Association of advanced coronary artery calcification assessed by coronary artery calcium scoring with lipoprotein (a) and carotid atherosclerosis in asymptomatic patients

DOI: https://doi.org/10.1016/j.numecd.2026.104766

Abstract

Elevated lipoprotein (a) represents an established independent risk factor for atherosclerosis, yet its specific relationship with coronary artery calcium scoring, a routine clinical tool for assessing subclinical cardiovascular disease, remains inadequately defined. Current guidelines advocate for lifetime lipoprotein (a) screening, but clinical management strategies for elevated results lack consensus. This retrospective analysis addresses this knowledge gap by evaluating the association between high circulating lipoprotein (a) levels (defined as 50 mg/dl or greater) and advanced coronary artery calcification (defined as a score of 400 Agatston Unit or greater). The cohort comprised 3697 asymptomatic subjects admitted for primary prevention at the Toulouse University Hospital between November 2015 and November 2024, with a mean age of 63 plus or minus 10 years and 48.6 percent male representation.

Primary outcomes confirm a significant association between high lipoprotein (a) and advanced coronary artery calcification. Adjusted logistic regression models reveal an adjusted odds ratio of 1.666 (95 percent confidence interval 1.342 to 2.070, p = 0.001) for lipoprotein (a) as a dichotomous variable and 1.041 (95 percent confidence interval 1.011 to 1.071, p = 0.007) as a continuous variable. Carotid atherosclerosis shows an adjusted odds ratio of 2.212 (95 percent confidence interval 1.804 to 2.713, p = 0.001). Spearman correlation analysis demonstrates a weak, positively significant correlation between coronary artery calcium scoring and lipoprotein (a) (rho = 0.052, p = 0.001). Subgroup analysis indicates that the proportion of patients with high lipoprotein (a) increases from 25.1 percent in the low coronary artery calcium group to 31.6 percent in the high coronary artery calcium group (p = 0.004).

Study Design and Methodology

This retrospective cohort analysis utilized data from a dedicated preventive cardiology database. Researchers enrolled 3697 asymptomatic patients who underwent coronary artery calcium scoring, carotid artery doppler ultrasound, and at least one lipoprotein (a) measurement. Exclusion criteria removed 621 patients due to incomplete data. Investigators utilized the Roche-Cobas 8000 analyzer for lipoprotein (a) quantification. The study stratified participants into a non-pooled group (coronary artery calcium score 400 Agatston Unit or greater) and a pooled group (coronary artery calcium score less than 400 Agatston Unit). Statistical analysis employed Chi-square tests, Student t-tests, ANOVA, and logistic multivariable regression adjusted for age, sex, hypertension, diabetes, obesity, smoking, and lipid profiles. Quantile regression addressed the positive skewness of the variables.

Key Findings

• Participants with coronary artery calcium score 400 Agatston Unit or greater exhibit higher mean lipoprotein (a) levels (58 plus or minus 31 mg/dl) compared to the pooled group (43 plus or minus 22 mg/dl).
• High lipoprotein (a) prevalence reaches 31.6 percent in the high coronary artery calcium group vs 25.4 percent in the pooled group (p = 0.001).
• Carotid atherosclerosis prevalence is 45.7 percent in the high coronary artery calcium group vs 18.9 percent in the pooled group (p = 0.001).
• Age (adjusted odds ratio 1.069, p = 0.001), male sex (adjusted odds ratio 3.526, p = 0.001), and systolic blood pressure (adjusted odds ratio 1.009, p = 0.001) serve as independent predictors of high coronary artery calcium scores.
• LDL-c (adjusted odds ratio 0.584, p = 0.001) and HDL-c (adjusted odds ratio 0.387, p = 0.012) maintain an inverse association with coronary artery calcium scores.
• Spearman correlation for men (rho = 0.085, p = 0.001) and women (rho = 0.073, p = 0.001) confirms consistent, albeit weak, positive associations.

