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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 Ultimate Guide to Cellular Longevity: NAD+, Methylation, and Senolytics 
Date:
September 10, 2026 10:57 AM
Introduction: Understanding Cellular Aging and Energy DeclineBiological aging represents a progressive decline in cellular maintenance, structural repair, and energy generation. Over decades, tissues experience an attrition of functional reserves, compromised stress resilience, and persistent low-grade systemic inflammation. At the cellular scale, biological degeneration is driven by a failure to generate bioenergetic fuel, repair genetic code, and clear metabolic waste.Cellular aging is characterized by interconnected biological disruptions known as the hallmarks of aging. These encompass genomic instability, epigenetic alterations, mitochondrial decay, loss of proteostasis, and cellular senescence. Rather than operating as isolated occurrences, these phenomena establish a self-reinforcing degenerative cycle: declining cellular power generation impairs enzymatic genetic repair, promoting the accumulation of damaged cells that enter irreversible growth arrest and poison surrounding healthy tissues. Mitigating cellular aging requires examining how microscopic bioenergetic pathways deteriorate and evaluating how targeted nutritional and biochemical interventions can restore cellular homeostasis. The Role of Mitochondria and ATP ProductionEvery biological function - from muscular contraction to continuous DNA replication - depends on adenosine triphosphate (ATP), the primary biochemical energy currency of living systems. Cells produce the vast majority of this energy within mitochondria through oxidative phosphorylation. Within these specialized organelles, metabolic intermediates derived from dietary carbohydrates and lipids donate high-energy electrons to the electron transport chain. The flow of these electrons across protein complexes establishes an electrochemical proton gradient across the inner mitochondrial membrane, driving ATP synthase to manufacture ATP.A youthful cell functions like an efficient municipal power grid, dynamically matching energetic demands with immediate ATP output. However, as biological aging progresses, mitochondrial efficiency declines. The electron transport chain becomes structurally leaky, inadvertently shedding electrons that react with ambient molecular oxygen to produce reactive oxygen species (ROS). While regulated levels of ROS participate in vital intracellular signaling, chronic excess induces widespread oxidative stress. Mitochondria are exceptionally vulnerable to this oxidative burden because they carry their own circular genetic material, known as mitochondrial DNA (mtDNA). Unlike nuclear DNA, mtDNA lacks the protective shielding of histone proteins and possesses rudimentary repair systems. As a result, mtDNA sustains cumulative oxidative damage, encoding increasingly defective electron transport chain proteins. This dynamic generates a bioenergetic deficit: degraded mitochondria synthesize progressively less ATP while emitting greater volumes of damaging free radicals. Deprived of optimal ATP reserves, cells lack the energy necessary to drive vital enzymatic repair cascades, accelerating structural degeneration and functional exhaustion. How Cellular Senescence Accelerates the Aging ProcessWhen healthy cells confront critical physiological damage - such as severe telomere attrition, persistent DNA double-strand breaks, or oxidative stress - they activate protective cell cycle arrest pathways governed primarily by the p53/p21^CIP1 and p16^INK4a/Rb molecular checkpoints. This defensive shutdown, termed cellular senescence, permanently prevents the replication of potentially premalignant or mutated cells.Senescent cells, colloquially known as "zombie cells," enter a state of permanent growth arrest while actively resisting programmed cell death (apoptosis). Over time, these cells accumulate within adipose depots, skeletal muscle, the vascular endothelium, and major organs, largely because immune surveillance and clearance pathways simultaneously lose functional efficiency. The systemic danger of senescent cells stems from their secretome. Rather than remaining biologically inert, senescent cells develop a hyperactive secretory state termed the Senescence-Associated Secretory Phenotype (SASP). The SASP is a destructive mixture of pro-inflammatory cytokines, chemokines, extracellular matrix-degrading matrix metalloproteinases (MMPs), and reactive oxygen species. Through this toxic secretome, even a small burden of senescent cells can impair whole-tissue architecture. SASP factors degrade surrounding structural proteins, induce insulin resistance in neighboring metabolic cells, and biochemically force adjacent healthy cells into secondary senescence. This persistent paracrine signaling fuels chronic, sterile, low-grade systemic inflammation, termed "inflammaging," which accelerates systemic tissue degeneration and elevates susceptibility to degenerative age-related pathologies. Nicotinamide Riboside (NR) and the NAD+ Salvage PathwayThe Biochemistry of NAD+ Depletion Over TimeNicotinamide adenine dinucleotide (NAD+) is an indispensable coenzyme present in every living cell. NAD+ fulfills a dual biological mandate: it serves as a central redox cofactor that shuttles electrons between cellular metabolic reactions, and it functions as an obligatory consumable substrate for regulatory enzymes that preserve cellular viability. In its redox capacity, NAD+ accepts electrons to form NADH during glycolysis, the tricarboxylic acid (TCA) cycle, and fatty acid beta-oxidation, subsequently donating those electrons to Complex I of the respiratory chain to power ATP synthesis.
The primary enzymatic driver of age-related NAD+ destruction is CD38, a membrane-bound glycohydrolase expressed on immune cells that is upregulated in response to chronic SASP exposure. Concurrently, lifelong genotoxic damage causes persistent activation of Poly(ADP-ribose) polymerase 1 (PARP-1), an enzyme that cleaves the glycosidic bonds of NAD+ to assemble branched poly(ADP-ribose) chains at DNA lesion sites. Because PARP-1 consumes NAD+ without directly recycling the molecule, chronic DNA damage depletes intracellular NAD+ pools, impairing bioenergetics and limiting sirtuin activity. How NR Efficiently Boosts Cellular NAD+ LevelsThe mammalian body maintains its NAD+ supply through three distinct biosynthetic routes: the de novo pathway from dietary L-tryptophan, the Preiss-Handler pathway from nicotinic acid (niacin), and the NAD+ Salvage Pathway. The de novo pathway requires substantial energy expenditure, consuming roughly sixty milligrams of dietary tryptophan to yield a single milligram of NAD+. The Preiss-Handler pathway, while effective, can induce cutaneous prostaglandin-mediated flushing at therapeutic intakes. Consequently, the salvage pathway serves as the primary mechanism for maintaining intracellular NAD+ pools.The salvage pathway recycles the breakdown product nicotinamide (NAM), which is released whenever NAD+-consuming enzymes execute their functions. Under normal conditions, cells convert free nicotinamide into nicotinamide mononucleotide (NMN) via the rate-limiting enzyme nicotinamide phosphoribosyltransferase (NAMPT), after which NMN adenylyltransferases (NMNAT1–3) complete the conversion into NAD+. However, NAMPT expression declines with advancing age, chronic inflammation, and metabolic stress, limiting the recycling capacity of the cell. Nicotinamide Riboside (NR) is a naturally occurring pyridine nucleoside that bypasses this enzymatic bottleneck. Upon cellular entry via equilibrative nucleoside transporters, NR is directly phosphorylated into NMN by nicotinamide riboside kinases (NRK1 and NRK2) using a single molecule of ATP. Because the NRK pathway remains intact and robust across the lifespan, NR provides an efficient alternative entry point into the NAD+ salvage cascade. Clinical evaluations in humans confirm the safety, bioavailability, and pharmacokinetics of oral NR supplementation. Randomized, double-blind, placebo-controlled trials reveal that oral NR chloride produces dose-dependent increases in steady-state whole blood NAD+ concentrations. Dosing regimens of 100 mg, 300 mg, and 1,000 mg daily elevate blood NAD+ levels by approximately 22%, 51%, and up to 142%, respectively, within two weeks of administration, maintaining these elevations throughout continuous use. High-resolution metabolomic analyses also demonstrate parallel elevations in nicotinic acid adenine dinucleotide (NAAD), establishing it as a reliable biomarker of active intracellular NAD+ synthesis without hepatic or systemic toxicity. Sirtuin Activation and DNA Repair MechanismsReplenishing intracellular NAD+ supports functions beyond mitochondrial ATP generation. NAD+ functions as an obligatory cofactor for sirtuins (SIRT1 through SIRT7), a family of class III histone and non-histone protein deacetylases that regulate stress resilience, metabolic homeostasis, and cell survival. Sirtuins couple the removal of acetyl groups from target lysine residues to the stoichiometric cleavage of NAD+, producing nicotinamide and O-acetyl-ADP-ribose. In states of NAD+ deficiency, sirtuin enzymes remain inactive regardless of cellular demand.In the nucleus, SIRT1 coordinates defense against cellular decline. When activated by restored NAD+ levels, SIRT1 deacetylates peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1a), the master transcriptional coactivator of mitochondrial biogenesis. This deacetylation stimulates mitochondrial replication and assembly, expanding functional respiratory capacity. Concurrently, SIRT1 deacetylates the p65 subunit of nuclear factor-kappa B (NF-kB), suppressing the transcription of pro-inflammatory cytokines. In the mitochondria, SIRT3 utilizes NAD+ to deacetylate metabolic enzymes and superoxide dismutase 2 (SOD2), enhancing the organelle's capacity to neutralize reactive oxygen species. At the same time, cellular NAD+ levels directly regulate genomic integrity through PARP-1. When genotoxic stress or oxidative damage induces single- or double-strand DNA breaks, PARP-1 binds to the damaged termini using its zinc-finger domains. Bound PARP-1 hydrolyzes NAD+ to synthesize extensive, negatively charged poly(ADP-ribose) polymers on itself and adjacent histones. This modification relaxes chromatin architecture and establishes an electrostatic scaffold that recruits base excision repair and homologous recombination complexes. Recent discoveries demonstrate close crosstalk between sirtuins and PARP-1 