Vitamin E is a group of 8 different nutrient compounds: 4 types of tocopherols and four types of tocotrienols. Both tocopherols and tocotrienols are types of vitamin E nutrients.
Image: Forms of Vitamin E
The most predominant form of vitamin E in the body is α-tocopherol. It comprises over 90% of the vitamin E found in the body. This form was first isolated from wheat germ oil. Interestingly, the “tokos” in α-tocopherol stands for “childbirth.”
Animal studies have revealed that a deficiency of α-tocopherol increases the risk of infertility. That’s why this nutrient is also known as anti-infertility vitamin or anti-sterility factor X.
Vitamin E is an essential nutrient, which means we need to obtain this nutrient through food sources.
Some foods rich in vitamin E are almonds, sunflower seeds, avocados, peanut butter, pine nuts, rainbow trout, and pumpkin.
Vitamin E is a potent antioxidant and protects our body from the damaging effects of free radicals.
Free radicals are unstable molecules that are harmful to the healthy cells in our bodies.
Vitamin E also has anti-aging properties.
Once vitamin E enters the body, it is absorbed by the intestines and stored in the adipose tissues, commonly known as body fat. On-demand, the adipose tissues are broken down to release vitamin E.
Here, it is important to know that the liver only acts on α-tocopherol and converts it into a form that is usable by the cells in the body. All other types of vitamin E are excreted out.
A healthy adult woman requires about 8 mg of vitamin E per day. In men and pregnant women, the requirement increases to 10 mg per day.
Vitamin E deficiency can result in a weakened immune system, muscle damage, vision loss, and nervous system-related disorders.
Many conditions like cystic fibrosis, short bowel syndrome, and chronic pancreatitis prevent effective absorption of fats, including the fat-soluble vitamin E. So, they can increase your risk for vitamin E deficiency.
Genetics is another important factor that contributes to vitamin E deficiency.
The TTPA gene is crucial for regulating vitamin E levels in the body. It contains instructions for the production of α-tocopherol transfer protein. This protein is responsible for the distribution of vitamin E obtained from the diet to all the cells and tissues of the body.
Any changes in this gene can affect the amount of the protein produced, and hence the vitamin E levels. People who have these changes are at a higher risk of vitamin E deficiency.
A simple genetic test can reveal your genetic status of vitamin E deficiency.
Most genetic tests provide your DNA information in the form of a text file called the raw DNA data. This data may seem like Greek and Latin to you.
At Xcode Life, can help you interpret this data. Upload your raw data and order a nutrition report.
Xcode Life then analyzes your raw data in detail to provide you with comprehensive nutrition analysis, including information on your vitamin E requirements.
Also Check Out: Gene Nutrition Report Walkthrough!
Vitamin E has gained popularity recently. The association between vitamin E and skin health is a key reason for its popularity.
Vitamin E is a fat-soluble nutrient. Both plant and animal sources are available:
Animal sources: fish and oysters, dairy products like butter and cheese, Plant sources: vegetable oils, nuts and seeds, and green vegetables like broccoli and spinach.
There are 8 different chemical forms of vitamin E found.
All of these have varied effects on the body. Out of these, alpha-tocopherol (α-tocopherol) is the most active form while gamma-tocopherol (γ-tocopherol) is the most common form found in foods consumed by North Americans.
Here are some of the significant functions of vitamin E:
Vitamin E as an antioxidant
Vitamin E is a proven anti-oxidant (substances that prevent oxidation). It helps prevent cell damage from free-radicals.
Free radicals are active molecules in the body that can harm the cells in the body and prevent the cells from staying healthy.
Free-radical damage is the most common reason for skin problems including aging of the skin, development of wrinkles, fine lines, and dark spots, and skin becoming loose and saggy.
Vitamin E in both dietary forms and topical forms (external application in the form of creams, gels, and serums) is beneficial for healthy skin.
