Water Soluble vitamins- Part 1

0:04 [music] Welcome to the week seven uh on uh the water-soluble vitamins. So we will be discussing about the watersoluble vitamins for the session. At the end of the session, the students will be able to uh understand the definition functions mechanism dietary requirements, ICMR, RDA, bioavailability, toxicity, food sources and stability of uh B1, B2, B3 and its critical role in uh carbohydrate metabolism, uh the energy

0:50 metabolism and the uh oxidation reduction reactions as well as neurological function, cellular respiration, ation and their NAD and NADP co-enzyme functions also. So coming to the water soluble vitamins uh these water-soluble vitamins are basically required in very small amounts and they must be supplied in everyday's diet. B complex we call it as the entire uh mechanism is like the range of vitamins include thamine which is B1, riboflavin which is B2, nasin B3, B6 is podoxin and folic acid uh biotin, cyanocobalamin which is the B12 and also vitamin C. So these all comprise the B complex and

1:35 vitamin C are considered to be the water soluble vitamins. So we are going to start with the first waters soluble vitamin which is the vitamin B1 the thamin. Thamin is a water-soluble vitamin that functions as an essential co-enzyme in the carbohydrate and energy metabolism. It is the first B vitamin to be discovered and it plays a very crucial role in nerve conduction and brain function. So if you see the uh chemical nature their forms and the activation process if you see uh the chemical nature is nothing but it has a pyramidan ring linked to a thosol ring by methyline bridge and it contains sulfur which is a theo and nitrogen active co-enzyme form

2:24 thamine thyroofphosphate which is TPP thamine pyroofhosphate also called as thamine diphosphate which is the TDP P and activation includes uh the thamine has to be converted to TPP which is a thamin pyroofhosphate by thamin phyrophosphocinise enzyme using the ATP which is the uh adinine trieptide or triphosphate and this is how the chemical nature and the activity and the activation takes place. The deficiency diseases include berry berry which is the wet berry berry uh which involves the cardiac uh process and dry berry berry which includes the neurological symptoms and there is something called warnicki

3:10 scarsov syndrome which is uh mostly commonly seen in alcoholics. So moving on to the functions of v vitamin B1. Uh B1 as a part of TPP is involved in various cycles of our uh carbohydrate metabolism, crep cycle and all that. The first role is as an energy metabolism. TPP which is a thamin pyroof phosphate is essential co-enzyme for oxidative decarboxilation which converts the pyroate to acetyl coa which this acetyl coa will then enter into the crep cycle. [snorts] Similarly in the crep cycle if you see uh as a TPP co-actor thin pyroofphosphate is acting as a co-actor for alpha ketoglutrate

3:55 dehydrogenase which would be converting the alpha ketoglutrate into saxinal coa. So if you see it starts from the oxidative decaroxilation and entering into the crep cycle as acetyl coa and also here in the crep cycle again it forms a saxinal coa by being a co-actor in the carbohydrate metabolism we could see that it enables the complete oxidation of glucose for ATP production without B1 pyrovate where it accumulates as lactic acidosis. So what happens is uh when there is a complete oxidation of glucose for ATP production uh this particular uh B1 will help in the uh

4:43 pyroate formation. If there is no pyroate the pyroate will get accumulated B1 is involved in that. So the there is a B1 deficiency this pyroate will accumulate and forms lactic acidosis. That's the major mechanism over there. And if you see uh the pentos phosphate pathway, TPP which is a thamin pyrophosphate plays a co major co-actor for trans keto enzyme and is essential for nucleic acid synthesis and NADPH production. nerve conduction if we see it maintains the myelin sheath integrity essential for sodium ion transport across neuronal membranes and also forming a major role in cardiac function where it is essential for heart muscle

