ID 1131 - Migdały

PL: Migdały
EN: Almonds
Pdf: almonds

Oświadczenie (2)

1. Charakterystyka żywności / składnika

The food that is the subject of the health claims is almonds. The Panel assumes that the claim refers to sweet almonds.
Almonds (Prunus amygdalus Batsch) contain about 40-50 % fat, of which 22 % are polyunsaturated fatty acids (PUFAs, mostly linoleic acid), 70 % are monounsaturated fatty acids (MUFAs, mostly oleic acid), and 8 % are saturated fatty acids (SFAs). The amount of fibre is about 9-12 %, 98 % of which is insoluble. In addition, almonds contain small amounts (0.1-0.2 g/100 g) of beta-sitosterol (Maguire et al., 2004; Spiller et al., 1992).
The Panel considers that the food, almonds, which is the subject of the health claims, is sufficiently characterised in relation to the claimed effects.

2.1. Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi (ID 1131)

The claimed effect is “maintains healthy blood total and LDL cholesterol and 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.

3.1. Utrzymanie prawidłowego stężenia cholesterolu LDL we krwi (ID 1131)

The references provided for the scientific substantiation of this claim included guidelines from a scientific body, human intervention studies on food/food constituents other than almonds (e.g. nuts, peanuts, fatty acids, oils) or almonds in combination with other foods/food constituents and/or effects other than blood cholesterol concentrations (e.g. coronary heart disease, blood pressure, weight loss, diabetes). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
One systematic review (Mukuddem-Petersen et al., 2005) and one meta-analysis (Fulgoni et al., 2002) of human intervention studies which assessed the effects of almond consumption on blood lipids were provided. However, the meta-analysis was provided as an abstract in conference proceedings only, and the limited information available did not allow the Panel to perform a full evaluation. The systematic review by Mukuddem-Petersen et al. (2005) included five (Abbey et al., 1994; Jenkins et al., 2002; Lovejoy et al., 2002; Sabate et al., 2003; Spiller et al., 1992) of the seven intervention studies selected by Fulgoni et al. (2002) and one additional study (Spiller et al., 1998) but provided no combined statistical analysis because of the large differences observed between the individual study designs. The study by Hyson et al. (2002), which had been provided separately in the consolidated list, was included only in the meta-analysis by Fulgoni et al. (2002).
Two of the intervention studies were either single arm (run-in taken as comparison, Spiller et al., 1992) or used 3-week sequential intervention periods in which all subjects received the interventions (e.g. peanuts, almonds, walnuts) in the same order with no wash-out period in between (Abbey et al., 1994). The Panel notes that these studies did not allow controlling for a time effect. An intervention study which assessed the effect of raw almonds vs. roasted almonds vs. roasted almond butter on blood lipids (no control group for non-almond interventions) was also provided (Spiller et al., 2003). In addition, one intervention study investigated the effects of a diet high in monounsaturated fatty acids (including 84 g/day of almonds) vs. a diet high in carbohydrates (Wien et al., 2003). The Panel notes that both diets were not comparable for macronutrient (e.g. total fat, carbohydrates) intake. The Panel considers that no conclusions can be drawn from these studies for the scientific substantiation of the claimed effect.
A total of six randomised, controlled intervention studies on the effect of almonds on blood lipids were presented (Jambazian et al., 2005; Jenkins et al., 2002; Lovejoy et al., 2002; Sabate et al., 2003; Spiller et al., 1998; Tamizifar et al., 2005). Five used a cross-over design and one used a parallel design (Spiller et al., 1998). Three of the studies tested the effects of two almond doses which ranged from 25 to 100 g/day. The number of subjects tested per intervention was between 13 and 30. The duration of the intervention was four weeks in all studies. One study used an olive oil-based diet and a cheese and butter-based diet as control (Spiller et al., 1998), one used muffins as control (Jenkins et al., 2002), one used a high-fat and a low-fat diet as controls (Lovejoy et al., 2002), two used an American Heart Association/National Cholesterol Education Program Step I diet with 30 E% from fat (Sabate et al., 2003; Tamizifar et al., 2005), and in one the control diet was not specified (Jambazian et al., 2005). Most of the studies observed a significant decrease in LDL-cholesterol concentrations with the almond diet compared to the control diet, with the exception of the studies by Lovejoy et al. (2002) and Spiller et al. (1998) in which the almond diet was compared to an olive oil diet. The studies by Jenkins et al. (2002) and Sabate et al. (2003) showed an effect on LDL-cholesterol
concentrations for the highest almond doses (50-100 g/day and about 54 g/day, respectively), but not for the lowest almond doses tested (25-50 g/day and about 27 g/day, respectively).
A more recent meta-analysis of randomised controlled trials (RCTs) (Phung et al., 2009), which investigated the effects of almonds on the blood lipid profile and which included three of the studies considered above (Lovejoy et al., 2002; Sabate et al., 2003; Tamizifar et al., 2005) plus two more recently published RCTs (Jenkins et al., 2008; Jia et al., 2006), tested the effect of different almond doses, ranging from 37 to 168 g/day, over four week interventions. In the randomised cross-over study by Jenkins et al. (2008) muffins were used as a control, and in a parallel design RCT by Jia et al., (2006) the control group did not receive any almonds. In a total of 142 participants no significant effects of almond consumption (between 25 and 168 g/day) on LDL- or HDL-cholesterol concentrations, or the LDL-to-HDL cholesterol ratio were found.
Hyson et al. (2002), using a randomised, cross-over design, compared the effects of whole almonds vs. almond oil in amounts corresponding to one half of daily total fat intake (14 E%) on blood lipids in 22 healthy women and men. Whole almonds and almond oil similarly reduced serum total cholesterol (by -4 %) and LDL cholesterol (by -6 %) compared to a typical American background diet. This study indicated that the effect of almonds on blood cholesterol can be explained by their fatty acid composition, as whole almonds did not have a significant effect on LDL-cholesterol concentrations beyond what was observed for almond oil.
The studies described showed that almonds consumed in amounts of more than 50 g/day and contributing up to 50 % of the total daily fat intake, significantly decreased total and LDL-cholesterol concentrations. At lower intakes, the effects were variable and mostly non-significant. The observed effects of almonds on blood cholesterol can be explained by the fatty acid composition of almonds and possibly by dietary modifications associated with high almond intakes. It is also apparent from the studies provided that the effect of almond consumption on blood cholesterol is influenced by the fatty acid composition of the background and control diets used in the studies, 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 almonds.
In weighing the evidence, the Panel took into account that the evidence provided did not establish that consumption of almonds had an effect on blood LDL-cholesterol concentrations beyond what could be expected from the fatty acid composition of almonds, and that the cholesterol-lowering effect of almonds could be attributed to their content in MUFAs and PUFAs.
The Panel concludes that a cause and effect relationship has not been established between the consumption of almonds and maintenance of normal blood LDL-cholesterol concentrations beyond what could be expected from the fatty acid composition of almonds.
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 (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).

Warunki i możliwe ograniczenia stosowania oświadczenia

28g raw or roasted almonds with skin per day