Vitamins are obtained from the different types of foods that we consume. If a diet is lacking a certain type of nutrient, a vitamin deficiency may occur. Vitamins are organic compounds that are traditionally assigned to two groups fat-soluble (hydrophobic) or water-soluble (hydrophilic). This classification determines where they act in the body. Water-soluble vitamins act in the cytosol of cells or in extracellular fluids such as blood; fat-soluble vitamins are largely responsible for protecting cellmembranes from free radical damage. The body can synthesize some vitamins, but others must be obtained from the diet.
One major difference between fat-soluble vitamins and water-soluble vitamins is the way they are absorbed in the body. Vitamins are absorbed primarily in the small intestine and their bioavailability is dependent on the food composition of the diet. Fat-soluble vitamins are absorbed along with dietary fat. Therefore, if a meal is very low in fat, the absorption of the fat-soluble vitamins will be impaired. Once fat-soluble vitamins have been absorbed in the small intestine, they are packaged and incorporated into chylomicrons along with other fatty acids and transported in the lymphaticsystem to the bloodstream to the liver. Water-soluble vitamins on the other hand are absorbed in the small intestine but are transported to the liver through blood vessels. (Figure 9.2 “Absorption of Fat-Soluble and Water-Soluble Vitamins”).
Figure 9.2 Absorption of Fat-Soluble and Water-Soluble Vitamins
Vitamin A is a generic term for a group of similar compounds called retinoids. Retinol is the form of vitamin A found in animal-derived foods, and is converted in the body to the biologically active forms of vitamin A: retinal and retinoicacid (thus retinol is sometimes referred to as “preformed vitamin A”). About 10 percent of plant-derived carotenoids, including beta-carotene, can be converted in the body to retinoids and are another source of functional vitamin A. Carotenoids are pigments synthesized by plants that give them their yellow, orange, and red color. Over six hundred carotenoids have been identified and, with just a few exceptions, all are found in the plant kingdom. There are two classes of carotenoids—the xanthophylls, which contain oxygen, and the carotenes, which do not.
In plants, carotenoids absorb light for use in photosynthesis and act as antioxidants. Beta-carotene, alpha-carotene, and beta-cryptoxanthin are converted to some extent to retinol in the body. The other carotenoids, such as lycopene, are not. Many biological actions of carotenoids are attributed to their antioxidant activity, but they likely act by other mechanisms, too.
Vitamin A is fat-soluble and is packaged into chylomicrons in small intestine, and transported to the liver. The liverstores and exports vitamin A as needed; it is released into the blood bound to a retinol-binding protein, which transports it to cells. Carotenoids are not absorbed as well as vitamin A, but similar to vitamin A, they do require fat in the meal for absorption. In intestinal cells, carotenoids are packaged into the lipid-containing chylomicrons inside small intestine mucosal cells and then transported to the liver. In the liver, carotenoids are repackaged into lipoproteins, which transport them to cells.
The retinoids are aptly named as their most notable function is in the retina of the eye where they aid in vision, particularly in seeing under low-light conditions. This is why night blindness is the most definitive sign of vitamin A deficiency. Vitamin A has several important functions in the body, including maintaining vision and a healthy immune system. Many of vitamin A’s functions in the body are similar to the functions of hormones (for example, vitamin A can interact with DNA, causing a change in protein function). Vitamin A assists in maintaining healthy skin and the linings and coverings of tissues; it also regulates growth and development. As an antioxidant, vitamin A protects cellular membranes, helps in maintaining glutathione levels, and influences the amount and activity of enzymes that detoxifyfreeradicals.
Retinol that is circulating in the blood is taken up by cells in the eye retina, where it is converted to retinal and is used to help the pigment rhodopsin, which is involved in the eye’s ability to see under low light conditions. A deficiency in vitamin A thus results in less rhodopsin and a decrease in the detection of low-level light, a condition referred to as night-blindness.
Insufficient intake of dietary vitamin A over time can also cause complete vision loss. In fact, vitamin A deficiency is the number one cause of preventable blindness worldwide. Vitamin A not only supports the vision function of eyes but also maintains the coverings and linings of the eyes. Vitamin A deficiency can lead to the dysfunction of the linings and coverings of the eye (eg. bitot spots), causing dryness of the eyes, a condition called xerophthalmia. The progression of this condition can cause ulceration of the cornea and eventually blindness.
Figure 9.3 Bitot Spot caused by vitamin A deficiency
Malnutrition-Bitot’s Spots (foamy, bubbly spots) / Bitot’s Spots caused by vitamin A deficiency by CDC / Nutrition Program
The common occurrence of advanced xerophthalmia in children who died from infectious diseases led scientists to hypothesize that supplementing vitamin A in the diet for children with xerophthalmia might reduce disease-related mortality. In Asia in the late 1980s, targeted populations of children were administered vitamin A supplements, and the death rates from measles and diarrhea declined by up to 50 percent. Vitamin A supplementation in these deficient populations did not reduce the number of children who contracted these diseases, but it did decrease the severity of the diseases so that they were no longer fatal. Soon after the results of these studies were communicated to the rest of the world, the World Health Organization (WHO) and the United Nations Children’s Fund (UNICEF) commenced worldwide campaigns against vitamin A deficiency. UNICEF estimates that the distribution of over half a billion vitamin A capsules prevents 350,000 childhood deaths annually.
In the twenty-first century, science has demonstrated that vitamin A greatly affects the immune system. What we are still lacking are clinical trials investigating the proper doses of vitamin A required to help ward off infectious disease and how large of an effect vitamin A supplementation has on populations that are not deficient in this vitamin. This brings up one of our common themes in this text—micronutrient deficiencies may contribute to the development, progression, and severity of a disease, but this does not mean that an increased intake of these micronutrients will solely prevent or cure disease. The effect, as usual, is cumulative and depends on the diet as a whole, among other things.
Growth and Development
Vitamin A acts similarly to some hormones in that it is able to change the amount of proteins in cells by interacting with DNA. This is the primary way that vitamin A affects growth and development. Vitamin A deficiency in children is linked to growth retardation; however, vitamin A deficiency is often accompanied by protein malnutrition and iron deficiency, thereby confounding the investigation of vitamin A’s specific effects on growth and development.
In the fetal stages of life, vitamin A is important for limb, heart, eye, and ear development and in both deficiency and excess, vitamin A causes birth defects. Furthermore, both males and females require vitamin A in the diet to effectively reproduce.
Vitamin A’s role in regulating cell growth and death, especially in tissues that line and cover organs, suggests it may be effective in treating certain cancers of the lung, neck, and liver. It has been shown in some observational studies that vitamin A-deficient populations have a higher risk for some cancers. However, vitamin A supplements have actually been found to increase the risk of lung cancer in people who are at high risk for the disease (i.e., smokers, ex-smokers, workers exposed to asbestos). The Beta-Carotene and Retinol Efficacy Trial (CARET) involving over eighteen thousand participants who were at high risk for lung cancer found that people who took supplements containing very high doses of vitamin A (25,000 international units) and beta-carotene had a 28 percent higher incidence of lung cancer midway through the study, which was consequently stopped.
