Beneficial effects of vaccenic acid on postprandial lipid metabolism and dyslipidemia: Impact of natural trans‐fats to improve CVD risk

Abnormal non‐fasting (postprandial) lipid metabolism has been recognized as a significant contributor to dyslipidemia and cardiovascular disease (CVD) risk. Clinically, impaired metabolism of lipoproteins following a meal (e.g. chylomicrons) has been demonstrated in a number of chronic diseases, including obesity, insulin resistance, as well as type 1 and 2 diabetes. Given the proposed effects of dietary trans fat to contribute to a lipid profile that increases CVD risk, there has been a public health campaign in many countries to eliminate these fatty acids from the food supply. In contrast, our group has recently reported novel lipid‐lowering benefits of a major naturally‐occurring trans fatty acid vaccenic acid (VA, shorthand lipid name 18:1 trans‐11), in an animal model of dyslipidemia and the metabolic syndrome. Studies to date have shown that dietary supplementation of VA effectively reduces not only fasting lipids, but also postprandial triacylglycerol and chylomicron concentrations in obese JCR:LA‐cp rats. Evidence from animal studies to date suggest that VA may down‐regulate hepatic fatty acid synthesis and directly influence lipogenesis in the intestine. The discovery of new bioactive properties of VA is supported by clinical studies which have provided increased momentum for industry applications. In this review we summarize the emerging beneficial view of natural trans fats that have distinct and differential properties compared to those synthetically produced in partially hydrogenated vegetable oils (PHVO), with a particular focus on fasting and postprandial lipid metabolism in CVD risk.     

Cholesteryl Ester Transfer Protein Impairs Triglyceride Clearance via Androgen Receptor in Male Mice

Elevated postprandial triacylglycerols (TAG) are an important risk factor for cardiovascular disease. Men have higher plasma TAG and impaired TAG clearance compared to women, which may contribute to sex differences in risk of cardiovascular disease. Understanding mechanisms of sex differences in TAG metabolism may yield novel therapeutic targets to prevent cardiovascular disease. Cholesteryl ester transfer protein (CETP) is a lipid shuttling protein known for its effects on high-density lipoprotein (HDL) cholesterol levels. Although mice lack CETP, we previously demonstrated that transgenic CETP expression in female mice alters TAG metabolism. The impact of CETP on TAG metabolism in males, however, is not well understood. Here, we demonstrate that CETP expression increases plasma TAG in males, especially in very-low density lipoprotein (VLDL), by impairing postprandial plasma TAG clearance compared to wild-type (WT) males. Gonadal hormones were required for CETP to impair TAG clearance, suggesting a role for sex hormones for this effect. Testosterone replacement in the setting of gonadectomy was sufficient to restore the effect of CETP on TAG. Lastly, liver androgen receptor (AR) was required for CETP to increase plasma TAG. Thus, expression of CETP in males raises plasma TAG by impairing TAG clearance via testosterone signaling to AR. Further understanding of how CETP and androgen signaling impair TAG clearance may lead to novel approaches to reduce TAG and mitigate risk of cardiovascular disease.     

The effectiveness of blood cholesterol lowering is a question of duration as well as magnitude

A high circulating LDL‐cholesterol level is a risk factor for cardiovascular disease. LDL‐cholesterol is cleared from the circulation by the LDL receptor and hence the more receptors an individual possesses the lower the circulating LDL‐cholesterol level will be. Statins increase the synthesis of new LDL receptors and hence reduce circulating LDL‐cholesterol levels and lower the risk of developing cardiovascular disease. However, low circulating levels of LDL resulting from 5 years of statin treatment are not as effective at lowering the risk of developing cardiovascular disease as lifelong exposure to low circulating levels of LDL resulting from loss of function mutations in the gene for PSCK9 a protein which breaks down the LDL receptor. This implies that the effectiveness of statins depends not only on the magnitude of cholesterol lowering but also on its duration.     

Resistance training with soy vs whey protein supplements in hyperlipidemic males

Background  

Most individuals at risk for developing cardiovascular disease (CVD) can reduce risk factors through diet and exercise before resorting to drug treatment. The effect of a combination of resistance training with vegetable-based (soy) versus animal-based (whey) protein supplementation on CVD risk reduction has received little study. The study's purpose was to examine the effects of 12 weeks of resistance exercise training with soy versus whey protein supplementation on strength gains, body composition and serum lipid changes in overweight, hyperlipidemic men.     

