Late-Night Overeating or Low-Quality Food Choices Late at Night Are Associated with Subclinical Vascular Damage in Patients at Increased Cardiovascular Risk.

Late-night overeating (LNO) is associated with several cardiovascular disease (CVD) risk factors. Limited data exist regarding the association between late-night (LN) systematic food consumption, LNO, and LN poor food quality with subclinical vascular damage (SVD) which precedes the onset of CVD. This study aimed to investigate the above associations with SVD in a large sample of adults, free of established CVD, with one or more CVD risk factors. In total, 901 adults (45.2% males) underwent anthropometric, dietary (through two 24 h dietary recalls) and vascular assessment. LN systematic eating was defined as consumption of food after 19:00 h in both dietary recalls and LNO was defined as systematic consumption of >40% of daily total energy intake (dTEI) after 19:00 h. Systematic LN food consumption was inversely associated with diastolic blood pressure (DBP) (−1.44 95% C.I. (−2.76, −0.12)) after adjusting for age, sex, hypertension, diabetes, dyslipidemia, smoking, BMI and dTEI. LNO was positively associated with existence of carotid plaques (1.70 95% C.I. (1.07, 2.68)), while LN increased consumption of red meat, refined grains and wine and low consumption of whole wheat grains was positively associated with Aix (Augmentation Index) (0.84 95% C.I. (0.09, 1.59)), after adjusting for all the mentioned confounders. Systematic LN eating is associated with lower DBP while systematic LNO and consumption of poor-quality food late at night, is associated with SVD. Further research is needed to define more accurately the impact of LN eating habits on vascular health.

Dietary sodium estimation methods: accuracy and limitations of old and new methods in individuals at high cardiovascular risk.

OBJECTIVE: Accurate and easy to use methods for dietary Na intake estimation in population level are lacking. We aimed at (i) estimating the mean Na intake in the group level using a variety of dietary methods (DM) and urinary methods (UM) and correlating them with 24-h urine collection (24UCol) and (ii) improving the accuracy of the existing DM. DESIGN: The most common DM (three 24-h dietary recalls (24DR) and FFQ) and UM (24UCol and spot urine collection using common equations) were applied. To improve the existing: (i) 24DR, discretionary Na was quantified using salt-related questions or adding extra 15 % in total Na intake and (ii) FFQ, food items rich in Na and salt-related questions were added in the standard questionnaire (NaFFQ). SETTING: National and Kapodistrian University of Athens, Greece. PARTICIPANTS: Totally, 122 high cardiovascular risk subjects (56·0 ± 12·6 years; 55·7 % males). RESULTS: Mean 24 h Na excretion (24UNa) was 2810 ± 1304 mg/d. Spot urine methods overestimated the 24UNa (bias range: -1781 to -492 mg) and were moderately correlated to 24UCol (r = 0·469-0·596, P ≤ 0·01). DM underestimated the 24UNa (bias range: 877 to 1212 mg) and were weakly correlated with 24UCol. The improved DM underestimated the 24UNa (bias range: 877 to 923 mg). The NaFFQ presented the smallest bias (-290 ± 1336 mg) and the strongest correlation with 24UCol (r = 0·497, P ≤ 0·01), but wide limits of agreement in Bland-Altman plots (-2909 mg; 2329 mg), like all the other methods did. CONCLUSIONS: The existing methods exhibit poor accuracy. Further improvement of the newly developed NaFFQ could be promising for more accurate estimation of mean dietary Na intake in epidemiological studies. Additional validation studies are needed.

Dietary sugars and subclinical vascular damage in moderate-to-high cardiovascular risk adults.

