11 replies to this topic

[fql]

I've heard this supplement is good and every anecdote (no science) I've read approved of MCT oil. Any comments?

http://www.amazon.co...60901,k:mct oil

Edited by juryben, 13 December 2012 - 02:30 AM.

[burgerking789]

I'm interested in adding it to my protein shakes. It's gaining a lot of popularity.

[LexLux]

Looks interesting, anyone know if the MCT oil supplements are cholesterol free? - 

 

Effects of beta-hydroxybutyrate on cognition in memory-impaired adults.

Reger MA1, Henderson ST, Hale C, Cholerton B, Baker LD, Watson GS, Hyde K, Chapman D, Craft S.

 

Abstract

Glucose is the brain's principal energy substrate. In Alzheimer's disease (AD), there appears to be a pathological decrease in the brain's ability to use glucose. Neurobiological evidence suggests that ketone bodies are an effective alternative energy substrate for the brain. Elevation of plasma ketone body levels through an oral dose of medium chain triglycerides (MCTs) may improve cognitive functioning in older adults with memory disorders. On separate days, 20 subjects with AD or mild cognitive impairment consumed a drink containing emulsified MCTs or placebo. Significant increases in levels of the ketone body beta-hydroxybutyrate (beta-OHB) were observed 90 min after treatment (P=0.007) when cognitive tests were administered. beta-OHB elevations were moderated by apolipoprotein E (APOE) genotype (P=0.036). For 4+ subjects, beta-OHB levels continued to rise between the 90 and 120 min blood draws in the treatment condition, while the beta-OHB levels of 4- subjects held constant (P<0.009). On cognitive testing, MCT treatment facilitated performance on the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog) for 4- subjects, but not for 4+ subjects (P=0.04). Higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02). Additional research is warranted to determine the therapeutic benefits of MCTs for patients with AD and how APOE-4 status may mediate beta-OHB efficacy.

 

Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor

Tadahiro Shimazu et al, Science 11 January 2013

 

Concentrations of acetyl?coenzyme A and nicotinamide adenine dinucleotide (NAD+) affect histone acetylation and thereby couple cellular metabolic status and transcriptional regulation. We report that the ketone body D-?-hydroxybutyrate (?OHB) is an endogenous and specific inhibitor of class I histone deacetylases (HDACs). Administration of exogenous ?OHB, or fasting or calorie restriction, two conditions associated with increased ?OHB abundance, all increased global histone acetylation in mouse tissues. Inhibition of HDAC by ?OHB was correlated with global changes in transcription, including that of the genes encoding oxidative stress resistance factors FOXO3A and MT2. Treatment of cells with ?OHB increased histone acetylation at the Foxo3a and Mt2 promoters, and both genes were activated by selective depletion of HDAC1 and HDAC2. Consistent with increased FOXO3A and MT2 activity, treatment of mice with ?OHB conferred substantial protection against oxidative stress.

 

How calorie restriction influences longevity: Protecting cells from damage caused by chronic disease

ScienceDaily, 6 December 2012

 

"Scientists have identified a novel mechanism by which a type of low-carb, low-calorie diet -- called a "ketogenic diet" -- could delay the effects of aging. This fundamental discovery reveals how such a diet could slow the aging process and may one day allow scientists to better treat or prevent age-related diseases, including heart disease, Alzheimer's disease and many forms of cancer."

[...]

"The findings could be relevant for a wide range of neurological conditions, such as Alzheimer's, Parkinson's, autism and traumatic brain injury -- diseases that afflict millions and for which there are few treatment options." ... "Identifying ?OHB as a link between caloric restriction and protection from oxidative stress opens up a variety of new avenues to researchers for combating disease," said Tadahiro Shimazu, a Gladstone postdoctoral fellow and the paper's lead author. "In the future, we will continue to explore the role of ?OHB -- especially how it affects the body's other organs, such as the heart or brain -- to confirm whether the compound's protective effects can be applied throughout the body."

 

Ketones can be bad for diabetics though...

 

Edited by LexLux, 31 May 2014 - 08:03 AM.