Atherogenic Dyslipidemia: Cardiovascular Risk and Dietary Intervention

Atherogenic dyslipidemia comprises a triad of increased blood concentrations of small, dense low-density lipoprotein (LDL) particles, decreased high-density lipoprotein (HDL) particles, and increased triglycerides. A typical feature of obesity, the metabolic syndrome, insulin resistance, and type 2 diabetes mellitus, atherogenic dyslipidemia has emerged as an important risk factor for myocardial infarction and cardiovascular disease. A number of genes have now been linked to this pattern of lipoprotein changes. Low-carbohydrate diets appear to have beneficial lipoprotein effects in individuals with atherogenic dyslipidemia, compared to high-carbohydrate diets, whereas the content of total fat or saturated fat in the diet appears to have little effect. Achieving a better understanding of the genetic and dietary influences underlying atherogenic dyslipidemia may provide clues to improved interventions to reduce the risk of cardiovascular disease in high-risk individuals.     

Molecular Biological and Clinical Understanding of the Statin Residual Cardiovascular Disease Risk and Peroxisome Proliferator-Activated Receptor Alpha Agonists and Ezetimibe for Its Treatment

Several randomized, double blind, placebo-controlled trials (RCTs) have demonstrated that low-density lipoprotein cholesterol (LDL-C) lowering by using statins, including high-doses of strong statins, reduced the development of cardiovascular disease (CVD). However, among the eight RCTs which investigated the effect of statins vs. placebos on the development of CVD, 56–79% of patients had the residual CVD risk after the trials. In three RCTs which investigated the effect of a high dose vs. a usual dose of statins on the development of CVD, 78–87% of patients in the high-dose statin arms still had the CVD residual risk after the trials. An analysis of the characteristics of patients in the RCTs suggests that elevated triglyceride (TG) and reduced high-density lipoprotein cholesterol (HDL-C), the existence of obesity/insulin resistance, and diabetes may be important metabolic factors which determine the statin residual CVD risk. To understand the association between lipid abnormalities and the development of atherosclerosis, we show the profile of lipoproteins and their normal metabolism, and the molecular and biological mechanisms for the development of atherosclerosis by high TG and/or low HDL-C in insulin resistance. The molecular biological mechanisms for the statin residual CVD risk include an increase of atherogenic lipoproteins such as small dense LDL and remnants, vascular injury and remodeling by inflammatory cytokines, and disturbed reverse cholesterol transport. Peroxisome proliferator-activated receptor alpha (PPARα) agonists improve atherogenic lipoproteins, reverse the cholesterol transport system, and also have vascular protective effects, such as an anti-inflammatory effect and the reduction of the oxidative state. Ezetimibe, an inhibitor of intestinal cholesterol absorption, also improves TG and HDL-C, and reduces intestinal cholesterol absorption and serum plant sterols, which are increased by statins and are atherogenic, possibly contributing to reduce the statin residual CVD risk.     

Obesity-Related Changes in High-Density Lipoprotein Metabolism and Function

In obese individuals, atherogenic dyslipidemia is a very common and important factor in the increased risk of cardiovascular disease. Adiposity-associated dyslipidemia is characterized by low high-density lipoprotein cholesterol (HDL-C) levels and an increase in triglyceride-rich lipoproteins. Several factors and mechanisms are involved in lowering HDL-C levels in the obese state and HDL quantity and quality is closely related to adiponectin levels and the bioactive lipid sphingosine-1-phosphate. Recent studies have shown that obesity profoundly alters HDL metabolism, resulting in altered HDL subclass distribution, composition, and function. Importantly, weight loss through gastric bypass surgery and Mediterranean diet, especially when enriched with virgin olive oil, is associated with increased HDL-C levels and significantly improved metrics of HDL function. A thorough understanding of the underlying mechanisms is crucial for a better understanding of the impact of obesity on lipoprotein metabolism and for the development of appropriate therapeutic approaches. The objective of this review article was to summarize the newly identified changes in the metabolism, composition, and function of HDL in obesity and to discuss possible pathophysiological consequences.     

