REVIEW ARTICLE
Fredrik Rosqvist1* and Sari Niinistö2
1Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University, Uppsala, Sweden; 2Finnish Institute for Health and Welfare, Helsinki, Finland
This scoping review for the Nordic Nutrition Recommendations 2023 summarizes the available evidence on fats and oils from a food level perspective. A literature search for systematic reviews (SRs) and meta-analyses was conducted in PubMed. There are few SRs and meta-analyses available that investigate the association between fats and oils (food level) and health outcomes; the majority report associations at the nutrient level (fatty acid classes). All identified SRs and meta-analyses were of low methodological quality, thus the findings and conclusions presented within this scoping review should be interpreted cautiously. Based on this limited evidence, the following results were indicated: the intake of olive oil may be associated with reduced risk of cardiovascular disease (CVD), type 2 diabetes (T2D), and total mortality in prospective cohort studies. The intake of butter was not associated with the risk of CVD but may be related to slightly lower risk of T2D and higher risk of total mortality in prospective cohort studies. For cancer, the evidence is sparse and primarily based on case-control studies. The intake of olive oil may be associated with reduced risk of cancer, whereas the intake of butter may be associated with increased risk of certain cancer types. Butter increases LDL-cholesterol when compared to virtually all other fats and oils. Palm oil may increase LDL-cholesterol when compared to oils rich in MUFA or PUFA but may not have any effect on glucose or insulin. Coconut oil may increase LDL-cholesterol when compared to other plant oils but may decrease LDL-cholesterol when compared to animal fats rich in SFA. Canola/rapeseed oil may decrease LDL-cholesterol compared to olive oil, sunflower oil and sources of SFA and may also reduce body weight compared to other oils. Olive oil may decrease some inflammation markers but may not have a differential effect on LDL-cholesterol compared to other fats and oils. The effect on risk markers likely differs depending on the type/version of oil, for example, due to the presence of polyphenols, phytosterols and other minor components. Taken together, based on the available evidence, oils rich in unsaturated fat (e.g. olive oil, canola oil) are to be preferred over oils and fats rich in saturated fat (e.g. butter, tropical oils).
Keywords: fats; oils; butter; olive oil; rapeseed oil; palm oil; vegetable oil; coconut oil; LDL cholesterol; diabetes; cardiovascular disease; mortality; cancer
Citation: Food & Nutrition Research 2024, 68: 10487 - http://dx.doi.org/10.29219/fnr.v68.10487
Copyright: © 2024 Fredrik Rosqvist and Sari Niinistö. This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material for any purpose, even commercially, provided the original work is properly cited and states its license.
Received: 8 March 2022; Revised: 10 June 2022; Accepted: 3 January 2024; Published: 9 February 2024
*Fredrik Rosqvist, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University, Husargatan 3, BMC, Box 564, 751 22 Uppsala, Sweden. Email: fredrik.rosqvist@pubcare.uu.se
Competing interests and funding: None
Dietary sources of fat are usually, and conveniently, defined by their fatty acid compositions as saturated (SFA), monounsaturated (MUFA) or polyunsaturated (PUFA) fat rich sources (illustrated in Fig. 1) as the degree of saturation is known to have a meaningful impact on important risk markers (e.g. blood lipids). Although the degree of saturation is likely to be the primary mediator in terms of health effects of dietary fats and oils, it is not the only factor. Vegetable oils may also contain different levels of other bioactive components, such as polyphenols, antioxidants, vitamins and phytosterols, potentially mediating parts of the overall health effect. These bioactive compounds may be more or less preserved depending on the degree of processing (1). Olive oil is a well-known example, where the level of polyphenols may vary widely due to agronomic factors (e.g. ripeness of the olives and cultivation conditions), extraction technology, and mixing of different fractions (2). In general, extra-virgin olive oil has the highest content of polyphenols whereas levels may be very low in refined olive oils. Similarly, the natural content of phytosterols (known to have beneficial effects on blood cholesterol levels) varies markedly between different fats and oils, being markedly higher in, for example, rapeseed and corn oil than in, for example, sunflower, soybean and olive oil (1). However, and similar to polyphenols on olive oil, the levels of phytosterols in oils will be affected by the cultivation conditions, extraction method, and degree of refinement (1). Thus, the overall health effect of various sources of fat may differ, even if the fatty acid composition is similar, due to complex interactions between nutrients, non-nutrients and physical structure (known as food matrix-effects). Furthermore, for some fats and oils, multiple fractions may be obtained. An illustrative example of this is palm oil, consisting of roughly equal parts of saturated and unsaturated fatty acids and is viewed as a source of saturated fat in the diet. However, multiple different fractions can be obtained from palm oil. These fractions have different physicochemical properties and differ markedly in their fatty acid composition (3). For example, compared to ‘palm oil’, ‘palm olein’ has a lower content of palmitic acid (and total SFA) and is semi-solid in room temperature, whereas both ‘super olein’ and ‘top olein’ are liquid in room temperature due to even lower contents of palmitic acid (and total SFA) (3). In contrast to ‘palm oil’, ‘palm stearin’ has a markedly higher content of palmitic acid (and total SFA) and is solid at room temperature (3). In extreme contrast to ‘palm oil’, ‘palm olein’ and ‘palm stearin’, palm kernel fractions (e.g. palm kernel oil and -olein) have a very low content of palmitic acid and is dominated primarily by lauric acid (~45%) but also myristic acid (~15%) (3). Finally, red palm oil (crude/unprocessed) has a high content of carotenoids, antioxidants, vitamin E, and phytosterols but has limited utility and is seldom used. Thus, in order to draw conclusions about the health effects of palm oil compared to other oils, it is important to know which fraction(s) that have been used. Palm oil is a so-called ‘tropical oil’, which means that it is a vegetable oil rich in saturated fat derived from the tropical zone. These vegetable oils (also including e.g. coconut oil) are distinctly different from the so-called ‘non-tropical oils’, which are instead characterized by their low content of saturated fat.
