Substitution Of Saturated Fatty Acids Research Articles

Dietary polyunsaturated fatty acids intake is negatively associated with hyperuricemia: The National Health and Nutrition Examination Survey 2003–2015

Background and aimsThe objective of this research was to explore the associations between dietary PUFAs intake and hyperuricemia risk. Methods and resultsBased on the National Health and Nutrition Examination Survey (NHANES) 2003–2015, all eligible individuals were divided into hyperuricemia and non-hyperuricemia groups based on diagnostic criteria for hyperuricemia (serum uric acid >420 μmol/L for men and >360 μmol/L for women). Multivariate-adjusted logistic regression was employed to explore the relationship between dietary PUFAs intake and hyperuricemia risk. Total PUFAs and their subtypes were modeled to isocalorically replace saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs). Higher intake of n-3 PUFAs, n-6 PUFAs, linoleic acid (LA), alpha-linoleic acid (ALA), and non-marine PUFAs intake correlated with decreased hyperuricemia risk, with adjusted odds ratio (OR) and 95% confidence interval (95%CIs) were 0.77 (0.63, 0.93), 0.75 (0.61, 0.92), 0.75 (0.61, 0.91), 0.69 (0.55, 0.87), and 0.73 (0.59, 0.91), respectively. Replacing 5% of total energy intake from SFAs with isocaloric PUFAs was associated with decreased odds of hyperuricemia in men (0.69 (0.57, 0.84)) and in individuals (0.81 (0.71, 0.92)). Similar trends were observed in the substitution of SFAs with non-marine PUFAs in men (0.87 (0.80, 0.94)) and in all individuals (0.92 (0.88, 0.98)). Sensitivity analyses exhibited consistent results with primary analyses. ConclusionHigher dietary intake of n-3 PUFAs, n-6 PUFAs, LA, ALA, and non-marine PUFAs was associated with decreased hyperuricemia risk. These results support the recommendation to substitute SFAs with PUFAs in diet.

Substitutions of saturated fat intakes with other macronutrients and foods and risk of NAFLD cirrhosis and all-cause hepatocellular carcinoma: a prospective cohort study

BackgroundShort-term trials have shown a reduction in liver fat when saturated fatty acids (SFAs) are substituted with polyunsaturated fatty acids (PUFA), or with low-glycemic carbohydrates. However, few cohort studies have been conducted to investigate the associations of replacing SFA and SFA-rich foods with different macronutrients and foods in more severe stages of liver disease; nonalcoholic fatty liver disease (NAFLD) cirrhosis and hepatocellular carcinoma (HCC). ObjectivesTo investigate associations between the substitution of SFA and SFA-rich foods with other macronutrients and foods and NAFLD cirrhosis and HCC in a middle-aged to elderly Swedish population of n = 77,059 males and females. MethodsTime-to-event analyses were performed to investigate associations between the food and macronutrient substitutions and NAFLD cirrhosis and HCC. Multivariable Cox regression models were constructed to estimate hazard ratios (HRs) with corresponding 95% confidence intervals (CIs). Statistical isocaloric and equal-mass substitutions were performed using the leave-one-out method. Prespecified nutrient and food substitutions of interest were SFA with carbohydrates, SFA with fiber, SFA with PUFA, butter with margarine and vegetable oils, unprocessed red meat with fish, and milk with fermented milk. ResultsOver a median follow-up of 24 y, 566 cases of NAFLD cirrhosis and 205 cases of HCC were registered. Overall, dietary substitutions showed no clear associations with either NAFLD cirrhosis or HCC. Substituting SFA with carbohydrates showed an HR of 0.87 (95% CI: 0.74, 1.02) for HCC and 1.00 (95% CI: 0.89, 1.11) for NAFLD cirrhosis. Substituting milk with fermented milk showed an HR of 0.93 (95% CI: 0.85, 1.01) for HCC and 0.97 (95% CI: 0.92, 1.03) for NAFLD cirrhosis. ConclusionsNo clear associations were observed between diet and NAFLD cirrhosis or HCC. Although accompanied by low precision, possible lowered risks of HCC by substituting SFA with carbohydrates or milk with fermented milk might be of interest, but needs replication in other cohorts.

A Review of Low-Density Lipoprotein-Lowering Diets in the Age of Anti-Sense Technology.

