Food oxalate: factors affecting measurement, biological variation, and bioavailability.

Food and nutrition professionals provide medical nutrition therapy for patients with kidney stones. If the stones contain oxalate or the patient has been diagnosed with hyperoxaluria, reduction of dietary oxalate may be appropriate. Differences in oxalate values for a single food may be due to analytical methods, and/or biological variation from several sources, including cultivar, time of harvest, and growing conditions. Bioavailability of food oxalate and, thus, urine oxalate, will also be affected by salt forms of oxalate, food processing and cooking methods, meal composition, and the presence of Oxalabacter formigenes in the patient's gut. Dietary advice for reducing urinary oxalate should include both reduction of dietary oxalate and simultaneous consumption of calcium-rich food or supplement to reduce oxalate absorption.

Metabolic syndrome in a multiethnic sample of school children: implications for the pediatric nurse.

There is lack of translational work that may assist the pediatric nurse in identifying the child who is at risk for metabolic syndrome. Early identification of the syndrome could assist pediatric health care providers in intervening and in lowering child health risks. Fasting serum insulin, metabolic syndrome criteria, and dietary intake were examined in a multiethnic sample of children aged 9-15 years. Forty-seven percent had two or more risk factors for metabolic syndrome, and 28% had three or more risk factors. Insulin levels were negatively correlated with the recommended dietary allowance. A regression model, including gender, age, race, body mass index, serum glucose, high-density lipoprotein cholesterol, triglycerides, and blood pressure, explained 48% of insulin variance.

Oxalate and phytate concentrations in seeds of soybean cultivars [Glycine max (L.) Merr.].

This study analyzed soybean seeds from 116 cultivars for total, insoluble, and soluble oxalate (Ox), phytate (InsP6), calcium (Ca), and magnesium (Mg) because of their potential beneficial or harmful effects on human nutrition. These cultivars were divided into four groups (A-D) on the basis of the year and geographic location where they were grown. Oxalate concentration ranged from about 82 to 285 mg/100 g of dry seed. The InsP6 concentration ranged from 0.22 to 2.22 g/100 g of dry seed. There was no correlation between Ox and InsP6 within or among the four groups of cultivars. There was a significant correlation between total Ox and Ca, but not Mg, in group D cultivars (r = 0.3705; p < 0.0005). No significant relationship was found in the group A-C cultivars. Eleven group D cultivars had InsP6 less than 500 mg/100 g, but all had total Ox of 130 mg/100 g or greater. Five cultivars from groups A-C had relatively low InsP6 (group B; < or =1.01 g/100 g) and low Ox (<140 mg/100 g). These cultivars could be useful for producing soy foods beneficial to populations at risk for kidney stones and for improved mineral bioavailability. The Ox and InsP6 concentrations of the cultivars indicate that choosing specific parents could generate seeds in succeeding generations with desirable Ox and InsP6 concentrations.

Ascorbate increases human oxaluria and kidney stone risk.

Currently, the recommended upper limit for ascorbic acid (AA) intake is 2000 mg/d. However, because AA is endogenously converted to oxalate and appears to increase the absorption of dietary oxalate, supplementation may increase the risk of kidney stones. The effect of AA supplementation on urinary oxalate was studied in a randomized, crossover, controlled design in which subjects consumed a controlled diet in a university metabolic unit. Stoneformers (n = 29; SF) and age- and gender-matched non-stoneformers (n = 19; NSF) consumed 1000 mg AA twice each day with each morning and evening meal for 6 d (treatment A), and no AA for 6 d (treatment N) in random order. After 5 d of adaptation to a low-oxalate diet, participants lived for 24 h in a metabolic unit, during which they were given 136 mg oxalate, including 18 mg 13C2 oxalic acid, 2 h before breakfast; they then consumed a controlled very low-oxalate diet for 24 h. Of the 48 participants, 19 (12 stoneformers, 7 non-stoneformers) were identified as responders, defined by an increase in 24-h total oxalate excretion > 10% after treatment A compared with N. Responders had a greater 24-h Tiselius Risk Index (TRI) with AA supplementation (1.10 +/- 0.66 treatment A vs. 0.76 +/- 0.42 treatment N) because of a 31% increase in the percentage of oxalate absorption (10.5 +/- 3.2% treatment A vs. 8.0 +/- 2.4% treatment N) and a 39% increase in endogenous oxalate synthesis with treatment A than during treatment N (544 +/- 131 A vs. 391 +/- 71 micromol/d N). The 1000 mg AA twice each day increased urinary oxalate and TRI for calcium oxalate kidney stones in 40% of participants, both stoneformers and non-stoneformers.

Oxalate and phytate of soy foods.

The consumption of foods made from soybeans is increasing because of their desirable nutritional value. However, some soy foods contain high concentrations of oxalate and/or phytate. Oxalate is a component of calcium oxalate kidney stones, whereas phytate is an inhibitor of calcium kidney stone formation. Thirty tested commercial soy foods exhibited ranges of 0.02-2.06 mg oxalate/g and 0.80-18.79 mg phytate/g. Commercial soy foods contained 2-58 mg of total oxalate per serving and 76-528 mg phytate per serving. Eighteen of 19 tofu brands and two soymilk brands contained less than 10 mg oxalate per serving, defined as a low oxalate food. Soy flour, textured vegetable soy protein, vegetable soybeans, soy nuts, tempeh, and soynut butter exhibited greater than 10 mg per serving. The correlation between oxalate and phytate in the soy foods was significant (r = 0.71, P < 0.001) indicating that oxalate-rich soy foods also contain higher concentrations of phytate. There also was a significant correlation, based on molar basis, between the divalent ion binding potential of oxalate plus phytate and calcium plus magnesium (r = 0.90, P < 0.001) in soy foods. Soy foods containing small concentrations of oxalate and moderate concentrations of phytate may be advantageous for kidney stone patients or persons with a high risk of kidney stones.

