Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Caloric Intake”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1992

Modulation of chemical toxicity by modification of caloric intake.

Caloric restriction increases maximum achievable lifespan and offsets the time to development of degenerative disease. Part of these desirable effects may result from positive modulation of toxic events. We have shown that when rodents are placed on a diet that is reduced in total calories by 40%, several beneficial changes on biochemical systems which impact on toxicologic processes are positively enhanced. Lipid metabolism is reduced and, therefore, the potential for lipoperoxidation is reduced. Additionally, activity of enzymes that produce free radicals as byproducts (cytochrome P4502C11) are also reduced. Concurrently, we have shown that the "effective" activity of catalase and the activity of superoxide dismutase (which are required for the detoxification of toxic oxygen radicals) are significantly increased by caloric restriction. The activities of enzymes of drug and xenobiotic metabolism are also altered by caloric restriction. The effect upon activity may be to either decrease or increase activity, dependent upon whether the enzyme activates compounds to intermediates which may be more toxic or whether the enzyme acts to reduce toxicity. We have also shown that caloric restriction may affect the initiation stage of carcinogenesis. Aflatoxin B1 binding to hepatic nuclear DNA was reduced by caloric restriction (caloric restriction reduced both major adducts that are formed upon exposure to aflatoxin B1). caloric restriction also reduced cytochrome P4502C11 which converts aflatoxin B1 to its toxic epoxide, and may partly explain the reduction in binding. These results suggest that caloric restriction may, in part, extend the time to development of degenerative disease by altering basic biochemical mechanisms of toxicity.

Animals↗
PubMed1982

Effects of excessive caloric intake and caloric restriction on body weight and energy expenditure at rest and light exercise.

The individual response to overeating and semistarvation on energy expenditure at rest and light work before and after a test meal was investigated. This response was related to the change in dry body weight, measured as weight (W) minus total body water (TBW). Experiments were performed on 9 non-obese subjects: (a) with a normal habitual energy intake; (b) (overfeeding) with an extra energy intake of 12 MJ per day for two weeks; and (c) (semistarving) with an energy intake of only 2.1 MJ per day for 2 weeks. Measurements of VO2, VCO2, W and TBW were obtained at the end of each of the three periods. It was found that the perturbation in energy intake from normal to 20-25 MJ per day increased the energy expenditure. The magnitude of this increase was highly individual and inversely related to the change in dry body weight. Energy expenditure, measured under the four standardized conditions, after 2 weeks of starvation was lower than that obtained after the preceding overeating period. This decrease was also roughly inversely related to the change in dry body weight. The results support the idea that part of the regulation of body energy content takes place by way of a change in the efficiency of energy utilization and that the response to a perturbed energy intake varies considerably between subjects.

Adult↗
PubMed1986

Caloric intake necessary for weight maintenance in anorexia nervosa: nonbulimics require greater caloric intake than bulimics.

In the past decade, patients with anorexia nervosa have been subdivided by the presence or absence of binging-and-purging behavior. Psychologic, physiologic, and premorbid weight differences have also been discovered between these subgroups. We now report that nonbulimic anorectics required 30-50% more caloric intake than bulimic anorectics to maintain a stable weight. This difference in caloric intake was independent of phase of illness; it was present at low weight and at intervals after weight restoration. Subjects were closely supervised on an inpatient hospital ward so that they could not binge or purge. Motor activity did not appear to explain these alterations in caloric requirements. Such differences in caloric intake could be trait related or a consequence of many years of starving or binging behavior. These findings are clinically relevant for advising eating disorder patients of caloric requirements necessary to maintain a normal weight.

Adult↗
PubMed2005

Fat intake reverses the beneficial effects of low caloric intake on skeletal muscle mitochondrial H(2)O(2) production.

