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Dietary Saturated Fats and Health: Are the U.S. Guidelines Evidence-Based?
Astrup, A, Teicholz, N, Magkos, F, Bier, DM, Brenna, JT, King, JC, Mente, A, Ordovas, JM, Volek, JS, Yusuf, S, et al
Nutrients. 2021;(10)
Abstract
The last decade has seen nearly 20 papers reviewing the totality of the data on saturated fats and cardiovascular outcomes, which, altogether, have demonstrated a lack of rigorous evidence to support continued recommendations either to limit the consumption of saturated fatty acids or to replace them with polyunsaturated fatty acids. These papers were unfortunately not considered by the process leading to the most recent U.S. Dietary Guidelines for Americans, the country's national nutrition policy, which recently reconfirmed its recommendation to limit saturated fats to 10% or less of total energy intake, based on insufficient and inconsistent evidence. Continuation of a cap on saturated fat intake also fails to consider the important effects of the food matrix and the overall dietary pattern in which saturated fatty acids are consumed.
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Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review.
Astrup, A, Magkos, F, Bier, DM, Brenna, JT, de Oliveira Otto, MC, Hill, JO, King, JC, Mente, A, Ordovas, JM, Volek, JS, et al
Journal of the American College of Cardiology. 2020;(7):844-857
Abstract
The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. Most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke. Although SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due to increasing levels of small, dense LDL particles, but rather larger LDL particles, which are much less strongly related to CVD risk. It is also apparent that the health effects of foods cannot be predicted by their content in any nutrient group without considering the overall macronutrient distribution. Whole-fat dairy, unprocessed meat, and dark chocolate are SFA-rich foods with a complex matrix that are not associated with increased risk of CVD. The totality of available evidence does not support further limiting the intake of such foods.
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The Impact of Dairy Products in the Development of Type 2 Diabetes: Where Does the Evidence Stand in 2019?
Guo, J, Givens, DI, Astrup, A, Bakker, SJL, Goossens, GH, Kratz, M, Marette, A, Pijl, H, Soedamah-Muthu, SS
Advances in nutrition (Bethesda, Md.). 2019;(6):1066-1075
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Abstract
The prevalence of type 2 diabetes (T2D) has increased rapidly. Adopting a heathy diet is suggested as one of the effective behaviors to prevent or delay onset of T2D. Dairy consumption has been recommended as part of a healthy diet, but there remains uncertainty in both the scientific community and the public about the effect of different dairy products on T2D risk. In a recent workshop, the evidence on dairy products and T2D risk was presented and discussed by a group of experts. The main conclusions from the workshop are presented in this position paper and are as follows. 1) Available evidence from large prospective cohort studies and limited randomized controlled trials (RCTs) suggests that total dairy consumption has a neutral or moderately beneficial effect on T2D risk. 2) Increasing evidence from prospective cohort studies indicates that yogurt is most strongly associated with a lower T2D risk, but evidence from RCTs is scarce. 3) Fatty acids from dairy (medium-chain, odd, and very long-chain SFAs as well as trans-palmitoleic acid) are associated with lower T2D risk and improved metabolic health, but more research is needed on studies that explore cause and effect relations to exclude the possibility that the dairy fatty acids simply serve as markers of overall dairy consumption. 4) The food matrix can be a stronger determinant of health effects than SFA content. This review further identifies research gaps in the existing knowledge and highlights key research questions that need to be addressed to better understand the impact of dairy consumption on future T2D risk.
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Effects of Full-Fat and Fermented Dairy Products on Cardiometabolic Disease: Food Is More Than the Sum of Its Parts.
Astrup, A, Geiker, NRW, Magkos, F
Advances in nutrition (Bethesda, Md.). 2019;(5):924S-930S
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Abstract
Current dietary recommendations to limit consumption of saturated fat are largely based on early nutrition studies demonstrating a direct link between dietary saturated fat, elevated blood cholesterol levels, and increased risk of cardiovascular disease. As full-fat dairy products are rich in saturated fat, these dietary guidelines recommend consumption of fat-free or low-fat dairy products in place of full-fat dairy. However, dairy products vary greatly in both their nutrient content and their bioactive ingredients, and research increasingly highlights the importance of focusing on whole foods (i.e., the food matrix) as opposed to single nutrients, such as saturated fat. In fact, the weight of evidence from recent large and well-controlled studies, systematic reviews, and meta-analyses of both observational studies and randomized controlled trials indicates that full-fat dairy products, particularly yogurt and cheese, do not exert the detrimental effects on insulin sensitivity, blood lipid profile, and blood pressure as previously predicted on the basis of their sodium and saturated fat contents; they do not increase cardiometabolic disease risk and may in fact protect against cardiovascular disease and type 2 diabetes. Although more research is warranted to adjust for possible confounding factors and to better understand the mechanisms of action of dairy products on health outcomes, it becomes increasingly clear that the recommendation to restrict dietary saturated fat to reduce risk of cardiometabolic disease is getting outdated. Therefore, the suggestion to restrict or eliminate full-fat dairy from the diet may not be the optimal strategy for reducing cardiometabolic disease risk and should be re-evaluated in light of recent evidence.
