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Rhesus monkeys inhibited their feeding in response to intragastric nutrient preloads, so as to maintain a constant caloric intake. There is a definite dose- response relationship to calories which does not depend on the volume, caloric concentration, or nature of the nutrient. This accurate control is accomplished even though some of the preload remains in the stomach throughout the feeding period.
There is a diurnal rhythm in ACTH responses to stressors that peaks, in nocturnally feeding rats, at the time of lights on, in the morning (AM). To determine whether this rhythm is subordinate to the rhythm in food intake, we tested the effects of removing food during the night or the day on ACTH responses in the AM or evening (PM) to the stimulus of restraint in 5-day-adrenalectomized rats. An overnight fast reduced the ACTH response to restraint with tail blood sampling in the AM to the low magnitude observed in the PM in rats fed ad libitum; by contrast, a fast of equivalent duration imposed during the day had no effect on the ACTH response to the stressor in the PM. Short term fasts did not alter the normal AM-PM rhythm in basal ACTH levels. The fasts did, however, significantly decrease the pituitary ACTH concentration at both times of day, suggesting that lack of food had stimulated ACTH secretion during the preceding 14 h. Providing calories by either gavage or manipulation of food presentation increased ACTH responses to restraint in fasted adrenalectomized rats in both the AM and PM. Although four of four experiments showed that provision of calories to fasted rats resulted in increased ACTH responses to the stimulus of restraint, none of the manipulations of caloric intake fully restored ACTH responses in fasted rats to the high amplitude observed in ad libitum fed rats in the AM. We conclude that 1) unlike the circadian rhythm in basal activity in the hypothalamic-pituitary-adrenalocortical (HPA) system, the diurnal rhythm in ACTH responsiveness to stimuli is tightly coupled to the endogenous rhythm in energy intake; and 2) caloric deprivation per se appears to activate the HPA system at some time during the 14- to 17-h fast, but does not produce the normal facilitation in the AM response to acute restraint that is induced by chronic or prior stimulation of the HPA axis.
The primary aim of this experimental investigation was to examine the effects of short-term dietary restriction on caloric consumption in eating disordered subjects. Subjects with bulimia nervosa, binge eating disorder, and overweight non-eating disordered subjects, attended a laboratory experiment during which they were randomly assigned to either a 1 h or a 6 h food deprivation condition prior to being served a multi-item buffet. The primary measure of interest was calories consumed during the laboratory experiment. Subjects deprived of food for 6 h consumed significantly more calories at the buffet compared to subjects in the 1 h food deprivation condition. However, caloric intake during the entire laboratory day was not affected by the experimental manipulation. Subjects in the longer deprivation condition apparently compensated at the buffet for the caloric restriction, but did not overcompensate.
Blood glucose, gastric inhibitory polypeptide (GIP), vasoactive intestinal polypeptide (VIP) and gastrin secretions were measured over a three-hour period following the ingestion by normal subjects of a mixed meal with two different caloric levels (1055 Kcal and 1192 Kcal). No VIP secretion was observed after either meal. Gastrin release was not modified by the increase of caloric intake (mainly carbohydrates and lipids), whereas GIP secretion was significantly more important after the meal with the highest caloric value (peak at 30 mm: 499.5 +/- 250.4 vs. 273.4 +/- 128.7 pg/ml and integrated response 53.3 +/- 20.5 vs. 28.2 +/- 9.9 ng X ml-1 X 180 min-1-p less than 0.05). This difference could not be attributed to glucose since the blood glucose levels were not significantly different. It is more probably related to the total amount of ingested food. This suggests the existence of rapid mechanisms of adaptation to the incoming load of the GIP-producing cells.
The interrelationship and reliability of three different activity measures were examined in 76 postmenopausal women. The women wore Large Scale Integrated (LSI) activity monitors, completed the Paffenbarger Activity Survey, and completed 3-day food logs for determination of caloric intake/expenditure. The Paffenbarger survey was assessed twice, a year apart. The results indicated that caloric intake was a very poor index of activity. The LSI activity monitoring and Paffenbarger survey were both effective, reliable measures of physical activity. However, they appeared to measure somewhat different aspects of physical activity. The LSI measured physical activity associated with movement, whereas the surveys measured the intensity component of energy expenditure. The research indicated that it is important to evaluate the characteristics of the activity of interest in order to select a physical activity tool for assessing activity patterns in older women.
