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  • Microfluidic chips advance neurodegenerative disease research

    Microfluidic chips advance neurodegenerative disease research

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    A review article published in the journal Nature Communications provides a detailed overview of recent developments in microfluidic chip models for neurodegenerative diseases.

    Study: Neuropathogenesis-on-chips for neurodegenerative diseases. Image Credit: luchschenF / ShutterstockStudy: Neuropathogenesis-on-chips for neurodegenerative diseases. Image Credit: luchschenF / Shutterstock

    Background

    Recent advancements in medical science have significantly increased human life expectancy, leading to a gradual risNeuropathogenesis-on-chips for neurodegenerative diseasesNeuropathogenesis-on-chips for neurodegenerative diseases in the aging population globally. This is accompanied by a concomitant increase in the prevalence of age-related neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis.

    Neurodegenerative diseases primarily affect the cognitive and behavioral abilities of older adults. With the accumulation of dysfunctional proteins as the primary initiating factor, these diseases share some common pathogenic characteristics, including specific neuronal loss, gliosis, neuroinflammation, oxidative stress, mitochondrial dysfunction, and early vascular damage.

    Despite advancements in medical science, the development of diagnostic and therapeutic interventions for neurodegenerative diseases remains a challenging task because of the complex multifactorial pathogenesis that progresses gradually.

    Microfluidic organs or organoids-on-chips have provided a unique opportunity to experimentally reproduce critical elements of distinct brain regions associated with neurodegenerative diseases. These miniaturized systems can be used for studying disease pathogenesis, drug development, drug screening, and primary biomedical research purposes.

    Microfluidic chip design  

    The ‘Campenot chamber,’ a compartmentalized in vitro system, was the first microfluidic chip application for brain research. With two fluidically separated chambers, this device is used to study the effects of nerve growth factors on axonal growth. Later, scientists invented several miniaturized systems of neuron-glia cells, the blood-brain barrier, and the neurovascular unit.

    Microfluidic chips typically contain two or more fluidically separated chambers that are connected by microchannels, porous membranes, or phase guides. These connections are required to maintain direct or indirect interactions between homogeneous or heterogeneous cell populations kept in these chambers.      

    The earliest microfluidic chip for the brain was designed by separating a neuronal soma from its neurites using microchannels. This design was used to study directional neurite growth. More advanced neural circuit models were developed later by incorporating multiple chambers for neuronal subpopulations.

    AD is characterized by the inclusion of misfolded amyloid-β (Aβ) and neurofibrillary tangles in pyramidal neurons, primarily in the hippocampus and cortex regions of the brain. b PD is characterized by Lewy body aggregates composed of misfolded α-synuclein and degeneration of dopaminergic neurons in the substantia nigra region of the brain. c ALS is characterized by including mutant TAR DNA-binding protein 43 (TDP-43) and other proteins, degeneration of motor neurons in the motor cortex and spinal cord, and muscle atrophy with dysfunctional proteins. d HD is characterized by including mutant Huntingtin protein (mHTT) and degeneration of medium spiny neurons in the basal ganglia, and corpus striatum of the brain. AD Alzheimer’s disease, ALS amyotrophic lateral sclerosis, BDNF brain-derived neurotrophic factor, EAL endosomal-autophagic-lysosomal pathway, GABA gamma-aminobutyric acid, HD Huntington’s disease, PSEN presenilin 1, SNCA synuclein alpha.AD is characterized by the inclusion of misfolded amyloid-β (Aβ) and neurofibrillary tangles in pyramidal neurons, primarily in the hippocampus and cortex regions of the brain. b PD is characterized by Lewy body aggregates composed of misfolded α-synuclein and degeneration of dopaminergic neurons in the substantia nigra region of the brain. c ALS is characterized by including mutant TAR DNA-binding protein 43 (TDP-43) and other proteins, degeneration of motor neurons in the motor cortex and spinal cord, and muscle atrophy with dysfunctional proteins. d HD is characterized by including mutant Huntingtin protein (mHTT) and degeneration of medium spiny neurons in the basal ganglia, and corpus striatum of the brain. AD Alzheimer’s disease, ALS amyotrophic lateral sclerosis, BDNF brain-derived neurotrophic factor, EAL endosomal-autophagic-lysosomal pathway, GABA gamma-aminobutyric acid, HD Huntington’s disease, PSEN presenilin 1, SNCA synuclein alpha.

    Current neuronal chips contain multiple chambers of different diameters positioned in various geometries. These models also include microchannels with patterned shapes and controlled fluid flow. These features allow for indirect and direct, asymmetric, and symmetric neuronal connections.     

    Extra pump systems and passive hydrostatic pressure can be incorporated into chips to control fluid flow. This helps create disease models by allowing a gradient of chemicals with varying concentrations throughout the cell compartments.  

    Porous membranes with different pore sizes, numbers, and positions can be used on chips as an interface between chambers to enable indirect interactions mediated by soluble chemicals and direct physical contact. This design has been used for mimicking the blood-brain barrier on chips.

    Application of microfluidic chips for neurodegenerative disease pathogenesis

    Microfluidic chips can be used for replicating several anatomical and physiological systems, including the neuromuscular junction, corticostriatal pathway, substantia nigra, blood-brain barrier, glymphatic system, neurovascular unit, and gut-brain axis.

    To provide mechanical, structural, and biochemical cues to cells, 3D extracellular matrix gel has been introduced on chips, which allows for studying cell morphology, migration patterns, signal transduction, and gene expression in the context of neurodegenerative diseases.

    Alzheimer’s disease-on-chips

    The application of microfluidic chips in Alzheimer’s disease research has provided valuable insights into distinct pathogenic features, including amyloid-beta and tau protein accumulation, mitochondrial dysfunction, and neuroinflammation.

    Several models of neurons-on-a-chip have been used to study tau propagation and amyloid-beta toxicity. By separating the soma and neurites, neurons-on-a-chip allow real-time visualization of proteinopathy.

    A gradient chip with interstitial flow has been used to study the effect of amyloid-beta oligomers on neurons. Inflammatory cytokine-mediated migration of microglia towards Alzheimer’s disease neurons and astrocytes has been observed using a 3D static neuroinflammation-on-a-chip model.

    Blood-brain barrier-on-a-chip has been developed to fully recapitulate amyloid plaque formation, neurofibrillary tangle formation, and increased permeability of the brain endothelial cells.

    Dynamic neurospheroid-on-a-chip has been developed by incorporating an osmotic pump that creates a flow of exogenous amyloid-beta to study axonal degeneration and cell death.

    Parkinson’s disease-on-chips

    Many studies have been conducted using Parkinson’s disease-on-a-chip to primarily recapitulate alpha-synuclein-related pathogenesis. The propagation of alpha-synuclein has been studied by co-culturing neuroglioma cells that express green fluorescent protein-tagged alpha-synuclein.

