How does dietary fiber affect on nutrients (carbohydrates, lipids, minerals and vitamins) absorption?

Contents

1. Interaction of dietary fibers with carbohydrates absorption
2. Interaction of dietary fibers with dietary lipids absorption
3. Interaction of dietary fibers with mineral absorption
4. Interaction of dietary fibers with Vitamins absorption
5. Other related topics

Interaction of dietary fibers with carbohydrates absorption

Most, though not all, the results of feeding or administering various preparations of dietary fibers, particularly in the soluble gel forms indicate that dietary fibers modulate the absorption of carbohydrates in the small intestine. Incorporating such preparation into carbohydrate-containing meal has been shown to reduce gastric emptying and post-prandial hyperglycemia and insulinemia in both normal and diabetic subjects.

There is some evidence to suggest that the activity of the pancreatic enzymes, amylase, lipase, trypsin and chymotrypsin can be altered in vitro by incubation with dietary fiber polymers. It is difficult to draw any firm conclusions from these studies.

The mode of action of insoluble dietary fibers is less well understood. It may interfere with enzymes access to carbohydrates substrates. High carbohydrate, high fiber diets have been shown to be effective in diabetes and to improve indices of diabetic control. Diets high in dietary fibers improve diabetic control independent of the amount of carbohydrates in the diet.

Interaction of dietary fibers with dietary lipids absorption

Both soluble and insoluble dietary fibers have been shown to alter fat absorption, with a decrease in apparent digestibility and increase in fecal fat. The increase in fecal fat is, however, nutritionally insignificant, with absorption remaining well over 95%.

There is some evidence that dietary fiber slower cholesterol absorption in the small intestine, demonstrated by both in vitro and in vivo experiments on the rat. It has been suggested that the action of dietary fiber in inhibiting cholesterol uptake in the small intestine is similar to that proposed for absorption of sugars. However, the interaction between soluble fiber and lipid micelles and reduced fluid movement in the presence of viscous fiber may also be important considerations. More studies are needed to elucidate the influence of dietary fibers on cholesterol absorption.

Interaction of dietary fibers with mineral absorption

In all discussion of the potential benefits of increasing the level of dietary fibers, at least one warning is always sounded: fiber interacts with dietary minerals, changing the micronutrients balance, and persons on marginal intakes may be at risk on increasing the dietary fiber intake. Dietary fiber can alter the absorption of calcium, zinc, iron, phosphorus and magnesium.

It is seen that not all fibers behave alike in affecting mineral bioavailability. Wheat bran is the most active. Fiber seems to have little or no nutritional consequences on persons on adequate mineral intake.

Interaction of dietary fibers with Vitamins absorption

Data on the effect of dietary fibers on vitamin in bioavailability is scarce. Vitamin A absorption appears to be increased with a formula diet containing guar, apple pectin, cellulose or bran.

Other related topics

1. What are the Dietary fibers?
2. Dietary fibers and related diseases
3. Bacterial flora and dietary fibers
4. Bile acids absorption and dietary fibers

Dietary fibers and related diseases

Contents

1. Introduction
2. High fiber diet and related diseases
3. Low fiber diet and related diseases
4. Other related topics

Introduction to Dietary fibers

Although the importance of dietary fibers was recognized only a few decades ago, throughout the history a few perceptible individuals have from time to time drawn attention to the need for fiber in the diet. Hippocrates commented on the laxative effect of coarse flour.

High fiber diet has a positive effect on following diseases

1. constipation
2. hemorrhoids
3. Anal fissure
4. irritable bowel disease
5. diverticular disease
6. High cholesterol
7. Diabetes
8. Obesity

High fiber diet has a negative/uncertain effect on following diseases

1. Colorectal cancers
2. Diverticular disease

Low fiber diet has a positive effect on following diseases

1. Coeliac disease
2. Pancreatic diseases
3. Vitamin deficiency diseases
4. Mineraldeficiency diseases

Low fiber diet has a negative/uncertain effect on following diseases

1. Fecal incontinence
2. Ileitis

Constipation and dietary fibers

Constipation can be defined as a bowel frequency of fewer than three motions per week or the need to strain more than 25% of the time during defecation. According to these criteria, bowel frequency is normal in 99% of the population. Most adults with an abnormally low bowel frequency are women.

