Two factors intrinsic to health are diet and sleep. These two behaviors may well influence one another. Indeed, that insufficient sleep adversely impacts dietary intakes is well documented. On the ...other hand, diet may influence sleep via melatonin and its biosynthesis from tryptophan. Experimental data exist indicating that provision of specific foods rich in tryptophan or melatonin can improve sleep quality. Whole diets rich in fruits, vegetables, legumes, and other sources of dietary tryptophan and melatonin have been shown to predict favorable sleep outcomes. Although clinical trials are needed to confirm a causal impact of dietary patterns on sleep and elucidate underlying mechanisms, available data illustrate a cyclical relation between these lifestyle factors. We recommend adopting a healthful diet to improve sleep, which may further promote sustained favorable dietary practices.
Dietary fat quality and fat replacement are more important for cardiovascular disease (CVD) prevention than is total dietary fat intake.
The aim was to evaluate the association between total fat ...intake and fat subtypes with the risk of CVD (myocardial infarction, stroke, or death from cardiovascular causes) and cardiovascular and all-cause death. We also examined the hypothetical effect of the isocaloric substitution of one macronutrient for another.
We prospectively studied 7038 participants at high CVD risk from the PREvención con DIeta MEDiterránea (PREDIMED) study. The trial was conducted from 2003 to 2010, but the present analysis was based on an expanded follow-up until 2012. At baseline and yearly thereafter, total and specific fat subtypes were repeatedly measured by using validated food-frequency questionnaires. Time-dependent Cox proportional hazards models were used.
After 6 y of follow-up, we documented 336 CVD cases and 414 total deaths. HRs (95% CIs) for CVD for those in the highest quintile of total fat, monounsaturated fatty acid (MUFA), and polyunsaturated fatty acid (PUFA) intake compared with those in the lowest quintile were 0.58 (0.39, 0.86), 0.50 (0.31, 0.81), and 0.68 (0.48, 0.96), respectively. In the comparison between extreme quintiles, higher saturated fatty acid (SFA) and trans-fat intakes were associated with 81% (HR: 1.81; 95% CI: 1.05, 3.13) and 67% (HR: 1.67; 95% CI: 1.09, 2.57) higher risk of CVD. Inverse associations with all-cause death were also observed for PUFA and MUFA intakes. Isocaloric replacements of SFAs with MUFAs and PUFAs or trans fat with MUFAs were associated with a lower risk of CVD. SFAs from pastries and processed foods were associated with a higher risk of CVD.
Intakes of MUFAs and PUFAs were associated with a lower risk of CVD and death, whereas SFA and trans-fat intakes were associated with a higher risk of CVD. The replacement of SFAs with MUFAs and PUFAs or of trans fat with MUFAs was inversely associated with CVD. This trial was registered at www.controlled-trials.com as ISRCTN 35739639.
