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Both fresh and processed foods make up vital parts of the food supply. Processed food contributes to both food security (ensuring that sufficient food is available) and nutrition security (ensuring that food quality meets human nutrient needs). This ASN scientific statement focuses on one aspect of processed foods: their nutritional impacts. Specifically, this scientific statement 1) provides an introduction to how processed foods contribute to the health of populations, 2) analyzes the contribution of processed foods to "nutrients to encourage" and "constituents to limit" in the American diet as recommended by the Dietary Guidelines for Americans, 3) identifies the responsibilities of various stakeholders in improving the American diet, and 4) reviews emerging technologies and the research needed for a better understanding of the role of processed foods in a healthy diet. Analyses of the NHANES 2003-2008 show that processed foods provide both nutrients to encourage and constituents to limit as specified in the 2010 Dietary Guidelines for Americans. Of the nutrients to encourage, processed foods contributed 55% of dietary fiber, 48% of calcium, 43% of potassium, 34% of vitamin D, 64% of iron, 65% of folate, and 46% of vitamin B-12. Of the constituents to limit, processed foods contributed 57% of energy, 52% of saturated fat, 75% of added sugars, and 57% of sodium. Diets are more likely to meet food guidance recommendations if nutrient-dense foods, either processed or not, are selected. Nutrition and food science professionals, the food industry, and other stakeholders can help to improve the diets of Americans by providing a nutritious food supply that is safe, enjoyable, affordable, and sustainable by communicating effectively and accurately with each other and by working together to improve the overall knowledge of consumers., (© 2014 American Society for Nutrition.)

Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene-nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient-genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.

Two experimetns were conducted to study the body pool size and turnover rate of carnitine in rats. The turnover of carnitine was determined by injection of a tracer dose of L-[methyl-14C] carnitine. In experiment 1, carnitine body pool size and turnover in rats fed a choline-deficient basal diet were compared with values obtained from rats fed the basal diet supplemented with choline. These rats were maintained at 22degrees. In experiment 2, carnitine body pool size and turnover were determined in cold-exposed (2degrees) rats fed the choline-deficient basal diet. Carnitine body pool sizes of rats maintained 22degrees and fed the choline-deficient basal diet and the choline-supplemented diet were 35.6 and 41.8 mumoles/100 g body weight, respectively. Carnitine body pool size of rats maintained at 2degrees and fed a choline-deficient basal diet were 6.6 and 56.1 days, for rats fed a choline-supplemented diet, 6.7 and 40.2 days, and for rats maintained at 2degrees and fed a choline-deficient diet, 2.9 and 36.4 days, respectively. Carnitine turnover times obtained with DL-[14C]carnitine in our previous study longer than turnover times obtained with DL-[14C]carnitine in our previous study (j. nutr. 104, 782-792). These observations suggest that D-carnitine is not metabolized the same way as L-carnitine, and that D-carnitine is not cleared from the body within 2 days after injection. The results also suggest that carnitine metabolism can be influenced by the amount of choline in the diet and by cold exposure.

Studies in vitro and with intact chicks support the view that liver is the major site of lipid biosynthesis in the chicken. Adipose tissue is relatively unimportant as a site of fatty acid biosynthesis in this species although it does have the ability to esterify fatty acids to triglycerides. The available evidence, therefore, suggests that in the chicken, and presumably other avian species, fatty acids are synthesized in liver and are transported as triglycerides in the plasma low-density lipoproteins to the adipose tissue for storage. Fasting, even for short periods of time, markedly depresses the capacity for hepatic lipogenesis in the chick. Food restriction for 2 hr. depresses hepatic lipogenesis by about 90% and refeeding for 1 hr./or/the intravenous administration of glucose or fructose restores the lipogenic capacity. Feeding diets high in fat or protein cannot be adequately explained on the basis of the reduction of dietary carbohydrate which accompanies increased dietary protein or fat levels. Dietary fat and protein appear to exert their effects on hepatic lipid synthesis by different mechanisms. The depression in hepatic fatty acid synthesis brought about by fasting or fat-feeding is accompanied, and probably preceded, by an increased plasma free fatty acid level. Under these conditions hepatic fatty-acyl CoA levels increase while free CoA levels are reduced. Long-chain acyl CoA derivatives are capable of inhibiting acetyl CoA carboxylase activity as well as citrate transport. The reduced availability of free CoA may limit the citrate cleavage reaction. Dietary alterations influence the hepatic lactate-pyruvate ratio of chicks, however the changes observed are not always consistent with the changes observed in rat liver. Chicks fed high-protein diets have a decreased hepatic lactate/pyruvate ratio indicative of a more oxidized cytoplasmic environment. This change in redox state may be associated with control of fatty acid synthesis in chicks fed high-protein diets. Thyroxine and glucagon affect hepatic fatty acid synthesis in the chick, however insulin appears to play a lesser role.