Most of the time management depends on the underline cause but general management is the same irrespective of the cause Dietary fiber increases the weight and size of your stool and softens it. A bulky stool is easier to pass, decreasing your chance of constipation. If you have loose, watery stools, fiber may also help to solidify the stool because it absorbs water and adds bulk to stool.

Hemorrhoids (piles) and dietary fibers

Individuals with constipation tend to strain while defecating so they are more vulnerable to develop hemorrhoids. Therefore prevention of constipation is the mainstay of treatment. For that dietary modification are required as discussed in above.

Anal fissures and dietary fibers

The management of the acute fissure is conservative. Stool softeners for those with constipation, increased dietary fiber, topical anesthetics, glucocorticoids, and sitz baths are prescribed and will heal 60 to 90% of fissures. Chronic fissures are those present for >6 weeks. These can be treated with modalities aimed at decreasing the anal canal resting pressure including nitroglycerin ointment (0.2%), applied three times a day, and botulinum toxin type A, up to 20 units, injected into the internal sphincter on each side of the fissure. Surgical management includes anal dilation and lateral internal sphincterotomy.

Irritable bowel disease (IBD) and dietary fibers

There are two types of IBD’s; crohn’s disease and ulcerative colitis. Among those crohn’s disease needs a dietary modification. Patients should be advised to eat a well-balanced diet with high fiber content. A low-fat, lactose-free or low-residue

Diet is required in those with steatorrhoea, hypolactasia or stricture. Elemental diets (containing amino acids and glucose) and polymeric diets have been shown to be almost as effective as prednisolone in treating active disease and can be a useful form of therapy in some patients.

Diverticular disease and dietary fibers

The term ‘diverticulosis’ simply describes the presence of diverticula; no symptoms need be present. Diverticulitis is the clinical syndrome that occurs on the rare occasions when a diverticulum becomes inflamed; it may be associated with local perforation leading to pericolitis. Diverticular disease encompasses all manifestations, including the muscular abnormalities in the colonic wall that usually accompany diverticulosis.

A high-fibre diet and/or bulking agents (e.g. bran, ispaghula) are recommended in diverticulosis. The amount of bran required is determined by trial and error, starting with a small dose.

High cholesterol and dietary fibers

Soluble fiber found in beans, oats, flaxseed and oat bran may help lower total blood cholesterol levels by lowering low-density lipoprotein, or "bad," cholesterol levels.

Diabetes and dietary fibers

Fiber, particularly soluble fiber, can slow the absorption of sugar, which for people with diabetes; can help improve blood sugar levels. A high-fiber diet may also reduce the risk of developing type 2 diabetes.

Obesity and dietary fibers

High-fiber foods generally require more chewing time, which gives your body time to register when you're no longer hungry, so you're less likely to over eat. Also, a high-fiber diet tends to make a meal feel larger and linger longer, so you stay full for a greater amount of time. And high-fiber diets also tend to be less "energy dense," which means they have fewer calories for the same volume of food.

Colorectal cancers and dietary fibers

Evidence that dietary fiber reduces colorectal cancer is mixed — some studies show benefit, some show nothing and even some show greater risk. If you're concerned about preventing colorectal cancer, adopt or stick with a colon cancer screening regimen. Regular testing and removal of colon polyps can prevent colon cancer.