Many early studies presented beneficial effects of polyunsaturated fatty acids (PUFA) on cardiovascular risk factors and disease. However, results from recent meta-analyses indicate that this effect ...would be very low or nil. One of the factors that may contribute to the inconsistency of the results is that, in most studies, genetic factors have not been taken into consideration. It is known that fatty acid desaturase (
gene cluster in chromosome 11 is a very important determinant of plasma PUFA, and that the prevalence of the single nucleotide polymorphisms (SNPs) varies greatly between populations and may constitute a bias in meta-analyses. Previous genome-wide association studies (GWAS) have been carried out in other populations and none of them have investigated sex and Mediterranean dietary pattern interactions at the genome-wide level. Our aims were to undertake a GWAS to discover the genes most associated with serum PUFA concentrations (omega-3, omega-6, and some fatty acids) in a scarcely studied Mediterranean population with metabolic syndrome, and to explore sex and adherence to Mediterranean diet (MedDiet) interactions at the genome-wide level. Serum PUFA were determined by NMR spectroscopy. We found strong robust associations between various SNPs in the
cluster and omega-3 concentrations (top-ranked in the adjusted model:
-rs174547,
= 3.34 × 10
;
-rs174550,
= 5.35 × 10
;
-rs1535,
= 5.85 × 10
;
-rs174546,
= 6.72 × 10
;
-rs174546,
= 9.75 × 10
;
- rs174576,
= 1.17 × 10
;
-rs174577,
= 1.12 × 10
, among others). We also detected a genome-wide significant association with other genes in chromosome 11:
(myelin regulatory factor)-rs174535,
= 1.49 × 10
;
(transmembrane protein 258)-rs102275,
= 2.43 × 10
;
(flap structure-specific endonuclease 1)-rs174538,
= 1.96 × 10
). Similar genome-wide statistically significant results were found for docosahexaenoic fatty acid (DHA). However, no such associations were detected for omega-6 PUFAs or linoleic acid (LA). For total PUFA, we observed a consistent gene*sex interaction with the
(deoxynucleotidyl transferase terminal interacting protein 2)-rs3747965
= 1.36 × 10
. For adherence to MedDiet, we obtained a relevant interaction with the
(malic enzyme 1) gene (a gene strongly regulated by fat) in determining serum omega-3. The top-ranked SNP for this interaction was
-rs3798890 (
= 2.15 × 10
). In the regional-wide association study, specifically focused on the
and
(fatty acid elongase) 2/
5 regions, we detected several statistically significant associations at
< 0.05. In conclusion, our results confirm a robust role of the
cluster on serum PUFA in this population, but the associations vary depending on the PUFA. Moreover, the detection of some sex and diet interactions underlines the need for these associations/interactions to be studied in all specific populations so as to better understand the complex metabolism of PUFA.
Insufficient sleep leads to overconsumption, but the factors contributing to this effect are poorly understood. Therefore, we assessed the influence of prolonged curtailment of sleep on free-living ...eating patterns linked with overconsumption and explored associations of these eating patterns with diet quality under different sleep conditions.
Sixty-five adults (47 females) participated in outpatient randomized crossover studies with two 6-week conditions: adequate sleep (7-9 h/night) and sleep restriction (-1.5 h/night relative to screening). Food records were collected over 3 nonconsecutive days, from which we ascertained data on eating frequency, midpoint, and window and intakes of energy and nutrients. Linear mixed models were used to assess the impact of sleep condition on change in eating pattern (sleep × week interaction) and the relation between eating patterns and dietary intakes (sleep × eating pattern interaction).
Sleep condition impacted the change in eating frequency across weeks, with eating frequency increasing in sleep restriction relative to adequate sleep (β = 0.3 ± 0.1;
= .046). Across conditions, eating more frequently tended to relate to higher energy intakes (β = 60.5 ± 34.6;
= .082). Sleep also influenced the relation of variability in eating midpoint with intakes of saturated fat (β = 6.0 ± 2.1;
= .005), polyunsaturated fat (β = -3.9 ± 2.0;
= .051), and added sugar (β = 17.3 ± 6.2;
= .006), with greater midpoint variability associated with more adverse changes in these diet quality components in sleep restriction vs adequate sleep.
Chronic short sleep increases eating frequency and adversely influences associations of variability in meal timing with components of diet quality. These findings help to explain how short sleep leads to overconsumption and obesity.
Registry: ClinicalTrials.gov; Name: Impact of Sleep Restriction in Women; URL: https://clinicaltrials.gov/ct2/show/NCT02835261; Identifier: NCT02835261 and Name: Impact of Sleep Restriction on Performance in Adults; URL: https://clinicaltrials.gov/ct2/show/NCT02960776; Identifier: NCT02960776.
Barragán R, Zuraikat FM, Tam V, RoyChoudhury A, St-Onge M-P. Changes in eating patterns in response to chronic insufficient sleep and their associations with diet quality: a randomized trial.
. 2023;19(11):1867-1875.
