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Search Term: " Sponge "
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 Secret to Gut Health: Feeding Your Microbiome for Maximum SCFAs 
Date:
September 11, 2026 01:29 PM
Your Complete Guide to Digestive Support: Building a Thriving Gut MicrobiomeWhen we talk about digestive health, the conversation usually stops at taking a daily probiotic or drinking enough water. But true microbiome health goes much deeper. It involves feeding the good bacteria you already have, ensuring your body can properly break down fats, and timing your supplements right.If you want to optimize your digestion, you need to understand how different fibers work, the magic of "postbiotics," and how specialized enzymes keep everything running smoothly. The Magic of Short-Chain Fatty Acids (SCFAs)To understand gut health, you have to understand a process called fermentation. When you eat dietary fiber that your stomach can't digest, it travels down into your colon. There, your gut bacteria feast on it.When these good bacteria eat fiber, they release beneficial byproducts called Short-Chain Fatty Acids (SCFAs) - most notably butyrate, acetate, and propionate. Think of SCFAs as the ultimate super-fuel for your digestive system. They provide the main energy source for the cells lining your colon, helping to keep the gut barrier strong and preventing "leaky gut." SCFAs also help calm inflammation throughout the body and play a massive role in healthy metabolism. But to get these benefits, you have to feed your microbiome the right type of fibers. The Ultimate SCFA-Boosting TrioNot all fibers are created equal. Some just add bulk to your stool, while others are "prebiotics" - meaning they actively feed your good bacteria. To maximize SCFA production, combining different types of prebiotic fibers is incredibly effective.Here is a functional combination that acts as a powerhouse for your microbiome:
Glucomannan vs. Psyllium: Which Fiber is Right for You?If you are looking to supplement with an isolated fiber for digestive support, you will likely encounter two heavyweight contenders: Glucomannan and Psyllium. Both are soluble fibers, meaning they dissolve in water to form a gel in your stomach, but they act a bit differently.
Can You Take Fiber With Vitamins?A very common question is whether you can take your daily fiber supplement alongside your morning vitamins.The short answer is no. You should separate them. Because soluble fibers (like psyllium, glucomannan, and even high doses of acacia) form a thick, sticky gel in your digestive tract, they act like a Sponge. If you take them at the exact same time as your daily vitamins or minerals, the fiber can bind to the nutrients. Instead of absorbing those vitamins into your bloodstream, your body will simply sweep them out in your next bowel movement. The Golden Rule: Take your vitamin and mineral supplements at least 1 hour before or 2 hours after taking a heavy fiber supplement. Beyond Fiber: The Benefits of Ox Bile for Fat DigestionFiber takes care of the carbohydrates, but what about the fats? Many people eat a healthy diet but still experience bloating, indigestion, or floating stools after a rich meal. This is often an issue with bile.Bile is a fluid produced by your liver and stored in your gallbladder. When you eat fats, your gallbladder squirts bile into your intestines. Think of bile like dish soap on a greasy frying pan—it emulsifies the fat, breaking it down into tiny droplets so your body can absorb it. If you have had your gallbladder removed, or if your liver is simply sluggish, your body might not release enough bile. This means fats pass through your system undigested, missing out on crucial fat-soluble vitamins (like Vitamins A, D, E, and K). This is where ox bile comes in. Taken as a supplement with meals, ox bile closely mimics human bile. The benefits include:
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6652) Grow Your Own Loofah Sponge (Yes, You Really Can!)
Date:
June 27, 2017 12:14 PM
Loofahs are usually purchased in the bath aisle, but they are actually a form of plant, otherwise called a sponge gourd. These sponges can be grown as well as purchased, and are used in the bath to exfoliate skin. This can keep skin from breaking out and help remove dead cells to give your skin a better appearance. To grow your own, you will need to buy Luffa seeds to plant, and allow 150 to 200 days for the loofah to grow. Once it dries out on the vine, it should be picked and the skin should be peeled. Key Takeaways:
"If you’ve been scrubbing your skin with your loofah sponge, you’re also adding trapped skin cells to the mix, giving the unwanted critters breakfast in bed, so to speak." Read more: https://draxe.com/loofah-sponge/
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=4893) Can Too Much Fiber Block Mineral Absorption ?
