STILEGE MAX TABLETS

Indications

• Selenium deficiency
• Supportive therapy in conditions requiring antioxidant support
• Potential adjunct in cancer prevention strategies

Dosage

Children: Refer to BNF for Children for specific dosing information.

Adults: Initially 100–500 micrograms daily, adjusted according to response and serum levels.

Mechanism of action

Selenium is metabolized to selenophosphate and selenocysteine, which are essential for the synthesis of selenoproteins. This process involves the incorporation of selenium into proteins through a specialized tRNA that recognizes the RNA sequence UGA, which is facilitated by SECIS structures and SBP-2 proteins. Key selenoproteins, like glutathione peroxidases, help protect cells from oxidative damage, thus playing a significant role in reducing the risk of diseases such as atherosclerosis and certain cancers.

Pharmacodynamics

Selenium is incorporated into various selenoproteins that perform essential functions, including antioxidant activity, redox balance, and regulation of thyroid hormones. Its role in antioxidant defense mechanisms is particularly important for protecting cells against reactive oxygen species (ROS). Selenium supplementation has been linked to improved immune function and potential cancer prevention.

Pharmacokinetics

Selenium is absorbed through the gastrointestinal tract, and its bioavailability can vary based on the source and form of selenium. Once absorbed, it is distributed to various tissues, where it is incorporated into selenoproteins. Selenium is primarily excreted through urine, and its half-life can depend on dietary intake and individual metabolism. Selenium status can be assessed through blood levels of selenoproteins and selenium itself.

Adverse effects

• Nausea
• Anaemia
• Aplastic anaemia
• Skin reactions
• Gastrointestinal disorders

Precautions

• Selenium supplementation should not be given unless there is good evidence of deficiency.
• Use caution in patients with a history of hypersensitivity to selenium or its compounds.

Pregnancy

Limited information is available regarding selenium supplementation during pregnancy. Consult specialist sources for guidance.

Breast-feeding

Limited information is available; the effect of selenium on copper levels in milk is conflicting, and its impact on the infant is unknown.

Storage

After opening, store in a refrigerator (2–8°C).

Formulations

• Tablets (e.g., L-Selenomethionine 200 micrograms, SelenoPrecise 100 micrograms)
• Capsules (e.g., Trientine dihydrochloride 250 mg)
• Injection solutions (e.g., Sodium selenite 50 micrograms per 1 ml)

Indications

• Hypertension
• Benign prostatic hyperplasia
• Urinary retention related to prostate enlargement

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines in the paediatric population.

Adults: Refer to the BNF for specific dosing recommendations based on individual clinical scenarios.

Mechanism of action

Alpha acts by selectively blocking alpha-1 adrenergic receptors, which are responsible for mediating vasoconstriction in blood vessels. By inhibiting these receptors, alpha promotes vasodilation, leading to a decrease in peripheral vascular resistance and subsequently lowering blood pressure. Additionally, this action can help alleviate urinary symptoms associated with an enlarged prostate.

Pharmacodynamics

The pharmacodynamics of alpha involve its competitive antagonism at alpha-1 adrenergic receptors, resulting in decreased vasoconstriction and increased blood flow. This mechanism is beneficial in conditions characterized by high blood pressure and urinary retention due to prostatic enlargement. The onset of action typically occurs within hours, with peak effects observed within a few days of consistent dosing.

Pharmacokinetics

Alpha is absorbed well from the gastrointestinal tract, with peak plasma concentrations achieved within 1-3 hours post-administration. The drug undergoes hepatic metabolism, primarily via cytochrome P450 enzymes, resulting in active and inactive metabolites. The elimination half-life varies, but it generally is around 6-12 hours, allowing for once-daily dosing in many cases. Renal excretion is a significant route for its metabolites, necessitating caution in patients with renal impairment.

Interactions

• maois, irreversible + alpha blockers: Severe (increases effects)
• ribociclib + alpha blockers: Severe (increases exposure)
• cobicistat + alpha blockers: Moderate (increases exposure)
• idelalisib + alpha blockers: Moderate (increases exposure)
• dronedarone + alpha blockers: Unknown (increases exposure)
• antifungals, azoles + alpha blockers: Unknown (increases exposure)
• crizotinib + alpha blockers: Unknown (increases exposure)
• imatinib + alpha blockers: Unknown (increases exposure)
• letermovir + alpha blockers: Unknown (increases exposure)
• clarithromycin + alpha blockers: Unknown (increases exposure)

Indications

• Cognitive impairment
• Dementia
• Memory enhancement
• Anxiety
• Peripheral vascular disease

Dosage

Children: Safety and efficacy in children have not been established. Use is not generally recommended without professional guidance.

Adults: Refer to specific product guidelines, as Ginkgo biloba is available in various forms including tablets, extracts, and teas. Typical doses range from 120 to 240 mg per day, divided into two or three doses.

Mechanism of action

The exact mechanism of action of Ginkgo biloba is not fully understood, but it is believed to enhance cerebral blood flow and improve circulation by inhibiting platelet-activating factor (PAF) and promoting vasodilation through nitric oxide release. Additionally, the antioxidant properties of flavonoids and terpenoids may protect neurons from oxidative stress and free radical damage.

Pharmacodynamics

Ginkgo biloba exhibits several pharmacodynamic effects, including increased blood flow to the brain, improved oxygen utilization, and enhanced glucose metabolism. It may also modulate neurotransmitter systems, including serotonin and dopamine, which could contribute to its effects on mood and cognitive function. The anti-inflammatory properties may further aid in neuroprotection.

Pharmacokinetics

Ginkgo biloba extracts are well-absorbed after oral administration. The bioavailability of its active constituents varies, and peak plasma concentrations occur within 1 to 4 hours post-ingestion. The elimination half-life of ginkgo flavonoids is approximately 4 to 5 hours, and metabolites are primarily excreted in urine. Factors such as age, health status, and concurrent medications can affect its pharmacokinetics.

Adverse effects

• Headache
• Dizziness
• Gastrointestinal upset
• Allergic skin reactions
• Palpitations

Interactions

• Anticoagulants (e.g., warfarin)
• Antiplatelet agents (e.g., aspirin)
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Certain antidepressants (e.g., selective serotonin reuptake inhibitors)

Precautions

• Use with caution in patients with bleeding disorders
• Monitor for potential interactions with other medications
• Discontinue use prior to surgery to reduce bleeding risk

Pregnancy

Not recommended due to insufficient safety data.

Breast-feeding

Lack of sufficient data, caution is advised.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Tablets
• Capsules
• Liquid extracts

Indications

• Osteoarthritis
• Rheumatoid arthritis
• Asthma
• Inflammatory bowel disease
• Chronic inflammatory conditions

Dosage

Children: Refer to established guidelines for appropriate dosing, as specific doses can vary based on formulation and clinical condition.

Adults: Refer to established guidelines for appropriate dosing, as specific doses can vary based on formulation and clinical condition.

Mechanism of action

Boswellic acids inhibit the enzyme 5-lipoxygenase, which is involved in the production of leukotrienes, inflammatory mediators. By blocking this pathway, boswellia reduces inflammation and may alleviate pain associated with conditions like arthritis and asthma.

Pharmacodynamics

Boswellia exhibits anti-inflammatory, analgesic, and potentially immunomodulatory effects. Its action on leukotriene synthesis is significant in conditions characterized by excessive inflammation. The anti-inflammatory effects may help in reducing symptoms of chronic inflammatory diseases, such as osteoarthritis and rheumatoid arthritis.

Pharmacokinetics

Boswellia is absorbed in the gastrointestinal tract and its bioavailability may be enhanced when taken with fatty meals. The metabolism and excretion pathways of boswellic acids are not fully elucidated, but they are believed to undergo hepatic metabolism. Their half-life may vary, necessitating multiple doses for sustained effects.

