I’ve kept an open mind on the question of coconut oil as a remedy for Alzheimer’s disease. It’s partly because I know about the ketogenic diet for children with epilepsy that doesn’t respond to drugs. Like coconut oil, the diet is high in fats called medium chain triglycerides,which are metabolized into chemicals called keytones, which the brain can use as fuel when there’s a problem with the glucose supply or the ability to use it. I’m not open-minded about journalists and influential bloggers who dismiss or deride the possibility that coconut oil is effective against Alzheimer’s because they don’t understand the hypothetical mechanism. Writing it off with a statement like there’s no evidence to support it” is meant to kill curiosity. But for every cat that curiosity kills, there’s a chance that a life can be improved b the fruits of curiosity about something for which there is currently no evidence.

The experts can pick the present study apart. It was a small sample, there were a lot of outcome measures, and one of the results might be due to regression to the mean. They can say that and more, and say this is a weak study. Without alleging outright fraud on the part of the authors, they can no longer say there’s no evidence the coconut oil, not much, and in not much time, can improve cognition impaired by  Alzheimers disease

Contents of this Post

1 A link to the study. as published. It’s a PDF and it’s in Spanish. I translated a tiny bit (in colored ink, in the margins). You should be able to make sense of the tables if you know Latin roots, Latin, or a romance language.
Link opens in a new window:
• 2 The cognitive test they used in the study. (They used a Spanish-language version.)
Link opens in a new window:
3  The study, as translated by the authors (the abstract), Google translate (the rest), and me (limited editing of Google’s work product).
Background: Alzheimer’s dementia is the most prevalent of the age-related dementias nowadays. As for treatment, there is no definitive cure, thus new therapies are needed. In this regard the medium chain triglycerides are a direct source of cellular energy and can be a nonpharmacological alternative to neuronal death for lack of cellular energy that occurs in Alzheimer patients.
Objective: to evaluate the impact of coconut oil in the development of Alzheimer’s dementia, in any degree of dementia. Also determine whether this improvement influences within variables such as sex and suffering or not Type II Diabetes Mellitus.
Material and methods: a prospective study was conducted in patients with Alzheimer’s dementia, with a control and an intervention group which was administered 40 ml/day of extra virgin coconut oil. The parameters evaluated were the mini test scores Lobo cognitive test, pre and post intervention in both groups.
Results: it was observed in subjects taking the product, a statistically significant increase in test score MECWOLF and therefore an improvement in cognitive status, improving especially women’s, those without diabetes mellitus type II, and severe patients.
Conclusion: this study, although preliminary, demonstrated the positive influence of coconut oil at the cognitive level of patients with Alzheimer’s, this improvement being dependent on sex, presence or absence of diabetes and degree of dementia.
(Nutr Hosp. 2015;32:2822-2827) DOI:10.3305/nh.2015.32.6.9707
Keywords: Alzheimer’s disease. Triglycerides. Coconut
AFA: Association of relatives and friends of Alzheimer’s.
DM II: Type 2 diabetes mellitus.
DTA: Alzheimer-type dementia.
AD: Alzheimer’s disease.
MEC: Mini-Mental State Examination.
WHO: World Health Organization.
Life expectancy has increased by leaps and bounds in the last century, which is causing problems social and health hitherto unknown by the growth in the elderly population. From Indeed, forecasts suggest that 50% of which now they are young they reach age 90, and of them between 40 and 60% suffer some kind of deficiency cognitive (DC), so there will be more demented in the population of which has never been if not find solutions to prevent or slow down your evolución (1,2).Within dementias disease highlights Alzheimer’s disease (AD) as the most prevalent, and it is representing between 60% and 70% of total cases (3), And clearly it is the most common in the elderly more than 80 years (4).
In Alzheimer’s can be set different stages, assuming overall there are three stages such as: mild, moderate and severe, They are ranging from silent appearance of the first symptoms to a very marked damage, which generates a point of no return for cognitive (5, 6) functions. It is a disease with no cure, multifactorial and multicausal, where the main risk factor aging is that coexists with many others such as vascular risk, hipertensión (7), Disorder-level lipid metabolism presence, hypercholesterolemia and Type II Diabetes Mellitus(NIDDM), tobacco addiction (8), and poor diet rich in fat and omega 3 (9).As for the etiology, the first theory that handled is the lack of the neurotransmitter acetilcolina (10,11), genética (12-14) with the cause, but now the accepted as the most prevalent is related to plates accumulation amyloid beta proteins (Amioide Aß) and tau protein in the patient’s brain as described in the early 15th century on (16).
Another alternative which is gaining currency is disorders at the metabolic level, especially those related with the insulin resistance in the brain, and it has been seen that there are receptors of this hormone level hippocampal especially that when activated by insulin allow use glucose by neurons, and it also appears that a series of enzymes that have an effect activated related detoxifying toxic action of amyloid plaques, which has been observed only in animal models(17).Therefore a therapeutic option could be metabolic processes through contribution to the diet of a food or nutrient, that counteracts neuronal death improving the patient at any stage of the disease, through providing alternative energy to glucose.
In this context ketone bodies which are produced from Medium Chain Triglycerides (MCT) They constitute an alternative source of energy to the lack of glucose for células (18,19).Coconut oil possibly has the greatest amount of food-derived MCTs. This oil contributes to the diet a high amount of these acids, since in its composition almost 90% are saturated fats highlighting among these which they are medium chain. Of these, approximately 45% is lauric acid and palmitic followed by myristic stearic and. Oleic acid is present with valueslower than 6% (20).
Thus, this study aims to assess the impact which has coconut oil in the evolution of AD. Also, if this improvement influences the degree dementia, and the variables of sex, and whether or not NIDDM is present.A prospective, longitudinal study was conducted, mixed, analytical and experimental. The period covered 21 days between the months of March and April 2015. Inclusion criteria were Alzheimer’s patients between 65 and 85 years, institutionalized in specialized Alzheimer centers located in the regions of the Bank and the Tavernes Valldigna (Valencia).As for exclusion, criteria were patients with an age younger than 65 or older than 85 years, noninstitutionalized, existence of other diagnosed pathologies that cause cognitive impairment, aversion to coconut product, and disability for a verbal response and therefore to be evaluated by the test.Patients included were divided into two groups, the control group, consisting of untreated patients, and the cases group, consisting of patients who underwent the intervention. In both groups the same characteristics in terms of number of NIDDM, degree of dementia, mean age, sex and other medication were present.The intervention consisted of administration coconut oil, in the patients group cases, for 21 consecutive days. Coconut oil extra virgin used in the study is comprised of lot of fatty acids of medium chain lauric, caprylic and capric, at 52% (m / m), 9% (m / m) and 7% (m / m) respectively. each boat containing 1 liter of extra virgin coconut oil, adminis Before the start of the intervention, it is individually evaluated cognitive impairment of all patients through a test of cognitive assessment, Mini-Examination (MMSE), which is a translation Spanish validated the MMSE test Folstein (MMSE) (21).