Date:
October 12, 2011 01:39 PM
Fiber Overview Fiber has always been known to be a helpful substance in many ways related to digestion and our bowel movements. In terms of how much is too much though we would need to look at first what fiber can do and how it works in the colon to have a broader point of view and to take all aspects into account before determining if too much fiber can cause health issues and specifically in this case, can cause a form of blockade for mineral absorption. What is Fiber and what does it do? Fiber, simply put is a substance that is found primarily in the outer layers of plants. Fiber is considered a carbohydrate and a special one at that because of its ability to stay intact even after passing through our digestive system unlike other carbohydrates that gets broken down by food and used for energy. For better understanding let’s talk more about its importance. For one, it has the ability to influence our digestive process in so many ways. It’s most evident importance and function is how it is able to regulate digestion and virtually slow the process down. With this, it is able to allow us to feel full longer which will cause less appetite therefore affecting weight and in turn overall health. With the same process it slows glucose processing as well which will aid in sugar levels and also helps nourish the colon’s lining to keep it from damage and maintain its health. However in a more practical sense, it aids in our digestion because of its Sponge like qualities. So if coupled with a good amount of water in the stomach it will aid and ease the stool and help bowel movements along. This is more known to many as a cleansing process which brings me back to the question, can it be too much and affect mineral absorption? Can too much affect absorption? A simple and most straight forward answer is “yes”. Yes it can, absolutely it can and “how?” you ask. As discussed above, one of the ways that fiber functions is aid with the cleansing process and the same Sponge like qualities are the primary reason why it can affect mineral absorption in the colon. The reason why fiber is effective for cleansing is because it absorbs bacteria and any other toxin or harmful substances in the colon and flushes it out therefore promoting good health however it can’t filter through its absorption process and select only those toxins, rather it absorbs both good and bad substances, the good in this case being the minerals. So before it can be absorbed by the body, fiber already caused it to be excreted. But this does not mean you stop taking fiber, remember the key words here are “too much” and all we need to do to avoid any mineral deficiency is to follow the right amount, we can check with our doctor for best advice but most experts believe getting somewhere around 30 – 35g maybe too much but then again most Americans does not even come close to that with their regular diets.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2506) Can You Take fiber With Vitamins?
Date:
September 06, 2011 03:10 PM
Fiber Overview Have you ever had a digestive problem, having hard time digesting food, feeling constipated or even constantly feeling bloated, if you have you probably have heard about fiber being possibly helpful to you, these days you are able to see lots of fiber enriched products in the market, it may be food in the grocery aisle or supplementation in the drug or health food store. Fiber has definitely reached a certain amount of popularity in mainstream natural remedies. It has shown great results in aiding in the relief of digestive tract problems through cleansing. And for many this is considered to be its main function, it allows in a way the purification of your digestive tract which leads to better health since toxins and harmful bacteria are flushed out from your system before it can make any damage. Now you may ask, what does this have to do with vitamin absorption? Fiber and How it works For us to understand what fiber’s relation is to vitamin absorption we need to look at first how it works. As mentioned above the key function of fiber is to cleanse the body and purify the digestive tract, in other words cleansing is the key when it comes to the relation of fiber to vitamin absorption. Looking into it with more detail, when fiber cleanses, it does take away toxins and harmful bacteria however with the same function or process it also may promote malabsorption as fiber does not have the ability to determine good from bad substances so in a way it will also flush out vitamins from the body before it can be absorbed. You see, the way fiber works is that it acts like a Sponge absorbing substances around it, with water it is able to create that cleansing effect as it absorbs water to help stool move along as it is softened by the liquid. Blocking certain vitamin absorption With how fiber works, if we are not careful the vitamins that we take in from the food we eat or from supplementation may not be absorbed by the body. So the answer to the question, if fiber can block vitamin absorption is yes it can. Fiber itself will not be the blockade, rather it is the characteristic it has and since it is not specifically a blockade we can work around that issue. We simply need to avoid taking too much fiber especially at times when we are also taking in either food that are high in vitamin content or vitamin supplementation itself that way the vitamins will stay long enough in our stomach for it to be absorbed by the body. Another thing to consider is, before allowing yourself to be scared of taking fiber is how much is too much fiber? Most researches have proven that 50 grams of fiber is more than should be consumed, however with that said most Americans does not reach that amount with their regular diet, in fact a regular American diet not infused with fiber rich foods only yields about 5 to 10g of fiber. The real question is, are you getting enough fiber to improve colon health because to much is impossible with out a fiber supplement.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2420) Does Eating Too Much Fiber Put On A Lot Of Flab?
