International Journal of Obesity (2006) 30, 704–710 & 2006 Nature Publishing Group All rights reserved 0307-0565/06 $30.00 www.nature.com/ijo
ORIGINAL ARTICLE Effects of peanut oil consumption on appetite and food choice SS Iyer1, LA Boateng2, RL Sales3, SB Coelho3, P Lokko2, JBR Monteiro3, NMB Costa3 and RD Mattes1 1 Department of Foods and Nutrition, Purdue University, West Lafayette, IN, USA; 2Food Research Institute, M.20 Accra, Ghana and 3Federal University of Vic- osa, MG, Brazil
Objective: Peanut consumption may improve lipid profiles without promoting weight gain. Both properties have been attributed to their high-unsaturated fat content. Mono and polyunsaturated fatty acids reportedly hold stronger satiety value than saturated fats and may help appetite control. This study investigated the effects of chronic peanut oil consumption on appetite and food choice. Research methods and procedures: A total of 129 healthy adults from three countries (Brazil, Ghana and US) were randomly assigned to one of four treatment arms: consumption of peanut oil, olive oil or safflower oil as 30% of individual resting energy expenditure (REE) for 8 weeks or no dietary intervention. Participants received no other dietary guidance. They completed appetite questionnaires eliciting information about hunger, fullness, desire to eat, and prospective consumption during all waking hours for 1 day at weeks 2 and 6 and for 1 or 3 days at weeks 0, 4 and 8. Diet records were completed at weeks 0, 4 and 8. Results: No differences in appetitive ratings were observed over the 8-week trial. There were no significant treatment by time interactions. Total caloric intake was significantly higher at week 8 relative to baseline (F ¼ 10.08, Po0.05). The increases for each treatment were: peanut oil ¼ 1977114; olive oil ¼ 2377121; safflower oil ¼ 274790; control ¼ 75771. Free-feeding intake, an index of dietary compensation, was reduced significantly at weeks 4 and 8 compared to baseline (F ¼ 9.08, Po0.00). The declines (compensation scores) were (kcals): peanut oil ¼ 2087105 (46%); olive oil ¼ 2357105 (50%); safflower oil ¼ 1867102 (44%). There were no significant differences across countries in appetite ratings. Discussion: A prior intervention with whole peanuts reported a dietary compensation score of 66% over 8 weeks, this compares to a 46% compensation score observed with peanut oil. Our data suggests that the lipid fraction in peanuts elicits a weak effect on satiety. International Journal of Obesity (2006) 30, 704–710. doi:10.1038/sj.ijo.0803180; published online 29 November 2005 Keywords: satiety; appetite; energy intake; peanut oil; free-feeding intake; dietary compensation
Introduction Data from multiple epidemiological studies including the Adventist Health Study,1 Nurses Health Study,2 Iowa Women’s Health Study3 and the Physicians Health Study4 reveal an inverse relationship between the frequency of nut consumption and cardiovascular disease risk. With a cohort of 26 473 subjects, the Adventist Health Study was the first to report a statistically significant inverse relation between frequency of nut consumption and body mass index (BMI). In the Nurses Health Study, women who rarely consumed nuts
Correspondence: Professor RD Mattes, Department of Foods and Nutrition, Purdue University, 212 Stone Hall, West Lafayette, IN 47907-1264, USA. E-mail:
[email protected] Received 27 May 2005; revised 29 August 2005; accepted 10 September 2005; published online 29 November 2005
had a BMI of 24.8 kg/m2 compared to 23.4 kg/m2 for women consuming nuts more than five times per week. Intervention trials5–9 provide additional support for an inverse relationship between nut consumption and both lipid profiles and BMI. In 2003, the Food and Drug Administration approved a qualified health claim for nuts stating that ‘Scientific evidence suggests, but does not prove that eating 1.5 ounces of most nuts per day as part of a diet low in saturated fat and cholesterol may reduce the risk of heart disease’. Peanuts are among the nine nuts identified in the health claim. Food disappearance data from 1990 to 1997 indicate that peanuts – as peanut butter, confections and whole peanuts account for 68% of total nut consumption, making them the most widely consumed nut in the United States.10 As a result of its high-energy density, fat has been implicated in the positive energy balance leading to overweight and obesity globally. Nuts are a rich source of fat,
