Research is fairly new regarding amount of B2 stored on the body (last 4 years). They have not quantified the amount yet, but the fact that it takes over 3 months to create a deficiency when animals are fed a purified diet suggests the stores are very high. You can create a deficiency of folic acid or B12, both stored in the liver in small quantities, in about 1-2 weeks, depending on circumstances of course. The other B vitamins that are not stored create a deficiency the very day they are not supplied by either food, supplement form or activated by other vitamins. You also correct those deficiencies the day you take or activate them. But correcting a B2 deficiency can take weeks, see information below.
The compound riboflavin or vitamin B2 as it is known is vital for the formation of two substances involved in the efficient utilization and biochemical conversion of the calories derived from the proteins, the fats and carbohydrates in food into a form that can be used by cells: riboflavin is found in flavin adenine dinucleotide (FAD) and in flavin mononucleotide (FMN); both compounds are part of the electron transport chain in the mitochondria. The energy levels in the body are reduced by a lack of riboflavin in the body. The formation of skin, nails and hair requires the presence of riboflavin.
Significant effects on the metabolism of the carbohydrates, fats and protein result from the existence of a riboflavin deficiency in the body. To be properly utilized in the human body, all these three basic food elements will require riboflavin for their bio-chemical conversion into usable metabolic energy. The utilization of carbohydrate decreases when there is insufficient riboflavin in the body, this may result in an increase in the consumption of carbohydrates as the human body tells itself to increase the intake of carbohydrates correct the diminished efficiency in carbohydrate metabolism.
The utilization of proteins also falls away in the even on a deficiency in the vitamin B2. A deficiency of riboflavin can lead to the greater excretion of proteins in the urine. The increased urinary output may also lead to the excretion of riboflavin along with the proteins in the urine, a vicious cycle begins as more protein has to be excreted and more riboflavin is released from the body - increasing the state of deficiency.
The human bodys requirement for riboflavin is also increased by high consumption of dietary fats. The fat will be deposited in the liver, in the kidneys, in the adrenal glands and along the arterial walls if insufficient riboflavin is supplied to handle the fat component of the diet.
A deficiency of riboflavin in the human body leads to a disruption in the activity of the thyroid gland and can induce birth defects in babies - defects that affect the nervous system, the skin, the skeletal system and the vascular system in general. The capacity to learn diminishes in young animals that suffer from a riboflavin deficiency during the developmental stages. A riboflavin deficiency in young developing animals have lasting effects as supplying adequate levels of riboflavin to older animals does not restore the capacity to learn to normal levels.
Physical symptoms such as inflammation in the tongue, in the lips or in the mouth can start to affect a person whose riboflavin demands in the metabolic process of the body exceeds the supply of the vitamin in the diet. Physical symptoms can also include eyes that become extremely sensitive to light and which burn or itch all the time, appearing bloodshot and teary at all times. Symptoms such as seborrheic - greasy scaling - dermatitis, begins to be apparent in the areas around the lips and the nose, in the skin around the eyes, in the skin behind the ears and in the scrotal sack. Many other factors can cause any of these physical symptoms. A riboflavin deficiency is indicated when all these symptoms affect a person at one time and the diet of the person is poor in nutrients.
The greatest importance must be paid to the changes in the skin that occur in and around the eyes. The eyes of animals can be affected by opacities as a result of riboflavin deficiency; these changes in the eyes are similar to the problems caused by cataracts in people. A riboflavin deficiency leads to the development of corneal opacity in some people. A test was conducted by doctors on twenty two people affected by cataracts, during these tests the doctors found that eight of these patients suffered from deficiencies of riboflavin at the cellular level.
