Dietary intakes and activity levels of stunted and non-stunted children in Kingston, Jamaica. Part 1. Dietary intakes.

The dietary intakes of stunted and non-stunted children were measured on enrollment to a longitudinal study of growth and development. Children aged 9-24 months were recruited by house to house survey of several poor areas of Kingston. All children with height for age less than -2 SD of the NCHS standards and weight for height below the standard median were enrolled. Alternate stunted children were matched for age and sex with the non-stunted child (height for age greater than -1 SD) living nearest. Dietary information was obtained by two 24-h recalls. Mean trainer-interviewer reliability was greater than 90 per cent throughout the study. Correlation between energy intakes on the 2 days was 0.68 (P less than 0.001). Stunted children had a significantly less varied diet, fewer dairy products and fruit than non-stunted children. Protein intakes met requirements. Energy intakes were similar in both groups and approximately 200 kcal below the recommended intake. Energy and protein intakes per kg were significantly higher in the stunted children than in non-stunted children (energy P less than 0.001, protein P less than 0.005). Greater morbidity in the stunted children could account for some, but not all, of this difference. Children with lower weight for height had lower intakes (energy P less than 0.05, protein P less than 0.01). Intakes were greater in children who lived in better housing, with more household possessions and whose mothers had more skilled occupations. Good reliability and the above associations indicate that the data are valid.

Dietary intakes and activity levels of stunted and non-stunted children in Kingston, Jamaica. Part I. dietary intakes

The dietary intakes and activity levels of stunted and non-stunted children were measured on enrolment to a longitudinal study of growth and development. Children aged 9-24 months were recruited by house to house survey of several poor areas of Kingston. All children with height for age < -2 SD of the NCHS standards and weight for height below the standard median were enrolled. Alternate atunted children were matched for age and sex with the non-stunted child (height for age > -1 SD) living nearest. Dietary information was obtained by two 24-h recalls. Mean trainer-interviewer reliability was > 90 percent throughout the study. Correlation between energy intakes on the 2 days was 0.68 (P < 0.001). Stunted children had a significantly less varied diet, fewer dairy products and fruit than non-stunted children. Protein intakes met requirements. Energy intakes were similar in both groups and approximately 200 kcal below the recommended intake. Energy and protein intakes per kg were significantly higher in the stunted children than in non-stunted children (energy P < 0.001, protein P < 0.005). Greater morbidity in the stunted children could account for some, but not all, of this difference. Children with lower weight for height had lower intakes (energy P < 0.05, protein P < 0.01). Intakes were greater in children who lived in better housing, with more household possessions and whose mothers had more skilled occupations. Good reliability and the above associations indicate that the data are valid.(AU)

Regulation of urinary dopamine by protein and NaCl. A model of extraneuronal amine formation in kidney.

Dopamine (DA) excretion correlates directly with NaCl intake, but in salt sensitive hypertensive subjects the DA response to NaCl is deficient. While the linkage between dietary NaCl and renal DA formation in normal or pathophysiological states is currently undefined, a model of renal amine production is proposed in which alterations in renal blood flow and/or renal tubular transport mechanisms account for both the normal and abnormal responses to dietary NaCl. This model derives, in part, from observations in experimental animals and in human subjects in which renal DA production is more highly correlated with renal serotonin (5-HT) formation than with indices of either sympathetic nervous system or adrenal medullary activity.

Protein and carbohydrate selection respond to changes in dietary saturated fatty acids but not to changes in essential fatty acids.