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705 consequently, their role in a healthful diet has been questioned. However, for multiple reasons, severe restriction of fat may not be advisable. For example, inclusion of highfat foods, including peanuts, on an energy restricted diet results in improved compliance, weight loss and increased vegetable consumption.11 While inclusion of nuts in an energy-controlled diet reportedly does not compromise weight loss, the influence of nut consumption on body weight in free-living, nondieting individuals is less well studied. In a recent intervention,8 participants were provided 500 (7136) kcals of whole peanuts with no dietary guidance for 8 weeks. Nonsignificant changes in body weight were observed due, in part, to dietary compensation for 66% of the energy from the peanuts. Peanuts are rich in protein (26% by weight) and dietary fiber (8.5%) and these components hold satiety effects that may moderate intake.8 The largest energy component of peanuts is their lipid fraction (49%) which is predominantly (40%) unsaturated fat. Evidence both from human and animal studies suggest that mono and polyunsaturated fatty acids are more readily oxidized than saturated fats and may be more satiating.12,13 Among unsaturated oils, MUFA are oxidized in preference to PUFA and may have stronger satiety effects. Therefore, a hypothesized candidate for the strong satiety effect of peanuts is its fatty acid content. However, there has been only limited study on the satiety effects of oils with varying composition or oils of similar fatty acid composition but different origin (e.g., peanut versus safflower oils which are predominantly MUFA and PUFA, respectively or peanut and olive oil, both rich sources of MUFA). Peanut oil is widely consumed in the US and holds greater nutritional significance in selected developing countries. Thus, its contribution to energy balance and total diet quality requires clarification. Further, contrasting effects of peanut consumption cross-culturally provides an opportunity to differentiate environmental versus physiological effects of oil consumption. This study investigated the effect of chronic peanut oil consumption on appetite and food choice in three countries – Ghana, Brazil, and the US.
Methods Subjects A total of 129 healthy adults (63 male and 66 female), age 2474 years (mean7s.d.) were recruited from three countries Brazil, Ghana, and the US (Table 1). Subjects were of normal weight and body composition (mean BMI 2272.5, body fat (%) 13.476.9). There were no significant differences of BMI across countries. Body weight was stable (change of o2.26 kg within the last 6 months). They were not taking medications known to influence study variables. All subjects were nonsmokers with no peanut allergy. They controlled the
Table 1
Baseline characteristics of participants
Age (years) Height (m) Weight (kg) BMI (kg/m2) Body fat (kg) Lean body mass (kg) Waist circumference (cm) Hip circumference (cm) Waist to hip ratio BMR (kcal)
25.0575.58 1.6870.09 62.67710.93 22.0972.58 13.4776.9 48.9070.87 75.5177.48 95.7778.62 0.7970.01 1551.407219.96
Values are mean7s.d. n ¼ 129.
purchase of at least half of their ingested food and obtained 30% or more of their energy from dietary fat. Additionally, participants evaluated experimental shakes containing the test oils during screening. Shakes were evaluated on a 13 point hedonic scale, with one being least palatable and 13 being most palatable. A score of 7 or above was required for eligibility. Only participants that rated four or more of the eight shakes as satisfactory were recruited. All study procedures were approved by appropriate Human Research Committees in each country.
Experimental design The study was an 8 week, parallel-group, intervention where participants received no dietary guidance except that they were required to consume a shake daily. The intervention was preceded by a 1 week baseline period. There were four treatment groups (1) Peanut oil; n ¼ 32; (2) Olive oil; n ¼ 32; (3) Safflower oil; n ¼ 33; and (4) No-oil control group; n ¼ 32. Treatments were randomized across participants within each country. The olive oil and safflower oil treatments provided comparable oleic and linoleic acid content to peanut oil; 45 and 32% (by weight) respectively. The amount of energy from oil in the load was approximately 30% of each individual’s resting energy expenditure. Resting energy expenditure was measured at baseline. Active treatment participants received a mean of 5277.2 g/day as peanut, olive or safflower oil for 8 weeks. Participants reported to the lab everyday for 8 weeks between 0900 and 1800 for consumption of the experimental shake. They were allowed to take shakes with them over the weekend or on occasions when they could not report to the laboratory. Shake palatability was monitored over the study to ensure only acceptable flavors were provided.