Glucose turnover and blood metabolites were measured in eight adult female beagles in the fed state, at 1 day of fasting, and at 7, 14, and 21 days of fasting. Glucose utilization decreased significantly from 1 to 7 days of fasting, but remained constant from 7 to 21 days, while blood ketones and plasma free fatty acids rose significantly during the same period. Plasma alanine, serine, and glycine fell with fasting, with the greatest decrease in alanine levels occurring between 7 to 14 days. Plasma branched chain amino acids rose significantly with fasting. It was concluded that the shifts in plasma metabolites and decreased glucose utilization could be indicative of decreased energy demands of the fasting dogs and/or a shift in substrate utilization with progressive fasting.

Young growing rats, chicks and pigs were fed diets containing graded levels of 1,3-butanediol (BD). Replacement of up to 20% of the dietary carbohydrate energy with BD did not affect body weight gain or food efficiency in these species. Blood beta-hydroxybutyrate levels were markedly elevated when BD was added to the diet. Plasma triglyceride response varied with species. In the rat, plasma triglyceride levels were decreased when BD was added to a high-carbohydrate diet. Plasma triglyceride levels were increased when BD-containing diets were fed to pigs and unchanged when chicks consumed diets containing BD. The hepatic lactate:pyruvate ratio was increased in rats fed BD and decreased in chicks fed BD. Hepatic long-chain acyl CoA levels were increased in rats, but not in chicks, fed BD. Addition of BD to a high-carbohydrate diet markedly decreased the rate of fatty acid synthesis, as measured in vitro or in vivo, in rat liver but not in rat or pig adipose tissue. Hepatic fatty acid synthesis in the chick was not affected by replacement of up to 18% of the dietary carbohydrate with BD. We propose that the hepatic conversion of BD to beta-hydroxybutyrate in the rat shifts the cytoplasmic redox state, reduces the glycolytic rate, and reduces substrate availability for fatty acid synthesis. Further, the concomitant shift in the mitochondrial redox state allows long-chain acyl CoA levels to increase. The overall effect is a decrease in the rate of fatty acid synthesis in livers of rats fed BD.

Concentrations of Na+,K+-ATPase enzyme units are lower in skeletal muscle and liver of adult obese (ob/ob) mice than in their lean counterparts. The present studies were designed to provide information on functional correlates of Na+,K+-ATPase in ob/ob mice. Obese mice had lower potassium (K+) content in muscle and liver and higher sodium (Na+) content in muscle and liver and higher sodium (Na+) content in muscle than lean counterparts. The calculated intracellular Na+/K+ ratio in muscle of obese mice was approximately twice as high as in muscle of lean mice. Oxygen consumption was measured in mice maintained at 14 degrees, 25 degrees, or 33 degrees for 40 min and injected with 0.3 or 0.9 microgram ouabain per g body weight. Ouabain, a specific inhibitor of Na+,K+-ATPase, decreased oxygen consumption less in obese mice (12%--25%) than in lean mice (19%--38%). These results suggest that Na+ pump activity may be reduced in obese mice.

