ON SALE UNTIL TOMORROW: Evidence-based Keto
Unbiased truth on keto and long-term effects on health, safety, pre-existing conditions, losing weight, and more.Learn the latest on keto
Human Effect Matrix
The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects medium-chain triglycerides has on your body, and how strong these effects are.
|Grade||Level of Evidence [show legend]|
|Robust research conducted with repeated double-blind clinical trials|
|Multiple studies where at least two are double-blind and placebo controlled|
|Single double-blind study or multiple cohort studies|
|Uncontrolled or observational studies only|
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
|Minor||Moderate See all 4 studies|
|Minor||- See study|
|Minor||- See study|
|Minor||- See study|
|Minor||- See study|
|Minor||- See study|
|Minor||- See study|
|Minor||- See study|
|Minor||- See study|
|-||- See study|
|-||- See study|
|-||- See study|
|-||- See study|
|- See study|
|-||- See study|
|-||- See study|
Everything you need to know about the keto diet
When we asked our users what they wanted us to cover, many of them mentioned the keto diet.
So we listened. We spent the year looking up the research on the ketogenic diet to help guide you in your journey.
With Evidence-based Keto, Examine.com gives you all the scientific research, but in understandable language with tons of informative infographics. No opinion, no bias, no conflict of interest.
If you’re interested in keto, this is a must-have unbiased source.
Scientific Research on Medium-chain triglycerides
Click on any below to expand the corresponding section. Click on to collapse it.
Medium chain triglycerides (MCTs) are a type of saturated fat in which the fatty acids have only 6-10 carbons. These fatty acids are referred to as medium chain fatty acids (MCFAs) and include:
Caproic acid (C6:0)
Caprylic acid (C8:0)
Capric acid (C10:0)
MCTs are not widely distributed in foods and can be found in limited quantities in dairy fat and tropical oils such as coconut oil and palm kernel oil. The richest dietary sources of caproic acid are butter (2 grams per 100 grams butter, or 2%) and various types of cheese (0.5%). Caprylic acid is most abundant in coconut oil (6.8%) and palm kernel oil (3.3%). Capric acid is most abundant in coconut oil (5.4%), palm kernel oil (3.7%), goat cheese (3.4%), and butter (2.5%).
The melting point of MCFAs is far lower than that of long-chain saturated fats, which explains why MCT oil is a liquid at room temperature while other saturated fats remain solid. The smaller size of MCFAs increases their solubility in water and the tendency for MCFAs to be ionized at neutral pH further increases their solubility in biological fluids (e.g., blood).
MCT oil is marketed as a supplement and is typically a combination of caprylic (50-80%) and capric acids (20-50%) sourced from coconut or palm kernel oil due to their relative abundance of these fatty acids compared to other foods. MCTs are produced by splitting and distilling the fatty acids from coconut or palm kernel oils, and then mixing the desired ratio of MCFAs with glycerin to form a triglyceride. This process can be achieved both through the use of chemical solvents and lipases.
The digestion and absorption of fatty acids is partly dependent on their length. Digestion for all triglycerides begins in the mouth and stomach with the action of lingual and gastric lipases and the type of fat does not appear to influence the rate of gastric emptying. Upon entering the small intestine, long-chain fatty acids stimulate the release of pancreatic lipase and bile, which together finish the digestive process and allow for long-chain fatty acids to be absorbed into the intestinal cells, packaged into chylomicrons, and excreted into the lymphatic system.
In contrast, MCFAs do not stimulate the release of pancreatic lipase and bile and passively diffuse through the intestinal cells into the portal vein. MCFAs are absorbed faster than long-chain fatty acids and at a rate similar to glucose, and it has been shown that an acute dose of 40 grams of MCTs fails to stimulate a chylomicron response.
However, it has been noted that MCFAs can account for 7-22% of the total fatty acid content of chylomicrons after five days of consuming a diet in which 40% of the calories are supplied by MCTs, suggesting that MCFAs can undergo the normal absorptive process of dietary fat when consumed in large enough quantities. The incorporation of capric acid was three- to four-fold greater than that of caprylic acid even though the diet contained nearly twice as much caprylic acid, strengthening the argument that fatty acid chain length plays a role in determining how the the fatty acids are digested and absorbed.
Chylomicrons enter systemic circulation from the lymph at a relatively slow rate and deliver their fatty acid contents mostly to tissues other than the liver, such as muscle and adipose tissues. The direct entry of MCFAs into portal circulation results in a near complete uptake by the liver, with almost none reaching systemic circulation.
Within the liver, MCFAs cross the mitochondrial membrane rapidly and without a need for carnitine, which is necessary for long-chained fatty acids to enter the mitochondria and undergo beta-oxidation. Beta-oxidation of the MCFAs results in an excess of acetyl-CoA that enters into various metabolic pathways. A fraction of this will enter the Krebs cycle and supply energy via the electron transport chain, but the amount of acetyl-CoA that can enter into the Krebs cycle is limited by the availability of other intermediates, especially oxaloacetate. Since the availability of acetyl-CoA determines the rate of ketogenesis, the excess supplied by MCFAs and not used in the Krebs cycle is redirected towards ketone production, with little to none being used for fat synthesis. This occurs even in the presence of anti-ketogenic regulators such as insulin.
