Differential Immunometabolic Effects of High-Fat Diets Containing Coconut, Sunflower, and Extra Virgin Olive Oils in Female Mice.

SCOPE: To compare the effects of three high-fat diets (HFDs) based on coconut, sunflower, or extra virgin olive oils (EVOOs) on adipose tissue, metabolism, and inflammation. METHODS AND RESULTS: Mice are fed for 16 weeks on their respective HFD. HFD based on coconut oil produces significantly lower body weight than EVOO- or sunflower oil-based HFDs. Furthermore, the coconut oil HFD leads to metabolic disturbances such as reduction of circulating leptin and adiponectin concentrations, hypertriglyceridemia, hepatomegaly, and liver triglyceride accumulation. Likewise, this diet produces an increase in serum pro-inflammatory cytokines (interleukin 6 [IL-6] and tumor necrosis factor-α [TNF-α]). In white (WAT) and brown (BAT) adipose tissue, the HFD based on coconut oil does not cause significant changes in the expression of studied proteins related to thermogenesis (uncoupling protein 1 [UCP-1]), mitochondrial biogenesis, and browning (peroxisome proliferator-activated receptor-γ coactivator 1α [PGC-1α] and nuclear factor E2-related factor 2 [Nrf2]). However, the HFD based on EVOO induces upregulation of UCP-1, PGC-1α, and Nrf2 expression in BAT, increases the expression of UCP-1 and PGC-1α in inguinal WAT, and enhances the expression of PGC-1α in epididymal WAT. CONCLUSIONS: An HFD based on coconut oil could reduce circulating leptin and adiponectin concentrations, increase the liver fat content, raise serum triglycerides, and promote inflammation by increasing circulating pro-inflammatory cytokines, while an EVOO-based HFD could increase thermogenic activity.

Misinformation in nutrition through the case of coconut oil: An online before-and-after study.

BACKGROUND AND AIMS: Despite recent scientific evidence indicating absence of cardiometabolic benefit resulting from coconut oil intake, its consumption has increased in recent years, which can be attributed to a promotion of its use on social networks. We evaluated the patterns, reasons and beliefs related to coconut oil consumption and its perceived benefits in an online survey of a population in southern Brazil. METHODS AND RESULTS: We conducted a before-and-after study using an 11-item online questionnaire that evaluated coconut oil consumption. In the same survey, participants who consumed coconut oil received an intervention to increase literacy about the health effects of coconut oil intake. We obtained 3160 valid responses. Among participants who consumed coconut oil (59.1%), 82.5% considered it healthy and 65.4% used it at least once a month. 81.2% coconut oil consumers did not observe any health improvements. After being exposed to the conclusions of a meta-analysis showing that coconut oil does not show superior health benefits when compared to other oils and fats, 73.5% of those who considered coconut oil healthy did not change their opinion. Among individuals who did not consume coconut oil, 47.6% considered it expensive and 11.6% deemed it unhealthy. CONCLUSIONS: Coconut oil consumption is motivated by the responders' own beliefs in its supposed health benefits, despite what scientific research demonstrates. This highlights the difficulty in deconstructing inappropriate concepts of healthy diets that are disseminated in society.

Effects of consumption of coconut oil or coconut on glycemic control and insulin sensitivity: A systematic review and meta-analysis of interventional trials.

