See Food and Fibromyalgia: What to Know. This is not a complete list of supplements. Some supplements that have been helpful in treating other conditions have not been widely studied in people with fibromyalgia, such as:.

Given the number of coexisting medical conditions typical for people with fibromyalgia, symptoms and treatments can vary considerably. See Fibromyalgia or Not? Supplements can make a major difference in a person's quality of life, but should not be taken without talking with the doctor first.

The doctor can alert the patient to potential side effects or interactions that could limit the effectiveness of medications being taken. Vijay Vad is a sports medicine specialist at the Hospital for Special Surgery in New York, where he specializes in back pain, knee arthritis, frozen shoulder, and general sports medicine.

Home Types Fibromyalgia Turmeric, Vitamin D, and Coenzyme Q10 for Fibromyalgia. Turmeric, Vitamin D, and Coenzyme Q10 for Fibromyalgia. By: Vijay Vad, MD, Sports Medicine Physician Peer-Reviewed.

In This Article: Dietary Supplements for Fibromyalgia Magnesium, Melatonin, and Probiotics for Fibromyalgia Turmeric, Vitamin D, and Coenzyme Q10 for Fibromyalgia.

Symptoms Relieved Everyone experiences fibromyalgia differently, but turmeric, vitamin C, and coenzyme Q10 are supplements that have shown benefits in easing fibromyalgia symptoms: See What You Need to Know About Fibromyalgia Turmeric. Used since ancient times, turmeric—with its active ingredient curcumin—has long been known for anti-inflammatory properties.

Turmeric is a shrub that produces an orange-colored spice used in curry powder. See Turmeric and Curcumin for Arthritis In one research study of 62 people with fibromyalgia, participants took four 42 mg tablets of a purified curcumin extract called Flexofytol for six weeks.

See How to Create a Fibromyalgia-Friendly Diet One study found that a group of 30 people given vitamin D supplements for 20 weeks experienced significant pain relief and improved daily functioning, compared with the control group. See Multi-Specialty Fibromyalgia Treatment One small study of people who took mg daily of coenzyme Q10—also called CoQ10—for 40 days showed a marked easing of fatigue, morning tiredness, and pain.

See Getting the Sleep You Need With Fibromyalgia Another research study also found an improvement in headache symptoms for women who took mg of coenzyme Q10 each day. Meat, fish, poultry, soybean oil, and canola oil are especially good sources of coenzyme Q Other Supplements to Consider This is not a complete list of supplements.

Some supplements that have been helpful in treating other conditions have not been widely studied in people with fibromyalgia, such as: Signs of a serious vitamin B12 deficiency are similar to fibromyalgia symptoms: muscle weakness, fatigue, sleep problems, paresthesia, anxiety, and depression.

Cellfood is a blend of minerals, enzymes, electrolytes, dissolved oxygen, and amino acids. Ginger, a natural anti-inflammatory, has been used to relieve muscle and joint pain in other conditions.

Boswellia, also known as frankincense, is an anti-inflammatory that has been used to improve function and reduce the pain of osteoarthritis.

A Double Blind, Randomized, Placebo Controlled Clinical Study Evaluates the Early Efficacy of Aflapin® in Subjects with Osteoarthritis of Knee.

Research Center for Environmental Determinants of Health RCEDH , Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran. Department of Nutrition, Faculty of Nutritional Sciences and Food Technologies, Isar Sq.

Box , Kermanshah, Iran. You can also search for this author in PubMed Google Scholar. Correspondence to Hadi Abdollahzad. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Reprints and permissions. Nachvak, S. et al. Effects of coenzyme Q10 supplementation on matrix metalloproteinases and DAS in patients with rheumatoid arthritis: a randomized, double-blind, placebo-controlled clinical trial.

Clin Rheumatol 38 , — Download citation. Received : 23 April Revised : 24 July Accepted : 30 July Published : 07 August Issue Date : December Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Abstract Objectives This study aimed to assess the effect of CoQ10 supplementation on serum matrix metalloproteinases MMPs and clinical parameters in rheumatoid arthritis RA patients.

Results A significant reduction was observed in both CoQ10 and placebo groups in the medians of serum MMP-1 0. Conclusions It seems that CoQ10 may provide a new complementary approach for RA patients. Access this article Log in via an institution.

Abbreviations ANCOVA: Analysis of covariance BMI: Body mass index CoQ Coenzyme Q10 DAS Disease activity score joints DMARDs: Disease-modifying anti-rheumatic drugs ESR: Erythrocyte sedimentation rate FIQ: Fibromyalgia Impact Questionnaire hs-CRP: High-sensitivity C-reactive protein IL-1β: Interleukine-1β IL Interleukine-6 MDA: Malondialdehyde MMPs: Matrix metalloproteinases MTX: Methotrexate TNF-α: Tumor necrosis factor-alpha VAS: visual analogue scale.

