Figure 1 The weighted quantile sum WQS regression model index weights for the WQS regression model that included A all catechins and B only Epigallocatechin and Epigallocatechin 3-gallate. The red dashed line indicates the inverse of the number of exposed variables in the model.

All the models were adjusted for age, gender, ethnicity, education level, marital status, poverty income ratio, body mass index, serum cotinine, alcohol drinking status, and history of diabetes or hypertension.

Moreover, we further explored the associations with the regression coefficients assumed to be negative in the two WQS models.

Unsurprisingly, the weight of Epigallocatechin in the models was zero and neither model is statistically significant Figure S1 and Table S3. The risk of OA reached a nadir when epigallocatechin at approximately Figure 2 The non-linear association of osteoarthritis with A Epigallocatechin intake and B Epigallocatechin 3-gallate intake in the US NHANES and , using the restricted cubic spline RCS regression analysis.

The model was adjusted for age, gender, ethnicity, education level, marital status, poverty income ratio, body mass index, serum cotinine, alcohol drinking status, and history of diabetes or hypertension.

CI, confidence interval; OR, odds ratio. In the subgroup analyses, we stratified all covariates and used multifactorial logistic regression models adjusted for all confounders except the variables themselves to analyze the association between daily dietary epigallocatechin and epigallocatechin 3-gallate intake and the prevalence of OA.

In addition, a multiplicative interaction term was added to each model for testing potential interactions, and the results indicated no significant interactions between daily dietary intake of epigallocatechin and epigallocatechin 3-gallate and the stratification variables Tables S1, 2.

Table 4 Interaction effect between physical activity and Epigallocatechin or Epigallocatechin 3-gallate intake on the risk of osteoarthritis in the US NHANES and Figure 3 The association between osteoarthritis and Epigallocatechin intake in different physical activity subgroups. In this study, the relationship between dietary catechins intake and the prevalence of OA was investigated for the first time, using the study cohort of participants from the NHANES database, including both OA and non-OA individuals.

Our results suggest that a J-shaped nonlinearly correlation between the intakes of epigallocatechin and epigallocatechin 3-gallate with the risk of OA, in which PA played a significant moderating effect.

Most studies have found that catechins have a positive effect on OA treatment. The mechanisms are not fully understood, but several possible mechanisms have been suggested.

Catechins could up-regulate the expression of nuclear factor erythrocyte 2-related factor 2 Nrf2 , oxygenase 1 HO-1 , NADPH quinone oxidoreductase 1 NQO1 , and other antioxidant enzymes, and improve the oxidative stress-induced chondrocyte dysfunction Moreover, catechins can effectively clear excessive ROS in cells, significantly reduce the expression of pro-inflammatory cytokines, reduce the expression of M1-type macrophages, and show an excellent promotion effect on the transformation of macrophages to M2 phenotype 27 , However, the relationship between catechins intake and the risk of OA has not been evaluated in any study.

In this research, we explored the associations between six catechins subclasses and the prevalence of OA, with multifactorial logistic regression and WQS regression model, and found that excessive intake of epigallocatechin and epigallocatechin 3-gallate increases the risk of OA in the general US population.

Several experimental animal studies and epidemiological studies have shown that tea polyphenols have dose-dependent toxicology and low and medium doses 0. Conversely, a high dietary dose 0. In addition, there have been case reports that excessive consumption of tea extract can cause liver damage 31 , It has been suggested that this may be related to the properties of tea polyphenols.

Mechanistically, studies have found that tea polyphenols can produce reactive oxygen species ROS through auto-oxidation. Low and medium doses of tea polyphenols produce low levels of ROS, which can activate Nrf2 to reduce oxidative stress, while high doses of tea polyphenols produce high levels of ROS, leading to apoptosis and tissue damage 33 — All the above research evidence suggests that the daily intake of dietary catechins should take into account the complementary and toxicological effects of dose relationships.

Noteworthy, our findings suggest that although catechins have some adjunctive therapeutic effects in the OA population, gallocatechin intake greater than Interestingly, in the present study, using the WQS regression model, we first explored the mixed effect of intake of all catechins on the prevalence of OA and the results showed that this model was not associated with the prevalence of OA.