Pancreatic disease and dietary fibers

The effect of dietary fiber on pancreatic enzymes was examined in vitro, employing different concentrations of cellulose, pectin, and wheat bran incubated with amylase, lipase, and trypsin. Ingestion of a high fiber diet was associated with a small but significant (p less than 0.01) increase in fecal weight and fecal fat excretion. All patients complained of increased abdominal flatulence with high fiber diet, however, no significant increase in frequency of bowel movements was noted. In vitro studies demonstrated reduction in pancreatic enzyme activity by increasing concentration of dietary fiber and its components. These data suggest that steatorrhea may be enhanced with the ingestion of high fiber diet in patients with exocrine pancreatic insufficiency on oral pancreatic enzyme therapy. Increase in fecal fat excretion may, in part, be related to reduction in the activity of pancreatic enzymes by the dietary fiber.

Coeliac disease and dietary fibers

In coeliac disease, the mucosa of the small intestine is abnormal. The condition improves morphologically and symptomatically with a gluten-free diet treatment of coeliac disease requires a gluten-free diet avoiding wheat, rye and barley products. Debate continues about the possible toxicity of oats, but commercial oat flours may be contaminated with wheat and are therefore probably best avoided. The diet is low in fiber, so regular addition of rice bran and ispaghula husks may be useful.

Other related topics

1. What are the dietary fibers?
2. How does dietary fiber affect on nutrients absorption?
3. Bacterial flora and dietary fibers
4. Bile acids absorption and dietary fibers

What are the dietary fibers? /Importance of dietary fibers

Contents

1. Introduction to dietary fibers
2. The dietary fiber hypothesis
3. Classification of dietary fibers
4. Effects of dietary fibers on gut physiology
5. Interaction of dietary fibers with other nutrients
6. Common food items rich in dietary fibers
7. Other related topics

Introduction to dietary fibers

Although the importance of dietary fibers was recognized only a few decades ago, throughout the history a few perceptible individuals have from time to time drawn attention to the need for fiber in the diet. Hippocrates commented on the laxative effect of coarse flour. The Persian physician Hakim (9^th century AD) wrote: “whet is beneficial. Chappatis containing more bran come out of the digestive tract quicker but less nutritious. Those containing little bran take along time to be excreted”.

The dietary fiber hypothesis

The dietary fiber hypothesis has two primary statements;

1. A diet rich in foods containing plant cell walls (dietary fiber) is protective against a range of diseases prevalent in western communities.
2. In some instances a diet poor in foods containing plant cell walls is a causative factor in the development of the disease and, in others, it provides the conditions where other etiological factors are more active

Classification of dietary fibers

Dietary fiber was initially defined as the skeletal remains of plant cells in the diet that are resistant to hydrolysis by digestive enzymes of humans. The definition was later extended to all polysaccharides and lignin in the diet that are not digested by the endogenous secretions, so as to embrace polysaccharides in some food additives.

Dietary fibers may be classified according to their chemistry or their physical properties such as the water-holding capacity, viscosity and providers of gel filtration or cation exchange absorbent matrix or catalytic surface.

Chemical classification

1. Simple polysaccharides (cellulose)
2. Complex polysaccharides (Lignin, cutin)

Classification according to the physical properties

1. Water soluble Fibers(Cllulose)
2. Non-soluble fibers (Cutin)

The macromolecular constituents of plant cell wall material fall into 3 groups;

1. The fibrillar polysaccharides (cellulose)
2. The matrix polysaccharides ( hemicelluloses, glycoproteins)
3. The encrusting polysaccharides (lignin)

Effects of dietary fibers on gut physiology

The effects of dietary fibers on gut physiology will depend on the;

1. structure and tissue types
2. nature of the intracellular compounds
3. form in which the food is taken (fresh, cooked or processed)
4. food particle size

Dietary fiber acts in the small intestine in three main physical forms: as soluble chains, as insoluble macromolecular assemblies and as swollen, hydrated, sponge like net-work.

Dietary fiber helps to regulate 4 central aspects of the digestive process;

1. Nutrient absorption
2. Sterol metabolism
3. caecal fermentation
4. stool weight

Different fibers affect each of these processes in different ways.

