Medium Chain Triglycerides (MCT Oils)

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-- J.R.R. Tolkien The Children of Hurin
- Medium Chain Triglycerides (MCT Oils) -

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Coconut Oil (Medium Chain Triglycerides, MCT)

See also Coconut Oil Recipes
   More posts by Dr. Newport
   Mitochondrial Dysfunction
   Dr. Sinatra

Note:

1. MCT oil may decrease the frequency and severity of myoclonus in patients with certain neurodegenerative diseases such as Alzheimer's disease, corticobasal syndrome (CBS, CBD, CBGD), and frontotemporal dementia (FTD).

2. MCT oils added to the diet may also reduce the frequency and severity of cold sores (herpes simplex virus-1) and other related herpes viruses such as herpes zoster (chicken pox/shingles).

Coconut oil:

Doctor says an oil lessened Alzheimer's effects on her husband
By Eve Hosley-Moore, Times Correspondent
In print: Wednesday, October 29, 2008

" In Alzheimer's disease, certain brain cells may have difficulty metabolizing glucose, the brain's principal source of energy. Without fuel, these precious neurons may begin to die. But researchers have identified an alternative energy source for brain cells — fats known as ketone bodies, explained Dr. Theodore VanItallie, a medical doctor and professor emeritus at the College of Physicians and Surgeons at Columbia University in New York City. He has been researching ketones for more than 35 years.

"Ketones are a high-energy fuel that nourish the brain," VanItallie said, explaining that when you are starving, the body produces ketones naturally. When digested, the liver converts MCT oil into ketones. In the first few weeks of life, ketones provide about 25 percent of the energy newborn babies need to survive.

"As Dr. Newport continued to read about MCT oil and the new medication, she discovered something surprising: Non-hydrogenated coconut oil is more than 60 percent MCT oil, and this medication derived its MCT oil from this readily available tropical tree."
http://www.tampabay.com/news/aging/article879333.ece

See also Scyllitol

Glucose Hypometabolism:

Note: ALA may also positively affect glucose metabolism.

Bioenergetics breakdown in Alzheimer's disease: targets for new therapies.
Int J Physiol Pathophysiol Pharmacol. 2011;3(2):133-9. Epub 2010 Jun 12.
Saxena U.
Source: R and D Strategy, Kareus Therapeutics SA, Switzerland.
Abstract

Alzheimer's disease is rapidly growing worldwide and yet there is no cure for it. Currently available drugs only provide symptomatic relief and do not intervene in disease process sufficiently enough to prevent or cure it. Characteristic features of this disease are decline in neuronal mass and cognitive functions. The most dominant hypothesis proposed for pathogenesis of this disease is called "amyloid hypothesis". It states that excessive production of amyloid peptides called abeta peptides (Aβ) is the underlying cause of neuronal death and dysfunction. However, recent drugs designed based on amyloid hypothesis have failed in clinical trails, demanding fresh assessment. Early and persistent molecular events in this disease progression are energy deficiency and high oxidative stress in the neurons. Our review will put together a disease model based on known human and animal data with regards to breakdown in neuronal energy generation. The model will integrate energy deficits as the cause of neuronal dysfunction and abeta peptide production culminating in catastrophic loss of cognitive functions. Finally, based on this model, we will also suggest enzyme targets in neuronal bioenergetics pathway for design and development of new disease modifying therapies.

PMID: 21760971 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/21760971
PMCID: PMC3134007
Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134007/?report=abstract
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134007/?tool=pubmed

Impaired Energy Metabolism Linked With Initiation Of Plaques In Alzheimer's Brain
ScienceDaily (Jan. 3, 2009)
"Here, for the first time we provide evidence linking impaired energy metabolism, an AD-relevant stress, with BACE1 translation mediated by eIF2α phosphorylation," says Dr. Vassar. "Our findings implicate phosphorylated eIF2α in both the initiation and progression of sporadic AD. Future experiments will determine whether inhibition of eIF2α phosphorylation could be an efficacious therapeutic approach for the prevention and treatment of AD..."
http://www.sciencedaily.com/releases/2008/12/081224215536.htm

Brain Starvation As We Age Appears To Trigger Alzheimer's: Improving Blood Flow
To Brain Is Preventive Strategy
ScienceDaily (Dec. 28, 2008)
"A slow, chronic starvation of the brain as we age appears to be one of the major triggers of a biochemical process that causes some forms of Alzheimer's disease..."
http://www .sciencedaily.com/releases/2008/12/081224215704.htm