    A gradient chip has been developed to manipulate intracellular alpha-synuclein expression in singularly trapped yeasts in the system with a galactose gradient. Dopaminergic neurons-on-a-chip have been developed to recapitulate mitochondrial dysfunction and neural degeneration caused by Parkinson’s disease-related mutations.     

    Substantia nigra and vascular barrier chips have been developed by co-culturing human-induced pluripotent stem cell-derived midbrain dopaminergic neurons, primary glia cells, and brain microvascular endothelial cells in chambers separated by porous membrane. This model has been used to study blood-brain barrier-on-a-chip dysfunction, progressive neuronal loss, neuroinflammation, and astrogliosis.  

    Amyotrophic lateral sclerosis on-chips

    Application of chemotactic and volumetric gradients on amyotrophic lateral sclerosis-on-chips has caused the successful formation of interactions between FUS-mutated motor neurons and mesangioblast-derived myotubes through microchannels.

    Many pathologies of amyotrophic lateral sclerosis have been recapitulated by co-culturing TAR DNA-binding protein 43 (TDP-43)-mutated motor neuron spheroid and muscle fibers in a 3D condition between two separate chambers.  

    A three-chamber-chip has been developed to create metabolic interactions between superoxide dismutase-mutated astrocytes and cortical neurons through microchannels in a glutamate gradient condition. 

    Muscle denervation pathology of amyotrophic lateral sclerosis has been studied using an open compartmentalized neuromuscular junction device that co-cultures optogenetic motor neurons and superoxide dismutase-mutated astrocytes as a spheroid.

    Huntington’s disease on-chips

    Early pathologies of Parkinson’s disease have been studied by forming synaptic connections between cortical axons and striatal dendrites through microchannels of different lengths and a separate synaptic channel.

    Corticostriatal on-a-chip has been developed to study how mutant huntingtin protein reduces the cortical axonal transport of brain-derived neurotrophic factors to trigger striatal neuron degeneration.

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  • Diet’s role in fighting vitiligo highlighted in new research

    Diet’s role in fighting vitiligo highlighted in new research

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    In a recent review published in the Journal of Cosmetic Dermatology, researchers collated available literature exploring the impacts of diet and nutritional interventions against vitiligo. Their dataset comprised 14 publications from three online scientific databases. Review findings highlight that vitiligo, a relatively rare autoimmune skin disorder, potentially develops in response to increased somatic reactive oxygen species (ROS) concentrations. While some heavy metals (Cd, Hg, and Pb) have been implicated in the development of the condition, the impacts of trace minerals like Zn and Cu remain uncertain and conflicting.

    Study: Exploring the impact of diet and nutrition on vitiligo: A systematic review of dietary factors and nutritional interventions. Image Credit: Master1305 / ShutterstockStudy: Exploring the impact of diet and nutrition on vitiligo: A systematic review of dietary factors and nutritional interventions. Image Credit: Master1305 / Shutterstock

    In general, diets and nutritional interventions rich in ROS-depleting molecules (such as vitamin C, B12, and D, polyunsaturated fatty acids (PUFAs), and antioxidants are observed to trigger beneficial vitiligo outcomes and reduce the burden of metabolism, cellular deterioration, and oxidative stress brought about by ROS. While unlikely to replace pharmacological and phototherapy interventions against vitiligo, dietary interventions present an essential step forward in reducing our reliance on these potentially side-effect-inducing clinical interventions. However, large-scale clinical trials are required before these interventions can become commonplace.

    What is vitiligo, and what do we know about its pathology?

    Vitiligo is a rare autoimmune disorder characterized by the loss of skin pigmentation in patches or blotches, usually around the mouth, hair, and eyes. It is estimated to affect between 0.004% and 2.28% of the global population, and while phototherapy and pharmacological interventions can reduce symptom visibility, no cure for the condition hitherto exists. While the mechanisms underpinning the development and progression of vitiligo remain to be elucidated, the condition is assumed to be caused by a combination of hormonal and genetic factors, particularly those pertaining to cellular deterioration (of melanocytes), metabolic imbalances, and oxidative stress.

    Heightened concentrations of reactive oxygen species (ROS) in tandem with reduced efficacy of the body’s normal antioxidant mechanisms is assumed to substantially exacerbate the disease, with research finding substantial differences in the per-erythrocyte ROS production volumes of patients with (much higher) and without vitiligo. A growing body of literature presents that, while physically harmless, vitiligo is associated with more severe comorbidities, including alopecia areata, atopic dermatitis, and psoriasis.

    As is the case in other chronic conditions characterized by altered ROS metabolism (some cancers and neurodegenerative conditions), diets are being explored for their potential antioxidant properties. Studies in various fields, including vitiligo research, support dietary interventions as natural, comparatively inexpensive, and generally side-effect-free alternatives to conventional clinical interventions (corticosteroids and calcineurin inhibitors), the latter of which are often costly and prone to side effects. Unfortunately, these studies are very recent and seemingly disconnected from each other, with a synthesis and holistic evaluation of the topic hitherto lacking.

    About the study

    In the present review (PROSPERO registration number CRD42023464740), researchers discuss up-to-date outcomes from studies and publications exploring the association between diet and vitiligo. Two independent reviewers collected papers from three online scientific repositories, namely PubMed, European PMC, and Google Scholar, using repository-optimized search strategies for publication acquisition and screening. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) guidelines were followed in the review’s methodological design and presentation.

    Of the 214 records originally found from keyword searches, 19 were found to be duplicates and were excluded. Title and abstract screening excluded 173 records, which was further curbed to the final publication set (n = 14) following full-text screening. The Rayyan platform was used to screen included publications. Elicit and PDF Gear platforms were subsequently used for data extraction, with critical variables including study identification details, methodological attributes, outcome measures, and a concise study summary.

    “…studies lacking complete or accessible full-text articles were excluded to maintain the robustness of our ability to thoroughly assess and synthesize the findings.”

    The Critical Appraisal Skills Programme (CASP) tool was employed to assess the quality and risk of bias of included publications. Data synthesis comprised outcomes categorization and consolidation, followed by their visual representation as pie charts or bar diagrams.

    Study findings

    The present review highlights the critical role of ROS and the body’s antioxidant mechanisms in the development and progression of vitiligo. ROS-producing heavy metals like cadmium (Cd), Mercury (Hg), and lead (Pb) are implicated as disease-causing substances. In contrast, the roles and impacts of micronutrients remain poorly understood, with studies presenting confounding and often contrasting results.

    Vitamin supplements, especially C, D, and B12, have been hypothesized as potential anti-vitiligo interventions due to their high antioxidant efficacy.

    “In a pilot study, the effectiveness of high-dose oral vitamin D supplementation on vitiligo repigmentation was investigated in 16 individuals with vitamin D deficiency vitiligo. Over half of the patients experienced 26%–75% repigmentation after consuming 35 000 IU daily.29 Supplementation is advised but dosing strategies aren’t established.”

