Vitamins and Minerals Exam 1

clinical assessment

i. A clinical assessment is based on medical history as well as signs (something that can be seen or detected by someone else) and symptoms (something the patient relays). This kind of assessment is low cost and non-invasive but can only detect advanced stages of deficiency or toxicity which is when signs and symptoms usually present themselves.

dietary assessment

A dietary assessment is based on diet and food habits and nutrient content of foods. A dietary assessment can be conducted using 3 methods: dietary records, 24h recalls, and food frequency questionnaires (FFQ). This kind of assessment is also simple and non-invasive and can identify early risk for deficiency or toxicity but that is dependent on accurate self-reporting

1. Which groups of food (from MyPlate) have the highest content of thiamin, riboflavin, and niacin per serving? Which two groups are good sources in all three vitamins? Can you choose one for vegetarians and one for non-vegetarians?

The highest sources of Thiamin are proteins (pork, beef, and fish) and grains (fortified grains and whole grains) on My-plate. The highest sources of Riboflavin are dairy (milk), grains (enriched bread and cereals), meat (beef, and liver), and almonds. The highest sources of niacin per serving come from beef (especially liver), chicken, turkey, tuna, salmon, peanuts, whole grains, and enriched grain products. Meat protein (beef) and enriched grains are good sources of all 3 vitamins. Non-vegetarians would be able to consume all three vitamins from meat sources and vegetarians from whole or enriched grains

1. What foods have high content of iodine? Does sea salt have iodine? What are goitrogens? In which foods are they found?

Foods that exist in seawater have highest amount of iodine. Seafood like shrimp, crab, fish and seaweed like kelp and nori. Sea salt has low amounts of iodine, table salt is iodized and has enough to meet iodine requirements. Goitrogens are compounds that exist in certain foods that interfere with production of thyroid hormones, by decreasing the level of iodine uptake. They are mostly found in cruciferous vegetables such as broccoli and cauliflower as well as in cassava

1. If a client/patient asks you, what vitamin supplement would you recommend: which one/s would you suggest? What general recommendations would you follow? What information would you need to make a recommendation?

I would not suggest a vitamin supplement to them without determining if there was a need for a vitamin supplement. I would do this by conducting a dietary assessment (like a food diary), and a clinical assessment based on any signs/symptoms that may be present or complaints made by the client. If the client is okay with having a blood test done, I would also do a biochemical test to determine if there is any deficiency. I would also have to take into consideration age, life status, and if they have any diseases that would make absorbing certain nutrients difficult

1. What alteration is caused by iodine deficiency during fetal development? This alteration is due to impairment of what function? What public health measure is used to prevent iodine deficiency?

Iodine deficiency during fetal development (because of maternal iodine deficiency) can result in cretinism. Cretinism can result in impaired development of the central nervous system which can lead to severe developmental delays, hearing loss, and movement disorders. It is an irreversible condition and is the most common cause of preventable brain damage in the world

For micronutrients and macronutrients: contrast the following characteristics: organisms capable of synthesizing them, amounts needed, type of chemical structure, and what they are used for in cell?

Macronutrients include carbohydrates, lipids, and proteins, and most (excluding some essential amino acids and essential fatty acids) can be synthesized by animals. Macronutrients are organic compounds that are needed in large amounts for both structural and energy functions. In contrast micronutrients are nutrients that are needed in small amounts, and most cannot be synthesized (aside for a few like niacin and vitamin D). Micronutrients are required to maintain optimal health, and some can participate in regulatory functions as coenzymes, like in the synthesis of ATP. There are two types of micronutrients - vitamins and minerals, vitamins are organic, and minerals are inorganic.

