Study reveals refined carbs heighten inflammation and cardiovascular risk

A recent Nutrients journal study assesses the possible interplay between inflammation, carbohydrate intake, and the development of atherosclerotic cardiovascular disease (ASCVD) development.

Study: The Impact of Dietary Carbohydrates on Inflammation-Related Cardiovascular Disease Risk: The ATTICA Study (2002–2022). Image Credit: Tatjana Baibakova / Shutterstock.com

How do carbohydrates affect inflammation?

The role of carbohydrates, a major source of dietary energy, in the manifestation of cardiovascular disease (CVD) remains unclear. Chronic inflammation influences the development of atherosclerosis, which is often associated with elevated levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α). These are inflammatory markers also associated with metabolic syndrome and insulin resistance.

CRP is a key predictor of cardiovascular events and systemic inflammation. Similarly, IL-6 and TNF-α have been associated with multiple health outcomes, including cancer and neurodegeneration.

Although the role of carbohydrates in insulin secretion and fat storage is well-documented, a direct link to inflammatory effects has not been established. Some studies have reported that a low-carbohydrate diet is associated with greater reductions in inflammatory marker levels compared to low-fat diets.

The type of carbohydrate is important. For example, fiber-rich and low-glycemic index foods can promote satiety, improve digestion, and regulate blood glucose levels. Conversely, consuming more refined carbohydrates could increase the risk of CVDs.

About the study

The current study assessed the role of carbohydrate intake on CVD risk through its impact on chronic systemic inflammation. The quantity and quality of carbohydrate intake were recorded and expressed as fiber content. The main hypothesis was that both the quality and quantity of carbohydrates influence the inflammatory process, which can ultimately lead to the development of CVDs.

The study design follows the ATTICA study, which was a prospective epidemiological study conducted between 2002 and 2022 and included three follow-up assessments in 2006, 2012, and 2022. The objectives of the ATTICA study were to record the distribution of various lifestyle, clinical, socio-demographic, biochemical, and psychological risk factors for CVD to determine the associations between these factors and CVD risk.

A total of 3,042 individuals from Attica, Greece, were invited to participate in the study. Balanced representation was ensured by stratifying participants based on specific characteristics like age, sex, and region, following the demographics of the 2001 census. At baseline, the study participants did not have preexisting CVD, chronic inflammatory conditions, or cancer.

Study findings

Throughout the 20-year study period, 36% of the study cohort experienced fatal or non-fatal CVD events, 40% of whom were male and 32% female. Of these CVD events, 71.7% and 4.3% were coronary heart disease (CHD) and stroke, respectively, with the remaining 24% comprising other CVD events like heart failure, peripheral arterial disease, and aortic disease. The 20-year CVD mortality rate in this cohort was 7.3% and 1.8% in men and women, respectively.

Individuals with CVD exhibited significantly higher levels of inflammatory markers. Being an obese older male and having a history of hypertension, hypercholesterolemia, or diabetes mellitus also increases the risk of CVD events.

When the study cohort was stratified by carbohydrate quantity or quality, no significant differences were observed regarding lifestyle factors, clinical characteristics, or inflammatory marker levels.

Carbohydrate intake alone was not associated with an increased risk of developing CVDs. However, considering both carbohydrate quantity and quality, along with inflammatory marker levels, was found to affect the risk of CVD. This association persisted when CVD risk factors, including sex, obesity, hypertension, hypercholesterolemia, diabetes, smoking, physical inactivity, and low adherence to the Mediterranean diet, were considered.

Mechanisms involved in the association between carbohydrate intake, inflammation, and CVD risk

Refined carbohydrate consumption contributes to hyperglycemia and hyperinsulinemia. Hyperglycemia produces reactive oxygen species (ROS) and contributes to chronic low-grade inflammation.

ROS activates nuclear factor κB (NF-κB), subsequently leading to the oxidative modification of low-density lipoprotein (LDL) cholesterol and the release of pro-inflammatory cytokines like IL-6 and TNF-α. TNF-α also induces the expression of adhesion molecules on endothelial cells, which can influence atherogenesis.

Refined carbohydrate consumption also affects the gut microbiota, a pathway through which inflammation is induced. High-sugar diets are often associated with the increased production of bacterial pro-inflammatory factors, which alter the epithelial barrier and ultimately induce systemic inflammation.

Carbohydrate intake was not directly associated with CVD risk, as higher consumption of whole grains and total dietary fiber was associated with reduced CVD risk. After ingestion, fibers form gels in the intestine, facilitating nutrient absorption and reducing high glucose levels after meals. Fiber also increases satiety, which supports weight management.

Conclusions

In agreement with the researchers’ hypothesis, the effect of inflammation on CVD was found to depend on both the quality and quantity of carbohydrate consumption. To this end, a low-fiber, high-carbohydrate diet appears to stimulate inflammatory processes involved in ASCVD risk.

Moreover, a high-carbohydrate, low-fiber diet has the potential to augment the adverse effects of specific inflammatory markers on CVD risk. This emphasizes the importance of personalized dietary recommendations, particularly for individuals with chronic systemic inflammation.

The strengths of the current study include the large cohort examining CVD epidemiology and the extensive follow-up period. The age and sex distribution of the study cohort were also representative of the urban Greek population.

Some limitations of the current study involve the inclusion of study participants with low CVD risk. Furthermore, the researchers could not isolate the specific effects of individual macronutrients on health outcomes.

Adjusting the intake of carbohydrates is often accompanied by protein and fat consumption adjustments to maintain consistent total energy intake. Thus, it is not possible to definitively attribute CVD risk solely to carbohydrate intake from the current study findings.