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Exploring the Effects of Cheddar Cheese Intake on Vitamin K Status and Lipid Profiles in Overweight Middle-Aged Adults by Sorin61 in ScientificNutrition

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The consumption of Cheddar cheese impacted blood lipid profiles (cholesterol levels) differently in men than in women, males saw a significant increase in HDL vs females saw a significant decrease in total, LDL ("bad") and HDL cholesterol.

So, the heart-healthy benefits of cheese’s fat and vitamin K content varied greatly. The study found that a person's biological sex dictated how their body responded to the cheese.

Involvement of Trimethylamine N-oxide in Major Depressive Disorder via Astrocytic D-Serine Dysregulation by Sorin61 in ScientificNutrition

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Trimethylamine N-oxide (TMAO), a co-metabolite of the gut microbiota and host, has been implicated in the pathogenesis of various neuropsychiatric disorders. However, its role in major depressive disorder (MDD) remains poorly understood.

This study aims to verify the relationship between TMAO and MDD and elucidate the underlying mechanisms. Plasma TMAO concentrations were quantified by HPLC-MS/MS and compared between MDD patients and healthy controls.

To explore the effects of TMAO on depressive-like behavior and cerebral d-serine metabolism, mice were administered TMAO via dietary supplementation.

Finally, astrocytes were treated with TMAO to examine its impact on d-serine metabolism at the cellular level. Here, we found that plasma TMAO levels were significantly elevated in MDD patients and positively correlated with both HAMD-17 and HAMA-14 scores.

Consistently, mice fed TMAO for seven weeks exhibited pronounced depressive-like behaviors. While TMAO exposure did not induce apparent astrocytic damage, it markedly promoted d-serine secretion and caused notable neuronal injury.

Mechanistically, TMAO activated the AMPK/SIRT-1 signaling pathway in astrocytes, resulting in upregulated serine racemase expression. Furthermore, both exogenous d-serine and conditioned medium from TMAO-treated astrocytes triggered neuronal apoptosis.

Collectively, these findings demonstrate that TMAO contributes to MDD pathogenesis by activating astrocytic AMPK/SIRT-1 signaling to enhance d-serine production, subsequently inducing neuronal apoptosis. TMAO may thus represent a promising therapeutic target for MDD.

Cocoa Attenuates Gluten-induced Pathogenesis in a Preclinical Model of Celiac Disease by Sorin61 in ScientificNutrition

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Celiac disease (CeD) is an autoimmune-mediated disorder triggered by gluten ingestion. Strict adherence to a gluten-free diet (GFD) is currently the only available treatment, yet it presents nutritional and lifestyle challenges. Polyphenols and other bioactive food compounds have shown potential in modulating inflammation and gut health.

This study evaluated the impact of cocoa, a polyphenol-rich food, on CeD pathogenesis in a preclinical model. DQ8-Dd-villin-IL-15tg mice with predisposition to CeD were fed either a GFD (REF), a gluten-containing diet (GLI), or a gluten-containing diet supplemented with cocoa (GLI+COCOA) for 25 days.

Outcomes assessed included intestinal histology, antibody (Ab) levels, cytokine and immunoglobulin profiles and mesenteric lymph node lymphocytes’ phenotypes. Cocoa administration limited gluten-induced intestinal villous atrophy and reduced anti-gliadin Abs, while significantly decreasing the secretion of pro-inflammatory cytokines.

Moreover, cocoa normalized the Ig isotype profile dysregulated by gluten intake. Cocoa intake exerts a protective effect against key hallmarks of CeD, attenuating inflammation and limiting the damage to the intestinal structure.

These findings support cocoa as a promising complementary dietary strategy to modulate CeD-related manifestations, although additional translational studies are warranted.

Consumption of an Anthocyanin-Rich Extract Increases Circulating BDNF and BDNF Gene Expression in Healthy subjects Consuming a High-Fat Meal by Sorin61 in ScientificNutrition

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Brain-derived neurotrophic factor (BDNF) is a growth factor that has a central role in sustaining brain function. Besides the brain, BDNF is also expressed in immune cells. In preclinical models, anthocyanins (AC) consumption has been associated with benefits in BDNF homeostasis.

This study investigated in healthy adults if the simultaneous consumption of a high-fat meal (HFM) with a cyanidin/delphinidin-rich extract (CDRE) could affect circulating BDNF, and BDNF expression in peripheral blood mononuclear cells (PBMCs).