Vitamin A Toxicity
Vitamin A toxicity, or hypervitaminosis A, is rare. Typically it requires you to ingest ten times the RDA of preformed vitamin A in the form of supplements (it would be hard to consume such high levels from a regular diet) for a substantial amount of time, although some people may be more susceptible to vitamin A toxicity at lower doses. The signs and symptoms of vitamin A toxicity include dry, itchy skin, loss of appetite, swelling of the brain, and joint pain. In severe cases, vitamin A toxicity may cause liver damage and coma.
Vitamin A is essential during pregnancy, but doses above 3,000 micrograms per day (10,000 international units) have been linked to an increased incidence of birth defects. Pregnant women should check the amount of vitamin A contained in any prenatal or pregnancy multivitamin to assure the amount is below the UL.
Dietary Reference Intakes for Vitamin A
There is more than one source of vitamin A in the diet. There is preformed vitamin A, which is abundant in many animal-derived foods, and there are carotenoids, which are found in high concentrations in vibrantly colored fruits and vegetables and some oils.
Some carotenoids are converted to retinol in the body by intestinal cells and liver cells. However, only minuscule amounts of certain carotenoids are converted to retinol, meaning fruits and vegetables are not necessarily good sources of vitamin A.
The RDA for vitamin A includes all sources of vitamin A. The RDA for vitamin A is given in mcg of retinol activity requirements (RAE) to take into account the many different forms it is available in. The human body converts all dietary sources of vitamin A into retinol. Therefore, 1 mcg of retinol is equivalent to 12 mcg of beta-carotene, and 24 mcg of alpha-carotene or beta-cryptoxanthin. For example, 12 micrograms of fruit- or vegetable-based beta-carotene will yield 1 microgram of retinol. Currently vitamin A listed in food and on supplement labels use international units (IUs). The following conversions are listed below:
1 IU retinol = 0.3 mcg RAE
1 IU beta-carotene from dietary supplements = 0.15 mcg RAE
1 IU beta-carotene from food = 0.05 mcg RAE
1 IU alpha-carotene or beta-cryptoxanthin = 0.025 mcg RAE
The RDA for vitamin A is considered sufficient to support growth and development, reproduction, vision, and immune system function while maintaining adequate stores (good for four months) in the liver.
Preformed vitamin A is found only in foods from animals, with the liver being the richest source because that’s where vitamin A is stored (see Table 9.2 “Vitamin A Content of Various Foods”). The dietary sources of carotenoids will be given in the following text.
Table 9.2 Vitamin A Content of Various Foods, per 100 gram
In the United States, the most consumed carotenoids are alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin. See Table 9.3 “Alpha- and Beta-Carotene Content of Various Foods” for the carotenoid content of various foods.
Table 9.3 Alpha- and Beta-Carotene Content of Various Foods, per 100 gram
Vitamin A (RAE mcg)
Source: 2010. USDA National Nutrient Database for Standard Reference, Release 23. US Department of Agriculture, Agricultural Research Service. http://www.ars.usda.gov/ba/bhnrc/ndl. Accessed April 16, 2019.
VITAMIN D FUNCTIONS AND HEALTH BENEFITS
Vitamin D refers to a group of fat-soluble vitamins derived from cholesterol. Vitamins D2 (ergocalciferol) and D3 (calcitriol) are the only ones known to have biological actions in the human body. The skin synthesizes vitamin D when exposed to sunlight. In fact, for most people, more than 90 percent of their vitamin D3 comes from the casual exposure to the UVB rays in sunlight. Anything that reduces your exposure to the sun’s UVB rays decreases the amount of vitamin D3 your skin synthesizes. That would include long winters, your home’s altitude, whether you are wearing sunscreen, and the color of your skin (including tanned skin). Less than thirty minutes of sun exposure to the arms and legs will increase blood levels of vitamin D3 more than orally taking 10,000 IU (250 micrograms) of vitamin D3.
Activated vitamin D3 (calcitriol) regulates blood calcium levels in concert with parathyroidhormone. In the absence of an adequate intake of vitamin D, less than 15 percent of calcium is absorbed from foods or supplements. The effects of calcitriol on calcium homeostasis are critical for bone health. A deficiency of vitamin D in children causes the bone disease nutritional rickets. Rickets is very common among children in developing countries and is characterized by soft, weak, deformed bones that are exceptionally susceptible to fracture. In adults, vitamin D deficiency causes a similar disease called osteomalacia, which is characterized by low BMD. Osteomalacia has the same symptoms and consequences as osteoporosis and often coexists with osteoporosis. Vitamin D deficiency is common, especially in the elderly population, dark-skinned populations, and in the many people who live in the northern latitudes where sunlight exposure is much decreased during the long winter season.
Observational studies have shown that people with low levels of vitamin D in their blood have lower BMD and an increased incidence of osteoporosis. In contrast, diets with high intakes of salmon, which contains a large amount of vitamin D, are linked with better bone health. A review of twelve clinical trials, published in the May 2005 issue of the Journal of the American Medical Association, concluded that oral vitamin D supplements at doses of 700–800 international units per day, with or without coadministration of calcium supplements, reduced the incidence of hip fracture by 26 percent and other nonvertebral fractures by 23 percent. A reduction in fracture risk was not observed when people took vitamin D supplements at doses of 400 international units.
Many other health benefits have been linked to higher intakes of vitamin D, from decreased cardiovascular disease to the prevention of infection. Furthermore, evidence from laboratory studies conducted in cells, tissues, and animals suggest vitamin D prevents the growth of certain cancers, blocks inflammatory pathways, reverses atherosclerosis, increases insulin secretion, and blocks viral and bacterial infection and many other things. Vitamin D deficiency has been linked to an increased risk for autoimmune diseases. Immune diseases, rheumatoid arthritis, multiple sclerosis, and Type 1 diabetes have been observed in populations with inadequate vitamin D levels. Additionally, vitamin D deficiency is linked to an increased incidence of hypertension. The bulk of scientific evidence touting other health benefits of vitamin D is from laboratory and observational studies and requires confirmation in clinical intervention studies. The VITAL study showed that vitamin D supplementation did not reduce risk of cancer and did not reduce risk of major cardiovascular events (heart attack, stroke, or cardiovascular death considered together).
Vitamin D Toxicity
Although vitamin D toxicity is rare, too much can cause high levels of calcium concentrations or hypercalcemia. Hypercalcemia can lead to a large amount of calcium to be excreted through the urine which can cause kidney damage. Calcium deposits may also develop in soft tissues such as the kidneys, blood vessels, or other parts of the cardiovascular system. However, it is important to know that the synthesis of vitamin D from the sun does not cause vitamin D toxicity due to the skin production of vitamin D3 being a tightly regulated process.
