Joint Joy

Joint Joy Uses, Dosage, Side Effects, Food Interaction and all others data.

Calcium citrate is a salt typically used as a source of calcium in a variety of over the counter supplements.

Increases plasma calcium levels leading to a decrease in calcium flux and increase in calcium deposition into bone

Chondroitin sulfate is a glycosaminoglycan considered as a symptomatic slow-acting drug for osteoarthritis (SYSADOA). The SYSADOA status suggested a pain relief and increased joint mobility after a relative long regular administration, as well as a long-lasting effect after the end of the treatment. Chondroitin sulfate is composed of alternating 1,3-N-acetyl-β-d-galactosamine and 1,4-β-d-glucuronic acid units which bear 4-O- and/or 6-O-sulfations at the N-acetylgalactosamine units disposed of in specific patterns. Depending on the predominating disaccharide unit, it will present different biological activities. Chondroitin sulfate is sold as an OTC dietary supplement in North America and it is a prescription drug under the EMA in Europe.

In clinical trials, chondroitin sulfate has been reported a significant pain relief. Some reports have shown no slow in joint damage. The effects of chondroitin sulfate have been very controversial. One of the characteristics of chondroitin is a slow onset of action with a maximal effect attained after several months. Chondroitin sulfate has been reported to have anti-inflammatory properties by reducing the synovitis and prevent proinflammatory cytokine up-regulation in arthritis models.

It is also registered an anabolic effect of chondroitin sulfate in which it induces the synthesis of hyaluronate in synovial cells, it increases type II collagen and proteoglycan synthesis.

Glucosamine is an amino sugar and a prominent precursor in the biochemical synthesis of glycosylated proteins and lipids. Glucosamine stimulates the production of proteoglycans and increases sulfate uptake by articular cartilage.

The administration of glucosamine, in theory, provides a building block towards the synthesis of glycosaminoglycans, slowing the progression of osteoarthritis and relieving symptoms of joint pain. Studies to this date examining the efficacy of glucosamine sulfate have been inconclusive. Glycosaminoglycans contribute to joint cartilage elasticity, strength, and flexibility. A systematic review of various studies and guidelines determined that modest improvements were reported for joint pain and function in patients taking glucosamine. A consistent joint space narrowing was observed, but with an unclear clinical significance.

Magnesium citrate is a low volume and osmotic cathartic agent. The cathartic action works primarily through the high osmolarity of the solution which draws large amounts of fluid into space where is used. Magnesium citrate is considered by the FDA as an approved inactive ingredient for approved drug products under the specifications of oral administration of a maximum concentration of 237 mg. It is also considered as an active ingredient in over-the-counter products.

The onset of action can be as early as 30 minutes after administration with a mean onset time of approximately 2 hours and a maximum action of 4 hours. The effect of magnesium citrate is highly dependent on the individual's hydration status.

Potassium chloride is a major cation of the intracellular fluid. It plays an active role in the conduction of nerve impulses in the heart, brain and skeletal muscle; contraction of cardiac skeletal and smooth muscles; maintenance of normal renal function, acid-base balance, carbohydrate metabolism and gastric secretion.

The potassium ion is in the principle intracellular cation of most body tissues. Potassium ions participate in a number of essential physiological processes including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal and smooth muscle, and the maintenance of normal renal function. The intracellular concentration of potassium is approximately 150 to 160 mEq per liter. The normal adult plasma concentration is 3.5 to 5 mEq per liter. An active ion transport system maintains this gradient across the plasma membrane. Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. The usual dietary intake of potassium is 50 to 100 mEq per day. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Such depletion usually develops as a consequence of therapy with diuretics, primarily or secondary hyperaldosteronism, diabetic ketoacidosis, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Depletion can develop rapidly with severe diarrhea, especially if associated with vomiting. Potassium depletion due to these causes is usually accompanied by concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. Potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent U-waves in the electrocardiogram, and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine. If potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long-term diuretic therapy, supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels. In rare circumstances (e.g., patients with renal tubular acidosis) potassium depletion may be associated with metabolic acidosis and hyperchloremia. In such patients, potassium replacement should be accomplished with potassium salts other than the chloride, such as potassium bicarbonate, potassium citrate, potassium acetate, or potassium gluconate.

Turmeric is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.