Acute caffeine effects on urine composition and calcium kidney stone risk in calcium stone formers.

PURPOSE: Caffeine increases urinary calcium (ca) excretion in nonstone formers. We designed a study to determine the effect of caffeine consumption on urinary composition in stone formers. MATERIALS AND METHODS: A total of 39 normocalcemic patients with calcium stones consumed caffeine (6 mg/kg lean body mass) after 14 hours of fasting. Urinary composition was compared 2 hours before and 2 hours after caffeine consumption. Control subjects included 9 nonstone formers studied contemporaneously with patients plus data from 39 nonstone formers from previous studies matched to each patient by level of fasting calcium/creatinine (Cr), gender and age. RESULTS: Caffeine increased urinary Ca/Cr, magnesium/Cr, citrate/Cr and sodium/Cr but not oxalate/Cr in stone formers and controls. The Tiselius stone risk index for calcium oxalate precipitation increased from 2.4 to 3.1 in stone formers and from 1.7 to 2.5 in nonstone formers. Of the 39 stone formers 32 had an increased Tiselius risk index after caffeine. Post-caffeine increases in Ca/Cr and Na/Cr were highly correlated. CONCLUSIONS: Caffeine consumption may modestly increase risk of calcium oxalate stone formation.

Homocysteine in a multi-ethnic sample of school-age children.

Cardiovascular disease is a major cause of morbidity and mortality in the United States and other developed countries; arterial lesions that are precursors of disease begin during childhood. Homocysteine levels have been associated with cardiovascular disease rates in adults, but information about levels in and impact on children is limited, particularly among various ethnic groups. This study examined the cardiovascular risk factors of a multi-ethnic sample of 100 9-15 year-old Native American, Hispanic, White, and mixed race children in rural central Washington. The mean fasting homocysteine level was 5.82 micromol/l (+/- 1.47), with no significant differences noted among ethnic groups. Mean dietary intake of folate, vitamin B6, and vitamin B12 exceeded current Recommended Dietary Allowances. Homocysteine levels did not show statistically significant correlations with cardiovascular risk factors. Homocysteine levels were not found to be a cardiovascular risk factor of importance, nor were significant ethnic differences found, in Native American, Hispanic and White children consuming adequate diets.

Dietary influences on urinary oxalate and risk of kidney stones.

Calcium oxalate is the most common constituent of kidney stones. Increases in urinary oxalate increase risk of calcium oxalate supersaturation more than increases in urinary calcium, as the physiological level of oxalate is about one-fifth to one-tenth that of urinary calcium. Urinary oxalate derives from two sources: endogenous synthesis and diet. Endogenous synthesis is proportional to lean body mass, and cannot be altered by any current treatment. Dietary oxalate is found in all plant foods. A single food may vary 2-15 fold in oxalate content, depending on variety and growth conditions. The salt form of oxalate, whether sodium, potassium, calcium or magnesium is likely to affect absorption, but has been little studied. Absorption of oxalate from food sources typically is 3-8% of its total oxalate in non-stone-forming individuals. Recent research shows that 40-50% of urinary oxalate comes from the diet of healthy individuals consuming typical diets with 150-250 mg/d dietary oxalate. However, a subpopulation of oxalate "hyperabsorbers" is found in most studies of stoneforming patients. It is likely that all stone formers will benefit from reduction of dietary oxalate, but especially hyperoxaluric stone formers.

Dietary animal and plant protein and human bone health: a whole foods approach.

Urinary calcium excretion is strongly related to net renal acid excretion. The catabolism of dietary protein generates ammonium ion and sulfates from sulfur-containing amino acids. Bone citrate and carbonate are mobilized to neutralize these acids, so urinary calcium increases when dietary protein increases. Common plant proteins such as soy, corn, wheat and rice have similar total S per g of protein as eggs, milk and muscle from meat, poultry and fish. Therefore increasing intake of purified proteins from either animal or plant sources similarly increases urinary calcium. The effects of a protein on urinary calcium and bone metabolism are modified by other nutrients found in that protein food source. For example, the high amount of calcium in milk compensates for urinary calcium losses generated by milk protein. Similarly, the high potassium levels of plant protein foods, such as legumes and grains, will decrease urinary calcium. The hypocalciuric effect of the high phosphate associated with the amino acids of meat at least partially offsets the hypercalciuric effect of the protein. Other food and dietary constituents such as vitamin D, isoflavones in soy, caffeine and added salt also have effects on bone health. Many of these other components are considered in the potential renal acid load of a food or diet, which predicts its effect on urinary acid and thus calcium. "Excess" dietary protein from either animal or plant proteins may be detrimental to bone health, but its effect will be modified by other nutrients in the food and total diet.