Medium-chain triglyceride (MCT) oil is commonly known for its potent ability to aid in fat loss. However, this oil contains much more benefits, which I will discuss in this article.
First and foremost, fatty acids can be divided into four groups. These are short-chain- (SCFAs), medium chain- (MCFAs), long chain- (LCFAs) and very long chain fatty acids (VLCFAs).
SCFAs are what is mostly produced by the gut bacteria, via fermentation of fibers, which are resistant to digestion. These fatty acids are between 1 and 5 carbons long.
MCFAs are mainly present in dairy, coconut and palm kernel and are between 6 and 12 carbons long. Lauric acid (the fatty acid which is most abundant in coconut oil) is 12 carbons long, but acts more like a long chain fatty acid, so it cannot really be seen as a MCFA.
LCFAs are between 13 and 21 carbons long and are present in most, if not all, foods. Some common LCFAs are palmitic acid, stearic acid, and linoleic acid.
VLCFAs consist of 22 carbons and more.
Each type of fatty acid is handled differently by the body and how they are handled determines if they are oxidized (burned for energy), stored as fat, incorporated into cell membranes, etc.
A fatty acid on its own is a free fatty acid, but they are most abundantly found as triglycerides, which is three fatty acids bound together on one glycerol.
MCT is three MCFAs connected to one glycerol. The difference between MCT and LCT (long chain triglycerides) is absorption, transportation, handling, and oxidation.
In the gut, during digestion, MCT is broken down into glycerol and three MCFAs, which is then directly absorbed in the duodenum and jejunum into the bloodstream and thereby transported to the targeted organs. MCT is then directly absorbed into the portal vein, transported rapidly to the liver for beta-oxidation, and thus increases diet-induced thermogenesis. LCT is absorbed via the intestinal lymphatic ducts and is transported by chylomicrons through the thoracic duct into the systemic circulation.
MCFAs are more efficiently absorbed than LCFAs. MCFAs also don’t require transporters in the blood, such as albumin or other fatty acid transporters as LCFAs do. Similarly, their uptake by cells requires neither fatty acid transport proteins, nor plasma membrane-embedded fatty acid translocase, nor cytosolic fatty acid-binding proteins. This provides a likely explanation of why octanoate (C8) is oxidized 5 times faster than oleate (C18:1-ω9), which is oxidized almost as fast as lauric acid. (1)
Another interesting fact about MCT, and probably the most important one, is that MCFAs do not interfere or inhibit the oxidation of glucose. LFCAs, except palmitic acid, inhibits pyruvate dehydrogenase by increasing pyruvate dehydrogenase complex (PDC). This inhibits the step where pyruvate is shuttled into the mitochondrial for oxidation, thus rather converting pyruvate to lactate, instead of to CO2 and ATP.
On a high-carbohydrate low-fat diet, oleate oxidation declines by 50%, whereas octanoate doesn’t (2). In contrast, MFCA oxidation goes on full speed in the presence of glucose oxidation and even creates ketones (3).
MCT oil shuns Fat
Because MCFAs are transported to the portal instead of the lymphatic system, very little is incorporated into adipose tissue and is mainly oxidized. MCFAs are also poor substrates for elongation, so they will not contribute insignificantly to the synthesis of new fat.
In this rat study, resting and norepinephrine (NE)-stimulated metabolic rates were 38.8% and 22.2% higher in MCT than in LCT fed rats, respectively (8). The increase in metabolic rate and thermogenesis is blocked by a β-adrenergic antagonist. The increase in metabolic rate is also due to an increase in uncoupling proteins (UCP3) activity and expression. UCP3 quenches free radical (prevents oxidative stress) and increases thermogenesis (9).
MCT oil inhibits lipogenesis at doses above 5g (12), and also decreases adipogenic genes such as PPARγ, CCAAT/enhancer binding protein alpha (CEBPα), including their downstream metabolic target genes, and adipose tissue lipoprotein lipase activity (LPL) (13).
In contrast to LCFAs (e.g., oleate), octanoate significantly raised the AMP level in the tissue (14). AMP increases AMPK, which increases the uptake of glucose, the oxidation of fats and glucose and inhibits lipogenesis. (15)
One of the most important things about MCT is that it doesn’t interfere with glucose oxidation, as longer chain fats do. For instance, capric acid (C10:0) increases the capacity for fatty acid oxidation without inhibiting glycolysis in skeletal muscle. This is because it doesn’t increase insulin resistance or PDK4. PDK4 inhibits pyruvate dehydrogenase which is the rate-limited step for pyruvate entry into the mitochondria. (16)
MCT oil goes synergistically with other foods to increase diet-induced thermogenesis and reduce body fat. Such foods include protein and chilies. Adding 30g of chili and 20g of MCT (instead of LCTs) to a meal increases DIT (diet-induced thermogenesis) by over 50% (17, 18).
