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Medical News Today
29-06-2025
- Health
- Medical News Today
Unsaturated fats may not always be anti-inflammatory, study finds
Unsaturated fats, such as those found in oily fish, nuts, seeds, avocados, and olive oil, are recommended as part of a healthful have linked these fatty acids to reduced levels of inflammation and lowered LDL ('bad') a new study suggests that both omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) are linked to increased levels of some inflammatory markers in the fish, nuts, seeds, avocados, and olive oil are all advocated as part of a healthful diet, mostly because of their high concentrations of unsaturated fatty acids. Studies suggest that unsaturated fatty acids, particularly omega-3, may reduce both inflammation, and levels of low-density lipoprotein, LDL or 'bad' cholesterol, which is linked to heart a new study has suggested that polyunsaturated fatty acids may actually increase levels of some inflammatory biomarkers in the blood research, which is published in The International Journal of Epidemiology, found that both omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) were associated with raised levels of glycoprotein acetyls (GlycA), biomarkers associated with increased cardiovascular to inflammatory biomarkers in the bloodThe researchers carried out their primary analysis on 2,802 participants from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort, which recruited a total of 14, 541 pregnant women residing in southwest England in 1991 and 1992, and has followed them and their offspring since then. They replicated their analysis using data from 12,401 participants in the UK Biobank.'Using two large datasets, ALSPAC and the UK Biobank, along with a genetic technique called Mendelian randomization, the researchers examined whether these fats cause changes in inflammation, rather than just being associated with it, exploring actual causality. This approach is especially powerful because it helps minimize the usual confounding factors found in nutrition studies, such as lifestyle or other dietary habits. In other words, the researchers went beyond asking who has more inflammation and what they eat and instead tried to determine whether the fats themselves were directly responsible.'— Thomas M. Holland, MD, MS, physician-scientist and assistant professor at the RUSH Institute for Healthy Aging, RUSH University, College of Health Sciences, Chicago, who was not involved in the researchers assessed the ALSPAC offspring after 24 years. In their analysis, they controlled for household social class at birth, maternal highest education qualification at birth, maternal and paternal smoking status during pregnancy, offspring sex at birth, type of drinker at age 24 , type of smoker at 24 , and at age in months at 24-year Crick, corresponding author, Institute for Molecular Bioscience, Queensland University, Australia, and MRC Integrative Epidemiology Unit, The University of Queesland, Australia, explained their research:'Dietary fatty acids were measured using levels of DHA, total omega-3 LA, total omega-6, and the omega-6:omega-3 ratio found in the blood. Inflammation was measured using substances in the blood called biomarkers and specifically we used the biomarkers C-reactive protein (CRP), Interleukin-6 (IL-6) and Glycoprotein Acetyls (GlycA).'Can omega-3s be inflammatory?The researchers found that in both cohorts, both omega-3 and omega-6 levels were associated with higher levels of told Medical News Today:'Surprisingly, the results showed that both omega-3 and omega-6 fatty acids were associated with higher levels of a marker called GlycA (a novel inflammatory marker), which reflects low-grade chronic inflammation. This was unexpected, especially for omega-3s, which are widely promoted as anti-inflammatory.''Omega-3s are found in dark fatty fish, like salmon and sardines, and in plant-based foods like flaxseeds, chia seeds, and walnuts. Most people think of them as calming to the immune system. Yet in this study, higher omega-3 levels were linked to more inflammation, not less, at least when GlycA was used as the measurement,' he to omega-3 fatty acid ratio could be keyIn the ALSPAC cohort, there was a consistent association between a higher omega-6:omega-3 ratio and all three inflammatory told us that this ratio is influenced by our changed diet:'This [finding] supports earlier findings that it's not just about how much omega-3 you consume; it's about how balanced your overall intake is. In fact, research highlights how this ratio has shifted dramatically in recent history. A century ago, people typically consumed a 4:1 ratio of omega-6 to omega-3. Today, due to modern diets rich in industrial seed oils, that ratio has ballooned to around 15:1 to 20:1. This shift creates a pro-inflammatory environment that could be contributing to chronic diseases, allergies, and autoimmune disorders.''Our findings suggest that it's not as simple as 'omega-3 is anti-inflammatory, and omega-6 is pro-inflammatory'. Just increasing the consumption of omega-3 through diet or supplements might not be enough to lower inflammation. Instead, our results suggest that it might be more useful to look at the balance or ratio between omega-6 and omega-3 in the diet. Improving the balance between the two fats could be a better method for people who want to reduce inflammation in their bodies.'