1. For vitamins and minerals: what characteristics do they share? In which aspects are they different?

Vitamins and minerals are similar in that they are both needed in small amounts, cannot be synthesized, are required for normal biochemical and physiological functions to sustain life and health, have regulatory functions, and are nutrients/food components. Vitamins differ from minerals because vitamins are organic while minerals are inorganic, and the regulatory functions of vitamins and minerals differ. Vitamins cannot be catabolized to generate ATP or be used to form structures, while minerals have structural functions and catalytic functions

1. B6 is necessary for the catalysis of chemical reactions that involve what two main types of substrates (which correspond to two different macronutrients)? Does B6 work the same way for those two types of substrates? For the better studied substrate: In which type of reactions is B6 a coenzyme?

a. B6 is necessary for the catalysis of chemical reactions that involve amino acids (that correspond to proteins) and glycogen (which corresponds to carbohydrates). B6 does not work the same way for both of these substrates. In glycogenolysis reactions the phosphate group of PLP facilitates the catalysis of the reaction between glycogen and phosphate ultimately forming glycogen and glucose-1-P. In reactions with amino acids, the aldehyde group of PLP is the facilitator of transamination, decarboxylation, and side chain removal reactions because it can bind to the amino group of an amino acid forming a Schiff base making the bonds around the alpha-carbon of the amino acid more susceptible to cleavage.

1. If more than 30% of the US population has an insufficient intake of vitamin C, why is scurvy not more common?

a. Because deficiency is likely noted before reaching the point where signs and symptoms can begin to present, therefore deficiency doesn't actually advance to scurvy

1. Name one nutrient for which intake below the RDA (or AI) is common AND which is associated with diseases of relatively high prevalence

a. Calcium intake is commonly below the recommendations for intake, and is associated with osteoporosis

1. What are DRIs? What are the four classical DRIs? Describe each one of them

a. DRIs are dietary reference intakes which are a common set of reference values that are grounded in relationships between nutrient intakes and indicators of adequacy, as well as the prevention of chronic diseases in apparently healthy populations. The four classical DRI's are RDA, AI, UL, and EAR. The RDA is the Recommended Dietary Allowance which is the average daily nutrient intake level that is sufficient to meet the nutrient requirements of about 98% of healthy individuals in a particular life stage and gender group. The AI is the adequate intake level which is the recommended average daily intake level when there is not enough information to establish and EAR or RDA. The UL is the tolerable upper limit which is the highest daily intake level that should not be exceeded to avoid toxicity. The EAR is the estimated average requirement which is the average daily intake level that is sufficient to meet the needs of about half of the healthy individuals in a particular life stage and gender group.

1. Which group of food is a good source of thiamin, riboflavin, and niacin in the US diet? Historically, has it always been the case? Why?

a. Enriched grains are a good source of thiamin, riboflavin, and niacin. This wasn't always the case because grains were not always enriched. The US began to enrich grains to prevent vitamin deficiencies.

1. If a colleague asks you about enzyme activation assays to evaluate the nutritional status of a vitamin (for example B6): How would you describe the general principle of the assay?

a. Enzyme activation assay measures activity of an enzyme for which micronutrient is a coenzyme with and without addition of the vitamin. If addition of the vitamin increases enzyme activity, then deficiency has been detected

1. What types of nutritional assessments can be used to assess the nutritional status of a micronutrient in individuals/patients? (Name main types)

a. There are 3 kinds of nutritional assessments that can be used to assess the nutritional status of a micronutrient: biochemical, clinical, and dietary.

1. Enzyme activation tests: What kind of laboratory test is this? Can you use an enzyme activation test to evaluate the nutritional status for vitamin B6 or K? How do these tests work in general? How does it work in this particular case?

a. Enzyme activation tests are functional tests that look at the activity of an enzyme for which a micronutrient is necessary. If activity of the enzyme increases after administration of the micronutrient, then that is indicative of a deficiency of that micronutrient. Enzyme activation test can be used to evaluate the nutritional status of B6 with the evaluation of alanine transaminase activity or aspartate transaminase activity, both of which require B6 because they require PLP as a coenzyme. Enzyme activation tests can't really be used to test for vitamin K deficiency because the tests for nutritional assessment focus on either the plasma/serum level of phylloquinone, time it takes for blood coagulation, or carboxylation of vitamin k-dependent proteins.