Caprylic acid is the most ketogenic MCFA, resulting in a blood ketone response about ~25% greater than an MCT oil mixture containing a 60% caprylic acid and 40% capric acid.  Additionally, a significant positive correlation was observed between blood ketone levels and the dose of caprylic acid, but not capric acid, suggesting that caprylic acid is driving the ketogenic effects of many commercial MCT oil products. 
MCTs do not undergo the same digestive and absorptive processes as long-chain fats. Instead, they are readily absorped into the portal vein and rapidly oxidized within the liver, resulting in the production of ketones. Caprylic acid appears to be the most ketogenic MCFA.
MCFAs readily crosses the blood-brain barrier via a combination of passive diffusion and a MCFA transporter that is used by some anticonvulsant drugs such as valproate. Capric acid is a non-competitive antagonist of the AMPA receptor, which is one of the three subsets of glutamate (excitatory) receptors. Caprylic acid does not affect AMPA receptor activity.
Several acute feeding studies in healthy men and women have reported that consuming 10-40 grams of MCTs alongside a standardized test meal significantly reduces energy intake at the following meal by 40-165 kcal compared to margarine, corn oil, and olive oil and lard. However, none of these studies reported significant differences in appetite or satiety ratings between the MCT and long-chain fat groups.
Two studies included a control group that ate the standardized test meal without any added fat. Compared to this group, the MCT supplementation significantly reduced energy intake at a later meal by 40-64% of the kcal supplied by the MCTs. Thus, there does not appear to be full compensation for the additional energy provided by the MCT oil. The effect on appetite is also mixed, with only one of the studies reporting significant reductions in hunger compared to the control.
A randomized crossover trial in six healthy men showed that increasing the ratio of MCT to long-chain fat in the diet from 0.5:1 to 2:1 while keeping total fat, carbohydrate, and protein intake constant over a two-week period resulted in a significant reduction in food intake averaging about 250 kcal per day.
In women with obesity administered a very low energy diet (~600 kcal/d) supplemented with either 10 grams of MCTs or long-chain fats for four weeks, hunger ratings were lower and satiety ratings were higher for up to 120 minutes after consuming the MCT supplemented meals during the first two weeks and up to 40 minutes after the meals thereafter, suggesting a diminished satiety effect over time. This is supported by the acute feeding study in women, which reported no significant difference in between MCTs and corn oil on subsequent energy intake among self-proclaimed dieters (actively trying to lose weight during the study).
However, a 12-week intervention in Chinese men and women with type-2 diabetes reported that adding 18 grams of MCTs into the diet resulted in a significant reduction in daily energy intake compared to adding 18 grams of corn oil.
MCTs appear to reduce energy intake when substituted for long-chained fats and compared to meals without any added fat, but the calories supplied are not fully compensated for compared to the no-fat condition. Evidence regarding appetite and satiety is mixed.
A high-fat, low-carbohydrate, low-protein ketogenic diet (typically a 3:1 or 4:1 ratio of fat to combined carbohydrate plus protein) has been in clinical use for over a century as a treatment option for children with epilepsy and current evidence suggests that it is very effective at reducing seizures. The anticonvulsive property of ketones is not completely understood but is likely related to neurotransmitter modulation, reduced neuronal excitability, enhanced energy production, and a direct antioxidant effect on the brain. However, adverse events such as stunted growth and bone loss, as well as a low palatability of the diet, limit adherence and the length of time that children may safely follow it.
Due to the ketogenic property of MCFAs, a high-MCT oil variant of the traditional ketogenic diet was introduced in the 1970s and investigated for its ability to increase the safety and tolerability of a traditional ketogenic diet while retaining its benefits for treating epilepsy. This diet was about 10% protein, 20% carbohydrate, 60% MCTs, and 10% long-chain fat and was found to be more palatable and allow for a greater diversity of foods.
Several early studies using the MCT oil diet found comparable seizure control to the traditional ketogenic diet but with intolerable gastrointestinal side effects in some children due to the high MCT oil intake.. In response, one group of researchers evaluated the effectiveness of a 30% MCT oil diet and reported comparable results between the traditional ketogenic diet, a 60% MCT oil diet, and a 30% MCT oil diet over three weeks. Although the 60% MCT oil diet was considered the most unpalatable and resulted in the greatest reports of diarrhea and vomiting, the 30% MCT oil diet was the best tolerated with few side effects.
One researcher has claimed that there are fewer incidents of kidney stones, hypoglycemia, ketoacidosis, constipation, low bone density, and growth retardation on a high-MCT oil diet compared to the traditional ketogenic diet. However, the author references a study that does not exist with himself as the author. In contrast to these claims, other research has reported no significant difference between a 45% MCT oil and traditional ketogenic diet for growth parameters, with both causing growth retardation despite a higher protein intake in the MCT oil group.
Only one randomized controlled trial to date has compared a 45% MCT oil diet to the traditional ketogenic diet for the treatment of epilepsy. It reported both diets to be equally effective at reducing seizures at 3-, 6-, and 12-month follow-ups, with no differences between groups. The children in the MCT oil diet group had a median reduction in seizure frequency of 30% after 12 months compared to baseline, with 22% achieving greater than 50% reduction and 10% greater than 90% reduction. However, the dropout rate and tolerability of both diets was similar, with 46% of the participants discontinuing treatment before 12 months and commonly reported adverse events being vomiting, diarrhea, abdominal pain, constipation, fatigue, hunger, and taste problems.
