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Supplementary material:Kinetics of absorptionStudies investigating CO need to consider the kinetics of blood βHB concentrations following MCFA (or CO) intake to maintain optimal ketone body production in AD patients, in addition to accounting for effective yet safe doses. For example, Axona?, containing the MCFA caprylic acid (C8H16O2), retailed as a medical food, has been reported to improve cognitive performance and elevate serum βHB two hours post administration ADDIN EN.CITE <EndNote><Cite><Author>Henderson</Author><Year>2009</Year><RecNum>2396</RecNum><DisplayText>(Henderson et al., 2009)</DisplayText><record><rec-number>2396</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2396</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Henderson, S. T.</author><author>Vogel, J. L.</author><author>Barr, L. J.</author><author>Garvin, F.</author><author>Jones, J. J.</author><author>Costantini, L. C.</author></authors></contributors><auth-address>Accera, Inc,, 380 Interlocken Crescent, Suite 780, Broomfield, Colorado 80021, USA. shenderson@.</auth-address><titles><title>Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer's disease: a randomized, double-blind, placebo-controlled, multicenter trial</title><secondary-title>Nutr Metab (Lond)</secondary-title></titles><pages>31</pages><volume>6</volume><dates><year>2009</year><pub-dates><date>Aug 10</date></pub-dates></dates><isbn>1743-7075 (Electronic)
1743-7075 (Linking)</isbn><accession-num>19664276</accession-num><urls><related-urls><url>;(Henderson et al., 2009). As per the prescription information available on the Axona? website (), the intake of Axona? has been prescribed once daily following a substantial meal. However, further studies are required to investigate the kinetics of elevated serum βHB concentrations several hours following Axona? administration, and whether the addition of longer MCFA (such as capric acid and lauric acid) to caprylic acid can potentially extend the duration of elevated serum βHB concentrations, in turn extending the duration of its beneficial effects per dose. Additionally, investigating the intake of multiple daily doses of MCFA may also serve as an alternative strategy to maintain a steady yet safe source of ketone bodies for the brain, serving as an alternative source of energy in AD as well as other glucose hypometabolism disorders ADDIN EN.CITE <EndNote><Cite><Author>Vandenberghe</Author><Year>2017</Year><RecNum>2569</RecNum><DisplayText>(Vandenberghe et al., 2017)</DisplayText><record><rec-number>2569</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2569</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Vandenberghe, C.</author><author>St-Pierre, V.</author><author>Pierotti, T.</author><author>Fortier, M.</author><author>Castellano, C. A.</author><author>Cunnane, S. C.</author></authors></contributors><auth-address>Research Center on Aging, Sherbrooke, Quebec, Canada; Departments of.
Pharmacology and Physiology and.
Medicine, Universite de Sherbrooke, Sherbrooke, Quebec, Canada; and.
Department of Biology-Health Sciences, Bishop's University, Sherbrooke, Quebec, Canada.</auth-address><titles><title>Tricaprylin Alone Increases Plasma Ketone Response More Than Coconut Oil or Other Medium-Chain Triglycerides: An Acute Crossover Study in Healthy Adults</title><secondary-title>Curr Dev Nutr</secondary-title></titles><pages>e000257</pages><volume>1</volume><number>4</number><keywords><keyword>acetoacetate</keyword><keyword>beta-hydroxybutyrate</keyword><keyword>coconut oil</keyword><keyword>ketones</keyword><keyword>medium-chain triglycerides</keyword><keyword>tricaprin</keyword><keyword>tricaprylin</keyword></keywords><dates><year>2017</year><pub-dates><date>Apr</date></pub-dates></dates><isbn>2475-2991 (Electronic)