This narrative review discusses an important issue, the primary role of diet in reducing low-density lipoprotein cholesterol (LDLc) concentrations in polygenic hypercholesterolemia. Two effective drugs, statins, and ezetimibe, that lower LDLc > 20% are relatively inexpensive and potential competitors to strict dieting. Biochemical and genomic studies have shown that proprotein convertase subtilisin kexin type 9 (PCSK9) plays an important role in low-density lipoprotein (LDL) and lipid metabolism. Clinical trials have demonstrated that inhibitory monoclonal antibodies of PCSK9 dose-dependently lower LDLc up to 60%, with evidence of both regression and stabilization of coronary atherosclerosis and a reduction in cardiovascular risk. Recent approaches using RNA interference to achieve PCSK9 inhibition are currently undergoing clinical evaluation. The latter presents an attractive option of twice-yearly injections. They are, however, currently expensive and unsuitable for moderate hypercholesterolemia, which is largely due to inappropriate patterns of eating. The best dietary approach, the substitution of saturated fatty acids by polyunsaturated fatty acids at 5% energy, yields > 10% lowering of LDLc. Foods such as nuts and brans, especially within a prudent, plant-based diet low in saturates complemented by supplements such as phytosterols, have the potential to reduce LDLc further. A combination of such foods has been shown to lower LDLc by 20%. A nutritional approach requires backing from industry to develop and market LDLc-lowering products before pharmacology replaces the diet option. Energetic support from health professionals is vital.

Abstract P059: Effects Of Saturated Fatty Acid On Lipoprotein(a): A Systematic Review And Meta-analysis

Background: Elevated lipoprotein(a) [Lp(a)] is a significant contributor to residual CVD risk. Replacement of saturated fatty acids (SFA) with mono- and polyunsaturated fatty acids (MUFA and PUFA), carbohydrates (CHO) has established effects on traditional lipid parameters related to CVD; however, the evidence for Lp(a) is inconsistent. Moreover, some evidence suggests replacing SFA with other macronutrients increases Lp(a). Objective: The aim was to conduct a systematic review and meta-analysis of randomized controlled trials (RCTs) to assess the effect of replacing SFA with MUFA, PUFA, trans fatty acids (TFA) and CHO on Lp(a). Methods: PubMed, Cochrane Central, ClinicalTrials.gov, and Web of Science were searched for RCTs with a duration of ≥13 days that included healthy adults ages 20-65 y and examined the effect of diets differing in SFA, MUFA, PUFA, or CHO on Lp(a). Exclusion criteria included changes in protein/alcohol and >10% weight loss in last 6 months. Diet comparisons were extracted from trials to assess the effect of substitution of SFA for other macronutrients. Data are presented as weighted means. Data were analyzed using a mixed model approach (SAS 9.4). Results: Twenty-seven articles met criteria for inclusion and data were available for analysis for 15 articles. There were 39 comparisons between SFA and other macronutrients. Lp(a) was measured by macra, polyclonal, or sandwich enzyme linked immunosorbent assay (ELISA), particle enhanced turbidimetric immunoassay, or radioimmunoassay. SFA was substituted for TFA ( k =6), MUFA ( k =9), and PUFA ( k =3). Five trials compared a high SFA diet with a high CHO diet. A total of 539 adults (44.7 + 31.6 y) were included in the pooled sample. Overall, the mean displacement of SFA for other macronutrients was 6.7% of kcals. Mean Lp(a) across the included studies was 100.5 + 100.3 mg/dl. Replacement of SFA with MUFA, PUFA or CHO did not significantly affect Lp(a). Lp(a) was 6.1 mg/dl (p=0.021; 95% CI: -11.3, -0.9) lower when SFA replaced TFA. Conclusions: Overall, substitution of SFA for other macronutrients did not impact Lp(a) concentrations. Lower levels of Lp(a) were observed when 5% of kcals from TFA were replaced with SFA, although the clinical relevance of this finding is unclear. Further research examining the effect of SFA replacement on Lp(a) is needed due to the methodological quality of the available data and heterogeneity in Lp(a) measurement methods utilized.

