By Dr A C Beynen*
Dr A C Beynen was professor of veterinary nutrition at the Faculty of Veterinary Medicine, Utrecht University, The Netherlands in the period of 1993-2007.
MCT stands for medium-chain triglycerides: liquid lipids consisting of saturated fatty acids with medium length, or having 6, 8, 10 or 12 carbon atoms. MCT oil is produced from selective fatty acids withdrawn from coconut or palm fat. A few marketed foods and treats contain MCT and promise to keep dogs mentally alert and active in their senior age. Some veterinary clinics endorse MCT-enhanced food to control seizures in canine epilepsy.
Contrary to longer-chain fatty acids in regular dietary lipids, MC fatty acids do not require post-digestion transport systems to reach, enter and cross the gut wall. Instead, they simply diffuse into the blood, straight into the liver, where they are scaled down into so-called ketone bodies. Once released into the bloodstream, ketones are preferentially taken up by the brain, then providing readily available energy so as to support brain metabolism and function.
Aged dogs fed a dry food containing 5.5% MCT had better brain function as measured in learning-ability and memory tests. Whether MCT reduces aging-related, behavioral problems is unknown. Dietary MCT marginally reduced the frequency of epileptic seizures in dogs at group level. Various individuals improved meaningfully, but spontaneous, MCT-independent, disease-activity changes cannot be excluded.
Promotional texts on the internet address home-made and commercial, ketogenic diets for dogs (1-4). Those diets, which are high in fat, moderate in protein and low in carbohydrates, stimulate production and utilization of ketone bodies after overnight fasting, but do not raise blood ketone bodies. Keto diets are believed to prevent and treat cancer in dogs. However, there is no evidence for efficacy. The proposed mechanism, depriving cancer cells of energy in the form of blood glucose, is fundamentally flawed.
Compared with man, fasting-induced ketogenesis in the dog appears miniscule, but actually is equivalent. Ketonemia and ketonuria are substantial in humans (5). In overnight-fasted dogs, blood content of ketone bodies is 14 times lower (6). However, per kg body weight, the fluxes through the pools in man and dog are similar (6).
Fatty acids, released by adipose tissue during fasting, enter hepatic β-oxidation. The acetyl-CoA formed can be converted by ketogenesis into acetoacetate (AA) and β-hydroxybutyrate (βHB). During prolonged starvation, the ketone bodies conceptually replace protein-derived glucose as fuel for the central nervous system, which has low capacity for fatty acid oxidation.
In dogs starved for two weeks, blood βHB rose from about 30 to 350 μmol/l (7). Fasting ketonemia is markedly reduced by oral administration of glucose and somewhat intensified by olive oil (8). A high-fat, carbohydrate-free diet did not influence plasma βHB in overnight-fasted, trained, racing huskies (9, 10), but induced a further rise during exhaustive exercise (10).
MCT and βHB
Dietary MCT increased βHB concentration in dogs’ blood sampled about 2 hours after feeding. After mixing about 13% MCT (> 95% C8) into dry food and replacing 5.5% tallow/lard by MCT (97% C8/ unreported composition), βHB was increased by 2.1, 3.9 and 1.3 times (11-13). Perhaps, the latter preparation was relatively high in C10 and/or C12, which are less ketogenic than C8 in rats (14). Commercial MCT preparations can differ markedly, some predominantly containing C12 (15). By comparison, corn oil, palm-kernel and coconut fat contain 0, 55 and 59% MC fatty acids (16).
Digestibility and metabolism
In dogs given 14C-labeled trioctanoin intraduodenally, radioactivity in portal venous blood was almost exclusively confined to the free-fatty acid fraction and that in hepatic venous blood to the aqueous extract (17). Radioactivity was not detected in lymph, while pancreatectomy markedly reduced 14CO2 in expired air (18).
Thus, pancreatic lipase hydrolyses of MCT oil so that its fatty acids can travel directly to the liver for β-oxidation and ketogenesis. In healthy dogs, the apparent total-tract digestibility of MCT oil (60% C8, 40% C10) was 1.3% units higher than that of corn oil (19). After micellization, absorption and mucosal re-esterification, the corn-oil fatty acids are carried by chylomicrons to adipose tissue via lymph.
Palatability and safety
Book chapters mention poor palatability of MCT (20, 21) and so do research articles for 15-22% MCT in dog food (22-24). For diets containing about 5% MCT acceptance issues were not reported (11-13, 19, 24).
In a 90-day study, dogs consumed dry food with 0, 5, 10 or 15% MCT, replacing tallow (24). There were no signs of toxicity by clinical observations. Feces consistency is not reported. The highest dose level depressed food intake.
Brain aging and epilepsy
Dogs with average age of 10 years were fed dry food containing either 5.5% tallow or MCT (97% C8) for 8 months (12, 25). During the feeding period, three types of cognitive tests were carried out. A food reward motivated the dogs to learn the tasks. There were 9-12 dogs per dietary treatment. The MCT-fed dogs outperformed the controls (12), perhaps due to increased respiration of their brain mitochondria (11).
Dogs with idiopathic epilepsy (n = 21) were subjected to a double-blinded, cross-over trial with feeding periods of three months (13). The dry foods contained either 5.5% lard or MCT (unreported composition). Mean seizure frequencies were 2.7 and 2.3/month for the control and test diet. The group-mean effect of MCT is not clinically relevant. When fed the MCT-diet, compared with the control diet, 10 dogs had ≥50% reduction in seizures.
List of references is available on request from the author (firstname.lastname@example.org)
* Dr Anton C Beynen writes this exclusive column on dog and cat nutrition every month. He is affiliated with Vobra Special Petfoods.