A systematic review of variations in circadian rhythm genes and type 2 diabetes.

BACKGROUND: Type 2 diabetes is a chronic disease that has severe individual and societal consequences, which is forecast to worsen in the future. A new field of investigation is variations in circadian rhythm genes, in conjunction with diet and sleep variables, associations with, and effects on, type 2 diabetes development. OBJECTIVE: This systematic review aimed to analyse all current literature regarding circadian rhythm gene variations and type 2 diabetes, and explore their interplay with diet and sleep variables on type 2 diabetes outcomes. This review was registered with PROSPERO (CRD42021259682). METHODOLOGY: Embase and Pubmed were searched on 6/8/2021/11/8/2021 for studies of all designs, including participants from both sexes, all ethnicities, ages, and geographic locations. Participants with risk alleles/genotypes were compared with the wildtype regarding type 2 diabetes outcomes. Studies risk of bias were scored according to the risk of bias in non-randomised studies - interventions/exposures criteria. RESULTS: In total, 31 studies were found (association n = 29/intervention n = 2) including >600,000 participants from various ethnicities, sexes, and ages. Variations in the melatonin receptor 1B, brain and muscle arnt-like 1 and period circadian regulator (PER) genes were consistently associated with type 2 diabetes outcomes. CONCLUSIONS: Individuals with variations in melatonin receptor 1B, brain and muscle arnt-like 1 and PER may be at higher risk of type 2 diabetes. Further research is needed regarding other circadian rhythm genes. More longitudinal studies and randomised trials are required before clinical recommendations can be made.

Genetics of caffeine and brain-related outcomes - a systematic review of observational studies and randomized trials.

CONTEXT: Although the stimulant and anxiogenic properties of caffeine are widely accepted, research on its specific effects on the brain remains controversial. Growing evidence shows that interindividual differences in caffeine response may be partly due to variations in genes such as CYP1A2 and ADORA2A, which have been used to identify individuals as "fast" or "slow" caffeine metabolizers and as having a "high" or "low" caffeine sensitivity, respectively. OBJECTIVE: The objective of this review was to identify, evaluate, and discuss current evidence on the associations between common genetic variants, caffeine consumption, and brain-related outcomes in humans. DATA SOURCES: PubMed and Embase databases were searched for relevant reports based on a predetermined search strategy. DATA EXTRACTION: Reports of observational and experimental studies on healthy adults who underwent (a) genetic analysis for polymorphisms in genes associated with caffeine metabolism and effects and (b) measurements of brain-related effects such as anxiety, insomnia, and cognitive performance associated with the consumption of caffeine (habitual intake or supplementation) were included. DATA ANALYSIS: Of the 22 records included, 15 were randomized controlled trials, 6 were cross-sectional studies, and 1 was a genome-wide association study. The main outcomes identified were cognitive performance (n = 9), anxiety (n = 7), and sleep disturbance/insomnia (n = 6). Polymorphisms in the CYP1A2 gene were associated with cognitive function, while variations in the ADORA2A gene were associated with anxiety and sleep disturbance. CONCLUSION: The present review has provided evidence that variability in the CYP1A2 and the ADORA2A genes may modulate the association between caffeine and brain-related outcomes. Future studies are warranted to investigate the specific polymorphisms implicated in each brain outcome, which cognitive functions are particularly related to caffeine (simple vs complex), whether there are gender differences in anxiety effects, and how habitual caffeine intake may influence the acute effects of caffeine. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration no. CRD42021257556.

The efficacy of genotype-based dietary or physical activity advice in changing behavior to reduce the risk of cardiovascular disease, type II diabetes mellitus or obesity: a systematic review and meta-analysis.