Dietary Reference Intake for Vitamin D
The Institute of Medicine RDAs for vitamin D for different age groups is listed in Table 10.4 “Dietary Reference Intakes for Vitamin D”. For adults, the RDA is 600 international units (IUs), which is equivalent to 15 micrograms of vitamin D. The National Osteoporosis Foundation recommends slightly higher levels and that adults under age fifty get between 400 and 800 international units of vitamin D every day, and adults fifty and older get between 800 and 1,000 international units of vitamin D every day. According to the IOM, the tolerable upper intake level (UL) for vitamin D is 4,000 international units per day. Toxicity from excess vitamin D is rare, but certain diseases such as hyperparathyroidism, lymphoma, and tuberculosis make people more sensitive to the increases in calcium caused by high intakes of vitamin D.
Table 9.4 Dietary Reference Intakes for Vitamin D
Infant (0–6 months)
Infants (6–12 months)
Children (1–3 years)
Children (4–8 years)
Children (9–13 years)
Adolescents (14–18 years)
Adults (19–71 years)
Adults (> 71 years)
* denotes Adequate Intake
Source: Ross, A. C. et al. The 2011 Report on Dietary Reference Intakes for Calcium and Vitamin D from the Institute of Medicine: What Clinicians Need to Know. J Clin Endocrinol Metab. 2011; 96(1), 53–8. http://www.ncbi.nlm.nih.gov/pubmed/21118827. Accessed October 10, 2017.
Dietary Sources of Vitamin D
Table 9.5 Vitamin D Content of Various Foods, per serving size
Vitamin D (IU)
Percent Daily Value
Tuna fish, canned in water, drained
Orange juice fortified with vitamin D
Milk, nonfat, reduced fat, and whole, vitamin D- fortified
Vitamin E occurs in eight chemical forms, of which alpha-tocopherol appears to be the only form that is recognized to meet human requirements. Alpha-tocopherol and vitamin E’s other constituents are fat-soluble and primarily responsible for protecting cell membranes against lipid destruction caused by free radicals, therefore making it an antioxidant. When alpha-tocopherol interacts with a free radical it is no longer capable of acting as an antioxidant unless it is enzymatically regenerated. Vitamin C helps to regenerate some of the alpha-tocopherol, but the remainder is eliminated from the body. Therefore, to maintain vitamin E levels, you ingest it as part of your diet.
Insufficient levels are rare (signs and symptoms of such conditions are not always evident) but are primarily the result of nerve degeneration. People with malabsorption disorders, such as Crohn’s disease or cystic fibrosis, and babies born prematurely, are at higher risk for vitamin E deficiency.
Vitamin E has many other important roles and functions in the body such as boosting the immune system by helping to fight off bacteria and viruses. It also enhances the dilation of blood vessels and inhibiting the formation of blood clotting. Despite vitamin E’s numerous beneficial functions when taken in recommended amounts, large studies do not support the idea that taking higher doses of this vitamin will increase its power to prevent or reduce disease risk.
Fat in the diet is required for vitamin E absorption as it is packaged into lipid-rich chylomicrons in intestinal cells and transported to the liver. The liver stores some of the vitamin E or packages it into lipoproteins, which deliver it to cells.
Vitamin E reduces the oxidation of LDLs, and it was therefore hypothesized that vitamin E supplements would protect against atherosclerosis. However, large clinical trials have not consistently found evidence to support this hypothesis. In fact, in the “Women’s Angiographic Vitamin and Estrogen Study,” postmenopausal women who took 400 international units (264 milligrams) of vitamin E and 500 milligrams of vitamin C twice per day had higher death rates from all causes.
Other studies have not confirmed the association between increased vitamin E intake from supplements and increased mortality. There is more consistent evidence from observational studies that a higher intake of vitamin E from foods is linked to a decreased risk of dying from a heart attack.
The large clinical trials that evaluated whether there was a link between vitamin E and cardiovascular disease risk also looked at cancer risk. These trials, called the HOPE-TOO Trial and Women’s Health Study, did not find that vitamin E at doses of 400 international units (264 milligrams) per day or 600 international units (396 milligrams) every other day reduced the risk of developing any form of cancer.
Oxidative stress plays a role in age-related loss of vision, called macular degeneration. Age-related macular degeneration (AMD) primarily occurs in people over age fifty and is the progressive loss of central vision resulting from damage to the center of the retina, referred to as the macula. There are two forms of AMD, dry and wet, with wet being the more severe form.
In the dry form, deposits form in the macula; the deposits may or may not directly impair vision, at least in the early stages of the disease. In the wet form, abnormal blood vessel growth in the macula causes vision loss. Clinical trials evaluating the effects of vitamin E supplements on AMD and cataracts (clouding of the lens of an eye) did not consistently observe a decreased risk for either. However, scientists do believe vitamin E in combination with other antioxidants such as zinc and copper may slow the progression of macular degeneration in people with early-stage disease.
The brain’s high glucose consumption makes it more vulnerable than other organs to oxidative stress. Oxidative stress has been implicated as a major contributing factor to dementia and Alzheimer’s disease. Some studies suggest vitamin E supplements delay the progression of Alzheimer’s disease and cognitive decline, but again, not all of the studies confirm the relationship. A recent study with over five thousand participants published in the July 2010 issue of the Archives of Neurology demonstrated that people with the highest intakes of dietary vitamin E were 25 percent less likely to develop dementia than those with the lowest intakes of vitamin E.
More studies are needed to better assess the dose and dietary requirements of vitamin E and, for that matter, whether other antioxidants lower the risk of dementia, a disease that not only devastates the mind, but also puts a substantial burden on loved ones, caretakers, and society in general.
Vitamin E Toxicity
Currently, researchers have not found any adverse effects from consuming vitamin E in food. Although that may be the case, supplementation of alpha-tocopherol in animals has shown to cause hemorrhage and disrupt blood coagulation. Extremely high levels of vitamin E can interact with vitamin K-dependent clotting factors causing an inhibition of blood clotting.
Dietary Reference Intakes for Vitamin E
The Recommended Dietary Allowances (RDAs) and Tolerable Upper Intake Levels (ULs) for different age groups for vitamin E are given in Table 9.6 “Dietary Reference Intakes for Vitamin E”.
Vitamin E supplements often contain more than 400 international units, which is almost twenty times the RDA. The UL for vitamin E is set at 1,500 international units for adults. There is some evidence that taking vitamin E supplements at high doses has negative effects on health. As mentioned, vitamin E inhibits blood clotting and a few clinical trials have found that people taking vitamin E supplements have an increased risk of stroke. In contrast to vitamin E from supplements, there is no evidence that consuming foods containing vitamin E compromises health.
Dietary Sources of Vitamin E
Add some nuts to your salad and make your own dressing to get a healthy dietary dose of vitamin E.
Image by rawpixel.com on unsplash.com / CC0
Vitamin E is found in many foods, especially those higher in fat, such as nuts and oils. Some spices, such as paprika and red chili pepper, and herbs, such as oregano, basil, cumin, and thyme, also contain vitamin E. (Keep in mind spices and herbs are commonly used in small amounts in cooking and therefore are a lesser source of dietary vitamin E.) See Table 10.7 “Vitamin E Content of Various Foods” for a list of foods and their vitamin E contents.
