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Diseases

Chronic inflammation — the quiet fire that fuels disease?

Sources: 22 · Article: 28 335 characters

Paul Clayton points out that a pro-inflammatory diet may increase the risk of acute pain becoming chronic.

  • Mild, short-term inflammation supports immunity, memory, and injury healing, while excessive or chronic inflammation can lead to depression and neurodegenerative diseases.
  • Clayton also links chronic inflammation with atrial fibrillation and sleep apnea.
  • Hubert Czerniak describes rheumatoid arthritis (RA) as a disease in which antibodies against cartilage trigger inflammation, pain, and joint swelling.

What the authors write

Paul Clayton

Mild, temporary inflammation supports immune surveillance, brain development, memory, and injury healing; excessive or chronic inflammation can lead to sickness behavior, depression, and neurodegenerative diseases.

„Social pain (loneliness, social defeat, anger) tends to make physical pain worse, especially nociplastic pain (22, 23)—probably by activating a shared neural network known as the “pain matrix” (23–25). The pain matrix is shaped by early-life trauma (26) and strengthened by neuroinflammation (27), which is affected by many lifestyle factors. Low-level, temporary inflammation is “normal” and entirely positive. It plays a role in immune surveillance and signaling, as well as in aspects of brain development, memory, and learning (28, 29). At higher levels, it is a key part of injury repair. If inflammation is excessive and/or chronic, but driven by a pro-inflammatory diet and/or substantial peripheral inflammation or repeated social defeat, it leads to sickness behavior, including loss of appetite, lethargy, apathy, lack of motivation, reduced activity, and reduced sociability (30). It can also lead to depression, brain aging, and neurodegenerative diseases (31, 32).”Ból społeczny (samotność, porażka społeczna, złość) ma tendencję do zaostrzania bólu fizycznego, zwłaszcza bólu nocyplastycznego (22, 23) – prawdopodobnie poprzez aktywację wspólnej sieci neuronowej znanej jako „macierz bólu” (23–25).Macierz bólu jest tworzona przez uraz we wczesnym okresie życia (26) i wzmacniana przez zapalenie nerwów (27), na które wpływa wiele czynników związanych ze stylem życia.Przejściowe zapalenie o niskim poziomie jest „normalne” i całkowicie pozytywne. Bierze udział w nadzorze immunologicznym i sygnalizacji wraz z aspektami: rozwoju mózgu, pamięci i uczenia się (28, 29), a na wyższych poziomach jest kluczowym elementem w naprawie urazów.Jeśli stan zapalny jest nadmierny i/lub przewlekły, ale wywołany dietą prozapalną i/lub znacznym zapaleniem obwodowym lub powtarzającą się porażką społeczną, prowadzi do zachowań chorobowych, w tym: utraty apetytu, letargu, apatii, demotywacji, zmniejszonej aktywności i zmniejszonej towarzyskości (30). Prowadzi również do: depresji, starzenia się mózgu i chorób neurodegeneracyjnych (31, 32).
Dlaczego boli nas coraz dokuczliwiej?
Paul Clayton

Paul Clayton points out that a pro-inflammatory diet may increase the risk of acute pain becoming chronic, and that dysbiosis may play a part.

„The industrial, pro-inflammatory diet probably distorts cellular responses to injury (64, 65), increasing the chances of chronic inflammation and pain developing—as epidemiological evidence shows (6–8). But that is not the whole story, because the modern diet also causes dysbiosis.”Przemysłowa, prozapalna dieta prawdopodobnie wypacza reakcje komórkowe na uraz (64, 65), zwiększając szanse na przejście do przewlekłego stanu zapalnego i bólu – co pokazuje epidemiologia (6–8). Ale to nie koniec historii, ponieważ współczesna dieta powoduje również dysbiozę.
Dlaczego boli nas coraz dokuczliwiej?
Paul Clayton

Paul Clayton links more frequent consumption of ultra-processed, pro-inflammatory foods with an increase in reports of chronic pain.