2475-2991 (Linking)</isbn><accession-num>29955698</accession-num><urls><related-urls><url>;(Vandenberghe et al., 2017). However, a relatively recent study on an Experimental Autoimmune Encephalomyelitis mouse model showed that lauric acid enhanced differentiation and proliferation of immune activating proinflammatory cells (T helper 1 and/or 17) and impaired their intestinal sequestration via a proinflammatory (p38-MAPK) pathway. In contrast, dietary short chain fatty acids (SCFA; C3, C4, C6) expanded gut T regulatory cells by suppression of proinflammatory pathways (JNK1 and p38) therefore ameliorating the proinflammatory signals in the gut PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IYWdoaWtpYTwvQXV0aG9yPjxZZWFyPjIwMTU8L1llYXI+
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ADDIN EN.CITE.DATA (Haghikia et al., 2015). SCFA are produced by the gut microbiota from dietary fibre, primarily comprising plant cell wall polysaccharides, oligosaccharides and resistant starches. Interestingly, studies have reported that the average western diet contains 20-25g fibre/day while a diet high in fruits and vegetables could contain up to 60g fibre/day, highlighting the importance of accompanying MCT intake with high fruit and vegetable intake. Clinical studies of ketone supplement dosage and effects on CMRA study conducted on mild to moderate AD patients found that 30g/d MCT supplementation for one month increased brain ketone consumption by 2-fold, without affecting glucose utilization PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Dcm90ZWF1PC9BdXRob3I+PFllYXI+MjAxODwvWWVhcj48
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ADDIN EN.CITE.DATA (Croteau et al., 2018). Further, a study assessing the impact of diet-induced moderate ketosis on CMRGlu and CMRAcAc in healthy adults following a four-day high fat KD (4.5:1; lipid: protein plus carbohydrates), reported an 8-fold increase in plasma ketones and a 24% decrease in plasma glucose equating to a 6-fold increase in CMRAcAc and a 20% decrease in CMRGlu respectively. This boost in CMRAcAc represented 17% of the whole brain energy requirements in healthy adults with a 2-fold difference across brain regions (12-24%) whereas the combined CMR of AcAc and βHB was estimated to represent about 33% of the brain’s energy requirements PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Db3VyY2hlc25lLUxveWVyPC9BdXRob3I+PFllYXI+MjAx
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ADDIN EN.CITE.DATA (Dayton et al., 1969; Leren, 1970; Turpeinen et al., 1979) that compared high intake of saturated fat with high intake of polyunsaturated fat. However, the literature cited was primarily based on studies that employed saturated fats predominantly comprising animal fats (palmitate and stearate, not laurate/myristate). Moreover, the study ADDIN EN.CITE <EndNote><Cite><Author>Keys</Author><Year>1957</Year><RecNum>2464</RecNum><DisplayText>(Keys et al., 1957)</DisplayText><record><rec-number>2464</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2464</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Keys, A.</author><author>Anderson, J.T.</author><author>Grande, F. </author></authors></contributors><titles><title>Prediction of serum-cholesterol responses of man to changes in fats in the diet. </title><secondary-title>Lancet</secondary-title></titles><pages>959-966</pages><dates><year>1957</year></dates><urls></urls></record></Cite></EndNote>(Keys et al., 1957) that involved CO, employed a hydrogenated variety of CO (likely to have high trans-fat content ADDIN EN.CITE <EndNote><Cite><Author>Hilditch</Author><Year>1929</Year><RecNum>2460</RecNum><DisplayText>(Hilditch and Vidyarthi, 1929)</DisplayText><record><rec-number>2460</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2460</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hilditch, T. P. </author><author>Vidyarthi, N. L. </author></authors></contributors><titles><title>The products of partial hydrogenation of higher monoethylenic esters</title><secondary-title>Proc. Roy. Soc. A</secondary-title></titles><pages>552-563</pages><volume>122</volume><number>790</number><dates><year>1929</year></dates><urls></urls></record></Cite></EndNote>(Hilditch and Vidyarthi, 1929)) instead of VCO or natural CO. Furthermore, the different properties (digestion and metabolism) of fatty acids based on carbon chain length PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5CcmFnZG9uPC9BdXRob3I+PFllYXI+MTk2MDwvWWVhcj48
