Coconut oil is a very potent antimicrobial. This is due to the lauric acid, which constitutes 50% of all the fats, contained in the compound. One study found that out of 30 straight chain fatty acids and derivatives tested, lauric acid was the most inhibitory saturated fatty acid against gram-positive bacteria.[1]When lauric acid is digested, it forms a monoester by combining with glycerol called monolaurin.[1] Lauric acid and monolaurin interfere with the survival of gram-positive bacteria in three ways: destruction of the cell membrane by physiochemical processes, interference with signal transduction and transcription, and stabilization of human cell membranes.[1]Bacteria have been unable to evolve resistance against the action of lauric acid through these mechanisms.[1]This is very important to human health because of the increased antibiotic resistant bacteria to other drugs.
Coconut oil’s medium chain triglycerides have also been shown to reduce symptoms associated with Alzheimer’s disease. Alzheimer’s disease is the most common cause of dementia worldwide and is a frequent problem among elderly individuals. The pathology of Alzheimer’s disease is characterized by atrophy in the frontal, temporal, and parietal regions of the brain.[2] In addition, a form of hypometabolism develops which decreases cerebral glucose metabolism.[2] Because glucose is the primary fuel for the brain, inhibition of the ability to use this substrate for energy puts the patient at risk for a decline in cognitive function.[2] Coconut oil’s medium chain fatty acids have been used as a therapeutic approach to treat this hypometabolism.[2] After digestion, medium chain triglycerides rapidly cross the double mitochondrial membrane and do not require the presence of Carnitine, unlike long-chain fatty acids.[2] This results in an excess of acetyl-coA, which follows various metabolic pathways in the mitochondria and the cytosol. As a result, ketone bodies are produced.[2]
Ketone bodies provide the body with an alternative energy source when glucose concentration is low.[2] These compounds consist of beta-hydroxybutrate, acetaoacetate, and acetone.[2] They bypass the glucose metabolism defects in Alzheimer’s patients and enter the tricarboxylic acid cycle in the mitochondria of neurons. As a result, they are rapidly converted to ATP and precursors of acetylcholine.[2]
This process has been used to treat other central nervous system disorders, including Epilepsy.[3] Using a ketogenic diet consisting of 88% fat, 10% protein, and 2% carbohydrates, one study showed that 53.9% of children with Refractory Epilepsy had more than a 75% reduction is seizure frequency 1 month after starting the diet.[3] However, compliance with this type of diet has been shown to be low in the general population with Alzheimer’s disease and other central nervous system disorders.[3] Therefore, Accera Inc. has manufactured a medium chain triglyceride called AC-1202 and is sold as a nutritional beverage. This provides a simple and safe method to induce elevated levels of ketone bodies without the compliance of a strict diet. The formula is derived from coconut oil. As a result, epileptic patients have an easy and convenient way to decrease their symptoms through the use of a coconut derivative.[2]
Medium chain triglycerides found in coconut oil decrease the risk of obesity through improvement of metabolic biomarkers.[4] AThe adult treatment panel 3 specifies criteria for diagnosing metabolic syndrome. Abdominal obesity, decreased HDL, and high blood pressure are 3 of several metabolic biomarkers that are used in the diagnosis. One study examined the effects of dietary coconut oil supplementation on anthropometric profiles of women who had abdominal obesity.[4] Over a 12-week period, two groups were given a hypocaloric diet and dietary supplements of either 30 mL of coconut oil or soybean oil.[4] They also walked 50 minutes per day. [4]Although both groups lost weight, the coconut oil group had a significant reduction of waist circumference over the soybean oil group.[4] As a result, dietetic supplementation with coconut oil seems to promote a reduction in abdominal obesity.[4]
In addition, improvements in cholesterol ratios were found with the coconut oil group, but not in the soybean group.[4] The coconut oil group had a higher level of HDL and a lower LDL: HDL ratio than the soybean oil group.[4] In contrast, the soybean oil group increased their total cholesterol, decreased their HDL cholesterol and increased their LDL cholesterol.[4] Lastly, they also increased their LDL: HDL ratio.[4] These improved metabolic biomarkers found in the coconut oil group decreases the risk for cardiovascular disease, the current number 1 cause of death in the United States.[5]
Another study found that medium chain triglycerides found in coconut oil were superior to intake of long chain fatty acids in terms of increasing metabolic rate and decreasing fat storage. [6]Researchers overfed rats containing 50% fat.[6] One group received MCT’s found in coconut oil, while another group were fed long chain triglycerides.[6] At the end of the 6-week study, rats in the MCT group gained 15% less weight than the LCT group, and total dissectible fat was significantly lower in the MCT group, as well as mean adipocyte size.[6] Lastly, resting and maximal norepinephrine stimulated oxygen consumptions were 39.7 and 22.1% higher in the MCT group than the LCT group, suggesting higher metabolic rates.[6]
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- ^ a b c d Kabara, Jon J.; Swieczkowski, Dennis M.; Conley, Anthony J.; Truant, Joseph P. (1972-07-01). "Fatty Acids and Derivatives as Antimicrobial Agents". Antimicrobial Agents and Chemotherapy. 2 (1): 23–28. ISSN 0066-4804. PMC 444260. PMID 4670656.
- ^ a b c d e f g h i j Costantini, Lauren C.; Barr, Linda J.; Vogel, Janet L.; Henderson, Samuel T. (2008-12-03). "Hypometabolism as a therapeutic target in Alzheimer's disease". BMC neuroscience. 9 Suppl 2: S16. doi:10.1186/1471-2202-9-S2-S16. ISSN 1471-2202. PMC 2604900. PMID 19090989.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b c Mak, S. C.; Chi, C. S.; Wan, C. J. (2016-12-20). "Clinical experience of ketogenic diet on children with refractory epilepsy". Acta Paediatrica Taiwanica = Taiwan Er Ke Yi Xue Hui Za Zhi. 40 (2): 97–100. ISSN 1608-8115. PMID 10910595.
- ^ a b c d e f g h i j Assunção, Monica L.; Ferreira, Haroldo S.; dos Santos, Aldenir F.; Cabral, Cyro R.; Florêncio, Telma M. M. T. (2009-07-01). "Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity". Lipids. 44 (7): 593–601. doi:10.1007/s11745-009-3306-6. ISSN 1558-9307. PMID 19437058.
- ^ "The Heart Foundation". www.theheartfoundation.org. Retrieved 2016-12-20.
- ^ a b c d e Baba, N.; Bracco, E. F.; Hashim, S. A. (1982-04-01). "Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride". The American Journal of Clinical Nutrition. 35 (4): 678–682. ISSN 0002-9165. PMID 7072620.