SHAKE OFF PHYTO FIBER COMBINATION PRODUCT POWDER

Indications

• Used as a sweetener in food products
• Management of hypoglycemia (under specific conditions)
• Potential use in metabolic studies

Dosage

Children: Refer to BNF for Children for specific dosing guidance based on age and clinical conditions.

Adults: Refer to BNF for specific dosing guidance based on clinical conditions and formulations.

Mechanism of action

Fructose is absorbed in the small intestine and transported to the liver where it is phosphorylated to fructose-1-phosphate. This compound is then further metabolized through the glycolytic pathway, providing an energy source. Fructose metabolism bypasses the main regulatory step of glycolysis, making it a quick source of energy.

Pharmacodynamics

Fructose does not elicit a significant insulin response compared to glucose, thus affecting glucose metabolism and insulin sensitivity differently. The metabolism of fructose can lead to the generation of triglycerides, which can impact lipid profiles and cardiovascular health if consumed in excess.

Pharmacokinetics

Fructose is rapidly absorbed from the gastrointestinal tract. Its absorption does not require insulin, and it is primarily metabolized in the liver. The half-life of fructose in the bloodstream is short, as it is quickly taken up and utilized by the liver and other tissues.

Contra-indications

• Fructose intolerance
• Hereditary fructose intolerance

Adverse effects

• Diarrhea
• Nausea
• Abdominal discomfort
• Hypoglycemia (in sensitive individuals)

Precautions

• Use with caution in patients with diabetes or insulin resistance
• Monitor blood glucose levels in diabetic patients

Pregnancy

Fructose is generally considered safe during pregnancy when consumed in normal dietary amounts.

Breast-feeding

Fructose is safe during breastfeeding; it is a natural sugar found in fruits and is metabolized by the body.

Storage

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

Formulations

• Liquid form
• Powder form
• As an ingredient in various food products

Indications

• Constipation
• Irritable bowel syndrome (IBS)
• Diverticular disease
• Cholesterol management
• Blood sugar control in diabetes

Dosage

Children: For children, it is recommended to consult a healthcare provider for appropriate dosing based on age and weight, as specific pediatric dosing

Adults: For adults, the typical dosage is 1 to 2 teaspoons (5 to 10 grams) of psyllium husk taken 1 to 3 times daily, mixed with at least 8 ounces of water or other liquid.

Mechanism of action

Psyllium husk acts as a bulk-forming laxative. It is not digested by the body, but when mixed with water, it expands and forms a viscous gel. This gel increases the bulk of the stool and triggers peristalsis, enhancing bowel movements. Additionally, it may slow down the absorption of carbohydrates and fats, contributing to its cholesterol-lowering and blood sugar-regulating effects.

Pharmacodynamics

The primary pharmacodynamic effect of husk is its ability to increase stool bulk and water content, which facilitates easier passage of stool through the intestines. This leads to improved bowel regularity and relief from constipation. Furthermore, psyllium husk has been shown to have a mild effect on lowering serum cholesterol levels, particularly low-density lipoprotein (LDL) cholesterol, and may improve glycemic control in patients with type 2 diabetes.

Pharmacokinetics

Psyllium husk is not absorbed systemically; it remains in the gastrointestinal tract, where it exerts its effects. The onset of action for bowel regulation typically occurs within 12 to 72 hours after ingestion, depending on the individual's digestive transit time and fluid intake. Adequate hydration is essential to maximize its efficacy and prevent potential gastrointestinal obstruction.

Adverse effects

• Bloating
• Abdominal cramping
• Diarrhea
• Nausea

Precautions

• Ensure adequate fluid intake when using husk to prevent gastrointestinal obstruction
• Monitor for allergic reactions in sensitive individuals

Pregnancy

Generally considered safe to use during pregnancy, but always consult a healthcare provider.

Breast-feeding

Considered safe while breastfeeding, but consult a healthcare provider for personalized advice.

Storage

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

Formulations

• Psyllium husk powder
• Psyllium husk capsules
• Psyllium husk granules

Indications

• Ethanol intoxication
• Detoxification in alcohol dependence
• Antiseptic and disinfectant
• Solvent in pharmaceutical preparations

Dosage

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

Adults: Refer to BNF for specific dosing information based on clinical indications.