The management of obesity

The prevalence and incidence of obesity is rising as current ways of managing obesity are proving to be ineffective. The preferred approach is to induce an energy deficit by decreasing energy intake through a low calorie diet and increasing energy expenditure through exercise. In order to provoke body weight loss the changes in lifestyle that this approach involves have to be sustained and while some individuals have the motivation to do this the vast majority of the population has not. Very low calorie diets are ineffective as the body adapts to them by lowering energy expenditure and altering the macronutrient composition of low calorie diets has no additional effect. The anti‐obesity drugs orlistat, sibutramine and rimonabant can provoke body weight loss but all suffer from side effects. However, the explosion in our understanding of the factors that regulate energy intake is likely to lead to the development of more effective drugs with fewer side effects. Bariatric or weight reducing surgery is highly effective at provoking body weight loss but there are obvious barriers to its widespread use.     

n‐3 PUFA Esterified to Glycerol or as Ethyl Esters Reduce Non‐Fasting Plasma Triacylglycerol in Subjects with Hypertriglyceridemia: A Randomized Trial

To date, treatment of hypertriglyceridemia with long‐chain n‐3 polyunsaturated fatty acids (n‐3 PUFA) has been investigated solely in fasting and postprandial subjects. However, non‐fasting triacylglycerols are more strongly associated with risk of cardiovascular disease. The objective of this study was to investigate the effect of long‐chain n‐3 PUFA on non‐fasting triacylglycerol levels and to compare the effects of n‐3 PUFA formulated as acylglycerol (AG‐PUFA) or ethyl esters (EE‐PUFA). The study was a double‐blinded randomized placebo‐controlled interventional trial, and included 120 subjects with non‐fasting plasma triacylglycerol levels of 1.7–5.65 mmol/L (150–500 mg/dL). The participants received approximately 3 g/day of AG‐PUFA, EE‐PUFA, or placebo for a period of eight weeks. The levels of non‐fasting plasma triacylglycerols decreased 28 % in the AG‐PUFA group and 22 % in the EE‐PUFA group (P < 0.001 vs. placebo), with no significant difference between the two groups. The triacylglycerol lowering effect was evident after four weeks, and was inversely correlated with the omega‐3 index (EPA + DHA content in erythrocyte membranes). The omega‐3 index increased 63.2 % in the AG‐PUFA group and 58.5 % in the EE‐PUFA group (P < 0.001). Overall, the heart rate in the AG‐PUFA group decreased by three beats per minute (P = 0.045). High‐density lipoprotein (HDL) cholesterol increased in the AG‐PUFA group (P < 0.001). Neither total nor non‐HDL cholesterol changed in any group. Lipoprotein‐associated phospholipase A2 (LpPLA2) decreased in the EE‐PUFA group (P = 0.001). No serious adverse events were observed. Supplementation with long‐chain n‐3 PUFA lowered non‐fasting triacylglycerol levels, suggestive of a reduction in cardiovascular risk. Regardless of the different effects on heart rate, HDL, and LpPLA2 that were observed, compared to placebo, AG‐PUFA, and EE‐PUFA are equally effective in reducing non‐fasting triacylglycerol levels.     

The impact of dietary mono‐ and poly‐unsaturated fatty acids on risk factors for atherosclerosis in humans

The fatty acid composition of the diet has various effects on atherosclerosis risk factors. Dietary saturated fatty acids (SFA) and trans‐unsaturated fatty acids increase the low‐density lipoprotein (LDL)‐/high‐density lipoprotein (HDL)‐cholesterol ratio in serum, while these fats do not have a significant bearing on serum triglyceride levels. By contrast, dietary monounsaturated fatty acids (MUFA), n‐6 polyunsaturated fatty acids (PUFA), and α‐linolenic acid (C18:3n‐3) similarly reduce LDL cholesterol concentrations, while their influence on serum HDL cholesterol and triglycerides is not appreciable. Dietary long‐chain n‐3 PUFA slightly increase serum LDL cholesterol concentrations, but are nevertheless considered salubrious with regard to serum lipids due to the distinct triglyceride‐lowering effects. MUFA‐rich compared to n‐6 PUFA‐rich diets strongly reduce the in vitro oxidizability of LDL. The available studies on this subject also suggest that n‐3 PUFA in the small amounts usually present in the diet are not unduly harmful. These findings are consistent with reports from observational studies: the amount of SFA is positively and the amount of MUFA and n‐6 PUFA in the diet is inversely associated with the risk of cardiovascular disease in most epidemiological studies. The available studies have had an impact on current dietary guidelines, which unanimously recommend that most of the dietary fat should be in the form of MUFA, while the amount of SFA and trans fatty acids in the diet should be as low as possible.     