[FW900]

 

Looks interesting, anyone know if the MCT oil supplements are cholesterol free? - 

 

Effects of beta-hydroxybutyrate on cognition in memory-impaired adults.

Reger MA1, Henderson ST, Hale C, Cholerton B, Baker LD, Watson GS, Hyde K, Chapman D, Craft S.

 

Abstract

Glucose is the brain's principal energy substrate. In Alzheimer's disease (AD), there appears to be a pathological decrease in the brain's ability to use glucose. Neurobiological evidence suggests that ketone bodies are an effective alternative energy substrate for the brain. Elevation of plasma ketone body levels through an oral dose of medium chain triglycerides (MCTs) may improve cognitive functioning in older adults with memory disorders. On separate days, 20 subjects with AD or mild cognitive impairment consumed a drink containing emulsified MCTs or placebo. Significant increases in levels of the ketone body beta-hydroxybutyrate (beta-OHB) were observed 90 min after treatment (P=0.007) when cognitive tests were administered. beta-OHB elevations were moderated by apolipoprotein E (APOE) genotype (P=0.036). For 4+ subjects, beta-OHB levels continued to rise between the 90 and 120 min blood draws in the treatment condition, while the beta-OHB levels of 4- subjects held constant (P<0.009). On cognitive testing, MCT treatment facilitated performance on the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog) for 4- subjects, but not for 4+ subjects (P=0.04). Higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02). Additional research is warranted to determine the therapeutic benefits of MCTs for patients with AD and how APOE-4 status may mediate beta-OHB efficacy.

 

Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor

Tadahiro Shimazu et al, Science 11 January 2013

 

Concentrations of acetyl?coenzyme A and nicotinamide adenine dinucleotide (NAD+) affect histone acetylation and thereby couple cellular metabolic status and transcriptional regulation. We report that the ketone body D-?-hydroxybutyrate (?OHB) is an endogenous and specific inhibitor of class I histone deacetylases (HDACs). Administration of exogenous ?OHB, or fasting or calorie restriction, two conditions associated with increased ?OHB abundance, all increased global histone acetylation in mouse tissues. Inhibition of HDAC by ?OHB was correlated with global changes in transcription, including that of the genes encoding oxidative stress resistance factors FOXO3A and MT2. Treatment of cells with ?OHB increased histone acetylation at the Foxo3a and Mt2 promoters, and both genes were activated by selective depletion of HDAC1 and HDAC2. Consistent with increased FOXO3A and MT2 activity, treatment of mice with ?OHB conferred substantial protection against oxidative stress.

 

How calorie restriction influences longevity: Protecting cells from damage caused by chronic disease

ScienceDaily, 6 December 2012

 

"Scientists have identified a novel mechanism by which a type of low-carb, low-calorie diet -- called a "ketogenic diet" -- could delay the effects of aging. This fundamental discovery reveals how such a diet could slow the aging process and may one day allow scientists to better treat or prevent age-related diseases, including heart disease, Alzheimer's disease and many forms of cancer."

[...]

"The findings could be relevant for a wide range of neurological conditions, such as Alzheimer's, Parkinson's, autism and traumatic brain injury -- diseases that afflict millions and for which there are few treatment options." ... "Identifying ?OHB as a link between caloric restriction and protection from oxidative stress opens up a variety of new avenues to researchers for combating disease," said Tadahiro Shimazu, a Gladstone postdoctoral fellow and the paper's lead author. "In the future, we will continue to explore the role of ?OHB -- especially how it affects the body's other organs, such as the heart or brain -- to confirm whether the compound's protective effects can be applied throughout the body."

 

Ketones can be bad for diabetics though...

 

 

 

I'm no expert on the subject but I've read that coconut oil contains no cholesterol (or no "bad" cholesterol) and can rise "good" cholesterol. MCT oil, is a refined coconut oil, so whatever is true of coconut oil could be translated to MCT oil.
 