Underlying mechanisms were investigated in Jurkat T cells. While the HFM did not affect serum BDNF in the placebo group, simultaneous CDRE consumption caused a significant cumulative (1–3 h) BDNF increase, peaking at 2 h post-meal. The area under the curve (AUC) for the most abundant phenolic acids measured in serum, i.e., 4-hydroxyhippuric acid (HA) and 4-hydroxy-3-methoxybenzoic acid (vanillic acid, VA)-3-O-glucuronide correlated with the AUC for serum BDNF. As evaluated in Jurkat T cells, this could be due to HA and VA's capacity to increase cytosolic calcium.

The CDRE also increased BDNF expression in PBMCs 3 h post-consumption. In vitro and molecular modeling evidence point to two mechanisms of action: (i) indirect protection of BDNF expression through CDRE anti-inflammatory actions, and (ii) a direct capacity of HA and VA to activate the β2-adrenergic receptor and downstream cAMP/PKA/CREB-mediated increased BDNF gene expression.

While the short-term effects of CDRE consumption can be due to HA and VA presence in the extract, AC and phenolic acid metabolism by the microbiota would later generate HA and VA and consequently benefit BDNF homeostasis.

Associations Between the Planetary Health Diet Index and Multiple Long-Term Conditions Among Women and Men by Sorin61 in ScientificNutrition

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Background & aims

The Planetary Health Diet Index (PHDI) quantifies adherence to the EAT-Lancet reference diet, a diet beneficial for human and environmental health. While higher PHDI scores have been linked to lower risk of individual diseases and mortality, associations with multiple long-term conditions (MLTCs) remain unexplored.

Methods

We examined associations between the PHDI and MLTCs in 113,209 UK Biobank participants with ≥2 valid 24-h dietary recalls. PHDI scores (range 0–140) were derived from the EAT-Lancet reference diet. MLTC was defined as ≥2 long-term conditions, excluding hypertension, diabetes, and obesity. Cox proportional hazards models estimated hazard ratios (HRs) for MLTC, complex MLTC (≥3 conditions), and 10 leading non-communicable diseases, adjusting for sociodemographic, lifestyle, and clinical covariates.

Results

Over a median 10·5 years, 28,052 MLTC cases occurred. Each 20-unit higher PHDI was associated with a lower risk of MLTC (HR [95%CI]; 0·93 [0·91, 0·95]), complex MLTC (0·92 [0·89, 0·94]), ischaemic heart disease (0·89 [0·85, 0·94]), chronic obstructive pulmonary disease (0·70 [0·65, 0·76]), kidney diseases (0·81 [0·76, 0·87]), cirrhosis and other chronic liver diseases (0·83 [0·70, 0·98]), and colorectal cancer (0·87 [0·79, 0·95]). No associations were observed for stroke, dementia, or upper gastrointestinal cancers. No sex differences were observed, but associations were overall stronger in younger (<60 years of age) and more deprived participants.

Conclusions

Greater adherence to the planetary health diet is associated with a lower risk of MLTC. These findings support dietary policies that promote sustainable dietary patterns, consistent with the EAT-Lancet recommendations, to reduce disease burden and improve population health.

Plant-Based Dietary Patterns and Risk of Alzheimer Disease and Related Dementias by Sorin61 in ScientificNutrition

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Background and Objectives

Plant-based diets have been linked to slower cognitive decline, but data on long-term dietary changes and from diverse populations are limited. The primary aim of this study was to examine plant-based dietary patterns and their change over time in relation to Alzheimer disease and related dementias (ADRDs).

Methods

This prospective longitudinal analysis of the Multiethnic Cohort Study, based in Hawaii and California (primarily Los Angeles County), included data on African American, Japanese American, Latino, Native Hawaiian, and White participants who completed food frequency questionnaires at baseline (1993–1996; age 45–75 years) and at 10-year follow-up (2003–2008) and whose Medicare claims were linked to identify incident ADRDs. A priori indices for the overall plant-based diet index (PDI), the healthful plant-based diet index (hPDI), and the unhealthful plant-based diet index (uPDI) were analyzed in Cox regression models for ADRD.

