MCTs play a unique role in T-helper 2-type (Th2) allergic responses via their stimulation of thymic stromal lymphopoietin (TSLP). The AMPA receptor GluR1 is thought to directly participate in the regulation of melatonin secretion.334https://doi.org/10.1046/j.1471-4159.2000.0750288.x This may be one of the factors, aside from neuronal oxidative stress, that plays into circadian rhythm disruptions and insomnia seen in Alzheimer’s disease. Octanoic acid’s effects on dendritic cells may also be seen in the skin, where it acts as an immune sensitizer. Because the body prefers to burn glucose for fuel when it is available, a diet filled with carbohydrates that convert to glucose in combination with long-chain fats, will encourage the development of adipose tissue. Medium-chain fatty acids have shown the capability to directly cross the blood-brain barrier, reaching levels 50% of that found in blood plasma, thereby providing neurons and astrocytes directly with an alternative energy source. This hypothesis is not well supported at this time, and I encourage any scientists reviewing this material to organize a study that would elucidate it further. Ironically, the very mechanism by which MCTs control seizure in models of epilepsy is the very means by which they can also induce cognitive decline. Without calcium, this phenomena is considerably less prominent.249https://alzres.biomedcentral.com/articles/10.1186/alzrt214 Nonetheless, antibodies to GluA3 AMPAR subunits as a result of autoimmunity also reduce their levels with or without tau’s involvement. Clearly, even in the absence of autoimmunity, the degradation of neurons induced by amyloid proteins can induce stress signals that lead to rampant neuroinflammation, and adding medium-chain triglycerides to this milieu is only going to throw oil on the fire. Ordinarily, only ions, water, and water-soluble molecules are allowed through the tight-junctions of the gut. As such, MCTs have a wide variety of effects on brain cell energy metabolism. Both animal and human trials have shown ketogenic diets have slight beneficial effects in mild-to-moderate Alzheimer’s disease. Only at extremely high levels of consumption would we see any AMPA-inhibitory effect. Currently, the only trials that have been performed in this area have focused on autoimmune encephalitis involving either NMDA or AMPA receptors. Once again, this is precisely what MCTs do in the brain in models of epilepsy. This is especially true for decanoic acid which is not well metabolized, due to the absence of CPT1 expression in the brain. Such plans include anergy, clonal deletion by activation, induced cell death, and antigen sequestration. overdevelopment). Repeated exposures to skin sensitizers such as octanoic acid leads to chronic allergic contact dermatitis, in part induced by upregulation of pro-inflammatory genes such as ATF3 and chemokine CXCL8.138https://www.ncbi.nlm.nih.gov/pubmed/27965148. Inhibition of glycolysis (i.e. Thus far, we have been focusing on MCT metabolism and the general risk for overconsumption. It should be abundantly clear that MCTs increase antigen uptake into Peyer’s patches, providing them access directly to the internal immune cascade. FoxO controls transcription of gluconeogenic enzymes and in the absence of insulin, it invokes hepatic glucose production. There were significantly fewer mitochondria, and those that survived were dysfunctional. While the study did a fantastic job of showing the physiological effects of ketone production from MCTs — a whopping 230% increase in brain ketone metabolism–it did have a few shortcomings in terms of the cognitive measures. This can result in swelling and, eventually, apoptosis (i.e. Unfortunately, quite severe complications can and do arise over time, even with intermittent use, and are almost never associated with the smoking gun that is medium-chain triglycerides. In this article, we are going to analyze medium-chain fats, specifically capric (C10) and caprylic (C8) acids, from all possible angles and connect dots that have never been connected before. It should be further concerning to find that capric acid is produced endogenously by colorectal tumors and has started to get attention as an early diagnostic biomarker for colorectal cancer. Considerable excretion of saturated, unsaturated and hydroxylated medium-chain fatty acids has also been seen, along with several conjugates such as suberylglycine, hexanovlglycine and octanoylcarnitine.386https://doi.org/10.1016/0009-8981(83)90246-2387https://link.springer.com/article/10.1007/BF03047374 