Patterns of chocolate consumption.

Although consumed in some form since at least 460 AD, cacao (Theobroma cacao) was not used in confectionery until the 19th century when the cocoa press was invented. Per capita consumption of chocolate confectionery in the United States is moderate (approximately 4.6-4.8 kg/y) compared with that of many northern European countries (approximately 7-10 kg/y). Eleven percent of the US population reported consuming chocolate candy on > or = 1 of the 3 d of recorded food intake in the US Department of Agriculture Nationwide Food Consumption Survey 1987-1988; < 1.0% consumed chocolate every day. The Western region of the United States contained the highest proportion of chocolate consumers. More whites than other racial groups were consumers. Chocolate was consumed by more people in the winter than in other seasons and more was consumed at snacks than at meals. The mean amount of chocolate consumed was approximately 30-90 g/d, depending on sex and age group. Chocolate candy was only a minor contributor (0.7-3.4%) to the overall dietary intake of total energy, fat, saturated fatty acids, and stearic acid.

Effects of calcium carbonate and hydroxyapatite on zinc and iron retention in postmenopausal women.

We measured the effect of calcium carbonate and hydroxyapatite on whole-body retention of zinc-65 in 11 and iron-59 in 13 healthy, postmenopausal women. In a single-blind, controlled, crossover study, each subject, on three occasions, ingested a standard test meal supplemented with iron-59 or zinc-65 and capsules containing placebo or 500 mg elemental calcium as calcium carbonate or hydroxyapatite. Whole-body countings were performed prior to, 30 min after, and 2 wk after each meal. Mean (SEM) zinc retention was 18.1 +/- 1.0% with placebo (control) and did not vary significantly with calcium carbonate (110.0 +/- 8.6% of control) or hydroxyapatite (106.0 +/- 7.9% of control). Iron retention, 6.3 +/- 2.0% with placebo, was significantly reduced with both calcium carbonate (43.3 +/- 8.8% of control, p = 0.002) and hydroxyapatite (45.9 +/- 10.0% of control, p = 0.003). Iron absorption may be significantly reduced when calcium supplements are taken with meals.

Effects of a milk chocolate bar per day substituted for a high-carbohydrate snack in young men on an NCEP/AHA Step 1 Diet.

This study compares the plasma cholesterol response with the isoenergetic substitution of a milk chocolate bar (46 g) given daily for a high-carbohydrate snack in healthy young men on a Step 1 Diet. Normocholesterolemic men (n = 42) were fed a Step 1 Diet for 21 d (run-in diet) followed by a 27-d experimental period during which they consumed the same diet plus either a milk chocolate bar or a high-carbohydrate snack; after this they consumed the run-in diet for 21 d followed by the other snack for 27 d. When subjects consumed a milk chocolate bar instead of the high-carbohydrate snack, high-density-lipoprotein (HDL) cholesterol was 0.08 +/- 0.03 mmol/L higher (P < 0.01) and plasma triglycerides were 0.06 +/- 0.03 mmol/L lower (P < 0.05). Substitution of a milk chocolate bar for a high-carbohydrate snack did not adversely affect the low-density-lipoprotein-(LDL) cholesterol response to a Step 1 Diet despite an increase in total fat and saturated fatty acid content of the diet. This response may be due to stearic acid.

The role of fatty acid saturation on plasma lipids, lipoproteins, and apolipoproteins: II. The plasma total and low-density lipoprotein cholesterol response of individual fatty acids.

Regression analyses were performed on individual data from our two previous clinical investigations to establish the cholesterolemic effects of individual fatty acids. Our principal objective was to determine the effects of stearic acid on plasma total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol levels. Our second objective was to determine the variation in the cholesterolemic response of individuals to changes (delta) in the major dietary fatty acids. The best-fitting linear regression equations relating delta TC and delta LDL (mg/dL) were as follows: delta TC = 2.3 delta C14:0 + 3.0 delta C16:0 - 0.8 delta C18:0 - 1.0 delta polyunsaturated fatty acids (PUFA) and delta LDL = 2.6 delta C14:0 + 2.9 delta C16:0 - 0.5 delta C18:0 - 0.7 delta PUFA, where delta fatty acid = change in intake expressed as percent of calories. Based on these equations, in which stearic acid has a significant, negative regression coefficient, and the other regression models analyzed, it appears that stearic acid has an independent cholesterol-lowering effect. Using the equation we developed, 75% of the actual cholesterolemic responses were within +/- 10 mg/dL of the predicted response. In summary, we have developed a predictive equation (similar to those developed by both Keys and Hegsted) to estimate changes in plasma TC and LDL cholesterol levels of young men in response to changes in dietary fatty acids. However, our predictive equation separates stearic acid from the other long-chain saturated fatty acids (SFA) and indicates that it has an independent cholesterol-lowering effect. Thus, stearic acid is a unique long-chain SFA because of its effect on plasma cholesterol level.

Tissue nonprotein sulfhydryl content and weight gain of rats as affected by dietary methionine level.