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Resistant starch and protein intake enhances fat oxidation and feelings of fullness in lean and overweight/obese women.
Gentile, CL, Ward, E, Holst, JJ, Astrup, A, Ormsbee, MJ, Connelly, S, Arciero, PJ
Nutrition journal. 2015;:113
Abstract
BACKGROUND Diets high in either resistant starch or protein have been shown to aid in weight management. We examined the effects of meals high in non-resistant or resistant starch with and without elevated protein intake on substrate utilization, energy expenditure, and satiety in lean and overweight/obese women. METHODS Women of varying levels of adiposity consumed one of four pancake test meals in a single-blind, randomized crossover design: 1) waxy maize (control) starch (WMS); 2) waxy maize starch and whey protein (WMS+WP); 3) resistant starch (RS); or 4) RS and whey protein (RS+WP). RESULTS Total post-prandial energy expenditure did not differ following any of the four test meals (WMS = 197.9 ± 8.9; WMS+WP = 188 ± 8.1; RS = 191.9 ± 8.9; RS+WP = 195.8 ± 8.7, kcals/180 min), although the combination of RS+WP, but not either intervention alone, significantly increased (P <0.01) fat oxidation (WMS = 89.5 ± 5.4; WMS+WP = 84.5 ± 7.2; RS = 97.4 ± 5.4; RS+WP = 107.8 ± 5.4, kcals/180 min). Measures of fullness increased (125% vs. 45%) and hunger decreased (55% vs. 16%) following WP supplemented versus non-whey conditions (WMS+WP, RS+WP vs. WMS, RS), whereas circulating hunger and satiety factors were not different among any of the test meals. However, peptide YY (PYY) was significantly elevated at 180 min following RS+WP meal. CONCLUSIONS The combined consumption of dietary resistant starch and protein increases fat oxidation, PYY, and enhances feelings of satiety and fullness to levels that may be clinically relevant if maintained under chronic conditions. This trial was registered at clinicaltrials.gov as NCT02418429.
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Personalized weight loss strategies-the role of macronutrient distribution.
Martinez, JA, Navas-Carretero, S, Saris, WH, Astrup, A
Nature reviews. Endocrinology. 2014;(12):749-60
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Abstract
A large number of different dietary approaches have been studied in an attempt to achieve healthy, sustainable weight loss among individuals with overweight and obesity. Restriction of energy intake is the primary method of producing a negative energy balance leading to weight loss. However, owing to the different metabolic roles of proteins, carbohydrates and lipids in energy homeostasis, diets of similar overall energy content but with different macronutrient distribution can differentially affect metabolism, appetite and thermogenesis. Evidence increasingly suggests that the fuel values of calories provided by distinct macronutrients should be considered separately, as metabolism of specific molecular components generates differences in energy yield. The causes of variation in individual responses to various diets are currently under debate, and some evidence suggests that differences are associated with specific genotypes. This Review discusses all available systematic reviews and meta-analyses, and summarizes the results of relevant randomized controlled intervention trials assessing the influence of macronutrient composition on weight management. The initial findings of research into personalized nutrition, based on the interactions of macronutrient intake and genetic background and its potential influence on dietary intervention strategies, are also discussed.
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Postprandial coagulation activation in overweight individuals after weight loss: acute and long-term effects of a high-monounsaturated fat diet and a low-fat diet.
Bladbjerg, EM, Larsen, TM, Due, A, Jespersen, J, Stender, S, Astrup, A
Thrombosis research. 2014;(3):327-33
Abstract
Diet is important in the prevention of cardiovascular disease, and it has been suggested that a high-MUFA diet is more cardioprotective than a low-fat diet. We hypothesised that the postprandial thrombotic risk profile is improved most favourably by a high-MUFA diet compared with a low-fat diet. This was tested in a parallel intervention trial on overweight individuals (aged 28.4 (SD 4.7) years) randomly assigned to a MUFA-diet (35-45% of energy as fat; >20% as MUFA, n = 21) or a low-fat (LF) diet (20-30% of energy as fat, n = 22) for 6 months after a weight loss of ~10%. All foods were provided free of charge from a purpose-built supermarket. Meal tests designed after the same principles were performed before and after the dietary intervention, and blood samples were collected at 8.00 h (fasting), 12.00 h, and 18.00 h and analysed for factor VII coagulant activity (FVII:C), activated FVII, fibrinogen, prothrombin fragment 1 + 2 (F1 + 2), D-dimer, plasminogen activator inhibitor (PAI:Ag), and thrombin activatable fibrinolysis inhibitor. There were significant postprandial increases in F1 + 2 and D-dimer before and after dietary intervention, with significantly lower values after 6 months. No significant differences were observed between the postprandial changes induced by the two diets. The postprandial decrease in FVIIC and PAI:Ag did not differ before and after intervention, irrespective of the diets. Our findings suggest postprandial coagulation activation in overweight subjects with more pronounced acute than long-term effects. We observed similar effects of the MUFA diet and the LF diet on the postprandial prothrombotic risk profile.