Aerobic Training in Young Men Increases the Transfer of Cholesterol to High Density Lipoprotein In Vitro: Impact of High Density Lipoprotein Size

Exercise training not only improves the plasma lipid profile but also reduces risk of developing coronary heart disease. We investigate whether plasma lipids and high density lipoprotein (HDL) metabolism are affected by aerobic training and whether the high-density lipoprotein cholesterol (HDL-C) levels at baseline influence exercise-induced changes in HDL. Seventy-one male sedentary volunteers were evaluated and allocated in two subgroups, according to the HLD-C levels (< or >40 mg/dL). Participants underwent an 18-week aerobic training period. Blood was sampled before and after training for biochemical analysis. Plasma lipids, apolipoproteins, HDL diameter, and VO₂ peak were determined. Lipid transfers to HDL were determined in vitro by incubating plasma samples with a donor lipid artificial nanoemulsion. After the 18-week period of aerobic training, the VO₂ peak increased, while the mean body mass index (BMI) decreased. HDL-C concentration was higher after the training period, but low-density lipoprotein cholesterol (LDL-C) and non-HDL-C did not change. The transfer of esterified cholesterol and phospholipids was greater after exercise training, but the triacylglycerol and unesterified cholesterol transfers were unchanged. The HDL particle diameter increased after aerobic training in all participants. When the participants were separated in low-HDL and normal-HDL groups, the postaerobic exercise increment in HDL-C was higher in the low-HDL group, while the transfer of esterified cholesterol was lower. In conclusion, aerobic exercise training increases the lipid transfers to HDL, as measured by an in vitro method, which possibly contributes to the classical elevation of the HDL-C associated with training.     

Increased Postprandial Triglyceride-Rich Lipoprotein Levels in Elderly Survivors of Myocardial Infarction

Postprandial triglyceride-rich lipoproteins (TRL) levels are a predictor for coronary atherosclerosis. The aim of the study was to compare fasting high density lipoprotein (HDL) cholesterol, plasma lipoprotein lipase (LPL) activity, and postprandial TRL between elderly survivors of myocardial infarction (MI) and healthy controls. A case-control study was performed in 44 elderly patients 65-85 years of age with a previous history of MI and 43 age- and sex-matched healthy controls. Each participant underwent physical examination and was given a standard oral fat load with subsequent blood sampling over the next 8 h. Total and chylomicron triglycerides were assessed by area under the curve (AUC), incremental are under the curve (AUCi) and triglyceride response (TGR). Elderly MI patients had significantly lower postheparin LPL activity (87.4 +/- 36.9 mU/ml) (mean +/- 1 SD) than healthy controls (106.0 +/- 29.0 mU/ml) (P = 0.014). Decreased postheparin LPL activity was accompanied by significant increased and delayed clearance of postprandial TRL. Fasting HDL cholesterol was significantly lower in elderly MI patients than controls (1.45 +/- 0.32 and 1.66 +/- 0.47 mmol/l, respectively, P = 0.048). Multiple regression analysis revealed postheparin LPL activity as an independent predictor for postprandial TRL and fasting HDL cholesterol. Logistic regressions analysis revealed HDL cholesterol, triglycerides measured 2 h after the oral fat load, and postheparin LPL activity as independent predictors for MI. Our findings indicate that decreased fasting HDL cholesterol is associated with increased postprandial triglyceridemia which could be a target for life-style and therapeutic interventions in patients at risk for cardiovascular disease.     

Impact of Lipoprotein Lipase Gene Polymorphism,S447X,on Postprandial Triacylglycerol and Glucose Response to Sequential Meal Ingestion

Lipoprotein lipase (LPL) is a key rate-limiting enzyme for the hydrolysis of triacylglycerol (TAG) in chylomicrons and very low-density lipoprotein. Given that postprandial assessment of lipoprotein metabolism may provide a more physiological perspective of disturbances in lipoprotein homeostasis compared to assessment in the fasting state, we have investigated the influence of two commonly studied LPL polymorphisms (rs320, HindIII; rs328, S447X) on postprandial lipaemia, in 261 participants using a standard sequential meal challenge. S447 homozygotes had lower fasting HDL-C (p = 0.015) and a trend for higher fasting TAG (p = 0.057) concentrations relative to the 447X allele carriers. In the postprandial state, there was an association of the S447X polymorphism with postprandial TAG and glucose, where S447 homozygotes had 12% higher TAG area under the curve (AUC) (p = 0.037), 8.4% higher glucose-AUC (p = 0.006) and 22% higher glucose-incremental area under the curve (IAUC) (p = 0.042). A significant gene–gender interaction was observed for fasting TAG (p = 0.004), TAG-AUC (P_interaction = 0.004) and TAG-IAUC (P_interaction = 0.016), where associations were only evident in men. In conclusion, our study provides novel findings of an effect of LPL S447X polymorphism on the postprandial glucose and gender-specific impact of the polymorphism on fasting and postprandial TAG concentrations in response to sequential meal challenge in healthy participants.     

