Whole food protection from age-related cognitive and neurodegenerative disorders - Medicinal Properties in Whole Foods

Townsend Letter for Doctors and Patients,  July, 2002  by Gina L. Nick

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"Functional foods," "nutraceuticals," "designer foods" and "medicinal foods" are terms that describe foods, and key ingredients isolated from foods, that have non-nutritive or tertiary functional properties. Researchers, healthcare practitioners, laypersons, and the popular media use these words interchangeably. The purpose of this article is to detail valid scientific information available on whole food neuroprotectants that may augment the age-associated risks of cognitive decline and Alzheimer's disease.

All age-related cognitive and neurodegenerative disorders are associated with mild to severe behavioral impairments that notably decrease quality of life (Hauser and Zesiewicz, 1996). Free radicals and the oxidative stress they generate offer one theory for the connection between age and the onset of neurdegenerative disorders and cognitive decline. While this hypothesis has been utilized extensively to explain the onset, progression, and increased incidence of heart disease and cancer (Rimm et al., 1996; Halliwell et al., 1995; Gey, 1993; Eastwood, 1999), it is likely to be most applicable to neurodegenerative disorders, because the brain is more vulnerable to oxidative stress. It utilizes very high amounts of oxygen while exhibiting reduced free radical scavenging capabilities over time (Ames et al., 1993; Benzi and Moretti, 1995; Cadet and Brannok, 1998; Halder and Bhaduri, 1998). Accordingly, diseases such as diabetes mellitus, hypertension, ischemic heart disease, and hyperlipidemia, all known to increas e the level of oxidative stress in the body, are associated with an increased risk for cognitive disorders (Meyer et al., 1988; Ihara et al., 1997; Bowling and Beal, 1995; Benzi and Moretti, 1995; Smith et al., 1997).

The increased recognition of the role that oxidative stress plays in the onset and progression of neurodegeneration has undoubtedly influenced the number of researchers studying the effects of antioxidant vitamins in altering or forestalling these neurodegenerative changes.

Experiments examining the effects of diets rich in select herbs, fruits, and vegetables on disease highly suggest that known (antioxidant) and unknown compounds within whole foods play a significant role in preventing cognitive decline over time (Ferro-Luzi and Branca, 1995; Goodwin and Brodwick, 1995; Martin et al., 2000; Joseph et al., 1995; Stoll et al., 1996; Halder and Bhaduri, 1998).

Oxidative Stress and Neurodegeneration

Neurons are extremely sensitive to free radical attacks, particularly as one ages. Hence, oxidative stress, which reportedly increases with age, offers one explanation for the inherent heterogeneity (multiple possible neurological and biochemical characteristics) of the disease. Christen (2000) explains that the brains of AD and other neurodegenerative disorder patients contain lesions typical of free radical damage including:

* DNA damage

* Protein oxidation

* Lipid peroxidation, and

* Advanced glycosylation end products.

In addition, there is a possible role for metal ions (iron, copper, zinc, and aluminum) in the generation of free radicals. Beta-amyloid aggregates found in the neurons of AD patients form free radicals in the presence of existing free radicals, leading to a cascade of damage. This beta-amyloid toxicity is reduced or eliminated by free radical scavengers including vitamin E, selegiline, and Ginkgo biloba, as well as desferrioxamine, an iron-chelating agent (Pappolla et al., 1997; Bruce et al., 1996; Bastianetto et al., 1998). Additionally, mitochondrial anomalies associated with AD may also contribute to the free radical cascade.

Free Radical Attack on Neurons

It has been estimated that free radicals may modify approximately 10,000 DNA base pairs every day (Ames et al., 1999). Neurons are particularly vulnerable to free radical attack because:

* They have a low glutathione content

* Their membranes are rich in vulnerable polyunsaturated fatty acids, increasing lipid peroxidation activity

* Brain metabolism consumes a great deal of oxygen, and

* Neurons are post-mitotic (do not divide), limiting their ability to repair chromosomal damage

The free radical hypothesis for the neurodegeneration evident in AD is supported by the fact that AD is an age-related disease and damage from reactive oxygen species is known to accumulate with age. Brain trauma can also result in free radical release and is a known cause for AD and dementia.

Metals and Alzheimer's

Metals play a major role in the production of free radicals. Particular attention is focused on iron, aluminum, mercury, copper, and zinc, which all catalyze the generation of free radicals under certain circumstances. Observations by many researchers provide evidence for the connection between iron and the onset and progression of AD. The concentration of reactive iron, capable of generating hydroxyl radicals, is elevated in the brains of Alzheimer's patients. Further, iron, transferrin, and ferritin are found in the brains of AD patients with a similar distribution pattern to senile plaques and neurofibrillary tangles (Smith et al., 1997).