Date:
September 02, 2011 11:33 AM
Many of us today has looked into fiber and its role in health and weight regulation, many researches also has backed up the claims of many companies that manufactures fiber supplements that fiber has benefits in both those areas. So whether you are someone who is an avid user of fiber or just someone who uses it occasionally, the question "Does too much fiber help me put on more flab?" might have come to mind a couple of times. I know it did for me, my reason was because I just simply felt heavier, for some they feel like they have a bigger pant size and these are just a few of the examples. Whatever the reason may be, for us to be able to answer that question with more accuracy, we need to examine two things. One is how fiber works in our body and two is how we gain weight in the first place and find out what the correlation is between the two. Fiber and how it works Many people use fiber for digestive purposes, more commonly for cleansing purposes and rightfully so because one of the main functions of fiber is to help alleviate the digestive tract through helping stool move along as long as there is ample amounts of water together with it. That is the catch because fiber works in such a way that when ingested into the intestines it absorbs the substances around it and it can do so as much as five times of its original weight. So with this, it can work both ways, if there is no water around to absorb, it absorbs solids therefore causing hardening of stool and move toward constipation for more severe instances. However with water around, it will absorb the liquid and create a flushing effect in our digestive tract aiding in the cleansing of toxins and other bacteria which could lead to more beneficial effects. Weight Gain or Flab Gain The formula for gaining weight is pretty simple. If you have worked out for any reason you might have come across the idea, calories equal energy and unused energy equals calories stored and calories stored equals weight gain. So when you gain weight it simply means you are taking in more calories that you can burn. That it is the only way you will gain weight and how does this relate to fiber intake? Fiber and weight gain According to researches too much fiber can cause weight gain and it does so because of its Sponge like properties. Going back to what we talked about above, it can cause stool hardening and constipation and that can cause some temporary weight gain and bloating making you feel like you have gained weight and your stomach bigger. That is one way. The other is when trying to increase fiber intake through fruits and vegetables or by other means, the additional calories that come along with it may cause the actual weight gain and the additional flab so fiber may be part of it but is not the direct culprit of the flab gain.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=2416) Activated Charcoal - Highly absorbent material to combat poisoning
Date:
April 24, 2008 02:44 PM
Activated charcoal has been treated by heat to open up millions of small spaces between the carbon atoms and turn it literally into an atomic Sponge that adsorbs both organic and organic impurities. This heat treatment is carried out in the absence of oxygen, so the charcoal cannot burn. Instead, what oxygen it did contain is driven off leaving behind all of these interstitial gaps that multiply the effective surface area by factors of ten. Since it is the surface area of the charcoal that determines its potency, then the greater this is the better. Activated charcoal has a massive surface area, and just ten grams has the same surface area as nine American football pitches or 77 tennis courts. Ten grams is just marginally more than a third of an ounce. The term adsorb has a different meaning to absorb, and while a real Sponge absorbs water by mopping it up through capillary action and suction, activation carbon adsorbs substances through a form of chemical attraction. You get rid of water from the Sponge by squeezing it, but that doesn’t work with activated charcoal, since the substances are bound to it, not just physically constrained. This huge surface area provides activated charcoal with innumerable bonding sites, and when chemicals that are attracted to carbon pass by they are attached to the surface. They cannot get free again, as water in a Sponge can, but are bound to the surface of the carbon. Because the digestive system has no effect on charcoal then whatever is bound to it passes naturally through the body. It is most effective at binding other carbon-based materials, and other substances with the right electronic arrangement, but others will just pass straight through. Because it is a chemical process, once all of the empty bonding sites have been taken up, the charcoal loses its effectiveness and has to be replaced. It is possible to regenerate it, but hardly worthwhile for you to do so because of the small quantities you use. Because of the way it works, activated charcoal can help people to recover from some forms of food poisoning. It can adsorb gases in the intestine and help to relieve the pain of excessive gas in the gut. It has many additional uses that will be touched on later, but for now we will look at its effect on poisons because that is where activated charcoal is of greatest benefit to us. It does not adsorb and neutralize all poisons, but is very effective with those that it can be sued for. Professor Touery proved a point when he drank a lethal dose of strychnine in front of colleagues at the French Academy of Medicine in 1831 and came through unscathed. He had mixed the strychnine with activated charcoal, and the fact that he lived after drinking a dose that would certainly have led to a very painful death within minutes testifies to the powerful effect of