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Results for “Caloric Intake”

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PubMed1985

Obesity and caloric intake: the National Health and Nutrition Examination Survey of 1971-1975 (HANES I).

Most published studies have failed to show a greater food intake in obese subjects than in nonobese. However, the sample sizes in most of these studies are small and the methodologies open to question. HANES I is based on a probability sample of 20,749 people, representative of the civilian noninstitutional population of the U.S. We analyzed a subsample of 6219 nonpregnant adults whose diet was not influenced by illness or drugs and who stated that their intake, estimated by dietary interview, represented their usual pattern. Neither the caloric intake nor the caloric intake adjusted for physical activity level and age was higher in the obese subjects. This suggests that, unless estimates of food intake differ in accuracy between obese and nonobese subjects, factors other than overeating should be given increased consideration in the etiology of obesity.

Adult↗

PubMed1986

[Caloric intake and weight gain according to the shift schedule of shift workers].

Survey involved 84 workers matched for age, socio-occupational and families status and divided into 3 groups : A : 27 shift workers on 3 days rotating shift, B : 47 shift workers on 5 days rotating shift, C : 20 days workers. Each subject was submitted to dietary survey by means of 24 hours recall, realised 3 times for shift workers and once for control. All workers were interviewed about caloric intake of the preceding day off caloric intake. Annual weight gain was studied through the use of occupational health service records. There was no significant difference between the 3 groups for working day caloric intake. Day-off intake was lower (p less than 0.05) in group A (day-off any day of the week). Annual weight gain was not different between the 3 groups. Shift workers with faster weight gain had a higher caloric intake on day-off and after evening meal.

Adult↗

PubMed1988

Quantitative therapeutic plan for the treatment of obesity and a simple method for estimating appropriate caloric intake by using previous rate of weight loss.

We have formulated an equation for the calculation of the caloric intake in a reducing diet that is suited to individual obese patients. We have designed a system in which the weight loss achieved after the intake of a fixed number of calories over a given period is used as a basis for the next weight-reducing plan for a given patient. We devised the formula Y = X - 1000 (b2/a2-b1/a1) for calculating the daily caloric intake (Y). X is the previous caloric intake; b1 is achieved weight loss (kg) in the previous period (a1 weeks); and b2 is the planned reduction in weight in the subsequent target period (a2 weeks).

Energy Intake↗

PubMed1985

Influence of caloric intake on the respiratory mode during mandatory minute volume ventilation.

Mandatory minute volume ventilation has been proposed as a method for weaning patients from ventilators. The purpose of this study was to delineate the influence of caloric intake on spontaneous ventilation in patients receiving mandatory minute volume ventilation. While the value of such ventilation remained unchanged, eight patients were studied at the following three different levels of daily caloric intake: (1) level A, mean of 223 kcal/sq m; (2) level B, mean of 1,380 kcal/sq m; and (3) level C, mean of 2,100 kcal/sq m. We performed gas exchange measurements and a 24-hour recording of ventilation with a monitoring system providing distinction between spontaneous and mechanical cycles. We found that the ventilatory mode was markedly dependent upon the nutritional intake; the percentage of spontaneous ventilation over 24 hours increased from 11 +/- 7 percent (+/- SE) during diet A to 50 +/- 9 percent during diet B and 79 +/- 8 percent during diet C. This increment paralleled the increase in production of carbon dioxide with caloric intake. We suggest therefore that the patient's ability to breathe spontaneously when receiving mandatory minute volume ventilation should be interpreted according to caloric intake.

Aged↗

PubMed1991

Maternal weight and sire group, not caloric intake, influence adipocyte volume in infant female baboons.

