Higher intake of high-fat cheese and high-fat cream was associated with a lower risk of all-cause dementia, whereas low-fat cheese, low-fat cream, and other dairy products showed no significant association. APOE ε4 status modified the association between high-fat cheese and AD. Our study's observational design limits causal inference.

BACKGROUND:Dementia is a growing public health concern, and although diet is a modifiable potential risk factor, the role of free sugar intake remains unclear. Excess sugar has been linked to metabolic and cardiovascular dysfunction, both associated with cognitive decline, but evidence regarding specific sugar sources is limited. OBJECTIVES:This study aimed to investigate the associations between free sugar intake, its dietary sources, and the risk of all-cause dementia, Alzheimer's disease, and vascular dementia, and to assess potential modification by apolipoprotein E (APOE) ε4 status. METHODS:We included 27,786 participants without dementia at baseline (mean age: 58 y; 61% females) from the Malmö Diet and Cancer Study, a population-based prospective cohort. Dietary intake was assessed using a validated diet history method. Dementia diagnoses were obtained from national registers and validated by memory clinic physicians. During a median follow-up of 25 y, 3224 participants (11.6%) were diagnosed with dementia. RESULTS:Free sugar intake was not significantly associated with all-cause dementia or Alzheimer's disease. However, a U-shaped association was observed for vascular dementia, with moderate intake (10%-12.5% of energy) associated with lower risk [hazard ratio (HR): 0.70; 95% confidence interval (CI): 0.52, 0.95]. Sugar-sweetened beverage intake showed no association with dementia risk. High chocolate intake was associated with lower risks of all-cause [HR for quintile 5 (Q5) compared with Q1: 0.81; 95% CI: 0.72, 0.91] and vascular dementia (HR for Q5 compared with Q1: 0.68; 95% CI: 0.50, 0.92), whereas high jam/marmalade intake was linked to a lower risk of all-cause dementia (HR: 0.86; 95% CI: 0.77, 0.97 for >10 servings per week compared with <0.5 servings per week). No significant interactions with APOE ε4 status were observed. CONCLUSIONS:Free sugar intake was not associated with overall dementia risk, but moderate intake may reduce the risk of vascular dementia. These findings suggest that future dietary guidelines for cognitive health should consider not only sugar quantity but also its food source.

The EAT-Lancet Commission introduced the planetary health diet to promote human health while reducing environmental impact. However, no study has yet examined how adherence to this diet is associated with risk of irritable bowel syndrome (IBS). This study aimed to investigate the association between the planetary health diet index (PHDI) and the risk of developing IBS. This prospective cohort study included 177,754 participants (mean age: 55.6 ± 7.93 years, 44.8

OBJECTIVES:To investigate the relation between adherence to dietary recommendations, the quantified intake of the components of these recommendations, and the risk of developing giant cell arteritis (GCA). METHODS:Participants in the Malmö Diet and Cancer Study cohort who subsequently developed GCA were identified through register linkage and validated in a structured review. Four controls, matched for age, sex, and year of inclusion, were selected per case. Diet quality was assessed using the Swedish Dietary Guidelines Score (SDGS, range 0-5). The relations for the SDGS, adherence to recommendations for each component and total intake of each component with development of GCA were assessed using logistic regression, adjusted for total energy intake, leisure-time physical activity and alcohol intake. Potential misreporters of total energy intake were excluded. RESULTS:There were 193 incident cases of GCA. High adherence to dietary guidelines (SDGS 4-5 vs 0-1) was associated with subsequent development of GCA (adjusted odds ratio 2.70; 95% CI 1.43-5.10). In adjusted models, adherence to recommended intake of added sugar, fish and shellfish and vegetables and fruit was associated with an increased risk of GCA. A reduced risk was seen with higher quantified consumption of added sugar, and an increased risk with higher intakes of fiber and fish and shellfish. CONCLUSIONS:An overall high diet quality was independently associated with an increased risk of GCA. This is compatible with the concept of an increased risk of GCA in subjects with a healthy metabolic profile, and of metabolic regulation of early disease mechanisms in GCA.

