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School of Physiology, Nutrition and Consumer Science, North-West University (Potchefstroom Campus), Potchefstroom, South Africa
1To whom correspondence should be addressed. E-mail: vgewo{at}puk.ac.za.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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50–100 g (1.5–3.5 servings) of nuts 
5 times/wk as part of a heart-healthy diet with total fat content (high in mono- and/or polyunsaturated fatty acids) of 35% of energy may significantly decrease total cholesterol and LDL cholesterol in normo- and hyperlipidemic individuals.
KEY WORDS: • lipids • lipoprotein • nuts • triacyglycerol
It is undisputed that dietary habits affect coronary risk factors and hence the risk of a coronary event. In the search for bioactive components in foods that favorably affect cardiovascular disease (CVD)2 risk, nuts have begun to attract attention (1).
Epidemiologic studies have consistently demonstrated an association between nut consumption and coronary heart disease (CHD) morbidity and mortality in different population groups (2). Compared with people who ate nuts < 1 time/wk, those who ate them 1–4 times/wk had a 25% reduced risk of dying from CHD; people who ate nuts 5 times/wk experienced an 50% reduction in risk (3). Nut consumption may not only offer protection against heart disease, but also increase longevity (4). Recently, the benefits of nuts were acknowledged by the U.S. FDA when they approved a qualified health claim that eating nuts (1.5 oz/d, 42.8 g/d) may reduce the risk of CHD (5).
There is substantial evidence that nuts may have favorable effects on CHD through a variety of mechanisms. The most extensively studied mechanism involves the lipid-lowering effects. Nuts are good sources of unsaturated fatty acids [monounsaturated fatty acids (MUFA) and PUFA] (Fig. 1), known for their favorable effects on blood lipids. Furthermore, evidence suggests that components in nuts further reduce total cholesterol (TC) and LDL cholesterol (LDL-C) concentrations beyond the effects predicted by equations based solely on fatty acid profiles (6,7). In particular, the magnitude of the cholesterol-lowering effect was shown to be 25% greater than would be predicted based on the fatty acid profiles of the test diets studied (2). Therefore, the possible mechanisms whereby nuts may improve lipid profiles do not rely exclusively on the beneficial action of unsaturated fatty acids (PUFA and MUFA) but may include the effects of fiber, micronutrients such as vitamin E and C, folic acid, copper, magnesium, plant protein (e.g., arginine), plant sterols, and phenolic components (2).
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Dietary intervention studies with 186 healthy or diseased (216 hypercholesterolemic, 66 hyperlipidemic, 30 type 2 diabetic) or mixed (95) subjects (312 men and 281 women) were included in this systematic review.
Studies
Studies were included if the objective was to investigate the independent effect of nuts on lipid concentrations and the study was conducted among humans. Trials were excluded when these independent effects could not be assessed and studies had incomplete or missing data.
Outcome measures
The main outcome measures were percentage differences between treatment and control groups for blood TC, LDL-C, HDL cholesterol (HDL-C), and triacyglycerols (TG).
Data sources
Dietary intervention trials with the primary objective of determining the effects of nuts on lipid concentrations were identified through Medline (8) (since inception to August 2004) and Web of Science (9) (from 1994 to August 2004) research databases, supplemented by contact with authors of papers and reference lists of relevant publications. Search terms used included MeSH terms (Medline): Nuts [MeSH] AND ("Lipoproteins"[MeSH] OR "Cholesterol"[MeSH]) OR "Triacylglycerol"[MeSH]) and key words (Web of Science): (nuts OR walnut* OR almond* OR pecan* OR macadamia* OR hazelnut* OR peanut* OR pistachio*) AND (cholesterol OR triacylglycerol OR lipoprotein).
Study selection and data extraction
Two reviewers independently assessed studies to determine eligibility, executed data extraction by using a prepiloted standardized form, and determined the quality of all of the identified intervention studies. Differences in data extracted or quality score were adjudicated by a third reviewer and then finalized in discussion among the 3 authors.