We tested the hypothesis that overfeeding with a high caloric (concentrated) formula increases growth without influencing adipocyte volume in preweaning infant baboons. Female infant baboons from three sires and 25 dams were fed either 67.5 kcal (normal formula) or 94.5 kcal (concentrated formula)/100 g Similac formula. Immediately before weaning (19 wk), adipocyte volume was measured in biopsied adipose tissue from omentum, flank, and popliteal depots. From birth until weaning, infants fed the concentrated formula consumed 20% more total calories, averaged 15% more calories/kg/wk, and gained 14% more weight than normally fed infants. Adipocyte volume differed significantly among different sites (omentum greater than popliteal greater than flank) and among different sire groups. Increased caloric intake alone did not increase adipocyte volume. There was a small but significant sire by infant formula interaction on adipocyte volume. When fed the concentrated formula, progeny from one sire had larger adipocytes than normally fed infants, whereas progeny from the other two sires had smaller adipocytes or adipocytes that were comparable to infants fed normal formula. Variability in adipocyte volume at 19 wk of age was best accounted for by maternal weight and sire group (omentum R2 = 0.334, p = 0.026; flank R2 = 0.532, p = 0.01; popliteal R2 = 0.482, p = 0.01) and not by caloric intake. These results suggest that the level of triglyceride deposition into adipocytes attained during preweaning growth is determined to a greater extent by genetic and other factors rather than caloric intake.

Adipose Tissue↗

PubMed1991

Relationships between weight and caloric intake of men who stop smoking: the Multiple Risk Factor Intervention Trial.

Data from 6,569 middle-aged men in the Multiple Risk Factor Intervention Trial were analyzed to determine whether the weight change associated with smoking cessation resulted primarily from appetite or metabolic alterations. The appetite hypothesis attributes weight gain to an enhanced appetite and subsequent increase in caloric intake. The metabolic change hypothesis attributes weight gain to a metabolic alteration and subsequent decrease in basic caloric needs. Caloric intake and weight changes were tabulated for men who quit smoking and were compared to similar changes in men who continued smoking over 12 months. The difference between caloric intake changes in men quitting smoking versus men continuing smoking, controlled for weight change, was attributed to the metabolic change hypothesis. Men who quit smoking consumed 103 calories per day less (95% confidence interval = 29 to 177) than men who continued smoking with similar body weight changes. The decrease in caloric intake attributed to smoking cessation was proportional to the number of cigarettes smoked prior to cessation [corrected].

Adult↗

PubMed1977

Postnatal growth of infants of less than 1.3 kg birth weight: effects of metabolic acidosis, of caloric intake, and of calcium, sodium, and phosphate supplementation.

Weekly increments of length, weight, head circumference, and skinfold thickness in response to a series of dietary changes were measured in 108 healthy infants who weighed less than 1.3 kg at birth. The serial manipulations included prevention of late metabolic acidosis, increased caloric intake, and calcium, sodium, and phosphorus supplementation. The study comprised four phases; the infants were divided into ten groups according to dietary regimen. AGA and SGA infants were studied separately. Growth in length was primarily influenced by a change to a formula providing a higher caloric intake and a 60:40 whey protein/casein ratio. Correction of late metabolic acidosis, sodium, and phosphorus supplementation had minor additive effects on growth in length. Increased caloric intake also influenced growth of head circumference, but only in AGA infants. Only the sodium intake was shown to influence body weight increments significantly with the range of caloric intake used in the study (132 to 160 calories/kg/day).

Acidosis↗

PubMedDate not supplied

Altered testosterone feedback in pubertal male rats raised on reduced caloric intake.

A study was conducted to explore the hypothesis that reduced caloric intake increases the negative feedback efficacy of testosterone on gonadotropin secretion. Daily subcutaneous injections of testosterone propionate in oil were administered to either age-matched (37-day-old) or weight-matched (mean = 178 g) ad libitum-fed (control) or underfed rats that received 60% of normal daily food intake from the age of 20 days. Daily doses of testosterone propionate ranged from 25 to 400 micrograms/100 g body weight. Results indicate that reduced caloric intake increases the suppression of serum LH by testosterone propionate in both age-matched and weight-matched underfed rats. On the other hand, the response of serum FSH concentrations to testosterone propionate was affected by reduced diet only in the weight-matched animals. Results suggest that the increased negative feedback of testosterone on LH secretion is a specific diet-induced effect and not merely the result of reduced growth. The altered response in FSH secretion, however, may represent age-associated changes in sensitivity to testosterone rather than diet-induced effects.

Animals↗

PubMed1995

Caloric intake stimulates growth hormone secretion in food-deprived rats with anterolateral deafferentation of the medial basal hypothalamus or administered antiserum to somatostatin.