5:30 energy production. The deficiency causes cardiac enlargement and heart failure which is nothing but the wet berry. As we can see in the amino acid metab apart from the carbohydrate metabolism crep cycle and all that even TPP is majorly involved in the amino acid metabolism as a co-actor for branch chain alpha keto acid dehydrogenase which is involved in the metabolism of lucin isolucin and valin. So when I talk about the uh mechanism of B1 the core mechanism involves here which is a thamin pyrophosphate which is the co-enzyme in most of the cases. So when we consume the dietary thamine it

6:16 is absorbed in the small intestine and here thamine pyrophosphocinise is being uh released along with ATP and this becomes the TPP as an active form which is thamine pyrophosphate. So when it comes to the different metabolisms, pyroate dehydrogenous complex we are going to talk about the pyroate which is getting converted to acetyl coa plus carbon dioxide and this acetyl coa enters into the crep cycle. Similarly in the crep cycle alpha ketoglutarate dehydrogenase forms alpha ketoglutarate and that gets converted to saxinal coa plus carbon dioxide. This again happens inside the crep cycle. trans keto pentos

7:04 phosphate pathway which is the NADPH plus nucleotide synthesis. This also we need B1 as a co-actor. When it comes to the RDA or ICMR recommendation which is nothing but uh from infant to uh elderly age group is being given and for every,000 kiloalorie diet there will be an increase in the uh B1 recommendation. So for infants it is 02 and uh for infants 7 to 12 months it is.3 and it keeps increasing as they grow and for adult men it is 1.2 mg per day and for adult women it is 1 mg per day uh and for pregnancy there is a.5

7:50 increase and so it becomes 1.5 mg per day and lactation it remains the same and for elderly who greater than 60 years it is 1.2 mg per day. So when we talk about the bioavailability the absorption rate includes about 80 to 95%age of absorption will be happening when your body is having a deficiency. So at a low intake the absorption is more and uh it decreases when you're consuming too much of the uh dosages which is a high dosages and the site of absorption is usually the small intestine where it happens through the active transport at low doses and passive diffusion at high doses. So the absorption also varies

8:36 according to the low or high dosages. Phosphorulation happens as it is absorbed as a free thamine phosphorolated to thyin pyroofhosphate in intestinal mucosa and liver and we don't require any dietary fat uh unlike fat soluble vitamins whereas fat water soluble vitamins don't require any fat for its absorption whereas water soluble fats soluble vitamins will be requiring fat for its absorption sim uh it is unlike to the water soluble vitamins. [snorts] So there are lot of enhancing factors for the absorption. If you see protein intake should be adequate and there should be an acidic pH where stomach

9:22 acid releases acids from the food [snorts] and uh these are some of the enhancing factors. Reducing factors include thaminise enzyme in the raw fish uh shellfish and ferns. These things will destroy the thamin. Similarly, tannins in tea and coffee, anti-histamin factors in beetlenuts, all that anti-thamin factors in beetlenuts will all reduce the thamine absorption in the body. Similarly alcoholism alcohol it severely impairs the absorption and increase the urinary excretion. So the that becomes the major cause of deficiency uh of B1 among alcoholics. When we talk about cooking losses 20 to

10:09 40%age of losses happens in the boiling water when it lost in the boiling water and it's destroyed by alkaline cooking like adding baking soda to it. [snorts] Toxicity of B1 is generally not much documented. If we see there is extremely safe limit that is uh we don't need any um upper limit being established because excess of consumption of water soluble vitamins will be excreted in the urine and similarly that is also documented or evident in B1 from food there is no toxicity that is being reported from the food sources and from supplements it's very rare only if there is an extremely high IV dose in clinical settings we

10:56 would be uh looking at the toxic uh toxic levels of B1. [snorts] So if we see uh the acute uh IV overdose could be because would lead to headache, weakness, allergic reactions, any anaphilaxis. Uh this is usually rare. uh it if it is uh case documented is only because of IV administration only and there is no chronic toxicity that is reported even at high uh oral doses. So the food sources include a weed germ uh which has the highest thamin content which is 1.88. That's why if you see processed foods and polished foods will

