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Low-fat dietary pattern and breast cancer mortality by metabolic syndrome components: a secondary analysis of the Women's Health Initiative (WHI) randomised trial.
Pan, K, Aragaki, AK, Neuhouser, ML, Simon, MS, Luo, J, Caan, B, Snetselaar, L, Mortimer, JE, Manson, JE, Kroenke, C, et al
British journal of cancer. 2021;(3):372-379
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BACKGROUND In the Women's Health Initiative (WHI) dietary modification (DM) randomised trial, the low-fat dietary intervention reduced deaths from breast cancer (P = 0.02). Extending these findings, secondary analysis examined dietary intervention influence on breast cancer mortality by metabolic syndrome (MS) components. METHODS In total, 48,835 postmenopausal women with no prior breast cancer were randomised to a low-fat dietary intervention or comparison groups. Four MS components were determined at entry in 45,833 participants: (1) high waist circumference, (2) high blood pressure, (3) high cholesterol and (4) diabetes history. Forest plots of hazard ratios (HRs) were generated with P-values for interaction between randomisation groups and MS component score. Primary outcome was death from breast cancer by metabolic syndrome score. RESULTS HRs and 95% confidence intervals (CI) for dietary intervention influence on death from breast cancer were with no MS components (n = 10,639), HR 1.09, 95% CI 0.63-1.87; with 1-2 MS components (n = 30,948), HR 0.80, 95% CI 0.62-1.02; with 3-4 MS components (n = 4,246), HR 0.31, 95% CI 0.14-0.69 (interaction P = 0.01). CONCLUSIONS While postmenopausal women with 3-4 MS components were at higher risk of death from breast cancer, those randomised to a low-fat dietary intervention more likely had reduction in this risk. REGISTRY ClinicalTrials.gov (NCT00000611).
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Short communication: Daily intake of 125 g of cheese for 2 weeks did not alter amount or distribution of serum lipids or desaturase indexes in healthy adults in an exploratory pilot study.
Høstmark, AT, Lunde, MSH, Hjellset, VT
Journal of dairy science. 2018;(11):9625-9629
Abstract
Regular cheese contains saturated fat, consumption of which may negatively influence the amount of serum lipids. The American Dietary Guidelines (https://health.gov/dietaryguidelines/2015/guidelines/) recommend consumption of low-fat food. However, we observed a negative association between cheese intake and serum triglycerides and a positive association with high-density lipoprotein cholesterol. Cheese intake was also inversely related to metabolic syndrome and blunted the harmful association of intake of soft drinks with serum lipids. Cheese contains calcium and factors that may inhibit desaturases, thereby partly explaining why cheese might not have negative effects on serum lipids. Thus, opposing forces seem to govern the cheese effect but will any of these prevail? In an exploratory pilot study, 17 healthy subjects participated in a 4-wk crossover trial without washout. During the first 2 wk, 9 subjects were randomly assigned to add 125 g/d of regular cheese to their habitual diet. After 2 wk, cheese intake was discontinued and the subjects were instructed to return to their habitual diet. The other 8 subjects followed their habitual diet during the first 2 wk, and then added 125 g/d of cheese for the next 2 wk. Mean values (mmol/L) before and after 2 wk on habitual (cheese) diet were as follows: serum triglycerides: 0.91 (0.89) and 0.95 (0.91); total cholesterol: 5.25 (5.16) and 5.08 (5.24); low-density lipoprotein cholesterol: 3.18 (3.17) and 3.09 (3.22); and high-density lipoprotein cholesterol: 1.71 (1.64) and 1.61 (1.66). The fatty acid pattern in total serum lipids and desaturase indexes did not change significantly in response to high cheese intake. Thus, an appreciable increase in daily cheese intake for 2 wk may not alter concentrations of serum lipids, estimates of desaturases, or the distribution of serum fatty acids.
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Marital discord, past depression, and metabolic responses to high-fat meals: Interpersonal pathways to obesity.