Adverse effects

• Nausea
• Diarrhea
• Abdominal pain
• Skin rash
• Allergic reactions

Interactions

• May interact with anticoagulants and antiplatelet drugs, increasing the risk of bleeding
• Potential interaction with NSAIDs, which may enhance gastrointestinal side effects

Precautions

• Use with caution in patients with a history of gastrointestinal disorders
• Monitor for allergic reactions, especially in patients with known sensitivities to resins or similar compounds

Pregnancy

Boswellia is generally not recommended during pregnancy due to a lack of safety data.

Breast-feeding

Insufficient information is available on the excretion of boswellia in human milk; caution is advised.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Capsules
• Tablets
• Extracts
• Topical preparations

Indications

• Osteoarthritis
• Rheumatoid arthritis
• Joint pain
• Cartilage repair
• Tissue engineering

Dosage

Children: Dosage for cartilage-related conditions in paediatric patients should be determined by a healthcare professional, taking into account the child's age, weight, and specific clinical situation.

Adults: Dosage for cartilage-related conditions is highly variable and should be determined by a healthcare professional based on individual patient needs and clinical guidelines.

Mechanism of action

Cartilage does not have a specific pharmacological mechanism of action as it is a biological tissue rather than a drug. However, it contributes to joint stability and mobility by reducing friction between bones during movement and absorbing shock. The chondrocytes within cartilage are responsible for maintaining the extracellular matrix, which is essential for the tissue's resilience and function.

Pharmacodynamics

The pharmacodynamics of cartilage is primarily related to its role in joint health and function. It helps to distribute loads across joint surfaces and acts as a cushion to protect bones from impact. The degradation of cartilage, often seen in conditions like osteoarthritis, leads to pain and decreased mobility due to increased friction and bone-on-bone contact. Cartilage also plays a role in the inflammatory response within joints, influencing the severity of conditions like rheumatoid arthritis.

Pharmacokinetics

As cartilage is a biological tissue, it does not have traditional pharmacokinetic properties like absorption, distribution, metabolism, and excretion observed in drugs. However, factors such as age, mechanical stress, and nutritional status can affect the health and maintenance of cartilage. The healing process of cartilage is slow due to its avascular nature, meaning it has limited blood supply and, therefore, a limited capacity for regeneration.

Pregnancy

Data on the safety of cartilage supplements during pregnancy is limited. It is advisable to consult a healthcare provider before use.

Breast-feeding

There is insufficient data on the safety of cartilage supplements during breastfeeding. Consultation with a healthcare provider is recommended.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Type 2 diabetes mellitus
• Dyslipidemia
• Metabolic syndrome
• Antioxidant support
• Anti-inflammatory conditions

Dosage

Children: Specific dosing for children should be determined by a healthcare professional based on individual circumstances and clinical guidelines.

Adults: Dosage varies based on formulation and indication. Commonly, 1-6 grams of powdered cinnamon can be used daily, though specific recommendations should be based on clinical guidelines and individual patient needs.

Mechanism of action

Cinnamon exerts its effects primarily through the modulation of insulin signaling pathways. Cinnamaldehyde enhances insulin sensitivity and may stimulate glucose uptake by cells. It also has antioxidant properties, which help in reducing oxidative stress. Additionally, components of cinnamon may inhibit enzymes involved in carbohydrate digestion, leading to a reduction in postprandial blood glucose levels.

Pharmacodynamics

Cinnamon demonstrates several pharmacodynamic effects, including anti-inflammatory, antioxidant, and antimicrobial activities. Its active compounds can help regulate blood glucose levels, improve lipid profiles by reducing triglycerides and LDL cholesterol, and exhibit potential benefits in metabolic syndrome and type 2 diabetes management.

Pharmacokinetics

The bioavailability of cinnamon compounds varies, but cinnamaldehyde is rapidly absorbed and metabolized in the liver. Its metabolites can be detected in plasma, and the half-life varies based on the dose and formulation. The onset of action for cinnamon extract may vary, and continuous consumption is often required to achieve significant clinical effects. Cinnamon is generally well-tolerated, with minimal adverse effects reported.

Adverse effects

• Allergic reactions
• Gastrointestinal discomfort
• Liver toxicity (with excessive consumption of Cassia cinnamon)

Precautions

• High doses may cause liver damage due to coumarin content in Cassia cinnamon.
• Caution in individuals with liver disease.

Pregnancy

Cinnamon is generally considered safe in food amounts during pregnancy, but high doses should be avoided.

Breast-feeding

Cinnamon is likely safe in food amounts while breastfeeding, but excessive use should be avoided.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Ground cinnamon
• Cinnamon sticks
• Cinnamon oil
• Cinnamon extract

Indications

• Bone health support
• Joint pain relief
• Weight management
• Anti-inflammatory effects
• Antioxidant support

Dosage

Children: Refer to specific product guidelines for dosing recommendations, as there are no standardized doses established.

Adults: Refer to specific product guidelines for dosing recommendations, as there are no standardized doses established.

Mechanism of action

Cissus quadrangularis exhibits several mechanisms of action, primarily attributed to its active compounds such as flavonoids, phenolic compounds, and triterpenoids. These compounds are known to possess anti-inflammatory, antioxidant, and analgesic properties. Cissus may promote the synthesis of collagen, thereby aiding in bone and connective tissue health. Additionally, it may modulate the activity of certain enzymes involved in metabolic processes, contributing to its weight management effects.

Pharmacodynamics

The pharmacodynamic effects of cissus are primarily related to its anti-inflammatory and analgesic properties. It is thought to inhibit the production of pro-inflammatory cytokines and increase antioxidant activity, which can alleviate pain and inflammation. Furthermore, the plant may play a role in regulating lipid metabolism and reducing oxidative stress, which can benefit overall metabolic health.

Pharmacokinetics

The pharmacokinetics of cissus are not extensively studied. However, it is generally understood that the active compounds in cissus are absorbed in the gastrointestinal tract, with their bioavailability influenced by various factors including formulation and individual metabolism. The elimination half-life and specific metabolic pathways remain largely unknown and require further research to clarify.

Adverse effects

• Gastrointestinal disturbances
• Headache
• Dizziness
• Allergic reactions

Interactions

• May enhance the effects of anticoagulants
• Potential interaction with antihyperglycemic agents

Precautions

• Use with caution in patients with diabetes
• Avoid use in pregnant or breastfeeding women unless advised by a healthcare professional

Pregnancy

Limited data on safety during pregnancy; consult a healthcare professional before use.

Breast-feeding

Insufficient data on safety during breastfeeding; consult a healthcare professional before use.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Powder
• Capsules
• Tinctures

Indications

• Skin aging and wrinkle reduction
• Joint pain and osteoarthritis
• Tendon and ligament injuries
• Bone health
• Wound healing

Dosage

Children: Refer to specific product guidelines or consult a healthcare professional for appropriate dosing based on the indication and formulation used.

Adults: Refer to specific product guidelines or consult a healthcare professional for appropriate dosing based on the indication and formulation used.

Mechanism of action

Collagen exerts its effects primarily by providing the necessary amino acids, such as glycine, proline, and hydroxyproline, that are crucial for the synthesis of new collagen in the body. It is thought to stimulate fibroblast proliferation, which leads to increased collagen production and improved tissue repair. Additionally, collagen may enhance the hydration of the skin and improve its elasticity.

Pharmacodynamics

Collagen supplementation may promote the synthesis of new collagen and improve the integrity of the extracellular matrix. This can lead to improved skin hydration, elasticity, and the reduction of wrinkles. In joint health, collagen may help reduce inflammation and pain, contributing to improved mobility and function. The effects can vary based on the source of collagen (bovine, porcine, marine) and the form of administration (powder, liquid, capsules).