The only study not involving children is a case study of a 43 year-old man with history of partial epilepsy who previously failed multiple trials of antiepileptic drugs. He reported a dramatic reduction in seizure frequency with the addition of four tablespoons (60 mL) of MCT oil daily and a recurrence of seizures after ten days of MCT oil discontinuation.
A high-fat (70% kcal), high-MCT oil (30-60% of kcal) diet with limited carbohydrate (20% kcal) and protein (10% kcal) is an effective alternative to the traditional therapeutic ketogenic diet used for the treatment of epilepsy in children. Both diets have comparable reductions in seizure frequency and adverse events, including growth retardation and gastrointestinal problems. Evidence in adults is lacking.
MCTs have been investigated for their ability to enhance cognition in several studies based on preliminary clinical trials and mechanistic data suggesting that ketogenic diets improve cognitive function in people with Alzheimer’s disease through increasing ketone use by the brain.
A double-blind crossover study involving 20 elderly adults with mild to moderate cognitive impairment or probable Alzheimer’s disease reported that consuming 40 mL of MCT oil (>95% caprylic acid) significantly improved performance on the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-cog) compared to an equal amount of fat from heavy whipping cream, but only among participants who did not contain the APOE4 variant. Those with the APOE4 variant performed significantly worse with MCT oil supplementation. However, there was no effect in either group for performance on the Stroop Color Word Test.
A follow-up randomized controlled trial assessed the effectiveness of consuming 20 g of MCT oil (>95% caprylic acid) daily for 90 days on cognitive performance in 140 Alzheimer’s disease patients. The MCT oil group had significantly greater improvement on the ADAS-cog than the placebo group after 45 days and nearly significant (p=0.077) improvement after 90 days. There was no difference between groups for the Mini-Mental State Examination (MMSE) or Clinical Global Impression of Change (CGIC) scores. As demonstrated by the previous study, when the participants were stratified by APOE4 genotype, only those who were APOE4 negative performed significantly better on the ADAS-cog test with MCT oil supplementation compared to the placebo group.
A third double-blind, randomized controlled trial involved four elderly adults with mild cognitive impairment who supplemented with 56 grams of commercial MCT oil or canola oil placebo per day for 24 weeks. No statistical tests were performed and no performance improvements in the ADAS-cog were noted.
Two studies have suggested that caprylic acid supplementation can enhance cognitive function after a single 40 mL dose and after daily dosing of 20 grams over 90 days among older adults with mild to moderate cognitive impairment and who are negative for the APOE4 variant.
A double-blind randomized controlled trial involving 78 healthy adults who consumed 10 grams of MCTs daily for 12 weeks reported no significant differences in fasting triglycerides or total cholesterol compared to those who consumed a blend of rapeseed and soybean oils. Similarly, a study of 18 healthy women reported that consuming 30 grams of MCT oil did not significantly alter triglycerides, total and LDL-cholesterol, apoA-1, apoB, or LDL particle size compared to lauric acid, although only lauric acid increased HDL-cholesterol.
Consuming 10% of calories from MCFAs was reported to have intermediate effects on total and LDL-cholesterol compared to myristic and oleic acid, with no difference in triglycerides. Additionally, the MCFA diet slightly lowered apoA-1 while myristic and oleic acids increased it, and all of the fats similarly raised apoB, leading to a significantly lower apoA-1 to apoB ratio in the MCFA group. There was no effect of MCFAs on lipoprotein(a).
However, consuming 40% of calories from MCT oil (relative to soybean oil) was found to significantly increase triglycerides by 42% and reduce HDL-c by 15% in just six days without effecting total or LDL-cholesterol levels. A 3-fold increase in fasting triglycerides was noted when participants were overfeeding. In either case, consuming a single meal with ~40 grams of MCTs had no effect on postprandial triglyceride levels. An early study also found that consuming 40% of calories from MCT oil significantly increased total cholesterol compared to corn oil but lowed cholesterol compared to butter.
In overweight and obese adults, consuming 18-24 grams of MCTs for 90 days in the context of a hypocaloric diet resulted in similar reductions in total cholesterol and LDL-c and increases in HDL-c as olive oil, with neither diet affecting triglycerides. Another study in obese men found that daily supplementation with 20 grams of MCT oil had no effect on the blood lipid profile compared to corn oil.
However, a study in overweight and obese men found that MCFAs significantly increases nearly all VLDL, IDL, and LDL subfractions compared to linoleic acid, which was associated with a significant reduction in VLDL, IDL, and LDL particle lipolysis and uptake in the liver and no modification to VLDL production. These findings are complemented by a study in rats showing that MCFAs lower lipoprotein lipase activation in adipose tissue.
Several studies by a group of researchers in Beijing, China have investigated a type of triglyceride in which the fatty acids are a mixture of long- and medium-chain fatty acids, so that it contains 13% MCFAs (e.g., 13 grams of MCFAs per 100 grams of the oil). Compared to purely long-chain triglycerides supplied by rapeseed and soybean oils, consuming 25-30 grams per day of this mixture (3-4 grams of MCFAs) has similar effects on triglycerides and cholesterol in healthy adults and significantly reduces triglycerides and LDL-cholesterol in hypertriglyceridemic adults.