[LexLux]

I've seen mixed reports on coconut oil since it does also contain long chain triglycerides. one might need to take 20-30g of refined MCTs spread out throughout the day (see first study bellow), which could translate to as much as 50g coconut oil. Good news is that MCTs provide energy and sate appetite. NOW has an MCT supplement and recommends a 15ml serving, a bottle is 32 oz (which is 63 servings/bottle). What I'm not sure of is whether it contains any LCTs. 

 

Stimulation of mild, sustained ketonemia by medium-chain triacylglycerols in healthy humans: estimated potential contribution to brain energy metabolism.

Courchesne-Loyer et al, Nutrition. 2013 Apr;29(4):635-40. doi: 10.1016/j.nut.2012.09.009. Epub 2012 Dec 28.

 

Abstract

 

OBJECTIVE:

In humans consuming a normal diet, we investigated 1) the capacity of a medium-chain triacylglycerol (MCT) supplement to stimulate and sustain ketonemia, 2) ¹³C-β-hydroxybutyrate and ¹³C-trioctanoate metabolism, and 3) the theoretical contribution of the degree of ketonemia achieved to brain energy metabolism.

 

METHODS: Eight healthy adults (26 ± 1 y old) were given an MCT supplement for 4 wk (4 times/d; total of 20 g/d for 1 wk followed by 30 g/d for 3 wk). Ketones, glucose, triacylglycerols, cholesterol, free fatty acids, and insulin were measured over 8 h during two separate metabolic study days before and after MCT supplementation. Using isotope ratio mass spectroscopy, ¹³C-D-β-hydroxybutyrate and ¹³C-trioctanoate β-oxidation to ¹³CO₂ was measured over 12 h on the pre- and post-MCT metabolic study days.

 

RESULTS: On the post-MCT metabolic study day, plasma ketones (β-hydroxybutyrate plus acetoacetate) peaked at 476 μM, with a mean value throughout the study day of 290 μM. Post-MCT, ¹³C-trioctanoate β-oxidation was significantly lower 1 to 8 h later but higher 10 to 12 h later. MCT supplementation did not significantly alter ¹³C-D-β-hydroxybutyrate oxidation.

 

CONCLUSIONS: This MCT supplementation protocol was mildly and safely ketogenic and had no side effects in healthy humans on their regular diet. This degree of ketonemia is estimated to contribute up to 8% to 9% of brain energy metabolism.

 

 

Role of Medium Chain Triglycerides (Axona®) in the Treatment of Mild to Moderate Alzheimer's Disease.

Sharma A et al, Am J Alzheimers Dis Other Demen. 2014 Jan 9. [Epub ahead of print]

Abstract

 

Treatment of Alzheimer's disease (AD) with acetylcholinesterase inhibitors or N-methyl-D-aspartate (NMDA) receptor antagonists provides symptomatic relief but do not prevent its progression. Thus, additional approaches aimed at slowing the progression of the disease have been investigated. Reports detailing reduced brain glucose metabolism in the early stages of AD led to the hypothesis that alternate energy sources aimed at increasing neuronal metabolism may protect neurons and thus benefit patients with AD. Medium-chain triglycerides (MCTs) are metabolized to ketone bodies that serve as an alternative source of energy for neurons. Data from clinical trials suggest that MCTs improve cognition in patients with mild to moderate AD in apolipoprotein E4-negative patients. Adverse events observed were mild and included minor gastrointestinal problems such as diarrhea, dyspepsia, and flatulence. However, since genomic profiles are not routinely conducted in patients with AD in a clinical setting, the role of MCTs in clinical practice seems to be minimal.

 

Edited by LexLux, 31 May 2014 - 05:32 PM.