Endotoxins increase gut permeability, activate TLR4, increase inflammation, and all of this is prevented by MCT consumption. A human equivalent dose of 0.71mg/kg of MCT oil increased survival rate to 100% when a lethal dose of endotoxins was injected into rats (19). MCT oil also reduced the ALT response by 90%, gut permeability by 70%, the endotoxin receptor (CD14) expression by about 70% and TNFα by 60%. This just indicates how powerful MCT oil is against endotoxins, because the rats were injected with endotoxins, whereas humans absorb it through the gut. Absorption rate via injection is 100%, whereas the absorption rate through the gut is significantly less. So if MCT protects against the harmful effect of injected endotoxins to such a significant degree, it will do so to a much greater extent against endotoxins in the gut. This is important because endotoxins contribute a great deal to fat gain and inflammation, and all kinds of disease. This is one of the reasons calorie restriction is healthy, because it reduces endotoxins and gut microbes (20). MCT oil provides these benefits without the need for calorie restriction.
MCT also increase extracellular protein kinase (ERK½), which is suppressed during stress, most likely due to reduced availability of fuel for ATP production. As a matter of a fact, ATP supplementation increases ERK, which shows how potent MCT oil is at boosting ATP levels. ERK½ stimulates the vitamin D receptor, which in turn releases cathelicidin, which is very potent anti-bacterial. Gut bacteria is associated with weight gain and I’ll be writing an article about it soon, so be on the lookout for that.
MCT oil consumption also results in smaller sized adipocytes, which is indicative of less systemic inflammation, improved insulin sensitivity, etc. For more info on saturated fat and inflammation, check out this article.
The anabolic & androgenic fat
Apart from the fact that MCT oil can be utilized and oxidized very rapidly for fuel, thus having the potential to maintain optimal exercise performance, it can also assist in building muscle and gaining strength.
MCT consumption significantly enhances phosphorylation level of Akt and its downstream molecule mTOR, suggesting that MCT increases insulin sensitivity and glucose utilization in the skeletal muscle. (15). mTOR is the anabolic signal for stimulating muscle growth.
MCT oil ingestion also improvements nitrogen balance, protein synthesis capacity and the RNA/protein ratio, which will improve hypertrophy. (21)
Caprylic acid is an androgen receptor agonist and inhibits ACTH stimulated CRH release, which lowers cortisol levels under stress (22, 30). And as we know by now, keeping cortisol low is essential for building muscle.
This study shows that giving the elderly 6g MCT, in combination with 1.2g leucine and vitamin D (cholecalciferol (20 μg)), increased muscle strength and function, more so than LCFs, which was mostly ineffective (23).
In high temperatures and most humidity conditions, maximal aerobic capacity is impaired by increasing serotonin and prolactin, as well as reducing dopamine (24). MCT restores optimal exercise performance under such conditions.
The Fat that fuels brain cells as a Nootropic
MCFAs are able to rapidly permeate the blood-brain barrier and supply energy.
Capric acid (C10), but not caprylic acid, has been found to stimulate glycolysis in astrocytes, thus resulting in an enhanced release of lactate into the extracellular space, which is considered a key energy source for neurons (25).
6g of MCT in combination with 1.2g leucine and vitamin D (cholecalciferol (20 μg)), also improved cognitive function in the elderly whereas the LCTs did not (26).
Acute hypoglycemia, such as which occurs during diabetes, impairs cognitive performance in tests of attention, short-term and delayed verbal memory, as well as working memory. MCT oil (40g dose) is shown to prevent the decline in cognitive performance during hypoglycemia in tests of immediate verbal memory, delayed verbal memory, and verbal memory recognition (during hypoglycemia in type I diabetes), by providing ketones to the hippocampus (a brain region particularly vulnerable to hypoglycemia) (27).
There has recently been an established link between mitochondrial dysfunction and high anxiety and depression. This is where MCFAs shine bright because they’re so easily utilized for fuel, even with mitochondrial dysfunction. MCFAs prevent a decline in the activity of the nucleus accumbens (NAc) and lower excessive prefrontal cortex (PFC) activity.
A decrease in NAc activity and excessive glutamate signals through PFC is pro-anxiety. Promoting NAc activity and antagonizing glutamate with ketamine is anti-anxiety.
MCT oil significantly enhanced GLT-1 (a glutamate transporter) and Na-K ATPase (which controls GLT-1 activity) in the mPFC, which increased the capability to uptake excessive glutamate in this brain region (28).
It has also been found that MCT oil prevents depression caused by a stress-induced down-regulation of the pERK½:ERK½ ratio.
As a cool side note: The activation of ERK1/2 activates C/EBPβ, which increases detoxification enzymes in the liver and contributes to liver protection and regeneration.
