Can coconut oil promote weight loss by increasing metabolism?

Question

Today, I expressed guilt for eating a large, coconut-based treat, not in keeping with a balanced diet (but quite delicious). I was assured by a friend that coconut oil isn't fattening.

Natural News repeats the claim.

Coconut oil primarily consists of medium-chain fatty acids. These triglycerides can speed up the metabolism because they are so easily digested and converted into energy. Long-chain fatty acids, like those in polyunsaturated oils, are more difficult for the body to break down and use for energy. Instead, long-chain fatty acids are usually stored as fat in the body.Several scientific studies have exhibited these principles.

One study examined the effect of medium-chain fatty acids on metabolism. Participants' metabolism was evaluated before and after a meal rich in these fats. On average, metabolism increased by 48 percent. In obese individuals, the increase was as high as an astounding 65 percent. Studies have shown this thermogenic effect can last for 24 hours.

A study published in the American Journal of Clinical Nutrition reported that medium-chain fatty acids were three times more effective at raising the metabolism than long-chain fatty acids. Researchers concluded that replacing long-chain fatty acids with medium-chain fatty acids was an effective method for weight loss. Another study from the same journal showed that eating medium-chain fatty acids increases metabolism and also helps burn off stored fat.

Is it true that coconut oil is less fattening (or even slimming) because it "increases metabolism"?

Answer 1

TL;DR = Coconut oil increases metabolism in the sense that it doesn't require your body to perform any additional work to metabolize the energy in the oil. Does it increase your metabolic efficiency overall? No. In fact, greater weight-loss is evident with Long-Chain Triglycerides than with Medium-Chain Triglycerides.

My emphasis in bold below...

--

Medium chain fatty acids found in coconut oil are absorbed by the GI tract (gastrointestinal) with ease. They do not require any pancreatic enzymes to break them down, which means less work for your pancreas. Next, medium chain fatty acids are shipped to the portal blood stream, directly to the liver, where they go directly into mitochondria without the use of the carnitine palmitoyl transferase, and are immediately oxidized for energy. MCFA (medium chain fatty acids) from coconut oil do not get packaged up with lipoproteins, and do not get transported to a variety of tissues and are not stored as body fat, they go directly to the liver and are metabolized for energy.

See: (Life Sciences 62 (14): 1203-1215)

In this article, medium chain fatty acids of 8-10 carbon long increases activity of lipase and thus absorb to the intestine at a much faster rate than long chain fatty acids. Study indicated that medium chain fatty acids do not need a lipoprotein for transport but can transport straight to the mitochondria via portal circulation for beta-oxidation. In this paper, other oxidative process such as omega-oxidation and peroxisomal-oxidation occurs in the liver. As seen before, long chain fatty acid need some sort of transport to other organ through the blood. Most often with long chain fatty acids, a carnitine shuttle is required to get the fatty acid into the mitochondria to do beta-oxdation. With medium chain fatty acids, a shuttle is not needed. Energy intake and stored from medium chain fatty acids metabolism is much more sufficient than long chain fatty acids. Appoximately 13% more energy intake compare to long chain fatty *acids* (Papamandjaris, Macdougall, Jones, p. 1209). We see than medium chain fatty acids metabolism is more efficient in which the intake and storing of energy is greater than that of long chain fatty acids.

Here is an abstract from another study involving rats: Clinical Nutrition Volume 14, Issue 1, February 1995, Pages 23–28

Protein and energy metabolism were examined in 34 partially hepatectomized rats (70%), receiving total parenteral nutrition (TPN). The TPN contained either long chain triglycerides (LCT) or triglycerides comprising both medium- (MCFA) and long chain fatty acids (LCFA) on the same carbon skeleton (MILT, medium- and long chain triglyceride). The rats were divided into 4 groups with and without glucose (G) supplementation: LCT+G, LCT-G, MLT+G, MLT-G. 3 days after surgery protein synthetic rate in skeletal muscle, as evaluated from in vitro incorporation of 14C-phenylalanine into muscle protein, was significantly higher in rats receiving MLT if compared to rats receiving LCT (p < 0.05). Rats receiving MLT lost significantly less weight during the study period when compared to the LCT group (p < 0.005). Increased leucine oxidation was observed in rats receiving TPN without glucose regardless of the type of fat emulsion used (p < 0.05). In conclusion, when given to partially hepatectomized rats TPN containing both MCFA and LCFA exerts a stimulatory effect on muscle protein synthesis and preserves body weight better than an emulsion containing LCT only.

For other information concerning Lipids and Energy Storage/Useage, see this wikibooks link.

Answer 2

Answer: Potentially yes. Probably still a good idea to avoid excess calories in general.

Coconut oil is composed of approximately 66% medium-chain triglycerides There are studies that indicate that MCTs may hold potential as weight loss agents.