CONTEXT: Despite clear evidence that adherence to dietary and physical activity advice can reduce the risk of cardiometabolic disease, a significant proportion of the population do not follow recommendations. Personalized advice based on genetic variation has been proposed for motivating behavior change, although research on its benefits to date has been contradictory. OBJECTIVE: To evaluate the efficacy of genotype-based dietary or physical activity advice in changing behavior in the general population and in individuals who are at risk of cardiovascular disease (CVD) or type II diabetes mellitus (T2DM). DATA SOURCES: MEDLINE, EMBASE, PsycInfo, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched up to January 7, 2022. Randomized controlled trials of a genotype-based dietary and/or physical activity advice intervention that aimed to change dietary and/or physical activity behavior were included. DATA EXTRACTION: Abstracts of 7899 records were screened, and 14 reports from 11 studies met the inclusion criteria. DATA ANALYSIS: Genotype-based dietary or physical activity advice was found to have no effect on dietary behavior in any of the studies (standardized mean difference [SMD] .00 [-.11 to .11], P = .98), even when analyzed by subgroup: "at risk" (SMD .00 [-.16 to .16, P = .99]; general population (SMD .01 [-.14 to .16], P = .87). The physical activity behavior findings were similar for all studies (SMD -.01 [-.10 to .08], P = .88), even when analyzed by subgroup: "at risk" (SMD .07 [-.18 to .31], P = .59); general population (SMD -.02 [-.13 to .10], P = .77). The quality of the evidence for the dietary behavior outcome was low; for the physical activity behavior outcome it was moderate. CONCLUSIONS: Genotype-based advice does not affect dietary or physical activity behavior more than general advice or advice based on lifestyle or phenotypic measures. This was consistent in studies that recruited participants from the general population as well as in studies that had recruited participants from populations at risk of CVD or T2DM. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration no. CRD42021231147.

Salt Taste and Salt Sensitive Hypertension in HIV.

PURPOSE OF REVIEW: To provide a summary of current literature and propose potential mechanistic models to help us understand the role of HIV infection/antiretroviral therapy (ART), salt taste sensitivity (STS), and salt sensitivity of blood pressure (SSBP) in hypertension development. RECENT FINDINGS: The epithelial sodium channel (ENaC) is the main protein/sodium channel for recognizing Na + in the tongue and mediates preference to low-medium salt concentrations in animals and humans. Considering the pressor response to oral salt in individuals with SSBP, poor STS may worsen blood pressure. Specific genetic variants in ENaC are linked to salt taste perception and hypertension. HIV infection, some ART, and specific antihypertensive drugs are associated with reduced STS and an increased liking for salty foods. Persons with HIV (PWH) on ART may have a decreased STS and are at a higher risk of developing salt-sensitive hypertension. Inflammation mediated by dietary salt is one of the drivers of poor STS and salt-sensitive hypertension among PWH.

The impact of genetic variability on the relationship between caffeine and cardiometabolic outcomes: A systematic review.

The relationship between caffeine consumption and cardiometabolic health has been reported, however with heterogenous results. Discrepancies in study results may be due to inter-individual variability between study participants. This systematic review aimed to identify the impact of genetics on the relationship between caffeine consumption and cardiometabolic outcomes. Electronic databases (PubMed and EMBASE) were searched for studies published until July 2021. Selected studies were of both intervention and observational design and included (1) analysis of at least one of the selected cardiometabolic outcome (type 2 diabetes, glucose/insulin levels, cardiovascular disease [CVD], blood pressure [BP] or hypertension, and blood lipid and catecholamine levels), (2) adults aged 18-65 years, and (3) genetic analysis of individuals consuming caffeine. Seventeen studies were included: four randomised controlled trials and an interventional and quasi-experimental study, six population-based prospective cohort studies, three cross-sectional studies, and three case-control studies. CYP1A2 rs762551 and ADORA rs5751876 were associated with glucose response when caffeine was consumed with carbohydrates. CYP1A2 rs762551 moderated the association between coffee intake and hypertension. Moreover, ADORA2A rs5751876 and the ADRA2B I variants moderated the associations between caffeine and BP. Studies that investigated the effects of genetic variations on CVD and caffeine consumption reported equivocal findings (CYP1A2) or warrant replication (COMT, ADORA and TRIB1). Elucidating the extent to which these genes moderate the association between caffeine and cardiometabolic outcomes will enable caffeine consumption advice to be tailored to specific individuals to optimise health.

Immediate pressor response to oral salt and its assessment in the clinic: a time series clinical trial.