The evaluation was conducted by staff schooled, with the patient in the sitting position and relaxed, in a quiet place enable a table to write and draw. After the intervention, again made an assessment of cognitive impairment, by the same process described above for determining previous administration, the same time and with the same examiner strip for each patient.

Statistical data processing
The analysis of data obtained from the study consisted in a hypothesis test where he assessed the differences found before and after the intervention, through the Microsoft Excel spreadsheet program and EPIDAT vs.4.1. Out of a population of 458 patients, 44 have met the criteria for the study: 22 cases and 22 controls. It was assumed the same deviation typical in the two populations; the difference was used obtaining a standardized mean δ = 0.632 which It is within the range of oscillation; It is the coefficient of samples 1 ratio. With this model, we calculated the value of significance and power, gaining that confidence 90% and potential between 60% -70%, it was validated the main objective of the study.

Ethical considerations
Volunteers and their families received information detailed oral and written information about the study, including a newsletter and a consent form individual. They were also instructed to not change their habits for 21 days duration. The study was developed in accordance with the Declaration Helsinki, prior approval of the protocol by the Committee on Human Research of the Commission Ethics in Experimental Research Valencia’s university.

They were included in the study 44 patients They met the criteria for inclusion of 458 patients evaluated. The average age was 79.32 years a standard deviation of ± 4.476 years, and 81.82% were women. The stadium was more prevalent Alzheimer’s grave with 63.64%. The general characteristics of the sample is listed in Table I.

