In this paper, we consider the control of energy balance in animals and man. We argue that patterns of mammalian feeding have evolved to control energy balance in uncertain environments. It is, therefore, expected that, under sedentary conditions in which the diet is rich in nutrients and abundantly available, animals and man will overeat. This suggests that no physiological defects are needed to induce overweight and ultimately obesity in man. Several considerations arise from these observations. The time period over which energy balance is controlled is far longer than allowed by most experiments. Physiological models of energy balance control often treat excess energy intake as a defect of regulation; ecological models view the same behaviour as part of normal energy balance control in environments where resources are uncertain. We apply these considerations to common patterns of human and animal feeding. We believe that the ecological perspective gives a more accurate explanation for the functionality of excess fat and the need to defend nutrient balance and avoid gross imbalances, as well as explaining hyperphagia in the face of plenty. By emphasising the common features of energy balance control in different mammalian species, the importance of changes in behaviour to accommodate changes in the environment becomes apparent. This also opens up possibilities for the control of body weight and the treatment of obesity in man.

The effect of the feeding period on larval development was investigated in European sea bass larvae by considering the expression level of some genes involved in morphogenesis. Larvae were fed a control diet except during three different periods (period A: from 8 to 13d post-hatching (dph); period B: from 13 to 18dph; period C: from 18 to 23dph) with two compound diets containing high levels of vitamin A or PUFA. European sea bass morphogenesis was affected by these two dietary nutrients during the early stages of development. The genes involved in morphogenesis could be modulated between 8 and 13dph, and our results indicated that retinoids and fatty acids influenced two different molecular pathways that in turn implicated two different gene cascades, resulting in two different kinds of malformation. Hypervitaminosis A delayed development, reducing the number of vertebral segments and disturbing bone formation in the cephalic region. These malformations were correlated to an upregulation of retinoic acid receptor γ, retinoid X receptor (RXR) α and bone morphogenetic protein (BMP)4. An excess of PUFA accelerated the osteoblast differentiation process through the upregulation of RXRα and BMP4, leading to a supernumerary vertebra. These results suggest that the composition of diets devoted to marine fish larvae has a particularly determining effect before 13dph on the subsequent development of larvae and juvenile fish.

Stearoyl-CoA desaturase (SCD) is a key enzyme that determines the composition and metabolic fate of ingested fatty acids, in particular the conversion of trans-vaccenic acid (TVA) to conjugated linoleic acid (CLA). The present study addressed the hypothesis that intestinal TVA absorption and biotransformation into CLA can be modulated by EPA and 3,10-dithia stearic acid (DSA) via altered SCD mRNA levels and desaturation indices (cis-9, trans-11-CLA:TVA and oleic acid:stearic acid ratios) in Caco-2 and T84 cells, two well-established in vitro models of the human intestinal epithelium. The study determined the effect of acute (3h with 0·3mm-EPA or 0·3mm-DSA) and acute-on-chronic (1 week with 0·03mm-EPA or -DSA, followed by respectively, 0·3mm-EPA or -DSA for 3h) treatments. In both cell lines, acute EPA treatment did not alter SCD desaturation indices, whereas the acute-on-chronic treatment affected these surrogate markers of SCD activity. This was associated with reduced sterol regulatory-element binding protein-1c and SCD mRNA levels. In contrast, acute and acute-on-chronic DSA treatments significantly reduced SCD desaturation indices without affecting SCD mRNA levels in Caco-2 cells. The present study on intestinal cells shows that the conversion rate of TVA to c9, t11-CLA is affected by other fatty acids present in the diet such as EPA, confirming previous observations in hepatic and mammary cell models.

