Alcohol use inhibits absorption of nutrients. – Not only is alcohol devoid of proteins, minerals, and vitamins, it actually inhibits the absorption and usage of vital nutrients such as thiamin (vitamin B1), vitamin B12, folic acid, and zinc.
Thiamin (vitamin B1) is involved in the metabolism of proteins and fat and the formation of hemoglobin. It is also essential to optimal performance for its role in metabolizing carbohydrates. Vitamin B12 is essential to good health. It helps maintain healthy red blood and nerve cells. Folic acid is an integral part of a coenzyme involved in the formation of new cells; a lack of it can cause a blood disorder called “megaloblastic anemia”, which causes a lowering of oxygen-carrying capacity and thus negatively affects endurance activities. Zinc is also essential to your energy metabolic processes. Since alcohol depletes your zinc resources, the effect is an even greater reduction of your endurance.
- 1 Does alcohol cause B12 deficiency?
- 2 Does alcohol deplete vitamin B6?
- 3 Does alcohol lower vitamin D?
- 4 Does alcohol deplete zinc?
- 5 Why is thiamine given to alcoholics?
- 6 How does alcohol deplete magnesium?
- 7 What electrolytes are depleted when you drink alcohol?
- 8 Why does alcohol deplete vitamin D?
What vitamin does alcohol deplete the most?
What Types of Vitamins are Depleted through Alcoholism? – While not all types of vitamin-intake are compromised as a result of alcohol consumption, there are several key vitamins of which alcoholics are often deprived while drinking. One of the most common and serous types of alcohol-related vitamin deficiency is lack of B vitamins like Thiamine, which is an essential vitamin for neurobiological health.
Vitamin C Magnesium Calcium Zinc Iron Potassium
All of these vitamins play a key role in the body’s chemistry and help to promote optimal physical and psychological health. They are key to fighting conditions like cancer, chronic pain, premature aging, diabetes, immunity issues and more. They also fight depression and central nervous system issues.
Does alcohol cause B12 deficiency?
Do Alcohol Affect B12 Levels? – The simple answer to this question is yes. Consumption of alcohol (of any kind) affects the level of B12 absorption in the body even if taken in moderate amounts. Studies show that even a little amount of alcohol can decrease vitamin B12 absorption by about 5-6%. Alcohol affects B12 absorption in the body in many ways.
Large amounts of alcohol irritate the mucosal linings in the stomach and intestines leading to a condition called gastritis which further leads to reduced absorption of B12 levels in the body. According to the National Institute of Alcohol Abuse and Alcoholism, alcohol consumption also prevents the body from fully utilizing the absorbed nutrients by altering their transport and storage. Gastritis reduces the production of hydrochloric acid which leads to the growth of intestinal bacteria. These bacteria use the B12 vitamins in the body thus leading to lesser amounts available for your use. Though small amounts of alcohol are believed to be appetite stimulants, excessive amounts can stop you from following a healthy diet which leads to vitamin B12 deficiency.
What nutrition does alcohol deplete?
Alcohol and nutrient absorption – Unlike food, alcohol is not digested. Instead, it is absorbed directly in the blood stream.11 Alcohol begins its journey through the digestive system in the mouth, where it then travels down the oesophagus to the stomach, where some of the alcohol is absorbed into the bloodstream.11 The stomach starts the breakdown of alcohol with an enzyme called alcohol dehydrogenase.12 The rest of the alcohol travels to the small intestine where the remainder gets absorbed.
Does alcohol deplete vitamin B6?
How Does Alcohol Deplete The Body Of B and C Vitamins? July 30, 2020 | Posted In When a person tries to recover from alcoholism, the body undergoes some major changes from within. Alcoholics experience deficiencies in key vitamins, and due to the lack of these vitamins, they often notice irritating symptoms as they continue to drink actively.
- These symptoms include inflammation of the skin, lethargy, dehydration, depression, and memory loss.
- Without the proper vitamins, pain and sickness can also occur in more severe instances for longer.
- Why Does Drinking Make You Vitamin Deficient? Many alcoholics tend to replace some of the calories they get from food with calories they get from drinking.
Calories are considered good for the body, but the ones that come from alcohol as well as junk food are known as empty calories. These calories contain minimal nutritional value. They can also prevent the body from absorbing important nutrients from other foods.
Your local facilities often compare alcohol to sugar. Once consumed, there is a temporary boost in energy, but then a large drop in energy from decreasing levels of blood glucose. When this happens, your body feels the need to consume more alcohol and grows a dependency to it. They also might turn to an intake in sugar for short-term energy, such as in junk foods.
For alcoholics to be able to overcome the urges of both alcohol and sugar, they will need to replenish their bodies with foods that are high sources of vitamins and nutrients. With vitamins, the body will experience more productive boosts of energy with no drops in blood glucose or cravings for alcohol or sugar.
Vitamin B1 can be found in cereal, nuts, and pork. Vitamin B3 can be found in cereal, seafood, and pork. Vitamin B5 can be found in whole grains, eggs, milk, and liver. Vitamin B6 can be found in nuts, bananas, and avocados. Vitamin B12 can be exclusively found in dairy products.
Vitamin C There are no other types of C vitamins; there is only one, which is simply known as vitamin C. Vitamin C promotes health in the teeth, skin, bones, and blood vessels. When the body is depleted of vitamin C, one may experience irritability, weakness, and fatigue in the muscles.
Vitamin C is strongly found in orange juice, with more vitamin C being present if the oranges used to make the juice were first frozen. Broccoli and cantaloupe are also foods that contain vitamin C. Nutrients are also an important part in recovering from alcohol. Many nutrients are needed to keep the body healthy and strong, and help reduce the risk of cancer and diabetes.
These nutrients include the following:
Calcium Iron Magnesium Potassium Zinc
As you can see, a proper recovery process does not simply involve removing alcohol from a person’s diet, but also adding healthy foods that are high in vitamins and nutrients that may have otherwise been lost from heavy drinking. A proper diet is necessary for the best chance at recovery and to prevent relapse.
Does alcohol deplete potassium and magnesium?
1. Introduction – Alcohol dependence among adults in the United States is estimated at 14%, Among heavy drinkers, alcoholic liver disease is estimated to develop in 15–30%, In patients who consume excessive amounts of alcohol, various types of disturbances are observed, i.e., electrolyte, acid-base, protein-caloric malnutrition, and vitamin deficiency,
Chronic alcohol abuse patients are malnourished not only because of a diet low in nutrients but also because alcohol impairs the absorption of essential nutrients and elements. In addition, ethanol metabolic pathways produce toxic metabolites (acetaldehyde and free radicals) that lead to cell damage as a result of oxidative stress,
The clinical picture of the observed disorders depends on the duration and amount of alcohol consumed. Most patients who develop electrolyte imbalance, metabolic acidosis, and hyponatremia are admitted to hospital. However, clinical symptoms of chronic alcohol consumption are also decreased levels of phosphate, magnesium, potassium, sodium and calcium, and other elements in blood plasma,
Electrolyte abnormalities develop as a result of chronic alcohol consumption during acute alcohol intoxication, but they are particularly important during alcohol withdrawal, It turns out that even during alcohol withdrawal, hypokalemia, hypomagnesemia, and hyponatremia are observed, Currently, it is believed that the toxic effects of alcohol on organs are mainly associated with the activity of alcohol metabolites, induction of oxidative stress, and translocation of intestinal endotoxins into the bloodstream,
These processes lead to cell damage and stimulation of inflammatory reactions releasing a large number of cytokines, among others such as TNF-alpha and IL-6, With continuous alcohol abuse, which stimulates hepatocytes to secrete some interleukins, such as IL-8, activating Kupffer cells by binding to toll-like receptors, other effects are impaired including defective tissue regeneration, hepatocyte necrosis, recruitment of neutrophils and immune cells, and liver fibrosis, Three pathways of alcohol metabolism. Each of the three pathways is responsible for the production of free radicals, which can damage lipids, proteins, carbohydrates, and DNA substrates, However, there are several endogenous enzymes that protect the body against the adverse effects of free radicals, including glutathione peroxidase (GPx), which neutralizes hydrogen peroxide and organic peroxides, glutathione reductase (GR), superoxide dismutase (SOD) and CAT,
Cofactors for antioxidant enzymes are trace elements such as selenium, manganese, copper, zinc, and iron. Selenium in the form of selenocysteine is present in the active center of GPx. In turn, manganese, copper, and zinc are components of the enzymes from the superoxide dismutase group (MnSOD, Cu/ZnSOD), which catalyze the reaction of the superoxide anion radical dismutation to hydrogen peroxide and oxygen.
Iron is a part of CAT that catalyzes the decomposition of hydrogen peroxide into water and oxygen. Zinc-dependent enzymes, in turn, are alcohol dehydrogenase, RNA polymerases, and fructose 1,6-bisphosphatase, which is allosterically regulated by zinc and could influence gluconeogenesis.
Does alcohol lower vitamin D?