Mechanism of action

Ethanol affects the brain’s neurons by altering their membranes, ion channels, enzymes, and receptors. It binds directly to GABA, glycine, NMDA, acetylcholine, and serotonin receptors, enhancing the inhibitory effects of GABA at GABAa receptors and blocking NMDA receptors for glutamate. This results in reduced excitatory neurotransmission, contributing to its sedative effects. Ethanol also acts as a dehydrating agent, disrupting osmotic balance across cell membranes, which enhances its anti-infective properties.

Pharmacodynamics

Ethanol produces cytotoxic effects through dehydration and precipitation of cellular components, leading to bacteriocidal and antifungal actions. It is metabolized primarily in the liver by alcohol dehydrogenase, with 90 to 98% of ethanol oxidized to acetaldehyde and further to acetic acid. The interaction of ethanol with various neurotransmitter receptors modulates neuronal signaling, which is responsible for its psychoactive effects. Chronic exposure leads to tolerance, characterized by adaptive changes in neurotransmitter systems.

Pharmacokinetics

Ethanol is rapidly absorbed from the gastrointestinal tract, with peak blood concentrations occurring approximately 30 to 90 minutes after consumption. It is distributed throughout body water, with a volume of distribution that varies based on fat and water content in the body. Ethanol is primarily metabolized in the liver, with a small fraction excreted unchanged in urine and breath. The elimination half-life can vary significantly based on individual metabolic rates and liver function.

Contra-indications

• Hypersensitivity to ethanol or any of its components
• Severe liver disease
• Active gastrointestinal bleeding
• Acute pancreatitis

Adverse effects

• Drowsiness
• Dizziness
• Nausea
• Vomiting
• Headache
• Impaired coordination
• Dependence and withdrawal symptoms with chronic use

Interactions

• Increased sedation with other CNS depressants (e.g., benzodiazepines, opioids)
• Inhibition of the metabolism of drugs metabolized by CYP2E1
• Potentially increased risk of gastrointestinal bleeding with nonsteroidal anti-inflammatory drugs (NSAIDs)
• May enhance the hypoglycemic effect of antidiabetic medications

Precautions

• Use with caution in patients with a history of alcohol use disorder
• Monitor for signs of liver function impairment
• Avoid use in pregnant women due to potential fetal harm
• Caution in patients with a history of seizure disorders

Pregnancy

Ethanol should be avoided during pregnancy due to the risk of fetal alcohol spectrum disorders.

Breast-feeding

Ethanol is excreted in breast milk; mothers should avoid alcohol consumption during breastfeeding.

Storage

Store in a cool, dry place away from light and tightly closed in its original container.

Formulations

• Oral solutions
• Topical antiseptic solutions
• Medicated syrups

Indications

• Type 2 diabetes mellitus
• Hyperglycemia
• Irritable bowel syndrome
• Constipation
• Dysbiosis

Dosage

Children: Refer to the BNF for Children for appropriate pediatric dosing, as it is not universally established.

Adults: Refer to specific clinical guidelines and local protocols for appropriate dosing, as it may vary based on the condition being treated.

Mechanism of action

Inulin functions primarily as a prebiotic, stimulating the growth of beneficial gut bacteria and enhancing gut health. It may improve insulin sensitivity and glycemic control by modulating gut hormones, leading to increased secretion of glucagon-like peptide-1 (GLP-1), which enhances insulin secretion and decreases glucagon levels. Additionally, it may slow gastric emptying, contributing to a reduction in postprandial blood glucose levels.

Pharmacodynamics

Inulin's pharmacodynamics involve its role in carbohydrate metabolism and its effects on gut microbiota. By promoting the growth of beneficial bacteria, it can lead to improved intestinal barrier function and reduced inflammation. Inulin also aids in the modulation of lipid metabolism, potentially lowering cholesterol levels. Its effects on insulin sensitivity can help improve glycemic control in patients with insulin resistance.

Pharmacokinetics

Inulin is not absorbed in the gastrointestinal tract; it remains intact until it reaches the colon. It is fermented by intestinal bacteria, producing short-chain fatty acids (SCFAs) that may have systemic effects. The fermentation of inulin results in an increase in stool bulk and may improve bowel regularity. The time to reach the colon varies, but fermentation typically begins within 24 hours of ingestion. The elimination route is primarily through feces, as it is not metabolized by human enzymes.