Intervention load The treatment oils were blended with skim milk and fruit or a flavoring. The food items used in the study were as follows: Equal (Manteno IL, US) Pineapple (Dole Packaged Food Cooperation, West Lake Village, CA) Chocolate (Nestle, International Journal of Obesity
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706 Solon, OH), Orange Juice (Minute Maid Company, Houston, TX), Chocolate Milk (Great Value, Bentonville, AR) Coffee (General Foods, Rye Brook, NY), Vanilla Essence (Great Value, Bentonville, AR), Peanut Oil (Hollywood, Melville, NY), Safflower Oil (Hollywood, Uniondale, NY), Olive Oil (Filippo Berio, Hackensack, NJ). A mixture of flour, skim milk and sugarcane or sweetener – mix flour; was blended in the shakes to mask the flavor of the oil. The mix flour was developed at The Federal University of Vic- osa, MG, Brazil. The energy content of the intervention load without treatment oils was 152735 kcal per 240 ml load. The macronutrient composition was: 30711 g carbohydrate; 872 g protein; 172 g fat. Inclusive of the treatment oils, the shakes provided a mean of 620 kcals per day.
Participants were asked to refrain from strenuous activity, alcohol and caffeine 24 h prior to assessment days. After a 12 h fast, participants arrived in the laboratory and rested for at least 10 min on a hospital bed. REE measurements were performed in the supine position for approximately 30– 45 min. Readings for the last 20–30 min were averaged as an estimate of REE. After the REE measurement, participants consumed an experimental shake. The load that received the highest palatability rating during screening was administered during both test sessions. Following consumption of the experimental shake, TEF was measured at 15 min intervals for 5 h. Participants were required to stay awake and refrain from unnecessary bodily movements throughout the measurement period.
Dietary assessment Dietary intake was assessed by diet records completed by participants at weeks 0, 4, and 8. Participants were trained to record every food item consumed, including water, along with portion sizes. For food mixtures, participants listed each ingredient separately. A model diet record was provided to serve as a guide for recording intake. Records were completed on three nonconsecutive days (2 weekdays and 1 weekend day). The diet records were analyzed by country-specific databases.
Appetitive ratings Hunger ratings were recorded on a 9-point categorical scale with 1 ¼ not at all hungry and 9 ¼ extremely hungry. Desire to eat, fullness, and thirst were rated on comparable scales. Appetite logs were completed every hour from the time participants awoke until sleep. Appetite logs were completed on three days along with the diet records at weeks 0, 4, and 8. One set of appetite logs was completed on weeks 2 and 6.
Anthropometric measurements Anthropometric measurements were taken at weeks 0, 4, and 8. Body height was measured with participants in a standing position. Body weight was measured in a fasting state with participants in light street clothes or gown. Bioelectrical impedance was used to measure body composition (Tanita Corporation of America Inc. Arlington Heights, IL; BIA model 310 used in Brazil).Waist circumference was measured by placing a nonstretch measuring tape around the abdomen, just above the hip bone. Hip circumference was measured around the largest portion of the hips. Blood pressure was measured with a random-zero sphygmomanometer. Heart rate was determined by palpating the radial artery. All measurements were taken by a single researcher at each test site.