Fig. 1. Compositional differences between various fats and oils. Values are taken from the Swedish, Finnish and US food databases which showed the amount of different types of fatty acids as grams per 100 g fat or oil which equals to percentages.
The aim of this scoping review is to describe the totality of evidence for the role of fats and oils for health-related outcomes as a basis for setting and updating food-based dietary guidelines in the Nordic Nutrition Recommendations (NNR) 2023 (Box 1). This scoping review primarily considers results at a food level perspective (i.e. studies reporting on specific food sources of fat, e.g. olive oil). Results from studies reporting at a nutrient level perspective (e.g. saturated fat) are considered in an accompanying paper (4).
Box 1. Background papers for Nordic Nutrition Recommendations 2023
This review follows the protocol developed within the NNR2023 project (5). The sources of evidence used in this review follow the eligibility criteria described previously (6). No de novo NNR2023 systematic review (SR) was performed for this paper, and no previously published qualified SRs reporting at a food level perspective were available (5, 7). However, one qualified SR primarily reporting at a nutrient level could be used as supporting evidence for the association between butter and cardiovascular disease (CVD) (8). A literature search for SR and meta-analyses was conducted in PubMed on 16 August 2021 (updated on 31 January 2022) using the following search string (“dietary fat”[Title/Abstract] odds ratio [OR] “dietary fats”[Title/Abstract] OR “vegetable oil”[Title/Abstract] OR “butter”[Title/Abstract] OR “ghee”[Title/Abstract] OR “corn oil”[Title/Abstract] OR “cottonseed oil”[Title/Abstract] OR “canola”[Title/Abstract] OR “olive oil”[Title/Abstract] OR “rapeseed oil”[Title/Abstract] OR “safflower oil”[Title/Abstract] OR “sunflower oil”[Title/Abstract] OR “sesame oil”[Title/Abstract] OR “soybean oil”[Title/Abstract] OR “plant oil”[Title/Abstract] OR “seed oil”[Title/Abstract] OR “cooking oil”[Title/Abstract] OR “margarine”[Title/Abstract] OR “flaxseed oil”[Title/Abstract] OR “palm oil”[Title/Abstract] OR “coconut oil”[Title/Abstract] OR “camelina oil”[Title/Abstract] OR “lard”[Title/Abstract] OR “mayonnaise”[Title/Abstract] OR “dietary fats”[Mesh] OR “plant oils”[Mesh] AND ((meta-analysis[Filter] OR systematicreview[Filter]) AND (humans[Filter]) AND (2011:2021[pdat])). For publications reporting results at both food- and nutrient level, primarily the food level perspective is considered in this paper. The search resulted in 961 hits. Study selection was done in duplicate and consensus was reached through discussion between the authors. The search was repeated without filtering for ‘Humans’ which resulted in an additional three papers of relevance. The quality of the included studies (Table 1) was evaluated using the tool AMSTAR 2, modified for NNR (5). The certainty of evidence was not assessed. Excluded studies are presented in Table 2. The topics discussed in this scoping review are, to a large degree, defined by the topics covered by the SRs. In case of multiple and overlapping SRs, we chose the most recent and most updated SRs over the older, or used both if they were complementary.
It is challenging to directly compare the intake of fats and oils between the Nordic and Baltic countries as food groupings and assessment methods are not harmonized. Food group definitions, and thus level of information, differ between countries. Furthermore, data was collected at different time points (from 2010 to 2020) using different instruments (2 × 24 h recall, 4-day web-based food record, and 7-day food record), and participation rate ranged between 33 and 90%. Finally, contribution of alcohol to total energy intake was not included in Latvia and Lithuania. However, based on available data (9) it appears that the intake of fats and oils is higher in Denmark (men: 47 g/day, women: 35 g/day) and Finland (men: 53 g/day, women: 38 g/day) than in Norway (men: 39 g/day, women: 24 g/day) and Iceland (men: ~20 g/day, women: ~15 g/day). Data for Sweden only includes ‘spreads on bread’ (being 13 g/day for men, 10 g/day for women) and is thus difficult to compare to the other countries. In the Baltic countries, intake appears higher in Estonia (men: ~26 g/day, women: 19 g/day) than in Latvia (men: 13 g/day, women: 11 g/day) and Lithuania (men:12 g/day, women: 9 g/day). However, there is a large standard deviation/range in all countries.
In a meta-analysis from 2014 (10) based on seven cohort studies (population ranged from n ~3,300 to n ~41,000 with follow-up durations ranging from 3.7 to 11.3 years), the intake of olive oil (top vs. bottom third) was associated with a 28% reduction in the risk for combined cardiovascular events (relative risk [RR] 0.72 [95% confidence interval [CI]: 0.57–0.91]), although with considerable heterogeneity (I2 = 75%). Results in the same direction were observed at the nutrient level for both ‘all MUFA combined’ (RR 0.91 [0.86–0.96], 30 studies) and ‘MUFA:SFA ratio’ (RR 0.93 [0.86–1.01], six studies). For CVD mortality, a risk reduction of 30% was indicated for higher compared to lower intake; however, substantial heterogeneity (I2 = 71%) caused by one study resulted in a statistically non-significant result (RR 0.70 [0.48–1.03]). Similar results, although of smaller magnitudes, were observed at the nutrient level for both ‘all MUFA combined’ (RR 0.88 [0.80–0.96], n = 14 studies) and ‘MUFA:SFA ratio’ (RR 0.91 [0.83–0.99], four studies). When looking at the risk of stroke separately, the intake of olive oil (highest vs. lowest third) was associated with a 40% reduction in risk (RR 0.60 [0.47–0.77]), without heterogeneity (I2 = 0%) but based on only two cohorts. When looking at the risk of coronary heart disease (CHD) separately, the intake of olive oil (highest vs. lowest third) was not associated with risk (RR 0.80 [0.57–1.14]), based on four cohorts with considerable heterogeneity (I2 = 77%). Another meta-analysis from 2014 based on the same data observed similar results for both stroke and CHD when exposure was expressed as ‘per 25 g/day increment’.