BACKGROUND: High blood pressure (BP) is associated with high-salt consumption especially in sub-Saharan Africa. Although the pressor effect of salt is viewed as a chronic effect, some studies suggest that a salty meal may increase BP immediately in some individuals, and that this effect may cause endothelial dysfunction. Therefore, the aim of our research was to study the immediate pressor response to oral salt (IPROS) and its determinants, with the expectation that a simple methodology may be devised to diagnose it in the clinic or in low-resource environments. METHODS: We conducted a time series trial at Livingstone Central Hospital. We present data in 127 normotensive participants who ingested 2 g of sodium chloride; their BP was monitored for 120 minutes in intervals of 10 minutes. Sociodemographic and clinical data were collected. Descriptive and inferential statistics were used for analyses of data. RESULTS: Median age was 30 years (interquartile range, 22-46 years) and 52% were female patients. An increase of ≥10 mmHg in mean arterial pressure (MAP), considered a clinically significant IPROS, was present in 62% of participants. Systolic BP 30 minutes after the salt load was a significant predictor of IPROS, avoiding the need to calculate MAP in the clinic setting. CONCLUSIONS: We confirm the presence of an IPROS in a high proportion (62%) of otherwise normotensive participants. The average time course for this response was 30 minutes and its duration was sustained for the 120-minutes period of study in most of the participants. Prediction of IPROS by ∆SBP (change in systolic blood pressure) at 30 minutes allows for easy assessment of possible responder status in the clinic. Our data indicate that the IPROS to oral salt-loads in the range currently consumed by the Western world and African populations in single meals may increase the 24-hour BP load, which is a risk factor for hypertension and target organ damage. The relevance of our findings indicates the need to include dietary sodium assessment in the diagnosis, prevention, and management of high BP.

Erythrocyte sodium buffering capacity status correlates with self-reported salt intake in a population from Livingstone, Zambia.

BACKGROUND: Salt impairs endothelial function and increases arterial stiffness independent of blood pressure. The mechanisms are unknown. Recent evidence suggests that there is a possible link between salt consumption and sodium buffering capacity and cardiovascular disease but there is limited evidence in the populations living in Sub-Saharan Africa. The aim of our study was to explore the relationship between erythrocyte sodium buffering capacity and sociodemographic, clinical factors, and self-reported salt consumption at Livingstone Central Hospital. METHODS: We conducted a cross sectional study at Livingstone Central hospital among 242 volunteers accessing routine medical checkups. Sociodemographic and dietary characteristics were obtained along with clinical measurements to evaluate their health status. Sodium buffering capacity was estimated by erythrocyte sodium sensitivity (ESS) test. We used descriptive and inferential statistics to describe and examine associations between erythrocyte sodium sensitivity and independent variables. RESULTS: The median age (interquartile range) of the study sample was 27 (22, 42) years. 54% (n = 202) and 46% (n = 169) were males and females, respectively. The majority (n = 150, 62%) had an ESS of >120%. High salt intake correlated positively with ESS or negatively with vascular sodium buffering capacity. CONCLUSIONS: Self-reported high salt intake was associated with poor vascular sodium buffering capacity or high ESS in the majority of middle-aged Zambians living in Livingstone. The poor vascular sodium buffering capacity implies a damaged vascular glycocalyx which may potentially lead to a leakage of sodium into the interstitium. This alone is a risk factor for the future development of hypertension and cardiovascular disease. However, future studies need to validate vascular function status when using ESS testing by including established vascular function assessments to determine its pathophysiological and clinical implications.

Nutrition knowledge, food choices and diet quality of genotyped and non-genotyped individuals during the COVID-19 pandemic.

Background: Severe obesity (body mass index ≥ 40 kg/m2) and non-communicable diseases, both influenced by diet, have been associated with COVID-19. Genotype-based personalised nutrition advice may improve nutrition knowledge and enhance behaviour change towards better diet quality compared with conventional recommendations. Aim: To investigate the nutrition knowledge, food choices and diet quality in genotyped and non-genotyped individuals during the COVID-19 pandemic. Methods: One hundred and twenty-three healthy UK adults were recruited using convenience sampling through social networks. The online questionnaire consisted of the General Nutrition Knowledge Questionnaire, the Food Choices Questionnaire, and the EPIC-Norfolk Food Frequency Questionnaire (FFQ). FFQ was used to calculate participant diet quality with the Diet Quality Index-International and socio-demographic and anthropometric data. Results: Median general nutrition knowledge, diet variety and diet balance scores were higher in genotyped compared with non-genotyped individuals (71.0 ± 11.0 vs. 61.0 ± 15.0, p = <.001, 18.00 ± 5.00 vs. 15.00 ± 5.00, p = .007 and 2.00 ± 4.00 vs. 0.00 ± 2.00, p = .025, respectively). Pooled sample multiple regression showed that health motive positively influenced while familiarity motive negatively influenced diet quality index scores (ß = .428, t = 4.822, p = <.001 and ß = -.356, t = -4.021, p = .001, respectively). Conclusions: Nutrition knowledge and diet quality indices of balance and variety were higher among genotyped compared with non-genotyped individuals; overall diet quality was similar between groups. This may be due to pandemic-specific factors, such as altered motives of food choice and availability.