„Rising consumption of pro-inflammatory, ultra-processed foods that drive inflammatory disease will therefore contribute to an increase in reports of chronic pain (31, 32). Ongoing damage to our social connections and repeated social defeat will increase these numbers (33, 34).”Rosnące spożycie prozapalnej, ultraprzetworzonej żywności, która napędza choroby zapalne, przyczyni się zatem do zwiększenia liczby zgłoszeń przewlekłego bólu (31, 32). Postępujące szkody w naszych kontaktach społecznych i powtarzające się porażki społeczne zwiększą te liczby (33, 34).
Dlaczego boli nas coraz dokuczliwiej?
Paul Clayton

Paul Clayton describes sleep apnea as a disorder in which inflammation plays a significant part and suggests that chronic inflammatory stress may precede it.

„Blood levels of various inflammatory cytokines correlate well with the severity of OSA (29–32), and it is reasonable to describe OSA as a disorder with a significant inflammatory component. This seems to be particularly linked to damage to the hippocampus and cerebral cortex (8–13, 33), as well as to later cardiovascular outcomes (22–24, 34).”Poziomy różnych cytokin zapalnych we krwi dobrze korelują z ciężkością OBS (29–32) i uzasadnione jest scharakteryzowanie OBS jako zaburzenia z istotnym komponentem zapalnym. Wydaje się, że jest to szczególnie związane z uszkodzeniem hipokampu i kory mózgowej (8–13, 33) oraz dalszymi sercowo-naczyniowymi punktami końcowymi (22–24, 34).
Wspomnienie Lorda Vadera, czyli o związku flory jelitowej z bezdechem nocnym
Paul Clayton

Paul Clayton identifies chronic inflammation as an important part of the progression of atrial fibrillation.

„Unlike anticoagulants (32), which prevent the formation of a clot inside the atrium. Let us move on to a very basic overview of the pathophysiology of atrial fibrillation progression. There is evidence that recurrent episodes of atrial fibrillation help it progress to a more advanced stage through interactions between electrical and structural remodeling (33, 34). This occurs alongside later changes in ongoing interactions between myocytes, fibroblasts, and endothelial cells (35). Chronic inflammation is central to this process.”W przeciwieństwie do antykoagulantów (32) przeciwdziałających tworzeniu się skrzepliny wewnątrzprzedsionkowej.Przejdźmy do bardzo podstawowego przeglądu patofizjologii progresji migotania przedsionków.Istnieją dowody, że nawracające epizody migotania przedsionków sprzyjają osiągnięciu przez nie kolejnego stadium zaawansowania poprzez interakcję między przebudową elektryczną i strukturalną (33, 34). To wszystko wraz z późniejszymi zmianami w toczących się interakcjach między: miocytami, fibroblastami i komórkami śródbłonka (35).Centralną częścią tego procesu jest przewlekły stan zapalny.
Twoje oszukane serce
Paul Clayton

Paul Clayton links chronic inflammatory stress with the development of atrial fibrillation, and higher inflammatory biomarkers with a greater risk of the disease.

„Although many additional factors may complicate the picture (such as diet, smoking, physical activity, and psychological factors), the evidence above suggests that chronic inflammatory stress is involved in the pathogenesis and rising incidence of atrial fibrillation (15, 16). Other inflammatory conditions may also trigger atrial fibrillation.”Chociaż istnieje wiele dodatkowych czynników zakłócających obraz (takich jak: dieta, palenie tytoniu, aktywność fizyczna, czynniki psychologiczne), powyższa mieszanka sygnalizuje, że przewlekły stres zapalny jest zaangażowany w patoetiologię i wzrost liczby przypadków migotania przedsionków (15, 16).Inne stany zapalne mogą również wywoływać migotanie.
Twoje oszukane serce
Paul Clayton

Paul Clayton describes neuroinflammation as an important cause of epilepsy and links it with oxidative stress.