activated charcoal as an potential antidote for poisoning. Ever medicine cabinet should have an emergency supply of activated carbon, especially those with young children in the household. However, this is not good news for the pharmaceutical companies who have reacted by refuting some of the claims made in its favor: they have claimed that it is not effective against arsenic. If that is so, then how did Michel Bertrand survive after swallowing 5 grams of arsenic trioxide – 150 times what is regarded as the lethal dose? He did this is 1813 after mixing it with activated charcoal, just as Professor Touery was to do 18 years later with ten times the lethal dose of strychnine. It is true, however, that it does not have this degree of activity with all poisons, and it has no effect on cyanide, alcohols, antifreeze (glycols) and lithium. It also has no effect on corrosive poisons such as the strong alkalis used in oven clearers, or hydrocarbons such as kerosene. The way it works is adsorb the poison and prevent it being released into the body. For that to happen, the poison must have an affinity for carbon, and its adsorption site, and not all substances possess that property. Those that do however are permanently bound and therefore safe. For charcoal to be effective in neutralizing a poison, it must be swallowed within an hour of taking the poison, or the poison will be too far advanced ion the digestive process for the charcoal to do any good. Keep in mind, though, that it is not selective, and activated charcoal can adsorb nutrients and other beneficial constituents of your body’s chemistry. It is important therefore that you take in only when necessary: you might need several doses if the poison was severe, but once it has done its job it is not meant to be used as a maintenance material to take ‘just in case’. Used like that, it can do harm. If charcoal can adsorb poisons then it makes sense to believe that it can also adsorb some of the harmful agents that cause food poisoning. Not all food poisoning of course, but certainly those organisms that emit toxins that are attracted to carbon. And this is, in fact, the case. Food poisoning is caused by bacteria rather than viruses, and is not the presence of the bacteria that make you vomit and feel very ill. As bacteria grow in your body they release toxins, or poisons, into your digestive system. These poisons are what make you ill. They can seriously affect the complete gastro-intestinal tract, causing vomiting, diarrhea, and inflammation and swelling of the small and large intestine. The latter can cause abdominal cramps and severe colic, and the severity of the symptoms depends very much upon the type of bacteria and the number of them in your body. Many of these toxins are attracted to carbon since they are frequently organic based, and activated charcoal can be used to adsorb them. Once adsorbed they lose their potency, and since carbon is not digested by the body, they are passed harmlessly through the colon and eliminated in the faeces. It can also be used to eliminate many other foreign bodies from your gut, including viruses and fungi and might possibly reduce the concentration of uric acid, which can bring relief to gout sufferers. Activated charcoal has many uses, and is normally available in capsule form. It can be dangerous to take too much, particularly if you suffer from intestinal problems that cause constipation, because the charcoal itself can have that effect. However, there is no better emergency treatment for accidental poisoning in the home, although, since it is not suitable for all poisons, you must still regard poisoning as an emergency and contact the emergency services.
Activated charcoal, or activated carbon as it is sometimes called, is also a good emergency treatment for vomiting and the other unpleasant effects of food poisoning. It deals with bacterial toxins in the same way as any other, though once again you must refer to your physician before or after using it – preferably the former.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1769) Milk Thistle May Help With Cirrhosis, Gallstones, and Hepatitis Liver Problems
Date:
November 14, 2007 12:34 PM
Milk thistle, botanically Silybum Adans, is a member of the daisy family that is native to the Mediterranean, the Middle East and North Africa but has also been introduced to California and parts of the eastern side of the USA, and can help with problems such as cirrhosis, gallstones and hepatitis. Although it has been recorded as being used in medieval times as a tonic for the liver, it is only relatively recently that its chemical components have been investigated. Analysis indicated the presence of hitherto unknown flavonoids which were given the name of silymarin. In general, flavonoids are strong antioxidants found in many fruits and vegetables that eat up the free radicals that cause so much damage to our bodies. Free radicals are very unstable molecules that are generated through pollution, such as smoking, car fumes, perticides etc, and that destroy body cells accelerating aging. They also oxidise the low density lipids (LDL) that carry water-insoluble cholesterol through the blood to the arteries where it is needed to repair damage, resulting in excess deposition and the atherosclerosis that can cause strokes and heart disease. Antioxidants mop these up like a Sponge, and are some of the healthiest types of molecules that we can consume. The silymarin group of flavonoids are particularly attracted to the liver where they act as antihepatoxic agents that prevent the liver from becoming poisoned. But why should the liver be poisoned I can hear you ask, and what are the poisons involved? Can we avoid them? It is a very relevant question, and one that will make you wonder, every time you leave your