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NSAIDs vs. Curcumin: Which One Relieves Joint Pain Without Stopping Healing?   
Date:
September 14, 2026 11:22 AM
Comparative Analysis of NSAIDs versus Curcumin in Musculoskeletal Tissue RepairPrimary Biological Mechanisms and Pharmacological TargetsManaging soft tissue and joint injuries presents a persistent therapeutic challenge in musculoskeletal medicine. Acute inflammation triggers pain, localized swelling, and mechanical disability, which routinely drives patients toward pharmacological relief. For decades, nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen, celecoxib, and diclofenac have served as primary clinical interventions. While these synthetic agents effectively extinguish acute pain signals, expanding cellular and clinical research indicates that their biochemical mechanism interrupts the fundamental repair cascades required for long-term connective tissue healing. In contrast, curcumin - a natural polyphenolic compound derived from the rhizomes of Curcuma longa (turmeric) - exhibits a distinct, multi-targeted regulatory profile that calms hyperactive inflammation while protecting the structural components of cartilage and tendon tissue.The functional divergence between these two compounds becomes clear when considering an intuitive mechanical analogy. Tissue trauma resembles damage to a commercial building, where initial inflammation functions as the construction and demolition crew tasked with clearing rubble, stabilizing the foundation, and laying down fresh structural framing. NSAIDs function like abruptly cutting electrical power to the entire work site: the noisy machinery stops instantly and the immediate disturbance ceases, but the construction workers lose the power necessary to clean the debris and erect permanent walls. Conversely, curcumin operates as an experienced site manager: it silences unnecessary chaos and prevents site vandalism while ensuring that the skilled workers - specifically chondrocytes in cartilage and tenocytes in tendons - remain fully active, supplied, and capable of completing the restoration. At the cellular level, NSAIDs exert their effects through the catalytic inhibition of cyclooxygenase enzymes, categorized as constitutive cyclooxygenase-1 (COX-1) and inducible cyclooxygenase-2 (COX-2). Membrane phosphoLipids damaged during injury release arachidonic acid, which COX enzymes convert into pro-inflammatory Lipid mediators known as prostanoids, most notably prostaglandin E2 (PGE2). Nonselective NSAIDs block both isoforms, while selective coxibs specifically target COX-2. By shutting off PGE2 production, NSAIDs rapidly elevate pain thresholds and blunt localized swelling. However, because PGE2 also functions as a vital signaling cue for cellular recruitment, angiogenesis, and cellular proliferation, this total enzymatic shutdown strips local repair cells of the baseline signals required to orchestrate tissue regeneration. Curcumin avoids this indiscriminate pathway paralysis by acting upstream on master transcriptional control switches rather than directly neutralizing isolated enzymes. Its primary therapeutic mechanism centers on the inhibition of Nuclear Factor-kappa B (NF-kB) and Activator Protein-1 (AP-1) signaling networks. Under acute stress or chronic inflammatory loads, the NF-kB protein complex is released from its cytoplasmic inhibitor, IkBa, and translocates directly into the cell nucleus, where it drives the transcription of catabolic cytokines such as interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-a), and interleukin-6 (IL-6). Curcumin blocks the phosphorylation and degradation of IkBa, effectively keeping NF-kB trapped in the cytoplasm. By preventing this nuclear entry, curcumin attenuates the expression of pro-inflammatory cytokines and downstream matrix-degrading enzymes while preserving baseline physiological functions. Furthermore, curcumin activates the nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidant response element (ARE) pathways, which upregulate endogenous cellular antioxidants to neutralize destructive reactive oxygen species (ROS) that induce cell death in injured joints.
The Mechanisms of NSAID-Induced Inhibition in Cartilage and Tendon RepairArticular cartilage and tendons are specialized, bradytrophic connective tissues characterized by relatively low basal metabolic rates and limited endogenous vascular supplies. These physical constraints make their cellular maintenance highly vulnerable to pharmaceutical disruptions. When synthetic compounds impair cell migration, survival, or extracellular matrix secretion, the intrinsic repair capacity of these structures is substantially degraded.Cartilage maintenance depends on chondrocytes, the sole cell type residing within articular joints, which are responsible for generating and maintaining the extracellular matrix of Type II collagen and water-binding proteoglycans such as aggrecan. Because adult articular cartilage lacks a direct vascular network, major defect repair relies heavily on the recruitment and chondrogenic differentiation of subchondral mesenchymal stem cells (MSCs) through endochondral ossification. Experimental evaluations demonstrate that systemic or intra-articular NSAID exposure halts this regenerative differentiation. Both nonselective NSAIDs and selective COX-2 inhibitors interfere with chondrocyte maturation and prevent successful tissue integration following cartilage transplantation or microfracture procedures. At the cellular level, common NSAIDs - including indomethacin, ketorolac, and diclofenac - induce cell cycle arrest in chondrocytes by blocking transition from the resting G0 phase to the proliferative G1. phase, substantially reducing viable cell numbers. Concurrently, NSAIDs downregulate Bone Morphogenetic Protein-2 (BMP-2), an essential anabolic signaling molecule that orchestrates matrix synthesis. Histological analyses in animal models reveal that NSAID administration causes a marked loss of extracellular proteoglycan content and widespread chondrocyte depletion, yielding elevated modified Mankin scores that signify advanced structural degeneration. In layman's terms, proteoglycans serve as water-absorbing structural sponges that grant cartilage its elastic shock absorption. When NSAIDs deplete these molecules, the joint surface dries out, becomes brittle, and rapidly wears down under routine mechanical friction. Tendon healing is similarly susceptible to disruption by NSAIDs. Tendons operate as high-tensile structural cables composed of longitudinally arranged Type I collagen fibers, maintained by specialized fibroblasts termed tenocytes and tenoblasts. Healing after acute rupture or chronic tear progresses through an initial inflammatory phase, followed by a proliferative phase of cell migration, and culminates in a lengthy remodeling phase of collagen alignment. In vitro and in vivo studies establish that NSAIDs directly suppress the migration and proliferative capacity of tenocytes during the critical early healing window. Without an adequate cellular workforce migrating into the wound bed, provisional collagen scaffolding cannot be synthesized effectively. The disruption is particularly pronounced at the enthesis, the specialized fibrocartilaginous junction where soft tendon inserts into rigid bone. Re-establishing this transition zone requires coordinated bone remodeling and chondrogenic differentiation, both of which are hindered by COX inhibition. In animal rotator cuff repair models, early administration of NSAIDs significantly delays collagen fiber organization and impairs mechanical integration at the insertion site, resulting in a measurable decline in load-to-failure strength and overall tendon toughness. Furthermore, while prolonged inflammation contributes to pathological degeneration, the transient synthesis of PGE2 during the initial hours following injury is essential for regulating localized microvascular flow and hyperemic nutrient delivery. By eliminating this early prostanoid pulse, NSAIDs starve the repair zone of oxygen and circulating factors precisely when the cellular metabolic demand is highest. Beyond direct biochemical cytotoxicity, systemic NSAIDs introduce a physical hazard known as analgesic arthropathy. In musculoskeletal biomechanics, pain functions as a protective feedback mechanism, forcing the patient to unload an injured joint or limb to prevent structural overload. By effectively blunting the pain reflex while simultaneously undermining the cellular synthesis of proteoglycans and collagen, NSAIDs create a deceptive state of perceived recovery. Patients prematurely resume unrestricted weight-bearing and strenuous activity, placing substantial, uncompensated mechanical forces onto compromised cartilage surfaces and unhealed tendon fibers. Over time, this recurring mechanical trauma accelerates joint space narrowing, promotes microfractures in the subchondral plate, and hastens functional joint breakdown. Chondroprotective and Tenogenic Mechanisms of CurcuminIn sharp contrast to the suppressive actions of synthetic COX inhibitors, curcumin exhibits a tissue-sparing, pro-regenerative biological profile. Rather than paralyzing cellular metabolism, curcumin modulates the microenvironment by suppressing destructive catabolic enzymes while supporting the baseline anabolic signals required for cartilage and tendon reconstruction.In articular cartilage, curcumin acts as a direct chondroprotective agent by dismantling the catabolic cascade induced by pro-inflammatory cytokines. When joint tissues are exposed to elevated IL-1ß and TNF-a, chondrocytes are provoked to synthesize matrix metalloproteinases - specifically collagenases such as MMP-1, MMP-3, and MMP-13 - along with aggrecanases like ADAMTS5. These enzymes function like enzymatic shears, systematically slicing through structural Type II collagen strands and degrading aggrecan cores. Curcumin suppresses the transcription and secretion of MMP-1, MMP-3, MMP-13, and ADAMTS5 by neutralizing NF-kB and AP-1 activation. Concurrently, it upregulates Cbp/p300 Interacting Transactivator with ED-rich tail 2 (CITED2), an essential transcriptional regulator that represses matrix metalloproteinases at the genomic level. In addition to halting extracellular degradation, curcumin protects chondrocytes from inflammatory apoptosis. Exposure to oxidative stress and inflammatory cytokines typically triggers programmed cell death by activating the intrinsic caspase cascade. Curcumin suppresses this apoptotic pathway by reducing the cleavage of executioner caspase-3, downregulating the pro-apoptotic factor Bax, and elevating anti-apoptotic Bcl-2 expression. Microscopic and histological analyses of osteoarthritic cartilage treated with curcumin consistently show robust Safranin O staining, intact surface regularity, preserved chondrocyte density, and significantly reduced Osteoarthritis Research Society International (OARSI) degradation scores. Within tendon biology, curcumin promotes active tissue regeneration (tenogenesis) rather than inert scar formation. In animal models of tendon rupture and surgical repair, curcumin guides tendon-derived stem and progenitor cells (TSPCs) toward mature tenocyte differentiation. This lineage-specific differentiation is orchestrated primarily through activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and Wnt/ß-catenin signaling cascades. As stem cells commit to the tenogenic pathway, they significantly upregulate crucial structural and phenotypic markers, including epithelial cell adhesion molecule (EpCAM), tenomodulin, and the master tendon transcription factor Scleraxis. Through this guided differentiation, curcumin supports the preferential synthesis and organized deposition of high-tensile Type I collagen fibers, the primary architectural building blocks of healthy tendons. Injured tendons typically fill with disorganized, loose Type III collagen, which forms a structurally inferior, compliant scar. Curcumin supplementation promotes the progressive maturation from primitive Type III collagen to densely packed, parallel Type I collagen fibrils, restoring native tensile strength and mechanical breaking force. A major clinical challenge following tendon surgery is the development of peritendinous adhesions, in which excessive fibrotic scar tissue binds the healing tendon to its synovial sheath, restricting range of motion and joint gliding. Postoperative tendon repair involves a balance between extrinsic healing (in which exterior fibroblasts infiltrate the defect and deposit messy scar tissue) and intrinsic healing (in which tenocytes within the tendon substance reconstruct the matrix). Curcumin suppresses excessive peritendinous inflammation and extrinsic fibrosis while accelerating intrinsic tenocyte repair. Biomechanical testing confirms that local or systemic curcumin administration yields lower adhesion scores, increased gliding distances, and superior functional mobility without sacrificing structural load-bearing capacity. Comparative Clinical Efficacy and Systemic Safety ProfilesTranslating cellular findings into clinical practice requires weighing therapeutic outcomes against systemic safety profiles. While synthetic NSAIDs deliver potent, rapid analgesia during acute musculoskeletal pain events, their chronic administration is constrained by systemic toxicities across multiple organ systems.In randomized, active-controlled clinical trials of knee osteoarthritis, optimized curcumin preparations have demonstrated clinical pain reduction and functional recovery comparable to standard therapeutic doses of NSAIDs. In a randomized, open-label parallel-arm study evaluating 139 patients with symptomatic knee osteoarthritis, subjects received either 500 mg of a bio-enhanced curcumin extract three times daily or 50 mg of diclofenac sodium twice daily for 28 consecutive days. Patients treated with curcumin demonstrated comparable improvements in pain intensity on the Visual Analogue Scale (VAS) and functional scores on the Knee Injury and Osteoarthritis Outcome Score (KOOS) at days 14 and 28, showing no statistically significant difference in therapeutic efficacy compared to diclofenac. However, the systemic tolerability profiles between the treatments diverged markedly. Overall adverse events occurred in only 13% of the curcumin group compared to 38% of the diclofenac cohort. In the diclofenac arm, 28% of patients developed dyspeptic symptoms severe enough to require concurrent treatment with H2-receptor antagonists or proton pump inhibitors to prevent mucosal ulceration, whereas no patients in the curcumin cohort required gastroprotective intervention. Furthermore, the curcumin cohort experienced a significant reduction in flatulence and digestive discomfort, demonstrating beneficial gastric and intestinal cytoprotective effects. These safety observations are consistent across broader systematic reviews and meta-analyses. Nonsteroidal anti-inflammatory agents inherently compromise gastrointestinal integrity by systematically depleting cytoprotective prostaglandins, leaving the gastric epithelium vulnerable to acid erosion and hemorrhage. In addition, systemic inhibition of renal and vascular COX enzymes by NSAIDs reduces renal perfusion and disrupts the balance between prostacyclin and thromboxane, elevating the risk of fluid retention, hypertension, and adverse cardiovascular thrombotic events. Curcumin does not suppress these physiological prostanoid pathways, making it free from ulcerogenic, nephrotoxic, and cardiotoxic properties at therapeutic dosages.