Contrasted central effects of n-3 versus n-6 diets on brain functions in diet-induced obesity in minipigs

ABSTRACT Introduction N3 polyunsaturated fatty acids (n-3 PUFAs) exert anti-inflammatory effects for the hypothalamus, but their extra-hypothalamic outcome lack documentation. We evaluated the central consequences of the substitution of saturated fatty acids with n-3 or n-6 PUFA in obesogenic diets. Methods Twenty-one miniature pigs were fed ad libitum obesogenic diets enriched in fat provided either as lard, fish oil (source for n-3 PUFAs), or sunflower oil (source for n-6 PUFAs) for ten weeks. The blood–brain barrier (BBB) permeability was quantified by CT perfusion. Central autonomic network was evaluated using heart rate variability, and PET 18FDG was performed to assess brain metabolism. Results BBB permeability was higher in lard group, but heart rate variability changed only in fish oil group. Brain connectivity analysis and voxel-based comparisons show regional differences between groups except for the cingulate cortex in fish oil vs. sunflower oil groups. Discussion : The minute changes in brain metabolism in obese pigs feed with fish oil compared with saturated fatty acids were sufficient to induce detrimental changes in heart rate variability. On the contrary, the BBB's decreased permeability in n-3 and n-6 PUFAs groups was protective against an obesity-driven damaged BBB.

Chilling injury is associated with changes in microsomal membrane lipids in guava fruit (Psidium guajava L.) and the use of controlled atmospheres reduce these effects

Abstract Storage of guava fruit cv ‘Media china’ at temperatures below 8 °C causes chilling injury associated with changes in cell membrane lipids. The aim of the present study was to evaluate the effects of two temperatures (4 and 10 °C) and three controlled atmospheres (air; 10 kPa O2; 5 kPa CO2 and 10 + 5 kPa of O2 and CO2) on microsomal lipid profiles in ripened fruit or fruit storage during three weeks. The study revealed that chilling injury is associated with a decrease in microsomal membrane volume and microsomal protein and phospholipids content (5%, 47% and 22%; respectively). Also, it was observed a decrease in Monogalactosyldiacylglycerol (MGDG), digalactosyldiacylglycerol (DGDG), Phosphatidylinositol (PI), phosphatidic acid (PA), cardiolipin (CL) contents and a substitution of saturated fatty acids (FA) for unsaturated FA in the microsomal membrane. Importantly, it was found that storing guava fruit 'Media China' at 10 °C under 5 kPa CO2 reduced chilling injury prevalence and increased shelf life, suggesting that these storage conditions maintained membrane functionality. Overall, these results indicate that CI is associated to deep alterations in membrane lipids pathway.

Apolipoprotein E gene polymorphism modifies fasting total cholesterol concentrations in response to replacement of dietary saturated with monounsaturated fatty acids in adults at moderate cardiovascular disease risk

BackgroundConsumption of ≤10% total energy from fat as saturated fatty acids (SFA) is recommended for cardiovascular disease risk reduction in the UK; however there is no clear guidance on the optimum replacement nutrient. Lipid-associated single-nucleotide polymorphisms (SNPs) have been shown to modify the lipid responses to dietary fat interventions. Hence, we performed a retrospective analysis in 120 participants from the Dietary Intervention and VAScular function (DIVAS) study to investigate whether lipoprotein lipase (LPL) and apolipoprotein E (APOE) SNPs modify the fasting lipid response to replacement of SFA with monounsaturated (MUFA) or n-6 polyunsaturated (PUFA) fatty acids.MethodsThe DIVAS study was a randomized, single-blinded, parallel dietary intervention study performed in adults with a moderate cardiovascular risk who received one of three isoenergetic diets rich in SFA, MUFA or n-6 PUFA for 16 weeks.ResultsAfter the 16-week intervention, a significant diet-gene interaction was observed for changes in fasting total cholesterol (P = 0.001). For the APOE SNP rs1064725, only TT homozygotes showed a significant reduction in total cholesterol after the MUFA diet (n = 33; −0.71 ± 1.88 mmol/l) compared to the SFA (n = 38; 0.34 ± 0.55 mmol/l) or n-6 PUFA diets (n = 37; −0.08 ± 0.73 mmol/l) (P = 0.004). None of the interactions were statistically significant for the other SNPs.ConclusionsIn summary, our findings have demonstrated a greater sensitivity of the APOE SNP rs1064725 to dietary fat composition, with a total cholesterol lowering effect observed following substitution of SFA with MUFA but not n-6 PUFA. Further large intervention studies incorporating prospective genotyping are required to confirm or refute our findings.Trial registrationThe trial was registered at www.clinicaltrials.gov as NCT01478958.