We previously reported differences in protein and carbohydrate selection patterns in post-weanling rats fed beef tallow or soybean oil-based diets. Two experiments were designed to determine the characteristic of the dietary fat which mediates the selection behavior. For each experiment, dietary fat was 20% (w/w) of diets and fatty acid profiles were obtained by blending fat sources. Rats were randomly assigned to diets (24% protein, 40% carbohydrate) which varied only in fatty acid composition. After 2 weeks, rats selected from 2 diets with the fat composition previously fed, but varying in their protein and carbohydrate composition (55% protein, 4% carbohydrate and 5% protein, 61% carbohydrate). Experiment 1 was designed to test the effect of relative (omega 6: omega 3 ratios of 1 and 20) and absolute (15% or 4% omega 6, 0.7% or 0.2% omega 3) differences in essential fatty acids on macronutrient selection patterns. Differences in dietary essential fatty acids had no effect on energy intake or the proportion of energy consumed as protein and carbohydrate. Experiment 2 examined the effect of differences in the level of saturated fat (3-10% diet (w/w] on protein and carbohydrate selection. Animals selecting from diets with higher levels of saturated fat consumed more energy as protein and less as carbohydrate than rats selecting from diets with lower levels of saturated fat (p less than 0.0001). Regression analysis was used to examine the relationship between percent protein or carbohydrate energy and classes of dietary fat. The strongest relationship existed between percent dietary saturated fat and percent protein or carbohydrate energy (p less than 0.0001). Polyunsaturated:saturated fat ratio was also weakly associated with percent protein and carbohydrate energy (p less than 0.05). Polyunsaturated, monounsaturated, omega 6 and omega 3 fatty acids were not significantly related to percent protein or carbohydrate energy. These results indicated that protein and carbohydrate selection patterns are altered in response to qualitatively different dietary fatty acids, and that the amount of saturated fat in the diet is the important characteristic of dietary fat mediating the behavioral alteration.

Nutritional factors in cataract.

Age-related cataract is a condition characterized by multiple mechanisms and multiple risk factors. The mechanisms that bring about a loss in transparency include oxidation, osmotic stress, and chemical adduct formation. Risk factors for cataract include diabetes, radiation (ultraviolet B, x-ray), certain pharmaceutical substances, certain nutritional states, and possibly acute episodes of dehydration. Interaction occurs between and among mechanistic factors and risk factors. Thus nutrition must be considered as one part of a tapestry of intertwined events and responses. Certain experimental models for nutritional cataract have been useful for study of the cataractogenic process but are probably not important factors in the human disease. Little current evidence supports significant roles in human senile cataract for imbalances of tryptophan or other amino acids, deficiencies of calcium or selenium, or excessive intake of selenium. Overconsumption of galactose is likely to be hazardous only in subjects with genetic inability to metabolize this sugar. Vitamins with antioxidant potential (riboflavin, vitamin E, vitamin C, carotenoids) deserve further research scrutiny to ascertain their significance in cataract etiology. Excessive caloric intake needs to receive added emphasis as a factor contributing to cataract. Diabetes increases the likelihood of cataract three- to four-fold. Obesity, defined as more than 20% overweight, is considered a major risk factor for non-insulin-dependent, or type II, diabetes (69, 73). Weight control can be recommended as a prudent, safe, economic, and effective means of lowering risk probability for diabetes and the associated complication of cataract.

Adaptation of the exocrine pancreas to diet.

Pancreatic adaptation represents dietary regulation of gene expression; dietary substrates alter the synthesis and mRNA levels of their respective digestive enzymes. The mechanisms whereby mRNA levels change are not understood, but they must be elucidated. Although the changes in synthesis of proteases, amylase, and lipase parallel the changes in their mRNA levels in response to respective substrates, the concomitant changes in the synthesis of the other enzymes can be discordant with mRNA levels. The evidence supports a pretranslational mechanism of the adaptation of proteases, amylase, and lipase to their respective substrates and suggests potential translational mechanisms of other enzymes in these adaptations. Changes in synthesis occur within hours after a dietary change, but whether mRNA levels also change so early is unknown. Rapid, adaptive changes may occur by a different mechanism from later adaptation, possibly by translational control or nuclear transport. The differential effects of acute and chronic caerulein administration support the possibility of multiple mechanisms of regulation by a single effector. The mediators of pancreatic adaptations have not yet been identified, except for adaptation to dietary protein. CCK appears to mediate protease adaptation through the feedback regulation of its release by dietary protein. Available evidence supports a role of insulin and glucose in the adaptation to carbohydrate and a role of secretin and ketones in the adaptation to dietary fat. Elucidation of the mediators of pancreatic adaptation to carbohydrate and fat and their mechanisms is needed.