„Diet or any other factors that cause intestinal inflammation are likely to drive neuroinflammation (27–38), and neuroinflammation appears to be an important cause of epilepsy (37). Given the consistent evidence and the importance of Gram-positive saccharolytic species, a ketogenic diet supplemented with prebiotic fiber may offer additional benefits for seizure control and gut health.”Dieta lub jakiekolwiek inne czynniki, które powodują zapalenie jelit, prawdopodobnie napędzają zapalenie układu nerwowego (27–38), a stan zapalny układu nerwowego wydaje się być istotną przyczyną padaczki (37). Zważywszy na harmonię dowodów i biorąc pod uwagę znaczenie Gram-dodatnich gatunków sacharolitycznych, dieta ketogeniczna z dodatkiem włókien prebiotycznych może przynieść dodatkowe korzyści pod względem kontroli napadów i zdrowia jelit.
Współdziałanie flory jelitowej z mózgiem
Hubert Czerniak

Hubert Czerniak describes RA as a disease in which antibodies against cartilage trigger inflammation, pain, swelling, and impaired joint function.

„However, when the body begins to see itself as an enemy, it starts producing antibodies against components of the joint itself—cartilage. The antibodies trigger inflammation, causing redness, swelling, pain, and impaired function. When an older person comes to the doctor with joint problems, they hear the word “degeneration.””Jednak, gdy organizm zaczyna postrzegać sam siebie jako wroga, zaczyna wytwarzać przeciwciała przeciw właśnie tym elementom stawu – chrząstkom. Przeciwciała wywołują zapalenie, a więc zaczerwienienie, obrzęk, ból i zaburzenie funkcji. Gdy przychodzi starszy człowiek do lekarza i ma problemy ze stawami, słyszy „zwyrodnienie”.
Reumatoidalne zapalenie stawów - poznaj prawdę o tej chorobie
Henryk Różański

Henryk Różański describes Hashimoto’s disease as thyroid inflammation associated with antibodies against the thyroid’s own components, which can lead to hypothyroidism.

„The production of antibodies against a person’s own thyroglobulin or peroxidase causes inflammation of the thyroid and lymphocyte infiltration, leading to hypothyroidism. Hashimoto’s disease affects about 2% of the population and can occur at any age.”Wytwarzanie przeciwciał przeciwko własnej tyreoglobulinie lub peroksydazie powoduje stan zapalny tarczycy, nacieki limfocytowe, co prowadzi do niedoczynności tarczycy. Choroba Hashimoto występuje u około 2% społeczeństwa. Dotyczy ludzi w każdym wieku.
Choroba Hashimoto, czyli przewlekłe autoimmunologiczne zapalenie tarczycy, część 1.
Henryk Różański

Henryk Różański describes lymphocyte attacks on thyroid cells as a cause of their damage or destruction.

„In this disease, lymphocytes fail to recognize thyroid cells as the body’s own and instead see them as foreign and carrying antigens, so they seek to destroy them. Hashimoto’s disease may occur with an enlarged thyroid, a thyroid of normal size, or an atrophied thyroid.”W przypadku choroby limfocyty nie rozpoznają komórek tarczycy jako własne, lecz obce, zawierające antygen i dlatego dążą do ich zniszczenia. Choroba Hashimoto może występować z wolem, z prawidłową wielkością tarczycy lub w postaci zanikowej tarczycy.
Choroba Hashimoto, czyli przewlekłe autoimmunologiczne zapalenie tarczycy, część 1.
Piotr Witczak

Piotr Witczak points out that obesity is accompanied by low-grade chronic inflammation and that limiting it may slow disease progression.

