Learn how you can benefit today from the NutraBlast Vitamins A & D3
What you'll discover on this page:
What is Vitamins A & D3?
Vitamin A is a fat soluble vitamin that is required for a number of bodily functions. This vitamin is needed to maintain good vision and a healthy immune system, as well as being essential for growth and development. Vitamin A describes a group of compounds that include retinol, retinoic acid, retinal, and a number of provitamin A carotenoids such as beta-carotene. All types of vitamin A contain a beta-ionone ring with an isoprenoid chain attached which is referred to as the retinyl group. Both structures are required for vitamin activity. Vitamin D3 is the common name for cholecalciferol. Vitamin D3 can be taken as a supplement to improve overall health or used to treat osteoporosis. It can also be used to treat conditions in which vitamin D3 levels may be low, such as in people who have underactive parathyroid glands, low levels of phosphate in the blood, or hereditary conditions in which the body doesn't respond to the parathyroid hormone. Vitamin D3 also encourages the kidneys to recycle phosphate back into the blood, which helps the blood stay at the right pH.
The History of Vitamins A & D3
The earliest clues to be discovered that led to the identification of Vitamin A and its deficiency date back as far as 1819, when a physiologist called Magendie found that malnourished dogs tended to develop corneal ulcers and their risk of death was increased. In 1912, an English biochemist called Frederick Gowland Hopkins found unknown factors present in milk that were not fats, proteins or carbohydrates, but were required to aid growth in rats. Hopkins was later awarded the Nobel Prize (in 1929) for this discovery. In 1917, Elmer McCollum from the University of Wisconsin–Madison along with Lafayette Mendel and Thomas Burr Osborne from Yale University discovered one of these substances while researching the role of dietary fats. In 1918, these “accessory factors” were described as fat soluble and in 1920, they were referred to as vitamin A. As carotenoids such as beta-carotene are converted to vitamin A in the body, researchers have attempted to establish how much of the carotenoids in the diet are equal to a certain amount of retinol. The reasoning behind this was that foods could then be compared to assess their different benefits. However, the accepted values of equivalences have changed over the years. For many years, a system was used where one international unit (UI) was classed as being equivalent to 0.3 μg of retinol, 0.6 μg of beta-carotene or 1.2 μg of other provitamin A carotenoids. In subsequent years, the retinol equivalent (RE) unit was introduced. Prior to 2001, a system was used where 1 RE was equivalent to 1 μg retinol, 2 μg β-carotene dissolved in oil, 6 μg β-carotene in normal food, or 12 μg of α-carotene, γ-carotene or β-cryptoxanthin in food. However, in 2001, the US Institute of Medicine recommended the use of a new unit, referred to as the retinol activity equivalent (RAE). This was advised because studies demonstrated that the amount of provitamin-A carotenoids absorbed was only half of what it was believed to be previously. According to the new classification, one μg RAE is equal to 1 μg retinol, 2 μg of β-carotene in oil, 12 μg of beta-carotene found in the diet, or 24 μg of the provitamin-A carotenoids α-carotene, γ-carotene and β-cryptoxanthin. The Nobel prize for chemistry for 1928 was awarded to Adolf Windaus “for his studies on the constitution of the sterols and their connection with vitamins” (1), the first person to receive an award mentioning vitamins. What was the contribution Windaus made to our knowledge of vitamins that deserved the highest scientific accolade? The vitamin in question was vitamin D. It had a long history before Windaus appeared on the scene. Rickets, the bone disease caused by vitamin D deficiency, was known in antiquity and was described in detail by F. Glisson in 1650 (2). Many causes and cures for rickets had been proposed. Although cod-liver oil had been used medicinally for a long time, D. Scheutte (2) in 1824 was the first to prescribe it for the treatment of rickets. It was not until 1906 that Hopkins (3) postulated the existence of essential dietary factors necessary for the prevention of diseases such as scurvy or rickets. The first scientific approach to the disease was made by McCollum and his co-workers. In their early research (4) in 1914, they isolated a fat-soluble, nonsaponifiable factor from butterfat, necessary for normal growth and prevention of the eye disease xerophthalmia in young rats. They named this factor “fat-soluble factor A,” later “vitamin A.” The notion of a fat-soluble essential dietary factor for health led Mellanby (5) in 1919 to experiment with puppies in which he succeeded in producing a bone disease by feeding them a diet of low-fat milk and bread. He diagnosed rickets by X-ray examination, bone-calcium assay, and histology of bone, and noted that the gross appearance of the dogs was quite similar to that of rachitic children. Even adding yeast to the dogs' diet (to provide the water-soluble B-vitamins) and orange juice (to prevent scurvy), did not prevent the appearance of rickets within 3–4 mo. Rickets was prevented by the addition of butterfat to their diet or, most effectively, of cod-liver oil. He wrote: “Rickets is a deficiency disease which develops in consequence of the absence of some accessory food factor or factors. It therefore seems probable that the cause of rickets is a diminished intake of an anti-rachitic factor, which is either [McCollum's] fat-soluble factor A, or has a similar distribution to it” (5). A landmark investigation was that of Hariette Chick and her co-workers (6) who, in 1922, working with malnourished children in a clinic in post-World War I Vienna, showed that rickets prevalent in the children could be cured by whole milk or cod-liver oil.