BACKGROUND:The EAT-Lancet planetary health diet emphasises plant-based foods while including moderate amounts of animal-sourced foods. Simulation-based modelling studies suggest that the diet can provide adequate micronutrients, but concerns remain about potential deficiencies as studies have used different methodologies and few have assessed nutrient intakes using both dietary and biomarker data in population-based studies. This study aimed to evaluate nutrient adequacy, defined as the ability of a diet to provide sufficient essential vitamins and minerals to meet physiological requirements, in relation to adherence to the EAT-Lancet diet and assess how methodological differences in measuring adherence impact the findings. METHODS:Data was derived from the Swedish Malmö Diet and Cancer cohort (baseline 1991-96), including 25 970 participants. Dietary intake was assessed through a validated diet history method, and nutrient intakes were calculated. Seven different EAT-Lancet diet scores were used to measure adherence. Associations with micronutrient intake and nutrient biomarkers in subgroups (folate, vitamin D, selenium, zinc, and haemoglobin) were evaluated using linear and logistic regression models. FINDINGS:Higher adherence to the EAT-Lancet diet was generally associated with nutrient intakes above recommended intake, although results varied by scoring method and modelling approach. Energy adjustment increased the likelihood of attaining nutrient adequacy, and higher adherence increased the likelihood of adequate intake for vitamin A, vitamin E, thiamine, vitamin B6, folate, vitamin C, calcium, magnesium, potassium, iron, and zinc. For nutrient biomarkers, higher adherence was linked to a reduced risk of folate deficiency, but a slightly increased risk of anaemia in women. No differences in deficiency risk were observed for selenium, zinc, or vitamin D among women, whereas men showed a slightly lower risk of vitamin D deficiency. For one score, there was a lower risk of zinc deficiency. INTERPRETATION:The EAT-Lancet diet can provide sufficient micronutrient intake without increasing deficiency risk, except for anaemia in women. Differences in outcomes between scoring methods and energy adjustment modelling highlight the need for standardised frameworks in assessing sustainable diets. FUNDING:The Swedish Heart-Lung Foundation, the Pålsson Foundation, Crafoord Foundation, the Agenda 2030 Graduate School, Lund University, the Independent Research Fund Denmark, and the Danish Diabetes Association.

Background Taurine has shown promise as a therapeutic agent for diabetic disorders, and circulating taurine concentration has consistently been lower in individuals with type 2 diabetes (T2D). However, it is unclear whether higher habitual taurine intake or plasma taurine concentration is associated with a lower risk of developing T2D. Objective To investigate associations of habitual taurine intake, its food source, and plasma taurine concentration with risk of incident T2D. Methods This prospective study included 23,456 individuals without diabetes from the Chinese Tianjin Chronic Low-grade Systemic Inflammation and Health (TCLSIH) cohort and 24,241 individuals without diabetes from the Swedish Malmö Diet and Cancer (MDC) cohort. Habitual taurine intake was assessed using a validated food frequency questionnaire in the TCLSIH cohort and a modified diet history method in the MDC cohort. Plasma taurine concentration was measured in a subsample of the MDC cohort. Incident T2D was identified through medical examinations and physician diagnoses in the TCLSIH cohort, and via registry linkage and rescreening in the MDC cohort. Multivariable Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results Over a median follow-up of 4.2 years (TCLSIH) and 24.6 years (MDC), 757 and 4,161 participants developed T2D, respectively. The fully adjusted HRs (95% CIs) for incident T2D comparing extreme quartiles of absolute taurine intake were 0.96 (0.73, 1.25) in the TCLSIH cohort and 1.08 (0.96, 1.21) in the MDC cohort. The corresponding pooled multivariable HR (95% CI) was 1.06 (0.95, 1.18). Such associations remained largely unchanged after adjusting taurine intake for total energy using both the residual and nutrient density methods. In addition, no significant association was observed for source-specific taurine and plasma taurine concentration. Conclusions Neither habitual taurine intake nor plasma taurine concentration was associated with risk of incident T2D in population-based settings.

Background: The global food system is a major contributor to climate change, accounting for about one-third of human-induced greenhouse gas emissions (GHGE). Shifting toward plant-based diets offers potential benefits for both planetary health and chronic disease prevention. However, epidemiological evidence linking dietary GHGE to health outcomes remains limited and inconsistent. Objective: To examine the associations between dietary GHGE and the risk of all-cause and cause-specific mortality, cardiovascular disease (CVD), and type 2 diabetes in a large Swedish cohort. Methods: This prospective cohort study included 22,388 adults (45–73 years) from the Malmö Diet and Cancer study. Dietary intake was assessed through a validated modified diet history method and linked to GHGE estimates using life cycle assessment data. Cox proportional hazards models were used to assess associations between GHGE and disease outcomes, adjusting for sociodemographic and lifestyle factors. Results: Over a mean follow-up of 28.5 years, 11,213 deaths, 5322 CVD cases, and 4324 diabetes cases were documented through registers. Higher GHGE were consistently associated with higher risk of diabetes (p > 0.001). For all-cause and CVD mortality, moderate positive associations were observed, particularly among participants with very high GHGE. When participants who reported substantial dietary changes prior to baseline were excluded, a significant linear association was observed for cancer mortality and CVD incidence. Conclusion: Diets with higher climate impact were associated with adverse health outcomes, especially diabetes incidence. These findings suggest that climate-friendly diets may also confer health benefits. Future studies should transparently report GHGE modelling approaches and clarify the roles of specific dietary components in improving both health and environmental outcomes.