Effect of Dietary Intake of Saturated Fatty Acids on the Development of Atrial Fibrillation and the Effect of Replacement of Saturated With Monounsaturated and Polyunsaturated Fatty Acids

The aim of the present study was to explore substitution of intake of saturated fatty acids (FAs) with monounsaturated and polyunsaturated FAs and incident atrial fibrillation (AF) in men and women. A total of 57,053 Danish participants aged 50 to 64 years were enrolled in the Diet, Cancer and Health cohort study in 1993 to 1997 and completed a semiquantitative food frequency questionnaire at baseline. Follow-up was registry-based and data were analyzed using Cox proportional hazards regression. The statistical model was formulated in such a way that 1 g/day of saturated FAs was replaced with 1 g/day of monounsaturated or polyunsaturated FAs while keeping total fat intake, total energy intake, and energy intake from protein and carbohydrates constant. During a median follow-up of 17 years, 5,175 incident cases of AF occurred. In men, there was a higher hazard of AF when total n-3 polyunsaturated FAs replaced dietary saturated FAs-hazard ratio per 1-g substitution of FAs of 1.08 (95% confidence interval 1.02 to 1.14) in a model adjusted for lifestyle factors. For other substitutions of FAs (monounsaturated, total or n-6 polyunsaturated FAs), no consistent nor statistically significant associations were found. In conclusion, we found a moderately higher risk of AF in men, but not in women, when total n-3 polyunsaturated FAs replaced dietary saturated FAs. Substitution of saturated FAs with monounsaturated, total or n-6 polyunsaturated FAs was not associated with the risk of AF.

Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse

A significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is unclear which fatty acids are most obesogenic. The objective of this study was to determine the obesogenic potency of LA vs. saturated fatty acids and the involvement of hypothalamic inflammation. Forty-eight mice were divided into four groups: low-fat or three high-fat diets (HFDs, 45% kcals from fat) with LA comprising 1%, 15% and 22.5% of kilocalories, the balance being saturated fatty acids. Over 12 weeks, bodyweight, body composition, food intake, calorimetry, and glycemia assays were performed. Arcuate nucleus and blood were collected for mRNA and protein analysis. All HFD-fed mice were heavier and less glucose tolerant than control. The diet with 22.5% LA caused greater bodyweight gain, decreased activity, and insulin resistance compared to control and 1% LA. All HFDs elevated leptin and decreased ghrelin in plasma. Neuropeptides gene expression was higher in 22.5% HFD. The inflammatory gene Ikk was suppressed in 1% and 22.5% LA. No consistent pattern of inflammatory gene expression was observed, with suppression and augmentation of genes by one or all of the HFDs relative to control. These data indicate that, in male mice, LA induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.

Abstract P273: Dietary Saturated Fatty Acids and Coronary Heart Disease Risk in a Dutch Elderly Population: Food Source and Carbon Chain Length Matter