during DNA repair. PARP-1 recruits SIRT1 to double-strand breaks, where SIRT1 deacetylates the chromatin-remodeling ATPase BRG1 to displace nucleosomes and facilitate homologous recombination. However, because PARP-1 and SIRT1 draw from the same intracellular NAD+ pool, severe NAD+ depletion forces a biological compromise: PARP-1 consumes the scarce remaining cofactor to address DNA damage, leaving sirtuins deactivated. Restoring NAD+ via NR prevents this deficit, enabling concurrent genomic repair and sirtuin-mediated metabolic defense. Quercetin: A Powerful Senolytic and mTOR RegulatorClearing Senescent "Zombie" Cells from TissuesThe accumulation of senescent cells has driven interest in senolytics: molecules that selectively eliminate senescent cells while sparing healthy, non-senescent populations. Senolytic agents exploit a specific vulnerability in senescent cells. Because senescent cells produce cytotoxic, pro-inflammatory SASP factors that would normally induce their own death, they become dependent on upregulated Senescent Cell Anti-Apoptotic Pathways (SCAPs) to survive. The SCAP network involves anti-apoptotic proteins (such as BCL-2 and BCL-xL), the PI3K/Akt kinase cascade, and cyclin-dependent kinase inhibitors.Quercetin is a polyphenolic flavonoid found in capers, red onions, apples, and the flower buds of Sophora japonica. Beyond its classical antioxidant properties, quercetin functions as a senolytic compound that exerts multi-target inhibitory effects across the SCAP network. By inhibiting the upstream PI3K/Akt survival axis and downregulating anti-apoptotic defenses, quercetin disrupts the signaling that protects senescent cells from intrinsic apoptosis. Deprived of these survival signals, senescent cells undergo programmed cell death. Preclinical studies demonstrate that senolytic protocols utilizing quercetin - often combined with the tyrosine kinase inhibitor dasatinib - reduce senescent cell burden across multiple tissues. This targeted clearance lowers circulating SASP factors, attenuates tissue fibrosis, restores endothelial reactivity, and improves functional health span. By removing senescent cells, quercetin mitigates the primary driver of chronic, low-grade inflammaging. Modulating the mTOR Pathway for Optimal AutophagyThe mechanistic Target of Rapamycin (mTOR) is an evolutionarily conserved serine/threonine protein kinase that coordinates cellular metabolism by balancing anabolic growth with catabolic recycling. Operating within two multiprotein complexes - mTORC1 and mTORC2 - the mTOR pathway integrates signals from amino acids, growth factors, and intracellular energy levels. In nutrient-rich environments, mTORC1 promotes protein synthesis, lipogenesis, and cellular growth, while suppressing catabolic breakdown. Conversely, nutrient scarcity downregulates mTORC1, activating autophagy.Autophagy is an intracellular degradation system that packages damaged organelles, misfolded protein aggregates, and biological debris into double-membraned autophagosomes for lysosomal degradation and recycling. A specialized branch of this pathway, mitophagy, selectively targets and clears damaged mitochondria. In modern metabolic conditions characterized by continuous caloric intake, mTORC1 can remain persistently active. This persistent signaling suppresses autophagy, causing damaged organelles and toxic aggregates to accumulate within tissues. Quercetin functions as a natural modulator of mTOR signaling. By inhibiting upstream PI3K/Akt signaling and activating intracellular energy sensors, quercetin attenuates overactive mTORC1, mimicking the metabolic effects of caloric restriction. This down-regulation relieves inhibition on the ULK1 autophagy initiation complex, stimulating both general autophagy and mitophagy. As autophagy proceeds, cells clear protein aggregates and eliminate damaged mitochondria, supporting cellular longevity and proteostasis. Enhancing Absorption: Phytosomes and Dietary FatsDespite the biological activities of quercetin identified in experimental models, its clinical translation has historically been limited by poor oral bioavailability. Raw quercetin aglycone is a crystalline, hydrophobic polyphenol with poor solubility in water and gastrointestinal fluids. When ingested in unformulated powder forms, quercetin molecules aggregate in the gut lumen, resisting dissolution and passive absorption. Consequently, the vast majority of an unformulated dose passes into the colon unabsorbed, where it undergoes microbial degradation without reaching meaningful systemic concentrations.To address these pharmacokinetic limitations, advanced delivery systems such as phytosomes were engineered. A phytosome is a 100% food-grade molecular complex where individual polyphenolic molecules are bound to dietary phospholipids, typically sunflower-derived phosphatidylcholine. Unlike a classical liposome - which encapsulates water-soluble compounds inside an aqueous core enclosed by a lipid bilayer - a phytosome forms an amphiphilic complex at the molecular level. The polar head of the phosphatidylcholine molecule forms hydrogen bonds with the hydroxyl groups of the quercetin molecule, while its lipophilic fatty acid tails extend outward. This structural arrangement shields the polar regions of the flavonoid, creating a lipid-compatible complex that integrates smoothly into the intestinal mucosa.
The Importance of Methylation in Healthy AgingVitamin B-Complex and Choline as Essential Methyl DonorsMethylation is an essential biochemical process occurring billions of times each second across all human tissues. It involves the transfer of a single-carbon unit - a methyl group consisting of one carbon atom bound to three hydrogen atoms - (CH3) - from a donor molecule to diverse recipients, including DNA, RNA, structural proteins, neurotransmitters, and membrane phospholipids. This transfer of one-carbon units is coordinated by the methionine-homocysteine cycle, which sustains genetic stability, detoxification pathways, and cellular repair.At the center of this pathway sits S-adenosylmethionine (SAM), the universal methyl donor in human biology. When a methyltransferase enzyme transfers a methyl group from SAM to an acceptor molecule, SAM is converted into S-adenosylhomocysteine (SAH). SAH functions as a potent competitive inhibitor of intracellular methyltransferases. To maintain functional methylation, SAH is rapidly hydrolyzed into homocysteine, a sulfur-containing amino acid that must be remethylated or cleared through transsulfuration. Homocysteine clearance proceeds through two distinct remethylation pathways. The primary route operates across most tissues via the enzyme methionine synthase, which requires vitamin B12 in its active methylcobalamin form. Methionine synthase transfers a methyl group from 5-methyltetrahydrofolate (5-MTHF, the active form of folate) to homocysteine, regenerating methionine. The ongoing production of 5-MTHF depends on the enzyme methylenetetrahydrofolate reductase (MTHFR), which utilizes riboflavin (vitamin B2) as a cofactor. Alternatively, excess homocysteine can be routed into the transsulfuration pathway by vitamin B6 (as pyridoxal-5'-phosphate) to synthesize cystathionine, cysteine, and ultimately the antioxidant glutathione. A secondary remethylation pathway, active predominantly in hepatic and renal tissues, bypasses folate entirely. In this route, dietary choline is oxidized to betaine (trimethylglycine or TMG). The enzyme betaine-homocysteine S-methyltransferase (BHMT) then transfers a methyl group from betaine directly to homocysteine, yielding methionine and dimethylglycine. When dietary intake of active B-vitamins or choline is insufficient, or when genetic variations like MTHFR polymorphisms reduce pathway flux, the methylation cycle slows. Homocysteine accumulates in circulation, promoting vascular and neurological inflammation, while SAM reserves decline, restricting cellular methylation capacity. Understanding DNA Methylation and Epigenetic HealthEvery somatic cell in an organism carries an identical genetic code. Cellular differentiation and tissue-specific functions are governed by the epigenome: a regulatory layer of chemical modifications that dictates gene expression without altering underlying DNA sequences. DNA methylation represents the primary and most stable epigenetic modification. In this process, DNA methyltransferase (DNMT) enzymes utilize methyl groups donated by SAM to add a methyl tag to cytosine bases adjacent to guanine residues, forming 5-methylcytosine within CpG dinucleotide sites.Under physiological conditions, DNA methylation maintains genomic stability and coordinates transcription. Methylation of promoter regions condenses chromatin, repressing transposable elements and silencing genes inappropriate for a given cell type. Conversely, hypomethylated promoters maintain an open chromatin state, allowing transcription factors to bind and initiate gene expression. During biological aging, this epigenetic landscape undergoes progressive dysregulation, a phenomenon termed "epigenetic drift". Aging cells experience global hypomethylation alongside focal hypermethylation of specific gene promoters. Global loss of methyl tags destabilizes the genome, activating retrotransposons and pro-inflammatory pathways. Simultaneously, hypermethylation at targeted promoter sites silences critical tumor suppressor genes and DNA repair complexes. This systematic change in DNA methylation patterns is consistent across populations, allowing researchers to develop molecular "epigenetic clocks". Algorithms such as the Horvath clock, PhenoAge, and GrimAge quantify biological age by profiling the methylation status of specific CpG sites across the genome. These clocks assess whether individuals are aging faster or slower than their chronological years. Ensuring a steady supply of methyl donors and preventing unnecessary SAM depletion supports DNMT activity, maintaining epigenetic patterns and genomic stability. How the Methylation Cycle Impacts Energy and Cognitive FocusBeyond long-term epigenetic regulation, the methylation cycle directly modulates immediate biochemical processes that govern daily energy, neurotransmission, and cognitive focus. Compromised methylation capacity frequently manifests as cognitive slowing, executive fatigue, and reduced physical stamina.A major consumer of methyl reserves is the endogenous synthesis of creatine. Approximately 40% of all SAM-derived methyl groups in the human body are utilized by guanidinoacetate N-methyltransferase (GAMT) in the liver to synthesize creatine. Creatine then translocates to the brain and skeletal