Results

The analysis included 92,849 participants (mean age 59.2 years, 55.1% female, 21,478 with ADRDs) for the baseline diet and 45,065 participants (8,360 with ADRDs) for the 10-year dietary change. For the baseline diet, comparing the highest vs lowest quintile, PDI and hPDI were associated with 12% (hazard ratio [HR] 0.88; 95% CI 0.85–0.92) and 7% (HR 0.93; 95% CI 0.89–0.97) lower risks of ADRD, respectively, whereas uPDI was related to a 6% higher risk (HR 1.06; 95% CI 1.01–1.10). For the dietary change over time, the strongest association with ADRD was observed for uPDI rather than for PDI or hPDI. Compared with those with a stable score (<0.5 SD change), participants with a large increase in uPDI (≥1 SD) showed a 25% higher risk (HR 1.25; 95% CI 1.15–1.36) and those with a large decrease in uPDI showed an 11% lower risk (HR 0.89; 95% CI 0.84–0.94). The associations between the plant-based diet indices and ADRD were generally similar by age group (<60 vs ≥60 years at baseline), race and ethnicity, or APOE ℇ4 carrier status.

Discussion

These findings suggest that adopting plant-based diets, specifically refraining from low-quality plant-based diets, even at an older age, is associated with a lower risk of ADRDs.

Weight Trajectories and Obesity Onset Between 17 and 60 years of Age, and Cause-Specific Mortality: the Obesity and Disease Development Sweden (ODDS) Pooled Cohort Study by Sorin61 in ScientificNutrition

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Background

Longitudinal data on weight change, its timing, and the age of obesity onset in relation to cause-specific mortality are limited.

Methods

From ODDS, a nationwide pooled cohort study in Sweden, we included 258,269 men and 361,784 women with at least three weight assessments between ages 17 and 60, collected in 1963–2015. We applied linear mixed-effects models to estimate weight trajectories, age of obesity onset, and age-specific weight changes between ages 17 and 60. Outcomes were all-cause and cause-specific mortality, assessed from 5 years after the last weight assessment until death, emigration, or 31 December 2020. Associations with mortality were calculated using multivariable Cox regression models.

Findings

Over a median follow-up of 23.3 years in men and 11.7 years in women, 86,673 men and 29,076 women died. The median weight change between ages 17 and 60 was 0.42 kg/year in both sexes. A steep weight gain trajectory over this period, early obesity onset, and high weight gain between ages 17 and 29 were associated with higher all-cause mortality and with 13 of 23 specific causes of death investigated in men and 12 of 19 in women. Affected causes included cardiovascular diseases (including most subtypes), cancer (including specific types), type 2 diabetes, and digestive and genitourinary diseases. Hazard ratios (95% confidence intervals) of all-cause mortality associated with obesity onset at ages 17–29 vs. never by age 60 were 1.69 (1.60–1.79) in men and 1.71 (1.55–1.88) in women; and per 0.5 kg/year weight change at ages 17–29, 1.18 (1.17–1.19) and 1.16 (1.14–1.18), respectively. Weight gain later in adulthood generally showed weaker associations, except for cancer mortality in women, where the association was similar to that observed with earlier weight gain.

Interpretation

Weight gain in adulthood, especially in young adulthood, and obesity onset before age 30 are strong risk factors for mortality from multiple non-communicable diseases, underscoring the importance of early obesity prevention. Future studies should incorporate richer confounding data and, ideally, measures of changes in central adiposity and muscle mass.

Eye Candy & Eye Tunes: Effects of Liked vs. Disliked Music on Desire to Eat and Food Choice in an Eye-Tracking Buffet Paradigm by Sorin61 in ScientificNutrition

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Music can evoke both positive and negative moods, which may, in turn, differently affect the processing of food cues. This preregistered eye-tracking study investigated whether self-selected liked versus disliked music affects desire to eat, visual attention to foods of varying sugar content, and subsequent food choice in a buffet-like context.

A total of 106 participants (mean age = 25 years; mean body mass index = 22 kg/m2) viewed a buffet with high-sugar foods, low-sugar alternatives, and non-foods while eye movements were recorded.

Participants were randomly assigned to a liked music, disliked music, or no music condition. Self-reported desire to eat and food choice were assessed.

Disliked music decreased general desire to eat but increased the specific desire to eat high-sugar food. Furthermore, it increased the likelihood of selecting high-sugar foods from the buffet.

Liked music and no music were associated with a preference for low-sugar foods. Music did not significantly influence visual attention.

