February 2013 Issue

Protecting Cognitive Function — Evidence Shows Diet and Lifestyle Factors Positively Affect the Aging Brain
By Densie Webb, PhD, RD
Today’s Dietitian
Vol. 15 No. 2 P. 58

Some degree of neurodegeneration, or the loss of functioning neurons in specific areas of the brain, occurs with age, but if the damage goes unchecked, it can lead to a decline in cognitive function that manifests as dementia or Alzheimer’s disease.1

Protecting cognitive function, otherwise known as neuroprotection, involves strategies designed to defend the central nervous system against these degenerative disorders. Diet and lifestyle factors are being recognized as important components of neuroprotection. It’s been estimated that almost one-half of Alzheimer’s disease cases worldwide and in the United States may be attributable to potentially modifiable risk factors.2

The Neurodegenerative Process
Amyloid beta protein (Aβ), a protein normally found in the brain, is important for brain functioning because it increases the plasticity of neurons (the ability to adapt) and aids the brain in creating memory balance (retaining important memories and disposing of unimportant ones). The most prominent theory on the cause of Alzheimer’s disease suggests that accumulation and aggregation of Aβ into plaques is toxic to neurons. As neurons die, they create twisted strands with another protein (tau) called tangles, which prevent neurons from communicating, and they begin to die. An immune defense system in place is designed to clear Aβ by activating an inflammatory response via specific immune cells, including cytokines. As Aβ builds up, inflammation increases, causing free radical damage to neurons. 

“Immunological and pathological activation of proinflammatory cells and a depletion of antioxidant systems are major factors in the pathogenesis of neurodegeneration like that in Alzheimer’s disease,” says Vincenza Frisardi, MD, PhD, of the department of neurological and psychiatric sciences at the University of Bari, Italy. Preventing oxidative damage and the resulting inflammation appear to be key factors in the prevention of neurodegeneration of any kind.

Diabetes and Insulin Resistance
Diabetes is a known risk factor for Alzheimer’s and dementia. In fact, according to Court Vreeland, DC, DACNB, owner of the Vreeland Clinic in Vermont and a presenter at the 2012 Food & Nutrition Conference & Expo in Philadelphia, it’s the No. 1 risk factor for neurodegenerative disorders. Insulin resistance and metabolic syndrome also put people at risk. “The connection is undeniable,” he says. “Eighty percent of patients with mild cognitive impairment and Alzheimer’s disease display impairment in glucose metabolism.”

Some researchers go so far as to refer to Alzheimer’s as “type 3 diabetes” because of the biochemical similarities of the two conditions.3 Impaired insulin signaling affects the expression and metabolism of Aβ-induced tangles in the brain. The same enzyme that breaks down Aβ also breaks down insulin; if the enzyme is being used to break down elevated insulin levels, less is available to break down Aβ. The intimate connection between glucose metabolism and cognitive function has resulted in the term “metabolic-cognitive syndrome,” referring to patients with metabolic syndrome plus cognitive impairment.4

Cardiovascular Disease Connection
Several risk factors for cardiovascular disease, such as elevated blood pressure, increased concentrations of homocysteine and cholesterol, and being overweight also are risk factors for cognitive impairment. Homocysteine may promote the generation of Aβ plaques and increase oxidative stress in the brain.5,6 People with hyperhomocysteinemia have more than twice the risk of developing Alzheimer’s disease than those with lower levels.7 Atherosclerosis, which is potentially reversible, results in decreased circulation to the brain (chronic brain hypoperfusion) and can contribute to neurodegeneration.8

While high blood pressure is a risk factor for neurodegeneration, blood pressure that’s too low may result in hypoperfusion and accelerated brain aging as well. In fact, Vreeland suggests that the slightly elevated blood pressure that typically occurs with age may be a beneficial compensatory action, allowing circulation to reach the deep recesses of the brain. Lowering blood pressure in an effort to help the heart, he says, may actually be harming the brain. If blood pressure is low, Vreeland suggests a reevaluation of a patient’s medications that affect blood pressure.

A recent review in the Journal of Alzheimer’s Disease concluded that obesity and overweight, which are recognized as risk factors for cardiovascular disease, also are associated with lower cognitive performance, cognitive decline, cognitive deficit, and dementia.