These effects appear to occur only in men, which the authors speculate may be owed to a deficiency in estrogen among the primarily postmenopausal women participating in the study. Additionally, the MCFA mixture group lost significantly more fat mass than the long-chain fat group in these studies, which may have impacted the oil’s effect on blood lipids. A reanalysis of the data by BMI status showed that only overweight and obese participants experienced significant reductions in triglycerides and LDL-cholesterol and were also the only groups to experience significant reductions in fat mass, supporting the notion that weight loss was the primary driver of the superior effect on blood lipids.
Low doses of MCT oil (10-20 grams) appear to have little to no effect on blood lipids in healthy adults. However, large doses (40% of kcal) appear to notably increase fasting triglyceride levels, especially when overfeeding.
One study in patients with hyperlipidemia reported that consuming ~10% of energy intake from MCT oil significantly increases total cholesterol (16%) and non-HDL cholesterol (19%) compared to corn oil without affecting fasting triglycerides and preventing an increase in postprandial triglycerides. However, consuming 43% of calories from MCTs, again in patients with hyperlipidemia, caused a significant increase in triglycerides (20-30%) and VLDL (26-38%) compared to both palm oil and high-oleic sunflower oil, as well as significant increases in total (12%) and LDL-cholesterol (14%) compared to sunflower oil only.
In people with type-2 diabetes, small doses of MCT oil (18 grams) have been reported to significantly reduce total cholesterol (12%), LDL-c (17%), and HDL-c (16%) relative to corn oil, with no difference in triglycerides. However, the MCT oil group also lost significantly more bodyweight that may have affected changes in blood lipids. Consuming 54-103 grams per day of MCT oil increased triglycerides in patients with type-2 diabetes only under weight-maintenance conditions; no effect was observed when the patients were eating in an energy deficit.
An inpatient feeding study compared weight-maintenance diets with 40% of calories supplied by MCTs or long-chain fats provided by partially hydrogenated shortening (Crisco), each consumed over a four-day period. The MCT diet significantly reduced triglycerides in participants with type-2 diabetes (-19%) but did not affect total and HDL-cholesterol. A double-blind randomized controlled trial involving people with type 2 diabetes reported that consuming 28% of kcal from MCTs had no effect on triglycerides or cholesterol levels relative to a common vegetable oil over two weeks.
In people with elevated triglyceride and cholesterol levels, MCT oil appears to increase blood lipids further, especially compared to oils high in polyunsaturated fatty acids. However, even large doses of MCT oil appear to have minor effects on the blood lipids of people with type-2 diabetes.
It has been suggested that any cholesterol-raising effect of MCTs is owed to the use of a comparator oil high in polyunsaturated fatty acids, which are well known to reduce blood cholesterol concentrations. Accordingly, MCTs may be relatively neutral compared to monounsaturated and long-chain saturated fatty acids, which has been shown via comparisons to olive oil, oleic and mystryic acids, and butter.
Most studies have compared MCTs to highly polyunsaturated seed oils such as corn and soybean oils. Further research is necessary to determine the effects of MCTs compared to other dietary fats.
Consuming 1 g/kg of MCT oil has been shown to raise insulin levels in healthy adults from a fasting level of 9.3 µU/mL to 17.7 after 30 minutes, 15.3 after one hour, and 15.4 after two hours, with a decline back to baseline thereafter. This was associated with a significant reduction in blood glucose of about 6-8 mg/dL. These observations have been replicated.
A small study involving 10 adults with type 2 diabetes reported significant increases in insulin sensitivity during a hyperinsulinemic-euglycemic clamp after four days of consuming 40 grams of MCTs prelative to shortening, which appeared to be owed to an increase in glucose uptake in peripheral tissues.
However, a follow-up study in five free-living adults with type 2 diabetes reported that consuming 15 mL of MCTs with each of three meals per day for one month had no significant effect on fasting blood glucose, fasting insulin, or insulin sensitivity compared to corn oil, but did significantly lower the 3-hour average postprandial blood glucose response by ~44%.
A 90 day randomized controlled trial using 18 grams of MCTs, relative to 18 grams of corn oil, in type 2 diabetics reported a 17% improvement in insulin sensitivity as assessed by HOMA-IR, while the control group experienced a worsening of sensitivty (7%); the difference between groups was significant. However, the MCT oil group also lost a significant amount of bodyweight that correlated with improvements in insulin sensitivity.
MCTs appear to improve insulin sensitivity in people with type 2 diabetes.
Medium-chain triglycerides (65% of coconut oil by weight), relative to long-chain fatty acids, appear to have a greater propensity for oxidation which is shown in animal studies on substrate utilization and has been demonstrated in humans. Consumption of medium-chain triglycerides in humans has once been noted to enhance oxidation of long-chain fatty acids in addition to medium chain fatty acids which is thought to have important implications for obesity as it has been observed obese persons have less long-chain fatty acid oxidation relative to lean counterparts, but no impairments in medium-chain oxidation are noted.
This may be related to the enzyme carnitine palmitoyltransferase (CPT), the rate limiting step in fatty acid oxidation, not being required for fatty acids of medium or short chain length.
Medium-chain triglycerides appears to be more readily oxidized via lipolysis ('fat burning') relative to longer chain fatty acids, which may be important in obesity as impaired long-chain fatty acid oxidation has been noted in obese persons
In animal studies in which the animals are overfed, there appears to be less weight gain associated with medium-chain fatty acid ingestion relative to long-chain fatty acid ingestion although a degree of weight gain is still present.
An increase in metabolic rate has been noted in otherwise healthy young women, which was detected on day 7 but failed to be present subsequently on day 14.
