Fat soluble vitamins-Part2

0:16 I welcome you all to the part two of fats soluble vitamins which is on vitamin E and K. At the end of the session, the student will be able to understand the introduction, functions, dietary requirements and recommended dietary elevances just like vitamin A and D, bioavailability, toxicity, food sources and stability of vitamin E especially toerol and its role as primary fats soluble antioxidant in human health. Vitamin K also has the same uh objective along with vitamin E. So all these things are going to be dealt in the upcoming slides. So uh the conceptual framework would be like this. So uh talking about the interaction of vitamin uh E and K

1:02 functions, dietary requirements and ICMR RDA bioavailability, food sources, stability, toxicity and conclusion of these vitamins. To start with vitamin E, it's a collective term of about eight fats soluble compounds, four tocopherols and four too trienols. Alpha tocopherol is the biologically most active and predominant form in human plasma and tissues. It is the body's most important lipid soluble antioxidant. uh the chemical form includes about tocoperol four uh four uh forms and tocotenol four form among that alpha tocopherol is the only form recognized to meet the human requirements. So the

1:50 structure of the vitamin E includes the chromol ring with a phal side chain where the tocoenol have unsaturated bonds which has three double bonds the side chain versus the tocophererals. Similar to vitamin D even vitamin E is stored in adipos tissue liver and cell membrane. Highest concentrations are present in adrenal glands. So the transport of vitamin E includes there they are absorbed in the small intestine transported via the kyomicrons which is the VLDL which is nothing but uh very low density lipoprotein and in lipo low density lipoprotein alpha TTP which is the alpha tocoperol transfer protein in

2:37 liver preferentially they retain alpha tocopherol the mechanism of vitamin E uh antioxidant action regeneration cycle includes a free radical chain reaction and how vitamin E breaks it. So PUFA uh in cell membranes which is the polyunsaturated fatty acids in the cell membranes are really highly vulnerable to free radical attack. When they are unchecked this triggers lipid peroxidation a destructive chain reaction destroying the cell membranes. So step one and uh the the processes include in this particular slide is given. In the step one the PUFA which is nothing but the polyunsaturated fatty

3:22 acid reacts with reactive oxygen species and a lipid radical is being generated and this free radical attacks the membrane polyunsaturated fatty acid. Whereas in the step two, this lipid radical along with oxygen forms a lipid peroxide radical where the chain reaction begins. And after this, the chain reaction includes the lipid peroxil radical with the vitamin E hydroxide forms the LO tocoperoxile radical and thereby the chain reaction is broken. Alpha tocopherol is physically embedded in the phospholipid billayer exactly where lipid peroxidation occurs making it uniquely positioned to act. So when

4:10 we talk about vitamin E uh regeneration cycle, vitamin C donates an electron and vitamin uh decreased vitamin uh and vitamin C uh as a part of dehydrocorbic acid and uh as well as a glutathione will regenerate this process. uh NADPH is uh regenerating the glutathione again and thereby the regeneration cycle continues. So this is how the vitamin C uh is involved as well as a glutathione is involved in the vitamin E uh regeneration cycle and there is two line defense system. The first line defense is on the vitamin E where it stops the lipid peroxidation

4:56 chain at the membrane level itself. Whereas in the second line uh coming to the glutathione and selenium. So the selenium forms the detoxifying uh it detoxifies the lipid hydroparoxides which is already formed. So therefore l plus this glutathione uh reacts to form lo which is a harmless one plus water is being released and this is via the glutathione peroxidase. So there is the two-line defense system that you can uh see in the slide. So when we talk about mechanism of vitamin E the site of action and the non-antioxidant functions include eriththroy membrane uh is a location