muscle, where it is phosphorylated into phosphocreatine. Phosphocreatine functions as a rapid energy buffer, donating a high-energy phosphate group to regenerate ADP into ATP in milliseconds during demanding physical or cognitive tasks. When methyl donor availability falls, endogenous creatine synthesis drops, depleting phosphocreatine reserves and increasing susceptibility to neuromuscular and cognitive fatigue. Methylation is equally central to central nervous system architecture. SAM provides methyl groups to convert phosphatidylethanolamine into phosphatidylcholine, the predominant phospholipid comprising neuronal cell membranes and the myelin sheaths that insulate axons. Intact myelin preserves rapid action potential conduction throughout the nervous system. Furthermore, free choline derived from this pathway is the direct precursor to acetylcholine, the neurotransmitter required for attention, working memory, and learning. The methylation cycle also governs monoamine neurotransmitter metabolism. SAM is required for the synthesis of adrenaline (epinephrine) from noradrenaline, while catechol-O-methyltransferase (COMT) relies on SAM to degrade dopamine and norepinephrine within the prefrontal cortex. Sluggish methylation disrupts this balance, contributing to cognitive fatigue, mood variability, and impaired mental performance. Building a Comprehensive Longevity ProtocolSynergizing NR, Quercetin, and Methylated B-VitaminsLongevity supplementation often falters when single molecules are administered in isolation, ignoring interconnected metabolic pathways. Designing an effective cellular longevity protocol requires combining complementary mechanisms that reinforce one another while preventing secondary metabolic deficits. The combination of Nicotinamide Riboside, Quercetin Phytosome, and Methylated B-Vitamins illustrates this multi-target synergy.This synergy is grounded in the direct biochemical intersection between the NAD+ salvage pathway and the methylation cycle. When high-dose NR is supplemented to boost systemic NAD+, sirtuins and PARP enzymes consume the newly synthesized cofactor, generating substantial quantities of free nicotinamide (NAM). This intracellular nicotinamide faces two primary metabolic fates: it can be recycled back into NAD+ through the NAMPT-dependent salvage loop, or it can be cleared via methylation. When the influx of nicotinamide exceeds salvage recycling capacity, the excess is cleared to avoid feedback inhibition of sirtuin enzymes. To accomplish this, the enzyme nicotinamide N-methyltransferase (NNMT) transfers a methyl group from SAM directly onto nicotinamide, forming 1-methylnicotinamide (1-MNA/MNAM), which is subsequently excreted in urine. Prolonged, high-dose precursor administration without nutritional methyl support can elevate NNMT flux, depleting intracellular SAM reserves. As methyl groups are consumed clearing nicotinamide, the cellular SAM-to-SAH ratio falls, which can elevate circulating homocysteine and reduce methyl availability for DNA methylation and neurotransmitter synthesis. Co-administering a fully methylated B-complex alongside choline or betaine addresses this potential bottleneck. Providing active methyl donors (such as 5-MTHF, methylcobalamin, and betaine) maintains the one-carbon donor pool. Even during increased NNMT activity, SAM pools remain stable, protecting DNA methylation fidelity and maintaining homocysteine within safe parameters. Quercetin reinforces this protocol through complementary mechanisms. By clearing senescent cells and reducing SASP-mediated inflammation, quercetin downregulates CD38, the primary enzyme responsible for age-related NAD+ degradation. Suppressing CD38 prevents unnecessary breakdown of newly synthesized NAD+, enhancing the efficiency of NR supplementation. Furthermore, while NR provides the NAD+ necessary to activate SIRT1-driven mitochondrial biogenesis, quercetin concurrently modulates mTORC1 to stimulate autophagy. This coordinated action ensures that newly generated mitochondria operate in an environment cleared of proteotoxic cellular debris. The Crucial Role of Magnesium Glycinate and Zinc in Cellular FunctionLongevity protocols require essential mineral cofactors to function efficiently. Without adequate divalent minerals acting as enzymatic cofactors and structural stabilizers, metabolic longevity pathways cannot operate at full capacity. Among these, magnesium and zinc are required for cellular repair, genomic stability, and energy production.Magnesium serves as an obligatory cofactor in over 300 enzymatic reactions, primarily through its interaction with ATP. In biological systems, ATP exists predominantly as a chelate with a divalent magnesium ion, forming biologically active Mg2+ -ATP. Every enzymatic reaction that synthesizes, transfers, or consumes cellular energy - including the enzymes of the NAD+ salvage pathway (NRK and NMNAT) and DNA polymerases - strictly requires Mg2+ -ATP as its substrate. Magnesium deficiency impairs these phosphorylation reactions, reducing the cellular utilization of NAD+ precursors. Additionally, magnesium is an essential cofactor for the enzymes that activate dietary B-vitamins into their active forms. Supplying magnesium as magnesium glycinate provides high gastrointestinal bioavailability, minimal laxative effect, and yields glycine to support inhibitory neurotransmission and restful sleep. Zinc serves as a vital structural component for more than 3,000 human transcription factors and enzymatic proteins. Its most prominent structural role in longevity occurs within zinc-finger motifs. These are specialized protein conformations stabilized by a zinc ion coordinated to cysteine and histidine residues. The DNA damage sensor PARP-1 utilizes three zinc-finger domains to identify, track, and physically bind to single- and double-strand DNA breaks. Without adequate intracellular zinc, PARP-1 cannot properly assemble or dock onto damaged chromosomes, impairing DNA repair and increasing genomic instability. Zinc is also an obligatory structural component of copper/zinc superoxide dismutase (Cu/Zn-SOD or SOD1), the primary cytosolic antioxidant enzyme that dismutates superoxide radicals into hydrogen peroxide, protecting mitochondrial membranes and nuclear DNA from premature senescence. Integrating Prebiotics (like Acacia and Inulin) for Gut-Derived Longevity MarkersA comprehensive cellular longevity framework must extend beyond somatic tissues to encompass the gut microbiome. The intestinal microbiome functions as a central regulator of systemic inflammatory tone, immune development, and metabolic signaling. Age-associated dysbiosis - characterized by the loss of beneficial commensals and an overgrowth of pathobionts - frequently leads to breakdown of the intestinal barrier.The gut epithelium consists of a single-cell monolayer sealed by tight junction proteins, including zonula occludens-1 (ZO-1), occludin, and claudins. When this physical barrier is disrupted by poor dietary fiber intake or dysbiosis, gut permeability increases. This allows lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, to enter the portal and systemic circulation. The resulting "metabolic endotoxemia" activates Toll-like receptor 4 (TLR4) on immune cells, inducing NF-kB and systemic pro-inflammatory cytokine production. This persistent gut-derived inflammation exacerbates the SASP, accelerates tissue senescence, upregulates CD38, and drains systemic NAD+ reserves.
These short-chain fatty acids, particularly butyrate, exert direct protective effects on systemic longevity. Butyrate provides the primary metabolic fuel for colonic epithelial cells, supplying more than 70% of their baseline energy needs and supporting mitochondrial function within colonocytes. Furthermore, SCFAs upregulate the expression of epithelial tight junction proteins (ZO-1, occludin, and claudin-1), restoring intestinal barrier integrity and preventing the translocation of inflammatory LPS into systemic circulation. Systemically absorbed butyrate also functions as an endogenous histone deacetylase (HDAC) inhibitor, suppressing pro-inflammatory gene expression and supporting regulatory T cell (T_reg) development. Reducing metabolic endotoxemia dampens systemic inflammation, protecting vascular function and preventing premature NAD+ depletion. Conclusion: The Integrated Cellular Longevity MatrixCellular longevity is achieved not by addressing isolated biomarkers in isolation, but by systematically supporting interconnected biological pathways. As bioenergetic capacity declines, cellular senescence accelerates, epigenetic patterns degrade, and gut barrier integrity weakens. A comprehensive approach addresses these biological vulnerabilities simultaneously.
Quercetin Phytosome clears senescent cells and modulates mTORC1, stimulating autophagy while dampening the inflammatory SASP cascade that accelerates CD38-mediated NAD+ destruction. Methylated B-vitamins, active folate, and choline replenish SAM reserves, balancing the methyl requirements of NNMT-mediated nicotinamide clearance, preserving epigenetic DNA methylation, and maintaining neurotransmitter production. Magnesium glycinate and zinc provide the structural and catalytic foundation required for ATP utilization, B-vitamin activation, and PARP-1 zinc-finger DNA repair docking. Finally, prebiotic fibers generate short-chain fatty acids like butyrate, reinforcing the intestinal barrier and preventing metabolic endotoxemia from fueling systemic inflammation. By coordinating energy replenishment, cellular waste clearance, epigenetic maintenance, and the suppression of systemic inflammation, this unified approach directly addresses the underlying drivers of cellular aging to support long-term physiological vitality.
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(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6650) "The Butyrate Paradox" Does Butyrate Trigger Apoptosis in Just Colon Cancer or All Cancers Throughout The Body?
Date:
November 20, 2025 12:16 PM
In the context of the colon, the paradox states that butyrate is a promoter of life for healthy colon cells but an inducer of death (apoptosis) for colon cancer cells. Regarding its effects on all cancers throughout the body, studies show that butyrate's pro-apoptotic (death-inducing) properties are not limited to colon cancer, but the paradox itself is largely defined by the unique metabolic environment of the colon. ?? Understanding the Butyrate Paradox in the ColonThe paradox is explained by a fundamental difference in how normal colonocytes and cancerous colonocytes get their energy, a phenomenon known as the Warburg Effect.
