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Why palm oil intake is of no health concern
Abstract
Palm oil is an oil with a widespread use in food industry, mainly in applications where texture, neutral taste and long shelf life are required. In the last few years some opinionates, non-governmental organizations as well as industries, mainly in France, Italy, Belgium and Norway have contributed to an escalation of negative publicity surrounding this oil. This article aims at critically scrutinizing the main dietary concerns about palm oil.
... The current demand for functional foods is attracting a wide range of customers around the world. In response, supermarkets and producers are adapting their products and have identified the growth potential of products which bear a 'free from' claim in their packaging [17]. Despite various statements against the consumption of palm oil, up to now there is no substantiated indication that consumption of palm oil in a balanced diet is related to any specific health concern. ...
... Despite various statements against the consumption of palm oil, up to now there is no substantiated indication that consumption of palm oil in a balanced diet is related to any specific health concern. In fact, it has been shown that replacing palm oil in food products or diets with fats higher in saturated FAs or with added sugar to compensate for the palatability and taste, will not provide a health benefit [17]. ...
... In this context, PO is a very popular fat, free from TFAs, with desirable physical properties (Wong and Radhakrishnan, 2012). However, in the last few years, use of this fat by the food industry as well as consumers has been criticized for its supposed negative effects on human health and the environment (Gambelli and Logman, 2015;Hrncirik and Van Duijn, 2011); hence, PO has become a 'specially monitored ingredient' (Greenpeace, 2018). These factors, together with increase in consumer demand for healthier foods, have led the food industry to replace PO in the recipes, and the 'no palm oil" logo became a powerful marketing tool. ...
This study reports an approach combining the use of tocols and fatty acids as variables to separate different bakery products with respect to the oil/fat used as ingredients. The tocol and fatty acid profiles were investigated in 12 biscuits prepared with different fats/oils. Based on different profiles, principal component analysis (PCA) was used to classify samples according to their fat/oil ingredients. The PCA found three components that are able to explain approximately 71% of total variance, and it proved useful in characterizing products. The tested approach was validated on 33 commercial bakery products prepared with different fats/oils to verify the information men-tioned on food labels.
Background:
Although saturated fatty acids (FAs) have been linked to cardiovascular mortality, it is not clear whether this outcome is attributable solely to their effects on low-density lipoprotein cholesterol (LDL-C) or whether other risk factors are also associated with FAs. The Western Alaskan Native population, with its rapidly changing lifestyles, shift in diet from unsaturated to saturated fatty acids and dramatic increase in cardiovascular disease (CVD), presents an opportunity to elucidate any associations between specific FAs and known CVD risk factors.
Objective:
We tested the hypothesis that the specific FAs previously identified as related to CVD mortality are also associated with individual CVD risk factors.
Methods:
In this community-based, cross-sectional study, relative proportions of FAs in plasma and red blood cell membranes were compared with CVD risk factors in a sample of 758 men and women aged ≥35 years. Linear regression analyses were used to analyze relations between specific FAs and CVD risk factors (LDL-C, high-density lipoprotein cholesterol, triglycerides, C-reactive protein, systolic blood pressure, diastolic blood pressure, heart rate, body mass index, fasting glucose and fasting insulin, 2-hour glucose and 2-hour insulin).
Results:
The specific saturated FAs previously identified as related to CVD mortality, the palmitic and myristic acids, were adversely associated with most CVD risk factors, whereas unsaturated linoleic acid (18:2n-6) and the marine n-3 FAs were not associated or were beneficially associated with CVD risk factors.
Conclusions:
The results suggest that CVD risk factors are more extensively affected by individual FAs than hitherto recognized, and that risk for CVD, MI and stroke can be reduced by reducing the intake of palmitate, myristic acid and simple carbohydrates and improved by greater intake of linoleic acid and marine n-3 FAs.