Aging is a risk factor for several pathologies, restricting one's health span, and promoting chronic diseases (e.g., cardiovascular and neurodegenerative diseases), as well as cancer. Telomeres are ...regions of repetitive DNA located at chromosomal ends. Telomere length has been inversely associated with chronological age and has been considered, for a long time, a good biomarker of aging. Several lifestyle factors have been linked with telomere shortening or maintenance. However, the consistency of results is hampered by some methodological issues, including study design, sample size, measurement approaches, and population characteristics, among others. Therefore, we aimed to systematically review the current literature on the effects of three relevant lifestyle factors on telomere length in human adults: physical activity, smoking, and sleep. We conducted a qualitative systematic review of observational and intervention studies using the Preferred Reporting Item for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. The systematic literature search covered articles published in MEDLINE and EMBASE databases (from 2010 to 2020). A total of 1400 studies were identified; 83 were included after quality control. Although fewer sedentary activities, optimal sleep habits, and non- or ex-smoker status have been associated with less telomere shortening, several methodological issues were detected, including the need for more targeted interventions and standardized protocols to better understand how physical activity and sleep can impact telomere length and aging. We discuss the main findings and current limitations to gain more insights into the influence of these lifestyle factors on the healthy aging process.
Background Insufficient sleep is associated with increased cardiovascular disease risk, but causality is unclear. We investigated the impact of prolonged mild sleep restriction (SR) on lipid and ...inflammatory profiles. Methods and Results Seventy-eight participants (56 women 12 postmenopausal; age, 34.3±12.5 years; body mass index, 25.8±3.5 kg/m
) with habitual sleep duration 7 to 9 h/night (adequate sleep AS) underwent two 6-week conditions in a randomized crossover design: AS versus SR (AS-1.5 h/night). Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol, triglycerides, and inflammatory markers (CRP C-reactive protein, interleukin 6, and tumor necrosis factor-α) were assessed. Linear models tested effects of SR on outcomes in the full sample and by sex+menopausal status (premenopausal versus postmenopausal women+men). In the full sample, SR increased high-density lipoprotein cholesterol compared with AS (β=1.2±0.5 mg/dL;
=0.03). Sex+menopausal status influenced the effects of SR on change in total cholesterol (
-interaction=0.04), LDL-C (
-interaction=0.03), and interleukin 6 (
-interaction=0.07). Total cholesterol and LDL-C decreased in SR versus AS in premenopausal women (total cholesterol: β=-4.2±1.9 mg/dL;
=0.03; LDL-C: β=-6.3±2.0 mg/dL;
=0.002). Given paradoxical effects of SR on cholesterol concentrations, we explored associations between changes in inflammation and end point lipids under each condition. Increases in interleukin 6 and tumor necrosis factor-α during SR tended to relate to lower LDL-C in premenopausal women (interleukin 6: β=-5.3±2.6 mg/dL;
=0.051; tumor necrosis factor-α: β=-32.8±14.2 mg/dL;
=0.027). Conclusions Among healthy adults, prolonged insufficient sleep does not increase atherogenic lipids. However, increased inflammation in SR tends to predict lower LDL-C in premenopausal women, resembling the "lipid paradox" in which low cholesterol associates with increased cardiovascular disease risk in proinflammatory conditions. Registration URL: https://www.clinicaltrials.gov; Unique identifiers: NCT02835261, NCT02960776.