[LexLux]

Some more Studies that I dug up -

 

Augmentation of Normal and Glutamate-Impaired Neuronal Respiratory Capacity by Exogenous Alternative Biofuels

Melissa D. Laird et al., December 2013, Volume 4, Issue 6, pp 643-651 

 

Abstract

Mitochondrial respiratory capacity is critical for responding to changes in neuronal energy demand. One approach toward neuroprotection is the administration of alternative energy substrates (“biofuels”) to overcome brain injury-induced inhibition of glucose-based aerobic energy metabolism. This study tested the hypothesis that exogenous pyruvate, lactate, β-hydroxybutyrate, and acetyl-l-carnitine each increase neuronal respiratory capacity in vitro either in the absence of or following transient excitotoxic glutamate receptor stimulation. Compared to the presence of 5 mM glucose alone, the addition of pyruvate, lactate, or β-hydroxybutyrate (1.0–10.0 mM) to either day in vitro (DIV) 14 or 7 rat cortical neurons resulted in significant, dose-dependent stimulation of respiratory capacity, measured by cell respirometry as the maximal O2 consumption rate in the presence of the respiratory uncoupler carbonyl cyanide-p-trifluoromethoxyphenylhydrazone. A 30-min exposure to 100 μM glutamate impaired respiratory capacity for DIV 14, but not DIV 7, neurons. Glutamate reduced the respiratory capacity for DIV 14 neurons with glucose alone by 25 % and also reduced respiratory capacity with glucose plus pyruvate, lactate, or β-hydroxybutyrate. However, respiratory capacity in glutamate-exposed neurons following pyruvate or β-hydroxybutyrate addition was still, at least, as high as that obtained with glucose alone in the absence of glutamate exposure. These results support the interpretation that previously observed neuroprotection by exogenous pyruvate, lactate, or β-hydroxybutyrate is at least partially mediated by their preservation of neuronal respiratory capacity.

 

 

3-Hydroxybutyrate methyl ester as a potential drug against Alzheimer's disease via mitochondria protection mechanism Junyu Zhang et al, Biomaterials Volume 34, Issue 30, October 2013, Pages 7552–7562

 

Abstract

Alzheimer's disease (AD) is induced by many reasons, including decreased cellular utilization of glucose and brain cell mitochondrial damages. Degradation product of microbially synthesized polyhydroxybutyrate (PHB), namely, 3-hydroxybutyrate (3HB), can be an alternative to glucose during sustained hypoglycemia. In this study, the derivative of 3HB, 3-hydroxybutyrate methyl ester (HBME), was used by cells as an alternative to glucose. HBME inhibited cell apoptosis under glucose deprivation, rescued activities of mitochondrial respiratory chain complexes that were impaired in AD patients and decreased the generation of ROS. Meanwhile, HBME stabilized the mitochondrial membrane potential. In vivo studies showed that HBME crossed the blood brain barrier easier compared with charged 3HB, resulting in a better bioavailability. AD mice treated with HBME performed significantly better (p < 0.05) in the Morris water maze compared with other groups, demonstrating that HBME has a positive in vivo pharmaceutical effect to improve the spatial learning and working memory of mice. A reduced amyloid-β deposition in mouse brains after intragastric administration of HBME was also observed. Combined with the in vitro and in vivo results, HBME was proposed to be a drug candidate against AD, its working mechanism appeared to be mediated by various effects of protecting mitochondrial damages.

 

Treatment with beta-hydroxybutyrate and melatonin is associated with improved survival in a porcine model of hemorrhagic shock 

Kristine E. Mulier et al, Resuscitation Volume 83, Issue 2, February 2012, Pages 253–258

 

Introduction

The neuroprotective ketone β-hydroxybutyrate (BHB) and the antioxidant melatonin have been found at elevated levels in hibernating mammals. Previous studies in rat models of hemorrhagic shock have suggested a benefit. We compared infusion of 4 M BHB and 43 mM melatonin (BHB/M) to 4 M sodium chloride and 20% DMSO (control solution) to evaluate for potential benefits in porcine hemorrhagic shock.

 

Methods

Hemorrhagic shock was induced to obtain systolic blood pressures <50 mmHg for 60 min. Pigs were treated with a bolus of either BHB/M (n = 9) or control solution (n = 8) followed by 4-h infusion of the either BHB/M or control solution. All animals were then resuscitated for 20 h after shock. Physiological data were continually recorded, and blood samples were taken at intervals throughout the experiment. Serum samples were analyzed via high resolution NMR for metabolomic response.