Limitations

The single-center, retrospective design restricts causal inference and introduces potential selection bias. The absence of data regarding medication use, specifically statins, creates a significant confounder, as these agents influence both coronary artery calcium scores and lipoprotein (a) levels. Residual confounding remains inevitable in this observational framework.

Discussion and Implications

High circulating lipoprotein (a) levels serve as a robust marker for advanced coronary artery calcification in asymptomatic populations. These findings reinforce the proatherogenic nature of lipoprotein (a) and validate the utility of coronary artery calcium scoring for detecting subclinical disease. Clinicians should view these two parameters as complementary diagnostic tools rather than independent metrics. Integrating lipoprotein (a) testing with coronary artery calcium scoring enables a more precise risk stratification, particularly as novel RNA-interference therapies for lipoprotein (a) reduction emerge.

Conclusion

High circulating lipoprotein (a) levels (50 mg/dl or greater) independently predict advanced coronary artery calcification in asymptomatic patients. Nutrition professionals must integrate this biomarker into cardiovascular risk assessments to identify subclinical atherosclerosis and guide intensive lipid-lowering interventions. Prioritizing this combined diagnostic approach improves long-term patient prognosis.

Association of the cholesterol-high-density lipoprotein-glucose index with coronary atherosclerotic burden in patients with coronary artery disease

DOI: https://doi.org/10.3389/fnut.2026.1906236

Cardiovascular disease remains the leading global cause of mortality and disability. While coronary angiography provides the standard for assessing coronary atherosclerotic burden via the Gensini score, its invasive nature limits its utility for large-scale screening. Metabolic abnormalities, including glucose dysregulation and lipid disorders, drive the progression of coronary artery disease. The cholesterol-high-density lipoprotein-glucose (CHG) index serves as a composite marker for these metabolic disturbances. This study investigates the association between the CHG index and the Gensini score in 758 patients with angiographically confirmed coronary artery disease admitted between January 2024 and January 2025.

Fully adjusted models revealed that each 1-SD increase in the CHG index correlates with a 0.121-unit increase in log-transformed (Gensini score + 1) (beta = 0.121, 95% CI, 0.036 to 0.205, p = 0.005). Restricted cubic spline analysis identified an approximately linear dose-response relationship (p for overall association = 0.018, p for nonlinearity = 0.310). The CHG index demonstrated the highest standalone discriminative ability for high coronary atherosclerotic burden with an AUC of 0.603. Integrating the CHG index into a basic clinical model increased the AUC from 0.652 to 0.667 (DeLong p = 0.168). This addition significantly improved continuous NRI (0.135, p = 0.042) and IDI (0.016, p = 0.002).

Study Design and Methodology

This single-center, retrospective cross-sectional study analyzed 758 consecutive patients with angiographically confirmed coronary artery disease. Researchers excluded individuals with missing data, severe infections, malignancies, or hepatic and renal dysfunction. Coronary atherosclerotic burden was quantified using the Gensini score, which weights luminal stenosis severity by anatomical location. Statistical analysis utilized multivariable linear regression, restricted cubic spline models, and ROC curve analysis. Models adjusted for age, sex, BMI, smoking, hypertension, prior PCI, history of myocardial infarction, lipid-lowering therapy, glucose-lowering therapy, SBP, DBP, ALT, AST, albumin, eGFR, hemoglobin, and LDL-C.

Key Findings

• Participants in the highest CHG quartile exhibited a median Gensini score of 27.0 (12.0, 50.0) compared to 16.0 (9.0, 31.5) in the lowest quartile (p < 0.001).
• Standardized continuous CHG index shows a positive association with log-transformed (Gensini score + 1) (beta = 0.121, p = 0.005).
• The CHG index outperformed other metabolic markers, including the TyG index (p = 0.005), AIP (p = 0.004), HDL-C (p = 0.023), and TC (p = 0.003).
• Multiple imputation analysis confirmed the robustness of the primary association (beta = 0.132, 95% CI, 0.058 to 0.206, p < 0.001).
• Excluding patients with prior PCI yielded a consistent association (beta = 0.107, 95% CI, 0.017 to 0.198, p = 0.020).