1. Does grain refinement affect the content of thiamin, riboflavin, and/or niacin? What is food fortification? What are enriched grain products?

a. Grain refinement affects the content of thiamin, niacin, and riboflavin, which are lost during refinement. Food fortification is when foods have vitamins or minerals not necessarily lost during refinement added to them to improve the nutritional quality of commonly consumed food and reduce the risk of deficiency in a population (milk being fortified with vitamin D). Enriched grain products are products that have had vitamins and minerals that were lost during the refinement process added back in.

1. What nutritional assessment methods would you use to diagnose a micronutrient deficiency in the clinical stage? Can you diagnose a deficiency before the clinical stage? If yes, what methods would you use?

a. In order to diagnose a nutrient deficiency at the clinical stage one would look at the medical history of the patients, as well as any signs that are physically present that would indicate a deficiency, or by taking note of symptoms the person may be feeling. Biochemical methods could also be used at this stage. A deficiency can be diagnosed prior to the clinical stage, and the best way to do that would be through a dietary assessment. One could have the person recall what they ate within the last 24hrs, have them keep a food journal for a few days, or fill out a food frequency questionnaire, all of which can indicate whether or not they have a deficiency depending on which foods they may or may not be eating. Biochemical methods can also be used to establish deficiency at this stage.

What are micronutrients = what are the main characteristics that define micronutrients?

a. Micronutrients are dietary components that are needed in small amounts and are essential meaning that they are not synthesized or not synthesized in adequate amounts and are necessary to maintain optimal health and to prevent deficiency syndromes. There are two types of micronutrients, vitamins which are organic and minerals which are inorganic. Micronutrients are also nonnutritive but aid in regulatory functions like gene regulation, and as coenzymes in various reactions including those necessary for ATP synthesis.

1. Which vitamin can be synthesized from a macronutrient in human cells? If it can be synthesized, why is it considered a vitamin? Is it essential or not (or "it depends")? How is this property/characteristic called? How this affects the requirements for this vitamin?

a. Niacin can be synthesized by the body from tryptophan, which is an amino acid that can be obtained from the consumption of the macronutrient protein. Niacin is conditionally essential, when consumption of B6 is low which is necessary for the pathway that converts tryptophan into niacin. The ability of niacin to be derived from tryptophan affects intake requirements by affecting how the RDA is calculated. The RDA for niacin includes calculations that account for the estimated niacin that will be made in the body from tryptophan consumption.

1. How can you use the knowledge about absorption and excretion of thiamin to explain why no UL has been established?

a. No UL for thiamin is established because its absorption and excretion mechanisms in our body prevent/reduce the risk of toxicity. Thiamin absorption is mediated by transport proteins, if we take in large amount the transporters will become saturated and the absorption of thiamin will remain constant regardless of if the thiamin concentration increases. And when Thiamin is filtered through the kidney most of it is reabsorbed by the transporters (ThTr1/2) by same mechanism as it was absorbed in intestines but whatever is extra will be excreted in urine i.e., the more we take it, the more it will be excreted and less will be absorbed to prevent toxicity.

1. Nutrient load test: What kind of laboratory test is this? Can you use a load test to evaluate the nutritional status for vitamin B6 or K? How do load tests work? How does it work in this particular case?

a. Nutrient load tests are functional tests which a macronutrient is administered, whose metabolism is dependent on the micronutrient of interest. The metabolites of the macronutrient are then measured (usually in the urine). A nutrient load test could be used to test for vitamin B6 deficiency with tryptophan loading. Vitamin B6 is essential for the metabolism of tryptophan to niacin. If there is excess xanthurenic acid in the urine, that indicates B6 deficiency because it indicates that the pathway to synthesis of Niacin could not be completed. Again, nutrient load tests are not generally used to evaluate the nutritional status of vitamin K, which instead can be measured using a static test, prothrombin time, or measuring the carboxylation of vitamin-K dependent proteins.