Effects of dietary protein intake on renal function in humans.

The effects of an acute protein load on renal hemodynamic responses and plasma glucagon levels were investigated in 31 patients with biopsy proven chronic glomerulonephritis (24 cases) or chronic renal failure (6 cases). After baseline clearance measurements, the subjects ingested a high protein meal consisting of 1.2 to 1.5 g protein/kg body weight in the form of cooked beef followed by a second set of measurements. This acute protein load resulted in a rise of both creatinine and PAH clearances (from 86.5 +/- 6.0 ml/min to 98.3 +/- 7.1 ml/min and 531.1 +/- 59.1 ml/min to 688.9 +/- 72.9 ml/min, respectively). This was associated with an elevation of plasma glucagon levels from 104.6 +/- 7.9 pg/ml to 134.5 +/- 7.5 pg/ml. From these data we suggest that the augmentation of renal function following a high protein intake may be mediated by the simultaneous rise of plasma glucagon levels, and that the glucagon concentration in the portal vein rather than in the peripheral blood has a pivotal role in this setting.

Effect of a high-protein meal on blood flow to transplanted human kidneys.

Renal blood flow in normal adults increases after protein ingestion. The mechanisms that create this hyperperfusion are unclear. A neurogenic factor in humans has not been definitively ruled out. Accordingly, we tested the hypothesis that a high-protein meal significantly increases renal blood flow to the denervated human kidney. We studied 11 transplant recipients (TR) with denervated kidneys and 4 kidney donors (KD) with a single innervated kidney. All subjects had normal urinalysis. Using noninvasive Doppler flowmetry that was previously validated, we determined renal blood flow (RQ, ml/min) after a 12-hr fast (F) and 1, 2, and 3 hr after a high-protein meal (500 ml) of 150 g protein, 30 g fat, and 30 g carbohydrate. The RQ (mean +/- SD, ml/min) at fasting and at 1, 2, and 3 hr postprandially was 409 +/- 100, 446 +/- 100, 493 +/- 122 (P less than 0.05 vs. F), and 500 +/- 123 (P less than 0.05 vs. F), respectively, for the TR, and was 654 +/- 60 (P less than 0.05 vs. TR), 667 +/- 86 (P less than 0.05 vs. TR), 776 +/- 80 (P less than 0.05 vs. F and TR), and 809 +/- 81 (P less than 0.05 vs. F and TR) for KD. We conclude that RQ in TR increases significantly after protein ingestion. Thus, in the noninstrumented, unanesthetized human with a transplanted kidney, neural control is not a factor in the increase in renal blood flow after a high protein meal.

Impact of protein malnutrition on exogenous reinfection with Mycobacterium tuberculosis.

Malnutrition may be a predisposing host factor in the development of exogenous-reinfection tuberculosis. Outbred Hartley guinea pigs were given isocaloric diets containing either 30% ovalbumin (control animals) or 10% ovalbumin (low-protein-fed [LP] animals). Equal numbers of control and LP animals were assigned to one of three infection groups: (i) primary pulmonary infection with a low-virulence, streptomycin-resistant (LVsr) isolate of Mycobacterium tuberculosis and then reinfection 6 weeks later by the same route with a high-virulence (HV) isolate; (ii) only the primary infection (LVsr isolate); and (iii) only the secondary infection (HV isolate). Each infection resulted in the development of 4 to 12 pulmonary tubercles. Guinea pigs were skin tested with purified protein derivative and killed 6 weeks after the second infection. Protein deprivation suppressed the dermal responses to purified protein derivative in all infection groups. Primary infection of well-nourished animals with the LVsr isolate induced significant protection against infection with the HV isolate in the reinfected group, based upon the numbers of viable mycobacteria in the lung and spleen. Protein malnutrition did not exacerbate disease in the reinfected group beyond that observed in malnourished animals infected with the HV isolate only, but neither did the infection with the LVsr isolate protect the LP animals against reinfection with the HV isolate. We conclude that malnutrition interferes with the protection normally afforded by primary infection but does not result in more severe disease in reinfected individuals than would be observed in singly infected subjects.

