PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Saturated Fats”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Should mono- or poly-unsaturated fats replace saturated fat in the diet?

The effects of diets differing in saturated, monounsaturated and polyunsaturated fatty acid composition (SAFA, MUFA and PUFA, respectively) on plasma lipoproteins and factor VIIc were investigated in 28 middle-aged men and women with mild to moderate hyperlipidaemia. The subjects were stabilized on a diet with a total fat content fairly typical of New Zealand, containing approximately 40% energy as fat, before entering a randomized cross-over trial of diets high in PUFA (20% energy; SAFA and MUFA 10% each) or a high MUFA diet (20% energy; SAFA and PUFA 10% each). After 6-week periods on each diet the subjects returned to a high SAFA diet. Body weight and blood pressure remained unchanged during the study. Total and LDL cholesterol, HDL cholesterol and the HDL2 subfraction were significantly lower on both the MUFA and the PUFA diet than on SAFA. However, there were no statistically significant differences in lipoprotein concentrations on the MUFA and PUFA diet. Factor VIIc concentrations were similar on the three diets. The proportion of PUFA in a MUFA diet appears to be a major determinant of the relative lipoprotein response to such a diet. In order to avoid a reduction in HDL-C when replacing SAFA with MUFA it may be necessary to ensure that PUFA does not provide more than about 8% total energy. Thus careful planning is needed to identify the most appropriate foods to replace those rich in SAFA in diets designed to reduce the lipoprotein-mediated risk of coronary heart disease.

Aged↗

Phytosterols, but not pectin, added to a high-saturated-fat diet modify saturated fatty acid excretion in relation to chain length.

The main objective of this article was to study how the excretion of saturated fatty acids (SFA) is modified after the consumption of a high-saturated-fat diet that was supplemented with phytosterol and pectin. We present the results of a longitudinal 4-week study on guinea pigs. Diets were supplemented with 0.33% of cholesterol and differed in the content of pectin (three levels) and of phytosterols (three levels). Seventy-two female Dunkin Hartley guinea pigs were randomly assigned to the treatment groups (8 animals/group). Addition of phytosterol resulted in a decrease of lauric (12:0) and myristic (14:0) excretions and in an increase of arachidic (20:0) and behenic (22:0) excretions. Palmitic (16:0) and stearic (18:0) acids did not show a clear change after phytosterol supplementation. Addition of pectin resulted in a decreased excretion of all SFA, although this was not significant. These results suggest that phytosterols added to a high-saturated-fat diet enhance the absorption of the most atherogenic fatty acids (lauric and myristic) after 1 week of treatment, as compared with the high-saturated-fat diet alone.

Animals↗

Dietary restriction of saturated fat and cholesterol decreases HDL ApoA-I secretion.

We examined the mechanisms responsible for the decrease in HDL cholesterol (HDL-C) levels after the consumption of a diet low in total fat, saturated fat, and cholesterol. Twenty-one subjects with a mean age of 58+/-12 years were placed on a baseline isocaloric diet (15% protein, 49% carbohydrate, 36% fat, and 150 mg/1000 kcals of cholesterol) and then switched to an NCEP Step 2 diet (15% protein, 60% carbohydrate, 25% fat, and 45 mg/1000 kcals of cholesterol). After 6 or 24 weeks on each diet, subjects received a 15-hour primed-constant infusion of [5,5,5-2H3]-L-leucine. HDL apoA-I and apoA-II tracer curves were determined by gas chromatography-mass spectrometry and fitted to a monoexponential equation. Compared with the baseline diet, consumption of the Step 2 diet lowered HDL-C mean levels by 15% (1.03+/-0.23 to 0.88+/-0.16 mmol/L, P<0.001), apoA-I by 12% (1.25+/-0.15 to 1.10+/-0.13 g/L, P<0. 001) and the TC/HDL-C ratio by 5% (0.145+/-0.04 to 0.137+/-0.03). No significant changes were observed in apoA-II levels and HDL particle size with diet. HDL apoA-I fractional catabolic rate did not change (0.219+/-0.052 to 0.220+/-0.043 pools/day, P=0.91) but HDL apoA-I secretion rate decreased by 8% (12.26+/-3.07 to 10.84+/-2.11 mg. kg-1. day-1, P=0.03) during consumption of the Step 2 diet. There was no effect of diet on apoA-II fractional catabolic rate or secretion rate. Our results indicate that the decrease in HDL-C and apoA-I levels during the isocaloric consumption of a Step 2 diet paralleled the reductions in apoA-I secretion rate.