Vitamin E and immunity - Vitamin E helps improve immune response and provide protection against various infections by keeping the immune cells healthy.
Vitamin E and lifestyle risks - Lifestyle risks like smoking, drinking, and UV exposure can harm the cells in the body. Vitamin E provides protection against these.
Vitamin E and degenerative diseases - Many studies have shown that taking the recommended amounts of vitamin E reduces the risk of developing diseases like cancer, high blood pressure, and coronary heart diseases. These promising early results are being further investigated.
The early 1900s was the time when some of the initial vitamins like vitamin A, B, C, and D were discovered. Scientists and biochemists were involved in intense research identifying what else these vitamins could and couldn’t do.
Herbert McLean Evans and Katherine Bishop were anatomists experimenting with rats at the University of California. They fed rats only milk and studied how the rats were progressing. While they found that the rats were growing healthier, they were not reproducing!
They tried modifying the diet and included some starch and animal fats. The female rats became pregnant but were unable to carry the pregnancy to full term.
That’s when they introduced lettuce as a part of the diet. Now they found that the rats got pregnant and delivered healthy babies.
It was then recorded that healthy and natural sources of food were important for fertility. A particular nutrient was extracted from lettuce and was named vitamin E in 1922.
Since the nutrient was related to fertility in rats, it was given a Greek name ‘Tocopherol’. In Greek, ‘toco’ meant birth, ‘pher’ meant carrying, and ‘ol’ referred to it being a chemical.
Upon consuming vitamin E rich foods or vitamin E supplements, it is absorbed in the body like any regular fat source that you eat. Vitamin E is absorbed by the small intestine and from here, it reaches the blood and is circulated around.
The liver absorbs most of the vitamin E from the blood. You should know that the liver only acts on alpha-tocopherol and converts it into a form that is usable by the cells in the body. All other types of vitamin E are sent (excreted) out.
The converted form of alpha-tocopherol is now sent out to the blood and reaches all the tissues and cells.
Excess vitamin E is stored in the adipose tissues (fat-storing tissues present in several locations in the body) just like how normal fat is stored and is used when needed.
The use of vitamin E in the cosmetics and skincare industry has become quite common. Every product in the market seems to have added vitamin E to it.
Are all of these actually beneficial?
No, says research.
Vitamin E needs to remain stable to be useful for your skin. Most generic skincare products use unstable vitamin E forms that get destroyed as soon as you expose the product to light and air.
Hence the products you religiously use may do nothing to your skin.
The next time you buy a vitamin E-enriched product, make sure the base nutrient used is an ester form of vitamin E (a type of compound produced from acids) that is more stable and is also easily absorbed by the skin.
You cannot get vitamin E toxicity by just consuming foods rich in vitamin E. You get it only when you consume excess supplements. Here is a list of maximum levels of vitamin E that your body can handle safely.
Vitamin E toxicity can lead to internal and external blood loss (hemorrhage). When you consume excess vitamin E supplements for a longer duration, the side effects get worse.
For normal healthy individuals, vitamin E deficiency is quite rare. These individuals can easily get their recommended values only from regular food that they eat.
If a person gets vitamin E deficient because of certain genetic and non-genetic reasons mentioned below, it can result in:
Genetically, few people can have higher levels of vitamin E in the body and a few others can have lower levels. You will have to plan your vitamin E intake based on your genetic design.
APOA5 gene - The APOA5 gene is responsible for producing (encoding) the Apolipoprotein A-V protein. This is important for transporting fats including vitamin E. There are two SNPs of this gene that alter the vitamin E needs in the body.
CYP4F2 gene - The CYP4F2 gene produces the CYP4F2 enzyme. This helps in breaking down vitamin E. A particular allele of the gene is known to result in higher levels of vitamin E in the body.
TTPA gene - The TTPA gene helps produce the alpha-tocopherol transfer protein. This helps in transferring vitamin E in the body. Few mutations of the TTPA gene can cause Ataxia with Vitamin E Deficiency (AVED). AVED is another very rare inherited disorder that can lead to vitamin E deficiency.