— Daisy CrickThe link between fatty acids and health is complexAlthough the study found an association between PUFAs and some of the 3 biomarkers, the authors emphasize that different biomarkers measure different aspects of inflammation, so by assessing only 3 biomarkers, they may have missed some important effects of PUFAs on inflammation. Further research using additional biomarkers is needed to better understand the relationship between PUFAs and told MNT that these findings should lead to further research: 'It is important to remember that the study measured just three inflammatory markers. The immune system is incredibly complex, and omega fatty acids might influence other pathways that weren't captured here. For example, omega-3s might still help resolve short-term inflammation or protect against specific diseases, even if they raise GlycA slightly. More research using a broader range of immune biomarkers will help clarify this relationship.'Despite this limitation, the findings highlight that there may be more to the relationship between fatty acids and health than previously thought.'The relationship between fatty acids and inflammation is complex and our findings only tell part of the story. Although we show that omega-3 fats are associated with increases in some biomarkers of inflammation, it does not rule out other potential beneficial effects of these fatty acids in the diet.'— Daisy Crick
Medscape
23-06-2025
- Health
- Medscape
Should CV Risk Equations Add Lp(a)?
Whether to measure Lp(a), a lipoprotein associated with increased cardiovascular risk, and how to use that information in risk assessment is a hot topic in cardiovascular medicine. The American Heart Association recently introduced the Predicting Risk of Cardiovascular EVENT (PREVENT) equations — an update to the pooled cohort equations. Neither risk calculator includes values for Lp(a). A recent study looked at whether adding Lp(a) to the PREVENT equations would improve risk prediction. It found that including the lipid parameter yielded a modest improvement at a population level but appeared to be more useful for personalized risk assessment, particularly among lower-risk individuals. 'Our results validate the PREVENT equations on a population level and show that they perform well, both in people with and without high levels of Lp(a),' lead author of the study, Harpreet Bhatia, MD, University of California San Diego, told Medscape Medical News . 'While I think our results would not support adding Lp(a) to the PREVENT equations, they confirm that on an individual-patient basis Lp(a) can add information,' he commented. Bhatia explained that the PREVENT risk equations are going to be the future paradigm of risk stratification in the primary prevention setting in the US, eventually replacing the pooled cohort equations which have been used for many years. The reason that Lp(a) wasn't included in either risk score, he suspects is because the datasets on which the risk equations are based would not have these values available. The PREVENT equations removed the consideration of race or ethnicity, as there is now acknowledgement that race is more of a social construct, but it is known that Lp(a) levels vary by ancestry, he said. Bhatia believes that Lp(a) should be routinely tested at least once in all adults; 'For those of us who practice preventive cardiology and lipidology, it can alter our clinical management.' Current American Heart Association/ American College of Cardiology cholesterol guidelines from 2018 do not recommend universal testing of Lp(a) but include it as a risk enhancing factor; updated guidelines are expected within the next year. Guidelines from the European Society of Cardiology and Canada and the US National Lipid Association do recommend measuring Lp(a). For the current study, Bhatia and colleagues examined data from the Multi-Ethnic Study of Atherosclerosis, a US study of 6670 people started in the year 2000, and the UK Biobank, a study of over 500,000 individuals from the UK started around 2006. Participants had no known cardiovascular disease at baseline and most had an Lp(a) measurement. Bhatia noted that his study used risk thresholds established for the pooled cohort equations, but it has not yet been decided what the cut points will be for the PREVENT equations. Low risk was defined as < 5%; borderline as 5%-7.5%; intermediate as 7.5%-20%, and high as ≥ 20% predicted 10-year risk for cardiovascular disease. 'PREVENT Equations Generally Do A Good Job' 'Essentially, what we saw was that the PREVENT equations generally do a good job of putting people into those 10-year risk categories across the board,' Bhatia said. However, they also found that within each category and across the board, if Lp(a) was high, then the cardiovascular risk was increased compared to individuals with a lower Lp(a) and sometimes quite significantly increased. The researchers also tried to establish whether Lp(a) could improve risk prediction on top of the PREVENT equations, using the Net Reclassification Index (NRI) which looks at the percentage of people who would be reclassified based on the new model (the proportion who move up minus the proportion who move down). They found that Lp(a) levels led to a modest improvement in risk prediction according to the NRI. In terms of atherosclerotic cardiovascular disease (ASCVD), including elevated Lp(a) on top of the PREVENT equations appropriately reclassified about 6% of people. With regard to coronary artery disease, which Lp(a) is most strongly associated with, the NRI was about 8%. Another measure of how well a new model predicts risk — the C index — found that the addition of Lp(a) did not significantly modify results. 