Alzheimer disease (AD) is a chronic neurodegenerative disorder and is one of the most common causes of dementia.1 It is characterized by progressive cognitive impairment, affecting memory, language, and visuospatial abilities.2 AD is a complex disease that has a long preclinical phase of several decades, similar to type 2 diabetes, heart disease, and other chronic conditions. As with other chronic diseases, the most recognized risk factor is an increase in age; however, impaired vascular health has been shown to be another major factor for cognitive decline, and interventions that decrease cardiovascular risk factors may improve cognitive health. Other considerations include lifestyle-related risk factors such as metabolic syndrome, obesity, diabetes, poor dietary habits, and mental and physical inactivity.
The manifestation of dementia usually occurs in people older than 65 years, concomitantly with other age-related health problems.3 The incidence of comorbidity with dementia is due to the fact that certain chronic disease states, such as hypertension and diabetes, actually increase the risk of vascular dementia and AD. Furthermore, an individual with multiple health conditions is known to experience additional physiological stress, which negatively affects resilience and repair, resulting in the increased risk of developing dementia.3,4
NEUROPATHOLOGY
The neuropathology of AD is characterized by neuronal loss and the progressive accumulation of extracellular amyloid [beta]-peptide (A[beta]) containing plaques and intracellular neurofibrillary tangles in the brain.5 Chronic inflammation and oxidative stress in the brain are also important factors in the pathophysiology of AD and result in neuronal dysfunction and death.6
Individuals with AD exhibit impaired glucose utilization in the brain, as evidenced by a consistent pattern of reduced cerebral metabolic rate of glucose in the hippocampus and prefrontal regions of the brain.5 This region-specific decline in brain glucose metabolism in AD has become a potential target for therapeutic intervention and has resulted in studies that have assessed the supplementation of ketone bodies, which are produced by the body during glucose deprivation and can be metabolized by the brain as a source of energy when blood glucose is impaired. The administration of ketone bodies or high-fat ketogenic food sources has the potential to augment a deficiency of glucose, the main energy substrate for the brain.
COCONUT OIL
Coconut, Cocos nucifera L. (Fam: Arecaceae) is a member of the palm tree family and is often referred to as "the tree of life." Although the tree is cultivated for providing numerous products, it is primarily grown for its medicinal and nutritional properties and is categorized as a highly nutritious "functional food."
Coconut oil is extracted by a hot- or cold-pressed technique from the coconut fruit, which is botanically classified as a "drupe." Coconut oil is recognized for containing high levels of medium-chain triglycerides, which are absorbed and metabolized through medium-chain fatty acids by the liver into ketone bodies. The ketone bodies serve as a potent alternative energy source for the brain and may be beneficial for those individuals developing or already experiencing memory impairment as in AD.7 In addition, recent studies have suggested that the use of coconut oil (extra virgin) may have significant positive effects on blood pressure, lowering of cholesterol levels, and regulation of blood glucose levels, which are risk factors for developing AD. The use of extra virgin coconut oil to prevent or treat AD holds promise and merits further research supported by large cohort clinical trials.
AUTHOR COMMENT
Current evidence supports the recognition that neurotransmitter balance, dietary and lifestyle habits, nutritional status, and metabolic mechanisms, which include inflammation, microbiota imbalance, oxidative stress, and impaired mitochondrial function, are important variables that affect brain function. Central to the focus of this article is the accumulated clinical research that points to nutritional status as an important modifiable factor associated with cognitive health and functional decline leading to cognitive impairment and dementia.
Cognitive impairment and dementia are not an inevitable consequence of the aging process. Implementation of preventable health care strategies that include evidence-based dietary plans can greatly reduce the incidence and delay of cognitive decline.
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