- 6.0 IRON DEFICIENCY ANEMIA 6.0.1 Introduction There are many types and causes of anemia. Iron deficiency anemia is the most common form of anemia and affects about 20.
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The Role of Thiamine Deficiency in Alcoholic Brain Disease. Peter. R. Martin, M. D., Charles K. Singleton, Ph. D., and Susanne Hiller–Sturmh. Martin, M. D., is professor of psychiatry and pharmacology at Vanderbilt. University School of Medicine and director of the Vanderbilt Addiction.
Center, Nashville, Tennessee. Charles. K. Singleton, Ph. D., is professor and chair in the Department of Biological. Science, Vanderbilt University, Nashville, Tennessee. Susanne. Hiller–Sturmh. Thiamine is a helper molecule. Because intermediate products of these pathways are needed for the.
DNA as well as brain chemicals), a reduction in thiamine can. Wernicke–Korsakoff syndrome, which is found predominantly in. Chronic alcohol consumption can result in thiamine deficiency by. Key. words: thiamine deficiency; alcoholic brain syndrome; chronic AODE (alcohol. Wernicke’s encephalopathy; Wernicke–Korsakoff. AODR (alcohol and other drug related).
Alcohol consumption can. Alcohol Research & Health. One of these. mechanisms involves the reduced availability of an essential nutrient, thiamine. This article describes. Specific actions of thiamine. Finally, the article explores the hypothesis. Thiamine deficiency is particularly important because it.
Alcohol Research & Health. WHAT IS THIAMINE. AND WHAT ARE THE CONSEQUENCES OF THIAMINE DEFICIENCY? Thiamine, also known as. B1, is an essential nutrient required by all tissues, including. The human body itself cannot produce thiamine but must ingest it.
Vitamin B12 (cobalamin) deficiency is a common cause of megaloblastic anemia, a variety of neuropsychiatric symp- toms, and elevated serum homocysteine. Glucose-6-phosphate dehydrogenase deficiency, the most common enzyme deficiency worldwide, causes a spectrum of disease including neonatal hyperbilirubinemia, acute.
Thiamine–rich foods include meat (e. In addition, many foods in the United States commonly are fortified. Humans require a minimum of 0.
Background Endemic cretinism, caused by severe iodine deficiency during pregnancy, is the world's most common preventable cause of mental retardation.
Hoyumpa 1. 98. 0). In the body, particularly. Singleton and Martin 2. In the tissues, thiamine. Proper functioning of.
In addition, inadequate functioning of the. Therefore, the resulting impairment in the functioning. The classical manifestations of thiamine deficiency–related. In the brain, thiamine.
Thiamine deficiency is the established. Wernicke–Korsakoff. WKS), but it also contributes significantly to other forms of alcohol–induced.
These disorders are discussed in the following sections. Wernicke’s. Encephalopathy and Korsakoff’s Psychosis WKS typically consists of. Wernicke’s. encephalopathy (WE) and a long–lasting and debilitating condition known. Korsakoff’s psychosis. WE is an acute life–threatening neurologic. In affluent countries, where people.
Singleton and Martin 2. WE is primarily found in alcoholics (Ragan et al. For example. patients with WE may be too confused to find their way out of a room or may. Many WE patients, however, do not exhibit all three. WE may be present even if the patient presents with only one or two. In fact, neuropathological studies after death indicate that many cases. Approximately 8. 0 to 9.
WE develop Korsakoff’s psychosis, a chronic neuropsychiatric. Victor. et al. Although these patients have problems remembering old information. For example, these patients. Because of these characteristic. Korsakoff’s psychosis also is called alcohol amnestic. It is still somewhat controversial, however, whether Korsakoff’s.
WE or whether it develops in fits and starts. WE. The role of thiamine in. WKS is supported by findings that giving this nutrient to. WKS reverses many of the acute symptoms of the disease, although. Singleton and Martin.