    Recently, researchers have begun exploring fatty acids such as saturated fatty acids (SFAs) and polyunsaturated fatty acids (PUFAs) for their beneficial effects on vitiligo patients. PUFAs, particularly, have been shown to exert a strong immunosuppressive influence on the disease. Alpha Lipoic acid (ALA) alongside narrow band (NB) ultraviolet B (UVB) light has further been shown to reduce and even reverse vitiligo symptoms compared to a placebo.

    While the present review highlights the present dearth of vitiligo-diet association research (only 14 publications met review inclusion criteria), substantial ongoing research will soon supplement our current knowledge in the field. While unlikely to dethrone corticosteroids and calcineurin inhibitors as the primary clinical interventions against vitiligo progression, studies have shown that the efficacies of both interventions are impressively bolstered by some dietary components, suggesting their future role as adjuncts.

    “Further large-scale clinical trials are warranted to establish strong evidence and protocols, and might also help reduce the dependency on pharmacological methods, which come with their own adverse effect profiles.”

    Journal reference:

    • Hadi, Z., Kaur, R., Parekh, Z., Khanna, S., Bin Khalil, A. B., Abbasi, H. Q., Ashfaque, F., Shah, D., Patel, V. J., & Hasibuzzaman, M. A. Exploring the impact of diet and nutrition on vitiligo: A systematic review of dietary factors and nutritional interventions. Journal of Cosmetic Dermatology, DOI – 10.1111/jocd.16277, https://onlinelibrary.wiley.com/doi/10.1111/jocd.16277

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  • Limoncella apple polyphenol extract shines in IBD liver damage study

    Limoncella apple polyphenol extract shines in IBD liver damage study

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    In a recent study published in the International Journal of Molecular Sciences, a group of researchers evaluated the efficacy of ‘Limoncella’ apple polyphenol extract (LAPE) in mitigating inflammatory bowel disease (IBD)-induced hepatotoxicity through its antioxidant and anti-inflammatory properties in a dinitro-benzenesulfonic acid (DNBS)-colitis mouse model.

    Study: Polyphenol-Rich Extract from ‘Limoncella’ Apple Variety Ameliorates Dinitrobenzene Sulfonic Acid-Induced Colitis and Linked Liver Damage. Image Credit: Marcin Rogozinski / ShutterstockStudy: Polyphenol-Rich Extract from ‘Limoncella’ Apple Variety Ameliorates Dinitrobenzene Sulfonic Acid-Induced Colitis and Linked Liver Damage. Image Credit: Marcin Rogozinski / Shutterstock

    Background  

    IBDs like Crohn’s disease (CD) and ulcerative colitis (UC) lead to persistent digestive inflammation, and over 35% of patients suffer from extraintestinal manifestations (EIMs), worsening their life quality. These EIMs include joint, skin, and eye issues, with primary sclerosing cholangitis as a prevalent liver complication. The gastrointestinal system’s connection to the hepatobiliary system exposes the liver to colitis-induced inflammation. Increased intestinal permeability in IBD allows gut flora to migrate to the liver, causing inflammation and damage. Polyphenols have shown promise in treating these issues due to their antioxidant, anti-inflammatory, and lipid-lowering properties. Notably, Limoncella apple polyphenols have demonstrated effectiveness in reducing colitis-induced liver damage, necessitating further research to clarify their mechanisms and potential in human IBD treatment.

    About the study 

    Chemicals like DNBS, myeloperoxidase (MPO), and other reagents were sourced from reputable suppliers, ensuring high purity for the study. For the investigation of LAPE, apples were harvested from Castelvetere del Calore, Italy, and processed using a method involving methanol to extract the polyphenols, which were then analyzed through high-performance liquid chromatography (HPLC) to identify the polyphenolic content.

    Male CD1 mice were housed under controlled conditions for the experimental model to ensure their well-being. The study followed ethical guidelines, with approval from relevant authorities. Colitis was induced in these mice using DNBS, and LAPE was administered to evaluate its therapeutic potential. Various concentrations of LAPE were tested to assess its effect on colonic inflammation and liver damage markers. Intestinal permeability was measured using fluorescein isothiocyanate (FITC)-conjugated dextran, while MPO activity assays and cytokine production measurements provided insights into the inflammatory response. 

    Histological analysis of colon and liver tissues, along with the assessment of serum biochemical markers, offered a further understanding of LAPE’s protective effects against colitis-induced damage. The study’s findings were rigorously analyzed, employing statistical methods to ensure the reliability of the results, pointing towards the potential benefits of LAPE in treating inflammatory conditions and their complications.

    Study results 

    The present study analyzed the polyphenolic composition of LAPE  using HPLC- Diode-Array Detection (DAD), revealing significant quantities of gallic acid, procyanidin B1, catechin, chlorogenic acid, and other polyphenols, indicating a rich polyphenolic profile beneficial for health. In experiments using the DNBS model of colitis in mice, LAPE showed promising anti-inflammatory properties by improving both macroscopic and histopathological damage caused by DNBS. Notably, LAPE administration led to a significant reduction in the colon weight/length ratio, an indicator of inflammation, and improved histological signs of colon injury, such as crypt loss and inflammatory cell infiltration.

    Further investigation into LAPE’s anti-inflammatory effects revealed a significant decrease in neutrophil infiltration, as measured by MPO activity, and a reduction in pro-inflammatory cytokines interleukin (IL)-1β and IL-6 in the colons of DNBS-treated mice. These findings underscore LAPE’s potential in modulating inflammatory responses within the gut.

    Moreover, LAPE’s role in restoring intestinal barrier function was highlighted by its ability to significantly reduce increased intestinal permeability in DNBS-treated mice, as indicated by lower serum levels of FITC-dextran. The study also found that LAPE treatment helped maintain β-catenin levels on the cell membrane, which is crucial for cell adhesion and maintaining intestinal barrier integrity.

    The research extended to examining LAPE’s impact on liver dysfunction and lipid accumulation associated with colitis. DNBS-induced colitis resulted in elevated serum liver enzymes like Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and increased lipid peroxidation, indicative of liver damage and oxidative stress. Remarkably, LAPE administration significantly reduced these effects, demonstrating its protective role against liver dysfunction and oxidative stress. Histological assessments further supported LAPE’s efficacy, showing reduced hepatic lipid accumulation and improved liver histopathology in DNBS-treated mice.