home, especially if you live in a big city or an industrialized area. Smoking cigarettes, working with volatile organic compounds that you can breathe in, such as paint and printing ink solvents, the exhaust fumes of cars and diesel engines, factory chimneys belching out tons of smoke, analgesics such as paracetamol, pesticides on your fruit and vegetables that you have failed to wash off, alcohol, etc, etc, etc… All of these have to be removed from your body or you will die, awash with all these poisons that you have ingested, some deliberately and some not. The organ that does this is your liver: the powerhouse chemical plant of your body that carries out millions of biochemical reactions every day. Your liver converts all of these poisons into molecules that can be flushed away through your body naturally. However it places great stresses upon it, and even your liver needs a rest sometimes, or even just a little rejuvenating tonic would keep it happy. Milk thistle has been used for just that purpose, especially when the liver has been toxified with excess alcohol, pesticide poisoning or even hepatitis. The silymarin initially coats the cells of the liver by binding to the cell membranes of the cell walls, so that the toxins are hindered from entering the cells. Its antioxidant properties then neutralise any free radicals present that are causing the damage to the liver cells. It also helps to stimulate the production of proteins to help the healing process, and reduces the fibrosis that is the development of fibrous masses outside the liver cells caused by damaged cells excreting materials such as collagens outside the cells into the general body of the liver. Finally, milk thistle helps to prevent the activity of the immune system in causing inflammation of the damaged cells. Silymarin acts very specifically on the liver, and is often used by physicians in the treatment of such liver conditions as jaundice, hepatitis, liver cancer and cirrhosis. In addition to its own effects it appears that it stimulates the production of glutathione that is also a very powerful natural tripeptide antioxidant produced by the body when it is under oxidative stress. Its effect on cancer and some diseases is not curative, but to allow the liver to continue to detoxify the body when otherwise it might fail and lead to toxicity problems from which the patient might not be able to recover. Due to the remarkable regenerative powers of the liver, milk thistle is able to stimulate it into repairing its damage and grow fresh cells to replace the damaged ones. This is the reason for its effectiveness in otherwise very serious degenerative diseases. It is often prescribed by doctors for patients who are taking a number of different medications. Which help the liver to metabolize these medications, since without it, it might struggle to provide the true efficacy of the prescribed drugs. So far we have been concentrating on the liver, but milk thistle has other properties not connected directly with the hepatic function. It can help to promote the production of bile in the gall bladder and so give the digestive system a boost when needed, where it also acts as a mild laxative. However, it can also help patients suffering from both lose stools and constipation due its effect. It can also help to relieve gallstones, though medical tests are generally carried out first to ensure that they are not too large for the milk thistle to handle. It is also an anti-inflammatory, and is useful in the treatment of acne and other inflammatory responses, and also for inflammations in the gall bladder, kidney and bladder. There are few serious side effects, although, as milk thistle rids the body of toxins, these toxins can cause problems such as diarrhea, headaches and abdominal pain. Keep in mind that you are releasing poisons from the liver into your system so that they can be expelled by the usual means, and they will put up a fight along the way. However, the milk thistle will usually win in the end. There currently appear to be no long term issues with taking milk thistle as a supplement over a long period, and it is good way to maintain a healthy liver. Keep in mind that the liver is the body’s chemical plant, where most of the biochemical reactions of life take place, and without we cannot survive. It makes sense, therefore, to look after your liver, and milk thistle is one way of doing that; some would say the best way.
So remember that, although milk thistle may help with cirrhosis, gallstones and hepatitis liver problems, you should be prepared for a short struggle before it wins the day. Always consult your family physician for a clear diagnosis before self prescribing herbs as treatment. Your physician can advise you as the correct course of action to take once diagnosed with a liver blood test first. But, to boost overall health and wellness milk thistle is a great herbal supplement to take on a daily basis.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1631) CHITOSAN: The Fiber that Binds Fat 
Date:
June 25, 2005 07:55 PM
Overview Chitosan is a natural product that inhibits fat absorption. It has the potential to revolutionize the process of losing weight and by so doing, reduce the incidence of some of the most devastating Western diseases we face today. Chitosan is indigestable and non-absorbable. Fats bound to chitosan become nonabsorbable thereby negating their caloric value. Chitosan-bound fat leaves the intestinal tract having never entered the bloodstream. Chitosan is remarkable in that it has the abilty to absorb an average of 4 to 5 times its weight in fat.60 The same features that allow chitosan to bind fats endow it with many other valuable properties that work to promote health and prevent disease. Chitosan is a remarkable substance whose time has come.