In rats, food deprivation inhibits episodic growth hormone (GH) secretion. On the basis of previous studies, we hypothesized that during a recovery from prolonged fasting, caloric intake stimulates the release of GH-releasing factor (GRF) and this process does not depend on the specific macronutrients in the meal, while protein in the meal acts to restore characteristic ultradian rhythmicity of GH secretion. To test this hypothesis, the effect of caloric intake on GH secretion was examined in fasted adult male Wistar rats devoid of somatostatin (SS) influence on GH secretion either by anterolateral deafferentation (ALC) of the medial basal hypothalamus (MBH) or administration of anti-SS goat serum (ASS). Rats were provided with an indwelling right atrial cannula and were deprived of food for 72 h. ALC was performed 2 weeks prior to the study. ASS was given i.v. 8 h and 7 h prior to refeeding, respectively. Serial blood specimens were collected every 10 min. In rats with ALC (ALC rats) or rats given ASS (ASS rats), the blood GH level revealed irregularly occurring small fluctuations, instead of the usual high bursts and low trough level. The baseline GH level and the mean GH level of fasted ALC rats or fasted ASS rats were significantly lower than those of fed ALC rats or fed ASS rats. Feeding the isocaloric mixed meal, the protein meal or the protein-deficient meal increased the GH pulse frequency, the pulse amplitude, the baseline GH level and the mean GH level in 72-h fasted ALC rats. These changes in GH secretory pattern persisted during the period of observation and were independent of the type of meal ingested. Following feeding the mixed meal, similar changes in the GH secretory pattern demonstrated in 72-h fasted ALC rats were also observed in 72-h fasted ASS rats, suggesting that the stimulation of GH secretion following caloric intake is not limited to ALC rats. Since the influence of SS on GH secretion has been largely eliminated in ALC or ASS rats, it is highly unlikely that the augmentation of GH secretion following feeding after prolonged food deprivation was the consequence of inhibition of SS secretion. Although GRF measurement was not performed, it is conceivable that the signal of caloric intake is conveyed to the MBH and acts to stimulate GRF release.

Animals↗

PubMedDate not supplied

Comparison of resting energy expenditures and caloric intake in children with severe burns.

Nutritional support is provided to children after severe burn injuries in amounts derived from empirical formulas or measurements of resting energy expenditure. To scrutinize these methods, indirect calorimetry measurements were performed on 74 survivors of burns (greater than or equal to 40% total body surface area) and compared to their actual caloric intake, percent weight change, and optimal caloric requirements formulated from the Curreri and Shriners' equations. These parameters showed that in spite of an initial deficit in actual caloric intake as compared to formulated goals, weight was maintained, whereas resting energy expenditures ranged from 30% to 40% below the actual caloric intake. Furthermore, a subgroup of patients (n = 42) who met +/- 20% of their formulated needs were stratified by extent of burn; this illustrated a significant weight gain in the more severely burned children. In conclusion, nutritional formulas in popular use overestimate caloric requirements in severe burns, whereas resting energy expenditure measurements require an additional factor of 30% to maintain body weight.

Body Weight↗

PubMed1990

A proxy approach to the determination of total caloric intake for use in cancer epidemiology.

In the absence of complete dietary information on a cohort of 472 early-stage breast cancer patients a caloric prediction technique was developed. Deriving an accurate caloric denominator would enable examination of individual nutrient effects by controlling for potential confounding by calories. Surrogate measures of mean daily caloric intake were generated from estimates of basal metabolic rate (BMR) predicted from age, height, weight, and physical activity. A validation study was undertaken to test the relationship between the BMR proxy terms and mean daily energy intake obtained from four-day food diaries for 51 subjects. Pearson correlation coefficients between the diary-derived and predicted values of caloric intake were computed (r = 0.43, p = 0.001). The results are in the range of what many researchers found when comparing self-reports of total caloric intake in validation and reliability studies of various dietary assessment tools. Because of the large heterogeneity of results across the ages represented in this study (25-77 yrs), it is recommended that small validation studies of this type be carried out in the subpopulations of interest.

Adult↗

PubMed1975

Caloric intake and unconjugated hyperbilirubinemia.