Does personalised nutrition advice based on apolipoprotein E and methylenetetrahydrofolate reductase genotype affect dietary behaviour?

Background: Dietary intake is linked to numerous modifiable risk factors of cardiovascular disease. Current dietary recommendations in the UK to reduce the risk of cardiovascular disease are not being met. A genotype-based personalised approach to dietary recommendations may motivate individuals to make positive changes in their dietary behaviour. Aim: To determine the effect of a personalised nutrition intervention, based on apolipoprotein E (ApoE, rs7412; rs429358) and methylenetetrahydrofolate reductase (MTHFR, rs1801133) genotype, on reported dietary intake of saturated fat and folate in participants informed of a risk genotype compared to those informed of non-risk genotype. Methods: Baseline data (n = 99) were collected to determine genotype (non-risk vs risk), dietary intake and cardiovascular risk (Q-Risk®2 cardiovascular risk calculator). Participants were provided with personalised nutrition advice via email based on their ApoE and MTHFR genotype and reported intake of folate and saturated fat. After 10 days, dietary intake data were reported for a second time. Results: Personalised nutrition advice led to favourable dietary changes, irrespective of genotype, in participants who were not meeting dietary recommendations at baseline for saturated fat (p < 0.001) and folate (p = 0.002). Only participants who were informed of a risk ApoE genotype met saturated fat recommendations following personalised nutrition advice. Conclusion: Incorporation of genotype-based personalised nutrition advice in a diet behaviour intervention may elicit favourable changes in dietary behaviour in participants informed of a risk genotype. Participants informed of a non-risk genotype also respond to personalised nutrition advice favourably but to a lesser extent.

Dietary Intake and TCF7L2 rs7903146 T Allele Are Associated with Elevated Blood Glucose Levels in Healthy Individuals.

INTRODUCTION: Type 2 diabetes (T2D) is a leading cause of global mortality with diet and genetics being considered amongst the most significant risk factors. Recently, studies have identified a single polymorphism of the TCF7L2 gene (rs7903146) as the most important genetic contributor. However, no studies have explored this factor in a healthy population and using glycated haemoglobin (HbA1c), which is a reliable long-term indicator of glucose management. This study investigates the association of the genetic polymorphism rs7903146 and dietary intake with T2D risk in a population free of metabolic disease. METHODS: T2D risk was assessed using HbA1c plasma concentrations and dietary intake via a validated Food Frequency Questionnaire in 70 healthy participants. RESULTS: T allele carriers had higher HbA1c levels than the CC group (32.4 ± 7.2 mmol/mol vs. 30.3 ± 7.6 mmol/mol, p = 0.005). Multiple regression reported associations between diet, genotype and HbA1c levels accounting for 37.1% of the variance in HbA1c (adj. R2 = 0.371, p < 0.001). The following macronutrients, expressed as a median percentage of total energy intake (TEI) in the risk group, were positively associated with HbA1c concentration: carbohydrate (≥39% TEI, p < 0.005; 95% CI 0.030/0.130) protein (≥21% TEI, p < 0.005, 95% CI 0.034/0.141), monounsaturated (≥15% TEI p < 0.05, 95% CI 0.006/0.163) and saturated fatty acids (≥13% TEI; p < 0.05, 95% CI 0.036/0.188). CONCLUSION: Carriers of the T allele showed significantly higher levels of HbA1c compared to non-carriers. Dietary intake affected T2D risk to a greater extent than genetic effects of TCF7L2rs7903146 genotype in a healthy population. The study focus on healthy individuals is beneficial due to the applicability of findings for T2D screening.

The Associations Between Bitter and Fat Taste Sensitivity, and Dietary Fat Intake: Are They Impacted by Genetic Predisposition?

