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Using the dual-pathway framework (Beach et al., 2022a), we tested a Neuro-immune Network (NIN) hypothesis: i.e., that chronically elevated inflammatory processes may have delayed (i.e., incubation) effects on young adult substance use, leading to negative health outcomes. In a sample of 449 participants in the Family and Community Health Study who were followed from age 10 to age 29, we examined a non-self-report index of young adult elevated alcohol consumption (EAC). By controlling self-reported substance use at the transition to adulthood, we were able to isolate a significant delayed (incubation) effect from childhood exposure to danger to EAC (β = −.157, p = .006), which contributed to significantly worse aging outomes. Indirect effects from danger to aging outcomes via EAC were: GrimAge (IE = .010, [.002, .024]), Cardiac Risk (IE = −.004, [−.011, −.001]), DunedinPACE (IE = .002, [.000, .008]). In exploratory analyses we examined potential sex differences in effects, showing slightly stronger incubation effects for men and slightly stronger effects of EAC on aging outcomes for women. Results support the NIN hypothesis that incubation of immune pathway effects contributes to elevated alcohol consumption in young adulthood, resulting in accelerated aging and elevated cardiac risk outcomes via health behavior.
Bupropion is not licensed as an antidepressant in the UK, limiting its use. We highlight bupropion’s distinct pharmacological profile and its potential benefits in treatment-resistant depression and people experiencing selective serotonin reuptake inhibitor-induced sexual dysfunction. The National Health Service repurposing medicines programme could improve equity of access for UK patients.
Inflammation and oxidative stress contribute to the progression of chronic diseases, and the volume of research in this area is rapidly expanding. Various dietary indices have been developed to determine the overall inflammatory or oxidative stress potential of a diet; however, few have been validated in cardiometabolic disease populations. This review aimed to explore the association between dietary indices and biomarkers of inflammation and oxidative stress in adults with cardiometabolic conditions. Four databases were systematically searched for literature in any language (Embase, CINAHL, CENTRAL, and MEDLINE) with 12,177 deduplicated records identified. Seventeen studies of adults with metabolic syndrome, cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease or chronic kidney disease were included. Fourteen studies were observational studies, one study was a clinical trial, and one was a randomised controlled trial. Four dietary indices were reported on with most studies (n=11) reporting on the dietary inflammatory index. The most reported biomarker was C-reactive protein. The findings were narratively synthesised. Results were inconclusive due to the heterogeneity of dietary indices and their use, disease states, and biomarkers reported. Only one study reporting on the dietary inflammatory index assessed all 45 parameters. Observational studies, particularly retrospective designs (n=7) are subject to recall and selection biases, potentially presenting overestimated results. Further research is required to determine the relationship between dietary indices and biomarkers of inflammation and oxidative stress in cardiometabolic disease populations. Future research should be rigorous, prospective, assess the full range of index parameters, and examine biomarkers the tool was developed for.
Helminth infection is highly prevalent in indigenous chickens reared in semi-scavenging/ scavenging systems in Bangladesh. Here, we estimated the prevalence of gizzard worm infection in indigenous chickens, the detection of the worm-induced pathologies, the development of ex vivo cultural protocol, and anthelmintic efficacy. We randomly collected and examined 390 chickens and isolated worms from the gizzard and proventriculus. The isolated worms were identified as Cheilospirura hamulosa Diesing, 1861. The overall prevalence of C. hamulosa was 33.1% (129 out of 390). Prevalence of the worm was almost similar in both sexes but significantly (p <0.05) higher in adult chickens (44.3%) and in the summer season (47.1%). In heavy infections, C. hamulosa destroyed the muscular layer of the gizzard. The presence of brown necrotic tissues and curd-like caseous materials was detected in the affected gizzards. In severe cases, the horny lining of the gizzard was inflamed, necrotized and marked by multiple holes and brick-red colored spots. Liquefied, fetid materials oozed out from the muscular layer in extensive cases. Histopathological examination showed marked infiltrations of eosinophils. In serum-supplemented M199 and DMEM, adult C. hamulosa survived well and reproduced. Levamisole (LEV) and ivermectin (IVM) efficiently killed the worm. However, albendazole (ABZ), mebendazole (MBZ) and piperazine (PPZ) did not kill the worms. Our results suggest that C. hamulosa is highly prevalent in semi-scavenging chickens in Bangladesh. LEV and IVM can be used to treat and control the infection in chickens.