A longstanding limitation of standard curcumin supplementation in clinical settings has been its low oral bioavailability. Native curcuminoids are highly lipophilic, poorly soluble in aqueous gastric fluids, and subject to rapid hepatic and intestinal phase II metabolism into inactive glucuronides and sulfates, leading to swift biliary and fecal excretion. Consequently, raw culinary turmeric powders struggle to achieve the therapeutic systemic circulating concentrations required to reach poorly vascularized joint and tendon compartments. Modern pharmacognosy has addressed this pharmacodynamic hurdle through advanced delivery formulations. Modern strategies - such as co-administration with the natural alkaloid piperine (which inhibits hepatic glucuronidation), micellar dispersions, phytosomal phosphoLipid complexes, and bio-enhanced submicron dispersions - elevate systemic blood bioavailability by ten- to thirty-fold compared to unformulated extracts. These modern delivery platforms ensure that therapeutic concentrations reach synovial fluid, subchondral bone, and fibrous tendon sheaths without requiring excessive oral dosing. Conclusions and Translational Clinical ImplicationsThe biological and clinical evidence reveals distinct physiological paths for NSAIDs and curcumin in orthopedic recovery. While NSAIDs remain powerful tools for the brief alleviation of acute, unmanageable pain, their ongoing administration during active tissue healing presents substantial biological compromises. Tendons and cartilage require a controlled, transient inflammatory cascade to signal cell recruitment, stimulate stem cell differentiation, and direct extracellular matrix synthesis. By completely shutting down cyclooxygenase enzymes and depleting local prostaglandins, NSAIDs disrupt this regenerative cascade. The resulting cellular consequences - including chondrocyte cell cycle arrest, proteoglycan loss, suppression of tenocyte migration, and weakened collagen tensile strength at the tendon-to-bone interface - demonstrate that pain relief from NSAIDs frequently comes at the cost of the structural integrity of healing connective tissues.In contrast, curcumin provides a tissue-preserving alternative that decouples pain and inflammation control from cellular suppression. Operating upstream at the level of NF-kB and AP-1 transcriptional activation, curcumin attenuates the expression of pro-inflammatory cytokines while leaving the physiological baseline of cellular metabolism intact. In cartilage, it actively represses the matrix-degrading enzymes MMP-1, MMP-3, MMP-13, and ADAMTS5, maintains water-binding proteoglycan content, and protects chondrocytes from inflammatory apoptosis. In damaged tendons, curcumin stimulates tenogenic differentiation of local stem cells via PI3K/Akt signaling, supports the proper maturation of dense Type I collagen fibers, and prevents restrictive peritendinous scar adhesions, preserving both joint mobility and mechanical breaking strength. From a translational perspective, these findings indicate that clinical protocols should reconsider relying on continuous NSAIDs as the default intervention for connective tissue injuries, post-surgical recovery, and chronic degenerative conditions. Where synthetic NSAIDs are deemed necessary, their use should be confined to short-term acute flare-ups to avoid interrupting early tissue remodeling. For long-term joint preservation, ongoing tendinopathy rehabilitation, and chronic osteoarthritis management, optimized bio-enhanced curcumin formulations deliver pain relief and functional restoration comparable to conventional pharmaceuticals, all while preserving the biological processes required for lasting musculoskeletal repair. References: NSAID therapy effects on healing of bone, tendon, and the enthesis The Detrimental Effects of Systemic Ibuprofen Delivery on Tendon Conservative management of symptomatic knee osteoarthritis - PMC Positives and negatives of nonsteroidal anti-inflammatory drugs in (PDF) Conservative management of symptomatic knee osteoarthritis Non-steroidal anti-inflammatory drugs influence cartilage healing Is Curcumine Useful in the Treatment and Prevention of ... - PMC - NIH Efficacy and mechanisms of curcumin in the treatment of osteoarthritis Biological actions of curcumin on articular chondrocytes - PubMed Curcumin slows osteoarthritis progression and relieves ... - PMC - NIH Do Nonsteroidal Anti-Inflammatory Drugs Have a Deleterious Effect Anti-inflammatory management for tendon injuries - friends or foes? The mechanistic role of curcumin on matrix metalloproteinases in Therapeutic effects of turmeric or curcumin extract on pain and Curcumin inhibits chondrocyte apoptosis and inflammation in ... - PMC Analysis of the mechanism of curcumin against osteoarthritis using Synergistic enhancement of tendon-to-bone healing via anti ... - PMC A Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial Safety and efficacy of curcumin versus diclofenac in knee osteoarthritis A randomized, pilot study to assess the efficacy and safety ... - PubMed Effectiveness of curcuminoids in the treatment of knee osteoarthritis THE EFFECTS OF TRADITIONAL STRENGTHENING EXERCISES Putting Some Muscle into Osteoarthritis | Annals of Internal Medicine Do Nonsteroidal Anti-Inflammatory Drugs Have a Deleterious Effect Calebin A, a Compound of Turmeric, Down-Regulates Inflammation The Effect of Non-Steroidal Anti-Inflammatory Drugs on Tendon-to Chiropractor in Toronto, ON, Canada :: Head and Neck Pain Investigation of the association of long-term NSAID use with ... - PMC Curcumin Improves Functional Recovery of Ruptured Tendon by Chemically modified curcumin (CMC2.24) alleviates osteoarthritis Curcumin improves age-related and surgically induced osteoarthritis (PDF) Curcumin Improves Functional Recovery of Ruptured Tendon Investigation of the effects of umbilical cord-derived mesenchymal Effect of curcumin-loaded polycaprolactone scaffold on Achilles Controlled release of curcumin from curcumin-loaded nanomicelles Efficacy and safety of combination of curcuminoid complex ... - PMC The efficacy of Curcuma Longa L. extract as an adjuvant therapy in
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6653) The Ultimate Guide to Cellular Longevity: NAD+, Methylation, and Senolytics 
Date:
September 10, 2026 10:57 AM
Introduction: Understanding Cellular Aging and Energy DeclineBiological aging represents a progressive decline in cellular maintenance, structural repair, and energy generation. Over decades, tissues experience an attrition of functional reserves, compromised stress resilience, and persistent low-grade systemic inflammation. At the cellular scale, biological degeneration is driven by a failure to generate bioenergetic fuel, repair genetic code, and clear metabolic waste.Cellular aging is characterized by interconnected biological disruptions known as the hallmarks of aging. These encompass genomic instability, epigenetic alterations, mitochondrial decay, loss of proteostasis, and cellular senescence. Rather than operating as isolated occurrences, these phenomena establish a self-reinforcing degenerative cycle: declining cellular power generation impairs enzymatic genetic repair, promoting the accumulation of damaged cells that enter irreversible growth arrest and poison surrounding healthy tissues. Mitigating cellular aging requires examining how microscopic bioenergetic pathways deteriorate and evaluating how targeted nutritional and biochemical interventions can restore cellular homeostasis. The Role of Mitochondria and ATP ProductionEvery biological function - from muscular contraction to continuous DNA replication - depends on adenosine triphosphate (ATP), the primary biochemical energy currency of living systems. Cells produce the vast majority of this energy within mitochondria through oxidative phosphorylation. Within these specialized organelles, metabolic intermediates derived from dietary carbohydrates and Lipids donate high-energy electrons to the electron transport chain. The flow of these electrons across protein complexes establishes an electrochemical proton gradient across the inner mitochondrial membrane, driving ATP synthase to manufacture ATP.A youthful cell functions like an efficient municipal power grid, dynamically matching energetic demands with immediate ATP output. However, as biological aging progresses, mitochondrial efficiency declines. The electron transport chain becomes structurally leaky, inadvertently shedding electrons that react with ambient molecular oxygen to produce reactive oxygen species (ROS). While regulated levels of ROS participate in vital intracellular signaling, chronic excess induces widespread oxidative stress. Mitochondria are exceptionally vulnerable to this oxidative burden because they carry their own circular genetic material, known as mitochondrial DNA (mtDNA). Unlike nuclear DNA, mtDNA lacks the protective shielding of histone proteins and possesses rudimentary repair systems. As a result, mtDNA sustains cumulative oxidative damage, encoding increasingly defective electron transport chain proteins. This dynamic generates a bioenergetic deficit: degraded mitochondria synthesize progressively less ATP while emitting greater volumes of damaging free radicals. Deprived of optimal ATP reserves, cells lack the energy necessary to drive vital enzymatic repair cascades, accelerating structural degeneration and functional exhaustion. How Cellular Senescence Accelerates the Aging ProcessWhen healthy cells confront critical physiological damage - such as severe telomere attrition, persistent DNA double-strand breaks, or oxidative stress - they activate protective cell cycle arrest pathways governed primarily by the p53/p21^CIP1 and p16^INK4a/Rb molecular checkpoints. This defensive shutdown, termed cellular senescence, permanently prevents the replication of potentially premalignant or mutated cells.Senescent cells, colloquially known as "zombie cells," enter a state of permanent growth arrest while actively resisting programmed cell death (apoptosis). Over time, these cells accumulate within adipose depots, skeletal muscle, the vascular endothelium, and major organs, largely because immune surveillance and clearance pathways simultaneously lose functional efficiency. The systemic danger of senescent cells stems from their secretome. Rather than remaining biologically inert, senescent cells develop a hyperactive secretory state termed the Senescence-Associated Secretory Phenotype (SASP). The SASP is a destructive mixture of pro-inflammatory cytokines, chemokines, extracellular matrix-degrading matrix metalloproteinases (MMPs), and reactive oxygen species. Through this toxic secretome, even a small burden of senescent cells can impair whole-tissue architecture. SASP factors degrade surrounding structural proteins, induce insulin resistance in neighboring metabolic cells, and biochemically force adjacent healthy cells into secondary senescence. This persistent paracrine signaling fuels chronic, sterile, low-grade systemic inflammation, termed "inflammaging," which accelerates systemic tissue degeneration and elevates susceptibility to degenerative age-related pathologies. Nicotinamide Riboside (NR) and the NAD+ Salvage PathwayThe Biochemistry of NAD+ Depletion Over TimeNicotinamide adenine dinucleotide (NAD+) is an indispensable coenzyme present in every living cell. NAD+ fulfills a dual biological mandate: it serves as a central redox cofactor that shuttles electrons between cellular metabolic reactions, and it functions as an obligatory consumable substrate for regulatory enzymes that preserve cellular viability. In its redox capacity, NAD+ accepts electrons to form NADH during glycolysis, the tricarboxylic acid (TCA) cycle, and fatty acid beta-oxidation, subsequently donating those electrons to Complex I of the respiratory chain to power ATP synthesis.