Pharmacokinetics

After oral administration, collagen peptides are absorbed in the gastrointestinal tract and enter the bloodstream. They can be transported to various tissues where they may be incorporated into the extracellular matrix. The half-life of collagen peptides is relatively short, and they are metabolized in the liver and other tissues. The bioavailability of collagen can vary based on the formulation and the presence of other dietary components.

Adverse effects

• Allergic reactions
• Skin rash
• Itching
• Gastrointestinal disturbances
• Nausea

Precautions

• Use with caution in individuals with fish allergies if derived from fish sources
• Monitor for allergic reactions

Pregnancy

Collagen is generally considered safe during pregnancy, but consult a healthcare professional before use.

Breast-feeding

Collagen is likely safe during breastfeeding, but consult a healthcare professional before use.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Formulations

• Powder
• Capsules
• Liquid

Indications

• Copper deficiency
• Occipital Horn Syndrome
• Menke's disease
• Contraception (via copper IUD)

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: Refer to the relevant clinical guidelines and BNF for specific dosing information.

Mechanism of action

Copper is absorbed from the gastrointestinal tract via high affinity copper uptake proteins and low affinity copper uptake proteins, likely being reduced to the Cu1+ form prior to transport. Inside enterocytes, it binds to the copper transport protein ATOX1, which facilitates its transport to copper transporting ATPase-1 on the Golgi membrane for incorporation into the Golgi apparatus. Once in systemic circulation, copper binds primarily to ceruloplasmin, albumin, and alpha 2-macroglobulin. It acts as a cofactor in a variety of oxidase enzymes and also influences sperm motility when released from copper IUDs, contributing to its contraceptive effect.

Pharmacodynamics

Copper is essential for the activity of many enzymes and plays a vital role in processes such as iron metabolism, neurotransmitter synthesis, and antioxidant defense. Copper ions, particularly when released from intrauterine devices, have been shown to decrease sperm viability, thereby impacting fertility.

Pharmacokinetics

Copper is absorbed from the gut and is predominantly transported in the plasma bound to proteins such as ceruloplasmin and albumin. The absorption efficiency can vary; however, a significant portion of dietary copper is usually absorbed. The body regulates copper levels through hepatic excretion and storage mechanisms, ensuring homeostasis. Excess copper can lead to toxicity, while deficiency results in various health issues.

Pregnancy

Copper is considered essential during pregnancy, but excessive intake should be avoided due to potential toxicity.

Breast-feeding

Copper is excreted in breast milk, and adequate maternal intake is important for infant development.

Storage

Store in a cool, dry place, away from moisture and heat.

Indications

• General wellness support
• Anti-inflammatory effects
• Antioxidant activity
• Digestive aid
• Support for immune function

Dosage

Children: Paediatric dosing should be determined based on the specific extract and its intended use. Consultation with a healthcare provider is recommended for accurate dosing.

Adults: Dosage varies widely depending on the specific extract and formulation. It is essential to follow the manufacturer's instructions or consult a healthcare professional for appropriate dosing.

Mechanism of action

The mechanism of action of herbal extracts can vary significantly based on their constituents. Commonly, they exert their effects through multiple pathways including modulation of neurotransmitter systems, interference with inflammatory processes, or direct antioxidant activity. Some extracts may activate certain receptors or inhibit enzymes related to disease processes.

Pharmacodynamics

The pharmacodynamics of extracts is complex due to the presence of multiple active compounds which can have synergistic or antagonistic effects. These compounds may influence cellular signaling pathways, alter gene expression, or modulate immune response. The overall pharmacological profile is determined by the specific composition of the extract, its concentration, and the biological target it interacts with.

Pharmacokinetics

The pharmacokinetics of extracts involves absorption, distribution, metabolism, and excretion of the active compounds. Generally, herbal extracts are absorbed in the gastrointestinal tract, with bioavailability influenced by factors such as formulation, the presence of food, and individual metabolic differences. Compounds may undergo hepatic metabolism, and elimination can occur through urine or feces, depending on their chemical nature.

Pregnancy

Consult a healthcare professional before use, as the safety of the extract during pregnancy has not been established.

Breast-feeding

Consult a healthcare professional before use, as the safety of the extract during breastfeeding has not been established.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Folate deficiency
• Megaloblastic anemia
• Prevention of neural tube defects in pregnancy
• Supplementation in patients on certain medications (e.g., methotrexate)

Dosage

Children: Refer to the BNF for Children for appropriate pa

Adults: Refer to specific guidelines or the BNF for appropriate adult dosing based on the indication.

Mechanism of action

Folate functions as a coenzyme in the conversion of homocysteine to methionine, a process that is vital for DNA synthesis and repair. It is involved in the one-carbon metabolism pathway, where it acts as a carrier of one-carbon units necessary for the synthesis of purines and thymidylate, thus supporting the production of nucleotides and DNA. This mechanism is particularly important in rapidly dividing cells.

Pharmacodynamics

Folate is critical for the formation of red blood cells and the proper functioning of the nervous system. It aids in the production of nucleic acids, which are essential for cell proliferation. Folate deficiency can lead to impaired DNA synthesis, resulting in megaloblastic anemia characterized by the presence of large, immature red blood cells in the bloodstream. Adequate folate levels are also associated with reduced risk of neural tube defects in developing fetuses.

Pharmacokinetics

Folate is absorbed in the proximal part of the small intestine, primarily in the jejunum, and is transported in the bloodstream bound to plasma proteins. It undergoes hepatic metabolism and is stored mainly in the liver. The elimination half-life varies, but dietary folate can be retained in the body for several weeks. Excess folate is excreted through the urine. The bioavailability of folate from food sources is lower compared to synthetic folic acid found in supplements.

Interactions

• folates+fluorouracil: Severe (increases risk of toxicity)
• folates+antiepileptics: Moderate (decreases concentration)
• folates+fosphenytoin: Moderate (decreases concentration)
• folates+phenobarbital: Moderate (decreases concentration)
• folates+phenytoin: Moderate (decreases concentration)
• folates+primidone: Moderate (decreases concentration)
• sulfasalazine+folates: Unknown (decreases absorption)

Pregnancy

Folate is essential for fetal development and is often recommended to prevent neural tube defects.

Breast-feeding

Folate is generally safe during breastfeeding, as it is important for both maternal and infant health.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• Tablets
• Injection

Indications

• Nausea and vomiting (including motion sickness and morning sickness)
• Gastrointestinal discomfort
• Osteoarthritis
• Inflammation
• Cold and flu symptoms

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations.

Adults: Refer to established guidelines for specific dosing; typically, doses range from 1 to 3 grams of dried ginger per day.

Mechanism of action

The active components of ginger, particularly gingerols, exert their effects primarily through the inhibition of pro-inflammatory cytokines and enzymes, such as cyclooxygenase and lipoxygenase. This action helps to reduce inflammation and pain. Additionally, ginger enhances gastrointestinal motility and has antiemetic properties, which are beneficial in treating nausea.

Pharmacodynamics

Ginger exhibits anti-inflammatory, antioxidant, and antinausea effects. Its ability to modulate the immune response and inhibit platelet aggregation contributes to its cardiovascular protective effects. The antiemetic properties of ginger are particularly effective in reducing nausea and vomiting associated with motion sickness and chemotherapy.

Pharmacokinetics

Ginger is rapidly absorbed in the gastrointestinal tract, with its active components being metabolized in the liver. The bioavailability of ginger compounds may vary, with gingerols being converted into shogaols during processing or heating. The elimination half-life and specific metabolic pathways have not been extensively studied, but the effects can be observed within 30 minutes to 2 hours after ingestion.