Adult↗

Effects of various combinations of omega 3 and omega 6 polyunsaturated fats with saturated fat on serum lipid levels and eicosanoid production in rats.

The effects of varying the ratio of polyunsaturated/saturated fatty acids (P/S) and omega 3/omega 6 polyunsaturated fatty acids (PUFA) of dietary fats on lipid metabolism were studied in rats using safflower oil (SFO), linseed oil (LSO), palm oil (PLO), and a 1:1 combination of these oils. The hypocholesterolemic and hypotriglyceridemic effects depended on the P/S ratio of dietary fats, LSO (omega 3 PUFA) being more effective than SFO (omega 6 PUFA). A similar pattern of the response was observed on liver cholesterol and triglyceride. The liver cholesterol-lowering effect of LSO, but not SFO, remained even when they were combined with PLO. The activity of liver delta 6-desaturase tended to be higher while that of liver phospholipase A2 was significantly lower in the LSO group than in the SFO or PLO groups. The aortic PGI2 production and the production by platelets of thromboxane A2 were significantly low in rats fed LSO accompanying a distinct reduction of arachidonate in tissue phospholipids. The depressing effect of LSO disappeared when it was combined with SFO but not with PLO. There were no significant differences in enzyme activities and eicosanoid production between SFO and PLO in spite of a large difference in their P/S ratio. Thus, lipid parameters examined were complicatedly regulated by the ratios of omega 3/omega 6 as well as P/S, suggesting an existence of an appropriate ratio for these variables.

Animals↗

Interactions of selenium deficiency, vitamin E, polyunsaturated fat, and saturated fat on azoxymethane-induced colon carcinogenesis in male F344 rats.

The effect of the interaction of selenium deficiency, excess vitamin E, and type of fat on colon carcinogenesis induced by azoxymethane (AOM) was studied in male F344 rats. The experimental diets, based on a Torula yeast diet and containing 20% stripped corn oil or 20% stripped lard, were as follows: 1) selenium deficient with adequate (50 mg/kg diet) vitamin E, 2) selenium deficient with excess (750 mg/kg diet) vitamin E, 3) selenium adequate with adequate vitamin E, and 4) selenium adequate with excess vitamin E. Starting at about 3 weeks of age, animals were fed the experimental diets, and at 7 weeks of age all animals except the vehicle-treated controls were given sc injections of AOM (15 mg/kg body wt) once weekly for 2 weeks. Animals were fed the experimental diets until termination of the experiment. Selenium deficiency significantly inhibited the incidence (percentage of animals with tumors) and multiplicity (tumors per animal) of colon adenocarcinomas and adenomas, whereas excess vitamin E had no effect on colon carcinogenesis. There was no interaction between the selenium status and vitamin E; the selenium status and type of fat; vitamin E and type of fat; and among selenium status, vitamin E, and type of fat.

1,2-Dimethylhydrazine↗

Stearoyl-CoA desaturase-1 mediates the pro-lipogenic effects of dietary saturated fat.

Dietary saturated fats have often been implicated in the promotion of obesity and related disorders. It has been shown recently that saturated fats act through the transcription factor SREBP-1c (sterol regulatory element-binding protein-1c) and its requisite coactivator, peroxisome proliferator-activated receptor-gamma coactivator-1beta (PGC-1beta), to exert their pro-lipogenic effects. We show here that a diet high in the saturated fat stearate induces lipogenic genes in wild-type mice, with the induction of the Scd1 (stearoyl-CoA desaturase-1) gene preceding that of other lipogenic genes. However, in Scd1-/- mice, stearate does not induce lipogenesis, and Srebp-1c and Pgc-1beta levels are markedly reduced. Instead, genes of fatty acid oxidation such as Cpt-1 (carnitine palmitoyltransferase-1) as well as Pgc-1alpha are induced. Mitochondrial fatty acid oxidation is increased, and white adipose tissue and hepatic glycogen stores are depleted in stearate-fed Scd1-/- mice. Furthermore, AMP-activated protein kinase is also induced by stearate feeding in Scd1-/- mice. These results indicate that the desaturation of saturated fats such as stearate by SCD is an essential step mediating their induction of lipogenesis. In the absence of SCD1, stearate promotes oxidation, leading to protection from saturated fat-induced obesity. SCD1 thus serves as a molecular switch in the promotion or prevention of lipid-induced disorders brought on by consumption of excess saturated fat.