Here, the transfer protein required to process vitamin E into cell-usable forms is absent or doesn’t function right. AVED results in vitamin E deficiency and individuals with these mutations are likely to require more vitamin E than recommended levels.
MTTP gene - The MTTP gene is responsible for producing a particular type of protein called microsomal triglyceride. This protein, in turn, helps produce beta lipoproteins. Beta lipoproteins carry fats in the food you eat from the intestine to the blood. These also carry fat-soluble vitamins like vitamin E.
There are about 60 different mutations of the MTTP gene that cause a condition called abetalipoproteinemia.This is a very rare inherited disease that hinders dietary fat absorption in the body.
People with abetalipoproteinemia are likely to require more vitamin E levels. They will need large doses of vitamin E supplements (5-10 grams a day) to prevent getting vitamin E deficient.
Vitamin K refers to a group of fat-soluble vitamins that play a role in blood clotting. It also helps your body make proteins for healthy bones and tissues.
Vitamin K is produced in our bodies by gut bacteria.
Two natural forms of this vitamin exist - vitamin K1 and vitamin K2. Vitamin K1, also called phylloquinone, is produced in plants. It is the main type of dietary vitamin K.
Vitamin K2, which is the main form stored in animals, has a number of subtypes referred to as menaquinones.
Vitamin K3, K4, and K5 are the synthetic forms (made artificially) of vitamin K.
A Danish scientist, Henrik Dam, aimed to study the effects of low cholesterol (fat-like substance present in the body) levels in the body, in 1929. He examined chickens that were fed a diet low in cholesterol.
After a few weeks, the chickens started developing hemorrhages (bleeding inside the body). However, restoring the cholesterol in their diets did not seem to reverse this.
It was then learned that another compound had been extracted from the food along with the cholesterol. That compound was the coagulation vitamin, which was described as vitamin K because it was first reported in a German journal as “Koagulations vitamin.”
It was only much later in 1974 that the exact function of vitamin K in the body was discovered.
During pregnancy, vitamin K does not cross the placenta (tissue that develops in the womb during pregnancy) to reach the developing baby, and the gut does not have any bacteria to make vitamin K before birth. After birth, vitamin K in breast milk is also not adequate enough.
Insufficient vitamin K levels can put the baby at a risk for a rare but serious disease called Haemorrhagic Disease of New-Born (HDN), also known as Vitamin K Deficiency Bleeding (VKDB)
Thus, vitamin K is administered to the baby at birth using either of the following ways:
So far, vitamin K administration to the newborns has not resulted in any noticeable side effects.
Most of the diets followed in the United States contain an adequate amount of vitamin K. Thus, reports of vitamin K deficiency in adults are very rare.
VKROC1 gene is located on the short or p-arm of chromosome 16.
The VKORC1 gene plays a vital role in the vitamin K cycle. The gene produces the enzyme (vitamin K epoxide) reductase that converts vitamin K to another form (from vitamin K epoxide to vitamin K) that is required for the blood clotting process.
Warfarin usage can interfere with this conversion. Warfarin is a blood thinner that is prescribed to treat blood clots and is advised for people with a high risk for stroke or heart diseases.
Since warfarin is a blood thinner (doing the opposite of what vitamin K does), it tends to inhibit the activity of the VKROC1 gene. This results in reduced vitamin K levels that can hamper the functioning of various blood clotting proteins.
The SNP rs9923231 can alter the activity of the enzyme vitamin K epoxide reductase. The C allele shows enhanced enzyme activity compared to the T allele, and thereby increases the availability of active vitamin K. The T allele, on the other hand, results in lower enzyme levels, and therefore less active clotting factors.
The GGCX gene is located on the p arm of chromosome 2.
It produces the enzyme Gamma-glutamyl carboxylase. This enzyme helps in the modification of several vitamin K-dependent proteins that are involved in blood clotting.
