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.
References
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)
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Regulation of neuron mitochondrial biogenesis and relevance to brain heath;
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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)
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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)
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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;
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