Mechanism of the Paradox
?? Apoptosis in Cancers Outside the ColonButyrate's ability to trigger apoptosis is not exclusive to the colon, as its core mechanism—Histone Deacetylase (HDAC) inhibition - is a potent anti-cancer strategy relevant to many tumor types.Evidence for Anti-Cancer Effects Beyond the ColonButyrate, or its sodium salt (sodium butyrate), has been shown in various in vitro (cell culture) and animal studies to inhibit proliferation and induce apoptosis in several non-colonic cancer cell lines, including:
Key Distinction: Local vs. Systemic ConcentrationThe challenge for non-colon cancers is delivery and concentration.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6629) Delta-8 THC Shows Promise in Combating Myocarditis
Date:
April 29, 2022 12:41 PM
Heart disease is the leading cause of death in America, and myocarditis is one of the most common causes. Researchers are constantly looking for new ways to combat this deadly disease, and Delta-8 THC may be a promising treatment. A recent study found that Delta-8 was able to slow down heart rate and reduce inflammation in mice with myocarditis. While more research is needed, these findings suggest that Delta-8 could be a valuable tool in the fight against heart disease. What is myocarditis and what are the symptoms? Myocarditis is a term used to describe inflammation of the heart muscle. This can occur for a variety of reasons, including infection or injury, and it can cause a wide range of symptoms. Some of the most common signs of myocarditis include shortness of breath, chest pain, and chest tightness. Other possible symptoms include dizziness, lightheadedness, fatigue, nausea, and weakness. If you experience any combination of these symptoms along with changes in your heart rate or blood pressure, it is important to seek immediate medical attention to determine whether you are suffering from myocarditis. Treatment will depend on the specific cause of your condition, but it typically involves anti-inflammatory medications and rest. Early diagnosis and treatment are essential for preventing the progression of the disease and reducing the risk of cardiovascular complications. What causes myocarditis and how is it diagnosed? Myocarditis is a condition characterized by inflammation and swelling of the heart muscle. This can lead to a number of symptoms, such as shortness of breath, chest pain, increased heart rate, and cough. There are many possible causes of myocarditis, including infections, autoimmune disorders, metabolic or nutritional disorders, or exposure to toxins or other irritants. In order to diagnose myocarditis properly, doctors will typically perform several different tests. These may include blood tests, scans of the heart using ultrasound or MRI technology, and electrocardiograms to assess heart activity. Ultimately, the treatment for myocarditis will depend on its underlying cause and the severity of symptoms. With proper care, however, most people can recover fully from this condition. How is myocarditis treated and what are the potential complications? Myocarditis is a condition that occurs when the heart muscle becomes inflamed. This can be caused by a viral infection, an autoimmune reaction, or other factors. Treatment for myocarditis generally involves addressing the underlying cause, if possible. For example, if the inflammation is due to a viral infection, antiviral medications may be prescribed. Corticosteroids may also be used to reduce inflammation. In some cases, heart surgery may be necessary to repair damage to the heart muscle. Complications of myocarditis can include heart failure and arrhythmias. With prompt and appropriate treatment, however, most people with myocarditis recover fully. What is Delta-8 THC and how does it work? Delta-8 THC is a chemical compound that is found in the Hemp plant. Unlike other forms of THC, which produce psychoactive effects by binding to cannabinoid receptors in the brain, Delta-8 simply activates these receptors without producing any noticeable effects on cognition or perception. While the precise mechanism of action for this compound remains somewhat unclear, scientists believe that Delta-8 works by interacting with specific neuroreceptors in the brain and body, thereby triggering a series of responses that ultimately lead to changes in mood or behavior. Furthermore, research suggests thatDelta-8 may also have antioxidant properties and may be effective at reducing inflammation in certain tissues. Overall, while more research is needed to fully understand the pharmacological effects of this compound, it seems clear that Delta-8 has great potential as a therapeutic agent and may hold benefits for patients suffering from certain mood disorders or neurological conditions. Delta-8, inflammation and relaxation Delta-8 is a cannabinoid that is found in hemp plants. This compound has a similar structure to Delta-9 THC, the main psychoactive compound in cannabis. However, Delta-8 is much less potent than Delta-9 and does not produce the same psychoactive effects. Instead, Delta-8 provides a more mild physical response that is associated with relaxation and relief from anxiety and pain. Research suggests that Delta-8 may also be effective in reducing inflammation. This anti-inflammatory effect may be due to the ability of Delta-8 to bind to CB2 receptors, which are found in high numbers in the immune system. As a result,Delta-8 may offer a unique combination of anti-inflammatory and relaxant effects. What are the findings: The results of recent studies suggest that delta-8, a type of cannabinoid found in cannabis plants, may play a role in reducing the symptoms of myocarditis. Myocarditis is a condition characterized by inflammation and damage to the heart muscle, which can lead to serious complications such as cardiac arrest if left untreated. Early research has shown that delta-8 may be able to help protect against this deterioration, as it was found to reduce levels of oxidative stress and inhibit pro-inflammatory signaling pathways. As more studies continue to explore the mechanisms underlying myocarditis, it is hoped that delta-8 will become an important tool for managing this deadly disease.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6398) Researchers reveal how the common curry spice turmeric kills coloncancer cells
Date:
April 19, 2019 02:20 PM
Studies are now showing that turmeric, which is a common spice found in curry, can actually help kill off colon cancer cells to help the disease from progressing. They believe that these healing properties are due to the curcumin content that is found within the spice itself. If you're searching for ways to take in adequate amounts of turmeric, try consuming turmeric tea. For a more savory option, turmeric tastes fantastic when sprinkled on roasted produce. Key Takeaways:
"In this study, published in the journal Nutrition Research, the researchers hypothesized that curcumin-induced ROS works against colon cancer by promoting apoptosis and inhibiting the cell cycle. They tested this through in vitro experiments involving Smd4 and p53 mutated HT-29 colon adenocarcinoma cells." Read more: https://www.naturalnews.com/2019-02-27-common-curry-spice-turmeric-kills-colon-cancer-cells.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6143) Can your dog be arrested for using a cannabis extract?
Date:
December 16, 2017 03:59 PM
Thomas McDermott, a Democrat and the Mayor of Hammond, Indiana, brought up the legality of using cannabidiol oil (CBD) for treating his Labrador retriever's arthritis at the BGD Legislative Conference in Indianapolis. At the conference was Republican Indiana Attorney General Curtis Hill who last month stated that the use of CBD was illegal in most circumstances in his state after a bill passed to allow epilepsy patients to legally use the oil for seizures. McDermott questioned Hill using a story about his dog that suffered from arthritis, noting that his vet recommended using CBD oil to treat the pain. He mentioned that the oil allowed his dog to move around more easily, had more energy, and had improved appetite. McDermott thought aloud that Hill was "grandstanding" on CBD, but Hill simply stated he was following the law as it was written. When McDermott asked if his dog was breaking the law, Hill responded that the Mayor himself was breaking the law - not the dog. McDermott was upset afterwards that Hill accused him for being a criminal for treating his dog with CBD, and he has no plans to change the therapy for his dog. Key Takeaways:
"The question Thomas McDermott wanted answered Wednesday doesn’t get asked often during policy discussions in Indiana: Could his Labrador retriever be breaking the law by using a pain remedy extracted from cannabis?" Read more: https://www.indystar.com/story/news/2017/12/13/can-your-dog-arrested-using-cannabis-extract/949429001/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5439) Scientists call on feds to allow research on CBD for pets
Date:
December 10, 2017 03:59 PM
Veterinarians, researchers and pet owners are looking to loosen federal regulations on the use of marijuana products to help treat sick animals. Medical issues in dogs, such as epilepsy, arthritis, anxiety, loss of appetite and inflammation could potentially by helped by marijuana-based drugs and extracts. Some people are already using marijuana extracts on their animals, such as those containing CBD, which is an element of marijuana that is not psychoactive. However, such extracts continue to be listed as Schedule 1 drugs by the Federal Drug Enforcement Administration, even when they contain little or no THC. THC is the active component in marijuana that causes intoxication. The Food and Drug Administration has warned that marijuana products for pets sold in animal hospitals or online pet stores are illegal, since such drugs are unapproved. The FDA has suggested it will pursue legal action against those in violation of the law. However, the policy-making body of the American Veterinary Medical Association, in conjunction with two group councils, is considering making a recommendation to the DEA for marijuana to be declassified as a Schedule 1 drug in order to enable research for both animal and human medical purposes. Declassification could also help prevent pet owners from accidentally overmedicating their animals in the absence of proper guidance from a medical professional. In September, Republican senator Orrin Hatch of Utah introduced a bill that would facilitate research on use of marijuana-based medications, concurring that the drug is over-regulated, although he continues to oppose recreational use of the drug,. Some veterinarians note that without sufficient evidence, it remains unsafe to use marijuana products on animals, with concerns about potential toxicity. Yet researchers are continuing to wait for clearance to proceed on various relevant studies, such as use of marijuana for dogs with osteoarthritis, pruritis and epilepsy. Some research on use of products with CBD has been stopped until federal approval is granted. Gaining approval has been difficult due to government requirements, which continue to be an obstacle to moving forward. Key Takeaways:
"The concern our membership has is worry about people extrapolating their own dosages, looking to medicate their pets outside the realm of the medical professional" Read more: https://www.aspentimes.com/news/scientists-call-on-feds-to-allow-research-on-cbd-for-pets/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5432) France is "decriminalizing" cannabis nationwide
Date:
June 11, 2017 11:14 AM
France appears poised to change the way it punishes cannabis users. While it seems France will continue levying fines against citizens found guilty of cannabis use, the prison elements will likely be removed soon. There are several reasons supporters of the change tout in their advocacy for the change. One, cannabis use is widespread among the populace. Two, many citizens feel the government should not mandate what they do or not do with their bodies. Three, cannabis has the potential to provide several medicinal benefits and research into these benefits would be aided by the move to destigmatize its use by removing the criminal aspect. Four, cannabis use has a low potential for abuse. And finally, it has been estimated a cannabis arrest consumed up to six hours of police office and magistrate time. By removing the criminal aspect of cannabis use, it would free the country's law enforcement to pursue other matters of greater risk to the populace. Read more: France is "decriminalizing" cannabis nationwide
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4810) Scientists Call for Restrictions on Ibuprofen & other OTC Painkillers After Deadly Risks Discovered
Date:
April 09, 2017 03:44 PM
Generally people know that medications can have negative side effects. But when it comes to over the counter pain medications it is often thought that they are safe to take. There are studies however that show that stuff like Ibuprofen actually have some pretty terrible side effects when taken to often, when taken with other drugs, or if you take too many at one time. If you take over the counter medications often you should see what you can do to wean yourself off of them. Key Takeaways:
"A recent study from Denmark that was published in the European Heart Journal has found that taking Ibuprofen, the popular over-the counter painkiller is linked to a 31% increased risk of cardiac arrest, among other things." Read more: http://www.healthnutnews.com/scientists-call-restrictions-ibuprofen-otc-painkillers-deadly-risks-discovered/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4386) How Not to Die from High Blood Pressure
Date:
February 15, 2017 12:59 PM
Not dying from high blood pressure can be a hard thing. By age 60, it impacts many more people. High blood pressure does not need to occur though. Researchers found that people that ate better diets had much lower blood pressure than people that did not. For people that eat a bad diet, their blood pressure will get higher. Key Takeaways:
"That’s why I created this new series of overview videos, which are basically taken straight from my hour-long live 2016 presentation HOW NOT TO DIE: The Role of Diet in Preventing, arresting, and Reversing Our Top 15 Killers." Reference: //nutritionfacts.org/video/how-not-to-die-from-high-blood-pressure/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3948) What are heart failure, heart attack and cardiac arrest?