'Our results suggest there does seem to be some improvement in risk prediction with Lp(a) for some individuals, particularly those at lower cardiovascular risk,' Bhattia said, an observation he described as 'intriguing'. He does not believe that new equations are needed that incorporate Lp(a). He pointed out that statin therapy for prevention is more strongly recommended in intermediate/higher risk patients, with a weaker recommendation for those at lower risk when there's the presence of an additional risk enhancing factor. 'It may be that someone at low risk in the equations with an elevated Lp(a) may be eligible for starting statins.' Bhatia already considers Lp(a) levels in this way in his clinic. He said that Lp(a) testing is simple and widely available, and the majority of people will only need to be tested once in their lifetime. He explained that most people who have low or high levels would stay in those categories long term, while people who have intermediate or borderline levels (30-50 mg/dL or 75-125 nmol/L) may need repeat testing if something changes that can affect Lp(a) levels longer term such as going through menopause, or the development of kidney or thyroid disease. Lp(a) Testing Worthwhile In an editorial accompanying the publication, Donald M. Lloyd-Jones, MD, Framingham Center for Population and Prevention Science, Boston University, Framingham, Massachusetts, and Amit Khera, MD, University of Texas Southwestern Medical School, Dallas, said the results are a useful validation of the PREVENT risk equations in contemporary broad populations and large real-world clinical samples. In terms of whether Lp(a) should be incorporated directly as a variable in the PREVENT equations, the editorialists have a similar view to Bhatia. 'That appears unnecessary,' they wrote. But, like Bhatia, they believe that Lp(a) should be measured once in everyone to help understand and individualize risk. 'Lp(a) is indeed a risk-enhancing, likely causal, factor for ASCVD. Its absence does not exonerate traditional risk factors, but its presence can amplify and personalize that risk, and help guide clinicians and patients regarding use and intensity of preventive therapies,' they concluded. Also commenting on this latest study, was Nathan Wong, PhD, from the University of California Irvine School of Medicine. He told Medscape Medical News that the analysis shows that the PREVENT risk score predicts ASCVD outcomes similarly in those with and without elevated Lp(a) levels. The stronger prediction of Lp(a) in lower risk people 'argues for the need to promote increased screening in the broader population, including those at lower risk' he said noting that most recommendations in the past have focused on people at higher risk such as those with a personal history of ASCVD. Wong agreed with Bhatia that the value of Lp(a) is more at the individual level than at the population wide level. But he does believe a risk score incorporating Lp(a) could be helpful for personalizing treatment strategies in certain individual patients, particularly for those with elevated Lp(a) levels who may not already be identified as high risk. Indeed, Wong and colleagues recently published such a score and showed that incorporating Lp(a) into ASCVD risk prediction models developed using a real-world clinic population moderately improves performance over 10 years, with good generalizability when applied to other US population cohorts. In that paper, a 25 mg/dL increment in Lp(a) was associated with a 23% increased risk for incident ASCVD. Levels ≥ 75 mg/dL conferred a near two-fold greater risk for ASCVD, including a 2.5-fold greater risk for stroke compared with Lp(a) levels < 25 mg/dL. They also demonstrated that adding Lp(a) to the pooled cohort equations ASCVD risk calculator correctly reclassified 45% of borderline-intermediate risk patients who experienced incident ASCVD as high-risk. However, about 24% who did not experience events were incorrectly reclassified high-risk (for an NRI of 21%). He cited a use case of a Black man aged 65 years with an Lp(a) of 80 mg/dL and a 10-year ASCVD risk of 18% without considering Lp(a) who would be up-stratified to 24% after factoring in Lp(a). 'Based on current guidelines, this person would now be clearly recommended for a statin to lower his ASCVD risk which may not have been as certain based on the risk not incorporating Lp(a),' he said. Recent studies have also shown identification of elevated Lp(a) levels can result in greater use of lipid-lowering therapy, he added. Wong also agreed with Bhatia on the distinction between risk prediction in populations vs individuals. 'We don't practice medicine on populations. We practice it on individuals and for certain individuals a risk score that incorporates Lp(a) can reclassify their risk category significantly dependent on how high their Lp(a) is,' he stated.