Food restriction is the most effective modulator of oxidative stress and it is believed that a reduction in caloric intake per se is responsible for the reduced generation of reactive oxygen species (ROS) by mitochondria. Hydrogen peroxide (H(2)O(2)) generation and oxygen consumption (O(2)) by skeletal muscle mitochondria were determined in a peculiar strain of rats (Lou/C) characterized by a self-low-caloric intake and a dietary preference for fat. These rats were fed either with a standard high-carbohydrate (HC) or a high-fat (HF) diet and the results were compared to those measured in Wistar rats fed a HC diet. H(2)O(2) production was significantly reduced in Lou/C rats fed a HC diet; this effect was not due to a lower O(2) consumption but rather to a decrease in rotenone-sensitive NADH-ubiquinone oxidoreductase activity and increased expression of uncoupling proteins 2 and 3. The reduced H(2)O(2) generation displayed by Lou/C rats was accompanied by a significant inhibition of permeability transition pore (PTP) opening. H(2)O(2) production was restored and PTP inhibition was relieved when Lou/C rats were allowed to eat a HF diet, suggesting that the reduced oxidative stress provided by low caloric intake is lost when fat proportion in the diet is increased.

Animals↗
PubMed1973

Diagnosis of Gilbert's syndrome: role of reduced caloric intake test.

Reduction in caloric intake to 400 a day for 72 hours resulted in a significant increase in the plasma bilirubin concentration in patients with Gilbert's syndrome and in normal subjects. This was due to an increase in unconjugated pigment. There was no significant increase in the bilirubin concentration in patients with liver disease or haemolytic anaemia.The increase in unconjugated bilirubin was signficantly greater in Gilbert's syndrome than in normals but only when the initial bilirubin concentration was raised. It was usually seen within 24 hours of reducing the caloric intake. An increase of 100% or more suggests that unconjugated hyperbilirubinaemia is due to Gilbert's syndrome. In the normal subjects the unconjugated bilirubin level did not exceed 1.0 mg/100 ml.The increase in unconjugated bilirubin concentration on reducing the caloric intake may be due to decreased hepatic bilirubin uridine diphosphate glucuronyl transferase activity, which was shown to be present in seven rats starved for 72 hours. The effect of a 400 calorie diet for 24 hours on the unconjugated bilirubin level may distinguish Gilbert's syndrome from other causes of unconjugated hyperbilirubinaemia.

Anemia, Hemolytic↗
PubMed1998

Caloric intake patterns of nonpurge binge-eating women.

Daily caloric intake of nonpurge binge-eating women was monitored over 28 days using food diaries to determine how caloric intake patterns were related to binge eating. The majority of participants had extreme fluctuations in daily caloric intake. Caloric intake for both nonbinge days and days preceding the highest-calorie binge days was significantly lower than caloric intake on binge days and highest-calorie binge days. The lower caloric intake was not low enough to cause physiological deprivation. Although there was not physiological deprivation of calories, the individual may have felt that she ate less than desired, which may have contributed to subsequent binge eating.

Adult↗
PubMed1989

An assessment of caloric intake as an indicator of physical activity.

Caloric intake has been suggested as a surrogate measure of physical activity, provided that energy balance is maintained. In this study we assessed caloric intake in relation to other measures of physical activity in a free-living population by a single 24-hr recall in white adult males, ages 22-79 years, examined in 1957-1960 as part of the U.S. Railroad Study. Intake was positively related to leisure time and occupational activity. Men with higher levels of caloric intake had lower exercise test heart rates indicating that they were probably more fit. Caloric intake was also significantly and inversely related to body mass index, the sum of the triceps and subscapular skinfold thickness measurements, blood pressure, and total serum cholesterol. These results suggest that caloric intake, even as measured in a 24-hr dietary recall, is an indicator of physical activity level. Therefore, caloric intake may be a useful indicator of physical activity in some population-based epidemiologic studies.

Adult↗
PubMed1975

Metabolic effects of increased caloric intake in man.