Of note, these urinary profiles are accompanied by a parallel low level of carnitine in both urine and plasma. We’ve already discussed how medium-chain fatty acids are catabolized by beta-oxidation, resulting in acetyl-CoA formation. It is also important to note that these natural sources of MCT do not contain large amounts of C8 and C10 fatty acids. This is one of the many ways in which MCTs can exacerbate neurodegeneration, and volume / frequency of intake matter greatly.29https://www.sciencedirect.com/science/article/abs/pii/0304394090906912. Contrary to popular belief, the effects are not so much related to ketones but, rather to inhibition of the glutamate-binding AMPA receptors and increase in mitochondrial biogenesis (i.e. Valproic acid can achieve these stages in 50% tested cases at 1.06 mmol in only 5-10 minutes. Without mucosal tolerance, there is increased risk for inflammatory damage to the gut mucosa as a result of “hyper-reactivity”. Indeed, Crohn’s disease has been shown to be most prominent in the ileum where there is an abundance of Peyer’s patches.118https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5083260/, As stated above, we see a peak in Peyer’s patch numbers between the ages of 15 and 25. As such, it serves as a defense mechanism preventing the disturbance of the local brain environment. So we now have overactive DC-mediated activation of both autoreactive T cells, and by virtue of their damage to the neurons themselves, antigen-type reactivity to self-proteins. It is extremely important to emphasize here that these issues arise on a very broad spectrum from no symptoms at all to full-blown metabolic shutdown. CO2 production) but also mitochondrial respiration, and this effect is amplified in accordance with individual metabolism of medium-chain fatty acids. As a matter of fact, one of my clients that suffers from this problem used to get significant pressure in his head after consuming any amount of caprylic acid. palmitic acid), With carnitine depletion, further have the potential of, With increased consumption, can accumulate in the brain (especially C10), inhibiting energy metabolism in the cerebral cortex, and ultimately. The answer to this question is beyond the scope of this article, but it includes a number of factors including dietary calcium intake, vitamin D and K status, as well as any compound that could potentially affect calcium homeostasis.295https://doi.org/10.1124/jpet.110.166363 One such compound is caprylic acid. Don’t wait – take action now! Though at least one study proved that consumption of up to 42g of MCT per day has not shown any significant side effects, this should not be interpreted as “carte blanche” for liberal and unrestrained use.21https://www.ncbi.nlm.nih.gov/pubmed/1913576822https://www.ncbi.nlm.nih.gov/pubmed/16753249 Nonetheless, we see MCTs cropping up in an almost endless array of foodstuffs ranging from protein powders to chocolate bars and, of course, coffee. Coconut Oil, Ketones and Alzheimer’s Disease. As it turns out, C10 has been found to employ the carnitine shuttle to improve beta-oxidation potential! MCTs produce this condition, regardless of whether or not symptoms are present. Epithelial cells in the choroid plexus are densely numbered with mitochondria and have enzymes for glycolysis and the citrate cycle, both of which are essential to varying degrees for the supply of energy to physiological functions such as the active transport process. As I will describe below, this ammonia is more likely to end up in the bloodstream when there is higher gut permeability – and MCTs have the distinct ability to degrade that gut barrier, thereby allowing more ammonia through. For that particular client, administration of L-carnitine resolved the issue, and the scientific literature confirms the ability of carnitine to enhance the excretion of medium-chain acyl carnitines, the most prominent of which is octanoylcarnitine from C8.87https://www.sciencedirect.com/science/article/abs/pii/000689939090046E. AMPAR modulation is quite messy and it can be difficult to gauge “which side” of the activation curve one is on. Though the brain loves glucose and thrives on it, it can also use ketones generated by the liver to satisfy its energetic requirements. Indeed, this effect may very well be one of the ways in which biohacker anecdotes of “improved cognitive function” have appeared — via higher glutamatergic signaling. This delicate balance only works when the immune system recognizes commensal bacteria from previous exposures. The