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Search Term: " Fibrosis "
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) Choline: The Liver’s Fat-Export Engine
Date:
June 24, 2026 11:48 AM
Without sufficient choline, the liver's ability to process and export fats grinds to a halt. The Liver’s Fat-Export MechanismThe primary reason the liver requires choline comes down to a specific molecule: phosphatidylcholine (PC).When you eat fats or liberate stored fatty acids, your liver processes them into triglycerides. To move these triglycerides out of the liver and deliver them to muscle or adipose (fat) tissue for energy or storage, the liver has to package them into transport vehicles called VLDL (Very Low-Density Lipoproteins). Phosphatidylcholine forms the essential outer shell of these VLDL transport "boats." If you don't have enough choline, your liver cannot manufacture this outer shell, meaning the boats cannot be built, and fat cannot leave the liver. What Happens When Choline is Deficient?When dietary choline drops below critical levels, a highly predictable cascade of liver dysfunction occurs:
Dietary Benchmarks & SourcesTo prevent fat accumulation and support proper VLDL export, the Food and Nutrition Board establishes specific Adequate Intake (AI) targets, though optimal metabolic and athletic performance may require a more robust baseline.
Summary: Choline acts as a critical logistics coordinator for liver health, serving as a non-negotiable raw material for exporting fat out of the organ. Specifically, the liver relies on choline to produce phosphatidylcholine, a molecule that forms the essential outer shell of Very Low-Density Lipoproteins (VLDL). Think of VLDLs as transport boats designed to safely carry triglycerides out of the liver and deliver them to the rest of the body for energy or storage. Without an adequate dietary supply of choline, the liver simply cannot build these outer shells, causing the entire transport system to grind to a halt and leaving processed fats stranded inside liver cells. When this export mechanism stalls, the stranded fat quickly triggers a highly predictable cascade of liver dysfunction. This buildup leads directly to fat accumulation - historically known as fatty liver disease and now classified as MASLD - which quickly overwhelms the cellular mitochondria. The resulting oxidative stress and cellular injury spark chronic inflammation (MASH), causing liver cells to die and potentially leading to permanent scarring or Fibrosis over time. Furthermore, a severe shortage of dietary choline starves the body's methylation cycle, forcing it to deplete vital SAMe pools in a desperate, structurally taxing attempt to manufacture its own phosphatidylcholine.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6643) Did you know that glutathione is not only great for liver health, but it also promotes beautiful, radiant skin?
Date:
December 07, 2023 12:12 PM
Did you know that glutathione is not only great for liver health, but it also promotes beautiful, radiant skin?Glutathione (GSH), often considered as an amino acid but actually a tripeptide, is an antioxidant primarily synthesized in the liver. Composed of cysteine, glutamic acid, and glycine, it plays a crucial role in the synthesis and repair of DNA and protein, as well as the synthesis of prostaglandins. With its involvement in various functions like amino acid transport, toxin and carcinogen metabolism, immune system function, prevention of oxidative cell damage, and activation of enzymes, it is undoubtedly the most important tripeptide in the body. While the benefits of supplementing with glutathione are numerous, two particularly compelling reasons are its positive impact on liver health and beautiful skin, which are the key focus of this article. However, before diving into the specifics of liver health and skin benefits, it's important to review the data on glutathione depletion and absorption. GSH depletion can occur due to various oxidative stressors such as radiation, v.infections, enviro toxins, household chemicals, heavy metals, surgery, inflammation, burns, septic shock, and dietary deficiencies of GSH precursors and enzyme cofactors. Additionally, research suggests that GSH levels tend to decline with age. The bioavailability of glutathione as a dietary supplement has encountered challenges in the past. Studies in the 1990s suggested that oral GSH might be inactivated by peptidases in the gut, as the levels of glutathione in the body did not seem to correlate with dietary intake, despite its presence in fruits, vegetables, and meats. Moreover, previous studies showed no significant increase in blood GSH levels when subjects were given high doses of 1,000-3,000 mg. As a result, alternative strategies like supplementation with NAC were used to boost GSH levels. In 2014, something interesting happened that changed the way we look at the bioavailability of GSH. A groundbreaking study published in the Journal of Agricultural and Food Chemistry shed new light on the old research. This study showed that GSH, when taken in its intact form as OPITAC, a yeast-derived glutathione by Kohjin/Mitsubishi, can actually be rapidly transported across intestinal epithelial cells. Once inside, it gets rapidly converted into oxidized glutathione (GSSG) and accumulates in red blood cells and the liver, with only a small presence in plasma. So, although the GSH was indeed absorbed, it didn't show up in blood plasma because it transformed into GSSG and stored in the red blood cells and the liver. The bottom line is, supplementing with GSH is an effective way to boost GSH levels in the body. This finding was further confirmed in another study that described how OPITAC, as a yeast-derived glutathione by Kohjin/Mitsubishi, is directly absorbed in its electrochemically reduced form in the intestine, then transported in the blood in bound forms, and eventually deposited into the liver in its reduced form. But here's where it gets even more significant. A six-month randomized, double-blinded, placebo-controlled trial involving 54 adults was conducted to investigate the effects of oral GSH supplementation (250 or 1,000 mg/day, as OPITAC glutathione, Kohjin/Mitsubishi) on GSH levels in various parts of the body, including blood, erythrocytes, plasma, lymphocytes, and exfoliated buccal mucosal cells. The results were astounding. After one, three, and six months, GSH levels in blood increased significantly compared to baseline in both dosage groups. At the six-month mark, GSH levels skyrocketed 30-35 percent in erythrocytes, plasma, and lymphocytes, and a mind-boggling 260 percent in buccal cells in the 1,000 mg group (P < 0.05). Even in the low-dose group, GSH levels in blood and erythrocytes increased by 17 and 29 percent, respectively (P < 0.05). This research clearly demonstrates that supplementation with GSH is not only effective for increasing GSH levels in the body but also for maintaining them. So, to sum it all up, the evidence speaks volumes - supplementing with GSH can have a profound impact on your body's GSH levels, and trust me, that's definitely a good thing! Liver HealthWhen it comes to our well-being, the liver is a true superhero. Let's dive into some fascinating details about this essential organ. Did you know that the liver is not only the largest reservoir of GSH (glutathione) but also a major site of GSH manufacture in the body? Pretty impressive, right? Special cells in the liver work tirelessly to synthesize GSH, which plays a crucial role in detoxification. Speaking of detoxification, the liver is a champion in this field. Its cells have sophisticated mechanisms to break down toxic substances, be it internal or external compounds. During the detoxification process, the liver attaches or conjugates the toxins to water-soluble substances. This attachment makes the toxic molecules more water-soluble, less harmful, and easier to eliminate via urine or bile. In fact, glutathione conjugation produces water-soluble mercaptates that are excreted via the kidneys, effectively detoxifying acetaminophen and nicotine. Isn't it amazing how this process helps our bodies get rid of harmful substances? But that's not all. Adequate levels of glutathione are crucial for the elimination of fat-soluble compounds, particularly heavy metals like mercury and lead. What's more, GSH serves as a cofactor for various peroxidase enzymes, aiding in the detoxification of peroxides generated from oxygen radical attacks on biological molecules. It also assists transhydrogenase enzymes in reducing oxidized centers on DNA, proteins, and other biomolecules. Talk about a multitasker! The practical significance of this liver superhero was demonstrated in a study involving workers exposed to lead. A group of five workers received GSH at 200 mg/day for 30 days, while five others served as the control group. The results were striking. The group receiving GSH showed a significant increase in ALA dehydratase activity (which is inhibited by lead) compared to the control group (p < 0.05). This indicates that GSH could be a valuable solution for treating patients with lead poisoning. So, let's take a moment to appreciate the remarkable liver and its incredible role in maintaining our health and well-being! Alcohol IntoxicationAlcohol consumption is widely recognized for its capability to induce hepatic steatosis, also known as fatty liver disease, and disrupt biomembranes due to hepatic lipid peroxidation. This can lead to various lifestyle-related diseases and even hepatic cirrhosis by diminishing hepatic physiological