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At least 163 records · Page 9Linked to original sources
PubMed1986

Hypotheses regarding caloric intake in cancer development.

The epidemiologic evidence on fats as related to cancer has until recently been equivocal. Some studies showed an inhibitory effect, some showed no effect, and a few showed a reduction in risk. More recently, however, epidemiologic inquiries have suggested that fats may be associated with increased risk of cancer of the breast, prostate, cervix, colon, rectum, larynx, and lung. The relationship is not a simple one. There is evidence that a high level of total calories ingested, regardless of whether the source is fats, carbohydrates, or proteins, increases risk. Still other studies suggest that calorie expenditure may be the important fact. Thus, obesity, derived from whatever source, may be etiologically related to some cancers. Fats being a potentially important contributor to obesity over the long term, may in this way increase risk.

Diet Surveys↗
PubMed1996

Effect of age and caloric intake on protein oxidation in different brain regions and on behavioral functions of the mouse.

The objective of this study was to determine if oxidative stress/damage is a possible causal factor in the senescence-related loss of brain functions in the mouse. If such a relationship indeed existed, it was expected that oxidative protein damage would increase with age within regions of the brain associated with senescence-related functional loss, and that calorie restriction, an intervention which retards certain aspects of age-associated functional loss, would reverse such increases. Dietary restriction was found to retard age-associated decline of sensorimotor coordination and improve performance of aged mice on an avoidance learning problem. Protein carbonyl concentration, one measure of protein oxidation, increased from 8 to 27 months of age in most regions of the mouse brain, with the most notable increases occurring in the striatum and hippocampus, regions of the brain strongly implicated in age-associated functional loss. Age-associated loss of protein sulfhydryls was more uniform across brain regions and did not involve the hippocampus. Dietary restriction resulted in reversal of the age-associated regional trends in carbonyl and sulfhydryl concentration, with the largest changes occurring within the striatum. Cross over studies in aged calorie restricted and ad libitum fed mice indicated that lowering of carbonyl content by calorie restriction could be induced or reversed within a time frame of 3 to 6 weeks. These findings suggest that the beneficial effects of dietary restriction upon brain function and life span may depend upon its ability to acutely reduce steady-state levels of oxidative stress.

Aging↗
PubMed1993

Effect of activation of the serotoninergic system during prolonged starvation on subsequent caloric intake and macronutrient selection in the Zucker rat.

Starvation or dietary restriction are known to modify post-fasting dietary self-selection. We have examined the effects of activation of the serotoninergic system and food deprivation on macronutrient self-selection following a period of starvation. Rats were starved for 4 days and either treated or not with dl-fenfluramine or fluoxetine. Starved untreated animals showed a post-fasting anorexia and an increased preference for carbohydrate intake, even though lipids remained the preferred source of calories. Treatment with fenfluramine or fluoxetine increased post-fasting anorexia, abolished the preference for carbohydrates and decreased lipid intake. Fluoxetine, but not fenfluramine, resulted in decreased protein intake as well. Following a 2-day refeeding period ad libitum, during which the animals were not treated with drugs, the anorectic effect of fenfluramine disappeared but that of fluoxetine remained unchanged. In addition, we noted that at an equimolar dose to dl-fenfluramine (100 mumol/kg/day) fluoxetine treatment resulted in the death of all the animals in the group by the second day of refeeding; no deaths were observed in any of the other groups. In conclusion, we confirm a post-starvation anorexia and increased carbohydrate intake following long-term fasting. In addition we show that activation of the serotoninergic system abolishes the increase in carbohydrate intake and potentiates post-starving anorexia.

Animals↗
PubMed1995

Low-fat diets do not lower plasma cholesterol levels in healthy men compared to high-fat diets with similar fatty acid composition at constant caloric intake.

In most studies reporting the effects of high-fat (HF) and low-fat (LF) diets on human plasma fatty acids (FA) and lipoprotein levels, the design involved adding to the diet an oil that had an FA composition (FAC) very different from the FAC of the control diet. Thus, it is difficult to determine if simply reducing the fat content of the diet without changing the dietary FAC changes the tissue FAC or alters plasma lipid levels. In this study, we fed diets that contained either 22 or 39% of calories from fat, but had no differences in their FAC, for 50 d to a group (n = 11) of healthy men (20-35 y). Thus, the polyunsaturated/saturated ratios (1.0) of the diets were identical as were the n-3/n-6 ratio and the monounsaturated-to-total fat ratios. The diets contained (wt% of total fat) approximately 28% saturated FA, 33% monounsaturated cis-FA, 6% monounsaturated trans-FA, 22% n-6 polyunsaturated FA, and 7% n-3 polyunsaturated FA, and 4% other minor FA. The diets consisted of natural foods and were formulated to contain 16 en% protein, either 45 or 62 en% carbohydrate (CHO) and at least the recommended daily allowance for all micronutrients. Both diets contained 360 mg of cholesterol per day. All subjects were given the HF diet for 20 d, and then six were placed on the LF and the other five remained on the HF diet for 50 d. The two groups were crossed-over for the remaining 50 d of the study. The subjects' baseline total cholesterol level was 173 mg/dl, after 50 d on the HF diet it was 177 mg/dl and after 50 d on the LF diet, 173 mg/dl. The differences were not significant, and there were no significant changes in either the LDL or HDL cholesterol levels with either diet. Triglyceride levels, and consequently very low density lipoprotein levels, rose significantly on the LF, higher CHO diet compared to the levels found in the subjects on the HF diet (91.5 and 66.4 mg/dl respectively, P < 0.002). The linoleic acid content of the plasma, platelets, and red blood cells was significantly (P < 0.05) reduced in the LF diet compared to HF diet, without any obvious physiological effects. Hence, many earlier observations indicating reductions in plasma lipid levels when people are on LF diets may be due to changes in the FAC of the diet, not the reduction in fat calories.

Adult↗
PubMed2006

Reductions in caloric intake and early postnatal growth prevent glucose intolerance and obesity associated with low birthweight.

AIMS/HYPOTHESIS: Low birthweight (LBW) and rapid postnatal weight gain, or catch-up growth, are independent risk factors for the development of obesity and diabetes during adult life. Individuals who are both small at birth and have postnatal catch-up growth are at the highest risk. We hypothesised that dietary interventions designed to attenuate catch-up growth in LBW subjects may have long-term beneficial consequences. MATERIALS AND METHODS: We used our previously described mouse model of LBW-associated diabetes, created by restricting maternal food intake to 50% during the last week of gestation. Control (C) dams and dams that had been subjected to undernutrition (U) were then provided either chow ad libitum after delivery or 50% food restriction on a per-day basis from delivery until weaning. We designated the resulting four groups control-control (CC), undernutrition-control (UC), control-undernutriton (CU) and undernutrition-undernutrition (UU), indicating the prenatal and postnatal experimental conditions, respectively. Carbohydrate metabolism and adiposity were assessed prospectively in offspring until age 6 months. RESULTS: Males that were small at birth and exhibited early postnatal catch-up growth developed glucose intolerance and obesity by age 6 months. In contrast, LBW mice without catch-up growth (UU) remained smaller than controls (CC), and glucose intolerance and obesity was prevented. Similarly, mice with normal birthweight that had blunted catch-up growth (CU) were leaner and had better tolerance test than CC mice. Catch-up growth during the first week of life correlated better than birthweight with glucose, fat mass and glucose tolerance up to 6 months of age. CONCLUSIONS/INTERPRETATION: Prevention of early catch-up growth reversed the development of glucose intolerance and obesity in our mouse model of LBW-associated diabetes.

Diet, Reducing↗