In 1920 Hopkins (7) found that the fat-soluble factor A in butterfat could be destroyed by heating and aeration. Butterfat so treated no longer had growth-promoting activity; the rats fed the treated butterfat developed xerophthalmia and died within 40–50 d. The key experiment was performed by McCollum and his co-workers (8) in 1922, when they observed that heated, oxidized cod-liver oil could not prevent xerophthalmia but could cure rickets in the rats. “This shows that oxidation destroys fat-soluble A without destroying another substance which plays an important role in bone growth” (8). They concluded that fat-soluble factor A consisted of 2 entities, one later called “vitamin A,” the other being the newly discovered antirickets factor. Because the water-soluble factors then discovered were termed vitamin B and the known antiscurvy factor was called vitamin C, they named the new factor vitamin D. In the meantime, an entirely different cure for rickets appeared, in the role of UV light. A long-standing tradition held that fresh air and sunshine were good for the prevention of rickets. Hess and Unger (9), in 1921, put forward the explanation of their clinical observations that “seasonal incidence of rickets is due to seasonal variations of sunlight.” In her work with children, Chick and her team (6), mentioned above, observed that sunlight would cure rickets just as well as cod-liver oil. The field received a new impetus when Huldschinsky (10) in 1919 argued that, if sunlight at the seaside or in the mountains can prevent or cure rickets, then artificial sunlight, simulating light at mountain heights (“Höhensonne”) should do the same. He exposed severely rachitic children to irradiation with a quartz-mercury lamp (emitting UV light) every other day for 2 to 20 min for 2 mo and observed great improvement, including fresh calcium deposition, as revealed by X-rays. He was careful to make sure that the children had not been exposed to sunlight or received any supplements to their diet during those months. The thinking at that point was that rickets can be prevented or cured by a component of butterfat or cod-liver oil that was distinct from the fat-soluble factor A (vitamin A). It can also be cured by an entirely different process, by sunlight or UV light irradiation simulating sunlight, perhaps as the result of generally improved health. This dichotomy was jolted by the most surprising observations, made simultaneously in 1924 in 3 different laboratories. Hume and Smith (11,12) found that rats suffering from rickets induced by a low-phosphate diet (13) benefited from irradiation by UV light, not only by irradiation of the rats themselves, but also by irradiation of the “air” in the glass jars from which they had been removed and then put back after irradiation. It turned out that it was the irradiated sawdust, feces, and spilt food left in the jars, which the rats later ate, and not the air that improved the rats' rickets. Goldblatt and Soames (14) observed that livers of irradiated rats were curative when fed to rachitic rats. Steenbock and Black (15) went a step further. They argued that because liver in the living rat is activated by UV light, perhaps liver removed from the animals can also be so activated. Indeed, both liver and muscle tissue from nonirradiated rats, after removal from the body and exposed to UV light “was found to have become activated, being both growth-promoting and bone-calcifying,” when fed to nonirradiated rachitic rats. The third laboratory that simultaneously reported the imparting of antirachitic properties to inert foods, such as wheat, lettuce, or cottonseed oil, was that of Hess and Weinstock (16,17). They also showed that in linseed oil, the antirachitic properties resided in the nonsaponifiable fraction and that activation occurred by UV irradiation in the absence of oxygen (18). The discovery that irradiation of food, in particular of whole milk (containing butterfat), could impart antirachitic potency led to tremendous advances in public health. The procedure, when adopted by producers, caused a rapid decline in the prevalence of rickets in children. It was well known at that time (1924) that certain animal fats, such as butterfat or cod-liver oil, were antirachitic without irradiation. What, then, was the substance in vegetable oils that could be activated by irradiation? In 