Subsequently, we focused on the mixed effect of intake of epigallocatechin and epigallocatechin 3-gallate, and unsurprisingly, there was significance between the model and the prevalence of OA.

Therefore, the results of the WQS regression model showed that the overall effect of all six catechins subclasses or epigallocatechin and epigallocatechin 3-gallate mainly resulted from Epigallocatechin suggesting that Epigallocatechin intakes are more important for studying the prevalence of OA in the general U.

Not alone, we found that there was no significant interaction effect in the intake of epigallocatechin and OA prevalence in age, gender, and ethnicity subgroups, while a significant interaction effect was found in the PA subgroup.

According to the Physical Activity PA Guidelines from the U. Department of Health and Human Services DHHS , maintaining a moderate intensity of physical activity each week can reduce OA risk and also have a positive effect on OA recovery 18 , Many reports have shown that high-intensity exercise itself is easy to cause joint strain, which has shown that high-intensity exercise is an increased risk of OA 19 , 37 , Similarly, our study found that intake of epigallocatechin hardly affected the protective effect of low PA on the risk of OA in the Low PA group.

However, in the Sufficiently PA group, the prevalence of OA was significantly higher in the epigallocatechin Q 3 group compared to the Q 1 group, and OA prevalence increased with the higher daily intake of epigallocatechin.

This study is a relatively large population study using three complementary methods to reveal the relationship between dietary catechin intake and the prevalence of OA in American adults. Under the premise that dietary catechins are now recommended as natural health products in daily life, we first found that excessive daily catechins intake will lead to an increase in the risk of OA.

However, further large-scale prospective studies and clinical trials are needed to confirm our findings and their underlying mechanisms. In addition, there are some limitations to our study. First, we used data from a cross-sectional survey.

The assessment of dietary catechin intake in this study can only reflect current intake status, but OA is a long-term developing disease, which may have biased our results. Second, dietary catechins intake data were collected through a hour dietary recall survey, which could lead to recall bias.

Third, our analysis was unable to conclude a causal relationship between dietary catechin intake and OA. Fourth, our population inclusion is limited by the NHANES database. It is unclear whether the relationship between dietary catechin intake and OA applies to other populations.

In summary, the results of this study suggested that epigallocatechin intake greater than In addition, PA showed a significant moderating effect on the relationship between epigallocatechin intake and the prevalence of OA.

Further inquiries can be directed to the corresponding authors. YF: Conceptualization. LL: Conceptualization. JG: Writing — original draft. YZ: Project administration. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Flavanones: Citrus phytochemical with health-promoting properties. This regulation resulted in the inhibition of liver fibrosis and bile duct adhesion-dependent changes by preventing the activation of astrocytes in the liver Zhong et al.

Finally, the mechanism between hepatic diseases and inflammatory effect of catechins were presented in Table 3. Pulmonary inflammation is caused by the inhalation or invasion of external contaminants. Sources of external pollutants mainly include tobacco smoke, toxins, bacteria, viruses, and particulates including heavy metals Adler and Li, The inflammatory response caused by cigarette smoke leads to chronic obstructive pulmonary disease COPD , and air pollution containing particulate matter PM , heavy metal, biomass fuels, carbon dioxide and ozone induce idiopathic pulmonary fibrosis Johannson et al.

In addition, it has been reported that various pulmonary viruses such as influenza virus, respiratory syncytial virus RSV , adenovirus, and coronavirus respond easily to the respiratory tract, and stimulate the inflammatory response of lung tissue, causing various symptoms such as tonsillitis, bronchitis, and pneumonia Lessler et al.

This viral lung injury causes secondary bacterial pneumonia, and inflammatory cytokines produced in the lung tissue have effects throughout the whole body Conti et al. Lung tissue is involved in the expression of inflammation by interacting with various cells, including epithelial cells and immune cells surrounding the airways and alveoli.

Airway epithelial cells secrete mucus to trap particles in the inhaled air as a physical system that repels external toxicants Knudsen and Ochs, To suppress pulmonary damage by inducers, antimicrobial peptides, proteases, cytokines and chemokines are secreted in pulmonary epithelial cells Wong et al.