A basal diet or a basal diet plus 1% of cholesterol and 0.33% cholic acid was fed to rats for varying lengths of time and (1) the activities of liver phosphoenolpyruvate-carboxykinase (PEP-CK), tyrosine transaminase (TT), and serine dehydratase (SD); (2) the rate of total hepatic protein synthesis and (3) the concentration of hepatic reduced glutathione (GSH) were quantitated. The specific activity of PEP-CK was significantly depressed by cholesterol plus cholic acid feeding, while the specific activity of TT was unchanged. No significant effect of dietary cholesterol plus cholic acid was found on the total liver activities. In contrast, SD specific activity was increased 3-fold. The rate of (U-14C)-L-leucine incorporation into total TCA precipitable protein following ingestion of cholesterol plus acid was significantly reduced when the data were expressed as dpm (U-14C)-L-leucine/mg protein. After correcting this expression for specific radioactivity of the liver tissue free leucine pool, no significant effect of dietary cholesterol plus cholic acid on hepatic protein synthesis existed. In fact, the amount of 14C-leucine incorporated into protein on a total liver basis was 50% greater for the cholesterol group. On a per gram of liver basis, the concentration of GSH in the liver of rats fed a cholesterol plus cholic acid diet was significantly decreased. Considering the liver enlargement in rats fed cholesterol plus cholic acid, total organ GSH was found to be significantly greater than for rats fed a basal diet.

Young female obese (ob/ob) and lean mice were fed a single diet containing 10 or 20% casein or were allowed to self-select from two diets containing 10 and 50, 20 and 60, or 30 and 70% casein for 3 weeks. Obese and lean mice offered a choice of two diets varying in protein-consumed 36% and 32%, respectively, of energy from protein. Although both obese and lean mice consumed more protein when allowed to self-select, each group maintained the same energy intake as observed when a single diet was fed. Because obese mice consumed more energy than lean mice, their self-selected intake of protein was 55% greater than observed in lean mice. The increased protein intake in self-selected obese mice was associated with a decreased tryptophan:large neutral amino acid ratio in their plasma. Average nitrogen retention was only slightly less in obese mice than in lean mice, but the sites of nitrogen deposition differed considerably. Obese mice retained only 35% of their nitrogen in the carcass (skeletal muscle and skeleton) while lean mice retained 58% of their nitrogen in the carcass. In summary, young obese mice allowed to self-select from two diets varying in protein and carbohydrate consumed more protein and more energy, but deposited less nitrogen in their carcasses, than lean mice. Hyperphagia in young obese mice is not directly linked to an increased demand for dietary protein.

The influence of fasting and diet composition on the time sequence of changes in hepatic lipogenic enzyme activities in coho salmon was investigated. Young coho salmon fed a high-carbohydrate diet for 3 weeks were then fasted for 2, 6, or 23 days. Liver preparations were assayed for fatty acid synthetase, citrate cleavage enzyme, malic enzyme, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities. Fasting the fish for 2 or 6 days did not influence the activities of these enzymes; however, by the end of the 23-day fast the activities of all these enzymes had decreased. Changing the diet of the fish from high-carbohydrate to high-fat had only a minimal influence on the activities of the hepatic lipogenic enzymes after 7 to 14 days. Longer-term studies demonstrated that high-fat diets did eventually depress lipogenic enzyme activities. The effect of fasting and feeding on the level of lipogenic enzyme activities was observed only after several weeks, in contrast to hours in the rat. This may reflect a difference between poikilothermous and homoiothermous animals.

This study was undertaken to establish the time sequence of lipogenic changes in adipose tissue of rats when converted from ad libitum feeding to meal-eating. Rats were fed a high carbohydrate diet 2 hours/day for 0 to 10 days (meal-eating). The high speed supernatant fraction from homogenized epididymal fat pads was assayed for citrate cleavage enzyme, acetyl CoA carboxylase, fatty acid synthetase and malic enzyme activities. The effects of meal-feeding on in vitro and in vivo rates of fatty acid synthesis in adipose tissue as well as the amounts of glycogen deposited in the adipose tissue were measured. During the first 10 days of meal-feeding, the lipogenic enzyme activities were actually decreased or unchanged in the meal-fed rats but during this time the in vitro and in vivo rates of fatty acid synthesis were progressively increased in the meal-fed rats. Glycogen levels in the adipose tissue of meal-fed rats were greater than the levels in the nibblers. The initial hyperlipogenesis observed in the meal-fed rat appears to be due to changes in substrate uptake by the adipose tissue and/or to alterations in enzyme activation in the adipose tissue rather than to changes in the quantity of enzyme present in the tissue.

