Psoriasis has been linked to various diet-related comorbidities such as metabolic syndrome, type 2 diabetes, and cardiovascular disease(1). Evidence for the role of diet in the management of psoriasis and its comorbidities is lacking, and there is no dietary guidance for people with psoriasis. This study aimed to characterise the dietary patterns and quality by adherence to the UK Eatwell guide and a Mediterranean-style diet in UK individuals living with psoriasis and assessed associations between diet quality and risk of psoriasis comorbidities, psoriasis severity and cardiometabolic risk markers.

Using the UK Biobank cohort, we identified 2,615 patients with psoriasis by self-report or health records at baseline, with a comparison group of 122,572 non-psoriasis participants who have valid dietary data. The dietary intake was assessed through online 24h-recalls (Oxford WebQ) conducted every 3-4 months over one year. The average nutrient and food groups intake were calculated from at least 2 recalls to determine adherence to the UK Eatwell Guide (Eatwell Score, range: 0-9(2)) and the Mediterranean-style diet (alternative Mediterranean diet (aMED) score(3), range: 0-9). Associations between diet quality and the risk of 13 selected comorbidities, psoriasis severity (assumed from treatment type), and cardiometabolic risk markers were evaluated using multivariate regression models, adjusted for confounders including age, sex, Townsend deprivation factor, physical activity levels, smoking, alcohol, supplement use and the reporting source of psoriasis.

Both psoriasis and non-psoriasis groups showed similar average scores for Eatwell (3.9±1.7 for both groups) and aMED (3.6±1.8 and 3.3±1.7, respectively). Higher Eatwell scores were associated with a 15% reduced risk of myocardial infarction (OR = 0.85, 95%CI: 0.74−0.98, P = 0.025) and 23% increased risk of osteoporosis (OR = 1.23, 95% CI: 1.05-1.45, P = 0.010) in participants with psoriasis. Additionally, higher Eatwell scores were associated with lower BMI (StdBeta, adjusted P: −0.049, 0.013) and improved plasma lipid profiles (cholesterol: −0.058, 0.004; LDL: −0.068, 0.001; triglycerides: −0.076, <0.001). A higher aMED score is positively associated with better plasma lipid profiles (cholesterol −0.051, 0.012; LDL −0.051, 0.012) in individuals with psoriasis fully adjusted. No significant association was found between diet quality and psoriasis severity. However, participants with the highest severity (on systemic treatment) had a 34% lower chance of meeting guidelines for fruit and vegetable intakes (5 servings/day) compared with those on no treatment or topical treatment only (OR = 0.66, 95% CI: 0.46−0.95, P = 0.024).

Our findings suggest that higher dietary quality is associated with a reduced risk of certain cardiometabolic diseases in people with psoriasis, emphasising the importance of dietary management in this population. Longitudinal and intervention studies are needed to further explore the role of diet in psoriasis and its associated health outcomes.

Psoriasis is a chronic inflammatory skin condition arising from gene-environment interactions(1). The role of diet in individuals living with psoriasis is poorly understood with research to date confined to relationships with Mediterranean diet adherence in southern European populations(2). Studies are yet to explore the role of dietary patterns in relation to psoriasis severity within a UKbased population. The Asking People with Psoriasis about Lifestyle and Eating (APPLE) study investigated associations between four diet quality indices and psoriasis severity, hypothesising that individuals with more severe psoriasis would report lower diet quality scores.

The APPLE study is an online cross-sectional study (King’s College London Research Ethics Committee LRS/DP-21/22-29257; NCT05448352). Eligible participants included adults residing in the UK with diagnosed psoriasis. Participants were recruited using social media (June 2022January 2024). Validated questionnaires were used to evaluate: 1) psoriasis severity, by the selfassessed simplified psoriasis index, and 2) diet quality, using a 147-item food frequency questionnaire (FFQ) to calculate the Mediterranean Diet Score (MDS), the Dietary Approaches to Stop Hypertension (DASH) score, the Healthy Diet Score (HDS) and the Plant-based Diet Indices (PDIs). Diet-psoriasis associations were adjusted for age, sex, smoking status, energy intake, alcohol use, anxiety/depression diagnosis, and body mass index (BMI)

A total of 270 participants completed the study, of which 82% were female, 85% of White-British ethnicity, with a median (interquartile range (IQR)) age of 40 years (20.0), and a median BMI of 25 kg/m2 (8.2). Univariate regression analyses revealed significant negative associations between the HDS, DASH, healthy PDI, original PDI and MDS and psoriasis severity following adjustment for all covariates except BMI (β =−0.179 to −0.254, P<0.05). Only the HDS remained statistically associated with psoriasis severity when adjusted including BMI (β = −0.152, P<0.05). Stepwise multiple linear regressions identified meat and poultry from the MDS as predictors for psoriasis severity (β =0.158, P<0.05), whilst fruits and nuts (β =−0.140, P<0.05) and legumes (β =−0.130, P<0.05) were negatively associated with disease severity.

Participants with lower diet quality scores report more severe psoriasis, with meat/poultry and fruit/nuts revealed as key dietary components that merit further investigation. Previous findings showed that olive oil and fish were independent predictors for psoriasis severity in a smaller Italian sample population(3), which were not replicated in this population, possibly due to very low fish intakes in the UK population(4).

This study contributes to the evidence examining the diet-psoriasis relationships. Randomised controlled trials are required to evaluate causal inferences in relation to the effect of dietary patterns on psoriasis severity.

Psoriasis is a chronic dermatological disease often linked with systemic conditions such as cardiovascular disease, obesity, and type 2 diabetes(1). Unlike many other systemic diseases, psoriasis lacks specific dietary recommendations for its management(2). To develop evidencebased dietary advice, profiling dietary intakes in this population group is paramount. As part of the Asking People with Psoriasis about Lifestyle and Eating (APPLE) study, we aimed to quantify macronutrient intakes and their food group sources and assess associations with psoriasis severity.

The APPLE study is a web-based cross-sectional survey recruiting UK-based adult volunteers with psoriasis (King’s College London Research Ethics Committee LRS/DP-21/22-29257; NCT05448352). Recruitment was between June 2022 and January 2024 through social media. Participants self-reported age, weight, height, and alcohol use, depression or anxiety diagnosis, as well as psoriasis severity by responding to the self-assessed Simplified Psoriasis Index (possible score range 0-70 points). Diet was self-reported with a validated 147-item food frequency questionnaire. Nutritional composition was determined using the Composition of Food Integrated Dataset(3).Linear models tested associations between food groups sources and psoriasis severity.

