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43 Cards in this Set

  • Front
  • Back
Water-Soluble Vitamins
Water soluble vitamins like fat soluble vitamins are essential organic substances needed for normal functions, growth and maintenance of the body tissues.



Unlike fat soluble vitamins---water soluble vitamins are not stored (or only small amounts) in the body therefore there is less risk of toxicity




Easily destroyed during cooking—through heat, light, air (air bubbles in water), and alkaline substances.




Water soluble vitamins can leach into cooking water therefore use the water to get the vitamins…where fat soluble vitamins leach into oils…that is why they recommend eating tuna in water and not oil.




Best way to keep vitamins in foods is by steaming, stir-frying, and microwaving.

Overview of Water-Soluble Vitamins
All B-vitamins form coenzymes which are a type of cofactor. Metals are another type of cofactor. Cofactors combined with inactive enzymes (apoenzymes) to form active enzymes (holoenzymes) that are able to catalyze specific reactions.



Grains are an important source of B-vitamins. Remember many of the B-vitamins are in the bran of the grain. Therefore enriched grains are adding back some of the B-vitamins that are lost during the process of whole grains.

Thiamin B1
Beriberi is a disease in which the body does not have enough thiamine (vitamin B1). This disease in not very prevalent in US due to enrichment of foods. Drinking heavily can lead to poor nutrition, and excess alcohol makes it harder for the body to absorb and store thiamine. There is also a genetic disease –very rare condition known as genetic beriberi is inherited (passed down through families). People with genetic beriberi lose the ability to absorb thiamine from foods. This can happen slowly over time and symptoms occur when the person is an adult. However, because doctors may not consider beriberi in nonalcoholics, this diagnosis is often missed.



Thiamin absorbed in the SI by sodium-dependent active absorption process. Transported by RBC in the coenzyme form of TPP where thiamin has two phosphates---page 442 biochesmits’s view




Very little stored (if stored in muscles, brain, liver and kidney)


Excess filterd by kidney and excreted in urine Pork, sunflower seeds and legumes

Thiamin Needs

•RDA:


1.2mg men,


1.1mg women




•DV:1.5mg




•AverageNorth American intake is 1.2-2.0mg/day




•NoUL

Functions of Thiamin

•Coenzyme form:


•thiamin pyrophosphate (TPP)




•Required for carbohydrate and branched chain amino acid metabolism


•Decarboxylation reactions --removal of carbon dioxide


•Glucose--> Pyruvate -->Acetyle-CoA


•Kreb’s cycle or Citric acid cycle (CAC)


•Alpha-ketoglutarate-->succinyl-CoA •Additional B-vitamins needed for these reactions




•Pentose phosphate pathway


• Coenzyme for transketolase


•Converts the 6-carbon glucose (DNA) to 5- carbon pentose (RNA)

Thiamin Deficiency
Impairs nervous, muscle, gastrointestinal and cardiovascular systems. Peripheral neuropathy and weakness, muscle pain and tenderness, enlargement of the heart, difficulty breathing, edema, anorexia and weight loss, poor memory and confusion.



Dry is related to nervous and muscular systems where wet has an additional symptom of the neurological and cardiovascular system where the heart may enlarge leading to congestive heart failure.




Wernicke-Korsakoff (pronounced vair-ni-kuh-kawr-suh-kawf) is cerebral beriberi mainly found in heavy drinkers of alcohol




-3 problems---alcohol decreases thiamin absorption, increase thiamin excretion




-Symptoms include changes in vision (double vision, crossed eyes, rapid eye movement), ataxia –inability to coordinate muscle activity during voluntary movements;Incoordination---imparied mential functions..symptoms improve with hihg doses of thiamin (especially those of the eye)

Types of Thiamin Deficiency

•Beriberi


•Impairs




•Symptoms


- Peripheral neuropathy


•Twotypes—wet and dry


•Wet-nervousand muscular


•Dry-wet symptoms plus neurological and cardio


•Congestiveheart failure •Wernicke-KorsakoffSyndrome


•Alcohol


1)decrease absorption


2)increases excretion


3)poor diet

RiboFlavin (B2)
¼of riboflavin comes from milk products. Rest inenriched grains as well as eggs and meat (liver).



