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Mealtime glycemic load is associated with risk for chronic disease. This study examined whether complementary foods (vinegar and peanut products) could lower postprandial glycemia without altering mealtime glycemic load. Eleven healthy subjects consumed two test meals (bagel and juice, glycemic load=81; or chicken and rice, glycemic load=48) under three conditions (control, vinegar, or peanut) using a randomized, crossover design. Vinegar or peanut ingestion reduced the 60-minute glucose response to both test meals by approximately 55%, but these reductions were significant only for the high-glycemic load meal. After consumption of the high-glycemic load meal, energy consumption for the remainder of the day was weakly affected by the vinegar and peanut treatments, a reduction of approximately 200 to 275 kcal (P=.111). Regression analyses indicated that 60-minute glucose response to the test meals explained 11% to 16% of the variation in later energy consumption. In conclusion, the addition of vinegar or peanut products to a high-glycemic load meal significantly reduced postprandial glycemia.

Objectives. We sought to determine prevalence rates of vitamin C deficiency and depletion in the United States. Methods. We used data from the Third National Health and Nutrition Examination Survey to assess intake of dietary, supplemental, and serum vitamin C. Results. Mean intakes and serum levels of vitamin C were normal; however, vitamin C deficiency and depletion were common (occurring among 5%–17% and 13%–23% of respondents, respectively). Smokers, those who did not use supplements, and non-Hispanic Black males had elevated risks of vitamin C deficiency, while Mexican Americans had lower risks. Conclusions. Health professionals should recommend consumption of vegetables and fruits rich in vitamin C and should recommend supplementation for individuals at risk of vitamin C deficiency.

Although popular and effective for weight loss, low-carbohydrate, high-protein, high-fat (Atkins) diets have been associated with adverse changes in blood and renal biomarkers. High-protein diets low in fat may represent an equally appealing diet plan but promote a more healthful weight loss. Healthy adults (n = 20) were randomly assigned to 1 of 2 low-fat (

We examined the effects of prenatal and postnatal nutrition on birthweight and insulin sensitivity, indicated by the glucose/insulin (G/I) ratio, in adult rats (F1 generation) and in their adult offspring (F2 generation). Rat pups (F1) whose dams consumed low-protein diets during gestation (malnourished) consumed either nutritionally adequate (control) or high-fat diets ad libitum post-weaning. The offspring of these rats (F2) were maintained on the same diets as their respective dams. Separate pups (F1) whose dams consumed high-fat diets during gestation (over-nourished) were maintained on high-fat diets post-weaning, as were their offspring (F2). Birthweights were significantly reduced in all fetally malnourished F1 animals. At approximately 70 d of age, fasting insulin sensitivity in over-nourished F1 rats was significantly reduced compared to controls regardless of whether they were malnourished or over-nourished in utero; however, fetally malnourished F1 rats consuming control diets post-natally had significantly greater fasting insulin sensitivity than control animals. At 30 and 120 min post-glucose load, insulin sensitivity was reduced 12-65% in both groups of over-nourished F1 rats as compared to the fetally malnourished F1 rats consuming the control diet. Birthweights were significantly lower in F2 animals whose dams (F1) were fetally malnourished and weaned to high fat diets. Insulin sensitivity was significantly reduced in all F2 animals versus control animals, regardless of dietary treatment. Thus, post-natal diets alter insulin sensitivity in fetally malnourished, adult rats; and maternal malnutrition during gestation results in insulin resistance in offspring, irrespective of offsprings' birthweight or diet.

Type 2 diabetes has reached epidemic proportions in many Native American communities in North America. The overwhelming majority of physicians, biomedical researchers, and medical ecologists continue to explain the astoundingly high prevalence rates of diabetes among Native Americans and other high prevalence populations in terms of yet-to-be-identified genetic factors. Recent experimental and epidemiological research, however, has brought to light an etiological alternative to the genetic-predisposition model. This body of research suggests that type 2 diabetes may result initially from fetal malnutrition and, in subsequent generations, be propagated via perturbations in the intrauterine environment. Native American populations at greatest risk for diabetes today are the ones most likely to have endured severe nutritional stress in their recent histories, thus experiencing the conditions that are most conducive to the diabetic developmental sequence. If further substantiated, the implications of the fetal-origin model of diabetes for diabetes intervention programs are profound.