BACKGROUND AND AIMS: The often purported claim that coconut fat is beneficial for cardiovascular health and was disputed in several recent meta-analyses. However, the evidence on the effects of coconut fat intake on glycemic control remains equivocal. We conducted a systematic review and meta-analysis in accordance with the PRISMA guidelines to determine the effects of dietary coconut fats on markers of acute and long-term glycemic control. METHODS AND RESULTS: PubMed, Scopus, ProQuest, and Web-of-Science databases were searched and the records were screened by three independent reviewers to identify interventional studies examining acute and long-term (i.e., >10 days) effects of coconut fat on glycemic control. DerSimonian-Laird random-effects meta-analyses were performed using the meta-package in R (4.0.2). Seven interventional studies on acute effects and 11 interventional studies on long-term effects of coconut fat were included. Meals with coconut fat acutely increased the incremental area under the curve (AUC) of glucose (p = 0.046) and decreased the incremental AUC of insulin (p = 0.037) vs. control meals. Long-term coconut fat intake increased HOMA-IR (p = 0.049), but did not significantly affect fasting glucose, insulin, or HOMA-ß vs. control meals. CONCLUSIONS: Coconut fat in meals seems to be associated with a diminished postprandial insulin response, resulting in a subtle increase in the postprandial glycemic response. Long-term intake of coconut fat seems to increase insulin resistance, yet does not seem to be beneficial for long-term glycemic control. Thus, our results disprove the popular claim that coconut fat improves glycemic control. REGISTRATION: PROSPERO registry (CRD42020183450).

Celecoxib exhibits therapeutic potential in experimental model of hyperlipidaemia.

Hyperlipidaemia is a major risk factor for cardiovascular diseases, the leading cause of death globally. Celecoxib attenuated hypercholesterolaemia associated with CCl4-induced hepatic injury in rats without improving liver function in our previous study. This present study investigated the lipid lowering potential of celecoxib in normal rats fed with coconut oil subjected to five deep-frying episodes. Male Sprague Dawley rats were randomly assigned to groups (n = 6 rats/group) which received physiological saline (10 mL/kg), unheated coconut oil (UO, 10 mL/kg) or heated coconut oil (HO, 10 ml/kg) for 60 days. Groups that received HO were subsequently treated with either physiological saline, atorvastatin (25 mg/kg), celecoxib (5 mg/kg) or celecoxib (10 mg/kg) in the last fifteen days of the experiment. Rats were sacrificed 24 hours after last treatment and blood and tissue samples collected for analysis. HO consumption produced significant hyperlipidaemia and elevation in marker enzymes of hepatic function. Celecoxib ameliorated the hyperlipidaemia as shown by the significantly (P<0.05) lower total cholesterol, triglycerides, low and very low density lipoprotein in the celecoxib-treated rats when compared with HO-fed rats that received saline. Celecoxib also reduced (P<0.05) alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and liver weight of hyperlipidaemic rats. Similarly, hepatocellular damage with the hyperlipidaemia was significantly reversed by celecoxib. However, serum TNF-α and IL-6 did not change significantly between the various groups. Taken together, data from this study suggest that celecoxib may exert therapeutic benefit in hyperlipidaemia and its attendant consequences.

Health effects of coconut oil: Summary of evidence from systematic reviews and meta-analysis of interventional studies.

BACKGROUND AND AIMS: Systemic review (SR) and meta-analysis (MA) of interventional studies are considered as the highest level of evidence for clinical decision making. Therefore, we systematically summarized all high-quality evidence on the usage of coconut oil for health-related benefits from SRs and MA. METHODS: PubMed®, Web of science®, SciVerse Scopus®, and EMBASE® databases were systematically searched to select SRs and SRs with MA of interventional studies reporting health-related clinical outcomes of coconut oil. Similar studies were grouped based on their respective clinical areas. A methodological quality appraisal was conducted for all included SRs and SRs with MA using the Critical Appraisal Checklist for Systematic Reviews. RESULTS: A total of seven papers were selected for inclusion in this review, consisting of three MA and one SR on cardio-metabolic health, one SR on oral health, and one SR and one MA each on skin health. Coconut oil significantly increases serum total cholesterol, low-density- and high-density- lipoprotein cholesterol levels compared to poly- and mono-unsaturated oils. Limited studies showed that topical use of coconut oil helps in the prevention and treatment of atopic dermatitis and oil pulling for the prevention of dental caries. All four studies on cardiometabolic health and the SR on oral health had a high score in the quality assessment, SR with MA on skin health fulfilled high-quality scoring whereas the SR on the same topic had a low-quality scoring. CONCLUSIONS: In summary, consistent and strong evidence shows that coconut oil has an adverse effect on the lipids parameters associated with cardio-metabolic health, with limited studies to conclude the effects of atopic dermatitis and oil pulling.