1925, Hess and his team (19) isolated sitosterol (then called phytosterol) from cottonseed oil, an abundant fraction in the nonsaponifiable portion of the oil. What appeared to the investigators to be sitosterol was inactive against rickets in rats. Upon irradiation by UV light, it became active. Similarly, cholesterol, isolated from rat brain and recrystallized to a state thought by the authors to be pure, was activated to become an antirachitic substance by irradiation. Therefore, at this time (1925), the conclusion was reached that the precursor of the active substance, susceptible to activation by UV light, was cholesterol. With amazing foresight, Hess et al. (19) proposed the hypothesis that “it would seem quite possible that the cholesterol [we now know that this is 7-dehydrocholesterol] in the skin is normally activated by UV-irradiation and rendered anti-rachitic—that the solar rays and artificial radiations can bring about this conversion. This point of view regards the superficial skin as an organ, which reacts to particular light waves rather than as a mere protective covering.” At this moment (1926) some doubts arose as to the purity of the “pure” cholesterol, convertible into the antirachitic substance. Heilbron et al. (20) had observed that the “pure” cholesterol samples showed spectroscopic absorption peaks in the UV region that could not have belonged to cholesterol. Cholesterol was known to have a single double bond and the 3 peaks found by Heilbron et al. (20) would have been due to 2 or 3 double bonds. The suspicion arose that “pure” cholesterol, as obtained from rat brain, contained a small amount of an impurity that may be the precursor of the vitamin. It was at this stage (in 1926) that A. F. Hess (in New York) asked the famous steroid chemist A. Windaus (in Göttingen, Germany) to collaborate on the question of the chemical structure of the antirachitic product formed by irradiation of the substance then thought to be cholesterol (21). A third investigator, who took part in this exceptionally amicable collaboration, was O. Rosenheim in London. Because physical methods, such as recrystallization, left the supposedly pure cholesterol unchanged, chemical methods were tried. Thus, Rosenheim and Webster, at a meeting of the Biochemical Society in London in 1926 (22) announced that “the precursor of vitamin D is not cholesterol itself, but a substance which is associated with and follows ‘chemically pure' cholesterol in all its stages of purification by the usual methods (saponification and recrystallization).” The investigators converted the “pure” cholesterol into its dibromide, recrystallized this, and recovered cholesterol upon treatment with sodium amalgam. When purified by this method, the recovered cholesterol, upon irradiation, had completely lost its antirachitic potency. The authors state (22): “According to information received from Prof. Windaus, a specimen of cholesterol [was] prepared by him at our suggestion [my italics] by the same procedure. Thus purified, cholesterol prepared in this way was no longer rendered anti-rachitic by irradiation with ultraviolet light. It is evident, therefore, that not cholesterol, but [another] substance is the immediate precursor of vitamin D.” From this report, it is clear that, in the close collaboration among Rosenheim, Hess, and Windaus, it was Rosenheim's team that performed the crucial experiment demonstrating that “pure” cholesterol contained an impurity that could be converted into the antirachitic vitamin photochemically. This was the essential clue that led to the identification of the vitamin D precursor or provitamin. Windaus and Hess (21) improved upon the chemical purification of the provitamin by the debromination of the cholesterol dibromide by zinc dust. Rosenheim and Webster (23) emphasized that the work resulted from mutual suggestions emanating from the 3 teams in London, Göttingen, and New York simultaneously, “according to a friendly arrangement.” With the discovery that “pure” cholesterol contained a small amount of an impurity that appeared to be the provitamin, the collaborative research began by the 3 groups on its identification. The impurity had the chemical properties of a steroid, being precipitable by digitonin and displayed a spectrum characteristic of the presence of 3 double bonds. Rosenheim and Webster (23) pointed