Neuropsychiatric disorders in preeclampsia (PE) women are prevalent and worsen PE outcome. Immune-related biomarkers including soluble sCD80 and cytotoxic T-lymphocyte antigen-4 (sCTLA-4) are not well studied in relation to depression, anxiety, and chronic fatigue due to PE.
Methods:
The aim is to study serum immune-inflammatory biomarkers of PE and delineate their associations with the Hamilton Depression (HAMD), Anxiety (HAMA), and Fibro-Fatigue (FF) rating Scale scores. sCD80, sCTLA-4, vitamin D, granulocyte-macrophage colony-stimulating factor, zinc, copper, magnesium, and calcium were measured in 90 PE compared with 60 non-PE pregnant women.
Results
PE women show higher depression, anxiety and FF rating scale scores as compared with control women. sCTLA-4, sCD80, and copper were significantly higher and zinc, magnesium, and calcium significantly lower in PE women than in controls. Multiple regression analysis showed that around 55.8%-58.0% of the variance in the HAMD, HAMA and FF scores was explained by the regression on biomarkers; the top 3 most important biomarkers were sCTLA-4, sCD80, and vitamin D. The sCTLA-4/sCD80 ratio was significantly and inversely associated with the HAMD/HAMA/FF scores. We found that around 70% of the variance in systolic blood pressure could be explained by sCTLA-4, vitamin D, calcium, and copper.
Conclusions:
The findings underscore that PE and depression, anxiety, and chronic fatigue symptoms due to PE are accompanied by activation of the immune-inflammatory response system. More specifically, disbalances among soluble checkpoint molecules seem to be involved in the pathophysiology of hypertension and neuropsychiatric symptoms due to PE.
Autoimmune processes have been documented in both childhood and adulthood patients with obsessive-compulsive disorder (OCD), with the pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) representing the paradigm of this model.
Given the limited information available, the present study aimed at assessing the characteristics of adult patients with OCD exposed to a previous group A β-hemolytic Streptococcus infection, together with some peripheral inflammatory biomarkers.
Materials and methods
Fifty-two subjects displaying antistreptolysin O (ASO) titer positivity were recruited from a sample of 247 adult OCD outpatients, diagnosed according to DSM-5 criteria and assessed by the Yale-Brown Obsessive-Compulsive Scale. Their clinical features were assessed and compared. The possible relationships between the different parameters were also examined.
Results
Thirty-six subjects who were on medication for OCD showed significantly lower ASO titers than the other. The neutrophil count was positively and negatively related to, respectively, the “distress associated with obsessive thoughts” item and to the patients’ age. The lymphocyte count and folic acid levels were higher in 30 subjects with no perinatal insults.
Conclusions
These results seem to suggest that OCD subjects with ASO titer-positivity show a chronic inflammatory state, in spite of no symptoms or recall of bacterial infections, that might be involved in both the onset and the maintenance of OCD, with immunological alterations being related to symptom dimension to be identified. They also support the notion of possible anti-inflammatory effects of some psychotropic compounds.
Growing evidence suggests that psychedelic-assisted therapies can alleviate depression, anxiety, posttraumatic stress, and substance use disorder, offering relatively safe profiles, enhanced efficacy, and lasting effects after a few applications. Athletes often experience high levels of stress and pressure, making them susceptible to these psychiatric conditions. However, the effects of psychedelic substances on athletic performance remain largely unknown. Before potential acceptance, evaluating their impact on physical and physiological measures beyond mental health outcomes is crucial. Here, we aim to explore this topic and highlight research directions to advance our understanding. Preclinical studies suggest that psilocybin/psilocin, lysergic acid diethylamide (LSD), N,N-dimethyltryptamine (DMT), and ayahuasca possess anti-inflammatory and anti-nociceptive properties. Studies investigating the effects of classical psychedelics or 3,4-methylenedioxymethamphetamine (MDMA) on factors such as muscle strength, motor coordination, locomotion, endurance, fluid and electrolyte balance, hormonal regulation, and metabolism are still scarce. While adhering to regulatory frameworks, further research in animal models, athletes, and non-athletes is needed to address these gaps, compare psychedelics with commonly used psychoactive drugs, and explore the potential prophylactic and regenerative benefits of specific interventions.