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B The bar graph shows the average bone surface density percentages. B The bar graphs show the average OARSI left and Makin right scores. To explore whether CoQmicelles affected the expression of inflammatory mediators and catabolic factors involved in OA progression, we immunochemically stained tissue samples for IL-1β, IL-6, and MMP The IL-1β and IL-6 levels were reduced in the CoQmicelle group compared to the vehicle group Fig 5A and 5B.

The level of the catabolic factor MMP13 was also decreased in the CoQmicelle group compared to the vehicle group Fig 5A and 5B. CoQmicelles also reduced the levels of mRNAs encoding catabolic factors in human OA chondrocytes Fig 7A. Thus, CoQmicelles protected against OA progression by inhibiting inflammation and the catabolic response.

A Representative images of immunohistochemical staining of IL-1β, IL-6, and MMP13 in the joint synovia of a WT group, a vehicle group, a CoQmicelle group, and a celecoxib group.

B The bar graphs show the average positive areal percentages for IL-1β, IL-6, and MMP Inflammatory cell death is well known to cause tissue destruction during OA progression.

To explore any role for CoQmicelles in this context, we immunohistochemically stained tissue samples for cell death markers including RIP1, RIP3, and phosphorylated-MLKL pMLKL. The expression of all markers was lower in the CoQmicelle group than the vehicle group Fig 6A and 6B.

CoQmicelles also reduced the levels of mRNAs encoding inflammatory cell death markers in human OA chondrocytes Fig 7B. A Representative images of immunohistochemical staining of RIP1, RIP3, and pMLKL in the joint synovia of a WT group, a vehicle group, a CoQmicelle group, and a celecoxib group.

B The bar graphs show the average positive areal percentages for RIP1, RIP3, and pMLKL. A The bar graphs show the levels of mRNAs encoding MMP1, MMP3, and MMP13 in chondrocytes.

B The levels of mRNAs encoding RIPK1 and RIPK3 in chondrocytes. Osteoarthritis OA is the most common form of degenerative arthritis associated with pain and cartilage destruction in older adults. The pathogenesis includes inflammation.

There is no cure; however, analgesic and anti-inflammatory medicines, such as corticosteroids and nonsteroidal anti-inflammatory drugs NSAIDs are available [ 31 — 33 ].

Several studies have shown that CoQ10 slows OA progression [ 17 , 18 , 22 ]. Although anti-oxidant and anti-inflammatory effects of CoQ10 have been reported [ 34 — 38 ], little is known about the effects of micellized-CoQ10 on OA.

We found that micellized-CoQ10 CoQmicelles inhibited OA development and progression. During OA, the activation of catabolic factors triggers bone and cartilage degradation, and pain.

MMPs are catabolic mediators which degrade extracellular matrix proteins, and cause inflammatory diseases such as OA. In OA, MMPs degrade cartilage and thus exacerbate OA.

MMP activation and overexpression induces tissue destruction. Increased MMP levels were observed in patients with OA and experimental animals with OA [ 39 ]. MMP levels are regulated by IL-1β, which is a key mediator of the inflammatory response.

IL-1β is well- known to play a crucial role in OA [ 40 ]. Chondrocytes are the only cells found in cartilage; the cells control the structure of the extracellular cartilage matrix. Chondrocyte inflammation induced by IL-1β triggers cartilage destruction.

We previously reported that MMP and IL-1β levels were increased in an OA animal model exhibiting such destruction [ 41 — 44 ]. CoQ10 exhibits clinical anti-oxidant and anti-inflammatory effects [ 35 , 45 ]. CoQ10 deficiency has been associated with various diseases and five clinical phenotypes, thus encephalomyopathy, severe infantile multisystemic disease, cerebellar ataxia, nephropathy, and isolated myopathy [ 46 ].

Previously, we reported that CoQ10 was therapeutic in patients with autoimmune diseases [ 20 , 47 ]. CoQ10 ameliorated OA symptom in animal mode by regulating inflammatory cytokines [ 21 ]. Chang et al. reported that CoQ10 is the key factor and therapeutic target for the patient with OA [ 17 ].

Drug encapsulation affords several benefits. Drug side-effects are reduced [ 26 ]. Although micellized-CoQ10 has been used to treat certain diseases, OA was not among the diseases.

Here, we investigated whether micellized-CoQ10 CoQmicelles affected OA progression compared to CoQ We found that CoQmicelles showed better chondroprotective effect than CoQ10 in OA rats.

Pain severity, bone erosion, and cartilage destruction were significantly decreased by CoQmicelles treatment of experimental rats. Micro-CT and safranin-O staining showed that bone erosion and cartilage destruction were reduced by CoQmicelles. OA-induced increases in catabolic mediators and MMPs were reduced by CoQmicelles.

The levels of pro-inflammatory cytokines, including IL-1β and IL-6, were also significantly decreased; the drug exhibited an anti-inflammatory activity. The role played by inflammatory cell death both pyroptosis and necroptosis in OA pathogenesis is well defined.

Several studies have reported increased inflammatory cell death during OA progression [ 48 , 49 ]. Phosphorylation of MLKL by the protein kinase RIPK3 induces necroptosis and OA progression [ 50 ].