The final sample (n = 270) primarily constituted mid-life (median (IQR) 40 (20) years), White-British (85%), female participants (82%) with psoriasis, of which 51% were living with overweight or obesity. Protein intake from animal sources (processed meat, poultry, and red meat) was significantly positively associated with psoriasis severity, adjusted for age, gender, smoking, alcohol use, energy intake, and diagnosed depression/anxiety (β between 0.133 and 0.225, P<0.05). Plant-based (excluding tree nuts) and tree nut sources of protein were inversely associated with psoriasis severity (adjusted β between −0.145 and −0.131, P<0.05). Protein from red meat and plant-based protein remained significantly associated with psoriasis when adjusting for BMI. Poultry and processed meat sources of n-6 polyunsaturated fatty acids were also positively associated with psoriasis severity (βbetween 0.125 and 0.133, P<0.05), whilst tree-nut sources were inversely associated with disease severity (β =−0.144, P<0.05), but associations were no longer significant when adjusting for BMI.

Our findings highlight that associations between psoriasis severity and protein and n-6 polyunsaturated fatty acids intakes depend on their source, suggesting that healthy plant-based diets warrant further investigation by randomised controlled trials for the dietary management of psoriasis.

Psoriasis is a chronic debilitating skin disease driven by pro-inflammatory immunological pathways. Research examining the effect of micronutrient supplementation on the severity of psoriasis has extensively focused on vitamin D and magnesium, yielding conflicting findings(1). As part of the Asking People with Psoriasis about Lifestyle and Eating (APPLE) study; micronutrients intakes were estimated in people with psoriasis for comparison with Reference Nutrient Intakes (RNIs) and to examine associations with psoriasis severity.

The APPLE study was a cross-sectional internet-based survey recruiting adult volunteers with psoriasis residing in the United Kingdom (King’s College London Research Ethics Committee LRS/DP-21/22-29257; NCT05448352). Volunteers were recruited between June 2022-January 2024 through social media. Psoriasis severity and diet were self-reported with validated tools, the self-assessed Simplified Psoriasis Index and a 147-item food frequency questionnaire. Micronutrient constituents were determined using the Composition of Foods Integrated Dataset (https://www.gov.uk/government/publications/composition-of-foods-integrated-datasetcofid).

The demographic characteristics of the study population (n = 270) comprised of a White-British (88%), middle-aged (median (IQR) age of 40 (20.0) years), female majority (82%), reporting a median body mass index (BMI) of 25.8 (8.2) kg/m2. Two-thirds (66%) of both males and females reported intakes below sex-specific RNIs for calcium. Approximately 80% of both males and females reported an iodine intake below 140 µg/day and more than 90% did not meet the 10 µg/day dietary recommendation for vitamin D. Most males (93%) and females (80%) did not meet the RNI for selenium intake. Two-thirds of women aged 18-50 years reported dietary iron intakes below the RNI of 14.8 mg/day. Intakes for other vitamin and minerals met dietary requirements. Magnesium (β = −0.197, P<0.01), copper (β = −0.174, P<0.01) and iron (β = −0.127, P<0.05) were significantly inversely associated with psoriasis severity, adjusted for age, sex, smoking, alcohol use, and diagnosed depression/anxiety. These associations with psoriasis severity were no longer significant when additionally adjusted for BMI.

There is a lack of studies examining dietary mineral intakes in populations with psoriasis, although some reports suggest people with psoriasis have a lower iron and magnesium status compared with control groups(2,3). Our preliminary data suggests that dietary screening of micronutrient intakes as part of routine care may be beneficial in people with psoriasis. Additional research is warranted to explore the effects of mineral intakes and physiological mineral status in people living with psoriasis. Minerals are key regulators of cellular and immunological responses which is of relevance to population groups with underlying immune-mediated conditions such as psoriasis.

Mechanistic studies and short-term randomised trials suggest that higher intakes of dietary flavonoids may protect against non-alcoholic fatty liver disease (NAFLD)(1–3). However, little research has been conducted at a population level, and to date no long term prospective study has assessed the associations between flavonoid intakes and NAFLD risk(4). We aim to perform the first population-based study with long-term follow-up on flavonoid consumption and NAFLD incidence.

In a prospective study, we assessed the associations between flavonoid intakes based on ≥2 24hour dietary assessments and NAFLD risk among 121,563 adults aged 40 to 69 years by multivariable regression analyses. Flavonoid intakes were assessed on three levels: a novel flavodiet score (FDS), flavonoid rich foods, and flavonoid subclasses. Cox proportional hazard models were used to assess NAFLD risk, and linear trend tests were used to test for significance. Additional sensitivity analysis was conducted using both a FDS excluding red wine, and non flavonoid containing equivalent foods as negative controls.

Over 10 years of follow-up, 1090 cases of NAFLD were observed. When compared to the lowest Quartile, the highest quartile (Q4) of the Flavodiet Score (FDS) was associated with a 20% lower risk of NAFLD (HR (95%CI): 0.80 (0.66−0.96), P trend=0.02). Additionally, higher apple intake was associated with a 22% lower risk of NAFLD (HR (95%CI): 0.78 (0.66 - 0.92), P trend=<0.01), while higher tea consumption was associated with a 13% lower risk of NAFLD (HR (95%CI): 0.87 (0.73 -1.03), P trend=0.046). Of the flavonoid subclasses, we observed that higher intakes of proanthocyanidins, theaflavins and thearubigins, flavonols and flavan-3-ols were also associated with lower risk.

In a large UK cohort, we demonstrate for the first time that flavonoid-rich diets, containing approximately 6-servings of flavonoid rich food per day, are associated with lower risk of NAFLD. As such, the consumption of flavonoid-rich foods may reduce the risk of NAFLD and its sequalae among middle-aged adults.

Chronic kidney disease (CKD) is highly prevalent among people with diabetes(1,2). While identifying modifiable risk factors to prevent a decline in kidney function among those living with diabetes is pivotal, there is limited evidence on dietary risk factors for CKD. In this study we examined the associations between healthy and less healthy plant-based diets (PBDs) and the risk of CKD among those with diabetes, and to identify potential underlying mechanisms.

