ABSTRACT
The Chair introduced "Pasteur's Quadrant" as a potentially useful paradigm for modern science. Developed by Princeton's Donald E Stokes, the quadrant is two-by-two matrix that classifies knowledge as fundamental and/or applied. The Chair also noted the effect of competitive pressures, and the necessity for cooperation among nutrition societies. The Presidents of The American Society for Nutritional Sciences (ASNS), The American Society for Clinical Nutrition (ASCN), The American Society for Parenteral and Enteral Nutrition (ASPEN), and the Chair of the Institute of Food Technologist's (IFT) Nutrition Division presented their views on how societies can prepare to meet their members' upcoming needs. The Director of the Center for Food and Nutrition Policy discussed the future role of nutrition societies and how they might interact with various interest groups. The Forum, which included an opportunity for audience participation, took place soon after the February 1996 release of "Meeting the Challenge: A Research Agenda for America's Health, Safety, and Food." Published by the Executive Office of the President's Office of Science and Technology Policy, the report highlights the importance of nutrition to our nation's health.
Subject(s)
Nutritional Physiological Phenomena , Societies, Scientific/trends , Humans , Nutrition Policy , Societies, Scientific/organization & administration , United StatesABSTRACT
When a new technology is introduced, scientists can help improve public understanding and acceptance. In the case of biotechnology, scientists should communicate more effectively: to provide accurate scientific data to facilitate policy analysis; to clarify issues in active political debate; to explain science to the lay public to dispel general ignorance and enable rational choice; to assist the media in producing more thoughtful journalism; to share expertise to allow beneficial applications in developing countries; and to advance scientific discovery.
Subject(s)
Biotechnology , Humans , ScienceABSTRACT
The relationship between adequate folate intake by pregnant women and reduced risk of delivering infants with neural tube defects (NTDs) has raised the public health issue of increasing folate intake among women of reproductive age. The U.S. Food and Drug Administration has proposed fortifying cereal and grain products with folate, although at a level less than half that recommended by its sister agency, the Centers for Disease Control and Prevention. We question the wisdom of fortifying foods with folate at this time, given a variety of uncertainties, which include the following: 1) the fact that neural tube defects seem to be a multifactorial group of disorders that are polygenic as well, so folate will not help in all or perhaps even in most cases; 2) the incidence of NTDs, which varies geographically, has been decreasing in the United States for years; 3) fortifying more food with folate may pose safety concerns for some not as risk for NTDs; 4) no dose-response relationship has been established between folate and NTDs; and 5) fortification in this case would represent a conceptually new intervention strategy for addressing what may be a metabolic abnormality where pharmacological doses of a nutrient may be required. Launching a major nutritional intervention before better understanding the relationship between nutrients and NTDs and without reasonable assurance that it will not shift health risks from one group (developing embryos) to another (primarily adults with pernicious anemia) might prove ineffective and/or harmful.
Subject(s)
Folic Acid/administration & dosage , Food, Fortified , Neural Tube Defects/prevention & control , Adult , Anemia, Pernicious/etiology , Arteriosclerosis/prevention & control , Centers for Disease Control and Prevention, U.S. , Female , Folic Acid/adverse effects , Humans , Incidence , Infant, Newborn , Neural Tube Defects/epidemiology , Neural Tube Defects/etiology , Pregnancy , Risk Factors , United States/epidemiology , United States Food and Drug AdministrationABSTRACT
The 1992 AAP policy of dietary fat and cholesterol restrictions in all children over two is based on incomplete evidence. The low-fat diet has never been demonstrated to be beneficial for prepubescent healthy children, and the unguided rapid implementation of numerical guidelines could lead to ill effects. Caution in the face of incomplete data was the hallmark of the 1983 and 1986 AAP Committee positions. Subsequent AAP policy change should have awaited either the direct clinical evidence they had previously considered necessary to demonstrate efficacy or the more general availability of the dietary guidance needed for safe implementation of strict numerical guidelines. We are neither calling for paralysis of policy nor do we wish to imply that 30% dietary fat is necessarily unhealthful for children. However, we do foresee the need for greater nutritional guidance for parents. In the absence of better nutrition education, zealous parents could switch a 2-year old immediately to a low-fat regimen to such an extent that the child might not achieve adequate nutrient intake to assure optimal growth and development. Moreover, current changes in lifestyle result in less parental supervision in all spheres of behavior, making closer dietary supervision less likely. A prudent pediatric guideline should encourage moderation and the gradual reduction of dietary fat intake throughout the early childhood years, achieving the numerical standards set for adults during adolescence. Such a policy has not been shown to foster atherosclerosis or to provide the yoke of unhealthful dietary habits that must be broken in adulthood.