The primary enzymatic driver of age-related NAD+ destruction is CD38, a membrane-bound glycohydrolase expressed on immune cells that is upregulated in response to chronic SASP exposure. Concurrently, lifelong genotoxic damage causes persistent activation of Poly(ADP-ribose) polymerase 1 (PARP-1), an enzyme that cleaves the glycosidic bonds of NAD+ to assemble branched poly(ADP-ribose) chains at DNA lesion sites. Because PARP-1 consumes NAD+ without directly recycling the molecule, chronic DNA damage depletes intracellular NAD+ pools, impairing bioenergetics and limiting sirtuin activity. How NR Efficiently Boosts Cellular NAD+ LevelsThe mammalian body maintains its NAD+ supply through three distinct biosynthetic routes: the de novo pathway from dietary L-tryptophan, the Preiss-Handler pathway from nicotinic acid (niacin), and the NAD+ Salvage Pathway. The de novo pathway requires substantial energy expenditure, consuming roughly sixty milligrams of dietary tryptophan to yield a single milligram of NAD+. The Preiss-Handler pathway, while effective, can induce cutaneous prostaglandin-mediated flushing at therapeutic intakes. Consequently, the salvage pathway serves as the primary mechanism for maintaining intracellular NAD+ pools.The salvage pathway recycles the breakdown product nicotinamide (NAM), which is released whenever NAD+-consuming enzymes execute their functions. Under normal conditions, cells convert free nicotinamide into nicotinamide mononucleotide (NMN) via the rate-limiting enzyme nicotinamide phosphoribosyltransferase (NAMPT), after which NMN adenylyltransferases (NMNAT1–3) complete the conversion into NAD+. However, NAMPT expression declines with advancing age, chronic inflammation, and metabolic stress, limiting the recycling capacity of the cell. Nicotinamide Riboside (NR) is a naturally occurring pyridine nucleoside that bypasses this enzymatic bottleneck. Upon cellular entry via equilibrative nucleoside transporters, NR is directly phosphorylated into NMN by nicotinamide riboside kinases (NRK1 and NRK2) using a single molecule of ATP. Because the NRK pathway remains intact and robust across the lifespan, NR provides an efficient alternative entry point into the NAD+ salvage cascade. Clinical evaluations in humans confirm the safety, bioavailability, and pharmacokinetics of oral NR supplementation. Randomized, double-blind, placebo-controlled trials reveal that oral NR chloride produces dose-dependent increases in steady-state whole blood NAD+ concentrations. Dosing regimens of 100 mg, 300 mg, and 1,000 mg daily elevate blood NAD+ levels by approximately 22%, 51%, and up to 142%, respectively, within two weeks of administration, maintaining these elevations throughout continuous use. High-resolution metabolomic analyses also demonstrate parallel elevations in nicotinic acid adenine dinucleotide (NAAD), establishing it as a reliable biomarker of active intracellular NAD+ synthesis without hepatic or systemic toxicity. Sirtuin Activation and DNA Repair MechanismsReplenishing intracellular NAD+ supports functions beyond mitochondrial ATP generation. NAD+ functions as an obligatory cofactor for sirtuins (SIRT1 through SIRT7), a family of class III histone and non-histone protein deacetylases that regulate stress resilience, metabolic homeostasis, and cell survival. Sirtuins couple the removal of acetyl groups from target lysine residues to the stoichiometric cleavage of NAD+, producing nicotinamide and O-acetyl-ADP-ribose. In states of NAD+ deficiency, sirtuin enzymes remain inactive regardless of cellular demand.In the nucleus, SIRT1 coordinates defense against cellular decline. When activated by restored NAD+ levels, SIRT1 deacetylates peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1a), the master transcriptional coactivator of mitochondrial biogenesis. This deacetylation stimulates mitochondrial replication and assembly, expanding functional respiratory capacity. Concurrently, SIRT1 deacetylates the p65 subunit of nuclear factor-kappa B (NF-kB), suppressing the transcription of pro-inflammatory cytokines. In the mitochondria, SIRT3 utilizes NAD+ to deacetylate metabolic enzymes and superoxide dismutase 2 (SOD2), enhancing the organelle's capacity to neutralize reactive oxygen species. At the same time, cellular NAD+ levels directly regulate genomic integrity through PARP-1. When genotoxic stress or oxidative damage induces single- or double-strand DNA breaks, PARP-1 binds to the damaged termini using its zinc-finger domains. Bound PARP-1 hydrolyzes NAD+ to synthesize extensive, negatively charged poly(ADP-ribose) polymers on itself and adjacent histones. This modification relaxes chromatin architecture and establishes an electrostatic scaffold that recruits base excision repair and homologous recombination complexes. Recent discoveries demonstrate close crosstalk between sirtuins and PARP-1 during DNA repair. PARP-1 recruits SIRT1 to double-strand breaks, where SIRT1 deacetylates the chromatin-remodeling ATPase BRG1 to displace nucleosomes and facilitate homologous recombination. However, because PARP-1 and SIRT1 draw from the same intracellular NAD+ pool, severe NAD+ depletion forces a biological compromise: PARP-1 consumes the scarce remaining cofactor to address DNA damage, leaving sirtuins deactivated. Restoring NAD+ via NR prevents this deficit, enabling concurrent genomic repair and sirtuin-mediated metabolic defense. Quercetin: A Powerful Senolytic and mTOR RegulatorClearing Senescent "Zombie" Cells from TissuesThe accumulation of senescent cells has driven interest in senolytics: molecules that selectively eliminate senescent cells while sparing healthy, non-senescent populations. Senolytic agents exploit a specific vulnerability in senescent cells. Because senescent cells produce cytotoxic, pro-inflammatory SASP factors that would normally induce their own death, they become dependent on upregulated Senescent Cell Anti-Apoptotic Pathways (SCAPs) to survive. The SCAP network involves anti-apoptotic proteins (such as BCL-2 and BCL-xL), the PI3K/Akt kinase cascade, and cyclin-dependent kinase inhibitors.Quercetin is a polyphenolic flavonoid found in capers, red onions, apples, and the flower buds of Sophora japonica. Beyond its classical antioxidant properties, quercetin functions as a senolytic compound that exerts multi-target inhibitory effects across the SCAP network. By inhibiting the upstream PI3K/Akt survival axis and downregulating anti-apoptotic defenses, quercetin disrupts the signaling that protects senescent cells from intrinsic apoptosis. Deprived of these survival signals, senescent cells undergo programmed cell death. Preclinical studies demonstrate that senolytic protocols utilizing quercetin - often combined with the tyrosine kinase inhibitor dasatinib - reduce senescent cell burden across multiple tissues. This targeted clearance lowers circulating SASP factors, attenuates tissue fibrosis, restores endothelial reactivity, and improves functional health span. By removing senescent cells, quercetin mitigates the primary driver of chronic, low-grade inflammaging. Modulating the mTOR Pathway for Optimal AutophagyThe mechanistic Target of Rapamycin (mTOR) is an evolutionarily conserved serine/threonine protein kinase that coordinates cellular metabolism by balancing anabolic growth with catabolic recycling. Operating within two multiprotein complexes - mTORC1 and mTORC2 - the mTOR pathway integrates signals from amino acids, growth factors, and intracellular energy levels. In nutrient-rich environments, mTORC1 promotes protein synthesis, lipogenesis, and cellular growth, while suppressing catabolic breakdown. Conversely, nutrient scarcity downregulates mTORC1, activating autophagy.Autophagy is an intracellular degradation system that packages damaged organelles, misfolded protein aggregates, and biological debris into double-membraned autophagosomes for lysosomal degradation and recycling. A specialized branch of this pathway, mitophagy, selectively targets and clears damaged mitochondria. In modern metabolic conditions characterized by continuous caloric intake, mTORC1 can remain persistently active. This persistent signaling suppresses autophagy, causing damaged organelles and toxic aggregates to accumulate within tissues. Quercetin functions as a natural modulator of mTOR signaling. By inhibiting upstream PI3K/Akt signaling and activating intracellular energy sensors, quercetin attenuates overactive mTORC1, mimicking the metabolic effects of caloric restriction. This down-regulation relieves inhibition on the ULK1 autophagy initiation complex, stimulating both general autophagy and mitophagy. As autophagy proceeds, cells clear protein aggregates and eliminate damaged mitochondria, supporting cellular longevity and proteostasis. Enhancing Absorption: Phytosomes and Dietary FatsDespite the biological activities of quercetin identified in experimental models, its clinical translation has historically been limited by poor oral bioavailability. Raw quercetin aglycone is a crystalline, hydrophobic polyphenol with poor solubility in water and gastrointestinal fluids. When ingested in unformulated powder forms, quercetin molecules aggregate in the gut lumen, resisting dissolution and passive absorption. Consequently, the vast majority of an unformulated dose passes into the colon unabsorbed, where it undergoes microbial degradation without reaching meaningful systemic concentrations.To address these pharmacokinetic limitations, advanced delivery systems such as phytosomes were engineered. A phytosome is a 100% food-grade molecular complex where individual polyphenolic molecules are bound to dietary phosphoLipids, typically sunflower-derived phosphatidylcholine. Unlike a classical liposome - which encapsulates water-soluble compounds inside an aqueous core enclosed by a Lipid bilayer - a phytosome forms an amphiphilic complex at the molecular level. The polar head of the phosphatidylcholine molecule forms hydrogen bonds with the hydroxyl groups of the quercetin molecule, while its lipophilic fatty acid tails extend outward. This structural arrangement shields the polar regions of the flavonoid, creating a Lipid-compatible complex that integrates smoothly into the intestinal mucosa.
The Importance of Methylation in Healthy AgingVitamin B-Complex and Choline as Essential Methyl DonorsMethylation is an essential biochemical process occurring billions of times each second across all human tissues. It involves the transfer of a single-carbon unit - a methyl group consisting of one carbon atom bound to three hydrogen atoms - (CH3) - from a donor molecule to diverse recipients, including DNA, RNA, structural proteins, neurotransmitters, and membrane phosphoLipids. This transfer of one-carbon units is coordinated by the methionine-homocysteine cycle, which sustains genetic stability, detoxification pathways, and cellular repair.At the center of this pathway sits S-adenosylmethionine (SAM), the universal methyl donor in human biology. When a methyltransferase enzyme transfers a methyl group from SAM to an acceptor molecule, SAM is converted into S-adenosylhomocysteine (SAH). SAH functions as a potent competitive inhibitor of intracellular methyltransferases. To maintain functional methylation, SAH is rapidly hydrolyzed into homocysteine, a sulfur-containing amino acid that must be remethylated or cleared through transsulfuration. Homocysteine clearance proceeds through two distinct remethylation pathways. The primary route operates across most tissues via the enzyme methionine synthase, which requires vitamin B12 in its active methylcobalamin form. Methionine synthase transfers a methyl group from 5-methyltetrahydrofolate (5-MTHF, the active form of folate) to homocysteine, regenerating methionine. The ongoing production of 5-MTHF depends on the enzyme methylenetetrahydrofolate reductase (MTHFR), which utilizes riboflavin (vitamin B2) as a cofactor. Alternatively, excess homocysteine can be routed into the transsulfuration pathway by vitamin B6 (as pyridoxal-5'-phosphate) to synthesize cystathionine, cysteine, and ultimately the antioxidant glutathione. A secondary remethylation pathway, active predominantly in hepatic and renal tissues, bypasses folate entirely. In this route, dietary choline is oxidized to betaine (trimethylglycine or TMG). The enzyme betaine-homocysteine S-methyltransferase (BHMT) then transfers a methyl group from betaine directly to homocysteine, yielding methionine and dimethylglycine. When dietary intake of active B-vitamins or choline is insufficient, or when genetic variations like MTHFR polymorphisms reduce pathway flux, the methylation cycle slows. Homocysteine accumulates in circulation, promoting vascular and neurological inflammation, while SAM reserves decline, restricting cellular methylation capacity. Understanding DNA Methylation and Epigenetic HealthEvery somatic cell in an organism carries an identical genetic code. Cellular differentiation and tissue-specific functions are governed by the epigenome: a regulatory layer of chemical modifications that dictates gene expression without altering underlying DNA sequences. DNA methylation represents the primary and most stable epigenetic modification. In this process, DNA methyltransferase (DNMT) enzymes utilize methyl groups donated by SAM to add a methyl tag to cytosine bases adjacent to guanine residues, forming 5-methylcytosine within CpG dinucleotide sites.Under physiological conditions, DNA methylation maintains genomic stability and coordinates transcription. Methylation of promoter regions condenses chromatin, repressing transposable elements and silencing genes inappropriate for a given cell type. Conversely, hypomethylated promoters maintain an open chromatin state, allowing transcription factors to bind and initiate gene expression. During biological aging, this epigenetic landscape undergoes progressive dysregulation, a phenomenon termed "epigenetic drift". Aging cells experience global hypomethylation alongside focal hypermethylation of specific gene promoters. Global loss of methyl tags destabilizes the genome, activating retrotransposons and pro-inflammatory pathways. Simultaneously, hypermethylation at targeted promoter sites silences critical tumor suppressor genes and DNA repair complexes. This systematic change in DNA methylation patterns is consistent across populations, allowing researchers to develop molecular "epigenetic clocks". Algorithms such as the Horvath clock, PhenoAge, and GrimAge quantify biological age by profiling the methylation status of specific CpG sites across the genome. These clocks assess whether individuals are aging faster or slower than their chronological years. Ensuring a steady supply of methyl donors and preventing unnecessary SAM depletion supports DNMT activity, maintaining epigenetic patterns and genomic stability. How the Methylation Cycle Impacts Energy and Cognitive FocusBeyond long-term epigenetic regulation, the methylation cycle directly modulates immediate biochemical processes that govern daily energy, neurotransmission, and cognitive focus. Compromised methylation capacity frequently manifests as cognitive slowing, executive fatigue, and reduced physical stamina.A major consumer of methyl reserves is the endogenous synthesis of creatine. Approximately 40% of all SAM-derived methyl groups in the human body are utilized by guanidinoacetate N-methyltransferase (GAMT) in the liver to synthesize creatine. Creatine then translocates to the brain and skeletal muscle, where it is phosphorylated into phosphocreatine. Phosphocreatine functions as a rapid energy buffer, donating a high-energy phosphate group to regenerate ADP into ATP in milliseconds during demanding physical or cognitive tasks. When methyl donor availability falls, endogenous creatine synthesis drops, depleting phosphocreatine reserves and increasing susceptibility to neuromuscular and cognitive fatigue. Methylation is equally central to central nervous system architecture. SAM provides methyl groups to convert phosphatidylethanolamine into phosphatidylcholine, the predominant phosphoLipid comprising neuronal cell membranes and the myelin sheaths that insulate axons. Intact myelin preserves rapid action potential conduction throughout the nervous system. Furthermore, free choline derived from this pathway is the direct precursor to acetylcholine, the neurotransmitter required for attention, working memory, and learning. The methylation cycle also governs monoamine neurotransmitter metabolism. SAM is required for the synthesis of adrenaline (epinephrine) from noradrenaline, while catechol-O-methyltransferase (COMT) relies on SAM to degrade dopamine and norepinephrine within the prefrontal cortex. Sluggish methylation disrupts this balance, contributing to cognitive fatigue, mood variability, and impaired mental performance. Building a Comprehensive Longevity ProtocolSynergizing NR, Quercetin, and Methylated B-VitaminsLongevity supplementation often falters when single molecules are administered in isolation, ignoring interconnected metabolic pathways. Designing an effective cellular longevity protocol requires combining complementary mechanisms that reinforce one another while preventing secondary metabolic deficits. The combination of Nicotinamide Riboside, Quercetin Phytosome, and Methylated B-Vitamins illustrates this multi-target synergy.This synergy is grounded in the direct biochemical intersection between the NAD+ salvage pathway and the methylation cycle. When high-dose NR is supplemented to boost systemic NAD+, sirtuins and PARP enzymes consume the newly synthesized cofactor, generating substantial quantities of free nicotinamide (NAM). This intracellular nicotinamide faces two primary metabolic fates: it can be recycled back into NAD+ through the NAMPT-dependent salvage loop, or it can be cleared via methylation. When the influx of nicotinamide exceeds salvage recycling capacity, the excess is cleared to avoid feedback inhibition of sirtuin enzymes. To accomplish this, the enzyme nicotinamide N-methyltransferase (NNMT) transfers a methyl group from SAM directly onto nicotinamide, forming 1-methylnicotinamide (1-MNA/MNAM), which is subsequently excreted in urine. Prolonged, high-dose precursor administration without nutritional methyl support can elevate NNMT flux, depleting intracellular SAM reserves. As methyl groups are consumed clearing nicotinamide, the cellular SAM-to-SAH ratio falls, which can elevate circulating homocysteine and reduce methyl availability for DNA methylation and neurotransmitter synthesis. Co-administering a fully methylated B-complex alongside choline or betaine addresses this potential bottleneck. Providing active methyl donors (such as 5-MTHF, methylcobalamin, and betaine) maintains the one-carbon donor pool. Even during increased NNMT activity, SAM pools remain stable, protecting DNA methylation fidelity and maintaining homocysteine within safe parameters. Quercetin reinforces this protocol through complementary mechanisms. By clearing senescent cells and reducing SASP-mediated inflammation, quercetin downregulates CD38, the primary enzyme responsible for age-related NAD+ degradation. Suppressing CD38 prevents unnecessary breakdown of newly synthesized NAD+, enhancing the efficiency of NR supplementation. Furthermore, while NR provides the NAD+ necessary to activate SIRT1-driven mitochondrial biogenesis, quercetin concurrently modulates mTORC1 to stimulate autophagy. This coordinated action ensures that newly generated mitochondria operate in an environment cleared of proteotoxic cellular debris. The Crucial Role of Magnesium Glycinate and Zinc in Cellular FunctionLongevity protocols require essential mineral cofactors to function efficiently. Without adequate divalent minerals acting as enzymatic cofactors and structural stabilizers, metabolic longevity pathways cannot operate at full capacity. Among these, magnesium and zinc are required for cellular repair, genomic stability, and energy production.Magnesium serves as an obligatory cofactor in over 300 enzymatic reactions, primarily through its interaction with ATP. In biological systems, ATP exists predominantly as a chelate with a divalent magnesium ion, forming biologically active Mg2+ -ATP. Every enzymatic reaction that synthesizes, transfers, or consumes cellular energy - including the enzymes of the NAD+ salvage pathway (NRK and NMNAT) and DNA polymerases - strictly requires Mg2+ -ATP as its substrate. Magnesium deficiency impairs these phosphorylation reactions, reducing the cellular utilization of NAD+ precursors. Additionally, magnesium is an essential cofactor for the enzymes that activate dietary B-vitamins into their active forms. Supplying magnesium as magnesium glycinate provides high gastrointestinal bioavailability, minimal laxative effect, and yields glycine to support inhibitory neurotransmission and restful sleep. Zinc serves as a vital structural component for more than 3,000 human transcription factors and enzymatic proteins. Its most prominent structural role in longevity occurs within zinc-finger motifs. These are specialized protein conformations stabilized by a zinc ion coordinated to cysteine and histidine residues. The DNA damage sensor PARP-1 utilizes three zinc-finger domains to identify, track, and physically bind to single- and double-strand DNA breaks. Without adequate intracellular zinc, PARP-1 cannot properly assemble or dock onto damaged chromosomes, impairing DNA repair and increasing genomic instability. Zinc is also an obligatory structural component of copper/zinc superoxide dismutase (Cu/Zn-SOD or SOD1), the primary cytosolic antioxidant enzyme that dismutates superoxide radicals into hydrogen peroxide, protecting mitochondrial membranes and nuclear DNA from premature senescence. Integrating Prebiotics (like Acacia and Inulin) for Gut-Derived Longevity MarkersA comprehensive cellular longevity framework must extend beyond somatic tissues to encompass the gut microbiome. The intestinal microbiome functions as a central regulator of systemic inflammatory tone, immune development, and metabolic signaling. Age-associated dysbiosis - characterized by the loss of beneficial commensals and an overgrowth of pathobionts - frequently leads to breakdown of the intestinal barrier.The gut epithelium consists of a single-cell monolayer sealed by tight junction proteins, including zonula occludens-1 (ZO-1), occludin, and claudins. When this physical barrier is disrupted by poor dietary fiber intake or dysbiosis, gut permeability increases. This allows lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, to enter the portal and systemic circulation. The resulting "metabolic endotoxemia" activates Toll-like receptor 4 (TLR4) on immune cells, inducing NF-kB and systemic pro-inflammatory cytokine production. This persistent gut-derived inflammation exacerbates the SASP, accelerates tissue senescence, upregulates CD38, and drains systemic NAD+ reserves.