out that the amount of the impurity must be very small (1:2000) and hence the vitamin itself must be biologically active in very small amounts. The work of the identification of the provitamin was greatly speeded up by the discovery of Heilbron et al. (20), already referred to, that the active impurity had 3 absorption peaks in the UV spectrum (269, 280, 293 nm). Thus, it was possible to purify the provitamin using the UV absorption peaks as a guide instead of the laborious animal tests. Windaus and Hess (21), by means of high-vacuum distillation and charcoal adsorption techniques, obtained the highly concentrated active fraction from “pure” cholesterol. Windaus and Hess (21) tested 30 different steroid preparations with more than 1 double bond from various plant sources for antirachitic activity upon irradiation. They hit upon ergosterol, a fungal steroid from ergot (Fig. 1), which when irradiated, was found to be highly active in curing rats suffering from rickets. The reasons for choosing this steroid for testing were as follows: 1) its UV spectrum matched that of the active fraction from “pure” cholesterol; 2) it was a steroid rapidly destroyed by oxidation, similar to the active fraction from cholesterol; 3) it produced the same color reaction with sulfuric acid as that fraction. Simultaneously and in consultation with Windaus and with Hess, Rosenheim and Webster (23) also determined that ergosterol was the provitamin D, convertible to vitamin D by UV irradiation.
The Top 4 Reasons You Need Vitamins A & D3
The most commonly cited lecithin benefits include:
1. Vision Support Retinal is the form of vitamin A needed for vision. When light shines on the retina, in the human eye, a molecule called rhodopsin is activated. The activated rhodopsin sends a signal to the brain that results in vision. Can you go blind from vitamin A deficiency? Vitamin A is a critical part of making the rhodopsin molecule. This is why a deficiency in vitamin A can cause night blindness and contribute to full blindness in some people — and why vitamin A is one of the most important eye vitamins. Vitamin A deficiency has been shown to play a role in xerosis of the cornea, corneal ulceration and “keratomalacia” (a full-thickness melting of the cornea that progresses rapidly to loss of the eye). Because it’s converted to retinal once consumed, a diet high in beta-carotene and other antioxidants found in plants has been shown to play a role in preventing macular degeneration, the leading cause of age-related blindness.
2. Immune Support Vitamin A is known as an immune-boosting vitamin because several immune system functions are dependent on sufficient vitamin A intake and antioxidant activity. Certain genes involved in immune responses are regulated by vitamin A. Deficiency in this vitamin can lead to increased infections and an overall weakened immune system. Vitamin A is also required for the development of T both-helper (Th) cells and B-cells. Beta-carotene supports immunity by acting as a powerful antioxidant and helpin prevent a variety of chronic illnesses. Researchers from the USDA Western Human Nutrition Research Center and Nutrition Department explain that “vitamin A deficiency impairs innate immunity by impeding normal regeneration of mucosal barriers damaged by infection, and by diminishing the function of neutrophils, macrophages, and natural killer cells.” (7) Some research suggests that in populations deficient in vitamin A, acquiring more appears to be effective in reducing cancer incidence. (8)
3. Skin Health and Cell Growth What is one of the first signs of vitamin A deficiency? Poor skin health, including dryness, breakouts, infections and irritation. Vitamin A is needed to support all of the epithelial (skin) cells both internally and externally. It is needed to form glycoproteins, a combination of sugar and protein, which help the cells bind together forming soft tissues. Due to this function, vitamin A is necessary for wound healing and skin regrowth. Because vitamin A is essential for skin health, deficiency can lead to a poor complexion even in younger people. Studies have proven that consuming vitamin A-rich foods can fight acne and improve overall skin health. Some of the best vitamin A foods for skin include berries, leafy greens, carrots and eggs, which also supply other important nutrients that protect the skin.