Vitamin K refers to a group of fat-soluble vitamins that are similar in chemical structure. Vitamin K is critical for blood function acting as coenzymes which play an essential role in blood coagulation (aka blood clotting). Blood-clotting proteins are continuously circulating in the blood. Upon injury to a blood vessel, platelets stick to the wound forming a plug. Without vitamin K, blood would not clot.
A deficiency in vitamin K causes bleeding disorders. It is relatively rare, but people who have liver or pancreatic disease, celiac disease, or malabsorption conditions are at higher risk for vitamin K deficiency. Signs and symptoms include nosebleeds, easy bruising, broken blood vessels, bleeding gums, and heavy menstrualbleeding in women. The function of the anticoagulant drug warfarin is impaired by excess vitamin K intake from supplements. Calcium additionally plays a role in activation of blood-clotting proteins.
Vitamin K is also required for maintaining bone health. It modifies the protein osteocalcin, which is involved in the bone remodeling process. All the functions of osteocalcin and the other vitamin K-dependent proteins in bone tissue are not well understood and are under intense study. Some studies do show that people who have diets low in vitamin K also have an increased risk for bone fractures.
Dietary Reference Intake and Food Sources for Vitamin K
The AI of vitamin K for adult females is 90 micrograms per day, and for males it is 120 micrograms per day. A UL for vitamin K has not been set. The Food and Nutrition Board (FNB) has not established an UL for vitamin K because it has a low potential for toxicity. According to the FNB, “no adverse effects associated with vitamin K consumption from food or supplements have been reported in humans or animals.”
Vitamin K is present in many foods. It is found in highest concentrations in green vegetables such as broccoli, cabbage, kale, parsley, spinach, and lettuce. Additionally, vitamin K can be synthesized via bacteria in the large intestine. The exact amount of vitamin K synthesized by bacteria that is actually absorbed in the lower intestine is not known, but likely contributes less than 10 percent of the recommended intake. Newborns have low vitamin K stores and it takes time for the sterile newborn gut to acquire the good bacteria it needs to produce vitamin K. So, it has become a routine practice to inject newborns with a single intramuscular dose of vitamin K. This practice has basically eliminated vitamin K-dependent bleeding disorders in babies.
Table 9.9 Dietary Sources of Vitamin K, per serving
Vitamin K (mcg)
Percent Daily Value
Summary of Fat-soluble Vitamins
Table 9.10 Fat-Soluble Vitamins
Recommended Intake for adults
Deficiency diseases and symptoms
Groups at risk of deficiency
Vitamin A (retinol, retinal, retinoic acid,carotene, beta-carotene)
Goodman GE, et al. The Beta-Carotene and Retinol Efficacy Trial: Incidence of Lung Cancer and Cardiovascular Disease Mortality During 6-year Follow-up after Stopping Beta-Carotene and Retinol Supplements. J Natl Cancer Inst. 2004; 96(23), 1743–50. http://jnci.oxfordjournals.org/content/96/23/1743.long. Accessed October 6, 2017.
Goodman M, Bostlick RM, Kucuk O, Jones DP. Clinical trials of antioxidants as cancer prevention agents: past, present, and future. Free Radic Biol Med. 2011; 51(5), 1068–84. https://www.ncbi.nlm.nih.gov/pubmed/21683786. Accessed October 5, 2017.
Waters DD, et al. Effects of Hormone Replacement Therapy and Antioxidant Vitamin Supplements on Coronary Atherosclerosis in Postmenopausal Women: A Randomized Controlled Trial. JAMA. 2002; 288(19), 2432–40. https://jamanetwork.com/journals/jama/fullarticle/195531. Accessed October 5, 2017.
All water-soluble vitamins play a different kind of role in energy metabolism; they are required as functional parts of enzymes involved in energy release and storage. Vitamins and minerals that make up part of enzymes are referred to as coenzymes and cofactors, respectively. Coenzymes and cofactors are required by enzymes to catalyze a specific reaction. They assist in converting a substrate to an end-product. Coenzymes and cofactors are essential in catabolic pathways and play a role in many anabolic pathways too. In addition to being essential for metabolism, many vitamins and minerals are required for blood renewal and function. At insufficient levels in the diet these vitamins and minerals impair the health of blood and consequently the delivery of nutrients in and wastes out, amongst its many other functions. In this section we will focus on the vitamins that take part in metabolism, blood function and renewal.
Figure 9.7 Enzyme Active Site for Cofactors
Coenzymes and cofactors are the particular vitamin or mineral required for enzymes to catalyze a specific reaction.
Vitamin C, also commonly called ascorbic acid, is a water-soluble micronutrient essential in the diet for humans, although most other mammals can readily synthesize it. Vitamin C’s ability to easily donate electrons makes it a highly effective antioxidant. It is effective in scavenging reactive oxygen species, reactive nitrogen species, and many other free radicals. It protects lipids both by disabling free radicals and by aiding in the regeneration of vitamin E.
In addition to its role as an antioxidant, vitamin C is a required part of several enzymes like signaling molecules in the brain, some hormones, and amino acids. Vitamin C is also essential for the synthesis and maintenance of collagen. Collagen is the most abundant protein in the body and used for different functions such as the structure for ligaments, tendons, and blood vessels and also scars that bind wounds together. Vitamin C acts as the glue that holds the collagen fibers together and without sufficient levels in the body, collagen strands are weak and abnormal. (Figure 9.8 “The Role of Vitamin C in Collagen Synthesis”)
Figure 9.8 The Role of Vitamin C in Collagen Synthesis
Vitamin C levels in the body are affected by the amount in the diet, which influences how much is absorbed and how much the kidney allows to be excreted, such that the higher the intake, the more vitamin C is excreted. Vitamin C is not stored in any significant amount in the body, but once it has reduced a free radical, it is very effectively regenerated and therefore it can exist in the body as a functioning antioxidant for many weeks.
The classic condition associated with vitamin C deficiency is scurvy. The signs and symptoms of scurvy include skin disorders, bleeding gums, painful joints, weakness, depression, and increased susceptibility to infections. Scurvy is prevented by having an adequate intake of fruits and vegetables rich in vitamin C.
Figure 9.9 Bleeding Gums Associated with Scurvy
Vitamin C’s ability to prevent disease has been debated for many years. Overall, higher dietary intakes of vitamin C (via food intake, not supplements), are linked to decreased disease risk. A review of multiple studies published in the April 2009 issue of the Archives of Internal Medicine concludes there is moderate scientific evidence supporting the idea that higher dietary vitamin C intakes are correlated with reduced cardiovascular disease risk, but there is insufficient evidence to conclude that taking vitamin C supplements influences cardiovascular disease risk. Vitamin C levels in the body have been shown to correlate well with fruit and vegetable intake, and higher plasma vitamin C levels are linked to reduced risk of some chronic diseases. In a study involving over twenty thousand participants, people with the highest levels of circulating vitamin C had a 42 percent decreased risk for having a stroke.