Reduction in caloric intake was associated with a greater absolute rise in the serum bilirubin concentration in patients with Gilbert's syndrome and partial hepatic bilirubin uridine diphosphate glucuronyltransferase (UDPG-T) dysfunction compared to patients with hemolytic unconjugated hyperbilirubinemia and normal subjects. Two patients with overt hemolysis but an exaggerated response to caloric deprivation had reduced UDPG-T activities comparable to Gilbert's syndrome. The UDPG-T activities in the other patients with hemolytic jaundice were normal. The combination of fasting and novobiocin in 2 normal subjects produced a greater increase in bilirubin level than either fasting or novobiocin alone. These data suggest that theunderlying UDPG-T dysfunction, rather than the prefasting level of unconjugated hyperbilirubinemia, is responsible for the diet-induced hyperbilirubinemia in Gilbert's syndrome. The diet test appears to differentiate Gilbert's syndrome from hemolytic jaundice as well as from normal subjects, irrespective of the initial serum bilirubin concentration.

Anemia, Hemolytic↗

PubMed1975

Effects of obesity and caloric intake on biliary lipid metabolism in man.

The effects of obesity and caloric intake on biliary lipid metabolism were investigated in a series of related studies. The degree of saturation of gallbladder bile with cholesterol was found to be significantly higher in a group of 23 obese healthy subjects than in a group of 23 nonobese controls matched for age, sex, and race. Bile was also significantly more saturated in 11 obese subjects before than after weight reduction. To determine whether supersaturated bile in obesity is due to excessive secretion of cholesterol or to deficient secretion of bile acids and phospholipids, the hepatic outputs of these three lipids were measured during constant duodenal infusion of formula in the same 11 subjects before and after weight reduction. Weight reduction resulted in significant reduction of cholesterol output but not of bile acid or phospholipid output. Moreover, very obese subjects were found to have cholesterol secretion rates markedly higher than less obese subjects previously studied by the same method. In obese subjects, bile was supersaturated with cholesterol despite increased bile acid pool sizes and increased secretion rates of bile acids and phospholipids. Supersaturated bile in the obese could therefore be attributed to a single defect in lipid secretion, namely, an excessive output of cholesterol. To determine whether the rate of caloric intake can account for the effects of obesity on biliary lipid composition and secretion, nine obese white men were studied on a weight maintenance diet and then during weight reduction on a 1,000 cal diet. As compared to weight maintenance, chronic caloric restriction resulted in reduced outputs of cholesterol, bile acids, and phospholipids, reduced bile acid pool size, and reduced synthesis and fecal excretion of cholesterol. Saturation of bile with cholesterol did not decrease during weight reduction, evidently because of the mobilization of cholesterol from adipose stores and the marked reduction in bile acid and phospholipid output observed during chronic caloric restriction. Acute alterations in caloric infusion rates did not fully reproduce the effects of chronic administration of high and low calorie diets. Likewise, chronic intake of hypercaloric diets by nonobese subjects did not reproduce the cholesterol hypersecretion characteristic of the obese. Thus, increased cholesterol secretion in obese subjects could not be fully explained by the amount of calories they ingested to maintain stable weight. It is concluded that obesity is characterized by excessive hepatic secretion of cholesterol which results in supersaturated bile.

Adipose Tissue↗

PubMed1982

Serum bile acids in Gilbert's syndrome before and after reduced caloric intake.

Fasting and postprandial serum bile acids were determined before and after reduced caloric intake in patients with Gilbert's syndrome. Cholic and chenodeoxycholic acid were determined by radioimmunoassay. In all patients there was a pronounced increase in serum bilirubin (mean increase, 140%) after caloric restriction. However, both fasting and postprandial levels of serum bile acids were within the normal range before and after reduced caloric intake. The results indicate that different mechanisms are involved in the hepatic uptake and secretion of bile acids and bilirubin. Moreover, the results show that determinations of serum bile acids can be used to assess liver function in patients with Gilbert's syndrome irrespective of the degree of hyperbilirubinemia.

Adolescent↗

PubMed1984

The infant's ability to self-regulate caloric intake: a case study.