The effects of six balanced diets for 3 weeks on dietary intake, growth, liver weight and fat, plasma cholesterol, total antioxidant capacity, liver glutathione status and antioxidant enzymes in growing male Wistar rats were studied. Ten rats per group were fed casein- and soyabean-based diets with or without 2·4% cholesterol-raising agent. Seven percent of the diet consisted of a cellulose–wheat starch mix (35:65; control diets), freeze-dried nori (nori diets) or konbu (konbu diets). The 7% dietary supplement of seaweeds was well accepted and induced normal growth rates in rats. Except for food intake, total and reduced glutathione and total antioxidant capacity, dietary cholesterol addition significantly affected (at least P<0·05) all parameters studied. Alga consumption affected total and reduced glutathione, glutathione reductase activity, plasma cholesterol, and total and cholesterol-adjusted total antioxidant capacity (at least P<0·05). A significant cholesterol–alga interaction was found for liver weight, total glutathione peroxidase (GSH-Px) and the Se-dependent GSH-Px:total GSH-Px ratio (at least P<0·05). GSH-Px activity increased in cholesterol-fed nori rats mainly as Se-dependent GSH-Px, while in konbu and control groups the GSH-Px activity was related to increases in both non-Se-dependent and Se-dependent GSH-Px activities. The decrease in the antioxidant status of konbu rats was related to the high As content of this alga, which led to a compensatory increase in glutathione reductase activity in these animals. In conclusion, although some antioxidant compounds are present in algae, other dietary compounds, such as As, induced poor antioxidant status in rats.

The present study evaluated the effect of dietary methionine on breast-meat accretion and protein expression in skeletal muscle of broiler chickens in vivo. All broilers received a common pre-test diet up to 21d of age, and were subsequently fed either a methionine-deficient (MD) or -adequate (MA) diet (3·1 V. 4·5g/kg diet) from age 21 to 42d. Dietary cystine levels were 3·7 V. 3·6g/kg diet for the MD and MA diet, respectively. Detrimental effects on carcass yield (P=0·004), abdominal fat percentage (P=0·001), and breast-meat weight (P=0·001), yield (P=0·001), and uniformity (P=0·002) were observed and validated in birds fed MD diets. Via tandem MS, a total of 190 individual proteins were identified from pectoralis major (PM) muscle tissue. From the former composite, peptides from three proteins were observed to be present exclusively in breast muscle from those chickens fed the MD diet (pyruvate kinase, myosin alkali light chain-1, ribosomal-protein-L-29). No proteins were observed to be uniquely expressed in chickens fed MA diets. Research is warranted to further explore the possibility of the proteins pyruate kinase, myosin alkali light chain-1, or ribosomal protein L-29, as potential biological indicators of differences in protein expression of PM of chickens in response to a dietary methionine deficiency.

Gender and dietary fatty acids are involved in the regulation of lipid metabolism, disturbances of which can lead to pathologies such as metabolic syndrome or CVD. Possible interactions between these factors were investigated in male and female hamsters fed diets rich in either saturated fatty acids (‘butter’ diet) or in α-linolenic acid (‘linseed oil’ diet). Gender effect predominated over the diet effect on cholesterol (CH) metabolism; compared to males, females exhibited lower concentrations of plasma total CH (−20%, P<0·001), LDL-CH (−40%, P<0·001) and HDL-CH (−16%, P<0·001), together with higher LDL receptor (+40%) and lower HDL receptor (−60%) hepatic content. Triacylglycerol (TG) metabolism was affected by diet above all: compared to animals fed the ‘butter’ diet, those fed the ‘linseed oil’ diet exhibited lower plasma (−23%, P=0·046) and liver TG (−20%, P=0·026) concentration which may result from both an increased β-oxidation (P<0·001), without any change in PPARα mRNA, and a decreased hepatic lipogenesis (P=0·023), without increased sterol response element binding protein 1c (SREBP1c) mRNA. The response to diet was much more pronounced in males than in females, without gender effect on the transcription level of PPARα and SREBP1c. Finally, the ‘linseed oil’ diet decreased the insulin resistance index (−80%, P<0·001) with a more marked effect in males, in relation to their higher hepatic PPARγ expression (+90%, P=0·012). In conclusion, in our model, the response of either TG or CH to dietary fatty acids is modulated differently by gender. The possible relevance of these interactions to dietary practice should be taken into account in man.

