| Literature DB >> 31454938 |
Eva Gesteiro1, Luis Guijarro2, Francisco J Sánchez-Muniz3, María Del Carmen Vidal-Carou4, Ana Troncoso5, Lluis Venanci6, Vicente Jimeno7, Joan Quilez8, Arturo Anadón9, Marcela González-Gross10.
Abstract
Internationally recognized Spanish experts in the food industry, nutrition, toxicology, sustainability, and veterinary science met in Madrid on July 2018 to develop a consensus about palm oil (PO) as a food ingredient. Their aim was to provide a useful, evidence-based point of reference about PO. Scientific evidence about the role of PO in food safety, nutrition and sustainability was analyzed. Main conclusions were: (1) RSPO foundation responded to the environmental impact of palm crops. The Amsterdam Declaration pursues the use of 100% sustainable PO in Europe by 2020. Awareness about choosing sustainable products will help to maintain local economies and environments in the producing countries; (2) evidence shows that a moderate intake of PO within a healthy diet presents no risks for health. No evidence justifies any change fat intake recommendations; (3) food industry is interested in assuring safe, sustainable and high-quality products. The use of certified sustainable PO is increasing; and (4) there is no evidence associating PO consumption and higher cancer risk, incidence or mortality in humans. Tolerable daily intake (TDI) for toxic contaminants (2-and 3-monochloropropanediols (MCPDs), glycidyl esters (GEs)) have been established by JECFA and EFSA. Consequently, the European Commission has modified the Contaminants Regulation for GEs and it is still working on 3-MCPDs'.Entities:
Keywords: 3MCPD; cardiovascular disease; communication; food industry; palm oil; palmitic acid; sustainability
Mesh:
Substances:
Year: 2019 PMID: 31454938 PMCID: PMC6770503 DOI: 10.3390/nu11092008
Source DB: PubMed Journal: Nutrients ISSN: 2072-6643 Impact factor: 5.717
Sustainable development goals (SDGs) (UN 2015–2030) [16].
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| No poverty | Affordable and clean energy | Climate action |
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| Zero hunger | Decent work and economic growth | Life below water |
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| Good health and well-being | Industry, innovation, and infrastructure | Life on land |
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| Quality education | Reducing inequality | Peace, justice, and strong institutions |
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| Gender equality | Sustainable cities and communities | Partnerships for the goals |
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| Clean water and sanitation | Responsible consumption and production |
Figure 1World population growth prospects [17].
Roundtable for Sustainable Palm Oil (RSPO) principles [18].
| 1. Behave ethically and transparently |
| 2. Operate legally and respect rights |
| 3. Optimize productivity, efficiency, positive impacts and resilience |
| 4. Respect community and human rights and deliver benefits |
| 5. Support smallholder inclusion |
| 6. Respect workers’ rights and conditions |
| 7. Protect, conserve and enhance ecosystems and the environment |
Figure 2Map of palm oil producing countries (United States Department of Agriculture (USDA), 2018).
Different criteria for fat intake recommendations for healthy adult population.
| WHO/FAO (2010) [ | FESNAD (2015) [ | AHA (2000) [ | |
|---|---|---|---|
| Total fat | 20%–35% | 20%–40% | 30% |
| SFA | <10% | The recommendations are reducing the SFA-rich foods intake. | <10% |
| MUFA | Calculated by difference | 12%–30% (27–67 g/day) 20%–25% (45–55 g/day) * | Calculated by difference |
| PUFA | 6%–11% | <10% | |
| PUFA W3 | 0.1%–1% (0.25–2.25 g/day) 0.5–1% | ||
| PUFA W6 | 0.5%–2% | 5%–10% (10–20 g/day) | |
| Trans-FAs | <1% | 2%–3% Reduce the intake as much as possible | |
| Cholesterol | <300 mg/day |
* PREDIMED study data. Modified from Gesteiro et al., (2018) [39]. Fatty acids (FAs): saturated (SFA), monounsaturated (MUFA); and polyunsaturated (PUFA).
