Typical Dietary Intake Research Articles

Database and Quick Methods of Assessing Typical Dietary Fiber Intakes using data for 228 Commonly Consumed Foods

To promote assessment of dietary fiber intakes in clinical settings, we established two objectives for this study: to provide a detailed database in grams per serving of fiber content and polymer composition for most fiber sources in the US diet, and to develop a quick method for estimating total fiber intakes. Data for 342 foods were condensed to 228 foods by combining similar foods. The comprehensive database developed includes pectin, hemicelluloses, and β-glucan contents of the soluble and insoluble fractions of fiber and the cellulose and Klason lignin contents of the insoluble fiber. Three fourths of the 228 foods contained 2.0 g fiber per serving or less; only 10% contained more than 3.0 g per serving. The quick method consists of multiplying the number of servings in each food group by the mean total dietary fiber content of foods in that group: 1.5 g for fruits (n=43), 1.5 g for vegetables (n=68), 1.0 g for refined grains (n=80), and 2.5 g for whole grains (n=13). Actual fiber values from the database should be used in the quick method if foodstuffs concentrated from grains, legumes, and nuts and seeds are consumed. Sample menus demonstrate that quick assessment of total fiber intake yielded results similar to the sum of individual values from the database. J Am Diet Assoc. 1997;97:1139–1148, 1151.

A comparison of dietary intake estimates in a population with chronic renal failure

The present study compares estimates of dietary intake of 40 patients with chronic renal failure. The study uses the modified diet history technique and a semiquantitative food frequency questionnaire. Both methods are used by a registered dietitian during personal interviews with the patients. Significantly more food items are recalled and significantly greater estimates of all nutrients tested (except cholesterol) are obtained using the food frequency questionnaire. Furthermore, results with this technique are more consistent with typical dietary intake for the Israeli population. Bias in patients' reporting of dietary intake causes the outcome of dietary intervention and evaluation of patient compliance difficult to assess. The food frequency questionnaire seems to produce less misclassification bias and therefore, may better estimate true dietary intake in patients with chronic renal failure.

Trans,trans-muconic acid as a biomarker of non-occupational environmental exposure to benzene.

Excretion of trans,trans-muconic acid (2,4-hexadienedioic acid; t,t-MA), a potential biomarker of low-level exposure to benzene, was determined in 32 smokers and 82 nonsmokers. In smokers the median background excretion of t,t-MA was 0.13 (0.06-0.39) mg/g creatinine and was significantly higher (P < 0.05) than the value of 0.065 (0.02-0.59) mg g creatinine in nonsmokers. For nonsmokers, the correlation between t,t-MA excretion and environmental exposure to benzene in ambient air, which was determined during the 8-day study period by personal diffusion samplers, was not significant (r = 0.164, P = 0.18). Nonsmokers living in the city tended to have higher t,t-MA excretion rates than nonsmokers living in the suburbs. However, the difference was only significant for nonsmokers from nonsmoking homes. For the same location (suburb or city), smoking at home leads to a marginal increase in t,t-MA excretion of the nonsmoking members of the household. In a further study with eight nonsmokers we found that dietary supplementation with 500 mg sorbic acid significantly increased (P < 0.001) the mean urinary t,t-MA excretion from 0.08 (0.04-0.12) to 0.88 (0.57-1.48) mg/24 h. Under study conditions 0.12% of the sorbic acid dose was excreted in urine as t,t-MA, thereby indicating that a typical dietary intake of 6-30 mg/day sorbic acid accounts for 10-50% of the background t,t-MA excretion in nonsmokers, and for 5-25% in smokers. As a consequence, sorbic acid in the diet is a significant confounding factor in assessing low-level benzene exposure if t,t-MA excretion in urine is used as a biomarker.

Formation of N-nitrosoiminodialkanoic acids and their unsuitability as biological monitors for endogenous nitrosation of dipeptides.

Nitrosation of dipeptides which do not contain imino acids leads to rearrangement and the formation of N-nitrosoiminodialkanoic acids. The optimum conditions for the nitrosation of dipeptides in buffer solutions occur at pH 2.0 (0.8-3.2% yield) and are not significantly catalysed by thiocyanate. In vitro nitrosation in gastric juice resulted in a lower yield. It was demonstrated that under normal gastric conditions, a maximum yield of 0.1 mumol total N-nitrosoiminodialkanoic acids/0.1 mol dipeptide would occur, 0.1 mol representing a typical dietary intake of dipeptide. This corresponds to a total concentration of approximately 20 micrograms/l N-nitrosoiminodialkanoic acids over a 24 h period. However, this figure may be significantly altered due to the fluctuation of nitrosation catalysts and inhibitors in gastric juice. Further studies showed that N-nitrosoiminodialkanoic acids are quantitatively excreted in urine when fed by gavage to rats. However, co-administration of the precursor dipeptide and nitrite resulted in negligible in vivo formation. The presence of N-nitrosoiminodialkanoic acids in normal human urine was not detected. Thus it was concluded that the monitoring of N-nitrosoiminodialkanoic acids in human urine is not a suitable method for biological monitoring of the endogenous nitrosation of dipeptides.

Nurse-training scheme for ex-tuberculosis patients.

<h3>Background</h3> Reducing intestinal phosphorus absorption is a cornerstone in CKD-MBD management. Yet, knowledge gaps include how CKD pathophysiology affects intestinal phosphorus absorption. <i>In vivo</i> rodent studies suggest that intestinal phosphorus absorption remains inappropriately normal in early-moderate CKD, despite declining 1,25-dihydroxyvitamin D (1,25D). We measured intestinal phosphorus absorption in patients with moderate CKD versus healthy adults using a direct radiotracer method. <h3>Methods</h3> Patients with CKD and healthy adults matched for age, sex, and race were enrolled in this 8-day controlled diet study: the first 6 days outpatient and the final 2 days inpatient. Oral and intravenous doses of ³³P and serial blood and urine sampling determined intestinal phosphorus absorption during the final 2 days. Secondary outcomes included fasting biochemistries and 24-hour urine phosphorus (uP). <h3>Results</h3> In total, <i>n</i>=8 patients with CKD (eGFR=29–55 ml/min per 1.73 m²) and <i>n</i>=8 matched healthy controls completed the study. On a controlled diet, no difference in fractional intestinal phosphorus absorption was detected between patients with CKD and healthy adults (0.69 versus 0.62, respectively; <i>P</i>=0.52), and this was similar for 24-hour uP (884 versus 935 mg/d, respectively; <i>P</i>=0.70). Fractional intestinal phosphorus absorption was not significantly related to 24-hour uP. Patients with CKD had higher serum intact PTH and intact FGF23 and lower 1,25D. The relationship between 1,25D and fractional intestinal phosphorus absorption was not statistically significant. <h3>Conclusions</h3> Intestinal phosphorus absorption with typical dietary intake did not differ in patients with moderate CKD compared with controls, despite lower serum 1,25D levels. In this setting, a relationship between 24-hour uP and fractional or absolute intestinal absorption was not evident. Further investigation is needed to determine what factors influence intestinal phosphorus absorption in CKD and the apparent lack of compensation by the intestine to limit phosphorus absorption in the face of declining kidney function and reduced 1,25D. Whether this is evident across a range of dietary phosphorus intakes, as well as CKD severity, also needs to be determined. <h3>Clinical Trial registry name and registration number:</h3> Phosphorus Absorption in Healthy Adults and in Patients with Moderate Chronic Kidney Disease, NCT03108222