    Conclusions 

    To summarize, IBDs like UC and CD cause chronic gastrointestinal inflammation, potentially leading to liver damage. Current treatments, often associated with adverse effects, highlight the need for safer alternatives. This study focuses on 

    LAPE, demonstrating its effectiveness in reducing intestinal and liver inflammation in a DNBS-induced colitis model in mice. LAPE not only alleviated colonic inflammation by decreasing inflammatory markers and improving histological damage but also enhanced intestinal barrier function, potentially through modulation of the Wnt/β-catenin signaling pathway. Additionally, it reduced liver damage, evidenced by lower liver enzyme levels and decreased lipid accumulation, likely via inhibiting the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. The findings suggest that a small daily intake of Limoncella apples could be beneficial for IBD patients, offering a natural approach to reduce both intestinal and liver inflammation.

    Journal reference:

    • Lama S, Pagano E, Borrelli F, et al. Polyphenol-Rich Extract from ‘Limoncella’ Apple Variety Ameliorates Dinitrobenzene Sulfonic Acid-Induced Colitis and Linked Liver Damage. International Journal of Molecular Sciences. (2024), DOI: 10.3390/ijms25063210, https://www.mdpi.com/1422-0067/25/6/3210 

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  • How culinary herbs and spices may boost gut health through polyphenols

    How culinary herbs and spices may boost gut health through polyphenols

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    In a recent study published in Nutrients, a group of researchers explored how regular polyphenol intake from diet affects gut microbiota composition in healthy adults.

    Study: Relationships between Habitual Polyphenol Consumption and Gut Microbiota in the INCLD Health Cohort. Image Credit: Danijela Maksimovic/Shutterstock.comStudy: Relationships between Habitual Polyphenol Consumption and Gut Microbiota in the INCLD Health Cohort. Image Credit: Danijela Maksimovic/Shutterstock.com

    Background 

    Polyphenols, found in a wide range of foods and drinks, are phytochemicals known for their potential health benefits, including their influence on gut microbiota.

    These compounds can impact health through direct cellular effects and by modifying gut microbial composition, producing bioactive metabolites that affect various physiological processes.

    However, the specific effects of habitual polyphenol consumption, particularly from everyday foods and culinary herbs and spices, on gut microbiota are not fully understood.

    Research indicates that polyphenols can enhance the abundance of beneficial bacteria and reduce harmful ones, contributing to improved gut health and potentially influencing broader health outcomes like inflammation, oxidative stress, and cardiovascular health.

    Further research is needed to clarify the effects of habitual polyphenol consumption on gut microbiota and its implications for human health.

    About the study 

    The present study conducted a secondary analysis of data from the International Cohort on Lifestyle Determinants of Health (INCLD Health), focusing on baseline data to examine the relationship between dietary polyphenol intake and gut microbiome composition.

    A subset of 96 participants was selected based on the completion of specific surveys and tests, excluding those with certain health conditions or antibiotic usage.

    Deoxyribonucleic acid (DNA) was extracted from faecal samples using a specific kit and sequenced to identify microbial DNA.

    The sequencing targeted the V4 viz fourth variable region of the 16S ribosomal ribonucleic acid (rRNA) gene, with subsequent processing to identify and classify microbial taxa. The data underwent filtering and normalization to ensure reliability using an online platform designed for microbiome data analysis.

    Polyphenol intake was quantified based on dietary data collected through a food frequency questionnaire, with an emphasis on identifying polyphenol content in various foods and beverages, excluding minimal polyphenol sources.

    The polyphenol intake assessment considered the total daily consumption and the frequency of herb and spice use known for their high polyphenol content. This approach allowed for a detailed analysis of polyphenol exposure from regular dietary habits.

    Statistical analysis explored gut microbiota diversity and its relation to polyphenol intake. This included examining differences in microbial diversity and abundance across varying levels of polyphenol consumption. 

    Study results 

    The study analyzed the characteristics and dietary habits of 96 participants, predominantly white, non-Hispanic females with normal cardiometabolic measures. Most were non-smokers and moderate alcohol consumers.

    Dietary polyphenol consumption varied, with flavonoids being the most consumed class. Commonly used herbs and spices include black pepper, cinnamon, ginger, onion, garlic, and turmeric, with varying polyphenol content.

    Microbial community analysis, stratified by polyphenol consumption, showed Firmicutes as the dominant phyla across all groups, without significant differences in microbial diversity or community structure between low, medium, and high polyphenol consumers.

    However, the abundance of specific microbial taxa varied with dietary polyphenol levels. Higher polyphenol consumption was associated with a greater abundance of Lactobacillus and Sutterella and a lower abundance of the Eubacterium ventriosum group, Ruminococcus torques group, Bacteroides, and Enterococcus.

    The frequency of polyphenol-rich herb and spice use similarly did not affect overall microbial diversity but influenced specific taxa abundance.

    High-frequency users showed a different microbial profile than low-frequency users, with variations in Lachnospiraceae UCG 004, Lachnotalea, and Lachnospiraceae UCG 001 abundance.

    Correlation analyses revealed significant relationships between total and specific classes of polyphenol consumption and microbial taxa. Lactobacillus and Sutterella abundance positively correlated with total polyphenol, flavonoid, and lignan consumption.

    Conversely, Eubacterium ventriosum, Ruminococcus torques group, Bacteroides, and Enterococcus abundances are inversely correlated with polyphenol intake.

    Specific polyphenol classes also showed varied correlations with different microbial taxa, highlighting the complex interplay between diet and gut microbiota.

    Conclusions 

    The study examined the link between dietary polyphenol intake and gut microbiota in healthy adults, focusing on consuming polyphenol-rich foods and herbs/spices.

    Findings revealed specific gut microbial patterns associated with polyphenol consumption levels, showing an increased abundance of beneficial microbes like Lactobacillus and Sutterella with higher polyphenol intake.

    Conversely, certain microbes showed an inverse relationship with polyphenol consumption, indicating complex interactions between diet and gut health. The study also identified potential microbial markers for polyphenol-rich herb and spice use.

    The findings highlight the complex interaction between dietary polyphenols and gut microbiota, indicating that polyphenols might influence gut health.

    This suggests a promising role for dietary polyphenols in gut health modulation, emphasizing the importance of further research to understand these relationships better.

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  • Microplastics and nanoplastics could be harming your heart health

    Microplastics and nanoplastics could be harming your heart health

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    In a recent study published in The New England Journal of Medicine, researchers investigated whether micro- and nano-plastics (MNPs) are detectable in atherosclerotic plaques.

    Study: Microplastics and Nanoplastics in Atheromas and Cardiovascular Events. Image Credit: chayanuphol/Shutterstock.comStudy: Microplastics and Nanoplastics in Atheromas and Cardiovascular Events. Image Credit: chayanuphol/Shutterstock.com 

    Background

    Plastic production has been constantly increasing and is likely to continue until 2050. Plastics can degrade and form MNPs, inducing toxic effects.

    Studies have demonstrated the entry of MNPs into the body through skin exposure, inhalation, and ingestion, as well as their interactions with tissues/organs. Further, MNPs have been detected in the placenta, liver, lungs, urine, blood, and breast milk. Recent preclinical reports implicate MNPs as a cardiovascular risk factor.