1. If a physician asks you how a nutrition load test to the evaluate nutritional status of a vitamin (for example B6) works: How would you explain the general principle of the test?

a. Nutrient load tests are test in which a macronutrient is administered, whose metabolism is dependent on the micronutrient of interest. The metabolites of the macronutrient are then measured (usually in the urine). An example would be the tryptophan load test which tests the nutritional status of vitamin B6, by evaluating the pathway that converts tryptophan to niacin, for which B6 is necessary. If B6 is deficient, then the pathway will not proceed properly.

1. How common are the deficiencies of pantothenic acid and biotin? What are the main symptoms? Why do you think that there is no EAR and RDA for these vitamins?

a. Pantothenic acid and biotin deficiencies are rare because both vitamins are found in a wide variety of foods and deficiencies really only happen when there are absorption issues like with alcohol intake or malnutrition. The main symptoms of pantothenic acid deficiency are burning foot syndrome, restlessness, insomnia, fatigue, cramping, nausea, and vomiting. The symptoms of biotin deficiency include dermatitis, alopecia, brittle nails, and neurological problems like muscle hypotonia and pain, lethargy, and depression. There is probably no EAR and RDA because deficiency is so rare and caused by secondary factors that there is not enough information to determine an EAR or RDA.

1. Pantothenic acid is a precursor for which two molecules? In which way these two molecules have a similar function? For which metabolic pathways are they necessary? In which cells are these metabolic pathways active? How can you relate the function with the food sources?

a. Pantothenic acid is a precursor of Coenzyme A which is important for fatty acid degradation and synthesis (active in adipocytes and liver cells) and for the conversion of carbohydrates to ATP and Acyl Carrier Protein, which is part of the fatty acid synthase complex (also active in adipocytes and liver cells). These two molecules are similar in that pantothenic acid as a component of coenzyme A and ACP facilitates the transfer of acyl groups to other molecules and they are both utilized for fatty acid synthesis. Being that pantothenic acid is utilized in the synthesis of fatty acids, it makes sense that pantothenic acid is found in almost all food sources.

1. What signs and symptoms are characteristic of the disease caused by niacin deficiency? What lab test would you request to confirm a niacin deficiency?

a. Pellagra is characterized by the 4 D's: Dermatitis (scaly, dark skin), Dementia (depression, fatigue, headache, disorientation, Diarrhea (and GI alterations), and Death. The lab test that would be requested to confirm niacin deficiency is the measurement of urinary excretion of metabolites of niacin, most importantly N-methyl nicotinamide. Urinary excretion of ~0.8 mg/day of N9 methyl nicotinamide and of ~0.5 mg of N9 methyl nicotinamide/1 g of creatinine are suggestive of poor (deficient) niacin status.

1. What kind of foods are the best sources of vitamin K? Why? Is breast milk a good source of vitamin K? Does formula have vitamin K? What medical procedure related to vitamin K is recommended for neonates?

a. Phylloquinone is the main source of vitamin K and is found in green leafy vegetables and oils such as soybean oil and olive oil. Menaquinones are found in animal products in small amounts and fermented foods such as yogurt and cheese. Breast milk is low in vitamin K and although formula contains added vitamin K, it is essential that newborns receive a vitamin K shot within 6 hours of birth to prevent vitamin K deficiency bleeding. This is because babies are born with very little vitamin K stored in their bodies and they do not yet have vitamin k synthesizing bacteria.

1. Riboflavin and Niacin are each precursor for which co-enzymes? What metabolic reactions need these co-enzymes, and therefore an adequate intake of B2 and B3? What enzyme/s need/s B1, B2, B3, and B5?

a. Riboflavin is a precursor of FMN and FAD, which are coenzymes for enzymes that catalyze oxidative reactions. FMN and FAD are bound to enzymes called flavoproteins. Flavins accept a pair of hydrogen atoms one at a time and donate them to other acceptors. Niacin is a precursor of NAD+ which plays a role in oxidative (generally catabolic) pathways like glycolysis, PHDC, beta-oxidation, and the citric acid cycle as an electron carrier. Niacin is also a precursor for NADP+, which plays a role in reductive (generally anabolic) pathways like synthesis of fatty acids, synthesis of cholesterol, and synthesis of nucleotides, as an electron carrier. Thiamin (B1) is necessary for pyruvate dehydrogenase, Riboflavin (B2) is necessary for glutathione reductase, Niacin (B3) is necessary for dehydrogenases, and pantothenic acid (B5) is necessary for acyl carrier protein.