Patients with bulimia (binge-purge syndrome) frequently complain that they consume a very restrictive diet to avoid gaining weight. To investigate this claim, 23 hospitalized bulimic patients were assessed daily for body weight, caloric intake, macronutrient diet content, activity measures, and body composition estimates during weight-stable periods. Bulimic patients ate fewer kilocalories per kilogram body weight (22.1 +/- 4.6 kcal/kg) than did age-matched normal women (29.7 +/- 6.5 kcal/kg) but had similar activity levels and body composition. Clinical variables, such as history of laxative abuse, anorexia, or obesity, and physiological characteristics, such as body weight, activity level, or dietary content, could not account for this difference in caloric consumption. Bulimic patients tended to eat a diet lower in fat and higher in protein than did control subjects. These results agree with observations of increased efficiency of caloric utilization in obese patients and support patient complaints of a tendency to gain weight easily.
A nutritional evaluation was performed in 72 patients with advanced solid tumors receiving chemotherapy: 35 patients (49%) were considered malnourished and 37 (51%) were considered normal. The malnourished group showed a significantly lower caloric intake than the normal group (1214 +/- 360 vs 2088 +/- 607; P less than 0.001) and a higher incidence of severe depression (16 of 27 patients [59%] vs six of 30 [20%]; P = 0.026). No significant difference was found between the normal and malnourished patients in reference to emesis, glucose tasting threshold, or tumor burden.
Previous reports have described a syndrome of paresthesias, weakness, seizures and hypophosphatemia in patients and animals receiving intravenous hyperalimentation. In this report we describe a group of five patients who developed this syndrome while on oral caloric intake and three patients who received only modest amounts of hyperalimentation therapy. As an experimental corollary, studies were performed in starved and normal dogs with calories infused via an intragastric catheter. The serum inorganic phosphorus (Pi) fell slightly in normal animals from 4.8-2.5 mg. %. In the starved dogs with diarrhea or vomiting the Pi fell gradually from 4.8-1.6. In starved dogs without gastrointestinal symptoms the Pi fell precipitously from 3.7-1.4 mg % on the first day of infusion and remained at that level. Approximately 50% of the starved animals developed the neurological syndrome; none of the normal animals had neurological symptoms.
The inverse relationship between smoking and body weight may be due in part to nicotine's effects on reducing hunger and eating. Male smokers and nonsmokers (n = 10 each), abstinent overnight from smoking and food, participated in four sessions, involving consumption of a liquid caloric load or water followed by nicotine (15 micrograms/kg) or placebo via nasal spray every 20 min for 2 h. Hunger and satiety ("fullness") ratings were obtained prior to each dose presentation. At the end of the two sessions involving the caloric load (simulating breakfast), subjects were also presented with typical lunch/snack food items varying in sweet taste and fat content for ad lib consumption. Results indicated that, for both smokers and nonsmokers, the hunger-reducing effects of nicotine occurred only following caloric load consumption, and there was no effect of nicotine on hunger afer water consumption. Smokers unexpectedly reported greater satiation than nonsmokers following the caloric load regardless of nicotine or placebo condition. Nicotine also resulted in less caloric intake during the meal, and the decrease was not specific to consumption of sweet, high-fat foods. These results indicate that nicotine reduces appetite, possibly helping to explain the influence of smoking on body weight.
UNLABELLED: We have compared, using non protein RQ method, energy expenditures of diarrheic patients with intraperitoneal or intraluminal suppuration and feed enterally (group II) or intravenously (group III). Five non suppurative diarrheic patients feed enterally were studied as control (group I). Carbohydrate, protein and fat intakes were not significantly different in the 3 groups of patients. Patients of group II metabolized significantly less of carbohydrate (p less than 0.01) and more of fat (P less than 0.01) than groups I and III patients. Carbohydrate and fat expenditures of patients of groups I and III were not significantly different. CONCLUSION: 1) There is a possible trouble of carbohydrate absorption in suppurative diarrheic patients. 2) Therefore caloric intake must be preferably parenteral in these patients.
Fifteen fullterm female infants were enrolled in each of two feeding groups and all but one completed the proposed period of observation to age 112 days. Formulas prepared from the same ingredients (fat-free milk solids, a mixture of corn and coconut oils, lactose, vitamins and minerals) were fed ad libitum to both groups. Formula concentration was 54 kcal/100 ml for one group and 100 kcal/100 ml for the other. A limited selection of commercially prepared strained foods was permitted after 28 days of age. Weighed intakes of food were recorded for each day of study. During the internal 8 through 41 days of age, the infants fed the 54 kcal/100 ml formula consumed a considerably greater quantity of food but fewer calories than did those fed the 100 kcal/100 ml formula. Those fed the 54 kcal/100 ml formula also gained less weight. These differences between feeding groups were statistically significant. After 41 days of age, mean caloric intakes (kcal/kg/day) and rates of gain in weight were similar for the two feeding groups. The data provide a basis of speculation on the possible difference in allocation of calories to growth and non-growth in the two groups.