Green tea, a plant rich in bioactive compounds, has been highlighted for its beneficial effects. In the present systematic review and meta-analysis of randomised controlled trials (RCTs), the impact of green tea on inflammatory and oxidative markers is investigated. Using pre-defined keywords, online databases (PubMed, Scopus, Web of Science Core Collection, and Google Scholar) were searched for relevant articles, published from inception up to February 2024. The outcomes included C-reactive protein (CRP), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), total antioxidant capacity (TAC), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPX). Analyses of subgroups, linear, and non-linear associations were also carried out. Out of 1264 records initially retrieved, 38 RCTs were included. Supplementation with green tea improved the following indicators: IL-1β (weighted mean difference (WMD): −0.10 pg/mL; 95% CI: −0.15, -0.06), MDA (WMD: −0.40 mcmol/L; 95 % CI: −0.63, −0.18), TAC (WMD: 0.09 mmol/L; 95% CI: 0.05, 0.13), SOD (WMD: 17.21 u/L; 95% CI: 3.24, 31.19), and GPX (WMD: 3.90 u/L; 95% CI: 1.85, 5.95); but failed to improve others, including CRP (WMD: 0.01 mg/L; 95% CI: −0.14, 0.15), IL-6 (WMD: −0.34 pg/mL; 95% CI:−0.94, 0.26), and TNF-α (WMD: −0.07 pg/mL; 95% CI: −0.42, 0.28). Supplementation with green tea can improve the body’s oxidative status. However, the results showed no significant effect of green tea on inflammatory markers, except for IL-1β. Further studies are needed to determine the effectiveness of green tea, particularly on inflammatory status.
A randomised parallel intervention study was conducted with male patients diagnosed with CHD. Participants were assigned to three groups: Group A abstained from alcohol (n 20), Group B consumed red wine (n 21) and Group C (n 16) consumed an alcoholic beverage without wine micro-constituents. Biological samples were collected at baseline, 4 and 8 weeks. Enzyme activities of acetyl-CoA:lyso-platelet-activating factor (PAF) acetyltransferase, cytidine 5’-diphospho (CDP)-choline:1-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase (PAF-cholinephosphotransferase), PAF-acetylhydrolase in leukocyte homogenates, serum lipoprotein-associated phospholipase-A2 and plasma markers of thrombosis were measured. PAF-, ADP- and collagen-induced platelet aggregation was measured in human platelet-rich plasma. Red wine consumption led to a 15·3 % reduction in LysoPAF-acetyltransferase activity at 4 weeks (P= 0·008) compared with baseline and Group A (P= 0·01). PAF-cholinephosphotransferase activity was reduced by 11·1 % at 8 weeks (P= 0·04) compared with baseline and by 24·9 % compared with Group C (P= 0·02). PAF-acetylhydrolase activity was reduced by 36·2 % at 8 weeks compared with baseline (P= 0·001) and compared with Group A (P< 0·000) and Group C (P= 0·009). Fibrinogen levels in Group B reduced by 6–9 % at 4 (P= 0·04) and 8 weeks (P= 0·01) compared with baseline while D-dimer in Group C increased by 16·1 % at 8 weeks (P= 0·005) compared with baseline. Platelet aggregation against PAF and collagen was reduced in Group B (82·6 and 35·4 %, respectively), and in Group C (158·4 and 37·1 %, respectively) compared with baseline and Group A (P< 0·05). In conclusion, moderate wine consumption improved the activity of PAF-metabolism enzymes regardless of ethanol and reduced platelet aggregation, probably through mechanisms different from those of ethanol.
Insulin-like growth factor 1 (IGF-1) is an important growth factor in childhood. We aimed to investigate the impact of food supplements for the treatment of moderate acute malnutrition (MAM) on serum IGF-1 (sIGF-1). Secondary analysis of a randomised 2 × 2 × 3 factorial nutrition trial was performed. Children aged 6–23 months with MAM received 2093 kJ/d as lipid-based nutrient supplement (LNS) or corn soy blend (CSB), containing either dehulled soya or soya isolate and different quantities of dried skimmed milk (0 %, 20 % or 50 % of total protein) for 12 weeks. The trial was double-blind with regard to soya and milk but not to matrix (LNS v. CSB). sIGF-1 was measured at inclusion and after 12 weeks of supplementation. Of 1609 children enrolled, 1455 (90 %) had sIGF-1 measured at both time points. During supplementation, sIGF-1 increased 6·7 (95 % CI 6·1, 7·3) ng/ml compared with an expected age-dependent decrease of 0·3 (95 % CI 0·2, 0·4) ng/ml. Children who received LNS v. CSB had a lower increase in sIGF-1 (–8 %, 95 % CI − 12, −3). The effect of LNS was partly attenuated when sIGF-1 was corrected for inflammation. Children who received soya isolate compared with dehulled soya had a higher increase in sIGF-1 (6 %, 95 % CI 1, 12). Milk content did not affect sIGF-1. Overall, sIGF-1 increased during supplementation. The lower increase with LNS v. CSB was only partly explained by increased inflammation with LNS and needs further investigation. Isolate v. dehulled soya led to a higher increase which may be due to antinutrients in dehulled soya.