The beneficial effect of olive oil on CVD indicated by meta-analyses of observational studies is supported by the ~5 year-long PREDIMED trial, where the risk of CVD (composite of myocardial infarction, stroke and death from cardiovascular causes) decreased by ~30% in the group receiving extra-virgin olive oil in the context of a Mediterranean diet compared to the control group (receiving advice on a low-fat diet).
In a meta-analysis from 2016 (11) based on cohort studies from Sweden, USA, Finland, and the Netherlands, there was no association between the intake of butter (per 14 g/day increment) and the risk for total CVD (RR 0.99 [0.96–1.02], n = 2 cohorts with n = 6,051 cases), stroke (RR 1.01 [0.98–1.03], n = 3 cohorts with n = 5,229 cases), CHD (RR 0.99 [0.96–1.03], n = 3 cohorts with n = 4,484 cases) or any CVD outcome (RR 1.00 [0.98–1.02], n = 4 cohorts with n = 9,783 cases), without heterogeneity (I2 = 0% for all). For stroke specifically, another meta-analysis from 2016 (12) based on largely the same data also did not observe any association (RR 1.00 [0.99–1.01] per 10 g/day increment). The null association between butter and CVD reported above is supported by findings by the US Dietary Guidelines Advisory Committee 2020 (8).
In a SR from 2018 (13), one single case-control study (n = 2,111 cases) from Costa Rica was identified comparing the intake of palm oil with soybean oil and ‘other oils’ regarding the risk of myocardial infarction. The results indicated that palm oil was associated with increased risk compared with ‘other oils’ (RR 1.26 [1.02–1.55]) and soybean oil with low (5%) levels of trans-fat (RR 1.33 [1.09–1.62]) but not when compared with soybean oil with high (22%) levels of trans-fat (RR 1.16 [0.86–1.56]). The certainty of evidence was graded as ‘very low’.
In a meta-analysis from 2017 (14) based on four cohort studies including 19,081 type 2 diabetes (T2D) cases among 183,370 participants from the US and Europe, high olive oil consumption compared to low showed a 16% reduced risk of T2D (RR 0.84 [0.77–0.92], I2 = 22%) when the duration of follow-up ranged from 4 to 22 years. Further, in a dose-response meta-analysis, 10 g increase of olive oil daily intake was associated with 9% lower risk (RR 0.91 [0.87–0.95]). In addition, a non-linear association was observed so that olive oil intake showed stronger protective association up to the 13 g daily intake (14). However, the quality of meta-evidence of these studies was graded as low (14). Moreover, a SR from 2015 (15) reported that olive oil was found to be protective from T2D in two randomized controlled trials (RCTs) among Spanish adults that compared Mediterranean diet supplemented with virgin olive oil or nuts to a control group who had been advised to comply with a low-fat diet (PREDIMED trial) (16, 17). In the olive oil group (n = 139; median age of participants = 67 years), the risk of T2D was 51% lower than in low-fat diet group (n = 134) during the median follow-up of 4 years (hazard ratio [HR] 0.49 [0.25–0.97]) (16). Also, later data based on a larger number of participants (n = 3,541) aged 55 to 80 years and having high cardiovascular risk showed protective effect for olive oil (HR 0.60 [0.43–0.85]) (17).
A meta-analysis from 2016 (11) based on 11 country-specific cohorts consisting of European and US populations, including altogether 201,628 participants with 23,958 cases, showed that 14 g increase of daily butter consumption was associated with lower risk of type 2 diabetes (RR 0.96 [0.93–0.99], I2 = 47%).
A meta-analysis from 2022 based on 45 large studies, including eight cohort studies with 12,461 cases in a total cohort of 929,771 subjects and 37 case-control studies with 17,369 cases and 28,294 controls, summarized that high olive oil consumption compared to low was associated with 31% reduced risk of having any type of cancer (RR 0.69 [0.62–0.77], I2 = 75%). However, when cohort and case-control studies were analyzed separately, there was no association among eight cohort studies (RR 0.90 [0.77–1.05], I2 = 52%), although a protective association was observed among 37 case-control studies (OR 0.65 [0.57–0.74], I2 = 67%). A protective overall association between higher olive oil intake and any type of cancer was seen both among Mediterranean (RR 0.69 [0.60–0.79], I2 = 70%) and non-Mediterranean participants (RR 0.49 [0.34–0.71], I2 = 49%) (18).
Similarly, high olive oil consumption was related to lower risk for developing a gastrointestinal cancer, that is, colorectal, esophageal, gastric, and pancreatic cancer in overall meta-analysis that combined two cohort and 13 case-control studies (RR 0.77 [0.66–0.89], I2 = 41%) as well as among 13 case-control studies (RR 0.72 [0.61–0.85], I2 = 39%), whereas a protective association was not observed in a meta-analysis of cohort studies (RR 0.97 [0.75–1.24], I2 = 21%) (18). Further, high intake of olive oil was protectively associated with upper aero-digestive cancer (laryngeal, nasopharyngeal, and oral/pharyngeal) among six case-control studies (RR 0.74 [0.60–0.91], I2 = 33%) and urinary tract cancer (prostate and bladder) in a meta-analysis including six case-control studies (RR 0.46 [0.29–0.72], I2 = 73%).