The cause of menstrual disturbance in athletes is still debated. Apart from the acute and chronic effects of exertion, other associated behavioral variables are suspected to play a key role. A longitudinal study with frequent blood sampling was undertaken to link information about nutrition and stress with a quantitative assessment of endocrine menstrual function in 18 endurance-trained athletes and 25 age-matched, nonathletic women. Four athletes did not show hormonal signs of follicular development. The 14 athletes with cyclic gonadal function did not differ from controls with regard to estradiol concentrations during the follicular phase and at midcycle. During the luteal phase, however, they showed significantly reduced areas under the estradiol and progesterone curves. Caloric intake, as assessed by nutritional diaries, correlated positively with the area under the progesterone curve during the luteal phase (rs = 0.70, P less than 0.01). Ratings of subjective stress in the area "partner, family, friends" correlated negatively with the luteal progesterone area (rs = 0.80; P less than 0.01). Data support the hypothesis that nutrition and stress may play a critical role in the genesis of menstrual disturbance in athletes.
This double-blind, cross-over trial was designed to assess the effects of megestrol acetate (MA) on cancer-induced cachexia. Forty consecutive malnourished patients with advanced non-hormone-responsive tumors receiving no antineoplastic treatment were randomized to receive MA 480 mg/day versus placebo for 7 days. During day 8, a cross-over was made until day 15. Appetite, pain, nausea, depression, energy, and well-being were assessed with a visual analog scale (0 to 100 mm) at 9:00 AM and 4:00 PM during days 6, 7, 13, and 14. Weight (W;kg), tricep skinfold (TS; mm), arm circumference (AC; cm), and calf circumference (CC; cm) were measured at days 1, 8, and 15. Caloric intake (CI; Kcal/day) was determined during days 6, 7, 13, and 14. In 31 evaluable patients, the percentual difference in appetite at 9:00 AM, appetite at 4:00 PM, energy, and well-being after MA was +15.1, +14, +3.2, and +5.2, versus -12 (P = 0.03), -5.1 (P = 0.015), -10 (P = 0.024), and -8.3 (not significant) after placebo. Percentual difference in W, TS, AC, and CC after MA was +0.2, +1, -0.1, and +0.4 versus -0.8 (P = 0.03), -0.8 (P = 0.001), -0.3 (not significant), and -0.5 (P = 0.04) after placebo. CI during MA was 3480 +/- 1574 (48-hour intake), versus 2793 +/- 1542 (P less than 0.001) during placebo. Patients and investigators blindly chose MA in 20 (66%, P = 0.023) and 28 cases (92%, P less than 0.001), placebo in eight and two cases, and made no choice in three and one cases, respectively. Toxicity consisted of mild edema and nausea in three and two cases, respectively. After mean follow-up of 27 +/- 13 days, on an open basis, an average increase in W and AC of 4.8 +/- 1.7 kg and 2.8 +/- 1.7 cm was observed, respectively. The authors conclude that MA is a powerful appetite stimulant with subjective and objective effects on nutritional status.
In the obese progeny of the SHR/N-cp strain of the rat the bile acid pool was at least twice as large as that in their lean littermates even when only 6 weeks old. The composition of the pool remained unchanged in the obese females, but in their male counterparts the proportion of cholic acid was significantly increased. Cholestyramine feeding reduced the pool size by 26% in the obese rats, but a similar effect also occurred in the lean animals. The obese rats consumed about 60% more food per day than their lean littermates. When obese females were pair-fed to the intake of their lean controls from 6 to 11 weeks of age, the bile acid pool remained significantly enlarged, although not to the same extent as in the obese rats fed ad lib. Plasma cholesterol levels were reduced but remained significantly higher than the levels in the lean animals. The marked hypertriglyceridemia exhibited by the obese rats fed ad libitum did not develop in their pair-fed counterparts. In contrast, there was a comparatively smaller reduction in plasma cholesterol and triglyceride levels in the obese rats fed cholestyramine. Hepatic steatosis persisted in the pair-fed animals as well as in those given cholestyramine. Restricting caloric intake significantly reduced the body weight gain of the obese rats but had little effect on the extent of their corpulence. These studies show that at least some of the characteristics of this congenic strain, including hypertriglyceridemia and hepatic and intestinal hypertrophy, are due mainly to excess dietary intake.(ABSTRACT TRUNCATED AT 250 WORDS)
Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated rats served as controls. All animals were fed lab chow for 15 postoperative days. At that time they were subdivided into two groups each. One DMNL and one control group continued to be fed lab chow until the termination of the experiment on postoperative day 116. A second DMNL and control group were fed a high-fat diet and 32% sucrose solution (HF/SS diet). All DMNL rats showed reduced body weight and linear growth, but the HF/SS diet depressed these parameters further below the levels of the chow-fed groups. Both DMNL and control rats fed HF/SS had more carcass fat, heavier epididymal fat pads, more carcass fat per calories eaten, higher plasma levels of glucose, glycerol and free fatty acids but lower insulin levels than chow-fed DMNL rats and controls. This occurred in the face of lower body weights and caloric intake. Neither growth hormone nor insulin showed lesion effects. Rats with DMNL exhibited the same inverse relationship between plasma insulin and free fatty acids as controls. The data indicate that DMNL rats respond to the HF/SS diet essentially like sham-operated controls, i.e., they develop dietary obesity. Although they do show some small deficits, their lipogenic capacity is actually significantly greater than that of HF/SS-diet fed controls.