Role of Physical Activity
Studies show an inverse relationship between physical activity and Alzheimer’s disease. Regular physical activity may indirectly protect against Alzheimer’s and dementia by reducing the risk of cardiovascular and cerebrovascular disease and diabetes, and directly protect against Alzheimer’s and dementia by increasing fuel delivery (oxygen and glucose) to the brain and stimulating the development of synapses and neuronal growth and survival.9-11

Supplements and Lifestyle Changes
“There are a lot of studies supporting the beneficial effects of the Mediterranean diet on prevention of cognitive decline,” Frisardi says. The associations reflect a lifetime of exposure to both the Mediterranean diet and other healthful behaviors, she explains. “However, changes in dietary preferences toward a Mediterranean-style diet in late life could slow the physiological processes of neurodegeneration, reinforce the immune system, and allow for a more rapid recovery from inflammatory diseases.”

Vreeland also suggests focusing on a low-glycemic-index diet to prevent elevated blood sugar levels and insulin resistance from developing.

A diet rich in vitamins E and C also may help prevent oxidative damage to neurons. One study found that vitamin E and vitamin C supplements taken together reduced the risk of Alzheimer’s disease by 78%.12 Omega-3s and vitamin D also may have protective effects due to their anti-inflammatory properties. Some studies have found that anti-inflammatory drugs may lower the risk of developing Alzheimer’s disease, but treating Alzheimer’s disease patients with anti-inflammatory drugs hasn’t been shown to improve symptoms or slow the disease’s progression. Two related factors consistently associated with a reduced risk of a decline in cognitive function are obesity prevention and weight loss and regular physical activity.

It’s best to recommend that patients begin taking preventive measures as early in life as possible. While early dietary intervention and lifestyle changes are the best approach for maintaining optimum cognitive function with age, changes in diet, physical activity, and possibly medications later in life may help reduce inflammation, prevent further oxidative damage, and improve circulation within the brain.

— Densie Webb, PhD, RD, is a freelance writer, editor, and industry consultant based in Austin, Texas.

 

References
1. Kumar GP, Khanum F. Neuroprotective potential of phytochemicals. Pharmacogn Rev. 2012;6(12):81-90.

2. Barnes DE, Yaffe K. The projected effect of risk factor reduction on Alzheimer’s disease prevalence. Lancet Neurol. 2011;10(9):819-828.

3. Akter K, Lanza EA, Martin SA, Myronyuk N, Rua M, Raffa RB. Diabetes mellitus and Alzheimer’s disease: shared pathology and treatment? Br J Pharmcol. 2011;71(3):365-376.

4. Panza F, Solfrizzi V, Logroscino G, et al. Current epidemiological approaches to the metabolic-cognitive syndrome. J Alzheimers Dis. 2012;30 Suppl 2:S31-S75.

5. Kruman II, Kumaravel TS, Lohani A, et al. Folic acid deficiency and homocysteine impair DNA repair in hippocampal neurons and sensitize them to amyloid toxicity in experimental models of Alzheimer’s disease. J Neurosci. 2002;22(5):1752-1762.

6. Selley ML. Increased homocysteine and decreased adenosine formation in Alzheimer’s disease. Neurol Res. 2004;26(5):554-557.

7. Van Dam F, Van Gool WA. Hyperhomocysteinemia and Alzheimer’s disease: a systematic review. Arch Gerontol Geriatr. 2009;48(3):425-430.

8. de le Torre JC. How do heart disease and stroke become risk factors for Alzheimer’s disease? Neurol Res. 2006;28(6):637-644.

9. Sigal RJ, Kenny GP, Wasserman DH, Castaneda-Sceppa C, White RD. Physical activity/exercise and type 2 diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(6):1433-1438.

10. Colcombe SJ, Kramer AF, McAuley E, Erickson KI, Scalf P. Neurocognitive aging and cardiovascular fitness: recent findings and future directions. J Mol Neurosci. 2004;24(1):9-14.

11. Mattson MP. Glutamate and neurotrophic factors in neuronal plasticity and disease. Ann NY Acad Sci. 2008;1144:97-112.

12. Zandi PP, Anthony JC, Khachaturian AS, et al. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study. Arch Neurol. 2004;61(1):82-88.

 

 


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