Psychiatric disturbances can also be induced by a riboflavin (vitamin B2) deficiency. Six young men were maintained on a riboflavin deficient diet during a riboflavin deficiency study carried out under 24 hour medical supervision - the men were given whole sets of psychological tests during the trial. The young men experienced very significant levels of psychological change as soon as the deficiency started to manifest itself in the body. The young men became depressed and suffered from an increase in lethargy. Some of them complained about suffering from imaginary pains and illnesses - a medical condition called hypochondriasis. When measured on hysteria and psychopathic deviate scales - their scores were all high, and some of them underwent measurable personality shifts that were very significant. However, none of the classic symptoms seen during riboflavin deficiency - including problems like dermatitis and inflammation in the eyes affected the young men before the experiment ended. The men were again supplemented with riboflavin following the period of testing -which lasted about two months - the psychiatric symptoms took longer than two weeks to completely dissipate and the young men were restored to normal.
High levels of riboflavin in the blood was studied by another group of researchers in another scientific study that measured the psychological effects of vitamins on people - the researchers associated high levels of riboflavin with greater extroversion, an ability to concentrate and general contentment with life.
The ability of the muscles to perform is beneficially affected by supplements of riboflavin (vitamin B2). This vitamin given as supplements in moderate amounts to young athletes resulted in an eleven per cent boost in their ability to resist fatigue. The neuromuscular irritability of several young athletes who were given 10 mg of vitamin B2 in another study was lowered -this irritability is a biochemical measurement connected to physical fatigue. Before the experiments began, at least eight of the athletes were deficient in riboflavin and this could have played a part in the results witnessed. A riboflavin supplementation regimen could benefit athletes as the results from the tests suggest an increased requirement for riboflavin during heavy physical training and exercise. Vitamin B2 may in particular be of benefit to athletes who are required to exercise in the cold, the results from some animal experiments suggests that riboflavin given in high doses actually enabled rats to swim in cold water for longer periods of time - this could be true of humans as well.
One of the ways in which riboflavin helps protect the body is by maintaining the functioning of the immune response and by helping in the detoxification of noxious chemicals in the body. People affected by a riboflavin (vitamin B2) deficiency also experience general decrease in cellular antibody production and a lowering of general cell level activity. The detoxification process in the liver is also actively aided by riboflavin, the vitamin helps detoxify hormonal chemicals like the estrogens and various other carcinogenic substances in the body, it also eliminates other harmful natural and synthetic chemicals that have found their way into the human body. There is general consensus among doctors that this vitamin may also be involved in the detoxification of the common poison, boric acid, this is based on the discovery that boric acid poisoning causes excessive levels of riboflavin to be found in the urine.
Carcinogens or cancer causing chemicals found in the human body are also actively detoxified by riboflavin. During one experiment, rats given such carcinogens were spared from developing liver tumors by giving them riboflavin in high doses. At the same time, a deficiency of the vitamin riboflavin can result in the stimulation of the growth of tumors in the body. One example of an increase in utilization and need of riboflavin is show in the fact that less amounts of riboflavin than normal is excreted if a person suffers from cancer of the stomach, breast cancer, uterine cancer, or cancers of the skin and the lungs. This connection between tumors and riboflavin excretion has been demonstrated in one study involving a thousand adults with various cancers, in eighty per cent of such people there was virtually no riboflavin excreted in the urine, notwithstanding the type of tumor they suffered from at the time.
The level of riboflavin (vitamin B2) required by active people is much more than the RDA for people who are less than active. Women who jogged twenty five to fifty minutes daily were placed on a controlled diet that included measurable amounts of riboflavin during on clinical investigation. The body of the women was subsequently tested for levels of the vitamin after the doses were varied during the study. A minimum of twice the RDA of riboflavin was required in the diet intake to raise the blood levels of riboflavin to levels that doctors considered an acceptable range for women. Therefore, it can be said that the bodys requirement for riboflavin is increased by physical exercise and metabolic requirements; this same requirement for riboflavin was increased in a weight loss diet as well.