Four diets containing 0 to 62% of energy from carbohydrate and 24% to 48% of energy from protein were fed to young dogs. Two of the diets (diets LPLC and HPLC) were carbohydrate-free and two of the diets (diets HPHC and HPLC) contained 46% to 48% protein. The influence of these diets on several parameters of glucose metabolism was ascertained. Following an intravenous glucose load, plasma glucose levels were higher in dogs fed carbohydrate-free diets (diets LPLC and HPLC) than observed in dogs fed carbohydrate-containing diets (diet LPHC and HPHC). Consumption of high-protein diets (diets HPHC and HPLC) also impaired glucose tolerance. Estimates of glucose utilization were obtained. Dogs fed carbohydrate-containing diets exhibited a higher rate of glucose utilization than did dogs fed the carbohydrate-free diets. Fasting the dogs for 48 hours reduced the glucose replacement rate in dogs fed the carbohydrate-containing diets but did not influence the rate of glucose utilization in dogs fed the carbohydrate-free diets. The activities of phosphoenolpyruvate carboxykinase (PEPCK) and of pyruvate carboxylase (PYCAR) in livers and kidneys of these dogs were influenced by the diets fed. Mitochondrial PEPCK and PYCAR activities in both liver and kidney were increased in dogs fed the carbohydrate-free diets. Consumption of the high-protein diets actually decreased the activities of PEPCK in liver and kidney mitochondria.

Accumulation of p-aminohippurate (PAH) and N-methylnicotinamide (NMN) by renal cortical slices was used to estimate transport capacity for organic anions and cations, respectively. In a previous study, renal organic anion transport appeared to be selectively depressed in animals rendered obese by high fat feeding. However, the effects of obesity could not be discretely separated from the effects of the 30% fat diet used to produce the obesity. Genetically obese hyperglycemic mice provided a model to determine the effect of obesity on renal transport systems without the complication due to diet. Accumulation of both PAH and NMN was depressed in renal cortical slices from genetically obese mice. Addition of plasma from thin or obese animals increased PAH accumulation by slices from thin animals. Accumulation by slices from obese animals was unaffected by addition of plasma. Oxygen consumption with acetate in the medium was less in kidneys from obese mice than kidneys from thin mice. Thus, in addition to inhibition of transport capacity, renal cortex of genetically obese mice has a biochemical defect that prevents response to stimulators. It is concluded that several renal functions are depressed in the genetically obese hyperglycemic mouse. Whether the depressed function results from the obesity or is concomitant with the gene for obesity is as yet undertermined.

Six semipurified canned diets ranging in composition from 0 to 62% of energy from carbohydrate and from 20% to 48% of energy from protein were fed to female beagle dogs for 8 months. Additionally, three commercial-type diets were also fed. The effects of these diets on growth, body composition and selected blood metabolite levels in the dogs were studied. The dogs readily consumed each of the nine diets fed. The level of carbohydrate, fat or protein in the diet did not influence body weight gain during the first 16 weeks nor was nitrogen balance affected by the diets. At the end of the 32-week study, dogs fed the high-carbohydrate (62% of energy) diet contained less body fat but an equal-free mass, than did dogs fed lower-carbohydrate (20--42% of energy) diets with a similar quantity of protein. Consumption of carbohydrate-free diets did not influence postprandial levels of circulating glucose or insulin in the dogs. Plasma cholesterol levels were elevated in dogs consuming in the diets high in fat but plasma triglyceride levels were not influenced by the diets fed. Consumption of high-protein (46--48% of energy) diets elevated plasma urea nitrogen levels but had minimal influence on plasma amino acid levels. The general response of these young dogs was not markedly influenced by consumption of diets ranging from carbohydrate-free to high-carbohydrate and from adequate-protein to high-protein.

