Scientific Opinion on the substantiation of health claims related to peanuts,
peanut oil and peanut butter manufactured exclusively from roasted
peanuts, and maintenance of normal blood LDL-cholesterol concentrations
(ID 1284) pursuant to Article 13(1) of Regulation (EC) No 1924/2006[sup]1[/sup]
EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA)2, 3
European Food Safety Authority (EFSA), Parma, Italy
Słowa kluczowe:
LDL-cholesterol
Peanut
health claims
peanut butter
peanut oil
1. Charakterystyka żywności / składnika
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Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi
The foods that are the subject of the health claim are peanuts, peanut oil and peanut butter.
Peanuts are seeds of the groundnut (Arachis hypogaea L.) belonging to the legume bean family. Peanuts and peanut oil contain about 49 % fat by weight (of which about 14 % are saturated fatty acids (SFAs), 51 % are monounsaturated fatty acids (MUFAs) (mostly oleic acid) and 33 % are polyunsaturated fatty acids (PUFAs) (mostly linoleic acid)), 16 % carbohydrates, 9 % fibre and 25 % protein.
Peanut butter is manufactured from roasted peanuts. Its composition may vary and it may contain added palm oil or partially hydrogenated vegetable oil. For peanut butter manufactured from roasted peanuts only, the fatty acid composition depicted above applies.
The Panel considers that whereas peanut butter, which is not manufactured exclusively from roasted peanuts is not sufficiently characterised in relation to the claimed effect because of its unknown fatty acid composition, the foods, peanuts, peanut oil and peanut butter manufactured exclusively from roasted peanuts, which are the subject of the health claim, are sufficiently characterised in relation to the claimed effect.
2. Znaczenie oświadczenia dla zdrowia człowieka
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Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi
The claimed effect is “helps achieve normal cholesterol levels by reducing blood total and LDL- cholesterol and thereby promoting heart health”. The Panel assumes that the target population is the general population.
Low-density lipoproteins (LDL) carry cholesterol from the liver to peripheral tissues, including the arteries. Elevated LDL-cholesterol, by convention >160 mg/dL (>4.1 mmol/L), may compromise the normal structure and function of the arteries.
The Panel considers that maintenance of normal blood LDL-cholesterol concentrations is a beneficial physiological effect.
3. Naukowe uzasadnienia wpływu na zdrowie człowieka - Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi
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Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi
Most of the references provided reported on the effects of different diets, some of which included peanuts (low vs. high fat diets, low SFAs, high MUFAs, high PUFAs, low/high in carbohydrates) or of foods other than peanuts (e.g. avocado, nuts in general or nuts other than peanuts) on different health outcomes (including blood cholesterol) which do not allow an assessment of the effects of peanut consumption (independently of other dietary manipulations) on blood cholesterol concentrations. Some references were narrative reviews which did not contain any primary data which could be used to substantiate the claim. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
Three intervention studies in humans on the effects of peanut consumption on blood cholesterol concentrations were provided (Alper and Mattes, 2003; Kris-Etherton et al., 1999; O'Byrne et al., 1997). The Panel notes that the study by Alper and Mattes (2003) lacked a control intervention, and considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
Kris-Etherton et al. (1999) compared the effects of an Average American Diet (AAD) with those of four cholesterol-lowering diets on blood lipids in 22 normocholesterolaemic subjects following a randomised, double-blind, five-period cross-over study design: an American Heart Association/National Cholesterol Education Program Step II diet and three MUFA-rich diets (olive oil (OO), peanut oil (PO), and peanuts and peanut butter (PPB)). The AAD, OO, PO and PPB diets were controlled for total fat (about 34 %), but the AAD was higher in SFAs (16 %) than the OO, PO and PPB diets (about 7 %). MUFA content in the AAD (11 %) and the Step II (12 %) diet was lower than in the three MUFA-rich diets (17-21 %). PUFAs were 9-10 % in the peanut diets and 6-7 % in the remaining three diets. Each diet was consumed for 24 days with wash-out periods of 4-11 days in between. All four intervention diets (the Step II and the three MUFA-rich diets) significantly decreased LDL-cholesterol concentrations when compared to the AAD diet, with no significant differences between the diets. The Panel notes that the effects of MUFAs on blood cholesterol concentrations may have been due to the replacement of SFAs. The Panel also notes that the OO, PO and PPB diets, which were controlled for their fatty acid composition, had similar effects on blood cholesterol concentrations.