Fatty acids undergo different metabolic fates depending on their chain length and degree of saturation. The purpose of this review is to examine the metabolic handling of medium chain fatty acids (MCFA) with specific reference to intermediary metabolism and postprandial and total energy expenditure. The metabolic discrimination between varying fatty acids begins in the GI tract, with MCFA being absorbed more efficiently than long chain fatty acids (LFCA). Subsequently, MCFA are transported in the portal blood directly to the liver, unlike LCFA which are incorporated into chylomicrons and transported through lymph. These structure based differences continue through the processes of fat utilization; MCFA enter the mitochondria independently of the carnitine transport system and undergo preferential oxidation. Variations in ketogenic and lipogenic capacity also exist. Such metabolic discrimination is supported by data in animals and humans showing increases in postprandial energy expenditure after short term feeding with MCFA. In long term MCFA feeding in animals, weight accretion has been attenuated. These differences in metabolic handling of MCFA versus LCFA are considered with the conclusion that MCFA hold potential as weight loss agents.

(more studies linked in the Wikipedia article)

Edit: Citing http://www.ncbi.nlm.nih.gov/pubmed/2739575 (Abstract):

To test whether excess dietary energy as medium-chain triglycerides (MCT) affects thermogenesis differently from excess dietary energy as long chain triglycerides (LCT), ten male volunteers (ages 22 to 44) were overfed (150% of estimated energy requirement) liquid formula diets containing 40% of fat as either MCT or LCT. Each patient was studied for one week on each diet in a double-blind, crossover design. Resting metabolic rate (RMR) did not change during either week of overfeeding. The thermic response to food (TEF) was greater on day 1 following a meal (1,000 kcal) containing MCT than following an isocaloric meal containing LCT (8 +/- .8% v 5.8 +/- .8% of ingested energy; P less than .05). Moreover, the TEF observed after a 1,000 kcal meal containing MCT increased significantly to 12% (+/- 1.3%) overfeeding. The TEF of the 1,000 kcal meal containing LCT was unchanged by five days of LCT overfeeding (6.6 +/- 1.0% of ingested energy). Energy expenditure during a 20-hour continuous enteral infusion of the diet on day 7 was also significantly higher with the MCT diet than with the LCT diet (15.7 +/- 1.7% v 7.3 +/- .9% of ingested energy; P less than .05). Our results demonstrate that excess dietary energy as MCT stimulates thermogenesis to a greater degree than does excess energy as LCT. This increased energy expenditure, most likely due to lipogenesis in the liver, provides evidence that excess energy derived from MCT is stored with a lesser efficiency than is excess energy derived from dietary LCT.

Edit2: TEF

Looking at the TEF increases. We get numbers of almost 100% increase in "Metabolism". However even for MCTs the "Metabolism" only eats a small fraction of the total energy.

Looking at both studies: weight accretion has been attenuated and excess dietary energy as MCT stimulates thermogenesis to a greater degree than does excess energy as LCT. That indicates that subjects may not have lost weight at all but only gained weight at a slower rate. Consumption of extra coconut oil could still result in weight gain compared to not eating it at all.

NYTimes and Livestrong both cite a Dr. Daniel Hwang

There are a lot of claims that coconut oil may have health benefits, but there is no concrete scientific data yet to support this.

Answer 3

Since weight loss requires consuming fewer calories, it makes little sense to consume more calories to do so. (It goes against the grain, lol). Calorifically, 1 gm of fat contains 9 calories vs 4 cal for 1 g of carbohydrate or protein so consuming equivalent amounts of fat in mass to that of protein or carbohydrate will always result in consuming more than twice the calories.

People who lose weight on high fat diets only do so by consuming overall fewer calories, and not thru some magic burning effect. There have been numerous claims of magic fat burning substances, and coconut oil is just one of the latest. Meta analyses of high fat diets show adverse health benefits with increased overall mortality from all causes.

• Low-Carbohydrate Diets and All-Cause Mortality: A Systematic Review and Meta-Analysis of Observational Studies, Hiroshi Noto mail, Atsushi Goto, Tetsuro Tsujimoto, Mitsuhiko Noda, Published: January 25, 2013, DOI: 10.1371/journal.pone.0055030

Coconut oil, like other saturated fats is atherogenic, and should be avoided:

These results suggest that consuming an HFD containing even a normal number of calories can cause insulin resistance, hypertension, and adipose accumulation even without obesity. High amounts of fat in diets apparently accelerate the development of atherosclerosis:

• High-fat diet without excess calories induces metabolic disorders and enhances atherosclerosis in rabbits. Waqar AB, Koike T, Yu Y, Inoue T, Aoki T, Liu E, Fan J. Atherosclerosis. 2010 Nov;213(1):148-55. doi: 10.1016/j.atherosclerosis.2010.07.051. Epub 2010 Aug 11.

Coconut oil is also the drug of choice to induce experimental atherosclerosis in test animals.

• Experimental canine atherosclerosis and its prevention. The dietary induction of severe coronary, cerebral, aortic, and iliac atherosclerosis and its prevention by safflower oil., McCullagh KG, Ehrhart A, Butkus A., Lab Invest. 1976 Apr;34(4):394-405.