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ADDIN EN.CITE.DATA (Bragdon and Karmen, 1960; McCarty and DiNicolantonio, 2016), have until recently, rarely been considered. For example, a recent systematic review and meta-analysis on the comparison of the effects of saturated MCFA (6-12 carbon atoms) versus saturated LCFA on lipid profiles showed that MCFA significantly increased plasma HDL-C as well as plasma concentrations of apolipoprotein A-1, the major protein component of HDL particles, compared to LCFA ADDIN EN.CITE <EndNote><Cite><Author>Panth</Author><Year>2018</Year><RecNum>2530</RecNum><DisplayText>(Panth et al., 2018)</DisplayText><record><rec-number>2530</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2530</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Panth, N.</author><author>Abbott, K.A.</author><author>Dias, C.B.</author><author>Wynne, K.</author><author>Garg, M.L.</author></authors></contributors><titles><title>Differential effects of medium and long-chain saturated fatty acids on blood lipid profile: a systematic review and meta-analysis</title><secondary-title>Amer J Clin Nutr</secondary-title></titles><volume>in press</volume><dates><year>2018</year></dates><urls></urls></record></Cite></EndNote>(Panth et al., 2018). This review underscores the importance of considering the effect of the saturated fatty acid chain length on lipid profiles and CVD risk and discusses points which may address concerns raised by the AHA. Needless to say, caloric intake always needs to be considered; if the caloric intake exceeds daily requirements, MCFA will tend to be stored in adipose tissue ADDIN EN.CITE <EndNote><Cite><Author>Hill</Author><Year>1990</Year><RecNum>2592</RecNum><DisplayText>(Hill et al., 1990)</DisplayText><record><rec-number>2592</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="1549837692">2592</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hill, J. O.</author><author>Peters, J. C.</author><author>Swift, L. L.</author><author>Yang, D.</author><author>Sharp, T.</author><author>Abumrad, N.</author><author>Greene, H. L.</author></authors></contributors><auth-address>Department of Pediatrics, Vanderbilt University, Nashville, TN.</auth-address><titles><title>Changes in blood lipids during six days of overfeeding with medium or long chain triglycerides</title><secondary-title>J Lipid Res</secondary-title></titles><periodical><full-title>J Lipid Res</full-title></periodical><pages>407-16</pages><volume>31</volume><number>3</number><keywords><keyword>Adult</keyword><keyword>Blood Glucose/metabolism</keyword><keyword>Cholesterol/blood</keyword><keyword>Chromatography, Gas</keyword><keyword>Diet</keyword><keyword>Fasting</keyword><keyword>Fatty Acids/administration & dosage/blood</keyword><keyword>Humans</keyword><keyword>Insulin/blood</keyword><keyword>Lipids/*blood</keyword><keyword>Liver/metabolism</keyword><keyword>Male</keyword><keyword>Triglycerides/*administration & dosage/blood</keyword></keywords><dates><year>1990</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>0022-2275 (Print)
0022-2275 (Linking)</isbn><accession-num>2187945</accession-num><urls><related-urls><url>;(Hill et al., 1990). It is also important to note that the beneficial effects of MCFA are modulated by the overall dietary pattern, as this influences MCFA transport to the liver via the portal vein ADDIN EN.CITE <EndNote><Cite><Author>Swift</Author><Year>1990</Year><RecNum>2420</RecNum><DisplayText>(Swift et al., 1990)</DisplayText><record><rec-number>2420</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2420</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Swift, L. L.</author><author>Hill, J. O.</author><author>Peters, J. C.</author><author>Greene, H. L.