We conducted a prospective analysis among 7,747 UK Biobank participants with prevalent diabetes (Type 1 and Type 2). Multivariable Cox proportional hazard regression models were used to examine the associations between healthful and unhealthful plant-based indices (hPDI and uPDI) and the risk of CKD. Fruits, legumes, nuts, tea and coffee, vegetables and whole grains were classified as healthy plant-based foods, whereas fruit juice, potatoes, refined grains, sugary drinks as well as sweets and desserts were classified as unhealthy plant-based foods. Animal-based foods used for the PDIs were grouped into meat, eggs, dairy products, animal fat, seafood or fish, and miscellaneous animal-based foods. Causal mediation analyses were further employed to explore the underlying mechanisms of the observed associations.

Among 7,747 study participants with diabetes, 1,030 developed incident CKD over 10.2 years of follow-up. The mean (SD) age was 58.8 (7.2) years, 6,910 (89.2%) were White, and 3,829 (49.4%) had a BMI over ≥30kg/m2. Higher adherence to a healthy PBD was associated with a 24% lower CKD risk (HRQ4 versus Q1: 0.76 [95%CI: 0.63−0.92], ptrend=0.002), while higher adherence to an unhealthy PBD was associated with a 35% higher risk (HRQ4 versus Q1: 1.35 [95%CI: 1.11-1.65], ptrend=0.006). The observed associations were predominantly mediated by markers of body fatness (proportion mediated: 11-25%) and kidney function (23-89%).

In this prospective cohort study of UK adults with diabetes, adherence to a healthy PBD was associated with lower CKD risk, whereas adherence to an unhealthy PBD was associated with a higher CKD risk. Associations were primarily mediated by markers of lower body fatness and improved kidney function.

Carrot consumption reduces tumour development in several animal models, possibly as sources of polyacetylenes, resistant starch, carotenes or other active constituents. In a recent systematic review and meta-analysis of prospective studies(1), we showed that carrot intake measured directly or using α-carotene as a marker of carrot intake was associated with reduced risk of cancer incidence. However, since the incidence of cancers among very old people (aged 85 and over) is lower than in those aged 65 to 85(2), it is of interest to understand how carrot intake affects cancer risk across different age groups. Here we compare the results from the Newcastle 85+ study3 and a meta-analysis of prospective studies1 of older adults aged 65-85 years at baseline.

In the Newcastle 85+ study(3) (n = 387, 65% women), baseline dietary carrot intake was assessed using a multiple-pass recall tool (2×24 h recalls) and α-carotene concentration measured in plasma samples by reverse phase high-performance liquid chromatography. Cancer incidence data were ascertained from medical records, and the association between carrot intake and α-carotene and cancer risk (any type) tested using multivariable Cox proportional hazard regression models. For the meta-analysis(1), mean ±SD of the reported upper age range at baseline in 50 studies (with 52000 cases) with data on carrot intake reported directly or indirectly (as α-carotene intake) was 68 ± 12 years, and in 30 studies (9331 cases) reporting plasma concentration of α-carotene it was 69 ± 9 years.

In the Newcastle 85+ study, the summary risk ratio (RR) for cancer incidence was 0.82 (95% CI: 0.24 – 2.79, n =129 cases, 258 non-cases) for consumption of ≥ 1 vs < 1 serving/day of carrots after adjusting for key confounders. RR for cancer for the highest compared with lowest quartile of plasma α-carotene was 0.68 (0.33 –1.39). The corresponding values comparing highest versus lowest exposure groups for the younger age groups in the meta-analysis(1) were: RRs (95% CI) for carrot intake 0·90 (0·87–0·94) and 0·80 (0·72–0·89) for plasma α-carotene. For most (67 of 80) of the individual studies included in the meta-analysis, the RRs were not statistically significantly different from 1, as was the case for the Newcastle 85+ study, due to small sample size and limited duration of the dietary records. However, the similarity of the RR values from the Newcastle 85+ study with the two corresponding independent datasets in the meta-analysis means that the results do not support a difference in effect between the age groups.

The association of carrot consumption with incident cancer in the very old does not differ from younger age groups of older adults. Carrot consumption should be encouraged among the very old, and the causal mechanisms further investigated.

Carotene-rich vegetables like carrots have been consistently associated with lowered cancer risk in observational studies(1). Beta-carotene, a phytochemical found in fruits and vegetables, is known for its antioxidant properties. In rodent trials, supplementation with carrot (containing both carotenes and polyacetylenes) significantly reduced tumour numbers in the APCMin/+ mouse model(2). However, human intervention trials with pure beta-carotene showed more adverse effects than benefits(3). This study aimed to investigate the impact of beta- and alpha-carotene supplementation (without polyacetylenes) on colorectal cancer using the APCMin/+ mouse model, which spontaneously develops intestinal tumours and an enlarged liver(4).

APCMin/+ mice were fed either a daily supplement of 10mg/kg mouse of a polyacetylene-free extract from carrots containing a beta- and alpha-carotene mixture, in a dose corresponding to the beneficial carrot supplementation, or the control diet, with a very low beta-carotene content (providing approx. 0.02mg/kg mouse/day). The 8-week supplementation commenced at 5 weeks of age. Tumour quantification in the small intestines of APCMin/+ mice was performed by histology of the entire small intestine, with one slide per 0.3mm, using the H&E staining method and Imagescope software.

Supplementation with carotenes had no significant effect on the total number of tumours (≥0.5 mm), showing no discernible difference between the control (n = 6) (20.5, 95% CI [14.69, 26.31]) and treatment (n = 8) (24.5, [19.21, 29.79]) group (P = 0.237). However, the liver weight, in % of body weight, showed a significant 25% decrease in the treatment group (n = 7) (4.78 95% CI [4.45, 5.15]) compared to controls (6.42, [5.71, 7.13]) (P<0.0003), reaching a level comparable with wildtype mice (4.48, [4.13, 4.83].