Recent meta-analyses have found no association between heart disease and dietary saturated fat; however, higher proportions of plasma saturated fatty acids (SFA) predict greater risk for developing type-2 diabetes and heart disease. These observations suggest a disconnect between dietary saturated fat and plasma SFA, but few controlled feeding studies have specifically examined how varying saturated fat intake across a broad range affects circulating SFA levels. Sixteen adults with metabolic syndrome (age 44.9±9.9 yr, BMI 37.9±6.3 kg/m2) were fed six 3-wk diets that progressively increased carbohydrate (from 47 to 346 g/day) with concomitant decreases in total and saturated fat. Despite a distinct increase in saturated fat intake from baseline to the low-carbohydrate diet (46 to 84 g/day), and then a gradual decrease in saturated fat to 32 g/day at the highest carbohydrate phase, there were no significant changes in the proportion of total SFA in any plasma lipid fractions. Whereas plasma saturated fat remained relatively stable, the proportion of palmitoleic acid in plasma triglyceride and cholesteryl ester was significantly and uniformly reduced as carbohydrate intake decreased, and then gradually increased as dietary carbohydrate was re-introduced. The results show that dietary and plasma saturated fat are not related, and that increasing dietary carbohydrate across a range of intakes promotes incremental increases in plasma palmitoleic acid, a biomarker consistently associated with adverse health outcomes.
Background:
Guidelines advocate changes in fatty acid consumption to promote cardiovascular health.
Purpose:
To summarize evidence about associations between fatty acids and coronary disease.
Data sources:
MEDLINE, Science Citation Index, and Cochrane Central Register of Controlled Trials through July 2013.
Study selection:
Prospective, observational studies and randomized, controlled trials.
Data extraction:
Investigators extracted data about study characteristics and assessed study biases.
Data synthesis:
There were 32 observational studies (530,525 participants) of fatty acids from dietary intake; 17 observational studies (25,721 participants) of fatty acid biomarkers; and 27 randomized, controlled trials (103,052 participants) of fatty acid supplementation. In observational studies, relative risks for coronary disease were 1.02 (95% CI, 0.97 to 1.07) for saturated, 0.99 (CI, 0.89 to 1.09) for monounsaturated, 0.93 (CI, 0.84 to 1.02) for long-chain ω-3 polyunsaturated, 1.01 (CI, 0.96 to 1.07) for ω-6 polyunsaturated, and 1.16 (CI, 1.06 to 1.27) for trans fatty acids when the top and bottom thirds of baseline dietary fatty acid intake were compared. Corresponding estimates for circulating fatty acids were 1.06 (CI, 0.86 to 1.30), 1.06 (CI, 0.97 to 1.17), 0.84 (CI, 0.63 to 1.11), 0.94 (CI, 0.84 to 1.06), and 1.05 (CI, 0.76 to 1.44), respectively. There was heterogeneity of the associations among individual circulating fatty acids and coronary disease. In randomized, controlled trials, relative risks for coronary disease were 0.97 (CI, 0.69 to 1.36) for α-linolenic, 0.94 (CI, 0.86 to 1.03) for long-chain ω-3 polyunsaturated, and 0.89 (CI, 0.71 to 1.12) for ω-6 polyunsaturated fatty acid supplementations.
Limitation:
Potential biases from preferential publication and selective reporting.
Conclusion:
Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.
Primary funding source:
British Heart Foundation, Medical Research Council, Cambridge National Institute for Health Research Biomedical Research Centre, and Gates Cambridge.
Palm oil (PO) may be an unhealthy fat because of its high saturated fatty acid content.
The objective was to assess the effect of substituting PO for other primary dietary fats on blood lipid-related markers of coronary heart disease (CHD) and cardiovascular disease (CVD).
We performed a systematic review and meta-analysis of dietary intervention trials. Studies were eligible if they included original data comparing PO-rich diets with other fat-rich diets and analyzed at least one of the following CHD/CVD biomarkers: total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, TC/HDL cholesterol, LDL cholesterol/HDL cholesterol, triacylglycerols, apolipoprotein A-I and B, very-low-density lipoprotein cholesterol, and lipoprotein(a).
Fifty-one studies were included. Intervention times ranged from 2 to 16 wk, and different fat substitutions ranged from 4% to 43%. Comparison of PO diets with diets rich in stearic acid, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) showed significantly higher TC, LDL cholesterol, apolipoprotein B, HDL cholesterol, and apolipoprotein A-I, whereas most of the same biomarkers were significantly lower when compared with diets rich in myristic/lauric acid. Comparison of PO-rich diets with diets rich in trans fatty acids showed significantly higher concentrations of HDL cholesterol and apolipoprotein A-I and significantly lower apolipoprotein B, triacylglycerols, and TC/HDL cholesterol. Stratified and meta-regression analyses showed that the higher concentrations of TC and LDL cholesterol, when PO was substituted for MUFAs and PUFAs, were not significant in young people and in subjects with diets with a lower percentage of energy from fat.