The SNP rs699664 influences the activity of the enzyme gamma-glutamyl carboxylase. The G allele produces a protein that is less active than the A allele. This results in lower levels of vitamin K which may lead to blood clotting issues.
Vitamin K deficiency can be very dangerous, as it could result in uncontrolled bleeding - which is the primary symptom.
Vitamin K toxicity is extremely rare. The natural forms of vitamin K (K1 and K2) don’t cause toxicity even when consumed in large quantities.
However, a synthetic form of vitamin K - vitamin K3 - is associated with toxicity and should not be used to treat vitamin K deficiency. K3 interferes with the body’s natural antioxidants which can result in cell damage. In infants, the toxicity manifests as jaundice and can result in hemolytic anemia (where the red blood cells are destroyed faster than they are produced) in adults.
Vitamin K deficiency is easily treatable using the drug phytonadione, which is essentially vitamin K1, that is given orally or subcutaneously (skin). The dosage for the drug varies based on the age, gender, and requirement of each patient. However, the best way to ensure you get the optimum recommended amount of vitamin K is through diet.
You must get your daily dose of green vegetables as they are natural sources and contain large amounts of vitamin K. These include:
Vitamin K is a fat-soluble vitamin that plays a major role in blood clotting. It is also essential for regulating blood calcium levels. Most newborns are born vitamin K deficient as this vitamin cannot cross the placenta. Hence, vitamin K needs to be administered either orally or through injection after birth. Though vitamin K deficiency in adults is pretty rare, it can potentially be life-threatening as it could lead to uncontrolled bleeding. Certain genetic types can put you at a risk for vitamin K deficiency, especially when on anticoagulants like warfarin. Vitamin K1 injections and oral supplements can bring vitamin K levels back to normal. However, in order to continually maintain adequate levels of vitamin K, dietary sources are the way to go!
The sun has always been the most important source of energy for all living beings in the world. The sun makes life possible.
Your body needs sunlight to stay healthy. Sunlight is the major source of vitamin D for human beings.
Vitamin D is a kind of fat-soluble vitamin needed by all living beings. This vitamin is also known as calciferol. Though it is present in a few food sources like fatty fish (salmon, tuna, sardines), mushrooms, and egg yolks, a majority of vitamin D is obtained from sunlight naturally.
Depending on their chemical composition, there are 5 different types of vitamin D available.
Out of these, Vitamin D2 and D3 are the major ones usually discussed.
Rickets is a condition that causes soft bones in children. The telltale signs of rickets are bowed legs, an abnormally large forehead, a curved spine, and stunted growth.
There are mentions of children born with deformed bones as early as in the first and second centuries AD. Though rickets was not identified as a specific medical condition until 1645, instances of children born with bone deformities were quite common.
Until the early 20th century, the reason and cure for rickets remained a mystery. Parents with newborns had no idea whether their child would grow up healthy or end up with bone deformities and stunted growth.
In 1914, Elmer McCollum, an American biochemist, identified that a certain additive in cod liver oil helped prevent rickets. He assumed it was vitamin A.
In 1922, he realized that cod liver oil without vitamin A, also prevented rickets. This led to the identification of a new 4th vitamin in history and this was named vitamin D. At that time, people did not realize sunlight could produce vitamin D.
That knowledge was brought forth by another American physician Alfred Hess who concluded “Light equals vitamin D”
The skin consists of two layers - the outermost layer, epidermis and the inner layer, dermis. The epidermis is made up of 5 layers. Vitamin D is produced using sunlight by the two innermost layers of the epidermis.
7-Dehydrocholesterol, also known as 7-DHC, is a chemical compound that is made in the skin in large quantities. 7-DHC reacts with the ultraviolet (UV) rays from the sun and is converted into vitamin D.