Furthermore, in a meta-analysis from 2022 (18) based on three cohort and 11 case-control studies, high versus low consumption of olive oil showed 33% lower risk of breast cancer (RR 0.67 [0.52–0.86], I2 = 83%). However, in a subgroup analysis by study design, this protective association was observed only among 11 case-control studies (RR 0.63 [0.45–0.87], I2 = 80%), while there was no association within the three cohort studies (RR 0.67 [0.29–1.56], I2 = 78%). In another meta-analysis from 2015 (19) based on five cohorts and 11 case-control studies (11,161 cases in over 150,000 women from Europe, the US and Iran), the highest versus lowest category of intake of vegetable oils, including olive, safflower seed, peanut, soya, corn, or mixed oil, was not associated with the risk of breast cancer (OR 0.88 [0.77–1.01]). However, there was substantial heterogeneity among studies (I2 = 74%). Neither dose-response meta-analysis (n = 12 studies with 6,253 cases in 73,842 women) did show any association between 10 g increment of daily vegetable oil intake and the risk of breast cancer (OR 0.98 [0.95–1.01]) (19). Subgroup analysis showed no indication that menopause or hormone receptor status may modify the association between vegetable oils and the risk of breast cancer (19).
In a meta-analysis of two large cohort studies including participants from Europe (1,303 cases in 301,107 women) and the US (1,531 cases in 205,863 women), consumption of butter was associated with increased risk of endometrial cancer (highest vs. lowest category RR 1.14 [1.03–1.26], I2 = 3%) (20). Also, high intake of butter showed association with increased risk of non-Hodgkin lymphoma in a meta-analysis of four case-control studies (RR 1.31 [1.04–1.65], I2 = 37%) (21). In contrast, butter intake showed no associations with the risk of esophageal squamous cell carcinoma (n = 4 case-control studies with severe heterogeneity I2 = 80%; high vs. low 1.77 [0.84–3.75]) (22), bladder cancer (n = 2 cohorts, 3 case-control studies; RR 1.00 [0.95–1.06], I2 = 6%) (23), or gastric cancer (n = 1 cohort, 2 case-control studies; highest vs. lowest category RR 1.35 [0.88–2.08], I2 = 55%) (24). Margarine was not associated with gastric cancer (n = 2 cohorts, 1 case control; highest versus lowest category RR 1.04 [0.51–2.21], I2 = 71%) (24).
A meta-analysis from 2014 (25) investigated the association between dairy foods and risk of Parkinson’s disease. Based on three effect sizes from two prospective cohorts (one from Finland, one from USA), the intake of butter (highest vs. lowest category) was not associated with the risk of Parkinson’s disease (RR 0.76 [0.51–1.13], I2 = 0.0%).
A meta-analysis from 2019 (26) investigated the association between food groups and risk of age-related macular degeneration in prospective cohort studies. The risk of developing age-related macular degeneration was not associated with the intake (higher vs. lower) of butter (RR 1.04 [0.93–1.16], n = 2 studies), margarine (RR 1.05 [0.91–1.21], n = 3 studies) or oils (RR 1.10 [0.98–1.23], n = 2 studies).
In a meta-analysis from 2021 (27) based on one prospective cohort and two case-control studies, higher butter consumption was associated with a 27% increased risk of endometriosis in the females compared to lower intake (1.27 [1.03–1.55], I2 = 0%). Studies included 1,173 endometriosis cases from the US and Europe.
A meta-analysis from 2021 (28) investigated the effects of olive oil on the main components of metabolic syndrome (obesity, insulin resistance or glucose intolerance, dyslipidemia, and high blood pressure) in healthy adults or subjects with at least one component related to metabolic syndrome. Olive oil had no effect on body composition (−0.02 [−0.10, 0.05], I2 = 18%) or glycemic profile (0.04 [−0.10, 0.18], I2 = 40%) or blood pressure (−0.00 [−0.06, 0.05], I2 = 37%) compared to other oils (e.g. sunflower oil, palm olein, cocoa butter, fish oil, cottonseed oil, butter, coconut oil, corn oil, soybean oil, safflower oil, canola oil).
In a meta-analysis from 2014 (10) based on five cohort studies (population ranged from n ~3,300 to n ~41,000 with follow-up durations ranging from 3.7 to 11.3 years), the intake of olive oil (top vs. bottom third) was associated with a 23% reduction in risk for all-cause mortality (RR 0.77 [0.71–0.84]). No heterogeneity was observed (I2 = 0%). Similar results, although of smaller magnitudes, were observed at the nutrient level for both ‘all MUFA combined’ (RR 0.89 [0.83–0.96], n = 17 studies) and ‘MUFA:SFA ratio’ (RR 0.90 [0.82–1.00], n = 10 studies).
In the PREDIMED trial, supplementation with extra-virgin olive oil in the context of a Mediterranean diet was associated with a non-significant 10% reduction in risk for total mortality (HR 0.90 [0.69–1.18]).
In a meta-analysis from 2016 based on two large studies consisting of European populations (nine country-specific cohorts, ~10 years of follow-up, ~28,000 events), the intake of butter was associated with a 1% increased risk for all-cause mortality per 14 g/day increment (RR 1.01 [1.00–1.03]) without heterogeneity (I2 = 0%). A previous meta-analysis from 2013 (29) based on partly the same data (one overlapping study) observed no association between intake of butter and all-cause mortality (RR 0.96 [0.85–1.08] per each additional serving/week), with considerable heterogeneity (I2 = 78%).