5:42 thereby RBC rich in PUFA which is polyunsaturated fatty acid and oxygen prevents the hemolytic anemia which is being formed. mitochondrial membranes which is the highest ROS production site in the cell uh and also in the lung epithelial cells if you see a first contact with the inhaled oxidants and pollutants are being observed in the neural neuronal membranes the brain is about 60%age fat which is highly vulnerable to the oxidative damage in the sperm membranes it is rich in polyunsaturated fatty acids protecting the reproductive function LDL particle particle which is a low density lipoprotein particle prevents LDL oxidation a key step in the artherosclerosis prevention

6:29 when we talk about the non-antioxidant mechanisms uh this particular mechanism has a role to play which is the protein kynise inhibition alpha tocoperol directly inhibits the protein kynise C thereby reducing the platelet aggregation and smooth muscle uh proliferation and also if we see uh the inflammatory uh regulators like uh uh they suppress these um cytoines and all that. So they suppresses the master inflammatory regulator which reduces interlucan one interlucan 6 tumor necrossing factor CRP which is uh C reactive protein and adhesion molecules are all being suppressed and

7:17 COX inhibition which is via the phospholipase A2 and cycllo oxygenase which reduces a proinflammatory prostaglandins and thromboxins which is uh in the A2 process gene regulation happens is modulating the genes for collagen synthesis, scavenger receptor, CD36 and connective tissue me maintenance are all because of the vitamin E and these are all independent of its antioxidant role. Vitamin E forms a a major chain breaking antioxidant wherein it stops the propagation of lipid peroxidation. They donate a hydrogen atom to lipid peroxide radical. Tcoeroxil radical is formed

8:04 which is really stable and non-reactive. Vitamin C regenerates the vitamin E at the membrane water interface. They are co- dependent and selenium detoxifies the remaining products byproducts which is the two-line defense and the non antioxidant role includes the protein kiny inhibition and anti-inflammatory suppression and gene expression regulation. So vitamin E has a lot of roles to play in our body and alpha tocoperol is the only form recognized to meet the human uh vitamin E requirements. So vitamin E requirements are very minimal and uh if you see the RDA it goes as the age grows and uh adults

8:52 starting from infants it is six and for adults greater than 70 years it is 22.5 uh international units per day. If it is the upper limit if you see it is 1,000 uh mg per day. So we can see that a lot of uh requirements that are being given especially for pregnancy it is 22.5 for lactation it is 28.5 international units per day and for adult men it is 15 international units. For adult women it is 12 international units. it can be easily met. Coming to the toxicity, uh vitamin E does not produce much toxic symptoms compared to vitamin A and D. But then

9:38 very large doses more than 1,000 to,500 international units per day in adults who are deficient in vitamin K may be associated with increased coagulopathy. In neonates, the large doses of more than 100 mg per kg per day has led to increased evidence of necrotising entrocolitis and sepsis presumably due to inhibition which has led to bacterial and fungal killing by neutrfils through antioxidant suppression of neutrfll derived free radical. So the vitamin E food sources include uh there are lot of food sources uh when we talk about the food include animal sources like egg yolk, butter, fish, salmon, chicken liver, plant oils uh

10:25 include wheat germ oil, sunflower oil, safflower oil, ground nut oil and mustard oil. Similarly, when we talk about the nuts, most of these nuts which give the oil are good in vitamin E. Sunflower seeds, almonds, hazelnuts, peanuts and peanut butter. And coming to fruits and vegetables, spinach, drumstick leaves, avocados and broccololis are very good sources of vitamin E. In Indian diet, especially in Tamil Nadu, we can see that groundut oil, cem oil, drumstick leaves, peanuts, curry leaves are good sources of vitamin E. Bioavailability includes about 20 to 80%age average 40% under normal conditions and they are primarily absorbed in small intestine primarily

11:11 junum and the mechanism include passive diffusion after misella solubilization. They require dietary fat about 5 to 10 g so that they get absorbed much more better and bile salts are also required for the absorption. Transport includes kyomicron transportation via the lymphatic circulation to the blood and to the liver. In the liver alpha transyrogen protein selectively retains the alpha tocopherol and they are redistributed via very low density lioprotein to the tissues. The storage include adipos tissue majorly as we saw in D and E uh in the liver and adrenal

