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The purpose of this systematic review was to evaluate the impact of saturated fatty acid chain lengths on the development of cardiovascular disease (CVD). The importance of replacement macronutrients is also discussed. PubMed, CINAHL, and Cochrane library were searched for relevant prospective cohort studies that measured SFA chain length via diet analysis through October of 2020. A second updated PubMed search was conducted from October 2020 to 7 August 2022. Five prospective cohort studies were added. All studies used food frequency questionnaires to assess dietary intake. For all five added studies, the main sources of saturated fat were palmitic and steric acid from meat and cheese. Most studies discovered an association with increased risk of CVD and long-chain saturated fatty acid intake, as well as a neutral (potentially beneficial) association with short- and medium-chain saturated fatty acids. Isocaloric substitutions were associated with a higher risk for CVD when saturated fats were replaced with refined carbohydrates and protein from meat, but a reduced or neutral impact when relaced with plant-based protein, unsaturated fat, or complex carbohydrates. When examining the impact of diet on CVD risk, it is critical to consider the macronutrient replacing saturated fat as well as the saturated fat chain length, whole foods, and diet patterns on CVD risk. The studies included in this review suggest that LCSFA (C12–18) may increase the risk for CVD development, while SCFA and MCFA (C4–-C10) may be more beneficial or neutral.

With the growing interest in non-dairy products, there has been a surge of interest in consumers seeking plant-based cheese alternatives spurred by a desire to improve individual health and achieve a more sustainable food supply. The aim of this study was to conduct a cross-sectional survey of non-dairy cheese alternatives available in the United States and to evaluate their nutritional content. A total of 245 non-dairy plant-based cheese alternatives were analyzed using their nutritional facts labels. The various cheese alternatives were based upon coconut oil (n = 106), cashews and coconut (n = 61), cashews (n = 35), oats (n = 16), almonds (n = 7), soy (n = 6), palm fruit oil (n = 5), and other blends (n = 9). Only 3% of these cheese alternatives had 5 g or more of protein, while 19%, 14%, and 1% were fortified with calcium, vitamin B12, and vitamin D, respectively. Almost 60% had high levels of saturated fat, while 15% had low sodium levels. The products based on cashews alone more commonly had the highest protein levels and the lowest sodium and saturated fat levels. Those containing coconut oil more commonly had higher saturated fat and sodium levels and were most frequently fortified with vitamin B12. Few of these products could be considered good dietary sources of either protein or calcium.

Coconut, Cocos nucifera L., is a tree that is cultivated to provide a large number of products, although it is mainly grown for its nutritional and medicinal values. Coconut oil, derived from the coconut fruit, has been recognised historically as containing high levels of saturated fat; however, closer scrutiny suggests that coconut should be regarded more favourably. Unlike most other dietary fats that are high in long-chain fatty acids, coconut oil comprises medium-chain fatty acids (MCFA). MCFA are unique in that they are easily absorbed and metabolised by the liver, and can be converted to ketones. Ketone bodies are an important alternative energy source in the brain, and may be beneficial to people developing or already with memory impairment, as in Alzheimer's disease (AD). Coconut is classified as a highly nutritious 'functional food'. It is rich in dietary fibre, vitamins and minerals; however, notably, evidence is mounting to support the concept that coconut may be beneficial in the treatment of obesity, dyslipidaemia, elevated LDL, insulin resistance and hypertension - these are the risk factors for CVD and type 2 diabetes, and also for AD. In addition, phenolic compounds and hormones (cytokinins) found in coconut may assist in preventing the aggregation of amyloid-β peptide, potentially inhibiting a key step in the pathogenesis of AD. The purpose of the present review was to explore the literature related to coconut, outlining the known mechanistic physiology, and to discuss the potential role of coconut supplementation as a therapeutic option in the prevention and management of AD.

Purpose We sought to determine the effects of dietary fat on insulin sensitivity and whether changes in insulin sensitivity were explained by changes in abdominal fat distribution or very low-density lipoprotein (VLDL) fatty acid composition. Methods Overweight/obese adults with normal glucose tolerance consumed a control diet (35 % fat/12 % saturated fat/47 % carbohydrate) for 10 days, followed by a 4-week low-fat diet (LFD, n  = 10: 20 % fat/8 % saturated fat/62 % carbohydrate) or high-fat diet (HFD, n  = 10: 55 % fat/25 % saturated fat/27 % carbohydrate). All foods and their eucaloric energy content were provided. Insulin sensitivity was measured by labeled hyperinsulinemic-euglycemic clamps, abdominal fat distribution by MRI, and fasting VLDL fatty acids by gas chromatography. Results The rate of glucose disposal (Rd) during low- and high-dose insulin decreased on the HFD but remained unchanged on the LFD (Rd-low: LFD: 0.12 ± 0.11 vs. HFD: −0.37 ± 0.15 mmol/min, mean ± SE, p  < 0.01; Rd-high: LFD: 0.11 ± 0.37 vs. HFD: −0.71 ± 0.26 mmol/min, p  = 0.08). Hepatic insulin sensitivity did not change. Changes in subcutaneous fat were positively associated with changes in insulin sensitivity on the LFD ( r  = 0.78, p  < 0.01) with a trend on the HFD ( r  = 0.60, p  = 0.07), whereas there was no association with intra-abdominal fat. The LFD led to an increase in VLDL palmitic (16:0), stearic (18:0), and palmitoleic (16:1n7c) acids, while no changes were observed on the HFD. Changes in VLDL n-6 docosapentaenoic acid (22:5n6) were strongly associated with changes in insulin sensitivity on both diets (LFD: r  = −0.77; p  < 0.01; HFD: r  = −0.71; p  = 0.02). Conclusions A diet very high in fat and saturated fat adversely affects insulin sensitivity and thereby might contribute to the development of type 2 diabetes. ClinicalTrials.gov Identifier NCT00930371.