This process happens in the arms, legs, and face. The produced vitamin D is then carried in the blood to the liver. Here it is converted into a pre-hormone (a chemical substance produced by glands that is later converted into hormones) known as calcifediol.
Calcifediol is then converted into calcitriol in the kidneys, which is the vitamin D form actually used by the body. From here, calcitriol is sent out for circulation.
More and more doctors and scientists globally are encouraging people to increase their vitamin D intake to prevent the severity of the COVID-19 infection.
With the vaccine for coronavirus still not approved or available, people are looking towards alternate solutions to boost their immunity. Vitamin D has emerged as a powerful nutrient to keep away infections.
There are a few notable studies conducted around the world that link vitamin D deficiency to an increased risk of developing COVID-19. Some studies say people living in areas that receive lesser amounts of sunlight see higher coronavirus deaths.
Few other studies point to the fact that people with vitamin D deficiency seem to have worse symptoms when they test positive for the infection.
While there could be links between vitamin D consumption and the effects of the coronavirus, as of now, there is no solid proof that the vitamin can completely prevent or cure the infection.
The National Institutes of Health has also given out a statement stating that there is no evidence vitamin D can treat COVID-19.
However, making sure you get your recommended dose of vitamin D will definitely keep your immune system healthy during this pandemic.
According to the Food and Nutrition Board, here are the daily recommended intake values of vitamin D.
Excess quantities of vitamin D are unsafe. When you consume excess vitamin D, the calcium levels in the body increase too. This condition is called hypercalcemia. Hypercalcemia can result in the below conditions:
Vitamin D toxicity can also cause hypercalciuria (excess calcium in the urine). Extreme cases of vitamin D toxicity can lead to renal failure, irregular heartbeat, and even death.
Overexposure to the sun does not usually cause vitamin D toxicity because the skin learns to regulate the amount of vitamin D it produces. However, excessive use of tanning beds and excess consumption of vitamin D supplements can both cause vitamin D toxicity.
When your vitamin D levels are low because of unhealthy eating habits and less/no exposure to sunlight, you can get vitamin D deficient with time.
In children, vitamin D deficiency is reflected as rickets disease. Children can also suffer from developmental delays and dental problems early on. In adults, this can cause a condition called osteomalacia. Osteomalacia causes soft and weak bones. Adults also develop dental issues because of vitamin D deficiency.
There are two genes that seem to affect vitamin D concentrations in the body. Variations in these genes can cause increased/decreased needs for vitamin D.
GC gene - The GC gene is responsible for making the Vitamin D binding protein (VDBP) that helps in transporting vitamin D. One particular variant (type) of the GC gene is known to cause vitamin D deficiency.
CYP27B1 gene - The CYP27B1 gene is responsible for making vitamin D active and available for use by the cells in the body. One particular type of this gene can cause lowered vitamin D levels in the body.
Vitamin A plays a very important role in the overall development and maintenance of the body. This fat-soluble vitamin is stored in the liver and is available externally in two forms
Vitamin A is known to support a variety of metabolic functions. It helps with better vision and improves your immunity. Getting the right dose of vitamin A also plays a role in keeping the skin and teeth healthy. The right amounts of vitamin A protect the skeletal system and the soft tissues in the body.
In pregnant women, right vitamin A levels help with tissue repair after delivery and also keeps the risks of infections low.
It took almost 130 years for researchers to identify the existence of vitamin A and understand its effects on the human body.
Early accounts of Vitamin A Deficiency (VAD) have only been recorded in terms of night blindness amongst children, soldiers, and sailors. Back then, the only solution offered was to consume cod liver oil or eat an excess of cooked liver. Doctors knew this worked, but didn’t understand why it worked.
There were innumerable studies that tried to understand the effects of nutritional deprivation on animals and human beings between the mid-1800s and 1900s.
In 1912, Sir Frederick Gowland Hopkins concluded in his clinical trial that an additional factor in milk apart from carbohydrates, fats, and proteins helped rats survive on only a dairy-based food plan. He won the Nobel Prize for this study later.