Introduction – It has long been known that excessive alcohol consumption has a negative impact on vitamin D status. Chronic alcoholism results in disturbed vitamin D metabolism and chronic alcoholics usually have low levels of serum 25-hydroxyvitamin D,
However, experimental studies in rats has determined that chronic ethanol treatment increases the serum levels of 25(OH)D, Although these observations from a laboratory animal model suggest a possible beneficial effect of long-term alcohol consumption on vitamin D status in humans, the evidence from population-based studies has been inconsistent,
In addition, little is known regarding specific alcohol consumption-related behaviors in Asian populations. As correlates vary somewhat depending on ethnicity and sex, further studies have been necessary to demonstrate the sex-specific association between alcohol consumption and vitamin D status in Asian populations.
Does alcohol deplete zinc?
Why Zinc May Be Helpful in Alcoholism Recovery – In many cases, the patient is advised to eat healthier – but they are often not provided in-depth information on what to eat. A general diet that is rich in both vitamins and minerals, as well as foods that offer enough protein, should be preferred.
Additionally, the inclusion of certain nutrients may offer additional benefits, including a faster recovery. Zinc, in particular, is an important mineral that is often overlooked in an alcoholism recovery diet. There are several reasons why a person should consider adding more zinc to their diet during recovery.
When a person suffers from alcoholism, their body is unable to absorb nutrients from food and supplements as effectively. This is why malnutrition is a common complication among men and women who are alcoholics. According to one study 6, heavy alcohol consumption can cause deficiencies in micronutrients, as well as general malnutrition.
Is vitamin B12 good for alcoholics?
Vitamin B-12 Deficiency Supplemental vitamin B-12 treats this deficiency, but can sometimes hide a folate deficiency, which is another somewhat common vitamin deficiency among alcoholics. Because of this, doctors sometimes recommend taking folate as well as vitamin B-12.
Do you take B12 before or after drinking?
Is Vitamin B12 Good For Hangovers? – The only reliable hangover cure is limiting alcohol intake in the first place. Nonetheless, taking vitamin B12 supplements before and after drinking alcohol may help replenish the amount of this essential nutrient in your body and allow it to recover faster from hangover symptoms,
Why is thiamine given to alcoholics?
Peter R. Martin, M.D., Charles K. Singleton, Ph.D., and Susanne Hiller–Sturmhöfel, Ph.D. – Peter R. 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–Sturmhöfel, Ph.D., is a science editor for Alcohol Research & Health.
A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol–induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism.
Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke–Korsakoff syndrome, which is found predominantly in alcoholics.
Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition.
Ey words: thiamine deficiency; alcoholic brain syndrome; chronic AODE (alcohol and other drug effects); Wernicke’s encephalopathy; Wernicke–Korsakoff psychosis; alcoholic cerebellar degeneration; AODR (alcohol and other drug related) structural brain damage; malnutrition; disease susceptibility; survey of research Alcohol consumption can damage the brain through numerous mechanisms, many of which are discussed in the articles in this issue of Alcohol Research & Health.
One of these mechanisms involves the reduced availability of an essential nutrient, thiamine, to the brain as a consequence of chronic alcohol consumption. This article describes the normal role of thiamine in brain functioning as well as the pathological consequences that result from thiamine deficiency.
Specific actions of thiamine on a cellular level then are reviewed, followed by a discussion of how alcohol affects the body’s processing and availability of thiamine as well as thiamine utilization by the cells. Finally, the article explores the hypothesis that people may differ in their sensitivity to thiamine deficiency and that different brain regions may be more or less sensitive to a deficiency in this important nutrient.
Thiamine deficiency is particularly important because it can exacerbate many of the other processes by which alcohol induces brain injury, as described in other articles in this issue of Alcohol Research & Health. WHAT IS THIAMINE AND WHAT ARE THE CONSEQUENCES OF THIAMINE DEFICIENCY? Thiamine, also known as vitamin B 1, is an essential nutrient required by all tissues, including the brain.
The human body itself cannot produce thiamine but must ingest it with the diet. Thiamine–rich foods include meat (e.g., pork) and poultry; whole grain cereals (e.g., brown rice and bran); nuts; and dried beans, peas, and soybeans. In addition, many foods in the United States commonly are fortified with thiamine, including breads and cereals.
Humans require a minimum of 0.33 milligrams (mg) thiamine for every 1,000 kilocalories (kcal) of energy they consume—in other words, people who consume a regular 2,000–kcal diet per day should ingest a minimum of 0.66 mg thiamine daily (Hoyumpa 1980).
To provide a safety margin, a daily intake of 1.1 mg thiamine is currently recommended for adult women and 1.2 mg for adult men.1 ( 1 Lower levels are recommended for children, and slightly higher levels are recommended for pregnant and breast–feeding women.) Studies have found that most healthy people typically consume 0.4 to 2.0 mg thiamine daily (Woodhill and Nobile 1972).
In the body, particularly high concentrations of thiamine are found in skeletal muscles and in the heart, liver, kidney, and brain (Singleton and Martin 2001). In the tissues, thiamine is required for the assembly and proper functioning of several enzymes that are important for the breakdown, or metabolism, of sugar molecules into other types of molecules (i.e., in carbohydrate catabolism).
Proper functioning of these thiamine–using enzymes is required for numerous critical biochemical reactions in the body, including the synthesis of certain brain chemicals (i.e., neurotransmitters); production of the molecules making up the cells’ genetic material (i.e., nucleic acids); and production of fatty acids, steroids, and certain complex sugar molecules.
In addition, inadequate functioning of the thiamine–using enzymes can interfere with the body’s defense against the damage (i.e., oxidative stress) caused by harmful, highly reactive oxygen molecules called free radicals. (For more information, see the section “Thiamine’s Actions in the Cell.”) Because thiamine and the thiamine–using enzymes are present in all cells of the body, it would be plausible that inadequate thiamine affects all organ systems; however, the cells of the nervous system and heart seem particularly sensitive to the effects of thiamine deficiency.
- Therefore, the resulting impairment in the functioning of the thiamine–using enzymes primarily affects the cardiovascular and nervous systems.
- The classical manifestations of thiamine deficiency–related heart disease include increased blood flow through the vessels in the body, heart failure, and sodium and water retention in the blood.
In the brain, thiamine is required both by the nerve cells (i.e., neurons) and by other supporting cells in the nervous system (i.e., glia cells). Thiamine deficiency is the established cause of an alcohol–linked neurological disorder known as Wernicke–Korsakoff syndrome (WKS), but it also contributes significantly to other forms of alcohol–induced brain injury, such as various degrees of cognitive impairment, including the most severe, alcohol–induced persisting dementia (i.e., “alcoholic dementia”).
These disorders are discussed in the following sections. Wernicke’s Encephalopathy and Korsakoff’s Psychosis WKS typically consists of two components, a short–lived and severe condition called Wernicke’s encephalopathy (WE) and a long–lasting and debilitating condition known as Korsakoff’s psychosis.
WE is an acute life–threatening neurologic disorder caused by thiamine deficiency. In affluent countries, where people normally receive adequate thiamine from their diets, thiamine deficiency is most commonly caused by alcoholism (Singleton and Martin 2001); accordingly, in these countries WE is primarily found in alcoholics (Ragan et al.1999).
The symptoms of WE include mental confusion, paralysis of the nerves that move the eyes (i.e., oculomotor disturbances), and an impaired ability to coordinate movements, particularly of the lower extremities (i.e., ataxia). For example, patients with WE may be too confused to find their way out of a room or may not even be able to walk.
Many WE patients, however, do not exhibit all three of these signs and symptoms, and clinicians working with alcoholics must be aware that WE may be present even if the patient presents with only one or two of them. In fact, neuropathological studies after death indicate that many cases of thiamine deficiency–related encephalopathy may not be diagnosed in life because not all the “classic” signs and symptoms are present or recognized.
Approximately 80 to 90 percent of alcoholics with WE develop Korsakoff’s psychosis, a chronic neuropsychiatric syndrome characterized by behavioral abnormalities and memory impairments (Victor et al.1989). Although these patients have problems remembering old information (i.e., retrograde amnesia), it is the disturbance in acquisition of new information (i.e., anterograde amnesia) that is most striking.
For example, these patients can engage in a detailed discussion of events in their lives but cannot remember ever having had that conversation an hour later. Because of these characteristic memory deficits, Korsakoff’s psychosis also is called alcohol amnestic disorder.
It is still somewhat controversial, however, whether Korsakoff’s psychosis always is preceded by WE or whether it develops in fits and starts, without an overt episode of WE. The role of thiamine in the development of WKS is supported by findings that giving this nutrient to patients with WKS reverses many of the acute symptoms of the disease, although in some people certain chronic neuropsychiatric consequences of previous thiamine deficiency may persist even with appropriate treatment (see Singleton and Martin 2001).
In the most severe cases, these persistent symptoms meet the criteria of full–blown Korsakoff’s psychosis. Other people may exhibit more subtle neurological signs and symptoms, such as abnormalities in a brain region called the cerebellum (as described in the following section) and an inflammation or degeneration of peripheral nerves (i.e., neuropathy) as well as changes in behavior and problems with learning, memory, and decisionmaking.