Low-Dose Coconut Oil Supplementation Induces Hypothalamic Inflammation, Behavioral Dysfunction, and Metabolic Damage in Healthy Mice.

SCOPE: Coconut oil (CO) diets remain controversial due to the possible association with metabolic disorder and obesity. This study investigates the metabolic effects of a low amount of CO supplementation. METHODS AND RESULTS: Swiss male mice are assigned to be supplemented orally during 8 weeks with 300 µL of water for the control group (CV), 100 or 300 µL of CO (CO100 and CO300) and 100 or 300 µL of soybean oil (SO; SO100 and SO300). CO led to anxious behavior, increase in body weight gain, and adiposity. In the hypothalamus, CO and SO increase cytokines expression and pJNK, pNFKB, and TLR4 levels. Nevertheless, the adipose tissue presented increases macrophage infiltration, TNF-α and IL-6 after CO and SO consumption. IL-1B and CCL2 expression, pJNK and pNFKB levels increase only in CO300. In the hepatic tissue, CO increases TNF-α and chemokines expression. Neuronal cell line (mHypoA-2/29) exposed to serum from CO and SO mice shows increased NFKB migration to the nucleus, TNF-α, and NFKBia expression, but are prevented by inhibitor of TLR4 (TAK-242). CONCLUSIONS: These results show that a low-dose CO changes the behavioral pattern, induces inflammatory pathway activation, TLR4 expression in healthy mice, and stimulates the pro-inflammatory response through a TLR4-mediated mechanism.

Effects of virgin coconut oil consumption on metabolic syndrome components and asymmetric dimethylarginine: A randomized controlled clinical trial.

BACKGROUND AND AIMS: There is some promising evidence regarding the beneficial effect of coconut oil on cardiometabolic risk factors. This study aimed to assess the effects of virgin coconut oil (VCO) consumption on metabolic syndrome (MetS) components, as well as, asymmetric dimethylarginine (ADMA) in adults with MetS. METHODS AND RESULTS: In this randomized controlled trial, 48 subjects, aged 20-50 years, with MetS were allocated into two groups; the intervention group was given 30 ml of VCO per day to substitute the same amounts of fat in their usual diet for four weeks. The control group was advised to follow their usual diet. VCO consumption significantly reduced serum levels of triglyceride (TG) (P = 0.001), very low-density lipoprotein (VLDL) (P = 0.001), and fasting blood sugar (FBS) (P = 0.015) compared to the control group. The levels of high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and total cholesterol (TC) were significantly increased in the VCO group when compared to the control group (P = 0.001). Circulatory ADMA also increased in the VCO group compared to the control group (P = 0.003). No significant differences were observed in the LDL-C/HDL-C ratio, anthropometric parameters, and blood pressure measurements between the two groups at the end of the study (P > 0.05). CONCLUSION: VCO consumption increased the values of HDL-C while reduced TG and FBS levels. Blood pressure and waist circumference did not change. However, levels of TC, LDL-C, and ADMA elevated by VCO consumption. Caution is warranted until the results of further studies become available to explain the long-term effects of VCO consumption. REGISTRATION NUMBER: IRCT20131125015536N11.

Borage Oil Enhances Lamellar Body Content and Alters Fatty Acid Composition of Epidermal Ceramides in Essential Fatty Acid-Deficient Guinea Pigs.