To investigate the effects of comparable dietary excess of fat or fructose and the combination of these two insults (mimicking ultra-processed foods) on interscapular brown adipose tissue (iBAT) whitening and markers of mitochondrial dynamics in adult male mice. Male C57BL/6 mice were randomly assigned into four groups according to the diet: control diet (C, following AIN-93M), high-fat diet (HF, 32% energy as lard), high-fructose diet (HFRU, 32% energy as fructose) or for high-fat/high-fructose diet (HF-HFRU, 32% as lard and 32% as fructose) for 12 weeks. Data were tested with one-way ANOVA and Dunnet T3 post-test (n=5 per analysis, significance level P < 0.05). All diets caused insulin resistance and iBAT whitening, albeit with overweight only in the HF and HF-HFRU groups. Principal component analysis indicated that the HFRU scores loaded next to inflammation (Nlrp3) and adipogenesis markers (Pparg), and the HF diet influenced more a mitochondrial gene (Tomm20). However, iBAT whitening in all groups was associated with deficits in mitochondrial dynamics (Ppargc1a, Dnml1, and Pink1), vascularization (Vegfa), and thermogenic markers (Bmp8b, and Ucp1). Similar increases in dietary saturated fat or fructose (32% as energy) and the combination of these two insults (32% / 32%) caused insulin resistance and brown adipocyte dysfunction (whitening) in adult mice after 12 weeks independent of being overweight. In comparison, the PC scores of the HFRU groups were closer to the HF-HFRU group than the HF group, implying a worse outcome and highlighting the importance of limiting saturated fat and fructose intake from ultra-processed foods. •High-fat diet and cumulative high-fat and high-fructose intake caused overweight.•High-fat or fructose and their cumulative intake caused brown adipocyte whitening.•Saturated fat impaired mitochondrial genes to cause brown adipocyte dysfunction.•Fructose, isolated or with fat, enhanced inflammatory and adipogenic genes.•High-fat and fructose intake found in ultra-processed foods should be discouraged. [Display omitted]

Background A cornerstone of conventional dietary advice is the recommendation to replace saturated fatty acids (SFA) with mostly n-6 polyunsaturated fatty acids (PUFA) to reduce the risk of coronary heart disease (CHD). Many clinical trials aimed to test this advice and have had their results pooled in several meta-analyses. However, earlier meta-analyses did not sufficiently account for major confounding variables that were present in some of those trials. Therefore, the aim of the study was to account for the major confounding variables in the diet heart trials, and emphasise the results from those trials that most accurately test the effect of replacing SFA with mostly n-6 PUFA. Design Clinical trials were identified from earlier meta-analyses. Relevant trials were categorised as ‘adequately controlled’ or ‘inadequately controlled’ depending on whether there were substantial dietary or non-dietary differences between the experimental and control groups that were not related to SFA or mostly n-6 PUFA intake, then were subject to different subgroup analyses. Results When pooling results from only the adequately controlled trials there was no effect for major CHD events (RR = 1.06, CI = 0.86–1.31), total CHD events (RR = 1.02, CI = 0.84–1.23), CHD mortality (RR = 1.13, CI = 0.91–1.40) and total mortality (RR = 1.07, CI = 0.90–1.26). Whereas, the pooled results from all trials, including the inadequately controlled trials, suggested that replacing SFA with mostly n-6 PUFA would significantly reduce the risk of total CHD events (RR = 0.80, CI = 0.65–0.98, P  = 0.03), but not major CHD events (RR = 0.87, CI = 0.70–1.07), CHD mortality (RR = 0.90, CI = 0.70–1.17) and total mortality (RR = 1.00, CI = 0.90–1.10). Conclusion Available evidence from adequately controlled randomised controlled trials suggest replacing SFA with mostly n-6 PUFA is unlikely to reduce CHD events, CHD mortality or total mortality. The suggestion of benefits reported in earlier meta-analyses is due to the inclusion of inadequately controlled trials. These findings have implications for current dietary recommendations.