Contra-indications

• Hypoglycemia
• Hypersensitivity to inulin or its components

Adverse effects

• Hypoglycemia
• Allergic reactions including rash, itching, or swelling
• Gastrointestinal disturbances such as nausea, vomiting, or diarrhea
• Injection site reactions

Interactions

• Insulin and other antidiabetic agents may increase the risk of hypoglycemia
• Certain medications like corticosteroids, diuretics, and thiazide diuretics may reduce the effectiveness of inulin

Precautions

• Monitor blood glucose levels closely, especially when initiating therapy or adjusting doses
• Caution in patients with renal impairment as clearance may be affected
• Use with caution in patients with liver dysfunction

Pregnancy

Inulin is generally considered safe during pregnancy; however, blood glucose levels should be monitored closely.

Breast-feeding

Inulin is excreted in breast milk, but it is typically considered safe during breastfeeding; consult with a healthcare provider for individualized advice.

Storage

Store in a refrigerator (2-8°C). Do not freeze. Keep out of reach of children.

Formulations

• Injectable forms (e.g., insulin syringes or pens)
• Inhalable formulations (in some regions)

Indications

• Constipation
• Irritable bowel syndrome
• Diverticulosis
• Hyperlipidemia
• Diabetes management

Dosage

Children: For children aged 6 to 12 years, the typical dosage is 1 to 2 teaspoons of psyllium husk mixed with water, 1 to 3 times a day. For children under 6 years, consult the BNF for Children for appropriate dosing guidelines.

Adults: The usual adult dosage is 3.5 to 7 grams (1 to 2 tablespoons) of psyllium husk taken with at least 240 ml of water, typically 1 to 3 times a day. Refer to the BNF for specific product formulations and dosing.

Mechanism of action

Psyllium works by absorbing water in the intestine to form a gel-like substance, which increases stool bulk and promotes peristalsis. This action helps to alleviate constipation and maintain bowel health. By enhancing fecal mass, psyllium also helps in reducing cholesterol absorption in the intestines.

Pharmacodynamics

Psyllium's pharmacodynamic properties are characterized by its ability to swell in water, producing a viscous gel that enhances stool consistency and frequency of bowel movements. It does not undergo metabolism in the body but influences gastrointestinal motility and fluid absorption.

Pharmacokinetics

Psyllium is not absorbed systemically as it is a soluble fiber. It passes through the gastrointestinal tract largely intact, with its primary action occurring in the intestines. The onset of action for constipation relief typically occurs within 12 to 72 hours after ingestion, depending on the individual’s hydration status and dosage.

Contra-indications

• Bowel obstruction
• Severe abdominal pain of unknown origin
• Fecal impaction
• Hypersensitivity to psyllium or any of its components

Adverse effects

• Abdominal cramping
• Diarrhea
• Nausea
• Vomiting
• Flatulence
• Esophageal obstruction
• Allergic reactions

Interactions

• May reduce absorption of concomitant medications if taken simultaneously
• Increased risk of gastrointestinal obstruction when taken with certain medications that can cause constipation

Precautions

• Ensure adequate fluid intake to prevent esophageal or intestinal obstruction
• Use with caution in patients with a history of gastrointestinal disorders
• Monitor for signs of allergic reactions

Pregnancy

Psyllium is generally considered safe for use during pregnancy, but it is always advisable to consult a healthcare provider before use.

Breast-feeding

Psyllium is not expected to pose a risk during breastfeeding, but consult a healthcare provider for personalized advice.

Storage

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

Formulations

• Powder for oral suspension
• Capsules
• Granules

Indications

• Hypertension
• Diabetes management
• Diuretic therapy
• Digestive health improvement
• Liver function support

Dosage

Children: Refer to established guidelines or consult with a healthcare professional for appropriate dosage.

Adults: Refer to established guidelines or consult with a healthcare professional for appropriate dosage.

Mechanism of action

The therapeutic effects of roselle are primarily attributed to its active compounds, such as anthocyanins, flavonoids, and organic acids. These constituents exhibit antioxidant properties, which help to reduce oxidative stress and inflammation in the body. Additionally, roselle may exert antihypertensive effects by promoting vasodilation and improving endothelial function, thereby reducing blood pressure. The diuretic effect is believed to be linked to the modulation of renal function and increased urine output.

Pharmacodynamics

Roselle has shown various pharmacodynamic effects, including antihypertensive, diuretic, lipid-lowering, and anti-inflammatory actions. The anthocyanins present in roselle are thought to contribute to its ability to lower blood pressure and improve lipid profiles by reducing LDL cholesterol levels. Furthermore, the plant's antioxidant properties enhance overall health by protecting cells from damage caused by free radicals.