There is some evidence that a higher vitamin C intake is linked to a reduced risk of cancers of the mouth, throat, esophagus, stomach, colon, and lung, but not all studies confirm this is true. As with the studies on cardiovascular disease, the reduced risk of cancer is the result of eating foods rich in vitamin C, such as fruits and vegetables, not from taking vitamin C supplements. In these studies, the specific protective effects of vitamin C cannot be separated from the many other beneficial chemicals in fruits and vegetables.
Vitamin C does have several roles in the immune system, and many people increase vitamin C intake either from diet or supplements when they have a cold. Many others take vitamin C supplements routinely to prevent colds. Contrary to this popular practice, however, there is no good evidence that vitamin C prevents a cold. A review of more than fifty years of studies published in 2004 in the Cochrane Database of Systematic Reviews concluded that taking vitamin C routinely does not prevent colds in most people, but it does slightly reduce cold severity and duration. Moreover, taking megadoses (up to 4 grams per day) at the onset of a cold provides no benefits.
Gout is a disease caused by elevated circulating levels of uric acid and is characterized by recurrent attacks of tender, hot, and painful joints. There is some evidence that a higher intake of vitamin C reduces the risk of gout.
Vitamin C Toxicity
High doses of vitamin C have been reported to cause numerous problems, but the only consistently shown side effects are gastrointestinal upset and diarrhea. To prevent these discomforts the IOM has set a UL for adults at 2,000 milligrams per day (greater than twenty times the RDA).
At very high doses in combination with iron, vitamin C has sometimes been found to increase oxidative stress, reaffirming that getting your antioxidants from foods is better than getting them from supplements, as that helps regulate your intake levels. There is some evidence that taking vitamin C supplements at high doses increases the likelihood of developing kidney stones, however, this effect is most often observed in people that already have multiple risk factors for kidney stones.
Dietary Reference Intakes for Vitamin C
The RDAs and ULs for different age groups for vitamin C are listed in Table 9.11 “Dietary Reference Intakes for Vitamin C”. They are considered adequate to prevent scurvy. Vitamin C’s effectiveness as a free radical scavenger motivated the Institute of Medicine (IOM) to increase the RDA for smokers by 35 milligrams, as tobacco smoke is an environmental and behavioral contributor to free radicals in the body.
Table 9.11 Dietary Reference Intakes for Vitamin C
Citrus fruits are great sources of vitamin C and so are many vegetables. In fact, British sailors in the past were often referred to as “limeys” as they carried sacks of limes onto ships to prevent scurvy. Vitamin C is not found in significant amounts in animal-based foods.
Because vitamin C is water-soluble, it leaches away from foods considerably during cooking, freezing, thawing, and canning. Up to 50 percent of vitamin C can be boiled away. Therefore, to maximize vitamin C intake from foods, you should eat fruits and vegetables raw or lightly steamed. For the vitamin C content of various foods, see Table 9.12 “Vitamin C Content of Various Foods”.
Table 9.12 Vitamin C Content of Various Foods, per serving
Thiamin is especially important in glucose metabolism. It acts as a cofactor for enzymes that break down glucose for energy production (Figure 9.7 “Enzyme Active Site for Cofactors” ). Thiamin plays a key role in nerve cells as the glucose that is catabolized by thiamin is needed for an energy source. Additionally, thiamin plays a role in the synthesis of neurotransmitters and is therefore required for RNA, DNA, and ATP synthesis.
The brain and heart are most affected by a deficiency in thiamin. Thiamin deficiency, also known as beriberi, can cause symptoms of fatigue, confusion, movement impairment, pain in the lower extremities, swelling, and heart failure. It is prevalent in societies whose main dietary staple is white rice. During the processing of white rice, the bran is removed, along with what were called in the early nineteenth century, “accessory factors,” that are vital for metabolism. Dutch physician Dr. Christiaan Eijkman cured chickens of beriberi by feeding them unpolishedricebran in 1897. By 1912, Sir Frederick Gowland Hopkins determined from his experiments with animals that the “accessory factors,” eventually renamed vitamins, are needed in the diet to support growth, since animals fed a diet of pure carbohydrates, proteins, fats, and minerals failed to grow. Eijkman and Hopkins were awarded the Nobel Prize in Physiology (or Medicine) in 1929 for their discoveries in the emerging science of nutrition.
Another common thiamin deficiency known as Wernicke-Korsakoff syndrome can cause similar symptoms as beriberi such as confusion, lossofcoordination, visionchanges, hallucinations, and may progress to coma and death. This condition is specific to alcoholics as diets high in alcohol can cause thiamin deficiency. Other individuals at risk include individuals who also consume diets typically low in micronutrients such as those with eating disorders, elderly, and individuals who have gone through gastric bypass surgery.
The RDAs and ULs for different age groups for thiamin are listed in Table 9.13 “Dietary Reference Intakes for Thiamin”. There is no UL for thiamin because there has not been any reports on toxicity when excess amounts are consumed from food or supplements.
Whole grains, meat and fish are great sources of thiamin. The United States as well as many other countries, fortify their refined breads and cereals. For the thiamin content of various foods, see Table 9.14 “Thiamin Content of Various Foods”.
Table 9.14 Thiamin Content of Various Foods, per serving
Riboflavin is an essential component of flavoproteins, which are coenzymes involved in many metabolic pathways of carbohydrate, lipid, and protein metabolism. Flavoproteins aid in the transfer of electrons in the electron transport chain. Furthermore, the functions of other B-vitamin coenzymes, such as vitamin B6 and folate, are dependent on the actions of flavoproteins. The “flavin” portion of riboflavin gives a bright yellow color to riboflavin, an attribute that helped lead to its discovery as a vitamin. When riboflavin is taken in excess amounts (supplement form) the excess will be excreted through your kidneys and show up in your urine. Although the color may alarm you, it is harmless. There are no adverse effects of high doses of riboflavin from foods or supplements that have been reported.
Riboflavin deficiency, sometimes referred to as ariboflavinosis, is often accompanied by other dietary deficiencies (most notably protein) and can be common in people that suffer from alcoholism. This deficiency will usually also occur in conjunction with deficiencies of other B vitamins because the majority of B vitamins have similar food sources. Its signs and symptoms include dry, scaly skin, cracking of the lips and at the corners of the mouth, sore throat, itchy eyes, and light sensitivity.
Dietary Reference Intakes
The RDAs for different age groups for riboflavin are listed in Table 9.15 “Dietary Reference Intakes for Riboflavin”. There is no UL for riboflavin because no toxicity has been reported when an excess amount has been consumed through foods or supplements.
Table 9.15 Dietary Reference Intakes for Riboflavin
Riboflavin can be found in a variety of different foods but it is important to remember that it can be destroyed by sunlight. Milk is one of the best sources of riboflavin in the diet and was once delivered and packaged in glass bottles. This packaging has changed to cloudy plastic containers or cardboard to help block the light from destroying the riboflavin in milk. For the riboflavin content of various foods, see Table 9.16 Riboflavin Content of Various Foods”.