These findings confirm the results from the human intervention trials by indicating that beta- and alpha-carotene do not confer any benefit for cancer prevention, while the decrease in liver weight suggests a potential beneficial effect on another aspect of liver health. Additional research is necessary to fully understand these relationships and uncover the underlying mechanisms behind these results. Specifically, beta-and alpha-carotene from carrots do not provide the reduction in tumour numbers in a mouse model of colon cancer found when feeding the corresponding dose of freeze-dried carrot. However, the carotenes significantly attenuate the liver enlargement also seen in this model.

Genetic disorders, including haemochromatosis and thalassaemia, can lead to iron overload and related adverse health outcomes, such as liver and cardiovascular disease(1,2).

Thalassaemia is one of the most common genetic blood disorders worldwide(1). It is characterized by impaired production of haemoglobin resulting in chronic anaemia. This, in turn, leads to an upregulation of dietary iron absorption causing iron overload. Standard treatment therefore includes iron chelation therapy with frequency depending on the velocity of body iron accumulation(1).

Some polyphenolic compounds have strong iron-chelating properties(3,4). We recently showed that a polyphenol supplement (PPS) consisting of grape juice extract, black tea and cocoa powder taken with an iron-rich meal or iron-fortified drink reduces iron absorption by ∼40 % in European adults with haemochromatosis(5).

Here we investigated the effect of this natural PPS on iron absorption from an iron-rich meal or iron-fortified drink in Thai adults with non-transfusion-dependent thalassaemia.

We performed a single-blind, placebo-controlled, cross-over study in 20 Thai adults with ironloading, non-transfusion-dependent thalassaemia. Each participant consumed, in partially randomized order, an iron-rich test meal (8 mg native iron) or an iron-fortified test drink (8 mg iron as FeSO4) extrinsically labelled with a stable iron isotope (2 mg 58Fe or 57Fe as ferrous sulphate [FeSO4]) with the PPS (2 mg grape juice extract, black tea and cocoa powder in equal parts) or the placebo (2 g maltodextrin). Fractional iron absorption (FIA) from each of the four test conditions was determined by measuring the incorporation of stable iron isotopes into erythrocytes using inductively coupled plasma mass spectrometry (ICP-MS)(6). Effects of treatment and matrix, as well as treatment x matrix interactions, were determined using 2-factorial repeated-measures ANCOVA.

Median (IQR) age of participants (n = 12 female; n = 8 male) was 26 (20–34) years; 12 (60 %) were alpha-thalassaemia and 8 (40 %) were beta-thalassaemia carriers. The PPS lowered FIA from the iron-rich test meal and iron-fortified test drink by 70 % and 35 %, respectively (treatment, p = 0.016; matrix, p = 0.116; treatment x matrix, p = 0.089; model adjusted for baseline haemoglobin). Median (IQR) FIA from the test meal consumed with the PPS and placebo was 0.36 (0.12–3.44) % and 1.37 (0.68–2.64) %, respectively. FIA from the test drink consumed with the PPS and placebo was 4.22 (2.42–15.3) % and 6.47 (3.00–14.0) %, respectively.

The findings from our study suggest that intake of this natural PPS alongside meals or drinks high in iron has the potential to lower iron absorption in people with non-transfusion-dependent thalassaemia. It remains to be investigated if long-term use of the PPS can reduce body iron accumulation and frequency of iron chelation therapy, as well as elicit potential cardioprotective effects, in people with non-transfusion-dependent thalassaemia.

Pernicious anaemia (PA) is characterised by vitamin B12 deficiency due to autoimmune-mediated destruction of gastric parietal cells and the consequent loss of intrinsic factor, a specific transporter for the intestinal uptake of vitamin B12. The aetiology of PA remains largely unknown, although genetic and environmental factors have been proposed to underpin the onset of PA(1). A significant proportion of PA patients exhibit iron deficiency, with approximately 50% of PA patients presenting with it before or at diagnosis and 61% subsequently, suggesting an association between the two(2). However, findings from traditional epidemiological studies are subject to confounding and reverse causality. For instance, these associations do not clarify whether iron deficiency contributes to the development of PA or is a consequence of the disease process. Given the profound prevalence of iron deficiency at diagnosis, we hypothesised that reduced iron levels may play a causal role in the onset of PA. We used a Mendelian randomisation (MR) approach to test the causal relationship between iron status and PA.

MR leverages the naturally randomised allocation of genetic variants among the population as instrumental variables to gauge the causal effect of an exposure on an outcome of interest(3). We conducted two-sample MR analyses to assess the association between genetically predicted iron levels and PA risk. We obtained genetic association data on iron status from the deCODE study(4). PA genetic association data was sourced from the R10 release of Finngen as our main analysis. The participant data consisted of 3,694 cases of PA and 393,684 controls. Our primary MR analysis method was the inverse-variance weighted approach with additional sensitivity analyses, including leave-one-out, Egger and weighted median analyses.

Four single nucleotide polymorphisms (SNPs) were strongly associated with systemic iron status and used as genetic instruments to proxy iron status in two-sample MR analyses. We found that genetically predicted higher iron status was not significantly associated with risk of PA (odds ratio per 1 standard deviation increase in serum iron: 1.12, 95% confidence interval 0.80 to 1.57, P = 0.49). Sensitivity analyses had consistent results, indicating that MR assumptions were not violated and that no single SNP drove the association.

This is the first study to test the hypothesis that iron deficiency is causally associated with an increased risk of PA. Our results show that genetically predicted lower iron levels were not associated with an increased risk of PA among individuals of Finnish ancestry. Further investigation is required to understand the manifestation of iron deficiency in PA. Iron deficiency may only be a consequence of PA due to the loss of parietal cells, which produce hydrochloric acid necessary for iron absorption. The frequent presence of iron deficiency before or at diagnosis may also reflect delays in diagnosing PA.

Adequate nutrition is important for health at all life stages with micronutrients having an important role in long term health, cognition, healthy development and ageing(1). The aim of this study was to estimate the prevalence of inadequate intakes and risk of excessive intakes of micronutrients among adults aged 19-64 years and 65 years and over, from a nationally representative sample of adults in Ireland.