Borage oil [BO: 40.9% linoleic acid (LNA) and 24.0% γ-linolenic acid (GLA)] reverses disrupted epidermal lipid barrier in essential fatty acid deficiency (EFAD). We determined the effects of BO on lamellar body (LB) content and LNA and GLA incorporation into epidermal ceramide 1 (CER1) and epidermal ceramide 2 (CER2), major barrier lipids. EFAD was induced in guinea pigs by a diet of 6% hydrogenated coconut oil (HCO) for 10 weeks (group HCO) or 8 weeks followed by 6% BO for 2 weeks (group HCO + BO). LB content and LNA and GLA incorporation into CER1 were higher in group HCO + BO than in group HCO. Small but significant levels of LNA, GLA, and their C20-metabolized fatty acids [dihomo-γ-linolenic acid (DGLA) and arachidonic acid (ARA)] were incorporated into CER2, where ARA was detected at a level lower than LNA, but DGLA incorporation exceeded that for GLA in group HCO + BO. Dietary BO enhanced LB content and differential incorporation of GLA into CER1 and DGLA into CER2.

Functional Characterization of Gomisin N in High-Fat-Induced Drosophila Obesity Models.

Gomisin N (GN) is lignin derived from Schisandra chinensis that has been reported to exhibit hepato-protective, anti-cancer, and anti-inflammatory effects. However, its role in whole-body energetic homeostasis remains unclear. In this study, we employed Drosophila melanogaster as a diet-induced obese model to elucidate the effects of GN on lipid and glucose metabolism by measuring climbing activity, triglyceride levels, and lifespan under a rearing condition of a high-fat diet (HFD) containing 20% coconut oil, with or without GN. Constant exposure of flies to an HFD resulted in increased body weight and decreased climbing activity, along with a shortened life span. Importantly, the administration of GN to HFD groups lowered their body weight and induced a specific upregulation of lipid storage droplet (Lsd)-2 and hormone-sensitive lipase (Hsl), in addition to improved lifespan. Importantly, GN in HFD groups appeared to downregulate heat shock protein Hsp90 family member (dGRP94), a key regulator of the endoplasmic reticulum stress response, which may also contribute to improved life span in the presence of GN. Taken together, these in vivo findings suggest that GN could serve as a useful agent for the prevention and treatment of obesity.

Effect of coconut oil on cardio-metabolic risk: A systematic review and meta-analysis of interventional studies.

BACKGROUND AND AIMS: High total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) could be major risk factors for cardiovascular disease burden among high risk populations especially in South Asians. This systematic review and meta-analysis aimed to quantify the effects of coconut oil compared with other oils and fats on cardio-metabolic parameters. METHODS: PubMed, Scopus and Web of Science were systematically searched. The main outcomes included are lipid and glycemic parameters. Subgroup analyses were performed to evaluate individual comparisons of vegetable oils and animal fat with coconut oil. Data were pooled using random-effects meta-analysis. RESULTS: Coconut oil consumption significantly increased TC by 15.42 mg/dL (95% CI, 8.96-21.88, p < 0.001), LDL-C by 10.14 mg/dL (95% CI, 4.44-15.84, p < 0.001) and high density lipoprorein cholesterol (HDL-C) by 2.61 mg/dL (95% CI, 0.95-4.26, p = 0.002), and significantly decreased glycosylated hemoglobin (HbA1c) by 0.39 mg/dL (95% CI, -0.50 to -0.27, p < 0.001) but, it had no effects on triglycerides (TG), (4.25 mg/dL; 95% CI, -0.49-8.99, p = 0.08) when compared with the control group. Sub-group analysis demonstrated that coconut oil significantly increased TC and LDL-C over corn, palm, soybean and safflower oils and not over olive oil. Compared with butter, coconut oil showed a better pattern in cardio-metabolic markers by significantly increasing HDL-C (4.38 mg/dL, 95% CI, 0.40 to 8.36, p = 0.03) and decreasing LDL-C (-14.90 mg/dL, 95% CI, -23.02 to-6.77, p < 0.001). CONCLUSIONS: Our results suggest that coconut oil consumption results in significantly higher TC, LDL-C and HDL-C than other oils. Consumption of coconut oil can be one of the risk factors for CVDs in South Asians.

The High-Fat Diet Based on Extra-Virgin Olive Oil Causes Dysbiosis Linked to Colorectal Cancer Prevention.