The association between early exposure to cow's milk products in infancy and risk for insulin dependent diabetes mellitus (IDDM) is controversial. We examined whether the ingestion of cow's milk-based infant formula altered the expression of the diabetic syndrome in the BB/Wor rat, an animal model of IDDM. Pregnant BB/Wor dams were obtained from the NIH contract colony at the University of Massachusetts and housed under semi-barrier conditions. Rat pups were intubated with 1 to 2 ml of commercially available cow's milk-based infant formula (Enfamil or Nutramigen) or sham intubated (controls) daily from day 12 to day 25 of life. Pups were weaned at day 25 and monitored for glucosuria daily through 120 days of life. All rats including dams consumed a milk-free rat chow and acidified water ad libitum throughout the study. The mean age of disease onset was 4 to 10 days earlier in Nutramigen-fed and Enfamil-fed rats relative to controls (84+/-3, 78+/-2 and 88+/-4 days, respectively); the mean age of disease onset was significantly different between controls and Enfamil-fed animals (p

When guinea pigs are fed tissue-saturating amounts of ascorbate, C1q concentrations are significantly higher than in those animals fed only enough ascorbate for adequate growth and for the prevention of scurvy. C1q is the recognition protein of the classical complement pathway, a system of blood proteins that constitutes an important part of host defense against pathogens. The observed effect of ascorbate nutriture on C1q concentrations is consistent with the known role of ascorbic acid in hydroxyproline biosynthesis. C1q is a hydroxyproline-containing protein with structural similarities to collagen.

In the guinea pig, ascorbate administration elevated plasma C1q values 30 to 50% over control values. To determine the effects of vitamin supplementation on C1q in man, healthy men and women ( n = 14) consumed placebo capsules for 4 weeks and ascorbate supplements, 1500 mg/d, for 4 weeks, in a double-blind, cross-over fashion. Subjects ate self-selected diets but were instructed to avoid vitamin C-rich foods during the 8-week experimental period. Fasting blood samples, collected at the start of the study and at the end of weeks 4 and 8, were analyzed for ascorbate and C1q, measured directly by immunodiffusion against anti-human C1q. Compared to placebo values, plasma ascorbate rose 92% following the 4-week supplementation period, and plasma C1q rose 18%. The rise in C1q following ascorbate administration was not significant ( P = 0.12). Furthermore, plasma ascorbate was not correlated with C1q ( r = 0.21, P = 0.14). Hence, in healthy men and women, ascorbate supplementation, at levels 25 times that which is recommended, did not significantly alter plasma Clq levels.

The biosynthesis of carnitine requires vitamin C as a cofactor for two separate hydroxylation steps. The majority of body carnitine (approximately 98%) is located in muscle and less than 0.5% is present in plasma. We examined the physiologic dynamics of plasma free carnitine and muscle total acid-soluble carnitine in vitamin C-depleted guinea pigs repleted with increasing amounts of vitamin C. Animals were fed a vitamin C-deficient diet for 3 weeks at which time symptoms of scurvy were evident. Animals were repleted with increasing doses of vitamin C, from 0.5 to 10.0 mg vitamin C/100 g body weight daily. Muscle total acid-soluble carnitine concentrations tended to correlate directly with plasma vitamin C (r = 0.41, P = 0.087) during the repletion phase of the study. Conversely, plasma free carnitine was inversely related to liver vitamin C (r = -0.54, P = 0.020) and to muscle total acid-soluble carnitine (r = -0.56, P = 0.015). Mean plasma free carnitine values fell 30% over the course of vitamin C repletion (P > 0.05) and mean muscle total acid-soluble carnitine rose by 30% (P > 0.05). These data suggest that elevated plasma free carnitine may indicate a low to marginal vitamin C status.