Energy expenditure assessment Resting energy expenditure (REE) and the thermogenic effect of feeding (TEF) were measured at baseline and week-8 by indirect calorimetry using a metabolic cart and a ventilated respiratory canopy (Sensor medics, VMax 29, Sensor medics Corporation, Yorba Linda, CA; Datex, Finland used in Brazil). Analyzers were calibrated with room air and standard calibration gas mixtures (74% CO2, 16% O2, balance N2 and 0% CO2, 26% O2, balance N2), energy expenditure was calculated based on the Weir equation (RMR kcal/day ¼ 3.94 (VO2)71.106 (V CO2) 1440).14 International Journal of Obesity
Statistics Treatment effects were tested by repeated measures analysis of variance (ANOVA). Reliability of subjective questionnaires was tested using Cronbach’s alpha. Statistical analyses were performed with the SPSS software package, release 11.5 (SPSS Inc. Chicago, IL). Dietary Compensation across the intervention was calculated using the following equation.15 Percent Dietary Compensation ¼
ðIntake without loadÞ ðIntake with loadÞ 100 Energy content of load
Results Mean daily hunger, fullness and desire to eat ratings at weeks 0, 2, 4, 6, and 8 are shown in Figure 1. Hunger and desire to eat ratings did not differ significantly at any time point over the intervention and no significant differences were detected between treatment groups. Mean ratings of fullness were significantly higher at week 6 (5.170.13) and week 8 (5.070.13) compared to week 2 (4.770.12) (F ¼ 3.480, Po0.008). There was no treatment effect on ratings of fullness. Appetitive ratings did not differ between the countries or by gender. Mean daily energy intake (kilocalories), at weeks 0, 4, and 8 is shown in Figure 2a. Intake at weeks 4 and 8 was significantly greater than intake at baseline (F ¼ 10.5, Po0.01). There was no significant treatment effect or a treatment by time interaction. Fat intake at week 4 and week
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TIME POINTS ACROSS INTERVENTION Figure 1 (a–c) Mean7s.e. hunger (a), fullness (b) and desire to eat (c) ratings at different time points across intervention (n ¼ 129).
8 was significantly higher than intake at baseline in all treatments except control (F ¼ 39.19, Po0.01) (Figure 2b). Protein and carbohydrate intake did not differ significantly across the intervention. Discretionary energy intake, at weeks 0, 4, and 8 is shown in Figure 3a. Energy intake at week 4 and week 8 was significantly lower than intake at baseline in all treatments except control (F ¼ 4.07, Po0.001). Discretionary energy intake with the peanut oil treatment decreased from 19867108 kcal at baseline to 17727113 kcal at week 4 and 17777126 kcal at week 8. This represented a compensation of 47 and 46% at weeks 4 and 8, respectively. Energy intake with the olive oil treatment decreased from 22047108 kcal at baseline to 18377112 kcal at week 4 and 19687126 kcal
at week 8. The corresponding compensation scores were 74 and 50%. Energy intake in the safflower oil treatment decreased from 18927104 kcal at baseline to 14987109 kcal at week 4 and 17067122 kcal at week 8. This represented a compensation for 87 and 44% of the safflower energy load at weeks 4 and 8, respectively. Participants in all three treatment groups significantly reduced habitual fat intake (Figure 3b) at weeks 4 and 8 by an average of 2373 and 2572 g, respectively compared to baseline (F ¼ 44.8; Po0.001). Fat intake declined from 7375 g at baseline to 5076 g at week 4 and to 4976 g at week 8 in the peanut oil treatment group. Fat intake in the olive oil treatment group decreased from 8375 g at baseline to 5176 g at week 4 and to 5876 g at week 8. Fat intake decreased from 7175 g at baseline to 5076 g at week 4 and to 3276 g at week 8 in the safflower oil group. Fat intake of participants in the control group increased from 6475 g at baseline to 6876 g at week 4 and 7076 g at week 8. There was a significant change in dietary fatty acid composition (Figure 4) in the three treatment groups across the intervention (Po0.01). MUFA and PUFA intakes were significantly higher in the intervention groups (Po0.001) compared to the control group. Participants in the olive oil International Journal of Obesity
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group had significantly higher intake of MUFA than the other three groups (Po0.01). MUFA intake in the peanut oil group was significantly higher than in the safflower (Po0.003) and control groups (Po0.001) and was significantly lower than in the olive oil group (Po0.003). Safflower oil consumption led to a significantly higher PUFA intake than the other interventions (Po0.001). PUFA intake was significantly higher in the peanut (Po0.00) and safflower oil (Po0.17) intervention groups compared to the control group. There were no significant differences between the three intervention groups with respect to SFA intake.
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Figure 3 (a, b) Mean Discretionary energy intake7s.e. (a) and Mean Discretionary fat intake7s.e. (b) at three time points across the intervention (n ¼ 129).Values a and b (Po0.01) are significantly different.