4. Reproductive Health While there’s some evidence that very high intake of supplemental vitamin A (leading to vitamin A toxicity) can lead to complications during pregnancy, vitamin A foods are definitely supportive of a healthy pregnancy and proper fetal development. It has been estimated that about 19 million pregnant women in low-income countries each year are affected by vitamin A deficiency, which can lead to many adverse health outcomes for both the mother and baby. (9) Among babies and children, vitamin A deficiency can also increase risk of mortality from infectious diseases due to low immune function, particularly measles, diarrhea, respiratory infections and malaria (especially in low-income countries). According to the Weston A. Price Foundation, traditional cultures emphasized that pregnant women should consume many vitamin A foods during pregnancy and while nursing, especially those with active vitamin A, such as liver, whole milk, eggs and butter. Regarding the low consumption of vitamin A-rich foods in many developed nations, the Weston A. Price Foundation website explains: “Worryingly, younger women are at particular risk. The older generation tended to eat more eggs, milk and liver, which are naturally rich in vitamin A, whereas the health-conscious youngsters on low-fat diets are relying heavily on the beta-carotene form of the nutrient.” (10) While getting active A is recommended during a woman’s reproductive years, foods with provitamin A/carotenoids can still be very healthy for pregnant or nursing women, especially green leafy vegetables and yellow/orange fruits, such as mangos and papaya.
Shocking Facts About Vitamins A & D3
You get it through diet and sunlight. Vitamin D is known as the “sunshine” vitamin because when your skin is exposed to the sun, your body manufactures it. Many people only need about 15 minutes of sun three times a week for their bodies to make adequate amounts of the vitamin, according to the National Institutes of Health. However, when you’re in a cloudy or shady area, or when you use sunscreen (which you should!) your body’s ability to make vitamin D is reduced. In addition, ethnic groups with darker skin also produce lower amounts. Fortunately, you can also get vitamin D from the food you eat. One of the best sources is fatty fish, including salmon and tuna. A 3-ounce serving of salmon contains about 450 international units (IU) of vitamin D. In addition to fish, most milk sold in the U.S. is fortified with about 100 IU per cup. Other foods that often have the nutrient added are orange juice, yogurt and breakfast cereal. The recommended dietary allowance (RDA) of vitamin D is 600 IU for people ages 1 through 70, and 800 IU for older adults. 2. It helps boost the immune system. Scientists from the University of Copenhagen recently determined that vitamin D is necessary to activate the immune system’s T-cells that identify and attack bad pathogens circulating throughout the body. Without enough of this vitamin, your body isn’t as effective in fighting infection. Your doctor may give you a blood test to determine if you have adequate levels of vitamin D in your system. If you don’t have enough of the nutrient, you may need to take a supplement, either over-the-counter or by prescription. As with any supplement, be sure to follow the doctor’s instructions carefully. It’s unusual for people to have too much of the vitamin, but it is possible. Vitamin D toxicity can lead to excess levels of calcium in the blood, which can cause nausea, vomiting and kidney problems. 3. It may help protect against chronic diseases. Not only does vitamin D help boost the immune system, research suggests it may also help protect against many autoimmune diseases, including multiple sclerosis (MS), rheumatoid arthritis and lupus. Interestingly, these diseases tend to be more prevalent in locations that are farther away from the equator, where people have less exposure to the sunlight the body needs to make vitamin D on its own. A study from the University of Toronto found that for patients who already have MS, those who took a high dose of vitamin D supplements had a decrease in relapse rates. There are also studies that show higher vitamin D intake is associated with a reduced risk of colorectal cancer. There is not enough evidence to recommend vitamin D to specifically prevent this disease, but more research is being done to examine the vitamin’s impact on this and other illnesses. 4. It is essential for strong bones and teeth. Vitamin D helps the body absorb calcium from the food you eat, which is important for normal bone growth and development. Without enough of the nutrient, bones can become brittle and soft. In fact, vitamin D deficiency is linked to osteoporosis in adults and rickets in children. 5. It might help you lose weight. A University of Minnesota clinical study found that people who started a diet with higher levels of vitamin D in their bodies were able to lose weight more successfully than people who were vitamin D-deficient, even though both groups were placed on a standardized reduced-calorie weight loss diet. Another study published in the American Journal of Clinical Nutrition featured women dieters who did not get enough calcium in their diets. It found that one group who took a calcium and vitamin D supplement as part of their diet had more fat loss than another group who did not take the supplement. If you are trying to lose weight, these studies suggest that having adequate amounts of the vitamin can help you with your efforts. Vitamin D has many benefits for the human body. Whether you get it through sunlight, diet, supplements, or a combination of all three, make sure you are receiving enough of this crucial nutrient. It’s an important part of a healthy lifestyle and diet.