- In affluent countries such as the United States, where other forms of malnutrition are uncommon, thiamine deficiency and the resulting 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 13 percent of alcoholics (Harper et al.1988).
These abnormalities include lesions in brain areas called the mamillary bodies, thalamus, hypothalamus, brain stem, and cerebellum (see figure 1). Other studies have found that only about 20 percent of alcoholics in whom the presence of WKS was confirmed at autopsy had been diagnosed with the disorder before death (Harper 1998).
|Figure 1 Brain regions affected by thiamine deficiency include the cerebellum, mamillary bodies, thalamus, hypothalamus, and brain stem.
Although WKS in developed countries occurs most commonly among alcoholics, other groups of patients are also at risk of developing the disease. For example, all people who are malnourished (e.g., because they are HIV infected or are undergoing cancer chemotherapy) or who have a metabolic disease leading to impaired thiamine absorption (i.e., uptake) or utilization can develop thiamine deficiency.
- Patients with severe kidney disease who are undergoing regular dialysis are also prone to encephalopathy, and a substantial portion of them have been found to suffer from thiamine deficiency (Hung et al.2001).
- Finally, patients who receive intravenous infusions of carbohydrates (e.g., the sugar dextrose) may experience episodes of thiamine deficiency, particularly if they are already at risk of receiving inadequate levels of this nutrient because they are alcoholics, as thiamine is used in the metabolism of those carbohydrates (see Ferguson et al.1997).
Cerebellar Degeneration Considerably more common than WKS among alcoholics is a condition called cerebellar degeneration, which typically develops after 10 or more years of heavy drinking (Charness 1993). In autopsy studies, 40 percent or more of alcoholics showed signs of this condition (Torvik 1987), which is characterized by shrinkage (i.e., atrophy) of certain regions of the cerebellum.
- This brain area is involved primarily in muscle coordination.
- It also is increasingly recognized for its role in various aspects of cognitive and sensory functioning (Parks et al.2003).
- Accordingly, cerebellar degeneration is associated with difficulties in movement coordination and involuntary eye movements, such as nystagmus.
Cerebellar degeneration is found both in alcoholics with WKS and in those without it, but because WKS patients typically have a higher degree of cerebellar atrophy, it appears likely that thiamine deficiency also is the predominant cause of cerebellar degeneration.
- The frequent occurrence of cerebellar degeneration in alcoholics is consistent with studies demonstrating that the cerebellum is particularly sensitive to the effects of thiamine deficiency.
- For more information on these studies, see the section “Differential Sensitivity of Various Brain Regions.”) As a result of this particular susceptibility, the effects of thiamine deficiency would be expected to appear first in the cerebellum, manifesting as cerebellar degeneration and its associated symptoms.
In a smaller number of patients, the consequences of insufficient thiamine then would progress to other brain regions and lead to more widespread brain dysfunction, including alcohol amnestic disorder or alcohol–induced persisting dementia. THIAMINE’S ACTIONS IN THE CELL To understand the mechanisms through which thiamine deficiency, whether induced by alcoholism or other causes, leads to brain damage, one first must understand the normal role of thiamine in the cell.
Investigations of this issue have focused on three enzymes that require thiamine as a cofactor. These enzymes are called transketolase, pyruvate dehydrogenase (PDH) and alpha–ketoglutarate dehydrogenase (α–KGDH); they all participate in the catabolism of sugar molecules (i.e., carbohydrates) in the body, as described in the following paragraphs.
Each of these enzymes consists of several components that must be assembled to yield the functional enzyme, and the addition of thiamine is a critical step in this assembly process. As a result, thiamine deficiency causes suboptimal levels of functional enzymes in the cell, in addition to interfering with the activity of those enzymes.
- Transketolase is an important enzyme in a biochemical pathway called the pentose phosphate pathway.
- In this set of biochemical reactions, a molecule called glucose–6–phosphate, which is derived from the sugar glucose, is modified by transketolase, yielding two products—a sugar called ribose–5–phosphate and a molecule called reduced nicotinamide adenine dinucleotide phosphate (NADPH) (see figure 2).
Both of these molecules are essential for the production of numerous other important molecules in the cell. Ribose–5–phosphate is needed for the synthesis of nucleic acids, complex sugar molecules, and other compounds. NADPH provides hydrogen atoms for chemical reactions that result in the production of steroids, fatty acids, amino acids, certain neurotransmitters, and other molecules.
|Figure 2 The thiamine–dependent enzyme transketolase is an important enzyme in the breakdown of glucose through a biochemical pathway called the pentose phosphate pathway. Glucose is first converted to a molecule called glucose–6–phosphate, which enters the pentose phosphate pathway where it is further modified by transketolase. During that reaction, two products are formed—the sugar ribose–5–phosphate and a molecule called reduced nicotinamide adenine dinucleotide phosphate (NADPH). Ribose–5–phosphate is needed for the synthesis of nucleic acids, complex sugar molecules, and other compounds called coenzymes that are essential for the functioning of various enzymes. NADPH provides hydrogen atoms for chemical reactions that result in the production of coenzymes, steroids, fatty acids, amino acids, and neurotransmitters. In addition, NADPH plays an important role in the synthesis of glutathione, a compound that is essential to the body’s defense against damage from oxidative stress. Reduced transketolase activity interferes with all these essential biochemical processes.
The other two enzymes requiring thiamine, PDH and α–KGDH, also participate in different steps of the breakdown and conversion of glucose–6–phosphate through two consecutive chains of biochemical reactions called glycolysis and the citric acid cycle (see figure 3).
- The main function of these pathways is the generation of a molecule called adenosine triphosphate (ATP), which provides energy for numerous cellular processes and reactions.
- Decreases in the activities of PDH and α–KGDH can result in reduced ATP synthesis, which in turn can contribute to cell damage and even cell death.
In addition, proper functioning of PDH is essential for the production of the neurotransmitter acetylcholine as well as for the synthesis of a compound called myelin, which forms a sheath around the extensions (i.e., axons) of many neurons, thereby ensuring the ability of these neurons to conduct signals.
|Figure 3 The thiamine–dependent enzymes pyruvate dehydrogenase (PDH) and a–ketoglutarate dehydrogenase (α–KGDH) participate in the metabolism of glucose through two biochemical reactions, glycolysis and the citric acid cycle. The main function of these two sets of reactions is to generate adenosine triphosphate (ATP), which provides energy for the cells. Reduced PDH and α–KGDH activity resulting from thiamine deficiency can lead to less ATP synthesis, which in turn can contribute to cell damage and even cell death. In addition, PDH is needed to produce the neurotransmitter acetylcholine and to generate myelin, a compound that forms a sheath around the extensions (i.e., axons) of many neurons, thereby ensuring proper neuronal functioning. The citric acid cycle and α–KGDH play a role in maintaining the levels of the neurotransmitters glutamate, gamma–aminobutyric acid (GABA), and aspartate, as well as in protein synthesis.
When thiamine levels decrease, the activity levels of all three enzymes are reduced to some extent. The specific reductions depend both on the enzyme and on the cell type studied (Singleton and Martin 2001). Overall, transketolase activity may be the most sensitive measure of thiamine deficiency.
- Studies using rats found that transketolase activity may be reduced as much as 90 percent in the brain regions that are most sensitive to thiamine deficiency (Gibson et al.1984).
- Substantial decline in transketolase activity resulting from thiamine deficiency has even been found in various brain areas of alcoholics who do not exhibit the clinical and neuropathological signs of WE (Lavoie and Butterworth 1995), suggesting that thiamine deficiency can cause adverse effects even before severe brain damage becomes obvious.
Thiamine Uptake Into the Cell Thiamine is ingested with the diet, and to exert its effects in the cells it must be transported from the gastrointestinal tract to the tissues and cells. This transport involves at least four steps:
Uptake from the intestine into the cells that line the intestine Transport out of those cells into the bloodstream Uptake from the blood into the tissues and cells; for thiamine transported to the brain this also includes crossing the blood–brain barrier Transport within the cells to the areas where the thiamine is needed (e.g., to the cell’s energy factories, the mitochondria, where PDH and α–KGDH act, or to the nucleus, where thiamine regulates gene activity).
These transport steps are accomplished by one or more thiamine transporter molecules. Researchers recently have identified and cloned the gene for a human thiamine transporter (see Singleton and Martin 2001). However, the characteristics of the thiamine transport process differ among different tissues and cell types, suggesting that variants of one transporter type or even different types of transporters may exist.
Indeed, a second thiamine transporter gene recently has been cloned (Rajgopal et al.2001). As will be described in more detail in the section “Differential Sensitivity to Thiamine Deficiency,” subtle variations in the transporter molecule among cells or among people, resulting in a reduced capacity to transport thiamine, may contribute to the differential sensitivity to thiamine deficiency.
Once taken up into the cells, thiamine first is modified by the addition of one or more phosphate groups. The compound containing two phosphate groups (thiamine diphosphate ) is the actual active molecule that serves as a cofactor for the various thiamine–requiring enzymes.