function. Nevertheless, animal studies have shown that hepatic damage caused by alcohol intoxication can be mitigated by glutathione (GSH), a powerful antioxidant found in cells. To further investigate the impact of GSH supplementation on the effects of alcohol intake, a human crossover comparative study was conducted. The study involved twenty healthy men and women who were grouped into three categories: placebo, 100 mg GSH (as OPITAC glutathione, Kohjin/Mitsubishi), and 30 mg curcumin. The study evaluated laboratory parameters, including breath alcohol concentration at different time intervals (20, 60, 120, and 180 minutes post-alcohol consumption) as measured by an alcohol checker. Additionally, subjective feelings were assessed through a questionnaire. During the study, all participants consumed whiskey in a quantity equal to their body weight multiplied by 1.25 mL, and were instructed to drink the entire sample within 10 minutes. The results revealed that the breath alcohol concentration in the group supplemented with GSH significantly decreased compared to the placebo and curcumin groups at 20 (p<0.01), 60 (p<0.01), 120 (p<0.05), and 180 (p<0.08) minutes post-consumption. Furthermore, the GSH group reported lower levels of "sleepiness," "headache," and "upset stomach" in the subjective feeling questionnaire. Importantly, the concentration of aspartate aminotransferase (AST), an indicator of alcohol-induced organ damage, was significantly lower in the GSH group after two months compared to the placebo group. The oral intake of GSH has demonstrated its effectiveness in reducing alcohol consumption-related stress and improving long-term hepatic function. These findings highlight the potential benefits of GSH supplementation in alleviating the detrimental effects of alcohol intoxication on the liver. Nonalcoholic fatty liver diseaseNonalcoholic fatty liver disease (NAFLD) is a condition characterized by the build-up of fat in the liver of individuals who consume little or no alcohol. Unfortunately, NAFLD is quite common, affecting nearly one-third of all American adults. Interestingly, it often presents without readily apparent signs or symptoms, sometimes resulting in complications, and can lead to liver inflammation and scarring as the fat accumulates. Additionally, NAFLD is typically associated with conditions such as insulin resistance, central obesity, reduced glucose tolerance, type-2 diabetes, and elevated triglyceride levels. Recognizing the substantial role glutathione (GSH) plays in phase 2 liver detoxification, a pilot trial was conducted to examine the therapeutic effects of GSH supplementation in patients with NAFLD. The trial included 29 individuals, and the patients were provided with daily oral supplementation of GSH at a dose of 300 mg (in the form of OPITAC glutathione, from Kohjin/Mitsubishi). The patients' clinical parameters were assessed before and after the GSH supplementation, and liver fat and Fibrosis were quantified as well. The primary goal of the study was to determine any changes in alanine aminotransferase (ALT) levels. The results indicated a significant decrease in ALT levels following the GSH supplementation. Furthermore, triglycerides, non-esterified fatty acids, and ferritin levels also showed a reduction. This pilot study provides promising evidence for the potential therapeutic effects of oral glutathione administration, even at practical doses, in patients diagnosed with NAFLD. However, further investigation through large-scale clinical trials is necessary to validate its efficacy. In summary, NAFLD is a prevalent condition with potential serious consequences, but studies like the aforementioned pilot trial shed light on potential treatment options such as GSH supplementation. The findings demonstrate the need for continued research in order to provide more conclusive evidence and expand our understanding of NAFLD management. Beautiful SkinBy activating melanocytes in the skin, there is a notable increase in melanin formation, resulting in various blemishes such as freckles, pigmentation, and UV-induced skin spots, commonly known as age spots or liver spots. This is especially prominent after prolonged sun exposure and tanning. Age spots appear when melanin becomes concentrated or "clumped" in areas that have had years of frequent sun exposure. Luckily, there are materials like glutathione that can prevent or improve such pigmentation-related skin conditions. Another aspect to consider is skin pigmentation, wrinkles, and pores. In a study conducted with eight women in their 30s or early 40s, each supplemented with 100 mg/day of GSH (as OPITAC glutathione, Kohjin/Mitsubishi) for two months, their skin conditions were evaluated using the Robo Skin Analyzer. Several parameters were analyzed, including skin brightness, the amount and area of skin pigmentation, number of pores, and number of wrinkles under the eyes. It was observed that all subjects' skin brightness improved when measured on the second day of the study. Additionally, over the course of the two months, both the amount and area of skin pigmentation decreased, leading to an improvement in blemishes and pigmentation. Not only did glutathione exhibit a whitening effect, but it also reduced the number of wrinkles under the eyes and minimized pores. Furthermore, a randomized, double-blind, two-arm, placebo-controlled study was conducted with 60 otherwise healthy medical students. The purpose was to investigate whether supplementing with 500 mg of glutathione daily for four weeks would affect the skin melanin index compared to a placebo. Melanin indices were measured at six different sites on the body. The results demonstrated that melanin indices consistently decreased at all six sites in subjects who received glutathione after four weeks. The reductions were statistically significant compared to those who received the placebo at two sites: the right side of the face and the sun-exposed left forearm (p = 0.021 and 0.036, respectively). This improvement was likewise reflected in the reduction of UV spots. Importantly, both glutathione and placebo were well-tolerated. In conclusion, oral administration of glutathione leads to a lightening of skin color in the tested subjects. Skin LighteningSkin lightening is a process that is of interest to many individuals who seek to achieve a more even and radiant complexion. In recent studies, the use of a lozenge containing GSH 500 mg was explored as a means of skin lightening through an open-label, single-arm trial. The focus of this trial was to evaluate the buccal mucosa as a route for GSH administration and its potential in relation to skin lightening. It is worth noting that substances absorbed through the buccal route have the advantage of entering directly into the systemic circulation, effectively bypassing the gastrointestinal tract. The trial involved thirty Filipino females with Fitzpatrick skin types IV or V who received a daily glutathione-containing lozenge for eight weeks. The results from this trial demonstrated a significant decrease in melanin indices from baseline to endpoint. What is fascinating is that this visible change became evident in as little as two weeks. It is important to highlight that during this trial, there were no recorded serious adverse events, and the laboratory examination findings remained normal. Based on these findings, the researchers concluded that the lozenge containing glutathione was deemed safe and effective in lightening the skin of Filipino women. In addition to the aforementioned buccal route administration, another interesting approach that emerged from the studies is the topical application of GSH. A double-blind randomized clinical trial35 conducted in Yogyakarta, Indonesia, involved 74 healthy Indonesian women, with an average age of 33.3 ± 5.9 years, to explore the potential benefits of topical GSH. The trial subjects received supervised applications of facial wash twice a day, along with day cream containing sunscreen and night cream. The subjects were divided into three groups based on the active ingredients of the tested products, which included GSH (as OPITAC glutathione, Kohjin/Mitsubishi) at concentrations of 0.1 percent and 0.5 percent, and a control group without GSH. Throughout the trial, the effects of the tested products on skin color and pigmentation were measured using colorimetry with Chromameter Minolta for L. Compared to the baseline measurements, there were significant increases in lightness (L) detected as early as week 2 for the group using GSH at 0.1 percent concentration. Interestingly, this increase was significantly higher compared to the group using GSH at the higher concentration of 0.5 percent, as well as the group without GSH. It is important to note that hyperpigmented lesions also showed improvement, particularly in the group using GSH at 0.5 percent concentration, which displayed superiority compared to the other groups at week 8. In conclusion, the skin care products containing GSH at 0.1 percent and 0.5 percent concentrations were found to be effective in lightening facial skin. The findings from these studies shed light on the potential benefits of GSH in achieving skin lightening, either through buccal administration or topical application. It is worth noting that these studies focused on specific populations and more research is necessary to explore its effectiveness and safety across different skin types and ethnicities. In summary, the administration of
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6592) What is liver cirrhosis? (and is alcohol always the cause of it?)