Results

BHB/M treatment significantly increased 24-h survival time when compared to treatment with control solution (100% versus 62%; p = 0.050), with a trend toward decreased volume of resuscitative fluid administered to animals receiving BHB/M. BHB/M-treated animals had lower base deficit and higher oxygen consumption when compared to animals receiving control solution. Serum metabolite profiles revealed increases in β-hydroxybutyrate (BHB), succinate, 2-oxovalerate and adipate with BHB/M treatment as compared with animals treated with control infusion.

 

Conclusion

Infusion of BHB/M conferred a survival benefit over infusion of control solution in hemorrhagic shock. BHB and its products of metabolism are identified in serum of animals subjected to shock and treated with BHB/M. Further preclinical studies are needed to clarify the mechanisms of action of this promising treatment strategy.

 

 

Not so good - could this be pathogenic in schizophrenia, or is it a biomarker? See two studies bellow - 

 

Novel Aspect of Ketone Action: β-Hydroxybutyrate Increases Brain Synthesis of Kynurenic Acid In Vitro

Iwona Chmiel-Perzyńska et al., July 2011, Volume 20, Issue 1, pp 40-50

 

Abstract

Ketone bodies formed during ketogenic diet or non-treated diabetes mellitus may exert neuroprotective and antiepileptic effects. Here, we assessed the influence of ketone body, β-hydroxybutyrate (BHB) on the brain synthesis of kynurenic acid (KYNA), an endogenous antagonist of glutamatergic and α7-nicotinic receptors. In brain cortical slices and in primary glial cultures, BHB enhanced KYNA production. KT 5270, an inhibitor of protein kinase A, has prevented this action. At hypoglycemia, under pH 7.0 and 7.4, profound (15 mM BHB), but not mild (3 mM) ketosis increased synthesis of KYNA. In paradigm resembling diabetic ketoacidosis in vitro (30 mM glucose, pH 7.0), neither mild nor profound ketosis influenced the production of KYNA. At pH 7.4 and in 30 mM glucose though, both mild and severe ketonemia evoked an increase of KYNA production. The activity of KYNA biosynthetic enzymes, KAT I and KAT II, in cortical homogenate was not altered by BHB (0.05–10.0 mM). However, in cultured glial cells exposed to BHB (10 mM), the activity of KATs increased. This effect was reversed by the co-incubation of cells with KT 5270. Presented data reveal a novel mechanism of action of BHB. Increased synthesis of KYNA in the presence of BHB is most probably mediated by protein kinase A-dependent stimulation of KATs expression/activity leading to an increase of KYNA formation. Ensuing attenuation of the excessive excitatory glutamate-mediated neurotransmission may, at least in part, explain the neuroprotective actions of BHB.

 

 

The kynurenic acid hypothesis of schizophrenia.

Erhardt S. et al, Physiol Behav. 2007 Sep 10;92(1-2):203-9. Epub 2007 May 21.

 

Abstract

In recent years progress in the field of schizophrenia research has led to the suggestion that dopamine only plays an intermediary role in the pathophysiology of the disease and that the main abnormalities lie elsewhere. In particular, deficits in brain glutamatergic systems are suggested to play a prominent role in the pathophysiology of the disease. Kynurenic acid is an endogenous glutamate antagonist with a preferential action at the glycine-site of the N-methyl-D-aspartate-receptor. Mounting evidence indicates that the compound is significantly involved in basal neurophysiological processes in the brain. Thus, pharmacologically elevated levels of kynurenic acid, in similarity to systemic administration of phencyclidine or ketamine, were associated with increased firing rate and burst firing activity of midbrain dopamine neurons, indicating per se that elevated levels of brain kynurenic acid is associated with psychotomimetic effects. Indeed, cerebrospinal fluid level of kynurenic acid was elevated in schizophrenic patients as compared to healthy controls. The present paper also describes a prostaglandin-mediated regulation of kynurenic acid formation as well as a relationship between brain kynurenic acid concentration and the excitatory responses of ventral tegmental area dopamine neurons by clozapine and nicotine. Our results suggest that kynurenic acid contributes to the pathogenesis of schizophrenia and link the dopamine hypothesis of schizophrenia together with the idea of a deficiency in glutamatergic function in this disease.