The levels of phosphate–free thiamine in the cell are relatively low and are tightly regulated by rapid conversion to the phosphorylated forms. Mechanisms of Thiamine Deficiency–Induced Cell Damage Thiamine deficiency can lead to cell damage in the central nervous system through several mechanisms. First, the changes in carbohydrate metabolism, particularly the reduction in α–KGDH activity, can lead to damage to the mitochondria.
Because the mitochondria produce by far the most energy required for cellular function, mitochondrial damage can result in cell death through a mechanism called necrosis (see Singleton and Martin 2001). Second, disturbances associated with thiamine deficiency in some cell types lead to apoptosis—a form of programmed cell death (or cell suicide) that serves to remove damaged cells from the organism (see Singleton and Martin 2001).
Third, altered carbohydrate metabolism can lead to a cellular state called oxidative stress (Calingasan et al.1999; Todd and Butterworth 1999), characterized by excess levels of highly reactive molecules called free radicals and/or the presence of insufficient levels of compounds to eliminate those free radicals (i.e., antioxidants, such as glutathione).
Oxidative stress can lead to various types of cell damage and even cell death. ALCOHOL’S EFFECTS ON THIAMINE UPTAKE AND FUNCTION As noted earlier, thiamine deficiency in affluent countries clearly is linked to alcoholism, occurring in up to 80 percent of alcoholics (e.g., Morgan 1982).
However, only a subset of these alcoholics develop brain disorders such as WKS. Moreover, identical twins (who share all of their genetic information) show greater similarity with respect to alcohol–induced brain disease than do fraternal twins (who share on average 50 percent of their genetic information).
These two observations have led to the conclusion that a genetic predisposition to thiamine deficiency and its effects may exist, as will be discussed in more detail in the section “Differential Sensitivity to Thiamine Deficiency.” Research over the past 30 years has identified several mechanisms through which alcoholism may contribute to thiamine deficiency.
Inadequate nutritional intake Decreased absorption of thiamine from the gastrointestinal tract and reduced uptake into cells Impaired utilization of thiamine in the cells.
Inadequate Nutritional Intake Although most people require a minimum of 0.33 mg thiamine for each 1,000 kcal of energy they consume, alcoholics tend to consume less than 0.29 mg/1,000 kcal (Woodhill and Nobile 1972). In fact, in an early study of 3,000 alcoholics admitted to hospitals because of alcohol withdrawal symptoms or other alcohol–related illnesses, 40 percent exhibited periodic thiamine deficiency during drinking binges, 25 percent exhibited prolonged thiamine deficiency with some periods of normal intake, and 35 percent exhibited continuous thiamine deficiency (Leevy and Baker 1968).
- A later study found that alcoholic patients had significantly lower average levels of a thiamine compound containing one phosphate group (i.e., thiamine monophosphate), but the average levels of free thiamine and ThDP were similar in alcoholics and control subjects (Tallaksen et al.1992).
- However, some of the alcoholics in that study had extremely high levels of free thiamine, suggesting that they may have had a problem in the steps that lead to the conversion of thiamine into its active, phosphate–containing form.
Decreased Uptake of Thiamine From the Gastrointestinal Tract Animal studies have helped elucidate the mechanisms of normal and alcohol–impaired thiamine uptake from the gastrointestinal tract into the blood and cells. To be used by the body, thiamine must cross a number of barriers, first transferring across the membranes of the cells lining the gut (i.e., enterocytes), then entering those cells, and then crossing the membranes at the other end of the cells to enter the bloodstream.
- At low thiamine concentrations, such as those normally found in the human body, this transfer is achieved by a specific thiamine transporter molecule that requires energy.
- This is called an active transport process and seems to be associated with the rapid addition of two phosphate groups by the enzyme thiamine diphosphokinase (TPK) once the thiamine is inside the cell.
At high thiamine concentrations, however, such as can be achieved after additional thiamine is administered, thiamine transport occurs through a passive process—that is, a mechanism that requires no energy. Acute alcohol exposure interferes with the absorption of thiamine from the gastrointestinal tract at low, but not at high, thiamine concentrations (Hoyumpa 1980).
- Furthermore, in studies using rats, the activity of the TPK enzyme from various tissues decreased with acute alcohol exposure to about 70 percent of the activity level in control animals, and with chronic alcohol exposure to about 50 percent (Laforenza et al.1990).
- Although no studies have addressed whether alcohol directly affects TPK in humans, indirect analyses have found that the ratio of phosphorylated thiamine (primarily ThDP) to thiamine is significantly lower in alcoholics than in nonalcoholics (Poupon et al.1990; Tallaksen et al.1992)—that is, that less thiamine is converted to ThDP.
This finding suggests that TPK is less active in the alcoholics. Thiamine malabsorption could become clinically significant if combined with the reduced dietary thiamine intake that is typically found in alcoholics, when other aspects of thiamine utilization are compromised by alcohol, or when a person requires increased thiamine amounts because of his or her specific metabolism or condition (e.g., in pregnant or lactating women).
- Impaired Thiamine Utilization The cells’ utilization of thiamine can be affected in different ways by chronic alcohol use.
- As mentioned earlier, once thiamine is imported into the cells, it is first converted into ThDP by the addition of two phosphate groups.
- ThDP then binds to the thiamine–using enzymes, a reaction that requires the presence of magnesium.
Chronic alcohol consumption frequently leads to magnesium deficiency, however (Morgan 1982; Rindi et al.1992), which also may contribute to an inadequate functioning of the thiamine–using enzymes and may cause symptoms resembling those of thiamine deficiency.
- In this case, any thiamine that reaches the cells cannot be used effectively, exacerbating any concurrently existing thiamine deficiency.
- Abstinence from alcohol and improved nutrition have been shown to reverse some of the impairments associated with thiamine deficiency, including improving brain functioning (Martin et al.1986).
Researchers also administered thiamine to alcoholic patients and laboratory animals and found that this treatment reversed some of the behavioral and metabolic consequences of thiamine deficiency (Victor et al.1989; Lee et al.1995). Most recently, researchers administered different thiamine doses for two days to a group of alcoholics undergoing detoxification, none of whom were diagnosed with WKS, and then tested the participant’s working memory.
These studies found that participants who received the highest thiamine dose performed best on tests of working memory (Ambrose et al.2001). DIFFERENTIAL SENSITIVITY TO THIAMINE DEFICIENCY Differences in Sensitivity Among People Several findings suggest that not all people are equally sensitive to thiamine deficiency and its consequences.
For example, although thiamine deficiency may occur in up to 80 percent of alcoholics (Tallaksen et al.1992; Hoyumpa 1980; Morgan 1982), only about 13 percent of alcoholics develop WKS (Harper et al.1988). This means that the severest consequences of thiamine deficiency develop only in a subset of people who consume alcohol and have poor nutrition on a chronic basis.
A possible explanation for this differential sensitivity is that some people are genetically predisposed to develop brain damage after experiencing repeated episodes of alcohol–related thiamine deficiency. To investigate this hypothesis, researchers have studied the activities of thiamine–using enzymes in patients with and without Korsakoff’s psychosis, arguing that variants of these enzymes may exist that could differ in their susceptibility to thiamine deficiency.
The results of these investigations, however, have been inconsistent.2 ( 2 The studies cited in this section mostly used enzymes isolated from skin or blood cells of the participants. Although it is not known whether the effects of thiamine deficiency on these cells are identical to those on brain cells, the thiamine–using enzymes in these cells should be similar to the enzymes in brain cells, which are not accessible to the researchers.
- Using such model systems to investigate mechanisms of cell function has a long tradition in research.) One study (Blass and Gibson 1977) compared the activity of transketolase, PDH, and α–KGDH derived from skin cells of people with and without Korsakoff’s psychosis.
- These investigators found that transketolase from the Korsakoff’s patients bound ThDP less avidly than did the enzyme from the control subjects.
Transketolase from the Korsakoff’s patients could function normally when sufficient thiamine or ThDP was present; under conditions of thiamine deficiency, however, the transketolase molecules would not be able to bind enough ThDP to maintain normal enzyme activity.
As a result, the Korsakoff’s patients would be more susceptible to developing complications of thiamine deficiency than would people with a transketolase variant that more readily binds ThDP. The investigators found no differences, however, between Korsakoff’s patients and control subjects in the ability of the PDH and α–KGDH enzymes to bind ThDP.
In another study (Mukherjee et al.1987), researchers studied transketolase activity in alcoholic men without Korsakoff’s psychosis and their sons who had not yet been exposed to alcohol (i.e., who were alcohol naive) and compared it with transketolase activity in nonalcoholic volunteers and their sons.
This analysis found that the enzyme from the alcoholic men and their sons also bound ThDP less strongly than did the enzyme from the healthy volunteers and their sons (fathers and sons were similar to each other in both groups). This finding suggests that the genetic makeup of alcoholics or those who are at risk of becoming alcoholic (e.g., sons of alcoholics who are still alcohol naive) might cause them to be more affected by thiamine deficiency than nonalcoholics.