Why Vitamins A & D3 Is The #1
Vitamin A is found in two primary forms: active Vitamin A and beta carotene. Active Vitamin A comes from animal-derived foods and is called retinol. This “pre-formed” Vitamin A can be used directly by the body; it does not need to first convert the Vitamin. The other type of Vitamin A, which is obtained from colorful fruits and vegetables, is in the form of “pro Vitamin A” carotenoids, which are converted to retinol by the body after the food is ingested. Beta carotene, a type of carotenoid which is found primarily in plants, needs to first be converted to active Vitamin A in order to be utilized by the body. Studies have repeatedly shown that antioxidants like Vitamin A are vital to good health and longevity; they benefit eye health, boost immunity, and foster cell growth. Nutrition experts and physicians recommend obtaining antioxidants like Vitamin A primarily by eating a well-balanced diet high in fruits, vegetables, and whole foods whenever possible, rather than from supplements. Vitamin D is a fat-soluble vitamin that is different from other vitamins because our bodies can make most of what we need with exposure to sunlight. Vitamin D is more than a vitamin in that is acts as a pro-hormone and effects hormone balance and immune regulation of the body. Most foods, unless they are fortified, are poor sources of vitamin D and there are only a small amount of vitamin D rich foods to choose from. Vitamin D plays a role in calcium absorption into the bones. A deficiency in vitamin D can result in a softening of the bones called osteomalacia or a bone abnormality called rickets. Some of the biggest vitamin D deficiency symptoms include: • Weakened immune system • Seasonal depression • Autoimmune disease • Cancer • Weak bones (osteopenia) • Skin issues eczema and psoriasis • Dementia People most prone to a vitamin D deficiency include those who live in northern regions with little sunlight exposure, people with darker skin, people on low fat diets and those taking steroids and weight loss medications. Vitamin D also helps with cell replication, and may play a role in the development of autoimmune conditions. The RDA for vitamin D is 600 IU/day and the Daily Value is 400 IU.
Top 3 Questions People Ask About Vitamins A & D3
There are a few frequently asked questions about these Vitamins A & D3.
1. What is Vitamins A? Vitamin A is a fat soluble vitamin that is required for a number of bodily functions. This vitamin is needed to maintain good vision and a healthy immune system, as well as being essential for growth and development.
2. . What is Vitamins D3? Vitamin D3 is the common name for cholecalciferol. Vitamin D3 can be taken as a supplement to improve overall health or used to treat osteoporosis. It can also be used to treat conditions in which vitamin D3 levels may be low, such as in people who have underactive parathyroid glands, low levels of phosphate in the blood, or hereditary conditions in which the body doesn't respond to the parathyroid hormone. Vitamin D3 also encourages the kidneys to recycle phosphate back into the blood, which helps the blood stay at the right pH.
3. How Is Vitamin D3 Different than Vitamin D? Vitamin D3, commonly known as the "sunshine vitamin," is cholecalciferol (coal’-i-kal-si’-fer-ul). It is either manufactured by the skin from sunlight (or the right tanning lamp) or provided as either a supplement or, modestly, by diet. Cholecalciferol is converted by the liver into a pre-hormone called Calcidiol (cal-si-die’-ol) that is then stored for use by various organs in the body. This is the substance that you want to obtain a measurement of when you order a Vitamin D3 test. The proper test is called 25(OH)D and measures the blood level of Calcidiol. The test name comes from its chemical name, 25-hydroxyvitamin D.
Tips for a Vitamins A & D3
Vitamin D is important for bones, muscles and overall health. It is made in our bodies through a series of processes that start when our skin is exposed to the sun’s ultraviolet (UV) radiation. Some Victorians are at risk of low vitamin D, particularly those with naturally very dark skin and those with little sun exposure. A balanced approach is required to ensure some sun exposure for vitamin D while minimising the risk of skin cancer.