The American Heart Association Dietary Guidelines for 2000: a summary report.

Recently, the American Heart Association published a revision of its dietary guidelines. The recommendations are based on new scientific findings, and address the contribution of growing rates of obesity, hypertension, and diabetes to heart disease in the United States. The guidelines for the general public are similar to dietary recommendations made by other health-related groups and government agencies and, therefore, place a greater emphasis on the adoption of healthy eating patterns and behaviors rather than a singular focus on dietary fat intake.

Effect of various levels of supplementation with sodium pivalate on tissue carnitine concentrations and urinary excretion of carnitine in the rat.

In previous studies, sodium pivalate has been administered to rats in their drinking water (20 mmoles/L; equivalent to 0.3% of the diet) as a way to lower the concentration of carnitine in tissues and to produce a model of secondary carnitine deficiency. Although this level of supplementation results in a marked decrease in carnitine concentration in a variety of tissues, it does not produce the classical signs of carnitine deficiency (i.e., decreased fatty acid oxidation and ketogenesis). The present study was designed (1) to determine if increasing the level of pivalate supplementation (0.6, 1.0% of the diet) would further reduce the concentrations of total and free carnitine in rat tissues without altering growth or food intake, and (2) to examine the effect of length of feeding (4 vs. 8 weeks) on these variables. Male, Sprague-Dawley rats were randomly assigned to either a control (0.2% sodium bicarbonate) or experimental diet (0.3, 0.6, 1.0% sodium pivalate) for either four or eight weeks. Animals (n = 6/group) were housed in metabolic cages; food and water were provided ad libitum throughout the study. Supplementation with sodium pivalate did not alter water intake or urine output. Ingestion of a diet containing 1.0% pivalic acid decreased food intake (g/day; P < 0.05), final body weight (P < 0.007), and growth rate (P < 0.001) after four weeks. The concentration of total carnitine in plasma, heart, liver, muscle, and kidney was reduced in all experimental groups (P < 0.001), regardless of level of supplementation or length of feeding. The concentration of free carnitine in heart, muscle, and kidney was also reduced (P < 0.001) in rats treated with pivalate for either four or eight weeks. The concentration of free carnitine in liver was reduced in animals supplemented with pivalate for eight weeks (P < 0.05), but no effect was observed in livers from rats treated for four weeks. Excretion of total carnitine and short chain acylcarnitine in urine was increased in pivalate supplemented rats throughout the entire feeding period (P < 0.001). Free carnitine excretion was increased during Weeks 1 and 2 (P < 0.01), but began to decline during Week 3 in experimental groups. During Weeks 6 and 8, free carnitine excretion in pivalate supplemented rats was less than that of control animals (P < 0.01). In summary, no further reduction in tissue carnitine concentration was observed when rats were supplemented with sodium pivalate at levels greater than 0.3% of the diet. Food intake (g/day) and growth were decreased in rats fed a diet containing 1.0% sodium pivalate. These data indicate that maximal lowering of tissue carnitine concentrations is achieved by feeding diets containing 0.3% sodium pivalate or less.

Importance of diet in maternal phenylketonuria.

Diet has long been recognized as the primary treatment modality for individuals with phenylketonuria (PKU) during infancy and childhood. Recent findings from the Maternal PKU Collaborative Study clearly indicate that dietary restriction of phenylalanine is also necessary to prevent the adverse effects of an elevated plasma phenylalanine concentration during pregnancy, which include microcephaly, physical anomalies, and mental retardation.

Vitamin D-deficient rickets: a multifactorial disease.

We present a case of an African-American child with vitamin D-deficient rickets. In addition to being solely breast-fed for the period of 1 year, he resided in New England, where exposure to ultraviolet light is limited owing to its northern latitude and long cold winters. He presented with classical signs of nutritional rickets and was immediately responsive to treatment with vitamin D supplementation.

Fish consumption and risk of sudden cardiac death.