Accumulating evidence demonstrates that whole peanuts hold strong satiety properties and have limited impact on body weight. In a 6-month intervention trial,5 25 hypercholesterolemic, post-menopausal women incorporated high-oleic cultivar peanuts into a low total fat, highmonounsaturated fat (LFMR) diet (27% energy from fat; 14% from MUFA). A cohort following a self-selected low fat diet (LF) served as controls. The LFMR diet group received prepackaged daily rations of dry roasted peanuts individualized to their energy requirements. Although both diets were designed to maintain weight, the LFMR group lost approximately 2.1 kg, as a consequence of decreasing discretionary energy intake, while the LF group maintained their weight. In another study, incorporation of peanuts into the habitual diets of free-living subjects for 8 weeks led to markedly lower
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Figure 4 Change in fatty acid composition across the intervention (n ¼ 129).
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709 than predicted weight gain.8 This was attributed to a combination of high-satiety value and inefficient use of energy from peanuts. In another arm of the same study, addition of peanuts to the customary diet prompted comments about the high-satiety value of the nuts. Finally, evidence indicates a diet, moderate in fat that includes nuts and olive oil improves compliance to a weight loss/weight control regimen.11 The components of peanuts accounting for their highsatiety value have not been identified. One candidate is its fatty acid profile. It has been argued that dietary fat elicits a weak satiety response compared to protein and carbohydrate.16–18 However, fatty acid chain length and saturation are hypothesized to influence appetite through their differential rates of oxidation.19 Fatty acid oxidation rates follow a hierarchy where MUFA4PUFA4SFA.12,13 Several acute feeding studies and one long term study have investigated the effect of saturation on indices of appetite in humans. A gastric infusion trial noted no effect of fatty acid on appetite, but a significant reduction of food intake with a linoleic acid infusion compared to oleic acid, stearic acid, or saline infusions.20 A second trial manipulated fatty acid type in a lunch meal and monitored energy intake and appetite through the rest of the day. Subjects consumed significantly more energy after consuming the lunch meal containing oleic acid blend than after the lunches containing linoleic and stearic-oleic acid blends respectively. However, in a replication of the study, the effects of these fatty acids on intake were not significantly different.21 Participants consumed significantly more energy in the first trial when provided the oleic acid, but no differences of intake were noted in the replication trial. A third trial22 compared the effects of muffin preloads rich in peanut oil or canola oil (both high in MUFA) with muffins rich in butter (rich in SFA). No differential satiety effects of the fat sources were observed. A trial documenting the longer-term effect (2-weeks) of eating diets containing fatty acids of varying saturation on appetite and energy intake reported higher satiety scores on an oleic acid diet (62.5719.2 mm) compared to a linoleic acid diet (46.1724.7). Energy intake did not differ between treatments.23 Thus, while evidence that fatty acids are not oxidized equally is strong; their differential effects on satiety and energy intake are not substantiated in humans. In line with existing literature, data from our study do not support a differential effect of diets containing peanut, olive or safflower oil on appetitive indices. We observed no change in hunger, desire to eat, or fullness across the intervention. These findings may be due to a true lack of effect of the tested fats or to insensitivity of the appetite assessment methods. The observed dietary compensation scores suggest that the tested fats do elicit behavioral responses. Compensation scores at week 4 were 47, 74 and 87% for peanut, olive and safflower oil treatments respectively. The corresponding values at week 8 were 46, 50, and 43%. The basis of the initially stronger compensation for the olive and safflower
oil treatments is not clear, there were no differences in reported appetitive sensations. This level of compensation is lower than previously reported with whole peanuts and tree nuts.8 This suggests that while the fat content contributes to compensation, other factors are also involved. The non-fat fraction of peanuts may potentiate their satiety inducing effects. Strong data indicate protein, due to its high metabolic cost, enhances satiety.24 By delaying gastrointestinal clearance and/or bulking, fiber enhances satiety.25 Magnesium, potassium, phosphorous and zinc are suggested thermogenic agents that could contribute satiety cues.26 Whole peanuts are rich in protein, fiber and the abovementioned micronutrients. Peanut oil is not a source of these components so may lack the satiety value of whole peanuts. In addition, it has been documented that