Contra-indications

• Gallstones
• Bleeding disorders
• Allergy to ginger or other plants in the Zingiberaceae family

Adverse effects

• Gastrointestinal disturbances (nausea, diarrhea, heartburn)
• Allergic reactions (skin rash, itching)
• Increased risk of bleeding

Interactions

• Anticoagulants (e.g., warfarin, aspirin)
• Antiplatelet agents
• Certain antihypertensives
• Diabetes medications (may enhance effects)

Precautions

• Use with caution in patients with diabetes, hypertension, or gallbladder disease
• Consult a healthcare provider before use in pregnancy or lactation

Pregnancy

Generally considered safe in food amounts, but high doses should be avoided due to potential effects on uterine contractions.

Breast-feeding

Considered safe in food amounts, but high doses should be avoided.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Dried ginger powder
• Ginger root (fresh)
• Ginger tea
• Ginger extract (liquid or capsule)
• Ginger oil

Indications

• Cognitive enhancement
• Memory disorders
• Tinnitus
• Peripheral vascular disease
• Anxiety
• Age-related macular degeneration

Dosage

Children: Safety and efficacy have not been established in children, so refer to specific guidelines if considering use in paediatric populations.

Adults: Refer to specific product guidelines, typically ranging from 120 to 240 mg of standardized ginkgo extract per day, divided into two or three doses.

Mechanism of action

The exact mechanism of action of ginkgo is not fully understood, but it is thought to involve several pathways. Ginkgo extracts contain flavonoids and terpenoids, which are believed to contribute to its pharmacological effects. These compounds may enhance cerebral blood flow by dilating blood vessels and reducing blood viscosity. Ginkgo also has antioxidant properties that help protect against oxidative stress, and it may modulate neurotransmitter systems, particularly those involving serotonin and dopamine.

Pharmacodynamics

Ginkgo exhibits various pharmacodynamic effects, including vasodilation, increased blood flow, and improved neurotransmission. It is noted for its ability to enhance cognitive function, particularly in older adults with mild cognitive impairment. The antioxidant properties of ginkgo help mitigate damage caused by free radicals, potentially reducing the risk of neurodegenerative diseases. Its effects on blood circulation can also alleviate symptoms associated with peripheral vascular disease.

Pharmacokinetics

Ginkgo is rapidly absorbed after oral administration, with peak plasma concentrations typically occurring within 1-3 hours. It undergoes extensive metabolism in the liver, primarily via cytochrome P450 enzymes. The elimination half-life of ginkgo components can vary, generally ranging from 4 to 12 hours. The bioavailability of ginkgo extracts can be influenced by formulation and individual patient factors, including age and health status.

Contra-indications

• Hypersensitivity to ginkgo or any of its components
• Active bleeding disorders
• Concurrent use with anticoagulants or antiplatelet agents

Adverse effects

• Gastrointestinal upset
• Headache
• Dizziness
• Allergic skin reactions
• Palpitations

Interactions

• Increased risk of bleeding when used with warfarin, aspirin, or other anticoagulants
• Potential interaction with selective serotonin reuptake inhibitors (SSRIs) and other antidepressants
• May affect the metabolism of certain drugs metabolized by cytochrome P450 enzymes

Precautions

• Use with caution in patients with a history of seizures
• Monitor for bleeding complications in patients with bleeding disorders
• Discontinue use prior to surgical procedures to reduce bleeding risk

Pregnancy

Limited data available, caution advised; consult healthcare provider.

Breast-feeding

Insufficient reliable information available regarding safety; consult healthcare provider.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Ginkgo biloba extract (standardized)
• Ginkgo leaf tablets
• Ginkgo capsules
• Ginkgo tinctures

Indications

• Fatigue
• Stress management
• Cognitive enhancement
• Immune support
• General well-being

Dosage

Children: Refer to specific product guidelines, as dosing in children should be determined by a healthcare professional.

Adults: Refer to specific product guidelines, as dosing can vary based on formulation and intended use.

Mechanism of action

Ginseng is thought to exert its effects through several mechanisms, including modulation of the hypothalamic-pituitary-adrenal (HPA) axis, enhancement of antioxidant activity, and regulation of neurotransmitter levels. Ginsenosides, the active compounds in ginseng, may influence cellular signaling pathways, promote neuroprotection, and enhance immune responses.

Pharmacodynamics

The pharmacodynamic effects of ginseng are attributed primarily to its active constituents, ginsenosides, which interact with various receptors and enzymes in the body. These interactions can lead to increased energy metabolism, improved cognitive function, enhanced physical performance, and modulation of the immune system. Ginseng may also exhibit adaptogenic properties, helping the body to maintain homeostasis under stress.

Pharmacokinetics

Ginsenosides undergo extensive metabolism in the body, primarily by the liver. Bioavailability can vary significantly based on the specific ginsenoside and the method of administration. Ginseng is usually administered orally, with effects typically observed within several hours after ingestion. The elimination half-life of ginsenosides can vary based on the specific compound and individual metabolism, with some studies suggesting that effects may persist for several hours to days.

Adverse effects

• Insomnia
• Headache
• Gastrointestinal disturbances
• Nervousness
• Hypertension
• Allergic reactions

Interactions

• May interact with anticoagulants (e.g., warfarin)
• May enhance the effects of caffeine
• May affect insulin levels and blood sugar control
• Potential interaction with immunosuppressants

Precautions

• Use with caution in patients with hypertension
• May cause sleep disturbances; avoid use before bedtime
• Should be used cautiously in patients with diabetes
• Consult a healthcare provider before use in individuals with autoimmune conditions

Pregnancy

Limited data available. Generally not recommended due to potential hormonal effects.

Breast-feeding

Limited data available. Consult a healthcare provider before use.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• Dried root
• Powdered extract
• Capsules
• Tinctures
• Teas

Indications

• Wound healing
• Skin ulceration
• Burns
• Psoriasis
• Dermatitis

Dosage

Children: Refer to the BNF for Children for appropriate dosing information based on the child's age and condition.

Adults: Refer to the BNF for specific formulations and dosing guidelines, as dosages may vary based on the condition being treated and the formulation used.

Mechanism of action

While there is no well-controlled data to formally substantiate the method of action, ongoing studies suggest that allantoin may induce a histological wound healing profile in animal models, leading to improved reestablishment of normal skin. This includes increased vasodilation, inflammatory cell presence, angiogenesis, fibroblast proliferation, and collagen deposition in treated wounds compared to untreated ones.

Pharmacodynamics

There is limited controlled data regarding the pharmacodynamic properties of allantoin. However, studies indicate that allantoin may possess moisturizing and keratolytic effects, increasing the extracellular matrix's water content and enhancing the desquamation of dead skin cells. These activities can promote cell proliferation and facilitate wound healing.

Pharmacokinetics

Specific pharmacokinetic data for allantoin in humans is limited. However, it is known to be applied topically, which suggests local absorption at the site of application. Systemic absorption is considered minimal due to its low molecular weight and hydrophilicity.

Pregnancy

There is limited data on the safety of allantoin in pregnancy. It is advisable to consult a healthcare professional before use.

Breast-feeding

Allantoin is generally considered safe during breastfeeding, but caution is recommended. Consult a healthcare professional before use.

Storage

Store at room temperature, away from direct sunlight and moisture. Keep out of reach of children.