Two hypotheses on the feedback regulation of pancreatic enzyme secretion.

We review the mechanisms underlying the feedback regulation of pancreatic enzyme secretion in response to a meal. Pancreatic enzyme secretion in the rat and pig is known to be regulated by a negative feedback mechanism mediated by intestinal trypsin and chymotrypsin. Such a mechanism has recently been noted in humans. The presence of these enzymes in the small intestine suppresses pancreatic enzyme secretion, whereas their removal increases it. Two novel peptides have been proposed to account for the stimulation of pancreatic enzyme secretion in response to feeding trypsin inhibitor. One was assumed to be present in rat pancreatic juice and the other to be spontaneously secreted from the rat small intestine. In either case, trypsin and trypsin inhibitors do not directly interact with the luminal surface of the small intestine, but their actions are mediated by a trypsin-sensitive, cholecystokinin-releasing peptide. This is a novel explanation of the well-recognized stimulation of pancreatic enzyme secretion in response to dietary protein intake.

Dietary treatment of familial hypercholesterolemia.

The principal goal of dietary treatment of familial hypercholesterolemia (FH) is the reduction of the plasma low density lipoprotein (LDL) cholesterol. This is best accomplished by enhancing the number of LDL receptors and, at the same time, depressing liver synthesis of cholesterol. Both cholesterol and saturated fat down-regulate the LDL receptor and inhibit the removal of LDL from the plasma by the liver. Saturated fat down-regulates the LDL receptor, especially when cholesterol is concurrently present in the diet. The total amount of dietary fat is also important. The greater the flux of chylomicron remnants into the liver, the greater is the influx of cholesterol ester. In addition, factors that affect LDL synthesis could be important. These include excessive calories (obesity) that enhance very low density lipoprotein (VLDL) and, hence, LDL synthesis, and weight loss and omega-3 fatty acids, which depress synthesis of VLDL and LDL. The optimal diet for treatment of children and adults has the following characteristics: cholesterol (100 mg/day), total fat (20% of kcalories, 6% saturated with the balance from omega-3 and omega-6 polyunsaturated and monounsaturated fat), carbohydrate (65% kcalories, two thirds from starch), and protein (15% kcalories). This low-fat high-carbohydrate diet can lower the plasma cholesterol 18% to 21%. It is also an antithrombotic diet, thrombosis being another major consideration in preventing coronary heart disease. Dietary therapy is the mainstay of treatment of FH to which various drug therapies can be added.

Digestion of hay protein in different segments of the equine digestive tract.

Mature ponies fitted with permanent ileal cannulas were used in a 3 X 3 Latin square experiment to quantify prececal, postileal and total tract digestion of hay protein. Coastal Bermuda grass (CB), containing 11.7% crude protein, and two qualities of alfalfa, containing 15.0% (low-protein alfalfa; LA) and 18.1% (high-protein alfalfa; HA) crude protein, were fed in coarsely chopped form at 2% of body weight daily. Total tract apparent digestibility of the N in HA (73.8%) was higher than that in CB (57.0%; P less than .05) and was slightly higher than that in LA (66.1%; P less than .10). Nitrogen in LA was apparently more digestible than that in CB (P less than .05). Apparent prececal digestibilities of N in LA and CB were 1.3% and 9.6%, respectively, and were lower (P less than .05), or tended to be lower (P less than .10), than the 21.0% observed for HA. In relative terms, an average of 9.4% of the total N digestion occurred in the upper tract when CB and LA were fed, whereas 28.5% of total N digestion occurred in the foregut when HA was fed. There was a slightly higher concentration of total plasma free amino acids (P less than .10) at 1 h postfeeding when horses were fed alfalfa. Also, N retention was higher when ponies were fed HA (P less than .05) than when LA or CB were fed. Apparent postileal N digestibility was 52.5% for CB, 65.7% for LA and 66.9% for HA. Differences were not significant, and the large intestine appeared to compensate for the inefficiency of N digestion in the upper tract.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of nutrition on ovulation rate in the ewe.