    In vitro findings indicate that some MNPs promote inflammation, oxidative stress, and apoptosis in endothelial cells. Moreover, animal studies support the role of MNPs in myocardial fibrosis, endothelial dysfunction, and cardiac function impairment.

    However, their clinical relevance remains unknown. There is no evidence to suggest the infiltration of MNPs in human vascular lesions or associations between MNP burden and cardiovascular disease.

    About the study

    In the present study, researchers investigated the presence of MNPs in atherosclerotic plaques and the associations between MNP burden and cardiovascular disease.

    Consecutive patients aged 18–75 with asymptomatic carotid artery stenosis indicated for carotid endarterectomy were screened. Patients with valvular defects, secondary causes of hypertension, malignant neoplasms, or heart failure were excluded.

    Besides, patients who had complications in the postoperative period were also excluded. Baseline clinical examinations were performed, and health records were accessed for clinical, demographic, and intervention data.

    Fasting blood specimens were collected for biochemical analyses. Participants were followed up after carotid endarterectomy.

    Surgically excised atheromatous plaque specimens were obtained at atherectomy. MNP abundance was measured using pyrolysis–gas chromatography–mass spectrometry, and results were validated using electron microscopy (EM) and isotope analysis.

    The primary endpoint was a composite of non-fatal stroke, non-fatal myocardial infarction, or death. Patients were grouped based on the presence/absence of MNPs in plaques.

    Cox regression was performed to assess associations between the presence of MNPs in plaques and composite endpoint incidence.

    Analyses were adjusted for sex, age, body mass index (BMI), creatinine, low- and high-density lipoprotein cholesterol, total cholesterol, triglycerides, hypertension, diabetes, and prior cardiovascular events.

    Findings

    The team screened 312 patients; of these, 47 were lost to follow-up or had missing data, and eight had a stroke or died before discharge.

    Overall, 257 subjects were followed up for an average of 33.7 months. Polyethylene was detectable in the excised carotid plaque of 150 patients; thirty-one of these also had measurable levels of polyvinyl chloride in the plaque.

    The average levels of polyethylene and polyvinyl chloride in plaques were 21.7 μg/mg and 5.2 μg/mg, respectively.

    Patients with these MNPs were younger, male, smokers, had dyslipidemia, cardiovascular disease, diabetes, and higher levels of creatinine, and were less likely to have hypertension compared to those without MNPs.

    Ten random plaque samples with both polyvinyl chloride and polyethylene were analyzed using EM. Transmission EM (TEM) revealed particles (foreign origin) smaller than one μm with jagged edges within foamy macrophages.

    Besides, the same slices were observed with scanning EM (SEM), and spectral X-ray maps were generated from particles resembling those observed with TEM.

    The maps indicated decreased carbon and oxygen in plaque samples and increased chlorine. Given the probable non-biologic nature of chlorine, this might confirm polyvinyl chloride deposits.

    The researchers performed the isotope analysis on 26 random plaque samples as petroleum-derived plastics exhibit lower δ13C values, i.e., the ratio between carbon-13 and carbon-12, than human tissues.

    This analysis revealed two distinct patient clusters. One cluster included patients with higher δ13C values; the other cluster showed lower values, perhaps due to MNP contamination. Lower values were more evident in plaques with MNPs.

    The primary endpoint event occurred in 30 and eight patients with and without evidence of MNPs, respectively. Patients with MNPs in plaques had a higher risk of the primary endpoint events than those without MNPs.

    Conclusions

    In patients with high-grade asymptomatic carotid stenosis indicated for carotid endarterectomy, those with MNPs in plaques had a higher incidence of the composite endpoint than those without MNPs.

    Notably, the results do not prove causality; the association between MNPs in plaques and the primary endpoint might also entail risks from exposure to unmeasured, residual, or other confounding variables.

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  • Research finds link between unhealthy eating and chronic pain severity, calls for comprehensive dietary support

    Research finds link between unhealthy eating and chronic pain severity, calls for comprehensive dietary support

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    In a recent study in Scientific Reports, researchers analyzed trends related to dietary and lifestyle habits among individuals living with chronic pain.

    Their results indicate that despite common suboptimal habits such as fast-food consumption and irregular mealtimes, many younger people, those with obesity, and individuals with extended pain expressed a desire to live healthier.

    These findings can help healthcare professionals address nutrition in pain management regimens.

    Study: Eating habits and the desire to eat healthier among patients with chronic pain: a registry-based study. Image Credit: fizkes/Shutterstock.comStudy: Eating habits and the desire to eat healthier among patients with chronic pain: a registry-based study. Image Credit: fizkes/Shutterstock.com

    Background

    Researchers believe that one in five adults worldwide lives with chronic pain, which should be treated using biopsychosocial strategies that address social, psychological, and biomedical factors and incorporate factors related to nutrition, stress reduction, sleep, exercise, and activity.

    Nutrition is closely related to chronic pain, with better nutrition correlating with better pain outcomes and vice versa. Diet can modulate inflammation, oxidative stress, gut health, and lipid and glucose metabolism while altering the central nervous system.

    Poor diet quality can also result from isolation and depression, which are commonly experienced by people living with chronic pain.

    Understanding dietary behaviors, particularly in terms of eating ultra-processed, nutrient-poor, and energy-rich foods, can help medical professionals treat chronic pain and encourage their patients to adopt more optimal dietary behaviors. However, large-scale surveys have not been used to investigate these factors.

    About the study

    Researchers recruited patients at a specialized pain and rehabilitation center in Sweden, many of whom had been diagnosed with neck pain, lower back pain, hypermobile Ehler-Danos syndrome, and fibromyalgia.

    To be included in the study, patients needed to fill up questionnaires, including self-reported height and weight, and to provide consent that their data could be utilized. Baseline information or data from before a consultation with a physician was used.

    Physical or functional impairments impacted the ability of several patients to work, and many also experienced psychosocial stresses like social isolation, depression, and anxiety.

    The researchers collected information about their pain, psychometric data, quality of life, physical disability, and socio-demographic backgrounds.

    The average pain intensity in the week preceding the survey was scored from 0 (meaning no pain) to 10 (meaning the worst possible pain level).

    Participants also provided information on when they had started feeling their current pain level and the locations of the body where they felt it, which was used to calculate a Pain Region Index (PRI).

    Depression and anxiety were each scored from 0 to 21, with a score over 10 indicating that the patient was depressed or anxious, respectively. Lifestyle factors included tobacco and alcohol consumption, adherence to regular mealtimes, and intake of fruit, vegetables, fast food, and confectionery.

    Participants were also asked to select their priorities from increasing exercise, eating healthier, ceasing smoking, reducing alcohol consumption, and reducing weight. They could also state that none of these were priorities.

    Statistical tests, correlation analysis, and regression modeling were used to analyze the data, and sensitivity analysis was used to evaluate bias due to missing data.