Formulations

• Topical cream
• Gel
• Ointment

Indications

• Osteoarthritis of the knee
• Viscosupplementation for joint pain
• Dry eye syndrome
• Ocular surgeries (e.g., cataract surgery)
• Wound healing

Dosage

Adults: Refer to specific guidelines or literature for adult dosing recommendations, as they can vary based on

Mechanism of action

Hyaluronate acts by increasing the viscosity and elasticity of synovial fluid in joints, leading to improved lubrication and shock absorption. It binds to water molecules, thus enhancing the hydration of tissues. In the context of osteoarthritis, it helps to restore the normal viscoelastic properties of the joint fluid, which can help alleviate pain and improve joint function. In ocular applications, it serves to lubricate the surface of the eye, aiding in the comfort and healing of the cornea.

Pharmacodynamics

Hyaluronate's pharmacodynamic effects are primarily related to its hydrophilic nature and its ability to form a gel-like consistency when mixed with water. This property allows it to provide mechanical support and cushioning in joints, reducing friction and wear in the articular cartilage. It also plays a role in cell signaling and tissue hydration, influencing cell proliferation and migration in wound healing.

Pharmacokinetics

Hyaluronate is administered via injection or topical application, depending on the indication. After injection into the joint space, it can remain for several weeks, but its half-life is influenced by factors such as the degree of synovial fluid viscosity and the presence of inflammation. Systemic absorption is minimal, and it is primarily metabolized by hyaluronidase enzymes found in various tissues, leading to fragmentation and clearance from the body. In ocular formulations, its retention time on the eye surface can vary based on the formulation and the presence of preservatives.

Contra-indications

• Hypersensitivity to hyaluronate or any component of the formulation
• Infection at the injection site
• Active skin diseases

Adverse effects

• Injection site reactions (pain, swelling, redness)
• Allergic reactions
• Joint effusion
• Increased joint pain
• Headache

Precautions

• Use with caution in patients with bleeding disorders
• Careful consideration in patients with a history of allergic reactions
• Not recommended for intra-articular injection in patients with active infections

Pregnancy

Safety in pregnancy has not been established. Use only if clearly needed and the potential benefits justify the risks.

Breast-feeding

It is not known if hyaluronate is excreted in human milk. Use with caution and only if clearly needed.

Storage

Store at 2-25 degrees Celsius. Protect from light. Do not freeze.

Formulations

• Sodium hyaluronate injection
• Hyaluronic acid gel

Mechanism of action

Glutathione (GSH) participates in leukotriene synthesis and acts as a cofactor for the enzyme glutathione peroxidase. It plays a critical role in detoxifying lipophilic toxins through conjugation, enhancing their excretion in bile. Glutathione is involved in detoxifying methylglyoxal, a toxic by-product of metabolism, through the glyoxalase enzyme pathway. Glyoxalase I and II catalyze the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione and then to reduced glutathione and D-lactate. GSH is also a cofactor for conjugation reactions mediated by glutathione S-transferase enzymes and can engage in non-enzymatic conjugation with certain reactive metabolites, such as N-acetyl-p-benzoquinone imine (NAPQI), thereby detoxifying them.

Pharmacodynamics

L-glutathione exerts its antioxidant effects by directly scavenging free radicals and reactive oxygen species, thus preventing cellular damage. It also maintains the activity of other antioxidants, such as vitamins C and E, and plays a crucial role in the regeneration of oxidized glutathione. Due to its involvement in various metabolic pathways, including the detoxification of harmful substances, it is essential for overall cellular health and function.

Pharmacokinetics

L-glutathione is absorbed in the gastrointestinal tract, but its bioavailability is variable due to rapid metabolism and degradation in the intestinal lumen. It is distributed throughout the body, with higher concentrations found in the liver, lungs, and erythrocytes. The metabolism of glutathione primarily occurs in the liver, where it undergoes conjugation and is involved in various metabolic pathways. Excretion occurs mainly through biliary routes, and it is also recycled through the action of enzymes that convert

Pregnancy

There is insufficient data on the safety of glutathione during pregnancy. It is advisable to use it only if clearly needed and after assessing the benefits and risks.

Breast-feeding

Limited information is available regarding the excretion of glutathione in human milk. Caution is advised when administering to breastfeeding women.

Storage

Store in a cool, dry place away from direct sunlight. Ensure the container is tightly closed to maintain product stability.

Indications

• Diabetic neuropathy
• Oxidative stress-related disorders
• Metabolic syndrome
• Weight management
• Liver health

Dosage

Children: Refer to specific product guidelines, as safety and efficacy in children have not been established.

Adults: Refer to specific product guidelines, as dosages may vary based on the formulation and indication.

Mechanism of action

Lipoic acid acts as a cofactor for mitochondrial enzyme complexes, particularly those involved in the Krebs cycle, enhancing energy production. It also possesses antioxidant properties, neutralizing free radicals and regenerating other antioxidants such as vitamins C and E. Additionally, lipoic acid can modulate various signaling pathways, including those related to insulin sensitivity and inflammation.

Pharmacodynamics

Lipoic acid has a dual role as a coenzyme and an antioxidant. By participating in the decarboxylation of alpha-keto acids, it aids in energy production. Its antioxidant properties contribute to the protection of cells from oxidative stress, which is implicated in various chronic diseases. Lipoic acid can improve insulin sensitivity, making it beneficial in managing glucose metabolism disorders.

Pharmacokinetics

After oral administration, lipoic acid is absorbed in the gastrointestinal tract, with peak plasma concentrations occurring within 30 to 60 minutes. It undergoes hepatic metabolism, primarily via reduction and conjugation, resulting in various metabolites. The elimination half-life is approximately 30 minutes to 2 hours, and it is excreted primarily in urine. The bioavailability of lipoic acid can be affected by food intake.

Adverse effects

• Nausea
• Vomiting
• Abdominal pain
• Skin rash
• Hypoglycemia

Interactions

• May enhance the effects of insulin and other antidiabetic medications
• May interact with heavy metal chelators

Precautions

• Use with caution in patients with diabetes due to the risk of hypoglycemia
• Monitor blood sugar levels in diabetic patients

Pregnancy

Safety during pregnancy has not been established; use only if clearly needed.

Breast-feeding

It is not known whether lipoic acid is excreted in human breast milk; caution is advised.

Storage

Store in a cool, dry place away from light.

Formulations

• Capsules
• Tablets
• Injectable solutions

Indications

• Manganese deficiency
• Bone health and development
• Antioxidant support
• Enzyme cofactor in metabolic processes

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations.

Adults: Refer to specific clinical guidelines or the BNF for appropriate dosing recommendations.

Mechanism of action

Manganese serves as a cofactor for several enzymes, including manganese superoxide dismutase (MnSOD), which protects cells from oxidative stress by catalyzing the dismutation of superoxide radicals into oxygen and hydrogen peroxide. It also participates in the activation of enzymes involved in carbohydrate, fat, and protein metabolism.

Pharmacodynamics

Manganese plays a role in various biochemical pathways, particularly in the metabolism of amino acids, cholesterol, glucose, and carbohydrates. It is crucial for bone formation and the maintenance of cartilage. Manganese also aids in the synthesis of glycosyltransferases, which are important for the formation of glycoproteins and proteoglycans.

Pharmacokinetics

Manganese is absorbed primarily in the small intestine, with absorption efficiency influenced by dietary factors and the presence of competing minerals. It is transported in the bloodstream bound to proteins such as alpha-2-macroglobulin and transferrin. Manganese is stored in the liver, pancreas, and bones, and is excreted primarily through bile and to a lesser extent in urine. Its half-life in the human body is not well defined due to its trace nature and variable absorption.

Pregnancy

Manganese is classified as a dietary mineral that is essential for human health, but excessive intake should be avoided during pregnancy as it may affect fetal development.

Breast-feeding

Manganese is present in breast milk, and normal dietary intake is considered safe during breastfeeding. However, excessive supplementation should be avoided.

Storage

Store in a cool, dry place, away from direct light and moisture.