Unsaturated fat replacement should be used to reduce the use of saturated fat and trans fatty acids in the diet. In this study, pea protein micro-gels (PPMs) with different structures were prepared by microparticulation at pH 4.0–7.0 and named as PPM (pH 4.0), PPM (pH 4.5), PPM (pH 5.0), PPM (pH 5.5), PPM (pH 6.0), PPM (pH 6.5), and PPM (pH 7.0). Pea protein was used as a control to evaluate the structure and interfacial properties of PPMs by particle size distribution, Fourier transform infrared spectroscopy (FTIR), free sulfhydryl group content, and emulsifying property. PPM (pH 7.0) was suitable for application in O/W emulsion stabilization because of its proper particle size, more flexible structure, high emulsifying activity index (EAI) and emulsifying stability index (ESI). The Pickering emulsion stabilized by PPM (pH 7.0) had a uniform oil droplet distribution and similar rheological properties to cream, so it can be used as a saturated fat replacement in the manufacture of ice cream. Saturated fat was partially replaced at different levels of 0%, 20%, 40%, 60%, 80%, and 100%, which were respectively named as PR0, PR20, PR40, PR60, PR80, and PR100. The rheological properties, physicochemical indexes, and sensory properties of low-saturated fat ice cream show that PPM (pH 7.0)-stabilized emulsion can be used to substitute 60% cream to manufacture low-saturated fat ice cream that has high structural stability and similar melting properties, overrun, and sensory properties to PR0. The article shows that it is feasible to prepare low-saturated fat ice cream with PPM (pH 7.0)-stabilized Pickering emulsion, which can not only maintain the fatty acid profile of the corn oil used, but also possess a solid-like structure. Its application is of positive significance for the development of nutritious and healthy foods and the reduction of chronic disease incidence.

Purpose Despite the important role of dietary fat in early childhood, our understanding of fat intake trends during this period is limited, particularly among Australian children. This study aimed to describe total and saturated fat (SFA) intake trends, food sources, and tracking in young Australian children. Methods Data of children at ages 9 months ( n  = 393), 18 months ( n  = 284), 3.5 years ( n  = 244), and 5 years ( n  = 240) from the Melbourne InFANT Program were used. Dietary intakes were collected via three 24-hour recalls. Food groups and nutrient intakes were calculated using the 2007 AUSNUT Food Composition Database. Descriptive statistics were used to summarize fat intake and key food sources of fat. Tracking of fat intake was examined using Pearson correlations of residualized fat scores between time points. Results Total and SFA intake (g/d) increased over time in early childhood. The percentage of energy from total fat decreased from 9 to 18 months but remained stable until 5 years of age. The percentage of energy from SFA decreased across early childhood. Milk and milk products were the primary sources of both total fat and SFA, followed by breads/cereals, and cakes/cookies. Slight to moderate tracking of fat was observed in most age groups. Conclusion This study described trends and food sources of young children’s fat intakes and showed that early fat intakes track up to age 5 years. The study will contribute to the development and refinement of fat recommendations in young Australian children and inform the design of interventions to improve fat intake.

PurposeTo derive dietary patterns based on dietary energy density (DED), free sugars, SFA, and fiber and investigate association with odds of overweight/obesity in young adults.MethodsCross-sectional data from 625 young Australian adults (18–30 years) were used. Dietary patterns were derived using reduced rank regression based on dietary data from a smartphone food diary using DED, free sugars, SFA, and fiber density as response variables. Multivariable logistic regression was used to investigate associations between dietary patterns and odds of self-reported overweight/obesity (BMI ≥ 25 kg/m2).ResultsTwo dietary patterns were identified (DP1 and DP2). DP-1 was positively correlated with DED, free sugars, and SFA, and inversely correlated with fiber density. It was characterized by higher sugar-sweetened beverages intake and lower vegetable intake, and associated with higher odds of overweight/obesity (OR: 1.22; 95% CI 1.05, 1.42). DP-2 was positively correlated with fiber density and free sugars, and inversely correlated with DED and SFA. It was characterized by higher sugar-sweetened beverages intake and lower non-lean red meat intake, and was not significantly associated with overweight/obesity.ConclusionAn energy-dense dietary pattern high in free sugars and SFA and low in fiber was associated with higher odds of obesity in young adults. These findings support dietary interventions that target reductions in energy-dense foods and sugar-sweetened beverages.

Background: Metabolic syndrome increases the risk of cardiovascular disease (CVD) over and above that related to type 2 diabetes. The optimal diet for the treatment of metabolic syndrome is not clear. Materials and Methods: A review of dietary interventions in volunteers with metabolic syndrome as well as studies examining the impact of dietary fat on the separate components of metabolic syndrome was undertaken using only recent meta-analyses, if available. Results: Most of the data suggest that replacing carbohydrates with any fat, but particularly polyunsaturated fat, will lower triglyceride(TG), increase high density lipoprotein (HDL) cholesterol, and lower blood pressure, but have no effects on fasting glucose in normal volunteers or insulin sensitivity, as assessed by euglycemic hyperinsulinemic clamps. Fasting insulin may be lowered by fat. Monounsaturated fat (MUFA) is preferable to polyunsaturated fat (PUFA) for fasting insulin and glucose lowering. The addition of 3–4 g of N3 fats will lower TG and blood pressure (BP) and reduce the proportion of subjects with metabolic syndrome. Dairy fat (50% saturated fat) is also related to a lower incidence of metabolic syndrome in cohort studies.