and lower AD risk. Perlmutter points to a 1997 study published in Neurology that examined the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on AD risk. “The patients who took NSAIDs for two or more years had a significantly lower risk of Alzheimer’s disease,” says Perlmutter. Indeed, the researchers concluded that the evidence suggests that one stage of the pathophysiology leading to AD is characterized by an inflammatory process. Other studies have also concluded that NSAIDs appear to protect against AD, as well as PD. Additional research is necessary before recommendations can be made for people to take NSAIDs to keep neurodegenerative disease at bay.
Oxidative Stress on the Mind The impact of oxidative stress on the brain is another crucial area catching researchers’ attention. Scientists have noticed that patients with AD tend to have lower antioxidant status. And now studies have shown oxidative damage to lipids, proteins, DNA, and RNA in multiple brain regions in late-stage AD, according to researchers from the University of Kentucky in a 2007 Archives of Neurology study. Recent autopsy findings on study patients with amnestic mild cognitive impairment demonstrate that oxidative damage may be an early event in the pathogenesis of AD. The researchers suggest that better antioxidants and agents used in combination to upregulate defense mechanisms against oxidation will be required to neutralize the oxidative component of the pathogenesis of AD.
Perlmutter sums it up: Neurodegenerative diseases represent the downstream effects of excessive free radical activity, supporting antioxidant approaches to brain protection and functional enhancement.
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