Neurons and Exercise

Neurons and Exercise

Monday, January 30, 2017

Benefits and Alternatives to Dietary Coconut Oil

My sister asked if I would recommend taking coconut oil in order to improve cognition for Alzheimer’s patients.  This question resulted in some research that found benefits and negative aspects of, and alternatives for ingesting coconut oil on a regular basis. Here is the short list of coconut oil benefits for the body:

·        Coconut oil is an alternative energy source for sugars and long chain fatty acids

·        Coconut oil can be converted to energy even in the presence of neurotoxic aluminum

·        Coconut oil promotes the generation of new mitochondria, called mitochondrial biogenesis1

Negative Aspects of Dietary Coconut Oil

There are several problems with ingesting large amounts of coconut oil regularly:

·        Lauric acid, comprising 50% of coconut oil, increases LDL by 16% in humans and LDL is linked to vascular disease, such as stroke and heart attack3

·        Coconut oil is a mixture of medium chain fatty acids as triglycerides

·        Coconut oil does not contain essential fatty acids (e.g. linoleic and alpha-linolenic acid)

·        Dietary coconut oil does not result in weight loss2

Better Alternatives to Dietary Coconut Oil

There are supplements that have the same benefits as dietary coconut oil and will result in better sugar and stored fat utilization.  These supplements are:

·        Dissolved silica (a.k.a. OSA) for lowering your body-burden of aluminum4-6

·        CoQ10 for improving your energy and cognition7

·        PQQ for increasing mitochondrial biogenesis and cognition7-9


There are also supplements that will lower LDL and triglycerides, both of which are linked to an increased risk of vascular disease, such as stroke and heart attack:


·        PA for reducing triglycerides by 15% and LDL by 8%10

·        EPA for reducing triglycerides by 5 to 10%11

·        Vitamin D for reducing triglycerides by 23%12

By lowering aluminum levels in your body, glycolysis and fat metabolism will return to normal.  This coupled with new mitochondria will allow you to metabolize or “burn” stored fat resulting in dieting with weight loss. Lowering triglycerides and LDL decreases the risk of vascular disease, heart attack, and stroke. 

Biochemistry of the Coconut Oil Diet

Since the Bayer and Hall processes for aluminum purification from bauxite were developed in 1888, there has been a steady increase in the amount of aluminum humans ingest. This aluminum upsets how our mitochondria produce energy from sugar and fat. Mitochondria are the organelles that produce energy in your body and they can be trained in one of two ways to utilize coconut oil for energy production:

·        Daily ingestion of coconut oil

·        Daily ingestion of aluminum

It may take several weeks before mitochondria become optimally adapted to metabolizing coconut oil for energy.  However, if you have been ingesting aluminum on a regular basis, your mitochondria may already be adapted.  Aluminum, at levels found in drinking water (108ppb), inhibits the first step in sugar metabolism (i.e. glycolysis) 13.  The biochemical response to the inhibition of glycolysis is the conversion of sugar to fat as triglycerides comprised of long chain fatty acids14.  Therefore your stored fat may be due to a combination of the sugar and aluminum you ingest.

Fat can be stored as adipose tissue or metabolized for energy.  However, aluminum also inhibits the production of L-carnitine required for movement of long chain fatty acids in stored fat to the mitochondria for conversion to energy15-19.  Therefore aluminum inhibits the production of energy from stored fat making fat loss impossible.  

Aluminum ingestion upsets both sugar and fat metabolism resulting in a lack of energy and cognition, vascular disease, along with obesity that does not respond to dieting15,19.

The good news is that although aluminum inhibits the production of energy from long chain fatty acids, it does not inhibit energy production from medium chain fatty acids, such as coconut oil20. Not surprisingly the cognition of some Alzheimer’s patients is improved within 90 minutes of ingesting 2 to 3 tablespoons of coconut oil mixed with whipped cream to make it more palliative21. Because of accumulated aluminum inhibiting glycolysis13, the mitochondria of Alzheimer’s patients have already adapted from sugar to dietary fat. Their improvement in cognition by ingesting coconut oil is quick but lasts only as long it takes to metabolize the dietary coconut oil. Therefore a steady diet of coconut oil is required for chronic improvement.

There are better solutions for improved cognition of AD patients, such as lowering aluminum ingestion and increasing aluminum excretion with silica water (i.e. Fiji Water or Silicade – See my book “Prevent Alzheimer’s, Autism, and Stroke”)4-6.  This will restore sugar and fat metabolism to normal. Also taking a daily supplement of the natural cofactors PQQ and CoQ10 will improve energy and cognition7-9.