Animals↗

Centrally fat-saturated three-dimensional magnetic resonance angiography of the abdomen using selective central fat-saturation of k-space.

PURPOSE: To assess the usefulness of centrally fat-saturated three-dimensional magnetic resonance (MR) angiography of the abdomen using an elliptical centric view order and selective placement of fat-saturation pulses in the central 30% portion of the k-space in terms of fat signal reduction, image contrast of post-contrast images, and breath-holding time. METHODS: Fat signal in abdomen and breath-holding time were compared between centrally fat-saturated three-dimensional sequence and partially fat-saturated three-dimensional sequence or conventional fat-saturated three-dimensional sequence. Abdominal contrast-enhanced centrally fat-saturated three-dimensional MR angiography was obtained at arterial and equilibrium phases, and image quality was quantitatively and visually evaluated. RESULTS: Centrally fat-saturated three-dimensional sequence suppressed fat signal, as did the conventional fat-saturated three-dimensional sequence, and the breath-hold was prolonged only by 1.5 seconds compared to the partially fat-saturated three-dimensional sequence. Contrast-enhanced centrally fat-saturated three-dimensional MR angiography provided abdominal MR arteriography with large signal difference between vessels and fat, while venous signal was insufficient at equilibrium phase. CONCLUSION: Abdominal contrast-enhanced centrally fat-saturated three-dimensional MR angiography using an elliptical centric view order and selective central fat-saturation of k-space reduced fat signal comparable to conventional fat-saturated three-dimensional sequence, and provided contrast-enhanced MR arteriography with high vascular contrast and minimum prolongation of breath-hold.

Abdomen↗

Regulation of guinea pig plasma low density lipoprotein kinetics by dietary fat saturation.

Dietary fat saturation has been shown to affect hepatic apoB/E receptor expression and to modify low density lipoprotein (LDL) composition and density in guinea pigs. The current studies were designed to investigate the independent and interactive effects of dietary fat saturation alterations in apoB/E receptor expression and LDL composition on in vivo LDL turnover kinetics, both receptor-mediated and receptor-independent. Guinea pigs were fed semi-purified diets containing 15% fat, either polyunsaturated corn oil (CO), monounsaturated olive oil (OL), or saturated lard, and injected with radioiodinated LDL isolated from animals fed the homologous diet. Blood samples were obtained over 33 h to determine apoLDL fractional catabolic rates (FCR) and flux rates. Compared to animals fed OL- or lard-based diets, intake of the CO-based diet resulted in a 50% decrease in LDL apoB pool size associated with a twofold increase in receptor-mediated FCR (P less than 0.001) and a 28% decrease in flux rate (P less than 0.05). Maximal LDL binding capacity of hepatic apoB/E receptors, determined in vitro, was twofold higher for animals fed the CO-based diet compared to guinea pigs fed the OL- and lard-based diets (P less than 0.01). There was a significant correlation between hepatic apoB/E receptor number and in vivo receptor-mediated LDL FCR (r = 0.987). Significant differences in LDL turnover were related to the source of LDL. When injected into animals fed a nonpurified commercial diet, the smaller, cholesteryl ester-depleted LDL isolated from animals fed the CO-based diet had a twofold higher FCR compared to larger LDLs from guinea pigs fed the OL- and lard-based diets, which had similar turnover rates. When LDL from animals fed the commercial diet was radiolabeled and injected into animals fed the three types of dietary fat, significant differences in LDL turnover were observed in the order CO greater than lard greater than OL, suggesting that intravascular processing and tissue uptake of the smaller LDL from animals fed the commercial diet varies depending on the dietary fat saturation fed to the recipient animals. These studies demonstrate that guinea pigs fed polyunsaturated fat diets lower plasma LDL levels in part by an increase in apoB/E receptor-mediated fractional LDL turnover and a decrease in apoLDL flux. In addition, fat saturation alters LDL composition and size which independently affect LDL turnover rates in vivo.

Animals↗

Availability of frequency-selective fat-saturation pulse (Fat-Sat) MRI in childhood optic neuritis.

A 2-year-old boy with acute optic neuritis, confirmed by gadolinium-DTPA enhancement of the optic nerve using frequency-selective fat-saturation pulse magnetic resonance imaging (Fat-Sat MRI), is reported. Because it is difficult in very young children to sufficiently evaluate visual acuity, visual field, and retroocular pain on eye movement, and visual evoked potential during wakefulness, Fat-Sat MRI will be useful for revealing optic nerve inflammation and for monitoring treatment.