In the study by O'Byrne et al. (1997), 20 postmenopausal hypercholesterolaemic women who previously consumed “high-fat” diets (34 E%, 11 E% SFA) were placed on a “low-fat” monounsaturated acid-rich diet (26 E%, 14 E% MUFA) for six months. Peanuts were the main source of MUFAs in the MUFA-rich diet, where subjects consumed 35-68 g per day of peanuts. Peanuts replaced about 28 g of lean cooked meat and 3-4 servings of oil or margarine. Sixteen women eating low-fat diets (24 E%) were also followed to monitor variations in serum lipids caused by seasonal variations. A total of 25 women completed the study (12 in the MUFA-rich diet and 13 in the low-fat control diet). Total fat intake was 26 E% in the peanut diet and 17 E% in the low-fat diet. This difference was accounted for by a higher intake of MUFAs in the peanut diet (14 % vs. 6 % of total energy). In women consuming the peanut diet, serum total cholesterol concentrations decreased by 7.4 % and LDL-cholesterol concentrations decreased by 9 % compared to the low-fat group (as calculated by Mukuddem-Petersen et al., 2005). The Panel notes that this study was not randomised, that intervention and control groups were not comparable at baseline with respect to body weight or blood cholesterol concentrations, and that the peanut diet group lost significantly more weight (about 3 kg) than the low-fat diet group during the intervention, which could explain at least in part the differences between groups with respect to changes in blood cholesterol concentrations. The Panel considers that only limited conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
In weighing the evidence, the Panel took into account that the evidence provided did not establish that consumption of peanuts has an effect on blood LDL-cholesterol concentrations beyond what could be
expected from the fatty acid composition of peanuts, that the cholesterol-lowering effect of peanuts could be attributed to the content of MUFAs and PUFAs in peanuts, and that part of the effect is due to the replacement of mixtures of SFAs in the diet by MUFAs and PUFAs, which are the prevalent fatty acids in peanuts.
The Panel concludes that a cause and effect relationship has not been established between the consumption of peanuts, peanut oil and peanut butter manufactured exclusively from roasted peanuts, and maintenance of normal blood LDL-cholesterol concentrations beyond what could be expected from the fatty acid composition of peanuts.
A claim on the replacement of mixtures of SFAs with cis-MUFAs and/or cis-PUFAs in foods or diets and maintenance of normal blood LDL-cholesterol concentrations has been assessed with a favourable outcome (EFSA Panel on Dietetic Products Nutrition and Allergies (NDA), 2011).
A claim on linoleic acid and maintenance of normal blood cholesterol concentrations has also already been assessed with a favourable outcome (EFSA Panel on Dietetic Products Nutrition and Allergies (NDA), 2009).
Wnioski
On the basis of the data presented, the Panel concludes that:
Whereas peanut butter which is not manufactured exclusively from roasted peanuts is not sufficiently characterised in relation to the claimed effect because of its unknown fatty acid composition, the foods, peanuts, peanut oil and peanut butter manufactured exclusively from roasted peanuts, which are the subject of the health claim, are sufficiently characterised in relation to the claimed effect.
The claimed effect is “helps achieve normal cholesterol levels by reducing blood total and LDL-cholesterol and thereby promoting heart health”. The target population is assumed to be the general population. Maintenance of normal blood LDL-cholesterol concentrations is a beneficial physiological effect.
A cause and effect relationship has not been established between the consumption of peanuts, peanut oil and peanut butter manufactured exclusively from roasted peanuts, and maintenance of normal blood LDL-cholesterol concentrations beyond what could be expected from the fatty acid composition of peanuts.
A claim on the replacement of mixtures of SFAs with cis-MUFAs and/or cis-PUFAs in foods or diets and maintenance of normal blood LDL-cholesterol concentrations has already been assessed with a favourable outcome. A claim on linoleic acid and maintenance of normal blood cholesterol concentrations has also already been assessed with a favourable outcome.