Interaction of dietary fibers with other nutrients

Most, though not all, the results of feeding or administering various preparations of dietary fibers, particularly in the soluble gel forms indicate that dietary fibers modulate the absorption of nutrients in the small intestine. Following dietary components are mainly affected;

1. carbohydrates
2. lipids
3. minerals
4. vitamins

Common food items rich in dietary fibers

1. Vegetables ( leafy vegetables)
2. pulses
3. cereals
4. legumes
5. fruits (banana, mango)

Other related topics

1. Dietary fibers and related diseases
2. How does dietary fiber affect on nutrients absorption?
3. Bacterial flora and dietary fibers
4. Bile acids absorption and dietary fibers

Potential effects of tea on health/medical benefits of tea/ importance of tea/ constituents/ chemical compound of tea /history of tea

Contents

1. History of Tea
2. health benefits of Tea
3. Constituents of Tea

• Protein
• Carbohydrates
• Lipids
• Vitamins
• Minerals
• Polyphenols
• Alkaloids

Tea plant

History of Tea

Tea has been the world’s most popular beverage, next to water. Emperor Shen Nang (2737 BC) is said to have used it as a beverage.

Tea is mentioned in Erh Ya, a Chinese dictionary 350 BC. The first monograph on tea was published by Lu Yu in 780 AD, who described the leaf and how and when it is plucked and explained how the leaf is manipulated in the hands, dried and sealed. The china tea plant was taken to Japan about 800 AD and regarded as a medicine for 500 years until green tea was developed and became a popular Japanese beverage.

In 1559 Europe was informed of tea by the Venetian writer, Gian Batista Ramusio. In England the first mention was by R L Wikham, in 1615.

Health benefits of Tea

Some of the health benefits are as follows;

1. Since caffeine relaxes the coronary vessels, it can be useful as a treatment for angina and myocardial infarction.
2. Useful in the treatment of bronchial asthma as the caffeine is a smooth muscle relaxant.
3. Tea can increase the gastric emptying therefore it is useful to relieve the post prandial distress.
4. There are evidences that tea is of value in gout.

Constituents of tea

The proportion in which the various constituents are present in the leaf will depend on the soil and climate and the stage of the leaf at harvest. The proportion of the constituents present in a cup of tea will be determined by the conditions under which the tea is brewed. Both brewing conditions and size of cup are subjected to considerable variation. In the discussion that follows on the composition of the extracted liquor, it is assumed that boiling water is added to black tea leaf in the ratio 100:1(weight for weight) and infused for 5 minutes, when about 35% of the solids are extracted. In estimating the daily intake of tea constituents, it is assumed that 5 to 6 cups (each of volume 170 ml) are consumed. Mai constituents are as follow;

1. Protein
2. Carbohydrates
3. Lipids
4. Vitamins
5. Minerals
6. Polyphenols
7. Alkaloids

Proteins and Tea

Although proteins constitute 5 to 23 % of black tea (dry weight), they make up less than 2% of the hot water-soluble solids, so that the daily intake is less than 70 mg. If milk is added, casein will complex with tea polyphenols, reducing the astringency but not interfering with the normal digestion of the protein.

Carbohydrates and Tea

Carbohydrates form only 4 to 5%of the solids in the liquor; hence it is considered as a low energy diet. Adding milk and sugar to the daily intake could give about I MJ (up to 10% of the daily energy intake).Ceylon tea has 1.4 to 5.7%ofsugars per dry weight of tea.

Lipids and Tea

Black tea has 2 to 3%of lipids, mainly phospholipids, glycolipids, sulpholipids, and triacylglycerols. The quantities extracted by water are negligible. The major fatty acids are linoleic and linolenic acids. These fatty acids are liberated in the free form during storage, when they become more easily extractable in hot water.

Vitamins and Tea

Each cup of tea provides 2.3 µg of thiamin, 21.5µg of riboflavin, and 127.5µg of niacin, 1.3µg folic acids, 21.4µg pantothenic acid, and 1.4µg biotin and 17µg inositol assuming 100% extraction into the liquor. Ascorbic acid in the fresh leaf is as high as in carrots but30 to 50% destroyed during manufacture and very little is extracted into the infusion.