Data synthesis
After careful scrutiny of selected studies, they received a rating based upon the methodology as it appeared in the publication. The following criteria for quality assessment of the dietary intervention trials were used (adapted from Verhagen et al.) (10): 1) the study was controlled; 2) randomization was performed; 3) justified sample size (20 participants or <20 with power calculation for TC or LDL-C); 4) good compliance; 5) single-blind study; 6) groups were similar at baseline for the most important prognostic indicators or differences in baseline characteristics were controlled for statistically; and 7) no order of treatment effect (applicable to crossover trials)
The following quality scores were assigned: 1 = if all of the above criteria were present; 2 = if controlled and two criteria were missing; 3 = if not controlled or 3 criteria were missing. Furthermore, the letter a was assigned for controlled feeding trials and b for studies conducted under free-living conditions. In addition, the nut studies that received a 3 rating were not considered when conclusions were drawn. No formal statistical analysis was performed due to large differences in study designs of the dietary intervention trials.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Two macadamia nut studies with higher quality scores are summarized in Table 1. Consumption of this nut diet significantly lowered TC (5%), LDL-C (5%), and TG (9%) concentrations compared with consumption of the average American diet (AAD) (19), but not compared with a low-fat high complex carbohydrate (CHO) (18) or Step I diet (19). The HDL-C concentration was not affected compared with those consuming a Step I diet or a low-fat high complex CHO diet (18,19). Compared with the AAD, consumption of the macadamia nut diet significantly decreased HDL-C concentrations (4%) (19).
In 2 studies of peanut consumption, there was a significant decrease in TC and LDL-C concentrations compared with consumption of a low-fat control diet (7%) (21) and with the AAD (11%) and Step II diet (2%; only for TC) (22), and there was a significant decrease in HDL-C concentrations compared with the low-fat diet (0.3%) (21). In the latter study (21), the modest reduction in HDL-C concentration was due to changes in the cholesterol content of the HDL3 subfraction. The ratio of TC:HDL-C and LDL-C:HDL-C decreased by 0.05–0.11 in the peanut intervention group compared with the low-fat control group (21). The TG concentrations decreased in both studies but this was significant only compared with the AAD (13%) and Step II diet (22%) (22). The lipid profile did not differ when consumption of the peanut diet was compared with the olive oil diet (22).
A feeding trial conducted by Rajaram et al. (24) showed that intakes of 72 g of pecans/d by subjects with normal-to-high cholesterol concentrations decreased serum TC (7%), LDL-C (10%), TG (11%) and increased HDL-C (6%), beyond that seen in the Step I diet (Table 1).
Walnuts are unique compared with other nuts because they contain predominantly (n-6) (linoleic acid) and (n-3) (
- linolenic acid) PUFAs rather than the MUFAs that predominate in most other nuts (Fig. 1) (38). In 4 of 7 studies of walnut consumption (40–84 g/d), there was a significant decrease in TC (4–12%) and LDL-C (6–16%) compared with consumption of Step I (26), Mediterranean (28,33), and Japanese (32) diets. Three studies showed no significant change in the lipid profile of hyperlipidemic subjects who followed a walnut intervention diet (41–78 g/d) compared with low-fat (27), Mediterranean (30), and Step I diets (31). In 1 study of walnut consumption, the HDL-C concentrations decreased significantly compared with consumption of a Step I diet (26). Despite the aforementioned significant decrease in HDL-C (26), the mean ratio of LDL-C:HDL-C was 2.5 ± 0.6 during consumption of the reference diet and decreased to 2.2 ± 0.7 during the walnut diet (P < 0.001). The ratio of TC:HDL-C also decreased from 4.0 ± 1.0 during consumption of the reference diet to 3.7 ± 1.0 during the walnut diet (P < 0.001) (26). In most of the walnut studies HDL-C was not significantly affected, as seen in the other nut studies. In addition, TG was not significantly affected by consumption of the walnut diets compared with their respective control diets.
No conclusions can be drawn from the studies performed using hazel and pistachio nuts because of insufficient reporting of data.
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The length of the dietary intervention periods of the clinical trials in this systematic review was sufficient to achieve stabilization of blood lipids (2–3 wk) (39). The sustainability of the outcomes cannot be evaluated, however, with duration periods of 4–6 wks (40).