Other investigators, however, have found no differences in the ability of transketolase from Korsakoff’s patients and healthy subjects to bind ThDP (Nixon et al.1984). Several reasons may explain these differences in findings. For example, if a study includes active alcoholics, toxic substances formed during alcohol degradation in the body (e.g., acetaldehyde or oxygen radicals) could conceivably damage the transketolase, leading to impaired transketolase activity even if the person does not have a genetic predisposition.
Moreover, processing of the samples being studied could have modified and deactivated the transketolase. Overall, researchers to date have found no consistent correlation between genetically determined transketolase variants and a person’s sensitivity to thiamine deficiency (McCool et al.1993). To determine whether a genetic predisposition to thiamine deficiency and resulting brain damage does indeed exist, more detailed molecular genetic studies are required.
Another possible explanation for the differences among people in their sensitivity to thiamine deficiency has focused on the assembly of functional transketolase. To yield a functional enzyme, two transketolase molecules—each of which is bound to ThDP and to magnesium—must come together.
- This assembly step is aided by an as yet unidentified “assembly factor,” which is probably also involved in the assembly of other thiamine–using enzymes.
- If this factor were defective, the final enzyme complex would be formed at a lower rate and would be unstable (Wang et al.1997).
- Researchers have identified at least one person with WKS whose cells showed enhanced sensitivity to thiamine deficiency and in whom the assembly factor was defective (Wang et al.1997).
Other mechanisms that could contribute to individual differences in the sensitivity to alcoholism could involve variability in the capacity for thiamine uptake into the cells or in the overall sensitivity to cell damage induced by oxidative stress. Differential Sensitivity of Various Brain Regions Various brain regions and even different cell types within one brain region may differ in their sensitivity to alcohol–induced damage as well as in their susceptibility to associated problems, including alcohol–related malnutrition (e.g., thiamine deficiency).
For example, as mentioned earlier, the cerebellum appears to be particularly sensitive to thiamine deficiency, as indicated by the high frequency of cerebellar degeneration in alcoholics. Autopsy studies have found that a region of the cerebellum known as the anterior superior cerebellar vermis most frequently exhibits alcohol–induced damage (Baker et al.1999).
Additional studies have found that the cerebellar vermis is particularly sensitive to the deleterious effects of thiamine deficiency (Baker et al.1999; Lavoie and Butterworth 1995; Victor et al.1989). For example, thiamine deficiency contributes to a reduction in the number and size of a certain cerebellar cell type called Purkinje cells in parts of the cerebellar vermis (Philips et al.1987).
The sensitivity of the cerebellum to alcohol–related damage was confirmed in a recent study in which investigators used an imaging technique called proton magnetic resonance spectroscopy (proton MRS) to determine the levels of certain molecules (i.e., metabolites) that reflect the functionality of the cells in various brain regions of alcoholics and nonalcoholics.
For example, one metabolite reflects nerve cell activity, another metabolite reflects the degradation and formation (i.e., turnover) of cell membrane components, and a third metabolite reflects cellular energy levels. The results of the analyses indicated that these metabolites are significantly reduced in the cerebellum of alcoholics, more so than in another brain region commonly affected by alcohol, the frontal white–matter cortex (Parks et al.2002).
Moreover, only some of these reductions in metabolite levels were reversed when the subjects were tested again after 3 weeks and then 3 months of abstinence. These findings suggest that the cerebellum, in particular the cerebellar vermis, is uniquely sensitive to alcohol’s effects, including alcohol–related thiamine deficiency, and therefore may be the initial target of alcohol–related damage.
This hypothesis is consistent with the clinical course of the neurocognitive deficits observed in alcoholics. Networks of nerve cells (i.e., neural pathways) extend from the cerebellum through brain regions called the basal ganglia and thalamus to the frontal lobe.
- These pathways mediate not only traditional cerebellar functions, such as motor control, but also perceptual– motor tasks, executive functions, and learning and memory, all of which are impaired in alcoholics (see Parks et al.2002).
- Accordingly, alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe, even early in the disease process when no cortical damage is detectable, by disrupting the neural pathways connecting the two brain regions.
As the alcoholism progresses and alcohol exposure persists, damage to the frontal lobe is also likely to occur, further interfering with the functions of that brain region. In addition to the cerebellum, numerous other brain regions and structures are damaged in people with WKS.
Although animal studies have suggested that thiamine deficiency may contribute to damage to these structures, the exact role of thiamine deficiency and the level of sensitivity of these structures to thiamine deficiency have not yet been determined. Further studies are certainly needed in this area. SUMMARY Thiamine deficiency, which is found in a large number of alcoholics, is an important contributor to alcohol–related brain damage of all kinds, not only WKS, as was commonly thought in the past.
Thiamine is an essential cofactor for several enzymes involved in brain cell metabolism that are required for the production of precursors for several important cell components as well as for the generation of the energy–supplying molecule ATP. Thiamine deficiency leads to significant reductions in the activities of these enzymes, and to deleterious effects on the viability of brain cells.
- Chronic alcohol consumption can cause thiamine deficiency and thus reduced enzyme activity through several mechanisms, including inadequate dietary intake, malabsorption of thiamine from the gastrointestinal tract, and impaired utilization of thiamine in the cells.
- Accordingly, thiamine deficiency can potentiate a number of processes associated with chronic alcohol consumption that are toxic to brain cells, as discussed in other articles in this journal issue.
It is important to note that these adverse effects of alcohol–induced thiamine deficiency, particularly the reduction of transketolase activity, can occur even in alcoholics who do not show evidence of WE or WKS. The extent to which alcohol exerts its detrimental effects on the brain and various other tissues may be genetically determined via individual differences in predisposition to thiamine deficiency disorders.
For example, some studies have suggested that there may be different variants of the genes encoding transketolase, which differ in their ability to bind the active form of thiamine, particularly at low thiamine concentrations. Such a genetic variation could be one explanation for why only a subset of alcoholics who experience thiamine deficiency develop the pathological consequences of that condition, such as WKS.
Additional genetic studies are necessary, however, to clarify the roles of different genetic variants and determine whether a genetically determined susceptibility does indeed exist. Various brain regions also differ in their sensitivity to alcohol’s effects, including alcohol–induced thiamine deficiency.
- The cerebellum appears to be particularly sensitive to the effects of thiamine deficiency and is the region most frequently damaged in association with chronic alcohol consumption.
- This heightened susceptibility is consistent with the cognitive deficits typically associated with alcoholism.
- These deficits are indicative either of cerebellar damage or of damage to the frontal lobes, which are connected to the cerebellum through neural pathways.
Accordingly, reversal of thiamine deficiency—for example, by administering thiamine at pharmacological levels—may not only ameliorate the consequences of cerebellar damage but improve some brain functions typically associated with the frontal lobe. REFERENCES AMBROSE, M.L.; BOWDEN, S.C.; and WHELAN, G.
Thiamin treatment and working memory function of alcohol–dependent people: Preliminary findings. Alcoholism: Clinical and Experimental Research 25(1):112–116, 2001. BAKER, K.G.; HARDING, A.J.; HALLIDAY, G.M.; et al. Neuronal loss in functional zones of the cerebellum of chronic alcoholics with and without Wernicke’s encephalopathy.
Neuroscience 91:429–438, 1999. BLASS, J.P., and GIBSON, G.E. Abnormality of a thiamine–requiring enzyme in patients with Wernicke– Korsakoff syndrome. New England Journal of Medicine 297:1367–1370, 1977. CALINGASAN, N.Y.; CHUN, W.J.; PARK, L.C.; et al. Oxidative stress is associated with region–specific cell death during thiamine deficiency.
Journal of Neuropathology and Experimental Neurology 58(9): 946–958, 1999. CHARNESS, M.E. Brain lesions in alcoholics. Alcoholism: Clinical and Experimental Research 17:2–11, 1993. FERGUSON, R.K.; SORYAL, I.N.; and PENTLAND, B. Thiamine deficiency in head injury: A missed insult? Alcohol and Alcoholism 32(4):493–500, 1997.
GIBSON, G.E.; KSIEZAK–READING, H.; SHEU, K.–F.R.; et al. Correlation of enzymatic, metabolic, and behavioral deficits in thiamine deficiency and its reversal. Neurochemical Research 9:803–814, 1984. HARPER, C. The neuropathology of alcohol–specific brain damage, or does alcohol damage the brain? Journal of Neuropathology and Experimental Neurology 57:101–110, 1998.
- HARPER, C.; RODRIGUEZ, M.; GOLD, J.; and PERDICES, M.
- The Wernicke–Korsakoff syndrome in Sydney—a prospective necropsy study.
- Medical Journal of Australia 149:718–720, 1988.
- HOYUMPA, A.M.
- Mechanisms of thiamine deficiency in chronic alcoholism.
- American Journal of Clinical Nutrition 33:2750–2761, 1980.
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Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. American Journal of Kidney Disease 38(5):941–947, 2001. LAFORENZA, U.; PATRINI, C.; GASTALDI, G.; and RINDI, G. Effects of acute and chronic ethanol administration on thiamine metabolizing enzymes in some brain areas and in other organs of the rat.