OBJECTIVES:This nested case-control study aimed to investigate the relationship between components of the Swedish food-based dietary guidelines (SDG) from 2015 and the risk of developing rheumatoid arthritis (RA). METHODS:Data were obtained from the prospective Malmö Diet and Cancer Study (MDCS) conducted 1991-1996. Diet was assessed at baseline using a validated diet history method. Incident RA cases until 2016 were identified through register linkage, followed by a validation process through review of medical records. For each case, 4 RA-free controls, matched for age, sex, and year of inclusion in the MDCS, were selected from the cohort. Adherence to the SDG was assessed using the SDG Score (SDGS) of 5 components. Multivariable logistic regression and restricted cubic splines (RCS) were applied to analyse the relationships among the SDGS, its components, and RA. RESULTS:A total of 305 incident RA cases (67% rheumatoid factor/anti-cyclic citrullinated peptide positive) were identified. Recommended intakes of vegetables and fruits (>400 g/day) and red and processed meat (<500 g/week) were associated with lower risks of RA, with multivariable-adjusted odds ratios of 0.64 (95% CI 0.43-0.94) and 0.60 (95% CI 0.38-0.97), respectively. RCS revealed a positive linear association for total intake of red/processed meat with RA development and a negative association for vegetables and fruits. The risk was higher by quartile of red and processed meat intake for seropositive, but not seronegative RA. CONCLUSIONS:Higher intake of red/processed meat associated with a higher risk of seropositive RA, whereas vegetables and fruit may reduce the risk of RA overall.

The Paleolithic Diet Fraction (PDF) estimates the proportion of absolute dietary intake derived from food groups included in the Paleolithic diet. In the Malmö Diet and Cancer Study (MDCS), higher PDF and lower systemic low-grade chronic inflammation (SLGCI) have been associated with lower cardiometabolic morbidity and mortality. We examined associations between PDF and SLGCI in the MDCS. The study population (n = 23,250; 63

Preclinical studies suggest that taurine may exert neuroprotective effects. However, its relevance to dementia risk in human populations remains unclear. We investigated the associations between mid-life dietary taurine intake, circulating taurine concentrations, and the risk of late-life all-cause dementia, Alzheimer's disease (AD), and vascular dementia (VaD) in a large prospective cohort. This study utilized data from 27 786 participants of the Malmö Diet and Cancer Study with baseline examination from 1991 to 1996. Dietary taurine intake was estimated from a detailed diet history and adjusted for energy intake. Plasma taurine concentration was measured in a subset of 3693 individuals. Dementia diagnoses were ascertained through the Swedish National Patient Register and validated by memory clinic physicians. Cox proportional hazards models assessed associations with dementia risk, adjusting for potential confounders including APOE ε4 status, lifestyle factors, and comorbidities. Over a median 25-year follow-up, 3224 participants developed dementia. No significant associations were found between dietary taurine intake or plasma taurine concentrations and the risk of all-cause dementia, AD, or VaD. Circulating taurine concentrations were only weakly correlated with dietary intake, suggesting a predominant role of endogenous taurine synthesis and metabolism. Our findings fail to support a protective role for taurine intake against dementia in humans. Further studies are warranted to examine potential effects under specific pathological conditions or with high-dose supplementation.

BACKGROUND:The impact of the environmentally sustainable EAT-Lancet diet on dementia risk remains poorly understood. The aim was to investigate associations between the EAT-Lancet diet and incident dementia. METHODS:Associations of the EAT-Lancet diet with all-cause dementia, Alzheimer's disease (AD), and vascular dementia (VaD) were investigated among 25,898 participants from the Malmö Diet and Cancer study, Sweden. Participants aged 45-73 years were recruited for the baseline examination between 1991 and 1996, and the mean follow-up time was 18 years. To assess robustness of estimations, we used seven previously constructed EAT-Lancet diet scores. Multi-adjusted Cox proportional hazard analyses were performed, with results presented per 10 % in increment scores. Additionally, we explored the potentially modifying effect of APOE ε4 status in this context. RESULTS:With one of the scores, higher adherence to the EAT-Lancet diet was associated with a reduced risk of AD and all-cause dementia. Moreover, the results suggest an interplay between the EAT-Lancet diet and APOE ε4 status. A risk-reducing effect was observed among APOE ε4 non-carriers with three of the scores in relation to AD, and with five of the scores in relation to all-cause dementia. No associations were observed among APOE ε4 carriers, or in relation to VaD. CONCLUSION:The results indicate a risk reducing effect of adhering to the EAT-Lancet diet among APOE ε4 non-carriers, and no negative effects on dementia risk were detected. Future studies should consider the potentially modifying effect of APOE ε4 status, and the implications of methodological differences in measuring adherence to the EAT-Lancet diet.