Both favorable and unfavorable changes in CHD/CVD risk markers occurred when PO was substituted for the primary dietary fats, whereas only favorable changes occurred when PO was substituted for trans fatty acids. Additional studies are needed to provide guidance for policymaking.
Palmitic acid (PA) has been widely used as an useful and effective additive to pulmonary surfactants (PS) such as Survanta and Surfaxin. Moreover, PA has well-known biological and physicochemical properties, and its simple chemical structure allows its manufacture at low cost. However, the role and significance of PA in PS formulations are still controversial. In the present study, the PS model preparation containing PA has been investigated to clarify its additional effect (molecular recognition and interaction in particular) employing the Langmuir monolayer technique. The elucidation of the PA effect is performed by comparison with the data from its analogue (or homologue) lipids; i.e. three fatty acids and four fatty alcohols. The surface pressure (π)-molecular area (A) and surface potential (ΔV)−A isotherms for the eight DPPC/fatty lipid systems containing a PS model peptide (Hel 13-5) have been measured. In addition, the morphology and phase behavior are examined with in situ fluorescence and ex situ atomic force microscopy. As a result, it is found that a balance between the hydrophilicity of the headgroup and the hydrophobicity of the tail group in the lipids is an important factor in pulmonary functions. In particular, the dissociation degree of the fatty acids, which depends on the pH or the surface pH, strongly affects their electrostatic interaction with positively charged Hel 13-5. The chain length is also significant and the carbon number 16 is found to be most appropriate. The present molecular-level information on the interaction between the lipids and Hel 13-5 in the presence of DPPC indicates that PA takes on a hydrophile–lipophile balance suitable for the PS preparation.
Background:
A reduction in dietary saturated fat has generally been thought to improve cardiovascular health.
Objective:
The objective of this meta-analysis was to summarize the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD; CHD inclusive of stroke) in prospective epidemiologic studies.
Design:
Twenty-one studies identified by searching MEDLINE and EMBASE databases and secondary referencing qualified for inclusion in this study. A random-effects model was used to derive composite relative risk estimates for CHD, stroke, and CVD.
Results:
During 5-23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.
Conclusions:
A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.
Besides measuring blood pressure and glucose levels, assessing the lipid spectrum is the method most commonly used to identify individuals at high risk of cardiovascular disease (CVD), as well as those who are likely to benefit most from lipid-lowering therapy. Although lowering LDL-cholesterol levels is the primary target of therapy in most clinical guidelines, accumulating evidence indicates that other lipoprotein-lipid measurements could provide a predictive value over and above that of LDL-cholesterol levels. For example, individuals treated with statins who achieve low LDL-cholesterol levels, but have high concentrations of either non-HDL cholesterol or apolipoprotein (apo) B, remain at increased cardiovascular risk. Similarly, individuals with low levels of either HDL cholesterol or apo A-I are also likely to experience cardiovascular events, despite having normal LDL-cholesterol levels. The residual cardiovascular risk, beyond that characterized by LDL-cholesterol levels alone, is exacerbated by physical inactivity and abdominal obesity, which are both increasingly prevalent risk factors for CVD. In this Review, we discuss the measurement of various lipoprotein-lipid parameters for the prediction of CVD risk, and their importance in identifying those patients who are likely to benefit from lipid-lowering therapy. The impact of recent studies on clinical guidelines is also considered.
Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.
We recently showed that a hypocaloric carbohydrate restricted diet (CRD) had two striking effects: (1) a reduction in plasma saturated fatty acids (SFA) despite higher intake than a low fat diet, and (2) a decrease in inflammation despite a significant increase in arachidonic acid (ARA). Here we extend these findings in 8 weight stable men who were fed two 6-week CRD (12%en carbohydrate) varying in quality of fat. One CRD emphasized SFA (CRD-SFA, 86 g/d SFA) and the other, unsaturated fat (CRD-UFA, 47 g SFA/d). All foods were provided to subjects. Both CRD decreased serum triacylglycerol (TAG) and insulin, and increased LDL-C particle size. The CRD-UFA significantly decreased plasma TAG SFA (27.48 ± 2.89 mol%) compared to baseline (31.06 ± 4.26 mol%). Plasma TAG SFA, however, remained unchanged in the CRD-SFA (33.14 ± 3.49 mol%) despite a doubling in SFA intake. Both CRD significantly reduced plasma palmitoleic acid (16:1n-7) indicating decreased de novo lipogenesis. CRD-SFA significantly increased plasma phospholipid ARA content, while CRD-UFA significantly increased EPA and DHA. Urine 8-iso PGF(2α), a free radical-catalyzed product of ARA, was significantly lower than baseline following CRD-UFA (-32%). There was a significant inverse correlation between changes in urine 8-iso PGF(2α) and PL ARA on both CRD (r = -0.82 CRD-SFA; r = -0.62 CRD-UFA). These findings are consistent with the concept that dietary saturated fat is efficiently metabolized in the presence of low carbohydrate, and that a CRD results in better preservation of plasma ARA.