Date:
May 02, 2019 11:59 AM
Cirrhosis is the advanced scarring of liver tissue. When the liver is injured, it will try repair itself, but this can lead to scarring (a.k.a. fibrosis). Advanced levels of scarring is cirrhosis. Excess drinking is a common cause of liver cirrhosis, but it isn't the only cause. A condition known as Nonalcoholic Fatty Liver Disease (NAFLD), actually the most common cause of liver disease in the U.S., can also lead to the disease. People who are overweight are at risk for NAFLD, so maintaining healthy weight is one way to prevent cirrhosis. Avoiding excess alcohol consumption is another. Finally, eating plenty of green leafy vegetables can protect the liver from damage. Key Takeaways:
"Each time that the liver is injured — whether by disease, excessive alcohol consumption, or fat cells that become toxins — it will try to repair itself." Read more: https://www.naturalnews.com/2019-03-26-what-is-liver-cirrhosis-and-is-alcohol-always-the-cause-of-it.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6235) Omega 3 Fatty Acid Found To Stop Liver Damage From Getting Worse
Date:
April 27, 2017 11:44 AM
Oregon State University researchers have determined an Omega 3 fatty acid can stop the progression of liver damage in lab animals for specific type of liver disease known a nonalcoholic steatohepatitis or NASH. The Omega 3 which produces this effect is docosahexaenoic acid or (DHA) a readily available dietary supplement. However, researchers caution this treatment will most generally be used clinically since the population rarely follows dietary recommendations on supplements. NASH is caused from consumption of the western diet high in sugar, cholesterol and fats and can lead to the development of liver cancer or cirrhosis. Key Takeaways:
"Characterised by liver inflammation, oxidative stress and fibrosis, NASH is a substantial risk factor for cirrhosis and liver cancer." Read more: http://www.news18.com/news/health-and-fitness/omega-3-fatty-acid-found-to-stop-liver-damage-from-getting-worse-1378455.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4490) Ease the load on your liver with these 7 foods
Date:
April 23, 2017 08:44 AM
Fatty liver disease can be caused by too much alcohol intake or an unhealthy lifestyle and diet. There are some foods that can help heal a fatty liver. Allison, found in garlic can detox your liver. Turmeric can decrease inflammation and is detoxifying. Dark leafy greens contain sulfur which contributes to a healthy liver. Green tea can decrease fat accumulation in the body and liver. Broccoli neutralizes liver toxins. Pineapples can reduce inflammation and reduce digestive stress on the liver. Blueberries are full of protective antioxidants and can fight lover cancer cells. Nutrient supplements and water are also a must for liver health. Key Takeaways:
"Liver problems like nonalcoholic fatty liver disease (NAFLD), liver fibrosis, and alcoholic liver disease are often caused by poor lifestyle choices. That’s why making positive changes to your diet is a huge step towards improved liver health. According to NaturalHealth365.com, these are some of the best foods and herbs for maintaining a healthy and happy liver." Read more: http://www.naturalnews.com/2017-04-20-8-easy-ways-to-reduce-the-toxic-load-on-your-liver.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4460) Eating These Foods Can Help You Get Your Daily Dose of Vitamin D - Pulmonary Fibrosis News
Date:
April 08, 2017 06:44 AM
Vitamins are important to everyone. If you do not have enough there can be linked bone pain or muscle weakness. if you are not getting enough vitamin D there are a few ways you can get more. going outside will help you get the "sunshine vitamin". Men and woman need 600-400 IU a day from the sun. Salmon, Milk, Eggs, Orange Juice, Yogurt, Cod Liver Oil, Cheerios, Beef Liver, Tuna, and supplements can all helkp you reduce your chance of getting Pulmonary Fibrosis Read more: Eating These Foods Can Help You Get Your Daily Dose of Vitamin D - Pulmonary Fibrosis News
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4374) CORDYCEP: MEANING AND BENEFITS
Date:
July 22, 2015 01:25 AM
Cordyceps is simply a fungus. Not typically kitchen friendly, but if health is your number one target, then it will make the best supplement in your system. Before we go deeper into its benefits let us first have a clear understanding of what this unpopular yet effective medicinal fungi is. What is Cordyceps? It is simply an ascomycete fungi genus with approximately four hundred species that are mainly parasitic. They weren't considered beneficial to health until a recent discovery of Cordyceps Sinensis popularly known as a caterpillar fungi (It attaches itself on the caterpillar). Despite limited research on its health benefits, Cordyceps seems to be the best remedy for most of the health complications related to poor diet, lack of exercise and more.
Let us take a look at some of its benefits. 1. A remedy for kidney disease - Cordyceps prevent rat's renal Fibrosis. This condition (renal Fibrosis) is evident in later stages of the organ. However, there is still need for more research on this fact. 2. Slows down Tumor Growth - There is some proof that Cordyceps trigger the immune system to combat cancer. Ability to improve the immune system was due to a result of research where there were some indications that Cordyceps slowed down tumor growth in many animals. 3. Increase libido - Lots of studies shows that Cordyceps raise the level of testosterone in rats. There are some claims that it also enhances sexual performance that is also yet to be proven. Apart from slowing down tumor growth, kidney disease and increasing sexual performance that are yet to be confirmed, Cordyceps have other numerous health benefits according to researchers that are, * Increase body oxygen uptake - Needed for maximum athletic performance. * Reduce the aging effects - Slows down aging that has remained a bother for centuries. * Strengthen muscles - For weight lifters and athletes looking to gain strong muscles with a little workout. * Improves lung function - Improves breathing needed for athletic performance * Good for the liver - Slows down liver complications that are known to lead to a liver transplant. There are also some claims that Cordyceps may replace the steroids when it comes to improving athletic performance and muscle building. Among these claims is that Cordyceps can enhance stamina needed mostly by sportsmen and women. Other researchers claim that it can tone muscles, increase energy and even reduce fatigue after a long time of work. In summary, the caterpillar fungi (Cordyceps) has a lot in store when it comes to solving health complications. However, these claims are yet to be confirmed. If the facts are as real as the researchers claim them to be, then Cordyceps will be at the top of the top list of best natural supplements ever discovered. https://en.wikipedia.org/wiki/Cordyceps //www.gnet.org/cordyceps-benefits/ //www.healthline.com/health/cordyceps-exercise-performance#1 //www.drugs.com/npp/cordyceps.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3179) Can Pancreatic Enzymes Help Reduce Pancreatic Stress?