Adipose Tissue↗

Comparison of short inversion time inversion recovery (STIR) and fat-saturated (chemsat) techniques for background fat intensity suppression in cervical and thoracic MR imaging.

The purpose of this study was to compare short inversion time inversion recovery (STIR) fast spin-echo (FSE), and fat-saturated T2-weighted FSE sequences in terms of uniformity of fat suppression and lesion conspicuity for magnetic resonance (MR) imaging of the neck and thorax. STIR FSE and fat-saturated T2-weighted FSE images were scored for uniformity of fat suppression (n = 40) and lesion conspicuity (n = 35). Five-point rank score analyses were utilized by three experienced radiologists. The mean scores of STIR and fat-saturated FSE techniques for uniformity of fat suppression were 4.3 and 2.3, respectively (P < 0.0001). The mean scores of STIR and fat-saturated FSE techniques for lesion conspicuity were 4.2 and 3.5, respectively (P < 0.0001). Insufficient fat suppression was prominent in the mandible, supraclavicular region, anterior mediastinum, epipericardial fat, and subdiaphragmatic fat. In addition, fat-saturated T2-weighted FSE showed inadvertent water suppression in 25%. The STIR FSE technique was superior to the fat-saturated FSE technique for cervical and thoracic MR imaging.

Adolescent↗

Effects of dietary N-3 and saturated fats on growth rates of the human colonic cancer cell lines SW-620 and LS 174T in vivo in relation to tissue and plasma lipids.

Ninety nude mice were inoculated subcutaneously with 1 x 10(7) cells of the human colonic cancer cell lines, SW-620 and LS174T. Tumour growth was assessed weekly for three weeks whilst the animals were receiving one of three diets: control (4.6% fat), coconut (20% fat, saturated fatty acids) and Maxepa (20% fat; n-3 fatty acids). At the end of the study SW-620 tumour weights (mean +/- SD, gm) were: control = 0.38 +/- 0.22, coconut = 0.43 +/- 0.31, Maxepa 0.20 +/- 0.16; the LS174T tumour weights were control = 1.33 +/- 1.27, coconut = 0.47 +/- 0.74, Maxepa = 0.38 +/- 0.56 (p less than 0.001, analysis of covariance). The Maxepa diet produced significant retardation in tumour growth (p less than 0.001). This was associated with reduced levels of linoleic acid and arachidonic acid in adipose tissue and tumour lipids with incorporation of n-3 fatty acids (all p less than 0.01 at least, analysis of variance). Moreover, the Maxepa diet produced significant reductions of plasma cholesterol, phospholipids and triglycerides (all p less than 0.01).

Adipose Tissue↗

Individual variability in cardiovascular disease risk factor responses to low-fat and low-saturated-fat diets in men: body mass index, adiposity, and insulin resistance predict changes in LDL cholesterol.

BACKGROUND: Although reductions in total and saturated fat consumption are recommended to reduce the risk of cardiovascular disease, individual variability in plasma lipid responses exists. OBJECTIVE: Our aim was to determine the effect of adiposity and insulin resistance on the lipoprotein response to diets lower in total and saturated fat than the average American diet (AAD). DESIGN: A randomized, double-blind, 3-period crossover controlled feeding design was used to examine the effects on plasma lipids of 3 diets that differed in total fat: the AAD [designed to contain 38% fat and 14% saturated fatty acids (SFAs)], the Step I diet (30% fat with 9% SFAs), and the Step II diet (25% fat with 6% SFAs). The diets were fed for 6 wk each to 86 free-living, healthy men aged 22-64 y at levels designed to maintain weight. RESULTS: Compared with the AAD, the Step I and Step II diets lowered LDL cholesterol by 6.8% and 11.7%, lowered HDL cholesterol by 7.5% and 11.2%, and raised triacylglycerols by 14.3% and 16.2%, respectively. The Step II diet response showed significant positive correlations between changes in both LDL cholesterol and the ratio of total to HDL cholesterol and baseline percentage body fat, body mass index, and insulin. These associations were largely due to smaller reductions in LDL cholesterol with increasing percentage body fat, body mass index, or insulin concentrations. Subdivision of the study population showed that the participants in the upper one-half of fasting insulin concentrations averaged only 57% of the reduction in LDL cholesterol with the Step II diet of the participants in the lower half. CONCLUSION: Persons who are insulin resistant respond less favorably to Step II diets than do those who are insulin sensitive.