Medscape
02-06-2025
- General
- Medscape
Fibrosis-4 Index Finds New Role in Rheumatoid Arthritis
Up to 20% of patients with rheumatoid arthritis (RA) had abnormal fibrosis-4 (FIB-4) index values, reflecting an indeterminate to high risk for liver fibrosis; a significant correlation was seen with insulin resistance but not with disease activity. METHODOLOGY: Researchers conducted a cross-sectional study to calculate FIB-4 index values in patients with RA and assess their relationship with disease characteristics and cardiovascular comorbidities. They recruited 465 adults with RA (mean age, 55 years; 81% women) between 2019 and 2021, all of whom had a disease duration of at least 1 year and were taking ≤ 10 mg/day of prednisone or an equivalent dose. The FIB-4 index was calculated using an equation considering age, platelet count, and alanine aminotransferase and aspartate aminotransferase levels, with the risk for fibrosis classified as low, indeterminate, or high on the basis of defined cutoff values. Participants underwent evaluations for disease activity, complete lipid profiles, the presence of metabolic syndrome, anthropometric parameters, and insulin resistance using the Homeostatic Model Assessment, as well as carotid ultrasound to detect subclinical carotid atherosclerosis. Cardiovascular risk was estimated using t he Systematic Coronary Risk Evaluation-2 (SCORE2) tool. TAKEAWAY: SCORE2 classified 66% of patients with RA as having low cardiovascular risk, 28% as having moderate cardiovascular risk, and 6% as having high cardiovascular risk; the prevalence of cardiovascular risk factors was generally high. FIB-4 values indicated an indeterminate risk for fibrosis in 18% of patients with RA and a high risk in 1%, whereas 81% had a low risk. Several factors, including age ( P < .001), cardiovascular risk measured by SCORE2 ( P < .001), and metabolic syndrome ( P = .008), showed positive correlations with FIB-4 values; however, in multivariable analysis, the presence of hypertension, insulin resistance indices, and statin use maintained significant positive associations. < .001), cardiovascular risk measured by SCORE2 ( < .001), and metabolic syndrome ( = .008), showed positive correlations with FIB-4 values; however, in multivariable analysis, the presence of hypertension, insulin resistance indices, and statin use maintained significant positive associations. Disease activity (measured by multiple scores), acute phase reactants, and the presence of rheumatoid factor or anti–citrullinated protein antibodies showed no significant association with FIB-4 values, whereas the presence of erosions at recruitment was associated with FIB-4 ( P = .044). IN PRACTICE: "This index may serve as a surrogate marker for CV [cardiovascular] risk and insulin resistance in patients with RA," the authors concluded. SOURCE: This study was led by Iván Ferraz-Amaro, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain. It was published online on May 21, 2025, in Rheumatology . LIMITATIONS: The cross-sectional design of this study prevented the establishment of causal relationships between variables. Data on hepatic ultrasound or liver biopsy were lacking. Information on cumulative methotrexate use was not collected. DISCLOSURES: This study was supported by a grant from Instituto de Salud Carlos III and additional funds from the European Union. Two authors reported receiving grants or research support and consultation fees from speaker bureaus associated with several pharmaceutical and healthcare companies, including AbbVie, Roche, and GSK.