„Obesity is accompanied by low-grade chronic inflammation, characterized by macrophage infiltration. Berberine improves insulin sensitivity. Similarly, metformin may reduce the production of nitric oxide, prostaglandins, and pro-inflammatory cytokines by inhibiting NF-κB activation in macrophages.”Otyłości towarzyszy przewlekły stan zapalny niskiego stopnia, charakteryzujący się naciekiem makrofagów. Berberyna poprawia wrażliwość na insulinę. Podobnie metformina może zmniejszać wytwarzanie tlenku azotu, prostaglandyn i cytokin prozapalnych poprzez hamowanie aktywacji NF-κB w makrofagach.
Metformina kontra berberyna w leczeniu chorób metabolicznych
M. Williamson i N. Moustaid-Moussa i L. Gollahon

M. Williamson, N. Moustaid-Moussa, and L. Gollahon list inflammation as a feature of metabolic diseases and cancer.

„Inflammation is a hallmark of metabolic disease and cancer. Acidosis has been implicated in many cases of pathogenesis by modulating activity in immune cells. Metabolic acidosis activation of the GCPR-Calcium-NFAT pathway may be contributing to the increasing cases of nonallergic respiratory disorders and autoimmune diseases worldwide ().”Inflammation is a hallmark of metabolic disease and cancer. Acidosis has been implicated in many cases of pathogenesis by modulating activity in immune cells. Metabolic acidosis activation of the GCPR-Calcium-NFAT pathway may be contributing to the increasing cases of nonallergic respiratory disorders and autoimmune diseases worldwide ().
Frontiers | The Molecular Effects of Dietary Acid Load on Metabolic Disease (The Cellular PasaDoble: The Fast-Paced Dance of pH Regulation)
Hubert Czerniak

Hubert Czerniak identifies dysbiosis as an early causal factor in the inflammatory process in the joints that he describes.

„We must not forget the digestive tract, because dysbiosis is an initiating cause. It is brought about by a change in the proportions of bacterial species in the gut, leading them to produce more acetate than butyrate. If we consume preservatives every day, we are harming our own bodies.”Nie wolno zapomnieć o przewodzie pokarmowym, bo elementem sprawczym na samym początku jest dysbioza. Tą wywołuje zmiana procentowego składu bakterii w jelitach, doprowadzająca do tego, że produkują one więcej octanów niż maślanów. Jeśli codziennie spożywamy konserwanty, to zabijamy własny organizm.
Reumatoidalne zapalenie stawów - poznaj prawdę o tej chorobie
Andrzej Frydrychowski

Andrzej Frydrychowski recommends limiting foods that he says increase inflammation, as well as regular exercise when joints are undernourished.

„It is essential to eliminate from the diet foods that increase inflammation, especially carbohydrates and gluten. Inflammation means an increased amount of free radicals, so their levels should be reduced. It is worth increasing vitamin C intake (e.g.”Niezbędne jest wyeliminowanie z diety produktów, które zwiększają stan zapalny, a więc przede wszystkim węglowodanów i glutenu. Stan zapalny to zwiększona ilość wolnych rodników, dlatego należy zmniejszyć ich ilość. Warto zwiększyć spożycie wit. C (np.
Artroza i co dalej?
Paul Clayton

Paul Clayton warns that in the study he describes, drug-based suppression of neutrophils after an injury was linked with a greater risk of chronic pain.

„A research team from McGill University (44) studied 98 patients with acute injuries and found that when immune cells known as “neutrophils” were suppressed by NSAIDs or steroids, pain was almost twice as likely to become chronic and lasted up to 10 times longer than in the control groups.”Zespół badawczy z McGill University (44) zbadał 98 pacjentów z ostrym urazem i odkrył, że gdy komórki odpornościowe – znane jako „neutrofile” – były hamowane przez NLPZ lub steroidy, prawdopodobieństwo, że ból stanie się przewlekły, było prawie 2 razy większe i będzie trwał do 10 razy dłużej niż w grupach kontrolnych.
Dlaczego boli nas coraz dokuczliwiej?

Research from PubMed · Europe PMC

We selected 10 studies with the best, positive results. This is a selection, not a full review of all research.

Total number of studies on this topic in PubMed: 139 972.

The review indicates that low-grade chronic inflammation is strongly associated with the development of obesity, cancer, and cardiovascular disease.

Aim of the study: Inflammation is an important physiological response of the organism to restore homeostasis upon pathogenic or damaging stimuli. However, the persistence of the harmful trigger or a deficient resolution of the process can evolve into a state of low-grade, chronic inflammation.