choroid plexus / blood-cerebrospinal fluid barrier, is absolutely critical for the clearance of both endogenous and exogenous organic acid products via the transport system. This mast cell degranulation in response to MCT may be effectively blocked by preventing receptor-mediated IgG responses.127https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670761 Considering these facts, it’s very clear that ingestion of in MCTs to any degree, with or without a food substance to which an allergy already exists, there is the potential for increased gut barrier permeability, absorption of antigen into Peyer’s patches, increased antibody production, and in extreme cases, the potential for anaphylaxis from any antigen to which one has been sensitized by MCT. However, there are plenty of keto-friendly sweeteners that you can use as sugar. EBV, HSV, etc. C10, in excess, has shown to have a wide range of neurological effects, not the least of which is the inhibition of mitochondrial cytochrome C activity by as much as 30% and complex II-III activity by 25%. Because Coconut Oil is a medium chain fatty acid (ie MCT), even though it is a saturated fat, it will not raise LDL cholesterol levels, and is not harmful to the diet. One of the issues with MCT oil containing both decanoic and octanoic acids is that CPT1 (carnitine palmitoyltransferase I), required for beta-oxidation of decanoic acid / C10 in mitochondria, is poorly expressed in the brain. and Naked Gun fame) brought his son, who was suffering from severe seizures, to Johns Hopkins Hospital in Baltimore. I was experiencing spontaneous, severe hypoglycemia, elevated ammonia in the brain (verified by testing), neurotransmitter disruptions which bordered on psychosis, and worst of all, hypothyroidism with sporadic dips in energy. The most common ones were stomach issues like discomfort, reflux, diarrhea, or nausea. Does this sound familiar? In the stomach, H. Pylori has been shown to induce gastritis via Peyer’s patch mediated translocation. It catabolizes proteins to form glucogenic amino acids and breaks down triglycerides, both of which may be used for glucose production. Decanoic acid increases paracellular transport of high molecular mass compounds across the tight junctions, with transport efficiency actually increasing with larger molecules. Sodium salts of these compounds are even more efficient in this respect. Further, carnitine levels in the blood are tightly regulated by the kidneys, so if there is any degree of kidney stress or disorder (e.g. This would further manifest as higher translocation of pathogenic bacteria via PPs.115https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885825116https://www.researchgate.net/publication/38018848_Nod2_regulates_the_host_response_towards_microflora_by_modulating_T_cell_function_and_epithelial_permeability_in_mouse_Peyer’s_patches In this way, MCTs are capable of gradually sensitizing a host to hyper-reactive immune responses to its own beneficial bacteria. Over time, such stress will deplete glutathione stores, thereby further decreasing available GSH for the beneficial conversion of S-hydroxylaminoglutathione to oxidized glutathione (GSSG). Truly, I would not have known to recognize their symptoms had I not experienced many of them first-hand. More often than not, it is combined with high-fat, low-carb diets that, at their extreme, become what is commonly known as “ketogenic”. In fact, AGEs are likely responsible for the majority of atherosclerosis and heart attacks in the world. Infections or autoimmune responses can only add oil to this fire. Yet other studies exist which clearly demonstrate the ability of capric (i.e. At that stage, they can either be further metabolized to ketones or enter the Citrate cycle for energy production.150http://www.jbc.org/content/262/27/13027151https://doi.org/10.1111/j.1471-4159.1988.tb01044.x When MCTs are administered with glucose, the brain has been shown to prefer glucose as its primary neuronal energy source.152https://doi.org/10.1002/jnr.10079153https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3900881/154https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390246155https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410436 Nonetheless, even though C8 and C10 have lower oxidation rates than glucose, they are taken up by neurons even in its presence. To be clear, in the early stages of Alzheimer’s, when symptoms are barely noticeable (if at all), a selective decrease in AMPARs has been noted. 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