Chitin, the precursor to Chitosan, was first discovered in mushrooms by the French professor Henri Braconnot in 1811.61 In the 1820’s chitin was also isolated from insects.62 Chitin is an extremely long chain of N-acetyl-D-glucoseamine
FIGURE 2. glucoseamine units. Chitin is the most abundant natural fiber next to cellulose and is similar to cellulose in many respects. The most abundant source of chitin is in the shells of shellfish such as crab and shrimp. The worldwide shellfish harvest is estimated to be able to supply 50,000 tons of chitin annually.63 The harvest in the United States alone could produce over 15,000 tons of chitin each year.64 Chitin has a wide range of uses but that is the subject of another book. Chitosan was discovered in 1859 by Professor C. Rouget.65 It is made by cooking chitin in alkali, much like the process for making natural soaps. After it
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---------------------------------- is cooked the links of the chitosan chain are made up of glucosamine units. Each glucosamine unit contains a free amino group. These groups can take on a positive charge which gives chitosan its amazing properties. The stucture of chitosan is represented schematically in Figure 2. Research on the uses of chitin and Chitosan flourished in the 1930s and early 1940s but the rise of synthetic fibers, like the rise of synthetic medicines, overshadowed the interest in natural products. Interest in natural products, including chitin and chitosan, gained a resurgence in the 1970s and has continued to expand ever since. Uses of Chit osan Some of Chitosan's major uses—both Industrial and Health and Nutritional—are listed in Tables 5 and 6. Water Purification Chitosan has been used for about three decades in water purification processes. 67 When chitosan is spread over oil spills it holds the oil mass together making it easier to clean up the spill. Water purification plants throughout the world use chitosan to remove oils, grease, heavy metals, and fine particulate matter that cause turbidity in waste water streams. Fat Binding/ Weight Loss Like some plant fibers, chitosan is not digestible; therefore it has no caloric value. No matter how much chitosan you ingest, its calorie count remains at
------------------------------ fibers, chitosan’s unique properties give it the ability to significantly bind fat, acting like a “fat Sponge” in the digestive tract. Table 7 shows a comparison of chitosan and other natural fibers and their ability to inhibit fat absorption. Under optimal conditions, Chitosan can bind an average of 4 to 5 times its weight with all the lipid aggregates tested.60 (NOTE: This assessment was made without the addition of ascorbic acid which potentiates this action even further.77 Studies in Helsinki have shown that individuals taking chitosan lost an average of 8 percent of their body weight in a 4-week period.76 Chitosan has increased oil-holding capacity over other fibers.108 Among the abundant natural fibers, chitosan is unique. This uniqueness is a result of chitosan’s amino groups which make it an acid absorbing (basic) fiber. Most natural fibers are neutral or acidic. Table 7 summarizes the in vivo effects in animals of various fibers on fecal lipid excretion. As can be seen from the results listed, ingestion of chitosan resulted in 5-10 times more fat excretion than any other fiber tested. D-Glucosamine, the building block of chitosan, is not able to increase fecal fat excretion. This is due to the fact that glucosamine is about 97 percent absorbed while chitosan is nonabsorbable. Fats bound to glucosamine would likely be readily absorbed along with the glucosamine. Chitosan, on the other hand, is not absorbed and therefore fats bound to chitosan can not be absorbed. Cholesterol Control Chitosan has the very unique ability to lower LDL cholesterol (the bad kind) while boosting HDL cholesterol (the good kind).78 Laboratory tests performed on rats showed that “chitosan depresses serum and liver cholesterol levels in cholesterol- fed rats without affecting performance, organ weight or the nature of the feces.”79 Japanese researchers have concluded that Chitosan “appears to be an effective hypocholesterolemic agent.”80 In other words, it can effectively lower blood serum cholesterol levels with no apparent side effects. A study reported in the American Journal of Clinical Nutrition found that Chitosan is as effective in mammals as cholestryramine (a cholesterol lowering drug) in controlling blood serum cholesterol without the deleterious side effects typical of cholestryramine. 81 Chitosan decreased blood cholesterol levels by 66.2 percent.82 It effectively lowered cholesterol absorption more than guar gum or cellulose.83 Laboratory test results indicated that a 7.5% chitosan formula maintained adequate cholesterol levels in rats, despite a dramatic increase in the intake of cholesterol. 84
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Fiber and Flab Overview 