However, excessive chronic inflammation stimulates macrophages to secrete inflammatory mediators and various enzymes and increases the number of lymphocytes, resulting in the destruction of the alveoli Ingersoll et al. PM continuously increases toxicity in respiratory organs Huang et al.

Intake of green tea catechins ameliorated PM 2. PM contains heavy metals, carbon monoxide and polycyclic aromatic hydrocarbons PAHs Shou et al.

Administration of catechins hydrate modulated benzo a pyrene-induced apoptotic toxicity and inflammation by regulating the expression of TNF-α, NF-κB, COX-2, BAX and caspase-3 in mice lung tissue Shahid et al.

Wang et al. Catechins have a high binding affinity with severe acute respiratory syndrome coronavirus 2 SARS-CoV-2 proteins containing 3-chymotrypsin-like cysteine protease 3CL , RNA-dependent RNA polymerase RdRp , and receptor-binding domain RBD , so they have the potential to act as an excellent multi-targeting agent to regulate COVID pandemic.

Mishra et al. In addition, catechins in green tea, coffee, and berries also act as a potent inhibitor of influenza A virus, preventing infection Kaihatsu et al. Catechin and epicatechin inhibited damage of mitochondrial complex I, reduced ATP level, and NO production in amiodarone-induced human lung fibroblasts Santos et al.

Finally, the mechanism between respiratory disease and inflammatory effect of catechins were presented in Table 4. Inflammatory bowel disease IBD is a chronic immune disease of unknown etiology related to the uncontrolled mucosal immune response of the intestinal microflora in the host intestine Takaishi et al.

IBD damages tight junction TJ proteins, resulting in altered intestinal permeability and impaired epithelial barrier function, and increased immune response due to changes in intestinal flora Lee, Alterations in the gut microbiota are responsible for influencing various diseases such as obesity, irritable bowel syndrome, tropical enteropathy, antibiotic-associated diarrhea, and vaginitis, and impair the digestion and absorption of nutrients, energy homeostasis, and maintenance of intestinal tissue of the host Musso et al.

Changes in the gut microbiota increase the inflammatory response by stimulating cytokine signaling pathways and indicate intestinal imbalances through changes in some microbial-derived metabolites such as short-chain fatty acids SCFAs Huda-Faujan et al.

Immune response eventually indicates damage to the intestinal tissue, causing nutritional abnormalities and an increase in inflammatory response Musso et al. Symptoms of IBD are reported as Crohn's disease CD and ulcerative colitis UC , and the immune pathology of IBD appears to be due to the overexpression of interferon-γ IFN-γ and TNF-α Rafa et al.

When the epithelial barrier is destroyed by an increase in the inflammatory response or infection of pathogenic bacteria, dendritic cells and macrophages are activated to react with antigens and present antigens to the surface through major histocompatibility complex MHC class II complexes Bedford et al.

This response promotes the differentiation of naive T cells into effector and regulatory T cells, and ultimately increases cytokines Leon et al.

Catechins can regulate intestinal microbial balance by modulating components of intestinal metabolites. Catechins absorbed through the intestinal tract exhibit various physiological activities, but unabsorbed catechin also plays an important role in the intestine Forester et al.

This is reported to play the role of prebiotics by stimulating the growth of symbiotic bacteria such as Lactobacillus plantarum using phenolic compounds as substrates and perturbing the function of the cytoplasmic membrane of gram-negative pathogenic bacteria such as Stenotrophomonas maltophila Liu et al.

In addition, catechin metabolites such as phenylvalerolactones, valerolactones, and phenylvaleric acids digested in the intestine promote the production of SCFAs by anaerobic fermentation to help improve intestinal health Santangelo et al.

EGCG reduced gut-derived endotoxin translocation and inhibited the loss of TJ proteins such as claudin-1, occludin, zonula occludens-1 ZO1 and hypoxia-inducible factor 1-alpha HIF-1α in HFD-induced diabetic mice Dey et al.

In addition, catechins reduce the inflammatory response by regulating the expression of NF-κB, MAPK, and nuclear factor erythroidrelated factor 2 Nrf2 in the intestine and the infiltration and proliferation of immune-related cells including neutrophils, macrophages, and T lymphocytes Fan et al.

