Nuts are rich sources of bioactive nutrients with potential to deliver metabolic and cardiovascular health benefits [1
]. Despite peanuts being a legume they share similar nutritional properties to other nuts. Peanuts are an excellent source of protein (approximately 25% of energy) and dietary fibre providing 5%–10% of daily fibre requirements in one serving (30 g), with potential satiety benefits for weight control [2
]. Other bioactive nutrients in peanuts such as vitamin E and polyphenols may benefit glucose regulation [3
] and inflammation [4
]. High oleic peanuts are also rich in phytosterols and monounsaturated fat, (providing up to 80% of the fatty acid composition) [6
] and they have demonstrated lipid lowering effects [7
]. In addition, high oleic peanuts oxidise less readily than regular, higher polyunsaturated peanut varieties (~28% polyunsaturated and 50% monounsaturated fatty acids) hence, have a longer shelf life and are the predominant type of peanut grown in Australia [6
Evidence suggests that both tree nut and peanut consumption is associated with lower body weight [8
]. Several large, cohort studies (the Adventist Health Study, the Iowa Womens’ Health Study and the Physicians Health Study) have shown significant inverse associations between the frequency of nut consumption and body mass index (BMI) [9
] Frequent nut consumption was also associated with reduced risk of weight gain in the SUN (Seguimiento University of Navarra) cohort after 6 years [12
]. In the Nurses’ Health Study II, participants who consumed nuts frequently (two or more times per week) had a 31% reduced risk of weight gain, or a 33% lower risk of obesity [13
] than those who rarely or never consumed nuts.
Similarly, evidence from intervention studies indicates that incorporating nuts into the diet has little impact on body mass and body fat [14
]. A systematic search of 23 clinical trials investigating the effect of chronic nut consumption (averaging ~15%–20% of energy requirements) on body mass demonstrated a small non-significant weighted mean decrease in body weight of 0.47 kg, BMI of 0.40 kg/m2
, and waist circumference of 1.25 cm [14
]; two of these studies assessed peanut intake [15
]. However, in most of the studies, nuts were used in iso-energetic diets so weight changes were not expected.
Several mechanisms outlined below have been proposed for the lack of weight gain observed with nut consumption, despite their high energy and fat content. These include reduced energy intake subsequent to increased satiety [2
], energy lost through faecal fat loss and a possible increase in energy expenditure [8
Nut consumption has also been associated with a reduced risk of type 2 diabetes; evidence to support this comes from large epidemiological studies [18
]. The Nurses’ Health Study demonstrated that consumption of nuts (~ 5 times per week), peanut butter (~5 times per week) or walnuts (~twice per week) was associated with a 24%, 21% and 15% lower risk respectively of developing type 2 diabetes compared with those who never or rarely ate nuts; the effect was greatest in those of healthy body weight [18
]. In addition, the Shanghai Women’s Health Study demonstrated that walnut consumption was associated with a 21% decreased risk of type 2 diabetes [20
]. Nut consumption has also improved glycaemic control and insulin sensitivity [21
]. A literature review [23
] revealed 14% weighted mean reductions in fasting insulin/glucose regulation and 34% reduction in homeostatic model assessment (HOMA) scores with nut consumption. However, the effects of nuts on insulin sensitivity are influenced strongly by changes in body weight; this may have accounted for the changes observed in one of the studies where subjects reduced body weight with nut consumption.
Clinical and epidemiological evidence also indicate that nut consumption can enable improvements in inflammatory markers, with daily doses of 30 g able to confer benefits [24
]. Mediterranean diets in which walnuts [26
], mixed nuts [27
] or pistachios [22
] replaced olive oil have demonstrated improvements in one or more of the inflammatory markers C-
reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and interleukin-6 (IL-6). Weighted mean reductions in ICAM-1 (9%), VCAM-1 (6%) and CRP (12%) were found from analysis of 27 intervention studies with nuts in a literature review [23
]. Studies which showed no benefits may have used an insufficient intake of nuts or intervention period.
Clinical trials have clearly shown that intakes of several varieties of nuts can lower total and low density lipoprotein (LDL) cholesterol by 9%–16%, even in the context of healthy diets [28
]. A pooled analysis of influences of nut consumption on blood lipids revealed the cholesterol lowering effects are greatest in individuals with higher baseline LDL levels or lower BMI [31
]. This pooled analysis estimated that a mean daily consumption of 67 g of nuts reduced LDL by 7%, triglycerides by 5% and reduced LDL:high density lipoprotein (HDL) by 8% [32
]. Nut consumption was also found to lower triglyceride levels, primarily in individuals with hypertriglyceridemia. Similarly, a walnut meta-analysis [32
] found that walnut-enriched diets significantly decreased total and LDL cholesterol by 5% and 7% respectively with a 5% reduction in triglycerides and no effect on HDL. These lipid lowering effects of nuts appear to be greatest when their intake is substituted for saturated fat in the diet rather than being added to the diet [31
The cholesterol lowering, anti-inflammatory and glucose regulating benefits of nuts have been attributed to their high content of unsaturated fat, possible weight reduction effect and bioactive compounds, including plant sterols, dietary fibre and antioxidants [30
]. Whilst previous studies have investigated the effect of peanut intake on body weight [15
], few have measured cardio-metabolic outcomes of peanuts and no research has previously been conducted with Australian high oleic peanuts.