Kiecolt-Glaser, JK, Jaremka, L, Andridge, R, Peng, J, Habash, D, Fagundes, CP, Glaser, R, Malarkey, WB, Belury, MA
Psychoneuroendocrinology. 2015;:239-50
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BACKGROUND Longitudinal studies have implicated both marital distress and depression in the development of the metabolic syndrome, a risk factor for diabetes and cardiovascular disease. This study addressed the impact of hostile marital interactions and a mood disorder history on obesity-related metabolic responses to high-fat meals. METHODS This double-blind, randomized crossover study included serial assessments of resting energy expenditure (REE), fat and carbohydrate oxidation, triglycerides, insulin, glucose, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) before and after two high-fat meals. During two separate 9.5h visits, 43 healthy married couples, ages 24-61 (mean=38.22), received either a high saturated fat meal or a high oleic sunflower oil meal, both 930kcal and 60g fat. The Structured Diagnostic Interview for DSM-IV assessed mood disorder history. Couples discussed a marital disagreement during both visits; behavioral coding of these interactions provided data on hostile marital behaviors. RESULTS Men and women who displayed more hostile behaviors and who also had a mood disorder history had significantly lower post-meal REE, higher insulin, and higher peak triglyceride responses than other participants, with nonsignificant effects for fat and carbohydrate oxidation. Participants with a mood disorder history had a steeper rise in postprandial IL-6 and glucose than those without a past history. Higher levels of hostile behaviors were associated with higher post-meal TNF-α. The two meals did not differ on any outcome assessed. CONCLUSIONS People spend about 18 of every 24h in a postprandial state, and dining with one's partner is a common daily event. Among subjects with a mood disorder history, the cumulative 6.75-h difference between high and low hostile behaviors translates into 128kcal, a difference that could add 7.6pounds/year. Our findings illustrate novel pathways through which chronic marital stress and a mood disorder history synergistically heighten the risk for obesity, metabolic syndrome, and cardiovascular disease.
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Proteome from patients with metabolic syndrome is regulated by quantity and quality of dietary lipids.
Rangel-Zúñiga, OA, Camargo, A, Marin, C, Peña-Orihuela, P, Pérez-Martínez, P, Delgado-Lista, J, González-Guardia, L, Yubero-Serrano, EM, Tinahones, FJ, Malagón, MM, et al
BMC genomics. 2015;(1):509
Abstract
BACKGROUND Metabolic syndrome is a multi-component disorder associated to a high risk of cardiovascular disease. Its etiology is the result of a complex interaction between genetic and environmental factors, including dietary habits. We aimed to identify the target proteins modulated by the long-term consumption of four diets differing in the quality and quantity of lipids in the whole proteome of peripheral blood mononuclear cells (PBMC). RESULTS A randomized, controlled trial conducted within the LIPGENE study assigned 24 MetS patients for 12 weeks each to 1 of 4 diets: a) high-saturated fatty acid (HSFA), b) high-monounsaturated fatty acid (HMUFA), c) low-fat, high-complex carbohydrate diets supplemented with placebo (LFHCC) and d) low-fat, high-complex carbohydrate diets supplemented with long chain (LC) n-3 polyunsaturated fatty acids (PUFA) (LFHCC n-3). We analyzed the changes induced in the proteome of both nuclear and cytoplasmic fractions of PBMC using 2-D proteomic analysis. Sixty-seven proteins were differentially expressed after the long-term consumption of the four diets. The HSFA diet induced the expression of proteins responding to oxidative stress, degradation of ubiquitinated proteins and DNA repair. However, HMUFA, LFHCC and LFHCC n-3 diets down-regulated pro-inflammatory and oxidative stress-related proteins and DNA repairing proteins. CONCLUSION The long-term consumption of HSFA, compared to HMUFA, LFHCC and LFHCC n-3, seems to increase the cardiovascular disease (CVD) risk factors associated with metabolic syndrome, such as inflammation and oxidative stress, and seem lead to DNA damage as a consequence of high oxidative stress.
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A low-fat dietary pattern and risk of metabolic syndrome in postmenopausal women: the Women's Health Initiative.