The present study aims to examine the effects of three different high-fat diet (HFD) on mice gut microbiota in order to analyse whether they create the microenvironmental conditions that either promote or prevent colorectal cancer (CRC). We evaluated colonic mucosa-associated microbiota in CD1 mice fed with HFD, based on 60% kcal from fat-containing coconut, sunflower or extra-virgin olive oil as the only source of fat. The main findings were as follows: (a) All HFD produced a decrease in the richness and diversity of the intestinal microbiota that was independent of mouse weight, (b) HFD switched Lactobacillus to Lactococcus. In general, the results showed that both sunflower- and coconut-HFD generated a pro-inflammatory intestinal microenvironment. In brief, coconut-HFD decreased Akkermansia and increased Staphylococcus, Prevotella and Bacteroides spp. abundance. Sunflower-HFD reduced Akkermansia and Bifidobacterium, while enhancing Sphingomonas and Neisseria spp. abundance. In contrast, EVOO-HFD produced an anti-inflammatory microenvironment characterised by a decreased Enterococcus, Staphylococcus, Neisseria and Pseudomonas spp. abundance. At the same time, it increased the Firmicutes/Bacteroidetes ratio and maintained the Akkermansia population. To conclude, EVOO-HFD produced changes in the gut microbiota that are associated with the prevention of CRC, while coconut and sunflower-HFD caused changes associated with an increased risk of CRC.

The Impact of Coconut Oil and Epigallocatechin Gallate on the Levels of IL-6, Anxiety and Disability in Multiple Sclerosis Patients.

BACKGROUND: Due to the inflammatory nature of multiple sclerosis (MS), interleukin 6 (IL-6) is high in blood levels, and it also increases the levels of anxiety related to functional disability. Epigallocatechin gallate (EGCG) decreases IL-6, which could be enhanced by the anti-inflammatory effect of high ketone bodies after administering coconut oil (both of which are an anxiolytic). Therefore, the aim of this study was to assess the impact of coconut oil and EGCG on the levels of IL-6, anxiety and functional disability in patients with MS. METHODS: A pilot study was conducted for four months with 51 MS patients who were randomly divided into an intervention group and a control group. The intervention group received 800 mg of EGCG and 60 mL of coconut oil, and the control group was prescribed a placebo. Both groups followed the same isocaloric Mediterranean diet. State and trait anxiety were determined before and after the study by means of the State-Trait Anxiety Inventory (STAI). In addition, IL-6 in serum was measured using the ELISA technique and functional capacity was determined with the Expanded Disability Status Scale (EDSS) and the body mass index (BMI). RESULTS: State anxiety and functional capacity decreased in the intervention group and IL-6 decreased in both groups. CONCLUSIONS: EGCG and coconut oil improve state anxiety and functional capacity. In addition, a decrease in IL-6 is observed in patients with MS, possibly due to the antioxidant capacity of the Mediterranean diet and its impact on improving BMI.

Virgin Coconut Oil Associated with High-Fat Diet Induces Metabolic Dysfunctions, Adipose Inflammation, and Hepatic Lipid Accumulation.

Obesity reaches an epidemic level worldwide, and this condition is associated with chronic low-grade inflammation and secondary comorbidities, largely driven by global changes in lifestyle and diet. Various dietary approaches are proposed for the obesity treatment and its associated metabolic disorders. Good taste, antioxidant functions, and vitamins have been attributed to virgin coconut oil (VCO). However, VCO contains a large amount of saturated fatty acids, and the consumption of this fat is associated with a number of secondary diseases. We evaluate the effects of VCO supplementation on biochemical, inflammatory, and oxidative stress parameters in rats fed with high-fat diet (HFD). After feeding with HFD for 12 weeks, the animals were supplemented with VCO for 30 days. HFD+VCO group increased in diet intake, weight gain, low-density lipoprotein cholesterol level, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. These findings were accompanied by increased in hepatic lipid profile and fat deposition in the liver. Adipocyte hypertrophy was observed in the HFD+VCO group, which was associated with elevated expression of tumor necrosis factor alpha (TNF-α) in adipose tissue. These results revealed that VCO associated with HFD induced important metabolic alterations, adipose inflammation, and hepatic lipid accumulation in rats.