Butter increases LDL-cholesterol when compared to basically all other fats/oil, as demonstrated in a SR from 2021 (30) and a network meta-analysis from 2018 (31). The difference in LDL-cholesterol (−0.25 to −0.42 mmol/L per 10 E% isocaloric exchange) is largest when butter is compared to oils rich in unsaturated fats (safflower oil, sunflower oil, rapeseed oil, flaxseed oil, corn oil, olive oil, and soybean oil), but butter increases LDL-cholesterol also in comparison to other sources of SFA (coconut oil, palm oil, and beef fat). Similar effects were observed for total cholesterol. Fewer differences are observed for triglycerides and high-density lipoprotein [HDL]-cholesterol. However, sunflower oil, soybean oil, and palm oil were observed to decrease triglycerides compared to butter (−0.04 to −0.06 mmol/L per 10 E% isocaloric exchange), and coconut oil was observed to increase HDL-cholesterol compared to butter (0.04 mmol/L per 10 E% isocaloric exchange).
The most recent meta-analysis (32) included studies using palm oil or palm olein, but not studies using palm stearin, palm kernel oil or red palm oil. Compared to MUFA-rich diets, palm oil increased LDL-cholesterol (0.24 mmol/L [0.06–0.42]) when based on n = 16 cross-over studies including a total of n = 365 participants, but decreased LDL-cholesterol (−0.28 mmol/L [−0.53 to −0.03]) when based on one parallel study including 60 participants. Compared to PUFA-rich diets, palm oil increased LDL-cholesterol (0.26 mmol/L [0.06–0.45]) when based on five cross-over studies including a total of 114 participants but not when based on three parallel studies including a total of 152 participants (0.54 mmol/L [−0.45 to 1.52]). Similar results, overall, were observed for total cholesterol. Palm oil increased HDL-cholesterol compared to PUFA-rich diets, both when based on five cross-over studies (0.08 mmol/L [0.01–0.15]) and when based on three parallel studies (0.08 mmol/L [0.00–0.16]). Compared to MUFA-rich diets, there was no difference in HDL-cholesterol when based on 16 cross-over studies (0.03 mmol/L [−0.01 to 0.07]), but palm oil increased HDL-cholesterol when based on one parallel study (0.18 mmol/L [0.09–0.27]). Finally, palm oil had no differential effect on apoA1 or apoB when compared to either MUFA-rich diets (n = 3 cross-over studies) or PUFA-rich diets (n = 2 cross-over studies and n = 1 parallel study).
A previous meta-analysis (3) included only studies using palm olein and found that palm olein decreased LDL-cholesterol when compared to other SFA-rich oils/fats (coconut, lard) (−0.50 mmol/L [−0.70 to −0.30]), but there was no difference when compared to MUFA-rich oils (olive oil, peanut oil, canola oil, high-oleic sunflower oil), PUFA-rich oils (soybean oil) or ‘all other oils’. Results were similar for total cholesterol whereas no differential effect was found for triglycerides. Palm olein increased HDL-cholesterol when compared to MUFA-rich diets (0.04 mmol/L [0.00 to 0.07]) and decreased HDL-cholesterol when compared to other SFA-rich oils (−0.06 mmol/L [−0.11 to −0.00]), whereas no differential effects were found when compared to PUFA-rich oils or ‘all other oils’.
A meta-analysis from 2019 (33) observed that coconut oil decreased LDL-cholesterol when compared to animal fats (butter, beef fat) (−0.37 [−0.69 to −0.05], n = 4), but increased LDL-cholesterol when compared to ‘all plant oils’ (0.26 [0.09 to 0.43], n = 13). Similarly, coconut oil increased LDL-cholesterol when compared to MUFA+PUFA-rich oils (0.34 [0.13 to 0.54], n = 10) as well as when compared to PUFA-rich oils only (0.43 [0.15 to 0.72], n = 5), but there was no difference when compared to MUFA-rich oils only (0.23 [−0.06 to 0.53], n = 5). Interestingly, when the type of coconut oil was considered, virgin/extra virgin coconut oil did not affect LDL-cholesterol compared to other fats/oils combined (−0.08 [−0.35 to 0.20], n = 5), whereas unspecified/all types of coconut oil increase LDL-cholesterol (0.20 [0.02 to 0.38], n = 12). Results were, overall, similar for total cholesterol whereas coconut oil raised HDL-cholesterol in all comparisons. Fewer differential effects were observed for triglycerides, but coconut oil increased triglycerides when compared to MUFA+PUFA-rich oils (0.21 [0.01 to 0.41], n = 10) as well as PUFA-rich oils only (0.31 [0.03 to 0.58], n = 5). Similarly, a meta-analysis from 2020 (34) observed that coconut oil increased both LDL and total cholesterol compared to palm oil (n = 4) and non-tropical vegetable oils (n = 16).
In a meta-analysis from 2019 (35) based on 27 randomized trials, olive oil had no differential effect on LDL-cholesterol compared to oils rich in n-3 PUFA (12 studies), n-6 PUFA (10 studies) or SFA (3 studies). When compared to ‘all other plant oils combined’, olive oil was found to increase LDL-cholesterol (n = 24 studies), but stratified analyses showed that this effect was only observed in studies lasting a maximum of 30 days (15 studies) and not in studies with longer duration (10 studies). Olive oil increased total cholesterol when compared to oils rich in n-3 PUFA (11 studies), n-6 PUFA (12 studies) and ‘all other plant oils combined’ (26 studies) but not when compared to SFA (3 studies). Olive oil increased both HDL-cholesterol and triglycerides when compared to oils rich in n-3 PUFA and ‘all other plant oils combined’ but not when compared to oils rich in n-6 PUFA or SFA. Finally, olive oil had no differential effect on apoA1 or apoB when compared to ‘all other plant oils combined’ (10 studies).