These short-chain fatty acids, particularly butyrate, exert direct protective effects on systemic longevity. Butyrate provides the primary metabolic fuel for colonic epithelial cells, supplying more than 70% of their baseline energy needs and supporting mitochondrial function within colonocytes. Furthermore, SCFAs upregulate the expression of epithelial tight junction proteins (ZO-1, occludin, and claudin-1), restoring intestinal barrier integrity and preventing the translocation of inflammatory LPS into systemic circulation. Systemically absorbed butyrate also functions as an endogenous histone deacetylase (HDAC) inhibitor, suppressing pro-inflammatory gene expression and supporting regulatory T cell (T_reg) development. Reducing metabolic endotoxemia dampens systemic inflammation, protecting vascular function and preventing premature NAD+ depletion. Conclusion: The Integrated Cellular Longevity MatrixCellular longevity is achieved not by addressing isolated biomarkers in isolation, but by systematically supporting interconnected biological pathways. As bioenergetic capacity declines, cellular senescence accelerates, epigenetic patterns degrade, and gut barrier integrity weakens. A comprehensive approach addresses these biological vulnerabilities simultaneously.
Quercetin Phytosome clears senescent cells and modulates mTORC1, stimulating autophagy while dampening the inflammatory SASP cascade that accelerates CD38-mediated NAD+ destruction. Methylated B-vitamins, active folate, and choline replenish SAM reserves, balancing the methyl requirements of NNMT-mediated nicotinamide clearance, preserving epigenetic DNA methylation, and maintaining neurotransmitter production. Magnesium glycinate and zinc provide the structural and catalytic foundation required for ATP utilization, B-vitamin activation, and PARP-1 zinc-finger DNA repair docking. Finally, prebiotic fibers generate short-chain fatty acids like butyrate, reinforcing the intestinal barrier and preventing metabolic endotoxemia from fueling systemic inflammation. By coordinating energy replenishment, cellular waste clearance, epigenetic maintenance, and the suppression of systemic inflammation, this unified approach directly addresses the underlying drivers of cellular aging to support long-term physiological vitality.
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(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6650) 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) Can DMAE Help With Cellular Cleanup?
Date:
May 28, 2026 01:38 PM
Yes, DMAE - and specifically its highly bioavailable pharmaceutical ester counterpart, centrophenoxine (meclofenoxate) - hits cellular cleanup mechanisms. However, the way it interacts with a stalled system in Parkinson's Disease (PD) is fundamentally different from standard macroautophagy upregulators like fasting or mTOR inhibitors. Instead of just forcing the cell to create more cleanup vesicles, DMAE addresses the structural and mechanical "traffic jams" that cause the system to stall in the first place. The Parkinson's Stagnation: An Autophagic Traffic JamIn Parkinson’s pathology, the primary breakdown in cellular quality control occurs within the autophagic-lysosomal pathway. The accumulation of misfolded a-synuclein proteins builds up into toxic aggregates (Lewy bodies). This doesn't just form static waste; it actively paralyzes the cell's transport machinery, halting macroautophagy, chaperone-mediated autophagy (CMA), and mitophagy (the clearing of damaged, radical-producing mitochondria).Here is how a healthy version of this pathway is structured: As shown above, a healthy cell relies on seamless transport where an autophagosome encapsulates debris and fuses with an acidic lysosome to form an autolysosome for enzymatic destruction. In a stalled Parkinson's state, this crucial fusion and trafficking step is paralyzed. How DMAE Alters Cleanup DynamicsDMAE approaches this bottleneck through two precise biochemical mechanisms:1. Re-greasing Vesicle Trafficking TracksTo build an autophagosome and move it to a lysosome, a neuron requires highly fluid Lipid membranes.
2. Direct a-Synuclein DisruptionClassically, DMAE is famous in longevity research for dissolving lipofuscin - the cross-linked "wear-and-tear" pigment aggregate that accumulates in aging cells. While lipofuscin is structurally distinct from the amyloid-like sheets of a-synuclein, modern molecular profiling has revealed that DMAE derivatives possess a powerful cross-over effect:
Mechanics of Clearance: DMAE vs. Traditional Autophagy Inducers
Summary: In Parkinson’s disease, cellular cleanup stalls because toxic accumulations of misfolded alpha-synuclein proteins physically paralyze the autophagic-lysosomal pathway, creating a mechanical traffic jam that prevents waste-carrying autophagosomes from fusing with digestive lysosomes. Rather than simply triggering the creation of more cleanup vesicles like standard autophagy inducers do, DMAE and its highly bioavailable derivative, centrophenoxine, address this bottleneck structurally. It serves as a direct biochemical precursor to vital membrane phosphoLipids like phosphatidylcholine, restoring Lipid bilayer fluidity and essentially "re-greasing the tracks" so stalled cellular transport machinery can resume normal trafficking and waste elimination. Beyond restoring membrane dynamics, DMAE compounds actively disrupt protein aggregation by changing the conformation of alpha-synuclein, which prevents individual monomers from stacking into the toxic, insoluble sheets that choke the cell's internal quality control. This action mirrors its well-documented ability to dissolve lipofuscin, the cross-linked "wear-and-tear" aging pigment that accumulates in aging cells. While free-base DMAE struggles to penetrate the central nervous system effectively due to competition with choline transporters, the lipophilic ester centrophenoxine easily crosses the blood-brain barrier, making it the superior vehicle for restoring neural membrane fluidity and clearing out stalled neurodegenerative debris.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6641) Beyond Choline: How DMAE Flushes Cellular Waste for Longevity
Date:
May 21, 2026 03:43 PM
How is DMAE and Methylation connected?Understanding the relationship between DMAE (dimethylaminoethanol) and the methylation cycle is a nuanced dive into nutritional biochemistry. While DMAE is a popular compound for cognitive and cellular health, its interaction with the body’s methyl pool is a critical factor to consider.DMAE and the Methylation ConnectionBiochemically, it is often considered important to support the methylation cycle when supplementing with DMAE. This is due to how the body processes DMAE to create choline.The "Methyl Drain"DMAE is a precursor to choline, but the conversion process requires the addition of methyl groups. Specifically, the body uses SAMe (S-adenosylmethionine), the universal methyl donor, to methylate DMAE into choline.If you supplement with high doses of DMAE without adequate methyl support, you may inadvertently "drain" your methyl pool. This can lead to:
Strategic Co-factorsTo balance this, many researchers suggest pairing DMAE with methyl donors to ensure the cycle remains fluid. Key co-factors include:
How DMAE Supports LongevityDMAE is often categorized as a "longevity" nutrient because of its impact on cellular waste and membrane integrity.1. Reduction of LipofuscinOne of the most cited longevity benefits of DMAE is its ability to reduce lipofuscin (often called "age spots" or "wear-and-tear pigment"). Lipofuscin is a metabolic waste product that accumulates in the heart, brain, and skin cells over time. High levels of lipofuscin can impair cellular function; DMAE helps the body flush these deposits, potentially slowing the cellular aging process.2. Membrane StabilizationDMAE acts as a free radical scavenger specifically within the cell membranes. By protecting the Lipid bilayer from oxidative stress, it helps maintain membrane fluidity. Flexible, healthy membranes are essential for efficient nutrient transport into the cell and waste removal out of the cell.3. Acetylcholine PrecursorWhile its primary longevity mechanism is cellular, DMAE’s role as a precursor to acetylcholine supports cognitive longevity. Maintaining healthy levels of this neurotransmitter is vital for focus, memory, and muscle control as the nervous system ages.4. Skin Health and "Lifting"In the context of physical appearance and anti-aging, DMAE is known for its "firming" effect. It is thought to increase the tone of the underlying skin muscles, providing a subtle "lift" and reducing the appearance of fine lines and sagging.Summary: While DMAE offers potent cellular cleaning and membrane protection, it functions best when the body has a robust supply of methyl donors to handle its conversion without taxing the system. Does DMAE efficiently convert to Acetylcholine?The conversion of DMAE (dimethylaminoethanol) into the neurotransmitter acetylcholine is a multi-step biochemical process. Because DMAE is not a direct precursor to acetylcholine, it must first be integrated into the phosphoLipid metabolism of the cell.To make this conversion efficient, the body requires specific methyl donors and enzymatic co-factors. The Two-Step Conversion Process1. The Methylation Step: DMAE to CholineDMAE is essentially a "dimethylethanolamine." To become choline (trimethylethanolamine), it requires the addition of a third methyl group.
2. The Acetylation Step: Choline to AcetylcholineOnce DMAE has been methylated into choline (or integrated into phosphatidylcholine), it must be acetylated by the enzyme Choline Acetyltransferase (ChAT).
Optimal Co-factors for EfficiencyTo maximize the "brain-boosting" effects of DMAE, the following nutrients are typically used to support the pathway:
The "Choline Sparer" EffectIt is worth noting that DMAE is often more efficient at crossing the blood-brain barrier than standard choline. However, because it "competes" for the same transport systems and enzymes, taking it alongside a high-quality choline source and a B-complex ensures that the body isn't forced to choose between building cell membranes and creating neurotransmitters.What is it better to consume choline or DMAE?Deciding between DMAE and choline depends entirely on whether your priority is systemic health (liver and cell membranes) or cognitive performance (acetylcholine production and focus). While choline is technically a "cheaper" raw material, the "efficiency" changes once you factor in how the body processes each compound.The Efficiency ComparisonEfficiency in this context is usually measured by how well a compound crosses the blood-brain barrier (BBB) and how many metabolic steps are required to reach the final goal: Acetylcholine.1. Choline Bitartrate (The "Budget" Option)
2. DMAE (The "Specialist")
3. Alpha-GPC & CDP-Choline (The "Premium" Options)
Cost-Efficiency Analysis
Which is better?
Summary: Supplementing with DMAE (dimethylaminoethanol) creates a unique biochemical dynamic in the body, particularly regarding cognitive performance and cellular longevity. While DMAE crosses the blood-brain barrier effectively, its conversion into the crucial neurotransmitter acetylcholine requires an additional methyl group, a process that can significantly drain the body's universal methyl donor, SAMe. To prevent this "methyl drain" and avoid issues like elevated homocysteine, it is highly beneficial to pair DMAE with strategic co-factors and methyl donors such as TMG (trimethylglycine) and methylated B-vitamins. Beyond its role in acetylcholine production, DMAE supports longevity through distinct cellular mechanisms that standard choline cannot replicate, specifically by neutralizing free radicals to stabilize cell membranes and flushing out lipofuscin, an age-related cellular waste product. When evaluating whether to replace DMAE with direct choline supplementation for cost and efficiency, the decision hinges on your specific physiological goals. Standard budget options like choline bitartrate are highly cost-effective for general liver health and systemic cell structures, but they suffer from very poor brain penetration. Conversely, premium forms like Alpha-GPC and CDP-Choline are far more efficient for cognitive optimization and memory because they cross the blood-brain barrier effortlessly without taxing the body's methylation cycle. Ultimately, while cheap choline salts cannot replicate DMAE's unique cellular cleaning properties, choosing a premium choline source is a more direct and biochemically efficient path for raw cognitive enhancement, especially if you want to avoid the multi-step metabolic cost associated with converting DMAE.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6638) Benefits of butyrate and other SCFAs which are produced by the friendly bacteria in the gut!
