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NSAIDs vs. Curcumin: Which One Relieves Joint Pain Without Stopping Healing?   
Date:
September 14, 2026 11:22 AM
Comparative Analysis of NSAIDs versus Curcumin in Musculoskeletal Tissue RepairPrimary Biological Mechanisms and Pharmacological TargetsManaging soft tissue and joint injuries presents a persistent therapeutic challenge in musculoskeletal medicine. Acute inflammation triggers pain, localized swelling, and mechanical disability, which routinely drives patients toward pharmacological relief. For decades, nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen, celecoxib, and diclofenac have served as primary clinical interventions. While these synthetic agents effectively extinguish acute pain signals, expanding cellular and clinical research indicates that their biochemical mechanism interrupts the fundamental repair cascades required for long-term connective tissue healing. In contrast, curcumin - a natural polyphenolic compound derived from the rhizomes of Curcuma longa (turmeric) - exhibits a distinct, multi-targeted regulatory profile that calms hyperactive inflammation while protecting the structural components of cartilage and tendon tissue.The functional divergence between these two compounds becomes clear when considering an intuitive mechanical analogy. Tissue trauma resembles damage to a commercial building, where initial inflammation functions as the construction and demolition crew tasked with clearing rubble, stabilizing the foundation, and laying down fresh structural framing. NSAIDs function like abruptly cutting electrical power to the entire work site: the noisy machinery stops instantly and the immediate disturbance ceases, but the construction workers lose the power necessary to clean the debris and erect permanent walls. Conversely, curcumin operates as an experienced site manager: it silences unnecessary chaos and prevents site vandalism while ensuring that the skilled workers - specifically chondrocytes in cartilage and tenocytes in tendons - remain fully active, supplied, and capable of completing the restoration. At the cellular level, NSAIDs exert their effects through the catalytic inhibition of cyclooxygenase enzymes, categorized as constitutive cyclooxygenase-1 (COX-1) and inducible cyclooxygenase-2 (COX-2). Membrane phospholipids damaged during injury release arachidonic acid, which COX enzymes convert into pro-inflammatory lipid mediators known as prostanoids, most notably prostaglandin E2 (PGE2). Nonselective NSAIDs block both isoforms, while selective coxibs specifically target COX-2. By shutting off PGE2 production, NSAIDs rapidly elevate pain thresholds and blunt localized swelling. However, because PGE2 also functions as a vital signaling cue for cellular recruitment, angiogenesis, and cellular proliferation, this total enzymatic shutdown strips local repair cells of the baseline signals required to orchestrate tissue regeneration. Curcumin avoids this indiscriminate pathway paralysis by acting upstream on master transcriptional control switches rather than directly neutralizing isolated enzymes. Its primary therapeutic mechanism centers on the inhibition of Nuclear Factor-kappa B (NF-kB) and Activator Protein-1 (AP-1) signaling networks. Under acute stress or chronic inflammatory loads, the NF-kB protein complex is released from its cytoplasmic inhibitor, IkBa, and translocates directly into the cell nucleus, where it drives the transcription of catabolic cytokines such as interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-a), and interleukin-6 (IL-6). Curcumin blocks the phosphorylation and degradation of IkBa, effectively keeping NF-kB trapped in the cytoplasm. By preventing this nuclear entry, curcumin attenuates the expression of pro-inflammatory cytokines and downstream matrix-degrading enzymes while preserving baseline physiological functions. Furthermore, curcumin activates the nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidant response element (ARE) pathways, which upregulate endogenous cellular antioxidants to neutralize destructive reactive oxygen species (ROS) that induce cell death in injured joints.