This study aimed to investigate the effect of adding high oleic peanuts to habitual diets of healthy overweight adults on cardio-metabolic measures (glucose, insulin, CRP and lipids), body composition and anthropometric measures and to determine if there are any relationships between these outcomes.
This is the first study to investigate the effect of Australian high oleic peanut consumption on cardio-metabolic measures, body composition, body mass or waist circumference. In addition, no previous peanut studies have measured inflammatory markers and no intervention studies have measured their effect on glucose regulation. The food diaries revealed ~50–70 g daily intake of peanuts, consumed by both men and women (6 days per week). The expected increase in energy intake from this amount of peanuts was 1400 kJ per day (assuming no other changes were made to the diet). The actual increase in energy intake was ~850 kJ (60% of the expected value) indicating that some of the peanuts were substituted for other foods in the diet. Additional monounsaturated fat consumed during the peanut phase accounted for ~90% of the additional energy consumed. The predicted weight gain for this increase in energy reported was 0.9 kg over 6 weeks and 1.9 kg over 12 weeks (calculated as 1 g body fat mass increase predicted for every additional 37 kJ consumed). The actual average weight gain over the whole period was only 0.5 kg (26% of expected), and no changes in waist circumference or body composition measures were observed. However, it is acknowledged that this predicted weight gain calculation does not take into account the dynamic nature of weight loss hence, may be overestimated.
Energy expenditure from physical activity remained the same for both phases so this did not contribute to the findings. Calculations revealed ~−1.1 g difference in body mass per unit (kJ) of total daily energy intake with peanut consumption compared with the control phase. The body mass per kJ would be expected to be the same for each phase, i.e.
, as energy changed body weight would expect to change proportionally. This was not observed; for every kJ consumed during the peanut there was less body weight change compared with the control phase. Similarly, eight weeks consumption of 89 g/day of peanuts compared with a nut free diet for 8 weeks by healthy subjects with no dietary compensation demonstrated a weight gain of only 1 kg which was 28% of the predicted 3.6 kg [40
]. A possible reason for less than predicted weight gain with additional energy intake was incomplete fat absorption from the peanuts. Fat contained within walled cellular structures of nuts has been found to be incompletely digested in the gut [41
] which is possibly compounded by incomplete mastication [42
In addition the body fat storage may have been limited as a result of the unsaturated fatty acids being oxidized. Unsaturated fats and have a greater thermogenic effect [43
] and are more readily oxidised [44
] than saturated fatty acids making them less readily stored in the adipose tissue. Further, peanut consumption for 8 weeks has elicited a small (5%) but significant increment in resting energy expenditure in obese individuals [40
]. A recent study with high-oleic peanuts has also revealed a greater increase in diet induced thermogenesis compared with conventional peanuts [45
] with MUFA intake suggested to contribute to the difference. Other studies have demonstrated an increase in diet induced thermogenesis and fat oxidation with MUFA possibly due to a higher stimulation of the sympathetic nervous system by MUFA than other fatty acids [46
Interestingly, in this study MUFA intake was inversely associated with body fat mass. It has been suggested that fat quality may have a stronger correlation with weight gain than fat quantity [47
]. Studies suggest a role for preferential oxidation and metabolism of dietary MUFA, which influences body composition hence ameliorating the risk of obesity [48
]. It is possible that a combination of these mechanisms contributed to inefficient energy utilisation or an increase in energy expenditure from thermic effect of consuming peanuts, demonstrating no body composition changes and a less than predicted increase in body weight. This study demonstrates that, despite a smaller than predicted increase in body weight, large doses of peanuts should not be added to the diet but should be substituted for other foods. In a previous study we observed a 10% reduction in energy intake over 4 days when high oleic peanuts were substituted for another snack food (potato crisps), indicating that peanuts have the potential to be included in a weight management diet when substituted for other snack foods [2
Surprisingly, lipid levels were not altered with high oleic peanut consumption, contrary to many other nut studies [31
]. However, the cholesterol lowering effects of nuts are shown to be greatest in individuals with higher baseline LDL and lower BMI [31
]. Obese individuals have demonstrated an attenuated cholesterol-lowering response to dietary manipulation of fatty acids compared with lean individuals [50
]. The subjects in this study were overweight or obese with an average BMI of 30.6 kg/m2
and had on average healthy baseline blood lipid levels. Nut consumption has also been found to lower triglyceride levels predominantly in individuals with hypertriglyceridemia [32
]. Similarly, Mukuddem-Peterson et al.