Poor sleep is a determinant of obesity, with overconsumption of energy contributing to this relationship. Eating behavior characteristics are predictive of energy intake and weight change and may ...underlie observed associations of sleep with weight status and obesity risk factors. However, relationships between sleep and dimensions of eating behavior, as well as possible individual differences in these relations, are not well characterized. Therefore, the aim of this study was to evaluate whether sleep behaviors, including duration, timing, quality, and regularity relate to dietary restraint, disinhibition, and tendency towards hunger and to explore whether these associations differ by sex. This cross-sectional study included 179 adults aged 20-73 years (68.7% women, 64.8% with BMI ≥ 25 kg/m
). Sleep was evaluated by accelerometry over 2 weeks. Eating behavior dimensions were measured with the Three-Factor Eating Questionnaire. Prolonged wake after sleep onset (WASO) (0.029 ± 0.011,
= 0.007), greater sleep fragmentation index (0.074 ± 0.036,
= 0.041), and lower sleep efficiency (-0.133 ± 0.051,
= 0.010) were associated with higher dietary restraint. However, higher restraint attenuated associations of higher WASO and sleep fragmentation with higher BMI (
-interactions < 0.10). In terms of individual differences, sex influenced associations of sleep quality measures with tendency towards hunger (
-interactions < 0.10). Stratified analyses showed that, in men only, higher sleep fragmentation index, longer sleep onset latency, and lower sleep efficiency were associated with greater tendency towards hunger (β = 0.115 ± 0.037,
= 0.003, β = 0.169 ± 0.072,
= 0.023, β = -0.150 ± 0.055,
= 0.009, respectively). Results of this analysis suggest that the association of poor sleep on food intake could be exacerbated in those with eating behavior traits that predispose to overeating, and this sleep-eating behavior relation may be sex-dependent. Strategies to counter overconsumption in the context of poor quality sleep should be evaluated in light of eating behavior traits.
Overall quality of dietary carbohydrate intake rather than total carbohydrate intake may determine the risk of cardiovascular disease (CVD).
We examined 6- and 12-mo changes in carbohydrate quality ...index (CQI) and concurrent changes in several CVD risk factors in a multicenter, randomized, primary-prevention trial (PREDIMED-Plus) based on an intensive weight-loss lifestyle intervention program.
Prospective analysis of 5373 overweight/obese Spanish adults (aged 55–75 y) with metabolic syndrome (MetS). Dietary intake information obtained from a validated 143-item semiquantitative food-frequency questionnaire was used to calculate 6- and 12-mo changes in CQI (categorized in quintiles), based on 4 criteria (total dietary fiber intake, glycemic index, whole grain/total grain ratio, and solid carbohydrate/total carbohydrate ratio). The outcomes were changes in intermediate markers of CVD.
During the 12-mo follow-up, the majority of participants improved their CQI by increasing their consumption of fruits, vegetables, legumes, fish, and nuts and decreasing their consumption of refined cereals, added sugars, and sugar-sweetened beverages. After 6 mo, body weight, waist circumference (WC), systolic and diastolic blood pressure (BP), fasting blood glucose, glycated hemoglobin (HbA1c), triglyceride levels, triglycerides and glucose (TyG) index, and TyG-WC decreased across successive quintiles of improvement in the CQI. After 12 mo, improvements were additionally observed for HDL cholesterol and for the ratio of total to HDL cholesterol. Favorable improvements (expressed in common units of SD and 95% CI) for quintile 5 compared with quintile 1 of CQI change were observed for most risk factors, including TyG-WC (SD −0.20; 95% CI −0.26, −0.15), HbA1c (SD −0.16; 95% CI −0.23, −0.10), weight (SD −0.12; 95% CI −0.14, −0.09), systolic BP (SD −0.11; 95% CI −0.19, −0.02) and diastolic BP (SD −0.11; 95% CI −0.19, −0.04).
Improvements in CQI were strongly associated with concurrent favorable CVD risk factor changes maintained over time in overweight/obese adults with MetS. This trial was registered as ISRCTN 89898870.
