Alzheimer's disease (AD) is currently the 6th leading cause of death in America according to the CDC. It affects over 5 million Americans and 50 percent of nursing home residents (2014), and is projected to spike to 16 million by 2050. It is considered an irreversible, progressive brain disorder that negatively affects thinking skills, memory, and language.

Researchers refer to a host of risk/environmental/biological factors leading to Alzheimer's including:

• Genetics
• Obesity/lack of exercise
• High blood pressure
• Exposure to heavy metals such as mercury and aluminum
• Reduced synthesis of acetylcholine
• Mitochondrial dysfunction and cellular energy production
• Increased oxidative stress
• Low-fat diets
• Extracellular amyloid deposits
• Man-made electromag-netic field exposure
• Tao protein abnormalities
• Smoking
• Impaired blood-brain barrier function
• Drugs such as statins and benzodiazepines
• Systemic inflammation

Alzheimer's will reach epidemic proportions unless we do something about it.

Pharmacologic Approaches (That Aren't Working)

In early 2012, Pfizer and Medivation announced that their new Alzheimer's drug, dimebon, was not only a complete failure, but also made patients worse in their trial. Statins were proposed to slow down the progression of Alzheimer's, but were found to have no effect on prevention or improving the course of the disease, and even had the reverse effect.

The Alzheimer's Association refers to five FDA certified drugs (three of which are cholinesterase inhibitors) for the treatment of symptoms associated with dementia. They dampen any excitement about these drugs with the following caveat:

"Cholinesterase inhibitors can't reverse Alzheimer's and won't stop the underlying destruction of nerve cells. Consequently, their ability to improve symptoms eventually declines as brain cell damage progresses."

Cholesterol is critical to our brain function, comprising 25 percent of its total mass. Cholesterol is used as an antioxidant, electrical insulator, functional component for all membranes, and a structural scaffold for the neural network in our brains.

Sadly, one in four Americans over age 55 are taking statin drugs, stripping their brains of the much-needed cholesterol and increasing their risk of diabetes by close to 50 percent.

Researchers reported in the British Medical Journal that taking benzodiazepines (prescribed for anxiety and insomnia) for three months or more was associated with a 51 percent increased risk of Alzheimer's disease. People under the care of assisted-living communities are on an average of 30 medications each. It's a wonder they have any brain function at all.

Alzheimer's: Type 3 Diabetes?

Researcher's began calling Alzheimer's "Type 3 diabetes" in the early 2000s, describing insulin resistance of the brain as a neuroendocrine disorder. Around that time, a Brown University neuropathologist, Suzanne de la Monte, blocked the path of insulin to rats' brains, damaging their neurons. Following the insulin, their brains showed classic signs of Alzheimer's.

Doctor de la Monte realized that insulin resistance can be connected with "target organs" and not others, which is why there isn't a direct correlation with type 2 diabetes and AD. However, there are cross-sectional and prospective associations between type 2 diabetes and moderate cognitive impairment, memory and executive functions, including vascular dementia. The bottom line is that diabetes doesn't "cause" Alzheimer's – environment, diet and lifestyle does.

Coconut Oil to the Rescue

Cold-processed organic virgin coconut oil is rich in short- and medium-chain fatty acids (MCFA). The length of the chain refers to the number of carbon atoms in the molecule, and shorter chain length allows fatty acids to be metabolized without extra energy (of the carnitine transport system). Long-chain fatty acids are more difficult to break down and are predominantly stored as fat.

In the 1960s, researchers vilified saturated fats, suggesting they were the cause of heart disease and stroke. Recent research demonstrates that diets high in processed and high-glycemic index foods cause systemic inflammation, leading to cardiovascular disease.

Unsaturated fats typically will go rancid in a matter of hours, even in the refrigerator. Coconut, on the other hand, is stable and can be stored at room temperature for over two years. Furthermore, Pacific islanders, who get 30-60 percent of their calories from coconut oil, have virtually no cardiovascular disease. Trans fats and hydrogenated oils (found in processed food) have spiked obesity and heart disease in America.

Coconut oil is known for a multitude of health-promoting and disease-fighting effects, such as:

• Killing viruses, bacteria, fungi, and yeasts
• Providing a nutritional source of quick energy
• Improving digestion and absorption of other nutrients
• Improving insulin secretion and utilization of blood glucose
• Reducing inflammation

How Coconut Oil Heals the Brain

Scientists have identified that insulin-resistant brain cells can trigger a cascade leading to AD. Positive Emission Tomography (PET) scans of the brains of Alzheimer's patients' brains show a disruption of the insulin signaling mechanism. Medium-chain fatty acids can act as a non-carbohydrate fuel source by enhancing the formation of ketone bodies (usually produced when you burn fat). Fatty acids can't pass the blood-brain barrier, but ketones can, directly feeding brain cells by bypassing the glucose pathway.

Over 98 percent of all small-molecule drugs and 100 percent of large-molecule drugs or genes cannot cross the blood-brain barrier.