BACKGROUND:The evidence linking sugar intake to cardiovascular disease risk remains largely inconclusive, with variations observed across different subgroups of sugar intake. In addition, studies on genetic markers of sugar intake are scarce, especially for different sugar subgroups. OBJECTIVE:This genome-wide association study (GWAS) aimed to investigate genetic variants associated with the intake of free sugars and sweet-tasting sugars (i.e., sucrose and monosaccharides) and to explore the relationship between sugar intake and cardiovascular disease risk using genetic markers. METHODS:We identified single-nucleotide polymorphisms (SNPs) associated with sugar intakes in two large cohorts: the Malmö Diet and Cancer Study (n = 25,660) and the UK Biobank (n = 141,437). We further examined whether the associations were independent of Body Mass Index (BMI), smoking status, and educational level. Finally, we investigated the genetic correlations between sugar intake and cardiovascular outcomes using data from different populations. RESULTS:For free sugar intake, GWAS-significant associations were found with SNPs in the FTO gene, in an intergenic region on chromosome 18, and near the FGF21 gene. For sweet-tasting sugar intake, the lead SNP was located near the FGF21 gene. The associations between sugar intake and the FTO SNPs were dependent on BMI, whereas this dependency was not observed for the FGF21-adjacent SNPs. Genetic correlations were found between both free sugar intake and sweet-tasting sugar intake and lower HDL cholesterol levels and heart failure risk, as well as higher log-triglyceride levels and risks of ischemic stroke and atrial fibrillation. CONCLUSION:The findings of this study indicate associations mainly between SNPs near the FGF21 gene and the FTO gene and both free and sweet-tasting sugar intake. Genetic correlations were found between both free sugar intake and sweet-tasting sugar intake and lower HDL cholesterol levels and heart failure risk, as well as higher triglyceride levels and risks of ischemic stroke and atrial fibrillation.

AIMS:Diet is a determinant of cardiovascular diseases (CVD) with coronary disease as predominant cause of pre-mature death. To analyse how diet was associated with coronary atherosclerosis, including plaque features. METHODS AND RESULTS:The cross-sectional population-based study using data from the Swedish CArdioPulmonary BioImage Study (SCAPIS) included 24 079 adults aged 50-64 years, recruited in 2013 to 2018 who were free of clinical cardiovascular disease. The recruitment and comprehensive examinations were conducted at six locations in Sweden. A dietary index (DI) based on a previously published anti-inflammatory DI including high proportion of plant-based foods, and low in red or processed meat and sugar-sweetened beverages was constructed. The reference group was within lowest DI tertile. Coronary atherosclerosis assessed by coronary computed tomography angiography, including any-, significant-, and adverse or high-risk coronary plaque, which is non-calcified with a significant stenosis ≥50%. Lowest, compared to highest DI tertile was associated with younger age, more often men (62.2% vs. 32.9%), higher high-sensitive C-reactive protein, more cardiometabolic risk and smokers, higher alcohol-, and higher energy-intake. In the highest and lowest tertile, coronary plaques were present in 36.3% and 44.3%, respectively, stenosis ≥ 50% in 3.7% and 6.0%. Non-calcified coronary plaques with stenosis ≥50% were present in 0.9% and 1.5% in highest and lowest tertiles. In multivariable analyses, the lowest tertile of DI was associated with high-risk plaque features after adjusting for age, sex, smoking, with waist circumference, triglycerides (TGs), and hypertension as possible mediators. CONCLUSION:A low-fibre diet with high red meat content was associated with high-risk plaques features, increased coronary calcification and significant stenosis. Waist circumference, TGs, and hypertension emerged as potential mediators of these associations, underscoring the role of metabolic and hemodynamic factors in the dietary impact on coronary atherosclerosis. Our findings strengthen the importance of cardioprotective dietary recommendations.