</author></authors></contributors><auth-address>Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232-2561.</auth-address><titles><title>Medium-chain fatty acids: evidence for incorporation into chylomicron triglycerides in humans</title><secondary-title>Am J Clin Nutr</secondary-title></titles><pages>834-6</pages><volume>52</volume><number>5</number><keywords><keyword>Chylomicrons/*metabolism</keyword><keyword>Fatty Acids/analysis/*metabolism</keyword><keyword>Food, Formulated/analysis</keyword><keyword>Humans</keyword><keyword>Triglycerides/analysis/*metabolism</keyword></keywords><dates><year>1990</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>0002-9165 (Print)
0002-9165 (Linking)</isbn><accession-num>2239759</accession-num><urls><related-urls><url>;(Swift et al., 1990). Supplementary table 1. Evidence from clinical trials on the effect of coconut oil on blood lipids and lipoprotein profilesReference (Country)SubjectsStudy design and lengthInterventionObservations (Mean ± standard deviation, mmol/L unless otherwise stated)LimitationsFisher et al, 1983 (USA) ADDIN EN.CITE <EndNote><Cite><Author>Fisher</Author><Year>1983</Year><RecNum>2546</RecNum><DisplayText>(Fisher et al., 1983)</DisplayText><record><rec-number>2546</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2546</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Fisher, E. A.</author><author>Blum, C. B.</author><author>Zannis, V. I.</author><author>Breslow, J. L.</author></authors></contributors><titles><title>Independent effects of dietary saturated fat and cholesterol on plasma lipids, lipoproteins, and apolipoprotein E</title><secondary-title>Journal of lipid research</secondary-title><alt-title>J Lipid Res</alt-title></titles><alt-periodical><full-title>J Lipid Res</full-title></alt-periodical><pages>1039-1 048</pages><volume>24</volume><dates><year>1983</year></dates><urls></urls></record></Cite></EndNote>(Fisher et al., 1983) 9 healthy men18-37 years old healthy weight normo-lipidemic Non-randomized, cross-over64 days (9-day oil then 9-day oil + cholesterol, 1-month wash out, 9-day alternate oil then 9-day alternate oil + cholesterol).Isocaloric diets providing 15%E protein, 54%E carbohydrate and 31%E fat.Fat sources: corn oil (corn), corn oil + 1g/day cholesterol (corn+), coconut oil (CO), coconut oil + 1g/day cholesterol (CO+).TC: CO (4.29±0.70) = CO+ (4.65±0.75) > corn (2.95±0.36) = corn+ (3.05±0.28)LDL-C+IDL-C: CO (2.72±0.65) = CO+ (3.00±0.72) > corn (1.76±0.41) = corn+ (1.78±0.44)VLDL-C: CO (0.52±0.23) = CO+ (0.67±0.26) > corn (0.34±0.18) = corn+ (0.39±0.18)HDL-C: CO (1.06±0.18) = CO+ (0.98±0.18) > corn (0.88±0.16) = corn+ (0.88±0.13)TG: CO (0.89±0.49) = CO+ (1.12±0.25) > corn (0.67±0.19) = corn+ (0.55±0.17)ApoE (mg/dL): CO (32.0±6.2) = CO+ (32.2±8.5) > corn (24.1±2.7) = corn+ (24.2±3.8); the coconut oil diet shifted ApoE towards lipoproteins of lower density (VLDL, IDL, and LDL) compared with the corn oil diet.No randomizationNo power calculation Small sample size Only men recruitedNot defined if coconut oil was refined or virgin.Mendis and Kumarasundaram, 1990(Sri Lanka) ADDIN EN.CITE <EndNote><Cite><Author>Mendis</Author><Year>1990</Year><RecNum>2547</RecNum><DisplayText>(Mendis and Kumarasundaram, 1990)</DisplayText><record><rec-number>2547</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2547</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Mendis, Shanthi</author><author>Kumarasundaram, Ravi</author></authors></contributors><titles><title>The effect of daily consumption of coconut fat and soya-bean fat on plasma lipids and lipoproteins of young normolipidaemic men</title><secondary-title>British Journal of Nutrition</secondary-title></titles><pages>547-252</pages><volume>63</volume><number>03</number><section>547</section><dates><year>1990</year></dates><isbn>0007-1145