We found that CoQmicelles reduced the expression of RIP1, RIP3, and phosphorylated MLKL in synovial tissue. Next, we examined whether CoQmicelle show therapeutic effect in human chondrocytes.

We found that CoQmicelle decreased mRNA level of MMP1, MMP3, MMP13, RIPK1, and RIPK3 in chondrocytes from OA patients. Our result demonstrated that CoQmicelle has therapeutic effect in not only animal model, but also in human. We explored whether CoQmicelles inhibited OA development and progression.

CoQmicelles reduced pain, bone erosion, and cartilage destruction. The levels of pro-inflammatory cytokines and catabolic factors were decreased in CoQmicelle-treated OA rats and human OA chondrocytes.

The levels of inflammatory cell death markers also decreased in CoQmicelle treated OA rats. Together, our findings suggest that CoQmicelles can be better choice than CoQ10 in clinical use to treat OA; the inflammatory response is downregulated. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field.

Article Authors Metrics Comments Media Coverage Peer Review Reader Comments Figures. Abstract Background Osteoarthritis OA is the most common degenerative joint disease and is characterized by breakdown of joint cartilage.

Methods Seven-week-old male Wistar rats were injected with monosodium iodoacetate MIA to induce OA. Results Oral supplementation with CoQmicelles attenuated OA symptoms remarkably, including pain, tissue destruction, and inflammation.

Conclusions CoQmicelles might usefully treat OA. Introduction Osteoarthritis OA is a common degenerative joint disease associated with aging. Materials and methods Animals Seven-week-old male Wistar rats were purchased from Central Laboratory Animal Inc.

Preparation of coenzyme Q10 CoQ10 -micelles Coenzyme Q10 CoQ10 , eicosapentaenoic acid EPA , and dipotassium glycyrrhizinate were purchased from Kaneka Nutrients USA , Phycoil Biotech Korea Inc.

Induction of osteoarthritis and treatment with CoQmicelles Animals were randomly assigned to the treatment or control groups before the study commenced. Assessment of pain and weight-bearing Nociception in MIA-treated rats was tested using a dynamic plantar aesthesiometer Ugo Basile, Italy.

In vivo microcomputed tomography micro-CT imaging and analysis Micro-CT imaging and analysis were performed using a benchtop, cone-beam animal scanner mCT 35; SCANCO Medical, Switzerland. Histopathological analysis Knee joints and dorsal root ganglions were collected from each group 3 weeks post-MIA induction.

Immunohistochemistry Paraffin-embedded sections were incubated at 4°C with the following primary monoclonal antibodies: Anti-IL-1β dilution, nb, Novus [USA] , anti-MMP dilution, ab, Abcam [USA] , anti-IL-6 dilution, nb, Novus , anti-RIP1 dilution, PA, Invitrogen [USA] , anti-RIP3 dilution, Invitrogen , and anti-phospho-MLKL dilution, Abcam.

Human articular chondrocyte differentiation Human articular cartilage was acquired from patients undergoing replacement arthroplasty or joint replacement surgery and digested with 0.

RNA isolation, cDNA synthesis, and real-time quantitative PCR RNA was extracted using the TRIzol reagent Molecular Research Center Inc. Ethics approval and consent of participate All experimental procedures were reviewed and approved by the Animal Research Ethics Committee of the Catholic University of Korea approval no.

Statistical analyses Data are presented as means ± standard errors of the means S. Results Preparation of coenzyme Qencapsulated micelles CoQmicelles To generate CoQmicelles, we combined three substances CoQ10, EPA, and dipotassium glycyrrhizinate Fig 1A , see the Methods.

Download: PPT. Attenuation of OA progression by CoQmicelles We administered CoQmicelles to MIA-induced OA rats; CoQ10 [ 21 ] and celecoxib [ 30 ] served as the positive control and micelle served as negative control. Fig 2. The therapeutic effects of CoQmicelles on OA progression.

Protective effects of CoQmicelles on knee joints of MIA-induced OA rats Micro-CT showed that the femora of OA rats were less damaged in the CoQmicelle than the vehicle group Fig 3A and 3B.

Fig 4. CoQmicelles protected against cartilage destruction during OA progression. CoQmicelles reduced the levels of inflammatory mediators and catabolic factors in the synovium of MIA-induced OA rats To explore whether CoQmicelles affected the expression of inflammatory mediators and catabolic factors involved in OA progression, we immunochemically stained tissue samples for IL-1β, IL-6, and MMP Fig 5.

The anti-inflammatory effects of CoQmicelles during OA progression. CoQmicelle administration reduced inflammatory cell death Inflammatory cell death is well known to cause tissue destruction during OA progression. Fig 6. The effect of CoQmicelles on inflammatory cell death during OA progression.

Fig 7. The effects of CoQmicelles on the expression levels of catabolic and necroptotic factors in chondrocytes. Discussion Osteoarthritis OA is the most common form of degenerative arthritis associated with pain and cartilage destruction in older adults.

Conclusions We explored whether CoQmicelles inhibited OA development and progression. Supporting information. S1 File. s DOCX.

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