Fat-soluble vitamins (4): Vitamins A, D, E, & k water-soluble

Download 72.5 Kb.
Size72.5 Kb.
Nutrition Lecture 7/8

  1. List the 13 vitamins that assist essential biochemical reactions within your body and classify the vitamins as fat-soluble and water soluble.

Fat-soluble vitamins (4): Vitamins A, D, E, & K

Water-soluble(9): Thiamin (B1), Riboflavin (B2), Nicotinic Acid (B3 aka Niacin), Pantothenic Acid (B5), Pyridoxine (B6), Folic Acid, Cobalamin (B12), Ascorbic Acid (C), & Biotin

  1. Describe vitamin digestion and absorption.

Fat-soluble vitamins are absorbed like lipids, meaning they require normal fat absorption (bile salts and pancreatic juice). They are transported to the liver in chylomicrons via the lymphatic system. Then they are transported in blood by lipoproteins or specific binding proteins.

Water-soluble vitamins are absorbed by the intestine and carried by the circulatory system to the specific tissues that they will be put to use. The different types of vitamin are differentiated by their solubility in water. They can be stored enough to last for several weeks.

In the forms they are absorbed, B vitamins are inactive. They have to undergo processing before they reach their functional state as coenzymes (compounds that unite with a protein, apoenzyme, to form an active enzyme). Vitamin C’s metabolism and working state (coenzyme or not) aren’t well understood.

  1. See attached table

  1. See attached table

  1. Describe the causes and treatments for Vitamin D deficiencies and toxicities (e.g., vitamin D/osteomalacia and hypercalcemia) and the current dietary recommendations.


Risk Factors - exclusively breast fed infants, dark skin, aging, covering all skin or using sunscreen whenever outside, fat malabsorption syndromes, inflammatory bowel disease, and obesity. Phenytoin (Dilantin), fosphenytoin (Cerebyx), phenobarbitol (Luminal), carbamazepine (Tegretol), and rifampin (Rimactane) all increase metabolism of Vitamin D. Cholesteyramine (Questran), colestipol (Colestid), orlistat (Xenical), mineral oil, and Olestra (fat substitute) all decrease intestinal absorption of Vitamin D.

Rickets – deficiency of Vitamin D in children. The developing bone has abnormal amounts of unmineralized osteoid which means that it’s significantly weaker (less rigid), so weak that the long bones of the legs actual bend under the weight of the body, leading to the “bowing.” In infants, this process may lead to delayed closure of fontanelles and rib cage deformation. In severe cases, hypocalcemia may cause seizures.

Osteomalacia – deficiency of Vitamin D in adults. Since adult bones are finished growing, the bones don’t bend, but they do lose strength, leading to higher risk of bone fracture. As more of the bone surface is covered by osteoid and recruitment of new osteoclasts is diminished, bone resorption is impaired and hypocalcemia develops. Hypocalcemia causes nerves to become more sensitive to depolarization. In sensory nerves, this effect leads to sensations of numbness, tingling, or burning; in motor nerves it leads to spontaneous contractions, tetany.

Muscle Weakness & Pain – deficiency causes muscle weakness & pain, especially in the Arab/Danish Muslim women living in Denmark. (no sun, skin covered)

Adequate Intake: 200 IU for infants to adults 50 years old (yo). 400 IU for 51-71 yo. 600 IU for those older. These levels are set to maintain serum levels of at least 37.5 nmol/L, which may be too low. Also note that the AI was set with the idea that there was no Vitamin D being synthesized in the skin.


Vitamin D toxicity induces hypercalcemia which could result in bone loss, kidney stones, and calcification of organs like the heart and kidneys if untreated over a long period of time. Cardiac arrhythmia may also be induced in patients taking digitalis (Digoxin).Two possible values for the upper limit: Food and Nutrition board – 2,000 IU/day & studies since 1997 – 10,000 IU/day.

  1. Describe thiamin’s key role in metabolism and be able to discuss the causes and treatments for thiamin deficiencies.

Thiamin (Vitamin B1) exists in the body as free thiamin, thiamin monophosphate (TMP), thiamin triphosphate (TTP), and thiamin pyrophosphate (TPP, aka thiamin diphoshate). Thiamin’s key role is because TPP is a required coenzyme for a few important enzymes: Pyruvate dehyrdogenase, alpha-ketoglutarate dehyrdogenase, branched chain ketoacid (BCKA) dehyrdogenase, and Transketolase. The first three of these enzymes comprise different enzyme complexes within mitochondria. Transketolase is critical in the pentose phosphate pathway. Transketolase decreases early in thiamin deficiency, so its activity in red blood cells is a useful measure.

Causes of deficiency:

Inadequate intake: main cause of thiamin deficiency in low-income populations whose diets are high in carbohydrate and low thiamin. Breast-fed infants whose mothers are thiamin deficient are also at risk. In industrialized countries, alcoholism is a cause of poor diet and the major cause of thiamin deficiency.