Results: This condition is strongly associated with the development of several increasingly prevalent and serious chronic conditions, such as obesity, cancer, and cardiovascular diseases, elevating overall morbidity and mortality worldwide. The current pandemic of chronic diseases underscores the need to address chronic inflammation, its pathogenic mechanisms, and potential preventive measures to limit its current widespread impact. The present review discusses the current knowledge and research gaps regarding the association between low-grade chronic inflammation and chronic diseases, focusing on obesity, cardiovascular diseases, digestive diseases, and cancer. We examine the state of the art in selected aspects of the topic and propose future directions and approaches for the field.

Low-Grade Chronic Inflammation: a Shared Mechanism for Chronic Diseases. · Physiology (Bethesda) 2025
Money for the studygovernment, public institutions · Agencia Nacional de Investigación y Desarrollo
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The review describes how chronic inflammation can damage blood vessels and organs and is linked with many chronic diseases.

Aim of the study: Reduced levels of physical activity in people's daily lives cause the development of metabolic syndromes or age-related disorders. Chronic inflammation is now understood to be an underlying pathological condition in which inflammatory cells such as neutrophils and monocyte/macrophages infiltrate into fat and other tissues and accumulate when people become obese due to overeating and/or physical inactivity.

Results: Chronic inflammation is also involved in sarcopenia that brings hypofunction in the elderly, dementia, osteoporosis, or cancer and negatively affects many chronic diseases and people's healthy life expectancy. In this paper, outlines of such studies are introduced in terms of homeostatic inflammation, which occurs chronically due to the innate immune system and its abnormalities, while focusing on the efficacy of exercise from aspects of immunology and oxidative stress. The preventative effects of functional food ingredients in combination with exercise are also introduced and described. The challenges and future directions in understanding the role of exercise in the control of chronic inflammation are discussed.

Chronic Inflammation as an Immunological Abnormality and Effectiveness of Exercise. · Biomolecules 2019
Money for the studygovernment, public institutions · Ministry of Education, Culture, Sports, Science and Technology of Japan
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The review indicates that signs of chronic inflammation in older people are associated with many age-related diseases.

Aim of the study: Acute inflammatory responses are essential for pathogen control and tissue repair but can also cause severe collateral damage. Tight regulation of the response is required to minimize host injury, but in the face of chronic infections and age-associated immune dysregulation, inflammatory processes may exert multiple detrimental effects on the organism.

Results: Acute inflammatory responses are essential for pathogen control and tissue repair but can also cause severe collateral damage. Tight regulation of the response is required to minimize host injury, but in the face of chronic infections and age-associated immune dysregulation, inflammatory processes may exert multiple detrimental effects on the organism. The signs of low level systemic inflammation commonly detectable in elderly people are associated with many chronic diseases of ageing and may even contribute to their causation. The purpose of this article is to review recent literature from the past two years providing new data on the inter-relationships between inflammatory status and chronic diseases of ageing.

Inflammation, ageing and chronic disease. · Curr Opin Immunol 2014
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The review describes inflammation as an important factor in the progression of many chronic diseases.

Aim of the study: Inflammation is a comprehensive array of physiological response to a foreign organism, including human pathogens, dust particles, and viruses. Inflammations are mainly divided into acute and chronic inflammation depending on various inflammatory processes and cellular mechanisms.

Results: Free radical productions from different biological and environmental sources are due to an imbalance of natural antioxidants which further leads to various inflammatory associated diseases. In this review article, we have outlined the inflammatory process and its cellular mechanisms involved in the progression of various chronic modern human diseases. In addition, we have discussed the role of free radicals-induced tissue damage, antioxidant defence, and molecular mechanisms in chronic inflammatory diseases/disorders. The systematic knowledge regarding the role of inflammation and its associated adverse effects can provide a clear understanding in the development of innovative therapeutic targets from natural sources that are intended for suppression of various chronic inflammations associated diseases.