A co-relation between Schistosoma japonicum (Sj) and liver cancer (LC) in humans has been reported in the literature; however, this association is circumstantial. Due to the inconclusive nature of this association, the International Agency for Research on Cancer has placed Sj in Group 2B for LC, signifying it to be a ‘possible carcinogen’. Many epidemiological, pathological and clinical studies have identified multiple factors, linked with Sj infection, which can lead to liver carcinogenesis. These factors include chronic inflammation in response to deposited eggs (which leads to fibrosis, cirrhosis and chromosomal instability at cellular level), hepatotoxic effects of egg-antigens, co-infection with hepatitis viruses, and up-regulation of glycolysis linked genes among others which predisposes hepatic tissue towards malignant transformation. The objective of this work is to present the current understanding on the association of Sj infection with LC. Mechanisms and factors linked with Sj infection that can lead to LC are emphasized, along with measures to diagnose and treat it. A comparison of liver carcinogenesis is also provided for cases linked with and independent of Sj infection. It appears that Sj, alone or with another carcinogen, is an important factor in liver carcinogenesis, but further studies are warranted to conclusively label ‘infection with Sj alone’ as a liver carcinogen.
Current evidence points to a research-practice gap in mental health. There is a specific unmet need to identify novel strategies to improve diagnostic criteria, especially when clinical manifestations overlap as in the case of bipolar (BD) and major depressive disorder (MDD). Based on the rapidly evolving notion that affective disorders are characterized by disrupted brain-body communication, current efforts of neuropsychiatric research are converging towards the identification of specific clusters of peripheral interconnected biomarkers. We argue that these can capture the complexity of the disease as they are linked to the fundamental pathophysiological mechanisms underlying BD or MDD, and can thus deliver an unbiased biosignature. Here we provide a critical viewpoint on the promises and challenges of biomarkers to identify reliable biosignatures of affective disorders. Novel methodological insight and relevant biomarkers are discussed with a main focus on immunometabolic derangements and disrupted redox balance. Major advancements are reviewed taking into consideration that an unbiased diagnosis can only derive from a deep understanding of how biological, psychological, and social factors interact ultimately affecting the clinical manifestation of affective disorders.
Peripheral inflammatory markers, including serum interleukin 6 (IL-6), are associated with depression, but less is known about how these markers associate with depression at different stages of the life course.
Methods
We examined the associations between serum IL-6 levels at baseline and subsequent depression symptom trajectories in two longitudinal cohorts: ALSPAC (age 10–28 years; N = 4,835) and UK Biobank (39–86 years; N = 39,613) using multilevel growth curve modeling. Models were adjusted for sex, BMI, and socioeconomic factors. Depressive symptoms were measured using the Short Moods and Feelings Questionnaire in ALSPAC (max time points = 11) and the Patient Health Questionnaire-2 in UK Biobank (max time points = 8).
Results
Higher baseline IL-6 was associated with worse depression symptom trajectories in both cohorts (largest effect size: 0.046 [ALSPAC, age 16 years]). These associations were stronger in the younger ALSPAC cohort, where additionally higher IL-6 levels at age 9 years was associated with worse depression symptoms trajectories in females compared to males. Weaker sex differences were observed in the older cohort, UK Biobank. However, statistically significant associations (pFDR <0.05) were of smaller effect sizes, typical of large cohort studies.
Conclusions
These findings suggest that systemic inflammation may influence the severity and course of depressive symptoms across the life course, which is apparent regardless of age and differences in measures and number of time points between these large, population-based cohorts.
Childhood adversity has been associated with increased peripheral inflammation in adulthood. However, not all individuals who experience early adversity develop these inflammatory outcomes. Separately, there is also a link between various internalizing emotional distress conditions (e.g. depression, anxiety, and fear) and inflammation in adulthood. It is possible the combination of adult emotional distress and past childhood adversity may be uniquely important for explaining psychopathology-related immune dysfunction at midlife.