Name one micronutrient for which intake in the US is commonly above the recommendations for maximum intake. What highly prevalent disease is associated with it?

a. Sodium intake is commonly above the recommendations for maximum intake and is associated with hypertension.

1. Why for some nutrients an RDA has been established while for others an AI exist? If, for a nutrient, information exists about the AI and RDA: Which one would you use to make a nutritional recommendation?

a. The Adequate Intake (AI) is set instead of an RDA (Recommended Dietary Allowance) when there is not enough research that has been conducted to be able to determine an EAR (Estimated Average Requirement) or RDA and is based on observed or experimentally determine approximations or estimates of nutrient intake by a group of healthy people. If information on both AI and RDA are available, I would use the RDA to make a nutritional recommendation, because it will be a more research-based intake level, and we know it will be enough for 98% of the population.

1. What groups of foods are the best sources of vitamin B6? How can you explain that those foods are good sources based on the functions of vitamin B6? What is the main function of B6 in those organs in humans?

a. The best food sources of vitamin B6 are animal products, particularly beef, liver, chicken, fish, and pork. These foods are good sources because animal (and human) muscle contain 75-80% of all the B6 in the body, primarily as its active form of PLP bound to glycogen phosphorylase. The liver stores about 5-10% of the vitamin. The phosphorylation of vitamin B6 (PLP) prevents its diffusion out of the cell, and because it's protein-bound, this prevents hydrolysis by phosphatases. In humans, the main function of B6, as PLP, is to act as a coenzyme for over 100 enzymes that are mostly involved in the metabolism of amino acids through transamination reactions, decarboxylation reactions, and removal of the amino acid side chain (or cleavage reactions). PLP in the muscle acts as a coenzyme to glycogen phosphorylase in the initial step of glycogenolysis, or the breakdown of glycogen, where the phosphate of PLP is used to catalyze this reaction for glucose production. This reaction also primarily takes place in the liver cells.

1. What disease is caused by deficiency of niacin? How frequent is it? Why? What groups or individuals have an increased risk?

a. The deficiency caused by Niacin is called pellagra, which is not very common in the U.S. due to the ability to synthesize it in the body and enrichment of grain products. The things that can cause a niacin deficiency are malnutrition or poor diet, malabsorption of tryptophan or niacin, alcoholism, or intake of drugs that can reduce the synthesis of niacin from tryptophan.

1. What two thyroid hormones exist? In which aspects do they differ? What are the most important effects of thyroid hormones?

a. The two thyroid hormones that exist are T3 and T4. They differ in the number of iodine molecules that they have, their activity levels, and their abundancy. T3 has 3 iodine molecules and is less abundant but is more active. T4 has 4 iodine molecules and is more abundant but is less active. T4 can be converted to T3 through a reaction that removes an iodine molecule. The most important effects of thyroid hormones are their effects on metabolism and development. Thyroid hormones can increase metabolic rate, cellular oxygen consumption, and body heat. They also are essential for normal development of the nervous system and normal growth and development of bone.