11:42 not have this weed germ part. So that becomes a loss of thamin. Sunflower seeds which is a very good source which has about 1.48 pork which is a lean pork has 90 whole wheat bread has got 34 and similarly brown rice green peas nuts have good amount of B1 and soybean also has about 0.87 87 mg of thyin per 100 grams. Even fortified cereals has about good amount of thyin in them. 0.5 to 1.5 5 mg based on the serving it is being uh seen. [snorts] Coming to the stability, thyon is the most unstable of all the B vitamins because it's very much sensitive to

12:28 heat, alkaline conditions and prolonged cooking. Polishing of rice removes the bran and the germ destroying up to 80%age of thyamine content. Major cause of berry biry in rice eating populations. We could see alkaline cooking uh includes like adding soda, baking soda to the vegetables will rapidly destroy the thamin. A common but harmful Indian cooking practice. So that is uh very much seen. Thamin leeches into the cooking water. Discarding the cooking water will cause about a significant loss of 20 to 40 percentage. That's uh the major uh part of B1 includes the berry berry uh dry berry

13:14 berry, wet berry berry and also we discussed about the warniki scars syndrome which is very much common among uh [snorts] the alcoholics and uh it leads to psychiatric uh issues also and toxicity is very rare. B2 next is the second uh water soluble vitamin and B2 is also called as riboflavin which is a water-soluble vitamin that serves as a precursor for two essential co-enzymes which is the FAD flavvenine ducleotide and FMN which is a flavven monucleotide and they are critical for cellular respiration and energy metabolism and oxidation reduction reactions.

14:01 So the chemical nature of this includes iso aloxxins ring which is attached to the ribbol and that's the sugar alcohol. It gives a characteristic yellow orange color to the food and the active co-enzyme forms include FMN which is the flavin monucleotide and FAD which is a flavin adinine ducleotide. The storage is seen primarily in liver, kidney and heart. uh body stores last only a few weeks. Okay. So if you see the uh there is a excess of uh storage doesn't happen. If it's excess it gets excreted in the urine only. The characteristic sign includes the urine turns bright yellow green fluorescent with supplementation

14:46 harmless and uh deficiency includes a ribboflavinosis which is uh obviously seen in angular stomatitis, keosis, glossitis, corial vascularization and saboric dermatitis which is common to B2 which is a riboflavven. [snorts] So when we talk about the functions similar to B1 it also has a very uh important uh function [snorts] in energy metabolism amino acid metabolism as a part of FMN flavin monucleotide. It is acting as electron carrier in mitochondrial electron transport chain and it's very much essential for ATP production. Amino acid metabolism forms a co-actor for amino acid oxidasis and

15:34 it gets involved in catabolism of amino acids also B6 activation also is very important uh with regard to B2. So when it comes to FMN it it is required for the conversion of B6 which is perodoxin to podoxal phosphate PLP which is active form. So we need B2 for that activation also. So uh FMN has those functions whereas FAD which is a flavven arinine ducleide has a lot of uh functions here which talks about energy metabolism and oxidative phosphorulation where we can see it accepts electron as FADH2. It transfers the electrons to

16:22 complex 2 of electron transport chain which in releases the ATP and it causes the ATP generation. Fatty acid oxidation includes uh it forms as a co-actor for asyl COA dehydrogenase which is the major first step in the beta oxidation of fatty acids under KB cycle. If we see it, it's a major co-actor for suinate dehydrogenase which is the complex 2 [snorts] that converts the suenate to fumemerate and also FAD acts as a major antioxidant function which involves as a co-actor for glutathione reductase regenerates the reduced glutathione which is GSH and uh in the folate metabolism it is