Joint Joy
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Joint Joy
Generic	Calcium Citrate + Withania Somnifera Extract + Vitamin B3 / Nicotinic Acid / Niacin + Magnesium Citrate + Glucosamine + Chondroitin Sulfate + Turmeric + Grape Seed Extract + Vitamin E / Tocopherol + Potassium Chloride
Weight	186.5mg
Type	Tablet
Therapeutic Class
Manufacturer	Neiss Labs Pvt Ltd
Available Country	India
Last Updated:	September 19, 2023 at 7:00 am

Uses

Calcium citrate is an ingredient found in a variety of supplements and vitamins.

For use as an over the counter calcium supplement.

Chondroitin sulfate, used with glucosamine, is indicated to alleviate pain and inflammation from primary osteoarthritis. This supplement is reported to improve joint function and slow disease progression. Osteoarthritis is characterized by progressive structural and metabolic changes in joint tissues, mainly cartilage degradation, subchondral bone sclerosis and inflammation of synovial membrane.

Studies have proposed the potential use of chondroitin sulfate as a nutraceutical in dietary supplements.

Indicated for the treatment of osteoarthritis of knee, hip, spine, and other locations. Also used as dietary supplement

Magnesium citrate is a laxative used in bowel preparation for colonoscopy or as a magnesium supplement.

Magnesium citrate has been used in bowel preparations prior to a colonoscopy as a cathartic agent.

It is also used in over-the-counter products to relieve occasional constipation.

Magnesium citrate can be one of the forms used for the administration of dietary supplements.

Potassium chloride is used for drug induced hypokalemia, liver cirrhosis, nausea, vomiting, cholera, diarrhoea, muscular weakness, paralysis, cardiac and congestive heart failure, diabetic ketoacidosis, ulcerative colitis, weakness, anorexia, drowsiness, Cushing's syndrome, pyloric stenosis, low blood pressure etc.

Joint Joy is also used to associated treatment for these conditions: Calcium Deficiency, Deficiency of Vitamin D3, Deficiency, Vitamin D, Folate deficiency, Hypocalcemia, Iron Deficiency (ID), OsteoporosisArthritis, Backache, Muscle Strain, Osteoarthritis (OA), Soreness, Muscle, Sprains, Eye lubrication, Joint supplementationArthritis, Backache, Joint Pain, Osteoarthritis (OA), Osteoarthritis of the KneeMigraineDehydration, Dry Mouth, Hypokalemia, Hypotonic Dehydration, Hypovolaemia, Isotonic Dehydration, Markedly Reduced Food Intake, Metabolic Acidosis, Hypodermoclysis, Mild Metabolic acidosis, Mild, moderate Metabolic Acidosis, Ocular edema, Acid-Base Balance, Bowel preparation therapy, Electrolyte replacement, Fluid replacement therapy, Hemodialysis Treatment, Hemofiltration, Parenteral Nutrition, Parenteral rehydration therapy, Plasma Volume Replacement, Urine alkalinization therapy, Fluid and electrolyte maintenance therapyOsteoarthritis (OA), Oral Nutritional Supplementation

How Joint Joy works

Calcium citrate increases plasma calcium levels. This reduces calcium flux from osteocyte activity by reducing the secretion of parathyroid hormone (PTH) . Calcium does this by stimulating a G-protein coupled calcium receptor on the surface of parathyroid cells. The reduction in calcium flux increases the amount of calcium deposited in bone resulting in an increase in bone mineral density. The reduction in PTH secretion also reduces the amount of vitamin D metabolized to its active form, calcidiol. Since calcidiol increases the expression of calcium dependent ATPases and transient receptor potential cation channel subfamily V member 6 (TRPV6) both of which are involved in calcium uptake from the gut, a reduction in calcidiol results in less calcium absorption. Additionally, TRPV5, the channel responsible for calcium reabsorption in the kidney, is downregulated when PTH secretion is reduced thus increasing calcium excretion via the kidneys. Another hormone, calitonin, is likely involved in the reduction of bone resorption during periods of high plasma calcium.

Chondroitin sulfate functions as a major component of the intricate extracellular matrix. It is proposed that chondroitin sulfate supply can provide new building blocks for the synthesis of new matrix components.

The anti-inflammatory effect of chondroitin sulfate is thought to be caused by the inhibition of the synthesis of inflammatory intermediates such as the inhibition of nitric oxide synthase, COX-2, microsomal prostaglandin synthase 1 and prostaglandin E2. It is reported also an inhibitory activity in the toll-like receptor 4 which will later inhibit inflammatory cytokines, NFkB and MyD88. This activity suggests a modulation of the MAP kinase pathway. On the other hand, some reports have pointed out an induction on the PKC/PI3K/Akt pathway in neuroblastoma.