Excess intake is excreted in theurine. If you take in excessive amounts of riboflavin—urine will be brightyellow and glow under a black light. But since limited absorption and rapidexcretion no UL.




HCL releases riboflavin from boundform. 60 to 65 % of the free riboflavin is absorbed via active transport orfacilitated diffusion in the SI. Just like thiamin little is stored in theliver, kidneys and heart.




Transported by protein carries in the blood.




Can be broken down by lighttherefore if in milk should be stored in opaque containers.

Riboflavin Needs

•Needs and Upper Level


•RDA:


1.3mg men,


1.1mg women




•DV: 1.7mg


•Average North American intake is 2.0-2.7mg/day




•No UL

Riboflavin Functions

Riboflavin plays a key role in energy metabolism. These coenzymes have oxidative and reductive functions. FAD is the oxidized form and when reduced to FADH2 it gains 2 electrons and 2 hydrogen's.




Other b-vitamin functions


1) formation of niacin from Tryptophan requires FAD




2) Active Vitamin b-6 coenzyme (pyridoxal phosphate) requires FMN




3) FAD is required for synthesis of the folate metabolite 5-methyl-tetrahydrofolate---indirectly participates in homocysteine metabolism Antioxidant function---remember antioxidant compound glutathione depends on FAD-containing enzymne glutahtione reductase

Riboflavin Functions

•Functions


•Coenzymes: flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD)




•Energy metabolism


•Kreb’s cycle (Citric acid cycle-CAC) •Succinate-->Fumerate


•Beta-oxidation


•Fatty acid to acetyl-CoA—the enzyme fatty acyldehydrogenase


•FMN shuttles H atoms to the electron transport system




•Other B vitamin functions


•Antioxidant function (glutathione synthesis)

Riboflavin deficiency

•Deficiency


•Ariboflavinosis


•Mouth


•Skin


•RBC


•Symptoms


•Inflammation


•Throat


•Mouth


•tongue




Deficiencies—primarily affect the mouth, skin and red blood cells




Symptoms include inflammation of the throat, mouth (stomatitis), tongue (glossitis) and cracking of the tissue around the corns of the mouth (angular cheilitis) and moist, red, scaly skin (seborrheic dermatitis)




Anemia, fatigue, confusions and headaches may also occur----since along the pathway of other B-vitamins may result from other deficiencies.

Niacin (B3)
•Two forms

•Nicotinicacid (niacin)


•Nicotinamide




•Foods


•Heatstable


•Availableas niacin or synthesized from tryptophan


•60mgtryptophan =1mg niacin


•1g of protein = 10mg tryptophan





•120grams of protein x 10 mg tryptophan / gram of protein = 1200 mg tryptophan


•1200mgtryptophan x (1 mg niacin/60mg tryptophan) = 20 mg niacin






Both forms are used to synthesize the niacin coenzymes nictotinacmide adenin dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP)




Available in foods as niacin or synthesized from tryptophan--such as in Poultry, meat and fish—about 25% from these sources---Also comes from enriched breads




Unlike other water-soluble vitamins---niacin is very heat stable and very little is lost in cooking. If niacin is synthesized from tryptophan




1) need 60mg of tryptophan to make 1 mg of niacin---protein is about 1% tryptophan therefore 1 gram of protein 10 mg of tryptophan




2) need riboflavin and vitamin B-6 Individuals with adequate protein intake meet the needs of niacin through tryptophan.