Foods items such as organ meats, sea foods and fishes, all dairy products and eggs, green leafy vegetables, wheat germ, whole grains and legumes form rich sources for riboflavin (vitamin B2). Heat does not degrade riboflavin in foods, however, soaking foods for long periods of time or cooking them in water can lead to substantial losses of the vitamin, as the vitamin is soluble in water and can leach away. Riboflavin is also degraded if it is exposed to strong light. There are a wide range of dosages of supplementary riboflavin, with tablets starting from one mg going up to hundreds of milligrams. There are no toxic side effects associated with riboflavin. The repeated failures experienced in many attempts to produce toxic reactions in the body of experimental animals using riboflavin has convinced researcher that no toxicity is connected to this compound. The absorption of this vitamin is increased and its rate of uptake in the body is hastened when it is consumed along with foods such as fiber rich vegetables.
Long term alcoholics are more likely to suffer from a deficiency of the vitamin B2. People who suffer from cataracts or sickle cell anemia are also much more likely to be affected by a deficiency of riboflavin.
Uptake of riboflavin by human-derived cultured liver cells is by means of a carrier-mediated, energy dependent,
Na+-independent system which appears to be regulated by an intracellular Ca2+/calmodulin mediated transduction pathway and by substrate level in the growth medium (Said et al., 1998). The liver is the major storage site of the vitamin and contains about one-third of the total body flavins, 7090% of which is in the form of FAD. Free riboflavin constitutes less than 5% of the stored flavins. Other storage sites are the spleen, kidney and cardiac muscle. These
depots maintain significant amounts of the vitamin even in severe deficiency states.
Riboflavin functions in the intermediary transfer of electrons in metabolic oxidation-reduction reactions as two coenzymes, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). The riboflavin coenzymes function with a large number of oxidases and dehydrogenases important in normal metabolism. Those enzymes that use FMN include glucose oxidase, L-amino acid oxidase and lactate dehydrogenase. Those that use FAD include D-amino acid oxidase, cytochrome reductase, succinic dehydrogenase and acylCoA dehydrogenases, L-gulonolactone dehydrogenase, x-glycerophosphate dehydrogenase and glutathione reductase. The activity of the last enzyme in the erythrocyte responds directly to changes in nutritional riboflavin status and is therefore used as a clinical parameter for that purpose.
The riboflavin coenzymes transfer electrons to the pyridine dinucleotides of the mitochondrial electron transport chain. Due to this role in energy metabolism, deficient intakes of riboflavin results in impaired efficiency of respiratory energy production. This may result in increases in feed intake by 10-15 percent. Reduced electron transport in riboflavin deficiency also results in specific pathologies in those tissues with the greatest normal respiratory rates.
In animals, riboflavin deficiency results in lack of growth, failure to thrive, and eventual death. Experimental riboflavin deficiency in dogs results in growth failure, weakness, ataxia, and inability to stand. The animals collapse, become comatose, and die. During the deficiency state, dermatitis develops together with hair loss. Other signs include corneal opacity, lenticular cataracts, hemorrhagic adrenals, fatty degeneration of the kidney and liver, and inflammation of the mucous membrane of the gastrointestinal tract. Post-mortem studies in rhesus monkeys fed a riboflavin-deficient diet revealed about one-third the normal amount of riboflavin was present in the liver, which is the main storage organ for riboflavin in mammals. About 28 million Americans exhibit a common sub-clinical stage. characterized by a change in biochemical indices (e.g. reduced plasma erythrocyte glutathione reductase levels). Although the effects of long-term subclinical riboflavin deficiency are unknown, in children this deficiency results in reduced growth. Subclinical riboflavin deficiency has also been observed in women taking oral contraceptives, in the elderly, in people with eating disorders, and in disease states such as HIV, inflammatory bowel disease, diabetes and chronic heart disease. The fact that riboflavin deficiency does not immediately lead to gross clinical manifestations indicates that the systemic levels of this essential vitamin are tightly regulated.
9^ a b Brody, Tom (1999). Nutritional Biochemistry. San Diego: Academic Press. ISBN 0-12-134836-9. OCLC 212425693 39699995 51091036 162571066 212425693 39699995 51091036.
10^ Powers J. Hilary. Riboflavin (vitamin B-2) and health, Review Article. Am J Clin Nutr 2003;77:135260