Neuhouser, ML, Howard, B, Lu, J, Tinker, LF, Van Horn, L, Caan, B, Rohan, T, Stefanick, ML, Thomson, CA
Metabolism: clinical and experimental. 2012;(11):1572-81
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OBJECTIVE Nutrition plays an important role in metabolic syndrome etiology. We examined whether the Women's Health Initiative (WHI) Dietary Modification Trial influenced metabolic syndrome risk. MATERIALS/METHODS 48,835 postmenopausal women aged 50-79 years were randomized to a low-fat (20% energy from fat) diet (intervention) or usual diet (comparison) for a mean of 8.1 years. Blood pressure, waist circumference and fasting blood measures of glucose, HDL-cholesterol and triglycerides were measured on a subsample (n=2816) at baseline and years 1, 3 and 6 post-randomization. Logistic regression estimated associations of the intervention with metabolic syndrome risk and use of cholesterol-lowering and hypertension medications. Multivariate linear regression tested associations between the intervention and metabolic syndrome components. RESULTS At year 3, but not years 1 or 6, women in the intervention group (vs. comparison) had a non-statistically significant lower risk of metabolic syndrome (OR=0.83, 95%CI 0.59-1.18). Linear regression models simultaneously modeling the five metabolic syndrome components revealed significant associations of the intervention with metabolic syndrome at year 1 (p<0.0001), but not years 3 (p=0.19) and 6 (p=0.17). Analyses restricted to intervention-adherent participants strengthened associations at years 3 (p=0.05) and 6 (p=0.06). Cholesterol-lowering and hypertension medication use was 19% lower at year 1 for intervention vs. comparison group women (OR=0.81, 95% CI 0.60-1.09).Over the entire trial, fewer intervention vs. comparison participants used these medications (26.0% vs. 29.9%), although results were not statistically significant (p=0.89). CONCLUSIONS The WHI low-fat diet may influence metabolic syndrome risk and decrease use of hypertension and cholesterol-lowering medications. Findings have potential for meaningful clinical translation.
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Interaction of PPARG Pro12Ala with dietary fat influences plasma lipids in subjects at cardiometabolic risk.
AlSaleh, A, O'Dell, SD, Frost, GS, Griffin, BA, Lovegrove, JA, Jebb, SA, Sanders, TAB
Journal of lipid research. 2011;(12):2298-2303
Abstract
The PPARγ2 gene single nucleotide polymorphism (SNP) Pro12Ala has shown variable association with metabolic syndrome traits in healthy subjects. The RISCK Study investigated the effect of interaction between genotype and the ratio of polyunsaturated:saturated (P:S) fatty acid intake on plasma lipids in 367 white subjects (ages 30-70 years) at increased cardiometabolic risk. Interaction was determined after habitual diet at recruitment, at baseline after a 4-week high-SFA (HS) diet, and after a 24-week reference (HS), high-MUFA (HM), or low-fat (LF) diet. At recruitment, there were no significant associations between genotype and plasma lipids; however, P:S × genotype interaction influenced plasma total cholesterol (TC) (P = 0.02), LDL-cholesterol (LDL-C) (P = 0.002), and triglyceride (TG) (P = 0.02) concentrations. At P:S ratio ≤ 0.33, mean TC and LDL-C concentrations in Ala12 allele carriers were significantly higher than in noncarriers (respectively, P = 0.003; P = 0.0001). Significant trends in reduction of plasma TC (P = 0.02) and TG (P = 0.002) concentrations occurred with increasing P:S (respectively, ≤0.33 to >0.65; 0.34 to >0.65) in Ala12 allele carriers. There were no significant differences between carriers and noncarriers after the 4-week HS diet or 24-week interventions. Plasma TC and TG concentrations in PPARG Ala12 allele carriers decrease as P:S increases, but they are not dependent on a reduction in SFA intake.
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Single nucleotide polymorphisms at the ADIPOQ gene locus interact with age and dietary intake of fat to determine serum adiponectin in subjects at risk of the metabolic syndrome.