In order to determine if increased caloric intake could be responsible for the insulin resistance and elevated plasma glucose, insulin, and triglyceride levels commonly associated with obesity, hypercaloric diets were fed for 3 wk to eight normal subjects, and the metabolic consequences of this diet were assessed before significant weight gain had occurred. One wk of increased caloric intake led to statistically significant increases in fasting plasma insulin (22 per cent), glucose (5 per cent), and triglyceride (30 per cent) levels, as well as an increased insulin response (20 per cent) to oral glucose. Since the average weight gain during this period was only 1.6 kg, the observed changes appear to be secondary to increased caloric consumption, not obesity. Most of these changes returned toward baseline values during the succeeding 2 wk of increased caloric intake, but statistically significant elevations of fasting plasma glucose (10 per cent), insulin (8 per cent) and cholesterol (15 per cent) levels were still seen at the end of the hypercaloric dietary period. On the other hand, insulin resistance, as estimated by direct measurement of insulin responsiveness, did not change as a result of 3 wk of increased caloric intake. These results indicate that acute increases in caloric intake can lead to elevated plasma glucose, insulin, cholesterol, and triglyceride levels. These changes occurred before significant weight gain had taken place, and raised the possibility that at least some of the abnormalities of carbohydrate and lipid metabolism attributed to obesity may be due to increased caloric intake. However, this conclusion would not seem to apply to the insulin resistance associated with obesity, as 3 wk of increased caloric intake did not produce any change in the responsiveness of these subjects to insulin's action.

Adult↗
PubMed2002

Voluntary alcohol drinking & caloric intake in rats exposed to crowding stress.

BACKGROUND & OBJECTIVES: Alcohol intake in animals is regulated in much the same way as intake of food. The effect of alcohol on feeding behaviour is not well documented. The objective of this study was to test whether alcohol was ingested as a source of calories after crowding stress in rats. METHODS: Male albino rats were exposed to crowding stress continuously for two weeks and the effect of stress on the body weight, food intake, voluntary alcohol consumption and caloric intake in terms of food and alcohol was studied. RESULTS: A significant decrease in the body weight was seen after one (P < 0.05), 7 and 14 days (P < 0.01) of stress compared to controls. Food intake decreased significantly (P < 0.01) after one day of stress and there was recovery after 7 days stress. Absolute alcohol intake (g/kg body weight) increased significantly (P < 0.001) after one day of stress. Prolonged stress for two weeks significantly (P < 0.01) increased the alcohol consumption. Total caloric intake in stressed rats decreased significantly (P < 0.001) after acute stress. After 14 days, stressed rats showed significant (P < 0.001) increase in total caloric intake compared to day one. INTERPRETATION & CONCLUSION: Crowding stress decreased the body weight gain throughout the period of stress. Chronic stress for two weeks increased the voluntary alcohol consumption and total caloric intake. Food intake alone seemed insufficient to provide the extra demand of energy due to prolonged stress and hence, the rats may be drinking increasing amounts of alcohol (when provided) to supply the extra energy required to combat stress.

Alcohol Drinking↗
PubMed2001

Comparison of caloric intake and weight outcomes of an ad lib feeding regimen for preterm infants in two nurseries.

BACKGROUND: Effects on caloric intake and weight gain of an ad libitum (ad lib) feeding regimen for preterm infants may be specific to a special care nursery. OBJECTIVE: To explore across two nurseries the similarity of effect on caloric intake and weight gain of an ad lib feeding regimen compared with a prescribed regimen and the similarity of effect of caloric intake on weight gain. METHODS: All infants participating in the multi-site randomized clinical trial (RCT) of the ad lib feeding regimen were <35 weeks gestational age at birth and had birth weight appropriate for gestational age. Data on caloric intake and weight gain were collected at two nurseries (A, n=22; B, n=78) with the same feeding regimen protocols. Two strategies were used to explore similarity of regimen effect on caloric intake and weight gain. Repeated measures analysis of variance (ANOVA) was used to examine the effect on caloric intake and weight gain of time, feeding regimen, and time-by-regimen interaction for each nursery. RESULTS: In both nurseries, regimen effects were reasonably consistent for caloric intake and weight gain. Caloric intake was lower across nurseries for infants fed ad lib. After accounting for caloric intake, the ad lib regimen did not affect weight gain. The time-by-regimen interaction effect on caloric intake was significant in both nurseries. Caloric intake for infants fed ad lib increased significantly over 5 days. CONCLUSIONS: Despite differences between nurseries in infant characteristics and in protocol implementation, the feeding regimen effect was consistent for caloric intake and weight gain. Further support was found for the development of infant self-regulatory capacity.