17:08 required for methile tetrahydro hydroolate enzyme uh and it converts the folate to active mthf with methile tetrahydropholate in ion metabolism. It helps mobilize the ion from feritin stores and deficiency worsens the iron deficiency anemia. So if we see even B2 uh FAD and FMN has these many functions which is very much important for our body. So coming to the mechanism of action uh when we consume the dietary riboflavin it is absorbed in the small intestine where it gets phosphorolated as FMN which is flavin monucleotide and this

17:54 FMN along with AM gets converted as FAD. This FAD or FMN acts as a redux enzyme where the cre reactions are being given there and it is involved in the electron transport chain where FADH2 is reduced and it accepts the electron and FADH2 therefore gets oxidized as FAD and this donates the electrons to electron transport chain. The particular enzyme reactions is seen in these particular metabolisms where beta oxidation is seen. [snorts] Beta oxidation of fatty acids from asile COA to enol COA. Asil COA dehydrogenase is dependent on FAD. In crep cycle suinate is converted to fummerate where

18:40 suinate dehydrogenase is again FAD dependent. In the electron transport chain complex, FADH2 is converted as co-enzyme Q which generates about 1.5 ATP per FADH2. [snorts] Glutathione reductase is uh nothing but antioxidant regeneration is FAD dependent again. So when we talk about ICMR's recommendation uh infants to uh elderly people there is a lot of uh increase in the recommendations from.3 till 1.4 for adult men and adult women it is 1.1 mg per day and for pregnancy it is 1.5 for lactation it is 1.7 and similarly for elderly it is 1.4 4 the energy

19:27 requirements are always linked to the uh FA um the B2 recommendations. So if you see 0.6 mg per,000 kilo calorie is being given and this is being sourced from ICMR nutrient requirements for Indians 2020. So when we talk about the bioavailability of these nutrients, bioavailability uh occurs with the 60 to 65%age under normal dietary conditions. That means when a person is not deficient of B2, [snorts] the uh absorption rate is really good and the site of absorption is upper small intestine where active transport mechanism takes place. The form includes the food riboflavin is

20:13 bound to proteins which is the FAD uh and FM. It is released by gastric acid and digestive enzymes before the absorption and uh similar to B1 even higher protein intake will enhance the riboflavin retention in tissues. So the form and the site is almost the same as that of the uh B1 um vitamin. The enhancing factors includes the adequate as gastric acid proteinrich food and small frequent meals. The reducing factors include UV light or sunlight which will destroy the riboflavin rapidly. Alkaline conditions include u the reducing uh effects. Even alcohol will absorb the uh impair the

21:00 absorption of B2. Photosensitivity most of the time it is light sensitive of all the B vitamins. Milk is uh stored in transparent bottles will lose up to 50%age of riboflavven in 2 hours of sunlight. So that is how its sensitivity is being uh analyzed. The thyroid hormone which is the hypothyroidism will will impair the conversion of ribboflow into FAD or FMN. So that becomes a major uh factor here. When we talk about the toxicity uh riboflavin toxicity is uh not really absorbed and there is no tolerable upper limit being established. Riboflavin B2

21:45 is extremely safe and there is no toxicity from food and there is no toxicity that has been ever reported from natural dietary sources. Also high doses of supplements even at pharmacological doses there is no significant adverse effects that has been reported absorption and excretion if you see intestinal absorption is limited and excess riboflavin is not at all stored and it is getting excreted through the urine it is causing a bright yellow urine. If there are any drugs which has an interaction if we see uh pheninoiaines and triccyclic anti-depressants are some of the u [snorts] drugs which can interfere with the riboflavin utilization. Please note

22:31 that ri rioflavin has no known toxicity. It is one of the safest nutrients that we are talking about. And the food sources of th rioflavin includes beef liver which is a highest source which is about 2.5 mg per 100 g. Milk comes the next and yogurt eggs are all there. Almonds forms a very good source which is 1.01 mg. Even mushrooms are good. Fortified cereals is the same as B1. Spinach cooked has good amount which is 0.21 mg per 100 gram. [snorts] Talking about the stability, uh riboflavin is the most light sensitive of all the uh vitamins. As uh discussed