The Mechanisms of NSAID-Induced Inhibition in Cartilage and Tendon RepairArticular cartilage and tendons are specialized, bradytrophic connective tissues characterized by relatively low basal metabolic rates and limited endogenous vascular supplies. These physical constraints make their cellular maintenance highly vulnerable to pharmaceutical disruptions. When synthetic compounds impair cell migration, survival, or extracellular matrix secretion, the intrinsic repair capacity of these structures is substantially degraded.Cartilage maintenance depends on chondrocytes, the sole cell type residing within articular joints, which are responsible for generating and maintaining the extracellular matrix of Type II collagen and water-binding proteoglycans such as aggrecan. Because adult articular cartilage lacks a direct vascular network, major defect repair relies heavily on the recruitment and chondrogenic differentiation of subchondral mesenchymal stem cells (MSCs) through endochondral ossification. Experimental evaluations demonstrate that systemic or intra-articular NSAID exposure halts this regenerative differentiation. Both nonselective NSAIDs and selective COX-2 inhibitors interfere with chondrocyte maturation and prevent successful tissue integration following cartilage transplantation or microfracture procedures. At the cellular level, common NSAIDs - including indomethacin, ketorolac, and diclofenac - induce cell cycle arrest in chondrocytes by blocking transition from the resting G0 phase to the proliferative G1. phase, substantially reducing viable cell numbers. Concurrently, NSAIDs downregulate Bone Morphogenetic Protein-2 (BMP-2), an essential anabolic signaling molecule that orchestrates matrix synthesis. Histological analyses in animal models reveal that NSAID administration causes a marked loss of extracellular proteoglycan content and widespread chondrocyte depletion, yielding elevated modified Mankin scores that signify advanced structural degeneration. In layman's terms, proteoglycans serve as water-absorbing structural sponges that grant cartilage its elastic shock absorption. When NSAIDs deplete these molecules, the joint surface dries out, becomes brittle, and rapidly wears down under routine mechanical friction. Tendon healing is similarly susceptible to disruption by NSAIDs. Tendons operate as high-tensile structural cables composed of longitudinally arranged Type I collagen fibers, maintained by specialized fibroblasts termed tenocytes and tenoblasts. Healing after acute rupture or chronic tear progresses through an initial inflammatory phase, followed by a proliferative phase of cell migration, and culminates in a lengthy remodeling phase of collagen alignment. In vitro and in vivo studies establish that NSAIDs directly suppress the migration and proliferative capacity of tenocytes during the critical early healing window. Without an adequate cellular workforce migrating into the wound bed, provisional collagen scaffolding cannot be synthesized effectively. The disruption is particularly pronounced at the enthesis, the specialized fibrocartilaginous junction where soft tendon inserts into rigid bone. Re-establishing this transition zone requires coordinated bone remodeling and chondrogenic differentiation, both of which are hindered by COX inhibition. In animal rotator cuff repair models, early administration of NSAIDs significantly delays collagen fiber organization and impairs mechanical integration at the insertion site, resulting in a measurable decline in load-to-failure strength and overall tendon toughness. Furthermore, while prolonged inflammation contributes to pathological degeneration, the transient synthesis of PGE2 during the initial hours following injury is essential for regulating localized microvascular flow and hyperemic nutrient delivery. By eliminating this early prostanoid pulse, NSAIDs starve the repair zone of oxygen and circulating factors precisely when the cellular metabolic demand is highest. Beyond direct biochemical cytotoxicity, systemic NSAIDs introduce a physical hazard known as analgesic arthropathy. In musculoskeletal biomechanics, pain functions as a protective feedback mechanism, forcing the patient to unload an injured joint or limb to prevent structural overload. By effectively blunting the pain reflex while simultaneously undermining the cellular synthesis of proteoglycans and collagen, NSAIDs create a deceptive state of perceived recovery. Patients prematurely resume unrestricted weight-bearing and strenuous