Subject(s)
Child Nutrition Sciences , Dietary Fats/administration & dosage , Nutrition Policy , Adolescent , Adult , Child , Child Nutrition Sciences/education , Child, Preschool , Growth Disorders/etiology , Humans , Nutritional Requirements , Parents/education , Pediatrics , Reproducibility of Results , Societies, Medical , United StatesSubject(s)
Dietary Fats, Unsaturated , Food , Nutritional Physiological Phenomena , Proteins , Fat Substitutes , Food Handling , Humans , Particle SizeABSTRACT
Taurine was long considered an end product of the metabolism of the sulfur-containing amino acids, methionine and cyst(e)ine. Its only clearly recognized biochemical role had been as a substrate in the conjugation of bile acids. Taurine is found free in millimolar concentrations in animal tissues, particularly those that are excitable, rich in membranes, and generate oxidants. Various lines of evidence suggest one major nutritional role as protecting cell membranes by attenuating toxic substances and/or by acting as an osmoregulator. The totality of evidence suggests that taurine is nonessential in the rodent, it is an essential amino acid in the cat, and it is conditionally essential in man and monkey. Absence from the diet of a conditionally essential nutrient does not produce immediate deficiency disease but, in the long term, can cause problems. Taurine is now added to many infant formulas as a measure of prudence to provide improved nourishment with the same margin of safety for its newly identified physiologic functions as that found in human milk. Such supplementation can be justified by the finding of improved fat absorption in preterm infants and in children with cystic fibrosis, as well as by salutary effects on auditory brainstem-evoked responses in preterm infants. Experimental findings in animal models and in human cell models provide further justification for taurine supplementation of infant formulas.
Subject(s)
Infant Food , Taurine/administration & dosage , Humans , Infant , Nutritional Requirements , Risk Factors , Taurine/deficiencyABSTRACT
The primary trihydroxy bile acid, cholate, both free and conjugated, is nontoxic in cultured human lymphoblastoid cells incubated in vitro. The primary dihydroxy bile acid, chenodeoxycholate, was more toxic at high concentrations than at low concentrations, but conjugation with taurine reversed it. The free secondary bile acids, deoxycholate and lithocholate, corresponding respectively to cholate and chenodeoxycholate, are extremely toxic, the latter more than the former. Conjugation with taurine reversed the toxicity, as did glycine. Neither free taurine nor free glycine added to unconjugated bile acids decreased toxicity.
Subject(s)
Bile Acids and Salts/metabolism , Taurine/metabolism , Bile Acids and Salts/toxicity , Cell Line , Cell Survival/drug effects , Humans , Kinetics , Structure-Activity Relationship , Taurine/toxicitySubject(s)
Aspartame/pharmacology , Brain Chemistry/drug effects , Dipeptides/pharmacology , Animals , Aspartame/metabolism , MiceSubject(s)
Taurine/physiology , Animals , Cats , Female , Haplorhini , Humans , Lymphocytes/drug effects , Milk/analysis , Parenteral Nutrition, Total , Rats , Retina/physiology , Time Factors , Vitamin A/pharmacology , Zinc/pharmacologyABSTRACT
The effect of dietary protein quantity and quality on the excretion of creatinine in preterm and term neonatal infants has been investigated. Whey protein predominant formulas result in increased creatinine excretion as compared with either casein protein predominant formulas or with pooled human milk in preterm infants (p less than 0.001 by ANOVA). The volume of human milk (170 versus 185 versus 200 ml/kg/day) appears to have little effect in these infants. In term infants, few differences among the feeding groups were observed, although creatinine excretion did increase with time. The pattern of creatinine excretion among feeding groups was similar regardless of whether or not the data were expressed in milligrams per deciliter or in milligrams per 24 hours. Small correlations of creatinine excretion with birth weight were observed, but these appeared to vary, depending on the type of feeding. These diet-induced differences in creatinine excretion indicate the need for caution in expressing other urinary metabolites, such as amino acids, relative to creatinine excretion.