Date:
February 14, 2017 10:59 AM
Though all types of heart trouble pose emergency threats to people's health, there are many differences between them in terms of both causes and symptoms. "Heart failure" refers to some loss of the heart's successful function as a pump; "congestive heart failure" applies more specifically to when blood flow has backed up, causing the swelling of veins. A "heart attack" occurs when blood flow to the heart is cut off - sometimes, this is caused by a spasm. But if the heart suddenly stops beating, that is a "cardiac arrest", and is a problem with the timed electrical signals that make the heart contract. Key Takeaways:
"Blockages causing heart attacks are mostly caused by a buildup of plaque in the arteries." Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3940) This Man Used Hemp Oil On Live TV To Draw Attention To His Granddaughter's Health
Date:
February 01, 2017 10:59 AM
The United States is not the only place where marijuana plant products are under fire. Even in Australia, it is nearly impossible to get CBD oil for treatment of medical conditions such as epilepsy. One particular case in Australia is gaining media attention. It is the case of 5-year-old Katelyn whose grandfather has been giving her CBD oil to help with her Dravet Syndrome seizures. Her grandfather is under threat of being arrested, but he says it is worth it if he gets his family better access to a drug that will greatly help with her condition. Key Takeaways:
"A millionaire philanthropist has taken hemp oil on national television to highlight his granddaughter's struggle to get treatment for her epilepsy, as the five-year-old-girl begs prime minister Malcolm Turnbull and state premiers to make medicinal cannabis more accessible." Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3865) 4 Best Ear Oil That Will Help Improve Hearing And Reduce Ringing.
Date:
March 12, 2014 08:03 PM
Ear ringing
Causes of ear ringing There are many causes of hear ringing, causes varies from one person to another. Some of the causes includes. Inner cell damage, this causes ear drum to echo sound even after the sound has been sent to the brain. This irritates ear and causes ear ringing. Other ear problems including ear diseases are among the major causes ear ringing. Treatment of ear ringing There are many possible treatment of this condition including drugs and allopathic treatments such as removing ear wax, finding any possible vascular disorders and treating them. You can also change medication you are on which may be the cause of Tinnitus. Though drugs themselves cannot cure Tinnitus, they may help reduce the severity of the symptoms. Changing lifestyle can also treat ear ringing and improve earing and ease ringing, for example, stress can exacerbate ear ringing. Reducing alcohol is another effective method to beat tinnitus, alcohol dilates blood vessels causing forceful blood flow to the inner ear. While those methods though effective, they cannot cure ear ringing, one of the method that has been proved to be efficient is use of essential oil. The aroma of essential oil enters the nose and stimulates the olfactory nerves. This then sends signals to the Limbic system (the control mechanism in the brain for memory and emotions). This sets in series of neuro-chemical impulses and response mechanisms that generate a natural healing response. Many essential oils contain healing properties. They assist in natural, are anti- inflammatory, pain relief, anxiety, reduce stress and assist the endocrine system in improving hearing and reducing ringing. The best oil to arrest ear ringing are;
Source
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3058) Health benefits of Bromelain and its mechanism of fighting inflammation
Date:
April 20, 2013 09:54 AM
Bromelain is a blend of enzymes found in the juice and the stems of pineapples and is often used as a health supplement to assist in various disorders and enhance overall health. Here are the health benefits of Bromelain. Improved Heart health Bromelain functions as a blood thinner by breaking down the fibrins thus helps prevent blood clotting. It allows blood to move more freely throughout the circulatory system. Thinner blood is linked with lower possibilities of stroke, cardiac arrest and other heart problems. Improved Breathing conditions Bromelain is linked to improved breathing conditions that occur as a result of thicker mucus like asthma. It has similar effects on mucus as it has on blood thus making mucus thinner and thus does not clog the bronchial tubes. Improved Immunity It serves as an immunity booster and helps certain immunity boosting receptors within the body. As a result it fortifies the immune response by improving the response of body's front-line immune defense called the T-cells. Improved digestion If the pancreas is not very active, it may produce insufficient quantities of enzymes, making the food we eat just getting digested partially. Consuming a bromelain supplement might help to cure any resulting digestive complaints like stomach upset, heartburn, diarrhea or indigestion. It is especially effective when used in in conjunction with other enzymes such as amylase and lipase because of its protease functions. Wound healing An external application of bromelain might help getting rid of undesirable skin tissues in the third-degree burns. Bromelain could also reduce inflammation due to insect bites and their stings. Alleviates Sinusitis Bromelain helps decreasing congestion and the cough that comes with sinusitis. Its anti-microbial attributes may wipe out viruses and bacteria associated with sinus infections. Relieves varicose veins and Hemorrhoids Bromelain is used as a complementary medicine in treating chronic venous insufficiency, hemorrhoids and varicose veins. Enhanced Acid-alkaline balance Bromelain can help in balancing the acidity and also the alkalinity in the small intestine. The anti-bacterial effects of bromelain helps relieving bacteria-related diarrhea connected with E. coli attacks and inflammatory bowel disease. Bromelain and Inflammation While inflammation aids mending the entire body during an injury, excessive swelling can result in health complications and speed up aging. Bromelain is beneficial in treating inflammation. The mechanism of how bromelain fights inflammation involves the inhibition of many bio-chemical responses and reactions that induce inflammation. Treatment with bromelain manages and regulates the activity of various bio-chemical messengers referred to as cytokines in our body. These cytokines are the chemical substances that trigger inflammation. By inhibiting the activity of cytokines, bromelain reduces the impulses that induce an inflammatory reaction. Bromelain also decreases the deposition of kinins, a by-product of inflammation and also prostaglandins, the hormone-like compounds found through the entire body Thus Bromelain assists fighting the majority of inflammation occurring after having a sports injury or after surgery, or from minor sprains and tendonitis. Certain kinds of arthritis which involve inflammation also benefits from bromelain, particularly in combination with some other typical anti-inflammatory medications. Do you take bromelain daily? If not, why not?
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2836) What Is 2000fu In Nattokinse?
Date:
December 29, 2012 11:48 AM
Nattokinase: History And Health Benefits Nattokinase is a proteolytic enzyme that naturally occurs in natto. It is a traditional fermented soybean dish and a well-known staple food in Japan. Natto is fairly easy to make since it only requires water, straw and soybeans. The straw that has the bacterium called bacillus subtilis natto will be mixed with the freshly steamed soybean and water. After that, it will be set for fermentation. During fermentation, natto develops its mild taste and it has a very strong odor like that in the blue cheese. In the year 1980, Dr. Hiroyuki Sumi was looking for a food that can effectively break up blood clots like those that can cause cardiac arrest and stroke. He discovered that natto can dissolve fibrin which is the type of protein that builds up in blood clots. In his laboratory experiment, he discovered that natto has the ability to completely dissolve fibrin clots after almost about 18 hours. Natto is low in cholesterol and it contains high quality protein and an excellent source of vitamin K, copper, iron, magnesium and manganese. Nattokinase works similarly like blood-thinning agent coumadin. People who have had vascular injury or those people who are in risk of elevated fibrinogen level formation can benefit from the fibrin-digesting effects of nattokinase. It also reduces the thickening of the arteries and helps to heal damaged blood vessels. What Does "FU" Mean in terms of Nattokinase? Companies that manufacture nattokinase supplements express its activity in terms of "FU" or fibrin units. This is entirely different from the IU measurement since it only indicates nattokinase activity base on the degradation of fibrin. But as of today, IU is being officially adopted by the Japanese when measuring nattokinase. The FU method doesn't have exact measure of nattokinase activity and is suspected to be erroneous. Because of that, IU standard is being used to accurately measure nattokinase. However, the FU measurement is still being widely used in labels. Most nattokinase supplements nowadays are in 100 mg capsule with 2,000-4,000 FU. As a precaution, it's best to consult a doctor first before taking nattokinase supplements for appropriate guidance and supervision with regards to its proper usage. Pregnant women including those people who have had stroke before or any other bleeding disorders must not take nattokinase supplements.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2795) Health Benefits Of Chamomile
Date:
December 03, 2012 07:56 AM
It is believed that ancient Egypt saw Chamomile as an effective cure for most illnesses. In the modern world too, this golden herb retains its healing properties and is used for treating many a disease and discomforts of the body. Most commonly, German chamomile blossoms are infused to prepare 'Chamomile tea' which is a fragrant concoction full of medicinal properties. The tea can be combined with honey to enhance the taste. Health Benefits Of Chamomile Tea Chamomile tea, supposedly, helps to bring about restful sleep. It is thus of great value for people suffering from insomnia and other sleep-related disorders. Due to its soothing and relaxing effects, it is generally taken before a person goes to bed. Since time immemorial, Chamomile has been considered a remedy for stomach ailments. Known to soothe gastric and bowel related problems, the herb is a blessing for people with stomach aches. All in all, Chamomile helps facilitate the complete digestion process by promoting bowel movement. For women facing menstrual cramps and nausea every month, Chamomile tea comes as a welcome relief. Research indicates that regular consumption of Chamomile tea increases the level of glycine in the body. Glycine is a compound that controls muscular spasms, thus it tends to calm menstrual cramps. A healthy cup of golden chamomile tea has also been found to combat the morning sickness of pregnancy. However nothing has been proven till now to this effect. Some studies suggest that this wonder herb accelerates the wound healing process too. Many researchers are of the belief that age-old Egyptians and Greeks used Chamomile flowers on wounds to speed up their healing time. Though there is no established evidence as such regarding this subject, history stands witness to the magical healing properties of Chamomile in more ways than one. Diabetes patients are also in for some good news concerning Chamomile tea. Many ongoing studies and surveys conducted worldwide are hinting at Chamomile playing a role in diabetes management. Consumed regularly in the form of tea, the herb may arrest complications arising out of diabetes and may also prevent hyperglycemia. What's more, the golden herbal tea prepared from chamomile is caffeine-free and will not be addictive in any way. However, it is always a good idea to take professional advice before going all-out for Chamomile. Some people may display allergic reactions to the herb and suffer side-effects. Therefore, it is best to try the herb first in small amounts before one decides to include chamomile tea in the daily routine of life. Besides its therapeutic uses, chamomile is being increasingly used as an ingredient in cosmetic products and is being considered a good friend of the skin. Since Chamomile is known to be a stress-buster, a cup of chamomile tea after a hectic work day might just prove to be the right beverage to save the evening. With its sedative, anti-inflammatory and anti-bacterial properties and benefits, Chamomile is sure to become more popular by the day. Used wisely, the golden herb is no less than gold itself.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2743) Carnitine Heart Energy!