Alcohol and Alcoholism 25:591–603, 1990. LAVOIE, J., and BUTTERWORTH, R.F. Related activities of thiamine–dependent enzymes in brains of alcoholics in the absence of Wernicke’s encephalopathy. Alcoholism: Clinical and Experimental Research 19:1073–1077, 1995. LEE, H.; TARTER, J.; HOLBURN, G.; et al. In vivo localized proton NMR spectroscopy of thiamine–deficient rat brain.
Magnetic Resonance Medicine 34:313–318, 1995. LEEVY, C.M., and BAKER, H. Vitamins and alcoholism. American Journal of Clinical Nutrition 21:1325–1328, 1968. MARTIN, P.R.; ADINOFF, B.; WEINGARTNER, H.; et al. Alcoholic organic brain disease: Nosology and pathophysiologic mechanisms.
- Progress in Neuro–psychopharmacological and Biological Psychiatry 10:147–164, 1986.
- MCCOOL, S.G.; PLONK, S.G.; MARTIN, P.R.; and SINGLETON, C.K.
- Cloning of human transketolase cDNAs and comparison of the nucleotide sequence of the coding region in Wernicke–Korsakoff and non–Wernicke–Korsakoff individuals.
Journal of Biological Chemistry 268:1397–1404, 1993. MORGAN, M.Y. Alcohol and nutrition. British Medical Bulletins 38:21–29, 1982. MUKHERJEE, A.B.; SVORONOS, S.; GHAZANFARI, A.; et al. Transketolase abnormality in cultured fibroblasts from familial chronic alcoholic men and their male offspring.
Journal of Clinical Investigation 79:1039–1043, 1987. NIXON, P.F.; KACZMAREK, M.J.; TATE, J.; et al. An erythrocyte transketolase isoenzyme pattern associated with the Wernicke–Korsakoff syndrome. European Journal of Clinical Investigation 14:278–281, 1984. PARKS, M.H.; DAWANT, B.M.; RIDDLE, W.R.; et al.
Longitudinal brain metabolic characterization of chronic alcoholics with proton magnetic resonance spectroscopy. Alcoholism: Clinical and Experimental Research 26(9):1368–1380, 2002. PARKS, M.H.; MORGAN, V.L.; PICKENS, D.R.; et al. Brain FMRI activation associated with self–paced finger tapping in chronic alcohol–dependent patients.
Alcoholism: Clinical and Experimental Research 27(4):704–711, 2003. PHILIPS, S.C.; HARPER, C.; and KRIL, J. A quantitative histological study of the cerebellar vermis in alcoholic patients. Brain 110:301–314, 1987. POUPON, R.E.; GERVAISE, G.; RIANT, P.; et al. Blood thiamine and thiamine phosphate concentrations in excessive drinkers with or without peripheral neuropathy.
Alcohol and Alcoholism 25:605–611, 1990. RAGAN, P.W.; SINGLETON, C.K.; and MARTIN, P.R. Brain injury associated with chronic alcoholism. CNS Spectrums 4(1):66–87, 1999. RAJGOPAL, A.; EDMONDSON, A.; GOLDMAN, I.D.; and ZHAO, R. SLC19A3 encodes a second thiamine transporter ThTr2.
Biochimica et Biophysica Acta 1537(3):175–178, 2001. RINDI, G.; CASIROLA, D.; POGGI, V.; et al. Thiamine transport by erythrocytes and ghosts in thiamine–responsive megaloblastic anemia. Journal of Inherited Metabolic Diseases 15:231–242, 1992. SINGLETON, C.K., and MARTIN, P.R. Molecular mechanisms of thiamine utilization.
Current Molecular Medicine 1(2):197–207, 2001. TALLAKSEN, C.M.E.; BOHMER, T.; and BELL, H. Blood and serum thiamin and thiamin phosphate esters concentrations in patients with alcohol dependence syndrome before and after thiamin treatment. Alcoholism: Clinical and Experimental Research 16:320–325, 1992.
- TODD, K., and BUTTERWORTH, R.
- Early microglial response in experimental thiamine deficiency: An immunohistochemical analysis.
- Glia 25:190–198, 1999.
- TORVIK, A.
- Brain lesions in alcoholics: Neuropathological observations.
- Acta Medica Scandinavica 717(Suppl.):47–54, 1987.
- VICTOR, M.; DAVIS, R.D.; and COLLINS, G.H.
The Wernicke–Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition, Philadelphia: F.A. Davis, 1989. WANG, J.J.–L.; MARTIN, P.R.; and SINGLETON, C.K. A transketolase assembly defect in a Wernicke–Korsakoff syndrome patient.
How quickly does alcohol deplete B12?
We have covered the relationship between vitamin D, alcohol, and depression. We want to talk about another negative side effect of alcohol related to vitamins. Dr. Joseph Bradley Oversees our Nutraceutical Education and Supplements Alcohol flushes vitamin B from your system.
- We need vitamin B to manufacture red blood cells.
- A lack of vitamin B often results in anemia.
- This makes a person feel weak and tired.
- Vitamin B-12 plays an important role in production brain chemicals that effect our mood and many other crucial brain functions.
- Low levels of B -12 and B-6 have been linked to depression.
Drinking alcohol regularly for more than two weeks decreases vitamin B12 absorption from the gastrointestinal tract. Vitamin B deficiency has been noticed in people who report suffering from depression. Vitamin B deficiency has also been linked to a poor response to antidepressant medication to make matters worth for alcoholics suffering with depression.
Evidence suggests that people with depression do better in treatment with higher levels of vitamin B12 in their system. One theory suggests that vitamin B12 deficiency increases the chances for a build up on the amino acid homocysteine, which may exacerbate depression. Many alcoholics are also deficient in vitamin B3, commonly known as Niacin.
In rehab centers around the country, during alcoholic withdrawals, some patients have been reported to spontaneously stop drinking in association with taking niacin supplements. This gave some the idea that alcoholism may be a manifestation of niacin deficiency.
The consumption of alcohol results in the formation of two very toxic compoundsacetaldehyde and malondialdehyde. These compounds generate massive free radicals that damage cells throughout the body. This causes that feeling of illness the next day. Proper antioxidants taken before a night of excessive drinking can minimize the hangover or damage to the body.
The older one gets the more damage these free radicals can have on the body. According to the National Institute of Mental Health depression affects 17 million Americans a year. People who have depression shouldn’t drink as it depresses the central nervous system.
Alcohol is a depressant. Why add fuel to the fire? Although alcoholic consumption may for a while dull the effects of stress hormones, it more than not leaves the user feeling worse than before because of how it depresses the brain and nervous system. The effects of alcohol on the central nervous system can be seen and measured in terms of human performance especially during field sobriety tests, where an individuals motor skills are radically hampered by excessive alcoholic consumption.
The questions I ask myself after researching all the above is, are clinics and rehab centers using vitamin B to treat alcoholism? Our drug facility does this. Sierra by the Sea supplements our therapeutic blend of activities with nutraceutical education and supplements.
How does alcohol deplete magnesium?
First, alcohol acts acutely as a Mg diuretic, causing a prompt, vigorous increase in the urinary excretion of this metal along with that of certain other electrolytes. Second, with chronic intake of alcohol and development of alcoholism, the body stores of Mg become depleted.
Should I take vitamin B if I drink alcohol?
From the earliest days of alcohol consumption in Ancient Egypt to modern-day Aperol spritz and craft beer crazes, humans have been dealing with the same problem — hangovers. Alcohol may relax you and make you feel great in the moment, but if you drink too much, you inevitably wake up the next morning (or afternoon) feeling awful.
- And unfortunately, the older you get, the worse alcohol tends to make you feel.
- This is why OnMi came up with a better solution in the form of an expertly crafted combination of vitamins: a Hangover Relief Patch,
- Just apply one an hour before you start drinking, then apply a fresh one the next morning.
Easy. But does it actually work? Can you take vitamins with alcohol ? Or is v itamins and alcohol interaction dangerous? OnMi dove into the scientific research out there to find the truth. Vitamins and Alcohol Interaction : An Answer Long story short, the answer to the question of ” can you take vitamins with alcohol ” is: yes, and it can even be beneficial to do so.
- Many people think this is because drinking alcohol negatively affects our body’s ability to absorb vitamins, but this meta-study found that the consumption of alcohol has no effect on our ability to absorb vitamins properly.
- The scientists concluded that the only culprits of a hangover are “alcohol and its metabolites”, meaning alcohol and the enzymes that break it down.
If hangovers are really just caused by alcohol and how it is metabolized, what, then, could one do to speed up the breakdown of alcohol to get it out in time to wake up with a smile on one’s face and a song in one’s heart? B vitamins are the star of the show here.
B vitamins are essential enzymes that get their rave on during the process of turning carbohydrates, such as alcohol, into energy. Thus, taking more B vitamins can assist your body in efficiently metabolizing alcohol to afford you the utmost of comfort the morning after a big night out. B vitamins and alcohol interaction is a completely safe combination that could improve your hangover.