Analyses were based on the National Adult Nutrition Survey II (NANS II) (2020-21) of 19-92 year olds in the Republic of Ireland (n 1000) (19-64y: 718, ≥65y: 282) (www.iuna.net). Food and beverage intake data (including nutritional supplements) were collected via two independent 24-hour telephone dietary recalls (at least 7 days apart, with each day of the week accounted for in the sampling plan). To assist with the recall, older adults (≥65years) were asked to record their foods the day before the dietary recall and all participants were provided with a photographic food atlas before the scheduled dietary recall. Nutrient intakes were estimated using Nutritics© based on UK food composition data which was updated to include recipes of composite dishes, nutritional supplements, fortified foods and generic Irish foods that were commonly consumed. Usual intakes of micronutrients were calculated via the NCI-method using SAS© Enterprise Guide. The prevalence of inadequate intakes of micronutrients (excluding energy under-reporters)(2) was estimated using estimated average requirements established by the US Institute of Medicine (IOM) (vitamin D)(3), the UK Department of Health (DOH) (thiamin, vitamin B12)(4) and the European Food Safety Authority (EFSA) (all other micronutrients)(5). The risk of excessive intake was evaluated by comparing intakes to tolerable upper intake levels (ULs) established by the US Food and Nutrition Board (vitamin C, iron)(6) and EFSA (all other micronutrients)(7).

Among those aged 19-64 years, a large proportion of adults had inadequate intakes of vitamin D (61%), vitamin C (41%), folate (37%), calcium (32%), zinc (28%), vitamin B6 (26%), riboflavin (23%), vitamin A (16%) and iron (8%; up to 14% for females). Similarly, a large proportion of adults aged 65 years and over had inadequate intakes of vitamin D (48%), vitamin C (43%), folate (36%), zinc (35%), calcium (31%), vitamin B6 (29%), riboflavin (21%), vitamin A (13%) and iron (11%; up to 13% for females).

The proportion of adults with intakes exceeding the UL was negligible for retinol, vitamins D, E, C, B6, preformed niacin, folic acid, calcium and iron (19-64y: <0.3%; ≥65y: <0.7%) and for zinc (19-64y: 2%; ≥65y: 1%).

These findings indicate that based on current dietary patterns, significant numbers of adults in Ireland have inadequate intakes of key micronutrients and highlight the need to investigate targeted dietary strategies to address these low intakes among this population group.

Fatty acids are essential molecules, which function as structural components, energy sources, and signaling mediators(1). Subcutaneous adipose tissue (SAT) is the largest fat depot and plays a crucial role in maintaining health and homeostasis(2,3). While regulation and health impacts of circulating fatty acid levels are well established, less is known about the regulation of fatty acid levels within adipose tissue itself. The aim of this study was to investigate the effect of dietary and genetic contribution to fatty acid contents in adipose tissue and identify the interaction between single nucleotide polymorphism (SNP) and diet on adipose fatty acids.

In 427 healthy female twins from TwinsUK, 18 types of fatty acids were measured in SAT biopsies alongside genotype, RNA-Seq and clinical phenotypes. Dietary intake was collected by food frequency questionnaire. The associations between dietary intake and adipose fatty acids were tested with linear mixed models, adjusting for age, smoking, physical activity, index of multiple deprivation, energy intake, and relatedness. Genome-wide association studies (GWAS) were performed adjusting for age.

The association between dietary scores, food intake, nutrient intake and fatty acid levels in adipose tissue were examined. Most dietary scores were positively correlated with polyunsaturated fatty acid (PUFA) but negatively correlated with trans-unsaturated fatty acid (TFA) (PFDR < 0.05). We highlighted the positive association between polyunsaturated margarine and fish intake and PUFA levels, as well as butter and cream intake and saturated fatty acid (SFA) levels (PFDR < 0.05). Negative associations between fresh red meat including lamb and beef, butter, and cream intake and PUFA levels in adipose tissue were observed (PFDR < 0.05). Regarding nutrient intake, PUFA, SFA, TFA, cholesterol, vitamin D, and vitamin E were correlated with fatty acid levels in adipose tissue (PFDR < 0.05). To reveal local genetic regulation of fatty acids in adipose tissue, we performed GWAS and identified 10 fatty acid-associated genetic loci across 13 fatty acids (i.e. palmitic acid/palmitoleic acid – at the SCD locus, dihomo-γ-linolenic acid/arachidonic acid at the FADS1 locus, P < 5 × 10-8). The integration of adipose gene expression data revealed the mediation effects of SCD and FADS1 expressions in the associations between FADS1 SNP and the conversion of unsaturated fatty acids. We took forward two GWAS lead SNPs (SCD SNP and FADS1 SNP) to test the SNP-by-diet interaction on adipose fatty acids. Milk intake showed SNP-by-diet interaction with FADS1 SNP for linoleic acid and docosapentaenoic acid levels (P < 0.001). The interactions between roasted potatoes/chips and FADS1

SNP were significant for dihomo-γ-linolenic acid/linoleic acid (P < 0.001).

Adipose fatty acid levels were regulated by both genetic variants and dietary intake. We found suggestive evidence for the interaction of genetic variant and diet.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major public health issue, with a recent estimated global prevalence of 30%(1). The pathogenesis of MASLD is complex, multifactorial, and incompletely understood(2). MicroRNAs (miRNAs) are small non-coding RNAs that typically inhibit gene expression as post-transcriptional regulators(3). MiRNAs are increasingly recognised for their potential as diagnostic biomarkers and therapeutic targets in liver diseases(3). The aim of this research was to consider the role of miRNAs in MASLD pathogenesis and their regulation by diet.

Liver RNA samples were extracted from male C57BL/6J mice (n = 6/group) fed for 8 weeks either a chow diet (CD) or 60% fat (high fat diet, HFD) and sent for RNA sequencing. The raw data obtained from next-generation sequencing (Novogene, Cambridge) were passed through a quality control pipeline. Differential expression analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and target predictions were performed in the R environment. Enriched GO terms were summarised and clustered by online tool Revigo. Rich factor (RF) was used to describe the intensity of dysregulated pathways, calculated as the ratio of differentially expressed genes (DEGs) to the total genes included in each pathway. MicroRNAs that targeted the DEGs were identified using two validated miRNA-mRNA interaction databases, Tarbase and miRTarbase.