1475-2662</isbn><urls></urls><electronic-resource-num>10.1079/bjn19900141</electronic-resource-num></record></Cite></EndNote>(Mendis and Kumarasundaram, 1990)25 healthy men20-26 years oldRandomized cross-over19 weeks (8-week feeding, 3-week wash out, 8-week feeding)Consumption of 2 high fat meals (lunch and dinner) containing either coconut fat or soya-bean oil and a low-fat high-carbohydrate breakfast.TC: Coconut (4.61±039) > Soya-bean (3.68±042)LDL-C: Coconut (2.84±0.37) = Soya-bean (2.27±0.36)HDL-C: Coconut (1.14±0.27) = Soya-bean (0.94±0.26)TG: Coconut (1.45±0.41) = Soya-bean (1.06±0.42)Only men recruitedHeber et al, 1992 (USA) ADDIN EN.CITE <EndNote><Cite><Author>Heber</Author><Year>1992</Year><RecNum>2548</RecNum><DisplayText>(Heber et al., 1992)</DisplayText><record><rec-number>2548</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2548</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Heber, D.</author><author>Ashley, J.M.</author><author>Solares, M.E.</author><author>Wang, H-J.</author><author>Alfin-Slater, R.B.</author></authors></contributors><titles><title>The effects of a palm-oil enriched diet on plasma lipids and lipoproteins in healthy young men</title><secondary-title>Nutrition Research</secondary-title><alt-title>Nutr Res</alt-title></titles><pages>53-59</pages><volume>12</volume><number>Suppl 1</number><dates><year>1992</year><pub-dates><date>1992</date></pub-dates></dates><urls></urls></record></Cite></EndNote>(Heber et al., 1992)9 healthy males22-43 years oldRandomized crossover13 weeks (2-week washout, 3x3-week diet)Substitution of 50% of total fat and 17.5% of total energy with either (P) palm oil, (CO) coconut oil or (HS) hydrogenated soybean oil.TC (change): CO significant increase; P and HS not significantLDL-C (change): CO significant increase; P and HS not significantHDL-C (change): P significant increase; CO and HS not significantTG (change): CO, P and HS not significantApoAI (change): CO, P and HS not significantApoB (change): CO, P and HS not significantSmall sample sizeDoes not compare dietsCox et al, 1995 (New Zealand) ADDIN EN.CITE <EndNote><Cite><Author>Cox</Author><Year>1995</Year><RecNum>2549</RecNum><DisplayText>(Cox et al., 1995)</DisplayText><record><rec-number>2549</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2549</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Cox, Charlotte</author><author>Mann, Jim</author><author>Sutherland, Wayne</author><author>Chisholm, Alexandra</author><author>Skeaff, Murray</author></authors></contributors><titles><title>Effects of coconut oil, butter, and safflower oil on lipids and lipoproteins in persons with moderately elevated cholesterol levels</title><secondary-title>Journal of lipid research</secondary-title><alt-title>J Lipid Res</alt-title></titles><alt-periodical><full-title>J Lipid Res</full-title></alt-periodical><pages>1787-1795</pages><volume>37</volume><dates><year>1995</year></dates><urls></urls></record></Cite></EndNote>(Cox et al., 1995)28 subjects (13 men, 15 women), 29-67 years old5.5-7.9 mmol/L TC< 3 mmol/L TGRandomized, cross-over, no wash out24 weeks (6-week run in + 3x6-week diet)Diets providing 17%E protein, 47%E carbohydrate, 36%E fat and cholesterol matched (300-350mg/day). Fat sources: coconut oil (CO) or butter (B), providing 20%E as SFA, or safflower oil (SA), providing 10%E PUFA and 10%E SFA.TC: B (6.8±0.9) > CO (6.4±0.8) > SA (6.1 ± 0.8)LDL-C: B (4.5±0.8) > CO (4.2±0.8) > SA (3.9±0.7)VLDL-C: B (0.65±0.65) = CO (0.54±0.51); B > SA (0.53±0.54); CO = SAHDL-C: B (1.4±0.4) = CO (1.5±0.4) = SA (1.4±0.3)ApoAI (mg/L): B (141±23) = CO (157±17) > SA (132±22)ApoB (mg/dL): B (86 ± 20) = CO (91±32) > SA (77±19)TG: B (2.0±1.3) > CO (1.8±1.0) = SA (1.7±1.0)Unbalanced male and female ratiosNo wash outCox et al, 1998(New Zealand) ADDIN EN.CITE <EndNote><Cite><Author>Cox</Author><Year>1998</Year><RecNum>2550</RecNum><DisplayText>(Cox et al., 1998)</DisplayText><record><rec-number>2550</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2550</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Cox, Charlotte</author><author>Sutherland, Waynne</author><author>Mann, Jim</author><author>Jong, S de</author><author>Chisholm, Alexandra</author><author>Skeaff, Murray</author></authors></contributors><titles><title>Effects