Studies show conflicting results regarding the protective effect of dietary fish and fish oil on certain types of cardiovascular disease. A recent epidemiologic study supports the hypothesis that moderate consumption (1-2 meals/week) of fish lowers the risk of sudden cardiac death in humans.

The diabetic diet: evidence for a new approach.

The dietary prescription for noninsulin-dependent diabetes mellitus remains an important component in the treatment of this disorder. Recent studies indicate that a diet high in monounsaturated fat and low in carbohydrate can produce a more desirable plasma glucose, lipid, and insulin profile.

Restricting food intake does not exacerbate the effects of a choline-deficient diet on tissue carnitine concentrations in rats.

Previous reports in animals indicate that choline deficiency alters carnitine metabolism. Recent studies in humans suggest that choline deficiency occurs in individuals during long term total parenteral nutrition. Malnutrition is also a frequent complication in this population. We therefore examined the effect of restricting the intake of a choline-deficient diet on carnitine concentrations in plasma and tissues. Adult male rats were randomly assigned to one of four dietary regimens: control, choline deficient, restricted control (85% of control), or restricted choline deficient for 42-43 d. At the end of the experimental period, restricted animals weighed significantly less than their respective controls (P < 0.01). Liver weight relative to body weight and fat concentration were greater in choline-deficient animals (P < 0.01 and 0.001, respectively). Choline-deficient rats fed free access had elevated plasma carnitine concentration (P < 0.01). Urinary carnitine excretion was elevated in both groups of choline-deficient rats (P < 0.01), while liver, heart and muscle carnitine concentrations were lower than in controls (P < 0.05). Restricting dietary intake reduced plasma carnitine concentration in choline-deficient animals (P < 0.01), but did not alter tissue or urine carnitine concentrations in either group. Restricted, choline-deficient animals did not exhibit a worsening of the sequelae of choline deficiency. We conclude that choline deficiency alters carnitine concentrations in plasma and tissues and that restricting the intake of a choline-deficient diet does not alter this effect in tissues.

Iron deficiency and infant development.

It has been shown that iron-deficient anemic infants are not as successful in tests of mental and motor development as their iron-sufficient age-matched counterparts. A recent study has confirmed that iron intervention can reverse developmental delays, while placebo-treated anemic infants showed no such improvement. The etiology of the developmental delay and its effect on later performance remain to be elucidated.

Breast-feeding protects against otitis media.

Although exclusive breast-feeding decreases infant mortality and morbidity in developing countries, its protective effects in infants living in industrialized nations have been more difficult to quantitate. A recent study provides strong evidence that exclusive breast-feeding for at least four months decreases the incidence of otitis media in the first year of life.

Cow's milk, diabetes, and infant feeding.

Recently, a link between the serum level of antibody to cow's milk protein and the onset of insulin-dependent diabetes mellitus in humans was reported. This observation renewed controversy regarding the suitability of cow's milk in infant diets.

Growth patterns in the first year of life: what is the norm?

The use of reference standards, such as those of the National Center for Health Statistics (NCHS), for determining the health and nutritional status of breast-fed infants and children has been questioned. A recent study found that the mean weight of formula-fed infants remained at about the 50th percentile throughout their first year, whereas that of breast-fed infants fell below the 50th percentile well before age one year. Although these children probably are not at nutritional risk, deviation from the national reference data could lead to unnecessary infant monitoring and testing as well as undue parental concern.

Treatment of iron-deficiency anemia complicated by scurvy and folic acid deficiency.

We present a case of a child with iron-deficiency anemia, folic acid deficiency, and scurvy. His anemia proved refractory to treatment with iron until he received both folic acid and vitamin C supplementation. This case illustrates the importance of the evaluation of ascorbic acid and folate status in treating iron-deficiency anemia initially refractory to iron supplementation, because multiple nutrient deficiencies may coexist.

Choline, an essential nutrient for humans.