1. Which disease is caused by deficiency of thiamin? What forms of the disease exist? How can you relate each form to some of the functions of thiamin?

a. The disease caused by deficiency of thiamin is Beri Beri. The forms of beri beri that exist are wet beriberi, dry beriberi, wernickes encephalopathy, and acute beriberi. i. Wet beriberi is characterized by heart failure which leads to peripheral and pulmonary edema. This type of beriberi is related to thiamin's function in ATP production as a cofactor for enzymes in the PDH complex, the citric acid cycle, and the electron transport chain. When ATP is low due to thiamin deficiency there is not enough energy to pump the heart, leading to heart failure. ii. Dry beriberi is characterized by peripheral neuropathy which is altered function of both sensory nerves (leading to muscle pain and "burning foot") and motor nerve (leading to muscle weakness). This type of beriberi relates to thiamins function in nerve transmission, which is to regulate sodium channels/permeability, and production of acetyl-coA which is a precursor for acetylcholine (neurotransmitter) and for the production of myelin iii. Wernicke's encephalopathy is more common in alcoholism and affects the central nervous system. It has 3 main symptoms which are abnormal eye movement, balance alterations, and cognitive impairment. This form of beriberi is also related to thiamin's function in the nervous system. iv. Acute beriberi is found in infants that are breastfed by a mother with thiamin deficiency resulting in lactic acidosis due to low activity of the pyruvate dehydrogenase complex. Lactic acidosis results in GI symptoms like nausea, anorexia, and vomiting. This form of beriberi relates to thiamins function as a cofactor in the pyruvate dehydrogenase complex.

1. A student had deep vein thrombosis (DVT) and pulmonary embolism. After that event, she was treated with warfarin to prevent recurrences. She had laboratory analyses to evaluate her coagulation at regular intervals: One day, her physician calls saying that the coagulation test had unexpected results and asked about changes in her diet. Why was the doctor inquiring about her diet? What alterations in the lab results may the physician have found? How would the alterations be related to the diet?

a. The doctor was inquiring about her diet to see if her vitamin K intake may have changed. The lab results could have indicated that the effect of warfarin was not as strong as normal, indicating an increase in vitamin K intake which could be caused by an increase in leafy green vegetables like spinach or kale, or it could have demonstrated that her blood was maybe too thin, indicating decreased consumption of vitamin K containing foods.

1. The enzymes that need thiamin as cofactor: In which metabolic pathways are they? Are those anabolic or catabolic pathways? Do they produce or use ATP?

a. The enzymes that need thiamin as a cofactor are involved in the pyruvate dehydrogenase complex, the citric acid cycle, the pentose phosphate pathway, as well as in the oxidation of alpha-ketoacids. These are catabolic pathways that ultimately produce ATP by either feeding into glycolysis, which in the presence of oxygen will lead to the citric acid cycle, or by feeding directly into the citric acid cycle through the conversion of a molecule like pyruvate or branched chain acyl-CoA to acetyl-coA.

1. What new type of DRI has been defined in the last 5 years? Describe it. For which micronutrient/s has it been used?

a. The new type of DRI is the CDRR, chronic disease risk reduction, which establishes an intake level above or below which can reduce the risk of chronic disease in a healthy population. Currently only set for sodium.

1. How to assess the nutritional status for vitamin K? Is there any functional test? If yes, how does it work?

a. The nutritional status for vitamin K can be measured using a static test, by checking the phylloquinone level in the plasma or serum which reflects recent intake of vitamin K. Nutritional status can also be assessed using two different functional tests. The first measures the time that it takes for blood to coagulate after inducing coagulation by the addition of calcium and tissue factor If coagulation takes longer than 25 seconds then deficiency of Vitamin K is possible but delayed coagulation time could also be the result of other factors and this method is insensitive because plasma prothrombin has to decrease by 50% before prothrombin time is affected. The next functional test would be to measure the percentage of uncarboxylated vitamin K dependent proteins, such as prothrombin or osteocalcin. However this is also unreliable because one protein could be 100% carboxylated while the other only carboxylated by 40%, so a combination of these tests should be used to determine vitamin K deficiency.