The Fe solubility test is a commonly used, easy and relatively cheap in vitro tool for predicting Fe bioavailability in food matrices. However, the outcome of a recent field trial comparing the effect on Fe status of Tanzanian infants of processed V. unprocessed complementary foods (CF), with otherwise the same composition, challenged the validity of this test for predicting Fe bioavailability. In the solubility test, significant more soluble Fe was observed in processed compared with unprocessed foods (mean 18·8 (sem 0·21) V. 4·8 (sem 0·23) %; V<0·001). However, in the field trial, no significant difference in Fe status was seen between processed and unprocessed CF groups after 6 months' follow-up. Therefore, twenty-four samples of these CF (twelve processed and twelve unprocessed batches) were analysed in triplicate for Fe availability using an in vitro digestion–Caco-2 cell culture method and results were compared with solubility results. Significantly more soluble Fe was presented to Caco-2 cells in the processed compared with unprocessed samples (mean 11·5 (sem 1·16) V. 8·5 (sem 2·54) % p=0·028), but proportionally less Fe was taken up by the cells (mean 3·0 (sem 0·40)p. 11·7 (sem 2·22) %; p=0·007). As a net result, absolute Fe uptake was lower (not significantly) in processed compared with unprocessed CF (mean 1·3 (sem 0·16) V. 3·4 (sem 0·83) nmol/mg cell protein; p=0·052). These data clearly demonstrate that the Fe solubility test was not a good indicator of Fe bioavailability in these particular food matrices. In contrast, the results of an in vitro Caco-2 model supported the effects observed in vitro.

Evidence from animal studies suggests that conjugated linoleic acid (CLA) modulates plasma and tissue appearance of newly synthesized PUFA. The effects of a 1·2g (0·5% energy) daily intake of the cis-9, trans-11 (c9, t11) isomer of CLA, trans-10,cis-12 (t10, c12) isomer of CLA or olive oil (placebo) on linoleic acid (LA) and linolenic acid (LNA) metabolism in healthy human volunteers was investigated. Fifteen subjects were fed an experimental diet and supplemented with c9,t11-CLA, t10, c12-CLA or placebo for 7d before consuming a tracer dose of U-[13C]La (50%Mg) And U-[13C]Lna (50Mg). Blood Samples Were Taken At 0, 2, 4, 6, 8, 24, 48, 72 and 168%h and analysed using high-precision MS. No differences between the groups in peak plasma [13C]LA (10·3–11·6% of dose), [13C]LNA (2·5–2·9% of dose), [13C]arachidonic acid (0·09–0·12% of dose), [13C]EPA (0·04–0·06% of dose) or [13C]Dha (0c·06–0·10% of dose) were detected. Concentration V. time curves (area under the curve) also showed no significant differences between groups. This suggests that, in healthy human subjects consuming a diet with adequate intake of essential fatty acids, CLA does not affect metabolism of LA or LNA

Tomatoes are an important part of the diet. Lycopene, the predominant carotenoid in tomatoes, is hypothesised to mainly mediate the health benefits of tomato products. Anticancer activity of tomato products and lycopene has been suggested by numerous studies. The aim of the present study was to investigate the effect of ingestion of three different tomato-based foodstuffs on plasma contents of lycopene, tocopherols and ascorbic acid. Because isomers of lycopene may have different biological activities, a special interest was to look how the lycopene isomer pattern is changed depending on the matrix of tomato products. Following a 2-week depletion phase volunteers ingested 12·5mg lycopene/d for 4 weeks comprising tomatoes, tomato juice or tomato purée. The basal levels of lycopene in plasma were comparable for all groups and decreased significantly during the 2 weeks of depletion to approximately half of the basal values. Following intervention, plasma lycopene concentration increased significantly. Conversely, supplementation did not significantly affect levels of tocopherols and ascorbic acid in plasma. Regarding isomers of lycopene, the (Z)-lycopene:(all-E)-lycopene plasma isomer ratio was significantly changed during the study for all groups. A remarkable enrichment of the relative contents of (5Z)-lycopene was observed during the depletion period, which supports the hypothesis that lycopene (Z)-isomers are formed within the human body after ingestion of (all-E)-lycopene. After dietary intervention with lycopene-rich products the isomer ratios returned to those observed at the start of the study. Further investigations will clarify the process of isomerisation in more detail.