Ingestion of medium-chain triglycerides in obese persons (BMI above 30 and and 9.9g MCTs) paired with a hypocaloric diet (578.4kcal) has been associated with a higher blood ketone body (beta hydroxy-butyrate) level and reduced nitrogen excretion which have been thought to exert protein sparing effects; this study noted that for weight loss obtained over 2 weeks, that a greater percentage (56%) was from fat mass relative to long chain triglycerides (22%) or low fat control (25%).
This section notes studies on coconut oil per se (65% medium-chain triglycerides, or MCTs) and supplemental MCTs themselves. In areas where long-chain triglycerides are used as an active control, the acronym LCT is used
The increase in long-chain fatty acid oxidation in obese persons has also been seen alongside an increase in fat oxidation in overweight persons (BMI 25-33) that may be independent of weight loss over 6 weeks (40% of diet as fat, 75% thereof being test oil) when medium-chain triglycerides are compared to the control of olive oil.
In women with abdominal obesity given either 30mL of coconut oil or 30mL of the control oil (soybean, both at 270kcal) for 12 weeks paired with a hypocaloric carbohydrate-rich diet and a walking regimen noted that while both groups experienced a similar reduction in weight and BMI only the coconut oil group reduced waist circumference (1.4cm). A reduction in waist circumference has been noted elsewhere with 1.7g daily in persons with an average BMI of 24.6-24.7 for 12 weeks to exceed control oil, although this study noted weight loss in both groups (MCT usage being associated with more weight loss and waist circumference loss).
One study compared 10 grams of MCTs to 10 grams of LCTs (both paired with a 2,200kcal intake and 60g fatty acids) and found that MCTs were associated with more fat loss after 12 weeks (3.86+/-0.3kg) than LCTs (2.75+/-0.2kg) only in persons with a BMI greater than 23, whereas there was no significant difference with persons with a lower BMI. This may be related to the aforementioned impairment in long-chain fatty acid oxidation noted in obese persons that may be alleviated with medium-chain triglycerides.
One study using a test bread (14g fatty acids of which 1.7g were MCTs) daily for 12 weeks noted that the body weight reduction in the MCT group was greater (6.1+/-0.5%) than the LCT group (4.5+/-0.5%) and a study in type II diabetics which noted improvements in HbA1c with consumption of 18g MCTs also noted a 2.6% weight loss over 90 days (132 to 128.6lbs average) where the control of LCTs was inactive.
There appears to be a fat reducing effect of coconut oil and MCTs that exceeds other oils used, which is more readily apparent in obese persons than lean persons. The magnitude of this effect is not astounding (with some studies not noting a weight reducing effect)
It has been reported that medium chain triglycerides in general, when replacing long chain fatty acids in the diet, do not appear to confer additional performance enhancing benefits or at least the benefits are highly controversial despite theoretically being a more readily catabolized source of fatty acids for energy production during exercise.
For studies assessing glycogen, there does not appear to be a significant interaction for for normal distance aerobic exercise or ultradistances with or without additional carbohydrates.
There is not a large amount of convincing evidence that calories from medium chain triglycerides and coconut oil are somehow better for performance than carbohydrates or long chain fatty acids, although the calories themselves may confer an ergogenic property
In conditions where the digestion, absorption, or transport of dietary fat is disturbed, MCT supplementation can alleviate symptoms and prevent malnutrition due to their unique ability to bypass most all digestive and absorptive processes necessary for long-chain fats. For example, benefits of MCT supplementation have been observed in people with biliary cirrhosis, pancreatic insufficiency, and short bowel syndrome.
Unpublished research in rats has failed to establish an LD50 for MCT oil, with the highest tested doses being a single bolus of 36 mL/kg and daily administration of 21.3 mL/kg over 30 days. A bolus of 36 mL/kg in rats corresponds to a human equivalent dose of 5.8 mL/kg, or about 400 mL (1.7 cups) for a 70 kg (154 lb) adult. Unpublished research also fed rats MCT oil at 5% in the diet for three months and failed to note any adverse effects. However, the oral LD50s of isolated caprylic acid and capric acid were 1.41 mL/kg and 3.73 mL/kg, respectively, in rats.
- Babayan V. Medium chain length fatty acid esters and their medical and nutritional applications. J Am Oil Chem Soc. (1981)
- Sigalet DL, Martin G. Lymphatic absorption of glucose and fatty acids as determined by direct measurement. J Pediatr Surg. (1999)
- Sigalet DL, Winkelaar GB, Smith LJ. Determination of the route of medium-chain and long-chain fatty acid absorption by direct measurement in the rat. JPEN J Parenter Enteral Nutr. (1997)
- USDA Food Composition Database Nutrient list for C6:0, C8:0, and C10:0.