Role of Antioxidants and Natural Products in Inflammation. · Oxid Med Cell Longev 2016
Money for the studyuniversity or foundation · Universiti Putra Malaysia
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The review indicates that inflammation is considered one of the main causes of many chronic diseases.

Aim of the study: Inflammation is considered as one of the major causes for the initiation of various chronic diseases such as asthma, cancer, cardiovascular disease, diabetes, obesity, inflammatory bowel disease, osteoporosis and neurological diseases like Parkinson's disease.

Results: Increasing scientific evidence has delineated that inflammatory markers such as TNF-α, IL-1, IL-6, IL-8 and CRP and different transcription factors such as NF-κB and STAT are the major key factors that regulate these inflammatory diseases. Food protein-derived bioactive peptides have been shown to exhibit anti-inflammatory activity by inhibiting or reducing the expression of these inflammatory biomarkers and/or by modulating the activity of these transcription factors. This review aims to discuss various molecular targets and underlying mechanisms of food protein-derived anti-inflammatory peptides and to explore their potential against various chronic inflammatory diseases. © 2015 Society of Chemical Industry.

The potential of food protein-derived anti-inflammatory peptides against various chronic inflammatory diseases. · J Sci Food Agric 2016
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The review describes how persistent inflammation may increase the risk of chronic diseases and contribute to mutations.

Aim of the study: Inflammation is a necessary part of the immune response. However, when inflammation persists, the resultant state of chronic inflammation may have a number of secondary consequences associated with increased risk of chronic disease.

Results: While frameshift and chromosomal mutations have been associated with chronic inflammation, much of the evidence reveals base pair substitution mutations associated with polymerase stalling near the lesions, and base pair mis-incorporation. There are also indirect effects of ROS/RNS through inhibition of DNA repair enzymes and/or effects on metabolic activation of known carcinogens. Certain disease states, including the Inflammatory bowel diseases, Crohn's disease and ulcerative colitis are associated with enhanced levels of chronic inflammation, and show evidence of enhanced levels of genetic damage in the colonic mucosa. Mutations may provide at least part of the cause of enhanced susceptibility to chronic diseases associated with chronic inflammation.

Chronic inflammation and mutagenesis. · Mutat Res 2010
Money for the studyuniversity or foundation · Auckland Cancer Society, New Zealand
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The review links chronic inflammation in kidney disease with wasting and a higher risk of death.

Aim of the study: Chronic inflammation is associated with cachexia and increased mortality risk in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Inflammation suppresses appetite and causes the loss of protein stores.

Results: In CKD patients, increased serum levels of pro-inflammatory cytokines may be caused by reduced renal function, volume overload, oxidative or carbonyl stress, decreased levels of antioxidants, increased susceptibility to infection in uremia, and the presence of comorbid conditions. Cachexia is brought about by the synergistic combination of a dramatic decrease in appetite and an increase in the catabolism of fat and lean body mass. Pro-inflammatory cytokines act on the central nervous system to alter appetite and energy metabolism and to provide a signal-through the nuclear factor-kappaB and ATP-ubiquitin-dependent proteolytic pathways-that causes muscle wasting. Further research into the molecular pathways leading to inflammation and cachexia may lead to novel therapeutic therapies for this devastating and potentially fatal complication of chronic disease.

Inflammation and cachexia in chronic kidney disease. · Pediatr Nephrol 2010
Money for the studygovernment, public institutions · NIDDK NIH HHS
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The review indicates that inflammatory markers are associated with the development of polycystic ovary syndrome.

Aim of the study: Polycystic ovarian syndrome (PCOS) is the most prevalent metabolic disorder in reproductive-age women. It is indeed a multifactorial condition evidenced by ovarian dysfunction, hyperandrogenaemia, infertility, hormonal imbalance and chronic anovulation. Experimental evidence infers that PCOS women are prone to cardiovascular problems and insulin resistance. To furnish the details about the association of inflammatory markers in PCOS.