Dietary reference intakes (DRIs) for vitamin C for healthy U.S. populations are currently being formulated by the Panel on Dietary Antioxidants and Related Compounds of the Food and Nutrition Board of the Institute of Medicine. A major task of the Panel is to analyze the evidence of adverse effects of high-dose vitamin C intakes to derive, if appropriate, a Tolerable Upper Intake Level (UL) for vitamin C. The present report details current and past research examining potential adverse effects of supplemental vitamin C. The available data indicate that very high intakes of vitamin C (2–4 g/day) are well tolerated biologically in healthy mammalian systems. Currently, strong scientific evidence to define and defend a UL for vitamin C is not available.

In a recent issue of Osteoporosis International, Carter et al. reported that subjects adhering to a ketogenic, lowcarbohydrate/high-protein (LCHP) diet for weight loss did not display increased bone turnover markers after 3 months compared to control subjects consuming a typical, unrestricted diet [1]. In this trial, weight loss averaged 6.4 kg versus 1.1 kg in the dieters and controls respectively (p=0.0008), whereas the mean urinary N-telopeptide increased by 1.6 versus 1.9 nmol BCE/mmol creatinine in the dieters and controls, respectively (p=0.86). Although this trial supports the view that high-protein diets do not adversely affect bone [2, 3], the dietary level of alkalizing minerals was not considered. High-protein diets generate excessive amounts of acid due to the obligatory catabolism of sulfur amino acids, and bone may respond by releasing basic salts into the circulation [4]. Hence, if high-protein intakes are not accompanied by an adequate intake of alkalizing minerals, which have a neutralizing effect in vivo, bone health may be adversely affected [4–6]. Here we discuss unpublished data regarding acid/base metabolism from our recent trial comparing ketogenic and nonketogenic LCHP diets [7]. In this trial, 19 adults (body mass index: 34.4T1.0 kg/m) were randomly assigned to a ketogenic LCHP diet (k-LCHP; 60% of energy as fat; 5% energy as carbohydrate) or to a nonketogenic LCHP diet (n-LCHP; 30% of energy as fat; 40% of energy as carbohydrate). The n-LCHP diet was composed mainly of low-fat dairy products, fruits and vegetables, and low-fat meats, whereas the k-LCHP diet consisted primarily of high-fat meats and some vegetables. The diets were similar in protein content (~20 g/mJ), but daily intakes of potassium (1,935 versus 3,535 mg) and calcium (715 versus 1,110 mg) were markedly different for the k-LCHP versus n-LCHP diets. Blood and urine samples were collected at baseline and at week 2. Weight loss, blood ketone concentrations and anion gap values, and urinary calcium concentrations at baseline and week 2 are shown in Table 1. The blood anion gap, the interval between the sum of blood cations and blood anions, is a direct indication of the acidity of blood. For comparison, Table 1 also displays values for urine calcium calculated from predictive equations based on the dietary protein:potassium ratio [8, 9]. These data indicate that n-LCHP diets are associated with lower acid loads and lower rates of calcium excretion as compared to k-LCHP diets. Moreover, anion gap values and urinary calcium were highly correlated (r=0.542, p=0.016). Since the predicted calciuria was similar to actual values, it would appear that potassium-rich foods favorably influence acid/base metabolism and reduce calciuria. Alexy et al. [10] have presented longitudinal evidence that inadequate intakes of alkalizing minerals from fruits and vegetables may adversely impact bone health. Also, based on data from Lewis et al. [11], the calcium-rich Osteoporos Int (2006) 17:1820–1821 DOI 10.1007/s00198-006-0214-y