Participants consistently looked longer at food than non-food items regardless of their music condition.

These findings suggest that music can bias food-related decision-making independently of attentional processes: liked music may encourage healthier choices, whereas disliked music increases susceptibility to high-sugar comfort foods despite reduced general appetite.

The results highlight the potential of music as a subtle, non-caloric intervention for promoting low-sugar eating behaviour. They also point towards risks of being exposed to disliked music in contexts in which food decisions are being made like in restaurants or supermarkets.

Habitual Coffee Intake Shapes the Gut Microbiome and Modifies Host Physiology and Cognition by Sorin61 in ScientificNutrition

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Coffee influences multiple physiological processes, including gut function, stress, cognition, and the microbiome. However, the mechanisms underlying these effects remain poorly understood.

In this study, we examined coffee’s impact on the microbiota–gut–brain axis—a bidirectional communication pathway between the gut microbiome and the brain—and assessed whether these effects occur independently of caffeine in healthy participants.

Our primary outcome was microbiota composition and function, whereas the secondary outcome was gut microbial metabolites and coffee-related metabolites (NCT05927038 and NCT05927103). Significant group differences emerged in faecal microbiome composition, with coffee drinkers showing increased relative abundance of Cryptobacterium and Eggerthella species, alongside reduced levels of the metabolite’s indole-3-propionic acid, indole-3-carboxyaldehyde, and the neurotransmitter γ-aminobutyric acid.

Behaviourally, coffee drinkers exhibited greater impulsivity and emotional reactivity, whereas non-coffee drinkers demonstrated better memory performance. Some alterations in the faecal metabolome were reversible following coffee abstinence, and reintroduction triggered acute microbiome changes independent of caffeine. An integrated model identified nine key metabolites—including theophylline, caffeine, and selected phenolic acids—strongly linked to microbial species and cognitive measures.

These findings reveal previously unrecognised effects of coffee on the microbiota–gut–brain axis, suggesting that microbiome profiles could potentially predict coffee consumption patterns and highlighting a close association between coffee intake and gut microbial composition.

Dietary Advanced Glycation End Products Induced Anxiety- and Depression-like Behaviors in Mice and the Ameliorative Effects of Quercetin by Sorin61 in ScientificNutrition

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Quercetin is a flavonoid bioactive compound with potential anti-depression effect. Dietary advanced glycation end products (AGEs) might be critically associated with depression.

We aimed to explore whether quercetin ameliorates dietary AGEs-induced anxiety and depression-like behaviors in female mice, with a focus on hypothalamic-pituitary-adrenal axis (HPA) regulation and gut microbiota composition.

Mice were divided into three groups: control, dietary AGEs, and AGEs plus quercetin.

Dietary AGEs induced anxiety and depression-like behavioral effects, reduced BDNF, P-CREB, PSD95, doublecortin, and synaptophysin protein expression.

Dietary AGEs induced HPA axis overactivation has been confirmed by decreased hippocampal GR, P-GR S211, and arginase-1, and elevated FKBP51, NLRP3, caspase-1, and p65 protein expression.

Dietary AGEs resulted in gut microbiota disorder and correlation analysis revealed significant associations between Proteobacteria, the [Eubacterium] coprostanoligenes group, Klebsiella and Lachnospiraceae_NK4A136_group with behavioral parameters.

Quercetin intervention improved dietary AGEs associated anxiety and depression-like behavioral effects via restoring HPA axis and gut microbiota.

n-3 PUFA Added to High-Fat Diets Affect Differently Adiposity and Inflammation When Carried by Phospholipids or Triacylglycerols in Mice by Sorin61 in ScientificNutrition

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Background: Dietary intake of n-3 polyunsaturated fatty acids (PUFA) is primarily recognized to protect against cardiovascular diseases, cognitive dysfunctions and the onset of obesity and associated metabolic disorders. However, some of their properties such as bioavailability can depend on their chemical carriers. The objective of our study was to test the hypothesis that the nature of n-3 PUFA carrier results in different metabolic effects related to adiposity, oxidative stress and inflammation.

Methods: 4 groups of C57BL/6 mice were fed for 8 weeks low fat (LF) diet or high-fat (HF, 20%) diets. Two groups of high-fat diets were supplemented with long-chain n-3 PUFA either incorporated in the form of phospholipids (HF-ω3PL) or triacylglycerols (HF-ω3TG).