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Effects of high-fat overfeeding on mitochondrial function, glucose and fat metabolism, and adipokine levels in low-birth-weight subjects.
Brøns, C, Jacobsen, S, Hiscock, N, White, A, Nilsson, E, Dunger, D, Astrup, A, Quistorff, B, Vaag, A
American journal of physiology. Endocrinology and metabolism. 2012;(1):E43-51
Abstract
Low birth weight (LBW) is associated with an increased risk of insulin resistance and downregulation of oxidative phosphorylation (OXPHOS) genes when exposed to a metabolic challenge of high-fat overfeeding (HFO). To elaborate further on the differential effects of HFO in LBW subjects, we measured in vivo mitochondrial function, insulin secretion, hepatic glucose production, and plasma levels of key regulatory hormones before and after 5 days of HFO in 20 young LBW and 26 normal-birth-weight (NBW) men. The LBW subjects developed peripheral insulin resistance after HFO due to impaired endogenous glucose storage (9.42 ± 4.19 vs. 5.91 ± 4.42 mg·kg FFM(-1)·min(-1), P = 0.01). Resting muscle phosphorcreatine and total ATP in muscle increased significantly after HFO in LBW subjects only, whereas additional measurements of mitochondrial function remained unaffected. Despite similar plasma FFA levels, LBW subjects displayed increased fat oxidation during insulin infusion compared with normal-birth-weight (NBW) subjects after HFO (0.37 ± 0.35 vs. 0.17 ± 0.33 mg·kg FFM(-1)·min(-1), P = 0.02). In contrast to NBW subjects, the plasma leptin levels of LBW subjects did not increase, and the plasma gastric inhibitory polypeptide (GIP) as well as pancreatic polypeptide (PP) levels increased less in LBW compared with NBW subjects during HFO. In conclusion, HFO unmasks dissociation between insulin resistance and mitochondrial dysfunction in LBW subjects, suggesting that insulin resistance may be a cause, rather than an effect, of impaired muscle OXPHOS gene expression and mitochondrial dysfunction. Reduced increments in response to HFO of fasting plasma leptin, PP, and GIP levels may contribute to insulin resistance, lower satiety, and impaired insulin secretion in LBW subjects.
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Acute differential effects of milk-derived dietary proteins on postprandial lipaemia in obese non-diabetic subjects.
Holmer-Jensen, J, Hartvigsen, ML, Mortensen, LS, Astrup, A, de Vrese, M, Holst, JJ, Thomsen, C, Hermansen, K
European journal of clinical nutrition. 2012;(1):32-8
Abstract
BACKGROUND/OBJECTIVES Postprandial lipaemia is an established risk factor for atherosclerosis. To investigate the acute effect of four milk-derived dietary proteins (alpha-lactalbumin, whey isolate, caseinoglycomacropeptide and whey hydrolysate) on postprandial lipaemia, we have conducted a randomized, acute, single-blinded clinical intervention study with crossover design. SUBJECTS/METHODS A total of 11 obese non-diabetic subjects (age: 44-74, BMI: 30-41.4 kg m(-2)) were included. On 4 different days the subjects ingested a high-fat meal with the following energy distribution: 66% energy from fat (100 g of butter), 15% of energy from carbohydrate (90 g of white wheat bread) and 19% of energy from protein (45 g of pure protein). Our primary variable was plasma triglyceride measured in the 8-h postprandial period. Secondarily, retinyl palmitate, non-esterified free fatty acids, glucose, insulin, glucagon, GLP-1 and GIP, active and total grehlin and cholecystokinin were measured. RESULTS We observed no statistically significant (P=0.8) differences between meals on our primary variable that is, triglycerides. Whey hydrolysate was associated with a significantly (P=0.02) smaller postprandial suppression of non-esterified free fatty acids compared with the other dietary proteins. CONCLUSION We did not observe significant differences in postprandial lipaemia to the four milk-derived dietary proteins. Whey hydrolysate caused less postprandial suppression of free fatty acids.
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The relevance of increased fat oxidation for body-weight management: metabolic inflexibility in the predisposition to weight gain.
Astrup, A
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2011;(10):859-65
Abstract
Cells, tissues and organisms have the ability to rapidly switch substrate oxidation from carbohydrate to fat in response to changes in nutrient intake, and to changes in energy demands, environmental cues and internal signals. In healthy, metabolically normal individuals, substrate switching occurs rapidly and completely; in other words, substrate switching is 'flexible'. A growing body of evidence demonstrates that a blunted substrate switching from low- to high-fat oxidation exists in obese individuals, as well as in pre-obese and post-obese, and that this 'metabolic inflexibility' may be a genetically determined trait. A decreased fat oxidation can lead to a positive energy balance under conditions of high-fat feeding, due to depletion of glycogen stores that stimulates appetite and energy intake through glucostatic and glucogenostatic mechanisms, e.g. hepatic sensing of glycogen stores. Several genetic polymorphisms and single-nucleotide polymorphisms have been identified that are associated with low-fat oxidation rates and metabolic inflexibility, and genetic identification of susceptible individuals may lead to personalized prevention of weight gain using fat oxidation stimulants ('fat burners') in the future.