 

 

Edited by LexLux, 31 May 2014 - 07:15 PM.

[LexLux]

Perhaps Niacin (or nicotinimide riboside) + glutamine + arginine could be protective against the increased beta-hydroybutyrate levels schizophrenics experience?THis article raises the intruiging prospect that schizophrenics suffer from low NAD levels. Resulting increases in BHB might explain the elevated Kynurenic Acid levels too.

 

The Niacin Flush Pathway in Recovery from Schizophrenia and how Arginine and Glutamine may Provide Added Benefit

W. Todd Penberthy, PhD, JOM Volume 27, Number 1, 2012

 

"Explanations for the Simultaneous Recovery from Acute Schizophrenia and the Niacin-Flush Response

 

Hoffer observed that treatment with high doses of the non-flush NAD precursor, nicotinamide, also frequently resulted in recovery from acute schizophrenia similar to recovery from pellagra dementia. While restoration of the nicotinic acid-mediated flush response does correlate with niacin-mediated recovery from schizophrenia, it does not necessarily mean that this effect was primarily the result of the flush response.It seems much more likely that the restoration of NAD levels is central to recovery, where NAD as NAD+, NADP+, NADH, and/or NADPH, may be restoring prostaglandin- flush pathways by one or a combination of the >450 reactions that require NAD for ac- tivity. There are several possible explanations for the observed reduced flush response. In this section we give consideration to each explanation and ultimately come to the conclusion that the reduced flush response is firstly an NAD deficiency, where PUFA reductions are likely to be secondary to this effect. This analysis concludes that schizo- phrenia is most likely not an essential fatty acid deficiency disease, but more of a NAD deficiency disease.

 

Firstly, the reduced niacin flush response observed in schizophrenia likely involves nia- cin receptor ligand mediated desensitization. A metabolic study of schizophrenia indicates a general increase in PUFA catabolism.31 Beta-hydroxybutryate levels were found to be elevated 2.6 fold. Beta-hydroxybutyrate is proposed to be the naturally occurring endogenous ligand for the high affinity nicotinic acid G-protein coupled receptor.32 Decreased levels of the GPR109a protein are observed in the brains of schizophrenics, as are increased GPR109a transcripts.33 Such ligand dependent receptor down-regulation (a.k.a., receptor desensitization) is a common theme with the G-protein coupled receptor protein superfamily. Thus, NAD may be simply restoring PUFA metabolism such that the levels of the beta-hydroxybutyrate ligand for the high affinity nicotinic acid G- protein coupled receptor are returned to normal levels. The GPR109a protein may then be expressed at correct levels, thus restoring the niacin-flush response to normal as well. This general alteration is surely a major contributor to the reduced flush response seen in schizophrenics."

Edited by LexLux, 01 June 2014 - 12:58 AM.

[Jimmy the hand]

I'm pretty certain the are NO long chain triglycerides in cocnut oil. Only medium chain triglycerides.

 

Cocnut oil is the healthiest choice for cooking bar none especially seeing as most vegetable oils are manufactured from GM crops.

[MenDis]

 

 

Ketogenic diets cause opposing changes in synaptic morphology in CA1 hippocampus and dentate gyrus of late-adult rats.

Balietti M1, Giorgetti B, Fattoretti P, Grossi Y, Di Stefano G, Casoli T, Platano D, Solazzi M, Orlando F, Aicardi G, Bertoni-Freddari C.