AlSaleh, A, O'Dell, SD, Frost, GS, Griffin, BA, Lovegrove, JA, Jebb, SA, Sanders, TA, ,
The American journal of clinical nutrition. 2011;(1):262-9
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BACKGROUND Adiponectin gene expression is modulated by peroxisome proliferator-activated receptor γ, which is a transcription factor activated by unsaturated fatty acids. OBJECTIVE We investigated the effect of the interaction between variants at the ADIPOQ gene locus, age, sex, body mass index (BMI), ethnicity, and the replacement of dietary saturated fatty acids (SFAs) with monounsaturated fatty acids (MUFAs) or carbohydrates on serum adiponectin concentrations. DESIGN The RISCK (Reading, Imperial, Surrey, Cambridge, and Kings) study is a parallel-design, randomized controlled trial. Serum adiponectin concentrations were measured after a 4-wk high-SFA (HS) diet and a 24-wk intervention with reference (HS), high-MUFA (HM), and low-fat (LF) diets. Single nucleotide polymorphisms at the ADIPOQ locus -11391 G/A (rs17300539), -10066 G/A (rs182052), -7734 A/C (rs16861209), and +276 G/T (rs1501299) were genotyped in 448 participants. RESULTS In white Europeans, +276 T was associated with higher serum adiponectin concentrations (n = 340; P = 0.006) and -10066 A was associated with lower serum adiponectin concentrations (n = 360; P = 0.03), after adjustment for age, BMI, and sex. After the HM diet, -10066 G/G subjects showed a 3.8% increase (95% CI: -0.1%, 7.7%) and G/A+A/A subjects a 2.6% decrease (95% CI: -5.6%, 0.4%) in serum adiponectin (P = 0.006 for difference after adjustment for the change in BMI, age, and sex). In -10066 G/G homozygotes, serum adiponectin increased with age after the HM diet and decreased after the LF diet. CONCLUSION In white -10066 G/G homozygotes, an HM diet may help to increase adiponectin concentrations with advancing age. This trial was registered at clinicaltrials.gov as ISRCTN29111298.
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Effect of changing the amount and type of fat and carbohydrate on insulin sensitivity and cardiovascular risk: the RISCK (Reading, Imperial, Surrey, Cambridge, and Kings) trial.
Jebb, SA, Lovegrove, JA, Griffin, BA, Frost, GS, Moore, CS, Chatfield, MD, Bluck, LJ, Williams, CM, Sanders, TA, ,
The American journal of clinical nutrition. 2010;(4):748-58
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BACKGROUND Insulin sensitivity (Si) is improved by weight loss and exercise, but the effects of the replacement of saturated fatty acids (SFAs) with monounsaturated fatty acids (MUFAs) or carbohydrates of high glycemic index (HGI) or low glycemic index (LGI) are uncertain. OBJECTIVE We conducted a dietary intervention trial to study these effects in participants at risk of developing metabolic syndrome. DESIGN We conducted a 5-center, parallel design, randomized controlled trial [RISCK (Reading, Imperial, Surrey, Cambridge, and Kings)]. The primary and secondary outcomes were changes in Si (measured by using an intravenous glucose tolerance test) and cardiovascular risk factors. Measurements were made after 4 wk of a high-SFA and HGI (HS/HGI) diet and after a 24-wk intervention with HS/HGI (reference), high-MUFA and HGI (HM/HGI), HM and LGI (HM/LGI), low-fat and HGI (LF/HGI), and LF and LGI (LF/LGI) diets. RESULTS We analyzed data for 548 of 720 participants who were randomly assigned to treatment. The median Si was 2.7 × 10(-4) mL · μU(-1) · min(-1) (interquartile range: 2.0, 4.2 × 10(-4) mL · μU(-1) · min(-1)), and unadjusted mean percentage changes (95% CIs) after 24 wk treatment (P = 0.13) were as follows: for the HS/HGI group, -4% (-12.7%, 5.3%); for the HM/HGI group, 2.1% (-5.8%, 10.7%); for the HM/LGI group, -3.5% (-10.6%, 4.3%); for the LF/HGI group, -8.6% (-15.4%, -1.1%); and for the LF/LGI group, 9.9% (2.4%, 18.0%). Total cholesterol (TC), LDL cholesterol, and apolipoprotein B concentrations decreased with SFA reduction. Decreases in TC and LDL-cholesterol concentrations were greater with LGI. Fat reduction lowered HDL cholesterol and apolipoprotein A1 and B concentrations. CONCLUSIONS This study did not support the hypothesis that isoenergetic replacement of SFAs with MUFAs or carbohydrates has a favorable effect on Si. Lowering GI enhanced reductions in TC and LDL-cholesterol concentrations in subjects, with tentative evidence of improvements in Si in the LF-treatment group. This trial was registered at clinicaltrials.gov as ISRCTN29111298.