It also lowers cortisone and increases glucocorticoid receptor mRNA, meaning lower cortisol levels, but increased sensitivity. (29) This shows the involvement of cortisol in depression. More on lowering cortisol here.
Saturated fat, with caprylic acid being the most potent, inhibits ACTH stimulates CRH release, thus inhibiting an increase in cortisol in periods of stress (30).
MCT oil will help you stay cool under stress.
Serotonin, similarly to cortisol, is also involved in depression, anxiety and mental slow down. MCT oil decreases the tryptophan to LNAA (large neutral amino acids), thus reducing brain serotonin synthesis (31). Serotonin is also involved in fibrosis, metabolic slowdown, and various other diseases. More on lowering serotonin here.
MCT oil reduces ammonia levels in cows. Ammonia reduces glutamate to GABA conversion and thus increases excitability and anxiety (32).
Revamps mitochondrial function
Many things can reduce mitochondrial function, such as PUFAs, inflammation, reactive oxygen species, cortisol, etc., but luckily mitochondrial function can be restored.
MCT oil increases the gene expression of tfam (a marker of mitochondrial biogenesis), uqcrc (Ubiquinol Cytochrome c Reductase; a respiratory chain protein on complex III), cox5b (Cytochrome c oxidase 5B; the last enzyme in the mitochondrial electron transport chain in complex IV), PGC-1α (a key regulator of energy metabolism and mitochondrial biogenesis) and mitochondrial membrane ATP synthase (the enzyme that converts ADP to ATP) (15).
It does so by increasing the activity of Akt and AMPK signaling pathways and inhibiting the TGFβ signaling pathway (15).
Mitochondrial biogenesis and function are negatively controlled by TGF-β signaling, which is mediated by Smad3. MCT hugely inhibits Smad3 and lowers TGFβ activity (15).
TGF-β signaling is required for normal tissue repair; however, excessive TGF-β signaling is involved in fibrosis, suppression of genes related to mitochondrial biogenesis and function, inhibition of complex IV and mitochondrial respiration; which in turn leads to increased ROS and decreased mitochondrial membrane potential, and a reduction of uncoupling protein 2 (UCP2; which increases thermogenesis) (15).
An increase in mitochondrial substrate flux, as seen with MCT oil, is often accompanied by higher ROS production; however, the mitochondria from MCFA-fed mice displayed a 32% decrease in hydrogen superoxide (H2O2) generation and a reduction in free radical leak. Which might explain the reduction in oxidative stress and inflammation seen in MCFAs consumption (33). So not only is MCT a readily available fuel, it’s also one of the safest fuels.
MCT increases ceramide, which is a waxy lipid molecule and is found in high concentrations within the cell membrane. But MCT only increases the ceramide with a chain length of C18 & C24, and it’s the chain length that has different effects (34). CER18:0 and CER24:0 are both involved in the synthesis of myelin and normal neural development. C18 has anti-tumor and cancer effects by inhibiting proliferation and inducing apoptosis (programmed cell death); whereas CER24:0 protects cells against damage and is anti-apoptotic. As seen in this study, MCT oil obliterates tumor growth (35).
MCT oil upgrades mitochondrial function, while also increasing the production of brand new mitochondrial.
Symbiotically improve insulins’ function
MCT doesn’t improve insulin sensitivity per se, but it does improve the function of insulin.
For instance, MCT oil reduces preprandial glycemic excursions by 45% in diabetic patients (36), by increasing insulin-mediated glucose disposal. It also improves insulin-stimulated glycogen synthesis rate by restoring the phosphorylation of GSK3β. This helps to lower blood glucose after a meal (by increasing muscle glucose uptake after a meal).
MCFAs, compared with LCTs, increases serum adiponectin levels by increasing the activity of the adiponectin gene (37). Adiponectin is anti-inflammatory and improves insulin sensitivity. So MCT oil can possibly improve insulin sensitivity over the long run congruent with the improvement to insulins’ function.
a) MCT oil is able to reverse fibrosis in the liver by lowering TGF-β and increasing mitochondrial biogenesis. It’s also able to improve liver health by lowering ALT and AST in a CYP450 dependent and non-CYP450 dependent manner (38). MCT oil is even effective at reversing alcohol-induced necrosis, inflammation, and fibrosis (even in the presence of continued alcohol consumption). The therapeutic effects may be explained, at least in part, by reduced endotoxemia and lipid peroxidation, which in turn result in decreased activation of NF-κB and reduced levels of TNFα and Cox-2 (39).
b) Significantly improves markers of metabolic syndrome (40).
c) MCT feeding was associated with low linoleate and low tocopherol requirements in rats. Reduced linoleate = reduced thrombosis formation and ROS/lipid peroxidation production (41). Sri Lanka has the lowest death rate from ischemic heart disease (because of their high MCFAs via coconuts).
d) Medium-chain fatty acids can be used as metabolic therapy in cardiac disease (42).