BACKGROUND AND AIMS: The association between dietary sugars and vascular damage has been scarcely examined out of the context of established cardiovascular disease. We aimed to investigate the association between different types of sugars with subclinical atheromatosis and arteriosclerosis, in individuals free of cardiovascular disease being, however, at moderate-to-high cardiovascular risk. METHODS AND RESULTS: Two 24-h dietary recalls were conducted to estimate sugars intake. Subclinical atheromatosis was assessed by B-mode ultrasonography and arteriosclerosis (arterial stiffness) via tonometry (carotid-to-femoral pulse wave velocity). Multiple logistic regression analysis was performed to determine the relationship of quartiles of total sugars, monosaccharides and disaccharides with atheromatosis and arteriosclerosis, adjusting for potential confounders [Odds Ratio (95%Confidence Interval)]. In 901 participants (52.4 ± 13.8 years, 45.2% males), total sugars intake was not associated with any type of subclinical vascular damage. Subjects at 4th quartile of lactose intake (15.3 ± 5.5 g/day) had lower probability to present atheromatosis compared to those at 1st quartile (0.00 ± 0.01 g/day) even in the fully adjusted model [0.586 (0.353-0.974)]. Subjects at 3rd quartile of total disaccharides intake and particularly sucrose (15.1 ± 2.2 g/day) had higher probability to present arteriosclerosis compared to those at 1st quartile (3.0 ± 1.9 g/day) even after adjustment for all potential confounders [2.213 (1.110-4.409)]. CONCLUSIONS: Overall, the present data suggest a distinct role of each type of sugars on vascular damage. These observations highlight the need for further studies investigating not only foods rich in sugars, but sugars as separate components of food as they probably contribute via different ways on the development of arterial pathologies.

Habitual consumption of instant coffee is favorably associated with arterial stiffness but not with atheromatosis.

OBJECTIVE: Epidemiological data suggest that moderate habitual coffee consumption associates with lower cardiovascular disease (CVD) risk; however scarce data exist regarding the association of coffee with subclinical vascular disease (SVD). We aimed at investigating the above association with habitual instant coffee consumption - a widely consumed coffee in Greece-in high CVD risk but free of established CVD adults. RESEARCH METHODS & PROCEDURES: In a cross-sectional design study we measured: (i) two 24 h dietary recalls to assess coffee consumption, (ii) arterial stiffness, by carotid to femoral pulse wave velocity - (PWV) and carotid compliance, arterial remodeling by carotid intima-media thickness (IMT), pressure wave reflection by augmentation index (AIx) and atheromatosis by carotid plaques. RESULTS: In 1041 participants (55.6% females, 53.6 ± 14.0 years), 30% habitually consumed instant coffee (0.53 ± 1.15 cups/day). Consumption of instant coffee was inversely associated with systolic blood pressure (ß = -1.19, p = 0.007), AIx (ß = -0.71, p = 0.043), PWV (ß = -0.22, p = 0.000) and IMT (ß = -0.01, p = 0.025), but these associations lost their significance after multiple adjustments for confounders. Instant coffee consumption was positively associated with carotid compliance independent from all possible confounders (ß = 0.005, p = 0.003). CONCLUSION: Habitual moderate instant coffee consumption is inversely associated with arterial stiffening and potential with arterial remodeling. These favorable vascular associations offer a potential pathophysiological link between habitual coffee consumption and lower incidence of CVD. Future studies are needed to examine the long-term effects of habitual instant coffee consumption on vascular structure and function.

Associations of dietary patterns with blood pressure and markers of subclinical arterial damage in adults with risk factors for CVD.

OBJECTIVE: Unhealthy diet is a modifiable risk factor leading to subclinical arterial damage (SAD), high BP and CVD. It was aimed to investigate the possible associations of dietary patterns (DPs) with SAD in adults having multiple CVD risk factors. DESIGN: Dietary intake was evaluated through two 24-h dietary recalls and principal component analysis was used to identify DPs. Oscillometry, applanation tonometry with pulse wave analysis and carotid ultrasound were used to assess peripheral and aortic BP, arterial stiffness and pressure wave reflections. SETTING: Laiko University Hospital, Athens, Greece. PARTICIPANTS: A total of 470 individuals (53·1 ± 14·2 years) with CVD risk factors were enrolled. RESULTS: A pattern characterised by increased consumption of whole-grain cereals, white meat and reduced consumption of sugar was positively associated with common carotid compliance (ß = 0·01, 95 % CI 0·00, 0·01), whereas a pattern high in refined cereals, red and processed meat was positively associated with brachial but not aortic systolic pressure (ß = 1·76, 95 % CI 0·11, 3·42) and mean arterial pressure (MAP) (ß = 1·18, 95 % CI 0·02, -2·38). Low consumption of low-fat dairy products, high consumption of full-fat cheese and butter was positively associated with MAP (ß = 0·97, 95 % CI 0·01, 1·95). Increased consumption of vegetables, fruits, fresh juices, fish and seafood was inversely associated with augmentation index (AIx) (ß = -1·01, 95 % CI -1·93, -0·09). CONCLUSION: Consumption of whole grains, white meat, fruits/vegetables, fish/seafood and avoidance of sugar was associated with improved SAD. Preference in refined grains, red/processed meat, high-fat cheese/butter and low intake of low-fat dairy products were associated with BP elevation. Future studies are needed to confirm the present findings.