Why an OnMi Patch is the Best for Vitamins and Alcohol Interaction So why not just buy B vitamins? Because OnMi has a better product for your Sunday Scaries. Turns out, your body may only be able to use 30% of the vitamins you buy in powder or capsule form.
Everything else gets flushed down the toilet along with all the money you spent buying those vitamins. Traditional vitamins have yet another downside: you have to swallow them. When your stomach’s already feeling queasy, forcing yourself to swallow a couple of pills along with your morning coffee can make you feel even more nauseated.
Even if you manage to keep things together, the nausea itself is far from pleasant. OnMi’s hangover patch solves both of those problems. It contains vitamins B1, B3, and B6, which your body desperately needs after a night on the town. Plus, we included guarana for a natural energy boost.
Because it’s a patch, there’s no pill-swallowing or additional nausea with which you have to deal. Perhaps most importantly, your body is still able to absorb up to 90% of the vitamins in the patch, making one patch far more effective than capsules and powders. Turns out the answer to the question of “can you take vitamins with alcohol ” was even better than you thought.
Can You Take Vitamins with Alcohol ? Yes, but You Need Water too. Even though the answer to ” can you take vitamins with alcohol ” is an emphatic “yes”, our patches can’t fix everything. If you apply one before you go out and a second one in the morning, you should feel better than you would otherwise, but there’s another aspect of hangovers that our patch can’t address — dehydration.
- Most people know this part, but since alcohol acts as a diuretic, drinking causes you to go to the bathroom a lot, and while alcoholic beverages are mostly water, they are not enough to replace the water you lose.
- Drink too much, and you’ll end up dehydrated.
- And if you’re already dehydrated when you start drinking, even a moderate amount of alcohol can leave you with a dry throat and a headache.
It may be possible to mask the feeling temporarily, but when your body’s short on water, the only thing that will actually help you feel better is more water. You must rehydrate. And since we still have yet to figure out a way to magically create dehydrated water, your only option is good, old-fashioned H2O.
What vitamins are depleted by caffeine?
“Do we have to give up coffee?” This is one of the most frequent questions we get from our newbie cleansers. And, unfortunately we have to be the bearer of bad news because after all this is a cleanse, and when we’re working on resetting the body’s system, part of this involves looking at what we’re dependent on for energy.
Although highly addictive, if you read any of the studies out there it quickly becomes confusing as to whether or not 1 cup of coffee a day will help prevent Alzheimer’s and colon cancer or if it’s the reason you can’t sleep, deal with anxiety, depression and even unwanted pounds. We firmly believe that taking a break from your Americano is not only beneficial, but also extremely empowering.
If you can kick your caffeine habit, what else is possible for you and your life? We say it all the time because it’s so true: The foods you love and crave the most are often times the foods causing the most problems in your health. Below are the top 7 reasons for replacing your beloved latte with a new non-caffeinated morning beverage.
- And, if you can’t even fathom a day without coffee, then consider it one more reason to take a break from it for a few weeks.
- Nudge, nudge! We know this is a hot topic for many people and we want to hear from you.
- Try it for yourself and tell us what happens.
- Notice how you feel, that is, after you come off your initial “coffee hangover.” You might just feel like a million bucks and have more energy than you’ve had in a long time.
With caffeine-free kisses, P.S. – Your caffeine addiction might show up in other forms like diet soda, energy drinks, or black tea, so don’t think you’re off the hook if you’re not a coffee drinker.
Coffee is acid-forming, Highly acidic, coffee wrecks havoc on your gut, affecting the natural balance of your flora.80% of our immune system is located in the gut, so you can imagine that when your digestive system out of whack, the rest of you is gonna be out of balance too. For optimal heath, we’re striving for an alkaline state, which means bye-bye acid forming drinks and foods. Coffee is full of chemicals, With all of our focus on the dirty dozen, we often lose sight of our favorite hot drinks, which are laden with nasty toxins. Coffee crops are sprayed heavily with pesticides, especially when imported from other countries. Coffee messes with your vanity, Yes, seriously! Most of us know that coffee is a diuretic, which means that it dehydrates the body. But did you know that dehydration could also lead to premature aging of the skin and kidneys. No thanks! We’d rather have vibrant glowing skin. Coffee leads to unwanted pounds, You’ve probably heard that coffee helps you lose weight. In reality, coffee spikes our blood sugar leading to higher levels of insulin in the body. After the spike in insulin, our blood sugar crashes and thus the nasty cycle begins. The blood sugar roller coaster and high levels of insulin send a signal to store excess sugar as fat. Avoiding the muffin top might be your motivation to ditch the coffee, but the way you feel when you kick the habitpriceless. Coffee strips your body of key vitamins, Maybe your thinking, “vitamins, schmitamins.” But here’s the deal, too much coffee depletes your supply of B vitamins, which is your natural source of energy. Caffeine also causes the body to dump other key nutrients like calcium, magnesium, potassium and iron. Have I made my case yet? Coffee can affect your mood, Instead of boosting your mood, caffeine actually produces stress hormones, which can trigger anxiety, irritability and insomnia. Most of us are already running around in a state of “fight or flight,” so ditching coffee is essential for helping us stay calm in our stressful lives. Coffee is void of nutrients, One of the key principles of the Conscious Cleanse is to focus on nutrient-dense food. Not only does coffee deplete the body of nutrients, it’s got nothing to give us in exchange short of a very temporary pick me up. Enough said! Coffee you’re fired!
If you liked this and would like learn more about the Conscious Cleanse, we invite you to join our online community! As a welcome-gift, we’ll send you our Green Smoothie eCookbook, a collection of more of our favorite easy smoothie recipes! We also share new recipes, free live calls with us, and more healthy lifestyle tips, plus let you know when our next group cleanse is coming.
Does alcohol deplete potassium?
Alcohol consumption historically has been found to reduce the amount of potassium excreted by the kidneys (e.g., Rubini et al.1955), although the body’s hydration state may help determine whether potassium excretion will increase or decrease in response to alcohol.
Do alcoholics need more magnesium?
Magnesium After Alcohol Withdrawal Treatment – Full Text View
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details.
Brief Summary: The primary purpose is to see if magnesium tablet supplementation will decrease elevated GGT enzyme activity in alcoholic patients immediately after they had been treated for alcohol withdrawal. The secondary aims are to find out whether supplementation decreases the activity of ASAT and ALAT enzymes, increases muscle strength, decreases blood pressure and decreases depressive symptoms among these patients.
Magnesium (Mg) deficiency is common among alcoholics. Animal studies have shown that magnesium deficiency aggravates the hepatic damage caused by alcohol. One study on chronic alcoholics suggested that magnesium supplementation over six weeks decreases abnormally high activities of three enzymes related to liver function: serum gamma-glutamyltransferase (GGT), aspartate-aminotransferase (ASAT) and alanine-aminotransferase (ALAT), and increases muscle strength,
- These results were, however, significant at the 5% level only when a 1-sided test was applied.
- It seems that magnesium supplementation may improve liver recovery after a drinking bout, but the evidence is not yet strong enough to warrant clear recommendations for clinical practice.
- Magnesium deficiency may also be one of the symptoms of depression and may aggravate hypertension.
The primary purpose of the present randomized, parallel group, double blind trial is to see if oral magnesium supplementation will decrease elevated GGT enzyme activity in alcoholic patients immediately after they had been treated for alcohol withdrawal.
Serum gamma-glutamyltransferase (GGT) activity
Secondary Outcome Measures :
- Aspartate-aminotransferase (ASAT) activity
- Alanine-aminotransferase (ALAT) activity
- Depressive symptoms
- Blood pressure
- Handgrip muscle strength
- Admission to treatment because of an acute alcohol withdrawal
- Elevated serum GGT (men>80, women >50)
- Age 20-64 years
- Fixed address and a telephone to facilitate follow-up
- Mg supplementation within the past two months ten 250 mg tablets or more
- History of heart rhythm disturbances
- Contraindications against Mg treatment
- Abnormally high serum creatinine
|Finnish Foundation for Alcohol Studies
|Helsinki, Finland, 00531
Finnish Foundation for Alcohol Studies
|Kari Poikolainen, Dr Med Sci
|Finnish Foundation for Alcohol Studies
Magnesium After Alcohol Withdrawal Treatment – Full Text View
Is magnesium high or low in alcoholics?
Background – Magnesium (Mg) deficiency is common among alcoholics, Even in cases with normal serum Mg levels marked intracellular deficiency may be present. Animal studies have shown that Mg deficiency aggravates the hepatic damage caused by alcohol,
- Mg treatment may help to normalize elevated enzyme activities and some other clinically relevant parameters, presented below, among alcoholics but the evidence is weak.
- A Norwegian study on chronic alcoholics suggested that Mg treatment over six weeks decreases abnormally high activities of three enzymes related to liver function: serum gamma-glutamyltransferase (S-GGT), aspartate-aminotransferase (S-AST) and alanine-aminotransferase (S-ALT), and increases handgrip muscle strength,
The above results were, however, significant at the 5% level only when a 1-sided test was applied. This may be related to the small sample size, 24 alcoholics in the treatment and 25 in the control group. In the treatment for alcohol withdrawal syndrome Mg administration has been questioned, and a randomized study found no effect of intramuscular Mg injections on withdrawal symptoms,
- However, long-term Mg treatment may help to restore liver function and other impairments after a drinking bout, but the evidence is not yet strong enough to warrant clear recommendations for clinical practice.