The purpose of this study was to determine whether carnitine metabolism or histamine degradation would be useful parameters for investigating the optimal requirement for vitamin C.Twenty-two non-scorbutic subjects with subnormal vitamin C status (plasma vitamin C28 mumol/L) were placed on a metabolic diet low in vitamin C for 3 weeks and repleted with graded doses of vitamin C: 10, 30 and 60 mg vitamin C daily (group 1) or 10,125 and 250 mg vitamin C daily (group 2) for weeks 1, 2 and 3, respectively. Fasting blood samples were collected weekly and analyzed for plasma vitamin C, plasma free carnitine and blood histamine.Group 1 subjects remained in a subnormal vitamin C state throughout the 3-week study, and blood histamine and plasma free carnitine were not impacted by the experimental treatment. Plasma vitamin C in group 2 subjects rose significantly during the study, and these subjects finished the study with an ample vitamin C status indicative of vitamin C intakes above the recommended dietary allowance. Both blood histamine and plasma free carnitine were inversely related to vitamin C status in group 2 subjects.These data indicate that blood histamine and plasma free carnitine are altered in individuals with subnormal, non-scorbutic vitamin C status and provide evidence that metabolic changes independent of collagen metabolism occur prior to the manifestation of scurvy. Thus utilizing scurvy as an end-point to determine vitamin C requirements may not provide adequate vitamin C to promote optimal health and well-being.

Histamine is a critical messenger molecule in times of stress, promoting alertness, blood flow, and healing (Kahlson et al., 1960; Schayer, 1962; White and Rumbold, 1988). Excess histamine, however, has a negative impact on circulatory and immunologic homeostasis (Schayer, 1962; Falus and Meretey, 1992) and aggravates inflammatory conditions of the gut (Rangachari, 1992) and respiratory tract (Doyle et al., 1994). Thus, antihistamine therapy is used for systematic treatment of certain diseases, including acid-peptic disorders (Feldman and Burton, 1990b), allergy (howarth, 1983; Schata et al., 1991; Naclerio, 1993), and inflammatory skin disorders (Giacosa et al.,1978).

The number of Americans with type 2 diabetes is expected to increase by 50% in the next 25 years; hence, the prevention of type 2 diabetes is an important objective. Recent large-scale trials (the Diabetes Prevention Program and STOP-NIDDM) have demonstrated that therapeutic agents used to improve insulin sensitivity in diabetes, metformin and acarbose, may also delay or prevent the onset of type 2 diabetes in high-risk populations. Interestingly, an early report showed that vinegar attenuated the glucose and insulin responses to a sucrose or starch load (1). In the present report, we …

We examined the effect of supplemental ascorbic acid on red blood cell glutathione. Subjects consumed self-selected vitamin C-restricted diets, and, under double-blind conditions, ingested placebo daily for week 1 (baseline), 500 mg L-ascorbate/d for weeks 2-3, 2000 mg L-ascorbate/d for weeks 4-5, and placebo daily for week 6 (withdraw). Mean red blood cell glutathione rose nearly 50% (P < 0.05) after the 500-mg period compared with baseline, and the changes from baseline for individual subjects ranged from +8% to +84%. However, the increases in plasma vitamin C and red blood cell glutathione were not correlated (r = 0.22). At the 2000-mg dosage, mean red blood cell glutathione was not significantly different from the value obtained at the 500-mg dosage. After the placebo-controlled withdraw period, red blood cell glutathione did not differ from baseline. These data indicate that vitamin C supplementation (500 mg/d) maintains reduced glutathione concentrations in blood and improves the overall antioxidant protection capacity of blood.

Background/Aims The offspring and grandoffspring of female rats fed low protein diets during pregnancy and lactation, but fed nutritionally adequate diets thereafter, have been shown to exhibit altered insulin sensitivity in adulthood. The current study investigates the insulin sensitivity of the offspring and grandoffspring of female rats fed low protein diets during pregnancy, and then maintained on energy-restricted diets post weaning over three generations. Methods Female Sprague Dawley rats (F0) were mated with control males and protein malnourished during pregnancy/lactation. F1 offspring were then weaned to adequate but energy-restricted diets into adulthood. F1 dams were fed energy-restricted diets throughout pregnancy/lactation. F2 offspring were also fed energy-restricted diets post weaning. F2 pregnant dams were maintained as described above. Their F3 offspring were split into two groups; one was maintained on the energy-restricted diet, the other was maintained on an adequate diet consumed ad libitum post weaning. Results F2 animals fed energy-restricted diets were insulin resistant (p < 0.05), while the insulin sensitivity of their F3 offspring equaled and surpassed that of controls on both the energy-restricted and adequate ad libitum postweaning diets (p < 0.05). Conclusion Maternal energy-restriction did not consistently program reduced insulin sensitivity in offspring over three consecutive generations. The reasons for this remain unclear. It is possible that the intergenerational transmission of developmentally programmed insulin resistance is determined in part by the relative insulin sensitivity of the mother during pregnancy/lactation.