23:17 earlier, if the milk is stored in a clear glass bottle, it loses up to 50%age of riboflavin within 2 hours of sunlight exposure. Always store in opaque containers which is relatively heat stable during normal cooking. uh the minimal losses during boiling and steaming compared to other B vitamins. So always uh normal cooking there will be it's relatively heat stable whereas uh if it's boiling or steaming there will be minimal loss. Alkaline conditions also rapidly destroy riboflavin. Adding the baking soda during cooking causes significant losses just like B1. UV light is the greatest enemy for uh riboflavin and uh it forms a fluoresence

24:03 and uh rapidly degrade under uh sun sunlight. Opaque packaging of milk and diary is essential to preserve this content. [snorts] So that's it with B2 which is rioflavin or a ribboflavinosis. If the uh child is having u a high berubin content the baby is born and they expose them to uh the light UV light and that also may cause some riboflavven deficiency. So that much heat sensitive it is. So next we move to the next third waters soluble vitamin which is commonly known as niacin that's it serves as a precursor for two critical enzymes which is NAD plus and

24:49 NADP which is a nicotenomide adinine ducleotide NAD and NADP plus is nicotenomide adinine duclotide phosphate. It is essential for over 400 oxidation reduction reactions in our body. So if you see the chemical forms uh they include nicotinic acid, nicotinomide both are dietary forms of nascin. Unique feature of this could be synthesized in the body from tryptophan. Uh the tryptophan amino acid gets converted as 60 mg of tryptophan is converted to 1 mg of nascin which is the one nascin equivalent. The active co-enzyme forms include NAD plus and NADPH

25:37 [snorts] storage is it is minimal and not significantly stored and the daily intake becomes an essential part. It can get converted as from tryptophan also that's a unique feature. So if your diet is good in protein and tryptophan it gets easily converted to nasin. [snorts] The functions include uh uh energy metabolism similar to the B1 and B2. NAD plus is an essential electron carrier in glycolysis crep cycle and B2 oxidation which generates the NAD H for electron transport and ATP production. Oxidation reduction uh is also taking place in in the similar way with over 400 enzyatic reaction and that's the largest

26:23 co-enzyme role of any vitamin. [snorts] Fatty acid synthesis uh NADPH forms formed from NADP+ is essential for hydrogen donor for fatty acid and cholesterol synthesis. The antioxidant defense uh happens via NADPH H which maintains a reduced glutathione via glutathione reductase which is essential for antioxidant production. [gasps] Lipid metabolism happens with pharmacological doses where high dose of nicotenic acid inhibits the lipolyis in adipos tissue that will reduce the very low density lipoprotein and low density lipoprotein thereby rising the HDL which is a good

27:09 cholesterol high density lipoprotein cholesterol serotin activation NADP uh NAD+ activates the serenins which is involved in aging ing inflammation and metabolic regulation as well as gene expression. NADPH is also essential for the synthesis of steroid hormones in the adinal glands and the gonads. The mechanism includes uh as discussed in the dietary nasin or tryptophan gets converted to 1 mg of nasin equivalent. It is absorbed in the small intestine gets converted to NAD plus and NADP+ in tissues. NAD+ and NADP+ acts as an electron acceptor and they carries electrons to the ETC which is electron

27:56 transport chain. It is involved in these many reactions in the glycolysis, crep cycle, electron transport chain, fatty acid synthesis, DNA repair and all that. So you can see the reactions over there. So the relation between tryptophan with nascin 60 mg of tryptophan is equivalent or getting converted to one mg or mill gram of nascin which is nothing but one nascin equivalent. So if you provide 60 g of protein to the person's diet they would provide about 600 mg of tryptophan. 600 mg of tryptophan can get converted to 10 nascin equivalent. The