Results: The inflammatory markers perform a substantial part in managing the functions of the ovary. Any disturbances in their levels can lead to ovarian dysfunction. Inflammatory markers are associated with PCOS pathogenesis. The interplay between inflammatory cytokines in the PCOS ovary strongly implies that inflammation is one of the most potent risk factors of PCOS. Inflammatory markers have a significant role in regulating the ovary. This manuscript highlights the significance of metabolic and inflammatory markers with PCOS. Since PCOS is always considered as a metabolic disorder, researchers can also consider focusing on the relationship between the inflammatory markers in PCOS to establish a new treatment or management of the disease and to improve women's health.

Association of metabolic and inflammatory markers with polycystic ovarian syndrome (PCOS): an update. · Arch Gynecol Obstet 2021
Money for the studygovernment, public institutions · VIT University, Indian Council of Medical Research
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studycombined analysis of many studies (meta-analysis)

“Not stated” does not mean nobody paid — the database does not always record it.

The study found that genetically predicted general obesity increased the risk of COPD, asthma, and allergic rhinitis.

Aim of the study: Obesity is heterogeneous; conventional anthropometric measures combine fat distribution, ectopic fat deposition, and muscle volume, limiting refined causal inference for chronic airway diseases. We used four magnetic resonance imaging (MRI)-defined obesity axes to assess their causal effects on chronic obstructive pulmonary disease (COPD), asthma, and allergic rhinitis (AR), and to evaluate mediation by circulating inflammatory proteins.

Results: Genetically predicted general obesity axis was associated with increased risks of COPD (OR = 1.125, 95% CI: 1.012-1.250), asthma (OR = 1.533, 95% CI: 1.426-1.647), and AR (OR = 1.624, 95% CI: 1.328-1.987). The lower-body fat axis was associated with higher risks of COPD (OR = 1.192, 95% CI: 1.088-1.306) and asthma (OR = 1.135, 95% CI: 1.052-1.224). No causal evidence was observed for the other obesity axes. Replication and meta-analysis largely supported these findings, except for general obesity and AR, which showed borderline pooled evidence (P = 0.055). Mediation analysis identified 17 candidate inflammatory pathways, of which 10 were significant. FLT3L mediated 18.17% of the effect of general obesity on COPD, and CXCL5 mediated 3.78% of its effect on asthma. CD40L receptor and LIFR mediated 5.59% and 12.65% of the lower-body fat-asthma effect, respectively, whereas CD40L receptor, CXCL10, IL-12B, OPG, and TNFRSF9 showed suppressive mediation in selected pathways.

Inflammation-Mediated Causal Effects of MRI-Defined Body-Composition Obesity Axes on Chronic Obstructive Pulmonary Disease, Asthma, and Allergic Rhinitis: A Mendelian Randomization Study. · Int J Chron Obstruct Pulmon Dis 2026
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyobservation of people

“Not stated” does not mean nobody paid — the database does not always record it.

In mice, Treg cell therapy effectively resolved chronic skin inflammation but only slightly slowed arthritis progression.

Aim of the study: Current therapies for autoimmune diseases rely largely on non-specific immunosuppression, which can lead to adverse effects such as malignancy and severe infections. Treg-based therapies have therefore attracted attention as a more targeted approach, particularly in preventive or early-stage settings.

Results: To investigate the basis of this difference, we performed microarray and GSVA-based pathway analyses. Under untreated conditions, skin and joint tissues exhibited distinct baseline pathway activity patterns, with the skin showing higher activity of the Hippo signaling pathway, a growth-regulatory pathway, and the joints displaying stronger enrichment of inflammation-related pathways, including complement- and angiogenesis-associated pathways. Following Treg administration, skin-but not joint-tissue showed pathway modulation, including increased Wnt and decreased IL-17 signaling pathway activity, consistent with a more reparative environment. These findings indicate that distinct inflammatory environments underlie differential responsiveness to Treg therapy across tissues, highlighting their context-dependent therapeutic potential in chronic autoimmune inflammation.