Hyperphosphataemia is associated with the diabetes-related cardiovascular risk factors

The serum phosphorus level is recently considered as one of the foretelling markers for the severity of cardiovascular diseases (CVD). We therefore investigated whether the serum phosphorus level in the diabetic patients against healthy individuals could act as a possible marker for identification of vulnerability to cardiovascular disease. One hundred and thirty two human subjects were involved in the study among which one hundred and four subjects are CVD patients and twenty eight were healthy individuals. The levels of the lipid profile and the glycemic status were significantly increased in the patients than those of the control subjects (Fasting glucose, FS=8.3 ± 0.3 vs. 6.1 ± 0.0 mmol/L; blood glucose 2 h after breakfast (STAB)=12.0 ± 0.5 vs. 8.5 ± 0.7, mmol/L; HbA1c (%),6.7 ± 0.2 vs. 5.4 ± 0.3; and Total cholesterol (TC)=189 ± 4.0 vs. 162 ± 7.0; low density lipoprotein cholesterol (LDL-C), 111 ± 3.8 vs. 96 ± 5.0; triacyglycerol (TG), 202 ± 9.0 vs. 118 ± 5.3 mg/dL, respectively. The serum phosphorus level was significantly increased in CVD patients (mg/dL, patient vs. control, 5.1 ± 0.10 vs. 3.7 ± 0.1). Simple regression analyses revealed a highly significant positive correlation between serum phosphorus and TC, TG and FG. Thus the results demonstrate that the serum phosphorus level might be another parameter which is closely associated with diabetes and could also be used as a possible marker for the risk of CVD.     

Farnesol Decreases Serum Triglycerides in Rats: Identification of Mechanisms Including Up-Regulation of PPARα and Down-Regulation of Fatty Acid Synthase in Hepatocytes

Obesity is associated with impaired fatty acid (FA) oxidation and increased de novo hepatic lipogenesis that may contribute to the development of hypertriglyceridemia, an important risk factor for the development of cardiovascular disease. Strategies to improve hepatocyte FA metabolism, including dietary interventions, are therefore important for the prevention of obesity-associated co-morbidities. Farnesol is consumed in the diet as a component of plant products. In the present study, we administered farnesol orally to rats for seven days and found significantly reduced serum triglyceride concentrations compared with controls. Potential mechanisms underlying the hypotriglyceridemic effect of farnesol were investigated using clone-9 cultured rat hepatocytes. Farnesol significantly upregulated expression of peroxisome proliferator-activated receptor alpha (PPARalpha) and the PPARalpha-regulated genes fatty acyl-CoA oxidase and carnitine palmitoyl transferase 1a, suggesting that increased hepatic FA oxidation may contribute to serum triglyceride lowering in rats. Farnesol did not change SREBP-1c mRNA levels, but significantly down-regulated fatty acid synthase (FAS) mRNA and protein levels and activity, indicating that attenuated lipogenesis may also contribute to hypotriglyceridemic effects of farnesol in vivo. Rescue experiments revealed that down-regulation of FAS by farnesol was not related to activation of PPARalpha, but rather was caused by a 9-cis retinoic acid mediated mechanism that involved down-regulation of retinoid X receptor beta. Diets rich in plant products are associated with a lower risk of cardiovascular disease. Our findings suggest that farnesol may contribute to this protective effect by lowering serum TG levels.     

International Society of Sports Nutrition position stand: protein and exercise

Position Statement  

The following seven points related to the intake of protein for healthy, exercising individuals constitute the position stand of the Society. They have been approved by the Research Committee of the Society. 1) Vast research supports the contention that individuals engaged in regular exercise training require more dietary protein than sedentary individuals. 2) Protein intakes of 1.4 – 2.0 g/kg/day for physically active individuals is not only safe, but may improve the training adaptations to exercise training. 3) When part of a balanced, nutrient-dense diet, protein intakes at this level are not detrimental to kidney function or bone metabolism in healthy, active persons. 4) While it is possible for physically active individuals to obtain their daily protein requirements through a varied, regular diet, supplemental protein in various forms are a practical way of ensuring adequate and quality protein intake for athletes. 5) Different types and quality of protein can affect amino acid bioavailability following protein supplementation. The superiority of one protein type over another in terms of optimizing recovery and/or training adaptations remains to be convincingly demonstrated. 6) Appropriately timed protein intake is an important component of an overall exercise training program, essential for proper recovery, immune function, and the growth and maintenance of lean body mass. 7) Under certain circumstances, specific amino acid supplements, such as branched-chain amino acids (BCAA's), may improve exercise performance and recovery from exercise.     

