The EAT-Lancet Diet Index, Plasma Proteins, and Risk of Heart Failure in a Population-Based Cohort.

BACKGROUND: The landmark EAT-Lancet Commission proposed that a planetary health diet is comprised mainly of plant-based foods. However, studies examining whether this diet is associated with heart failure (HF) are currently lacking. In addition, the potential proteomics mechanism on the association between diet and HF warrants further elucidation. OBJECTIVES: This study aims to both examine the association between the EAT-Lancet diet index and risk of HF and identify plasma proteins underlying such an association. METHODS: This prospective cohort study included 23,260 participants. HF cases during the follow-up were identified through the Swedish national register. An EAT-Lancet diet index (score range: 0-42) was created to assess adherence to the EAT-Lancet reference diet. In a subcohort (n = 4,742), fasting plasma proteins were quantified. RESULTS: During a median follow-up of 25.0 years, 1,768 incident HF cases were documented. After adjusting for sociodemographic, lifestyle, diabetes, hypertension, use of lipid-lowering drugs, and body mass index, the HR per 3-point increase of the EAT-Lancet diet index was 0.93 (95% CI: 0.88-0.97). This association was robust in several sensitivity analyses. Among the included 136 plasma proteins, a total of 8 proteins (AM, GDF15, IL6, TIM, CTSD, CCL20, FS, and FUR) were both inversely associated with the EAT-Lancet diet index and positively associated with risk of HF; the overall proteomic score mediated 9.4% (95% CI: 2.2%-32.1%) of the association. CONCLUSIONS: Higher adherence to the EAT-Lancet diet was associated with a lower risk of HF. The identified eight plasma proteins provide information on potential pathways mediating such an association.

Clusters of carbohydrate-rich foods and associations with type 2 diabetes incidence: a prospective cohort study.

BACKGROUND: About one in ten adults are living with diabetes worldwide. Intake of carbohydrates and carbohydrate-rich foods are often identified as modifiable risk factors for incident type 2 diabetes. However, strong correlation between food variables can make it difficult to identify true associations. The purpose of this study was to identify clusters of carbohydrate-rich foods and analyse their associations with type 2 diabetes incidence in the Malmö Diet and Cancer Study cohort in southern Sweden. METHODS: Dietary intake of 26 622 participants was assessed using a validated three-part diet history method: a 7-day food diary, a 168-item food frequency questionnaire, and a 60-minute interview. K-means clustering analysis identified five clusters from 21 food variables. The Cox proportional hazard regression model was applied to calculate hazard ratios (HR) and 95% confidence intervals (CI) of the association between clusters and incident type 2 diabetes. RESULTS: The cluster analysis resulted in five clusters; high vegetables/low added sugar, high sugar-sweetened beverages, high juice, high fruit, and high refined carbohydrates/low fruit & vegetables (reference). During mean follow-up of 18 years, 4046 type 2 diabetes cases were identified. After adjustment for potential confounding (including lifestyle, body mass index, and diet), a high fruit cluster (HR 0.86; 95% CI 0.78, 0.94) was inversely associated with type 2 diabetes compared to the reference cluster. No other significant associations were identified. CONCLUSIONS: A dietary pattern defined by a high intake of fruits was associated with a lower incidence of type 2 diabetes. The findings provide additional evidence of a potential protective effect from fruit intake in reducing type 2 diabetes risk. Future studies are needed to explore this association further.

The EAT-Lancet diet, genetic susceptibility and risk of atrial fibrillation in a population-based cohort.