Blood Sugar Linked To Normal Cognitive Aging
ScienceDaily (Dec. 31, 2008)
"Maintaining blood sugar levels, even in the absence of disease, may be an important strategy for preserving cognitive health, suggests a study published by researchers at Columbia University Medical Center (CUMC)..."
http://www .sciencedaily.com/releases/2008/12/081230072238.htm

Brain fuel metabolism, aging, and Alzheimer's disease.
Nutrition. 2011 Jan;27(1):3-20. Epub 2010 Oct 29.
Cunnane S, Nugent S, Roy M, Courchesne-Loyer A, Croteau E, Tremblay S, Castellano A, Pifferi F, Bocti C, Paquet N, Begdouri H, Bentourkia M, Turcotte E, Allard M, Barberger-Gateau P, Fulop T, Rapoport SI.

Abstract

Lower brain glucose metabolism is present before the onset of clinically measurable cognitive decline in two groups of people at risk of Alzheimer's disease--carriers of apolipoprotein E4, and in those with a maternal family history of AD. Supported by emerging evidence from in vitro and animal studies, these reports suggest that brain hypometabolism may precede and therefore contribute to the neuropathologic cascade leading to cognitive decline in AD. The reason brain hypometabolism develops is unclear but may include defects in brain glucose transport, disrupted glycolysis, and/or impaired mitochondrial function. Methodologic issues presently preclude knowing with certainty whether or not aging in the absence of cognitive impairment is necessarily associated with lower brain glucose metabolism. Nevertheless, aging appears to increase the risk of deteriorating systemic control of glucose utilization, which, in turn, may increase the risk of declining brain glucose uptake, at least in some brain regions. A contributing role of deteriorating glucose availability to or metabolism by the brain in AD does not exclude the opposite effect, i.e., that neurodegenerative processes in AD further decrease brain glucose metabolism because of reduced synaptic functionality and hence reduced energy needs, thereby completing a vicious cycle. Strategies to reduce the risk of AD by breaking this cycle should aim to (1) improve insulin sensitivity by improving systemic glucose utilization, or (2) bypass deteriorating brain glucose metabolism using approaches that safely induce mild, sustainable ketonemia.

PMID: 21035308 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/21035308

As far as I can determine, the test "FDG-PET" ([(18)F]-fluoro-deoxyglucose positron emission tomography) detects areas of the brain experiencing glucose hypometabolism.

Typical cerebral metabolic patterns in neurodegenerative brain diseases.
Mov Disord. 2010 Jul 28. [Epub ahead of print]
Teune LK, Bartels AL, de Jong BM, Willemsen AT, Eshuis SA, de Vries JJ, van Oostrom JC, Leenders KL.

Department of Neurology, University Medical Center Groningen, Groningen, The Netherlands.

Abstract

The differential diagnosis of neurodegenerative brain diseases on clinical grounds is difficult, especially at an early disease stage. Several studies have found specific regional differences of brain metabolism applying [(18)F]-fluoro-deoxyglucose positron emission tomography (FDG-PET), suggesting that this method can assist in early differential diagnosis of neurodegenerative brain diseases.We have studied patients who had an FDG-PET scan on clinical grounds at an early disease stage and included those with a retrospectively confirmed diagnosis according to strictly defined clinical research criteria. Ninety-six patients could be included of which 20 patients with Parkinson's disease (PD), 21 multiple system atrophy (MSA), 17 progressive supranuclear palsy (PSP), 10 corticobasal degeneration (CBD), 6 dementia with Lewy bodies (DLB), 15 Alzheimer's disease (AD), and 7 frontotemporal dementia (FTD). FDG PET images of each patient group were analyzed and compared to18 healthy controls using Statistical Parametric Mapping (SPM5).Disease-specific patterns of relatively decreased metabolic activity were found in PD (contralateral parietooccipital and frontal regions), MSA (bilateral putamen and cerebellar hemispheres), PSP (prefrontal cortex and caudate nucleus, thalamus, and mesencephalon), CBD (contralateral cortical regions), DLB (occipital and parietotemporal regions), AD (parietotemporal regions), and FTD (frontotemporal regions).The integrated method addressing a spectrum of various neurodegenerative brain diseases provided means to discriminate patient groups also at early disease stages. Clinical follow-up enabled appropriate patient inclusion. This implies that an early diagnosis in individual patients can be made by comparing each subject's metabolic findings with a complete database of specific disease related patterns. (c) 2010 Movement Disorder Society.