How good is the evidence for the lipid hypothesis?

The evidence for the lipid hypothesis is weak. After 20 years of follow‐up, the Nurses Health Study, a prospective cohort study, was no longer able to demonstrate an association between intakes of saturated fat and risk of developing coronary heart disease. Randomised controlled trials with statins have shown that lowering LDL‐cholesterol levels by 23% can reduce the risk of developing cardiovascular disease but reducing saturated fat can only reduce cholesterol levels by 10%. This issue can only be resolved by carrying out randomised controlled dietary trials with CVD endpoints. Although there are scientific difficulties standing in the way of such trials, it is the opinion of this author that these can be overcome. Whether there is the political will to fund them is another matter although some of the money currently spent on prospective cohort studies would be far better spent on randomised controlled trials.     

Postprandial Lipid Responses do not Differ Following Consumption of Butter or Vegetable Oil when Consumed with Omega-3 Polyunsaturated Fatty Acids

Dietary saturated fat (SFA) intake has been associated with elevated blood lipid levels and increased risk for the development of chronic diseases. However, some animal studies have demonstrated that dietary SFA may not raise blood lipid levels when the diet is sufficient in omega‐3 polyunsaturated fatty acids (n‐3PUFA). Therefore, in a randomised cross‐over design, we investigated the postprandial effects of feeding meals rich in either SFA (butter) or vegetable oil rich in omega‐6 polyunsaturated fatty acids (n‐6PUFA), in conjunction with n‐3PUFA, on blood lipid profiles [total cholesterol, low density lipoprotein cholesterol (LDL‐C), high density lipoprotein cholesterol (HDL‐C) and triacylglycerol (TAG)] and n‐3PUFA incorporation into plasma lipids over a 6‐h period. The incremental area under the curve for plasma cholesterol, LDL‐C, HDL‐C, TAG and n‐3PUFA levels over 6 h was similar in the n‐6PUFA compared to SFA group. The postprandial lipemic response to saturated fat is comparable to that of n‐6PUFA when consumed with n‐3PUFA; however, sex‐differences in response to dietary fat type are worthy of further attention.     

Efficacy and safety of turmeric and curcumin in lowering blood lipid levels in patients with cardiovascular risk factors: a meta-analysis of randomized controlled trials

Background

Dyslipidemia is an important and common cardiovascular risk factor in the general population. The lipid-lowering effects of turmeric and curcumin are unconfirmed. We performed a meta-analysis to assess the efficacy and safety of turmeric and curcumin in lowering blood lipids in patients at risk of cardiovascular disease (CVD).

Methods

A comprehensive literature search was conducted on PubMed, Embase, Ovid, Medline and Cochrane Library databases to identify randomized controlled trials (published as of November 2016) that assessed the effect of turmeric and curcumin on blood lipid levels including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Pooled standardized mean difference (SMD) with 95% confidence interval (CI) was used to assess the effect.

Results

The analysis included 7 eligible studies (649 patients). Turmeric and curcumin significantly reduced serum LDL-C (SMD = ?0.340, 95% confidence interval [CI]: ?0.530 to ?0.150, P < 0.0001) and TG (SMD = ?0.214, 95% CI: ?0.369 to ?0.059, P = 0.007) levels as compared to those in the control group. These may be effective in lowering serum TC levels in patients with metabolic syndrome (MetS, SMD = ?0.934, 95% CI: ?1.289 to ?0.579, P < 0.0001), and turmeric extract could possibly have a greater effect on reducing serum TC levels (SMD = ?0.584, 95% CI: ?0.980 to ?0.188, P = 0.004); however, the efficacy is yet to be confirmed. Serum HDL-C levels were not obviously improved. Turmeric and curcumin appeared safe, and no serious adverse events were reported in any of the included studies.

Conclusions

Turmeric and curcumin may protect patients at risk of CVD through improving serum lipid levels. Curcumin may be used as a well-tolerated dietary adjunct to conventional drugs. Further research is required to resolve uncertainties related to dosage form, dose and medication frequency of curcumin.