Author information

 

Abstract

Ketogenic diets (KDs) have beneficial effects on several diseases, such as epilepsy, mitochondriopathies, cancer, and neurodegeneration. However, little is known about their effects on aging individuals. In the present study, late-adult (19-month-old) rats were fed for 8 weeks with two mediumchain triglycerides (MCT)-KDs, and the following morphologic parameters reflecting synaptic plasticity were evaluated in stratum moleculare of hippocampal CA1 region (SM CA1) and outer molecular layer of hippocampal dentate gyrus (OML DG): average area (S), numeric density (Nv(s)), and surface density (Sv) of synapses, and average volume (V), numeric density (Nv(m)), and volume density (Vv) of synaptic mitochondria. In SM CA1, MCT-KDs induced the early appearance of the morphologic patterns typical of old animals (higher S and V, and lower Nv(s) and Nv(m)). On the contrary, in OML DG, Sv and Vv of MCT-KDs-fed rats were higher (as a result of higher Nv(s) and Nv(m)) versus controls; these modifications are known to improve synaptic function and metabolic supply. The opposite effects of MCT-KDs might reflect the different susceptibility to aging processes: OML DG is less vulnerable than SM CA1, and the reactivation of ketone bodies uptake and catabolism might occur more efficiently in this region, allowing the exploitation of their peculiar metabolic properties. Present findings provide the first evidence that MCT-KDs may cause opposite morphologic modifications, being potentially harmful for SM CA1 and potentially advantageous for OML DG. This implies risks but also promising potentialities for their therapeutic use during aging.

PMID:  18593281 [PubMed - indexed for MEDLINE]

 

 

 

Effect of two medium chain triglycerides-supplemented diets on synaptic morphology in the cerebellar cortex of late-adult rats.

Balietti M1, Fattoretti P, Giorgetti B, Casoli T, Di Stefano G, Platano D, Aicardi G, Lattanzio F, Bertoni-Freddari C.

Author information

 

Abstract

Ketogenic diets (KDs) have shown beneficial effects in experimental models of neurodegeneration, designating aged individuals as possible recipients. However, few studies have investigated their consequences on aging brain. Here, late-adult rats (19 months of age) were fed for 8 weeks with two medium chain triglycerides-supplemented diets (MCT-SDs) and the average area (S), numeric density (Nv(s)), and surface density (S(v)) of synapses, as well as the average volume (V), numeric density (Nv(m)), and volume density (V(v)) of synaptic mitochondria were evaluated in granule cell layer of the cerebellar cortex (GCL-CCx) by computer-assisted morphometric methods. MCT content was 10 or 20%. About 10%MCT-SD induced the early appearance of senescent patterns (decreased Nv(s) and Nv(m); increased V), whereas 20%MCT-SD caused no changes. Recently, we have shown that both MCT-SDs accelerate aging in the stratum moleculare of CA1 (SM CA1), but are "antiaging" in the outer molecular layer of dentate gyrus (OML DG). Since GCL-CCx is more vulnerable to age than OML DG but less than SM CA1, present and previous results suggest that the effects of MCT-SDs in the aging brain critically depend on neuronal vulnerability to age, besides MCT percentage.

 

  PMID: 19455680

[PubMed - indexed for MEDLINE]

 

Complex effects at play here; MCT may be bad for certain parts of the hippocampus and good for others.

[Pallas]

I used this stuff during my morning fast. It would keep my brain fueled whilst skipping meals.

 

However there can be some nasty disaster pants if you don't slowly acclimate your dosages upwards. I remember having 4 tablespoons and going to the gym for a squat session. Worked my glutes more then usual that day. 

[Major Legend]

lol...at least subjectively I figured out that MCT oil/ or virgin coconut oil is best taken when you are undergoing some kind of mild ketosis, otherwise I don't feel any immediete effects. On the other hand I get a slight high if I take butter and coconut oil together whilst being on ketosis.

 

About ketosis: better to strike a balance, personally I tried total ketosis and started having some really weird rashes all over me, putting some carbs in solved that problem.

 

I also make my own hydrating topical solution with it, its the best oil for dry inflamed skin.

 

Its a must have in my opinion, next to curcurmin.

[Metagene]

This could be a potential issue with MCT supplementation:


Dietary medium-chain triglycerides promote oral allergic sensitization and orally induced anaphylaxis to peanut protein in mice

http://www.ncbi.nlm....les/PMC3563838/