Date:
May 22, 2013 10:43 AM
Pancreatic enzymes are crucial for the purpose of breaking down fats, carbohydrates and proteins. A healthy pancreas will produce about 8 cups of pancreatic juice daily. This is released into the duodenum helping neutralize any acid. This potion of the stomach is at the entrance of the small intestines. The lack of these fluids could cause a myriad of problems depending on the functions that are carries out. The question however is; can pancreatic enzymes help reduce pancreatic stress? One of the best ways to answer this is to find out what these enzymes are and do exactly.
Lipase is a pancreatic enzyme that breaks down fats. The lack of this enzyme causes a shortage of fat soluble vitamins and diarrhea evident by fatty stools. Protease breaks down proteins in the body. It is also crucial in keeping the system clear of protozoa and yeast among many other parasites. The lack of the same will cause a rise on toxicity in the stomach due to faulty digestion. The individual will also be at risk due to infections. Amylase will break down carbohydrates and is commonly found in the saliva. The lack of the same will cause diarrhea due to the presence of starch that is undigested in the colon.
This is common in patients that have developed pancreatic cancer. The lack of pancreatic juice in the body will cause pancreatic stress. This calls for doctors to find a way to help induce the functionality of this juice into the body. This is the reason why pancreatic enzymes are used to help along with the breaking down of these body substances. This partly answers the question, can pancreatic enzymes help increase pancreatic stress? Some other effects that could come with the lack of these enzymes include cystic Fibrosis, pancreatitis, duodenal tumors and Whipple procedure. Some of the symptoms of these conditions brought by the lack of the enzymes include cramps, gas, indigestion, weight loss and diarrhea.
These enzymes given by doctors may also be given along some acid reducing medication. These enzymes should be taken carefully to ensure that they work optimally. Added enzymes will ease pancreatic stress by balancing the digestive system. The body in turn will not think it needs more enzymes and reduce its demands on the pancreas. Some of the things to keep in mind when using these are;
The most common side effect of these enzymes is constipation. They are however the best way to deal with indigestion due to the lack of the pancreatic fluid in the body. Have you had your pancreatin today to boost digestion and eliminate food allergies?
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2842) Serrapeptidase: Natural NSAID
Date:
March 27, 2012 03:26 PM
Serrapeptase, also known as Serratia peptidase is a proteolytic (protein-splitting) bioactive enzyme found in the intestines of the silk worm. This silk-worm enzyme is widely used in Europe and Japan in clinical therapy for relieving pain and inflammation. When the silk worm leaves the cocoon, it regurgitates the serrapeptase in to create a hole in the cocoon for its escape. It was soon discovered that serrapeptase enzyme has a unique property to dissolve dead material consisting protein without even harming the living tissue. This property of dissolving dead tissue can be used in treating many health conditions. How Serrapeptase work? Protein is the main component of most of the fibrous materials in the body. Once these fibrous materials out-live their purpose or are over-grown, they start causing serious disease conditions involving Fibrosis. Fibrosis is an abnormal thickening and scarring of connective tissue caused by infection, injury, surgery or lack of oxygen. Serrapeptase works as an anti-fibrotic and helps in relieving the conditions in connective tissue scarring and thickening has occurred. Health Benefits of Serrapeptase: This proteolytic enzyme is considered an alternative to NSAIDS (Non Steroidal Anti-Inflammatory Drugs) that are used to treat osteoarthritis, rheumatoid arthritis and other inflammatory conditions. Serrapeptase has been used to treat fibromyalgia, colitis, Inflammatory Bowel Diseases, varicose veins, ovarian cysts, ear and throat infections, enlarged prostate and postoperative inflammation. Studies have shown its effective results in prevention and removal of arterial plaque. Serrapeptase in relieving Pain: Pain and Inflammation Reduction: Serrapeptase is a great anti-inflammatory and analgesic agent. It reduces the inflammation and gives relief from the pain. It works by blocking the release of pain inducing amines from the inflamed tissues. Due to its pain relieving and anti-inflammatory properties, serrapeptase is used in treatment as an alternative to NSAIDS. This enzyme gives relief from mild to moderate pain like headache and backaches. Hence it is used all the inflammatory conditions such as colitis, sinusitis, arthritis and many more. Cardiovascular Health: Serrapeptidase has an anti-fibrotic and fibrinolytic action that prevents and treats the accumulation of plaque in the arteries. Plaque is the accumulated deposits of cholesterol, fatty substances, cellular waste products, fibrin and calcium. Excessive plaque formation impairs the normal blood flow and cause partial or complete blockage, which also results in arteriosclerosis. Serrapeptidase helps to prevent build-up of plaque in the body. Due to its fibrinolytic action, it also helps in dissolving of proteins and breaking down atherosclerotic plaques. The dissolved deposits are eliminated from the body. Hence, serrapeptidase prevents coronary artery diseases and improves cardiovascular health.
Relieving Sinusitis: Due to its anti-inflammatory and mucus dissolving properties, Serrapeptidase is very beneficial for chronic sinusitis sufferers. Serrapeptidase helps in thinning and expelling the thickened mucus secretion present in nasal cavities of sinusitis sufferer.
Promoting Healing: Serrapeptidase helps in reducing the recovery time in any injuries, wounds or surgery. It promotes healing in post-operative wounds by reducing the inflammation and pain. Serrapeptidase is available in the form of supplements. If you are taking NSAIDS for any healthy condition, substitute it with serrapeptidase supplement
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2621) Your Thyroid, Iodine, And Radiation, What You Need To Know!