Indications

• Hypertriglyceridemia
• Cardiovascular disease prevention

Mechanism of action

Omega-3 fatty acids exert their effects through multiple mechanisms. They compete with arachidonic acid for incorporation into cell membranes, leading to the production of eicosanoids with lower pro-inflammatory potential. This results in decreased levels of pro-inflammatory mediators such as prostaglandin E2 and leukotrienes. They also activate peroxisome proliferator-activated receptors (PPARs), which regulate inflammatory gene expression and inhibit the production of inflammatory cytokines like TNF and IL-1β. Omega-3 fatty acids also promote the generation of resolvins and protectins, which have further anti-inflammatory effects.

Pharmacodynamics

Omega-3 fatty acids are metabolized into smaller fatty acid units, impacting various physiological functions. They are known to reduce plasma triglyceride levels, increase cholesterol levels, and exhibit antiarrhythmic properties. These fatty acids also play a role in inhibiting platelet aggregation, prolonging bleeding time, and reducing plasma fibrinogen levels. As constituents of phospholipids, they are integral to cell membrane structure and function, and they are involved in the formation of eicosanoids, which are critical signaling molecules across multiple body systems.

Pharmacokinetics

Omega-3 fatty acids are absorbed in the gastrointestinal tract and incorporated into chylomicrons, which are transported in the lymphatic system and subsequently released into the bloodstream. They are distributed widely throughout body tissues, particularly in the heart, brain, and retina. The metabolism occurs primarily in the liver, where they undergo beta-oxidation and can be converted into various bioactive lipid mediators. The half-life of omega-3 fatty acids can vary based on the specific fatty acid and individual metabolism.

Adverse effects

• Nausea
• Diarrhea
• Abdominal pain
• Fishy aftertaste
• Belching
• Increased bleeding time

Interactions

• Anticoagulants
• Antiplatelet agents
• Blood pressure medications

Precautions

• Use with caution in patients with bleeding disorders
• Monitor for signs of bleeding in patients taking anticoagulants
• Consider potential effects on lipid levels

Pregnancy

Omega-3 fatty acids are generally considered safe during pregnancy, but it's advisable to consult a healthcare provider for individual recommendations.

Breast-feeding

Omega-3 fatty acids are excreted in breast milk; consult a healthcare provider for guidance.

Storage

Store in a cool, dry place, away from direct sunlight. Keep tightly closed.

Formulations

• Capsules
• Softgels
• Liquid formulations

Indications

• Enhancement of bioavailability of other drugs
• Potential anti-inflammatory agent
• Antioxidant
• Neuroprotective agent
• Possible anticancer properties

Mechanism of action

Piperine enhances the bioavailability of various compounds by inhibiting certain drug-metabolizing enzymes, particularly cytochrome P450 enzymes, thereby reducing their metabolism and increasing their absorption in the gastrointestinal tract. It also influences various transport proteins, which can affect the pharmacokinetics of drugs.

Pharmacodynamics

Piperine exhibits various pharmacological effects, including anti-inflammatory, antioxidant, and neuroprotective activities. It has been shown to modulate multiple signaling pathways involved in inflammation and oxidative stress, potentially contributing to its therapeutic effects.

Pharmacokinetics

Piperine is well absorbed after oral administration, with its bioavailability enhanced due to its ability to inhibit metabolic enzymes. It is metabolized primarily in the liver, with a relatively short half-life which can vary based on the presence of food and other substances.

Pregnancy

Piperine should be used with caution during pregnancy; consult healthcare professionals before use.

Breast-feeding

Limited information is available regarding piperine use during breastfeeding; consult healthcare professionals before use.

Storage

Store in a cool, dry place, away from direct sunlight.

Indications

• Depression
• Anxiety disorders
• Sleep disorders
• Seasonal affective disorder

Dosage

Children: Refer to established guidelines for specific dosing recommendations for children, as data on pediatric dosing is limited.

Adults: Refer to established guidelines for specific dosing recommendations, as dosages may vary based on formulation and specific condition being treated.

Mechanism of action

Quadrangularis exerts its effects primarily through the modulation of neurotransmitters in the brain, particularly serotonin, dopamine, and norepinephrine. Hyperforin is believed to inhibit the reuptake of these neurotransmitters, leading to increased levels in the synaptic cleft. Additionally, hypericin has been shown to exhibit anti-inflammatory and antiviral properties, which may contribute to its overall therapeutic profile.

Pharmacodynamics

The pharmacodynamic effects of quadrangularis include its ability to elevate mood, reduce anxiety, and improve sleep quality. The herb may also have neuroprotective effects, potentially benefiting cognitive function. Side effects can include gastrointestinal disturbances, fatigue, and photosensitivity, particularly with prolonged use.

Pharmacokinetics

Quadrangularis is bioavailable following oral administration, with peak plasma concentrations typically occurring within 1 to 2 hours. The herb is metabolized in the liver, primarily by cytochrome P450 enzymes, and its metabolites are excreted via urine. The half-life of active components can vary, influencing dosing frequency and duration of action.

Pregnancy

The safety of quadrangularis during pregnancy has not been established. It is advisable to avoid use unless clearly needed.

Breast-feeding

Information on the excretion of quadrangularis in breast milk is not available. Use with caution and consult a healthcare provider.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Dosage

Children: Refer to specific formulations and preparations for recommended dosing in children, as it varies widely by plant and intended use.

Adults: Refer to specific formulations and preparations for recommended dosing, as it varies widely by plant and intended use.

Mechanism of action

The mechanism of action varies significantly depending on the specific root being referred to. Many plant roots contain bioactive compounds such as alkaloids, flavonoids, and glycosides, which can modulate various biochemical pathways in the body. For instance, certain roots may inhibit enzymes involved in inflammation or microbial growth, while others may enhance immune responses or modulate neurotransmitter activity.

Pharmacodynamics

Pharmacodynamics will differ based on the specific root and its active compounds. Generally, roots may exhibit anti-inflammatory, analgesic, antimicrobial, or antioxidant effects. The pharmacodynamic profile will also depend on factors such as dosage, preparation method (e.g., decoction, tincture), and the specific condition being treated. For example, some roots may interact with cellular receptors, while others may exert their effects through modulation of gene expression.

Pharmacokinetics

The pharmacokinetics of a root extract will vary with the specific plant. Typically, factors such as absorption, distribution, metabolism, and excretion are influenced by the chemical composition of the root, the method of preparation, and the route of administration. Many active compounds are absorbed in the gastrointestinal tract, metabolized in the liver, and excreted via urine or feces. The bioavailability of these compounds can be affected by their solubility and stability.

Pregnancy

The safety of root during pregnancy has not been established. Consult a healthcare professional before use.

Breast-feeding

It is unknown whether root is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

Store in a cool, dry place away from direct sunlight and moisture.

Indications

• Anxiety
• Depression
• Skin wounds
• Inflammation
• Aromatherapy for relaxation

Dosage

Children: Refer to relevant guidelines and literature for specific dosing recommendations, as rose extracts vary widely in concentration and formulation.

Adults: Refer to relevant guidelines and literature for specific dosing recommendations, as rose extracts vary widely in concentration and formulation.

Mechanism of action

The essential oil from rose contains various compounds such as phenyl ethanol, geraniol, and citronellol, which may exert their effects through the modulation of neurotransmitter systems. It is believed to influence the central nervous system, promoting relaxation and reducing anxiety. Additionally, rose extracts possess antioxidant properties, which may contribute to their anti-inflammatory effects.

Pharmacodynamics

Rose extracts have been shown to have anxiolytic and antidepressant effects, likely through the enhancement of serotonin and dopamine levels in the brain. The anti-inflammatory properties are attributed to the inhibition of pro-inflammatory cytokines and modulation of immune responses. The antioxidant activity helps protect cells from oxidative stress.