28:42 conversion of tryptophan to nascin also requires thamine, riboflavin and podoxin. So all are interconnected and they require B1, B2, B6 for this particular conversion of uh tryptophan to nascin. Coming to the uh RDA, the infants uh require about 2 mg of uh nascin per day and it goes as they grow and for adult men it is uh 16 mg for adult women it is 14 mg and for pregnant it is 17 and for lactating women it is 18. So that's how it goes uh as they grow. So coming to the bioavailability

29:29 uh the absorption rate is about 100%age from the animal sources and supplements and the major side of absorption is small intestine and the nascin is always bound to the cereals especially in the maze or the corn. The nasin is bound as niacetin and it's completely unavailable unless it is treated with alkali. Nixelation which is the traditional Mexican practice of soaking corn in lime water releases the bound nasin and that helps in the prevention of pelgra. This is called nixalization. So it happens mostly with Mexican practice. Uh tryptophan conversion happens with 60 mg of dietary tryptophan converts to 1 mg of nascin requires B2,

30:17 B6 and iron as a co-actor. The high protein intake will enhance the nyin availability to the body and also alkaline treatment of cereals will enhance the availability. Reducing factors include alusins in excess in joir or sorghum diet where that will inhibit the tryptophan thereby nyin conversion does not take place and similarly alcoholics and also prolonged cooking will uh affect the B3 which is nascin. When we talk about the Indian relevance, jawar which is a sorghum based diets are high in lucin that will inhibit the nasin synthesis from tryptophan contributing to pelgra risk in south India.

31:05 So moving on to the toxicity. Uh acute toxicity happens only with the pharmacological doses of higher than 50 mg of uh nascin given. And the symptoms include nasin flush where you can observe intense skin flushing, redness, burning, tingling sensation, prostaglandin or mediated which is harmless but uncomfortable. proritis which which happens with severe itching of the skin. Uh there would be GI disturbances like uh gastrointestinal disturbances including nausea, vomiting and diarrhea. All these are toxic effects with regard to nasin which is B3. Chronic toxicity include when the intake

31:50 is above uh 3,000 mg per day. It would lead to hepattoxicity where the liver gets damaged. The elevated liver enzymes would be seen and that's the most severe or serious concern. Hyperglycemia would occur which leads to impairing uh insulin sensitivity and that worsens the diabetic condition. Hyperurismia where you can see uh there is a rise in the uric acid level which would lead to gout. Hypotension which is a low blood pressure would lead to the dizziness. So the average upper limit of nasin or nicotenomide includes 35 mg per day from supplements and nicotenomide 900 to,000 mg per day.

32:36 Toxicity happens only from high dose supplements and food sources are completely safe. So you don't have to worry about the food sources that you're going to talk about. So food sources include chicken breast uh which is about the highest 14.8 8 mg nin equivalent beef liver, tuna, ground nuts, whole wheat, brown rice, mushrooms, soybean all comes in the next. [snorts] So when we are going to talk about the stability, nasin is highly stable. They're resistant to heat, light, oxygen, acid and alkali. Uh would lead to minimal cooking loss. The main loss happens via water leeching. up to 40% is lost and can be covered by using cooking

33:22 water. The bound nascin uh called as niacin in corn and sorghum is makes it unavailable. Therefore there needs a alkaline treatment uh to prevent the pelgra. The process is called nixelamalization. A refining of the cereals will reduce the nasin. So prefer whole grains over the polished cereals. With this uh the conclusion would be for this particular three vitamins would be B1 is easily destroyed by heat and alkali. So the deficiency leads to ber whereas in riboflavin they are sensitive to light. So the destruction on exposure causes a ribboflavinosis. Vitamin B3 which is nasin is highly stable but its bioavailability varies

34:10 and the deficiency would lead to pelgra. Uh that comes to the end of the part one uh video of uh water-soluble vitamins. We still have more vitamins to discuss.