Methods
Using data from the Midlife in the United States (MIDUS) study (n = 1255), we examined whether internalizing, defined as past 12-month emotional distress symptomatology and trait neuroticism, moderated associations between childhood adversity and heightened inflammation in adulthood. Using latent variable modeling, we examined whether transdiagnostic or disorder-specific features of emotional distress better predicted inflammation.
Results
We observed that childhood adversity only predicted adult inflammation when participants also reported adult internalizing emotional distress. Furthermore, this moderation effect was specific to the transdiagnostic factor of emotional distress rather than the disorder-specific features.
Conclusions
We discuss the possibility that adult internalizing symptoms and trait neuroticism together may signal the presence of temporally stable vulnerabilities that amplify the impact of childhood adversity on midlife immune alterations. The study highlights the importance of identifying emotional distress in individuals who have experienced childhood adversity to address long-term immune outcomes and enhance overall health.
Recent theories have implicated inflammatory biology in the development of psychopathology and maladaptive behaviors in adolescence, including suicidal thoughts and behaviors (STB). Examining specific biological markers related to inflammation is thus warranted to better understand risk for STB in adolescents, for whom suicide is a leading cause of death.
Method:
Participants were 211 adolescent females (ages 9–14 years; Mage = 11.8 years, SD = 1.8 years) at increased risk for STB. This study examined the prospective association between basal levels of inflammatory gene expression (average of 15 proinflammatory mRNA transcripts) and subsequent risk for suicidal ideation and suicidal behavior over a 12-month follow-up period.
Results:
Controlling for past levels of STB, greater proinflammatory gene expression was associated with prospective risk for STB in these youth. Similar effects were observed for CD14 mRNA level, a marker of monocyte abundance within the blood sample. Sensitivity analyses controlling for other relevant covariates, including history of trauma, depressive symptoms, and STB prior to data collection, yielded similar patterns of results.
Conclusions:
Upregulated inflammatory signaling in the immune system is prospectively associated with STB among at-risk adolescent females, even after controlling for history of trauma, depressive symptoms, and STB prior to data collection. Additional research is needed to identify the sources of inflammatory up-regulation in adolescents (e.g., stress psychobiology, physiological development, microbial exposures) and strategies for mitigating such effects to reduce STB.
This study aimed to elucidate the association between the platelet-to-lymphocyte ratio (PLR) and the risk of attention deficit hyperactivity disorder (ADHD) in children aged 6–14 based on National Health and Nutrition Examination Survey (NHANES) data.
Method
We utilized data from NHANES 2013–2014 for analysis, with PLR as the independent variable and ADHD as the dependent variable. Weighted logistic regression was used to construct the relationship model. The subgroup analysis with stratification and adjustment for confounding factors was conducted to explore the association between PLR and ADHD risk in children aged 6–14. Finally, the restricted cubic spline (RCS) analysis was carried out to explore the non-linear relationship between PLR and ADHD.
Results
The study included 1455 samples with 91 ADHD cases. A significant positive association (OR > 1, P < 0.05) was observed between PLR and ADHD risk in the multivariate weighted logistic regression model. Race and asthma status remarkably influenced the relationship between PLR and ADHD (P for interaction<0.05). The positive association between PLR and ADHD risk was particularly significant (P < 0.05) in boys, children born to mothers aged 20–29, and children with asthma. The RCS curve indicated a non-linear association between PLR and ADHD risk (P-non-linear = 0.0040), with OR > 1 when PLR ≥ 106.40.
Conclusion
Increased PLR elevated the risk of ADHD, especially in males, children born to mothers aged 20–29, and children with asthma, with 106.40 possibly being an effective threshold for PLR’s impact on ADHD risk.
Mastitis in dairy cows is an important factor restricting the healthy development of dairy industry. Natural extracts have become a research hotspot to alleviate and prevent diseases because of their unique properties. The purpose of this study was to investigate the effects of resveratrol (RES) on the mitochondrial biosynthesis, antioxidation, and anti-inflammatory in bovine mammary epithelial cells (BMECs) and its mechanism involved. Blood samples were collected from six healthy cows and six mastitis affected cows, respectively, and lipopolysaccharide (LPS) was used to treat BMECs to construct inflammation models, gene interference is achieved by transfection. The results showed that messenger RNA (mRNA) expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) was down-regulated and mitochondrial biogenesis-related gene expression was disrupted in the blood of mastitis cows and LPS-induced BMECs. RES is the best active substance to activate PGC-1α. The addition of RES can effectively alleviate the production of BMECs reactive oxygen species (ROS) and mitochondrial damage induced by LPS, and improve the antioxidation and anti-inflammatory ability, while the alleviation effect of RES is inhibited after interfering with protein kinase AMP-activated catalytic subunit α 1 (PRKAA1). In summary, our study emphasizes that PRKAA1 is a key gene mediating the activation of PGC-1α by RES, which regulates mitochondrial biosynthesis, inhibits ROS release, attenuates mitochondrial damage, and improves mitochondrial antioxidant capacity through the activation of PGC-1α by PRKAA1, thus attenuating the inflammatory response in BMECs.