Adipose Tissue↗

Effects of a low fat diet with and without intermittent saturated fat and cholesterol ingestion on plasma lipid, lipoprotein, and apolipoprotein levels in normal volunteers.

Diets low in saturated fat and cholesterol are recommended to the American public for improving plasma lipoprotein patterns and reducing the risk of heart disease. However, since dietary intake cannot always be controlled, the effects of different degrees of dietary saturated fat lowering and occasional high saturated fat and cholesterol meals on the expected lipoprotein pattern improvement of these diets needs to be defined. In the current study, we compared lipid, lipoprotein, and apolipoprotein levels in 14 young normal volunteers on a metabolic ward when they were consuming a high saturated fat diet (42% fat), an AHA Phase II diet (25% fat), and a third diet which approximated the AHA Phase I diet (30% fat). The latter actually consisted of intermittent ingestion of meals high in saturated fat and cholesterol on the background of an AHA Phase II diet (Intermittent Saturated Fat diet). When compared to the high saturated fat diet, the AHA Phase II diet significantly reduced total, low density lipoprotein (LDL), and high density lipoprotein (HDL) cholesterol, apoB, and apoA-I levels, and improved the LDL/HDL cholesterol ratio, whereas the intermittent saturated fat diet lowered total and LDL cholesterol and apoB levels, and also improved the LDL/HDL cholesterol ratio. When compared to the AHA Phase II diet, the intermittent saturated fat diet raised total and HDL cholesterol levels. Thus, in these normal volunteers, intermittent saturated fat ingestion, in the context of an overall 30% fat diet and a 25% fat diet, did not differ with respect to the effect on improving the LDL/HDL cholesterol ratio.

Adult↗

Effect of dietary fat saturation on lipid metabolism, arachidonic acid turnover and peritoneal macrophage oxidative stress in mice.

We investigated the effects of a saturated fat diet on lipid metabolism and arachidonic acid (AA) turnover in mouse resident peritoneal macrophages. The pro-oxidative effect of this diet was also studied. Female C57BL/6 mice were weaned at 21 days of age and assigned to either the experimental diet containing coconut oil (COCO diet), or the control diet containing soybean oil as fat source (10 mice per group). The fat content of each diet was 15% (w/w). Mice were fed for 6 weeks and then sacrificed. The concentration of total lipids, triglycerides, (LDL+VLDL)-cholesterol, thiobarbituric acid-reactive substances (TBARS) and reduced glutathione were increased in the plasma of mice fed the COCO diet, without changes in phospholipid or total cholesterol concentrations compared to control. The concentrations of total cholesterol, free and esterified cholesterol, triglycerides, and TBARS were increased in the macrophages of COCO-fed mice, while the content of total phospholipids did not change. The phospholipid composition showed an increase of phosphatidylcholine and a decrease of phosphatidylethanolamine. The [3H]-AA distribution in the phospholipid classes showed an increase in phosphatidylcholine and phosphatidylethanolamine. Incorporation of [3H]-cholesterol into the macrophages of COCO-fed mice and into the cholesterol ester fraction was increased. The COCO diet did not affect [3H]-AA uptake but induced an increase in [3H]-AA release. The COCO diet also enhanced AA mobilization induced by lipopolysaccharide. These results indicate that the COCO diet, high in saturated fatty acids, alters the lipid metabolism and AA turnover of peritoneal macrophages in female mice and also produces a significant degree of oxidative stress.

Animals↗

Dietary fat saturation produces lipid modifications in peritoneal macrophages of mouse.