Fatty acid composition (%) of the different palm oil and kernel oil fractions.
| Fatty Acid | Palm Oil | Palm Stearin | Palm Olein | Palm Superolein | Palm Kernel Oil | Palm Kernel Stearin | Palm Kernel Olein |
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| C6:0 | ND | ND | ND | ND | ND-0.8 | ND-0.2 | ND-0.7 |
| C8:0 | ND | ND | ND | ND | 2.4–6.2 | 1.3–3.0 | 2.9–6.3 |
| C10:0 | ND | ND | ND | ND | 2.6–5.0 | 2.4–3.3 | 2.7–4.5 |
| C12:0 | ND-0.5 | 0.1–0.5 | 0.1–0.5 | 0.1–0.5 | 45.0–55.0 | 52.0–59.7 | 39.7–47.0 |
| C14:0 | 0.5–2.0 | 1.0–2.0 | 0.5–1.5 | 0.5–1.5 | 14.0–18.0 | 20.0–25.0 | 11.5–15.5 |
| C16:0 | 39.3–47.5 | 48.0–74.0 | 38.0–43.5 | 30.0–39.0 | 6.5–10.0 | 6.7–10.0 | 6.2–10.6 |
| C16:1 | ND-0.6 | ND-0.2 | ND-0.6 | ND-0.5 | ND-0.2 | ND | ND-0.1 |
| C17:0 | ND-0.2 | ND-0.2 | ND-0.2 | ND-0.1 | ND | ND | ND |
| C17:1 | ND | ND-0.1 | ND-0.1 | ND | ND | ND | ND |
| C18:0 | 3.5–6.0 | 3.9–6.0 | 3.5–5.0 | 2.8–4.5 | 1.0–3.0 | 1.0–3.0 | 1.7–3.0 |
| C18:1 | 36.0–44.0 | 15.5–36.0 | 39.8–46.0 | 43.0–49.5 | 12.0–19.0 | 4.1–8.0 | 14.4–24.6 |
| C18:2 | 9.0–12.0 | 3.0–10.0 | 10.0–13.5 | 10.5–15.0 | 1.0–3.5 | 0.5–1.5 | 2.4–4.3 |
| C18:3 | ND-0.5 | ND-0.5 | ND-0.6 | 0.2–1.0 | ND-0.2 | ND-0.1 | ND-0.3 |
| C20:0 | ND-1.0 | ND-1.0 | ND-0.6 | ND-0.4 | ND-0.2 | ND-0.5 | ND-0.5 |
| C20:1 | ND-0.4 | ND-0.4 | ND-0.4 | ND-0.2 | ND-0.2 | ND-0.1 | ND-0.2 |
| C20:2 | ND | ND | ND | ND | ND | ND | ND |
| C22:0 | ND-0.2 | ND-0.2 | ND-0.2 | ND-0.2 | ND-0.2 | ND | ND |
| C22:1 | ND | ND | ND | ND | ND | ND | ND |
| C22:2 | ND | ND | ND | ND | ND | ND | ND |
| C24: 0 | ND | ND | ND | ND | ND | ND | ND |
| C24:1 | ND | ND | ND | ND | ND | ND | ND |
Source: Codex Alimentarius (2015) [49].
Figure 3sn-2 hypothesis. Modified from Gesteiro et al. (2018) [39].
Reviews on the effect of palm oil on cardiovascular health.
| Reference | Type of Study and Aims | Results and Conclusions |
|---|---|---|
| Bester et al. [ | Review. To identify the benefits and risks of four edible oils (olive, sunflower, fish and palm oils) for cardiovascular health. | The studies reviewed here suggest that all four oils could be suitable for inclusion in a healthy diet. Beneficial effects have been identified for each one, although in some cases there remains some dispute. |
| In the case of palm oil, the bulk of the studies have addressed its effects on the serum lipid profile, concluding that the lipid profile is unaffected, and can even reduce atherosclerosis and prevent cardiac ischaemia. The few studies addressing the effect of palm oil on arrhythmogenesis are inconclusive, although it can apparently have a slight anti-arrhythmogenetic effect. | ||
| The studies performed with extracts of the tocotrienol-rich fraction of palm oil suggest that it may offer protection against myocardial ischaemia-reperfusion injury. However, these effects require further study with dietary supplementation models. | ||
| Studies with red palm oil (RPO), which contains the same components as refined oil but also contains more micronutrients, confirm the above-described effects of palm oil, enhanced by the presence of more micronutrients. It has also been shown that dietary supplementation with RPO offers protection against myocardial ischaemia-reperfusion injury. Again, however, further studies with RPO are needed to fully confirm these effects on risk factors of ischaemia and cardiac arrhythmias. | ||
| In conclusion, palm oil has shown only a mild effect on the lipid profile, and so there is no saying whether its consumption would have any beneficial effect in persons at cardiovascular risk (CVR). Nonetheless, it could be useful for some people to consume this oil, since it is one of the few oils to have demonstrated protective effect against myocardial ischaemia-reperfusion injury. | ||
| Teng et al. [ | Single-blind randomized crossover trial (n = 10 healthy males) comparing the effects of high intake of fat (50 g) rich in palmitic acid of both plant (palm olein) and animal (pork lard) origin versus consumption of a fat rich in oleic acid (virgin olive oil) on lipaemia, plasma glucose, insulin and adipocytokines. | The serum triglyceride (TG) concentration was significantly lower after consumption of pork lard than after consumption of olive oil or palm olein (meal effect |
| Levels of plasma glucose, insulin and adipocytokines [interleukin-6 (IL-6), tumoral necrosis factor-α (TNF-α), interleukine-1β (IL-1β) and leptin] were unaffected by the type of fat consumed. In the case of plasma IL-1β, there was such a change over time after taking 3 meals with a high-fat diet ( | ||