Extra-virgin olive oils (EVOO), high in phenolic compounds with antioxidant properties, could be partly responsible for the lower mortality and incidence of cancer and CVD in the Mediterranean region. The present study aims to measure oxidative DNA damage in healthy human subjects consuming olive oils with different concentrations of natural phenols. A randomised cross-over trial of high-phenol EVOO (high-EVOO; 592mg total phenols/kg) V low-phenol EVOO (low-EVOO; 147mg/kg) was conducted in ten postmenopausal women in Florence. Subjects were asked to substitute all types of fat and oils habitually consumed with the study oil (50g/d) for 8 weeks in each period. Oxidative DNA damage was measured by the comet assay in peripheral blood lymphocytes, collected at each visit during the study period. Urine samples over 24h were collected to measure the excretion of the olive oil phenols. The average of the four measurements of oxidative DNA damage during treatment with high-EVOO was 30% lower than the average during the low-EVOO treatment (p=0·02). Urinary excretion of hydroxytyrosol and its metabolite homovanillyl alcohol were significantly increased in subjects consuming high-EVOO. Despite the small sample size, the present study showed a reduction of DNA damage by consumption of an EVOO rich in phenols, particularly hydroxytyrosol.

The aim of this human intervention study was to evaluate the Δ9-desaturation of trans-11–18:1 (trans-vaccenic acid; tVA) to cis-9,trans-11–18:2 (c9,t11 conjugated linoleic acid; CLA) and of trans-12–18:1 (t12) to cis-9,trans-12–18:2 after a short-term (7d) and a long-term (42d) supplementation period. The conversion rates of both trans-18:1 isomers were estimated by lipid analysis of serum and red blood cell membranes (RBCM). Subjects started with a 2-week adaptation period without supplements. During the 42d intervention period, the diet of the test group was supplemented with 3g/d of tVA and 3g/d of t12. The diet of the control group was supplemented with a control oil. Serum tVA and t12 levels in the test group increased by fivefold and ninefold after 7d, respectively, and by eight- and 12-fold after 42d, respectively, when compared with the adaptation period (p≤0·002). The serum c9,t11CLA levels increased by 1·7- and 2·0-fold after 7d and 42d, respectively (p≤0·001). After 42d, the test group's RBCM c9,t11CLA content was elevated by 20% (p=0·021), whereas in the control group it was decreased by 50% (p=0·002). The conversion rate of tVA was estimated at 24% by serum and 19% by RBCM. No increase in c9,t12–18:2 was observed in the serum and RBCM, and thus no conversion of t12 could be determined. In conclusion, the endogenous conversion of dietary tVA to c9,t11CLA contributes approximately one quarter to the human CLA pool and should be considered when determining the CLA supply.

Malnutrition is common in pulmonary tuberculosis (TB), and may impair survival. The objective of this study was to assess effects of multi-vitamin/mineral (MVM) and zinc (Zn) supplementation during TB treatment on mortality. Patients diagnosed with sputum-positive pulmonary TB in Mwanza, Tanzania, were randomised, using a two-by-two factorial design, to Zn (45mg) or placebo, and MVM (vitamins A, B, C, D, E, and selenium and copper) or placebo. Survival status was ascertained at the end of the 8-month TB treatment and supplementation period. Of 499 TB patients, 213 (43%) had HIV. The mean weight gain at 7 months was 6·88kg (95% CI 6·36, 7·41). Zn and MVM combined, but neither alone (interaction, p=0·03), increased weight gain by 2·37kg (95% CI 0·91, 3·83), irrespective of HIV status. Survival status at 8 months was determined for 422 patients (84·6%), of which fifty-two (12·3%) had died. Among fifty-two deaths, there were no effects of MVM (relative risk (RR) 0·73; 95% CI 0·43, 1·23) and Zn (RR 0·76; 95% CI 0·46, 1·28). However, among HIV co-infected patients, marginally significant effects of both MVM (RR 0·60; 95% CI 0·34, 1·05) and Zn (RR 0·63, 95% CI 0·37, 1·08) were seen, and MVM and Zn combined reduced mortality (RR 0·29; 95% CI 0·10, 0·80; interaction ratio 0·52). In conclusion, supplementation with MVM, including Zn, during treatment of pulmonary TB may reduce mortality in those co-infected with HIV. A randomised trial of the effect of the combined intervention used in this study should be conducted in a different setting to confirm the finding.