activity, placing substantial, uncompensated mechanical forces onto compromised cartilage surfaces and unhealed tendon fibers. Over time, this recurring mechanical trauma accelerates joint space narrowing, promotes microfractures in the subchondral plate, and hastens functional joint breakdown. Chondroprotective and Tenogenic Mechanisms of CurcuminIn sharp contrast to the suppressive actions of synthetic COX inhibitors, curcumin exhibits a tissue-sparing, pro-regenerative biological profile. Rather than paralyzing cellular metabolism, curcumin modulates the microenvironment by suppressing destructive catabolic enzymes while supporting the baseline anabolic signals required for cartilage and tendon reconstruction.In articular cartilage, curcumin acts as a direct chondroprotective agent by dismantling the catabolic cascade induced by pro-inflammatory cytokines. When joint tissues are exposed to elevated IL-1ß and TNF-a, chondrocytes are provoked to synthesize matrix metalloproteinases - specifically collagenases such as MMP-1, MMP-3, and MMP-13 - along with aggrecanases like ADAMTS5. These enzymes function like enzymatic shears, systematically slicing through structural Type II collagen strands and degrading aggrecan cores. Curcumin suppresses the transcription and secretion of MMP-1, MMP-3, MMP-13, and ADAMTS5 by neutralizing NF-kB and AP-1 activation. Concurrently, it upregulates Cbp/p300 Interacting Transactivator with ED-rich tail 2 (CITED2), an essential transcriptional regulator that represses matrix metalloproteinases at the genomic level. In addition to halting extracellular degradation, curcumin protects chondrocytes from inflammatory apoptosis. Exposure to oxidative stress and inflammatory cytokines typically triggers programmed cell death by activating the intrinsic caspase cascade. Curcumin suppresses this apoptotic pathway by reducing the cleavage of executioner caspase-3, downregulating the pro-apoptotic factor Bax, and elevating anti-apoptotic Bcl-2 expression. Microscopic and histological analyses of osteoarthritic cartilage treated with curcumin consistently show robust Safranin O staining, intact surface regularity, preserved chondrocyte density, and significantly reduced Osteoarthritis Research Society International (OARSI) degradation scores. Within tendon biology, curcumin promotes active tissue regeneration (tenogenesis) rather than inert scar formation. In animal models of tendon rupture and surgical repair, curcumin guides tendon-derived stem and progenitor cells (TSPCs) toward mature tenocyte differentiation. This lineage-specific differentiation is orchestrated primarily through activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and Wnt/ß-catenin signaling cascades. As stem cells commit to the tenogenic pathway, they significantly upregulate crucial structural and phenotypic markers, including epithelial cell adhesion molecule (EpCAM), tenomodulin, and the master tendon transcription factor Scleraxis. Through this guided differentiation, curcumin supports the preferential synthesis and organized deposition of high-tensile Type I collagen fibers, the primary architectural building blocks of healthy tendons. Injured tendons typically fill with disorganized, loose Type III collagen, which forms a structurally inferior, compliant scar. Curcumin supplementation promotes the progressive maturation from primitive Type III collagen to densely packed, parallel Type I collagen fibrils, restoring native tensile strength and mechanical breaking force. A major clinical challenge following tendon surgery is the development of peritendinous adhesions, in which excessive fibrotic scar tissue binds the healing tendon to its synovial sheath, restricting range of motion and joint gliding. Postoperative tendon repair involves a balance between extrinsic healing (in which exterior fibroblasts infiltrate the defect and deposit messy scar tissue) and intrinsic healing (in which tenocytes within the tendon substance reconstruct the matrix). Curcumin suppresses excessive peritendinous inflammation and extrinsic fibrosis while accelerating intrinsic tenocyte repair. Biomechanical testing confirms that local or systemic curcumin administration yields lower adhesion scores, increased gliding distances, and superior functional mobility without sacrificing structural load-bearing capacity. Comparative Clinical Efficacy and Systemic Safety ProfilesTranslating cellular findings into clinical practice requires weighing therapeutic outcomes against systemic safety profiles. While