A total of 1087 DEGs were found in HFD fed mice relative to CD (adjusted P<0.05) and their biological functions were examined using GO and KEGG enrichment analyses. In aggregate, significantly enriched components and functions included: small molecule metabolic processes, collagen-containing extracellular matrix and lipoprotein particles, and oxidoreductase activity. Circadian rhythm was the most enriched pathway (RF = 0.29) among 12 enriched KEGG pathways, which also included fatty acid degradation (RF = 0.21), PPAR signalling (RF = 0.16), retinol (RF = 0.17) and cholesterol metabolism (RF = 0.22) pathways. Indeed, out of the 34 genes that comprise the KEGG circadian rhythm pathway, 10 (29%) were found dysregulated by HFD, including the critical. Period genes (Per2, Per3). Further exploration in human found hsa-miR-133a-3p targets PER2 and PER3 via examination of validated miRNA-mRNA interaction databases. In addition to circadian rhythm, hsa-miR-133a-3p was found to target genes that function in macroautophagy, cold-induced thermogenesis, and insulin response pathways.

Peripheral clocks of circadian rhythm (liver, pancreas, adipose tissue and muscle) are regulated by miRNAs that contribute to the pathogenesis of MASLD through disruption of lipid metabolism and the insulin response. Future work includes the confirmation of miR-133a-3p expression and the related pathways in mouse liver and human primary hepatocytes.

The International Agency for Research on Cancer classified processed meats (PMs) as “carcinogenic” and red meat as “probably carcinogenic” for humans(1). The possible relationship between colorectal cancer (CRC) risk and processed meats (PMs), along with the specific compound contributing to this association have not been established yet. Nitrosyl-heme and heme iron have been proposed as potential-related compounds. The aim of this study was to assess the association of nitrosyl-heme and heme iron intake with CRC risk among participants from the European Prospective Investigation into Cancer and Nutrition (EPIC) Spain study.

This prospective study included 38,262 subjects (61.5% females) from the EPIC-Spain study. Food consumption was assessed by a validated diet history questionnaire(2). Dietary intake of nitrosylheme and heme iron was estimated by matching PMs intake and composition data based on laboratory analyses conducted using a High Performance Liquid Chromatography method(3). In brief, the daily intake of nitrosyl-heme and heme iron was determined by multiplying the intake of each PM (in grams/day) by its corresponding content of nitrosyl-heme and heme iron, and then summing up the estimated intakes from all PMs. The proportional hazards models were used to examine the association between sex-specific tertiles of nitrosyl-heme and heme iron intake and CRC risk and 95% confidence intervals (CIs) were computed using Cox regression. Age served as the time scale, stratified by age and centre with adjustments for sex, energy intake, body mass index (BMI), waist circumference, education, smoking, physical activity in MET-h/week, lifetime alcohol consumption, dietary fibre, calcium intake, and family CRC history. Homogeneity of location subtype risk was also assessed. Interactions with smoking, BMI, physical activity, and alcohol were examined and sensitivity analyses were also conducted excluding the first three years of follow-up.

During a mean follow-up of 16.7 years, 577 CRC were identified. We found no overall association between nitrosyl-heme (T3 vs T1; HR: 0.98 (95% CI: 0.79-1.21)) or heme iron intakes (T3 vs T1; HR: 0.88 (95% CI: 0.70-1.10)) with CRC risk, nor according to tumour subtypes. However, we found a non-statistically significant positive association between nitrosyl-heme intake and proximal colon, HR =1.03; 95% CI, (0.65-1.61) and rectum cancer, HR = 1.04; 95% CI, (0.70-1.56).

Our study found no evidence supporting a link between nitrosyl-heme or heme iron intake and CRC risk in Spanish subjects from the EPIC cohort. As these results are novel and preliminary, more heterogeneous studies are necessary to provide more convincing evidence on their role in colorectal carcinogenesis.

Patients with end stage kidney disease (ESKD) on hemodialysis (HD) should follow a strict diet during the inter-dialytic period(1). Compliance to treatment, including diet, is key for optimal disease management and health outcomes and to protect against malnutrition(2,3). The objective of this study was to assess renal nutrition-related knowledge, compliance with dietary guidelines, adherence to treatment and risk of malnutrition among patients with ESKD in Lebanon.

A convenience sample of 119 patients with ESKD on HD was recruited from the dialysis units of the Lebanese American University Medical Center-Rizk Hospital (LAUMC-RH) and Hammoud Hospital University Medical Center (HHUMC) in Lebanon. Demographic characteristics, 24 hour-recall and a validated food frequency questionnaire(4) were collected from participants, while anthropometrics including weight status in the past 3 months, as well as biochemical data were collected from medical charts. Bioelectrical impedance tests were conducted on the patients, 30 mins after HD hemodialysis session, to assess body composition. Nutrition knowledge was assessed using a validated questionnaire(5), whereby “poor knowledge” corresponds to <70% correct answers. Compliance to treatment (HD sessions, medications, fluids, and diet) was collected from participants using the End-Stage Renal Disease Adherence Questionnaire (ESRD-AQ)(6)) (Kim et al., 2010) and scored using the tool guide. Accordingly, adherence was classified as “poor” (scores <500), “moderate” (scores: 500-799), or “good” (scores: 800-1000).

100 of the 119 participants (85.5%) were found to have malnutrition according to the Global Leadership Initiative on Malnutrition (GLIM) criteria(7). Malnourished patients were mostly found with lower education (57%), poor nutrition knowledge (68%), poor to moderate overall compliance (82%), and with no adequate caloric intake (67%). Weight loss was the most common phenotypic criterion among malnourished patients, whereby 22% of malnourished patients had weight loss of > 3Kg in the past 3 months. Malnourished patients with weight loss had a higher (p = 0.008) prevalence of poor overall compliance (36%), compared to those with mild or no weight loss (14%). Additionally, malnourished people with poor compliance tended to be younger (<55 years of age) and with lower levels of income and education (p<0.05).

Malnutrition rates are alarmingly high among patients with ESKD in our sample and are linked with low nutrition knowledge and poor adherence to treatment, including dietary compliance. Future studies with a larger more representative cohort are required to confirm our results. Accordingly, intervention trials targeting knowledge and adherence among ESKD patients in Lebanon are warranted to prevent malnutrition and to achieve better clinical outcomes.

While some studies have suggested that moderate alcohol consumption may be beneficial for rheumatoid arthritis (RA) prevention(1), the role of competing events have not been considered and may lead to misinterpretation of the magnitude of the risk between alcohol intake and RA incidence. We aimed to investigate the relationship between alcohol consumption and RA incidence when the competing risk of death is accounted for in the survival analysis.