| Fattore and Fanelli [ | Review of the scientific evidence on the relationship between palm oil and adverse health effects. | The main reason why consumption of palm oil is associated with adverse health effects is that it contains relatively high concentrations of saturated fatty acids (SFAs), particularly palmitic acid, which in turn have been associated with increased risk of coronary heart disease (CHD) and some types of tumor. However, recent research on the subject has reconsidered the negative role of dietary SFAs as a CVR factor and has shown that not only the type of fat but also the structure of the TGs plays an important part in cholesterolaemia. |
| Some studies have concluded that modification of the type of fat, or modification combined with reduction (but not only reduction) appear to reduce the incidence of cardiovascular events in high-risk subjects. Moreover, most studies posit a possible protective effect from partial replacement of SFAs by polyunsaturated (PUFAs) as opposed to the adverse effect of SFAs | ||
| The process of interesterification, which causes a reordering of palmitic acid and does not occur naturally in native oil, could be associated with potentially adverse health effects and hence is to be discouraged. | ||
| As for its role in the development of cancer, the studies are few and the evidence unconvincing. | ||
| Despite these uncertainties, this review does not demonstrate a negative role of palmitic acid in health, and much less native palm oil, which is a complex alimentary matrix in which palmitic acid is only one of the components. Palm oil also contains other FAs, chiefly oleic acid, along with antioxidant compounds, which may have compensatory effects. | ||
| Fattore et al. [ | Systematic review and meta-analysis of dietary intervention assays, to evaluate the effect on lipid markers for CHD and cardiovascular disease (CVD) of replacing palm oil with other primary dietary fats. The review includes a total of 51 intervention studies ranging in duration from 2 to 16 weeks, in which palm oil-rich diets were compared with diets rich in other fats, and in which at least one or more of the following CHD or CVD biomarkers were determined: total cholesterol (TC), cholesterol transported by low density lipoproteins (LDLc), cholesterol transported by high density lipoproteins (HDLc), TC/HDLc ratio, TG, apolipoprotein (Apo) A-I and Apo B. | Levels of TC, LDLc, Apo B, HDLc and Apo A-I were significantly higher in palm oil-rich diets than in diets rich in stearic acid, monounsaturated fatty acids (MUFAS) and PUFAs whereas most of these biomarkers were significantly lower than in diets rich in myristic and lauric acids. |
| Comparison of the effect of palm oil-rich diets with diets rich in trans-FAs showed that HDLc and Apo-A-I concentrations were significantly higher, while Apo B, and TG concentrations and TC/HDLc ratio were lower. | ||
| This meta-analysis indicates that replacement of palm oil by other fats (SFAs, MUFAs, PUFAs) produces both favorable and unfavorable changes in biomarkers for CVD and CHD. However, when palm oil was replaced by trans-FAs, only favorable changes were found. | ||
| The results do not support an association between palm oil replacement and reduction of mortality from CVD. They rather suggest a need for fresh comparative research and also call for caution in the development of policies for the general population that promote the use of some specific fats over others. More solid evidence is required as to the effects of palm oil on health and on the socio-economic consequences before embarking on such policies. | ||
| Voon et al. [ | Randomized crossover trial of 5 weeks with a total of 45 volunteers. To assess the effects of a (typical Malaysian) diet containing a high proportion of protein and supplemented with virgin olive oil, palm olein or coconut oil on arteriosclerosis markers (cell adhesion molecules, lipid inflammatory mediators and thrombogenicity indices) in healthy adults. | SFA-enriched diets (palm olein and coconut oil), and also a diet with virgin olive oil, containing high levels of oleic acid, have similar effects on arteriosclerosis markers, such as cell adhesion molecules and prostaglandin E2 (PGE2) and thromboxane B2 (TXB2)/Prostaglandin F1α (PGF1α) thrombogenicity indices. |
| Only the diet supplemented with virgin olive oil exhibited a lower level of the leukotriene B4 (LTB4) pro-inflammatory marker than the other two diets assayed. | ||