humans compensate more readily for a solid challenge over a liquid one.15 Therefore, rheology becomes an important variable when comparing whole peanuts to peanut oil. Incorporating whole peanuts and peanut oil into meals controlled for rheology and macronutrient composition will provide a more realistic comparison of the role of peanut oil on appetite. The treatment oils were administered as a percentage of individual REE, thus posing a comparable challenge to each participant and giving equal opportunity for dietary compensation. Experimental data and dietary information from free-living humans, document that people can consume up to 150 g of fat in a single meal.27 The dietary fat challenge in the present intervention ranged from 30 to 80 g. Therefore, it may not be considered extreme. Participants across all treatment groups significantly decreased (albeit, not precisely) habitual energy intake. This is consistent with a physiological sensitivity to the fat ingestion, but not to fatty acid source or saturation.20–23 A greater reduction of self-selected fat intake was noted with the safflower oil treatment. We can only speculate on an explanation. Safflower oil is a rich source of PUFA while the peanut and olive oils have higher MUFA content. The effect of fat composition on taste perception and fat specific satiety is not well characterized in humans.28 Sensitivity to linoleic acid is associated with lower preference for fat in rats.29 Whether this is altered through dietary experience is not known, but there is suggestive evidence in humans.30 One trial in humans noted that sensitivity to linoleic acid, but not oleic acid, is associated with lower self-selected fat intake when assessed in a single meal, but not over a day.23 No affect was observed on energy intake. There is evidence that linoleic acid induces a greater CCK release compared to oleic acid,31 but this would be expected to reduce total energy intake rather than fat alone. Finally, the Food and Drug Administration has approved a qualified health claim for nuts suggesting consumption of up to 1.5 ounces per day may be healthful and the Dietary Approaches to Stop Hypertension eating plan recommends the inclusion of 4–5 servings/week of nuts, seeds and dry beans.32 The present findings do not challenge these International Journal of Obesity
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710 recommendations. Both refer to whole nuts where other constituents, such as fiber and protein, contribute to reductions of cardiovascular disk risk and appetite moderation.33 In addition, the current challenge of 620 kcal/day as peanut oil markedly exceeds the energy level of the recommended portions. Given other evidence of beneficial health effects of unsaturated oils, determination of the compensatory dietary response to regular consumption of smaller amounts of nut, peanut, oil warrants further evaluation.
References 1 Fraser GE, Sabate J, Beeson WL, Strahan TM. A possible protective effect of nut consumption on risk of coronary heart disease. The Adventist Health Study. Arch Intern Med 1992; 152: 1416–1424. 2 Hu FB, Stampfer MJ, Manson JE, Rimm EB, Colditz GA, Rosner BA et al. Frequent nut consumption and risk of coronary heart disease in women: prospective cohort study. BMJ 1998; 317: 1341–1345. 3 Ellsworth JL, Kushi LH, Folsom AR. Frequent nut intake and risk of death from coronary heart disease and all causes in postmenopausal women: the Iowa Women’s Health Study. Nutr Metab Cardiovasc Dis 2001; 11: 372–377. 4 Albert CM, Gaziano JM, Willett WC, Manson JE. Nut consumption and decreased risk of sudden cardiac death in the Physicians Health Study. Arch Intern Med 2002; 162: 1382–1387. 5 O’Byrne DJ, Knauft AD, Shireman R. Low fat-monounsaturated rich diets containing High-Oleic Peanuts improve serum lipoprotein profiles. Lipids 1997; 32: 687–695. 6 Rajaraman S, Burke K, Connell B, Myint T, Sabate J. A monounsaturated fatty acid–rich pecan enriched diet favorably alters the serum lipid profile of healthy men and women. J Nutr 2001; 131: 2275–2279. 7 Fraser GE, Bennett HW, Jaceldo KB, Sabate J. Effect on body weight of a free 76 Kilojoule (320 calorie) daily supplement of almonds for six months. J Am Coll Nutr 2002; 21: 275–283. 8 Alper CM, Mattes RD. Effects of chronic peanut consumption on energy balance and hedonics. Int J Obes Relat Metab Disord 2002; 26: 1129–1137. 9 Alper CM, Mattes RD. Peanut consumption improves indices of cardiovascular disease risk in healthy adults. J Am Coll Nutr 2003; 22: 133–141. 10 USDA. Center for nutrition policy and promotion. The role of nuts in a healthy diet. Insight 2000; 23: 1–2. 11 McManus K, Antinoro L, Sacks F. A randomized controlled trial of a moderate-fat, low-energy diet compared with a low fat, lowenergy diet for weight loss in overweight adults. Int J Obes Relat Metab Disord 2001; 25: 1503–1511. 12 Piers LS, Walker KZ, Stoney RM, Soares MJ, O’Dea K. The influence of the type of dietary fat on postprandial fat oxidation rates: monounsaturated (olive oil) vs saturated fat (cream). Int J Obes Relat Metab Disord 2002; 26: 814–821.