Analysis of Variance↗
PubMed1976

Effects of marihuana use on body weight and caloric intake in humans.

Body weight and caloric intake were measured in a group of heavy and casual marihuana users prior to, during and following 21 days of marihuana smoking under research ward conditions. A group of control subjects were studied under identical conditions, but they did not smoke marihuana. Both heavy and casual marihuana users had a significant increase in caloric intake and gained weight during the marihuana smoking period. Heavy and casual users gained an average of 3.7 and 2.8 lbs respectively during the first 5 days of marihuana smoking. In contrast, control subjects gained only a small amount of weight (0.2 lbs) during the same time interval. Water retention did not appear to be a major factor in weight gain by the marihuana users. These findings are in agreement with both anecdotal reports and previous experimental data that marihuana use is associated with increased caloric intake and weight gain.

Body Weight↗
PubMed1999

Adaptive role of caloric intake on the degenerative disease processes.

Carcinogenicity and aging are characterized by a set of complex endpoints, which appear as a series of molecular events. Many of these events can be modified by caloric intake. Since most of these processes determine an organism's ability to cope with various environmental stressors, it is not surprising that a relationship (in the presence of a constant nutrient density) exists between caloric intake and time-to-tumor and/or life span. Our studies have clearly shown that generally, the greater the caloric intake, the greater the body weight, the higher the incidence of spontaneous tumor occurrence, the greater the susceptibility to chemical carcinogens, and the shorter the life span. It is also recognized that variables other than body weight influence the life span and carcinogenesis. We have focused our attention on the questions of how and to what extent caloric intake modifies those homeostatic processes believed to be critical in determining the ability of an organism to cope with endogenous and exogenous stresses such as chemical, physical, and biological carcinogens. The response of an organism to its environment can be divided into four categories--physiological, metabolic, molecular, and cellular. We have found that, from a physiological perspective, decreasing caloric intake causes body temperature in rodents to be decreased by 0.5 to 1.8 degrees C and water consumption to be increased by 80%, as is running activity. However, metabolic output per gram of lean body mass is not altered. Reproductive capacity declines, whereas the ECG waveform is preserved as caloric intake decreases. Alterations in these and other physiological functions suggests that energy intake serves as a signal to up-regulate or down-regulate functions related to the flight-or-fight response observed in placental mammals. A number of key metabolic pathways are altered as a function of lowered caloric intake, even though the rate of food consumption per gram of lean body mass remains steady during body weight decreases caused by decreasing caloric intake. Pharmacological compartmentalization, however, is altered. As caloric intake declines, changes occur in the expression of a number of drug-metabolizing enzymes, with the most striking effect seen in sex-specific growth hormones and liver-dependent phase I and phase II enzymes. Additionally, oxidative stress (free-radical and mediated damage to macromolecules) appears to decrease as a function of reduced caloric intake. A number of molecular processes also change with changes in energy consumption. Our studies have shown that, regardless of the source and nature of DNA damage, DNA repair is better preserved and/or enhanced when caloric consumption decreases. In addition, the fidelity of DNA replication increases and oncogene expression is stabilized, P53 gene expression is increased, and apoptosis is elevated by up to 500% with decreased caloric intake. At the cellular level, cell proliferation is decreased in direct proportion to lower energy intake in some but not all tissues. Studies have also shown an enhancement in immune capacity, changes in IGF1, and accelerated rates of wound healing proportionate to declines in energy consumption. Our most recent findings, however, have shown that the benefits associated with decreases in caloric intake only occur in the presence of sufficient nutrient quality and density. In the absence of proper nutrition, however, sensitivity to carcinogens and toxic substances appears to be enhanced. These findings are supported by independent studies. These observations have led us to conclude that, in certain organisms, when caloric intake is decreased, there is an up-regulation of those processes that modulate the responses to a wide range of environmental stressors. This response allows for a better survival rate and a down-regulation of reproductive activity. It is our belief that, during periods of environmental stress, these systems may be essential to perpetu

Adaptation, Physiological↗
PubMed2003

Caloric intake in medical ICU patients: consistency of care with guidelines and relationship to clinical outcomes.

