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BACKGROUND: The neural mechanisms of anorexia nervosa (AN), a severe and chronic psychiatric illness, are still poorly understood. Altered body state processing, or interoception, has been documented in AN, and disturbances in aversive interoception may contribute to distorted body perception, extreme dietary restriction, and anxiety. As prior data implicate a potential mismatch between interoceptive expectation and experience in AN, we examined whether AN is associated with altered brain activation before, during, and after an unpleasant interoceptive state change. METHODS: Adult women remitted from AN (RAN; n = 17) and healthy control women (CW; n = 25) underwent functional magnetic resonance imaging during an inspiratory breathing load paradigm. RESULTS: During stimulus anticipation, the RAN group, relative to CW, showed reduced activation in right mid-insula. In contrast, during the aversive breathing load, the RAN group showed increased activation compared with CW in striatum and cingulate and prefrontal cortices (PFC). The RAN group also showed increased activation in PFC, bilateral insula, striatum, and amygdala after stimulus offset. Time course analyses indicated that RAN responses in interoceptive processing regions during breathing load increased more steeply than those of CW. Exploratory analyses revealed that hyperactivation after breathing load was associated with markers of past AN severity. CONCLUSIONS: Anticipatory deactivation with a subsequent exaggerated brain response during and after an aversive body state may contribute to difficulty predicting and adapting to internal state fluctuation. Because eating changes our interoceptive state, restriction may be one method of avoiding aversive, unpredictable internal change in AN.

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The objective of this work was to quantify the contribution of fortification (defined here as adding nutrients beyond traditional enrichment standards) to dietary nutrient intakes in the United States. A list of fortified foods was developed that was relevant at the time of the analyses, and prefortification (naturally occurring) nutrients in the fortified foods were determined from industry-supplied data. Using dietary data from the 1989-1991 Continuing Survey of Food Intakes by Individuals (CSFII), intakes of nine nutrients were determined both as reported in the CSFII (i.e., postfortification) and also by using prefortification nutrient levels for the identified fortified foods. We report data for the total population age >/= 1 y based on respondents (n = 11,710) with 3 d of dietary data, as well as select age/gender subgroups. All data were weighted. Fortification substantially increased the intakes of all nutrients examined except calcium, in all age/gender groups but especially in children. In numerous cases, fortification was responsible for boosting median or 25th percentile intakes from below to above the RDA. The breakfast cereal category was responsible for nearly all the intake of nutrients from fortified foods, except vitamin C for which juice-type beverages made as great or a greater contribution. These data from 1989 to 1991 serve as a useful baseline with which to compare contributions of fortification as the practice expands. The large contribution of fortification even in 1989-1991 suggests that continued monitoring of fortification practices, using methods such as those presented here, is important.

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A group of 12 research scientists participated in a roundtable discussion on the health implications of milkfat in balanced diets. Four subjects areas were addressed: contributions of dairy foods and other fat sources to diets in the United States; influence of individual fatty acids on coronary heart disease risk; dairy foods and coronary heart disease risk; and health implications of low fat diets. The purpose of the meeting was twofold. First, the researchers evaluated the impact of fatty acids, milkfat and dairy foods on coronary heart disease risk, based on currently available evidence. They met this objective by considering statements of "fact" that were accepted, modified or rejected upon discussion. Final statements are presented in this report. Second, the group identified research questions that must be addressed to better define the role of dietary fats (in general) and milkfat (in particular) in varied diets. Critical study design considerations were high-lighted. Participants agreed that standard-fat dairy foods can fit into diets meeting contemporary fat intake guidelines; the guiding principles of balance, variety and moderation were stressed. More research is needed to understand fully the impact on blood lipid profiles (and on other indicators of disease risk) of butter and other sources of milkfat in mixed-fat diets.

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In this paper we have described physiological factors that are likely to influence iron bioavailability, reviewed chemical properties of iron important to its absorption, and addressed the question posed in the title. Intestinal transit times, luminal pH, and diffusion barriers resulting from gastrointestinal mucus may affect absorption. The tendency of iron to form large-molecular-weight species and to bind to macromolecules may limit its absorption. Iron solubility following in vitro gastrointestinal digestion is a reliable predictor of ascorbic acid effects on bioavailability but not of protein effects. Solubility of low-molecular-weight iron is better than simple solubility for predicting iron bioavailability.

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The availability of iron from 59Fe-labeled polymeric ferric hydroxides and low-molecular-weight ferric complexes (LMW iron) was compared by using ligated rat duodenal segments, in vivo. The effect of iron status was assessed by using iron-adequate (Hb 12.3-15.5 g/dl) and iron-deficient (Hb 8.1-10.6 g/dl) rats for each iron treatment. Analysis of data from the animal experiment showed: less (P less than 0.01) iron from polymers [6.8% (iron adequate) and 7.7% (iron deficient)] was transferred to the carcass than from LMW iron [29.2% (iron adequate) and 47.9% (iron deficient)] and iron-deficient animals absorbed more iron than iron-adequate rats from LMW iron but not from polymeric iron. Solubility studies showed that these data could not be attributed to solubility differences between polymers and LMW iron. The results of this experiment suggest that in the intestine factors or conditions that depolymerize iron or prevent polymer formation could enhance iron absorption.

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Availability to rats of Fe in isolated ferric hydroxide polymers was assessed. Polymers were prepared by hydrolyzing an 59Fe-labeled ferric nitrate solution with base (KHCO3). After isolation by gel filtration, the polymers were characterized by spectrophotometric, dialysis, and ultracentrifugation methods. In a split-plot design experiment, Fe-adequate (Hb 11.4-14.0 g/dl) or Fe-deficient (Hb 4.7-9.6 g/dl) male Sprague-Dawley rats (10/treatment) were dosed by stomach tube with one of the following 59Fe-labeled solutions: polymers, Fe(NO3)3 (low-molecular-weight control), polymers + citrate, or Fe(NO3)3 + citrate. As expected, Fe-deficient animals absorbed more Fe than adequate animals (P less than 0.01). There was no difference in absorption of Fe between polymers and low-molecular-weight control doses (P greater than 0.05). In Fe-adequate animals, citrate significantly depressed the uptake of Fe both from Fe(NO3)3 and polymers. These results indicate 1) that polymerization of Fe species prior to ingestion is not a likely means by which Fe is rendered unavailable and 2) that the effect of citrate on Fe absorption may depend on the Fe status of the animal.

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