synthetic NSAIDs deliver potent, rapid analgesia during acute musculoskeletal pain events, their chronic administration is constrained by systemic toxicities across multiple organ systems.In randomized, active-controlled clinical trials of knee osteoarthritis, optimized curcumin preparations have demonstrated clinical pain reduction and functional recovery comparable to standard therapeutic doses of NSAIDs. In a randomized, open-label parallel-arm study evaluating 139 patients with symptomatic knee osteoarthritis, subjects received either 500 mg of a bio-enhanced curcumin extract three times daily or 50 mg of diclofenac sodium twice daily for 28 consecutive days. Patients treated with curcumin demonstrated comparable improvements in pain intensity on the Visual Analogue Scale (VAS) and functional scores on the Knee Injury and Osteoarthritis Outcome Score (KOOS) at days 14 and 28, showing no statistically significant difference in therapeutic efficacy compared to diclofenac. However, the systemic tolerability profiles between the treatments diverged markedly. Overall adverse events occurred in only 13% of the curcumin group compared to 38% of the diclofenac cohort. In the diclofenac arm, 28% of patients developed dyspeptic symptoms severe enough to require concurrent treatment with H2-receptor antagonists or proton pump inhibitors to prevent mucosal ulceration, whereas no patients in the curcumin cohort required gastroprotective intervention. Furthermore, the curcumin cohort experienced a significant reduction in flatulence and digestive discomfort, demonstrating beneficial gastric and intestinal cytoprotective effects. These safety observations are consistent across broader systematic reviews and meta-analyses. Nonsteroidal anti-inflammatory agents inherently compromise gastrointestinal integrity by systematically depleting cytoprotective prostaglandins, leaving the gastric epithelium vulnerable to acid erosion and hemorrhage. In addition, systemic inhibition of renal and vascular COX enzymes by NSAIDs reduces renal perfusion and disrupts the balance between prostacyclin and thromboxane, elevating the risk of fluid retention, hypertension, and adverse cardiovascular thrombotic events. Curcumin does not suppress these physiological prostanoid pathways, making it free from ulcerogenic, nephrotoxic, and cardiotoxic properties at therapeutic dosages.
A longstanding limitation of standard curcumin supplementation in clinical settings has been its low oral bioavailability. Native curcuminoids are highly lipophilic, poorly soluble in aqueous gastric fluids, and subject to rapid hepatic and intestinal phase II metabolism into inactive glucuronides and sulfates, leading to swift biliary and fecal excretion. Consequently, raw culinary turmeric powders struggle to achieve the therapeutic systemic circulating concentrations required to reach poorly vascularized joint and tendon compartments. Modern pharmacognosy has addressed this pharmacodynamic hurdle through advanced delivery formulations. Modern strategies - such as co-administration with the natural alkaloid piperine (which inhibits hepatic glucuronidation), micellar dispersions, phytosomal phospholipid complexes, and bio-enhanced submicron dispersions - elevate systemic blood bioavailability by ten- to thirty-fold compared to unformulated extracts. These modern delivery platforms ensure that therapeutic concentrations reach synovial fluid, subchondral bone, and fibrous tendon sheaths without requiring excessive oral dosing. Conclusions and Translational Clinical ImplicationsThe biological and clinical evidence reveals distinct physiological paths for NSAIDs and curcumin in orthopedic recovery. While NSAIDs remain powerful tools for the brief alleviation of acute, unmanageable pain, their ongoing administration during active tissue healing presents substantial biological compromises. Tendons and cartilage require a controlled, transient inflammatory cascade to signal cell recruitment, stimulate stem cell differentiation, and direct extracellular matrix synthesis. By completely shutting down cyclooxygenase enzymes and depleting local prostaglandins, NSAIDs disrupt this regenerative cascade. The resulting cellular consequences - including chondrocyte cell cycle arrest, proteoglycan loss, suppression of tenocyte migration, and weakened collagen tensile strength at the tendon-to-bone interface - demonstrate that pain relief from NSAIDs frequently comes at the cost of the structural integrity of healing connective tissues.In