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PubMedDate not supplied

Qualitative versus quantitative caloric intake: are they equivalent paths to successful aging?

With the increasing demands placed on our society to perform better for longer, in addition to the large increase in the old segment of our population, a race has begun to forestall or reverse the ubiquitous declines that emerge from growing old. Currently, little is known about the mechanisms responsible for the neuronal degeneration seen during both normal aging and neurodegenerative disease; however, among the prime candidates responsible for producing these effects are free radicals. It has been hypothesized that brain aging results from a progressive inability to cope with such insults as oxidative stress and inflammation. As a result, this inability provides a fertile environment for the subsequent development of neurodegenerative disease. Therefore, if the preservation of neuronal function and associated cognitive and motor performance during aging will enhance the probability of aging successfully, then it is of crucial importance to find ways to preserve or decrease the responsiveness of the brain to these insults. The purpose of this review is to discuss two strategies, caloric restriction and antioxidant supplementation (through foods and supplements), both proven to be successful at protecting the brain from age-related oxidative insults. The two interventions will be compared and contrasted in terms of their effectiveness, safety, and generalization capacity for human treatment.

Aged↗
PubMed1984

The relationships of transcephalic impedance, head growth and caloric intake to outcome in preterm infants.

Twenty-two preterm infants with birth weights less than 1 400 g were measured weekly with transcephalic impedance and occipital-frontal head circumference. Mean caloric intake/kg/day was calculated weekly. All infants were assessed at one year of age with Bayley Mental and Motor Scales and neurological assessment. Univariate and multivariate analyses were performed indicating that transcephalic impedance was the most powerful of the three measures as a predictor of sequelae.

Birth Weight↗
PubMed1958

Importance of caloric intake during renal failure.

Loss of excretory function in acute renal failure results in the retention of catabolites and fluid. In the absence of available carbohydrate, endogenous fat and protein become the main caloric sources. This results in the rapid accumulation of keto acids and nitrogenous wastes. By providing readily available non-nitrogenous calories, protein catabolism is reduced, complete oxidation of fat is obtained and energy is provided to drive potassium into the intracellular compartment. The patient should be encouraged to eat despite his apathy, fear of vomiting and characteristically paranoid mood. Tube or parenteral feeding is complicated by the need to restrict fluid. Numerous small feedings are more successful than large meals. Hard candy and alcohol are often acceptable sources of calories, fat emulsions seldom. Oral hygiene aids feeding, and tranquilizers and anticholinergics are useful. If the patient does not take food by mouth, tube feeding may be carried out. Because of the bleeding tendency so often occurring in uremia, tube feeding may be contraindicated if it causes erosion of the pharynx or esophagus. Intravenous infusion of invert sugar, glucose and alcohol may be necessary if nutrition cannot be accomplished by other means.

Acute Kidney Injury↗
PubMed1984

Caloric intake and Na+-K+-ATPase: differential regulation by alpha 1- and beta-noradrenergic receptors.

This study examined the effects of diet and treatment with noradrenergic receptor antagonists on weight gain and indices of Na+-K+-adenosine triphosphatase (ATPase) activity in the rat. When rats were fed a palatable cafeteria diet, their caloric consumption increased by about 80%, but they did not gain weight significantly. Ouabain binding and K+-p-nitrophenylphosphatase (NPPase) activity were increased in brown adipose tissue and soleus. These indices remained elevated after the rats were returned to a regular diet. When rats were fasted for 3 days, they lost weight, and the indices of Na+-K+-ATPase activity were markedly reduced in brown adipose tissue and soleus. After refeeding the fasted rats gained weight three times more rapidly than nonfasted rats with similar food intake. Indices of Na+-K+-ATPase activity remained as low as they had been when the rats were fasting. There was a consistent negative correlation between weight gain per calorie eaten and brown adipose tissue NPPase activity. Changes in Na+-K+-ATPase could therefore be involved in the effects of overfeeding and fasting on metabolic efficiency. Desmethylimipramine binding was increased by cafeteria diet and decreased by fasting, consistent with changes in sympathetic nervous system activity. Treatment with prazosin, an alpha 1-noradrenergic receptor antagonist, reduced Na+-K+-ATPase in either control or cafeteria diet-fed rats but did not alter the effect of cafeteria diet feeding. By contrast, treatment with propranolol, a beta-receptor antagonist, prevented the increase in Na+-K+-ATPase during cafeteria diet feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Nitrophenylphosphatase↗
PubMed1990

Quantitative contribution of factors regulating rat colonic crypt epithelium: role of parenteral and enteral feeding, caloric intake, dietary cellulose level and the colon carcinogen DMH.

To elucidate the role and quantitative contribution of several exogenous factors which may regulate colon crypt mitotic activity, proliferative zone height (PZH) and crypt height, groups of rats were subjected to various feeding regimens both with and without treatment with the colon carcinogen, 1,2-dimethylhydrazine (DMH). The rats were divided into two major groups and one group was given eight weekly injections of DMH base at 9.5 mg kg-1 body weight. Throughout this period and for two additional weeks the rats were isocalorically fed either a defined nutritionally complete diet with different levels of dietary cellulose or they were parenterally (i.v.) fed a nutritionally complete liquid formula with different caloric levels. The rats were then injected with colchicine 3 h prior to sacrifice to arrest and to collect dividing cells at metaphase. The results of multiple regression analysis of all data were interpreted to indicate that parenteral feeding caused dramatic suppression of the colon crypt height (CH) and of the number of metaphase figures per crypt (MC). Increased cellulose intake stimulated CH but suppressed MC. The CH was also stimulated by DMH. CH was positively correlated to PZH and MC. The MC was suppressed by cellulose intake and negatively correlated to PZH but was positively correlated to CH. The PZH was positively correlated to CH. These findings were related to the role of luminal food, functional workload, kcal intake and treatment with DMH on the measured colon crypt parameters. A quantitative assessment of factors that regulate the measured colonic crypt parameters was accomplished.