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The data obtained in the Test Mec-Lobo show a value of 11.61 ± 6.85 and 11.42 ± 7.39 for both groups at baseline. As for the score to the end of the study was 16.13 ± 7.59 for the group cases and 11.56 ± 7.12 for the control group, with a percentage much higher improvement for the case group (P <0.05). This data is presented in Table II.

Screen Shot 2016-03-03 at 7.32.30 PMAfter obtaining the results on the amount changes in the two study groups were analyzed these as parameters sex (Table III), the presence or absence of NIDDM (Table IV) and baseline state dementia (Table V).

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We can see that there are no significant differences between the percentage of improvement between men and women.

As for patients with DM II we see that percentage of improvement was greater for patients who received coconut oil and had no diagnosis of NIDDM.

By baseline stage of dementia, in Table V can be observed as in the case group, improvement rates were higher in states of more advanced disease.

The Alzheimer risk factors are numerous and of these perhaps it highlights the influence you may have a metabolic disorder related with the use of glucose as is the DMII (8). This is confirmed because today one of the causes etiological disease is handled more It is a kind of brain that type II diabetes trigger neuronal death. Therefore this, coupled with the lack of drugs and therapies not pharmacological (TNFs) to cure the disease, suggested that alternative of contributing to the patients a food or nutrient that supplies a source of energy needed to slow death neuronal, that isn’t glucose.

From here arises interest ketone bodies, which are obtained of triglyceride metabolism. Of these, which are metabolized faster and more many are undoubtedly the medium chain, ie, those containing AGCM22-24. In fact, in literature there already published scientific papers, as it has been proven the benefit of these fatty acids, although what was administered was all an extract of a single triglyceride, namely the caprílico (18, 19). The results obtained are good, all based on the improvement that seen in the MoCA and MMSE tests. This meant the recent departure to the health product market Axona® pharmaceutical based on this triglyceride, but, despite the expected improvement was confirmed, if administered alone, as in publications above, to Alzheimer patients in mild, and also they appear intestinal problems such as diarrhea and flatulence.

Therefore, for our study a non-drug product sought (not produce these side effects related many cases with excipients) and that is rich in these triglycerides, to apply both patients mild, moderate and deep as. In this it meaning conventionally assumed that the food which contains more coconut oil it is also not only is the caprylic in this oil, but also found to lauric acid, the palmitic, stearic, myristic and acid to oleic among others, all medium-chain. This It supposed to be a much more complete product which, according to sources and experience itself, does not produce any level problem side or adverse effects.

After administering the oil for 21 days, could corroborate far published extracts dry of caprylic [we] observed statistically significant improvement in the patients, in some cases a very striking way, compared to the results reported in patients who are didn’t have the intervention.

Moreover, in the study design, also I wanted to assess what influence could have the oil in deeper degrees of dementia, and data obtained were even more surprising as you can see in the results section, although in this case, since it is not a significant sample, We need to replicate with a larger population. The physiological explanation for this, since in these patients there is an even greater decrease of neurons and synaptic connections along with a poor peripheral nerve innervation, it could be based theory that really TGCMs not increase metabolic activity; that inhibit gene expression of an enzyme braking half oxidative stress somehow the aging, and even revirtiéndolo, made improvement explain our results, not only in mild and moderate, but also, and more cases intensity in the profundos (19); but otherwise side could also be because to greater progress disease, metabolic disorder greater the brain and therefore can exert greater effect Product (18, 19). Thanks We appreciate the financial support provided by the Foundation Jose Navarro who has given all oil coconut used in the study valued at 3212.0 euros, as well as centers where did the AFA the study and a neuropsychologist our Good Alma (Soul) Group.