Finally, the mechanism between gastrointestinal GI tract and inflammatory effect of catechins were presented in Table 5. It is generally considered that safe for ingestion of low-dose catechins or green tea preparations that contain large amounts of catechins Church et al.

In particular, administration of catechins has been reported to have a protective effect on liver tissue in various hepatic toxicity disease models such as HFD, carbon tetrachloride, acetaminophen, and D-galactosamine Kim et al. However, recent studies have reported hepatic toxicity by intake of dietary supplements containing high doses of catechins or green tea.

In a rodent model, ingestion of high concentration catechins increased serum alanine aminotransferase ALT and bilirubin content, and caused gastrointestinal GI tract toxicity Galati et al. presented in liver and GI toxicity in beagle dogs Isbrucker et al.

According to Mazzanti et al. Although the numerous studies related to hepatic toxicity of high doses of catechins are reported, the mechanism of hepatotoxicity is unclear.

In conclusion, chronic inflammation is associated with various diseases, and the persistence of inflammation systemically indicates dysfunction and damage of various organs.

Plant-derived catechins impart anti-inflammatory and inflammatory response stabilization based on excellent antioxidant activity.

This review provides convincing evidence that catechins and plant materials rich in catechins are effective in suppressing inflammatory stress in the short and long term through an inflammatory mechanism in in vivo studies. Therefore, catechins themselves or nutraceutics with catechins can be used as strong anti-inflammatory agents or functional food materials with excellent physiological activity.

However, some in vivo and clinical studies have continuously reported that high doses of catechins and green tea extract cause safety concerns and risks of hepatic damage and liver necrosis. Considering these reports, additional studies should be conducted to confirm the empirical evidence of hepatotoxicity pathway, or to make guidelines for stably ingesting catechins by limiting intake so that it does not induce toxicity.

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Warner, E.

EGCG also appears to have better bioavailability, which is how well your body can absorb and use it. RA involves inflammation that damages the lining of your joints—the synovium.

In the synovium is a type of cell called a fibroblast. In RA, synovial fibroblasts are produced at high levels and destroy the cartilage around joints. This causes pain and disability.

Scientists theorize the surge in fibroblasts is caused by immune system substances involved in the overactive inflammation of RA. These include:. These excess fibroblasts then influence the activity of immune cells called leukocytes and signaling chemicals called cytokines and chemokines.

That allows the fibroblasts to invade the cartilage and begin destroying it. A review of natural products for treating autoimmune arthritis suggests that green tea catechins slow these inflammatory processes. It cites a rat study in which green tea significantly reduced levels of TNFα and IL-1ß.

It also decreased the activity of certain chemokine receptors in the joints. A study of RA fibroblast activity used human synovial tissues from the knees and hips.

Researchers found both EGCG and ECG inhibited IL-1ß activity, but EGCG was more effective. Other laboratory research has noted that:. A large-scale, real-world study in looked at green and black tea consumption and RA. Researchers analyzed data from more than participants.

They concluded people who drank a lot of tea had less active RA than those who drank less or no tea. This trend was strongest in women, non-smokers, and people older than A review of literature on RA and diet found evidence that:. A study with a thousand participants found that green tea and coffee both appeared to help prevent RA.

Green, white, and black teas all come from the Camellia sinensis plant. One of the main differences between them is length of the oxidation process the tea leaves undergo, which begins as soon as a leaf is picked.

The sooner this process is stopped, the more antioxidants and less caffeine the tea has. Animal studies have shown the anti-inflammatory effect of green tea extract to be superior to that of black tea extract. Green, black, and white teas come in different varieties. Research suggests that doses of up to mg a day may be safe.

But side effects are more likely at this level. Green tea extract may be more effective when taken on an empty stomach. For quality green tea, avoid grocery-store tea bags. They tend to be lower quality and not as fresh as other teas. Look for better quality teas in:. You may be able to find high-quality tea bags.

But loose-leaf teas generally yield better results. You may also get a lot of sugar. Brewing green tea properly can maximize its benefits. Green tea may become bitter if it steeps for too long. To get a consistent therapeutic dosage, green tea extract supplements may be the best option.