1,2-Dimethylhydrazine↗
PubMed2005

Increased caloric intake soon after exercise in cold water.

We examined the acute effect of cold-water temperature on post-exercise energy intake (EI) for 1 h. In a randomized, crossover design, 11 men (25.6 +/- 5 y) exercised for 45 min on a submersed cycle ergometer at 60 +/- 2% VO2max in 33 degrees C (neutral) and 20 degrees (cold) water temperatures, and also rested for 45 min (control). Energy expenditure (EE) was determined using indirect calorimetry before, during, and after each condition. Following exercise or rest, subjects had free access to a standard assortment of food items of known caloric value. EE was similar for the cold and neutral water conditions, averaging 505 +/- 22 (+/- standard deviation) and 517 +/- 42 kcal, respectively (P = NS). EI after the cold condition averaged 877 +/- 457 kcal, 44% and 41% higher (P < 0.05) than for the neutral and resting conditions, respectively. Cold-water temperature thus stimulated post-exercise EI. Water temperature warrants consideration in aquatic programs designed for weight loss.

Adult↗
PubMed1989

[Effects of various caloric intakes on nitrogen metabolism of the body, the muscles and the viscera during total parenteral nutrition with aminoacidic solution enriched with branched-chain amino acids].

Nitrogen metabolism was studied in ten injured/septic patients by means of a two compartment model, differentiating muscle from non muscle (central) tissue. During fasting muscle tissue loses a consistent amount of aminoacids which is retained in part by central tissue, giving rise to a positive nitrogen balance, whilst three methyl histidine and body nitrogen output are elevated. Total parenteral nutrition (glucose 15 kcal kg-1 day-1, nitrogen 0.30 g kg-1 die-1) improved body nitrogen balance and three methyl histidine excretion, but did not affect significantly either muscle or central nitrogen balance. Increasing caloric support to 30 kcal kg-1 day-1 did not showed any further effect on body nitrogen balance and three methyl histidine, while it improved significantly vs basal muscle nitrogen balance, but did not affect central nitrogen balance.

Amino Acids, Branched-Chain↗
PubMed1999

The relationships of animal age and caloric intake to cellular replication in vivo and in vitro: a review.

This brief review examines aging at the cellular level as expressed by cell replication rates in vivo, clone size limits in vitro, and cell function in several tissues and organs. Studies are presented in which in vivo and in vitro cell replication measurements were made for several cell types and organs in relation to animal age, diet, life span, and specific age-related pathologies. Among the events examined that affect cell replication and cell survival in vitro and in vivo over a lifetime are oxidative damage, telomere shortening, and hormone and hormone receptor level changes. Long-term caloric restriction (CR) is favorable or protective for all of these events when measured in later life and comparisons are made to ad libitum (AL)-fed animals, and it is accompanied by more youthful rates of cell replication. It is proposed that in vivo and in vitro measures of cellular replication constitute biomarkers of aging when applied to comparisons of CR and AL diet rodents, where they correlate with the delay of disease and extension of life span. Longitudinal studies are needed to confirm this. The occurrence of certain age-related pathophysiologic states, such as immune (T cell) insufficiency, cataract, and senile osteopenia/osteoporosis, are accompanied by major diminishments of replication rates, numbers, and functions of the essential cell types in the organs and tissues involved. However, direct evidence is lacking that diminished cell replication in specific organs contributes to the limitation of life span.

Aging↗
PubMed2003

Growth hormone-mediated breakdown of body fat: insulin and leptin responses to GH are modulated by diet composition and caloric intake in old rats.

This work was performed to elucidate whether growth hormone (GH)-mediated loss of adipose tissue and responses in plasma insulin and leptin are modulated by diet composition. 12-month-old rats were first fed a high-fat (HF) diet or a low-fat (LF) diet for 14 weeks. After that, GH or saline was administered to rat groups that were maintained on either HF or LF diets or that were switched from the HF to the LF diet. All 6 groups had free access to food. One additional saline group was pair-fed with the GH group that was switched from the HF to the LF diet. The caloric consumption of this latter group was also translated to yet another GH group receiving restricted amounts of the HF diet. GH was given in a total dose of 4 mg/kg/d for three weeks. After sacrifice, blood was collected and tissues were excised. In groups injected with saline, the weight of excised adipose tissue was 60 +/- 4.7, 41 +/- 3.8 and 50 +/- 4.5 g in animals that continued with the HF diet, LF diet, or that were switched from HF to LF, respectively. Corresponding figures after GH treatment were significantly (p < 0.05) decreased to 38 +/- 2.7, 30 +/- 2.3, and 31 +/- 2.7 g, respectively. Pair-feeding had no effect, whereas only 26 +/- 3.0 g of adipose tissue was retrieved in rats fed restricted amounts of HF diet while receiving GH. In this group, plasma insulin and leptin were also significantly (p < 0.05) depressed compared with other GH groups, especially to the group fed the unrestricted HF diet (203 +/- 35 vs. 1345 +/- 160 pmol/l and 9.3 +/- 1.2 vs. 31 +/- 4.4 micro g/l). In conclusion, this study shows that GH mediates breakdown of adipose tissue under a variety of dietary conditions, and that induction of hyperinsulinemia can be prevented if GH treatment is combined with restricted feeding of a diet which is relatively low in carbohydrates and rich in fat. This will also promote a fall of plasma leptin.

Adipose Tissue↗
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↗