Another two meta-analyses from 2019 compared the effects of different types of olive oil (36, 37). Olive oil with a high content of polyphenols decreased both LDL-cholesterol and oxidized LDL-cholesterol compared with olive oil with a low content of polyphenols or ‘refined’ olive oil. Furthermore, olive oil with a high content of polyphenols increased HDL-cholesterol when compared with olive oil with low content of polyphenols but not when compared to ‘refined’ olive oil. No differential effect was observed for diastolic blood pressure, but olive oil polyphenols may decrease systolic blood pressure.
A meta-analysis from 2020 (38) observed that canola oil decreased LDL-cholesterol when compared to olive oil (−0.17 [−0.29 to −0.04], n = 9), sunflower oil (−0.14 [−0.23 to −0.05], n = 11), sources of SFA (−0.49 [−0.70 to −0.28], n = 10) as well as all ‘other edible oils’ (−0.23 [−0.33 to −0.14], n = 35). Results were similar for total cholesterol. Canola oil had no differential effect on HDL-cholesterol or apoA1 compared to olive oil, sunflower oil, sources of SFA or ‘other edible oils’. Canola oil decreased apoB when compared to sources of SFA (−0.09 [−0.16 to −0.02], n = 4) and ‘other edible oils’ (−0.03 [−0.06 to −0.01], n = 14), but not when compared to olive oil (0.01 [−0.07 to 0.08], n = 2) or sunflower oil (0.01 [−0.04 to 0.07], n = 3). Canola oil had no differential effect on either systolic or diastolic blood pressure compared to olive oil, sunflower oil, sources of SFA or ‘other edible oils’.
Based on a network meta-analysis (a technique for comparing three or more interventions simultaneously) from 2018 (31), the effect of flaxseed oil on LDL-cholesterol is similar to that of most other fats/oils (safflower oil, sunflower oil, rapeseed oil, hempseed oil, corn oil, olive oil, soybean oil, palm oil, coconut oil, beef fat, and lard), but lowers LDL-cholesterol in comparison to butter (−0.37 mmol/L per 10 E% isocaloric exchange). Effects were similar for total cholesterol. Flaxseed oil had no differential effects on HDL-cholesterol or triglycerides compared to any other fats/oils. However, all comparisons are based on only 1–2 studies. Another meta-analysis from 2016 (39) indicates that flaxseed oil may lower diastolic (−4.1 mmHg [−6.8 to −1.4]), but not systolic (−4.6 mmHg [−11.9 to 2.6]), blood pressure; however, the type of comparison was not specified. Finally, a SR and meta-analysis from 2021, based on nine RCTs, found no differential effect of flaxseed oil on total cholesterol, LDL-cholesterol, HDL-cholesterol or triglycerides compared to other oils (sunflower oil, safflower oil, corn oil) in patients with dyslipidemia-related diseases (40).
A SR from 2015 (41) investigated the effects of oils rich in oleic acid (primarily high-oleic sunflower oil, but also safflower, olive, and canola oil) on cardiovascular risk factors when compared to other fats and oils (primarily palm oil, but also butter, cocoa butter, lard, and margarines with high content of trans fat). Based on 23 comparisons from 17 crossover interventions (8 studies in hyper- and nine studies in normocholesterolemic subjects), high-oleic oils reduced LDL-cholesterol, apoB, and total cholesterol when compared to oils/fats rich in saturated fat in the majority of comparisons, whereas no differential effect was observed for triglycerides, HDL-cholesterol or apoA1. When compared to trans-fat-containing oils/fats, high-oleic oils decreased total- and LDL-cholesterol, apoB and triglycerides in all or almost all comparisons, whereas HDL-cholesterol and apoA1 were increased in the majority of comparisons. High-oleic oils had no differential effect on any lipoprotein marker compared to oils rich in PUFA.
The largest available meta-analysis from 2015 (42) (n = 15 RCTs), including altogether 541 participants in the olive oil groups and 731 in control groups, showed that olive oil compared to control oil or diet reduced levels of c-reactive protein (CRP) (mean difference 0.64 mg/L [−0.96, −0.31], I2 = 66%). Also, olive oil decreased concentration of interleukin 6 (IL-6) (mean difference −0.29 pg/mL ([−0.7, −0.02], seven RCTs with a total of 416 subjects in olive oil and 441 in control groups, I2 = 62%)) as well as improved endothelial function (mean difference 0.76% ([0.27–1.124]; eight RCTs with 335 subjects in olive oil and 516 in control groups, I2 = 26%)). The study duration varied from four to 208 weeks. However, a considerable heterogeneity among studies indicates that results of this meta-analysis should be interpreted with caution.
In a meta-analysis from 2019 based on seven RCTs, flaxseed oil compared to placebo did not affect plasma CRP levels (−0.67 mg/L [−2.00, 0.65], I2 = 83%). Participants in these studies were healthy, overweight, obese, prediabetic or patients with chronic diseases (43). Also, in two other meta-analyses, flaxseed oil did not affect circulating inflammatory markers (CRP, IL-6, TNF-α, or high sensitive CRP) compared to other vegetable oils (44, 45). In contrast, in a meta-analysis from 2021 including participants with dyslipidemia related diseases, flaxseed oil reduced IL-6 (−0.35 pg/mL [−0.67, −0.03], I2 = 52%) and high sensitive CRP (−1.54 mg/L [−2.59, −0.49], I2 = 33%) compared to other vegetable oils (sunflower, safflower or corn), while there was no effect on CRP or TNF-α (40).