Choline is required to make essential membrane phospholipids. It is a precursor for the biosynthesis of the neurotransmitter acetylcholine and also is an important source of labile methyl groups. Mammals fed a choline-deficient diet develop liver dysfunction; however, choline is not considered an essential nutrient in humans. Healthy male volunteers were hospitalized and fed a semisynthetic diet devoid of choline supplemented with 500 mg/day choline for 1 wk. Subjects were randomly divided into two groups, one that continued to receive choline (control), and the other that received no choline (deficient) for three additional wk. During the 5th wk of the study all subjects received choline. The semisynthetic diet contained adequate, but no excess, methionine. In the choline-deficient group, plasma choline and phosphatidylcholine concentrations decreased an average of 30% during the 3-wk period when a choline-deficient diet was ingested; plasma and erthrocyte phosphatidylcholine decreased 15%; no such changes occurred in the control group. In the choline-deficient group, serum alanine aminotransferase activity increased steadily from a mean of 0.42 mukat/liter to a mean of 0.62 mukat/liter during the 3-wk period when a choline-deficient diet was ingested; no such change occurred in the control group. Other tests of liver and renal function were unchanged in both groups during the study. Serum cholesterol decreased an average of 15% in the deficient group and did not change in the control group. Healthy humans consuming a choline-deficient diet for 3 wk had depleted stores of choline in tissues and developed signs of incipient liver dysfunction. Our observations support the conclusion and choline is an essential nutrient for humans when excess methionine and folate are not available in the diet.

Abnormal liver function in malnourished patients receiving total parenteral nutrition: a prospective randomized study.

A prospective study was performed in clinically malnourished patients in which liver function was tested during a 4-week period of total parenteral nutrition (TPN). The purpose was to determine if concomitant intravenous lipid administration would reduce liver function abnormalities noted to occur frequently in patients receiving TPN. Twenty-five patients were randomly assigned to receive either daily infusions of 200 cc of a 20% lipid emulsion with TPN or TPN without lipid for the first week. In the subsequent 3 weeks all patients received daily intravenous lipid. The early lipid treatment group received 0.7 g lipid/kg BW/day and approximately 280 mg of choline/day from the lecithin emulsifier throughout the entire study period. Liver function tests were performed twice in the first week, then weekly thereafter. There were significant (p less than 0.05) elevations in liver function tests in the early lipid treatment group (for aspartate aminotransferase in weeks 1, 2, and 3, and lactic acid dehydrogenase in weeks 2 and 3). Alkaline phosphatase activity was elevated at weeks 2, 3, and 4 for the lipid-treatment group and at week 1 for the lipid-restricted group. The two groups had a similar elevation in gamma-glutamyltransferase activity. Analysis of covariance demonstrated that the overall duration of TPN, and not the presence or absence of intravenous lipid, was significantly related to the elevations in both alkaline phosphatase and gamma-glutamyltransferase (GGT) levels. In contrast, the early intravenous administration of lipid was significantly related to the increase in aspartate aminotransferase levels. The peak increase in AST was noted at day 7 in the lipid-administration group.(ABSTRACT TRUNCATED AT 250 WORDS)

Choline: an essential dietary nutrient?

Choline (trimethyl-beta-hydroxyethylammonium) is a quaternary amine which is widely distributed in plants and animals. It contains three methyl groups which are important in a number of metabolic reactions, including the synthesis of methionine and carnitine. Choline is also a component of the phospholipids phosphatidylcholine and sphingomyelin, important constituents of all cell membranes. Finally, choline is necessary for the synthesis of the neurotransmitter acetylcholine. Although this compound is considered an essential nutrient in numerous mammalian species, this has not been established for humans.

TPN cholestasis in premature infants: the role of parenteral nutrition solutions.

In conclusion, cholestatic liver disease is a frequent complication in low birthweight infants who receive parenteral nutrition. The etiology of this disorder is probably multifactorial. Although the composition of parenteral nutrition solutions may play a role in the development of cholestasis, at this time, there are limited data to suggest how to change parenteral solutions to alter the course of this disease. Further work is necessary to elucidate therapies to prevent and treat this disorder.