1. How is the secretion of thyroid hormones regulated? What is goiter? How does iodine deficiency cause goiter?

a. The secretion of thyroid hormones is regulated by thyroid stimulating hormone, which is secreted when the thyroid hormones become too low. TSH is then subject to negative feedback by T3 and T4, so when sufficient thyroid hormones have been produced they can go back stop the secretion of TSH. In order to make these hormones, iodine is needed. When there is not a sufficient amount of iodine available, goiter can occur. This is a disease in which the thyroid gland becomes enlarged as a result of thyroid deficiency. Increased TSH production stimulates growth of the thyroid gland, which would allow for more efficient iodine uptake and partially compensate for the low amount of thyroid hormones. Goiter is reversible once iodine is administered.

1. What is the name of the syndrome caused by riboflavin deficiency? What are the 3 organs or systems most affected? Which system is affected by deficiency of B2 as well as B3?

a. The syndrome caused by riboflavin deficiency is called ariboflavinosis and it affects the mouth (oral inflammation, pharyngitis, mouth and tongue inflammation, and cheilosis), the skin (seborrheic dermatitis, which is red, painful, scaly skin around the naso-labial fold, eyes, ears, and scrotum), and the nervous system (dysfunction of peripheral nerves). The skin is affected by deficiency of B2 (riboflavin) and B3 (niacin) both resulting in dermatitis.

1. Which are the two most common type of laboratory assays used to assess the nutritional status of this group of vitamins? How can you relate those two types to the physical properties of these vitamins and their functions?

a. The two most common laboratory tests to assess nutritional status in these group of vitamins are urine tests and enzyme activation tests. These can be related with their physical properties because vitamins such as thiamin, riboflavin, pantothenic acid and biotin are excreted as the same rate as the intake; they are all saturable and only a certain amount can be absorbed by the body, therefore can be excreted in the urine. This is different with niacin because unlike the other vitamins, niacin is not saturable, so it is able to absorb as much as it can take.

1. How common is thiamin deficiency in the US? Why? What population groups have higher risk? Why?

a. Thiamin deficiency is rare in the US because intake is generally adequate due to the enrichment of grain products, where thiamin is restored after grain refinement. However, population groups that have a higher risk of deficiency are the elderly and malnourished people due to inadequate intake, and people who have malabsorption issues due to inflammatory diseases, certain cancers, liver disease, surgery, the use of diuretics, and/or alcoholism. Alcoholism is the most common risk factor for a thiamin deficiency in the US due to the increased likelihood of a poor diet, inadequate intake, decreased absorption because of the inhibition of thiamin transporters, and decreased activation of TDP or TDP formation.

1. What are vitamers? What are pro-vitamins? Give examples

a. Vitamers are related chemical compounds that accomplish required biochemical functions and prevent deficiency syndrome. An example of a vitamer is Retinals, retinoids, and retinoic acid which are vitamers of Vitamin A. Pro-vitamins are compounds that can metabolized to vitamins like beta-carotenes being metabolized to pro-vitamin A.

1. What are vitamers? What is the most stable form of vitamin B6? Which B6 vitamers are the active forms as coenzymes?

a. Vitamers are related chemical compounds that accomplish required biochemical functions and prevent deficiency syndrome. The most stable form of vitamin B6 is pyridoxine and the vitamers that act as coenzymes are pyridoxyl phosphate and pyridoxamine phosphate.

Deficiency of B6 affects mainly which 3 systems/organs? What are the signs and symptoms in each? How common is the deficiency?

a. Vitamin B6 deficiency is rare in the US, its deficiency mainly affects skin and mucosa, nervous system, and Blood. The sign and symptoms are: i. Skin and Mucosa: Seborrheic dermatitis, cheilosis (angular chelitis, glossitis) ii. Nervous system: Depression, confusion, peripheral neuropathy, Weakness, fatigue, seizure iii. Blood: Anemia (hypochromic, microcytic)

1. How is B6 absorbed? What percentage of vitamin B6 from the diet is absorbed, in average? How does the mechanism of absorption of B6 relate to the efficiency of absorption?

a. Vitamin B6 is absorbed through passive diffusion, which cannot allow the phosphorylated vitamers to pass through the membrane, due to having a negative charge. They are dephosphorylated and absorbed, they will exit the enterocytes and enter the blood circulation as their non-phosphorylated forms. Most B6 is taken up by the liver where PN, PM, and PL will be phosphorylated and then PN and PM will be converted to PLP. PLP binds to proteins for storage, which has 5-10% of the body's B6. B6 will also leave the liver in the form of PL and enter muscle cells where it will be converted back to PLP and bound to glycogen phosphorylase. 5-10% of PLP is located in the liver and 75-80% in the muscle. The mechanism of absorption would make B6 absorption more efficient because there is no potential for saturation of transporters.