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13 Jones JH, Schoeller DA. Polyunsaturated: saturated ratio of diet fat influences energy substrate utilization in the human. Metabolism 1988; 37: 145–151. 14 Weir JB. New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol Lond 1949; 109: 1–9. 15 DiMeglio DP, Mattes RD. Liquid versus solid carbohydrate: effects on food intake and body weight. Int J Obes Relat Metab Disord 2000; 24: 794–800. 16 Rolls BJ. Carbohydrates, fats and satiety. Am J Clin Nutr 1995; 61: 960S–967S. 17 Stubbs RJ, van Wyk MC, Johnstone AM, Harbron CG. Breakfasts high in protein, fat or carbohydrate: effect on within-day appetite and energy balance. Eur J Clin Nutr 1996; 50: 409–417. 18 Stubbs RJ. Peripheral Signals affecting food intake. Nutr 1999; 15: 614–625. 19 Friedman MI, Tordoff MG, Ramirez I. Integrated metabolic control of food intake. Brain Res Bull 1986; 17: 855–859. 20 French S, Mutuma S, Francis J, Read N, Meijer G. The effect of fatty acid composition on intestinal satiety in man. Int J Obes 1998; 22: 82S. 21 Lawton CL, Delargy H J, Brockman J, Smith FC, Blundell JE. The degree of saturation of fatty acids influences post-ingestive satiety. Br J Nutr 2000; 83: 473–482. 22 Alfenas RC, Mattes RD. Effect of fat sources on satiety. Obes Res 2003; 11: 183–187. 23 Kamphuis MM, Westerterp-Plantenga MS, Saris WH. Fat specific satiety in humans for fat high in linoleic acid vs fat high in oleic acid. Eur J Clin Nutr 2001; 55: 499–508. 24 Robinson SM, Jaccard C, Persaud C, Jackson AA, Jequier E, Schutz Y. Protein turnover and thermogenesis in response to high protein and high carbohydrate feeding in men. Am J Clin Nutr 1990; 52: 72–80. 25 Burton-Freeman B. Dietary fiber and energy regulation. J Nutr 2000; 130: 272S–275S. 26 Astrup A, Toburo S, Christensen NJ, Quaade F. Pharmacology of thermogenic drugs. Am J Clin Nutr 1992; 55: 246S–248S. 27 Blundell JE, Macdiarmid JI. Passive Over consumption, Fat intake and short-term energy balance. Ann of NY Acad Sci 1997; 827: 392–405. 28 Mattes RD. Fat taste and lipid metabolism in humans. Physiol & Behav (in press). 29 Gilbertson TA, Liu L, York DA, Bray GA. Dietary fat preferences are inversely correlated with peripheral gustatory fatty acid sensitivity. Ann NY Acad Sci 1998; 30: 165–168. 30 Kamphuis MMJW, Saris WHM, Westerterp-Plantenga MS. The effect of addition of linoleic acid on food intake regulation in linoleic acid tasters and linoleic acid non-tasters. Br J Nutr 2003; 90: 199–206. 31 Beardshall K, Frost G, Morarji Y, Domin J, Bloom SR, Calam J. Saturation of fat and cholecystokinin release: implications for pancreatic carcinogenesis. Lancet 1989; 2: 1008–1010. 32 Sacks FM, Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP et al. A dietary approach to prevent hypertension: a review of the Dietary Approaches to Stop Hypertension (DASH) Study. Clin Cardiol 1999; 22: III6–III10. 33 Kris-Etherton PM, Yu-Poth S, Sabate J, Ratcliffe HE, Zhao G, Etherton TD. Nuts and their bioactive constituents: effects on serum lipids and other factors that affect disease risk. Am J Clin Nutr 1999; 70: 504S–511S.