Despite the well-established observation that substitution of saturated fats for carbohydrates or unsaturated fats increases low-density lipoprotein (LDL) cholesterol in humans and animal models, the relationship of saturated fat intake to risk for atherosclerotic cardiovascular disease in humans remains controversial. A critical question is what macronutrient should be used to replace saturated fat. Substituting polyunsaturated fat for saturated fat reduces LDL cholesterol and the total cholesterol to high-density lipoprotein cholesterol ratio. However, replacement of saturated fat by carbohydrates, particularly refined carbohydrates and added sugars, increases levels of triglyceride and small LDL particles and reduces high-density lipoprotein cholesterol, effects that are of particular concern in the context of the increased prevalence of obesity and insulin resistance. Epidemiologic studies and randomized clinical trials have provided consistent evidence that replacing saturated fat with polyunsaturated fat, but not carbohydrates, is beneficial for coronary heart disease. Therefore, dietary recommendations should emphasize substitution of polyunsaturated fat and minimally processed grains for saturated fat.
Prospective epidemiologic studies have generated mixed results regarding the association between saturated fatty acid (SFA) intake and risk of ischemic heart disease (IHD) and stroke. These associations have not been extensively studied in Asians.
The aim of this study was to test the hypothesis that SFA intake is associated with the risk of cardiovascular disease mortality in Japanese whose average SFA intake is low.
The Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC Study) comprised 58,453 Japanese men and women who completed a food-frequency questionnaire. Participants were aged 40-79 y at baseline (1988-1990) and were followed up for 14.1 y. Associations of energy-adjusted SFA intake with mortality from stroke (intraparenchymal and subarachnoid hemorrhages and ischemic stroke) and heart diseases (IHD, cardiac arrest, and heart failure) were examined after adjustment for age, sex, and cardiovascular disease risk and dietary factors.
We observed inverse associations of SFA intake with mortality from total stroke [n = 976; multivariable hazard ratio (95% CI) for highest compared with lowest quintiles: 0.69 (0.53, 0.89); P for trend = 0.004], intraparenchymal hemorrhage [n = 224; 0.48 (0.27, 0.85); P for trend = 0.03], and ischemic stroke [n = 321; 0.58 (0.37, 0.90); P for trend = 0.01]. No multivariable-adjusted associations were observed between SFA and mortality from subarachnoid hemorrhage [n = 153; 0.91 (0.46, 1.80); P for trend = 0.47] and heart disease [n = 836; 0.89 (0.68, 1.15); P for trend = 0.59].
SFA intake was inversely associated with mortality from total stroke, including intraparenchymal hemorrhage and ischemic stroke subtypes, in this Japanese cohort.
This review summarizes recent findings on the metabolism and biological functions of saturated fatty acids (SFA). Some of these findings show that SFA may have important and specific roles in the cells. Elucidated biochemical mechanisms like protein acylation (N-myristoylation, S-palmitoylation) and regulation of gene transcription are presented. In terms of physiology, SFA are involved for instance in lipogenesis, fat deposition, polyunsaturated fatty acids bioavailability and apoptosis. The variety of their functions demonstrates that SFA should no longer be considered as a single group.
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.