Minerals and Tea

Most minerals are present in the leaf and many are extracted into the infusion. Its sodium content is low. The fluoride content varies widely, being 100 parts per million, between 40 and 80% of this being extracted in the water (about 0.1 mg per cup), giving less than 1 mg per day.

Polyphenols and Tea

Polyphenols constituent about 15 % (w/w) of black tea and the amount is varying according to the variety of tea, its geographical origin and environmental conditions.

Alkaloids and Tea

Tea also provides alkaloids. Black tea contains 1 to 5% caffeine, 0.05% theobromine and 0.0002% to 0.0004% theophylline. About 80% of the caffeine is extracted during brewing, giving a daily intake of about 0.3 g.

VITAMIN A/Retinol/Carotene (Digestion/absorption/storage/transport/functions/recommended intakes/common food items/ Can you die from excess/toxicity

Vitamin A is the generic descriptor for compounds with vitamin A activity, namely all-trans retinol and its derivatives, retinal and retinoic acid, which are the naturally occurring vitamers. During the past few years a great deal of research into production of synthetic compounds with vitamin a activity has given rise to the term “retinoids” which is a generic term that includes both naturally occurring compounds with vitamin A activity, as well as synthetic analogues of retinol, with or without biological activity.

The dominant feature of the molecules of the vitamin a family is the conjugated double bond system which gives the molecule a high extinction coefficient. The basic structure also makes it extremely hydrophobic, a property that presents a major problem to animals that have to obtain it from the diet and transport it in an aqueous medium to target tissue.

Structure of the retinol

Digestion and absorption of Vitamin A/Retinol/Carotene

Vitamin a exists as an ester in the food and it is hydrolyzed in the duodenum in the presence of bile salts. Since both retinol and carotenes are highly unsaturated they tend to oxidized.

Absorption of both retinols and carotenes are facilitated by the presence of fat in the diet, being associated with micelles formed during fat digestion. Utilization of both retinol and beta-carotene is also enhanced by dietary protein and zinc. About 90% of dietary retinol is absorbed and 60% to 70% of beta-carotene is also absorbed.

Excessive intake of either retinol or beta-carotene decreases vitamin E status. Vitamin E, a powerful anti-oxidant, protects retinol and beta-carotene from oxidation.

Storage of Vitamin A/Retinol/Carotene

Hepatic vitamin A (95% as esters of long chain acids, chiefly palmitate) represents 90% of the body reserves of the Vitamin A. Mammalian liver has an exceptional capacity to store retinol over a wide range of dietary intakes. However, the plasma level remains remarkably constant.

Transport of Vitamin A/Retinol/Carotene

Retinol is mobilized from liver and transported in plasma to target cells as a complex with retinol binding protein (RBP), which is a single polypeptide of molecular weight about 21,000 and one binding site. Free retinol-RBP complex disappears from circulation quickly, being lost in the urine.

Recommended intakes of vitamin A/Retinol/Carotene

Infants are born with small stores and depend on breast milk to lay down their stores in the liver. A well nourished mother secretes about 60µg retinol per deciliter of milk, providing 50µg/kg body weight of infant.To provide an average secretion of milk of 650ml the recommended daily allowance (RDA) for lactating women is 850µg retinol/day. Poorly fed mothers provide only 30 to 40µg/kg infant weight in India and less than 20µg/kg in Jordan.