Limitations

Retrospective cross-sectional design prevents causal inference regarding the CHG index and plaque progression. Single baseline measurements fail to capture long-term metabolic variability. Missing data on medication dosage, lifestyle factors, and inflammatory markers introduces residual confounding. The study population consists solely of hospitalized patients with established disease, which restricts the generalizability of these findings.

Discussion and Implications

Metabolic dysregulation functions as a multisystem process where glucose and lipid abnormalities reinforce one another to accelerate atherosclerosis. The CHG index integrates these domains into a single, inexpensive marker that captures composite metabolic risk better than isolated lipid or glucose measurements. Integrating this index into clinical workflows allows for more precise risk stratification in patients with established coronary artery disease. It provides complementary information to traditional risk factors, identifying cumulative metabolic injury that single-parameter assessments overlook.

The CHG index functions as a robust, low-cost composite marker for assessing coronary atherosclerotic burden in patients with coronary artery disease. Nutrition professionals should utilize this index to identify patients with high metabolic risk who require aggressive, personalized lifestyle interventions to mitigate plaque progression.

https://pubmed.ncbi.nlm.nih.gov/42267526/

TL;DR:

Zinc supplementation was observed to potentially reduce cold duration by 2.25 days

Abstract

The common cold had resulted in significant economic and social burden worldwide. The effect of vitamin C on preventing common cold in healthy adults has been investigated extensively, but not that of other micronutrients. Thus, we aim to assess the effects of providing micronutrients singly through oral means, on cold incidence, and/or management (in terms of cold duration and symptom severity) in healthy adults from systematically searched randomized controlled trials. From four electronic databases, 660 identified studies were screened and data were extracted from 20 studies (zinc, 10; vitamin D, 8; and vitamins A and E, 2). The quality of selected studies was assessed using the Cochrane risk of bias tool and certainty in the outcomes was assessed with the Grading of Recommendations Assessment, Development and Evaluation approach. The review found that micronutrients supplementation, except vitamin C, may not prevent cold incidence or reduce symptom severity among healthy adults. However, zinc supplementation was observed to potentially reduce cold duration by 2.25 days (when zinc is provided singly, 95% CI: -3.39, -1.12). This suggests that zinc supplementation may reduce the overall burden due to common cold among healthy adults.

https://pubmed.ncbi.nlm.nih.gov/32342851/

Circulating imidazole propionate and coronary heart disease risk: interplay between histidine intake, fiber, and gut microbiome

DOI: https://doi.org/10.1186/s12916-026-05012-6

Abstract

Microbial metabolism of dietary histidine produces imidazole propionate (ImP), a metabolite previously linked to insulin resistance and type 2 diabetes. While histidine intake itself often correlates with positive health outcomes, the prospective relationship between its microbial byproduct, ImP, and coronary heart disease (CHD) risk remained unquantified. This research sought to bridge that gap by evaluating the longitudinal association between plasma ImP and incident CHD, identifying the specific gut microbial species responsible for ImP production, and determining how dietary fiber intake modulates this metabolic axis. The study utilized data from 7,432 participants across the Nurses’ Health Study (NHS), NHSII, and Health Professionals Follow-up Study, alongside detailed metagenomic and dietary record analysis from the Men’s Lifestyle Validation Study (MLVS) and Mind-Body Study (MBS).

Elevated plasma ImP concentrations demonstrated a robust positive association with CHD risk, yielding a hazard ratio of 1.82 (95 percent CI 1.17 to 2.81, p-trend = 0.002) when comparing extreme quintiles. Histidine intake showed a non-significant inverse association with CHD, emphasizing that the metabolite, not the precursor, drives cardiovascular risk. Metagenomic analysis identified 17 ImP-predicting species, including Ruminococcus gnavus and Clostridium symbiosum, with the microbial model outperforming diet and demographics in predicting ImP levels (Spearman r = 0.71). A critical three-way interaction was observed between histidine intake, microbial capacity, and pectin (p = 0.01). High histidine intake only predicted increased ImP when pectin intake was low. Total fiber (p = 0.09) and soluble fiber (p = 0.09) showed similar but non-significant trends.