Niacin Needs

•Needs and Upper Level


•RDA: 16mg men, 14mg women


•RDA expressed as niacin equivalents




•DV: 20mg


•U.S. intake exceeds RDA


•UL: 35 mg


applies only to supplements and fortification

Absorption, transportation, and excretion of Niacin
Niacinequivalents to account for performed niacin in foods and niacin synthesized from tryptophan. Niacin is usuallyunderestimated due to not knowing how much tryptophan is in all foods….whichsupplies half the niacin equivalents in the diet.



Absorption is in the stomach and SIthrough active transport and passive diffusion—almost all of niacin is consumed




Transported via the portal vein tothe liver, stored and delivered to the body’s cells.

Niacin Functions

•Functions


•Coenzymes: NAD+ and NADPH


•Oxidation-reduction reactions


•Required in at least 200 reactions especially ATP production


•NAD+ is required for catabolism of carbohydrate, fat and protein






Just like riboflavin—niacin is an active participants in oxidation-reduction reactions. NAD acts as an electron and hydrogen acceptor in glycolysis and Citric acid cycle.




NAD is regenerated under both aerobic and anaerobic conditions.




NAD is regenerated when pyruvate is converted to lactate. In aerobic conditions NADH + H+ donates electrons and hydrogen to acceptor molecules in the electron transport chain---making ATP

Niacin Deficiency

•Deficiency


•Pellagra


•3 D’s


•Dermatitis, Diarrhea, Dementia


•4th D if not treated = Death •Pharmacological use


•Nicotinic Acid: lowers Triglycerides, increases HDL-C






Because many metabolic pathways use NAD+ or NADPH + H+ a deficiency in niacin can cause wide spread damage to the body. Pellagra—causes a rash on the skin as well as around the neck




Niacin is also prescribed by physicians to increase HDL and lower triglycerides. When combined with other factors like diet, exercise and other cholesterol-lowering meds, nicotinc acid may reduce the risk of heart attack but still under going testing. In order to get this reaction need 1 to 2 grams daily (60 times the RDA)

Pantothenic Acid
Pantothenic acid in many food----Meat, milk and many vegetables because part of coenzyme A (CoA)



Unprocessed foods better sources of pantothenic acids than processed foods because milling, refining, freezing, heating, and canning can reduce pantothenic acid in foods.




Absorption—released during digestion in SI.




Transported throughout the body to red blood cells.




Storage minimal and excretion through urine

Pantothenic Acid Needs
Needs and Upper Level



•AI: 5mg




•DV: 10mg




•No UL—no known toxicity

Pantothenic Acid Functions

•Functions


•Coenzyme A (acetyl-CoA)


•Kreb’s cycle


•acyl carrier protein


•Increase chain length




Pantothenicacid is required for the formation of coenzymeA—which is a part of acetyl-CoA—remember the breakdown of carbs, proteins,alcohol and fat. Needed to enter Kreb’s cycle




Also forms part of compound callacyl carrier protein---attaches to fatty acids and shuttles them through themetabolic pathway designed to increase their chain length.

Pantothenic Acid Deficiencies
Deficiency—is very rare and only observed when deficiency was experimentally induced---symptoms include headache, fatigue, impaired muscle coordination, and GI tract disturbances.
Biotin
Biotin is widely distributed in foods free and as biocytin (biotin bound to lysine in proteins) Whole grains, eggs, nuts and legumes



We excrete more biotin than we consume—therefore it appears that bacteria in the Large intestine which synthesizes biotin.




Absorption—the enzyme biotinidase release biotin from protein and lysine and absorbed in the small intestine.




Stored in small amounts in the muscles, liver and brain Excreted mostly in the urine some in bile.

Biotin Nees

•Needs and Upper Level




•AI: 30 micrograms




•DV: 300 micrograms




•No UL

Biotin Functions

•Functions


•Coenzyme in carboxylase reactions (adds CO2) •Pyruvate --> oxaloacetate


•Breakdown of some AA to use as energy •Carboxylation of acetyl-CoA to form malonyl-CoA so fatty acids can be synthesized






When glucose low—oxaloacetate is the starting point for gluconeogenesis AA---threonine, leucine, methionine, and isoleucine Also thought to help with DNA folding leading to gene stability.