Date:
November 15, 2025 11:14 AM
Of course. The short-chain fatty acids (SCFAs) produced by your gut bacteria are powerful metabolites with wide-ranging, systemic benefits. While there are three main SCFAs - Butyrate, Acetate, and Propionate - each has slightly different functions. Butyrate, in particular, is a superstar for gut health. Here is a list of their most important benefits, categorized by body system. 1. Gut Health & Integrity (The Primary Benefit)This is where SCFAs do their most direct and important work.
2. Immune System RegulationYour gut houses over 70% of your immune system, and SCFAs are the main molecules that "talk" to it.
3. Brain Health (The Gut-Brain Axis)SCFAs are a critical communication link between your gut and your brain.
4. Metabolic HealthSCFAs play a major role in regulating your metabolism, energy balance, and blood sugar.
5. Cardiovascular & Liver Health
At-a-Glance: The "Jobs" of Each SCFA
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6628) What else does Akkermansia Muciniphila do for the body?
Date:
November 05, 2025 03:58 PM
1. Supports Metabolic Health (A Major Benefit)This is the second most-studied benefit after gut integrity. Higher levels of Akkermansia are consistently linked to a healthier metabolic profile.
2. Modulates the Immune SystemAkkermansia acts as a key communicator between your gut and your immune system.
3. Promotes a Healthy Microbiome (Cross-Feeding)Akkermansia isn't just a solo artist; it's a team player.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6625) 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) Understanding Benfotiamine: The Fat-Soluble, Bioavailable and Physiologically Active Form of Thiamine
Date:
July 27, 2023 12:12 PM
What if there existed a form of thiamine that was more bioavailable and physiologically active than the conventional form we all know about? Well, that form does exist, and it is called Benfotiamine. Benfotiamine has been gaining popularity lately, especially among people dealing with diabetes and other metabolic disorders. But what exactly is Benfotiamine, and what makes it different? Lets explore Benfotiamine, its bioavailability, and its physiological effects. Thiamine, also known as Vitamin B1, is a nutrient that plays a crucial role in energy production, nerve function, and metabolism. It is a water-soluble vitamin, which means it dissolves in water and is not stored by the body. However, conventional forms of thiamine have a limited ability to cross cell membranes and are easily excreted out of the body, rendering it ineffective for some individuals. This is where Benfotiamine comes in; it is a modified form of Vitamin B1 that is fat-soluble, highly bioavailable, and because cells are wrapped in Lipid fat this form of B1 is capable of crossing cell membranes with ease. Since our cell membranes are composed of Lipids, fat-soluble nutrients can easily penetrate the cell barrier and get into living cells where the vitamin is needed. Upon entering the bloodstream, benfotiamine is converted to thiamin pyrophosphate (TPP), the biologically active co-enzyme of thiamin, which is responsible for energy metabolism. By raising the blood levels of TPP, benfotiamine has been shown to support glucose metabolism, reduce oxidative stress and inflammation, and protect against the damage caused by high levels of advanced glycation end products (AGEs). In addition to its bioavailability, benfotiamine has been shown to have several physiological effect on the body. One of the key enzymes that benfotiamine influences is transketolase, which is involved in the pentose phosphate pathway, a metabolic pathway that generates NADPH, a vital molecule that protects cells against oxidative stress. By stimulating transketolase, benfotiamine supports the diversion of excess glucose to the pentose phosphate pathway, thereby reducing the production of reactive oxygen species and increasing the production of NADPH. Another significant benefit of benfotiamine is that it helps protect the nervous system. Chronic high blood glucose levels are known to cause oxidative stress and to damage the peripheral and central nervous systems. However, benfotiamine has been shown to help lower oxidative stress markers and reduce the risk of nerve damage. This can in turn help reduce pain, numbness, and tingling sensations associated with nerve damage, making it a promising adjunct therapy for people with diabetic neuropathy. In Summary: benfotiamine is a modified and bioavailable form of thiamine that offers unique benefits compared to conventional forms of Vitamin B1. Its fat-solubility enables it to cross cell membranes, raise levels of thiamin pyrophosphate, stimulate the transketolase enzyme, and support proper glucose metabolism. Its notable effects on the nervous system make it an attractive therapeutic agent for people with diabetic neuropathy. If you're seeking an alternative and highly effective form of thiamine, benfotiamine is definitely worth considering. Give it a try today!
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6580) The Many Health Benefits of Copper Glycinate
Date:
October 25, 2022 04:49 PM
You may not realize it, but copper is essential for many different bodily functions. This trace mineral is involved in energy production, iron metabolism, connective tissue syntheses, and neurotransmitter production. Copper is also critical for bone health, cardiovascular health, Lipid metabolism, neurological health, skin health, and free radical protection. Keep reading to learn more about the many health benefits of copper. Copper and Energy Production One of the most important roles that copper plays in the body is in energy production. Copper is a key component of mitochondria, which are known as the "powerhouses of the cell." The mitochondria produce ATP (adenosine triphosphate), which is the energy currency of the cell. Therefore, without adequate copper levels, your cells would not be able to produce enough ATP for optimal function. Copper and Iron Metabolism Another important role of copper is in iron metabolism. Copper is necessary for the absorption and utilization of iron in the body. Iron is a key component of hemoglobin, which carries oxygen around in the blood. Therefore, without adequate copper levels, your body would not be able to properly utilize iron, leading to anemia or other problems. Copper and Connective Tissue Synthesis Copper is also necessary for the synthesis of collagen and elastin, two proteins that make up connective tissue. Connective tissue includes things like skin, tendons, ligaments, and cartilage. Therefore, copper is necessary for healthy skin as well as strong tendons and ligaments. As you can see, copper plays many vital roles in the body. If you are deficient in copper, you may experience fatigue, anemia, weak bones or connective tissue, problems with Lipid metabolism or neurological function, or poor skin health. To ensure that you are getting enough copper in your diet, eat foods like liver, oysters, lobster, dark chocolate, avocados, almonds, mushrooms ,or leafy green vegetables. You can also take a copper supplement if needed.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6526) The Many Benefits of Glucomannan - Konjac Root
Date:
October 20, 2022 03:19 PM
If you're looking for a dietary supplement that can help with everything from maintaining intestinal regularity to promoting satiety, look no further than glucomannan. This soluble, bulk-forming fiber is derived from the konjac root and has a host of potential health benefits. Read on to learn more about glucomannan and how it can help you achieve your health goals. What is Glucomannan? Glucomannan is a type of dietary fiber that is classified as a soluble, gel-forming fiber. It is derived from the corm (or bulbous root) of the konjac plant, which is native to Asia (1). In its natural state, glucomannan is a white, powdery substance that can be dissolved in water. Once it comes into contact with water, it forms a viscous gel. This gel-like quality is what makes glucomannan so effective at promoting satiety and maintaining intestinal regularity (2). Health Benefits of Glucomannan In addition to promoting satiety and maintaining intestinal regularity, glucomannan may also offer other health benefits. For example, research suggests that glucomannan can help to support healthy Lipid levels already within the normal range (3). Additionally, glucomannan may help to support healthy blood sugar levels already within the normal range (4). And because glucomannan can help you feel full after eating fewer calories (5), it may also be helpful as part of a weight management plan that includes a healthy diet and exercise program. If you're looking for a dietary supplement that has a host of potential health benefits, look no further than glucomannan. This soluble, bulk-forming fiber derived from the konjac root can help promote satiety and maintain intestinal regularity, as well as support healthy Lipid and blood sugar levels already within the normal range.* What's more, glucomannan is a convenient addition to any weight management plan that includes a healthy diet and exercise program.* Add this versatile supplement to your routine today and start reaping its many rewards tomorrow.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6511) The Health Benefits of Berberine
Date:
September 12, 2022 04:22 PM
Berberine is a natural constituent of herbs such as goldenseal, Oregon grape, and barberry. Clinical studies have demonstrated that berberine helps to support already normal glucose and Lipid metabolism.* Because berberine is known for its limited bioavailability, this product includes caprate (C10, a medium-chain triglyceride) to promote optimal absorption and maintenance of gastrointestinal comfort during berberine supplementation.* Berberine has a long history of use in Traditional Chinese Medicine and Ayurveda for supporting already normal liver function and healthy digestion.* It is also one of the most well-studied botanicals for already normal glucose metabolism support, with research indicating it may work by activating an AMPK-dependent pathway.* Berberine May Help To Support Normal Glucose Metabolism* Berberine is a plant alkaloid with a long history of use in Traditional Chinese Medicine for promoting already normal liver function.* extraction process ensures a consistent level of berberine from batch to batch. In addition, this product provides 500 mg of berberine hydrochloride per vegetarian capsule. Several clinical studies have demonstrated that berberine can help to support normal glucose metabolism in already healthy individuals when taken at dosages of 900 mg to 1,500 mg per day.* In a placebo-controlled human clinical trial involving subjects with prediabetes who were given 500 mg of berberine two times daily for 12 weeks, researchers observed improvements in already normal fasting blood sugar, HbA1c, and triglyceride levels (as well as increases in HDL-cholesterol) compared to placebo group.* May Also Help To Support Lipid Metabolism* In addition to its effects on already normal glucose metabolism, berberine has also been shown to help support Lipid metabolism in already healthy individuals. In a 12-week, double-blind, placebo-controlled human clinical trial involving subjects with mild elevations in LDL cholesterol who were given 500 mg of berberine two times daily, researchers noted statistically significant decreases in total cholesterol and LDL cholesterol levels (along with increases in HDL cholesterol) compared to placebo group.* Berberine is a potent botanical extract that has been traditionally used for supporting liver function and healthy digestion. Additionally, it is one of the most well studied botanicals for supporting already normal glucose metabolism. Numerous clinical trials show that it can help maintain already normal levels of fasting blood sugar as well as HbA1c and triglycerides. Furthermore, berberine has also been shown to promote already healthy Lipid metabolism by supporting already normal levels of total cholesterol, LDL cholesterol, and HDL cholesterol. Therefore, if you are looking for an herbal supplement to support your overall health and well being, berberine is definitely worth considering.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6443) Vectomega: The Revolutionary Omega-3 Supplement
Date:
July 26, 2022 02:55 PM
Fish oil is good for the heart, brain, and helps maintain overall health and wellness Fish oil is a dietary supplement that is derived from fish body tissue. It is rich in omega-3 fatty acids, which are considered to be beneficial for the heart, brain, and overall health and wellness. Numerous studies have shown that fish oil can help to reduce the risk of heart disease, stroke, and cognitive decline. It has also been shown to be effective in managing diabetes, arthritis, and other chronic conditions. Vectomega Omega-3 fatty acids are essential for human health, but unfortunately, our bodies cannot produce them on their own. As a result, we must obtain omega-3s through our diet or through supplements. Vectomega is an innovative omega-3 supplement that provides all the benefits of fish oil without the unpleasant taste or risk of fishy burps. Unlike other omega-3 supplements, Vectomega is bound to phosphoLipids, which enhances absorption. In addition, Vectomega contains fish peptides, which are a natural source of omega-3s. Best of all, Vectomega has zero rancidity, ensuring that you get the freshest possible omega-3s every time you take it. If you're looking for a high-quality omega-3 supplement, look no further than Vectomega.
The human brain is comprised of 60% fat, making omega-3 essential for healthy cognitive function. Unfortunately, the Standard American Diet is notoriously low in omega-3, which can lead to cognitive decline and an increased risk for Alzheimer's disease. The good news is that omega-3 supplements can help to improve brain health. One high-quality option is vectomega, which contains a potent form of omega-3 called DHA. DHA has been shown to improve memory and protect against age-related cognitive decline. In addition, vectomega helps to support heart health by reducing inflammation and improving circulation. It can also improve eye health by reducing the risk for macular degeneration and dry eye syndrome. Overall, vectomega is an excellent way to support brain, heart, and eye health. Reduce pain with EPA from fish oil There are many ways to reduce pain, but one of the most effective is to take fish oil supplements. Fish oil contains omega-3 fatty acids, which are known to be anti-inflammatory. EPA, or eicosapentaenoic acid, is a type of omega-3 fatty acid that is particularly effective at reducing inflammation. In fact, studies have shown that EPA is more effective than ibuprofen at reducing pain and inflammation. And unlike ibuprofen, fish oil has no side effects. So if you're looking for a natural way to reduce pain and inflammation, fish oil is a great option. Just make sure to choose a high-quality supplement that contains a significant amount of EPA like vectomega. If you're looking for a high-quality omega-3 supplement, look no further than Vectomega. This revolutionary product provides all the benefits of fish oil without the unpleasant taste or risk of fishy burps. In addition, Vectomega contains peptides which are not found in fish oil or krill oil. These peptides play a vital role in mood, immune system function, focus, and overall health! Don't miss out on this incredible supplement. Start taking Vectomega today!