Increased requirement: strenuous physical exertion, fever (malaria), pregnancy, breastfeeding, HIV-infection, and adolescent growth are all conditions requiring increased thiamin intake.

Excessive loss: kidney failure requiring dialysis & alcoholics have high fluid intake and urine flow rate which exacerbate their already low intake.

Anti-thiamin factors: certain plants like tea, coffee, and betel nuts have anti-thiamin factors. Certain raw freshwater fish, raw shellfish, ferns, and African silkworms (Nigeria – high protein food) have thiaminases that break down thiamin in food.

Diseases of deficiency: thiamin deficiency affect cardiovascular, nervous, muscular, and GI systems. Beriberi, the result of severe deficiency, has 3 different types

Dry (paralytic or nervous) beriberi - result of inactivity and low-calorie intake. Mainly peripheral neuropathy: “burning feet syndrome,” hyperreflexia, diminished sensation & weakness in arms & legs, muscle pain & tenderness, and difficulty rising from a squatting position. Severely deficient individuals may experience seizures.

Wet (cardiac) beriberi – result of severe physical activity & high carb intake. All the neurologic symptoms of dry with additional cardiovascular symptoms: rapid heart rate, enlargement of heart, edema, difficulty breathing, and ultimately congestive heart failure.

Cerebral beriberi – seen in alcoholics (mostly), stomach cancer (gross malnutrition), and AIDS (gross malnutrition). Wernike’s Triad - abnormal eye movements, stance & gait abnormalities, and abnormalities in mental function – apathetic state/profound memory disorder (Korsakoff’s amnesia/psychosis). Wernike’s disease if no amnesia present. Wernike-Korsakoff syndrome if amnesia present.

3. Describe the main function of each vitamin and their major food sources.

fat-soluble vitamin

biological activity

major dietary sources

Vitamin A (retinoids) & provitamin A (carotenoids)

3 metabolically active forms: Retinol - hormone, retinal(retinaldehyde) - precursor of visual pigment rhodopsin, & Retinoic acid - affecting growth of epithelia; Vision, growth

liver, egg yolks, fish oil, and fortified milk

Vitamin D (calcitrol, cholecaciferol, and ergocalciferol)

facilitate absorption of calcium and phosphorus. Maintain optimum calcification of bone

most dairy products, egg yolks, liver, and fish

Vitamin E (tocopherol)

Antioxidant: prevent breakdown of vitamin A and unsaturated fatty acids

vegetable oil, nuts, wheat, and green leafy vegetables

Vitamin K (quinones)

prothrombin and other blood clotting factors

liver & green leafy vegetables

H20-soluble vitamin

biological activity

major dietary sources

Vitamin B1 (Thiamin)

active coenzyme thiamine pyrophosphate(TPP): carbohydrate metabolism - pyruvate dehyrdogenase, amino acid metabolism - decarboxylation of AA's, neurotransmitter synthesis - Acetyl-CoA --> Acetylcholine

whole grain cereals, legumes, nuts, lean pork, and yeast

Vitamin B2 (Riboflavin)

active coenzymes Flavin Mononucleotide (FMN) and Flavin Dinucleotide (FAD): B-oxidation & electron transport chain

milk and milk products

Vitamin B3 (Niacin: Nicotinic Acid & Nicotinamide)

active coenzymes Nicotinamide Adenine Dinucleotide (NAD) and Nicotinamide Adenine Dinucleotide Phosphate (NADP): carbohydrate metabolism, electron transport chain, fatty acid synthesis

enriched breads and animal proteins

Vitamin B5 (Pantothenic Acid)

component of Coenzyme A, component of Acyl carrier protein (ACP) in fatty acid synthesis, and protein acetylation

meat, milk, and many vegetables

Vitamin B6 (Pyridoxine)

50 enzymes involved with carb, fat, and protein metabolism. Blood cell Synthesis - Hemoglobin, Niacin Synthesis - from Tryptophan, & Neurotransmitter Metabolism: production of Serotonin, GABA, and norepi

meat, fish, and poultry

Vitamin B12 (Cyanocobalamin)

required for the function of Folate-dependent enzyme, Methionine synthase, and the enzyme that catalyzes conversion of L-methylmalonyl-CoA to succinyl-CoA.

meat, poultry, and eggs (req IF for absorption)

Vitamin C (Ascorbic acid)

antioxidant - non-specific reducing agent, structural integrity - collagen synthesis, enhancing mineral absorption - non-heme ferrous Iron (2+), vital cell component synthesis - thyroxine, epi, carnitine, norepi, serotonin, bile acids, steroid hormones, and purine bases for DNA synth. Growth of bones and teeth. Maintenance of subcutaneous tissues and walls of blood vessels, and wound healing.