- Bach AC, Babayan VK. Medium-chain triglycerides: an update. Am J Clin Nutr. (1982)
- Ghosh S, Bhattacharyya DK. Medium-chain fatty acid-rich glycerides by chemical and lipase-catalyzed polyester-monoester interchange reaction. J Amer Oil Chem Soc. (1997)
- Mu H, Porsgaard T. The metabolism of structured triacylglycerols. Prog Lipid Res. (2005)
- Mansbach CM 2nd, Gorelick F. Development and physiological regulation of intestinal lipid absorption. II. Dietary lipid absorption, complex lipid synthesis, and the intracellular packaging and secretion of chylomicrons. Am J Physiol Gastrointest Liver Physiol. (2007)
- McLaughlin J, et al. Fatty acid chain length determines cholecystokinin secretion and effect on human gastric motility. Gastroenterology. (1999)
- Symersky T, et al. The effect of equicaloric medium-chain and long-chain triglycerides on pancreas enzyme secretion. Clin Physiol Funct Imaging. (2002)
- You YQ, et al. Effects of medium-chain triglycerides, long-chain triglycerides, or 2-monododecanoin on fatty acid composition in the portal vein, intestinal lymph, and systemic circulation in rats. JPEN J Parenter Enteral Nutr. (2008)
- Iber FL. Relative rates of metabolism MCT, LCT and ethanol in man. Z Ernahrungswiss Suppl. (1974)
- Borel P, et al. Chylomicron beta-carotene and retinyl palmitate responses are dramatically diminished when men ingest beta-carotene with medium-chain rather than long-chain triglycerides. J Nutr. (1998)
- Swift LL, et al. Medium-chain fatty acids: evidence for incorporation into chylomicron triglycerides in humans. Am J Clin Nutr. (1990)
- Rubio-Gozalbo ME, et al. Carnitine-acylcarnitine translocase deficiency, clinical, biochemical and genetic aspects. Mol Aspects Med. (2004)
- Bach A, Phan T, Metais P. Effect of the fatty acid composition of ingested fats on rat liver intermediary metabolism. Horm Metab Res. (1976)
- Bach A. Oxaloacetate deficiency in MCT-induced ketogenesis. Arch Int Physiol Biochim. (1978)
- McGarry JD, Foster DW. Regulation of hepatic fatty acid oxidation and ketone body production. Annu Rev Biochem. (1980)
- Yeh YY, Zee P. Relation of ketosis to metabolic changes induced by acute medium-chain triglyceride feeding in rats. J Nutr. (1976)
- Bach A, et al. Ketogenic response to medium-chain triglyceride load in the rat. J Nutr. (1977)
- McGarry JD, Foster DW. The regulation of ketogenesis from octanoic acid. The role of the tricarboxylic acid cycle and fatty acid synthesis. J Biol Chem. (1971)
- Vandenberghe C, et al. Tricaprylin alone increases plasma ketone response more than coconut oil or other medium chain triglycerides: an acute crossover study in healthy adults. Curr Dev Nutr. (2017)
- Adkison KD, Shen DD. Uptake of valproic acid into rat brain is mediated by a medium-chain fatty acid transporter. J Pharmacol Exp Ther. (1996)
- Chang P, et al. Seizure control by decanoic acid through direct AMPA receptor inhibition. Brain. (2016)
- Van Wymelbeke V, Louis-Sylvestre J, Fantino M. Substrate oxidation and control of food intake in men after a fat-substitute meal compared with meals supplemented with an isoenergetic load of carbohydrate, long-chain triacylglycerols, or medium-chain triacylglycerols. Am J Clin Nutr. (2001)
- Rolls BJ, et al. Food intake in dieters and nondieters after a liquid meal containing medium-chain triglycerides. Am J Clin Nutr. (1988)
- St-Onge MP, et al. Impact of medium and long chain triglycerides consumption on appetite and food intake in overweight men. Eur J Clin Nutr. (2014)
- Van Wymelbeke V, et al. Influence of medium-chain and long-chain triacylglycerols on the control of food intake in men. Am J Clin Nutr. (1998)
- Stubbs RJ, Harbron CG. Covert manipulation of the ratio of medium- to long-chain triglycerides in isoenergetically dense diets: effect on food intake in ad libitum feeding men. Int J Obes Relat Metab Disord. (1996)
- Krotkiewski M. Value of VLCD supplementation with medium chain triglycerides. Int J Obes Relat Metab Disord. (2001)
- Han JR, et al. Effects of dietary medium-chain triglyceride on weight loss and insulin sensitivity in a group of moderately overweight free-living type 2 diabetic Chinese subjects. Metabolism. (2007)
- Martin K, et al. Ketogenic diet and other dietary treatments for epilepsy. Cochrane Database Syst Rev. (2016)
- Lima PA, Sampaio LP, Damasceno NR. Neurobiochemical mechanisms of a ketogenic diet in refractory epilepsy. Clinics (Sao Paulo). (2014)
- Masino SA, Rho JM. Mechanisms of Ketogenic Diet Action. . ()
- Groleau V, et al. Long-term impact of the ketogenic diet on growth and resting energy expenditure in children with intractable epilepsy. Dev Med Child Neurol. (2014)
- Bergqvist AG, et al. Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic diet. Am J Clin Nutr. (2008)
- Huttenlocher PR, Wilbourn AJ, Signore JM. Medium-chain triglycerides as a therapy for intractable childhood epilepsy. Neurology. (1971)
- Huttenlocher PR. Ketonemia and seizures: metabolic and anticonvulsant effects of two ketogenic diets in childhood epilepsy. Pediatr Res. (1976)