of dietary coconut oil, butter and safflower oil on plasma lipids, lipoproteins and lathosterol levels</title><secondary-title>European Journal of Clinical Nutrition</secondary-title><short-title>Dietary fat type and lathosterol levels</short-title></titles><pages>650-654</pages><volume>52</volume><dates><year>1998</year></dates><urls></urls></record></Cite></EndNote>(Cox et al., 1998)37 healthy pacific island Polynesians (24 men and 17 women)19-72 years old4.2-7.5 mmol/L TC < 3 mmol/L TGSequential, cross over, no wash out24 weeks (6-week run in + 3x6-week diet)Diet providing 17%E protein, 47%E carbohydrate, 36%E fat and cholesterol matched (250±300 mg/d).Fat sources: (B) Butter, 39g butter + palmitic acid rich (~17g palmitic acid); (CO) Coconut oil, 39g coconut oil (~17g lauric acid); (SA) Safflower, 24g safflower oil (~17g linoleic acid)TC: B (5.61±0.96) = CO (5.47±0.91) > SA (5.10±0.93)VLDL-C: B (0.34±0.18) = CO (0.41±0.36) = SA (0.45±0.45)LDL-C: B (4.08±0.89) > CO (3.79±0.75) > SA (3.50±0.84)HDL-C: B (1.16±0.24) = CO (1.21±0.27) > SA (1.06±0.21)ApoAI (g/L): B (1.23±0.18) = CO (1.33±0.28) > SA (1.15±0.14)ApoAII (g/L): B (0.34±0.08) = CO (0.35±0.08) = SA (0.35±0.08)ApoB (g/L): B (1.00±0.22) > CO (0.87±0.38) = SA (0.76±0.18)TG: B (1.86±0.89) = CO (1.61±0.93) = SA (1.77±.25)No randomizationNo wash outUnblindedAssuncao et al, 2009 (Brazil) ADDIN EN.CITE <EndNote><Cite><Author>Assuncao</Author><Year>2009</Year><RecNum>2551</RecNum><DisplayText>(Assuncao et al., 2009)</DisplayText><record><rec-number>2551</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2551</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Assuncao, M. L.</author><author>Ferreira, H. S.</author><author>dos Santos, A. F.</author><author>Cabral, C. R., Jr.</author><author>Florencio, T. M.</author></authors></contributors><auth-address>Faculdade de Nutricao, Universidade Federal de Alagoas, Maceio, AL 57072-970, Brazil.</auth-address><titles><title>Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity</title><secondary-title>Lipids</secondary-title></titles><pages>593-601</pages><volume>44</volume><number>7</number><keywords><keyword>Abdominal Fat/*drug effects</keyword><keyword>Adiposity/drug effects</keyword><keyword>Adult</keyword><keyword>Body Mass Index</keyword><keyword>Body Weight/drug effects</keyword><keyword>Body Weights and Measures</keyword><keyword>*Cocos/chemistry</keyword><keyword>Dietary Fats, Unsaturated/*pharmacology/therapeutic use</keyword><keyword>Dietary Supplements</keyword><keyword>Double-Blind Method</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Lipids/blood</keyword><keyword>Obesity/blood/*diet therapy/physiopathology</keyword><keyword>Young Adult</keyword></keywords><dates><year>2009</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>1558-9307 (Electronic)
0024-4201 (Linking)</isbn><accession-num>19437058</accession-num><urls><related-urls><url>;(Assuncao et al., 2009)40 women20–40 years old>88cm waist circumfe-renceRandomized,double-blind, clinical trial12 weeksS: 30 mL of soy bean oilCO: 30mL of coconut oilBoth combined with a balanced hypocaloric diet and a 50min daily walk. TC (change): S significant increase; CO not significantLDL-C (change): S significant increase; CO not significantHDL-C (change): S significant decrease; CO not significantLDL-C/HDL-C (change): S significant increase; CO not significantTG (change): S and CO not significantNo power calculationSmall sample sizeOnly womenDoes not compare dietsVoon et al, 2011(Malaysia) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Wb29uPC9BdXRob3I+PFllYXI+MjAxMTwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA (Voon et al., 2011)45 apparently healthy subjectsCrossover, 3 x 3 Latin-square, no wash out18 weeks (3-week standardization, 3x5-week intervention)Diet containing 30%E fat, 1/3 from either palmitic acid (16:0) rich palm olein (PO), lauric and myristic acid (12:0+14:0) rich coconut oil (CO) or oleic acid (18:1) rich virgin olive oil (VOO), 20%E protein and 50% carbohydrate.TC: VOO (4.65±0.71) < CO (4.95±0.69); PO (4.81±0.74) = VOO; PO = COLDL-C: VOO (3.06±0.64) < CO (3.30±0.75); PO (3.20±0.71) = VOO; PO = COHDL-C: VOO (1.28±0.23) < CO (1.37±0.30); PO (1.31±0.26) = VOO; PO = COTG: PO (0.85±0.31) = VOO (0.84±0.37) = CO (0.90±0.39)No wash outCardoso et al, 2015(Brazil) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5DYXJkb3NvPC9BdXRob3I+PFllYXI+MjAxNTwvWWVhcj48