citrus fruits

Folate (Folacin & Folic Acid)

transfer of one carbon units, deamination of AA's, & Purine/Pyrimidine synthesis

leafy green vegetables

Biotin (biotin - free-form & biolytic -inactive)

coenzyme in fat and carb metabolism. 3 main enzyme: Acetyl CoA Carboxylase, Pyruvate Carboxylase (Regulator in Gluconeogenisis), and propionyl CoA Carboxylase

cauliflower, egg yolks, and liver

  1. Describe (and name as appropriate) the deficiency state, clinical occurrence, and common clinical features associated with each of the vitamins. Classic examples would include: Vitamin C/scurvy and thiamin/beriberi.

fat-soluble vitamin

deficiency state (in bold) & clinical features

Clin. Occurrence (def.)

toxicity features

Vitamin A (retinoids) & provitamin A (carotenoids)

night blindness, xeropthalmia, poor growth, dry skin

third world children & severe low intake

fetal malformation, skin changes, & pain in bones

Vitamin D (calcitrol, cholecaciferol, and ergocalciferol)

Rickets - bone has abnormal amounts of unmineralized osteoid --> "bowing" of long bones (under weight of child). In severe cases, hypocalcemia may cause seizures. Osteomalacia - increase in unmineralized osteoid content in adults --> more prone to bone fractures. Bone resorption impaired --> hypocalcemia --> nerves more sensitive to depol --> in sensory nerves numbness, tingling, & burning; in motor nerves, increased spontaneous contraction or tetany

inadequate sun exposure, inadequate intake, & renal disease

growth retardation, kidney damage, calcium deposits in soft tissue

Vitamin E (tocopherol)

hemolysis & nerve destruction

cholestatic liver disease (especially children)

muscle weakness, fatigue, inhibition of Vitamin K metabolism

Vitamin K (quinones)


Warfarin anticoagulant, Long-term antibiotics (especially with TPN), & newborn infants

anemia and jaundice

H20-soluble vitamin

deficiency state

Clinical Occurrence (deficiency)

Vitamin B1 (Thiamin)

Beriberi: Dry (neurologic-peripheral neuropathy) Wet (cardiac) & Wernike-Korsakoff syndrome Cardiac: Heart failure

refeeding after starvation

Vitamin B2 (Riboflavin)

Arabinoflavinosis: cheilosis, angular stomatitis (fissures at corners of mouth), nasolabial dermatitis, photophobia, corneal vascularization. B-complex deficiency: cheilosis, angular stomatitis, & glossitis


Vitamin B3 (Niacin: Nicotinic Acid & Nicotinamide)

Pellagra – bilateral dermatitis particularly in areas exposed to sunlight, glossitis, dementia, diarrhea, irritability, mental confusion, eventually delirium or psychotic symptoms

poor diet

Vitamin B5 (Pantothenic Acid)

Fatigue, headaches, weakness, motional swings, impaired muscle coordination, muscle cramps, GI disturbances. Dermatitis, glossitis, & anorexia

Rare, excess egg white ingestion & TPN (?)

Vitamin B6 (Pyridoxine)

Neurologic: convulsions & B-complex deficiency: cheilosis, angular stomatitis, & glossitis

only with pyridoxine-antagonist drugs (isoniazid, cycloserine, penicillamine)

Vitamin B12 (Cyanocobalamin)

Pernicious Anemia (when secondary to idiopathic gastric atrophy) Hematologic: Pancytopenia, Neurologic: subacute combined with degeneration, Peripheral neuropathy, & glossitis

Achlorhydria, Terminal ileal disease or resection, bacterial overgrowth, Diphyllobothrium latum, & pancreatic insufficiency

Vitamin C (Ascorbic acid)

Scurvy: red swollen, bleeding gums, perifolluiclosis, poor wound healing, purpura, & swelling of joints

infants, elderly, & alcoholics with very poor intake

Folate (Folacin & Folic Acid)

Hematologic: Megaloblastic Anemia (Pancytopenia & glossitis)

pregnancy, poor intake, & malabsorption

Biotin (biotin - free-form & biocytin -inactive)

Dermatitis, glossitis, & anorexia

Rare, excess egg white ingestion & TPN (?)

Directory: Nutrition
Nutrition -> Human Nutrition Question Bank
Nutrition -> Indiana Department of Education idoe/cacfp child Nutrition Programs Policy Instruction 11-17
Nutrition -> 2013 Student Placement (Nutrition & Claims Innovation) in a Global Nutrition Business
Nutrition -> We must check your application
Nutrition -> Glossary of Terms Specific for Human Digestion and Nutrition a acute Having a short and relatively severe course adipocyte
Nutrition -> Author: Weston A. Price
Nutrition -> Rachel Forst Nutrition in India From: Secretary of Health, India To: Minister of Finance, India Introduction
Nutrition -> Review of Nutrition Cluster Experiences and Learning for Transition
Nutrition -> Nj senate Commerce Committee Contact List
Nutrition -> Nutrition Knowledge and Competency Framework for Medical Graduates

Share with your friends:

The database is protected by copyright ©dentisty.org 2019
send message

    Main page