    Findings

    Of the 2,152 people included in the study, about 72% were women, 84% had been born in a Nordic country, 20% had been to university, and less than a third were satisfied with their socioeconomic status. On average, they were 46.1 years old, and more than half were obese or overweight.

    More than 50% said they had been in pain for five years or more, reported high pain intensity and spatial extent of pain, and had either depression or anxiety or both. One in three were categorized as clinically emotionally distressed.

    Based on statistical testing, people who said they desired to eat healthier (PD) were more likely to be young than those who did not (PND), had a higher BMI, reported a longer duration of pain, had greater spatial pain extent and emotional distress, and were less satisfied with their socioeconomic status.

    Slightly over 27% of participants reported having irregular mealtimes; these were twice as common among PD participants than among PND participants.

    The PD group also reported lower fruit and vegetable intake and higher confectionary and fast-food consumption. Notably, the PD group reported lower alcohol consumption frequency than the PND group and were slightly more likely to consume tobacco.

    Correlation analysis suggested that mealtime regularity was significantly associated with pain scores, duration, and PRI, but also varied with obesity and social and demographic factors. The pain score was significantly associated with all suboptimal eating habits.

    Even in the regression model, the desire to eat healthier was significantly associated with suboptimal dietary habits.

    Multivariate regression analysis also showed that the PD group was, on average, aged between 18 and 29, more likely to be obese, and more likely to have a higher PRI.

    Conclusions

    The effectiveness of lifestyle interventions, including dietary ones, depends on the motivations and desires of the intervention group.

    These findings show that many people with suboptimal eating habits want to adopt healthier behaviors, indicating an opportunity for healthcare professionals to intervene using behavior change and education strategies to help manage chronic pain.

    Journal reference:

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  • How can food influence the severity of menopausal hot flashes?

    How can food influence the severity of menopausal hot flashes?

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    In a recent review published in Nutrients, researchers reviewed scientific literature from the previous five years, especially genome-wide association studies (GWAS), to identify mechanisms and nutrients related to menopause hot flashes.

    Study: Menopause Hot Flashes and Molecular Mechanisms Modulated by Food-Derived Nutrients. Image Credit: fizkes/Shutterstock.comStudy: Menopause Hot Flashes and Molecular Mechanisms Modulated by Food-Derived Nutrients. Image Credit: fizkes/Shutterstock.com

    Background

    The etiology of vasomotor symptoms (VMS), such as hot flashes, is unknown; however, they may be molecular and polygenic.

    Food provides bioactive compounds and nutrients to the human body, digested via several enzymatic biological pathways. The compounds can stimulate molecular signaling pathways, which activate effector protein molecules controlling hot flashes experienced by menopausal women.

    About the review

    In the present review, researchers explored the biological mechanisms underlying menopause hot flashes and related food-derived nutrients.

    Introduction

    Menopause refers to a physiological process that affects women at 50 years of age, characterized by a year of amenorrhea with no additional pathological or physiological factors.

    The menopausal transitional phase, occurring between irregular menstrual periods and menopause, precedes this one year.

    Menopausal transition symptoms include monthly irregularities, hot flashes, sleeplessness, sweating, vertigo, palpitation, tinnitus, headache, memory issues, mood changes, lack of focus, skin changes, genitourinary atrophy, and body weight changes.

    Hot flashes, a common menopausal transitional feature, may present with palpitations, night sweats, irritability, and anxiety and lasts two to four minutes.

    Hot flashes might occur infrequently or at least once per hour and are frequently associated with worse life quality, decreased productivity, reduced mood, embarrassment, exhaustion, anxiety, sleep disruption, social isolation, and impaired memory performance.

    Hormone therapies are highly effective in treating hot flashes but are not always feasible. Future studies on pathways underlying menopause hot flashes could aid in developing targeted therapies, as foods might alter the processes of menopause hot flashes and regulate their effects.

    Nutritional compounds and pathways involved in menopause hot flashes

    Several biochemical pathways and compounds cause hot flashes, a frequent symptom of menopause. These pathways differ from individual to individual and involve thermoregulatory processes controlled by the parasympathetic and sympathetic nervous systems.

    Thermoregulatory processes, such as the upregulation of neuropeptides like kisspeptin and neurokinin B, help to dissipate heat during menopause.

    Nutritional compounds that modulate signaling pathways, such as nutrients that modulate the kisspeptin-gonadotropin-releasing hormone (GnRH) pathway; nutrients that modulate the aryl hydrocarbon receptor (AHR) signaling; catechol estrogens and estrogen sulfotransferase; and nutrients that modulate the inflammatory-oxidative stress biomarker, may cause hot flashes.

    Compounds linked to hot flashes include genistein, docosahexaenoic acid (DHA), polyunsaturated fatty acid (PUFA), saturated fatty acid (SFA), β-carotene, curcumin, folic acid (Pteroyl-L-glutamic acid), vitamin B12, high-fat diet components, tryptophan metabolites, apigenin, chrysin, epicatechin, quercetin, resveratrol, and vitamin E.

    Genistein boosts GnRH production via regulating kisspeptin receptors, sirtuin 1 (SIRT1), protein kinase c γ (PKCγ), and makorin ring finger protein 3 (MKRN3). DHA, PUFA, and SFA promote GnRH mRNA expression.

    Palmitate disrupts hypothalamic function in GnRH neurons by regulating spexin (SPX) and its receptors, galanin receptor 2 (GALR2) and galanin receptor 3 (GALR3), through pathways involving protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and Toll-like receptor 4 (TLR4).

    β-carotene, curcumin, tryptophan metabolites, and high-fructose diet (HFD) components such as cholesterol, fructose, and palmitic acid activate aryl hydrocarbon receptors (AHR) and folic acid and vitamin B12 inhibit their transcriptional activity.

    Vitamin E lowers hot flashes over the week and enhances antioxidant status by boosting total antioxidant capacity (TAC). Higher ghrelin levels are associated with an increased risk of hot flashes in women in the early and late stages of menopause.

    Hot flashes are associated with insulin resistance in postmenopausal women, and the relationship between the two depends on the leptin-adiponectin interaction.

    Low estrogen activation of glucose transporter 1 (GLUT) may cause hot flashes, a frequent central nervous system symptom. Studies have demonstrated significant connections between SNPs in numerous genes, including aryl hydrocarbon receptor (AHR), aryl hydrocarbon receptor repressor (AHRR), aryl hydrocarbon receptor nuclear translocator (ARNT), catechol-O-methyltransferase (COMT), and cytochrome P450 (CYP) enzymes such as CYP1 A2, CYP3A4, and CYP19 A1.

    These symptoms are most prevalent among African American women, Asian women, and white women of Hispanic and non-Hispanic heritage in the United States.