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ADDIN EN.CITE.DATA (Cardoso et al., 2015)116 (63.2% males) 62.4 ± 7.7 years old100% hypertense94.5% dyslipidemicNon-randomized clinical trial6 monthsStage 1: 3 months intensive nutritional treatment.Stage 2: 3 months either on the standard diet (SD, n=22) or on the standard diet + 13mL/day extra virgin coconut oil (VCO, n=92).TC (change): VCO (0.15±0.92) = SD (0.29±0.82)LDL-C (change): VCO (0.10±0.81) = SD (0.07±0.85)HDL-C (change): VCO (0.08±0.19, p<0.01) > SD (-0.03±0.22)TG (change): VCO (-0.02±0.80) = SD (0.26±0.82) ApoA (mg/dL, change): VCO (4.7±12.7, p<0.01) = SD (-3.9 ±2.7, p=0.20)ApoB (mg/dL, change): VCO (6.4±17.6, p<0.01) = SD (7.4±18.1, p=0.07)No randomizationUnequal numbers in treatment (VCO) vs control (SD).Subjects were on lipid-lowering and/or anti-hypertensive drugs.Vijayakumar et al, 2016(India) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5WaWpheWFrdW1hcjwvQXV0aG9yPjxZZWFyPjIwMTY8L1ll
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ADDIN EN.CITE.DATA (Vijayakumar et al., 2016)200 males and females on standard medical care with stable CAD and controlled diabetes and lipid levels.Randomized, single blinded, clinical trial2 yearsSubjects were supplied with either coconut oil (CO) or sunflower oil (SO) as cooking media to account for 15% of their daily energy intake.TC (change): CO and SO not significantLDL-C (change): CO and SO not significantVLDL-C (change): CO and SO not significantHDL-C (change): CO and SO not significantTG (change): CO and SO not significantSubjects were on statins.Khaw et al, 2018(United Kingdom) ADDIN EN.CITE <EndNote><Cite><Author>Khaw</Author><Year>2018</Year><RecNum>2555</RecNum><DisplayText>(Khaw et al., 2018)</DisplayText><record><rec-number>2555</rec-number><foreign-keys><key app="EN" db-id="0w9vvr9elstpwvez5vpxzssnzdfrfew0drwp" timestamp="0">2555</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Khaw, K. T.</author><author>Sharp, S. J.</author><author>Finikarides, L.</author><author>Afzal, I.</author><author>Lentjes, M.</author><author>Luben, R.</author><author>Forouhi, N. G.</author></authors></contributors><auth-address>Department of Public Health and Primary Care, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Medical Research Council Epidemiology Unit, University of Cambridge School of Clinical Medicine, Cambridge, UK.
BBC Television 'Trust Me I'm a Doctor', BBC Glasgow, Glasgow, UK.
Winton Centre for Evidence Communication, University of Cambridge, Cambridge, UK.
Aston Medical Research Institute, Aston Medical School, Aston University, Birmingham, UK.</auth-address><titles><title>Randomised trial of coconut oil, olive oil or butter on blood lipids and other cardiovascular risk factors in healthy men and women</title><secondary-title>BMJ Open</secondary-title></titles><pages>e020167</pages><volume>8</volume><number>3</number><edition>2018/03/08</edition><keywords><keyword>*blood lipids</keyword><keyword>*coconut oil</keyword><keyword>*dietary fats</keyword><keyword>*olive oil</keyword><keyword>*randomized trial</keyword></keywords><dates><year>2018</year><pub-dates><date>Mar 6</date></pub-dates></dates><isbn>2044-6055 (Electronic)