Date:
June 27, 2011 03:34 PM
What is Potassium Iodide Good for?Potassium iodide is a white salt especially formulated to combat iodine deficiency. It is extensively utilized as iodized salts and also comes in pill form. It is medically noted for its protective effects when taken orally, for it has been proven to produce many health benefits. Also, it has been tied to nuclear medicine, which relies on the process of radioactive decay in the diagnosis and treatment of disease. Alkali metal salts such as sodium iodide and potassium iodide are extensively used in food and drug industries to promote dietary intake of the trace mineral iodine, which is a chemical element necessary to support human life. Nutraceutical companies prefer potassium iodide as it attracts water molecules at a lesser rate than sodium iodide. In fact, it is the most commercially significant form of iodide. Reverses Iodine Deficiency Endemic goiter is a global health concern caused by iodine deficiency, which is prevalent in regions where animal products and plant-based foods are very low in iodine. Delays in physical development are the most visible medical signs in children suffering from iodine deficiency. Many countries have relied on iodized salts that contain potassium iodide to boost iodine intake and reverse deficiency. Inhibits Radioiodine Uptake Potassium iodide has long been recommended by the scientific community to combat the deleterious effects of radioactive materials, most notably radioiodine. The thyroid gland has an affinity for iodine compounds, and its uptake of radioiodine have been linked to cancer and many other diseases. In nuclear medicine, potassium iodide is used to inhibit the uptake of radioisotopes taken internally. Promotes Thyroid Health The proper functioning of the thyroid gland is dependent on iodine, and thus this trace mineral always determines thyroid health. For one, it is a major component of tissues that make up the thyroid gland. Also, it is absolutely necessary in the synthesis of thyroid hormones. Regular intake of potassium iodide is a safe way to supply the body with iodine, whether in table salts or nutritional supplements. Remedies Fungal Infections Solutions that contain potassium iodide have been the subject of research on fungal diseases, such as sporotrichosis or rose gardener’s disease. Several fungi found in soils often afflict human beings and cause skin infections characterized by nodular boil-like lesions that progress to skin ulcerations. Oral administration of potassium iodide remedies infections and eradicates the fungus that causes them. Provides Numerous Benefits Potassium iodide has been reported to display antimicrobial properties. It is utilized as an antibiotic in surgical science. It has been noted to reduce Fibrosis of soft tissues and excessive formation of blood vessels in body organs. It stimulates the production of saliva and mucus in the event of respiratory infections. It also acts as a detox agent for several toxic chemicals found in the systemic circulation.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2348) Juniper Berries
Date:
September 04, 2009 12:17 PM
The juniper plant is a coniferous plant which is part of the genus Juniperus of the cypress family. There are approximately 50-67 different species of juniper, which are distributed widely throughout the northern hemisphere. Among these locations include the Artic, south to tropical Africa in the Old World, and to the mountains of Central America. Juniper berries were used in ancient Greece as a diuretic. In Europe, the scent of juniper berries was used to help ward off the plaque. Nicholas Culpeper, a seventeenth-century herbalist, recommended the use of juniper as an appetite stimulant. Native Americans used juniper berries as a survival food during the cold winter months. The berries were dried and ground and then made into cakes. Some tribes even roasted the berries, ground them, and then used them as a coffee substitute. The tea was recommended to be used by Jethro Kloss for kidney, prostate, and bladder disorders, and for dropsy and digestive diseases. The berries and oil of the juniper plant were listed in the U.S. Pharmacopoeia from 1820 to 1873. They were also listed in the National Formulary until 1960. Juniper berries contain a volatile oil that has traditionally been used to treat conditions of the urinary tract. The berries of the juniper plant are often used to increase the flow of urine. They are also beneficial for ridding the body of uric acid, which may crystallize in the kidneys. They are also used to dissolve kidney stones and sediment in the prostate. Juniper berries are also recommended for treating digestive problems, indigestion, gas, and to cleanse the blood. The berries may even help to stimulate the appetite. This herb contains natural insulin which is responsible for helping to restore the pancreas when no permanent damage has occurred. Juniper may be applied directly to wounds as a poultice for healing and infection prevention. One study that was done using animals found that juniper acts as an effective diuretic. The berries are believed to stimulate the flow of urine and the filtration process. The volatile oils, which are found in the juniper berries, are responsible for increasing the glomerular filtration rate of the kidneys. Juniper berries are often used for their diuretic properties. This herb is not recommended for use by pregnant women as it may increase uterine contractions. The berries of the juniper plant are used to provide anodyne, antispasmodic, aromatic, astringent, carminative, diuretic, emmenagogue, nephritic, and stimulant properties. The primary nutrients found in juniper are copper, sulfur, and vitamin C. Primarily, juniper is extremely beneficial in dealing with adrenal gland problems, bed-wetting, bleeding, colds, diabetes, edema, hypoglycemia, infection, kidney infections, kidney stones, pancreatic problems, uric acid irritations, urinary problems, uterine problems, and water retention. Additionally, this herb is very helpful in treating acne, ague, hay fever, allergies, arthritis, arteriosclerosis, insect and snake bites, blood impurities, bursitis, catarrhal inflammation, colic, coughs, convulsions, uterine and stomach cramps, cystic Fibrosis, fungus, gas, gonorrhea, gout, bleeding gums, irregular menstruation, excessive mucus, prostate problems, rheumatism, scurvy, sores, tuberculosis, typhoid fever, urinary incontinence, and worms. For more information on the many beneficial effects provided by juniper, please feel free to contact a representative at your local health food store.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2073) Milk Thistle May Help With Cirrhosis, Gallstones, and Hepatitis Liver Problems
Date:
November 14, 2007 12:34 PM
Milk thistle, botanically Silybum Adans, is a member of the daisy family that is native to the Mediterranean, the Middle East and North Africa but has also been introduced to California and parts of the eastern side of the USA, and can help with problems such as cirrhosis, gallstones and hepatitis. Although it has been recorded as being used in medieval times as a tonic for the liver, it is only relatively recently that its chemical components have been investigated. Analysis indicated the presence of hitherto unknown flavonoids which were given the name of silymarin. In general, flavonoids are strong antioxidants found in many fruits and vegetables that eat up the free radicals that cause so much damage to our bodies. Free radicals are very unstable molecules that are generated through pollution, such as smoking, car fumes, perticides etc, and that destroy body cells accelerating aging. They also oxidise the low density lipids (LDL) that carry water-insoluble cholesterol through the blood to the arteries where it is needed to repair damage, resulting in excess deposition and the atherosclerosis that can cause strokes and heart disease. Antioxidants mop these up like a sponge, and are some of the healthiest types of molecules that we can consume. The silymarin group of flavonoids are particularly attracted to the liver where they act as antihepatoxic agents that prevent the liver from becoming poisoned. But why should the liver be poisoned I can hear you ask, and what are the poisons involved? Can we avoid them? It is a very relevant question, and one that will make you wonder, every time you leave your home, especially if you live in a big city or an industrialized area. Smoking cigarettes, working with volatile organic compounds that you can breathe in, such as paint and printing ink solvents, the exhaust fumes of cars and diesel engines, factory chimneys belching out tons of smoke, analgesics such as paracetamol, pesticides on your fruit and vegetables that you have failed to wash off, alcohol, etc, etc, etc… All of these have to be removed from your body or you will die, awash with all these poisons that you have ingested, some deliberately and some not. The organ that does this is your liver: the powerhouse chemical plant of your body that carries out millions of biochemical reactions every day. Your liver converts all of these poisons into molecules that can be flushed away through