The aim of the present study was to test the hypothesis that maternal intake of antioxidant vitamins is associated with maternal and cord plasma levels at delivery. Women were recruited in early pregnancy in Aberdeen Maternity Hospital and habitual diet during pregnancy was assessed by a food-frequency questionnaire mailed at 34 weeks gestation. Blood samples were taken at recruitment (n 1149) and maternal (n 1149) and cord blood samples (n 747) taken at delivery for analyses of vitamins A, C, E and β-carotene. Maternal plasma levels of vitamin E and β-carotene at delivery were significantly higher than levels in early pregnancy while levels of vitamins A and C were significantly lower. Positive correlations were observed for maternal levels of all the vitamins between early pregnancy and delivery. At delivery, maternal plasma concentrations of vitamins A, E and β-carotene were significantly higher than cord levels, while maternal levels of vitamin C were significantly lower. There were significant correlations between maternal and cord plasma concentrations for β-carotene and vitamin C but not for vitamins A or E. Maternal dietary intakes were positively correlated with maternal plasma levels of vitamins C, E and β-carotene in early pregnancy, with maternal plasma levels of β-carotene and vitamin C at delivery and with cord plasma levels of β-carotene and vitamin C. The results from the present study show that, in this population, maternal diet influences cord plasma levels of β-carotene and vitamin C, but not vitamins A and E.

Triacylglycerol (TG) lowering effects of n−3 long-chain PUFA (n−3 LCPUFA) have been repeatedly demonstrated, but studies investigating the individual effects of EPA or DHA on plasma TG and lipoproteins in man are rare. The effects of a new DHA-rich, almost EPA-free microalgae oil (Ulkenia sp.) on plasma lipids and several safety parameters were investigated in a double-blind, placebo-controlled, parallel design intervention study. Normolipidaemic vegetarians (eighty-seven females, twenty-seven males) consumed daily microalgae oil (0·94g DHA/d) or olive oil (as placebo) for 8 weeks. DHA supplementation decreased plasma TG by 23% from 1·08 (sem 0·07) to 0·83 (sem 0·04) mmol/l (p<0·001). Absolute TG decreases after DHA supplementation were inversely correlated to baseline TG concentrations (r −0·627, p<0·001). Plasma total, LDL and HDL cholesterol increased significantly in the DHA group, resulting in lower TG:HDL cholesterol and unchanged LDL:HDL and total cholesterol:HDL cholesterol ratios. The intake of DHA-rich microalgae oil did not result in any physiologically relevant changes of safety and haemostatic factors. In conclusion, DHA-rich oil from microalgae Ulkenia sp. was well tolerated and can be considered a suitable vegetarian source of n−3 LCPUFA. Although DHA supplementation improved some CHD risk factors (plasma TG, TG:HDL cholesterol ratio), LDL cholesterol increased. Therefore, the overall effects of this intervention on CHD risk deserve further investigation.