Chickens (1,200 g) were fasted 1, 4, or 8 days. Significant decreases occurred in total body protein and fat with fasting, with the greatest energy loss from fat. Glucose production determined with either [2-3H] or [6-3H] glucose injected simultaneously with [U-14C] glucose remained constant with fasting at 10 to 13 mg/minute/kg body weight which is much higher than reported for mammals. Blood lactate and glycerol were unchanged with fasting, while pyruvate increased and plateaued. Plasma alanine, serine and glycine levels were extremely high compared to values in fasted mammals. Blood beta-hydroxybutyrate increased dramatically with fasting (350 to 3,500 nm/ml), while acetoacetate remained constant. The hepatic lactate: pyruvate ratio was unchanged with fasting, while the beta-hydroxybutyrate:acetoacetate ratio increased. These ratios have been reported to influence phosphoenolpyruvate (PEP) and glucose production in mammals. Hepatic and renal phospyoenolpyruvate carboxykinase (PEPCK) levels remained constant, while hepatic lactate dehydrogenase increased with fasting. Beta-Hydroxybutyrate dehydrogenase levels were very low at all times. The results indicate little glucose sparing adaptation per kg in the fasting chicken.

Female obese (ob/ob) and lean mice were weaned at 21 days of age, placed in wire-mesh cages maintained at 25 to 30 degrees, and fed a high-fat or a high-carbohydrate diet for 21 days. The body energy balance procedure was utilized to determine the maintenance energy requirements, and the efficiency of dietary energy utilization, above maintenance, in these mice. Heat production of each mouse was measured weekly in a gradient-layer calorimeter. Regressions of changes in body energy per kg3/4 on metabolizable energy intake per kg3/4 indicated that the maintenance energy requirement averaged 72 kcal/kg3/4/day for obese mice and 124 kcal/kg3/4/day for lean mice. Diet composition did not influence the maintenance energy requirements, but utilization of energy, above maintenance, in obese mice fed the high-fat diet was 41% more efficient than observed in obese mice fed the high-carbohydrate diet and 38 to 71% more efficient than observed in lean mice. Heat production, per unit body weight was lower in obese mice than in lean mice. The lowest heat production was observed in obese mice fed the high-fat diet. The 40% lower maintenance energy requirement of the obese mice is a major factor contributing to the high efficiency of energy retention in these mice. Consumption of a high-fat diet further improved the ability of the obese mice to retain dietary energy.

The influence of dietary 1,3-butanediol (BD) on body weight gain, blood and liver metabolites, and on lipogenesis in pigs and chicks was studied. Body weight gain and energy intake of both pigs and chicks were depressed when the dietary energy derived from BD exceeded about 20 percent. Circulating beta-hydroxybutyrate and acetoacetate levels were markedly increased by dietary BD. Plasma triglyceride levels were increased in pigs and unchanged in chicks fed BD-containing diets. In vitro rates of fatty acid synthesis and the activities of fatty acid synthetase and malic enzyme in pig adipose tissue were not affected by the dietary BD. Neither addition of 18 percent dietary energy in the form of BD to the diet nor addition of BD to the incubation buffer affected glucose conversion to fatty acids by chick liver slices. Dietary BD did not affect long-chain acyl CoA levels in freeze-clamped chick liver but did increase the free CoA levels slightly. The hepatic lactate: pyruvate ratio was decreased when chicks were fed a BD-containing diet.

Rats, chicks and pigs were fed diets containing safflower oil or tallow. Plasma triglyceride levels were elevated when tallow, rather than safflower oil was added to the diet of rats, unchanged in chicks and lowered when tallow, rather than safflower oil was fed to pigs. The rate of fatty acid synthesis in rat and chick liver was higher, whereas the rate of lipogenesis in adipose tissue preparations from rats and pigs was lower when tallow, rather than safflower oil was fed. These results indicate that there are species-specific, as well as organ-specific, metabolic responses to various dietary fats.