The anabolic effect of chondroitin sulfate is suggested to be caused by the inhibition of metalloproteinases such as MMP-1, -3 and -13 as well as ADAMTS-4 and -5.

The mechanism of action of glucosamine in joint health is unclear, however there are several possible mechanisms that contribute to its therapeutic effects. Because glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, glucosamine supplements may help to rebuild cartilage and treat the symptoms of arthritis. Some in vitro studies show evidence that glucosamine reduces inflammation via inhibition of interferon gamma and Nuclear factor kappa B subunit 65 (NF-κB p65), improving the symptoms of arthritis and joint pain. Clinical relevance is unknown at this time.

It mainly works through its property of high osmolality which will draw large amounts of fluid into the colonic lumen. There is also a possible stimulation of fluid excretion by cholecystokinin release and activation of muscle peristalsis.

Supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels.

Dosage

Joint Joy dosage

500 mg tablet three times daily or as directed by the physician. A single dose of 1500 mg daily may also be effective. Obese individuals may need higher doses, based on body weight.

Oral:Dosage must be adjusted to the individual needs of each patient.

Adults: In severe deficiencies 3-6 tablets or 4-8 teaspoonful or 25-50 mmol per day orally in divided doses for some days with fruit juice, sweet or plain water.
Children: ½-1 teaspoonful twice daily or 1-3 mmol/kg body weight a day in several divided doses.

Patient should take Potassium chloride with meals.

Intravenous:

Severe acute hypokalaemia:

Adult: If serum potassium level >2.5 mEq/L, give at a rate not exceeding 10 mEq/hr in a concentration of up to 40 mEq/L. Max dose: 200 mEq/24 hr. If serum potassium level <2 mEq/L, may infuse at a rate of up to 40 mEq/hr. Continuous cardiac monitoring is essential. Max dose: 400 mEq/24 hr.

75 mg KCl equivalent to 1 mmol K+

Side Effects

Safety studies with Glucosamine show no demonstrable toxicity. Rarely occurring side effects like mild & reversible intestinal flatulence are almost like placebo.

GI ulceration (sometimes with haemorrhage and perforation or with late formation of strictures) following the use of enteric-coated K chloride preparation; hyperkalaemia. Oral: Nausea, vomiting, diarrhoea and abdominal cramps. IV: Pain or phloebitis; cardiac toxicity.

Toxicity

Patients taking more than 4g of calcium a day are at risk of hypercalcemia and metabolic alkalosis . Chronic intake of calcium supplements is associated with adverse gastrointestinal symptoms such as constipation and flatulence .

Chondroitin sulfate does not present a carcinogenic potential. On tolerability assays, it has been shown to present great safety and good tolerability without significant severe side effects.

The oral LD50 of glucosamine in rats is >5000 mg/kg. Symptoms of an overdose with glucosamine may include nausea, vomiting, abdominal pain, and diarrhea (common side effects of this drug). Severe and life-threatening hypersensitivity reactions to glucosamine may occur in patients with a shellfish allergy or asthma.

The occurrence of overdose with magnesium citrate is very unlikely but some of the signs of the presence of overdose are diarrhea or severe stomach pain.

The administration of oral potassium salts to persons with normal excretory mechanisms for potassium rarely causes serious hyperkalemia. However, if excretory mechanisms are impaired, of if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can result. It is important to recognize that hyperkalemia is usually asymptomatic and may be manifested only by an increased serum potassium concentration (6.5-8.0 mEq/L) and characteristic electrocardiographic changes (peaking of T-waves, loss of P-wave, depression of S-T segment, and prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9-12 mEq/L).

Precaution

Diabetics are advised to monitor blood glucose levels regularly while taking Glucosamine. No special studies were formed in patients with renal and/or hepatic insufficiency. The toxicological and pharmacokinetic profile of the product does not indicate limitations for these patients. However, administration to these patients with severe hepatic or renal insufficiency should be under appropriate medical supervision.

Renal or adrenocortical insufficiency; cardiac disease; acute dehydration; extensive tissue destruction. Pregnancy. Ensure adequate urine output; monitor plasma-potassium and other electrolyte concentrations. Discontinue treatment if severe nausea, vomiting or abdominal distress develops. Accumulation of potassium may occur in renal impairment.

Interaction

There have been no reports of significant drug interactions ofGlucosamine with antibiotics, antidepressants, antihypertensives, nitrates, antiarrhythmics, anxiolytic, hypoglycaemic agents, anti-secretives.

Potassium-sparing diuretics, ACE inhibitors, ciclosporin and potassium-containing drugs. Antimuscarinics delay gastric emptying time consequently increasing risk of GI adverse effects esp of solid oral dosage forms.

