Coconut oil: an overview of cardiometabolic effects and the public health burden of misinformation.

Recent data from meta-analyses of randomized clinical trials (RCTs) suggest that dietary intake of coconut oil, rich in saturated fatty acids, does not result in cardiometabolic benefits, nor in improvements in anthropometric, lipid, glycemic, and subclinical inflammation parameters. Nevertheless, its consumption has surged in recent years all over the world, a phenomenon which can possibly be explained by an increasing belief among health professionals that this oil is as healthy as, or perhaps even healthier than, other oils, in addition to social network misinformation spread. The objective of this review is to present nutritional and epidemiological aspects related to coconut oil, its relationship with metabolic and cardiovascular health, as well as possible hypotheses to explain its high rate of consumption, in spite of the most recent data regarding its actual effects.

Effects of nutritional interventions on the severity of depressive and anxiety symptoms of women in the menopausal transition and menopause: a systematic review, meta-analysis, and meta-regression.

IMPORTANCE: Depression and anxiety may significantly affect women during the menopausal transition. In addition to traditional treatment strategies such as hormone therapy, antidepressants, and psychotherapy, nutritional interventions have been increasingly studied, but there is no consensus about their role in this patient population. OBJECTIVE: This systematic review and meta-analysis aimed to evaluate the effect of nutritional interventions on the severity of depressive (DS) and anxiety (AS) symptoms in women during the menopausal transition or menopausal years. EVIDENCE REVIEW: Electronic search using databases PubMed, Cochrane, and Embase to identify articles indexed until January 31, 2021, focusing on randomized placebo-controlled trials documenting the effect of diet, food supplements, and nutraceuticals on DS and AS. FINDINGS: Thirty-two studies were included (DS, n = 15; AS, n = 1; DS and AS combined, n = 16). We found two studies that demonstrated data combined with other interventions: one with lifestyle interventions (vitamin D plus lifestyle-based weight-loss program) and another with exercise (omega 3 plus exercise). The pooled effect size favored the intervention group over placebo for both DS and AS (DS: standardized mean difference, -0.35 [95% confidence interval, -0.68 to -0.03; P = 0.0351]; AS: standardized mean difference, -0.74 [95% CI, -1.37 to -0.11; P = 0.0229]). There was significant heterogeneity in the pooled results, which can be attributed to differences in assessment tools for depression and anxiety as well as the variety of nutritional interventions studied. The subgroup analysis showed a statistically significant effect of menopausal status (perimenopausal or menopausal) but not the type or duration of nutritional intervention. Older age was the only significant predictor of the effect size of nutritional interventions in the meta-regression. CONCLUSIONS AND RELEVANCE: Nutritional interventions are promising tools for the management of mood/anxiety symptoms in women during the menopausal transition and in postmenopausal years. Because of significant heterogeneity and risk of bias among studies, the actual effect of different approaches is still unclear.

The effects of coconut oil on the cardiometabolic profile: a systematic review and meta-analysis of randomized clinical trials.

BACKGROUND: Despite having a 92% concentration of saturated fatty acid composition, leading to an apparently unfavorable lipid profile, body weight and glycemic effect, coconut oil is consumed worldwide. Thus, we conducted an updated systematic review and meta-analysis of randomized clinical trials (RCTs) to analyze the effect of coconut oil intake on different cardiometabolic outcomes. METHODS: We searched Medline, Embase, and LILACS for RCTs conducted prior to April 2022. We included RCTs that compared effects of coconut oil intake with other substances on anthropometric and metabolic profiles in adults published in all languages, and excluded non-randomized trials and short follow-up studies. Risk of bias was assessed with the RoB 2 tool and certainty of evidence with GRADE. Where possible, we performed meta-analyses using a random-effects model. RESULTS: We included seven studies in the meta-analysis (n = 515; 50% females, follow up from 4 weeks to 2 years). The amount of coconut oil consumed varied and is expressed differently among studies: 12 to 30 ml of coconut oil/day (n = 5), as part of the amount of SFAs or total daily consumed fat (n = 1), a variation of 6 to 54.4 g/day (n = 5), or as part of the total caloric energy intake (15 to 21%) (n = 6). Coconut oil intake did not significantly decrease body weight (MD -0.24 kg, 95% CI -0.83 kg to 0.34 kg), waist circumference (MD -0.64 cm, 95% CI -1.69 cm to 0.41 cm), and % body fat (-0.10%, 95% CI -0.56% to 0.36%), low-density lipoprotein cholesterol (LDL-C) (MD -1.67 mg/dL, 95% CI -6.93 to 3.59 mg/dL), and triglyceride (TG) levels (MD -0.24 mg/dL, 95% CI -5.52 to 5.04 mg/dL). However, coconut oil intake was associated with a small increase in high-density lipoprotein cholesterol (HDL-C) (MD 3.28 mg/dL, 95% CI 0.66 to 5.90 mg/dL). Overall risk of bias was high, and certainty of evidence was very-low. Study limitations include the heterogeneity of intervention methods, in addition to small samples and short follow-ups, which undermine the effects of dietary intervention in metabolic parameters. CONCLUSIONS: Coconut oil intake revealed no clinically relevant improvement in lipid profile and body composition compared to other oils/fats. Strategies to advise the public on the consumption of other oils, not coconut oil, due to proven cardiometabolic benefits should be implemented. REGISTRATION: PROSPERO CRD42018081461.