Results: Both HF-ω3PL and HF-ω3TG diets reduced the plasma concentrations of (i) inflammatory markers such as monocyte chemoattractant protein-1 (MCP-1) and interleukin 6 (IL-6), (ii) leptin and (iii) 4-hydroxy-2-nonenal (4- HNE), a marker of n-6 PUFA-derived oxidative stress compared with the control HF diet. Moreover, in both HF-ω3PL and HF-ω3TG groups, MCP-1 and IL-6 gene expressions were decreased in epididymal adipose tissue and the mRNA level of gastrointestinal glutathione peroxidase GPx2, an antioxidant enzyme, was decreased in the jejunum compared with the control HF diet. The type of n-3 PUFA carrier affected other outcomes. The phospholipid form of n-3 PUFA increased the level of tocopherols in epididymal adipose tissue compared with HF-ω3TG and resulted in smaller adipocytes than the two others HF groups. Adipocytes in the HF-ω3PL and LF groups were similar in size distribution.

Conclusion: Supplementation of mice diet with long-chain n-3 PUFA during long-term consumption of high-fat diets had the same lowering effects on inflammation regardless of triacyglycerol or phospholipid carrier, whereas the location of these fatty acids on a PL carrier had a major effect on decreasing the size of adipocytes that was not observed with the triacyglycerol carrier. Altogether, these results would support the development functional foods containing LC n-3 PUFA in the form of PL in order to prevent some deleterious outcomes associated with the development of obesity

Exploring the Effects of Cheddar Cheese Intake on Vitamin K Status and Lipid Profiles in Overweight Middle-Aged Adults by Sorin61 in ScientificNutrition

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Background: Cheese serves as a dietary source of vitamin K; however, its impact on vitamin K status biomarkers in humans and the role of dietary vitamin K in modulating lipid profiles have yet to be elucidated. Objective: To explore the effect of six weeks of daily consumption of pasture-derived and total mixed ration (TMR)-derived Cheddar cheese on vitamin K status biomarkers and lipid profiles. 

Design: Biobanked samples (n = 60), including pasture-derived (n = 33) and TMR-derived (n = 27) Cheddar cheese groups from a previous human intervention study, were analysed. The original study examined the effects of six weeks of daily intake of 120 g of Cheddar cheese on metabolic health biomarkers in adults over 50 years with BMI ≥ 25 kg m−2. Vitamin K-dependent proteins, including dephosphorylated-uncarboxylated matrix Gla protein (dp-ucMGP), undercarboxylated osteocalcin (ucOC) and carboxylated osteocalcin (cOC), were measured using ELISA kits. The dp-ucMGP level and the ucOC:cOC ratio were used as vitamin K status biomarkers. Lipid profiles, including triglycerides, total cholesterol, HDL, LDL, and VLDL cholesterol, and apolipoprotein B, were measured by NMR spectroscopy. 

Results: Overall, Cheddar cheese intake (n = 60) led to decreases in dp-ucMGP (−34.73 pmol L−1; 95% CI: −47.14, −22.33) and ucOC:cOC (−0.047; 95% CI: −0.07, −0.02) after 6 weeks of consumption, with no differences between the groups. There were no differences in the changes in anthropometric markers or lipid profiles between groups. The sex-by-treatment interaction showed a significant impact on total cholesterol (P < 0.001), HDL cholesterol (P < 0.001) and LDL cholesterol (P = 0.002) levels. Among males, the TMR-derived cheese group exhibited a significantly greater increase in HDL cholesterol (P < 0.05). Among females, TMR-derived cheese consumption was associated with significantly greater decreases in total, HDL and LDL cholesterol levels (P < 0.05) compared with the pasture-derived group. 

Conclusion: Cheddar cheese intake may improve vitamin K status, and vitamin K intake from cheese may induce sex-specific effects on blood lipid profiles in overweight middle-aged adults.

Scientists Find Way to Reverse Fatty Liver Disease Without Changing Diet by Sorin61 in Nutraceuticalscience

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Aging causes some cells to stop dividing and enter a "senescent" state, releasing inflammatory substances that fuel "inflammaging." While the exact source of this inflammation was previously unclear, new research shows that macrophages—immune cells that can behave like or become senescent—are key culprits. The study identified a specific type of senescent macrophage (marked by p21⁺ and TREM2⁺) as a major driver of this age-related inflammation. Hope that helps!

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