Inconsistent trial results could possibly be explained in a number of ways. The lack of significant change in the lipid profile when the almond diet was compared with the olive oil–based diet could be the result of the similarities in fatty acid composition of these 2 diets (13) (Table 2). The possible explanation for the increase in HDL-C in the Jenkins study (14) could be the low-fat (26%) content of the control diet compared with the intervention diet (36%). Consumption of low-fat diets was shown to decrease HDL-C concentrations (22). The absence of an effect in the study of Lovejoy et al. (15) may be linked to the similarities in fatty acid distribution of the almond and control diets (MUFA provided by olive and canola oil) as seen in the study of Spiller et al. (13). Also, it was the only nut study with diabetic subjects (15), which may suggest that other mechanisms came into play. Notably, almond consumption in the 2 aforementioned almond studies did not differ from consumption of the olive oil control diets (13,15). Thus, we speculate that like the nut diets, the olive oil control diets may also have additional cholesterol-lowering effects that may extend beyond their fatty acid composition (e.g., phytosterols and flavonoids).
In the macadamia nut intervention, which was compared with consumption of the AAD, there were significant decreases in the lipid profile (19). This nut diet and the AAD diet had the same percentage of total fat (35% TF); however, the control diet was high in SFA (14 vs. 9%) and low in MUFA (12 vs. 20%) (Table 2). The absence of a beneficial lipid effect when comparing consumption of the macadamia nut diet with the low-fat high complex CHO (18), or Step I diet (19) may be due in part to the high concentration of palmitoleic acid (16:1) (38). A study by Nestel et al. (41) showed that palmitoleic acid behaves like an SFA, not a MUFA in its effect on LDL-C in hypercholesterolemic men. The lack of effect of the nut diet intervention by Colquhoun and researchers (18) may be explained by the large contrast between the very high concentration of TF (42%), SFA (11%), and low concentrations of CHO (39%) compared with the low-fat high complex CHO control diet (21% TF, 9% SFA, and 57% CHO) (Table 2). Curb and collaborators (19) concluded that the interpretation of the decrease in HDL-C may be difficult, and further investigation of HDL-C effects in longer-term macadamia nut studies with close attention to other dietary components is warranted.
It is evident from the 2 peanut intervention studies (21,22) that the TC and LDL-C concentrations of both hyper- and normocholesterolemic subjects were significantly improved except in comparison with an olive oil control diet (22). Epidemiologic and clinical data indicate that the inverse relation between HDL-C and premature atherosclerosis is stronger for HDL2-C than for HDL3-C (42,43), although HDL3-C decreased the concentration of HDL2-C, and apolipoprotein A-1 did not change in O’Byrne’s study. The resultant ratio of LDL-C:HDL-C was lower and the protective role of HDL-C was, therefore, not compromised (21). The significant decrease in TG could be ascribed to consumption of the Step II control diet, which caused a significant increase in TG concentrations (22).
Pecan consumption decreased TC and LDL-C concentrations compared with a Step I diet. The increase in HDL-C and decrease in TG concentrations may be ascribed in part to the decreasing effect of the HDL-C and increasing effect of TG with consumption of the low-fat Step I diet (28 vs. 40% provided by the pecan diet) (Table 2).
It is clear from the walnut interventions that the decreasing effect on TC and LDL-C concentrations extended beyond the cholesterol-decreasing effect that occurs with the consumption of Step I (26), Mediterranean (28,33), and Japanese (32) diets. We speculate that subjects in the study by Sabate and investigators (26) had the greatest improvement because the intervention had the largest dosage of walnuts (i.e., 84 g/d). In 2 walnut intervention trials (64–78 g/d) compared with consumption of low-fat (27) and Step I diets (31), the lipid profiles were not affected, possibly because of the large difference in the percentage of fat between the nut diet (38 and 45% respectively) and the control diets (30 and 33%, respectively). Also, it is evident from all of the walnut studies that the significantly favorable change in the lipid profile did not occur when the total percentage of fat in the diet was >37% (27,31). Nevertheless, the beneficial results in TC and LDL-C concentrations were evident when consumption ranged from 40 to 84 g walnuts/d. In the study by Munoz et al. (30), consumption of the walnut diet compared with the Mediterranean diet did not affect the lipid profile, probably as a result of the small sample size (n = 10). Generally, most of the walnut diets did not affect HDL-C concentrations compared with the aforementioned control diets (27,28,30–33). In a study by Sabate and investigators (26), there was a significant decrease in HDL-C, even though the TC:HDL-C and LDL-C:HDL-C ratios were favorable. The decrease in HDL-C may be ascribed to the high PUFA (17 vs. 10%), low SFA (6 vs. 9%) and MUFA (7 vs. 9%) content of the walnut diet compared with the control diet. SFA and MUFA increase HDL-C, whereas high intakes of PUFA (>10%) decrease HDL-C (44).