In the most severe cases, these persistent symptoms meet the criteria. Korsakoff’s psychosis. Other people may exhibit more. In affluent countries such. United States, where other forms of malnutrition are uncommon, thiamine. WKS occur most commonly among alcoholics. To date. there are only a few estimates of how common WKS is among alcoholics.
In autopsy. studies, brain abnormalities characteristic of WKS were present in approximately. Harper et al. These abnormalities include lesions. Other studies have found that only about 2.
WKS was confirmed at autopsy had been. Harper 1. 99. 8). Thus, the clinical presentation.
Figure 1. Brain regions affected by thiamine deficiency include the cerebellum. Although WKS in developed.
For example, all people who are malnourished. HIV infected or are undergoing cancer chemotherapy). Patients with severe. Hung et al. Finally, patients who receive intravenous infusions of carbohydrates.
Ferguson et al. Cerebellar Degeneration. Considerably more common. WKS among alcoholics is a condition called cerebellar degeneration, which. Charness 1. 99. 3).
This brain area is involved primarily in muscle coordination. Accordingly, cerebellar degeneration. Cerebellar degeneration is found both in alcoholics. WKS and in those without it, but because WKS patients typically have a.
The frequent occurrence. In a smaller number of patients, the consequences of insufficient. THIAMINE’S. ACTIONS IN THE CELLTo understand the mechanisms.
Investigations of this issue have focused on three enzymes that. These enzymes are called transketolase, pyruvate.
PDH) and alpha–ketoglutarate dehydrogenase (. Each of these enzymes. In this. set of biochemical reactions, a molecule called glucose–6–phosphate. NADPH) (see figure. Both of these molecules are essential for the production of numerous other.
Ribose–5–phosphate is needed for. In addition, NADPH plays an important role in the synthesis of glutathione.
Glucose is first converted to a molecule called glucose–6–phosphate. During that reaction, two products are formed—the. NADPH). Ribose–5–phosphate. NADPH provides hydrogen atoms for chemical reactions. In addition, NADPH plays an important role.
Reduced transketolase activity. The other two enzymes requiring. PDH and . The main function of these pathways is the generation. ATP), which provides energy for. Decreases in the activities of PDH. In addition, proper functioning. PDH is essential for the production of the neurotransmitter acetylcholine.
The citric acid cycle and . Thus, the thiamine–using. Figure 3. The thiamine–dependent enzymes pyruvate dehydrogenase (PDH) and. The main function of these two sets of reactions. ATP), which provides energy for.
In addition, PDH is needed to produce. The citric acid cycle and.
The specific. reductions depend both on the enzyme and on the cell type studied (Singleton. Martin 2. 00. 1). Overall, transketolase activity may be the most sensitive. Studies using rats found that transketolase. Gibson et al. Substantial decline. WE (Lavoie and Butterworth 1. Thiamine Uptake. Into the Cell.
Thiamine is ingested with. This transport involves. Uptake from the intestine. Transport out of those.
Uptake from the blood. Transport within the. PDH and . Researchers recently. Singleton. and Martin 2. However, the characteristics of the thiamine transport process. Indeed. a second thiamine transporter gene recently has been cloned (Rajgopal et al. As will be described in more detail in the section “Differential.
Sensitivity to Thiamine Deficiency,” subtle variations in the transporter. Once taken up into the cells. The levels of phosphate–free thiamine in the cell are relatively.
Because. the mitochondria produce by far the most energy required for cellular function. Singleton and Martin 2. Second, disturbances associated with thiamine. Singleton and Martin 2. Third, altered carbohydrate metabolism can. Calingasan et al.
Todd. and Butterworth 1. However, only a subset. WKS. Moreover, identical.
These two observations. Differential Sensitivity to Thiamine Deficiency.” Research over the past 3. The most important of these mechanisms (as discussed. Hoyumpa 1. 98. 0) include: Inadequate nutritional. Decreased absorption. Impaired utilization. Inadequate Nutritional.