BACKGROUND: The EAT-Lancet Commission proposed a global reference diet with both human health benefits and environmental sustainability in 2019. However, evidence regarding the association of such a diet with the risk of atrial fibrillation (AF) is lacking. In addition, whether the genetic risk of AF can modify the effect of diet on AF remains unclear. This study aimed to assess the association of the EAT-Lancet diet with the risk of incident AF and examine the interaction between the EAT-Lancet diet and genetic susceptibility of AF. METHODS: This prospective study included 24,713 Swedish adults who were free of AF, coronary events, and stroke at baseline. Dietary habits were estimated with a modified diet history method, and an EAT-Lancet diet index was constructed to measure the EAT-Lancet reference diet. A weighted genetic risk score was constructed using 134 variants associated with AF. Cox proportional hazards regression models were applied to estimate the hazard ratio (HR) and 95% confidence interval (CI). RESULTS: During a median follow-up of 22.9 years, 4617 (18.7%) participants were diagnosed with AF. The multivariable HR (95% CI) of AF for the highest versus the lowest group for the EAT-Lancet diet index was 0.84 (0.73, 0.98) (P for trend < 0.01). The HR (95% CI) of AF per one SD increment of the EAT-Lancet diet index for high genetic risk was 0.92 (0.87, 0.98) (P for interaction = 0.15). CONCLUSIONS: Greater adherence to the EAT-Lancet diet index was significantly associated with a lower risk of incident AF. Such association tended to be stronger in participants with higher genetic risk, though gene-diet interaction was not significant.

Adherence to the EAT-Lancet diet and risk of coronary events in the Malmö Diet and Cancer cohort study.

BACKGROUND: The EAT-Lancet Commission proposed a globally environmentally sustainable dietary pattern featuring mainly plant-based foods in 2019. However, evidence on this dietary pattern in preventing coronary events is minimal. OBJECTIVES: We aimed to examine the association between the EAT-Lancet diet and risk of coronary events. METHODS: The Malmö Diet and Cancer cohort study (recruited between 1991 and 1996) included 23,877 participants aged 44.5-73.6 y (62.5% women) without CVDs and diabetes at baseline. A modified diet history was used to collect the dietary data. An EAT-Lancet diet index (range, 0-42 points) was applied on the basis of 14 food components scored 0 (nonadherence) to 3 (adherence). Coronary events were extracted from the registers. Cox proportional hazards models were used to estimate the HRs and 95% confidential intervals (CIs). RESULTS: Over a median of 24.9 y of follow-up, 3031 coronary events occurred (incidence rate: 5.89/1000 person-years). After adjusting for age, sex, dietary assessment methods, season, total energy intake, leisure-time physical activity, alcohol consumption, smoking status, educational level, and BMI, the multivariable HR (95% CI) for coronary events among participants who had the highest adherence to the EAT-Lancet diet index (≥23 points, 8.1%) was 0.80 (0.67, 0.96) compared with those who had the lowest adherence (≤13 points, 9.7%) (P-trend = 0.01 across 5 groups of the EAT-Lancet diet). The inverse association was consistent in men and women and was robust after excluding those with misreported energy and significant diet changes or excluding coronary events occurred within the first 2 y of follow-up. CONCLUSIONS: Our data indicate that adherence to the EAT-Lancet diet was associated with a lower risk of coronary events.

Adherence to the EAT-Lancet diet, genetic susceptibility, and risk of type 2 diabetes in Swedish adults.

BACKGROUND AND AIMS: In 2019, the EAT-Lancet Commission proposed a mainly plant-based diet that nurtures human health and supports environmental sustainability. However, its association with type 2 diabetes (T2D) has not been widely studied, and it remains unclear whether genetic susceptibility for T2D can modify this association. The aim was therefore to investigate the association between the EAT-Lancet diet and risk of T2D and assess whether the association differs by the genetic predisposition to T2D. METHODS: A total of 24,494 participants from the Malmö Diet and Cancer study were analyzed. Dietary intake was assessed using a modified diet history methodology, and an EAT-Lancet diet index (range from 0 to 42 points) was constructed based on the EAT-Lancet reference diet. National and local registers were used to identify T2D cases during follow-up. Cox proportional hazards regression model was applied to estimate the association between the EAT-Lancet diet index and risk of T2D. Genetic predisposition to T2D was captured based on 116 single nucleotide polymorphisms. RESULTS: During a median of 24.3 years of follow-up, 4197 (17.1 %) T2D cases were documented. Compared with those with the lowest adherence to the EAT-Lancet diet (≤13 points), participants who had the highest adherence (≥23 points) showed an 18 % (95 % CI: 4 %-30 %) lower risk of T2D (P for trend <0.01). There was no significant multiplicative interaction between genetic predisposition to T2D and the EAT-Lancet diet index (P = 0.59). Also, no significant additive interaction between the genetic risk and the EAT-Lancet diet was seen (P = 0.44). The highest risk was observed among the 22.9 % of the individuals with high genetic risk and low EAT-Lancet diet score (HR = 1.79; 95 % CI: 1.63, 1.96). CONCLUSIONS: Our findings indicate that high adherence to the EAT-Lancet diet was associated with decreased risk of incident T2D among people with different genetic risks.