contrast, curcumin provides a tissue-preserving alternative that decouples pain and inflammation control from cellular suppression. Operating upstream at the level of NF-kB and AP-1 transcriptional activation, curcumin attenuates the expression of pro-inflammatory cytokines while leaving the physiological baseline of cellular metabolism intact. In cartilage, it actively represses the matrix-degrading enzymes MMP-1, MMP-3, MMP-13, and ADAMTS5, maintains water-binding proteoglycan content, and protects chondrocytes from inflammatory apoptosis. In damaged tendons, curcumin stimulates tenogenic differentiation of local stem cells via PI3K/Akt signaling, supports the proper maturation of dense Type I collagen fibers, and prevents restrictive peritendinous scar adhesions, preserving both joint mobility and mechanical breaking strength. From a translational perspective, these findings indicate that clinical protocols should reconsider relying on continuous NSAIDs as the default intervention for connective tissue injuries, post-surgical recovery, and chronic degenerative conditions. Where synthetic NSAIDs are deemed necessary, their use should be confined to short-term acute flare-ups to avoid interrupting early tissue remodeling. For long-term joint preservation, ongoing tendinopathy rehabilitation, and chronic osteoarthritis management, optimized bio-enhanced curcumin formulations deliver pain relief and functional restoration comparable to conventional pharmaceuticals, all while preserving the biological processes required for lasting musculoskeletal repair. References: NSAID therapy effects on healing of bone, tendon, and the enthesis The Detrimental Effects of Systemic Ibuprofen Delivery on Tendon Conservative management of symptomatic knee osteoarthritis - PMC Positives and negatives of nonsteroidal anti-inflammatory drugs in (PDF) Conservative management of symptomatic knee osteoarthritis Non-steroidal anti-inflammatory drugs influence cartilage healing Is Curcumine Useful in the Treatment and Prevention of ... - PMC - NIH Efficacy and mechanisms of curcumin in the treatment of osteoarthritis Biological actions of curcumin on articular chondrocytes - PubMed Curcumin slows osteoarthritis progression and relieves ... - PMC - NIH Do Nonsteroidal Anti-Inflammatory Drugs Have a Deleterious Effect Anti-inflammatory management for tendon injuries - friends or foes? The mechanistic role of curcumin on matrix metalloproteinases in Therapeutic effects of turmeric or curcumin extract on pain and Curcumin inhibits chondrocyte apoptosis and inflammation in ... - PMC Analysis of the mechanism of curcumin against osteoarthritis using Synergistic enhancement of tendon-to-bone healing via anti ... - PMC A Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial Safety and efficacy of curcumin versus diclofenac in knee osteoarthritis A randomized, pilot study to assess the efficacy and safety ... - PubMed Effectiveness of curcuminoids in the treatment of knee osteoarthritis THE EFFECTS OF TRADITIONAL STRENGTHENING EXERCISES Putting Some Muscle into Osteoarthritis | Annals of Internal Medicine Do Nonsteroidal Anti-Inflammatory Drugs Have a Deleterious Effect Calebin A, a Compound of Turmeric, Down-Regulates Inflammation The Effect of Non-Steroidal Anti-Inflammatory Drugs on Tendon-to Chiropractor in Toronto, ON, Canada :: Head and Neck Pain Investigation of the association of long-term NSAID use with ... - PMC Curcumin Improves Functional Recovery of Ruptured Tendon by Chemically modified curcumin (CMC2.24) alleviates osteoarthritis Curcumin improves age-related and surgically induced osteoarthritis (PDF) Curcumin Improves Functional Recovery of Ruptured Tendon Investigation of the effects of umbilical cord-derived mesenchymal Effect of curcumin-loaded polycaprolactone scaffold on Achilles Controlled release of curcumin from curcumin-loaded nanomicelles Efficacy and safety of combination of curcuminoid complex ... - PMC The efficacy of Curcuma Longa L. extract as an adjuvant therapy in
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6653) The Role of Vitamin B12 in Energy Production 
Date:
May 29, 2024 11:28 AM
The Role of Vitamin B12 in Energy ProductionVitamin B12, or cobalamin, is crucial for red blood cell production, DNA synthesis, and nervous system health. Among its many roles, one of the most vital is its contribution to energy production and metabolism. This article delves into how Vitamin B12 affects energy levels, with a particular focus on its importance for vegetarians and vegans.