In a meta-analysis from 2021, coconut oil intake compared to meals without coconut oil increased insulin resistance (HOMA-IR mean difference 0.55 [0.00–1.10], I2 = 64%), but did not affect fasting plasma glucose (mean difference 2.05 mg/dL, [−0.14, 4.25], I2 = 7%), insulin (mean difference 0.31 mIU/L [−2.59, 3.20], I2 = 28%) or HOMA-β (mean difference 17.09 [−44.31, 10.13], I2 = 82%) (46). This meta-analysis consisted of 11 RCTs, in which the number of participants ranged from 9 to 92 in intervention groups and the duration of the interventions varied from 3 to 28 weeks.
In a SR from 2019 (47) results from eight RCTs that compared the effect of palm oil on glucose metabolism in interventions that lasted from 3 to 7 weeks and the number of participants in intervention groups ranged from 15 to 100 participants were presented. Palm oil compared to other vegetable oils was not seen to affect fasting plasma glucose or insulin levels (47).
In a meta-analysis from 2019 (48) based on 22 RCT studies including 1,078 participants, canola oil reduced body weight 0.3 kg (−0.52, −0.08) compared to many other types of vegetable oils, fish oil or control diet in interventions of varying durations from three to 28 weeks. These studies were done in several countries around the world including Finland and Sweden and there was no heterogeneity between the studies (I2 = 0%). However, canola oil was not observed to affect BMI or other anthropometric measures.
In a meta-analysis from 2021 in participants with dyslipidemia related diseases, flaxseed oil intake did not affect body weight (n = 4 RCT), BMI (n = 8 RCT) or waist-to-hip ratio (n = 2 RCT), but it reduced waist circumference (n = 4 RCT) 1.61 cm [−2.69, −0.53], I2 = 50%, compared to other vegetable oils (40).
Based on the current evidence, vegetable oils rich in unsaturated fat (e.g. olive oil, canola/rapeseed oil) are to be preferred over tropical plant oils containing a high percentage of SFA such as coconut oil and palm oil as well as SFA-rich animal fats like butter. This is in line with several other fat recommendations in national dietary guidelines (e.g. USA 2020–2025 (49), Canada 2018 (50), Netherlands 2015 (51), and Germany 2015 (52)).
Non-tropical vegetable oils are rich in unsaturated fatty acids, and should be used as their dietary source. Particularly, the essential fatty acids, n−6 linoleic acid (LA) and n−3 alpha-linolenic acid (ALA), must be obtained from the diet since the human body is not capable of synthesizing them. Several vegetable oils are good sources of LA, whereas only a few oils are rich in ALA (Table 3). Good sources of ALA are canola/rapeseed, linseed, hempseed, soybean and walnut oils. For example, the recommended daily amount of both n-6 PUFA and n-3 PUFA can be obtained by 2–3 tablespoon of canola/rapeseed oil. In a Nordic context, rapeseed oil may thus be considered as the primary source of added fat due to its nutritional profile as well as being locally produced. However, olive oil may entail additional health benefits beyond fatty acid composition (e.g. polyphenols) (36, 37) and may also be used frequently. Unfortunately, very few studies are available that specifically investigates health effects of rapeseed oil. However, based on individual RCTs, rapeseed oil decreases liver fat content during isocaloric conditions compared to olive oil (53), and a diet rich in canola oil was found to decrease abdominal fat even when compared to diets with higher content of PUFA (blends of corn oil, safflower oil and flaxseed oil) (54). Furthermore, meals rich in rapeseed oil increased 24-h fat oxidation compared to meals rich in palm oil (55), and diets rich in rapeseed oil markedly improve blood lipid profile compared to butter (56, 57). Rapeseed oil has a higher content of phytosterols compared to many other oils (1), perhaps explaining the LDL-cholesterol reducing effect of rapeseed oil compared to both olive oil and sunflower oil demonstrated in a recent meta-analysis (38). Finally, a rapeseed oil-based margarine was used in the Lyon Diet Heart Study, a secondary prevention trial testing an ALA-enriched Mediterranean diet in patients having survived a first acute myocardial infarction (58, 59). A striking protective effect was observed on the risk of recurrence (50–70% reduction) after 4 years of follow-up. Although these positive results cannot be ascribed specifically to rapeseed oil, it further supports the role of rapeseed oil as part of a cardioprotective diet. Vegetable oils are 100% fat and therefore include a high energy content. Although adding healthy plant oils to the diet will improve the overall fat composition of the diet, it will also increase the energy content and density of the diet. Thus, from the perspective of weight management, it is advisable to use healthy plant oils in moderate amounts.