1. Christensen K, Double Hammer, Raul R, Vaupel JW. Ageing Populations:
the challenges ahead. Lancet. 2009; 374 (9696):
p. 1196-1208.
2. Bullain S, M. Corrada Dementia in the oldest old. continuum
(Minneap Minn). 2013; 19 (2): p. 457-469.
3. World Health Organization. Dementia: A priority
public health. Washington D.C. .: 2013.
4. M. Martín-Carrasco Biomarkers in Alzheimer’s disease:
definition, diagnostic significance and clinical utility.
Psicog. 2009; 1 (2): p. 101-114.
5. Vargas SB. The person beyond the world of memories:
impact of non-pharmacological therapies on quality of life
of people with Alzheimer’s disease [master’s thesis].
National university of Colombia; 2014.
6. Donoso A. Alzheimer’s disease. Rev Chil Neuropsiquiatr.
2003; 41 (2): p. 13-22.
7. Patterson C, Feightner J, Garcia A C. General risk Macknig
factors for dementia: A systematic review evidence. Alzheimers
Dement. 2007; 3 (7): p. 341-347.
8. Anstey KJ, von Sanden C, Salim A, & R. Smoking O’Kearn as
a risk factor for dementia and cognitive decline: a meta-analysis
of prospective studies. Am J Epidemiol. 2007; 166 (4):
p. 367-378.
9. Issa AM, Mojica WA, Morton SC, Traina S. The efficacy of omega-3
on cognitive function fatty acids in aging and dementia: a
systematic review. Dement Geriatr Cogn. 2006; 21 (2): p. 88-89.
10. Shen ZX. Brain cholinesterases: II. The molecular and cellular
of Alzheimer’s disease basis. Med Hypotheses. 2004; 63 (2):
p. 308-21.
11. Wenk GL. Neuropathologic Changes in Alzheimer’s Disease.
J Clin Psychiatry. 2003; 64 (9): p. 7-10.
12. Nistor M, Don M, Alpha- and beta M. Parekh-secretase activity
as a function of age and beta-amyloid in Down syndrome and
Normal brain. Neurobiol Aging. 2007; 28 (10): p. 1493-1506.
13. Lott IT, Head E. Alzheimer disease and Down syndrome: factors
in pathogenesis. Neurobiol Aging. 2005; 26 (3): p. 383-389.
14. Polvikoski T, Sulkava R, Haltia Apolipoprotein E M., dementia,
and deposition of beta-cortical amyloid protein. New Engl
J Med. 1995; 333 (19): p. 1242-1247.
15. Hardy J, Allsop D. Amyloid deposition as the main event in
the etiology of Alzheimer’s disease. Trends Pharmacol Sci.
1991; 12 (10): p. 383-388.
16. Mudher A, S. Alzheimer’s disease Lovestone-do tauists and
Baptists finally shake hands? Trends Neurosci. 2002; 25 (1):
p. 22-26.
17. Jagua A, Avila A. Insulin and Alzheimer’s disease: a
Type 3 diabetes? Rev Med Univ Nac Colomb. 2007; 55 (1):
p. 6-70.
18. Douglas Maynard S, Gelblum J. Retrospective case studies of
the efficacy of caprylic triglyceride in mild-to-moderate Alzheimer’s
disease. Neuropsych Dis Treat. 2013; 9: p. 1629-1635.
19. Andrew Farah B. Effects of caprylic triglyceride on cognitive
performance and cerebral glucose metabolism in mild Alzheimer’s
disease: a single-case observation. Front Aging Neurosci.
2014; 6 (133): p. 1-4.
20. Bezar J, Bugaut M, Clement G. Triclyceride composition of
coconut oil. J Am Chem Soc 1971 Oil.; 48: p. 134-139.
21. Lobo A, J Ezquerra, Burgada FG, Room A. The Mini- Review
Cognitive. Actas Esp Psiquiatr. 1979; 7: p. 189-202.
22. Aas M. Organ and subcellular distribution of fatty acid activating
enzymes in the rat. Biochim Biophys Acta 1971.; 231:
p. 32-47.
23. Metges CG, Wolfram G. Medium and longchain triglycerides
Labelled With 13C: a comparison of oxidation after oral or parenteral
administration in human. J Nutr. 1991; 121: p. 131-136.
24. JN Odle, Benevenga NJ, Crenshaw TD. Utilization of mediumchain
triglycerides by neonatal piglets: chain length of even
and odd-carbon fatty acids and apparent digestion / absorption
and hepatic metabolism. J Nutr. 1991; 121: p. 605-614.
25. S Sircar, Kansra U. Choice of cooking oils – myths and realities.
J Indian Med Assoc. 1998; 96 (10): p. 304-307.