PMID: 20669302
http://www.ncbi.nlm.nih.gov/pubmed/20669302

Fluorodeoxyglucose-Positron Emission Tomography in the differential diagnosis of early-onset dementia: a prospective, community-based study

Peter K Panegyres, Jeffrey M Rogers, Michael McCarthy, Andrew Campbell and Jing Shan Wu

1 Neurodegenerative Disorders Research, 185 York St, Subiaco WA, Australia
2 Neurosciences Unit, Health Department of Western Australia, Perth WA, Australia
3 Department of Nuclear Medicine, Royal Perth Hospital, Perth WA, Australia
4 WA PET/Cyclotron Service, Sir Charles Gairdner Hospital, Perth WA, Australia

BMC Neurology 2009, 9:41doi:10.1186/1471-2377-9-41

Background

The aim of this study was to evaluate the diagnostic accuracy of positron emission tomography (PET) using F18 fluorodeoxyglucose (FDG) in the differential diagnosis of early-onset Alzheimer's disease (AD) and other dementias in a community-dwelling population.
Methods

A prospective sample of 102 individuals presenting consecutively to a primary care centre for examination of suspected early-onset dementing diseases. The mean age of symptom onset of dementia in our patients was 60.06 ± 4.28 years (mean ± 1SD, 95% lower confidence intervals (CI) 54.75, upper 63.37). Patients were evaluated using standard clinical criteria for the diagnosis of dementia. Functional neuroimaging data was obtained and nuclear medicine physicians blind to the clinical diagnosis generated FDG-PET diagnoses. Final clinical diagnoses based on all available data were then established and compared against PET diagnoses.
Results

Forty-nine patients received a final clinical diagnosis of early-stage AD (MMSE score 20.97 ± 5.10). There were 29 non-AD demented patients, 11 depressed patients and a miscellaneous group of 13 patients. Among patients with AD, the sensitivity and specificity of FDG-PET was 78% (95% CI: 66–90%) and 81% (95% CI: 68–86%), respectively. The positive likelihood ratio (PLR) for a FDG-PET scan positive for the diagnosis of AD was 4.11 (95% CI: 2.29–7.32) and negative likelihood ratio (NLR) for a negative FDG-PET scan in the absence of AD was 0.27 (95% CI: 0.16–0.46). The pre-test probability was 48% and post-test probability was 79.02%. The specificity of FDG-PET in the differential diagnosis of other dementias, including frontotemporal dementia, was greater than 95%.

Recruitment methods in this study provide a sample that may be more representative of patients in the general population and indicate that FDG-PET imaging can contribute to the diagnosis of AD in younger adults with major increases in the positive likelihood rates and post-test probability.
Conclusion

The high specificity of FDG-PET suggests this technique might help in the diagnosis of frontotemporal dementia and other forms of early-onset dementia...
http://www.biomedcentral.com/1471-2377/9/41

Ketone bodies are selectively used by individual brain regions.
Science. 1979 Jul 20;205(4403):325-7.
Hawkins RA, Biebuyck JF.
Abstract

Close study of 3-hydroxybutyrate uptake by brain suggests that its metabolism is limited by permeability. Furthermore, the permeability characteristics vary from region to region; areas known to have no blood-brain barrier show the highest rate of utilization. The results imply that rather than substitute fuels, ketone bodies should be considered supplements which partially supply specific areas but are incapable of supporting the entire energy requirement of all brain regions.

PMID: 451608 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/451608?dopt=AbstractPlus

It is interesting that the idea of using ketone bodies as a "subsitute fuel" was around in 1979. I haven't read the whole paper, so I don't know the context. It probably was not in regards to combating glucose hypometabolism. So, what fuels the brains of people when they are starving? Is it the conversion of muscle protein to glucose? I have to wonder if more modern imaging technology agrees with this paper from 1979.

Posts and articles from Dr. Mary Newport about MCT oil and coconut oil:

Doctor says an oil lessened Alzheimer's effects on her husband
Eve Hosley-Moore, Times Correspondent
St. Petersburg Times
In Print: Wednesday, October 29, 2008
"After two weeks of taking coconut oil, Steve Newport's results in an early onset Alzheimer's test gradually improved says his wife, Dr. Mary Newport. Before treatment, Steve could barely remember how to draw a clock. Two weeks after adding coconut oil to his diet, his drawing improved. After 37 days, Steve's drawing gained even more clarity. The oil seemed to "lift the fog," his wife says..."
http://www.tampabay.com/news/aging/article879333.ece

More posts by Dr. Newport

Dr. Newport's web site: http://www.coconutketones.com
Dr. Newport's blog: http://coconutketones.blogspot.com
Dr. Newport's April 2009 "update" (.pdf version)
Dr. Newport's September 2009 "Diet guidelines" (.pdf version)

Update 11/15/2009:

I thought I should bring Dr. Newport's Thursday, October 29, 2009 blog entry to your attention. There are some very intriguing ideas here. And, they involve supplements that could easily be obtained by the average person who would like to pursue these ideas further.Here is an excerpt:

I hear from some people who are very discouraged because they do not see improvement in their loved one with Alzheimer's. About half of the people in the MCT oil studies declined minimally rather than improving, but declined less than the people who took the placebo. So this strategy may be worthwhile continuing even if results are not obvious in the beginning. Also, some people improve rather slowly but over two to three months, the changes may become more apparent, or perhaps you will see that things are not worse.