Regulatory T cells exhibit differential therapeutic effects across tissues during chronic autoimmune inflammation. · Int Immunol 2026
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyanimal study

“Not stated” does not mean nobody paid — the database does not always record it.

Perspectives and opinion materials

The content below presents the authors’ opinions, interpretations and hypotheses. It is not treated as equal to scientific studies and systematic reviews.

Orthomolecular Medicine News Service Opinion material
„In schizophrenia the chronically elevated inflammatory parameters indicate that ongoing inflammation is causing the signs and symptoms of schizophrenia. Schizophrenia = chronic brain inflammation = chronic encephalitis. [137] Many of the symptoms seen in acute encephalitis brain are also seen in the chronic encephalitis brain of the schizophrenic patient, including alterations in consciousness, confusion, hallucinations, and cognitive impairment.”In schizophrenia the chronically elevated inflammatory parameters indicate that ongoing inflammation is causing the signs and symptoms of schizophrenia. Schizophrenia = chronic brain inflammation = chronic encephalitis. [137] Many of the symptoms seen in acute encephalitis brain are also seen in the chronic encephalitis brain of the schizophrenic patient, including alterations in consciousness, confusion, hallucinations, and cognitive impairment.
Schizophrenia Is Chronic Encephalitis... and Niacin Cures It
Orthomolecular Medicine News Service Opinion material
„Niacin was found to reduce oxidative stress and inflammation in rats with chronic renal failure (Cho 2009), to inhibit acute vascular inflammation and improved endothelial function (Wu 2010, Wu 2012), to alter lipoprotein particle size and distribution, and to reduce inflammatory markers in patients with coronary artery disease (Kuvin 2006). Niacin increased anti-inflammatory markers and decreased pro-inflammatory markers in mice with high-fat diet-induced obesity and rats with ulcerative colitis, respectively (Wanders 2013, Salem 2017).”Niacin was found to reduce oxidative stress and inflammation in rats with chronic renal failure (Cho 2009), to inhibit acute vascular inflammation and improved endothelial function (Wu 2010, Wu 2012), to alter lipoprotein particle size and distribution, and to reduce inflammatory markers in patients with coronary artery disease (Kuvin 2006). Niacin increased anti-inflammatory markers and decreased pro-inflammatory markers in mice with high-fat diet-induced obesity and rats with ulcerative colitis, respectively (Wanders 2013, Salem 2017).
The Vital Role of NAD+ and Niacin in Longevity and Well-being
Orthomolecular Medicine News Service Opinion material
„Inflammation and coronary artery disease: insights from genetic studies. Can J Cardiol. 2012;28(6):662–6. 46.Boland J, Long C. Update on the Inflammatory Hypothesis of Coronary Artery Disease. Curr Cardiol Rep. 2021 Jan 6;23(2):6. 47.Sun M, Zhu S, Wang Y, Zhao Y, Yan K, Li X, et al. Effect of inflammation on association between cancer and coronary artery disease. BMC Cardiovasc Disord. 2024 Jan 24;24(1):72. 48.Kong P, Cui ZY, Huang XF, Zhang DD, Guo RJ, Han M. Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Signal Transduct Target Ther. 2022 Apr 22;7(1):131. 49.Wolf D, Ley K.”Inflammation and coronary artery disease: insights from genetic studies. Can J Cardiol. 2012;28(6):662–6. 46.Boland J, Long C. Update on the Inflammatory Hypothesis of Coronary Artery Disease. Curr Cardiol Rep. 2021 Jan 6;23(2):6. 47.Sun M, Zhu S, Wang Y, Zhao Y, Yan K, Li X, et al. Effect of inflammation on association between cancer and coronary artery disease. BMC Cardiovasc Disord. 2024 Jan 24;24(1):72. 48.Kong P, Cui ZY, Huang XF, Zhang DD, Guo RJ, Han M. Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Signal Transduct Target Ther. 2022 Apr 22;7(1):131. 49.Wolf D, Ley K.
A Holistic Approach to ASCVD:Summary of a Novel Framework and Report of 10 Case Studies

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