Understanding Vitamin B12Vitamin B12 is a water-soluble vitamin that is naturally found in animal products such as meat, dairy, and eggs. It is primarily responsible for converting food into ATP (adenosine triphosphate), which the body uses for energy. B12 is also crucial in the formation of red blood cells, which carry oxygen to every part of the body, and in maintaining the health of nerve cells.
The Science Behind Energy ProductionRole in MetabolismVitamin B12 is a key player in metabolism, a complex set of chemical reactions in our body that convert food into energy. One of the primary ways B12 contributes to metabolism is through its involvement in the Krebs cycle, a series of reactions that produce ATP (adenosine triphosphate), the body's primary energy currency. During the Krebs cycle, Vitamin B12 helps convert fats and proteins into energy, ensuring that the body has a constant supply of fuel to perform everyday tasks.
DNA Synthesis and Cell DivisionVitamin B12 is also essential for DNA synthesis and cell division. It works closely with folate (Vitamin B9) to synthesize DNA during cell division. Rapidly dividing tissues, such as red blood cells, require an adequate supply of B12. A deficiency in this vitamin can lead to megaloblastic anemia, a condition where red blood cells are larger than normal and not as effective in transporting oxygen, thereby causing fatigue and weakness.
The Challenge for Vegetarians and VegansB12 SourcesOne of the significant challenges for vegetarians and vegans is getting enough Vitamin B12, as it is predominantly found in animal products. Plant-based diets generally lack this vitamin, putting individuals at risk of deficiency. However, several fortified foods and supplements can help prevent this deficiency.
Fortified Foods and SupplementsMany plant-based milk alternatives, breakfast cereals, and nutritional yeasts are now fortified with Vitamin B12. For instance, a cup of fortified soy milk can provide about 50% of the daily recommended intake of B12. Additionally, B12 supplements are readily available and can be an effective way for vegetarians and vegans to ensure they get their daily dose. It's crucial to choose a supplement that meets the dietary needs and preferences of the individual.
Symptoms of DeficiencyA lack of Vitamin B12 can result in various health problems like fatigue, weakness, constipation, loss of appetite, and weight loss. In severe cases, it may lead to neurological issues such as numbness and tingling in the hands and feet, balance difficulties, depression, confusion, and memory loss. Given these risks, it's essential for vegetarians and vegans to monitor their B12 levels.
Benefits of Adequate B12 IntakeEnhanced Energy LevelsAdequate intake of Vitamin B12 can significantly enhance energy levels. Since B12 is involved in converting food into ATP, sufficient levels of this vitamin can help ensure that the body efficiently produces and uses energy. Individuals who maintain appropriate B12 levels often report feeling more energetic and less fatigued.
Improved Metabolic FunctionBy ensuring a sufficient supply of B12, vegetarians and vegans can support their metabolic functions. A well-functioning metabolism is crucial for maintaining body weight, supporting muscle function, and ensuring overall vitality. Improved metabolic function also means better handling of the foods consumed, leading to more stable energy levels throughout the day.
Better Mental HealthVitamin B12 is essential for producing neurotransmitters that regulate mood. Adequate levels of B12 can help prevent mental health issues such as depression and brain fog, which are often associated with fatigue and low energy levels. Regular intake of B12, either through diet or supplements, can contribute to better mental clarity and emotional well-being.
Optimal Nervous System FunctionB12 is crucial in maintaining the myelin sheath, a protective coating around nerves. A healthy nervous system ensures that signals travel efficiently between the brain and the rest of the body. This not only helps in preventing neurological issues but also ensures that the body's energy systems operate smoothly.
How to Ensure Adequate B12 IntakeRegular Blood TestsFor vegetarians and vegans, regular blood tests are an effective way to monitor B12 levels. These tests can help identify a deficiency early on, allowing individuals to take corrective measures before any severe symptoms manifest.