STUDY OBJECTIVES: To assess the consistency of caloric intake with American College of Chest Physicians (ACCP) recommendations for critically ill patients and to evaluate the relationship of caloric intake with clinical outcomes. DESIGN: Prospective cohort study. SETTING: Adult ICUs at two teaching hospitals. PARTICIPANTS: Patients with an ICU length of stay of at least 96 h. MEASUREMENTS AND RESULTS: On ICU admission, severity of illness (ie, simplified acute physiology score II) and markers of nutritional status (ie, serum albumin level and body mass index) were recorded. The route of feeding (ie, enteral or parenteral), actual caloric intake (ie, percentage of ACCP recommendations: 0 to 32% [tertile I]; 33 to 65% [tertile II]; >/==" BORDER="0"> 66% [tertile III]), and evidence of GI intolerance (ie, gastric aspirate levels, >/==" BORDER="0"> 100 mL) were recorded daily. The following outcomes were assessed: status on hospital discharge (alive vs dead); spontaneous ventilation before ICU discharge (yes vs no); and ICU discharge without developing nosocomial sepsis (yes vs no). The average caloric intake among 187 participants was 50.6% of the ACCP targets and was similar in both hospitals. Caloric intake was inversely related to the mean number of gastric aspirates >/==" BORDER="0"> 100 mL/d (Spearman rho = -0.04; p = 0.06), but not to severity of illness, nutritional status, or route of feeding. After accounting for the number of gastric aspirates >/==" BORDER="0"> 100 mL, severity of illness, nutritional status, and route of feeding, tertile II of caloric intake (vs tertile I) was associated with a significantly greater likelihood of achieving spontaneous ventilation prior to ICU discharge. Tertile III of caloric intake (vs tertile I) was associated with a significantly lower likelihood of both hospital discharge alive and spontaneous ventilation prior to ICU discharge. CONCLUSIONS: Study participants were underfed relative to ACCP targets. These targets, however, may overestimate needs, since moderate caloric intake (ie, 33 to 65% of ACCP targets; approximately 9 to 18 kcal/kg per day) was associated with better outcomes than higher levels of caloric intake.

APACHE↗
PubMed2004

Age-related decline in caloric intake and motivation for food in rhesus monkeys.

Human studies have documented age-related declines in caloric intake that are pronounced at advanced ages. We examined caloric intake from a longitudinal study of aging in 60 male and 60 female rhesus monkeys (Macaca mulatta) collected for up to 10 years. Monkeys were provided a standardized, nutritionally fortified diet during two daily meals, and intake was measured quarterly. About half of the monkeys were on a regimen of caloric restriction (CR) representing about a 30% reduction in caloric intake compared to controls (CON) of comparable age and body weight. CR was applied to determine if this nutritional intervention retards the rate of aging in monkeys similar to observations in other mammalian studies. Following reproductive maturity at 6 years of age, there was a consistent age-related decline in caloric intake in these monkeys. Although males had higher intake than females, and CON had higher intake compared to CR, the sex and diet differences converged at older ages (>20 years); thus, older CR monkeys were no longer consuming 30% less than the CON. When adjusted for body weight, an age-related decline in caloric intake was still evident; however, females had higher intake compared to males while CR monkeys still consumed less food, and again differences converged at older ages. Motivation for food was assessed in 65 of the monkeys following at least 8 years in their respective diet groups. Using an apparatus attached to the home cage, following an overnight fast, monkeys were trained to reach out of their cage to retrieve a biscuit of their diet by pushing open a clear plastic door on the apparatus. The door was then locked, and thus the biscuit was irretrievable. The time spent trying to retrieve the biscuit was recorded as a measure of motivation for food. We observed an age-related decline in this measure, but found no consistent differences in retrieval time between CR and CON groups of comparable age and time on diet. The results demonstrate an age-related decline in food intake and motivation for food in rhesus monkeys paralleling findings in humans; however, we found no evidence that monkeys on a long-term CR regimen were more motivated for food compared to CON. Examining the relationship of selected blood proteins to food intake following 7-11 years on the study, we found a negative correlation between globulin and intake among males and females after accounting for differences in age. In addition, a positive correlation was observed between leptin and intake in males.