] also reported no changes in blood lipid levels in individuals with obesity with either walnut or cashew consumption. In addition, the lipid lowering effects of nuts are greatest when they are substituted for saturated fat in the diet [31
]; in the current study there were no differences in saturated fat intake.
This study demonstrated no differences in glucose or insulin levels with consumption of high oleic peanuts. Similarly several other studies have not shown benefits with consumption of pistachios, almonds and walnuts on fasting glucose or insulin [51
]. Some short-term intervention studies have shown benefits of nut consumption on glucose homeostasis [22
] and insulin secretion [21
]. However, when adjustments were made for weight reduction in one of these studies no changes in insulin sensitivity were found [62
The effects of nuts on insulin sensitivity are influenced strongly by changes in body weight which may have accounted for the changes observed in one of these studies. As there were no changes in body composition in this current study, improvements in glucose regulation were less likely. Improvements in glucose regulation have also been demonstrated when nuts are included as part of an intervention diet such as the Nordiet [21
] or a Mediterranean diet [26
], with benefits partly attributable to other components of these diets. In the current study an increase in MUFA correlated with a decrease in insulin. A recent review [48
] has outlined studies determining the effect of MUFA on insulin resistance, demonstrating improved insulin sensitivity and glucose regulation following MUFA-rich diets in both healthy [64
] and diabetic individuals [67
]. However, these benefits are more likely to be observed in subjects of lower body weight [52
Consumption of high oleic peanuts in the chronic study did not affect the inflammatory marker C
-reactive protein (CRP) when compared with the nut free diet. Similarly, 12 weeks of hazelnut consumption (60 g) resulted in minimal effect on inflammatory markers and cell adhesion molecules in this group of healthy, normocholesterolemic overweight and obese individuals [71
]. In addition, in a recently published review [23
], we identified that 50% of nut studies demonstrated no significant differences in inflammatory markers. One of the suggested reasons for this was recruitment of healthy individuals who may only demonstrate limited improvements. Subjects in this study were healthy with a mean baseline CRP of 1.5 mg/L, well below the cut off of 3.0 mg/L for of cardiovascular disease risk [71
]. In addition, central adiposity is associated with increased CRP levels and it is possible that those with a central adiposity may not demonstrate improvements in inflammatory markers without weight loss [72
]. Both male and female subjects in this study displayed central adiposity. Two other nut studies also demonstrated no change but did observe reductions in other inflammatory markers, IL-6 and VCAM-1 with large doses (65–100 g) of pistachios and walnuts respectively [22
]. It is possible in the study that other inflammatory markers were improved with high oleic peanut consumption.
A minimum nut dose of 30 g may be required to elicit benefits for inflammatory markers [23
]. The current study used a relatively large dose of nuts (~50–70 g), so this was not likely to be a limiting factor. A more likely reason is the population studied; subjects had CRP levels within the normal range for a healthy population at baseline. Despite no observed improvements in cardio-metabolic outcomes, epidemiological studies suggest that prolonged peanut consumption in this population may help to maintain cardio-metabolic health over time [1
A strength of this study was the randomised, controlled cross-over design which assessed the effects of high oleic peanuts in the same individuals, hence reducing between subject variability. Another strength was high compliance with the consumption of peanuts and with the nut free diet, as assessed by food diary entries and returned peanut packages. The study also controlled for physical activity levels, with subjects requested to maintain similar physical activity levels throughout the study.
One of the limitations of the study was the inability to double-blind the intervention; however, data collection and data entry was blinded to minimise investigator bias. Another limitation was the high dose (actual intake of 50–70 g for both males and females) of peanuts used as proof of concept. A dose of 42 g/day recommended by The American Heart Association for reduction of cardiovascular disease (CVD) may still provide some cardio-metabolic benefits; however, this needs to be confirmed with further investigation. This study did not include a washout period; however, the control phase was a habitual (nut free) diet for 12 weeks, allowing sufficient time for reversal of any effects of peanut consumption [74
]. Another limitation was only one blood sample was taken at each intervention period which would not have detected intra-individual variation of lipids.
Due to budget constraints, it was not possible to measure fat excretion and energy expenditure directly, which may have provided information on a possible mechanism for the observed weight maintenance and body fat despite an increase in energy intake. Future studies should consider these outcomes.