Does Sodium Intake Induce Systemic Inflammatory Response? A Systematic Review and Meta-Analysis of Randomized Studies in Humans

Experimental studies suggest that sodium induced inflammation might be another missing link leading to atherosclerosis. To test the hypothesis that high daily sodium intake induces systemic inflammatory response in humans, we performed a systematic review according to PRISMA guidelines of randomized controlled trials (RCTs) that examined the effect of high versus low sodium dose (HSD vs. LSD), as defined per study, on plasma circulating inflammatory biomarkers. Eight RCTs that examined CRP, TNF-a and IL-6 were found. Meta-analysis testing the change of each biomarker in HSD versus LSD was possible for CRP (n = 5 studies), TNF-a (n = 4 studies) and IL-6 (n = 4 studies). The pooled difference (95% confidence intervals) per biomarker was for: CRP values of 0.1(-0.3, 0.4) mg/L; TNF-a -0.7(-5.0, 3.6) pg/mL; IL-6 -1.1(-3.3 to 1.1) pg/mL. Importantly, there was inconsistency between RCTs regarding major population characteristics and the applied methodology, including a very wide range of LSD (460 to 6740 mg/day) and HSD (2800 to 7452 mg/day). Although our results suggest that the different levels of daily sodium intake are not associated with significant changes in the level of systemic inflammation in humans, this outcome may result from methodological issues. Based on these identified methodological issues we propose that future RCTs should focus on young healthy participants to avoid confounding effects of comorbidities, should have three instead of two arms (very low, "normal" and high) of daily sodium intake with more than 100 participants per arm, whereas an intervention duration of 14 days is adequate.

Dietary sodium and cardiovascular morbidity/mortality: a brief commentary on the 'J-shape hypothesis'.

The last decade, a growing number of evidence support J-shape or inverse - instead of positive linear -- associations between dietary sodium intake and cardiovascular morbidity/mortality. A careful evaluation of these studies leads to the following observations: less accurate methods for dietary sodium assessment are usually used; most studies included high-risk participants, enhancing the possibility of a 'reverse causality' phenomenon. However, these limitations do not explain all the findings. Few carefully designed randomized clinical trials comparing different levels of sodium intake that address the issue of the optimal and safe range exist; therefore, current guidelines recommend a higher cut-off instead of a safe range of intake. Given the demonstrated harmful effects of very low sodium diets leading to subclinical vascular damage in animal studies, the 'J-shape hypothesis' cannot yet be either neglected or verified. There is a great need of well-designed general population-based prospective randomized clinical trials to address the issue.

Levels of dietary sodium intake: diverging associations with arterial stiffness and atheromatosis.