Toxemia of pregnancy is characterized by a combination of at least two of the following clinical symptoms: hypertension, edema, and proteinuria. In three successive trials over three consecutive years, the dietary intakes of a selected number of young pregnant women attending a Maternal and Infant Care Clinic at Tuskegee Institute were evaluated for protein, amino acids, and total calories. Women with toxemia were identified, and women without toxemia served as controls. The toxemic group generally consumed more protein than the controls, but values were statistically significant only in the first trial. However, all essential amino acids were consumed in significantly greater amounts by the toxemic group. Protein and essential amino acids were consumed in adequate amounts (at least two-thirds of the RDA) by both groups but in amounts smaller than the national average. Non-essential amino acids were also consumed in adequate amounts, with the toxemic group consuming larger quantities than the controls. Caloric intakes were adequate for young pregnant women. The relationships of glucosuria and of toxemia to protein and amino acid intake were similar and were opposite to the relationship of anemia to protein and amino acid intake. Meats and grains contributed the greatest quantity of protein and amino acids to the diet in all groups. Data seem to imply that any relationship of protein and amino acids with toxemia of pregnancy is a complex one involving several possibly interrelated nutritional parameters.
Although the dysregulation of physiological signals and mechanisms controlling cell proliferation has been a major focus in cancer research, recent evidence suggests that explicit evaluation of apoptosis or physiological cell death may be equally important in understanding multistage carcinogenesis. Dietary restriction of rodents is well known to reproducibly retard development of spontaneous and chemically induced tumors. We reasoned that the decrease in metabolic and hormonal trophic factors induced with this intervention could promote selective cell deletion via apoptosis. To pursue this possibility, we quantified the spontaneous apoptotic rate in liver sections from diet-restricted (DR) and ad libitum-fed (AL) 12-month-old male C57BL/6 x C3H F1 mice, a murine strain known to develop a high incidence of spontaneous liver tumors by 18 months of age. The identification of hepatocyte apoptotic bodies was facilitated by in situ end-labeling immunohistochemistry. The basal rate of proliferation of hepatocytes was quantified utilizing proliferating cell nuclear antigen immunohistochemistry. The incidence of apoptotic bodies and total proliferating cell nuclear antigen-positive cells was enumerated in 14 mice/group by scoring 50,000 random hepatocytes/liver and expressed as the mean incidence/100 cells. When the comparison was made between diet groups, the apoptotic rate was significantly higher in the DR mice relative to the AL mice, while the proliferation rate was significantly lower (P < 0.01 and P < 0.05, respectively). The increase in spontaneous level of apoptosis and the decrease in proliferation rate in livers of DR mice were associated with a significantly lower rate of spontaneous hepatoma over a 36-month period. In summary, the results suggest that caloric intake may modulate the basal turnover rates of cell death and proliferation in a direction consistent with a cancer-protective effect in the DR mice and a cancer-promoting effect in AL mice.
The extent and time course of caloric compensation for surreptitious dilutions and supplements to the energy value of the diet were examined in free-living normal-weight adults. Ten subjects were provided lunches containing approximately 66% more or less calories than their customary midday meal for 2-wk periods which were interposed between 1-wk baseline or recovery periods. Diet records were kept throughout the study. Total energy intakes did not differ among the three control periods (weeks 1, 4, and 7) or between any of these periods and when subjects were provided the low-calorie meal. Total energy intake was significantly higher relative to all other periods when subjects ingested the high-calorie meal. To the extent that compensation occurred, it was apparent immediately and did not appear to change over the 2-wk study periods. The results suggest that humans compensate more readily for decreases than for increases in caloric intake.