Pharmacokinetics

The pharmacokinetics of roselle have not been extensively studied, but it is known that the bioactive components, particularly anthocyanins, are absorbed in the gastrointestinal tract. The peak plasma concentration and half-life of these compounds can vary based on the form of roselle consumed (e.g., tea, extracts). Factors such as dosage, preparation method, and individual metabolism can influence the absorption and bioavailability of roselle's active ingredients.

Adverse effects

• Gastrointestinal disturbances
• Allergic reactions
• Hypotension

Interactions

• May interact with antihypertensive medications
• May interact with diabetes medications

Precautions

• Use with caution in individuals with hypotension
• Monitor blood sugar levels in diabetics

Pregnancy

Limited data available. Consult a healthcare provider before use.

Breast-feeding

Limited data available. Consult a healthcare provider before use.

Storage

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

Formulations

• Dried flowers
• Teas
• Extracts
• Capsules

Mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate. The sedative effects of ethanol are mediated through binding to GABA receptors and glycine receptors (alpha 1 and alpha 2 subunits). It also inhibits NMDA receptor functioning. In its role as an anti-infective, ethanol acts as an osmolyte or dehydrating agent that disrupts the osmotic balance across cell membranes. ... Ethanol is known to affect a large number of membrane proteins that participate in signaling pathways such as neurotransmitter receptors, enzymes, and ion channels, and there is extensive evidence that ethanol interacts with a variety of neurotransmitters. The major actions of ethanol involve enhancing the inhibitory effects of gamma-aminobutyric acid (GABA) at GABAa receptors and blockade of the N-methyl-D-aspartate (NMDA) subtype of glutamate, an excitatory amine acid (EAA) receptor. Animal studies indicate that the acute effects of ethanol result from competitive inhibition of glycine binding to NMDA receptor and disruption of glutamatergic neurotransmission by inhibiting the response of the NMDA receptor. Persistent glycine antagonism and attenuation of glutamatergic neurotransmission by chronic ethanol exposure results in tolerance to ethanol by enhancing EAA neurotransmission and NMDA receptor upregulation. The latter appears to involve selective increases in NMDA R2B subunit concentrations and other molecular changes in specific brain loci. The abrupt withdrawal of ethanol thus produces a hyperexcitable state that leads to the ethanol withdrawal syndrome and excitotoxic neuronal death. GABA-mediated inhibition, which normally acts to limit excitation, is eliminated during ethanol withdrawal syndrome and further intensifies this excitation. In addition, NMDA receptors function to inhibit the release of dopamine in the nucleus accumbens and mesolimbic structures, which modulate the reinforcing action of addictive xenobiotics such as ethanol. By inhibiting NMDA receptor activity, ethanol could increase dopamine release from the nucleus accumbens and ventral tegmental area and could thus create dependence. Chronic ethanol administration also results in tolerance, dependence, and an ethanol withdrawal syndrome, mediated, in part, by desensitization and or downregulation of GABAa receptors. The development of alcoholic ketoacidosis (AKA) requires that a combination of physical and physiologic events occur. The normal response to starvation and depletion of hepatic glycogen stores is for amino acids to be converted to pyruvate. Pyruvate can serve as a substrate for gluconeogenesis, be converted to acetyl-CoA, which can enter the Krebs cycle or can be utilized in various biosynthetic pathways (eg, fatty acid, ketone bodies, cholesterol, and acetylcholine) ... Ethanol metabolism generates NADH, resulting in an excess of reducing potential. This high redox state favors the conversion of pyruvate to lactate, diverting pyruvate from being a substrate for gluconeogenesis. To compensate for the lack of normal metabolic substrates, the body mobilizes fat from adipose tissue and increased fatty acid metabolism as an alternative source of energy. This response is mediated by a decrease in insulin and an increased secretion of glucagon, catecholamines, growth hormone, and cortisol. Fatty acid metabolism results in the formation of acetyl-CoA and it combines with the excess acetate that is generated from ethanol metabolism to form acetoacetate. Most of the acetoacetate is reduced to beta-hydroxybutyrate due to the excess reducing potential or high redox state of the cell. Volume depletion interferes with the renal elimination of acetoacetate and beta-hydroxybutyrate, and contributes to the acidosis. An elevated lactate concentration may result from shunting from pyruvate or

Pharmacodynamics

Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations. Ethanol also binds to GABA, glycine, NMDA receptors and modulates their effects. Ethanol is also metabolised by the hepatic enzyme alcohol dehydrogenase.