A relationship between bitter and fat taste sensitivity, CD36 rs1761667 and TAS2R38 has been demonstrated. However, research is scarce and does not take diet into account. This study aimed to explore associations between genetics, fat and bitter taste sensitivity and dietary fat intake in healthy UK adults. A cross-sectional study was carried out on 88 Caucasian participants (49 females and 39 males aged 35 ± 1 years; body mass index 24.9 ± 0.5 kg/m2). Bitter taste sensitivity was assessed using phenylthiocarbamide (PTC) impregnated strips and the general Labeled Magnitude Scale. Fat taste sensitivity was assessed by the Ascending Forced Choice Triangle Procedure and dietary intake with a semi-quantitative food frequency questionnaire. Genotyping for rs713598, rs1726866, rs10246939, and rs1761667 was performed. Participants with TAS2R38 PAV/PAV diplotype perceived PTC strips as more bitter than groups carrying AVI haplotypes (AVI/AVI, P = 1 × 10-6; AVI/AAV, P = 0.029). CD36 rs1761667 was associated with fat taste sensitivity (P = 0.008). A negative correlation between bitter taste sensitivity and saturated fat intake was observed (rs = -0.256, P = 0.016). When combining the CD36 genotypes and TAS2R38 diplotypes into one variable, participants carrying both TAS2R38 AVI haplotype and CD36 A allele had a higher intake of saturated fat compared to carriers of CD36 GG genotype or TAS2R38 PAV/PAV and PAV/AAV diplotypes (13.8 ± 0.3 vs. 12.6 ± 0.5%TEI, P = 0.047) warranting further exploration in a larger cohort.

HIV-positive demonstrate more salt sensitivity and nocturnal non-dipping blood pressure than HIV-negative individuals.

BACKGROUND: High dietary salt and a lack of reduced blood pressure (BP) at night (non-dipping) are risk factors for the development of hypertension which may result in end-organ damage and death. The effect of high dietary salt on BP in black people of sub-Saharan Africa living with HIV is not well established. The goal of this study was to explore the associations between salt sensitivity and nocturnal blood pressure dipping according to HIV and hypertension status in a cohort of adult Zambian population. METHODS: We conducted an interventional study among 43 HIV-positive and 42 HIV-negative adults matched for age and sex. Study participants were instructed to consume a low (4 g) dietary salt intake for a week followed by high (9 g) dietary salt intake for a week. Salt resistance and salt sensitivity were defined by a mean arterial pressure difference of ≤5 mmHg and ≥ 8 mmHg, respectively, between the last day of low and high dietary salt intervention. Nocturnal dipping was defined as a 10-15% decrease in night-time blood pressure measured with an ambulatory blood pressure monitor. RESULTS: The median age was 40 years for both the HIV-positive and the HIV-negative group with 1:1 male to female ratio. HIV positive individuals with hypertension exhibited a higher BP sensitivity to salt (95%) and non-dipping BP (86%) prevalence compared with the HIV negative hypertensive (71 and 67%), HIV positive (10 and 24%) and HIV-negative normotensive (29 and 52%) groups, respectively (p < 0.05). Salt sensitivity was associated with non-dipping BP and hypertension in both the HIV-positive and HIV-negative groups even after adjustment in multivariate logistic regression (< 0.001). CONCLUSIONS: The results of the present study suggest that high dietary salt intake raises blood pressure and worsens nocturnal BP dipping to a greater extent in hypertensive than normotensive individuals and that hypertensive individuals have higher dietary salt intake than their normotensive counterparts. Regarding HIV status, BP of HIV-positive hypertensive patients may be more sensitive to salt intake and demonstrate more non-dipping pattern compared to HIV-negative hypertensive group. However, further studies with a larger sample size are required to validate this.

Genetic predisposition to salt-sensitive normotension and its effects on salt taste perception and intake.