- Mg deficiency may also be a cause of depression,
- Mg ions regulate calcium ion flow in neuronal calcium channels, helping to regulate neuronal nitric oxide production.
In Mg deficiency, neuronal requirements for Mg may not be met, causing neuronal damage which could manifest as depression. Rapid recovery from depression has been seen in some cases after Mg treatment, Depressive symptoms are common among alcoholics during withdrawal from alcohol and often disappear during abstinence without any specific drug treatment,
It thus seems possible that Mg supplementation might also be useful in diminishing depressive symptoms among alcoholics after withdrawal. To clarify the clinical importance of the above, we studied the effect of oral Mg treatment in alcoholics, after treatment for alcohol withdrawal symptoms, in a randomized, parallel group, double-blind trial.
Confounders were included in the analyses, when appropriate,
What electrolytes are depleted when you drink alcohol?
Abstract – The present review summarizes the current knowledge on the multiple effects of alcohol overconsumption on the kidney function as well as on water, electrolyte and acid-base homeostasis. In contrast to the well known transitory diuretic effects, the overall long-term effect of chronic alcohol overconsumption is water and salt retention with expansion of extracellular volume.
Furthermore, depletion of magnesium, phosphate and calcium is also frequently found in alcohol-dependent patients. These electrolyte disturbances may be associated with the alcohol-induced hypoparathyroidism and parathyroid hormone resistance of the skeletal muscle as well as with the decrease of serum osteocalcin.
Metabolic acidosis with lower arterial blood pH and plasma bicarbonate concentrations was revealed in alcoholic patients upon admission and a significant correlation between chronic alcohol overconsumption and increased incidence of hyperuricemia and gout attacks was also reported.
Alcohol seems to have dual effects on the blood pressure. Increased blood pressure was demonstrated in men above 80 g and in women above 40 g ethanol consumption daily. In contrast, young adults consuming only 10 to 20 g per day had lower blood pressure than the abstinent group indicating a J-curve relationship.
This is in line with the lowered risk for coronary heart disease associated with regular consumption of small alcohol amounts. The mechanisms responsible for the association between alcohol overconsumption and postinfectious glomerulonephritis have not been elucidated yet.
Why does alcohol deplete vitamin D?
In compromising normal liver function, explains Sampson, alcohol interferes with the conversion of both dietary and endogenously produced vitamin D into its active metabolites. As a consequence, heavy drinkers have low blood levels of activated vitamin D.
Why do alcoholics lack thiamine?
Alcohol and Thiamine Deficiency – Normal thiamine uptake by the brain appears to just slightly exceed the amount required for proper brain functioning. Consequently, any reduction in thiamine availability could have serious effects on brain metabolism and may result in brain lesions and cognitive dysfunction.
In alcoholics, several factors may contribute to thiamine deficiency. First, nutritional thiamine deficiency can occur in alcoholics because of their poor eating habits. Alcoholics may eat nothing for days, and when they do eat, their food often is high in carbohydrates and low in vitamins such as thiamine.
In addition, high carbohydrate intake further depletes the already low thiamine levels, because two enzymes involved in the breakdown of carbohydrates (i.e., pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase) are thiamine-requiring enzymes.
- Second, alcoholics may develop a thiamine deficit because of impaired thiamine absorption from the intestine ( Hoyumpa 1980 ).
- Alcohol damages the lining of the intestine and directly inhibits the transport mechanism that is responsible for thiamine absorption in the intestinal tract ( Gastaldi et al.1989 ).
Also contributing to reduced thiamine uptake may be a nutritional deficiency of the vitamin folic acid, which commonly occurs in alcoholics as a consequence of poor nutrition. Studies in rats found that folic acid-deficient animals absorbed thiamine less efficiently than did healthy rats and that restoration of folic acid intake reversed the thiamine malabsorption ( Howard et al.1974 ).
Third, during chronic alcohol exposure, the activity of thiamine-metabolizing enzymes in the brain is compromised. To serve as a cofactor for the enzymes involved in energy production and lipid synthesis, thiamine must be converted into an active form by the enzyme thiamine pyrophosphokinase. Excessive alcohol consumption results in a significant decrease in thiamine pyrophosphokinase activity ( LaForenza et al.1990 ).
In addition, alcohol consumption increases the activity of the enzymes that break down activated thiamine in the brain ( LaForenza et al.1990 ). Through these mechanisms, alcohol could reduce the activity of thiamine-dependent enzymes and affect brain metabolism even in the presence of adequate nutrition and thiamine absorption.
Why do alcoholics need more vitamin C?
Discussion – Severe vitamin C deficiency causes the clinical features of scurvy. Scurvy is rarely seen in the UK, and so it is important for clinicians to be able to recognise its clinical features when it presents in high-risk individuals. The table below illustrates common (in italics) and uncommon signs and symptoms that have been reported in vitamin C deficient states.
|Signs or associations
|Purpura, petechia, ecchymosis, perifollicular hyperkeratosis, alopecia, splinter haemorrhages
|Dry, brittle skin, bruises
|Conjunctival haemorrhage, intraocular haemorrhage
|Dry eyes, blurred vision
|Gingivitis, loss of teeth
|Recurrent chest infections in smokers
|Cardiac hypertrophy, cardiac failure, haemopericardium, coronary artery disease, anaemia
|Gastrointestinal (GI) system
|Jaundice, upper GI bleeds
|Loss of appetite, weight loss, diarrhoea
|Urinary tract infections
|Seizures, pseudoparalysis, neuropathy
|Haemarthrosis, scorbutic rosary (chest wall deformity seen in children), pathological fractures, dislocations, osteopenia
|Myalgia ( especially legs ), arthralgia
|Irritability ( in children ), fever
Chronic alcoholism can lead to vitamin C deficiency in several ways: (1) malnutrition through self-neglect or poverty, (2) malabsorption from chronic diarrhoea secondary to alcohol or chronic pancreatitis and (3) increased urinary excretion of vitamin C caused by alcohol.2 Features of vitamin C deficiency such as malaise, loss of appetite, diarrhoea, a propensity towards bleeding and jaundice could be easily masked and attributed to coexisting liver disease.
- Symptoms and complications of alcoholic liver disease could also be worsened by untreated vitamin C deficiency.
- Within the UK, it is common practice to give hospitalised chronic alcohol abusers high doses of intravenous vitamins, often over 2–3 days to treat vitamin deficiencies and prevent complications such as Wernicke-Korsakoffs’ syndrome.
Vitamins B 1, B 2, B 3, B 6 and C are given intravenously in the form of a commercial preparation commonly known as ‘high-dose Pabrinex’. Pabrinex is the only licensed intravenous preparation containing vitamin C and the various vitamin Bs in the British National Formulary.
- It comes in a set of either two 5 mL ampoules or two 10 mL ampoules.
- High-dose Pabrinex’ refers to the 10 mL ampoules—it is ampoule 2 which contains 1000 mg of vitamin C.
- Usually 4–6 doses are administered over 2–3 days.
- Patients are then given oral thiamine (100–300 mg daily) and vitamin B compound tablets (1–2 tablets twice daily).
The normal body store of vitamin C is estimated to be 1500 mg in an average healthy man and the clinical features of scurvy usually occurs after 3 months of vitamin C deficiency when levels fall below 0.1 mg/dL.3 Therefore, many physicians would assume the commonly used regimen described above would be more than adequate to correct vitamin C deficiency.
This case report however highlights the inadequacy of this regimen and demonstrates chronic alcohol abusers who are at risk of longstanding vitamin C deficiency may need a prolonged course of vitamin C supplementation either intravenously or orally, especially in those who are acutely ill or critically unwell.
This is possibly because vitamin C is a negative acute phase reactant and there is increased use of vitamin C in the cellular processes involved in inflammation and tissue repair, particularly in acute critical illness and infectious states. Further GI and renal losses of vitamin C (eg, from intestinal failure or emergency renal replacement therapy) in the critically ill chronic alcoholic patient may also occur and contribute to a vitamin C-deficient state.
Does alcohol affect vitamin d3?
Vitamin D and Serotonin – Higher levels of vitamin D can increase serotonin. As a neurotransmitter, serotonin helps the brain to relay message form one area to the other and is believed to be highly influential in a a variety of psychological functions.
Most of our brain cells are influenced directly or indirectly by serotonin. Cells in the brain related to mood, sexual desire, appetite, sleep, learning, memory and a lot of social behavior are effected by serotonin levels. A lack of serotonin would, as you can see from the above examples, would seemingly have a strong case as a major factor in terms of depression.
Low production of serotonin in the brain can lead to depression when we consider that the serotonin isn’t reaching it’s receptor site. So there you go. Alcoholic consumption lowers vitamin D levels in the body. Lower D levels can effect serotonin production.