Subject(s)
Amino Acids/urine , Creatinine/urine , Dietary Proteins/pharmacology , Infant Food , Infant Nutritional Physiological Phenomena , Infant, Newborn , Infant, Premature , Milk, Human , Animals , Cattle , Humans , Infant , Milk Proteins/pharmacologySubject(s)
Taurine/metabolism , Animals , Antioxidants/metabolism , Bile Acids and Salts/metabolism , Blood Platelets/metabolism , Brain/metabolism , Humans , Kinetics , Lymphocytes/metabolism , Membranes/metabolism , Nutritional Physiological Phenomena , Retina/metabolism , Retinitis Pigmentosa/metabolismABSTRACT
Homocystinuria, an inherited disorder associated with premature atherosclerosis, represents a severe form of methionine intolerance. To analyze the importance of milder forms of methionine intolerance in the genesis of vascular disease, the relation between provokable methionine intolerance and coronary artery disease was investigated. In a group of 138 men, aged 31 to 65 years (mean 53), referred for cardiac catheterization, plasma homocystine was measured before and 6 hours after an oral l-methionine load (0.1 g/kg). Thirty-nine subjects found to have normal coronary arteries had a mean post-load plasma homocystine level of 0.59 +/- 0.37 mumol/liter. A criterion at the 95th percentile (1.64 SD above the mean) was selected and applied to the remaining 99 subjects with coronary artery disease (0.70 +/- 0.68 mumol/liter). Sixteen (16%) of 99 subjects with coronary artery disease exceeded this level as compared with 1 (2%) of 39 subjects without coronary artery disease (p less than 0.04). The risk of coronary artery disease in men with provokable methionine intolerance was increased sevenfold as estimated by the odds ratio. By correlation matrix and multivariate regression analyses, provokable homocystinemia was predictive of coronary artery disease and was independent of tobacco smoking, hypertension, diabetes mellitus, serum cholesterol and age. It is proposed that men with mild methionine intolerance exposed to the high methionine content of the Western diet may develop intermittent homocystinemia and thus may be at greater risk for the development of coronary artery disease.
Subject(s)
Coronary Disease/etiology , Metabolic Diseases/complications , Methionine/blood , Adult , Aged , Coronary Disease/blood , Homocystine/blood , Humans , Male , Metabolic Diseases/blood , Metabolic Diseases/physiopathology , Methionine/metabolism , Middle Aged , RiskABSTRACT
Taurine is one of the most abundant amino acids in mammals and there is increasing evidence for the importance of taurine during development. Plasma taurine kinetics in a rhesus monkey was studied using [1,2-13C2]taurine. Taurine in plasma was derivatized to its dimethylaminomethylene methyl ester, separated on a gas chromatographic column, and the [M+2+H]+/[M+H]+ ion ratio was measured by ammonia chemical ionization mass spectrometry. The results were comparable to those obtained from the simultaneous radioisotope tracer study using [35S]taurine. This stable isotope method requires only 200 microliters of plasma for precise and accurate determination and is suitable for taurine kinetic studies in human infants.
Subject(s)
Taurine/blood , Animals , Carbon Isotopes , Kinetics , Macaca mulatta , Male , Mass SpectrometryABSTRACT
Biopterin and neopterin concentrations were measured by reverse-phase high pressure liquid chromatography in milks of man, cow, rabbit, cat, and rat and in commercial formulas widely used in North America. There was wide variation of concentration among species. Higher concentrations of biopterin were present in human milk (392.0 +/- 158.6 pmol/ml) than were present in all milk formulas analyzed (2.6-50.6 pmol/ml).