Age Group	Basal need (µg)	Safe limit (µg)
Infants	180	350
1-6 years	200	400
6-15 years	270-350	400-600
Adult male	300-400	500-600
Adult female	270-330	500
pregnancy	Normal+100	Normal+100
lactating	Normal+180	Normal+350

Recommended dietary allowance of vitamin A in retinol equivalents (RE)

Function of Vitamin A/Retinol/Carotene

Vitamin A exists in three forms; retinol: retinal (aldehyde): retinoic acid. It has three main functions;

1. Visual function; this is the first to be deranged in deficiency.
2. systemic function; promoting growth and maintenance of tissues
3. Reproductive function

Vitamin A toxicity (hypervitaminosis)

Infants and young children are more vulnerable for Vitamin A toxicity. Bulging of fontanelles, irritability, severe headache and vomiting are features of acute toxicity of Vitamin A. Painful extremities, dry skin, sparse hair and hydrocephalus are some of the features of chronic Vitamin a toxicity. Therefore Infants and young children can die from Vitamin a toxicity. Adults can also be affected, but less frequently than that of youngest.

Common sources of Vitamin A/Retinol/Carotene

The dietary sources of vitamin a fall into two categories;

1. Vitamin A (all-trans retinol or preformed vitamin A)
2. Provitamin A (carotenoid precursors)

Common food items are as follows;

Chicken eggs

Green vegetables

Organ meat

1. preformed vitamin A ( milk and milk products, eggs, shell fish, liver and organ meats)
2. Provitamin A ( dark green leafy vegetables, red and yellow vegetables and fruits)

What are the plant poisons? /Importance of plant poisons

If the whole or part of a plant, when brought into contact with the body in quantities likely to be brought into such contact, is capable of acting d3eleteriously because of chemical substances, singly, cumulatively or due to hypersensitivity, such as a plant may be referred to as a poisonous plant

Many of the poisonous plants have medicinal qualities. Some well known examples are cinchona, Ipecacuanha and opium. Many such plants are used in Aurvedhic medicine after boiling in cow’s milk and other agents which are though to detoxify them.

Classification of plant poisons

Several classifications are available but no one is perfect.

· The following classification is based on the main system that is affected by the plant poison. But there can be an overlap as well.

1. Neurotoxin (opium, cannabis, strychnine)
2. Cardio-toxin (yellow oleander)
3. Gastrointestinal irritants (Gloriosa superba, Adenia palmate)
4. General cellular toxin (manioc, Adenia palmate)

· Classification according to the chemical constituents of the plant poison

1. Alkaloids (strychnine, cocaine)
2. Glycosides (yellow oleander)
3. Glycoprotein (Ricin)
4. Oxalates (Dieffenbachia)

· Classification according to the botanical family to which the plant belongs

1. Euphorbiaceae (manioc)
2. Passifloraceae(Adenia palmate)
3. Apocyanaceae (yellow oleander, nerium oleander)
4. Lilliaceae (Gloriosa superba)
5. Loganiaceae (strychnos nux vomica)

Autopsy features

Autopsy features are often non specific. They will depend on the poison and the pathophysiology it causes.

Smell of poison

Poison/seeds in stomach

Features of dehydration

Features of cyanide poisoning

Manioc/Manihot utilissma/ Cassava

Manioc poisoning occurs due to the presence of a cyanogenic glycoside (CG), linamarine and the enzyme linase in the leaves and root of the plant. The CG occurs in two forms; autolysable and hydrolysable. In the presence of the enzyme linase the autolysable form is autolysed to form HCN (hydrocyanic).When exposed the hydrolysable form is hydrolyzed and release HCN. This HCN is highly toxic.

Gloriosa superba

All parts of the plant are poisonous. Accidental poisoning can occur as the tuber resemble the sweet potato.The main poisonous agent is the alkaloid, colchicine. This chemical is used to treat gout.

Adenia palmata/ Modecca palmate

The plant is common in moist areas. The fruit resembles passion fruits. Therefore accidental poisoning in children occurs. The toxic effects are due to;

Cyanogenic glycoside (and enzyme emulsion that release HCN)

Free HCN

Toxalbumin

Hypersensitivity reaction

Thevetia peruviana (yellow oleander)

Poisoning is due to the ingestion of seeds of the yellow oleander. The toxic substance is a cardiac glycoside (thevetin, cerberine) Consumin 2-8 seeds may cause death of an adult.