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6421) The Truth About Sugar: How It's Digested, Metabolized, and Why Too Much Can Be Dangerous
Date:
June 25, 2022 10:13 AM
What is glycation and what does it do to the body? Glycation is a process that occurs when glucose binds to proteins, Lipids, or nucleic acids. This can damage tissues and lead to the formation of advanced glycation end products (AGEs). AGEs are toxic compounds that contribute to the development of chronic diseases, such as diabetes, atherosclerosis, and Alzheimer’s disease. The body has mechanisms to prevent glycation, but these become less effective with age. Additionally, certain lifestyle choices, such as smoking and a high-sugar diet, can increase the risk of glycation. Therefore, it is important to be aware of the risks and take steps to protect the body from this damaging process. How does sugar cause glycation? Sugar causes glycation in several ways. First, when sugar is present in the bloodstream, it can attach to proteins and Lipids, forming new molecules called advanced glycation end products (AGEs). Once formed, AGEs can accumulate in tissues and cause damage. Second, sugar can also indirectly cause glycation by promoting inflammation. Inflammation triggers a release of immune system chemicals that can damage tissues. Third, sugar can also impair the body's ability to regenerate tissues. This is because glycation damages DNA, making it difficult for cells to divide and multiply properly. over time, this leads to a decrease in the body's ability to heal wounds and repair damaged tissues. As a result, sugar plays a significant role in the development of conditions such as diabetes and Alzheimer's disease. How can you prevent glycation from happening? There are several ways to help prevent glycation from occurring. First, it is important to control blood sugar levels by eating a healthy diet and maintaining a healthy weight. Exercise can also help to regulate blood sugar levels and prevent glycation. In addition, antioxidants may help to protect against glycation by scavenging sugar molecules before they can attach to other molecules. By taking these steps, you can help to prevent glycation and the age-related conditions that are associated with it. Should we be worried about sugar intake? Sugar is a complex topic, and there is still a lot of scientific research to be done in order to understand all of its implications. However, based on the current evidence, it seems that we should be at least somewhat concerned about our sugar intake. Numerous studies have linked sugar consumption to an increased risk of obesity, type 2 diabetes, heart disease, and certain types of cancer. And while sugar itself is not necessarily bad for you, the truth is that most of us consume far more sugar than we need. The average American consumes over 150 pounds of sugar every year, which is well above the recommended limit. So, while you don't need to eliminating sugar entirely from your diet, it is important to be aware of how much sugar you're consuming and to make sure that you're not overdoing it. What are some healthy alternatives to sugar? Sugar is a common ingredient in many processed foods, and it can be difficult to avoid. However, consuming too much sugar can lead to weight gain, cavities, and other health problems. Thankfully, there are a few healthy alternatives that can be used in place of sugar. Stevia is a popular choice, as it is derived from a plant, has no calories, and does not elevate blood sugar levels. Xylitol and erythritol are both sugar alcohols that have a lower calorie content than sugar and do not cause cavities. These substitutes can be found in most supermarkets, and they can help to make healthier choices when it comes to sweetening food and drink. So, while you don't need to eliminating sugar entirely from your diet, it is important to be aware of how much sugar you're consuming and to make sure that you're not overdoing it. There are a few healthy alternatives that can be used in place of sugar. Stevia is a popular choice, as it is derived from a plant, has no calories, and does not elevate blood sugar levels. Xylitol and erythritol are both sugar alcohols that have a lower calorie content than sugar and do not cause cavities. Our suggestion is Kal brand Stevia, it is a no after taste stevia with over 1800 servings, this is VitaNet's Recommendation. Try a sugar alternative in your next recipe and see how it tastes! You might be surprised at how good it can be.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6413) Vitamin D Linked to Heart Health: Study Shows Promise in Preventing Cardiovascular Disease
Date:
April 26, 2022 10:18 AM
What is Vitamin D and why is it important for heart health? Vitamin D is an essential nutrient that plays various important roles in the body, including helping to maintain healthy bones and supporting immune function. In recent years, scientists have also begun to uncover the critical role that Vitamin D can play in promoting cardiovascular health. Vitamin D is involved in the regulation of several important cardiovascular processes, including blood pressure and Lipid metabolism. Studies have shown that individuals with lower levels of Vitamin D are at increased risk for heart disease and stroke. Therefore, ensuring adequate vitamin D levels through diet, sun exposure, or supplementation may help to protect against heart conditions and improve overall cardiovascular health. The study on Vitamin D and heart health Researchers at the University of South Australia have recently conducted a study exploring the link between vitamin D and heart health. They found that individuals with higher levels of vitamin D in their blood were less likely to suffer from cardiovascular diseases, such as heart attacks, than those with lower levels. The results suggest that vitamin D plays an important role in protecting the heart and maintaining efficient cardiovascular function. This is important not only for preventing or mitigating the effects of heart disease, but also for overall health and well-being. Overall, the results of this study highlight the importance of ensuring adequate levels of vitamin D to safeguard our hearts and keep us healthy. How to get more Vitamin D in your diet While vitamin D-3 is essential for good health, many people struggle to get enough of this important nutrient through their diet alone. With so many factors affecting our ability to absorb nutrients from food, it can be difficult to maintain healthy levels of vitamin D through regular meals. However, research suggests that we may be able to get enough of this vital nutrient by taking supplements or getting outside on sunny days. For example, studies show that simply spending time in sunlight for a few minutes each day can go a long way toward maintaining adequate vitamin D levels in the body. Additionally, many foods are fortified with vitamin D-3, including dairy products and some types of bread and cereal. Ultimately, the best way to ensure adequate vitamin D-3 levels is through a combination of dietary sources and appropriate supplementation. So don't be afraid to take that extra step or buying a supplement – your health will thank you! Bottom line: Vitamin D is a promising nutrient for heart health Vitamin D-3 is a nutrient that is continually been getting attention for its potential benefits to heart health. This nutrient can be obtained through certain foods, such as oily fish and eggs, but many individuals also supplement with vitamin D-3 on a regular basis. Preliminary research suggests that this nutrient may help to lower cholesterol levels and reduce inflammation in the arteries, two important contributors to cardiovascular disease. Additionally, studies have shown that vitamin D-3 can help to strengthen the immune system, which further enhances overall heart health by keeping the body healthy and strong. Overall, when it comes to promoting heart health, vitamin D-3 seems like a promising nutrient that deserves further scientific study and exploration. Assist Mineral absorption Vitamin D is an important nutrient that helps the body absorb calcium and phosphorus. It also plays a role in maintaining strong bones and muscles. Unfortunately, foods are a relatively poor source of vitamin D. The best way to get this nutrient is through exposure to sunlight. However, too much sun exposure can lead to skin damage, so many people choose to take a supplement instead. Vitamin D supplements are available in both liquid and pill form. They are typically taken once a day, and they can help people maintain adequate levels of vitamin D without exposing themselves to the harmful effects of the sun. Vitamin D-3 is involved in over 300 enzymatic processes in the body As we already know, vitamin D is a fat-soluble vitamin that plays an important role in bone health and calcium absorption. Vitamin D-3, the form of vitamin D found in supplements, is involved in over 300 enzymatic processes in the body. These processes include cell proliferation, immunomodulation, and regulation of gene expression. Vitamin D-3 has also been shown to have anti-inflammatory and neuroprotective effects. Supplementation with vitamin D-3 has been shown to improve bone density and reduce the risk of fractures, particularly in older adults. In addition, vitamin D-3 supplementation has been shown to improve muscular strength and reduce the risk of falls in older adults. While most people can get adequate amounts of vitamin D from exposure to sunlight, those who don't get enough sun exposure or have dark skin are at risk for vitamin D deficiency. Supplementation with vitamin D-3 is an effective way to ensure adequate intake of this important nutrient.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6393) Study identifies a natural preservative in the arjun tree
Date:
May 17, 2019 03:56 PM
Terminalia arjuna has been studied closely by researchers from India and New Zealand. Commonly known as the arjun tree, this plant was used on chevon sausages to test the properties of preservation. The study suggest that the it produced significantly lower values for total plate count, psychrophilic count, yeast and mold count, and free fatty acid values. The results showed an improved lipid oxidative stability and storage quality while refrigerated, thus suggesting that the arjun tree can be a novel natural meat preservative. Key Takeaways:
"Researchers from India and New Zealand explore the potential of Terminalia arjuna as a novel natural preservative in meat products." Read more: https://www.naturalnews.com/2019-04-09-study-identifies-a-natural-preservative-in-the-arjun-tree.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6329) Pu-erh tea has hepatoprotective and antioxidant properties
Date:
May 14, 2019 04:25 PM
Yunnan Tasly Deepure Biological Tea Group Company recently collaborated with scientists from Tianjin University of Commerce on research into the health benefits of pu-erh tea. The research involved rats on a high fat diet, and discovered that pu-erh tea can help defend your liver against oxidative stress and high glucose levels. Pu-erh tea also appears to be able to protect rats from weight and body fat increases and prevent lipid peroxidation. These results suggest pu-era tea has great potential for preventing fatty liver disease. Key Takeaways:
"The results showed that the treatment with Pu-erh tea extract prevented the increases of body weight and fat index, reduced oxidative stress, and inhibited lipid peroxidation — all of which contributed to the protection of the liver in rats." Read more: https://www.naturalnews.com/2019-04-16-pu-erh-tea-has-hepatoprotective-and-antioxidant-properties.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6317) Polysaccharide extract from reishi mushrooms found to have hypolipidemic, antioxidant, and antiapoptotic properties
Date:
May 08, 2019 01:29 PM
A recent study published in the Journal of Medicinal Food found that some properties of the Reishi Mushroom can fight obesity. The study was conducted by a Chinese research team at Hunan Agricultural University. It involved feeding mice high fat diets and then studying how the compounds of the mushrooms combated the weight gain over the course of a 12 week research project. The mushrooms exhibited helpful properties at both dosage levels that were tested. Key Takeaways:
"In mice, treatment with reishi mushroom polysaccharides, in both doses, significantly reduced the body weight increases caused by the feeding with a high-fat diet." Read more: https://www.naturalnews.com/2019-03-27-reishi-mushroom-hypolipidemic-antioxidant-antiapoptotic.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6280) A species of hawthorn has been found to control abnormally highblood sugar levels
Date:
May 02, 2019 02:45 PM
A team of researchers from the Middle East have found that a species of hawthorn, Crete hawthorn, has the ability to lower elevated levels of glucose in the blood. They have published their findings in the journal BMC Complementary and Alternative Medicine. Along with its effects on blood glucose, called its anti-hyperglycemic property, it also has hyperlipidemic properties, that is, the ability to protect the body against high levels of fat such as cholesterol in the blood. They carried out the study using mice that were induced with hyperglycemia through feeding them alloxan. The mice were then divided into two groups, one group receiving Crete hawthorn extracts and the other given a chemical for control. They also used another animal model to understand its hyperlipidemic properties and to investigate whether the plant had antioxidant and antimicrobial properties. The results of the findings were that Crete hawthorn had important antioxidant properties due to its containing phenols and flavonoids. They also found that it had antimicrobial properties because it acted against bacteria such as E. Coli and Staphylococcus aureus, among others. Key Takeaways:
"The mice were then divided into groups, with some receiving an ethanol extract from Crete hawthorn leaves while others were given glibenclamide for positive control." Read more: https://www.naturalnews.com/2019-03-12-hawthorn-controls-high-blood-sugar-levels.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6243) Fenugreek reduces menopausal symptoms
Date:
May 02, 2019 01:55 PM
According to a study in Phytotherapy Research, the nutrient fenugreek may help ease the symptoms associated with menopause without the unpleasant side effects of traditional hormone replacement therapy. Study participants who consumed 1,000 milligrams of fenugreek extract daily reported a significant improvement in headaches, hot flashes, insomnia, and night sweats, as well as an overall improvement in quality of life. Researchers concluded that fenugreek extract is a safe and effective treatment alternative for menopausal women. Key Takeaways:
"Furthermore, the researchers found fenugreek extract treatment is safe and plays a role in the management of lipid profile in menopausal women." Read more: https://www.naturalnews.com/2019-03-15-fenugreek-reduces-menopausal-symptoms.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6238) Catechins in green tea found to improve symptoms of metabolicsyndrome in obese people
Date:
April 25, 2019 04:43 PM
Green tea not only tastes good, but it also has very beneficial health factors. Among these factors includes the fact that it contains catechins, which are polyphenols that are a good barrier to diabetes and stress. These catechins can also help with metabolic syndrome, which is a syndrome that causes people to have higher than normal levels of abdominal fat and a slowed down metabolism. This could potentially lead to lowered rates of obesity when consumed by the public. Key Takeaways:
"In this study, the researchers wanted to determine if catechins were beneficial for reducing abdominal fat and improving metabolic syndrome." Read more: https://www.naturalnews.com/2019-02-27-catechins-improve-symptoms-of-metabolic-syndrome-in-obese-people.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6183) Why Fibre: The One Effective Macronutrient For Constipation AndWeight Loss
Date:
April 25, 2019 04:31 PM
Fiber is a critical macronutrient that can help to alleviate constipation by increasing the size and weight of the stool. However, consuming too much fiber can cause discomfort, gas and bloating. The recommended daily intake of fiber for adults is 25 grams for women and 35 grams for men. Unfortunately, most people take in only about 15 grams of fiber per day. It's important to drink plenty of water so that the body can absorb fiber properly without any negative effects. While fiber is not a magic pill, it can aid in weight loss by eliminating toxins, boosting gut health, and balancing blood sugar. Key Takeaways:
"This means that a lack of fibre can invite a host of health problems ranging from plummeting sugar and lipid profiles, overeating which can in turn lead to obesity, constipation and gut dysbiosis which can pave way for even more serious illnesses." Read more: https://www.ndtv.com/health/why-fibre-the-one-effective-macronutrient-for-constipation-and-weight-loss-2003400
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6181) Moms, add more leucine and omega-3s to your diet to boostantioxidant levels in your children's liver
Date:
April 22, 2019 04:16 PM
When you have an imbalance of antioxidants within your system, this often leads to oxidative stress. An increase in oxidative stress unfortunately leads to many forms of cancer. Research has emerged that showed leucine and omega-3's have the ability to fight off this oxidative stress by increasing the amount of antioxidants that are found in the liver. Both of these can be found in the form of a nutritional supplement at most mainstream health and wellness stores. Key Takeaways:
"Expectant mothers need a wide range of nutrients for them and their child to stay healthy." Read more: https://www.naturalnews.com/2019-02-27-moms-add-more-leucine-omega-3s-to-your-diet.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6148) Fiber reduces inflammation, reducing risk of inflammatory diseasesand the rate of mortality
Date:
April 17, 2019 01:45 PM
Chances are, you or someone you love has dealt with the ramifications of cardiovascular disease (CVD) in some way. While there may not be any way to completely safeguard you and your loved ones from early mortality due to CVD, research is now showing that fiber consumption may play a promising role. A recent study showed that those who consume more fiber are much less likely to face an early demise due to the presence of CVD. Key Takeaways:
"A study reports that having a fiber-rich diet lowers the risk of contracting chronic CVDs and Type 2 diabetes, as well as some cancers and inflammatory diseases like rheumatism." Read more: https://www.naturalnews.com/2019-02-27-fiber-reduces-inflammation-reducing-risk-of-inflammatory-diseases-and-the-rate-of-mortality.html
CBD can reduce inflammation and east pain through out the body as well!