Balanced DietA well-rounded, balanced diet that includes fortified foods can help meet the daily recommended intake of Vitamin B12. Incorporating a variety of B12-fortified foods into every meal ensures a steady supply of this vital nutrient.
Considering SupplementsFor those who struggle to get enough Vitamin B12 through diet alone, supplements are an excellent option.
Choosing the Right Supplement: Methyl B12When selecting a Vitamin B12 supplement, methylcobalamin, or methyl B12, is often recommended as the best form. It has superior bioavailability compared to cyanocobalamin, making it easier for the body to absorb and utilize. Methyl B12 doesn't need conversion in the body to be effective, leading to quicker uptake and immediate benefits. For vegetarians and vegans at higher risk of B12 deficiency, methyl B12 is especially beneficial for maintaining optimal B12 levels effectively. Including this form in your supplement routine can boost energy, mental clarity, and support metabolic and nervous system functions.
Awareness and EducationRaising awareness about B12 is key for vegetarians and vegans to prevent deficiencies. Health programs can educate on maintaining adequate levels through diet and supplements.
Are You Ready For More Energy?Vitamin B12's role in energy production and metabolism is indisputable. Vegetarians and vegans can struggle to get enough B12 from plant-based diets, but fortified foods and supplements offer solutions. Understanding B12's importance and taking action can boost energy, metabolism, and well-being. Regular monitoring, a balanced diet, and appropriate supplementation are key strategies to prevent deficiency and maintain optimal health.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6604) The 7 Proven Health Benefits of CBD Oil
Date:
May 06, 2019 03:30 PM
CBD oil has come into the spotlight recently with some amazing health benefits, so much so it is set to be sold in major retail pharmacy's such as CVS inthe very near future. CBD has many uses in the field of medicine, particularly as an over the counter remedy that if needed of long term, is safer than many of the current produces that are used as pain relievers, or that reduce anxiety and depression. One of the incredible things it does is to relieve cancer treatment symptoms, such as nausea and pain. It has also shown to improve neurological health and to stabilize blood sugars for those with diabetes. Key Takeaways:
"Although the use of medical marijuana is still a politically and emotionally charged topic, research shows that there may be huge benefits of the CBD oil." Read more: https://www.longevitylive.com/live-healthier/7-proven-health-benefits-cbd-oil/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6263) Turmeric (Curcumin),The Healing Root.
Date:
June 06, 2017 12:14 PM
A staple of Ayruvedic medicine, practiced in India, besides being a flavoring agent and useful for coloring fabrics, Turmeric is a highly nourishing herb, specifically a rhizome, with antibacterial, antiviral, anti-inflammatory and anticarcinogenic properties, to name a few. Hormonal imbalance, obesity and hypertension are a few other areas that can benefit from Turmeric use. Easy to incorporate into the diet, even small amounts are beneficial. A traditional golden milk, make with coconut milk, is tasty and provides many nutrients. Turmeric is an inexpensive way to boost your health every day and even makes a beautiful addition to the garden, should you decide to grow it. Key Takeaways:
"it has only been recently that people throughout the rest of world have discovered the many uses turmeric has for health and well being and as a tasty addition to culinary delights. This little root can help our bodies in miraculous ways and also healing our pets." Read more: http://uk.blastingnews.com/health/2017/06/turmeric-curcuminthe-healing-root-001741961.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4781) Can MSM Help Improve Joint Health?