Pharmacokinetics

The pharmacokinetics of rose extracts are not well-documented due to variations in preparation and formulation. However, the constituents are generally absorbed through the skin or mucous membranes when used topically or in aromatherapy. The bioavailability and half-life of specific compounds can vary widely, influenced by factors such as formulation, dosage, and individual metabolism.

Pregnancy

Insufficient data on the safety of rose during pregnancy. Consult healthcare provider before use.

Breast-feeding

Limited information available. Consult healthcare provider before use.

Storage

Store in a cool, dry place away from direct sunlight.

Indications

• Digestive disorders
• Inflammation
• Menopausal symptoms
• Cognitive enhancement
• Antimicrobial support

Dosage

Children: Refer to established herbal guidelines or consult a healthcare provider for appropriate dosing.

Adults: Refer to established herbal guidelines or consult a healthcare provider for appropriate dosing.

Mechanism of action

The active components of sage, including flavonoids, phenolic acids, and essential oils, interact with various biological pathways. They exhibit antioxidant activity by scavenging free radicals and modulating redox status, which helps to protect cells from oxidative stress. Additionally, sage components may modulate neurotransmitter systems, particularly through interactions with acetylcholine receptors, potentially enhancing cognitive function.

Pharmacodynamics

Sage demonstrates a range of pharmacological effects, mainly attributed to its bioactive compounds. Its anticholinergic properties can influence cognitive function and mood, while its anti-inflammatory and antimicrobial actions can contribute to gastrointestinal health and overall immune support. The herb has also been shown to have potential benefits in managing menopausal symptoms and may influence glucose metabolism.

Pharmacokinetics

The pharmacokinetics of sage is not extensively characterized in clinical studies. However, it is known that the bioactive compounds are absorbed through the gastrointestinal tract following ingestion. Factors such as the method of preparation (e.g., infusion, tincture) can influence the bioavailability and pharmacokinetic profile of these compounds. Generally, the effects of sage are expected to manifest within a few hours after ingestion, with a duration of action that may vary depending on the formulation and dose.

Adverse effects

• Allergic reactions
• Gastrointestinal upset
• Dizziness
• Headache

Interactions

• May interact with anticoagulants, increasing the risk of bleeding
• Potential interaction with diabetes medications, affecting blood sugar levels

Precautions

• Use with caution in individuals with hormone-sensitive conditions
• May cause drowsiness; caution advised when driving or operating machinery
• Consult healthcare provider before use if pregnant or breastfeeding

Pregnancy

Sage should be avoided during pregnancy due to potential uterine stimulant effects.

Breast-feeding

Sage is generally considered safe in small amounts while breastfeeding, but high doses should be avoided.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Dried leaves
• Essential oil
• Tincture

Indications

• Major depressive disorder
• Obsessive-compulsive disorder
• Panic disorder
• Social anxiety disorder
• Post-traumatic stress disorder
• Premenstrual dysphoric disorder

Dosage

Children: Refer to the BNF for Children for specific dosing recommendations.

Adults: Refer to the BNF for specific dosing recommendations.

Mechanism of action

Sertraline selectively inhibits the reuptake of serotonin in the synaptic cleft, thereby increasing serotonin availability to bind to postsynaptic receptors. This action enhances serotonergic neurotransmission, which is believed to contribute to its antidepressant effects.

Pharmacodynamics

The pharmacodynamic effects of sertraline are primarily attributed to its ability to increase serotonin concentrations in the synaptic cleft. This leads to enhanced serotonin receptor activation, which is associated with mood elevation, anxiety reduction, and improved emotional regulation. The onset of therapeutic effects may take several weeks, as the full clinical benefit develops gradually.

Pharmacokinetics

Sertraline is well-absorbed after oral administration, with peak plasma concentrations typically occurring within 4 to 6 hours. It has a large volume of distribution and is extensively metabolized in the liver, primarily by cytochrome P450 enzymes. The elimination half-life ranges from 22 to 36 hours, allowing for once-daily dosing. Sertraline is excreted mainly as metabolites in urine.

Pregnancy

Use during pregnancy only if the potential benefit justifies the potential risk to the fetus. Limited data are available on the safety of serata in pregnancy.

Breast-feeding

It is not known whether serata is excreted in human milk. Caution should be exercised when administering serata to nursing mothers.

Storage

Store at room temperature, away from light and moisture. Keep out of reach of children.

Indications

• Osteoarthritis
• Rheumatoid arthritis
• Cancer
• Cardiovascular diseases
• Skin disorders

Dosage

Children: Refer to specific product guidelines and consult a healthcare provider for appropriate dosing in children.

Adults: Refer to specific product guidelines, as dosages may vary widely depending on the formulation and intended use.

Mechanism of action

The exact mechanism of action of shark cartilage is not fully understood. It is believed to work by inhibiting angiogenesis, the process through which new blood vessels form from pre-existing vessels, which is crucial for tumor growth and metastasis. The compounds within shark cartilage may also modulate immune responses and exhibit anti-inflammatory effects.

Pharmacodynamics

Shark cartilage is thought to exert its effects through various biological pathways, primarily by interacting with the immune system and influencing cellular communication. It may have anti-inflammatory effects that reduce swelling and pain, particularly in joint disorders. Additionally, its potential anti-cancer properties are attributed to its ability to inhibit the growth of blood vessels that supply tumors.

Pharmacokinetics

The pharmacokinetics of shark cartilage have not been well-studied. It is generally consumed as an oral supplement, and its bioavailability may vary depending on the formulation. The components of shark cartilage, including glycosaminoglycans, are likely to be absorbed through the gastrointestinal tract, but the extent of absorption and metabolism remains unclear. Further research is needed to elucidate the pharmacokinetic profile of shark cartilage.

Pregnancy

There is limited data on the safety of shark products during pregnancy. Consult healthcare providers for personalized advice.

Breast-feeding

Limited data on the safety of shark products during breastfeeding. Consult healthcare providers for personalized advice.

Storage

Store in a cool, dry place away from direct sunlight. Ensure proper sealing to maintain freshness.

Mechanism of action

Selenium is first metabolized to selenophosphate and selenocysteine. Selenium incorporation is genetically encoded through the RNA sequence UGA. This sequence is recognized by RNA ste loop structures called selenocysteine inserting sequences (SECIS). These structures require the binding of SECIS binding proteins (SBP-2) to recognize selenocystiene. The specialized tRNA is first bound to a serine residue which is then enzymatically processed to a selylcysteyl-tRNA by selenocystiene sythase using selenophosphate as a selenium donor. Other unidentified proteins are required as part of the binding of this tRNA to the ribosome. Selenoproteins appear to be necessary for life as mice with the specialized tRNA gene knocked out exhibited early embryonic lethality. The most important selenoproteins seem to be the glutathione peroxidases and thioredoxin reductases which are part of the body's defenses againts reactive oxygen species (ROS). The importance of selenium in these anti-oxidant proteins has been implicated in the reduction of atherosclerosis by preventing the oxidation of low density lipoprotein. Selenium supplementation is also being investigated in the prevention of cancer and has been suggested to be beneficial to immune function. Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. Prior to occurrence of apoptosis, Se compounds alter the expression and/or activities of signaling molecules, mitochondria-associated factors, transcriptional factors, tumor suppressor genes, and cellular reduced glutathione. Mechanistic studies have demonstrated that the methylselenol metabolite pool has many desirable attributes of chemoprevention, whereas the hydrogen selenide pool with excess of selenoprotein synthesis can lead to DNA single-strand breaks. To elucidate the effects of Se on cytotoxic events, it should be remembered that the chemical forms and the dose of Se, and the experimental system used, are determinants of its biological activities. This mini-review focuses on elucidation of the molecular mechanisms of cancer prevention by Se with the apoptotic approach. /Selenium/ Selenium status can also influence thyroid hormone function via the deiodinase enzymes. Selenium is a critical component of the deiodinase enzymes, including iodothyronine 5'-deiodinases, which convert the prohormone thyroxine (T4) to the active circulating form, triiodothyronine (T3). Selenium is also a component of GPX, the main enzyme responsible for protecting thyroid cells against oxidative damage. GPX is involved in the detoxification of hydrogen peroxide, which is produced in the thyroid during the conversion of T4 to T3. /Selenium/ Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low in the organism. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenium may have a role in hepatic heme metabolism that is related to GPX or lipid peroxidation. Selenocysteine is specifically found in some proteins (e.g., glutathione peroxidase); selenomethionine appears to randomly substitute for methionine in protein synthesis. This appears to be an additional mechanism for intermediate- or chronic-duration toxicity. Skin, hair, and nail damage are significant indicators of chronic selenium overexposure. The mechanism causing these integumentary effects is unclear, but could be related to the high selenium concentrations in these tissues as a consequence of the substitution of selenium for sulfur in certain amino acids, including the disulfide bridges that pr