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6137) Take better care of your heart by eating more almonds
Date:
April 02, 2019 02:00 PM
A recent study showed that nuts are good snacks that can improve triglyceride and cholesterol levels. This study was done with 837 people and showed that the people who benefited the most were those with overall elevated total cholesterol. The results support the idea that eating nuts will lower the risk of heart disease. Other heart healthy snacks recommended include carrots, cucumbers, celery sticks and hummus, along with fruits such as whole apples, pears, peaches or bunches of grapes, oatmeal, and soy protein were listed. Key Takeaways:
"Among participants who consumed at least 45 grams (g) of almonds per day, a 0.212 mmol/L decrease in total cholesterol was seen. Furthermore, those who have high levels of total cholesterol and consumed at least 45 g of almonds every day experienced a 0.271 mmol/L in total cholesterol." Read more: https://www.naturalnews.com/2019-01-28-take-better-care-of-your-heart-by-eating-more-almonds.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6108) Can Apple Cider Vinegar really help you lose weight?
Date:
February 19, 2019 07:53 AM
People have trusted apple cider vinegar to help them shed those unwanted pounds for many years now after a fly by night company brought claims of its benefit to lose weight. But, have we all been duped or can apple cider vinegar really help those pounds come off? In a test conducted using mice and rats, weight loss did occur when given apple cider vinegar. Scientist say that it is true and yu can lose weight when using this product! Key Takeaways:
"They reported that acetic acid could prevent the build-up of body fat and lipids in the animals." Read more: https://www.naturalnews.com/2018-12-20-can-acv-really-help-you-lose-weight.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6041) The Arjun tree holds potential for lowering blood sugar andcholesterol levels
Date:
January 08, 2019 09:58 AM
According to the Journal of Ayurveda and Integrative Medicine, Arjun Tree extract may have benefits for moderating your blood sugar and also your cholesterol levels. Diabetics are at dramatically higher risk of dying from heart conditions, perhaps because hyperglycemia tends to raise blood pressure and damage the circulatory system. The study in question focused on Wistar rats that received a high-fat diet, and found that Arjun Tree extract improved insulin sensitivity and liver triglycerides, and exhibited a pronounced anti inflammatory effect. Key Takeaways:
"In this study, which was published in the Journal of Ayurveda and Integrative Medicine, the researchers were able to determine that Arjun tree extracts exhibit anti-hyperglycemic and anti-hyperlipidemic activity." Read more: https://www.naturalnews.com/2018-12-24-arjun-tree-lowers-blood-sugar-and-cholesterol-levels.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5942) Rutin: A Flavonoid for Your Heart, Brain & Blood Health
Date:
December 21, 2018 09:42 AM
Rutin, a bioflavonoid associated with foods such as figs, citrus fruits, buckwheat and especially apples, has many beneficial properties. It can help keep your blood vessels supple and prevent brittleness or leakage. Its antioxidant and anti inflammatory properties can help reduce arthritis symptoms and even cancer, and it may be able to encourage apoptosis among cancer cells. Rutin may also help guard against metabolic problems by helping to moderate levels of blood sugar, insulin, and lipid accumulation. Key Takeaways:
"Rutin, of the the most important constituents of apple nutrition and some other foods, has a wide array of beneficial effects on our health." Read more: https://draxe.com/rutin/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5919) Compelling study confirms the therapeutic effects of curcumin inremoving fluoride from our bodies
Date:
December 03, 2018 02:03 PM
According to statistics recently released by the CDC, 66.3% of U.S. citizens are being exposed to fluoride poisoning through the country's public water supplies. The good news is that a study in Pharmacognosy Magazine points to curcumin as a natural solution to this growing problem. According to this Indian study, curcumin can protect our brains from fluoride poisoning. If you cannot afford to install a whole-house water filter in your home, curcumin may be a safe and affordable option to protect your family from the dangerous neurological effects of fluoride. Key Takeaways:
"The researchers looked specifically at fluoride-induced toxicity on the mice’s brains, including the chemical’s impact on lipid peroxidation, or rancidity, in brain tissue. They also evaluated markers of malondialdehyde, or MDA, a well-known marker of oxidative stress and oxidative damage, in the brains of mice from each test group." Read more: https://www.naturalnews.com/2018-11-26-curcumin-removing-fluoride-from-the-body.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5869) Scientists: Taking EPA and DHA omega-3s reduces your risk ofcardiac death
Date:
November 27, 2018 08:51 AM
Mainstream media likes to emphasize medicine as the solution to our modern health crisis, but often downplays diet's role. The western diet is the cause of many cardiac issues, and it makes sense that it is also the solution. Omega 3 fatty acids have been shown to lower your risk of heart disease and cardiac death. Specifically, the compounds EPA and DHA are linked to a reduction in risk. Supplementing your diet with EPA and DHA omega 3 fatty acids is a low risk option with no negative side effects. Key Takeaways:
"A recent study published in the Journal of Clinical Lipidology has shown that omega 3 fatty acids can, and do, help reduce the risk of heart disease and cardiac death. Specifically, the compounds EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) were linked to an overall eight percent reduction in risk." Read more: https://www.naturalnews.com/2018-11-13-taking-epa-and-dha-omega-3s-reduces-your-risk-of-cardiac-death.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5862) Another study finds turmeric and curcumin to be a safe, effectivetreatment for lowering cholesterol and protecting the heart
Date:
November 19, 2018 09:36 AM
Turmeric and its much-lauded, health-giving component, curcumin, have had a health buzz about them for a long time. The health benefits to those that use turmeric and consequently curcumin, have long been noted. But, though its benefits for a wide array of bodily systems, including the cardiovascular, are not disputed, it has heretofore not been understood if turmeric, or more specifically curcumin, does some of its wonders by lowering Lipid levels. The Second Affiliated Hospital of Chongqing Medical University has now performed a meta-analysis of available data, surrounding turmeric and curcumin, as a means of filling the knowledge gap. The researchers began by filtering the data, searching for studies revolving around turmeric, cholesterol and triglycerides. To ensure the data was all the more compelling and germane, the researchers trimmed down the parameters even more, allowing for only those tests that involved subjects laboring under the effects of metabolic syndrome or type 2 diabetes. In these cases possible negative effects to the heart would prove particularly relevant. The meta-analysis revealed that turmeric and curcumin had positive effects to impart on the levels of serum triglycerides apparent in its user-subjects. The two components also positively impacted the low-density lipo-protein cholesterol levels of the user-subjects. The researchers theorized that positive chemical activity was initiated by the components, thereby causing the beneficial aspects. Other cholesterol and Lipid markers were not affected. In general, turmeric and curcumin have been shown to limit oxidative stress and inflammation as well as benefit the blood vessel lining, all of which can prevent a serious cardiac event. Key Takeaways:
"Turmeric and curcumin are two substances most known for their wide array of health benefits."
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5844) Virgin coconut oil improves your lipid profile
Date:
November 06, 2018 09:51 AM
New studies at the Federal University of Nigeria, have shown that virgin coconut oil could possibly improve cholesterol levels within our bodies. Scientist used rats in this animal study and supplemented the subjects diets with virgin coconut oil. They then observed a number of factors including antioxidant levels, kidney and liver function, and even cardiovascular risk factors. it showed that the animals who were supplemented the virgin coconut oil had improved all functions of the liver, kidneys, and antioxidant levels. It also showed to have reduce the level of malondialdehyde. Key Takeaways:
"People have found a use for every part of the coconut tree, from the leaves down to its roots. It can be processed into many forms, from food and medicine to fuel, timber, and even oil." Read more: https://www.naturalnews.com/2018-11-04-virgin-coconut-oil-improves-your-lipid-profile.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5817) The Remarkable Antioxidant Benefits of Liposomal Vitamin C
Date:
September 07, 2018 10:53 AM
Vitamin C is an essential vitamin for immune function. However, our bodies do not make Vitamin C on it's own and does not store it at all. However, a recently developed lipid called Liposomal Vitamin C is said to help. Liposomal Vitamin C offers another way to absorb Vitamin C by shuttling itself into the blood stream without digestion. Liposomal Vitamin C can be dispersed intravenously, meaning it goes straight into the blood stream, which offers a faster distribution and absorption of the Vitamin C. Key Takeaways:
"Despite the advantages of taking a multivitamin or getting your vitamin C through various nutritious foods, liposomal vitamin C offers another way to absorb this immune-boosting vitamin, and it may be the most beneficial." Read more: https://www.myhdiet.com/healthnews/cancer-news/the-remarkable-antioxidant-benefits-of-liposomal-vitamin-c/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5753) Sea buckthorn oil can promote liver health and decrease the storageof body fat
Date:
September 06, 2018 09:52 AM
More study is now being done regarding lesser known fruits and vegetables, not only for the betterment of human understanding, but also to potentially augment the list of natural alternatives to pharmaceuticals for the improvement of human health. Healthy lipids and fatty acids have been on the nutrition radar for a while now, as these items are known for having useful bioactive ingredients, including high vitamin content, making them useful for human consumption. Sea buckthorn oil is a new face on the lipid list, but offering some impressive credentials. For example, the plant shows high levels of vitamin A and E, phytosterols and unsaturated fatty acids. One study suggests that the type of oil used by humans effects how much vitamin A the liver stores. The ware-housing effect was considerably upped when rats were given sea buckthorn oil as opposed to soybean oil. Sea buckthorn oil has other pluses too. It can reverse GERD and possibly ulcers, also lower cholesterol and promote heart health. It also reduces inflammation, making it useful for sore inflamed, reddened skin. Key Takeaways:
"Lesser known fruits and plants have been gradually taking the spotlight in alternative medicine as natural remedies to various health conditions and improving overall nutrition." Read more: https://www.naturalnews.com/2018-09-01-sea-buckthorn-oil-can-promote-liver-health.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5749) Bitter melon extract found to help treat diabetes with its anti-obesity effects
Date:
July 26, 2018 09:09 AM
Bitter melon may be an unusual thing to incorporate into your diet. But, you may want to look into some recipes. It turns out that there is a wealth of study data that shows that bitter melon is a potent health ally, particularly when it comes to individuals who are fighting a losing battle with weight and some of the chronic conditions that go with it. There's scientific proof attesting to the fact that bitter melon aids the body in balancing its metabolism with lipid intake. It also benefits a syndrome marked by high levels if glucose in the blood and weight gain around the middle. It also tends to dampen the body's accumulation of adipose tissue. So, while it may not be a taste treat, it may be beneficial, nonetheless, to put some bitter melon on your plate. Key Takeaways:
"Bitter melons may taste unpleasant to some people, but its health benefits cannot be denied." Read more: https://www.naturalnews.com/2018-06-13-bitter-melon-extract-found-to-help-treat-diabetes-with-its-anti-obesity-effects.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5679) Dyslipidemia Causes + 5 Tips to Manage It Naturally
Date:
January 02, 2018 08:59 AM
Dyslipidemia causes 5 plus tips to manage it naturally. This is a group of disorders characterized by changes in plasma lipids or lipoproteins. This included two that they are familiar with. The two are cholesterol and triglycerides. The goal for people over 20 is to have cholesterol levels that are under 200 milligrams per deciliter. There are an estimated 99 million Americans that are dealing with blood cholesterol levels higher than what is considered the healthy range. Key Takeaways:
"However, in my opinion, one of the things you should focus on most is avoiding processed foods that increase cholesterol due to how they cause inflammation." Read more: https://draxe.com/dyslipidemia/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5473) Vitamin E: A Closer Look at Tocotrienols
Date:
October 21, 2017 10:14 AM
Researchers have made an estimate and guessed that there are 75 trillion cells in the body. Each of those cells is surrounded by a membrane that is bean shaped. This membrane is made up of dense rows of fatty acids. These require protection from lipid peroxidation. Vitamin E is one of the popular antioxidants. Vitamin E is shaped like a tadpole, which is the perfect shape to do this job. There are two forms of Vitamin E. Key Takeaways:
"In this study, researchers found that alpha-tocopherol, when co-administered with tocotrienols, reduced tocotrienols’ inhibitory effect on HMGR." Read more: http://www.nutritionaloutlook.com/vitamins-minerals/vitamin-e-closer-look-tocotrienols
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5355) Olive oil for a healthy heart
Date:
July 30, 2017 04:14 PM
The use of olives or olive oil in a diet has been proven to reduce the number of lipid peroxidation in the bloodstream. Olive oil can help blood vessels from clotting together. It is digested well by the stomach and has been proven to help ward off certain cancers. It also helps bone health and has been used by people with memory issues and has shown that it does help. The fatty acids are also great for the skin as they nourish it well. Key Takeaways:
"The antioxidant and anti-inflammatory properties of olives provide protection against cancer since chronic oxidative stress and chronic inflammation are the key factors in the development of cancer." Read more: https://news.statetimes.in/olive-oil-healthy-heart-2/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5062) Mediterranean Diet found to slash risk of dementia by 35%
Date:
July 22, 2017 09:14 AM
According to a study by the University of California following a Mediterranean diet could significantly reduce the risk of dementia. Other studies seem to agree that a diet low in meat and dairy but is rich in fresh fruit and vegetables, beans, nuts, and healthy fats significantly reduce the risk of cognitive decline. There are some studies showing that there is marked improvement in cognition when a person strictly adhered to the diet as well as decreasing inflammation, reducing obesity, healthier lipid panels and such. Key Takeaways:
"The Mediterranean diet, which includes mostly oily fish, vegetables and nuts, has long been touted as a highly effective diet scheme against a plethora of diseases." Read more: http://www.naturalnews.com/2017-07-19-mediterranean-diet-found-to-slash-risk-of-dementia-by-35.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=5014) Why You Need Choline And How To Get It
Date:
June 12, 2017 12:14 PM
choline, a vital, vitamin-like nutrient, is overestimated in its importance. involved in the metabolic process, the transport of lipids, and synthesis of neurotransmitters, just to name a few. both low levels and high levels of choline have negative health risks. a recent study found that choline is also vital to bone health in humans. low levels of choline have been linked to low bone density.Choline deficiency was found to be common in middle aged men and older women. The body can synthesize some choline on its own, but most of your choline comes from your diet, so make sure you eat choline risk foods and get your daily dose of bone building nutrients! Key Takeaways:
"They discovered that the average choline intake was significantly lower than the daily recommended intake — 255 mg/d for women and 259 mg/d for men aged 46–49 years, and for older adults 71-74 years, the intake was 265 mg/d for women and 258 mg/d for men." Read more: https://www.informationng.com/2017/06/need-choline-get.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4819) Why Are Diabetics More Prone to Heart Diseases?