Data from the UK Women’s Cohort Study (UKWCS), a prospective cohort study of 35,372 middleaged women established between 1995 and 1998, was used for the analyses(2). Alcohol intake was assessed at baseline by asking for the number of specified units of each type of alcoholic beverage (beer, wine, sherry, and spirits) consumed per week. Cases who developed RA were identified through linkage with Hospital Episode Statistics (HES) up to March 2019 (International Classification of Diseases, ICD-10 code M05-M06). Data linkage with the Health and Social Care Information Centre (HSCIC) allowed cause of death to be identified using ICD codes (9th/10th version). We used directed acyclic graphs, competing risk regression modelling, and subgroup analyses to examine the effect of alcohol intake on RA incidence.

Among 29,830 women linked to the HES data (666,857 person-years), 255 cases of rheumatoid arthritis were identified, with a median follow-up of 22.5 years. After adjustment for confounders, in both competing risk regression and cox proportional hazards models, regular drinking was associated with a reduced risk of RA. In the competing risk model, with occasional drinkers (less than 1 serving of alcohol per week) as the reference, the subhazard ratios (SHRs) for non-drinkers were: SHR, 0.67, 95% CI: 0.43-1.07; regular drinkers: SHR, 0.70, 95% CI: 0.53−0.94. Every additional unit of alcohol per week was associated with a 3% lower risk of rheumatoid arthritis (SHR (95% CI): 0.97(0.96−0.99)). BMI modified the linear associations between alcohol intake and risk of RA(Pinteraction=0.01). The incidence of RA in participants with a BMI < 30 kg/m2 (227 cases, 27,015 participants) was 2% lower for each additional serving of alcohol consumed per week (0.98(0.96−0.99)),no statistically significant effect was seen for alcohol in those with a BMI 30+kg/m2, though numbers were smaller in this group.

Higher consumption of n-3 polyunsaturated fatty acids (PUFAs) is associated with reduced severity of cardiovascular disease (CVD) and autoimmunity(1). The n-3 index (O3I), which correlates to n-3 PUFA habitual intake, is a useful clinical biomarker in determining cardiovascular risk(2). Individuals with an O3I <4% are considered to have higher cardiovascular risk, with 4-8% characterised as medium risk. The desirable O3I is >8% and deemed low risk for a cardiovascular event(3). Yet, little is known about O3I in systemic lupus erythematosus (SLE) patients who have a higher risk of CVD associated with their disease. This analysis aimed to determine the O3I of SLE patients, and its associations with disease activity.

A non-fasted blood sample was collected from SLE patients (n = 15) and healthy participants (n = 15). Isolated red blood cells were used to determine O3I and expressed as %. Habitual intake of fish, a rich source of n-3 PUFAs was assessed by questionnaire. Disease activity of SLE patients was assessed by a clinician using the British Isle Lupus Assessment Group (BILAG), Systemic Lupus Activity Measure-Revised (SLAM-R) and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Mann-Whitney U was used to evaluate O3I differences between SLE patients and healthy participants. Spearman’s rank coefficient assessed associations between O3I and SLE disease activity.

SLE patients had an O3I of 4.38% and categorised to have a medium risk of a cardiovascular event, which was significantly lower compared to healthy participants for cardiovascular risk (5.48%; p<0.01). Some 67% SLE patients (n = 10) reported to never/rarely consume fish (≤1 portion per month) whereas 53% healthy participants (n = 8) reported that they consumer >2 portions of fish per month. Correlation analysis showed O3I was negatively associated with BILAG (rho=−0.061), SLAM-R (rho=−0.215) and SLEDAI (rho=−0.122); albeit these associations were not significant (p>0.05).

This is the first report of O3I in SLE patients and identified lower O3I compared to healthy participants, suggesting that SLE patients might benefit from increasing fish consumption to reduce their risk of CVD. Further research is required to fully elucidate associations between O3I and SLE disease activity.

Findings from animal models suggest early exposure to polyunsaturated fatty acids (PUFAs) during pregnancy may influence developmental plasticity including adiposity(1). Birth cohort studies examining associations between offspring weight and maternal n-3 PUFA status or maternal fish intakes, the richest dietary source of n-3 PUFAs have been few and have yielded inconsistent findings. Some have reported lower weight at birth and throughout childhood with increasing maternal fish intakes and n-3 PUFA status(2), whilst others have observed positive or null associations(3,4). These have focused on the first few years of life and have been conducted within low fish-consuming populations. Our study provides novel data by examining associations between maternal fish consumption and prenatal PUFA (n-3 & n-6) status and offspring weight at birth and throughout childhood (7 & 13 years) in a high fish-eating population.

Pregnant women were enrolled in the Seychelles Child Development Study Nutrition Cohort 2 between 2008-2011. Serum PUFAs were quantified in maternal blood collected at 28-weeks’ gestation and in cord blood collected at delivery using gas-chromatography tandem mass spectrometry. Maternal fish consumption was assessed at 28-weeks’ gestation using a Fish Use Questionnaire. Childbirth weight (kg) was measured at delivery and classified according to WHO growth standards(5) (n = 1185). Child height (m), weight (kg), waist and hip circumference (cm) were recorded at 7 (n = 1167) and 13 (n = 878) years. Statistical analysis was conducted using logistic and multiple linear regression adjusting for child sex, gestational age, maternal age, BMI, alcohol use, socioeconomic status, and parity. Models at 7 & 13 years were additionally adjusted for child height and fish intakes.

Women were consuming on average 8.49 ± 4.51 fish meals/week during pregnancy. No significant associations were found between maternal fish intakes and anthropometric outcomes at birth, 7 & 13 years. No significant associations were observed between maternal PUFAs and offspring weight at birth. At both 7 & 13 years, however, higher maternal total n-6 PUFAs were associated with increased child weight [7yr; β = 0.070, p = 0.003, 13yr; β = 0.097, p = 0.004], waist circumference [7yr; β = 0.086, p = 0.003, 13yr; β = 0.105, p = 0.004], and hip circumference [7yr; β = 0.062, p = 0.027, 13yr; β = 0.090, p = 0.013]. No significant associations were found between cord n-6 PUFAs and birth weight. In quartile analysis, cord docosahexaenoic acid (DHA; C22:6n-3) concentrations <0.071mg/ml were associated with a higher risk of large for gestational age (LGA; >90th percentile) when compared to cord DHA concentrations >0.129mg/ml [OR 4.17, p = 0.017]. There were no significant associations between cord PUFAs and anthropometric outcomes at 7 & 13 years.