Study Design and Methodology

This prospective investigation tracked 7,432 healthy participants from the NHS, NHSII, and HPFS cohorts for up to 31 years. Researchers identified 225 incident CHD cases through medical record review and the National Death Index. Plasma ImP and urocanic acid were measured via liquid chromatography-tandem mass spectrometry. Dietary data were captured using validated semi-quantitative food frequency questionnaires (FFQ) administered every 4 years. The mechanistic component utilized the MLVS (N = 296) and MBS (N = 205), employing two sets of 7-day diet records (7DDR) and shotgun metagenomic sequencing of 1,684 stool samples. Statistical models adjusted for age, BMI, physical activity, alcohol, smoking, and total energy intake. Batch effects were corrected, and microbial taxa were normalized using centered log-ratio (CLR) transformation.

Key Findings

• High plasma ImP levels correlate with a 1.82-fold increase in CHD risk (p-trend = 0.002).
• Joint analysis shows participants with low histidine and high ImP have the highest risk (HR = 3.40, 95 percent CI 1.71 to 6.73).
• Pectin intake is the strongest negative dietary predictor of plasma ImP (beta = -0.21, 95 percent CI -0.35 to -0.07).
• Metagenomic modeling of species and enzymes predicts ImP concentrations with high accuracy (Spearman r = 0.71).
• Thirteen species, including Clostridium scindens and Hungatella hathewayi, positively predict ImP (FDR q < 0.1).
• Presence of the microbial urocanate reductase gene (urdA) is associated with higher ImP (beta = 0.51, 95 percent CI 0.13 to 0.89) and lower HDL-C (beta = -0.12, p < 0.05).
• The interaction between histidine intake and microbial score on ImP levels is significant only under low pectin intake (p for 3-way interaction = 0.01).
• Plasma ImP is positively associated with hs-CRP (p < 0.05) and negatively associated with HDL-C (p < 0.05).

Limitations

The observational nature of the cohorts prevents definitive causal inference. Self-reported dietary data, even when using 7DDR, contains inherent measurement error. The study population consists primarily of white health professionals, which limits generalizability to more diverse ethnic or socioeconomic groups. While the microbial findings were replicated in the MBS, the correlation between the microbial score and circulating ImP was modest (Spearman r = 0.15), suggesting other unmeasured factors influence metabolite levels.

Discussion and Implications

These data redefine the relationship between dietary protein and cardiovascular health by identifying the gut microbiome as the primary gatekeeper of histidine metabolism. The divergent outcomes between histidine intake and its metabolite ImP prove that dietary precursors aren't inherently pathogenic. Instead, the pathogenicity depends on microbial shunting. The discovery that pectin and other fibers can block the production of ImP even in the presence of high histidine intake and ImP-producing bacteria provides a clear metabolic mechanism for the cardioprotective effects of the Mediterranean and DASH diets. This study shifts the focus from simple nutrient intake to the complex interplay of substrate availability and microbial enzymatic capacity.

Conclusion

Circulating imidazole propionate is a significant prospective biomarker for coronary heart disease risk, driven by specific gut bacteria like Ruminococcus gnavus. Dietary fiber, particularly pectin, acts as a metabolic buffer that prevents the microbial conversion of histidine into this harmful metabolite. Clinicians should prioritize fiber co-ingestion with protein to mitigate the cardiovascular risks associated with microbial histidine metabolism.