Date:
November 09, 2013 05:58 PM
What is MSM
What are the Benefits of MSM Physical strain and Osteoarthritis (OA) may lead to swelling and joint pain. The pain caused by OA can be relieved using MSM. From the research done; MSM is believed to have anti-inflammatory effects. Many people especially the old suffer from joint disease. The OA affected joints suffer from uneven loading, which results to altered lines of weight bearing. Cartilage starts to form to compensate for the uneven load, this leads to formation of deformities and roughening in the surface of the joint. The operation of the joint inflame is affected because the socket and the ball rub unevenly due to the friction of outgrowths of bone and cartilage, called osteophytes.Up to date no cure for OA has been found therefore, the treatment available only eases the symptoms. How Sulfhur Helps our Body Sulfur is delivered into our bodies by MSM in a usable way. Sulphur helps in maintaining the connective tissue structure by forming cross linkages. This therefore means that sulphur strengthens the joint tissues.Sulphur is very important for the good health of the joints.Glycosaminoglycans (GAGs) are the crucial building blocks of joint cartilage. GAG molecules are held together by the disulfide bonds. As the name suggests, the disulfide bonds are bonds between 2 atoms of sulphur. Disulfide bridges reduce the conformational flexibility of the GAG chains, hence making the cartilage resilient and firm. Thus the integrity of the cartilage depends on sulphur. References:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2885) Fennel Seeds 
Date:
November 12, 2009 04:47 PM
The fennel plant is native to the southern areas of Europe and Asia Minor. The herb is now cultivated in the United States and Great Britain. It was used anciently in many civilizations. Used in ancient Egypt, this herb aids in digestion and flatulence. In Italy, fennel was used to bring surgical patients out of anesthesia. Fennel was recommended by Hippocrates and Dioscorides to increase milk production in nursing mothers. The ancient Greeks used this herb for weight reduction, while the seventeenth-century herbalist Nicholas Culpeper also recommended this herb for losing weight. Fennel is extremely helpful in weight reduction, as it suppresses the appetite. This herb aids in stabilizing the nervous system and can be used as a sedative for small children. Fennel can be used to expel phlegm from the throat, eliminate toxins from the body, and purify the blood. This herb is known for its ability to fortify the immune system and be good for the eyes. Additionally, fennel aids in digestion, improves night vision, relieves gas, expels worms, improves the quality of milk in nursing mothers, and cleans the bladder and liver. This herb has been used to stimulate menstruation and can help too soothe the smooth muscles of the digestive tract, as it aids in digestion and related problems.
Research on rats has found that the fennel seeds have estrogenic effects on the genital organs. The herb has been found to promote the production of milk in nursing mothers. Fennel is good for digestion, colic, and other stomach complaints. This herb contains essential oils that have a composition similar to catnip and peppermint. Additionally, this herb can be very helpful in treating excessive appetite, asthma, constipation, convulsions, coughs, uterine cramps, gout, kidney ailments, absence of lactation, liver disorders, lung disorders, and nervous disorders. For more information on the many beneficial effects provided by this herb, please feel free to contact a representative from your local health food store.
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The initials MSM stands for methyl- sulfonyl – methane commonly known as sulfur. MSM is white sulfur powder which is organic. MSM comes from the ocean and is soluble in water. It is a food commonly found in meats, vegetation, plants and dairy products. In the human body, it is the third largest nutrient. Sulfur is very important in human body; it plays a very critical role in the production of collagen which acts as a building block of skin, joints, nails, hair and other connective tissues.
Fennel is a plant species that is part of the genus Foeniculum. A member of the family Apiaceae, this plant is a hardy, perennial, umbelliferous herb. The plant has yellow flowers and feathery leaves. It is generally found growing on the shores of the Mediterranean, but it has become widely naturalized elsewhere. Now, the plant can be found growing wild in many parts of the world, especially on dry soils near the sea-coast and on river-banks. The plant is highly aromatic and flavorful. It is actually one of the primary ingredients of absinthe. Some species of fennel possess a swollen, bulb-like stem base, which is used as a vegetable. Fennel is used as food plant by some moth and bird species. 
The seeds of the fennel plant are used to provide anorectic, antacid, anti-inflaamtory, antimicrobial, antispasmodic, carminative, diuretic, estrogenic, expectorant, galactagogue, sedative, and stimulant properties. The primary nutrients found in this herb are calcium, magnesium, niacin, potassium, sodium, sulfur, vitamins A, C, B1, and B2. Primarily, fennel is extremely beneficial in dealing with abdominal cramps, colic, gas, gastric disorders, indigestion, intestinal problems, and weight-related conditions. 