BACKGROUND: Recent epidemiological evidence suggests a J-shaped, rather than the classical linear, association between dietary sodium (Na) intake and cardiovascular (CV) disease. Numerous animal studies have shown the acceleration of atheromatosis in a low-salt diet but data in humans are scarce. Our aim was to test the hypothesis that in a cohort of patients who are CV-free, yet at increased CV risk, moderate Na intake is associated with lower prevalence of atheromatosis and arterial stiffening than those at very low Na intake. METHODS: Two 24-h dietary recalls were conducted to estimate Na intake. Atheromatosis (carotid and femoral plaques) was assessed by B-mode ultrasonography and arterial stiffness through tonometry (carotid-to-femoral pulse wave velocity, cf-PWV). RESULTS: In 901 individuals (age: 52.4 ± 13.8 years, 45.2% males), only females at 3rd and 4th quartile of total Na intake (derived from food and discretionary salt) had significantly lower probability to present femoral plaques than those at 1st quartile (751.0 ± 215.5 mg/day), even in the full-adjusted model [0.462(0.229-0.935) and p = 0.032 3rd quartile; 0.274(0.118-0.638) and p = 0.003 4th quartile]. On the contrary, male and female individuals at 3rd quartile had significantly higher probability to present arterial stiffness (PWV >10 m/s) than those at 1st quartile [1.991(1.047-3.785) and p = 0.036]. CONCLUSIONS: Overall, the present data suggest that very low Na intake is associated with: a) accelerated atheromatosis, verifying findings from animal models, and providing a possible explanation of the modern epidemiology and b) lower arterial stiffness, which is in line with previous human findings, therefore suggesting a diverging effect of Na in the two major arterial pathologies.

Moderately increased alcohol consumption is associated with higher pressure wave reflections and blood pressure in men.

BACKGROUND AND AIMS: Increased alcohol consumption has been associated with CVD risk. Subclinical arterial damage (SAD) precedes the onset of cardiovascular disease (CVD), and allows early identification and study of the pathophysiology of CVD. Reliable, noninvasive vascular biomarkers are available for the early detection of SAD and reclassification of CVD risk. To investigate the association of alcohol consumption with multiple SAD biomarkers and central hemodynamics in a large sample of Greek adults with CVD risk factors. METHODS AND RESULTS: This cross-sectional study was conducted with 938 participants (43.5% men) and collected data on SAD biomarkers, central hemodynamics, and dietary intake. Multiple linear regression analysis was performed according to sex after adjusting for several confounders. In men, alcohol consumption of 20-30 g/d was positively associated with mean, diastolic, and peripheral systolic blood pressure (BP). The consumption of >30 g/d was positively associated with the augmentation index. In women, no statistically significant associations were found between alcohol consumption and BP or SAD indices. No statistically significant associations were found between alcohol consumption and arterial compliance or distensibility in both sexes. CONCLUSION: In men even a small deviation from the current recommendation for alcohol consumption is associated with both higher BP indices and pressure wave reflections. The absence of association in women might be due to very low alcohol intake, even in the high consumption group. More studies are needed to verify our findings and establish the above associations in each sex.

Current Data on Dietary Sodium, Arterial Structure and Function in Humans: A Systematic Review.

BACKGROUND: Subclinical arterial damage (SAD) (arteriosclerosis, arterial remodeling and atheromatosis) pre-exists decades before cardiovascular disease (CVD) onset. Worldwide, sodium (Na) intake is almost double international recommendations and has been linked with CVD and death, although in a J-shape manner. Studies regarding dietary Na and major types of SAD may provide pathophysiological insight into the association between Na and CVD. OBJECTIVES: Systematic review of data derived from observational and interventional studies in humans, investigating the association between dietary Na with (i) atheromatosis (arterial plaques); (ii) arteriosclerosis (various biomarkers of arterial stiffness); (iii) arterial remodeling (intima-media thickening and arterial lumen diameters). DATA SOURCES: Applying the PRISMA criteria, the PubMed and Scopus databases were used. RESULTS: 36 studies were included: 27 examining arteriosclerosis, four arteriosclerosis and arterial remodeling, three arterial remodeling, and two arterial remodeling and atheromatosis. CONCLUSIONS: (i) Although several studies exist, the evidence does not clearly support a clinically meaningful and direct (independent from blood pressure) effect of Na on arterial wall stiffening; (ii) data regarding the association of dietary Na with arterial remodeling are limited, mostly suggesting a positive trend between dietary Na and arterial hypertrophy but still inconclusive; (iii) as regards to atheromatosis, data are scarce and the available studies present high heterogeneity. Further state-of-the-art interventional studies must address the remaining controversies.