| The results indicate that it could be premature labelling palm olein and coconut oil as “bad oils” because of their contribution to increased CVR based solely on their effects on the serum lipid profile. | ||
| Odia et al. [ | Review of experimental studies in animals and humans on the association between palm oil and its constituents and serum lipid profile and CVD. | Many scientific studies, both in animals and human beings, clearly show that consumption of palm oil does not cause a rise in serum TC levels and that it is not atherogenic. Apart from palmitic acid, palm oil is composed of oleic and linoleic acids and also contains vitamins A and E, which are powerful antioxidants. It has been demonstrated scientifically that palm oil protects the heart and blood vessels from plaque and ischaemic lesions. |
| Consumed as part of a healthy, balanced diet, it does not cause increased CVR. Replacing this oil with others rich in MUFAs and PUFAs would not produce any additional benefit. | ||
| This review concludes that more longitudinal studies are required to assess the impact on CVR of diets containing palm oil in comparison with diets containing other oils accepted as “beneficial for cardiovascular health”, such as olive oil, analyzing lipid parameters as risk markers. | ||
| Imoisi et al. [ | Review on palm oil: composition and health implications. | Prospective epidemiological studies have shown that the level of plasma TGs, especially after eating, is a major factor in the pathogenesis of CHD. Palm oil is considered as to raise TC and to increase the CVR because of its SFA content (44% palmitic acid and 5% stearic acid). However, there is a growing body of scientific evidence indicating that the effect of palm oil on TC is relatively neutral compared to other fats and oils. Palm oil raises TC only when an excess of dietary cholesterol is present in the diet. |
| Palm oil stimulates the synthesis of HDLc and the elimination of LDLc. | ||
| Palm oil is rich in vitamin E (particularly tocotrienols), which can reduce serum TC concentrations and has powerful antioxidant effects. These benefits occur especially from non-oxidized palm oil. Oxidized palm oil can have an adverse effect on lipid profile, FFAs and phospholipids. | ||
| In conclusion, consumption of palm oil as a fat source in the diet does not pose any additional risk of CHD when consumed in realistic quantities as part of a healthy diet. Consumption of oxidized palm oil should be avoided owing to its adverse effects on lipid profiles. | ||
| Mancini et al. [ | Review on the functional role of palm oil and palmitic acid in the development of obesity, type 2 diabetes mellitus, CVD, and cancer. It also discusses the atherogenic potential of palmitic acid and its stereospecific position in TGs. | As to the possible effects of palm oil-rich diets on CVR in humans, the studies reviewed here report conflicting results. The main criticisms of these may be summarized as follows: (a) considerable qualitative and quantitative heterogeneity of FA concentrations in the diets; (b) differences in selection criteria used to form the trial and control groups; (c) wide age range addressed in the studies; and (d) little attention is paid to other dietary components which could confound the direct effects of FAs on blood lipid markers. |
| To date no clear evidence has been found to demonstrate beyond a doubt the association of consumption of palm oil with increased CVR, particularly in normo-cholesterolaemic subjects, assuming the recommended intake of PUFAs. | ||
| Moreover, the percentage of palmitic acid at position sn-2 on the TG is smaller in palm oil than in animal fats, which supports the hypothesis that palm oil has little atherogenic potential in the context of a balanced diet, and that the alleged adverse effects may be due to a dose-response ratio. | ||
| This review posit the need to carry out more rigorous research to define the advantages and disadvantages of palm oil consumption as regards CVR. | ||
| Sun et al. [ | Systematic review on the effect of palm oil consumption on blood lipids compared with other cooking oils, based on data from clinical trials (minimum duration 2 weeks, comparing the effects of palm oil consumption with that of other oils such as; low-SFA vegetable oils, partially hydrogenated vegetable oils containing trans-FAs and animal fats). | Palm oil significantly increased LDLc by 0.24 mmol/L (95% CI: 0.13, 0.35 mmol/L; I(2) = 83.2%) compared with other low-SFA vegetable oils. This effect was observed in randomized but not in non-randomized trials. Moreover, among randomized trials, only modest differences in study results were observed regarding the effects of palm oil versus LDLc. SFAs from palm oil appear to have the same effects on LDLc as animal fat. |