The effect of dietary methionine level on tissue nonprotein sulfhydryl content (NPSH) and weight gain was systematically evaluated in young adult rats (approximately 360 g) fed amino acid diets. In 28-day feeding experiments, weight gain and liver and skeletal muscle NPSH increased, but blood NPSH decreased as dietary methionine rose from 0 to 0.8%. The requirement for weight maintenance (0.2% methionine) did not sustain maximum liver and skeletal muscle NPSH, whereas the requirement for maximum weight gain (0.6% methionine) did. Maximum skeletal muscle NPSH was attained by 0.4% methionine and maximum liver NPSH by 0.5% methionine. In another experiment, diets containing 0.4, 0.5, and 0.6% methionine were fed for 1, 8, 29, and 50 days. Liver and skeletal muscle NPSH were lower, whereas blood NPSH was higher with the 0.4% methionine diet. These differences in NPSH were significant at all times for liver, at 8 days for skeletal muscle, and at 29 days for blood. Weight gain did not differ significantly among the groups at any time. In all experiments, weight gain was similar with 0.4 and 0.5% methionine even though liver NPSH was 40-50% higher with 0.5% methionine. The data suggest that tissue NPSH may serve as a cysteine reservoir and spare dietary sulfur-containing amino acids during marginal intake. Also, weight gain may be an unreliable measure of sulfur-containing amino acid needs under some circumstances.

Variable predictions of protein quality by chemical score due to amino acid analysis and reference pattern.

The amino acid composition of five protein samples (casein, beef, wheat flour, peanut flour and soy protein isolate) was obtained from several sources: various routine analytical procedures, manufacturer's fact sheets, and published data. The amino acid profile from each source was scored against three reference patterns, each based on an estimate of human essential amino acid requirements. Protein quality ratings based on chemical score were variable. Both the chemical score and predicted first-limiting amino acid for a given protein often differed with data source and choice of reference pattern. Some of the predictions contradicted those previously validated by bioassays. The variability in protein quality ratings was reduced somewhat by expressing the data as essential amino acid indices. But this also reduced the degree of difference in protein quality among the various proteins. Although the amino acid profile of food proteins provides an important perspective on their nutritive value, it appears that the imprecision and uncertain accuracy of routine hydrolysis and analytical procedures confound the use of amino acid data for regulating protein quality. The situation is further complicated because human essential amino acid requirements have been variably interpreted, which has led to different reference patterns.

Hyperactivity: is candy causal?

Adverse behavioral responses to ingestion of any kind of candy have been reported repeatedly in the lay press. Parents and teachers alike attribute excessive motor activity and other disruptive behaviors to candy consumption. However, anecdotal observations of this kind need to be tested scientifically before conclusions can be drawn, and criteria for interpreting diet behavior studies must be rigorous. Ingredients in nonchocolate candy (sugar, artificial food colors), components in chocolate candy (sugar, artificial food colors in coatings, caffeine), and chocolate itself have been investigated for any adverse effects on behavior. Feingold theorized that food additives (artificial colors and flavors) and natural salicylates caused hyperactivity in children and elimination of these components would result in dramatic improvement in behavior. Numerous double-blind studies of the Feingold hypothesis have led to the rejection of the idea that this elimination diet has any benefit beyond the normal placebo effect. Although sugar is widely believed by the public to cause hyperactive behavior, this has not been scientifically substantiated. Twelve double-blind, placebo-controlled studies of sugar challenges failed to provide any evidence that sugar ingestion leads to untoward behavior in children with Attention-Deficit Hyperactivity Disorder or in normal children. Likewise, none of the studies testing candy or chocolate found any negative effect of these foods on behavior. For children with behavioral problems, diet-oriented treatment does not appear to be appropriate. Rather, clinicians treating these children recommend a multidisciplinary approach. The goal of diet treatment is to ensure a balanced diet with adequate energy and nutrients for optimal growth.

Effects of equimolar doses of L-methionine, D-methionine and L-methionine-dl-sulfoxide on plasma and urinary amino acid levels in normal adult humans.

Plasma and urinary amino acid levels were measured in four normal adult subject administered equimolar quantities (0.0605 mmol/kg body wt) of L-methionine, D-methionine and L-methionine-dl-sulfoxide in a randomized crossover design. Plasma total methionine concentrations increased significantly (P less than 0.05) over base line (3.7 +/- 1.2 mumol/dl; mean +/- SD) after loading with each compound. Mean peak plasma methionine levels were 9.8 +/- 1.1, 14.4 +/- 2.3 and 5.2 +/- 1.0 mumol/dl after loading with L-methionine, D-methionine and L-methionine sulfoxide, respectively. D-Methionine accounted for the increased plasma levels seen after D-methionine loading. None of the three compounds affected plasma cystine, cysteine or taurine concentrations. Plasma methionine sulfoxide concentrations were not affected by loading with D- or L-methionine but increased significantly after ingestion of L-methionine sulfoxide. Urinary methionine excretion was 20 times higher after ingestion of D-methionine than after ingestion of L-methionine or L-methionine sulfoxide, with the increase due to D-methionine excretion. Urinary excretion of methionine sulfoxide and its N-acetyl derivatives was not significantly higher after loading with methionine sulfoxide. The data indicate that adult humans do not utilize D-methionine efficiently as a methionine source but probably do utilize L-methionine-dl-sulfoxide.