Intake. Although most people require. Woodhill and Nobile 1. In. fact, in an early study of 3,0. Leevy and Baker 1. A later study. found that alcoholic patients had significantly lower average levels of a thiamine. Th. DP were similar in alcoholics and. Tallaksen et al. However, some of the alcoholics in.
Decreased Uptake. Thiamine From the Gastrointestinal Tract. Animal studies have helped. To be used by the. At low thiamine concentrations, such as those normally found. This is called an active transport process and. TPK) once the thiamine is inside the cell.
Furthermore, in studies. TPK enzyme from various tissues decreased with.
Laforenza et. al. Although no studies have addressed whether alcohol directly affects. TPK in humans, indirect analyses have found that the ratio of phosphorylated. Th. DP) to thiamine is significantly lower in alcoholics than. Poupon et al. 1. 99. Tallaksen et al. 1. Th. DP. This finding suggests that TPK is less.
Thiamine malabsorption could. Impaired Thiamine. Utilization. The cells’ utilization.
As mentioned. earlier, once thiamine is imported into the cells, it is first converted into. Th. DP by the addition of two phosphate groups. Th. DP then binds to the thiamine–using. Chronic alcohol. consumption frequently leads to magnesium deficiency, however (Morgan 1.
Rindi et al. 1. 99. In this case, any thiamine that reaches the cells cannot. Abstinence from alcohol. Martin et al. Researchers also administered thiamine to alcoholic patients and laboratory. Victor et al. Most.
WKS, and then tested the participant’s working memory. These studies. found that participants who received the highest thiamine dose performed best. Ambrose et al. 2.
DIFFERENTIAL SENSITIVITY. TO THIAMINE DEFICIENCYDifferences. Sensitivity Among People. Several findings suggest. Hoyumpa 1. 98. 0; Morgan 1.
WKS (Harper et al. This means that the severest consequences.
A possible explanation for this. To investigate this hypothesis, researchers have studied. Korsakoff’s psychosis, arguing that variants of these enzymes may exist. The results. of these investigations, however, have been inconsistent. The studies cited in this section mostly used enzymes isolated from skin or. Although it is not known whether the effects. Using such model.
One study (Blass and Gibson. PDH, and . These.
Korsakoff’s patients bound. Th. DP less avidly than did the enzyme from the control subjects. Transketolase. from the Korsakoff’s patients could function normally when sufficient. Th. DP was present; under conditions of thiamine deficiency, however. Th. DP to maintain.
Vitamin D deficiency soars in the U. S., study says. Three- quarters of U. S. The trend marks a dramatic increase in the amount of vitamin D deficiency in the U.
S., according to findings set to be published tomorrow in the Archives of Internal Medicine. Between 1. 98. 8 and 1. National Health and Nutrition Examination Survey) had 3. D, the blood level a growing number of doctors consider sufficient for overall health; a decade later, just 2.
The slide was particularly striking among African Americans: just 3 percent of 3,1. Lack of vitamin D is linked to rickets (soft, weak bones) in children and thinning bones in the elderly, but scientists also believe it may play a role in heart disease, diabetes and cancer. She notes that the Institute of Medicine (IOM) defines insufficiency as less than. Using that as a threshold, some 1. U. S. Using a sunscreen with as little as a 1. D production by 9. Some food sources are salmon, tuna, mackerel and vitamin D- fortified dairy products, such as milk.
IOM recommends that people get 2. International Units (IU) of vitamin D daily, but it's reviewing whether to increase that recommendation in the wake of new studies. An update is expected in May 2.
Ginde believes that whatever those recommendations turn out to be, blacks should take double the amount of vitamin D supplements, because they have more melanin or pigment in their skin that makes it harder for the body to absorb and use the sun's ultraviolet rays to synthesize vitamin D. He adds that people should also take greater amounts of vitamin D in the winter when there's less sunlight. Jim Fleet, a professor of foods and nutrition at Purdue University who wasn’t involved in the study, agrees with Picciano that failing to consider differences in the vitamin D testing methods (used during the two survey periods) was .