Development of an EAT-Lancet index and its relation to mortality in a Swedish population.

BACKGROUND: Current global food systems threaten human health and environmental sustainability. In 2019, the EAT-Lancet Commission on healthy diets from sustainable food systems defined the first global reference diet to improve both areas, but there is no consensus on how to quantify the EAT-Lancet reference diet as a diet index, and its relation to mortality has not been widely studied. OBJECTIVES: We sought to develop a new dietary index to quantify adherence to the EAT-Lancet diet and assess its association with mortality in a large, population-based Swedish cohort. We also examined food components included in the index and their individual associations with mortality. METHODS: We used the Malmö Diet and Cancer cohort (n = 22,421; 45-73 years old at baseline). Dietary data were collected using a modified diet history method. The EAT-Lancet index was developed based on intake levels and reference intervals of 14 food components defined in the EAT-Lancet diet (0-3 points per component; 0-42 points in total). Associations with mortality were examined based on registers during a mean of 20 years of follow-up and were adjusted for potential confounders. RESULTS: Divided into 5 adherence groups, the highest adherence to the EAT-Lancet diet (≥23 points) was associated with lower all-cause mortality (HR, 0.75; 95% CI, 0.67-0.85), cancer mortality (HR, 0.76; 95% CI, 0.63-0.92), and cardiovascular mortality (HR, 0.68; 95% CI, 0.54-0.84) than the lowest adherence (≤13 points). Several food components included in the index contributed to the observed reductions in mortality. CONCLUSIONS: We developed a new dietary index to investigate adherence to the EAT-Lancet diet. The findings indicate a 25% lower risk of mortality among those with the highest adherence to the EAT-Lancet diet, as defined using our index, which adds to the evidence base for the development of sustainable dietary guidelines.

Co-benefits from sustainable dietary shifts for population and environmental health: an assessment from a large European cohort study.

BACKGROUND: Unhealthy diets, the rise of non-communicable diseases, and the declining health of the planet are highly intertwined, where food production and consumption are major drivers of increases in greenhouse gas emissions, substantial land use, and adverse health such as cancer and mortality. To assess the potential co-benefits from shifting to more sustainable diets, we aimed to investigate the associations of dietary greenhouse gas emissions and land use with all-cause and cause-specific mortality and cancer incidence rates. METHODS: Using data from 443 991 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, a multicentre prospective cohort, we estimated associations between dietary contributions to greenhouse gas emissions and land use and all-cause and cause-specific mortality and incident cancers using Cox proportional hazards regression models. The main exposures were modelled as quartiles. Co-benefits, encompassing the potential effects of alternative diets on all-cause mortality and cancer and potential reductions in greenhouse gas emissions and land use, were estimated with counterfactual attributable fraction intervention models, simulating potential effects of dietary shifts based on the EAT-Lancet reference diet. FINDINGS: In the pooled analysis, there was an association between levels of dietary greenhouse gas emissions and all-cause mortality (adjusted hazard ratio [HR] 1·13 [95% CI 1·10-1·16]) and between land use and all-cause mortality (1·18 [1·15-1·21]) when comparing the fourth quartile to the first quartile. Similar associations were observed for cause-specific mortality. Associations were also observed between all-cause cancer incidence rates and greenhouse gas emissions, when comparing the fourth quartile to the first quartile (adjusted HR 1·11 [95% CI 1·09-1·14]) and between all-cause cancer incidence rates and land use (1·13 [1·10-1·15]); however, estimates differed by cancer type. Through counterfactual attributable fraction modelling of shifts in levels of adherence to the EAT-Lancet diet, we estimated that up to 19-63% of deaths and up to 10-39% of cancers could be prevented, in a 20-year risk period, by different levels of adherence to the EAT-Lancet reference diet. Additionally, switching from lower adherence to the EAT-Lancet reference diet to higher adherence could potentially reduce food-associated greenhouse gas emissions up to 50% and land use up to 62%. INTERPRETATION: Our results indicate that shifts towards universally sustainable diets could lead to co-benefits, such as minimising diet-related greenhouse gas emissions and land use, reducing the environmental footprint, aiding in climate change mitigation, and improving population health. FUNDING: European Commission (DG-SANCO), the International Agency for Research on Cancer (IARC), MRC Early Career Fellowship (MR/M501669/1).