11:56 glands as well as in the cell membranes. The factors affecting the bioavailability includes dietary fat which is very much important and bile salt should be adequate. Mild heat processing is uh will enhance the vitamin E absorption. emulsified supplement forms and vitamin C which helps to regenerate the vitamin E are all uh very much needed to enhance the vitamin E absorption in our body. Along with that adequate protein intake is very much needed. What are the factors that decrease the uh vitamin E absorption? So we have some uh factors which do uh affect the vitamin E absorption. So fat-free diet when there is uh zero fat in your diet

12:42 or nil fat in your diet and malabsorption conditions like crohn's disease, celiac disease, cystic fibrosis, choleistasis, liver disease are all going to reduce the vitamin E absorption. A beta lipoproteinia which is impaired kyomicron formation and drugs like cholesterime or statat mineral oil can affect the vitamin E absorption. Similarly, highdose iron supplements also decrease the vitamin E. Vitamin E is very much sensitive to uh oxygen, UV light and heat. So, they can easily get destroyed during storage and cooking. Repeated reheating of oils because oil is very good source of vitamin E when you start reheating or repeated reheating of these oils. Up to

13:27 80%age loss can occur with regard to vitamin E and they may become harmful. So we have to store them in airtight dark containers and they no normally prefer gentle cooking. Uh especially steaming would be uh the ideal way of uh preserving the vitamin E from the sources. Refining milling will remove the vitamin E rich parts especially the germ and the outer layers of the cereals. And uh that's it with vitamin E. So we we are moving to vitamin K. Vitamin K is the last fats soluble vitamin that functions as an essential co-actor for the enzyme glutam caroxilase which activates the

14:14 vitamin K dependent proteins which is involved in blood coagulation bone metabolism and vascular calcification prevention. Chemical forms include the phyloenon which is the K2 menon which is uh the MK4 to MK13 and this is being synthesized by the bacteria uh from our own body uh present and fermented foods animal tissues. K3 is nothing but menadon which is a synthetic form. It could be toxic and it is no longer being used. The key mechanism include it's a co-actor for caroxilation of glutamate uh gamma caroxylutamate residues activates the coagulation

14:59 proteins and bone proteins. The storage include there is a limited hepatic storage for this particular vitamin. So the body stores turnover rapidly within 3 to 5 days unlike vitamin A and D. It is absorbed with dietary fat transported via kyomicrons uh especially K1 mainly in the liver which is a phyloenon K2 is the menon. So K2 is in the extra hypatic tissues like bone and arteries. So coming to the mechanism of vitamin K if you see uh this particular uh cycle will help you to understand better. So that dietary vitamin K uh in the reduced form vitamin KH2 hydrochinone forms a

15:47 co-actor for gamma glutam caroxilize enzyme where glutamate residues are in the protein and this gamma caroxyl glutamate residues are formed they again chilate with the calcium ions where the protein becomes biologically active. This vitamin K forms epoxide which is the usable form and then it forms this VK enzyme which is the vitamin K epoxide reductase. Thereby vitamin K K gets regenerated and the cycle gets continued. So there are uh certain vitamins which are dependent uh on vitamin K uh proteins which are dependent on vitamin K. Factor 2 which is the prothroin

16:33 factor 7 9 uh 10 protein C protein S osteocalin matrix GL protein everything is dependent on this so factor 2 prothroin is converted to thrombin and they cleave the fibbrronogen into fibbrin clot similarly factor 7 initiates the extrinsic coagulation pathway factor 9 a part of intrinsic contact pathway factor 10 The common pathway forms the prothroinous complex. Protein C forms a anti-coagulant inactivates the factors uh 5 A and 8A. The protein S forms a co-actor for protein C. Osteocalin which is nothing but uh resulting in the bone mineralization binds the hydroxy