Introduction: The association between dietary saturated fatty acids (SFA) and the risk of coronary heart disease (CHD) is heavily debated and appears to be more complex than initially thought. The food source and carbon chain length of SFA, as well as the macronutrient replacing SFA in the diet may affect the association between dietary SFA and CHD. Hypothesis: We assessed the hypothesis that the association between dietary SFA and incident CHD is dependent on the food source of SFA, the carbon chain length of SFA, and the substituting macronutrient. Methods: From the Rotterdam Study, we included 4,722 healthy men and women, aged 55 years or older. Baseline (1998-1993) SFA intake was assessed using a validated food frequency questionnaire. Incident CHD comprised fatal and non-fatal myocardial infarctions and coronary mortality up to January 2011, and was assessed through digital linkage with municipality records and general practitioners. We used multivariable Cox’ proportional hazard models to calculate CHD risks for higher intakes of total SFA, SFA from specific food sources, SFA differing in carbon chain length, and for higher intakes of other macronutrients at the expense of total SFA. Results: During a median follow up of 16.3 years 569 CHD events occurred. Median total SFA intake was 15.7 en% per day, and the top three food sources were cheese (20.0%), meat (17.8%), and milk and milk products (13.1%). Total SFA intake was not significantly associated with CHD risk (Hazard Ratio (HR) per 5 en%: 1.13, 95%CI: 0.94, 1.22). Neither was SFA from specific food sources, although the data suggested an increased CHD risk for a higher intake of SFA from meat (HR per 1 en%: 1.06, 95%CI: 0.99, 1.14). Regarding SFA differing in carbon chain lengths, a higher CHD risk was observed for C16:0 intake (HR 1en% : 1.18, 95%CI: 1.03, 1.35), but not for the remaining SFA. No significant associations with CHD risk were observed for each 5% lower intake of energy from SFA and a concomitant higher intake of 5% of energy from carbohydrates (HR 5en% : 0.90: 0.80, 1.02), polyunsaturated fatty acids (HR 5en% : 0.90, 95%CI: 0.71, 1.15), cis -monounsaturated fatty acids (HR 5en% :1.09, 95%CI: 0.98, 1.22), or vegetable protein (HR 5en% : 0.88, 95%CI: 0.50, 1.53).The exception was substitution of SFA with animal protein, which was associated with higher CHD risk (HR 5en% : 1.24, 95%CI: 1.01, 1.51). Conclusions: In this Dutch elderly population, with a high median intake of total SFA, the association between SFA intake and CHD risk depends on the SFA food source and carbon chain length. Future intervention studies are needed to determine the importance of the SFA food sources, and to confirm that C16:0 is more strongly related with CHD risk than other SFA.

Insulin resistance determines a differential response to changes in dietary fat modification on metabolic syndrome risk factors: the LIPGENE study

Previous data support the benefits of reducing dietary saturated fatty acids (SFAs) on insulin resistance (IR) and other metabolic risk factors. However, whether the IR status of those suffering from metabolic syndrome (MetS) affects this response is not established. Our objective was to determine whether the degree of IR influences the effect of substituting high-saturated fatty acid (HSFA) diets by isoenergetic alterations in the quality and quantity of dietary fat on MetS risk factors. In this single-blind, parallel, controlled, dietary intervention study, MetS subjects (n = 472) from 8 European countries classified by different IR levels according to homeostasis model assessment of insulin resistance (HOMA-IR) were randomly assigned to 4 diets: an HSFA diet; a high-monounsaturated fatty acid (HMUFA) diet; a low-fat, high-complex carbohydrate (LFHCC) diet supplemented with long-chain n-3 polyunsaturated fatty acids (1.2 g/d); or an LFHCC diet supplemented with placebo for 12 wk (control). Anthropometric, lipid, inflammatory, and IR markers were determined. Insulin-resistant MetS subjects with the highest HOMA-IR improved IR, with reduced insulin and HOMA-IR concentrations after consumption of the HMUFA and LFHCC n-3 diets (P < 0.05). In contrast, subjects with lower HOMA-IR showed reduced body mass index and waist circumference after consumption of the LFHCC control and LFHCC n-3 diets and increased HDL cholesterol concentrations after consumption of the HMUFA and HSFA diets (P < 0.05). MetS subjects with a low to medium HOMA-IR exhibited reduced blood pressure, triglyceride, and LDL cholesterol levels after the LFHCC n-3 diet and increased apolipoprotein A-I concentrations after consumption of the HMUFA and HSFA diets (all P < 0.05). Insulin-resistant MetS subjects with more metabolic complications responded differently to dietary fat modification, being more susceptible to a health effect from the substitution of SFAs in the HMUFA and LFHCC n-3 diets. Conversely, MetS subjects without IR may be more sensitive to the detrimental effects of HSFA intake. The metabolic phenotype of subjects clearly determines response to the quantity and quality of dietary fat on MetS risk factors, which suggests that targeted and personalized dietary therapies may be of value for its different metabolic features. This study was registered at clinicaltrials.gov as NCT00429195.