Computer-Based Training in Eating and Nutrition Facilitates Person-Centered Hospital Care: A Group Concept Mapping Study.

Studies have shown that computer-based training in eating and nutrition for hospital nursing staff increased the likelihood that patients at risk of undernutrition would receive nutritional interventions. This article seeks to provide understanding from the perspective of nursing staff of conceptually important areas for computer-based nutritional training, and their relative importance to nutritional care, following completion of the training. Group concept mapping, an integrated qualitative and quantitative methodology, was used to conceptualize important factors relating to the training experiences through four focus groups (n = 43), statement sorting (n = 38), and importance rating (n = 32), followed by multidimensional scaling and cluster analysis. Sorting of 38 statements yielded four clusters. These clusters (number of statements) were as follows: personal competence and development (10), practice close care development (10), patient safety (9), and awareness about the nutrition care process (9). First and second clusters represented "the learning organization," and third and fourth represented "quality improvement." These findings provide a conceptual basis for understanding the importance of training in eating and nutrition, which contributes to a learning organization and quality improvement, and can be linked to and facilitates person-centered nutritional care and patient safety.

Long-term effects of a computer-based nutritional training program for inpatient hospital care.

RATIONALE: A previous short-term study showed that a computer-based training in eating and nutrition increased the probability for hospital inpatients at undernutrition (UN) risk to receive nutritional treatment and care without increasing overtreatment (providing nutritional treatment to those not at UN risk). The aim of this study was to investigate if a computer-based training in eating and nutrition influences the precision in nutritional treatment and care in a longer-term perspective. METHOD: A preintervention and postintervention study was conducted with a cross-sectional design at each time points (baseline and 7 months postintervention). Hospital inpatients >18 years old at baseline (2013; n = 201) and follow-up (2014; n = 209) were included. A computer-based training was implemented during a period of 3 months with 297 (84%) participating registered nurses and nurse assistants. Undernutrition risk was screened for using the minimal eating observation and nutrition form-version II. Nutritional treatment and care was recorded using a standardized protocol. RESULTS: The share of patients at UN risk that received energy-dense food (+25.2%) and dietician consultations (+22.3%) increased between baseline and follow-up, while fewer received oral nutritional supplements (-18.9%). "Overtreatment" (providing nutritional treatment to those not at UN risk) did not change between baseline and follow-up. CONCLUSION: The computer-based training increased the provision of energy-dense food and dietician consultations to patients at UN risk without increasing overtreatment of patients without UN risk.

Short-term effects of a computer-based nutritional nursing training program for inpatient hospital care.

RATIONALE: This study aimed to explore whether a computer-based training in eating and nutrition for hospital nursing staff can influence the precision in nutritional treatment and care. METHOD: A pre-intervention and post-intervention study was conducted with a cross-sectional design at each time point. The settings were one intervention (IH) and two control hospitals (CH1 and CH2). Hospital inpatients >18 years old at baseline (2012; n = 409) and follow-up (2014; n = 456) were included. The computer-based training was implemented during a period of 3 months in the IH with 297 (84%) participating registered nurses and nurse assistants. Nutritional risk was screened for using the Minimal Eating Observation and Nutrition Form. Nutritional treatment and care was recorded using a standardized protocol RESULTS: In the IH, there was an increase in the share of patients at UN risk that received energy-dense food (+16.7%) and dietician consultations (+17.3%) between baseline and follow-up, while fewer received feeding assistance (-16.2%). There was an increase in the share of patients at UN risk that received energy-dense food (+19.5%), a decrease in oral nutritional supplements (-30.5%) and food-registrations (-30.6%) in CH1, whereas there were no changes in CH2. 'Overtreatment' (providing nutritional treatment to those not at UN risk) was significantly higher in CH2 (52.7%) than in CH1 (14.3%) and in the IH (25.2%) at follow-up. CONCLUSION: The computer-based training seemed to increase the probability for patients at UN risk in the IH to receive nutritional treatment without increasing overtreatment.