your body naturally. However it places great stresses upon it, and even your liver needs a rest sometimes, or even just a little rejuvenating tonic would keep it happy. Milk thistle has been used for just that purpose, especially when the liver has been toxified with excess alcohol, pesticide poisoning or even hepatitis. The silymarin initially coats the cells of the liver by binding to the cell membranes of the cell walls, so that the toxins are hindered from entering the cells. Its antioxidant properties then neutralise any free radicals present that are causing the damage to the liver cells. It also helps to stimulate the production of proteins to help the healing process, and reduces the Fibrosis that is the development of fibrous masses outside the liver cells caused by damaged cells excreting materials such as collagens outside the cells into the general body of the liver. Finally, milk thistle helps to prevent the activity of the immune system in causing inflammation of the damaged cells. Silymarin acts very specifically on the liver, and is often used by physicians in the treatment of such liver conditions as jaundice, hepatitis, liver cancer and cirrhosis. In addition to its own effects it appears that it stimulates the production of glutathione that is also a very powerful natural tripeptide antioxidant produced by the body when it is under oxidative stress. Its effect on cancer and some diseases is not curative, but to allow the liver to continue to detoxify the body when otherwise it might fail and lead to toxicity problems from which the patient might not be able to recover. Due to the remarkable regenerative powers of the liver, milk thistle is able to stimulate it into repairing its damage and grow fresh cells to replace the damaged ones. This is the reason for its effectiveness in otherwise very serious degenerative diseases. It is often prescribed by doctors for patients who are taking a number of different medications. Which help the liver to metabolize these medications, since without it, it might struggle to provide the true efficacy of the prescribed drugs. So far we have been concentrating on the liver, but milk thistle has other properties not connected directly with the hepatic function. It can help to promote the production of bile in the gall bladder and so give the digestive system a boost when needed, where it also acts as a mild laxative. However, it can also help patients suffering from both lose stools and constipation due its effect. It can also help to relieve gallstones, though medical tests are generally carried out first to ensure that they are not too large for the milk thistle to handle. It is also an anti-inflammatory, and is useful in the treatment of acne and other inflammatory responses, and also for inflammations in the gall bladder, kidney and bladder. There are few serious side effects, although, as milk thistle rids the body of toxins, these toxins can cause problems such as diarrhea, headaches and abdominal pain. Keep in mind that you are releasing poisons from the liver into your system so that they can be expelled by the usual means, and they will put up a fight along the way. However, the milk thistle will usually win in the end. There currently appear to be no long term issues with taking milk thistle as a supplement over a long period, and it is good way to maintain a healthy liver. Keep in mind that the liver is the body’s chemical plant, where most of the biochemical reactions of life take place, and without we cannot survive. It makes sense, therefore, to look after your liver, and milk thistle is one way of doing that; some would say the best way.
So remember that, although milk thistle may help with cirrhosis, gallstones and hepatitis liver problems, you should be prepared for a short struggle before it wins the day. Always consult your family physician for a clear diagnosis before self prescribing herbs as treatment. Your physician can advise you as the correct course of action to take once diagnosed with a liver blood test first. But, to boost overall health and wellness milk thistle is a great herbal supplement to take on a daily basis.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1631) Turmeric and Alzheimer’s Disease
Date:
May 10, 2007 12:38 PM
Turmeric and Alzheimer’s Disease
In
Compare these findings to people over the age of 65 living in the
So what are people who are living in
Q. How can curry prevent these changes in the brain? Isn’t that a lot to expect from a spice?
A. Evidently, it’s not too much to expect from this spice. Curry comes from the turmeric plant – Curcuma longa is the plant’s official name. Curcumin, a plant compound in turmeric, is the source of curry’s instantly recognizable bright yellow pigment. When it comes to the scientific research of Curcuma longa, the terms curcumin and turmeric are both used. Both refer to the same thing- tumeric extract.
There have been more than 1300 studies on tumeric and its health benefits for humans. Research has shown tumeric is able to help the body get rid of cancer-causing toxins. Turmeric also blocks estrogen receptors and enzymes that promote cancer. And it’s been found to stop the growth of new blood vessels in cancerous tumors – an important factor in keeping cancer from getting larger and spreading throughout the body.
But one of turmeric’s most exciting health benefits is its ability to reduce, prevent, and stop inflammation. While inflammation is a normal and needed response to injury or disease, chronic inflammation can cause damage to tissues. And researchers are now finding inflammation plays a huge role in Alzheimer’s disease.
Q. I’ve always heard that Alzheimer’s disease was caused by complex growths in the brain called plaques and tangles. How can simple inflammation cause such a devastating disease?
A. You are right. Plaques and tangles are indeed the hallmarks of Alzheimer’s disease. But researchers looking at the brain damage caused by Alzheimer’s have always noted the presence of inflammation wherever plaques and tangles form. In the past, this inflammation was thought to be simply a consequence of Alzheimer’s disease. Now scientists believe the inflammation itself starts a chain reaction ultimately contributing to the development of Alzheimer’s disease.
` When cells in the brain are disrupted by inflammation, amyloid, and a protein normally found in the brain, beings to act chaotically. This chaos results in the creation of beta-amyloid, protein that is toxic to cells in the brain. Sticky deposits of beta0amyloid build up and collect around the cells, making dense clumps or plaques. Because the brain can’t break the plaques down and get rid of them, they stay right where they are and slowly accumulate.
Tangles result when long protein fibers that act like scaffolding for brain cells begin to twist and tangle. The cell is damaged and eventually dies. But the tangled proteins remain in the brain even after the dead neuron has been cleared away. And inflammation might be the culprit causing the long protein fibers to start tangling.
The consequence of these abnormalities of protein in the brain is more than the cell death they cause. They also act as roadblocks interfering with electrochemical messengers being shot from cell to cell. Therefore, the remaining healthy cells’ activity is diminished as well.
Research of identical twins has repeatedly shown that if one twin has Alzheimer’s disease, the other has a 60% chance of developing the disease, too. Scientists from the Karolinska Institute in
In fact, the inflammatory process might occur years before the onset of Alzheimer’s, and be the result of any number of infections people can contract. That’s why current research is searching for ways to protect brain cells from inflammation. And why some countries have low rates of Alzheimer’s disease, like
Q. Why curry? Couldn’t other lifestyle difference account for the low rates of Alzheimer’s disease in
A. That’s a good question. When researchers begin studying a disease, like Alzheimer’s, they look for trends to help them determine how and why the disease occurs. For example, we all now know the connection between cigarettes smoking and long cancer. But, it wasn’t until the 1930’s that doctors noticed the trend fro cigarette smokers to have more lung cancer than people who didn’t smoke.
So it has been with researchers studying Alzheimer’s disease. They know Alzheimer’s disease has an important connection to inflammation. They also know turmeric reduces inflammation. And when researchers noticed these trends – that people in India eat high amounts of curry from turmeric and have very little Alzheimer’s disease – they began to theorize that turmeric might be able to prevent or even treat the illness. And the research they designed around these trends has unequivocally found turmeric to be on common denominator.
Q. What have the turmeric studies shown so far?
A. Simply amazing findings are coming from curry research. Not only does turmeric slow down cancer growth, it’s also been found to correct the cystic Fibrosis defect in mice, help prevent the onset of alcoholic liver disease, and may slow down other serious brain diseases like multiple sclerosis.