The inclusion of nuts altered the fatty acid composition of the diet (45), which may in turn favorably affect lipid concentrations. Similar to what has been done by other authors (1), we compared the actual observed changes with the predicted changes in LDL-C and TC concentrations (Fig. 2) based on differences in the dietary fatty acid composition in the individual nut and control diets; we used the predictive equation of Mensink and Katan (
TC = 1.51%energy from SFA/d –0.12%energy from MUFA/d –0.60%energy from PUFA) (6). There were significantly greater reductions in LDL-C and TC concentrations of 0.11 and 0.12 mmol/L, respectively, with the nut diets combined compared with the predicted changes.
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7 g/100 g of dietary fiber, of which 25% is soluble fiber (46). Brown et al. (46) conducted a meta-analysis of 67 controlled trials to quantify the cholesterol-lowering effect of major dietary fibers. They concluded that 2–10 g/d of soluble fiber was associated with small but significant decreases in TC. Rimm and Stampfer (47) suggested that plasma -tocopherol concentrations 27.5 µmol/L may be necessary to reduce cardiovascular risk by a dietary intake of 15–30 mg of vitamin E. Arginine, the second most abundant amino acid found in nut proteins, may account for the hypocholesterolemic effect observed in animal studies (48). In addition, this effect was seen in human intervention trials when the dosage of arginine in the diet appeared to be very high (6–21 g/d of arginine) (49). Nuts are also sources of phytosterols (38) and other phytochemical compounds such as polyphenols and ellagic acid, with possible serum cholesterol–modulating effects (50–54). In particular, studies showed that 2 g of plant sterols/d significantly reduces cholesterol absorption, which in turn decreases plasma TC and LDL-C concentrations (50,52). It is apparent that fiber, vitamin E, arginine, phytosterols, and phenolic components from realistic amounts of nuts are not sufficient to exert individual hypocholesterolemic effects (55). In essence, it is possible that there are multiple small effects that contribute, and these are mediated by more than the lipid-lowering fatty acid composition. Some of the limitations of this review include the fact that the independent effects of the type of nut diets and the type of control diets may mask some potential effects or accentuate others. There were also differences in the study populations whose lipid profile may be altered due to underlying disease, poorly designed studies (sample size, control, duration, size of intervention), publication bias, and insufficient reporting of results.
This systematic review highlights the evidence from well-designed nut intervention studies. As alluded to previously, most of these nut intervention diets are in fact heart healthy diets. In this regard, consumption of moderate-fat diets (35% of energy) containing 50–100 g/d of nuts, especially almonds, peanuts, pecan nuts, or walnuts, significantly lowered TC (2–16%) and LDL-C (2–19%) concentrations to a greater degree than observed for consumption of lower-fat, cholesterol-lowering diets without nuts or changes in dietary fatty acid profiles. At this stage, the evidence for macadamia nuts is less convincing. On the basis of the results of these nut intervention studies, it is appropriate to recommend that normo- and hyperlipidemic individuals consume a variety of nuts (50–100 g) at least 5 times/wk. Therefore, future food-based dietary strategies for improving plasma lipid concentrations should consider the lipid-lowering effect of nuts.
Future research should use quality feeding studies with larger sample sizes and longer duration to investigate the effects of nuts on HDL-C and TG concentrations. In particular, this should apply to mixed nuts and those individual nuts not yet considered. The unique nutrient and nonnutrient composition of nuts requires further research to elucidate the possible mechanisms responsible for the LDL-C–lowering effect.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Manuscript received 15 March 2005. Initial review completed 15 April 2005. Revision accepted 8 June 2005.
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LITERATURE CITED |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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