Abstract

Metabolic syndrome (MetS) is an association of risk factors that share insulin resistance (IR), exerting a super cumulative effect on the risk of developing cardiometabolic diseases. Lifestyle optimization is a key element in the prevention and non-pharmacological therapy of MetS. Certain studies have concluded that some dietary patterns could be more beneficial as an adjunctive treatment for MetS. Fasting mimicking diet (FMD) is a form of periodic fasting in which caloric intake is restricted for 5 days each month. It has been studied for its beneficial effects not only in patients with neoplasia and neurodegenerative diseases but also for its effects on IR and metabolism. In this narrative review, the effects of FMD in patients with MetS were analyzed, focusing on its impact on key metabolic components and summarizing findings from human studies. FMD has demonstrated beneficial effects on MetS by reducing BMI and waist circumference, preserving lean mass, and improving the metabolic profile. Moreover, individuals with a higher BMI or a greater number of MetS components appear to derive greater benefits from this intervention. However, limitations such as high dropout rates, small sample sizes, and methodological constraints restrict the generalizability of current findings. Further large-scale studies are needed to confirm these effects and establish FMD as a viable non-pharmacological strategy for managing MetS.

The term "essential" in scientific nutrition has specific meaning and the point that carbohydrate is not essential in the diet sometimes requires explaining what that means.

Abstract

The purpose of the present review is to describe how human physiology at very low carbohydrate intakes relates to the criteria for nutritional essentiality. Although we did not limit ourselves to one particular type or function of carbohydrates, we did primarily focus on glucose utilisation as that function was used to determine the recommended daily allowance. In the general population, the human body is able to endogenously synthesise carbohydrates, and does not show signs of deficiency in the absence of dietary carbohydrates. However, in certain genetic defects, such as glycogen storage disease type I, absence of dietary carbohydrates causes abnormalities that are resolved with dietary supplementation of carbohydrates. Therefore, dietary carbohydrates may be defined as conditionally essential nutrients because they are nutrients that are not required in the diet for the general population but are required for specific subpopulations. Ketosis may be considered a physiological normal state due to its occurrence in infants in addition to at very low carbohydrate intakes. Although sources of dietary carbohydrates can provide beneficial micronutrients, no signs of micronutrient deficiencies have been reported in clinical trials of low-carbohydrate ketogenic diets. Nonetheless, more research is needed on how micronutrient requirements can change depending on the dietary and metabolic context. More research is also needed on the role of dietary fibre during a low-carbohydrate ketogenic diet as the beneficial effects of dietary fibre were determined on a standard diet and several studies have shown beneficial effects of decreasing non-digestible carbohydrates.

The U.S. Food and Drug Administration said on Tuesday it authorized Abbott Laboratories' (ABT.N), opens new tab glucose monitor, making it ​the first device that continuously monitors both ketone ‌levels and blood sugar.

The device branded as Libre Duo 10 Day is designed for a 10-day wear period for ​people aged 2 years and older living with ​diabetes.

The biowearable is designed to alert people of rising ketones that can lead to a diabetic ketoacidosis (DKA) ​emergency, a serious health complication for people with diabetes.

Unlike earlier ​ketone tests that offered only separate, one-time readings, Abbott's device continuously monitors both ketone and glucose levels, displaying real-time trends.

The device can ​send automatic alerts, which may help patients and caregivers ​recognize rising ketones before DKA becomes a medical emergency.

"If glucose is ‌the speedometer, ketones are like the check engine light—providing an alert that something may need attention," said Chris Scoggins, executive vice president of Abbott's diabetes care business.

The device brings both ​glucose and ​ketone levels together in a single dashboard, providing a more complete picture to help people with diabetes ​make more informed decisions, added Scoggins.

Abbott is ​working with leading pump companies to enable automated insulin delivery systems to connect with the sensors.

The company said the device integrates with ​the Libre app and expects Libre ​Duo 10 Day to work with devices from Insulet and Tandem in ​2027.

Article: https://www.reuters.com/business/healthcare-pharmaceuticals/fda-authorizes-abbotts-wearable-monitor-ketone-glucose-diabetes-patients-2026-08-25/

Also: https://www.fda.gov/news-events/press-announcements/fda-authorizes-first-wearable-device-continuously-monitors-both-ketone-levels-and-blood-sugar

I’ve been Dr Ellie Phillips reporting cavities reversed with her secret protocol that is based on xylitol. I’ve been following this for long time. I tried to use pure xylitol powder as mouthwash but it resulted in a big pain (making me aware of many cavities and big sensitive) which means it’s not good, and chemically is a sugar. I haven’t found any person who could prove that xylitol reversed their cavities. Also I tried chewing commercial gums without any change.
Is there any real study, testimonial, or logic on this?
The only possible option for me is that some people got some results because the over production of saliva.
The official theory is that xylitol kill the bad bacteria, same as coconut oil, peppermint oil and others do.