The effect of nutrition on ovulation rate in the ewe is reviewed with particular reference to the role of protein and energy and the time of effect during the cycle. Ovulation rate is increased by both protein and energy. In the case of protein this was shown to be accompanied by increased plasma levels of FSH and androstenedione at about the time of luteolysis, while levels of LH were unaffected. Increased hepatic oxidative enzyme activity is proposed as a mechanism by which nutrient intake may influence ovulation rate.

Heligmosomoides polygyrus (Nematoda): the influence of dietary protein on the dynamics of repeated infection.

The influence of the protein component in the diet of the host on the population dynamics of gastrointestinal helminth infection was studied by using a mouse-H. polygyrus experimental model. Mice fed a 2% (by mass) protein diet ad libitum maintained body weight during the experiment, but gained weight steadily when fed a diet containing 8% (by mass) protein. When repeatedly infected with 5, 10, 20 or 40 larvae every 2 weeks, the mice fed the 2% (by mass) protein diet accumulated adult worms in direct proportion to exposure to the infective stages. Under similar infection régimes, mice fed an 8% (by mass) protein diet acquired a partly effective immunity to reinfection by the nematode. Acquired immunity was principally manifest as a reduction in the survival of adult worms, although a slight increase in the mortality rate and/or the development time of the tissue-dwelling larval phase was observed. Worm fecundity per head was significantly depressed in hosts fed the 8% protein diet. In conclusion, in these experiments it is demonstrated that the nutritional status of the host can influence the population dynamics of helminth infection.

Dietary protein, enhancement of N-nitrosomethylurea-induced mammary carcinogenesis, and their effect on hormone regulation in rats.

The effect of supplemental dietary protein (casein) fed with high fat diets was investigated using the N-nitrosomethylurea-induced mammary tumor model. Isocaloric diets containing casein and corn oil at 19 and 15% (normal protein-high fat) or 33 and 15% (high protein-high fat) were fed ad libitum to Sprague-Dawley mother rats. Female offspring continued on the diet. Food consumption and growth curves were similar over the entire growth period. N-Nitrosomethylurea (50 mg/kg body weight) or saline was administered at 7 and 8 weeks of age via the tail vein. Dietary protein had no effect on serum prolactin or growth hormone throughout the estrous cycle: Prior to carcinogen administration, at 7 weeks old, proestrus at 5 p.m., serum prolactin was 231.6 +/- 141.0 (SE) ng/ml (12 rats) versus 292.2 +/- 141.0 (13 rats) for normal versus high protein diet groups, respectively. No difference was noted after carcinogen injection at 9, 13, 28, and 33 weeks of age. Similarly no effect was noted on serum growth hormone activity. Tumor latency was 7 weeks and incidence was 100% in normal protein (24 rats) and high protein (39 rats) groups 28 weeks after carcinogen treatment. The number of tumors per rat (4.38 +/- 0.37 versus 2.87 +/- 0.35, P less than 0.002) and average tumor weight (17.97 +/- 2.63 versus 9.94 +/- 2.92 g) were significantly greater in the high protein group. Study indicates that diet or carcinogen treatment did not alter hormone regulation during the estrous cycle. However, supplemental dietary protein increased the effect of high fat diets enhancing the mammary tumor burden.