- Trauner DA. Medium-chain triglyceride (MCT) diet in intractable seizure disorders. Neurology. (1985)
- Sills MA, et al. The medium chain triglyceride diet and intractable epilepsy. Arch Dis Child. (1986)
- Schwartz RH, et al. Ketogenic diets in the treatment of epilepsy: short-term clinical effects. Dev Med Child Neurol. (1989)
- Schwartz RM, Boyes S, Aynsley-Green A. Metabolic effects of three ketogenic diets in the treatment of severe epilepsy. Dev Med Child Neurol. (1989)
- Liu YM. Medium-chain triglyceride (MCT) ketogenic therapy. Epilepsia. (2008)
- Liu YM, Wang HS. Medium-chain triglyceride ketogenic diet, an effective treatment for drug-resistant epilepsy and a comparison with other ketogenic diets. Biomed J. (2013)
- Neal EG, et al. Growth of children on classical and medium-chain triglyceride ketogenic diets. Pediatrics. (2008)
- Neal EG, et al. A randomized trial of classical and medium-chain triglyceride ketogenic diets in the treatment of childhood epilepsy. Epilepsia. (2009)
- Azzam R, Azar NJ. Marked Seizure Reduction after MCT Supplementation. Case Rep Neurol Med. (2013)
- Reger MA, et al. Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. Neurobiol Aging. (2004)
- Henderson ST, et al. Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer's disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutr Metab (Lond). (2009)
- Rebello CJ, et al. Pilot feasibility and safety study examining the effect of medium chain triglyceride supplementation in subjects with mild cognitive impairment: A randomized controlled trial. BBA Clin. (2015)
- Cunnane SC, et al. Can Ketones Help Rescue Brain Fuel Supply in Later Life? Implications for Cognitive Health during Aging and the Treatment of Alzheimer's Disease. Front Mol Neurosci. (2016)
- Tsuji H, et al. Dietary medium-chain triacylglycerols suppress accumulation of body fat in a double-blind, controlled trial in healthy men and women. J Nutr. (2001)
- Tsai YH, et al. Mechanisms mediating lipoprotein responses to diets with medium-chain triglyceride and lauric acid. Lipids. (1999)
- Temme EH, Mensink RP, Hornstra G. Effects of medium chain fatty acids (MCFA), myristic acid, and oleic acid on serum lipoproteins in healthy subjects. J Lipid Res. (1997)
- Swift LL, et al. Plasma lipids and lipoproteins during 6 d of maintenance feeding with long-chain, medium-chain, and mixed-chain triglycerides. Am J Clin Nutr. (1992)
- Hill JO, et al. Changes in blood lipids during six days of overfeeding with medium or long chain triglycerides. J Lipid Res. (1990)
- HASHIM SA, ARTEAGA A, VAN ITALLIE TB. Effect of a saturated medium-chain triglyceride on serum-lipids in man. Lancet. (1960)
- St-Onge MP, et al. Medium chain triglyceride oil consumption as part of a weight loss diet does not lead to an adverse metabolic profile when compared to olive oil. J Am Coll Nutr. (2008)
- Tremblay AJ, et al. Dietary medium-chain triglyceride supplementation has no effect on apolipoprotein B-48 and apolipoprotein B-100 kinetics in insulin-resistant men. Am J Clin Nutr. (2014)
- van Schalkwijk DB, et al. Dietary medium chain fatty acid supplementation leads to reduced VLDL lipolysis and uptake rates in comparison to linoleic acid supplementation. PLoS One. (2014)
- Turkenkopf IJ, Maggio CA, Greenwood MR. Effect of high fat weanling diets containing either medium-chain triglycerides or long-chain triglycerides on the development of obesity in the Zucker rat. J Nutr. (1982)
- Kasai M, et al. Effect of dietary medium- and long-chain triacylglycerols (MLCT) on accumulation of body fat in healthy humans. Asia Pac J Clin Nutr. (2003)
- Xue C, et al. Consumption of medium- and long-chain triacylglycerols decreases body fat and blood triglyceride in Chinese hypertriglyceridemic subjects. Eur J Clin Nutr. (2009)
- Zhang YH, et al. Medium- and long-chain fatty acid triacylglycerol reduce body fat and serum triglyceride in overweight and hypertriglyceridemic subjects. Zhonghua Yu Fang Yi Xue Za Zhi. (2009)
- Liu Y, et al. A good response to oil with medium- and long-chain fatty acids in body fat and blood lipid profiles of male hypertriglyceridemic subjects. Asia Pac J Clin Nutr. (2009)
- Barrett-Connor E. Sex differences in coronary heart disease. Why are women so superior? The 1995 Ancel Keys Lecture. Circulation. (1997)
- Zhang Y, et al. Medium- and long-chain triacylglycerols reduce body fat and blood triacylglycerols in hypertriacylglycerolemic, overweight but not obese, Chinese individuals. Lipids. (2010)
- Asakura L, et al. Dietary medium-chain triacylglycerol prevents the postprandial rise of plasma triacylglycerols but induces hypercholesterolemia in primary hypertriglyceridemic subjects. Am J Clin Nutr. (2000)
- Cater NB, Heller HJ, Denke MA. Comparison of the effects of medium-chain triacylglycerols, palm oil, and high oleic acid sunflower oil on plasma triacylglycerol fatty acids and lipid and lipoprotein concentrations in humans. Am J Clin Nutr. (1997)
- UZAWA H, et al. HYPERGLYCERIDEMIA RESULTING FROM INTAKE OF MEDIUM CHAIN TRIGLYCERIDES. Am J Clin Nutr. (1964)
- Eckel RH, et al. Dietary substitution of medium-chain triglycerides improves insulin-mediated glucose metabolism in NIDDM subjects. Diabetes. (1992)