Nerium oleander

All parts of the plan are poisonous. It contains a cardiac glycoside (oleandrin, nerin0 as the poison.

Strychnos nux vomica

It contains one of the most deadly known poisons and it is called strychnine (an alkaloid). The quantity of poison in one seed could be lethal.

What are the EICOSANOIDS? Importance of EICOSANOIDS

The term Eicosanoids refers to the oxidative metabolites of the Essential fatty Acids (EFA) containing 20 carbon atoms (in Greek Eicosa means twenty), and includes prostaglandins, prostacyclins, thromboxanes and leukotrienes. Prostaglandins (PG) were discovered by von Euler at about the same time that Burr and Burr discovered the EFA. The material was so named on the mistaken assumption that it originated from the prostate gland. There are more than 100 neutral PGs, isomers and their metabolites. Thromboxanes, prostacyclins and leukotrienes are derivatives of the PGs.

Eicosanoids Formation

The Eicosanoids formation may proceed through one of several alternative enzymatic routes. The precursor highly unsaturated fatty acids (HUFA) are esterified with cholesterol. They are made accessible on a stimulus reaching the cell surface, and acylhydrolases release the poly unsaturated fatty acids (PUFA) from the membrane, which will then be metabolized along one of three enzymatic routes.

1. The cyclooxygenase pathway
2. 5-lipooxygenase pathway
3. 12-lipooxygenase pathway

Dietary Fatty acids and Eicosanoids Metabolism

Desaturation and elongation of the essential fatty acids, linoleic (18:2,n-6) and alpha-linolenic (18:3,n-3) lead to the formation of dihomo-gamma-linolenic acid, DHLA (20:3,n-6), arachidonic acid, AA (20:4, N-6) and timnodonic acid (20:5,n-3;5,8,11,14,17-eicosa pentaenoic acid) more commonly known as EPA.these fatty acids are the precursors of prostaglandins of the 1,2 and 3 series, respectively. AA and EPA may be converted to leukotrienes of the 4 and 5 series, respectively. DHLA lacks a double bond at C5 and it is therefore not a substrate for 5-lipooxygenase.

Eicosanoids and Hemostasis

The major cyclooxygenase product in platelets is TXA2, a potent and important inducer of platelet aggregation and vaso-constriction. TXA2, formed during platelet activation, is highly unstable, with half life of 30 seconds, being rapidly hydrolyzed to inactive TXB2. Platelet aggregation is probably induced by prostaglandin endoperoxide PGG2 also. In vascular tissue the major eicosanoid released is prostacyclins, PGI2, a potent vasodilator and an inhibitor of platelet aggregation.

Greenland Eskimos have a low incidence of thrombotic episodes such as myocardial infarction, of atherosclerosis, of rheumatoid arthritis, of psoriasis and their bleeding tendancy is higher than that of other people.This has been attributed to high intake of fish food, containing large amount of EPA and its derivatives.

Lipid peroxidation and impact on Eicosanoids production

Many studies have implicated oxygen radicals and lipid peroxidation in various diseases. Poly unsaturated fatty acid (PUFA) is one component of cells that is liable to damage by free radicals. Attack by free radicals may result in;

1. The loss of PUFA cell membrane, with lowered ability to produce Eicosanoids.
2. The formation of lipid peroxides and related compounds which can themselves cause damage to other cellular component.

Above process can lead to formation of cancers.

Eicosanoids deficiency

Acute deficiency of essential fatty acids (EFA) in children results in growth failure and increased susceptible to infection. A chronic deficiency (a low ratio of EFA to non-essential fatty acids in the body) causes faulty structure of cell membranes and increased prevalence of chronic degenerative diseases such as atherosclerosis.

Requirements of Eicosanoids

In children, the minimal daily requirement of n-3 fatty acids has been estimated as 0.54% of total dietary energy.In adults it ranges from 0.2% to 0.3%. maximum being 0.5% to 1%, of total dietary energy.