Table 9.16 Riboflavin Content of Various Foods, per serving
Niacin is a component of the coenzymes NADH and NADPH, which are involved in the catabolism and/or anabolism of carbohydrates, lipids, and proteins. NADH is the predominant electron carrier and transfers electrons to the electron-transport chain to make ATP. NADPH is also required for the anabolicpathways of fatty-acid and cholesterol synthesis. In contrast to other vitamins, niacin can be synthesized by humans from the amino acid tryptophan in an anabolic process requiring enzymes dependent on riboflavin, vitamin B6, and iron. Niacin is made from tryptophan only after tryptophan has met all of its other needs in the body. The contribution of tryptophan-derived niacin to niacin needs in the body varies widely and a few scientific studies have demonstrated that diets high in tryptophan have very little effect on niacin deficiency. Niacin deficiency is commonly known as pellagra and the symptoms include fatigue, decreased appetite, and indigestion. These symptoms are then commonly followed by the four D’s: diarrhea, dermatitis, dementia, and sometimes death.
The RDAs and ULs for different age groups for Niacin are listed in Table 9.17 “Dietary Reference Intakes for Niacin”. Because Niacin needs can be met from tryptophan, The RDA is expressed in niacin equivalents (NEs). The conversions of NE, Niacin, and tryptophan are: 1 mg NE= 60 mg tryptophan= 1 mg niacin
Niacin can be found in a variety of different foods such as yeast, meat, poultry, red fish, and cereal. In plants, especially mature grains, niacin can be bound to sugar molecules which can significantly decrease the niacin bioavailability. For the niacin content of various foods, see Table 9.18 “Niacin Content of Various Foods”.
Table 9.18 Niacin Content of Various Foods, per serving
Pantothenic acid forms coenzyme A, which is the main carrier of carbon molecules in a cell. Acetyl-CoA is the carbon carrier of glucose, fatty acids, and amino acids into the citric acid cycle (Figure 9.14“Pantothenic Acid’s Role in the Citric Acid Cycle”). Coenzyme A is also involved in the synthesis of lipids, cholesterol, and acetylcholine (a neurotransmitter). A Pantothenic Acid deficiency is exceptionally rare. Signs and symptoms include fatigue, irritability, numbness, muscle pain, and cramps. Pantothenic acid can be seen on many ingredients lists for skin and hair care products; however there is no good scientific evidence that pantothenic acid improves human skin or hair.
Figure 9.14 Pantothenic Acid’s Role in the Citric Acid Cycle
Pantothenic Acid (Vitamin B5) makes up coenzyme A, which carries the carbons of glucose, fatty acids, and amino acids into the citric acid cycle as Acetyl-CoA.
Dietary Reference Intakes
Because there is little information on the requirements for pantothenic acids, the Food and Nutrition Board (FNB) has developed Adequate Intakes (AI) based on the observed dietary intakes in healthy population groups. The AI for different age groups for pantothenic acid are listed in Table 9.19 “Dietary Reference Intakes for Pantothenic Acid “.
Table 9.19 Dietary Reference Intakes for Pantothenic Acid
AI Males and Females mg/day)
Infants (0–6 months)
Infants (7–12 months)
Children (1–3 years)
Children (4–8 years)
Children (9–13 years)
Adolescents (14–18 years)
Adults (> 19 years)
Micronutrient Information Center: Pantothenic Acid. Oregon State University, Linus Pauling Institute. http://lpi.oregonstate.edu/mic/vitamins/patothenic-acid . Updated in July 2013. Accessed October 22, 2017.
Pantothenic Acid is widely distributed in all types of food, which is why a deficiency in this nutrient is rare. Pantothenic Acid gets its name from the greek word “pantothen” which means “from everywhere”. For the pantothenic acid content of various foods, see Table 9.20 Pantothenic Acid Content of Various Foods”.
Table 9.20 Pantothenic Acid Content of Various Foods, per serving
Pantothenic Acid (mg)
Percent Daily Value
Yogurt, plain nonfat
Whole wheat bread
Micronutrient Information Center: Pantothenic Acid. Oregon State University, Linus Pauling Institute. http://lpi.oregonstate.edu/mic/vitamins/patothenic-acid . Updated in July 2013. Accessed October 22, 2017.
Biotin (Vitamin H or B8)
Biotin is required as a coenzyme in the citric acid cycle and in lipid metabolism. It is also required as an enzyme in the synthesis of glucose and some nonessential amino acids. A specific enzyme, biotinidase, is required to release biotinfrom protein so that it can be absorbed in the gut. There is some bacterial synthesis of biotin that occurs in the colon; however this is not a significant source of biotin. Biotin deficiency is rare, but can be caused by eating large amounts of egg whites over an extended period of time. This is because a protein in egg whites tightly binds to biotin making it unavailable for absorption. A rare genetic disease-causing malfunction of the biotinidase enzyme also results in biotin deficiency. Symptoms of biotin deficiency are similar to those of other B vitamins, but may also include hair loss when severe.
Dietary Reference Intakes
Because there is little information on the requirements for biotin, the FNB has developed Adequate Intakes (AI) based on the observed dietary intakes in healthy population groups. The AI for different age groups for biotin are listed in Table 9.21 “Dietary Reference Intakes for Biotin”.
Vitamin B6 is the coenzyme involved in a wide variety of functions in the body. One major function is the nitrogen transfer between amino acids which plays a role in amino-acid synthesis and catabolism. Also, it functions to release glucose from glycogen in the catabolic pathway of glycogenolysis and is required by enzymes for the synthesis of multiple neurotransmitters and hemoglobin (Figure 9.15 “The Function of Vitamin B6 in Amino Acid Metabolism”).
Vitamin B6 is also a required coenzyme for the synthesis of hemoglobin. A deficiency in vitamin B6 can cause anemia, but it is of a different type than that caused by insufficient folate, cobalamin, or iron; although the symptoms are similar. The size of red blood cells is normal or somewhat smaller but the hemoglobin content is lower. This means each red blood cell has less capacity for carrying oxygen, resulting in muscle weakness, fatigue, and shortness of breath. Other deficiency symptoms of vitamin B6 can cause dermatitis, mouth sores, and confusion.
Figure 9.15 The Function of Vitamin B6 in Amino Acid Metabolism
Vitamin B6 coenzyme is essential for the conversion of amino acid methionine into cysteine. With low levels of Vitamin B6, homocysteine will build up in the blood. High levels of homocysteine increases the risk for heart disease.
Vitamin B6 Toxicity
Currently, there are no adverse effects that have been associated with a high dietary intake of vitamin B6, but large supplemental doses can cause severe nerve impairment. To prevent this from occurring, the UL for adults is set at 100 mg/day.
Dietary Reference Intakes
The RDAs and ULs for different age groups for vitamin B6 are listed in Table 9.23 “Dietary Reference Intakes for Vitamin B6“.
Table 9.23 Dietary Reference Intakes for Vitamin B6
Vitamin B6 can be found in a variety of foods. The richest sources include fish, beef liver and other organ meats, potatoes, and other starchy vegetables and fruits. For the Vitamin B6 content of various foods, see Table 9.24 Vitamin B6 Content of Various Foods”.