Date:
November 24, 2012 10:56 AM
An Amino Acid Carnitine is an amino acid that our body manufactures for the purpose of carrying fatty acids into cells so that these acids are converted to energy. Before you begin to lose interest from the scientific sentence that you just read, here's what Carnitine does, simply put - it helps your body create energy. Improve Heart Energy! Carnitine is more commonly known as L-Carnitine, and since it does help your body creates energy, it has been extensively researched and scientists have come to the conclusion that using L-Carnitine as a supplement will help your heart improve its functioning and thus reduce the risk of heart disease. Although it sounds too good to be true, it is a scientific fact and has been proved by numerous studies. For people who are already suffering from any kind of heart disease, L-Carnitine, used in tandem with other prescribed medication can help by increasing the effects of the medication by quite a large amount, and making the heart function effectively and treating any disease symptoms that the patient might have. To be more specific, it helps the heart from conditions that result in lower blood supply to the heart, like angina pectoris, myocardial infarction and cardiac arrest. It can thus be seen that Carnitine not only helps improve heart energy, but can also be life saving by removing these deadly conditions. For those who wish to make the most of Carnitine's heart friendly benefits, it is widely available as a nutritional supplement, and one does not need a prescription to get it. However, like with any supplement, it must be used in moderate amounts, as per the recommended dosage, it is impossible to overdose but taking more does not mean it will work better.. Although no conclusive bad effects have been linked to this supplement use, it is always better to be safe than sorry, and by using Carnitine wisely, you can improve your heart energy and keep it in prime shape.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2737) The Major Health Benefits Of Hemp
Date:
April 06, 2012 07:47 AM
Hemp Protein Hemp is the only food with the largest amount of protein available on earth. It is easily digestible and it is the only food with a wide range of proteins. These include important fatty acids and amino acids. It is the only food that supplies the human body with all dietary needs at once. Thus, it is the only food that is capable of sustaining human life alone without other nutritional supplements. Apart from being a good source of proteins, hemp supplies the body with important minerals and vitamins. However, the most important component of this food is the essential fatty acids. These include the alpha-linolenic (omega 3) and linoleic acids (omega 6). These two categories of fat are important in the body because human body is not capable of manufacturing them. Therefore, they have to be consumed in the daily meals. The ratio of omega 6 to omega 3 in hemp is 3:1. This is close to the 4.0 on average as the optimum recommendation of the world health organization for a human diet. It plays an important role in various organs of the body including: Heart health Hemp has important nutrients are that are essential for the good health of the human heart. These are the essential fatty acids which play a very important role in ensuring the health of the heart. Several studies have revealed that substituting saturated fats with healthy polyunsaturated reduced risk of cardiac arrest. Such fats are found in hemp and are important in preventing sudden cardiac arrhythmia. They also reduce levels of cholesterol in the blood. Hemp has important fats that also decrease build-up of cellular in the arteries. This is very important as it is associated with a condition known as atherosclerosis. Phytosterol contained in hemp plays an important role in reducing cholesterol in the blood by about ten percent. Brain health Human brain has a large portion that includes essential fat acids. Since hemp supplies the body with these fats, it becomes essential for brain health. It is also vital for proper memory function. Diseases such as Parkinson's and Alzheimer's are preventable with consumption of hemp. The Omega 3 and omega 6 fatty acids also help in delaying or reducing neurological effects that come with these diseases. This improves the kind of life led by individuals with such diseases. Skin health Essential fatty acids play an important role in ensuring healthy skin. Perhaps, this is why hemp seed has been used as an ingredient in various cosmetic products. The Lipids allow the acids to permeate via the skin. Hemp component in the cosmetic products help to nourish the skin directly. Hemp is also very beneficial to people with psoriasis and eczema skin conditions. These are just the major benefits of hemp in the human body. Others include increasing of metabolic rate and energy levels, improving immunity and organic function, among others. Hemp is also crucial in the prevention of degenerative diseases and this proves why it is crucial for positive human health. This food provides a lasting solution to various health complications and you may as well try it and enjoy its benefits.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2628) Fight Night Blindness, Boost Eye And Vascular Health With Bilberry
Date:
March 19, 2008 09:01 PM
Weakness of blood vessels is often seen during the aging process when blood vessels become fragile. Dark bilberry fruit has been shown to reduce blood vessel permeability, improve capillary resistance, and provide antioxidant properties, to scavenge free radicals. One way to fight the aging process of the body is to promote health in the vascular system by eating nourishing foods, exercising, and learning how to handle stress. Evidence shows that eating five servings or more a day of fruit and vegetables can reduce the risk of heart disease, cataracts, and some other disorders that related to blood vessel health. The dark pigment in fruits and vegetables has many health advantages. A lot of people think that the only way to improve blood vessel health is to reduce blood cholesterol, minimizing the risk of a heart attack. That is an essential goal, but blood vessels should also have strength and integrity to maintain their health in order to carry nutrients and oxygen through the body to feed the tissues. As we age, eye function begins to diminish and causes a lot of people to fear that they are losing their eyesight. The blood vessels decline in function, but there are other factors such as the reduction of arrestin and rhodopsin. arrestin is a protein while rhodopsin is the light sensitive pigment that can be found in the retina. The dark pigment of fruits and vegetables is extremely important to blood vessels and the health of the structures and proteins of the eyes. Brilliant colored fruits and vegetables may prevent strokes, heart disease, and help long-term vision because they improve integrity of blood vessels. Bilberry fruit has been studied for over 40 years for its supportive effects on blood vessel health, blood circulation, and lymph flow. Blood vessels in the brain, heart, eyes, stomach, veins in the legs, and actually anywhere in the body have the potential to leak. In many regions bilberry extract has been used to support individuals with microcirculatory disorders including varicose veins, atherosclerosis, and degenerative retinal conditions including macular degeneration and cataracts. Diabetes, atherosclerosis, poor diet, lack of exercise, smoking, excess alcohol and an inability to handle stress can all contribute to blood vessel disorders and cause the capillary’s membrane to thicken, therefore, increasing capillary permeability causing edema and leaking of fluid. During the aging process, oxidative damage occurs by free radicals in the eyes, which then causes a loss in the transparency of the lens. Symptoms that occur because of this are blurred vision, increased sensitivity to glare, reduced visual acuity, color perception, and light sensitivity. When the eye structure begins to break down, vision impairment and cataract formation result. Bilberry extract has been shown to improve vision and twilight vision, helping the retina adapt to darkness and glare. With aging, a gradual degenerative process is experienced which is caused by free radical damage to our body’s genetic material, cell membranes, and tissues. Free radicals attack blood vessel endothelial cells, and they begin to rupture. Antioxidants help to prevent AMD and reduce the damage of the retina’s photo receptors. In summary, blood vessel health is an important part of age management. By improving diet, managing stress, exercising, and supplementing with bilberry extract, one can promote the health of blood vessels throughout the body, and therefore, support the eyes.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1726) Green Coffee For Protection Against Oxidative Stress
Date:
November 17, 2007 11:46 AM
It is recorded that coffee drinking originated in Ethiopia in North East Africa, from where Arab traders introduced the plant to the Middle East. From there it moved to Turkey in the 15th century, where it was highly prized as a daily beverage due its invigorating properties. It is also believed that the infamous Captain John Smith introduced the plant to Virginia. The Brazilian coffee trade was due largely to the introduction of the bean to that country by the French in 1727, and the Boston Tea Party of 1773 rendered it the only non-alcoholic drink worth consuming by the patriots of 18th century America. Now over 50% of Americans drink coffee daily, although this seems a somewhat conservative estimate, and the tea houses of England have largely been replaced by coffee shops and the ubiquitous Starbucks. So much for the history of a beverage that has been prized for its stimulant properties, but recent research has established that not only is coffee a stimulating drink, but that it is a strong antioxidant due to its polyphenol content. However, not all forms of coffee have this property, only the green coffee bean before it has been roasted. Polyphenols are very powerful antioxidants that scavenge the free radicals that destroy body cells, and not only accelerate aging but also threaten the health of your cardiovascular system and the health of other major organs. Free radicals are compounds with a spare electron. Normally the electrons in all stable molecules come in pairs, and any free electron without a partner is like a lovelorn bachelor. It will seek a mate, and take it from wherever it can find one. Usually it secures its partner by stealing an electron from one of our body cells. This can totally destroy the cell, as it might anybody who has its partner stolen, and cell destruction is not a good thing. It is the destruction of body cells that promotes the appearance that aging brings: the wrinkles and the loss of energy that is generated by healthy cellular activity. Antioxidants destroy these free radicals, and come in a number of different guises. Vitamins A, C and E are all powerful antioxidants, as are many of the compounds that are essential to our biochemistry such as beta carotene and polyphenols. These polyphenols are found in practically all plants to a greater or lesser degree, and another rich source is grapes, and those found in green coffee beans are what are known as hydroxycinnamic acids the most abundant of which is caffeic acid. Another is chlorogenic acid, and together they form a very potent team in preventing the oxidation by free radicals of LDL (low density lipoprotein). Low density lipoproteins are those that carry cholesterol from the liver to areas of the body that need first aid due to damage, such the arterial walls. However, this can be attacked by free radicals and oxidized which results in the deposition of excess cholesterol that can build up till it eventually constricts, and sometimes completely blocks, the major cardiac arteries. This is a serious condition known as atherosclerosis that can eventually lead to cardiac disease and arrest or to strokes if the artery is in the brain. Not only do chlorogenic and caffeic acid help to prevent this from occurring, but they also help to prevent the cellular degeneration caused by the free radicals. They must be extracted from the green coffee bean because roasting or heating in any way, including brewing, destroys them. In fact, brewed coffee contains some potentially harmful substances called diterpenes that some believe can increase your chances of coronary disease by up to fifth if you drink coffee regularly over your lifetime. It is also believed that green coffee extract can reduce the risk of diabetes due to