Salt sensitivity is an independent CVD and mortality risk factor, which is present in both hypertensive and normotensive populations. It is genetically determined and it may affect the relationship between salt taste perception and salt intake. The aim of this study was to explore the genetic predisposition to salt sensitivity in a young and a middle-aged adult population and its effects on salt taste perception and salt intake. The effects of Na loading on blood pressure (BP) were investigated in twenty normotensive subjects and salt sensitivity defined as the change in BP after 7 d of low-Na (51·3 mmol Na/d) and 7 d of high-Na diet (307·8 mmol Na/d). Salt taste perception was identified using the British Standards Institution sensory analysis method (BS ISO 3972:2011). Salt intake was assessed with a validated FFQ. DNA was genotyped for SNP in the SLC4A5, SCNN1B and TRPV1 genes. The subjects with AA genotype of the SLC4A5 rs7571842 exhibited the highest increase in BP (∆ systolic BP=7·75 mmHg, P=0·002, d=2·4; ∆ diastolic BP=6·25 mmHg, P=0·044, d=1·3; ∆ mean arterial pressure=6·5 mmHg, P=0·014, d=1·7). The SLC4A5 rs10177833 was associated with salt intake (P=0·037), and there was an association between salt taste perception and salt sensitivity (r s 0·551, P=0·041). In conclusion, there is a genetic predisposition to salt sensitivity and it is associated with salt taste perception. The association between salt taste perception and discretionary salt use suggests that preference for salty taste may be a driver of salt intake in a healthy population and warrants further investigation.

Salt-sensitive hypertension: mechanisms and effects of dietary and other lifestyle factors.

Salt sensitivity, which is an increase in blood pressure in response to high dietary salt intake, is an independent risk factor for cardiovascular disease and mortality. It is associated with physiological, environmental, demographic, and genetic factors. This review focuses on the physiological mechanisms of salt sensitivity in populations at particular risk, along with the associated dietary factors. The interplay of mechanisms such as the renin-angiotensin aldosterone system, endothelial dysfunction, ion transport, and estrogen decrease in women contributes to development of salt sensitivity. Because of their effects on these mechanisms, higher dietary intakes of potassium, calcium, vitamin D, antioxidant vitamins, and proteins rich in L-arginine, as well as adherence to dietary patterns similar to the DASH (Dietary Approaches to Stop Hypertension) diet, can be beneficial to salt-sensitive populations. In contrast, diets similar to the typical Western diet, which is rich in saturated fats, sucrose, and fructose, together with excessive alcohol consumption, may exacerbate salt-sensitive changes in blood pressure. Identifying potential mechanisms of salt sensitivity in susceptible populations and linking them to protective or harmful dietary and lifestyle factors can lead to more specific guidelines for the prevention of hypertension and cardiovascular disease.

[Socioeconomic status and risky health behaviors in Croatian adult population]. / Socioekonomski status i rizicna zdravstvena ponasanja odrasle hrvatske populacije.

INTRODUCTION AND AIM: Based on the previous research, there is strong association between low socioeconomic status (SES) and high morbidity and mortality rates. Even though association between SES and risky health behaviors as the main factors influencing health has been investigated in Croatian population, some questions are yet to be answered. The aim of this study was to investigate the presence of unhealthy diet, physical inactivity, smoking and excessive drinking in low, middle, and high socioeconomic group of adult Croatian population included in the cohort study on regionalism of cardiovascular health risk behaviors. We also investigated the association between SES measured by income, education and occupation, as well as single SES indicators, and risky health behaviors. SAMPLE AND METHODS: We analyzed data on 1227 adult men and women (aged 19 and older at baseline) with complete data on health behaviors, SES and chronic diseases at baseline (2003) and 5-year follow up. Respondents were classified as being healthy or chronically ill. SES categories were derived from answers to questions on monthly household income, occupation and education by using two-step cluster analysis algorithm. RESULTS: At baseline, for the whole sample as well as for healthy respondents, SES was statistically significantly associated with unhealthy diet (whole sample/healthy respondents: p = 0.001), physical inactivity (whole sample/healthy respondents p = 0.44/ p = 0.007), and smoking (whole sample/healthy respondents p < 0.001/p = 0.002). The proportion of respondents with unhealthy diet was greatest in the lowest social class, smokers in the middle and physically inactive in the high social class. During the follow up, smoking and physical inactivity remained statistically significantly associated with SES. In chronically ill respondents, only smoking was statistically significantly associated with SES, at baseline and follow up (p = 0.001/p = 0.002). The highest share of smokers was in the middle social class. DISCUSSION AND CONCLUSION: Results of our study show that risky health behaviors are associated with SES and are divergently represented across socioeconomic groups of adult Croatian population. There is an obvious need for interventions targeting the specific socioeconomic group and behavior characteristic of that group.