Purpose Adding salt to foods, a novel indicator for studying habitual sodium intake, has been positively associated with multiple diseases and mortality. However, little is known about its association with liver-related disorders. This study aimed to investigate the associations of adding salt to foods with risks of metabolic dysfunction-associated steatotic liver disease (MASLD), cirrhosis, and hepatocellular carcinoma (HCC). Methods This prospective cohort study included 492,265 participants from the UK Biobank without prevalent liver diseases at baseline. The frequency of adding salt to foods was collected using a self-reported question, and incident liver-related disorders were identified through electronic health records. Multivariable Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the outcomes. Results Over a median follow-up of 13 years, 7,005 incident MASLD cases, 5,546 cirrhosis cases, and 413 HCC cases occurred. After adjusting for sociodemographic characteristics, lifestyle factors, personal history of diseases, and diet factors, the HRs (95% CIs) of MASLD across the increasing frequency of adding salt to foods were 1.00 (reference) for never/rarely, 1.08 (1.02, 1.14) for sometimes, 1.22 (1.13, 1.31) for usually, and 1.40 (1.27, 1.53) for always, with a P for trend < 0.0001. Such association was partly driven by adiposity. Also, similar positive associations were observed for cirrhosis and HCC. Conclusions A higher frequency of adding salt to foods was associated with increased risks of MASLD, cirrhosis, and HCC. Reducing adding salt to foods at the table could be included in public health initiatives to promote liver health.

BACKGROUND:Whether dairy intake is related to type 2 diabetes (T2D) remains unclear, as does potential metabolic mechanisms for this association. OBJECTIVES:We aimed to examine the association between high dairy intake and risk of T2D and identify plasma metabolites reflecting dairy intake. METHODS:This prospective cohort study included 26,461 Swedish individuals recruited between 1991 and 1996 and followed up until 31 December, 2020, with available data on dairy intake at baseline and linked registers. Plasma metabolites were measured in a subsample (n = 893) using mass spectrometry. Associations of dairy intake with risk of T2D were assessed using Cox proportional hazards models, with results presented as hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS:A total of 4552 new-onset incident T2D cases were documented during a median follow-up of 24.3 y. Increased risk of T2D was observed among participants consuming high nonfermented milk (>1000 g/d compared with <200 g/d; HR: 1.40; 95% CI: 1.12, 1.74) and cheese (>100 g/d compared with <20 g/d; HR: 1.23; 95% CI: 1.07, 1.41), although decreased risk of T2D was observed among those with high fermented milk (>300 g/d compared with 0 g/d; HR: 0.88; 95% CI: 0.74, 1.03), cream (>50 g/d compared with <10 g/d; HR: 0.77; 95% CI: 0.64, 0.92), and butter (>50 g/d compared with 0 g/d; HR: 0.82; 95% CI: 0.71, 0.94). Such associations were slightly attenuated after additional adjustment for BMI. In addition, we identified metabolite profiles for nonfermented milk (n = 45), fermented milk (n = 48), cheese (n = 12), cream (n = 27), and butter (n = 46); no overlap between metabolites was found. CONCLUSIONS:In this cohort of Swedish adults, high intakes of nonfermented milk and cheese are positively associated with risk of T2D, although high intakes of fermented milk, cream, and butter are inversely associated. Metabolomics provides novel insights into understanding the metabolic pathways of these associations.

BACKGROUND:Human diets account for 30% of greenhouse gas emissions (GHGE). Reporting dietary GHGE with or without energy standardization yields different outcomes, often resulting in conflicting conclusions regarding associations with micronutrient intake. OBJECTIVES:This study aims to compare methods of reporting dietary GHGE, with and without consideration of energy intake, and their respective associations with micronutrient intake. METHODS:Data were sourced from the Malmö Diet and Cancer Study, a cohort involving 25,970 participants. GHGE were estimated based on life cycle assessment data. The study explores different methods of reporting dietary climate impact: GHGE per day, GHGE per 1000 kcal, and with different energy adjustments. Association with micronutrient intake was modeled as daily intake and per 1000 kcal using linear regression models. RESULTS:Diets with higher GHGE per day were associated with a higher daily intake of all 17 examined micronutrients. When energy was included in the model, the results for GHGE per 1000 kcal aligned well with those for GHGE per day. However, using GHGE per 1000 kcal generally showed that higher GHGE were linked to lower daily micronutrient intake. Different methods of adjusting for energy intake yielded estimates with varying directions and magnitudes of associations. CONCLUSIONS:This study highlights the implications of energy intake when assessing the impact of dietary GHGE and demonstrates that the choice of GHGE modeling approach might have important consequences for the results and interpretation. The method of choice for modeling dietary GHGE in relation to micronutrient intake needs to be carefully considered in future studies.