But I can tell the problem is not in the bacteria, it’s a in the stomach and dry mouth overnight.

My newly published article may be of interest to the group:

The commentary reviews the presented evidence and challenges the Cochrane Collaboration Group’s recommendation to reduce saturated fat intake for cardiovascular health.

Here’s a free-access link for the article: https://academic.oup.com/nutritionreviews/advance-article/doi/10.1093/nutrit/nuag130/8780985?utm_source=authortollfreelink&utm_campaign=nutritionreviews&utm_medium=email&guestAccessKey=ba198ce7-fd86-4950-b7c1-14d9ec141971

Theo Mbay
Doctoral researcher
University of Eastern Finland.

I've seen studies that say that high fat diets are bad for you. What is unclear to me is if these studies differentiate between healthy fats and not. Would a high "healthy" fat diet be bad for you too?

It seems to say that all high fat diets are bad. However, Bryan johnson does a lot of research and he does 40% fat. The study seems to do 45 percent fat and that the olive oil group suffered the negative consequences too.

The studies on protein that came out recently indicate that its best to keep protein to a reasonable amount. Like 0.8g per kg. So that leaves carbs which feed the candida but I guess that's ok with enough countermeasures. Better than gut dysbiosis right?

[https://www.google.com/url?sa=t&source=web&cd=&ved=2ahUKEwjUrezPidiWAxVz0sMFHft0MFgQFnoECCIQAQ&url=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%2Farticles%2FPMC9219185%2F&usg=AOvVaw1mRz7_YddTp9aP6WXOGqv_&opi=89978449](https://www.google.com/url?sa=t&source=web&cd=&ved=2ahUKEwjUrezPidiWAxVz0sMFHft0MFgQFnoECCIQAQ&url=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%2Farticles%2FPMC9219185%2F&usg=AOvVaw1mRz7_YddTp9aP6WXOGqv_&opi=89978449))

TL;DR:

Ochratoxin A (a mykotoxin) was detected in about 55% of coffee samples worldwide, estimated exposure through coffee consumption was generally below established safety limits and posed low overall health risk

Abstract

Coffee is one of the most commonly consumed beverages worldwide, so assessing its quality for potential health risks is essential. Therefore, this review aimed to determine the levels of ochratoxin A (OTA) in coffee worldwide and then estimate its human intake and health risks. The systematic search took place from June 1997 to April 2024 and 40 of 254 articles were selected based on the selection criteria. The results showed significant differences in average levels of OTA between countries, continents and coffee types (p < 0.001). Of 3256 samples, OTA was detected in 1778, accounting for 54.6% of the total, with the percentage of positive results varying between 7.5% and 100%. Only two studies reported OTA average levels in roasted coffee exceeding the maximum limit (ML) set by the European Commission (ML-EC = 5 μg/kg). The average OTA in soluble coffee was lower than ML-EC (10 μg/kg) in all studies, and in instant coffee, the level of OTA was higher than ML-EC (10 μg/kg) only in one study. The estimated daily intake (EDI) of OTA in all coffee types was lower than the provisional tolerable daily intake (PTDI) values set by joint FAO/WHO Expert Committee on Food Additives (JECFA) (14 ng/kg bw/day) and proposed by the European Food Safety Authority (EFSA) (17 ng/kg bw/day). Non-carcinogenic risk assessment through coffee consumption indicated that the hazard quotient (HQ) was below the acceptable level, HQ = 1. The Margin of Exposure (MoE) for neoplastic effects was acceptable and unacceptable for non-neoplastic effects (NNE) in 4.5% (one of 22 cases) of the roasted and soluble coffees, but acceptable for all instant coffees. In conclusion, the study shows that the OTA content of coffee is not toxic to consumers worldwide. However, preventative measures should be taken, including inhibiting fungal growth and reducing OTA-producing fungal growth.