Since hyperinsulinemia tracks from childhood to adulthood and is associated with diabetes risk, identifying modifiable conditions during gestation that may impact insulin metabolism in offspring is important. We conducted a pilot study to investigate associations between maternal weight gain and infant insulin concentrations in an underserved population at high risk for diabetes. Mexican or Native American women with an infant

Background Isoflavones are gaining popularity as alternatives to hormone replacement therapy. However, few guidelines exist to inform the public as to an appropriate dose. This case involves a postmenopausal woman who experienced a hypertensive crisis while consuming a high-dose isoflavone supplement as part of a research protocol. Case Presentation The participant was part of a placebo-controlled crossover trial to investigate the potential synergism of the antioxidant activity of soy isoflavones and vitamin C. Upon entry into the study, this healthy, well-nourished, normotensive postmenopausal woman (51 years old), consumed the first of four randomly assigned treatments (500 mg vitamin C plus 5 mg/kg body weight soy isoflavones). During this treatment, the participant's systolic blood pressure spiked to a recorded 226/117 mmHg, necessitating medical intervention and discontinuation of study participation. Two plausible mechanisms for this hypertensive crisis are discussed. Conclusion Due to the availability and increasing popularity of soy supplements, practitioners should be aware of the potential side effects associated with their use. Practitioners counseling clients who are consuming soy isoflavone supplements should advise them that elevated blood pressure may be a potential side-effect to consider and monitor.

Poor consumption of vitamin C-rich foods has led to a rise in subclinical vitamin C deficiency in the United States. We used the 1994-96 Continuing Survey of Food Intakes by Individuals to assess vitamin C intake in a sample of 25- to 90-year-olds (n=5290). After stratifying by age and sex, we divided the sample into three groups based upon mean vitamin C intake: low (0-30mg), marginal (30.1-60mg), and desirable (>60.1 mg). ANOVA with post hoc Scheffe's analyses was used for comparisons. Across all age groups, leading sources of vitamin C were vitamin C-rich fruit juices, low-vitamin C vegetables, vitamin C-rich fruits, and vitamin C-fortified fruit drinks. On average, 17% of adults had low vitamin C intakes. Among males, the highest percentage with low vitamin C intake was the elderly (21% of 75- to 90-year-olds), whereas among females it was younger women (23% of 25- to 44-year-olds). Across age categories and sexes, we found consistent dietary differences. Adults with desirable vitamin C intake consumed significantly more vitamin C-rich fruit juice, low-vitamin C vegetables, beef and ground beef dishes, low-fiber breads/rolls, condiments, and french fries. Those with low vitamin C intake consumed significantly more soft drinks, table sweeteners, coffee/tea, and alcohol. Regarding nutrients, adults with desirable vitamin C intake consumed significantly more energy-adjusted fiber, iron, magnesium, folate, and vitamin B 6 , A, and C; those with low vitamin C intakes consumed significantly more energy-adjusted cholesterol, saturated fat, and total fat. Our data indicate that a considerable proportion of American adults are drastically under-consuming vitamin C and have an increased risk for atherosclerosis due to low antioxidant intakes and high intakes of saturated fat. Adults who did consume desirable vitamin C relied upon juice and a variety of low vitamin C-containing foods. Further education with the Food Guide Pyramid—emphasizing vegetables and fruits rich in vitamin C—is warranted.