The majority of research has focused on the association between trans unsaturated fatty acids (TUFA) from hydrogenated vegetable oils and heart disease even though TUFA are also produced from hydrogenated fish oil. We compared the acute effect of three solid fats on postprandial cholesterol, triacylglycerol (TAG) and NEFA concentrations in normocholesterolaemic males. Eight healthy male volunteers consumed each of the three 40g fat meals (partially hydrogenated fish oil (PHFO), palm oil and lard) in random order and blood samples were drawn at 2, 4, 6 and 8h thereafter for lipid analysis. The postprandial response in plasma TAG, TAG-rich lipoprotein-TAG (TRL-TAG), total cholesterol and plasma NEFA, measured as the area under the postprandial curve, was not significantly different between the three meals (p>0·05), which varied in MUFA, PUFA and TUFA content. There was no marked elevation of longer-chain fatty acids (C20–22, cis or trans isomers) into the TRL-TAG fraction following the PHFO meal even though they provided 40% of the total fatty acids in the PHFO meal. The postprandial TRL-TAG response to PHFO was expected to be higher, as it is higher in TUFA, lower in PUFA and similar in saturated fatty acid composition compared with the lard and palm oil test meals. The absence of a higher postprandial response following ingestion of PHFO could be as a result of reduced absorption and increased oxidation of long-chain fatty acids (both cis and trans isomers)

The aim of the study was to provoke cephalic and metabolic responses by oral fat stimulation with different high-fat meals in the postprandial state. A randomized parallel design was executed with three groups of subjects (twenty-six women and ten men; twelve subjects per group). Oral fat stimulation was achieved by the modified sham feeding (MSF) technique. Five hours after a high-fat breakfast, the subjects were given one of three test meals in random order: a high-fat lunch, water or the same lunch as the MSF. The main fat sources in the high-fat lunch and MSF were olive oil, linoleic oil and oleic oil. For 3h after the test meal, blood samples were taken for analysis of metabolite, and visual analogue scales of appetite profile were completed. A cephalic response appeared to be achieved by MSF in that we observed a relative increase in insulin and glucose; this response lasted up until 90min, indicating possible vagal stimulation. NEFA increased significantly after MSF compared with water ingestion in the case of olive oil (p<0·0001) and linoleic oil (p<0·05), but not with oleic oil. MSF provoked a significantly higher increase in triacylglycerol and glycerol levels compared with water ingestion in the case of linoleic oil (p<0·05). Satiety was significantly increased in the eating condition and in the MSF condition (p<0·0002, all oils) compared with water ingestion. We conclude that cephalic and perhaps vagal stimulation by different fats increased the concentrations of the metabolites and stimulated satiety, with linoleic oil showing the strongest response.

Relative validity and reproducibility of a semi-quantitative food-frequency questionnaire (FFQ) for measuring preschool children's usual Ca intake were assessed using parents or guardians as a proxy. Estimated diet records (EDR; 3d) were used as the reference method and reproducibility was measured by repeated FFQ administrations 5 weeks apart. From 2095 preschool children (2·5–6·5 years) randomly selected in Flanders (Flemish region of Belgium), 1052 returned a FFQ and EDR. Stringent exclusion procedures reduced the sample for validity analyses to 509 children. From a separate sample of 244 preschool children, 124 returned two FFQ, of whom sixty were included in the reproducibility analysis. Mean Ca intakes were 838 (sd 305) and 777 (sd 296) mg/d for EDR and FFQ respectively, indicating a mean difference of 60·9 (sd 294·4) mg/d (p<0·001). Pearson's correlation was 0·52. Cross-classification analysis of the FFQ and EDR classified 83%of the subjects in the same or adjacent category and 2·4% in extreme quartiles. Actual values for surrogate FFQ quartiles showed a progressive increase in Ca intake (p<0·001). The FFQ correctly identified 77% of the children consuming less Ca than the age-specific RDA (800mg/d). Correlation between repeated administrations was 0·79. No significant difference between mean Ca intakes was established by two administrations (23·8 (sd 161·2) mg/d). Cross-classification of repeated administrations classified 93·4% of the subjects in the same or adjacent category and no subjects in extreme categories. This FFQ tended to underestimate preschool children's Ca intake when administered by a proxy. However, it demonstrated good repeatability and fairly good ability to classify subjects into extremes of Ca intake.