its effect on your blood glucose levels. Evidence is coming to light that some polyphenols, including chlorogenic acid, might have inhibiting properties on the activity of glucose-6-phosphate, otherwise known as Robison Ester, which is involved in the metabolism of blood glucose and which is affected by diabetes which reduces its concentration. Chlorogenic acid is though to be able to redress this imbalance and not only reduce blood glucose levels, but increase the glycogen stored in the liver as an emergency energy source for the body. Green coffee bean extract also possesses other beneficial properties, not the least of which is its effect in increasing the metabolism of fats in relation to carbohydrates. This assists in weight loss and also increases stamina. The decrease in the risk of diabetes of up to 50% in men, and slightly less in women, could be due to a combination of the regulation of glucose-6-phosphate and the regulation of blood glucose levels and glucose and weight management in general. The vast majority of diabetes patients are overweight. In animal studies, the presence of chlorogenic acid appears to reduce the hyperglycemic peak that arises through the action of glucagon, a hormone used to counter hypoglycemia. The fact that chlorogenic acid reduced this sugar peak indicates its potential use in reducing abnormally high blood glucose levels. Another effect of this was an increase in the animal’s glycogen level and in the level of glucose-6-phosphate in the liver. This indicates a reduction in glycogenolysis, by which glycogen is ultimately converted to glucose-6-phosphate and glucose, thus increasing the blood glucose levels and also of gluconeogenesis which is the production of glucose from carbohydrates and some glucogenic amino acids. In other words, green coffee bean extract can help to regulate blood glucose levels by preventing the liver from producing glucose from glycogen and carbohydrates. However, the biochemistry apart, it must be stressed that these benefits are not obtained by drinking coffee, and it has to be repeated that the active agents in providing them are destroyed by the roasting and brewing processes. It is only the green coffee beans that can be used for protection of oxidative stress of human body cells and the gradual degradation into premature aging and many other related conditions.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1635) Recognizing the Signs: Roadmap to a Healthy Heart
Date:
June 13, 2005 10:06 AM
Recognizing the Signs: Roadmap to a Healthy Heart by Louis McKinley Energy Times, January 2, 2004 From time immemorial, people have tuned into life's lessons that come from the heart. Sadly, times are changing: If you're like most inhabitants of today's harried world, you may be too distracted to detect important clues about your cardiovascular circumstances. And while heart lessons may be more complicated than simply connecting the physiological dots, understanding those heart messages are imperative for improving and maintaining your heart health. Every cell in your body relies on heart-powered blood flow to keep it supplied with nutrients, oxygen, hormones and other natural chemicals necessary for survival. Without that supply of life-giving substances, few cells in the body-including those within the heart itself-can survive very long. And just as damage to a major roadway can cause mayhem with traffic patterns, damage to blood vessels and the heart can wreak a lumpy cardiovascular havoc that blocks the passage of blood and endangers your heart's well-being. Your Heart Disease Chances Within the last ten years, scientific research performed by investigators around the world has focused on the specific factors that most strongly influence your chances of developing heart disease and suffering either a heart attack or a stroke. While much of your risk depends on your genetic inheritance and family history, several factors that determine your heart health are within your control. The most important factors you can do something about include: * Smoking: free radicals generated by burning tobacco causes significant damage to blood vessels and other cells * Lack of exercise: the human body is designed for consistent, moderate physical activity; without exercise, the body slacks off in creating antioxidant protection for arteries * Diabetes: when excess blood sugar persists, physiological processes begin that endanger the heart and arteries * Cholesterol: when oxidized (a chemical process that has been compared to a kind of internal rusting), cholesterol can form artery-blocking plaque; antioxidant nutrients like vitamin C and natural vitamin E may help the body limit this process * High blood pressure: excessive pressure within the blood vessels raises the risk of damage to the heart and arteries; a program of weight loss and exercise can help control blood pressure * Being overweight: the extra body fat carried around your middle is linked to a greater risk of heart problems Heart Attack Signs Do you think you know what a heart attack feels like? Well, if you think it feels like a dramatic pain somewhere in your chest that knocks you to the floor, you're probably wrong. "Most heart attacks do not look at all like what one of my colleagues calls the 'Hollywood' attack-the heart attack you see on television or in the movies," warns Julie Zerwic, MD, professor of surgical nursing who has studied what happens when people develop heart disease and suffer damage to their hearts. "The symptoms [of heart problems] are not necessarily dramatic. People don't fall down on the floor. They don't always experience a knife-like, very sharp pain. In fact, many people describe the sensation as heaviness and tightness in the chest rather than pain," she says. And, if you're a woman experiencing a heart attack, you may not even feel discomfort specifically in your chest. Instead you may experience a severe shortness of breath. The apparent ambiguity of the discomforts caused by a heart attack lead many people to either ignore them or take hours to realize they need to go to the emergency room at the hospital. Consequently, much fewer than half of all individuals undergoing a heart attack actually go to a hospital within an hour of the start of the attack. That delay can be a fatal mistake. "Timing is absolutely critical," laments Dr. Zerwic. "If treatment starts within a hour after the onset of symptoms, drugs that reestablish blood flow through the blocked coronary artery can reduce mortality by as much as 50%. That number drops to 23% if treatment begins three hours later. The goal is to introduce therapy within two hours." However, in Dr. Zerwic's research, only 35% of non-Hispanic whites go to the hospital within an hour of the start of a heart attack. And among African-Americans, the number of people going to the hospital right away drops to a frighteningly low 13%. Often, people will lie down or use a heating pad to relieve the tightness they feel in the chest," says Dr. Zerwic. "They may take some medicine and wait to see if that works. All these steps postpone needed treatment." Signs of a possible heart attack include: * Chest discomfort: Heart attacks most frequently cause discomfort in the center of the chest that can either go away after a couple of minutes (and come back) or persist. The discomfort may feel like strong pressure, fullness or pain. * Upper body discomfort: An attack may set off pain or discomfort in either or both arms, and/or the back, neck, jaw or stomach. * Shortness of breath: Chest discomfort is frequently accompanied by shortness of breath. But it's important to note that shortness of breath can take place even in the absence of chest discomfort. * Other signs: You can also break out in a cold sweat, or feel nauseated or light-headed. A Woman's Sleep Signs If you are a woman who suddenly experiences a marked increase in insomnia and puzzling, intense fatigue, you may be in danger of an imminent heart attack. In an attempt to understand how women's symptoms of heart problems differ from those of men, researchers talked to more than 500 women in Arkansas, North Carolina and Ohio who had suffered heart attacks. (Technically, what they had experienced is referred to as acute myocardial infarction.) They found that chest pain prior to a heart attack was only reported by about 30% of the women surveyed. More common were unusual fatigue, sleep disturbances and shortness of breath (Circulation Rapid Access, 11/3/01). "Since women reported experiencing early warning signs more than a month prior to the heart attack, this [fatigue and sleep problems] could allow time to treat these symptoms and to possibly delay or prevent the heart attack," says researcher Jean C. McSweeney, PhD, RN, nursing professor at the University of Arkansas for Medical Sciences in Little Rock. In Dr. McSweeney's study, more than nine out of ten women who had heart attacks reported that they had had new, disturbing physical problems more than a month before they had infarctions. Almost three in four suffered from unusual fatigue, about half had sleep disturbances, while two in five found themselves short of breath. Other common signs included indigestion and anxiety. "Women need to be educated that the appearance of new symptoms may be associated with heart disease and that they need to seek medical care to determine the cause of the symptoms, especially if they have known cardiovascular risks such as smoking, high blood pressure, high cholesterol, diabetes, overweight or a family history of heart diseases," says Dr. McSweeney. Dr. McSweeney warns that, until now, little has been known about signs that women are having heart trouble or heart attacks. The fact that most of Western medicine's past attention has been on heart problems in men has obscured the warning signs in women. As part of Dr. McSweeney's studies, she and her fellow researchers have discovered that more than 40% of all women who suffer a heart attack never feel any chest discomfort before or during the attack. "Lack of significant chest pain may be a major reason why women have more unrecognized heart attacks than men or are mistakenly diagnosed and discharged from emergency departments," she notes. "Many clinicians still consider chest pain as the primary symptom of a heart attack." Vitamins for Diabetes and Heart Disease Having diabetes significantly raises your chance of heart disease, which means that keeping your blood sugar levels under control can reduce your chances of suffering a heart attack. Today, 17 million Americans have diabetes and, as the country's population in general gains weight and fails to exercise, the number of people suffering this problem continues to grow. The first line of defense against diabetes consists of exercise and weight control. All you have to do is take a brisk walk for 30 minutes a day to drop your chances of diabetes (American Journal of Epidemiology 10/1/03). "We have found that men and women who incorporate activity into their lifestyles are less likely to develop type 2 diabetes than those who are sedentary. This finding holds no matter what their initial weight," said Andrea Kriska, PhD, professor of epidemiology at University of Pittsburgh Graduate School of Public Health. To help your body fight the development of diabetes, researchers also recommend vitamin C and natural vitamin E. Researchers working with lab animals at the University of California at Irvine have found that these antioxidant vitamins can help insulin (the hormone-like substance secreted by the pancreas) reduce harmful blood sugar. In addition, these vitamins shrink the chances of organ damage that can be caused by diabetes (Kidney International 1/03). In this investigation, these vitamins also helped reduce blood pressure, another risk factor that raises heart disease risk. "Blood pressure was lowered to normal, and free radicals were not in sufficient numbers to degrade the sugars, proteins and nitric oxide," notes Nick Vaziri, MD, professor of medicine at the University of California. "We think this shows that a diet rich in antioxidants may help diabetics prevent the devastating cardiovascular, kidney, neurological and other damage that are common complications of diabetes." Free Radical Blues Dr. Vaziri and his group of researchers found that untreated diabetes raised blood pressure and increased the production of free radicals, caustic molecules that can damage arteries and the heart. Free radicals can change blood sugar and other proteins into harmful substances, boosting tissue and heart destruction. In Dr. Vaziri's work with lab animals, he found that treating diabetes with insulin lowered blood pressure and helped keep sugar and