These findings suggest lower cord DHA, an n-3 PUFA, may be associated with higher risk of LGA at birth whilst higher n-6 PUFAs during pregnancy may be associated with adiposity development throughout childhood. Future work is needed to determine the potential long-term metabolic consequences of such associations.

Pernicious anaemia (PA) is characterised by vitamin B12 deficiency due to autoimmune-mediated loss of gastric parietal cells and intrinsic factor, a specific transporter for the intestinal uptake of vitamin B12. PA is typically managed with lifelong intramuscular hydroxocobalamin injections every 2-3 months. However, this regimen lacks robust scientific validation and fails to account for varied symptomatic responses among patients, with many requiring more frequent injections(1).

The Pernicious Anaemia Society (PAS) is a patient-driven charity that identified 10 research priorities for PA through a James-Lind Alliance Priority Setting Partnership(2). PAS members were surveyed to build a PA Research Repository, exploring diagnostics, treatment, family histories, and comorbidities. This project aims to better understand and manage the condition by addressing these priorities and characterising a cohort of patients.

An online survey was designed using SurveyMonkey comprising 21 questions to collect data on demographics, mode and timing of PA diagnosis, diagnosed comorbidities, family history of PA or other autoimmune conditions, and management (type, regime and patient satisfaction). All questions were compulsory. The survey was sent to 3,482 PAS members (April-September 2022) via the PAS newsletter, email, and website. Chi-square tests were used to investigate associations between gender and survey responses. The study protocol and procedures received a Favourable Ethical Opinion.

Completed surveys were received from 1,191 PAS members (34% response rate). Among these, 971 (81%) had a confirmed PA diagnoses, and the cohort was predominantly UK-based (92%) females (81%) aged 23-90 years, with a wide age of onset (10 to 80 years, mean 49 years). Diagnoses were typically based on low serum B12 (40%), positive intrinsic factor (31%), and/or parietal cell autoantibodies (13%), with 7% diagnosed via the now obsolete Schilling test. Diagnostic delays were common, 39% of participants reported waiting ≥3 years for a diagnosis. Over half (59%) reported other micronutrient deficiencies upon diagnosis. Half reported additional autoimmune diseases, with one-third having family with PA or other autoimmune conditions. Treatment primarily involved hydroxocobalamin intramuscular injections (77%), with 48% following the recommended guidelines and 52% injecting more frequently. Females had higher prevalence rates of Hashimoto’s disease (27% vs 7%), asthma (33% vs 20%), and iron deficiency (49% vs 35%) (all p < 0.05).

This survey has established the first-ever PA research repository of over 1,000 participants offering initial insight into the complexities of PA, from varied age-of-onset and familial clustering to diagnostic challenges and treatment variability. These results support the need for improved diagnostic and treatment strategies, supporting the research recommendations made in the recent vitamin B12 deficiency NICE guidelines(3). It also highlights the potential of collaborative research with a patient-driven charity. Collaborative efforts aim to advance patient-centred PA research, improve treatment evaluation, and develop evidence-based approaches to managing this complex condition.

Vegan and vegetarian diets, lacking animal-based foods, increase the risk of vitamin B12 deficiency(1). Yet, there is limited current data on its prevalence among European ancestry individuals in Western Europe or the USA. This study aimed to provide a consensus on the prevalence of B12 deficiency among vegans and vegetarians of European ancestry residing in Western Europe or the USA.

We identified studies from our systematic review of “Functional Vitamin B12 Status Among Adult Vegans” to develop a narrative review of the prevalence of B12 deficiency based on biomarkers of B12 status among vegan and vegetarians. We then used pooled data from National Diet and Nutrition Survey (NDNS)(2) to calculate UK-specific prevalence information on B12 deficiency and insufficiency using the new NICE(3) criteria among vegan/vegetarian women of child-bearing age (WCBA) (age 18-45) compared with older women.

A total of six studies (2013-2022) with data on the prevalence of B12 deficiency were identified.

These studies were conducted on participants from UK, Norway, Spain, Czech Republic and US. Nearly all used different cut-offs to define B12 deficiency. Among vegans and vegetarians, the reported prevalence of deficiency ranged from 5-52% and 6-14%, respectively. Studies from Norway(4) and Finland(5) highlight low prevalence (5%) and no difference between dietary groups, possibly due to widespread supplement usage. The USA(6), indicated a higher prevalence of inadequate B12 intake among vegans and vegetarians compared to omnivours, with 8% of vegans and 6% of vegetarians exhibiting serum B12 levels < 148pmol/l. Similarly, results from Spain(7) noted subclinical deficiencies in 11% of participants, in both vegans and vegetarians. In the Czech Republic(8), cobalamin deficiency was noted in 15% of vegans, with 17% exhibiting deficiency (Serum B12< 100 ng/L). Notably, regular supplementation significantly reduced deficiency rates, emphasising its role in maintaining normal B12 levels. In the UK(9), only one publication reported B12 deficiency rates (SerumB12 <118pmol/L) among male vegans (52%) and vegetarians (7%). Using data from the NDNS and NICE guidelines, the prevalence of B12 deficiency was (defined as serum B12 < 133pmol/L and Holo-TC <25pmol/L) at 5-8% among vegetarian WCBA (Age 18-45); appropriate data on vegans was not available. B12 insufficiency (potential deficiency), defined by NICE as serum B12 < 258 pmol/L and Holo-TC < 70 pmol/L, translated to 75% of vegetarians within the WCBA cohort being defined as insufficient compared to 39% among older vegetarian women. A similar but more pronounced trend emerges for Holo-TC insufficiency, with 90% of vegetarians exhibiting inadequate Holo-TC < 70 pmol/L, compared to 58% of older women vegetarians and 65% of omnivores.

Few studies report B12 deficiency among Western European vegans and vegetarians, particularly for vegan WCBA. Existing data suggest a high risk can be mitigated with appropriate supplementation or adequately fortified foods.