Volume of Distribution

After intramuscular administration of chondroitin sulfate, the apparent volume of distribution was 0.40 ml/g. When administered orally, the apparent volume of distribution changed to 0.44ml/g.

Results of a pharmacokinetic study of 12 healthy volunteers receiving three daily consecutive oral administrations of glucosamine sulfate soluble powder demonstrated glucosamine distribution to extravascular compartments. Human pharmacokinetic data for glucosamine is limited in the literature, however, a large animal model study of horses revealed a mean apparent volume of distribution of 15.4 L/kg. Concentrations of glucosamine ranged from 9-15 microM after an intravenous dose, and 0.3-0.7 microM after nasogastric dosing. These concentrations remained in the range of 0.1-0.7 microM in the majority of horses 12 hours after dosing, suggesting effectiveness of a once-daily dose. In rats and dogs, radioactivity from a C-14 labeled dose of glucosamine is detected in the liver, kidneys, articular cartilage, and other areas.

Elimination Route

The percentage of calcium absorbed varies inversely with intake . Tmax of about 3.5-5h varying with formulation .

Chondroitin sulfate is absorbed from the gastrointestinal tract. The absorbed portion reaches a ratio of 10% as unchanged chondroitin sulfate and 90% as depolymerized low-molecular-weight derivatives. This absorption depends on the sulfation status. The bioavailability of chondroitin sulfate ranges from 10-20% following oral administration. Reports have shown a consistent accumulation of the compound in joint tissue. The steady-state is attained after 3-4 days and it takes around 3-6 months to obtain the maximal effect.

After intramuscular administration of chondroitin sulfate, the peak plasma level of 3.8 mcg/ml was reached after 90 min. When given orally, the peak plasma concentration of 4.6 mcg/ml was reached after 240 min.

In a pharmacokinetic study, glucosamine was 88.7% absorption by the gastrointestinal tract. Absolute oral bioavailability was 44%, likely due to the hepatic first-pass effect. In a pharmacokinetic study of 12 healthy adults receiving oral crystalline glucosamine, plasma levels increased up to 30 times the baseline levels and Cmax was 10 microM with a 1,500 mg once-daily dose. Tmax was about 3 hours. AUC was 20,216 ± 5021 after a 15,000 mg dose.

Mean plasma concentration of magnesium after administration of oral doses of magnesium citrate are reported to be of around 0.7 mmol/L and the concentration in saliva rested in 0.28 mmol/L. In reports, it has also been proven that the absorption and bioavailability of magnesium are greater when administered in the form of magnesium citrate when compared with other forms such as magnesium ocude.

Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine.

Half Life

The approximate half-life of chondroitin sulfate and its derivative metabolites is 15 hours. After intramuscular administration of chondroitin sulfate in humans, the elimination half-life of the chondroitin sulfate was of 275 min. When administered orally, the elimination half-life was presented at 310 min.

The estimated half-life for glucosamine is 15 hours after an oral dose. After a bolus intravenous injection of 1005 mg crystalline glucosamine sulfate, the parent drug has an apparent half life of 1.11 hours.

The study of the half-life of magnesium citrate is very difficult due to the half-life of the available isotopes for magnesium.

Elimination Route

Cleared via the kidneys but largely reabsorbed (98-99%) under normal conditions .

Chondroitin sulfate is excreted in the urine as intact polymers and as partial degradation products. After intramuscular administration, about 37% of the administered dose is excreted by urine during the first 24 hours as high- and low-molecular-weight derivatives.

Fecal excretion of glucosamine in a pharmacokinetic study was 11.3% within 120 hours after administration. Urinary elimination was found to be 1.19% within the first 8 hours post-administration.

After oral administration of magnesium citrate, there is a 40% increase in urine excretion of magnesium. Magnesium citrate is also widely eliminated via the feces because, when present in the bowel, it relaxes the bowel and pulls water into the intestine which increases bowel movement and a significant portion of this agent gets excreted by this via.

Potassium is a normal dietary constituent and, under steady-state conditions, the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake.

Pregnancy & Breastfeeding use

Women who are pregnant or who could become pregnant should not supplement with glucosamine. Glucosamine has not been studied enough to determine their effects on a developing fetus. And no studies have evaluated the use of Glucosamine during pregnancy or lactation. It should be taken with caution and medical advice during pregnancy and lactation.

Category C: Either studies in animals have revealed adverse effects on the foetus (teratogenic or embryocidal or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the foetus.