Chia seeds have gained attention for their potential anti-inflammatory properties, which may be attributed to their high content of omega-3 fatty acids, dietary fibre, and antioxidants. This study aims to provide an overview of the current understanding regarding the effects of chia seeds on inflammatory markers, specifically C-reactive protein (CRP), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α). A comprehensive literature search was conducted on PubMed, Scopus, Web of Science, Cochrane, and Google Scholar up to June 2024. Randomized controlled trials (RCTs) assessing the effect of chia seed on CRP or/and IL-6 or/and TNF-α. Data were extracted and analysed using a random-effects model, and reported as weighted mean differences (WMD) with 95% confidence intervals (CI). Subgroup and sensitivity analyses were also performed. Four RCTs involving 210 participants were included in the meta-analysis. The results showed that chia consumption significantly decreased CRP (WMD: –0.64 mg/dl; 95% CI: –1.24, –0.04; P = 0.03). But it had no significant effect on IL-6 (WMD: 0.29 pg/dl; 95% CI: –0.40, 0.98; P = 0.41), and TNF-α (WMD: 0.05%; 95% CI: –0.21 to 0.30; P = 0.72). Chia consumption can significantly decrease CRP, but no significant effect was observed on IL-6 and TNF-α. To prove our findings, more studies with a larger sample size are needed.
Markers of inflammation and cannabis exposure are associated with an increased risk of mental disorders. In the current study, we investigated associations between cannabis use and biomarkers of inflammation.
Methods
Utilizing a sample of 914 participants from the Avon Longitudinal Study of Parents and Children, we investigated whether interleukin-6 (IL-6), tumor necrosis factor α (TNFα), C-reactive protein (CRP), and soluble urokinase plasminogen activator receptor (suPAR) measured at age 24 were associated with past year daily cannabis use, less frequent cannabis use, and no past year cannabis use. We adjusted for a number of covariates including sociodemographic measures, body mass index, childhood trauma, and tobacco smoking. We found evidence of a strong association between daily or near daily cannabis use and suPAR.
Results
We did not find any associations between less frequent cannabis use and suPAR. We did not find evidence of an association between IL-6, TNFα or CRP, and cannabis use.
Conclusions
Our finding that frequent cannabis use is strongly associated with suPAR, a biomarker of systemic chronic inflammation implicated in neurodevelopmental and neurodegenerative processes is novel. These findings may provide valuable insights into biological mechanisms by which cannabis affects the brain and impacts the risk of serious mental disorders.
Metabolic dietary patterns, including the Empirical Dietary Index for Hyperinsulinaemia (EDIH) and Empirical Dietary Inflammatory Pattern (EDIP), are known to impact multiple chronic diseases, but the role of the colonic microbiome in mediating such relationships is poorly understood. Among 1,610 adults with faecal 16S rRNA data in the TwinsUK cohort, we identified the microbiome profiles for EDIH and EDIP (from food frequency questionnaires) cross-sectionally using elastic net regression. We assessed the association of the dietary pattern-related microbiome profile scores with circulating biomarkers in multivariable-adjusted linear regression. In addition, we used PICRUSt2 to predict biological pathways associated with the enriched microbiome profiles, and further screened pathways for associations with the dietary scores in linear regression analyses. Microbiome profile scores developed with 32 (EDIH) and 15 (EDIP) genera were associated with higher insulin and homeostatic model assessment of insulin resistance. Six genera were associated with both dietary scores: Ruminococcaceae_UCG-008, Lachnospiraceae_UCG-008, Defluviitaleaceae_UCG-011 Anaeroplasma, inversely and Negativibacillus, Streptococcus, positively. Further, pathways in fatty acid biosynthesis, sugar acid degradation, and mevalonate metabolism were associated with insulinaemic and inflammatory diets. Dietary patterns that exert metabolic effects on insulin and inflammation may influence chronic disease risk by modulating gut microbial composition and function.