(3H)-Ouabain binding to liver and kidney preparations was utilized to estimate the number of Na+, K+-ATPase enzyme units in livers and kidneys from rats fed 2% corn oil supplemented or fat-free diets. The specific (3H)-ouabain binding in liver and kidney preparations from fatty acid deficient rats was increased approximately 40%, but the affinity of the binding sites for ouabain (Kd-value) remained unchanged. The increased concentration of Na+, K+-ATPase enzyme units observed in the essential fatty acid deficient rats may contribute to the reduced body fat accumulation and elevated heat production observed in these animals.

The influence of glycerol on the rates of fatty acid snythesis in liver slices from rats and chickens in pieces of adipose tissue from rats was first studied. Then the effect of dietary glycerol on lipid metabolism in rats and cheickens was examined. Media containing 3 or 10 mM glycerol depressed the rate of glucose conversion to fatty acids in rat liver slices. However, media containing up to 25 mM glycerol did not influence the rate of fatty acid synthesis in chick liver slices. The inhibitory action of glycerol in rat liver slices might occur at the level of glucose (or glycogen) conversion to pyruvate because glycerol did not inhibit pyruvate or acetate conversion to fatty acids. Rats and chickens were fed glycerol containing diets for either 3 days or 3 weeks. Feeding diets containing 20.5 parts glycerol (22% of dietary energy) to rats or chickens did not influence the growth rate of the animals. However, substitution of 42.2 parts glycerol (43% of dietary energy) for glucose in the diet significantly depressed food intake and growth rate in both rats and chickens. The activities of citrate cleavage enzyme, fatty acid synthetase and malic enzyme in livers of rats fed the glycerol-containing diets were dramatically increased. However, this stimulation of enzyme activity occurred without a concomitant increase in the in vivo rate of fatty acid synthesis in the rat liver. In the chicken, unlike the rat, dietary glycerol did not stimulate but instead decreased hepatic malic enzyme and fatty acid synthetase activities. No significant differences in adipose tissue lipogenic enzyme activities or in the rates of fatty acid synthesis were observed in rats fed glycerol-containing diets. The lipogenic response to glycerol feeding depends on the species as well as the organ.

From 7-day food diaries of a cross-sectional sample of American children (n = 657), breakfast consumption patterns were assessed and related to average daily nutrient intake patterns. Results indicated that few of the children skipped breakfast and that breakfast consumption made a significant contribution to the average child's daily nutrient intake. Further, children who had ready-to-eat cereals at breakfast three or more times during the 1-wk period were found to have consumed significantly less (p less than 0.001) fat and cholesterol and significantly more (p less than 0.001) fiber, thiamin, niacin, riboflavin, iron, folacin, pyridoxine, and vitamins B12, A and D than those who had no ready-to-eat cereal at breakfast. Average total daily intakes of the same groups had fewer significant differences. Comparison of the average nutrient composition of the three types of consumed breakfasts revealed that the average breakfast containing presweetened or nonsweetened ready-to-eat cereal had a higher content of sixteen nutrients and a lower content of five nutrients than did the average breakfast including no ready-to-eat cereal.

The possible involvement of Na+,K+-ATPase in the etiology of obesity in the obese (ob/ob) mouse was explored. The number of Na+,K+-ATPase enzyme units in skeletal muscle, liver, and kidneys from 4- and 8-wk-old obese and lean mice was estimated from saturable [3H]ouabain binding to particulate fractions. Neither phenotype nor age altered the Kd value for ouabain binding in these three tissue preparations. The total number of [3H]ouabain binding sites in hindlimb muscles was 35--55% lower in 4- and 8-wk-old obese mice than in their lean counterparts. However, the total number of [3H]ouabain binding sites in liver and kidneys of obese mice was similar to values observed in their lean counterparts. Because it has been suggested that ob/ob mice are hypothyroid, we investigated the response of Na+,K+-ATPase in these mice to thyroid hormone treatment (approximately 5 microgram thyroxine/day for 2 wk). The number of [3H]ouabain binding sites in the three tissues increased in both obese and lean mice injected with this relatively large dose of thyroxine, but the obese mice were 2--3 times more responsive than lean mice.