If you are considering giving up on this, you might consider the possibility that this strategy could at least stabilize or slow down the process for your loved one. Hopefully we will be able to learn why some people improve and others don't. After attending the American College of Nutrition Conference at the beginning of October, I have some ideas about why this happens. It could be that the cells are so depleted of the various substances they need to make energy inside the cell that the cells don't recover simply by providing ketone. I learned more about other disease processes where there is also a problem with energy production in mitochondria, the organelles inside of the cells that manufacture ATP, the very basic energy that drives the whole function of the cell. Each cell has hundreds to thousands of mitochondria.

Dr. Stephen Sinatra discussed several dietary supplements that help people with severe congestive heart failure by providing certain substances involved in manufacturing ATP in the mitochondria in the cells. In the case of congestive heart failure, the cardiac cells have become depleted of these substances and are not making enough ATP to keep the cell going. Three of the supplements we have been giving Steve for quite some time, CoQ10, L-carnitine and magnesium, but the fourth I did not know about, D-ribose. D-ribose is a simple sugar normally made inside the cell from glucose, and is one of the building blocks for ATP. It makes sense that if glucose cannot even get into the cell that the cell will not be able to make D-ribose, which is critical to making ATP. It is not stored elsewhere in the body and it is not present in any quantity in foods, but is used by body builders and available as a supplement. For people with cardiac diseases, Dr. Sinatra recommends taking about 5 - 7 grams of D-ribose per day. It comes in a powder (disappears without much taste in coffee or any drink) or chewable tablet (not so good to my tastebuds.) I have many questions about it, such as does it cross the blood brain barrrier and how does it enter the cell, and of course, it is safe? I have not been able to find out much about it. If there is a chemist or other scientist out there with more information about D-ribose, I would appreciate hearing from you. When I learn more I will post something about it.

Dr. Sinatra has a book called, "The Sinatra Solution: Metabolic Cardiology" that discusses these supplements in detail, but is very technical. I believe that this strategy could help people with AD since the mitochondria work the same as far as producing enery in all of the cells. After reading up about this, part of the problem in AD may be that the cells become depleted of these substances, such as CoQ10, from some of the medications our people with AD are often on (anti-depressants, statins.) Also the whole process of making energy in the mitochondria depends on being able to get glucose (or ketone bodies as an alternative) into the cells in the first place and this is not happening...

http://coconutketones.blogspot.com/

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References:

In Parkinson's Disease, Brain Cells Abandon Mitochondria
ScienceDaily (Oct. 8, 2010) — In a study that sheds new light on the causes of Parkinson's disease, researchers report that brain cells in Parkinson's patients abandon their energy-producing machinery, the mitochondria. A shutdown in fuel can have devastating effects on brain cells, which consume roughly 20 percent of the body's energy despite making up only 2 percent of body weight... researchers, now show that a root cause of Parkinson's disease may lie in 10 gene sets related to energy production that spur neurons in the brain to "divorce" their mitochondria and related energy-producing pathways..."The most exciting result from our study for me is the discovery of PGC-1alpha as a new therapeutic target for early intervention in Parkinson's disease. PGC-1alpha is a master switch that activates hundreds of mitochondrial genes, including many of those needed to maintain and repair the power plants in the mitochondria,"... FDA-approved medications [Actos, CoQ10] that activate that PGC-1alpha are already available for widespread diseases like diabetes. These medications may jumpstart the development of new Parkinson's drugs; instead of having to start from scratch, pharmaceutical companies may be able to dust off their drug libraries and find look-alike drugs capable of targeting PGC-1alpha in the brain. "As we wrap up our first year of publishing the journal, the new study from Zheng et al. exemplifies the goal of Science Translational Medicine, applying knowledge and technology from different fields-such as neuroscience, genomics and bioinformatics-to achieve new discoveries,"...
http://www.sciencedaily.com/releases/2010/10/101006151557.htm

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Updated: July 2, 2012
Inception: July 2, 2012