Always read the labels on supplements. To make sure a supplement contains the amounts of catechins and caffeine claimed on the label, look for a seal of approval from a third-party testing organization.

ConsumerLab and USP are common ones. Even natural products can cause side effects. Any time you add something to your regimen, you should know and watch for the potential side effects. Talk to your healthcare provider before taking any supplement, as it may not be safe for you based on your medical history or other treatments.

Possible side effects of green tea tend to be more common at higher dosages. Most of them have to do with caffeine. They include:. Green tea is less likely to cause these symptoms than other caffeinated beverages.

Liver toxicity has been noted in animal studies. Still, if you have liver disease, talk to your healthcare provider about the potential risks. One animal study suggests it may cause abnormal fatty tissue deposits in the mother and baby.

The caffeine in green tea may also be a concern. Tannic acid in green tea may stain your teeth. Green tea may cause other medications to work differently than intended. It might lessen the effects of:. Catechins in green tea appear to help prevent and relieve symptoms of RA. Researchers believe this is due to catechins that block the inflammatory process and cells responsible for immune over-activity.

Dietary green tea can be effective medicinally. Green tea is generally more effective than black tea because of its higher antioxidant levels. You can get medicinal levels from a few cups a day. Select high-quality tea and be sure to brew it properly with simmering water and a short steep time.

Or, for a more consistent dosage, choose a high-quality green tea extract supplement. Check with your healthcare provider before using green tea medicinally. Watch for side effects and be aware of any possible drug interactions. RA is a serious and potentially debilitating disease.

Correction - August 23, : This article was updated to clarify that oxidation time, rather than harvest time, is one of the differences between the types of tea. Fechtner S, Singh A, Chourasia M, Ahmed S.

Molecular insights into the differences in anti-inflammatory activities of green tea catechins on IL-1β signaling in rheumatoid arthritis synovial fibroblasts. Toxicol Appl Pharmacol. Ospelt C. Synovial fibroblasts in RMD Open. Dudics S, Langan D, Meka RR, et al.

Natural products for the treatment of autoimmune arthritis: their mechanisms of action, targeted delivery, and interplay with the host microbiome. Int J Mol Sci. Lee SY, Jung YO, Ryu JG, et al. Often used in skincare because of its ability to calm redness and irritation, rose hip also shows potential for supporting joint health and reducing the symptoms of arthritis.

The fruit of the dog rose Rosa canina , rose hips are rich in antioxidants, including vitamin C, giving them anti-inflammatory properties.

They also contain galactolipids, which help to protect our cartilage and ease the symptoms of osteoarthritis and rheumatoid arthritis. Willow bark tea is famous for containing salicin, which was the original source of aspirin. As a natural painkiller, willow bark has traditionally been used to treat everything from headaches to menstrual pains.

It is also effective in easing the joint pain associated with osteoarthritis. Like the other herbs on our list, willow bark can also help to reduce inflammation, ease stiffness, and help to keep our joints healthy.

Nettle tea is a popular herbal remedy that is used to treat many conditions, including joint and muscle pain. It contains several compounds that help to fight inflammation, ease pain, and protect against oxidative stress. Often used as a general tonic for our health, nettle tea is also high in nutrients, including magnesium, calcium, and potassium.

At NutraTea, we like to combine different herbs to create herbal tea blends that are specifically designed to support different areas of your health. When it comes to healthy joints, our go-to blend is NutraJoint , which contains both curcumin from turmeric and green tea.

Curcumin is more easily absorbed into the body when it is combined with piperine from black pepper, which is also an anti-inflammatory in its own right. NUTRA JOINT Rated 4. While our NutraJoint blend is focused on joint health and flexibility, NutraBone is aimed at supporting bone health, including joint mobility.

NUTRA BONE Rated 5. NUTRA DEFENCE IMMUNE SUPPORT. NUTRA FLOW URINARY TRACT HEALTH. NUTRA GLYCEMIA BLOOD SUGAR SUPPORT.

NUTRA HEAD MIGRAINE SUPPORT. NUTRA RELEASE WATER RETENTION. HEALTHY WELLBEING PREMIUM BLENDS. WINTER WELLNESS PREMIUM BLENDS. Turmeric Turmeric has become a popular herbal remedy for arthritis sufferers and exercise enthusiasts alike.