To the Editor. —Although the press coverage that coincided with publication of the article by Dr Norris and colleagues 1 indicated that cow's milk was not linked to diabetes, it must be emphasized that these authors actually did not examine the relationship of early exposure to cow's milk protein and development of IDDM. Rather, they examined early eating patterns of first-degree relatives of patients with IDDM who had high plasma levels of autoantibodies to insulin, GAD 65 , and IA-2. Subjects with high levels of these β-cell autoantibodies (BCAs) were not more likely to have had early exposure to cow's milk protein when compared with the non-BCA subjects. However, the presence of high titers of autoantibodies is not considered a selective predictor of IDDM. Only 5% to 22% of subjects with these antibodies progress to diabetes, 2-4 which indicates that β-cell damage may be partial or even reversible in most cases. Norris and colleagues

This paper provides indirect evidence that ascorbate nutriture affects plasma concentrations of complement component C1q in the guinea pig. C1q is a protein with a hydroxyproline-rich region similar in structure to collagen. It is essential for complement-mediated lysis of pathogens and may also facilitate phagocytic activity of macrophages and neutrophils. Since C1q is the only hydroxyproline-containing protein in the euglobulin fraction of plasma, it can be quantified indirectly by precipitating this fraction, hydrolyzing it and estimating hydroxyproline colorimetrically. We investigated the effect of ascorbate nutriture on protein-bound hydroxyproline (PBH) in the euglobulin fraction of plasma of young male guinea pigs. The animals had been depleted of ascorbate for 3 wk to produce scurvy and then repleted (6 wk) as follows: 0.5, 2.0 and 10.0 mg ascorbate/100 g body weight per d or 10 g ascorbate per liter of drinking water. PBH values were significantly correlated (P less than 0.001) with dietary ascorbate (+ 0.74) and with liver ascorbate (+ 0.75). Plasma PBH was significantly higher (P less than 0.01, Scheffé's test) in guinea pigs fed ample ascorbate (10.0 mg/100 g body weight per day) or tissue-saturating levels (10 g/L of drinking water) than in those fed adequate (2.0 mg/100 g body weight) or suboptimal (0.5 mg/100 g body weight) levels. These data are consistent with the known biochemical role of ascorbic acid in hydroxyproline biosynthesis and suggest a possible link between ascorbate and the immune response via C1q.

This study shows that guinea pigs fed 100 times the amount of vitamin C needed for growth and for prevention of scurvy have elevated levels of complement component C1q. C1q is a plasma protein rich in hydroxyproline, an amino acid whose biosynthesis requires ascorbate. C1q is essential for host defense against pathogens, both as a component of the classical complement pathway and as an opsonin in the phagocytosis process. We measured C1q in vitamin C-depleted guinea pigs that had been repleted for 4 wks with the following daily doses of ascorbate (mg/100 g body wt): 0.50 (suboptimal), 2.0 (adequate), 10 (ample) and 50 (tissue saturating). We measured C1q in three ways: indirectly by quantifying protein-bound hydroxyproline and directly by hemolytic assay and by immunodiffusion against anti-C1q. Regardless of the method, plasma C1q was 30-50% higher in animals fed tissue-saturating ascorbate than in those fed adequate or suboptimal amounts of the vitamin (p less than 0.05, one-way analysis of variance, least significant difference test). These data confirm and significantly extend earlier work that provided indirect evidence for a relationship between C1q and ascorbate nutriture in the guinea pig. They are consistent with a possible relationship between ascorbate nutriture and host defense.