    Conclusion

    To conclude, based on the review findings, several variables, including food-derived nutrients and molecular pathways, impact hot flashes, a frequent symptom of menopause.

    These symptoms are a primary concern for women, and understanding the underlying causes is critical. Modifying these processes may help relieve hot flash symptoms.

    Hot flashes may be associated with lower estrogen levels, hypothalamic processes, adipocyte-derived hormones, the kisspeptin-GnRH pathway, aryl hydrocarbon receptor signaling, glucose availability, inflammatory-oxidative stress, catechol estrogens, and estrogen sulfotransferase.

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  • Flavonol-rich diet linked to lower mortality and disease risk, study shows

    Flavonol-rich diet linked to lower mortality and disease risk, study shows

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    In a recent prospective cohort study published in the journal Scientific Reports, researchers investigated the association between flavonol intake and cause-specific and all-cause mortality risk in adults in the United States. They found that an elevated dietary intake of flavonol is associated with a lower risk of all-cause mortality as well as Alzheimer’s disease (AD), cancer, and cardiovascular disease (CVD)-related mortality risk.

    Study: Flavonol-rich diet linked to lower mortality and disease risk, study shows. Image Credit: sematadesign / ShutterstockStudy: Flavonol-rich diet linked to lower mortality and disease risk, study shows. Image Credit: sematadesign / Shutterstock

    Background

    Flavonoids are biologically active polyphenolic compounds found in various plant-based foods. Among the six subclasses of flavonoids, flavonols are the most prevalent and active. Primary flavonols like quercetin, kaempferol, myricetin, and isorhamnetin are abundant in tea, onions, and berries. The consumption of flavonoids is known to potentially enhance endothelial function, maintain nitric oxide status, and influence biological processes relevant to lipid metabolism, platelet function, inflammation, oxidative stress, and blood pressure. Additionally, flavonoids are also known to exhibit anti-tumor effects by targeting key molecules and pathways, leading to apoptosis and inhibiting cell growth and metastasis.

    However, the relationship between flavonol intake and mortality risk has not been studied thoroughly so far. Therefore, using data from the National Health and Nutrition Examination Survey (NHANES) database, researchers in the present study explored the relationship between flavonol intake (total flavonol, kaempferol, myricetin, isorhamnetin, and quercetin), all-cause mortality risk, and cause-specific mortality risk (AD, CVD, cancer, and diabetes mellitus (DM)).

    About the study

    The study included 11,679 individuals aged≥ 20 who completed questionnaires, in-person assessments, and laboratory tests. The exclusion criteria were lack of flavonol intake and missing basic and demographic information. Flavonol intake data for the present study were derived from the US Department of Agriculture Survey Food and Beverage Flavonoid Values database (2003–2004). Detailed dietary interviews were conducted to capture information on foods and beverages consumed in the preceding 24 hours. The precise amounts of total flavonols were estimated in various foods, and the daily flavonol intake of participants was calculated.

    For mortality analysis, data from the National Death Index file and the 2019 Public Access Link mortality dataset were used. Mortality was categorized by causes such as cancer, CVD, DM, AD, and other causes, as per the International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) codes. Follow-up was conducted from the interview date to either the date of death or the study’s conclusion on December 31, 2019. Participants were stratified based on sociodemographic variables, including age, sex, race/ethnicity, marital status, education level, poverty ratio, alcohol consumption, body mass index (BMI), disease history, and the presence of various health conditions. Statistical analysis involved the use of Cox regression, Fine and Gray competing risks regression models, hazard ratios (HR), chi-square tests, and sensitivity analyses.

    Results and discussion

    Participants with the highest total flavonol intake tended to be male, younger, Non-Hispanic White, married, educated, above the poverty line, alcohol consumers, with BMI 18.5–30.0 kg/m2 and had a history of DM, hypertension, hyperlipidemia, congestive heart failure, coronary heart disease, angina, heart attack, and stroke. Increasing total flavonol intake showed a declining trend in all-cause mortality as well as AD, cancer, and CVD-specific mortality (p < 0.05 for all). Similar decreasing trends were observed for isorhamnetin, kaempferol, and quercetin intakes across various mortality categories, while myricetin intake exhibited a decreasing trend in AD mortality.

    While higher age was associated with a significant increase in all-cause mortality, female gender was found to be significantly linked to a lower risk of all-cause mortality. Conversely, a history of diseases was significantly associated with a higher risk of all-cause mortality.

    Further, higher total flavonol intake, particularly isorhamnetin, kaempferol, myricetin, and quercetin, was found to be associated with a reduced risk of all-cause and mortality owing to AD, CVD, cancer, and other causes. However, no correlation was found between flavonol intake and DM-specific mortality (p>0.05). The findings from the subgroup and sensitivity analyses aligned with the study’s main findings.

    Although the study is strengthened by its use of a multiple confounder-adjusted competing risks model to address competing risks of death, the study is limited by missing flavonol intake data, potential lack of generalizability, lack of data on primary food sources and dietary patterns, and the lack of exclusion of micronutrient supplement intake.

    Conclusion

    In conclusion, the present study establishes an association between dietary flavonol intake and overall mortality as well as cancer, AD, and CVD-specific mortality risk in US adults. The findings suggest that flavonol intake could be employed as an independent and reliable predictor of disease survival, offering patients the potential for health- and risk-management through dietary modifications.

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  • Can dietary patterns impact stomach cancer risk?

    Can dietary patterns impact stomach cancer risk?

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    In a recent review published in Frontiers in Oncology, researchers investigated eating patterns and indices related to gastric cancer and explored their association with stomach cancer risk.

    Study: Review of dietary patterns and gastric cancer risk: epidemiology and biological evidence. Image Credit: Peakstock/Shutterstock.comStudy: Review of dietary patterns and gastric cancer risk: epidemiology and biological evidence. Image Credit: Peakstock/Shutterstock.com

    Background

    Gastric cancer is a common cancer worldwide, accounting for considerable global mortality. Despite attempts to minimize Helicobacter pylori prevalence and enhance food storage, the incidence and fatality rates of stomach cancer have decreased.

    Epidemiological studies have found links between eating habits and stomach cancer risk. Individual dietary components, on the other hand, have produced inconsistent results in terms of the stated risk of stomach cancer.

    Assessing eating patterns yields more reliable effect estimates and outcomes, emphasizing the need for comprehensive cancer prevention recommendations.

    About the review

    In the present review, researchers reviewed existing data on the impact of diet on gastric cancer risk.

    Diet patterns can be posteriori (formed from cohort population data) or a priori (created using existing information about food, nutrients, and illness). Posteriori patterns are determined using statistical approaches such as principal component analysis, factor analysis, and cluster analysis.

    A priori patterns may derive from country-specific standards, chronic disease-preventive diets, or cultural eating habits.

    Association between a posteriori eating patterns and stomach cancer

    In case-control studies, healthy eating patterns minimized the risk of stomach cancer, but an “unhealthy” dietary pattern raised the risk.