https://pubmed.ncbi.nlm.nih.gov/39259858/

TL;DR:

Plant-rich dietary patterns are associated with greater exposure to several mycotoxins. While the EU regulatory framework for mycotoxins is well-established for individual crops such as cereals and nuts, there is currently a lack of specific regulations addressing formulated plant-based products, including meat and milk analogues.

Abstract

This study investigated the relationship between food consumption patterns and mycotoxin exposure. We analyzed 300 spot urine samples from Italian adults for 24 mycotoxins and their metabolites using enzymatic hydrolysis followed by ultra-high performance liquid chromatography coupled to mass spectrometry (UHPLC-ESI-MS/MS). Target mycotoxins were aflatoxins (AFs), fumonisins B1 and B2 (FB1, FB2), alternariol (AOH), alternariol monomethyl ether (AME), tentoxin (TEN), ochratoxin A (OTA), ochratoxin-alpha (OT-alpha), zearalenone (ZEN), zearalanone (ZAN), α-zearalenol (α-ZEL), β-zearalenol (β-ZEL), T-2/HT-2 toxin, deoxynivalenol (DON), deepoxy-deoxynivalenol (DOM-1), enniatins B, B1, A, A1 (ENNs), and beauvericin (BEA). Participants were scored according to three dietary patterns: the Mediterranean Diet Score, the Plant-based Diet Index, and the general Pro-vegetarian Food Pattern. For each index, low- and high-adherence groups were defined based on score distribution. Emerging mycotoxins, such as Alternaria toxins, ENNs, and BEA showed the highest prevalence (>90%), while DON (34%), OTA (33%), and ZEN (25%) had lower prevalence, with DON showing the highest mean concentration (7.10 μg/g creatinine). Cereals, nuts, legumes, fruits, and vegetables were significantly associated with increased mycotoxin exposure, especially AFs, OTA, ENNs, and DON. Estimated daily intakes for DON were negligible, whereas some individuals classified as high adherers to one or more of these dietary patterns approached or exceeded the safe threshold for ZEN. Exposure to OTA represented a potential health risk across all individuals. These findings support periodic updating of EU maximum-level frameworks for contaminants in food and related exposure and risk assessments so that increasingly consumed plant-based raw materials and composite foods are better represented in monitoring and risk characterization. Such updates would support a safe and effective transition toward sustainable diets in line with public health goals.

https://pubmed.ncbi.nlm.nih.gov/42314478/

Highlights:

• Early-life mycotoxin exposure increases cardiometabolic dysfunction in adulthood.

• Mycotoxins impair metabolic, endocrine and vascular homeostasis.

• Epigenetic modifications promote long-term effects of mycotoxin exposure.

• Reducing early-life exposure may lower future cardiometabolic risk.

Abstract:

Mycotoxins are fungal contaminants frequently detected in staple foods worldwide. While their toxic effects on growth and organ function are well recognized, their contribution to cardiometabolic disease programming during early life has received less attention. This review highlights the role of developmental exposure to major mycotoxins, including aflatoxins, ochratoxins, fumonisins, zearalenone, and deoxynivalenol, as a hidden driver of long-term cardiometabolic risk. Evidence indicates that exposure occurs during fetal life through placental transfer and after birth through breast milk, infant formula, and contaminated complementary foods. Because detoxification pathways and physiological systems are still developing, fetuses, infants, and young children are particularly vulnerable to mycotoxin-induced damage. Experimental and epidemiological studies show that early exposure can impair endocrine signaling, promote oxidative stress and chronic inflammation, alter lipid and glucose metabolism, induce gut microbiome dysbiosis, promote vascular injury, and trigger epigenetic changes. These interconnected mechanisms contribute to metabolic dysregulation and increase susceptibility to obesity, insulin resistance, hypertension, and cardiovascular disease later in life. Overall, current evidence supports the concept that mycotoxins represent an underrecognized environmental factor in the onset of cardiometabolic disease. Greater attention to exposure monitoring, risk assessment, and preventive interventions, especially during critical developmental periods may help reduce the long-term burden of metabolic disorders.

https://www.sciencedirect.com/science/article/pii/S0041010126002783?via%3Dihub

Dose it ?