Biotin Deficiency




•Deficiency


•Genetic


•Biotinase enzyme deficiency


•Consumption


•Anticonvulsant meds


•Malabsorption


•Excessive consumption of raw eggs (avidin)



Deficiency very rare---but genetic defect has low amounts of the biotinidase. Happens within months of birth symptoms including skin rash, hair loss, convulsions, low muscle tone and impaired growth)—treated by regular dose of biotin supplements. Deficiencies from anticonvulsant meds, malabsorption in those with severe intestinal diseases, and the regular ingestion of raw eggs (more than a dozen) daily. Raw eggs contain a protein (avidin) that binds biotin liming absorption. Cooking eggs denatures the protin avidin
Vitamin B-6 (pyridoxine)

•Threecompounds—


•Pyridoxal,pyridoxine, and pyridoxamine




All3 forms need to be phosphorlated to become active B-6




B-6is stored in the muscle tissue of animals---Meat,fish, poultry, fortified cereals, potatoes---whole grains are a good source butlost during refining grains and not added during enrichment most F/Vpoor sources except potatoes and bananas carrots are a few exceptions.

Vitamin B-6 Needs

•RDA:1.3mg women, 1.7mg men



•DV:2mg




•UL:100mg•Irreversiblenerve damage




2 to 6 grams a day can for 2+months can cause irreversible nerve damage---start with numbing in hands andfeet

Absorption of Vitamin B-6

Absorption by passive diffusion


---Transported via the portal vein tothe liver where it is phosphorylated. Phosphorylated forms transported in the blood bound to albumin.B-6 is stored in muscles but excessis excreted in the urine.

Vitamin B-6 Functions

•Functions


•Inmetabolism


•PLPcoenzyme involved in amino acid metabolism


•Glycogenolysis


•Synthesisof compounds


•Heme,


•neurotransmitters,


•B-vitamin(niacin from tryptophan)•Inimmune function and gene expression








Thesynthesis of nonessential amino acids. Without PLPevery AA would be essentialPLP is also needed for the releaseof glucose from glycogen. In this way, PLP helps maintain blood glucoseconcentration.




RBC—PLP catalzyes a stp in the synthesis of heme, tohold iron in place




PLP is required for the synthesisof several neurotransmitters: serotonin from tryptophan, dopamine andnorepinephrine from tyrosine, and gamma aminobutyric acid (GABA) from glutamicacid.




Niacin from tryptophan

Vitamin B-6 Deficiency

•Deficiency


•Rarein North America


•Symptoms


•Seborrheicdermatitis


•Microcytichypochromic anemia---decreased hemoglobin systhesis


•Convulsions


•Depression


•confusion




Deficiency---rare but some meds maycause deficiencies




—When deficiency dose occursymptoms include dermatitis and microcytic hypochromic anemia which decreaseshemoglobin synthesis




Certain meds (L-DOPA for Parkinson;isoniazid for tuberculosis; theophylline for asthma) can decrease PLP in theblood and therefore may need to have supplementation

Folate
Folate(generic name) vs. Folic Acid (synthetic form)



Namederived from Latin word folium meaning “leaf”. Folate is the generic name givenbecause of leafy green vegetables being excellent sources.




Sources = Legumes,leafy green vegetables, avocados, and oranges (green vegetables)




Foods fortified with folic acid orsupplements are refereed to as folicacid.

Folate Needs



•RDAand DV: 400 micrograms


•UL:1 mg


•Maymask B-12 deficiency


•Concernis with synthetic sources

Folate Functions
•Synthesisand maintenance of new cells •Exchangeof single carbon groups

•Formedfrom central coenzyme form: tetrahydrofolicacid (THFA)


•DNAsynthesis


•uracil→thymine—needTHFA


•B-12is needed to recycle folate


•Aminoacid metabolism


•Homocystine tomethionine•Neurotransmittersynthesis


•Possibleprevention of depression

Folate Deficiency
•Although fortified deficiency occurs

•Low intake, malabsorption, increased requirements, use of certain meds


•Since need Folate to make DNA if deficient DNA cannot divide normally to become a mature RBC therefore cells continue to become larger and retain nuclei.