We investigated the effects of a saturated fat diet on mice lipid metabolism in resident peritoneal macrophages. Male C57BL/6 mice were weaned at 21 days of age and assigned to either the experimental diet, containing coconut oil (COCO diet), or the control diet, containing soybean oil as fat source. Fat content of each diet was 15% (w/w). Mice were fed for 6 weeks until sacrifice. In plasma of mice fed the COCO diet, the concentration of triglyceride, total cholesterol, HLD- and (LDL+VLDL)-cholesterol, and thiobarbituric acid-reactive substances (TBARS) increased, without changes in phospholipid concentration, compared with the controls. In macrophages of COCO-fed mice, the concentration of total (TC), free and esterified cholesterol, triglyceride, phospholipid (P) and TBARS increased, while the TC/P ratio did not change. The phospholipid compositions showed an increase of phosphatidylcholine and phosphatidylserine + phosphadytilinositol, a decrease of phosphatidylethanolamine, and no change in phosphatidylglycerol. (3)H(2)O incorporation into triglyceride and phospholipid fractions of macrophages increased, while its incorporation into free cholesterol decreased. Incorporation of [(3)H]cholesterol into macrophages of COCO-fed mice and the fraction of [(3)H]cholesterol ester increased. COCO diet produced an increase in myrystic, palmitic and palmitoleic acids proportion, a decrease in linoleic and arachidonic acids and no changes in stearic and oleic acids, compared with the control. Also, a higher relative percentage of saturated fatty acid and a decrease in unsaturation index (p <0.001) were observed in macrophages of COCO-fed mice. These results indicate that the COCO-diet, high in saturated fatty acids, alters the lipid metabolism and fatty acid composition of macrophages and produces a significant degree of oxidative stress.

Animals↗

Men and women differ in lipoprotein response to dietary saturated fat and cholesterol restriction.

A diet restricted in saturated fat and cholesterol is recommended for subjects with elevated LDL cholesterol concentrations before and during drug therapy. Gender differences in lipoprotein subspecies response to such diets have not been studied in detail. We examined the effects of a diet low in total fat, saturated fat and cholesterol (Therapeutic Lifestyle Changes, TLC, diet: 26% of energy as fat, 4% as saturated fat, and 45 mg cholesterol/4.2 MJ), compared with an average American diet (AAD: 35% of energy as fat, 14% as saturated fat, and 147 mg cholesterol/4.2 MJ), on plasma lipoprotein subspecies in men and women. Each diet period lasted 6 wk. Body weight was kept constant during each diet period. Men (n = 19) and postmenopausal women (n = 14) >40 y old with moderate hypercholesterolemia participated in this study. Plasma lipoprotein concentrations were assessed by standardized methodology, and lipoprotein sizes were determined by gradient gel electrophoresis and NMR spectroscopy. The TLC diet resulted in greater reductions in total cholesterol and plasma apolipoprotein B concentrations in men than in women (-19% vs. -12%, P < 0.05, and -18% vs. -9%, P < 0.05, respectively). Postprandial triacylglycerol and LpAI:AII concentrations were reduced in men, but not in women (-15% vs. 8%, P < 0.05, and -9% vs. -2%, respectively, P < 0.05). Similar decreases in LpAI concentrations and LDL and HDL particle size were observed in men and women. These data are consistent with the concept that middle aged/elderly men may have a more favorable lipoprotein response to a low fat, low cholesterol diet than postmenopausal women.

Dietary Fats↗

Maternal diet rich in saturated fat during breastfeeding is associated with atopic sensitization of the infant.

OBJECTIVE: To investigate the impact of maternal diet during breastfeeding on atopic sensitization of infants at risk. DESIGN: Prospective cohort study. SETTING: Turku University Central Hospital, Finland. SUBJECTS AND METHODS: Altogether 114 infants with a family history of atopic disease were followed during their first year of life. The mothers completed a 4 day food record during breastfeeding just before the infants were 3 months old. Atopic sensitization of the infants was determined by a positive skin prick test result at 12 months. RESULTS: Positive skin prick test reactivity to at least one antigen was detected in 27/114 (24%) infants at 12 months. The energy intake of the mothers was low, mean 8.0 MJ/day (95% CI 7.7-8. 3), and the proportion of energy derived from fat was high, mean 36. 6 E% (95% CI 35.6-37.6). Atopic mothers had a higher intake of total fat and saturated fat and a lower intake of carbohydrate as a percentage of total energy intake than non-atopic mothers; P=0.017, P=0.050, P=0.004 respectively. Maternal intake of saturated fat during breastfeeding was associated with atopic sensitization of the infant, OR=1.16 (95% CI 1.001-1.36); P=0.048 irrespective of the maternal atopic status. CONCLUSIONS: Our results show that an unbalanced maternal diet during breastfeeding may be a risk factor underlying the later development of atopic sensitization of the infant regardless of maternal atopic disease. The observation thus extends findings implying that early nutrition programmes the subsequent health of the child to the risk of developing atopic disease. SPONSORSHIP: Academy of Finland and National Technology Agency.

Breast Feeding↗