Coconut oil intake and its effects on the cardiometabolic profile - A structured literature review.

In recent years, health professionals and laypersons have disseminated misinformation regarding the consumption of coconut oil. Those encouraging the supplementation of coconut oil argue that it provides health benefits and protective cardiovascular effects. Our article examines the effects of coconut oil intake on the cardiometabolic profile by exploring various lipid indices, as well as potential non-lipid effects, such as weight loss. The majority of randomized controlled trials show that coconut oil intake or its supplementation increases low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDLC), and total cholesterol when compared with other vegetable oils. Lauric acid, a medium-chain fatty acid and the main constituent of coconut oil, increases LDL-C and HDL-C concentrations, since it plays a main role as a substrate for apolipoprotein (apo)A1 and apoB synthesis, which are the key molecules in HDL-C and LDL-C particles, respectively.Despite some findings demonstrating an increase in HDL-C, definitive long-term clinical trials are imperative to ascertain whether this effect is clinically relevant. In addition, coconut oil intake has failed as a weight loss strategy and should not be considered as a supplementation strategy to increase satiety and/or thermogenesis.If one desires to include coconut oil in the diet, then we suggest that it should be limited and encompassed within the current recommendations of SFA intake, which are up to 10% of total caloric intake.

Dietary coconut oil ameliorates skin contact hypersensitivity through mead acid production in mice.

Coconut oil is used as a dietary oil worldwide, and its healthy effects are recognized by the fact that coconut oil is easy to digest, helps in weight management, increases healthy cholesterol, and provides instant energy. Although topical application of coconut oil is known to reduce skin infection and inflammation, whether dietary coconut oil has any role in decreasing skin inflammation is unknown. In this study, we showed the impact of dietary coconut oil in allergic skin inflammation by using a mouse model of contact hypersensitivity (CHS). Mice maintained on coconut oil showed amelioration of skin inflammation and increased levels of cis-5, 8, 11-eicosatrienoic acid (mead acid) in serum. Intraperitoneal injection of mead acid inhibited CHS and reduced the number of neutrophils infiltrating to the skin. Detailed mechanistic studies unveiled that mead acid inhibited the directional migration of neutrophils by inhibiting the filamentous actin polymerization and leukotriene B4 production required for secondary recruitment of neutrophils. Our findings provide valuable insights into the preventive roles of coconut oil and mead acid against skin inflammation, thereby offering attractive therapeutic possibilities.

Non-polar lipid carbonyls of thermally oxidized coconut oil induce hepatotoxicity mediated by redox imbalance.

Thermal oxidation products of edible oils including aldehydes, peroxides and polymerized triglycerides formed during the cooking process are increasingly debated as contributory to chronic degenerative diseases. Depending on the oil used for cooking, the source of fatty acids and its oxidation products may vary and would have a differential influence on the physiological process. Coconut oil (CO) is a medium chain triglyceride-rich edible oil used in South India and other Asia Pacific countries for cooking purposes. The present study evaluated the biological effects of thermally oxidized coconut oil (TCO) as well as its non- polar hexane (TCOH) and polar methanol (TCO-M) sub-fractions in male Wistar rats. Results showed an increase in the thiobarbituric acid reactive substances (TBARs) and conjugated diene levels in TCO, which was extracted to TCOH fraction. The animals consumed TCO and its hexane and methanol fractions had a considerable increase in weight gain. However, serum and hepatic triglycerides were increased only in animals with TCO and TCOH administration. In these animals, the hepatic redox balance was disturbed, with a reduction in GSH and a concomitant increase in thiobarbituric acid reactive substances (TBARs). Increased incidence of microvesicles in hepatic histological observations also supported this assumption. Together, the study shows that TCO consumption is unhealthy, where the nonpolar compounds generated during thermal oxidation may be involved in the toxic insults.