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.

Relationships between adiponectin levels, the metabolic syndrome, and type 2 diabetes: a literature review

ABSTRACT Elevated hepatic glucose production, impaired insulin secretion, and insulin resistance - abnormalities of glucose metabolism typically found in subjects with obesity - are major factors underlying the pathogenesis of type 2 diabetes (DM2) and the metabolic syndrome (MS). Adiponectin is a major regulator of glucose and lipid homeostasis via its insulin-sensitizing properties, and lower levels seems to be associated with the development of DM2 and MS. The purpose of this review is to clarify the mechanisms whereby adiponectin relates to the development of DM2 and MS and the association between polymorphisms of the adiponectin gene, circulating levels of the hormone, and its relationships with DM2. In addition, the impact of dietary lipids in the circulating levels of adiponectin will be addressed. According to the literature, circulating adiponectin levels seem to decrease as the number of MS components increases. Lower adiponectin concentrations are associated with higher intra-abdominal fat content. Therefore, adiponectin could link intra-abdominal fat with insulin resistance and development of MS. Therapeutic strategies that target the MS and its components, such as lifestyle modification through physical activity and weight loss, have been shown to increase adiponectin concentrations. Possible roles of diets containing either low or high amounts of fat, or different types of fat, have been analyzed in several studies, with heterogeneous results. Supplementation with n-3 PUFA modestly increases adiponectin levels, whereas conjugated linoleic acid supplementation appears to reduce concentrations when compared with unsaturated fatty acid supplementation used as an active placebo.

Relationships between adiponectin levels, the metabolic syndrome, and type 2 diabetes: a literature review.

Elevated hepatic glucose production, impaired insulin secretion, and insulin resistance - abnormalities of glucose metabolism typically found in subjects with obesity - are major factors underlying the pathogenesis of type 2 diabetes (DM2) and the metabolic syndrome (MS). Adiponectin is a major regulator of glucose and lipid homeostasis via its insulin-sensitizing properties, and lower levels seems to be associated with the development of DM2 and MS. The purpose of this review is to clarify the mechanisms whereby adiponectin relates to the development of DM2 and MS and the association between polymorphisms of the adiponectin gene, circulating levels of the hormone, and its relationships with DM2. In addition, the impact of dietary lipids in the circulating levels of adiponectin will be addressed. According to the literature, circulating adiponectin levels seem to decrease as the number of MS components increases. Lower adiponectin concentrations are associated with higher intra-abdominal fat content. Therefore, adiponectin could link intra-abdominal fat with insulin resistance and development of MS. Therapeutic strategies that target the MS and its components, such as lifestyle modification through physical activity and weight loss, have been shown to increase adiponectin concentrations. Possible roles of diets containing either low or high amounts of fat, or different types of fat, have been analyzed in several studies, with heterogeneous results. Supplementation with n-3 PUFA modestly increases adiponectin levels, whereas conjugated linoleic acid supplementation appears to reduce concentrations when compared with unsaturated fatty acid supplementation used as an active placebo.

Effect of dietary lipids on circulating adiponectin: a systematic review with meta-analysis of randomised controlled trials.

Different dietary interventions have been identified as potential modifiers of adiponectin concentrations, and they may be influenced by lipid intake. We identified studies investigating the effect of dietary lipids (type/amount) on adiponectin concentrations in a systematic review with meta-analysis. A literature search was conducted until July 2013 using databases such as Medline, Embase and Scopus (MeSH terms: 'adiponectin', 'dietary lipid', 'randomized controlled trials (RCT)'). Inclusion criteria were RCT in adults analysing adiponectin concentrations with modification of dietary lipids. Among the 4930 studies retrieved, fifty-three fulfilled the inclusion criteria and were grouped as follows: (1) total dietary lipid intake; (2) dietary/supplementary n-3 PUFA; (3) conjugated linoleic acid (CLA) supplementation; (4) other dietary lipid interventions. Diets with a low fat content in comparison to diets with a high-fat content were not associated with positive changes in adiponectin concentrations (twelve studies; pooled estimate of the difference in means: -0·04 (95% CI -0·82, 0·74) µg/ml). A modest increase in adiponectin concentrations with n-3 PUFA supplementation was observed (thirteen studies; 0·27 (95% CI 0·07, 0·47) µg/ml). Publication bias was found by using Egger's test (P= 0·01) and funnel plot asymmetry. In contrast, CLA supplementation reduced the circulating concentrations of adiponectin compared with unsaturated fat supplementation (seven studies; -0·74 (95% CI -1·38, -0·10) µg/ml). However, important sources of heterogeneity were found as revealed by the meta-regression analyses of both n-3 PUFA and CLA supplementation. Results of new RCT would be necessary to confirm these findings.