Folate is a required coenzyme for the synthesis of the amino acid methionine, and for making RNA and DNA. Therefore, rapidly dividing cells are most affected by folate deficiency. Red blood cells, white blood cells, and platelets are continuously being synthesized in the bone marrow from dividing stem cells. When folate is deficient, cells cannot divide normally A consequence of folate deficiency is macrocytic or megaloblastic anemia. Macrocytic and megaloblastic mean “big cell,” and anemia refers to fewer red blood cells or red blood cells containing less hemoglobin. Macrocytic anemia is characterized by larger and fewer red blood cells. It is caused by red blood cells being unable to produce DNA and RNA fast enough—cells grow but do not divide, making them large in size. (Figure 9.17 “Folate and the Formation of Macrocytic Anemia”)
Figure 9.17 Folate and the Formation of Macrocytic Anemia
Folate is especially essential for the growth and specialization of cells of the central nervous system. Children whose mothers were folate-deficient during pregnancy have a higher risk of neural-tube birth defects. Folate deficiency is causally linked to the development of spina bifida, a neural-tube defect that occurs when the spine does not completely enclose the spinal cord. Spina bifida can lead to many physical and mental disabilities (Figure 9.18 “Spina Bifida in Infants” ). Observational studies show that the prevalence of neural-tube defects was decreased after the fortification of enriched cereal grain products with folate in 1996 in the United States (and 1998 in Canada) compared to before grain products were fortified with folate.
Additionally, results of clinical trials have demonstrated that neural-tube defects are significantly decreased in the offspring of mothers who began taking folate supplements one month prior to becoming pregnant and throughout the pregnancy. In response to the scientific evidence, the Food and Nutrition Board of the Institute of Medicine (IOM) raised the RDA for folate to 600 micrograms per day for pregnant women. Some were concerned that higher folate intakes may cause colon cancer, however scientific studies refute this hypothesis.
Figure 9.18 Spina Bifida in Infants
Spina bifida is a neural-tube defect that can have severe health consequences.
Dietary Reference Intakes
The RDAs and ULs for different age groups for folate are listed in Table 9.25 “Dietary Reference Intakes for Folate”. Folate is a compound that is found naturally in foods. Folic acid however is the chemical structure form that is used in dietary supplements as well as enriched foods such as grains. The FNB has developed dietary folate equivalents (DFE) to reflect the fact that folic acid is more bioavailable and easily absorbed than folate found in food. The conversions for the different forms are listed below.
1 mcg DFE = 1 mcg food folate
1mcg DFE = 0.6 mcg folic acid from fortified foods or dietary supplements consumed with foods
1 mcg DFE = 0.5 mcg folic acid from dietary supplements taken on an empty stomach
Folate is found naturally in a wide variety of food especially in dark leafy vegetables, fruits, and animal products. The U.S. Food and Drug Administration (FDA) began requiring manufacturers to fortify enriched breads, cereals, flours, and cornmeal to increase the consumption of folate in the American diet. For the folate content of various foods, see Table 9.26 “Folate Content of Various Foods”.
Vitamin B12 contains cobalt, making it the only vitamin that contains a metal ion. Vitamin B12 is an essential part of coenzymes. It is necessary for fat and protein catabolism, for folate coenzyme function, and for hemoglobin synthesis. An enzyme requiring vitamin B12 is needed by a folate-dependent enzyme to synthesize DNA. Thus, a deficiency in vitamin B12 has similar consequences to health as folate deficiency. In children and adults vitamin B12 deficiency causes macrocytic anemia, and in babies born to cobalamin-deficient mothers there is an increased risk for neural-tubedefects. In order for the human body to absorb vitamin B12, the stomach, pancreas, and small intestine must be functioning properly. Cells in the stomach secrete a protein called intrinsic factor that is necessary for vitamin B12 absorption, which occurs in the small intestine. Impairment of secretion of this protein either caused by an autoimmune disease or by chronic inflammation of the stomach (such as that occurring in some people with H.pylori infection), can lead to the disease pernicious anemia, a type of macrocytic anemia. Vitamin B12 malabsorption is most common in the elderly, who may have impaired functioning of digestive organs, a normal consequence of aging. Pernicious anemia is treated by large oral doses of vitamin B12 or by putting the vitamin under the tongue, where it is absorbed into the bloodstream without passing through the intestine. In patients that do not respond to oral or sublingual treatment vitamin B12 is given by injection.
Vitamin B12 Relationship with Folate and Vitamin B6
Vitamin B12 and folate play key roles in converting homocysteine to amino acid methionine. As mentioned in Figure 9.19 “ Vitamin B6 Functional Coenzyme Role”, high levels of homocysteine in the blood increases the risk for heart disease. Low levels of vitamin B12, folate or vitamin B6 will increase homocysteine levels therefore increasing the risk of heart disease.
Figure 9.20 The Relationship Between Folate and Vitamin B12
When there is a deficiency in vitamin B12 , inactive folate (from food) is unable to be converted to active folate and used in the body for the synthesis of DNA. Folic Acid however (that comes from supplements or fortified foods) is available to be used as active folate in the body without vitamin B12. Therefore, if there is a deficiency in vitamin B12 macrocytic anemia may occur. With the fortification of foods incorporated into people’s diets, the risk of an individual developing macrocytic anemia is decreased.
Dietary Reference Intakes
The RDAs and ULs for different age groups for Vitamin B12 are listed in Table 9.27 “Dietary Reference Intakes for Vitamin B12.
Table 9.27 Dietary Reference Intakes for Vitamin B12
Vitamin B12 is found naturally in animal products such as fish, meat, poultry, eggs, and milk products. Although vitamin B12 is not generally present in plant foods, fortified breakfast cereals are also a good source of vitamin B12. For the vitamin B12 content of various foods, see Table 9.28 “Vitamin B12 Content of Various Foods”.
Choline is a water-soluble substance that is not classified as a vitamin because it can be synthesized by the body. However, the synthesis of choline is limited and therefore it is recognized as an essential nutrient. Choline is needed to perform functions such as the synthesis of neurotransmitter acetylcholine, the synthesis of phospholipids used to make cell membranes, lipid transport, and also homocysteine metabolism. A deficiency in choline may lead to interfered brain development in the fetus during pregnancy, and in adults cause fatty liver and muscledamage.
Dietary Reference Intakes
There is insufficient data on choline so the FNB has developed AIs for all ages in order to prevent fatty liver disease. The AI and UL for different age groups for choline are listed in Table 9.29 “Dietary Reference Intakes for Choline”.
Choline can be found in a variety of different foods. The main dietary sources of choline in the United States consist of primarily animal based products. For the Choline content of various foods, see Table 9.30 “Choline Content of Various Foods”.
Egg yolk, wheat, meat, fish, synthesis in the body
Synthesis of neurotransmitters and cell membranes, lipid transport
Non-alcoholic fatty liver disease, muscle damage, interfered brain development in fetus
Liver damage, excessive sweating, hypotension
Do B-Vitamins Supplements Provide an Energy Boost?