17:20 appatite matrix GL protein uh it prevents the vascular and soft tissue calcification. So there is a warerin mechanism that we should remember here is warerins are anticoagulants. They block the vko enzyme which is a vitamin K epoxide uh enzyme. It inhibits the vitamin K recycling clotting factors. They remain inactive. So thereby leading to therapeutic anti-coagulation. So the ICMR which is the uh recommended dietary allowances of vitamin A uh K includes uh wide range of values starting from infancy it is 5 to 10 and for adult it is um 55 mg per day for

18:09 adult women it is 55 mg per day it's the same and for pregnancy and lactation also it remains the same whereas for elderly it is 65 m per day a bit high And coming to the bioavailability of vitamin K, their absorption and transport includes about uh 80 to 10 to 80 percentage are highly variable which are tightly bound and they are forming a chloroplast membrane in raw leafy grains especially low bio accessibility. Absorption rate with regard to K2 is uh generally higher than K1 and it has a long halflife. Similarly, the site of absorption is small intestine uh especially the junum

18:56 and elium. The mechanism of absorption includes passive diffusion after myelar solubilization with bile salts. As I uh told already dietary fat about 5 to 10 g is needed for these absorption along with bile salts. Hence uh we require this for absorption. transportation takes place via kyomicrons lymphatic circulation to the liver and then they are redistributed via very low density lipoprotein. The enhancing factors include dietary fat of 5 to 10 gram per meal, cooking vegetables with oil, adequate bile salts and gut microb where the bacteria plays a very important role in synthesizing K2 which is a menquinon

19:42 and also MK7 form has long halflife and fermented foods all these are enhancing factors. When we talk about the reducing factors, fat-free diet, raw vegetables, choleistasis or liver disease, broadspectctrum antibiotics, drugs, choleic thyroamine, orally stat, mineral oil, fat malabsorption syndrome. So coming to the comparison of K1 and K2 K1 is phyocenon and K2 is menon. The K halflife of K1 versus K2 is the K1 has about 1.5 hours whereas menon has about 72 hours. The tissue distribution

20:29 includes it's in mainly in the liver whereas K2 is uh distributed in the extra hypatic like bone and arteries. The bioavailability is really really low with regard to K1 especially it is from the raw vegetables whereas this one is about u high and their uh higher bet and better tissue uptake is because of K2 and their bioavailability is really good. K1 is best for blood coagulation because their main role is blood coagulation and K2 is best for bone health and vascular protection. So the bioavailability is better than K K1 when it comes to K2. Toxicity uh unlike other fats soluble

21:15 vitamins, vitamin K is not stored in the body. Therefore toxicity is rarely seen. Menodon and its water-soluble forms have been connected with hemoliotic anemia. Other toxic symptoms include vomiting, thrombosis and jaundice. Excessive doses administered to the mother prior to delivery can result in jaundice by hemolyis antagonism for bilary metabolism or can lead to direct hepattose toxicity. Food sources include um kale uh which is cooked spinach, collard greens, broccoli, soybean oil, drumstick leaves, coriander leaves, curry leaves and fenugreek leaves. So if you see a spinach has the highest, broccoli is uh

22:01 good and fenugreek leaves as the highest and curry leaves also has the highest which is 265 mg. Animal and fermented sources include the na natto which is the fermented soya bean and then uh Adam cheese has some good amount whereas egg yolk has about 32 mg per 100 g. Chicken which is from the dark meat has about 10 m. Beef liver, butter also has good amount of uh K2. The Indian food sources include drumstick leaves which is the muring forms the major source which is an excellent K1 source. Curry leaves we call it as carvula which is having a regular K1 intake. Coriander leaves, fenugreek leaves, Italy and dosa which