1. Balietti, M., et al.; A ketogenic diet increases succinic dehydrogenase (SDH) activity and recovers age-related decrease in numeric density of SDH-positive mitochondria in cerebellar Purkinje cells of late-adult rats; Micron; 41(2):143-48 (2010)

2. Johnston, C.S., et al.; Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets; Am. J. Clin. Nutr.; 83:1055-61 (2006)

3. Tsai, Y.H., et al.; Mechanisms mediating lipoprotein responses to diets with medium chain triglyceride and lauric acid; Lipids; Sep.; 34(9):895-905 (1999)

4. Edwardson, J.A., et al.; Effect of silicon on gastrointestinal absorption of aluminum; The Lancet; 342(8865):211-12 (1993)

5. Carlisle, E.M., and Curran, M.J.; Effect of dietary silicon and aluminum on silicon and aluminum levels in rat brain; Alzheimer Dis. Assoc. Disord.; 1(2):423-30 (2013)

6. Davenward, S,, et al.; Silicon-rich mineral water as a non-invasive test of the 'aluminum hypothesis' in Alzheimers disease; J. Alzheimer's Dis.; 33(2):423-30 (2013)

7. Nakani, M., et al.; Effect of pyrroloquinoline quinone (PQQ) on mental status of middle-aged and elderly persons; Food Style; 21 13(7):50-3 (2009)

8. Chowanadisai, W., et al.; Pyrroloquinoline quinone stimulates mitochondrial biogenesis through cAMP response element-binding protein phosphorylation and increased PGC-1 alpha expression; J. Biol. Chem.; Jan.; 285(1):142-52 (2010)

9. Onyango, I.G., et al.; Regulation of neuron mitochondrial biogenesis and relevance to brain heath; Biochim Biophys Acta; jan.; 1802(1):228-34 (2010)

10. Bernstein, A.M., et al.; Purified palmitoleic acid for the reduction of high-sensitivity C-reactive protein and serum lipids: a double blinded, placebo controlled study; J.Clin. Lipidol.; 8(6):612-7 (2014)

11. Harris, W.S.; n-3 Fatty acids and serum lipoproteins: human studies; A. J. Clin. Nutr.; 65(suppl.):1645S-54S (1997)

12. Rejnmark, L., et al.; Simvastatin does not affect vitamin D status, but low vitamin D levels are associated with dyslipidemia; Results from a randomized, contolled trial: Internat. J. Endrocrin.; Article ID 957174 (2010)

13. Lai, J.C., and Blass, J.P.; Inhibition of brain glycolysis by aluminum; J. Neurochem.; Feb.; 42(2):438-46 (1984)

14. Mailloux, R.J., et al.; Hepatic response to aluminum toxicity: Dsylipidemia and liver diseases; Exper. Cell Res.; 317:2231-2238 (2011)

15. Gaballa, I.F., et al.; Dyslipidemia and disruption of L-carnitine in aluminum exposed workers; Egyptian J. Occup. Med.; 37(1):33-46 (2013)

16. Lemire, J., et al.; The disruption of L-carnitine metabolism by aluminum toxicity and oxidative stress promotes dyslipemia in human astrocytes and hepatic cells; Toxicol. Lett.; Jun.; 203(3):219-26 (2011)

17. Waly, M. I-A., et al.; Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal; Mol. Psychiatry; 9:358-70 (2004)

18. Waly, M. I-A., and Deth, R.; Neurodevelopmental toxins deplete glutathione and inhibit folate and vitamin B12-dependent methionine synthase activity – a link between oxidative stress and autism, FASEB J.; 22:894 1 (2008)

19. Fritz, I.B., Kaplan, E., Yue, K.T.; Specificity of carnitine action on fatty acid oxidation by heart muscle; Am. J. Physiol.; Jan.; 202:117-21 (1962)

20. Heo, K.N., et al.; Medium-chain fatty acids but not L-carnitine accelerate the kinetics of [14C]triacylglycerol utilization by colostrum-deprived newborn pigs; J. Nutr.; 132:1989-1994 (2002)

21. Reger, M.A., et al.; Effects of beta-hydroxybutyrate on cognition in memory-impaired adults; Neurobiol. Aging; Mar.; 25(3):311-4 (2004)