Researchers from the
And now the UCLA Alzheimer’s Disease Research Center (ADRC) is using turmeric in clinical trials and studying the effect of this powerful spice in patients diagnosed with this devastating disease. Clinical trials are the gold standard of medical research. But it’s rare in Alzheimer’s disease. And it’s even more rare when all-natural herbs and spices like turmeric are used in hopes the positive benefits will be discovered. The head of the UCLA’s research team was recently interviewed and stated that setting out to hopefully prove turmeric’s ability to prevent and treat Alzheimer’s disease was “tremendously exciting.”
Q. I recently read that one of the non-steroidal anti-inflammatory drugs (NSAID) was found to prevent Alzheimer’s disease. Is this true?
A. Scientists recently studied ibuprofen, one of the NSAIDs investigated for Alzheimer’s disease Prevention. Ibuprofen belongs to a family of drugs that includes naproxen, indomethacin, nabumetone, and several others. These drugs are used most often to get rid of headaches, mild arthritis, and other kinds of pain and inflammation.
In the studies, the average dose of ibuprofen was 800mg a day. Patients took the product for two years. While the results suggested that ibuprofen might reduce the risk of developing Alzheimer’s, ibuprofen’s side effects are too harmful to be a valid lifelong prevent aid treatment. Ibuprofen, like other NSAIDs, can cause gastrointestinal bleeding when used at high dosages over a long period of time. Long term use of ibuprofen can also lead to analgesic nephropathy, a kind of kidney damage caused by NSAIDs.
As we discussed earlier, turmeric appears to block and break up brain plaques that cause the disease and helps reverse some of the damage already present. Ibuprofen does not provide any protection against free radical damage. No anti-inflammatory medicine can do this.
Q. If I eat curry will I be protected against Alzheimer’s disease? There aren’t many foods or recipes I make that require curry, do I need to eat it every day? And how much do I need?
A. If you enjoy Indian cuisine, by all means, enjoy these delicious foods. You’ll benefit your brain and your appetite. But you make a good point, American meals rarely contain curry. That’s why supplements that contain extracts are suddenly quite popular. In fact, there are numerous turmeric/curcumin supplements on the market today.
But like all nutritional supplements, some turmeric supplements are superior to others. You need to read their labels to make sure the turmeric extract you are buying will provide the protection you need. Look for high-potency turmeric extract from turmeric (Curcuma longa) rhizome. And make sure the extract is standardized to contain 90% curcuminoids, the active ingredient in turmeric responsible for the positive research findings.
Conclusion
Researchers once thought that preventing for Alzheimer’s disease would elude them for decades. In fact, several scientists privately speculated the disease might never be ameliorated. They thought the origin of the disease was too complex and the symptoms of the disease were too profound.
That’s why ongoing research on turmeric is so exciting. A safe, natural, and effective way to protect against Alzheimer’s disease almost seems too good to be true. But, the nation of
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1535) Spectral RS - new hair regrowth formula from Divine Skin
Date:
July 27, 2006 09:49 AM
For those who are "in the know" Spectral.DNC® has acquired an almost legendary status with a loyal following for one simple reason — it delivers results unlike any other topical treatment in the world. Following in those footsteps the DS Laboratories scientific team has developed a new formula that is conservatively rated for thinning hair and delivers remarkable performance for hair re-growth. Spectral.RS® is a breakthrough formula for the treatment of thinning hair and diffuse hair loss. Spectral.RS® uses a proprietary nanosome technology as the delivery vehicle of active compounds directly into target cells. Spectral.RS® works by improving the nutrition, circulation, and metabolism of the hair follicle and preventing perifollicular Fibrosis.
Spectral RS® should be applied twice per day, whether your hair has been washed or not. Since there is no possibility of side effects, it is possible to apply Spectral RS® three times per day to accelerate the results. With twice per day use, a bottle of Spectral RS® will last approximately 30 days. For best results, it is important to apply Spectral RS® regularly without skipping applications.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1331) The healing power of borage oil
Date:
June 19, 2006 01:27 PM
Borage oil, extracted from the seed of the blue, star shaped borage flower, is gaining much attention by alternative health practitioners and main stream medicine alike for its profound medicinal properties. Whereas the oil is getting all the redit, it is actually the oil’s active component, gamma linoleic acid (GLA), which has drawn the interest of researchers. The majority of the early studies done on GLA, dating back to the late 1940’s, were conducted with the oil of evening primrose. For rezones cited in the title, more bank for the buck, borage seed oil is now thought to be s superior source of GLA compared to evening primrose oil. Other plants forms and food concentrates that contain appreciable amounts of GLA include black currant seed oil and spirulina. Why GLA Supplementation? A body with healthy biochemistry has the ability to produce GLA from the most essential fat linoleic acid. Linoleic acid is found most abundantly in the omega 6 family of oils, including safflower, sunflower, and corn oil. While it has been estimated that a majority of Americans and Europeans consume far to many omega 6 fatty acids in proportion to the beneficial omega 3 fatty acids (by approximately 10:1). Most biochemists agree optimal ratio of omega 6 to omega 3 fatty acids should be approximately 1:1. Despite the obvious over consumption of omega 6 oils rich in linoleic acid, some individuals lack the ability to convert linoleic acid to the much needed GLA. As is the example with many of our modern day nutrient deficiencies, the adulteration of our food supply by today’s processing methods has much to do with the faulty fat metabolism suffered by many. A prime example is the hydrogenation process utilized to convert liquid polyunsaturated oils into semi-solid, altered saturated fats for use as margarine and commercially processed foods. Hydrogenation is accomplished by subjecting the oils to temperatures in excess of 250 C, and bombarding them with hydrogen ions in the presence of the heavy metal nickel, which irreversibly changes the chemical structure of the fatty acid molecule from a healthful “cis” configuration to a dangerous “trans” configuration. When these products are eaten in excess they are known, in some cases, to block the enzymatic conversion of linoleic acid to GLA. In addition to the damaging effects of hydrogenation, certain essential fatty acid nutrient cofactor deficiencies may exist to further complicate the conversion. Vitamins pro-A, A, C, E, B-2, B-3, B-6, pantothenic acid, B-12 biotin and the minerals calcium, magnesium, potassium, sulfur and zinc are all involved in essential fatty acid (EFA) metabolism. Particular interest should be given to those afflicted with diabetes, cystic Fibrosis, asthma, alcoholism, multiple sclerosis. For a myriad of reasons, including cofactor deficiencies, these individuals lack the enzymatic ability to convert linoleic acid to GLA and must obtain a direct source of GLA for proper hormonal regulation. In addition, excessive consumption of animal fats containing acachidonic acid competes for the same metabolic pathways occupied by GLA, thus minimizing its biological action. These potential negating effects can simply be diverted to consuming a food source or supplement containing GLA which bypasses any previously necessary enzymatic conversion and floods the metabolic pathways with beneficial GLA. Nutrient deficiency should also be addressed. Here lies the true power of GLA. Prostaglandins, biochemical regulators Whereas GLA is the power, the prostaglandins deliver the punch in this biological equation. Just as linoleic acid is normally converted to GLA, GLA is further converted into the prostaglandin E1 (PGE1). Many of the benefits derived from GLA supplementation