A case study which illustrates the infant's ability to regulate caloric intake through adjustments in formula intake is presented. A daily record of infant formula and supplemental food intake of a normal, bottle-fed male infant was kept from 1 week to 9 months after birth. The infant's physical growth was assessed at regular intervals. Measurements included weight, recumbent length, head circumference, and skinfold thicknesses. Feeding was ad libitum, and caregivers were highly responsive to the infant's satiety behaviors. Under these conditions, the infant adjusted his caloric intake as supplemental foods were added to his diet by progressively decreasing the volume of formula consumed. His growth was well canalized and tracked very close to the 50th centile of NCHS weight and length standards. The regularity of his growth attests to the adequacy of his intake for meeting energy needs without excess energy storage. This suggests that to avoid overfeeding the bottle-fed infant, caregivers should attempt to facilitate the infant's self-regulation of intake.

Energy Intake↗

PubMedDate not supplied

Glucose and insulin responses in relation to insulin dose and caloric intake 12 h after acute physical exercise in men with IDDM.

Acute exercise in insulin-dependent diabetic patients may perturb glycemic control, and adjustments of insulin and diet might be required to avoid postexercise hypoglycemia. The aim of this study was to assess the role of alterations in insulin dose or caloric intake on blood glucose and free-insulin levels during 12 h after an evening bout of exercise. Nine insulin-dependent diabetic men (28-42 yr of age) receiving two daily injections with a combination of intermediate-acting and soluble insulin participated in the study. Patients were randomly assigned to four treatment protocols: A, 50% reduction in intermediate-acting insulin dose; B, 50% reduction in soluble insulin dose; C, extra caloric intake (1700 kJ) 1 h after exercise; and D, no change. Exercise consisted of 45 min of cycling at 60% of maximal oxygen uptake at each occasion. Glucose and insulin responses were similar for the four protocols. There was a significant (P less than .001) time effect found regardless of treatment, with lowest blood glucose values 75 min after exercise. Hypoglycemia occurred in six of the nine patients at some time during the study, with half of the occurrences on the control night (protocol D). Consistent individual plasma insulin and glucose patterns were observed independent of protocol used. In some patients, hypoglycemia was evident after reductions in insulin dose, and in others it was evident on the night increases in caloric intake were to occur; thus, none of the interventions were totally adequate in preventing exercise-induced hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

[Carcinogenesis: influence of caloric intake restriction].

In experimental animals, restriction of caloric intake is associated to a decreased incidence in the number and size of both spontaneous and induced tumors. Epidemiologic evidence of a similar effect in humans is not conclusive. However, some dietary recommendations regarding calories, protein and fiber content may be made in order to help prevent cancer development in human subjects.

Animals↗

PubMed1992

Effects of tobacco smoking on caloric intake.

Reduced body weight due to smoking may be an important factor inhibiting smoking cessation and promoting relapse after cessation in some smokers. It is popularly believed that smoking decreases body weight by suppressing appetite. However, cross-sectional studies show that, despite their lower body weights, smokers do not eat less than non-smokers or ex-smokers and, in fact, tend to eat slightly more. Similarly, laboratory studies show no acute effects of smoking or nicotine intake via other means on caloric intake in smokers, although intake of non-smokers may be reduced after nicotine. In contrast, longitudinal studies show that eating consistently increases in the first weeks after stopping smoking, but may recede to pre-cessation levels with longer-term abstinence, while resumption of smoking after cessation is accompanied by a reduction in eating. A similar pattern of results is seen for self-reported hunger and some, but not all, constituents of diet. Thus, there appear to be no acute or chronic effects of smoking on eating in smokers maintaining regular smoking, but changes in eating are observed concomitant with changes in smoking status (i.e. cessation or relapse). Although tolerance to anorectic effects of nicotine is one potential explanation, these findings may be more parsimoniously explained by viewing changes in eating due to smoking as secondary to an alteration in the set point around which body weight is regulated. According to this notion, cessation is accompanied by increased eating only until a new, higher body weight set point is reached, while relapse (and perhaps initiation of smoking) decreases eating only until a lower set point is reached. Implications of these findings and a set point explanation for them are discussed.

Energy Intake↗