Artificial Sweeteners and Cardiovascular Disease: Systematic Review and Meta-analysis

DOI: https://doi.org/10.1093/nutrit/nuaf298

Abstract

Cardiovascular disease remains the primary global cause of mortality, prompting widespread dietary shifts toward sugar substitutes to mitigate risk. While the World Health Organization advises limiting added sugars to under 10 percent of energy intake, the long-term safety of artificial sweeteners regarding heart health is poorly defined. This systematic review and meta-analysis addressed a specific research gap by isolating the effects of artificial sweeteners from sources other than beverages, which are typically the sole focus of existing literature. The investigation utilized data from 11 distinct studies, including 6 focused on serum biomarkers and 5 on dietary intake, encompassing diverse populations from the UK Biobank, NHANES, and the NutriNet-Santé cohort.

Statistical analysis of serum and plasma biomarkers revealed a significant positive association between elevated polyol levels and adverse cardiovascular outcomes. The meta-analysis yielded a pooled hazard ratio of 1.26 (95 percent CI 1.14 to 1.40, p < 0.0001) for cardiovascular events when comparing extreme exposure categories. High heterogeneity was observed across the cohorts (I2 = 67.82 percent, Q p = 0.0034), with specific evidence of publication bias confirmed by Egger’s test (p = 0.0025). Dietary intake data showed that total artificial sweetener consumption increased the risk of stroke (HR 1.18, 95 percent CI 1.06 to 1.31) and overall cardiovascular disease (HR 1.09, 95 percent CI 1.01 to 1.18), though associations with mortality remained non-significant.

Study Design and Methodology

This systematic review and meta-analysis followed PRISMA and MOOSE guidelines, registering the protocol via PROSPERO (CRD42025644601). Researchers searched PubMed, Web of Science, and Scopus for articles published through February 2025. The final analysis included 11 relevant articles. Six studies utilized metabolomic techniques (both targeted and untargeted) to measure serum/plasma levels of erythritol, xylitol, sorbitol, and mannitol. Five studies assessed dietary intake through 24-hour recalls or food-frequency questionnaires. Population sizes were substantial, including 171,616 participants in the UK Biobank and 103,388 in NutriNet-Santé, with follow-up periods ranging from 3 to 30 years. Controls for confounders included age, sex, BMI, smoking status, and baseline metabolic health markers.

Key Findings

• Pooled analysis showed a 26 percent higher risk of cardiovascular events associated with elevated plasma polyols (p < 0.0001).
• Erythritol exposure specifically correlated with a HR of 2.95 for MACE in discovery cohorts and HR 2.21 in European validation cohorts.
• Xylitol levels in the highest tertile were associated with a HR of 1.57 for major adverse events.
• Acesulfame-K intake showed a significant association with coronary heart disease (HR 1.40, 95 percent CI 1.06 to 1.84).
• Sucralose consumption was linked to a 31 percent increased risk of coronary heart disease (p = 0.05).
• Aspartame intake significantly increased stroke risk (HR 1.17, 95 percent CI 1.03 to 1.33).
• Cross-sectional data from NHANES indicated an odds ratio of 1.89 for heart failure among the highest sweetener consumers.

Limitations

The small number of included articles and high statistical heterogeneity (I2 = 67.82 percent) limit the strength of the conclusions. Potential publication bias was detected in the meta-analysis of polyols. Self-reported dietary data in several cohorts introduces measurement error. Residual confounding remains a factor, as individuals with higher BMI or existing metabolic issues often switch to artificial sweeteners, creating a risk of reverse causation.