Can you die from excess/toxicity of vitamins (Hypervitaminosis)? / How people die from excess/toxicity of vitamins (Hypervitaminosis)?

Frankly speaking anything can kill a person if it is consumed in excess amount and it is true for the vitamins as well. Fortunately deaths due to vitamin toxicity are very rare. There are two type of vitamin; fat soluble vitamins: water soluble vitamins. Usually fat soluble vitamin can cause vitamin toxicity as they are accumulated in the adipose/fat tissues of the body.

Fat soluble vitamins

1. Vitamin A
2. Vitamin D
3. Vitamin E
4. Vitamin F
5. Vitamin K

Water soluble vitamins

1. Vitamin B1 (Thiamin)
2. Vitamin B2 (Riboflavin)
3. Niacin/Nicotinic acid/Nicotinamide
4. Pantothenic acid
5. Vitamin B6 (Pyridoxine)
6. Vitamin B12 (Cyanocobalamine)
7. Folic acid
8. Vitamin H (Biotin)
9. Vitamin C (Ascorbic acids)

Vitamin A toxicity

Infants and young children are more vulnerable for Vitamin A toxicity. Bulging of fontanelles, irritability, severe headache and vomiting are features of acute toxicity of Vitamin A. Painful extremities, dry skin, sparse hair and hydrocephalus are some of the features of chronic Vitamin a toxicity. Therefore Infants and young children can die from Vitamin a toxicity. Adults can also be affected, but less frequently than that of youngest.

Vitamin D toxicity

The safety margin for vitamin D is large, and vitamin D toxicity is usually observed only in patients taking doses 40,000 IU daily.

Vitamin E toxicity

High doses of vitamin E (>800 mg/d) may reduce platelet aggregation and interfere with vitamin K metabolism and are therefore contraindicated in patients taking warfarin. Nausea, flatulence, and diarrhea have been reported at doses >1 g/d.

Vitamin K toxicity

Parenteral(Intravenous) doses of the water-soluble vitamin K derivative (menadione)have been reported to cause hemolytic anemia and hypobilirubinemia in infants. Toxicity from dietary phylloquinones and menaquinones has not been described. High doses of vitamin K can impair the actions of oral anticoagulants.

Vitamin B1 (Thiamin) toxicity

Although anaphylaxis has been reported after high doses of thiamine, no adverse effects have been recorded from either food or supplements at high doses. Thiamine supplements may be bought over the counter in doses of up to 50 mg/d.

Vitamin B2 (Riboflavin) toxicity

Because the capacity of the gastrointestinal tract to absorb riboflavin is limited (20 mg if given in one oral dose), riboflavin toxicity has not been described.

Niacin toxicity

Prostaglandin-mediated flushing has been observed at daily doses as low as 50 mg of niacin when taken as a supplement or as therapy for hypertriglyceridemia.There is no evidence of toxicity from niacin derived from food sources. Flushing may be accompanied by skin dryness, itching, and headache. Premedication with aspirin may alleviate these symptoms. Nausea, vomiting, and abdominal pain also occur at similar doses of niacin.

Vitamin B6 (Pyridoxine) toxicity

The safe upper limit for vitamin B6 has been set at 100 mg/d, although no adverse effects have been associated with high intakes of vitamin B6 from food sources only. When toxicity occurs, it causes a severe sensory neuropathy, leaving patients unable to walk. Some cases of photosensitivity and dermatitis have also been reported.

Vitamin C (Ascorbic acids) toxicity

Taking 2 g of vitamin C in a single dose may result in abdominal pain, diarrhea, and nausea; doses >3 g have been reported to elevate blood levels of ALT, lactic acid dehydrogenase, and uric acid. Since vitamin C may be metabolized to oxalate, it is feared that chronic, high-dose vitamin C supplementation could result in an increased prevalence of kidney stones.

CAN YOU DIE FROM MANIOC POISONING?

CAN YOU DIE FROM VITAMIN C POISONING?