Dietary and policy recommendations frequently focus on reducing saturated fatty acid consumption for improving cardiometabolic health, based largely on ecologic and animal studies. Recent advances in nutritional science now allow assessment of critical questions about health effects of saturated fatty acids (SFA). We reviewed the evidence from randomized controlled trials (RCTs) of lipid and non-lipid risk factors, prospective cohort studies of disease endpoints, and RCTs of disease endpoints for cardiometabolic effects of SFA consumption in humans, including whether effects vary depending on specific SFA chain-length; on the replacement nutrient; or on disease outcomes evaluated. Compared with carbohydrate, the TC:HDL-C ratio is nonsignificantly affected by consumption of myristic or palmitic acid, is nonsignificantly decreased by stearic acid, and is significantly decreased by lauric acid. However, insufficient evidence exists for different chain-length-specific effects on other risk pathways or, more importantly, disease endpoints. Based on consistent evidence from human studies, replacing SFA with polyunsaturated fat modestly lowers coronary heart disease risk, with ~10% risk reduction for a 5% energy substitution; whereas replacing SFA with carbohydrate has no benefit and replacing SFA with monounsaturated fat has uncertain effects. Evidence for the effects of SFA consumption on vascular function, insulin resistance, diabetes, and stroke is mixed, with many studies showing no clear effects, highlighting a need for further investigation of these endpoints. Public health emphasis on reducing SFA consumption without considering the replacement nutrient or, more importantly, the many other food-based risk factors for cardiometabolic disease is unlikely to produce substantial intended benefits.
DE NOVO: lipogenesis is the biological process by which C2 precursors of acetyl-CoA are synthesized into fatty acids. In human subjects consuming diets higher in fat (> 30 % energy), lipogenesis is down regulated and extremely low; typically < 10 % of the fatty acids secreted by the liver. This percentage will increase when dietary fat is reduced and replaced by carbohydrate, although the extent of carbohydrate-induced lipogenesis is dependent on the type of carbohydrate (monosaccharide v. polysaccharide) and the form in which the carbohydrate is fed (liquid meals, solid less-processed food). Clearly, massive overconsumption of carbohydrate can also increase lipogenesis. A second related phenomenon that occurs when dietary fat is reduced is hypertriacylglycerolaemia. This rise in blood triacylglycerol concentration could be due to increased de novo lipogenesis or to reduced clearance of lipid from the blood. The present paper will review the metabolic mechanisms leading to the elevations in blood triacylglycerol concentration that occur with dietary fat reduction. Studies considered will be those investigating fatty acid synthesis in subjects chronically fed low-fat high-carbohydrate diets and studies in which data were obtained in both the fasted and fed states. Also summarized will be data from subjects who had consumed diets of different carbohydrate types, as well as the most recent data from postprandial studies investigating factors that affect the magnitude of the rise in blood lipids following a meal. Given the changing availability of carbohydrate in the food supply, it will be important to understand how the balance of fat and carbohydrate in the diet influences lipogenesis, and the relative contribution of the process of de novo lipogenesis to the escalating incidence of obesity observed around the world.
A new experimental approach was used to determine whether a eucaloric, low fat, high carbohydrate diet increases fatty acid synthesis. Normally volunteers consumed low fat liquid formula diets (10% of calories as fat and 75% as glucose polymers, n = 7) or high fat diets (40% of calories as fat and 45% as glucose polymers, n = 3) for 25 d. The fatty acid composition of each diet was matched to the composition of each subject's adipose tissue and compared with the composition of VLDL triglyceride. By day 10, VLDL triglyceride was markedly enriched in palmitate and deficient in linoleate in all subjects on the low fat diet. Newly synthesized fatty acids accounted for 44 +/- 10% of the VLDL triglyceride. Mass isotopomer distribution analysis of palmitate labeled with intravenously infused 13C-acetate confirmed that increased palmitate synthesis was the likely cause for the accumulation of triglyceride palmitate and "dilution" of linoleate. In contrast, there was minimal fatty acid synthesis on the high diet. Thus, the dietary substitution of carbohydrate for fat stimulated fatty acid synthesis and the plasma accumulation of palmitate-enriched, linoleate-deficient triglyceride. Such changes could have adverse effects on the cardiovascular system.
Palmitoylethanolamide (PEA), the naturally occurring amide of ethanolamine and palmitic acid, is an endogenous lipid that modulates pain and inflammation. Although the anti-inflammatory effects of PEA were first characterized nearly 50 years ago, the identity of the receptor mediating these actions has long remained elusive. We recently identified the ligand-activated transcription factor, peroxisome proliferator-activated receptor-alpha (PPAR-alpha), as the receptor mediating the anti-inflammatory actions of this lipid amide. Here we outline the history of PEA, starting with its initial discovery in the 1950s, and discuss the pharmacological properties of this compound, particularly in regards to its ability to activate PPAR-alpha.
L'huile de palme va disparaître des produits alimentaires de la marque Casino
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