The purpose of this study was to investigate the association between dietary patterns and sexual maturation among Korean children. A cross-sectional study was conducted in 422 boys and 365 girls aged 9–12 years living in Seoul, Korea. Three-day food records were obtained, and pubertal stages were determined with a questionnaire using Tanner stages. Body fat was measured by bioelectrical impedance analysis, and bone mass content at the right calcaneus was measured by portable dual-emission X-ray absorptiometry. Exploratory factor analysis with a Varimax rotation was applied to identify dietary patterns using twenty-four food groups. Four distinct dietary patterns – ‘rice and Kimchi’, ‘shellfish and processed meat’, ‘pizza and drinks’ and ‘milk and cereal’ – were obtained. Twenty-six per cent (24% stage 2, 2% stage 3) of boys had genital development, and 79% (63% stage 2, 16% stage 3) of girls showed breast development. In boys, genital development was weakly positively associated with ‘shellfish and processed meat’ dietary factor scores (odds ratio 1·65, CI 0·95, 2·89, pfor trend 0·07) after adjusting for confounders. In girls, breast development was significantly positively associated with the factor score of ‘shellfish and processed meat’ (odds ratio 1·88, CI 1·08, 3·26, p for trend 0·05). These results suggest that dietary patterns were related to body composition and sexual maturation among the Korean children. Further investigations are needed to identify components of the foods consumed in high amounts in these patterns and how they are related to sexual maturation.

This prospective study investigated the relationship between the consumption of fish and intake of long-chain n−3 fatty acids and the risk of coronary heart mortality in 2775 men and 2445 women aged from 30 to 79 years who were free of CHD and had participated in a health examination survey from 1967 to 1972. In total, 335 men and 163 women died of CHD during a follow-up until the end of 1992. A dietary history interview method provided data on habitual consumption of fish and other foods over the preceding year at baseline. The intakes of long-chain n−3 fatty acids were calculated on the basis of food composition values of Finnish foods. Higher consumption of fish was associated with a decreased risk of CHD among women, whereas no significant association was seen among men. The relative risk between the highest and the lowest quintile for fish consumption was 1·00 (95% CI 0·70, 1·43; p for trend 0·83) for men and 0·59 (95% CI 0·36, 0·99; p for trend 0·02) for women in analysis adjusting for age, energy intake, geographical area, BMI, serum cholesterol, blood pressure, smoking, occupation and diabetes; however, after adjustment for dietary confounders this association was no longer significant. The intake of n−3 fatty acids was not significantly associated with the risk of CHD in either men or women. In conclusion, our results for women are in line with the suggested protective effect of fish consumption against CHD but a similar association was not, however, found in men.

We previously showed that neonatal leptin treatment programmes higher body weight and food intake in adult rats. Here we investigate whether leptin treatment during lactation affects the anorectic effect of leptin on adult rats and their hypothalamic leptin receptors (OB-Rb) and whether those changes could have consequences on intermediary metabolism. When the offspring were born, pups were divided into two groups: the Lep group, injected daily with leptin (8μg/100g body weight, subcutaneously) for the first 10d of lactation, and the control group, injected daily with saline. After weaning (day 21), body weight and food intake were monitored until the rats were 150d old. Food intake was higher in the Lep group (approximately 14%, p<0·05) from day 133 onwards, and body weight was higher (approximately 10%, p<0·05) from day 69 onwards, compared with the control group. At 150d of age, the rats were tested for food intake in response to either leptin (05mg/kg body weight intraperitoneally; groups CL and LepL) or saline (groups CSal and LepSal). The CL group showed a decrease in food intake, but no response was observed in the LepL group, suggesting leptin resistance. The Lep group demonstrated a decrease in OB-Rb expression (−40% p<0·05), hyperleptinaemia (+78%, p<0·05), hyperinsulinaemia (+100%, p<0·02), hypertriacylglycerolaemia (+17%, p<0·05) and a higher protein content in the body (+16%, p<0·05) without changes in fat mass and glycaemia. We conclude that neonatal leptin treatment programmes both hyperleptinaemia and hyperinsulinaemia in adulthood, which leads to leptin resistance by reducing the expression of the hypothalamic leptin receptor.