Date:
May 28, 2017 07:14 PM
Diabetes Mellitus is a chronic disease that can lead to many dangerous complications, including coronary heart disease, cerebro-vascular disease, retinopathy, nephropathy, and neuropathy. Of these complications, coronary heart disease is of one of the most worrisome. Having diabetes doubles the risk of heart disease in men and triples the risk in women. This is because people with diabetes have vessel blockages that make them more susceptible to cardiac problems. It is important for people with diabetes to manage their risk by monitoring their blood sugar and lipid levels. They can do this by making lifestyle changes, such as exercising, avoiding smoking, and having appropriate screened tests performed. Read more: Why Are Diabetics More Prone to Heart Diseases?
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4718) Major Depressive Disorder Treatment Looks to Role of Lipids
Date:
May 15, 2017 06:44 AM
People with major depressive disorder often have a hard time because it's not easy to treat it. There are many medications but they often have very unpleasant side effects or just don't work at all. Patients usually have to keep trying new ones or higher doses just to keep themselves feeling somewhat normal. The role of lipids in their treatment is now being looked at. Hopefully this will help those who suffer from this disorder. Read more: Major Depressive Disorder Treatment Looks to Role of Lipids
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4618) How Do Dietary Cholesterol and Sterols Impact Your Cholesterol Levels?
Date:
May 10, 2017 11:44 AM
The Medical News Bulletin addresses the issue of cholesterol and its impact on the body. Many of the cholesterol levels in the human body can be attributed to the diet habits a person has on a daily basis, as well as plat sterols. As many people already know, cholesterol levels can be significant indicators of overall cardiac health among adults and controlling it seems to be key in longevity. According to the author of the article, the use of plant sterols assist greatly in reducing cholesterol levels. Key Takeaways:
"A new research study by Canadian scientists revealed that variations in cholesterol absorption and synthesis at an inter-individual level have a significant influence on plasma lipid levels in healthy individuals." Read more: https://www.medicalnewsbulletin.com/dietary-cholesterol-vs-plant-sterol-intake-cholesterol-metabolism/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4581) 10 Foods your liver loves you to consume
Date:
April 13, 2017 11:44 AM
The liver has an important role in keeping us healthy and filtering our systems. An unhealthy liver can lead to many diseases such as hepatitis, cirrhosis, cancer and cardiovascular disease. There are many foods that help the liver function well and guard against disease. These include dark leafy vegetables, broccoli, garlic, walnuts, blueberries, turmeric, pineapple, green tea and avocados. Fresh vegetables and fruits of any kind are beneficial as is limiting alcohol intake and being careful to stay away from toxins. Key Takeaways:
"Adopting healthy lifestyle changes such as regular exercise, lower alcohol intake and less exposure to toxins may help promote liver health. Avoiding foods that are high in fat, sugar and preservatives do your liver a huge favor." Read more: http://www.naturalnews.com/2017-04-02-7-foods-your-liver-loves-you-to-consume.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4402) Garlic helps lower cholesterol in diabetes patients
Date:
March 20, 2017 08:44 AM
A study recently published in the Pakistan Heart Journal would seem to indicate that eating garlic lowers cholesterol in diabetes patients. The study involved a sample group of thirty patients, with ages ranging from thirty to sixty years old. The patients were administered a dose of three hundred milligrams of a local garlic product for eight weeks, and showed improved rates of cholesterol. It is noted that statins are good for lowering cholesterol, but readers uncomfortable with statins might want to consider red rice yeast, which has also demonstrated effectiveness in lowering cholesterol. Key Takeaways:
"A report published in 2017 in Pakistan Heart Journal suggests that eating garlic can help improve the cholesterol status in patients with type 2 diabetes mellitus." Read more: http://www.foodconsumer.org/newsite/Nutrition/Food/garlic_helps_lower_cholesterol_in_diabetes_patients_0316170206.html
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4232) LOOK WHAT HAPPENS TO YOUR BODY AFTER CONSUMING THIS SUPER FOOD!!
Date:
March 04, 2017 10:19 AM
After consuming one amazing super food, the effect it has on your body is really amazing. The food is called Quinoa and it is amazing for you. It has a very delicious taste and offers so many different benefits. It is rich in vitamins and minerals that are great for your body. https://www.youtube.com/watch?v=CEJFA_MQHBwKey Takeaways:
"Quinoa or quinoa is a superfood that can not be missing from your shopping list, not only for its delicious taste but also for its many health benefits."
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4069) Fat discovery could ease inflammation for diabetics
Date:
February 20, 2017 02:59 PM
It turns out that fat discovery could ease inflammation for diabetics. Inflammation is a reason many diabetic people experience things like heart attacks and strokes. A possible trigger has been identified though. Over the last 20 years the amount of people with diabetes has gotten very high. There is progress being made to help these people. Key Takeaways:
"The researchers also plan to take a look at existing drug compounds that change the Lipid composition in cells." Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3984) Ways to Decrease the Risk of Heart Attack
Date:
February 20, 2017 12:59 PM
There are ways to decrease the risk of having a heart attack. A heart attack is a life changing event that hurts a lot of people and getting rid of the risks is one important way to avoid having this terrible thing happen. Eating right and exercise are two really important things. Replace burger with something like fish and eat more fruits and veggies. Key Takeaways:
"New evidence shows that an enteric-coated 81 milligram Aspirin daily decreases the risk of a second coronary attack." Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3983) Fibre supplement boosts weight loss and lowers blood sugar in obese adults: Study
Date:
February 11, 2017 10:59 AM
Fiber is important for the body. It helps keep our digestion regular. It can be found in foods and there are also supplements you can take. They contribute to weight loss and lower blood sugar in adults according to the study mentioned here. This would help out diabetics and others. Key Takeaways:
"Researchers think that the high viscosity of PGX might have caused participants to decrease their food intake, which then lead to significant weight loss, Lipid, insulin, and glucose reductions." Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3923) Heart health: why low cholesterol is no longer the focus
Date:
December 18, 2016 02:59 PM
One of the main focuses in healthcare today is lowering cholesterol. While it is one of the few things about improving heart health that you can change fairly easily, it is not the only factor involved. Most doctors look to the total cholesterol to give an idea of a person’s health, but the HDL is actually the most important value to know. By consuming more foods like fish, vegetables, and nuts, we can help increase our HDL levels. This will, in turn, lower our LDL and total cholesterol values. We should be focusing on our good cholesterol, not total cholesterol. Key Takeaways:
"Foods that feature in the Mediterranean diet pyramid, such as fish, olive oil, vegetables and nuts, can increase ‘good’ HDL cholesterol and reduce inflammation, a biochemical trigger in the development of cardiovascular disease, high blood pressure, cancer, HIV, type-2 diabetes and Alzheimer’s." Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3668) Is sweet potato tea is the next weight-loss wonder?
Date:
December 14, 2016 06:59 AM
The superfood status of sweet potatoes continues to grow. In addition to having fewer calories than a regular potato and containing vitamin A, vitamin B, and antioxidants, researchers are saying that the water they are boiled in could be super healthy as well. A study found that the proteins extracted from sweet potatoes when they are boiled can help with weight loss and Lipids. This has lead t further research on how best to get the proteins out of the used water and insert them into an more easily digested medium. Key Takeaways:
"“Finding alternative uses for the sweet potato proteins in wastewater could be good for the environment and industry, and also potentially for health.”" Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3638) Heart Disease and Poor Gut Health Go Hand In Hand
Date:
December 07, 2016 02:59 PM
A new mechanism has been discovered that connects phosphatidyl choline (also called lecithin), a common dietary fat, along with intestinal microflora, to an increased risk of heart disease. The study shows that the heart risk of people with a diet high in the Lipid depends on how the micro-organisms that live in their digestive tracts metabolize it. When lecithin and choline were fed to mice, the substances were converted to a heart disease-forming product by the intestinal microbes. In humans, higher blood levels of choline and the heart disease forming microorganism products are strongly associated with increased cardiovascular disease risk. Key Takeaways:
"Finding Balance: Empower Yourself with Tools to Combat Stress and Illness,” discuss heart disease and stomach bugs, and how the bacteria in your gut affects your health." Reference:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3591) The Health Benefits of Grape Seed Extract
Date:
November 14, 2016 10:20 PM
Grape seed extract is most commonly a waste product produced by the grape juice and winery industry. This is because grape seed extract doesn't go into finished drinks. Grape seed contains a wide variety of health-enhancing ingredients like protein, carbohydrates and Lipids (healthy fats). Immune systemA study done on healthy volunteers found that grape seed considerably increased the levels of antioxidants in the blood. So, another one of the benefits of grape seed is it helps boosts the immune system to fight against harmful compounds which may reduce the risk of chronic diseases including breast, stomach, colon, prostate and lung cancer.
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Do you want to improve your heart health, support brain function, and maintain your overall health? If so, then you need to start taking Vectomega! This revolutionary Omega-3 supplement is unlike any other on the market. Instead of using fish oil, Vectomega uses phosphoLipids to bind the Omega-3s. This makes them more effectively absorbed by the body and means that you only need to take one tablet a day!* Plus, Vectomega contains peptides which are not found in fish oil or krill oil. These peptides play a vital role in mood, immune system function, focus, and overall health! Don't miss out on this incredible supplement. Start taking Vectomega. 
Brain, Heart, and Eye Health 
A recent study has shown that Vitamin D may play a role in preventing cardiovascular disease. The study, which was conducted by researchers at the University of Edinburgh, looked at data from over 10,000 adults. They found that those who had the highest levels of Vitamin D were less likely to develop heart disease or have a stroke. This is great news for those looking to improve their heart health! 
What is a depression?
What is thyroid glands.jpg )
Importance of selenium
Royal jelly is a gelatin-held substance, which is normally emitted from the cephalic organs of the working drones for the expansion of the ruler honeybee. The hugeness of this white substance for ruler honeybee could be comprehended with a truth that without it, the monarch bumblebee and other working drones will not prosper.
What is a tamanu?
Green tea is made from the leaves of Camellia Sinensis, which is recognized for its health benefits. The nonfermented product is obtained by leaf desiccation that contains potent, polyphenolic antioxidants, with a flavanolic structure referred to as green- tea catechins, including epigallocat-echin-gallate (EGCG). Studies have shown that drinking EGCG prevents carcinogenesis in rodent organs. Studies have shown it had a significant chemoprotective effect against DMBA-induced mammary tumorigenesis in rats. Human breast cancer cell proliferation inhibition by green tea appeared mediated in part by (CKI). Mutagenesis was inhibited at concentration levels equivalent to human daily consumption.
A rich source of recuperating mixes, flax seed has been grown for more than 7000 years. Initially grown in Europe, the plant's tan seeds were customarily used to plan salves for aggravated skin and mending slurries for stoppage. Rich in essential oils, or Efas, flax seed oil is utilized to anticipate and treat coronary illness and to assuage a mixture of incendiary issue and hormone-related issues, incorporating fruitlessness. 
Pantethine (bis-pantethine or co-chemical pantethine) is a dimeric type of pantothenic harsh corrosive (vitamin B5). It is made out of two particles of pantothenic harsh corrosive connected by cysteamine crossing over aggregations. The monomer of this compound is regarded as pantetheine and is a halfway in the generation of Coenzyme A by the form. Pantethine is acknowledged the all the more naturally animated type of vitamin B5, yet it is less stable, disintegrating over the long haul in the event that it is not kept refrigerated most vitamins B5 supplements are subsequently as calcium pantothenate, a salt of pantothenic harsh corrosive. 
What is Lecithin
Dopa Mucuna has become used as an aphrodisiac. Which is still used to raise and help libido in both women and men. However it's an alternative treatment peculiarity now is extremely popular used as it provides potential and valuable results in managing Parkinson along with conditions. Pots include seeds called velvet beans or mucuna beans, these are glowing brown or black. Dopa Mucuna is generally be able to recover soil fertility and decrease weed infestation. In society medicine seeds can be used healing different conditions and disease. Mucuna beans have been used as a coffee alternate (ground and roasted) in Brazil, Central America, and other countries. 
Cholesterol is a Lipid, or a fat, which is produced by the liver. Though many know it not, cholesterol is essential for the normal function of the body. Amazingly, each and every cell of the body contains cholesterol in its outer layer. This Lipid serves several critical functions. Most importantly, cholesterol aids in building and maintaining cell membranes. The compound also determines which elements can pass through a cell membrane and which cannot; put differently, it determines cell permeability. The compound is also essential in the production of sex hormones, including androgens and estrogens. 