Fat/oil | Portion | Linoleic acid (n-6 PUFA) g/portion | Alpha-linolenic acid (n-3 PUFA) g/portion |
Canola/rapeseed oil | 1 Tbsp. (14 g) | 3.1 | 1.5 |
Olive oil | 1 Tbsp. (14 g) | 1.5 | 0.1 |
Sunflower oil | 1 Tbsp. (14 g) | 8.7 | 0.1 |
Soybean oil | 1 Tbsp. (14 g) | 7.3 | 1.0 |
Linseed oil | 1 Tbsp. (14 g) | 1.8 | 7.5 |
Hempseed oil | 1 Tbsp. (14 g) | 7.4 | 2.6 |
Sesame oil | 1 Tbsp. (14 g) | 5.8 | 0.1 |
Walnut oil | 1 Tbsp. (14 g) | 7.4 | 1.5 |
Palm oil | 1 Tbsp. (14 g) | 1.3 | 0.0 |
Coconut oil | 1 Tbsp. (14 g) | 0.3 | 0.0 |
Butter | 1 Tbsp. (15 g) | 0.2 | 0.1 |
Margarine, 40% | 1 Tbsp. (15 g) | 1.0 | 0.5 |
Margarine, 60% | 1 Tbsp. (15 g) | 1.9 | 0.6 |
Margarine, 70% | 1 Tbsp. (15 g) | 2.4 | 0.9 |
Butter mix, 40% | 1 Tbsp. (15 g) | 0.6 | 0.3 |
Butter mix, 60% | 1 Tbsp. (15 g) | 0.9 | 0.3 |
Butter mix, 75% | 1 Tbsp. (15 g) | 0.8 | 0.4 |
Examples of recommended quantities | |||
Daily minimum intake* with an average expenditure of 2,000 kcal | 5.6 g (2.5 E%) | 1.1 g (0.5 E%) | |
Intake with 2,000 kcal during pregnancy and lactation | 8.9 g (4.0 E%) | 2.2 g (1 E%) | |
1For margarine and butter mixes, an average of LA and ALA is calculated. Values are from Finnish, Swedish, and US national food databases. | |||
*Because minimum requirements of cis-PUFA for adults are not known, the estimates are based on threshold intake data from children. The recommendation for essential fatty acids, that is, LA and ALA, is 3E% of which at least 0.5E% should be ALA. Recommended energy percentages were calculated as kcal of 2,000 kcal. Then, recommended intake of LA and ALA as grams were calculated based on that 1 g fat yields 9 kcal energy. For example, calculation for LA: 2.5% of 2,000 kcal = 50 kcal; thus, 50 kcal / 9 kcal = 5.6 g. |
Processing of oils, such as extraction method, cold-pressing, heating and refining, has no effect on fatty acid composition of oils but they impact on how other bioactive compounds are preserved (2). Refining, however, removes taste, unwanted compounds, and reduces oxidation products that will induce further oxidation if not removed. Further, cooking temperature, light exposure during storage as well as storage temperature and time influence bioactive compounds in oils since they are sensitive to heating and light. Light and heat are also factors that increase oxidation. In general, oils are suitable for frying and cooking (despite their relatively high content of unsaturated fatty acids) (60), but they should not give smoke at high temperatures when cooked. The temperature during normal pan frying is typically 140–175°C, and negative effects of frying vegetable oils high in unsaturated fatty acids are marginal even at 200 °C for extended time periods (60).
Further systematic investigations would be desirable of different consumption levels of vegetable oils in relation to disease outcomes, mortality, blood lipids as well as overweight and obesity among both adults and children. Current evidence indicates that the type/version (e.g. high or low in polyphenols) of oil may affect risk markers which suggests importance of degree of processing and advantageous health effects of bioactive components. Further studies are needed to clarify the effect of these minor components on health. Margarines and butter mixes are commonly used products in the Nordic countries; however, there is scarce evidence about their overall health effects compared to other sources of dietary fat. Margarines may differ a lot regarding both fat content and fatty acid composition (i.e. which oils/fats that have been used), and more specific studies are needed. As the oils/fats that are used in margarine production are typically highly refined, the levels of bioactive compounds (e.g. polyphenols) may potentially be lower in margarines compared to less refined versions of the parent oils/fats. On the other hand, many beneficial components could be added in margarines, for example, antioxidants, vitamin D or plant sterols and stanols. Furthermore, oils/fats used in margarine production are often interesterified (i.e. fatty acids are rearranged within the triglycerides) to achieve desirable physical structure/functionality. Although no negative effects of interesterification have been indicated in short-term human studies, the evidence is scarce and more studies are warranted. For similar reasons (physical structure), margarines typically contain a variable fraction of tropical oils (e.g. palm, coconut) influencing both the fatty acid and sustainability profile. However, vegetable oil-based margarines usually contain less saturated and trans-fat (levels of trans-fat are very low to absent) than butter or butter mixes, and could therefore be considered a healthier choice as the fatty acid composition is likely the primary factor determining the overall health effect. Margarines with a higher fat content (compared to lower) are generally better sources of essential fatty acids (Table 3).
The main limitation is that there were no recent qualified SRs available reporting at a food level perspective, and neither was a de novo NNR2023 SR performed for this topic. Overall, there were few SRs available, and many included SRs had low or critically low confidence, thus the summarized evidence should be interpreted with caution. Furthermore, only few fats/oils (olive oil, butter) have been investigated in relation to disease outcomes in SRs; for example, there was no SR concerning canola/rapeseed oil and disease outcomes. Thus, evidence of olive oil was emphasized in relation to disease outcomes. Furthermore, there were hardly any SRs that included margarines, butter mixes or shortenings. All studies that filled inclusion criteria were done in adults, and therefore evidence of health effects of fat and oils among vulnerable groups, that is, children, adolescents, pregnant and lactating women could not be taken into consideration. There were no SRs available for several diseases, for example, autoimmune diseases, asthma, and allergies. Most of the evidence on disease outcomes are based on observational data, and although statistical adjustment for potential confounders are typically performed, residual confounding likely remains. Data on dietary intake are most often self-reported, and various degrees of misreporting, and thus misclassification, can be expected. Another general limitation that can be discussed is the statistical modelling of the dietary data, where specific substitution models are generally not available, which may hamper the overall interpretation and advice on practical implementation. Evidence was identified in scientific literature only since 2011 and the search was done in one database. Therefore, there might be some relevant older studies which did not meet inclusion criteria. Furthermore, as the search only included SRs and meta-analyses, there may be individual studies of high quality (not included in any SR) that has not been considered.
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