are a result of the hormonal regulatory action of the prostaglandins. Just like the “parent” precursors they are made from, the hormone-like prostaglandins orchestrate a host of important biochemical activities. Their general regulatory effects include the control of arterial muscle tone, sodium excretion through the kidneys, blood platelet “Stickiness,” inflammatory response and the immune function, just to name a few. The list may be endless as scientists continue to discover the regulating effects of prostaglandins. One way in which GLA has shown to decrease the probability of allergic and inflammatory conditions is by competing with arachidomic acid, which when left unchecked may potentiate a hyperimmune response. Healing Power As a result of the powerful regulating effects derived from the conversion of GLA to healthful prostaglandins, borage oil and other GLA supplements have shown to be beneficial in the treatment and relief of many classic and modern day health problems. The disease of diabetes, cystic Fibrosis, asthma, multiple sclerosis are thought to be helped by bringing about a balance in an otherwise faulty fatty acid metabolism. According to a study released in the journal diabetes care, supplementation with GLA has shown promise in the reversal of diabetic neuropathy (a condition where the nerves degenerate and symptoms of pain and numbness follow). The study concluded that all diabetics should be considered for dietary protocol of GLA. Other conditions shown to benefit include high blood pressure, high cholesterol, skin conditions, arthritis, allergies, weight loss, improved behavior of hyperactive children and increased strength of hair and nails. Cited in the book, Super Nutrition For Menopause, written by the renowned nutritionist Ann Louise Gittleman, is one of the most popular applications of GLA supplementation in the relief of menstrual pain. Sufferers use a maintenance does up to the seventh day prior to menstruation, then double the dose for the duration of their menstruation. Dietary restrictions of meat, dairy and eggs during this time has also shown to compliment this regiment. Many would agree with Ms. Gittleman’s credo in allowing mother nature to cure our ails before relying on synthetic drugs which often come with side effects. More Bang for the Buck Now comes the challenge of acquiring a GLA supplement suited to meet your needs. With the help of the information below you may maximize your desired result while at the same time stretching your dollars. Lets take a look at the facts. We will limit out narrative to the tree most popular forms of GLA supplementation: 1) borage oil, 2) evening primrose oil and 3) black current seed oil. Potency is an important factor, as the higher the GLA content per gram, the more likelihood of greater biological activity. Borage oil contains 24% GLA, or 240mg per 1000 mg capsules. Black current seed oil contains 18%, or 180mg per 1000 mg capsule and evening primrose oil contains 10% GLA, or 100mg per 1000 mg capsule. While black currant seed may appear to run a close second to borage and have a slight edge on evening primrose, it contains a potent GLA inhibitor and should be considered last on the list. equally, if not more important than potency, is purity. Make it a practice not to purchase any oil product unless full disclosure of the method of extraction is printed on the label. If it is not, you may assume that the oil has been extracted in one of the following ways. Unfortunately, the popular use of the chemical hexane to extract oils is not required for disclosure. This method employs submerging cracked seed in a gasoline like substance (Hexane) and then slowly allowing it to evaporate off yielding 90% oil recovery. This is the most common method used to extract evening primrose oil because of the incredibly small, hard seed and low oil content. The second creative ploy is the claim that the oil has simply been extracted by a new high-tech method called supercritical fluid extraction (SCFE). This process “pregrinds” the seeds then subjects them to pressures of 6000 – 10000 psi in the presence of the gas CO-2. Under such intense pressure CO-2 gas becomes a liquid in which the seeds are submerged, ultimately yielding a 95% oil recovery. Look for oils that are labeled as “expeller pressed” without the damaging effects of light, heat and oxygen. The products should be contained in opaque (light resistant) bottles to protect them from the damaging effects of light. Optimally, you should find them in the refrigerated section of your local health food store. Due to the higher percentage of oil contained in the borage seed, as compared to evening primrose and black current, borage is typically priced well below the others making it the most potent and economical choice. All things considered an expeller pressed borage oil, contained in an opaque plastic bottle, may provide you the absolute best source of unadulterated GLA supplementation. One company that provides such a product and always fulfills the quality requirements listed is Barlean’s Organic Oils. Their organic flax oil and borage oils are available at VitaNet.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1316) Dr. Verghese, M.D. Liver Detoxifier & Regenerator Fact Sheet
Date:
December 07, 2005 12:16 PM
Dr. Verghese, M.D. Liver Detoxifier & Regenerator Fact Sheet Neil E. Levin, CCN, DANLA 02/10/05 LIKELY USERS: People with exposure to toxins that stimulate liver activity; People with exposure to infections that may have damaged liver tissue KEY INGREDIENT (S): Milk Thistle extract (Silymarin), Glutathione, NAC, Bupleurum extract, Grape Seed Extract, Dandelion Root extract, Artichoke Leaf, Schisandra and about a dozen additional herbs, along with synergistic ingredients MAIN PRODUCT FEATURES: This formula was developed by a physician based on his clinical experience.
Artichoke leaf has antioxidant properties and restores healthy growth to liver cells. Bupleurum may promote normal cell growth, immune function and is a staple of Chinese liver formulas. Dandelion Root may serve as a natural down-regulator of inflammatory chemicals in the body. NAC supports liver Glutathionestores (antioxidant, detoxifier, heavy metal chelator). Schisandra protects liver cells from toxins and may help to regenerate damaged cells. Milk thistle’s antioxidant Silymarin improves liver function tests and protects liver cells against oxidative damage. It also protects liver cells by blocking and removing toxins from the liver. Silymarin aids in regenerating injured liver cells and blocks Fibrosis. OTHER IMPORTANT ISSUES: Samuel Verghese, M.D. (AM), Ph.D., BCIA-EEG, DAAPM, holds a degree in Alternative Medicine and specializes in Nutritional, Ayurvedic and other Alternative Health Solutions. He is certified as a BCIA-EEG Associate Fellow. AMOUNT TO USE: Three or more capsules a day, preferably with meals. COMPLEMENTARY PRODUCTS: Antioxidants (supports liver detoxification), Alpha Lipoic Acid, EGCg Green Tea Extract, Astragalus, medicinal mushrooms (shiitake, reishi), SAM-e (may improve bile flow and promotes methylation to detoxify chemicals), TMG, lecithin, thymus glandular extract, Cordyceps. AVOID: acetaminophen, alcohol, iron supplements (also red meat, fortified flour) CAUTIONS: This formula should not be used by pregnant women, nursing mothers children or those with liver problems unless recommended under the supervision of a healthcare professional. Please notify your physician about your supplement use if you are using any drugs! Disclaimer: These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure or prevent any disease. REFERENCES:
1. Salmi HA, Sarna S. Effect of silymarin on chemical, functional and morphological alterations of the liver. A double-blind controlled study. Scand J Gastroenterol 1982;17:517–21.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=980) CARBON TETRACHLORIDE TESTING AND SILYMARIN 
Date:
July 12, 2005 09:59 AM
CARBON TETRACHLORIDE TESTING AND SILYMARIN Carbon tetrachloride is used in laboratory tests to assess the ability of a substance to actually protect the liver from any potentially damaging compound. Increasing the dosages of carbon tetrachloride takes the liver through fatty infiltration, Fibrosis and eventually cirrhosis. During these tests, administering Milk Thistle extract resulted in effective protection of liver tissue from the toxic effects of the chemical.
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