Although some marketers claim taking a vitamin that contains one-thousand times the daily value of certain B vitamins boosts energy and performance, this is a myth that is not backed by science. The “feeling” of more energy from energy-boosting supplements stems from the high amount of added sugars, caffeine, and other herbal stimulants that accompany the high doses of B vitamins. As discussed, B vitamins are needed to support energy metabolism and growth, but taking in more than required does not supply you with more energy. A great analogy of this phenomenon is the gas in your car. Does it drive faster with a half-tank of gas or a full one? It does not matter; the car drives just as fast as long as it has gas. Similarly, depletion of B vitamins will cause problems in energy metabolism, but having more than is required to run metabolism does not speed it up. Buyers of B-vitamin supplements beware; B vitamins are not stored in the body and all excess will be flushed down the toilet along with the extra money spent.
B vitamins are naturally present in numerous foods, and many other foods are enriched with them. In the United States, B-vitamin deficiencies are rare; however in the nineteenth century some vitamin-B deficiencies plagued many people in North America. Niacin deficiency, also known as pellagra, was prominent in poorer Americans whose main dietary staple was refined cornmeal. Its symptoms were severe and included diarrhea, dermatitis, dementia, and even death. Some of the health consequences of pellagra are the result of niacin being in insufficient supply to support the body’s metabolic functions.
Myint PK, et al. Plasma Vitamin C Concentrations Predict Risk of Incident Stroke Over 10 Years in 20,649 Participants of the European Prospective Investigation into Cancer, Norfolk Prospective Population Study. Am J Clin Nutr. 2008; 87(1), 64–69. http://www.ajcn.org/content/87/1/64.long. Accessed September 22, 2017.
The market is flooded with advertisements for “super antioxidant” supplements teeming with molecules that block free radical production, stimulate the immune system, prevent cancer, and reduce the signs of aging. Based on the antioxidant-supplement industry’s success, the general public appears to believe these health claims. However, these claims are not backed by scientific evidence; rather, there is some evidence suggesting supplements can actually cause harm. While scientists have found evidence supporting the consumption of antioxidant-rich foods as a method of reducing the risk of chronic disease, there is no “miracle cure”; no pill or supplement alone can provide the same benefits as a healthy diet. Remember, it is the combination of antioxidants and other nutrients in healthy foods that is beneficial. In this section, particular antioxidants functioning in the body are reviewed, to understand how they work together to protect the body against free radicals, and to explore the best nutrient-rich dietary sources of antioxidants. One dietary source of antioxidants is vitamins. In the discussion of antioxidant vitamins, the focus will be on vitamins E, C, and A.
There are many different antioxidants in food, including selenium, which is one of the majorantioxidants. However, the antioxidants you may be the most familiar with are vitamins. The “big three” vitamin antioxidants are vitamins E, A, and C, although it may be that they are called the “big three” only because they are the most studied.
Table 9.32 Some Antioxidants Obtained from Diet and Their Related Functions
While our bodies have acquired multiple defenses against free radicals, we also use free radicals to support its functions. For example, the immune system uses the cell-damaging properties of free radicals to kill pathogens. First, immune cells engulf an invader (such as a bacterium), then they expose it to free radicals such as hydrogen peroxide, which destroys its membrane. The invader is thus neutralized. Scientific studies also suggest hydrogen peroxide acts as a signaling molecule that calls immune cells to injury sites, meaning free radicals may aid with tissue repair when you get cut.
Free radicals are necessary for many other bodily functions as well. The thyroid gland synthesizes its own hydrogen peroxide, which is required for the production of thyroid hormone. Reactive oxygen species and reactive nitrogen species, which are free radicals containing nitrogen, have been found to interact with proteins in cells to produce signaling molecules. The free radical nitric oxide has been found to help dilate blood vessels and act as a chemical messenger in the brain. By acting as signaling molecules, free radicals are involved in the control of their own synthesis, stress responses, regulation of cell growth and death, and metabolism.
Sources of Free Radicals in the Environment
Substances and energy sources from the environment can add to or accelerate the production of free radicals within the body. Exposure to excessive sunlight, ozone, smoke, heavy metals, ionizing radiation, asbestos, and other toxic chemicals increase the amount of free radicals in the body. They do so by being free radicals themselves or by adding energy that provokes electrons to move between atoms. Excessive exposure to environmental sources of free radicals can contribute to disease by overwhelming the free radical detoxifying systems and those processes involved in repairing oxidative damage.
Oxidative stress refers to an imbalance in any cell, tissue, or organ between the amount of free radicals and the capabilities of the detoxifying and repair systems. Sustained oxidative damage results only under conditions of oxidative stress—when the detoxifying and repair systems are insufficient. Free radical-induced damage, when left unrepaired, destroys lipids, proteins, RNA, and DNA, and can contribute to disease. Oxidative stress has been implicated as a contributing factor to cancer, atherosclerosis (hardening of arteries), arthritis, diabetes, kidney disease, Alzheimer’s disease, Parkinson’s disease, schizophrenia, bipolar disorder, emphysema, and cataracts.
Aging is a process that is genetically determined but modulated by factors in the environment. In the process of aging, tissue function declines. The idea that oxidative stress is the primary contributor to age-related tissue decline has been around for decades, and it is true that tissues accumulate free radical-induced damage as we age. Recent scientific evidence slightly modifies this theory by suggesting oxidative stress is not the initial trigger for age-related decline of tissues; it is suggested that the true culprit is progressive dysfunction of metabolic processes, which leads to increases in free radical production, thus influencing the stress response of tissues as they age.
Phytochemicals are chemicals in plants that may provide some health benefit. Carotenoids are one type of phytochemical. Phytochemicals also include indoles, lignans, phytoestrogens, stanols, saponins, terpenes, flavonoids, carotenoids, anthocyanidins, phenolic acids, and many more. They are found not only in fruits and vegetables, but also in grains, seeds, nuts, and legumes. Many phytochemicals act as antioxidants, but they have several other functions, such as mimicking hormones, altering absorption of cholesterol, inhibiting inflammatory responses, and blocking the actions of certain enzymes.
Phytochemicals are present in small amounts in the food supply, and although thousands have been and are currently being scientifically studied, their health benefits remain largely unknown. Also largely unknown is their potential for toxicity, which could be substantial if taken in large amounts in the form of supplements. Moreover, phytochemicals often act in conjunction with each other and with micronutrients. Thus, supplementing with only a few may impair the functions of other phytochemicals or micronutrients. As with the antioxidant vitamins, it is the mixture and variety of phytochemicals in foods that are linked to health benefits.
Chapter 13 Lifespan Nutrition From Pregnancy to the Toddler Years
Chapter 14 Lifespan Nutrition During Childhood and Adolescence
Chapter 15 Lifespan Nutrition in Adulthood
Chapter 17 Food Safety
Chapter 18 Nutritional Issues
Chapters and sections were borrowed and adapted from the above existing OER textbooks on human nutrition. Without these foundational texts, a lot more work would have been required to complete this project. Thank you to those who shared before us.