An in vitro study of choline uptake by intestine from neonatal and adult rats.

We studied choline uptake by slices of adult and 10-day-old rat intestine which were exposed on their mucosal surface to radiolabeled choline. Both neonatal and adult intestine transported choline. Choline uptake was observed in duodenum, jejunum, ileum, and colon of the adult rat. In the small intestine, choline uptake consisted of two components: a saturable and a nonsaturable process. The kinetic variables for saturable transport (Km, Vmax) were not significantly different in adult and neonatal small intestine. Some of the transported choline was converted to phosphatidylcholine, glycerophosphocholine, phosphocholine, and betaine. However, most of the transported choline (79-85%) was not metabolized within the intestinal slice during a 15-min period. We conclude that the capacity for choline transport in the rat small intestine is present early in neonatal life. The characteristics of this transport mechanism for choline are similar in the neonate and in the adult small intestine. Neonates should therefore be able to absorb the large amounts of unesterified choline that are present in milk.

Plasma choline concentration in humans fed parenterally.

Choline is an essential nutrient for some mammals; it is used for membrane and neurotransmitter synthesis. We analyzed plasma samples, obtained periodically during TPN therapy, for choline concentration. Malnourished patients referred to a nutrition support service were prospectively assigned to be treated with daily infusions of amino acids with, and without, supplemental daily infusions of lipid emulsion for a period of 1 wk. After the first week, all subjects received intravenous lipid, and most were offered enteral food supplements. Initial plasma choline concentrations in the 25 malnourished patients were significantly lower than those measured in plasma samples from 23 hospitalized patients known to be eating well (6.5 +/- 0.6 vs 9.7 +/- 0.7 nmol/ml; mean +/- SEM; p less than 0.001). During the first week of TPN therapy, plasma choline concentrations in the lipid-restricted group tended to decrease (from 7.3 +/- 1.0 to 4.7 +/- 0.5 nmol/ml; mean +/- SEM; p less than 0.05), while in the lipid-supplemented group plasma choline tended to increase (from 5.6 +/- 0.5 to 6.2 +/- 0.7 nmol/ml; mean +/- SEM; p less than 0.05). Plasma choline concentration increased during wk 2-4, when all patients were treated with lipid emulsions, and some were offered enteral foods. We conclude that malnourished humans who eat no choline have diminished stores of plasma (and possibly tissue) choline.

Choline, phosphatidylcholine and sphingomyelin in human and bovine milk and infant formulas.

Choline is a precursor for the biosynthesis of phosphatidylcholine (lecithin), sphingomyelin, and choline plasmalogens--all essential constituents of membranes. Choline is also needed to make acetylcholine, a major neurotransmitter. The major choline-containing compounds of human milk (unesterified choline, phosphatidylcholine, sphingomyelin) were measured in samples obtained from mothers of full-term infants. Unesterified choline concentrations were highest (greater than 600 nmol/ml) during the first week of lactation, but thereafter remained relatively constant at 70-200 nmol/ml. There was no difference among foremilk, middle milk and hind milk, nor was there a diurnal pattern of variation in unesterified choline concentrations. Milk phosphatidylcholine and sphingomyelin concentrations remained relatively constant throughout lactation (100-200 nmol/ml). Hind milk always contained more of these phospholipids than did foremilk or middle milk. There was no consistent diurnal pattern of variation in milk concentrations of phosphatidylcholine or sphingomyelin. Milk contained no phospholipase activity capable of forming free choline from phosphatidylcholine or sphingomyelin. Bovine milk contained approximately the same concentrations of choline, phosphatidylcholine and sphingomyelin as did human milk from mothers more than 15 d postpartum. The same was true of "humanized" infant formulas made from cow's milk. Soy protein-based formulas had much more unesterified choline (up to 650 nmol/ml) and much less sphingomyelin than did mature human milk.