Green Tea Green tea comes from the same plant as black, white, and oolong tea. Ginger Warming ginger is another great tea to ease aches and pains and support your joint health. Rose Hip Often used in skincare because of its ability to calm redness and irritation, rose hip also shows potential for supporting joint health and reducing the symptoms of arthritis.

Willow Bark Willow bark tea is famous for containing salicin, which was the original source of aspirin.

Green tea and its extracts exert many different types of beneficial actions in the problem of joint and osteoarthritis pain by changing the chemicals in a damaged joint to point towards healing and shutting down toxic factors. It is the same line of research that cancer researchers are seeing as well.

Green tea is a very beneficial food source for health conscious individuals. A July study in the medical journal Scientific Reports 6 , found that the anti-obesity effect of green tea differs depending on composition of fats or fatty acids in the diet.

They suggested that green tea would have a better weight reducing effect in diets that consists of more healthy fats such as olive oil that contains abundant unsaturated fatty acid, especially oleic acid.

One of the reasons for this reduction in benefit is in the inability of the green tea to handle the inflammatory response to the bad fats. Similarly then, green tea will have a hard time dealing with the bad inflammation in you joints. Above we talked about research that showed green tea has an anti-inflammatory effect.

That positive effect works best in repairing old damage, not the new damage you are creating with a diet rich is toxic fats. Ingestion of a tea rich in catechins leads to a reduction in body fat and malondialdehyde-modified LDL in men.

The American journal of clinical nutrition. Mechanisms of body weight reduction and metabolic syndrome alleviation by tea. Green Tea Extracts Epigallocatechingallate for Different Treatments.

BioMed Research International. Green tea Camellia sinensis for patients with knee osteoarthritis: A randomized open-label active-controlled clinical trial. Clinical Nutrition. Reactive oxygen species production triggers green tea-induced anti-leukaemic effects on acute promyelocytic leukaemia model.

Cancer letters. Saturated fatty acid attenuates anti-obesity effect of green tea. Scientific reports. When should I involve a Prolotherapist in my care? Call Us: Email Us. Take our Pain Quiz Regenerative Treatments H3 Prolotherapy What does H3 mean?

Stem Cell Therapy Platelet Rich Plasma PRP LPIT - Neural Prolotherapy Nerve Release Injection Therapy Cervical Curve Correction Are you a good candidate? Book an Appointment Subscribe Log in. Home » Prolotherapy News » Nutrition and Chronic Pain » Green tea and joint pain.

Green tea and joint pain Marion Hauser, MS, RD In our medical practice we specialize in the non-surgical treatment of degenerative joint disease with a comprehensive program of regenerative medicine injections. Keep lid tightly secured to ensure freshness.

Sign up to receive special offers from Cosequin ® and Nutramax Laboratories Veterinary Sciences, Inc. Nutramax - 30 Years of Unmatched Quality Email Signup International Español. Previous Product. SKU: EQNASUP Categories: Horse , Joint Health , Powder Tags: Horse , Joint Health.

Description Additional information Directions for Use Active Ingredients Description. What is Cosequin ® ASU Plus? Patent No. For use under U. Quick View. Additional information patents U. Patent Nos. As osteoarthritis progresses, cartilage erosion is one of the biggest factors in painful, sore joints.

Findings from one research study suggested that green tea just might aid in relief from pain. The very same catechin that may help combat inflammation — EGCG — may also slow the progression of osteoarthritis and may help lessen the pain it causes by helping to reduce cartilage loss and inflammation-causing cytokines.

Rheumatoid arthritis RA , on the other hand, is associated with an overactive immune system. There is evidence that synovial fibroblasts are innate immune cells.

A phenomenon, sometimes called synovial fibroblast activity , can destroy joint cartilage and lead to joint pain. However, when you drink green tea, the catechins may calm the immune system — and may help limit the impact of inflammation, cartilage destruction and that synovial fibroblast activity.

Green tea is even recommended by the Arthritis Foundation. Thanks to its powerful catechins, green tea is considered one of the most beneficial brews for those living with any kind of arthritis.

Potential benefits of green tea on different kinds of joint pain may come down to one key ingredient: catechins.