This additional factor was narrowed-down to be a fat-soluble nutrient in 1918 and was finally identified as vitamin A in 1920.
In 1931, the International Conference on Vitamin Standards was first held in London and the league set to make standards and recommended values for all identified vitamins, including vitamin A.
Though people all over the world have become conscious about their nutritional intake, WHO states that about 250 million preschool children are still diagnosed with VAD. Making the right change in food habits, identifying the effects of one’s genes in his/her vitamin A requirements and taking vitamin A supplements, if needed, will all help bring down the risk of VAD.
We humans cannot produce vitamin A in our body, hence it is called an essential vitamin. We need to obtain it through diet or supplements. Vitamin A can be derived from both plant and animal sources.
Animal sources provide vitamin A in its active form, retinol, while plant sources provide vitamin A as carotene, an inactive form, which in-turn needs to be converted into the active form, retinol.
The genetics of some individuals predispose them to less efficient conversion of biologically inactive carotene to active retinol. They are usually advised to consume animal sources of vitamin A or take vitamin A supplements or consume higher amounts of plant sources to compensate for lowered conversion efficiency.
We will look into more details of specific genes that influence this predisposition in the following sections.
Everyone knows carrots are a good source of vitamin A and that they can improve general eyesight.
Did you know where this idea stemmed from?
During World War II, the British government ordered citywide blackouts to prevent German bomber flights from identifying their targets. On the other side, the British defenses were safeguarding a secret Intercept Radar System that helped their British flyers see better despite blackouts. To keep this information a secret, the British Ministry let out official information stating their flyers were able to see better in the dark because of excess consumption of carrots!
This detail has taken deep roots and is believed to date.
According to the U.S Department of Health & Human Services, here are the recommended values of vitamin A at every stage in life.
When you consume more vitamin A than recommended every day, here are some of the possible side effects recorded.
When your Daily Value Intake of vitamin A is consistently lesser than the suggested levels, you could be at a higher risk of developing the below conditions.
Insufficient dietary intake
A key source of vitamin A to the body is the food we consume. Naturally, not including enough of vitamin A rich foods is a top non-genetic reason for Vitamin A Deficiency (VAD). Not taking enough vitamin A can be a result of an unhealthy lifestyle, lack of awareness on the importance of nutrients, or poverty/unavailability of food.
People who suffer from chronic diarrhea and respiratory infections are also prone to having lower levels of vitamin A in the body.
Avoiding animal sources of vitamin A
Though vitamin A is available in both plant and animal sources, vegans have to depend exclusively on fruits and vegetables for their vit A needs. When vegans don’t plan their diet well and don’t consciously include enough carotenoid-rich foods, they can be prone to VAD.Veganism is hence a growing cause of concern as a non-genetic influence for VAD. If you follow a vegan lifestyle, you should be working on carefully choosing your food sources to prevent nutritional deficiencies.
Infants whose mothers show signs of VAD end up not getting enough Vitamin A in breast milk and hence are at a higher risk of developing VAD related health complications.
Mutations in both the TTR gene and the RBP4 gene can cause low levels of retinol in the body. The TTR gene produces a protein called transthyretin that transports vitamin A internally. The RBP4 gene (Retinol Binding Protein 4) produces the RBP4 transporting protein that delivers vitamin A from the liver to the tissues around.
RBP works with transthyretin in the plasma and prevents the kidneys from filtering out excess vitamin A.
Two gene variations can cause VAD.
BCMO1 gene – The BCMO1 gene helps encode enzymes that convert the carotenes from plant-based food sources into forms that can be used by the human body.
CYP26B1 gene – This gene is responsible for bringing down the active form of vitamin A called retinoic acid. The SNP rs2241057 with G variant in this gene can cause an increased breakdown of retinoic acid and hence can result in lowered vitamin A levels in the body.
Here is what you should do to maintain the right levels of vitamin A in the body.