Ketogenic diets are one of the most effective approaches to treat drug-resistant epilepsy, although the mechanism is poorly understood. Furthermore, coconut oil contains a high percentage of phenolic acids (also known as polyphenols) that are known to be powerful antioxidants. Phenolic compounds are known to inhibit the aggregation of amyloid-b peptide, a common pathology of AD. Lauric and capric acids found in coconut oil are believed to be involved in reducing insulin resistance and increasing HDL cholesterol levels.

Alzheimer's and Coconut Oil from a TCM Standpoint

Dementia in Chinese medicine has a number of differential diagnoses:

• Spleen qi deficiency, with phlegm and stagnating blood obstructing the orifices to the brain
• Liver qi stagnation, with entanglement of qi, accumulation of phlegm, and blood stagnation
• Hot phlegm clogging the orifices
• Spleen and kidney yang deficiency, with phlegm and stagnating blood obstructing the orifices to the brain
• Deficiency of liver and kidney yin, with phlegm and stagnating blood obstructing the orifices and with generation of internal wind
• Qi and blood stagnation, obstructing the orifices to the brain

We can approach this syndrome using herbs to disperse qi and blood, tonify qi, yin and/or yang, or resolve phlegm accumulation. Huperzine A is an appropriate herb to treat AD, with solid science to back it up, along with common tonic herbs for brain support such as ginseng, astragalus, atractylodes, dioscorea, rehmannia, lycium fruit, cistanche, and morinda. Coconut oil has the properties of lubrication and can be used as a yin tonic. In classical Chinese medicine, it's considered an Earth (Sp/St) element. It can handle the high temperatures of cooking, but the most effective therapeutic approach is to take it by the tablespoon at room temperature. Studies have recommended a daily intake of three to five tablespoons for a 160-pound man.

Pacific islanders hail coconut oil as being the cure for all illnesses, and have been using it in their traditional medicines for centuries. Try taking coconut oil yourself for a few weeks, and then recommend it to all of your Alzheimer's patients and any others complaining of memory issues.

References

1. Craft S, Cholerton B, Baker L. "Insulin and Alzheimer's disease: untangling the web." Journal of Alzheimer's Disease, 2013; 33(Suppl. 1), S263–S275.
2. de la Monte SM, Wands JR. "Review of insulin and insulin-like growth factor expression, signaling, and malfunction in the central nervous system: relevance to Alzheimer's disease." Journal of Alzheimer's Disease, 2005; 7(1):45–61.
3. de la Monte SM, Wands JR. "Molecular indices of oxidative stress and mitochondrial dysfunction occur early and often progress with severity of Alzheimer's disease." Journal of Alzheimer's Disease, 2006; 9(2):167–181.
4. de la Monte SM, Wands JR. "Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed." Journal of Diabetes Science and Technology, 2008; 2(6):1101-1113.
5. de la Monte SM, Tong, M. "Brain metabolic dysfunction at the core of Alzheimer's disease." Biochem Pharmacol, 2014; 88:548–559.
6. DeDea L. "Can coconut oil replace caprylidene for Alzheimer disease?" Journal of the American Academy of Physician Assistants, 2012; 25:19.
7. Fernando WM, Martins IJ, Goozee KG, Brennan CS, Jayasena V, Martins RN. "The role of dietary coconut for the prevention and treatment of Alzheimer's disease: potential mechanisms of action." British Journal of Nutrition, 2015 Jul 14;114(1):1-4.
8. Gillette-Guyonnet S, Secher M, Vellas, B. "Nutrition and neurodegeneration: epidemiological evidence and challenges for future research." British Journal of Clinical Pharmacology, 2013; 75:738–755.
9. Kashiwaya Y, Bergman C, Lee JH, et al. "A ketone ester diet exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and tau pathologies in a mouse model of Alzheimer's disease." Neurobiology of Aging, 2013; 34:1530–1539.
10. Kaunitz H, Dayrit C. "Coconut oil consumption and coronary heart disease." Philppine Journal of Internal Medicine, 1992; 30:165-171.
11. Kumar PD. "The role of coconut and coconut iol in coronary heart disease in Kerala, South India." Tropical Doctor, 1997; 27:215-217.
12. Reger MA, Henderson ST, Hale C, et al. "Effects of beta-hydroxybutyrate on cognition in memory-impaired adults." Neurobiology of Aging, 2004, 25:311–314.
13. Seneff S, et al. "Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet." European Journal of Internal Medicine, 2011.
14. Steen E, Terry BM, Rivera EJ, et al. "Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease—is this type 3 diabetes?" Journal of Alzheimer's Disease, 2005;7(1):63–80.
15. Swaminathan A, Jicha GA. "Nutrition and prevention of Alzheimer's dementia." Frontiers in Aging Neuroscience, 2014 Oct 20;6:282.
16. Yang G, Wang Y, Tian J, Liu J. "Huperzine A for Alzheimer's disease: a systematic review and meta-analysis of randomized clinical trials." PLoS ONE, 2013 Sept 23;8:e74916. doi: 10.1371/journal.pone.0074916

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