| Palm oil increased HDLc by 0.02 mmol/L compared with the low-SFA vegetable oils, and by 0.09 mmol/L compared with oils containing trans-FAs. | ||
| In conclusion, the consumption of palm oil results in a higher level of LDLc than that of low-SFA vegetable oils, and in a higher level of HDLc if compared with the effect of oils containing trans-SFAs. This would tend to support the recommendation to reduce the use of palm oil and replace it with low-SFA and trans-FA vegetable oils. | ||
| In the case of foods that are consumed in small quantities which are made using trans-FAs for their sensory characteristics, palm oil can be an alternative thanks to its better effects on HDLc. | ||
| Marangoni et al. [ | Summary of the symposium‘s conclusions on the use of palm oil in the food industry, produced by experts from several Italian medical and nutritional scientific societies and collected by the nutrition foundation of Italy. Toxicological and environmental issues were not considered. | The main conclusions of the Symposium may be summarized thus: |
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There is no evidence on the specific health effects of palm oil consumption as compared with other SFA-rich fats. | ||
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The stereospecific distribution of SFAs in the TG molecules of palm oil limits their rate of absorption and their metabolic effects. | ||
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International guidelines indicate that SFA intake should be less than 10% of total energy, within a balanced diet. Within these limits, there is no reason to expect palm oil consumption to have any effect on human health (and especially on CVD or cancer risk). | ||
| Palm oil intake does not appear to be a public health priority in Italy, in light of its overall effects and available consumption data. |
Apo, apolipoprotein; CHD, coronary heart disease; CVD, cardiovascular disease; CVR, cardiovascular risk; FAs, fatty acids; FFAs, free fatty acids; HDLc, cholesterol transported by high density lipoproteins; IL, interleukin; LDLc, cholesterol transported by low density lipoproteins; MUFAs, monounsaturated fatty acids; PUFAs, polyunsaturated fatty acids; RPO, red palm oil; SFAs, saturated fatty acids; TC, total cholesterol; TG, triglyceride.
Figure 4Technological and economic difficulties in replacing palm oil.
3-MCPD and glycidil ester (GE) levels in different oils and fats.
| Mean Content (mg/kg) (2009) | Maximum Content (mg/kg) (2009) | Mean Content (ppm) (2011) | Maximum Content (ppm) (2011) | Mean Content (mg/kg) (2019) | Maximum Content (mg/kg) (2019) | |
|---|---|---|---|---|---|---|
| Canola oil | 0.3 | 1.5 | 1 | 1 | 1.03 (*) | N |
| Soya oil | N | N | 0.5 | 0.6 | N | N |
| Sunflower oil | 1 | 5.7 | 2 | 4 | 1.82 | 2.05 |
| Corn oil | 2.8 | 7 | 7 | 9 | 0.9 | 1.55 |
| Coconut oil | N | N | 7 | 7.5 | Nd | Nd |
| Palm oil | 4.5 | 13 | 6 | 14 | 6.22 (*) | N |
| Sesame oil | N | N | N | N | 1.6 | 1.63 |
| Safflower oil | N | N | N | N | 2.78 (*) | N |
| Extra virgin olive oil | N | N | N | N | Nd | Nd |
| Refined olive oil 1° | N | N | N | N | 0.78 | 1.11 |
| Refined olive oil 0.4° | N | N | N | N | 0.95 | 1.22 |
| Fried extra virgin olive oil | N | N | N | N | 0.93 | 1.72 |
Prepared by authors, based on Mathäus et al., 2011 [104]; Willits, 2013 [105]; and Custodio-Mendoza et al., 2019 [106]; N: non- determined; Nd: Non detectable; (*) Data from a single oil sample.
Maximum levels of 3-MCPD and GE (Regulation 2018/290) [115].
| Foodstuffs | Maximum Level (μg/kg) | |
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| 4.1.1 | Hydrolysed vegetable protein | 20 |
| 4.1.2 | Soy sauce | 20 |
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| 4.2.1 | Vegetable oils and fats placed on the market for the final consumer or for use as an ingredient in food with the exception of the foods referred to in 4.2.2 | 1000 |
| 4.2.2 | Vegetable oils and fats destined for the production of baby food and processed cereal-based food for infant and young children | 500 |
| 4.2.3 | Infant formula, follow-on formula and foods for special medical purposes intended for infants and young children (powder) | 75 until 30 June 2019. |
| 4.2.4 | Infant formula, follow-on formula and foods for special medical purposes intended for infants and young children (liquid) | 10.0 until 30 June 2019. |