1. Why is vitamin K called vitamin K? What are the main functions of vitamin K? How do its functions relate to signs and symptoms of deficiency?

a. Vitamin K is named after the Danish word Koagulation, which means coagulation. Its main functions are to promote bloodclotting and coagulation as well as assist with bone remodeling to transform calcium into hydroxyapetite. SIgns and symptoms of deficiency include easy bruising, internal bleeding, and (when severe) hemorrhaging. Can also be at higher risk of bone fractures.

1. How do vitamin K antagonists work? How are cows related to the discovery of an antagonist of vitamin K?

a. Warfarin a.k.a coumadin is blood thinner drug, is a competitive antagonist of vitamin K. The drug prevents the carboxylation of coagulation factors by interfering with the recycling of vitamin K. In the 1930's farmers were dealing with bleeding issues of their cows. One of the farmers delivered cow's blood to Karl Paul Link's laboratory to be examined. The scientist discovered the substance in the hay called coumarin, that turned into blood thinner when interfered with fungus that was spoiling the hay. When experimenting multiple versions of this reaction, number 42 was the most potent. Which then became rat poisoning. After exploring, scientist wanted to experiment this blood thinner with human patients that had blood clotting that was causing heart attack and stroke. The experiment was successful, which now is prescribed drug warfarin

1. For water soluble and fat-soluble vitamins, how do the physical property of solubility relate to: how they are absorbed? How they circulate in the blood? How are they excreted?

a. Water soluble vitamins are absorbed into enterocytes via protein mediated facilitated diffusion because they cannot freely pass through the hydrophobic environment of the cell membrane. Because they require a protein transporter, once the proteins become saturated absorption is limited, which reduces the risk of toxicity. Because they are water soluble, they are able to circulate in the blood free or bound to transport proteins. Water soluble vitamins are not generally stored (except for folate and b12) and are lost or excreted in the urine when absorption capacity is reached. Fat soluble vitamins are able to be absorbed through simple diffusion through the membrane. Fat-soluble vitamins circulate in the lymph and then the blood and they are encased in lipoproteins or are carried around on transport proteins. Fat-soluble vitamins are stored in the liver, adipose tissue, and cell membranes. They can be metabolized to more polar metabolites and then excreted in bile and feces or urine. Toxicity is more common with fat soluble vitamins because when there is an excess of water-soluble vitamins they can be lost in the urine where fat soluble vitamins must be metabolized first.

1. Does B6 need to be digested? Which vitamers? Why?

a. Yes, vitamin B6 does need to be digested. PLP, PMP, and PNP need to be dephosphorylated to PL, PM, and PN because phosphate has a negative charge that would make absorption difficult, which are absorbed into cells by passive diffusion.

biochemical assessment

i. uses two types of tests: static and functional. A static test measures the concentration of micronutrients present in the blood, blood cells, tissues, and urine which can give an idea of the persons recent intake of the nutrient. A functional test measures the metabolism of a nutrient or the activity of an enzyme for which a nutrient is necessary. Some kinds of functional tests include nutrient load tests in which a macronutrient is administered, whose metabolism is dependent on the micronutrient of interest. The metabolites of the macronutrient are then measured (usually in the urine), and enzyme activation assay (measures activity of an enzyme for which a micronutrient is a coenzyme with and without addition of the vitamin. If addition of the vitamin increases enzyme activity, then deficiency has been detected.)