Pharmacodynamics

Selenium is incorporated into many different selenoproteins which serve various functions throughout the body.

Mechanism of action

Copper is absorbed from the gut via high affinity copper uptake protein and likely through low affinity copper uptake protein and natural resistance-associated macrophage protein-2. It is believed that copper is reduced to the Cu1+ form prior to transport. Once inside the enterocyte, it is bound to copper transport protein ATOX1 which shuttles the ion to copper transporting ATPase-1 on the golgi membrane which take up copper into the golgi apparatus. Once copper has been secreted by enterocytes into the systemic circulation it remain largely bound by ceruloplasmin (65-90%), albumin (18%), and alpha 2-macroglobulin (12%). Copper is an essential element in the body and is incorporated into many oxidase enzymes as a cofactor. It is also a component of zinc/copper super oxide dismutase, giving it an anti-oxidant role. Copper defiency occurs in Occipital Horn Syndrome and Menke's disease both of which are associated with impaired development of connective tissue due to the lack of copper to act as a cofactor in protein-lysine-6-oxidase. Menke's disease is also associated with progressive neurological impairment leading to death in infancy. The precise mechanisms of the effects of copper deficiency are vague due to the wide range of enzymes which use the ion as a cofactor. Copper appears to reduce the viabilty and motility of spermatozoa. This reduces the likelihood of fertilization with a copper IUD, producing copper's contraceptive effect. The exact mechanism of copper's effect on sperm are unknown. The reason for the less severe reaction when the foreign body is at a distance from the retina has been proposed to be ... that near the retina & its blood vessels there is greater oxygen tension than at a distance, which causes metallic copper to oxidize to toxic copper compounds more rapidly close to or in contact with the retina than at a distance. Furthermore, the abscess formation that is characteristic of copper undergoing oxidation close to the retina & choroiod can be attributed to attraction of polymorphonuclear leukocytes from these nearby vascular tissues, which become heavily infiltrated. Liquefaction & disorganization of the vitreous body has been explained on the basis of copper catalysis of oxidation of ascorbic acid, leading to depolymerization of the hyaluronic acid of the vitreous humor. Changes in protein & hexosamine content have also been related to decrease in viscosity of the vitreous humor. Increased content of amino acids in the vitreous humor has been consistent with proteolysis of the vitreous body, but decreased concentration in the aqueous humor has suggested suppression of secretion of amino acids by the ciliary body under the influence of copper.

Pharmacodynamics

Copper is incorporated into many enzymes throughout the body as an essential part of their function. Copper ions are known to reduce fertility when released from copper-containing IUDs.

Mechanism of action

There is no well controlled data that can formally substantiate the method of action. However, ongoing studies suggest that there may exist a histological wound healing profile induced by allantoin in rats that leads to the amelioration and fastening of the reestablishment of normal skin. This facilitation of wound healing is supported by observations that wounds inflicted to rat subjects to which topical allantoin preparations were applied histologically demonstrated increased vasodilation, presence of inflammatory exudates, number of inflammatory cells, angiogenesis, fibroblast proliferation, and increased collagen deposition when compared to rat subjects with wounds that did not receive any allantoin administration.

Pharmacodynamics

There is no well controlled and appropriate data that can formally substantiate the pharmacodynamic properties of allantoin. Nevertheless, ongoing studies suggest that allantoin possesses moisturizing and keratolytic effects, as well as abilities to increase the water content of the extracellular matrix and enhance the desquamation of upper layers of dead skin cells, all of which are activities that can promote cell proliferation and facilitate wound healing.

Mechanism of action

Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion. It participates in the detoxification of methylglyoxal, a toxic by-product of metabolism, mediated by glyoxalase enzymes. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. GSH is a cofactor of conjugation and reduction reactions that are catalyzed by glutathione S-transferase enzymes expressed in the cytosol, microsomes, and mitochondria. However, it is capable of participating in non-enzymatic conjugation with some chemicals, as it is hypothesized to do to a significant extent with n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450 reactive metabolite formed by toxic overdose of acetaminophen. Glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein sulfhydryl groups which would otherwise be toxically adducted. The preferred medical treatment to an overdose of this nature, whose efficacy has been consistently supported in literature, is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and allow a usable GSH pool.

Mechanism of action

Omega-3 fatty acids mediate anti-inflammatory effects and increased levels of EPA or DHA has shown to decrease the levels of PGE2 and 4 series-LT. Eicosapentaenoic acids compete with constitutive levels of arachidonic acid in cell membranes for the same desaturation enzymes and produce 3-series prostaglandins and thromboxanes, and 5-series leukotrienes which have low pro-inflammatory potential. The alteration in leukotriene biosynthesis due to higher concentration of omega-3 fatty acids compared to arachidonic acid underlies the anti-inflammatory effects. EPA and DHA also give rise to resolvins and related lipid signalling molecules such as protectins via cyclooxygenase and lipoxygenase pathways, which have anti-inflammatory effects. They inhibit transendothelial migration of neutrophils and inhibit TNF and IL-1β production. Omega-3 fatty acids also decrease adhesion molecule expression on leukocytes and on endothelial cells and decrease intercellular adhesive interactions. Omega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator-activated receptor (PPAR) gamma that regulates inflammatory gene expression and NFκB activation. PPAR alpha activation is also associated with induction of COX-2 expression. The role of EPA and DHA in reducing triglyceride levels include inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase, increased mitochondrial and peroxisomal-beta-oxidation in the liver, decreased lipogenesis in the liver, and increased plasma lipoprotein lipase activity. They also may reduce triglyceride synthesis because they are poor substrates for the enzymes responsible for TG synthesis, and EPA and DHA inhibit esterification of other fatty acids.

Pharmacodynamics

Omega-3 fatty acids are triglycerides that get broken down into smaller fatty acid units. They act to reduce plasma triglyceride levels however increase the cholesterol levels and are thought to possess potent antiarrythmic effects. Polyunsaturated fatty acids including eicosapentaenoic and docosahexaenoic acid mediate important cellular function such as inhibition of platelet function, prolongation of bleeding time, anti-inflammatory effects and reduction of plasma fibrinogen. Polyunsaturated fatty acids are components of the phospholipids that form the structures of the cell membranes and also serve as energy source. They form eicosanoids which are important signalling molecules with wide-ranging functions in the body's cardiovascular, pulmonary, immune and endocrine systems. DHA tends to exist in high concentrations in the retina, brain (via uptake by Mfsd2a as a transporter), and sperm.