22:48 is coming under the fermented food has a modest K2. curd yogurt though they are very small but they have good amount of K2 coming to the stability uh vitamin K is stable to normal heat and freezing but they're very sensitive to UV light alkaline pH and oxidation steaming and boiling causes minimal loss with cooking with oil improves the K1 absorption fermentation increases the K2 storage importance includes you should avoid sunlight while storing K1 and greens is better absorbed when cooked with oil. K2 in fermented foods is highly stable. Key facts is there is no upper limit for K1 or K2. They are very safe but only K3 is toxic because they are in the supplement form. So therefore

23:34 the requirement is approximately 55 mg per day. K2 has a better bioavailability than K1. The consistent intake needed with warerin. To conclude, uh, vitamin E and K both are vital fats soluble vitam antioxidants. Especially E forms a fats soluble antioxidant that protects a cell membrane from oxidative damage with adequate intake achievable through a balanced diet and minimal risk of toxicity from natural sources. Vitamin K forms an essential nutrient for blood coagulation and bone health. Especially they are safely obtained from the diet with consistent intake being crucial for maintaining the normal physiological functions. Thank you. Happy learning.

24:20 >> Water soluble vitamins dissolve instantly. But fats soluble vitamins play by completely different rules. How does this one trait change their journey? Let's track a single molecule of vitamin A entering your gut alongside your dietary fats. Because it's hydrophobic, it can't dissolve in digestive fluids. It has to physically merge with dietary lipids and bio salts just across your intestinal wall. Inside the cell, it's packed into a massive lipid carrier complex so it can navigate the bloodstream. Here's the problem. Water- soluble vitamins are easily filtered by your kidneys and peed out. But where do these fatbound molecules go if they can't be excreted? The carriers deposit them into long-term storage in the liver while vitamin E settles in

25:06 atapost tissue. Because they aren't easily excreted, taking excessive amounts means they accumulate in your tissues, creating toxicity risks. But in normal doses, they are essential. Vitamin A targets vision and immunity. Vitamin D maintains bone health. Vitamin E provides antioxidant protection. And vitamin K drives blood clotting. So what happens to that single fatbound vitamin A molecule we tracked from your lunch all the way into your liver? It doesn't get flushed away. It simply waits safely inside those fat reserves until your body actually needs it for your eyes. How does vitamin A deficiency systematically dismantle the human eye? Let's track a single vitamin A molecule from your plate down into your digestive

25:51 tract. Because it's fat soluble, it needs dietary fat to be absorbed. Once inside, it travels to your liver's stellate cells for storage. Here, it converts into retinol, retinol, and retinoic acid. Unless a malabsorption disorder blocks the pipeline, the active form retinol travels straight to your eye. It binds with a retinal protein to capture dim light, creating a pigment called rodopsin. But capturing light means nothing if the eyes's physical surface breaks down. That's the second pathway. Retinoic acid enters the cornea and conjunctiva. It regulates genes to keep these epithelial tissues moist and immune defended. Watch what happens when this pipeline runs dry. First rodopsin production crashes causing night

26:37 blindness. Then the surface dries out accumulating dead keratin into foamy patches known as beto spots. Left untreated this ends in irreversible keratomalia and permanent blindness. But you can restore the flow. Animal sources like liver or carotenoids from leafy greens paired with dietary fat will reverse early symptoms and protect your vision. and that single molecule of vitamin A from the beginning. By maintaining a varied diet, it navigates safely from plate to retina, keeping your vision sharp and your eyes protected. We build our modern lives mostly indoors, shielded from the sun. But that exact lifestyle actively starves us of a nutrient critical to our physical

27:22 framework. To understand why our skeleton fails without it, we have to look deep inside the gut. Vitamin D operates less like a standard vitamin and more like a potent hormone. Whether it enters as D2 from food or D3 synthesized directly in your skin, it targets the intestine. Actively unlocking cellular gates to absorb calcium and phosphorus into your bloodstream. But natural synthesis is easily blocked. Limited UV exposure drastically reduces how much your skin produces. Darker skin naturally filters UV rays while fat malabsorption disorders can block dietary uptake from the inside. When this absorption fails, bone integrity collapses. In children,