Adiponectin is gaining renewed interest since, in addition to its possible protective role against insulin resistance and arteriosclerosis, recent studies suggest other additional favorable effects. ...However, the influence of gene-diet interactions on plasma adiponectin levels is still little understood. We analyzed the association between plasma adiponectin levels and various metabolic traits in a high-cardiovascular risk Mediterranean population, as well as the genetic effect of four candidate single-nucleotide polymorphisms (SNPs) in the adiponectin gene (
) and their interactions with the Mediterranean dietary pattern. Additionally, we explored, at the genome-wide level, the SNPs most associated with plasma adiponectin levels, as well as gene-diet interactions with the Mediterranean diet. In the 954 participants studied (aged 55-80 years), plasma adiponectin levels were strongly associated with plasma HDL-C concentrations (
= 6.6 × 10
) and inversely related to triglycerides (
= 4.7 × 10
), fasting glucose (
= 3.5 × 10
) and type 2 diabetes (
= 1.4 × 10
). Of the four pre-selected
candidate SNPs, the one most associated with plasma adiponectin was the -11391G > A (rs17300539) promoter SNP (
= 7.2 × 10
, in the multivariable adjusted model). No significant interactions with the Mediterranean diet pattern were observed for these SNPs. Additionally, in the exploratory genome-wide association study (GWAS), we found new SNPs associated with adiponectin concentrations at the suggestive genome-wide level (
< 1 × 10
) for the whole population, including the lead SNP rs9738548 (intergenic) and rs11647294 in the
(Vesicle Amine Transport 1 Like) gene. We also found other promising SNPs on exploring different strata such as men, women, diabetics and non-diabetics (
= 3.5 × 10
for rs2850066). Similarly, we explored gene-Mediterranean diet interactions at the GWAS level and identified several SNPs with gene-diet interactions at
< 1 × 10
. A remarkable gene-diet interaction was revealed for the rs2917570 SNP in the
(Opioid Binding Protein/Cell Adhesion Molecule Like) gene, previously reported to be associated with adiponectin levels in some populations. Our results suggest that, in this high-cardiovascular risk Mediterranean population, and even though adiponectin is favorably associated with metabolic traits and lower type 2 diabetes, the gene variants more associated with adiponectin may be population-specific, and some suggestive gene-Mediterranean diet interactions were detected.
The relation between taste perception, diet, and adiposity remains controversial. Additionally, there is a lack of knowledge on the polymorphisms influencing taste given the scarcity of genome-wide ...association studies (GWASs) published.
We studied the relation between perception of the basic tastes, i.e., sweet, salty, bitter, sour, and umami (separately and jointly in a “taste score”), and anthropometric measurements in older subjects with metabolic syndrome (MetS). GWASs were undertaken to identify genes associated with basic tastes and their score.
Taste perception was cross-sectionally determined by challenging subjects (381 older individuals with MetS) with solutions (5 concentrations) of the basic tastes with the use of standard prototypical tastants (phenylthiocarbamide and 6-n-propylthiouracil, NaCl, sucrose, monopotassium glutamate, and citric acid, for bitter, salt, sweet, umami, and sour, respectively). Taste perception intensities were expressed on a scale. A total taste score was derived.
The total taste score was inversely associated with body weight, body mass index, and waist circumference (P < 0.05). Subjects having a total taste score higher than or equal to the median (11 points for concentration V) were less likely to be classified as obese than subjects below the median (OR: 0.36; 95% CI: 0.22, 0.59; P < 0.001). Associations were similar, albeit less strong, for some taste qualities. In the GWASs, the highest associations were for bitter taste (rs1726866-TAS2R38, with P = 7.74 × 10−18 for phenylthiocarbamide and P = 3.96 × 10−19 for 6-n-propylthiouracil). For other tastes, several single-nucleotide polymorphisms (SNPs) exceeded the P threshold of 1 × 10−5. However, the top-ranked SNPs independently explained a low percentage of taste variability, hence their use as single proxies for the association between taste perception and adiposity is limited.
We found a strong inverse association between greater taste perception and body weight, body mass index, and waist circumference in older subjects with MetS and identified some taste-related SNPs. It would be advantageous to identify additional genetic proxies for taste and to develop polygenic scores. Data used in this study were derived from the clinical trial PREDIMED PLUS at baseline, registered at http://www.isrctn.com as ISRCTN89898870.
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