- Airhart S, et al. A Diet Rich in Medium-Chain Fatty Acids Improves Systolic Function and Alters the Lipidomic Profile in Patients With Type 2 Diabetes: A Pilot Study. J Clin Endocrinol Metab. (2016)
- Hayes KC. Medium-chain triacylglycerols may not raise cholesterol. Am J Clin Nutr. (2000)
- Pi-Sunyer FX, Hashim SA, Van Itallie TB. Insulin and ketone responses to ingestion of medium and long-chain triglycerides in man. Diabetes. (1969)
- Tamir I, et al. Effects of a single oral load of medium-chain triglyceride on serum lipid and insulin levels in man. J Lipid Res. (1968)
- Yost TJ, et al. Dietary substitution of medium chain triglycerides in subjects with non-insulin-dependent diabetes mellitus in an ambulatory setting: impact on glycemic control and insulin-mediated glucose metabolism. J Am Coll Nutr. (1994)
- Souza PF, Williamson DH. Effects of feeding medium-chain triacylglycerols on maternal lipid metabolism and pup growth in lactating rats. Br J Nutr. (1993)
- Lieber CS, et al. Difference in hepatic metabolism of long- and medium-chain fatty acids: the role of fatty acid chain length in the production of the alcoholic fatty liver. J Clin Invest. (1967)
- Johnson RC, et al. Medium-chain-triglyceride lipid emulsion: metabolism and tissue distribution. Am J Clin Nutr. (1990)
- Watkins JB, et al. Diagnosis and differentiation of fat malabsorption in children using 13C-labeled lipids: trioctanoin, triolein, and palmitic acid breath tests. Gastroenterology. (1982)
- Metges CC, Wolfram G. Medium- and long-chain triglycerides labeled with 13C: a comparison of oxidation after oral or parenteral administration in humans. J Nutr. (1991)
- Schoeller DA, et al. 13C abundances of nutrients and the effect of variations in 13C isotopic abundances of test meals formulated for 13CO2 breath tests. Am J Clin Nutr. (1980)
- Papamandjaris AA, et al. Endogenous fat oxidation during medium chain versus long chain triglyceride feeding in healthy women. Int J Obes Relat Metab Disord. (2000)
- Binnert C, et al. Influence of human obesity on the metabolic fate of dietary long- and medium-chain triacylglycerols. Am J Clin Nutr. (1998)
- Carnitine Palmitoyltransferase 1A Deficiency.
- Geliebter A, et al. Overfeeding with medium-chain triglyceride diet results in diminished deposition of fat. Am J Clin Nutr. (1983)
- Dulloo AG, et al. Differential effects of high-fat diets varying in fatty acid composition on the efficiency of lean and fat tissue deposition during weight recovery after low food intake. Metabolism. (1995)
- Crozier G, et al. Metabolic effects induced by long-term feeding of medium-chain triglycerides in the rat. Metabolism. (1987)
- Lavau MM, Hashim SA. Effect of medium chain triglyceride on lipogenesis and body fat in the rat. J Nutr. (1978)
- Papamandjaris AA, White MD, Jones PJ. Components of total energy expenditure in healthy young women are not affected after 14 days of feeding with medium-versus long-chain triglycerides. Obes Res. (1999)
- Roynette CE, et al. Structured medium and long chain triglycerides show short-term increases in fat oxidation, but no changes in adiposity in men. Nutr Metab Cardiovasc Dis. (2008)
- Assunção ML, et al. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. (2009)
- Clegg ME. Medium-chain triglycerides are advantageous in promoting weight loss although not beneficial to exercise performance. Int J Food Sci Nutr. (2010)
- Does medium chain triglyceride play an ergogenic role in endurance exercise performance?.
- Hawley JA, Brouns F, Jeukendrup A. Strategies to enhance fat utilisation during exercise. Sports Med. (1998)
- Horowitz JF, et al. Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise. J Appl Physiol. (2000)
- Misell LM, et al. Chronic medium-chain triacylglycerol consumption and endurance performance in trained runners. J Sports Med Phys Fitness. (2001)
- Goedecke JH, et al. The effects of medium-chain triacylglycerol and carbohydrate ingestion on ultra-endurance exercise performance. Int J Sport Nutr Exerc Metab. (2005)
- Angus DJ, et al. Effect of carbohydrate or carbohydrate plus medium-chain triglyceride ingestion on cycling time trial performance. J Appl Physiol. (2000)
- Kehayoglou K, et al. The effect of medium-chain triglyceride on 47 calcium absorption in patients with primary biliary cirrhosis. Gut. (1973)
- Harrison JE, et al. Effect of medium chain triglyceride on fecal calcium losses in pancreatic insufficiency. Clin Biochem. (1973)
- Tandon RK, Rodgers JB Jr, Balint JA. The effects of medium-chain triglycerides in the short bowel syndrome. Increased glucose and water transport. Am J Dig Dis. (1972)
- Traul KA, et al. Review of the toxicologic properties of medium-chain triglycerides. Food Chem Toxicol. (2000)
- Nair AB, Jacob S. A simple practice guide for dose conversion between animals and human. J Basic Clin Pharm. (2016)
- White MD, Papamandjaris AA, Jones PJ. Enhanced postprandial energy expenditure with medium-chain fatty acid feeding is attenuated after 14 d in premenopausal women. Am J Clin Nutr. (1999)