2044-6055 (Linking)</isbn><accession-num>29511019</accession-num><urls><related-urls><url>;(Khaw et al., 2018)91 healthy subjects (2/3 women)50–75 yearsRandomized, unblinded, parallel4weeksSubjects consumed 50g/daily of either (VCO) organic extra virgin coconut oil, (EVO) organic unfiltered extra virgin olive oil and (B) organic unsalted butter.LDL-C (change): B (0.33±0.48) > VCO (?0.09±0.49) = EVO (?0.06±0.39)HDL (change): VCO (0.28±0.29) > B (0.09±0.27) = EVO (0.10±0.15)TG (change): VCO (0.07±0.58) = B (?0.001±0.36) = EVO (?0.03±0.27)TC/HDL-C (change): B (0.10±0.41) > VCO (?0.26±0.36) = EVO (?0.13±0.32)non HDL-C (change): B (0.33±0.51) > VCO (?0.06±0.44) = EVO (?0.07±0.42)ShortUnblinded13% of subjects reported less than 75% compliance.= represents no significant difference between interventions, > represents significantly higher values for the intervention on the left of the sign and < represents significantly lower values for the intervention on the left of the sign. ApoAI, apolipoprotein AI; ApoB, apolipoprotein B; ApoE, apolipoprotein E; B, butter; BF, beef fat; CAD, coronary artery disease; change, increase or decrease from baseline values to post-intervention values; CO, coconut oil; %E, percentage energy; EVO, extra virgin olive oil; HDL-C, high density lipoprotein cholesterol; HS, hydrogenated soybean oil; IDL-C, intermediary density lipoprotein cholesterol; LDL-C, low density lipoprotein cholesterol; P, palm oil; PO, palm olein; PUFA, polyunsaturated fatty acids; S, soy bean oil; SA, Safflower; SD, standard diet; SFA, saturated fatty acids; SO, sunflower oil; TC, total cholesterol; TG, triglycerides; VCO, extra virgin coconut oil; VLDL-C, very low density lipoprotein cholesterol; VOO, virgin olive oil.ReferencesCroteau, E., Castellano, C.A., Richard, M.A., Fortier, M., Nugent, S., Lepage, M., Duchesne, S., Whittingstall, K., Turcotte, E.E., Bocti, C., Fulop, T., Cunnane, S.C., 2018. Ketogenic Medium Chain Triglycerides Increase Brain Energy Metabolism in Alzheimer's Disease. J Alzheimers Dis 64, 551-561.Dayton, S., Pearce, M., Hashimoto, S., Dixon, W., Tomiyasu, U., 1969. A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis. Circulation 40, II-1-II-63.Haghikia, A., Jorg, S., Duscha, A., Berg, J., Manzel, A., Waschbisch, A., Hammer, A., Lee, D.H., May, C., Wilck, N., Balogh, A., Ostermann, A.I., Schebb, N.H., Akkad, D.A., Grohme, D.A., Kleinewietfeld, M., Kempa, S., Thone, J., Demir, S., Muller, D.N., Gold, R., Linker, R.A., 2015. Dietary Fatty Acids Directly Impact Central Nervous System Autoimmunity via the Small Intestine. Immunity 43, 817-829.Hilditch, T.P., Vidyarthi, N.L., 1929. The products of partial hydrogenation of higher monoethylenic esters. Proc. Roy. Soc. A 122, 552-563.Hill, J.O., Peters, J.C., Swift, L.L., Yang, D., Sharp, T., Abumrad, N., Greene, H.L., 1990. Changes in blood lipids during six days of overfeeding with medium or long chain triglycerides. J Lipid Res 31, 407-416.Keys, A., Anderson, J.T., Grande, F., 1957. Prediction of serum-cholesterol responses of man to changes in fats in the diet.. Lancet, 959-966.Leren, P., 1970. The Oslo diet-heart study. Eleven-year report. Circulation 42, 935-942.McCarty, M.F., DiNicolantonio, J.J., 2016. Lauric acid-rich medium-chain triglycerides can substitute for other oils in cooking applications and may have limited pathogenicity. Open Heart 3, e000467.Morris, J.N., Ball, K.P., Antonis, A., Brigden, W.W., Burns-Cox, C.J., Fulton, M., Haigh, M., Hall, G.J.L., Hanington, E., Heady, J.A., MCallen, P.M., Pilkington, T.R.E., Royston, G.R., Sharland, D.E., Sowry, G.S.C., Wilson, C., 1968. Controlled trial of soya-bean oil in myocardial infarction. The Lancet 292, 693-700.Panth, N., Abbott, K.A., Dias, C.B., Wynne, K., Garg, M.L., 2018. Differential effects of medium and long-chain saturated fatty acids on blood lipid profile: a systematic review and meta-analysis. Amer J Clin Nutr in press.Sacks, F.M., Lichtenstein, A.H., Wu, J.H.Y., Appel, L.J., Creager, M.A., Kris-Etherton, P.M., Miller, M., Rimm, E.B., Rudel, L.L., Robinson, J.G., Stone, N.J., Van Horn, L.V., American Heart, A., 2017. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. Circulation 136, e1-e23.Turpeinen, O., Karvonen, M.J., Pekkarinen, M., Miettinen, M., Elosuo, R., Paavilainen, E., 1979. Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study. Int J Epidemiol 8, 99-118. ................
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