28:07 poor mineralization causes skeletal deformities, a condition known as ricketetts. In adults, fully formed bones lose their mineral density, becoming dangerously soft. This is called osteomalacia. Reversing this deficiency requires a strategic triad. First, safe sunlight exposure. Second, dietary intake through fatty fish or fortified foods. And finally, clinical supplementation to avoid calcium overload. Ultimately, your skeleton's structural integrity relies entirely on securing this hormone through a deliberate balance of sun, diet, and clinical. Every second, your cells are under constant microscopic attack from oxidative damage. To stop that destruction, your body relies on a

28:52 built-in chemical shield to protect the membrane. This fats soluble molecule embeds itself directly into the cell membrane, defending vulnerable polyunsaturated fatty acids from breaking down. That active protective compound is alpha tcopherol, the primary form of vitamin E. But because it relies entirely on dietary fat to enter your system, true dietary deficiency is incredibly rare in healthy adults. Instead, severe drops are usually triggered by fat malabsorption disorders, genetic transport defects, or premature birth. When that biological shield drops, unprotected nerve and muscle membranes begin to physically degrade. This causes profound weakness, loss of coordination, and severe numbness and tingling in your hands and feet. To prevent this structural damage, you don't need extreme megaosing. Highdose medical supplements carry risks and should only be used for diagnosed

29:39 clinical needs. For most people, a very diet of nuts, seeds, leafy greens, and adequate dietary fat is all it takes to maintain your cellular antioxidant shield, keeping your nervous system seamlessly protected from the inside out. You get a sudden cut or take a minor fall that tests your skeleton. What single invisible nutrient seals that leak and keeps your bones dense? It's vitamin K. It acts as the essential key, activating specific proteins that turn on your body's natural coagulation cascade to stop bleeding. Simultaneously, it activates different proteins that pull in calcium to mineralize and harden bone. But having this nutrient in your gut doesn't guarantee it reaches your blood. Because vitamin K is strictly fat soluble, adult

30:26 deficiencies rarely start with a bad diet. Instead, gastrointestinal malabsorption or prolonged antibiotics wipe out the gut bacteria producing it. And while adults have reserves, newborns start entirely at zero. With extremely limited transfer across the placenta, infants are highly vulnerable to vitamin K deficiency bleeding. That biological gap makes standard clinical prophylaxis at birth an absolute necessity. To prevent deficiency long-term, you need K1 from dark green leafy vegetables and K2 from fermented foods. Crucially, you must consume them alongside dietary fats to actually unlock their absorption. So, the next time that cut perfectly clots and your bones hold strong, you can think that early

31:12 prophylaxis, leafy greens, and properly absorbed fats. Vitamins A, D, E, and K are absolute survival essentials, but they play by entirely different biological rules, walking a dangerous tightroppe between devastating deficiency and hidden toxicity. First, the architects. Vitamin A anchors your vision and immune system. Without it, your eyes literally fail to adjust to darkness. Vitamin D drives calcium absorption. Miss out and your very bones soften and weaken. Next, the rapid response defenders. Vitamin E shields your cell membranes from damage. A severe drop leads to muscular and neurological breakdown. And vitamin K controls your blood clotting. Without it, you face uncontrollable bleeding. But here is the biological catch to getting them. They are fat soluble. They

31:58 cannot cross your gut lining without hitching a ride on dietary fat molecules. So if you have a gastrointestinal disorder or eat an extreme zero fat diet, you can starve of these vitamins regardless of your vegetable intake. And that same mechanism creates a dangerous double-edged sword. Because they dissolve in fat, your body doesn't flush out the excess, it stores it in tissue. That makes highdose isolated supplement pills a fast track to dangerous toxicity. The safest move? A colorful whole food diet paired with healthy fats. It gives your body exactly what it needs for vision, bones, protection, and clotting with zero risk of overload.