•Usually don’t leave bone marrow but if do called macrocytes.


•Result in a form of anemia •Megaloblastic (macrocytic) anemia




•NeuralTube Defects


•Maternaldeficiency of folate plus genetic predisposition


•Allwomen capable of getting pregnant urged to take in 400 micrograms of folic acid •Currentfortification yields about 200 micrograms of folic acid daily


Vitamin B-12 (cobalamin)

•Unique


•Animalproducts only


•Containsa mineral (cobolt)






B-12 Needs
Needsand Upper Level

•RDA:2.4 micrograms


•DV:6 micrograms


•Averageintake is 2-3 times RDA


•NoUL





Absorption,transport, storage, and excretion of B-12

•Freevitamin binds to R-protein


•Releasedby pancreatic lipases


•Freevitamin then binds with intrinsic factor




In food B-12 is bound to protein. Therefore HCl and pepsin release B-12 from these proteins. The free B-12 binds to R-protein in the stomach. In the SI, pancreatic lipases release B-12 from the R-protein. The B-12 then binds with intrinsic factor (a proteinlike compound produced by the parietal cells in the stomach) that enhances B-12 absorption. The B-12 intrinsic factor complex travels to the ileum where it is absorbed and transported to the liver.




Unlike other water soluble vitamins—can be stored in the liver and “recycled” for years

Vitamin B-12 Functions

•Functions


•Cofactorin 2 enzymatic reactions


•Formationof methionine from homocysteine


•Enzymemethylmalonylmutase needed for fatty acid metabolism

Vitamin B-12 Deficiency

•Deficiency


•PerniciousAnemia


•Inadequateproduction of intrinsic factor•MacrocyticAnemia


•Littleor no stores of B-12


•Identicalto folate deficiency due to interrelationship




•Neurologicalchanges


•Producednerve degeneration




•Elevatedplasma Homocysteine concentrations •Leadto CVD


•Cognitivedysfunction and osteoporotic fractures

Person at Risk for Vitamin B-12 Deficiency

•OlderAmericans (20%)


•Atrophicgastritis


•Noanemia but neurological problems & ↑ Homocysteine




•Malabsorption


Treatment


•Monthlyinjections


•Nasalgel


•Veryhigh oral doses (1-2mg)


•Passivediffusion




•Vegans

Vitamin C (Ascorbic Acid)

•Foods


•Citrusfruits, peppers, and green vegetables




•Needsand Upper Level


•RDA:90 mg men, 75 mg women


•Smokersneed an additional 35 mg/day •DV:60 mg


•UL:2 g




•Absorption—SIby active transport for ascorbic acid & facilitated diffusion for dehydroascorbicacid


•Decreasesas intake increases


•70to 90% absorbed

Vitamin C Functions

•Functions


•Reduction-oxidationreactions (electron donor)


•Cofactorfor metalloenzymes




•Collagensynthesis


•Connectivetissue such as tendons and ligaments


•Neededin wound healing too




•Synthesisof other vital compounds


•AA,neurotransmitters, hormone thyroxine




•Antioxidantactivity


•Ironabsorption-moderately faciliate


•Immunefunction—high levels of Vit Cin WBC

Vitamin C Deficiency

•Deficiency


•Changesin connective tissue—first signs scurvy •Signsof connective tissue failure


•Researchto prevent Cancer and heart disease •Notconclusive


•Mayhelp




•Excess


•100mgor more daily


•Excreted


•1000mgdaily


•Doesnot prevent or treat the common cold


•Mayreduce symptoms modestly maybe 1 day