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Gene expression changes in mononuclear cells in patients with metabolic syndrome after acute intake of phenol-rich virgin olive oil.
Camargo, A, Ruano, J, Fernandez, JM, Parnell, LD, Jimenez, A, Santos-Gonzalez, M, Marin, C, Perez-Martinez, P, Uceda, M, Lopez-Miranda, J, et al
BMC genomics. 2010;:253
Abstract
BACKGROUND Previous studies have shown that acute intake of high-phenol virgin olive oil reduces pro-inflammatory, pro-oxidant and pro-thrombotic markers compared with low phenols virgin olive oil, but it still remains unclear whether effects attributed to its phenolic fraction are exerted at transcriptional level in vivo. To achieve this goal, we aimed at identifying expression changes in genes which could be mediated by virgin olive oil phenol compounds in the human. RESULTS Postprandial gene expression microarray analysis was performed on peripheral blood mononuclear cells during postprandial period. Two virgin olive oil-based breakfasts with high (398 ppm) and low (70 ppm) content of phenolic compounds were administered to 20 patients suffering from metabolic syndrome following a double-blinded, randomized, crossover design. To eliminate the potential effect that might exist in their usual dietary habits, all subjects followed a similar low-fat, carbohydrate rich diet during the study period. Microarray analysis identified 98 differentially expressed genes (79 underexpressed and 19 overexpressed) when comparing the intake of phenol-rich olive oil with low-phenol olive oil. Many of these genes seem linked to obesity, dyslipemia and type 2 diabetes mellitus. Among these, several genes seem involved in inflammatory processes mediated by transcription factor NF-kappaB, activator protein-1 transcription factor complex AP-1, cytokines, mitogen-activated protein kinases MAPKs or arachidonic acid pathways. CONCLUSION This study shows that intake of virgin olive oil based breakfast, which is rich in phenol compounds is able to repress in vivo expression of several pro-inflammatory genes, thereby switching activity of peripheral blood mononuclear cells to a less deleterious inflammatory profile. These results provide at least a partial molecular basis for reduced risk of cardiovascular disease observed in Mediterranean countries, where virgin olive oil represents a main source of dietary fat. Admittedly, other lifestyle factors are also likely to contribute to lowered risk of cardiovascular disease in this region.
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Changes in C-reactive protein from low-fat diet and/or physical activity in men and women with and without metabolic syndrome.
Camhi, SM, Stefanick, ML, Ridker, PM, Young, DR
Metabolism: clinical and experimental. 2010;(1):54-61
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Change in high-sensitivity C-reactive protein (CRP) from low-fat diet (diet) and physical activity (PA) interventions is relatively unknown for adults with metabolic syndrome. The objective of the study was to assess CRP change (DeltaCRP) with diet and/or PA in men and women with and without metabolic syndrome. Men (n = 149) and postmenopausal women (n = 125) with elevated low-density lipoprotein cholesterol and low high-density lipoprotein cholesterol were recruited into a 1-year randomized controlled trial. Treatment groups were as follows: control, diet (reduced total fat, saturated fat, and cholesterol intake), PA (45-60 minutes at 60%-85% maximum heart rate), or diet + PA. Weight loss was not an intervention focus. Metabolic syndrome was defined using the American Heart Association/National Heart, Lung, and Blood Institute criteria. Stored plasma samples were analyzed for CRP. Change in CRP was compared between treatments, within sex and metabolic syndrome status, using analysis of covariance, including covariates for baseline CRP and body fat change. For women with metabolic syndrome (n = 39), DeltaCRP was greater in diet vs control (-1.2 +/- 0.4, P = .009), diet + PA vs control (-1.3 +/- 0.4, P = .006), and diet + PA vs PA (-1.1 +/- 0.4, P = .02). Women with metabolic syndrome receiving the diet component (diet or diet + PA) had greater DeltaCRP compared with those who did not (control or PA) (P = .001). Change in CRP was not significantly different between intervention groups in men overall, women overall, men with (n = 47) or without metabolic syndrome (n = 102), or women without metabolic syndrome (n = 86). Low-fat diet may be the most effective treatment for reducing CRP in women with metabolic syndrome.