protein from changing into dangerous chemicals, but allowed the free radicals to subvert nitric oxide, a chemical the body uses to protect itself from free radicals. In this investigation, adding vitamins C and E to insulin insulated the body's sugars, proteins and nitric oxide from oxidative assault. This produces a double advantage: Lowering the risk of heart disease and other damage to the body from diabetes. Maitake, an Oriental mushroom that has been shown to have many health benefits, can also be useful for people with diabetes who are trying to avoid cardiovascular complications. Laboratory studies in Japan demonstrate that maitake may help lower blood pressure while reducing cholesterol (Biological & Pharmaceutical Bulletin 1997; 20(7):781-5). In producing these effects, the mushroom may also help the body reduce blood sugar levels and decrease the risk of tissue damage. No Smoking! Tobacco smoke is one of the most notorious causes of heart problems. In the same way a hard frost exerts a death grip on a highway, the smoke from cigarettes can freeze up arteries and hamper their proper function. A healthy artery must stay flexible to comfortably allow adequate circulation. But "...when blood vessels are exposed to cigarette smoke it causes the vessels to behave like a rigid pipe rather than a flexible tube, thus the vessels can't dilate in response to increased blood flow," says David J. Bouchier-Hayes, MD, professor of surgery at the Royal College of Surgeons in Ireland, who has studied the deleterious effects of tobacco. This rigidity is called endothelial dysfunction. When arteries are rigid, blockages gum up vessels, clots and other impediments to blood flow appear, and your risk of heart attack and stroke increases (Circulation 2001 Nov 27; 104(22):2673). This condition can also cause chest pain (angina) similar to that caused by a heart attack, and should be evaluated by a knowledgeable health practitioner. Although all experts recommend you stop smoking to lower your heart disease risk, some studies have found that Pycnogenol(r), a pine bark extract that helps the body fight inflammation, may ease some of smoking's ill effects. In a study of platelets, special cells in the blood that can form dangerous blood clots, researchers found that Pycnogenol(r) discouraged platelets from sticking together (American Society for Biochemical and Molecular Biology 5/19/98). By keeping platelets flowing freely, this supplement may alleviate some of the heart-threatening clots that tobacco smoke can cause. In Ayurvedic medicine, a traditional therapy from India, an herb called guggul has also been used to lower the risk of blockages in arteries. This herb, derived from the resin of the mukul tree, has been shown to reduce cholesterol by about 25%. People taking this herb have also reduced their triglycerides (harmful blood fats) by the same amount (Journal Postgraduate Medicine 1991 37(3):132). The Female Version of Heart Disease
For one thing, women often don't suffer from the crushing chest pain that for most people characterizes a heart attack; instead, many women experience back pain, sweating, extreme fatigue, lightheadedness, anxiety or indigestion, signs that can be easily misread as digestive troubles, menopausal symptoms or indicators of aging. The genders also differ in how heart disease poses a threat. While men seem most endangered by the buildup of blockages in arteries, women apparently are more at risk from endothelial dysfunction. But more study needs to be done since, in many cases, researchers have been unable to pin down the precise mechanism that causes many women to die of heart disease. Scientists have found that the number of women in their 30s and 40s who are dying from sudden cardiac arrest is growing much faster than the number of men of the same age who die of this cause. But research by the Oregon Health & Sciences University and Jesse E. Edwards Cardiovascular Registry in St. Paul, Minnesota, shows that while doctors can pinpoint the coronary blockages that kill men, they can't find specific blockages in half of the female fatalities they have studied (American Heart Journal 10/03). "This was an unexpected finding. However, the study underscores the need to focus on what is causing these younger women to die unexpectedly because the number of deaths continues to increase," says Sumeet Chugh, MD, a medical professor at Oregon. Since the failure of arteries to relax probably contributes to heart disease in many women, eating red berries, or consuming supplements from berries such as chokeberry, bilberry or elderberry, may be important in lowering women's heart disease risk. These fruits help arteries expand and allow blood to flow freely. Red berries are rich sources of flavonoids, polyphenols and anthocynanins. The anthocyanins are strong antioxidants that give the berries their color. Research at the Indiana University School of Medicine have found that these chemicals can interact with nitrous oxide, a chemical produced by the body, to relax blood vessels (Experimental Biology conference 5/20/02). Working Out As researchers work to devise lifestyle roadmaps that can steer you around the perils of heart disease, they are finding that exercise is a key path to avoiding cardiovascular complications. A 17-year study of about 10,000 Americans found that those who exercised and kept their weight down (or took weight off and kept it off) experienced a significantly lower risk of heart problems (Preventive Medicine 11/03). "The fact is that those who both exercised more and ate more nevertheless had low cardiovascular mortality," says Jing Fang, MD, of the Albert Einstein College of Medicine in the Bronx, New York. Burning calories in physical activity may be the secret to reducing heart disease risk and living longer, she says. Dr. Fang's research used information collected from the First National Health and Nutrition Examination Survey in 1975 and then computed how much people exercised, how their body mass indices varied and which of these folks died of heart disease during the next two decades. In the study, more than 1,500 people died of heart disease. Those who worked out and consumed more calories cut their risk of heart disease death in half. Exercise Is Essential "Subjects with the lowest caloric intake, least physical activity, and who were overweight or obese had significantly higher cardiovascular mortality rates than those with high caloric intake, most physical activity, and normal weight," Dr. Fang notes. The individuals in the study who were overweight and didn't exercise had a bigger risk of heart disease even if they tried (and succeeded) at eating less. "This suggests that heart disease outcome was not determined by a single factor, but rather by a compound of behavioral, socioeconomic, genetic and clinical characteristics," according to Dr. Fang. According to researchers, if your job requires a great deal of physical activity, your health will be better if you get another job. Exercise on the job not only doesn't decrease your risk of heart disease, it may actually raise it. The reason: On-the-job activity is linked to heart-endangering increases in job stress. Research into this subject, performed at the Keck School of Medicine of the University of Southern California, found that while recreational exercise slowed hardening of the arteries, workers who had to exert themselves during the workday had arteries that were blocked at a younger age (American Journal of Medicine 7/03). In this study, researchers examined about 500 middle-aged employees as part of what is called the Los Angeles Atherosclerosis Study. "We found that atherosclerosis progressed significantly faster in people with greater stress, and people who were under more stress also were the ones who exercised more in their jobs," says James Dwyer, PhD, professor of preventive medicine at the Keck School. According to Dr. Dwyer, "This suggests that the apparent harmful effect of physical activity at work on atherosclerosis-and heart disease risk-may be due to the tendency of high-activity jobs to be more stressful in modern workplaces. "It appears from our findings that the psychological stresses associated with physically active jobs overcomes any biological benefit of the activity itself." Playful Workouts On the other hand, the scientists found that heart disease drops dramatically among those who exercise the most in their spare time. In the study, people who vigorously worked out at least three times a week had the lowest risk. But even those who just took walks enjoyed better heart health than people whose most strenuous activity was working the TV remote. Dr. Dwyer says, "These results are important because they demonstrate the very substantial and almost immediate-within one or two years-cardiovascular benefit of greater physical activity." Lowering your risk of heart disease is substantially up to you. Listen to what your heart tells you it needs; then, exercise your right to fetch some cardiovascular necessities.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=321) Ellagic Active - Raspberry Extract - Promotes Healthy Cells ... 
Date:
June 01, 2005 01:22 PM
You may think raspberries are strictly a summertime indulgence. Yet scientists know this simple fruit is far more valuable than a delicious snack or gourmet dessert. Raspberries have the highest content of ellagitannins— amazing health compounds— which are converted into ellagic acids in the body. These compounds are highly regarded for their positive effects on the growth and regulation of various cells and tissues, including those in the breast, pancreas, esophageal, skin, colon and prostate. Ellagic acid is also a powerful antioxidant (even stronger than vitamin C) that supports DNA integrity and promotes overall cell health, according to animal and in-vitro research. Source Naturals offers ELLAGIC ACID in response to a breakthrough in cell research. We strive to be ahead of mainstream nutritional science and are passionate about our commitment to informed health choices. Protective Benefits Dieticians have long stressed the importance of the consumption of fruits and vegetables for general health and well-being, but now these food items are being recognized as even greater contributors to human health. We know that ellagic acid binds to DNA, and acts as a shield, protecting DNA and increasing the expression of the enzyme p21, which arrests division of cells with DNA damage. Raspberries contain phytochemicals that provide protective action: One study showed that ellagic acid was able to induce the production of NAD(P)H:quinone reductase (QR), a major detoxification enzyme. Ellagic acid acts as a free radical scavenger to “bind” irritant-causing chemicals, making them inactive. Ellagic acid stimulates the activity of the enzyme glutathione-S-transferase that supports healthy cell growth. Extensive Research Raspberry is also a traditional remedy in support of the gastrointestinal and respiratory tract. It is used to promote healthy blood vessels, as a mouth and throat remedy and is said to help maintain a “normal, balanced feeling” in the stomach. Research studies on the protective effects of ellagic acid have been extensive—there are approximately 126 published studies. Berries also contain a natural form of salicylates, which provide cardio support. British researchers analyzed the blood of subjects and found salicylates were present from dietary sources, including raspberries and blackberries. Researchers at the National Center for Health Statistics (NCHS) in Hyattsville, Maryland established a connection between reduced health risks and increased intake of salicylates. Animal tests also suggest that red raspberry may reduce levels of glucose (blood sugar) to support normal blood sugar levels. Potent Defense Research in the past decade has determined that ellagic acid is one of the most exciting and promising compounds for its striking effect on cell division, regeneration and growth. While ellagic acid has been found to occur naturally in 46 different foods, red raspberry has been identified as having the highest natural content. Each tablet contains 300 mg of raspberry leaf extract (40% ellagitannins), which is ten times higher than other raspberry products. Source Naturals again joins forces with your natural foods retailer to bring you this unparalleled supplement.
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Ear ringing is a clinical problem that affects 1 out of 5 people. It is also known as tinnitus and it can be a symptom of condition such as ear injury, hearing loss and circulatory disorder. There are many causes of this condition which can aggravate to completely hear loss.