    A comprehensive meta-analysis revealed that greater compliance with “prudent” diet patterns was related to a lower incidence of stomach cancer [odds ratio (OR) 0.8].

    In contrast, increased compliance with Western diets increased the risk of total stomach cancer (odds ratio, 1.5). The association between poor eating habits and stomach cancer risk was more robust for cardia stomach cancers (OR, 2.1) than for distal stomach cancers (OR, 1.4).

    Other meta-analyses showed that individuals consuming healthy foods had decreased stomach cancer risks (OR, 0.7) considerably.

    In contrast, following unhealthy diets increased stomach cancer risk (OR, 1.6). A 2017 meta-analysis found that “Western” diets increase gastric cancer risk.

    However, meta-analytical research of 13 case-control studies and eight studies of the prospective cohort type found that those abiding by “prudent” diets had a lower chance of developing stomach cancer.

    A priori dietary patterns, dietary indices, and gastric cancer

    The relationship between eating habits and stomach cancer risk is complicated and nuanced. There is limited research on the link between high health eating index (HEI) or alternate HEI (AHEI) scores and the risk of stomach cancer.

    A comprehensive review and meta-analysis found that higher adherence to HEI and AHEI dietary patterns was associated with a lower risk of total cancer-specific mortality.

    New case-control research from Iran found that eating the dietary approaches to stop hypertension (DASH) diet was related to a 54% lower incidence of stomach cancer.

    The DASH diet’s components, such as excessive salt intake, red meat consumption, and fruits, have been linked to an increased risk of stomach cancer.

    A Markov cohort state-transition model projected that a low sodium-DASH diet reduced stomach cancer risk by 25% in men and 21% in women.

    Meta-analyses indicate that Mediterranean diet (MD) followers are less likely to develop stomach cancer.

    MD vitamins and fibers reduce H. pylori colonization, whereas polyphenol-rich foods and extra-virgin olive oil (EVOO) reduce inflammation by inhibiting free radicals and lowering oxidative stress.

    Omega-3 fatty acids reduce triglyceride levels and inflammation, methionine reduces body weight and insulin resistance, branched-chain amino acids improve insulin sensitivity, and short-chain fatty acids reduce trimethylamine N-oxide (TMAO) and inflammation and regulate autoimmunity factors.

    Patterns based on biological markers

    Inflammation increases gastric cancer risk, particularly among men. Pro-inflammatory foods increase the incidence of intestinal and diffuse cancer subtypes.

    The upregulation of cytokines and chemokines, which recruit several hematopoietic and progenitor cell types to inflamed stomach tissues, may cause chronic inflammation.

    Gastric cancer-related inflammation includes inflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α). IL-1 has an anti-tumor impact, whereas IL-6 is associated with tumor progression, invasion, and metastasis.

    The ketogenic diet (KD) is associated with anti-cancer treatment in advanced gastric cancer patients. The KD alters glucose metabolism and inhibits insulin signaling and insulin-like growth factor 1 (IGF-1), the primary energy source for tumor cells. KD reduces nicotinamide adenine dinucleotide phosphate (NADPH) generation to increase oxidative stress in tumor cells.

    Ad libitum KD therapy inhibits hypoxia-related and growth-driven proteins, influencing tumor progression.

    Ketones enter cancer cells by monocarboxylate transporters (MCTs), limit lactate export, reduce cancer survival time, and prevent the activation of NLR family pyrin domain containing 3 (NLRP3), nuclear factor kappa B (NF-kB) and Signal transducer and activator of transcription 3 (STAT3) activation, lowering IL-1β expression.

    The review findings indicate that dietary patterns can influence gastric cancer risk by influencing metabolites, gut microbiota, inflammation, and immune function.

    Inconsistency in results might be owing to various factors such as meal types, recollection bias, overall energy consumption, and other confounders. Large-scale prospective cohort studies could improve the validity of the findings.

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  • Unlocking the health benefits of Valentine’s Day chocolates

    Unlocking the health benefits of Valentine’s Day chocolates

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    Valentine’s Day is here and plenty of couples are celebrating, but for some, chocolate is their one true love. Elvira de Mejia, professor of food science at the University of Illinois Urbana-Champaign’s College of Agricultural, Consumer and Environmental Sciences (ACES), investigates the health benefits of dark, white, milk, and even Valentine’s Day chocolates.

    With Valentine’s Day on the way, let’s dive into chocolate! What are the healthy compounds in chocolate and how do they work in our bodies?

    Chocolate contains more phenolic compounds -; especially flavonoids (flavanols) such as catechin and epicatechin -; than any other food. These compounds have very high anti-inflammatory and antioxidant properties in our bodies. As we know, oxidative stress and inflammation are two of the main factors that affect the development of chronic diseases, including cardiovascular diseases. So the main components in cocoa are responsible for mediating inflammation and oxidative stress.

    What are the differences between dark, milk, and white chocolate?

    What we call cocoa or cacao is the dry, fully fermented seed of the fruit that is later developed into chocolate. So chocolate is really a solid made by combining the products of cocoa liquor and cocoa butter, alongside lots of sugar. The percentages of cacao on chocolate packages represent the proportion of cocoa liquor. The type of chocolate consumed in the U.S. is mainly milk chocolate, which typically contains only 10 to 12% of cocoa liquor. Sweet, bittersweet, or dark chocolate should have at least 35% of cocoa liquor, which is where you start to see health benefits. White chocolate contains only cocoa butter, at least 20% by weight, but not cocoa liquor. This makes it less recommended for consumption since it doesn’t contain those healthy compounds.

    How much chocolate do we need to eat in order to see health benefits?

    There are many studies showing chocolate’s health benefits related to diabetes, immune response, cardiovascular diseases, reduction of hypertension, and atherosclerosis. Several of these studies tested the effects of 30 to 50 grams of chocolate per day, but there have been reports of positive health responses for myocardial infarction with only 7.5 grams per day. Other studies claim one to three servings per month, or one to two servings per week, can significantly lower rates of heart failure hospitalization or death compared to no chocolate in the diet. As of now, however, there are no official recommendations for chocolate consumption.

    So, when we consume Valentine’s Day chocolates, do they contain the same healthy compounds?

    We have to be careful about the content of sugar and cocoa butter because of the calories and saturated fat they may include. Also, milk products added to chocolate, for example, can reduce the bioavailability of beneficial compounds when proteins and phenolic compounds interact with one another. It’s okay to enjoy Valentine’s Day chocolates, but as small amounts of a balanced diet! Avoid white or milk chocolate and try to eat dark chocolate whenever possible, so that you can reap some of the health benefits while having fun and celebrating Valentine’s Day.

    Source:

    University of Illinois Urbana-Champaign’s College of Agricultural, Consumer and Environmental Sciences (ACES)

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