Oleate prevents saturated-fatty-acid-induced ER stress, inflammation and insulin resistance in skeletal muscle cells through an AMPK-dependent mechanism

Although the substitution of saturated fatty acids with oleate has been recommended in the management of type 2 diabetes mellitus, the mechanisms by which oleate improves insulin resistance in skeletal muscle cells are not completely known. Here, we examined whether oleate, through activation of AMP-activated protein kinase (AMPK), prevented palmitate-induced endoplasmic reticulum (ER) stress, which is involved in the link between lipid-induced inflammation and insulin resistance. Studies were conducted in mouse C2C12 myotubes and in the human myogenic cell line LHCN-M2. To analyse the involvement of AMPK, activators and inhibitors of this kinase and overexpression of a dominant negative AMPK construct (K45R) were used. Palmitate increased the levels of ER stress markers, whereas oleate did not. In palmitate-exposed cells incubated with a lower concentration of oleate, the effects of palmitate were prevented. The induction of ER stress markers by palmitate was prevented by the presence of the AMPK activators AICAR and A-769662. Moreover, the ability of oleate to prevent palmitate-induced ER stress and inflammation (nuclear factor-kappa B [NF-κB] DNA-binding activity and expression and secretion of IL6) as well as insulin-stimulated Akt phosphorylation and 2-deoxyglucose uptake was reversed in the presence of the AMPK inhibitor compound C or by overexpression of a dominant negative AMPK construct. Finally, palmitate reduced phospho-AMPK levels, whereas this was not observed in oleate-exposed cells or in palmitate-exposed cells supplemented with oleate. Overall, these findings indicate that oleate prevents ER stress, inflammation and insulin resistance in palmitate-exposed skeletal muscle cells by activating AMPK.

Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects

Background: The influence of the quality of dietary fat on some aspects of lipid metabolism—i.e. lipoprotein concentrations, post-prandial lipids and LDL size—is not completely understood, especially in healthy individuals. Objectives: Aim of this study was to evaluate the effects of different types of dietary fat (monounsaturated vs. saturated fatty acids, and n-3 or placebo supplementation) on fasting lipoproteins, LDL size and post-prandial lipids in healthy people. Design: One hundred and sixty-two individuals were randomly assigned to follow two isoenergetic diets, one rich in saturated fatty acids (SFA diet) and the other in monounsaturated fatty acids (MUFA diet). Each group was further randomised to receive supplementation with fish oil (3.6 g/day) or placebo. Results: The type of diet significantly affected LDL cholesterol and triacylglycerol content, which was higher with the SFA diet and lower with the MUFA diet. The changes between the two diets were statistically significant for cholesterol ( P<0.01) and triacylglycerol ( P<0.03). VLDL cholesterol and triacylglycerol were significantly reduced and LDL cholesterol significantly increased by fish oil supplementation. Plasma triacylglycerol was significantly lower in those taking n-3 fatty acids, also 1 and 3 h after a test-meal. Neither type of diet nor n-3 supplementation affected LDL size. Conclusions: A moderate substitution of saturated fatty acids with monounsaturated fatty acids has beneficial effects on lipid metabolism also in healthy individuals. A moderate supplementation of long-chain n-3 fatty acids in healthy individuals reduces both fasting and post-prandial triacylglycerol concentrations but increases LDL cholesterol, irrespective of the type of diet.

Omega-3 and omega-6 PUFA's have different effects on the phospholipid fatty acid composition of rat myocardial muscle when added to a saturated fatty acid dietary supplement

Changes in the type of dietary lipid intake can alter the fatty acid composition of cardiac membrane phospholipids. Generally these changes reflect the fatty acid composition of the diet, but important metabolic alterations also occur. These metabolic alterations between fatty acids are influence by competition for common metabolic pathways of conversion. However, the efficacy of omega-3 PUFA's is much greater than that of omega-6 PUFA's as a relatively small amount of fish oil added to a diet rich in saturated animal fats was most effective in changing membrane composition. Conversely almost total substitution of saturated fatty acids by omega-6 PUFA's was required to significantly alter cardiac membrane fatty acid profiles. These results agree with the difference in physiological efficacies of omega-3 and omega-6 PUFA's noted previously, and strengthen the view that dietary lipids can influence cardiac function via changes in membrane fatty acid composition.

Plasma cholesterol responsiveness to saturated fatty acids

The variability in responsiveness to saturated fatty acids has not been studied systematically. For this reason data from three dietary studies carried out in our laboratory were pooled and used to evaluate how individuals vary in their responses in plasma concentrations of total cholesterol and low-density-lipoprotein cholesterol to the substitution of saturated fatty acids for unsaturated fatty acids. The data showed a marked variability in response. Some patients demonstrated a striking rise in cholesterol levels whereas others had more modest increases. This finding points to the need for further investigation on this issue.