Age Factors↗
PubMed2003

Exercise, body mass index, caloric intake, and cardiovascular mortality.

BACKGROUND: The association of physical inactivity and elevated body mass index (BMI) with cardiovascular disease (CVD) risk is well established. The relationship of dietary caloric intake and CVD risk is less certain. METHODS: The epidemiologic follow-up of the First National Health and Nutrition Examination Survey (1971-1992) was examined to determine the relationship of caloric intake, BMI, and physical activity to CVD mortality. Of 14,407 participants, 9790 subjects aged 25 to 74 years met inclusion criteria. The CVD mortality rate was the outcome. RESULTS: During the 17 years of follow-up, there were 3183 deaths, 1531 of which were due to CVD (9.11/1000 person-years). People with relatively less physical activity, lower caloric intake, and who were overweight (BMI 25 to 29.9 kg/m(2)) and obese (BMI > or =30 kg/m(2)) had a less favorable baseline CVD risk profile than did those who were more active and of normal weight and had greater caloric intake. Age- and race/ethnicity-adjusted CVD mortality rates were highest among those with the least physical activity and lowest caloric intake, and who were overweight or obese. Moreover, subjects of normal weight who exercised most were more likely to have high caloric intake and lower CVD mortality (5.9 vs 14.7 per 1000 person-years, p =0.01) than subjects who were obese and exercised least. In Cox regression analysis, controlling for relevant CVD risk factors, least physical activity was independently associated with increased CVD mortality (hazard ratio=1.32, 95% confidence interval [CI]=1.13-1.53); and obesity was associated with increased CVD mortality (hazard ratio=1.24, 95% CI=1.06-1.44). Although highest dietary caloric intake was associated with reduced CVD mortality (hazard ratio=0.83, 95% CI=0.74-0.93), after adjusting for physical activity and BMI, there was no significant association of highest caloric intake with CVD mortality (hazard ratio=0.91, 95% CI=0.81-1.01). CONCLUSIONS: In this large general population sample, lower levels of physical activity and obesity were independently associated with decreased CVD survival. Moreover, when BMI, physical activity, and other relevant characteristics were taken into account, caloric intake was not related to CVD mortality.

Adult↗
PubMed1987

Caloric intake, body weight, and cancer: a review.

The literature is reviewed for evidence concerning the relation between caloric intake, body weight, and cancer. Convincing experimental data regarding caloric intake and benign and malignant tumor incidence have been available since the 1940s and demonstrate that caloric restriction significantly reduces tumor incidence for a variety of tumor types in several animal models. Some epidemiological investigations provide evidence for a positive calorie-cancer association in humans, although it is difficult (in these studies) to separate the effects of calories per se from those of dietary fat. A larger number of investigations have evaluated body weight alone, and high relative body weight or high caloric intake has been associated with increased risk of cancer of the breast, colon, rectum, prostate, endometrium, kidney, cervix, ovary, thyroid, and gallbladder. In contrast, lung, bladder, and stomach cancers appear to be inversely associated with body weight, and some prospective studies of men demonstrate greater total cancer mortality among lean individuals. However, in their analyses, few of these latter investigations considered the effects of cigarette smoking, antecedent illness, or competing causes of death. While the relations between caloric intake, other dietary macronutrients (e.g., fat), and body weight are complex and require further investigation, a complete review of the data suggests that reducing caloric intake and relative body weight may lead to a considerable decrease in cancer risk in humans.

Animals↗