A series of experiments were conducted to examine the effect of single oral doses of ascorbic acid on body temperature in healthy guinea pigs. Fifteen male guinea pigs (approximately 200 g) were fed a nonpurified diet designed for rabbits (a scorbutogenic diet) ad libitum and received orally 2 mg L-ascorbic acid/100 g body wt daily. After acclimation, rectal temperatures were recorded hourly following five separate ascorbate dosage treatments: 0 (control dosage), 2, 10 or 50 mg ascorbic acid/100 g body wt, or 50 mg ascorbic acid and 0.07 mg indomethacin/100 g body wt. Mean body temperature was significantly elevated (P less than 0.05) after 1 h in animals receiving either the 10 or 50 mg dosage (+ 0.27 +/- 0.05 and + 0.41 +/- 0.07 degree C, respectively) compared to that in animals receiving the 2 mg dosage (-0.07 +/- 0.05 degree C), the recommended daily intake for guinea pigs. Changes in body temperature of animals receiving the 50 mg dosage plus indomethacin did not differ significantly from those reported with the 2 mg dosage. Thus, a single oral dose of ascorbic acid at levels 5-25 times the recommended intake, can elevate body temperature significantly in healthy guinea pigs, a phenomenon which is inhibited by indomethacin administration.

In the rat, acute stress induces a rapid mobilization of tissue ascorbate, de novo synthesis of ascorbate in liver, and a rise in plasma and urinary ascorbate levels, culminating in elevated total-body ascorbate levels. In human beings, the enhanced metabolism of ascorbic acid after stress results in a rapid fall in ascorbate stores because of the body's inability to synthesize ascorbate in vivo. The physiologic relevance of these changes has not been established, but Chatterjee et al have postulated that ascorbate mobilization during stress may be a natural defense mechanism for the detoxification of excess histamine, an inflammatory substance that is synthesized and released by most tissues in response to chemical, physical, or immunologic stress. Histamine-induced vasodilation and increased vascular permeability promote the "fight-or-flight" response and healing. Excess histamine, however, has a negative impact on circulatory and immunologic homeostasis. Chronic administration of 2 g of L-ascorbate per day has significantly lowered blood histamine levels by 40% in healthy adults; this reduction in histamine was inversely related to leukocyte chemotaxis, a measure of immune responsiveness. In this study, we examined whether 500 mg ascorbate daily, a level that could be obtained in a carefully planned diet, had an antihistamine effect

Background Peanut consumption favorably influences satiety. This study examined the acute effect of peanut versus grain bar preloads on postmeal satiety and glycemia in healthy adults and the long-term effect of these meal preloads on body mass in healthy overweight adults. Methods In the acute crossover trial (n = 15; 28.4 ± 2.9 y; 23.1 ± 0.9 kg/m2), the preload (isoenergetic peanut or grain bar with water, or water alone) was followed after 60 min with ingestion of a standardized glycemic test meal. Satiety and blood glucose were assessed immediately prior to the preload and to the test meal, and for two hours postmeal at 30-min intervals. In the parallel-arm, randomized trial (n = 44; 40.5 ± 1.6 y, 31.8 ± 0.9 kg/m2), the peanut or grain bar preload was consumed one hour prior to the evening meal for eight weeks. Body mass was measured at 2-week intervals, and secondary endpoints included blood hemoglobin A1c and energy intake as assessed by 3-d diet records collected at pre-trial and trial weeks 1 and 8. Results Satiety was elevated in the postprandial period following grain bar ingestion in comparison to peanut or water ingestion (p = 0.001, repeated-measures ANOVA). Blood glucose was elevated one hour after ingestion of the grain bar as compared to the peanut or water treatments; yet, total glycemia did not vary between treatments in the two hour postprandial period. In the 8-week trial, body mass was reduced for the grain bar versus peanut groups after eight weeks (−1.3 ± 0.4 kg versus −0.2 ± 0.3 kg, p = 0.033, analysis of covariance). Energy intake was reduced by 458 kcal/d in the first week of the trial for the grain bar group as compared to the peanut group (p = 0.118). Hemoglobin A1c changed significantly between groups during the trial (−0.25 ± 0.07% and −0.18 ± 0.12% for the grain bar and peanut groups respectively, p = 0.001). Conclusions Compared to an isoenergetic peanut preload, consumption of a grain bar preload one hour prior to a standardized meal significantly raised postmeal satiety. Moreover, consumption of the grain bar prior to the evening meal was associated with significant weight loss over time suggesting that glycemic carbohydrate ingestion prior to meals may be a weight management strategy.