It is often deceived by the frequency of drinking, by the admission of guilt, remorse, by reason of his feelings and his desire to be corrected.

He is convinced that a reprimand is sufficient to make change. This conduct is harmful: it is not to condemn the drinker or sermon, but is contrary to normal treatment, effective and appropriate.

The drinker is found his game and tries to defend itself with weapons used and other times, like denying that you have a problem with drinking, protesting against such accusations skirts.

Current use excuses and bragging about his ability to hold the drink and work.

The control is better placed than anyone to encourage the patient to consult a specialist.

You should not try to convince a closed person, which will be limited to a discussion, to be angry and upset, as an excuse to quickly end the interview.

Take a firm and unchanging, repeating to convince his reasons against the excuses of the drinker. We recommend visiting the specialist, you will make it easier to attend, will closely follow developments and try to reinstate your job

The desire for alcohol during withdrawal, pain suppression and the high rate of relapse is due to adaptation and dependence on changes in brain chemistry caused by his long-term use of alcohol. Alcohol acts as a depressant on the central nervous system and causes relaxation and euphoria. In the brain, a small group of chemical messengers, called neurotransmitters, is responsible for changes in behavior after drinking alcohol. Of special interest to researchers are the neurotransmitter gamma aminobutérico acid (GABA, gamma amino butyric acid), dopamine and serotonin.

Genetic factors.

In people with severe alcoholism, researchers have located a gene that affects the function of a nerve-cell structure known as the dopamine D2 receptor (DRD2), which, in turn, influences the activity of dopamine. This gene is also found in people with attention deficit disorder, who are at increased risk for alcoholism, and is also present in people with Toilette syndrome and autism. The association of this gene with these neurological problems leading some experts to believe that the dopamine D2 receptor gene is not a primary cause of alcoholism, but that people with this gene is more likely to drink to treat behavioral and psychological symptoms of their neurological disorders. In addition, a main study did not find any connection whatsoever between the DRD2 gene and alcoholism. More work is needed in this area.

Depression and anxiety.

Some people drink to relieve anxiety or depression, and theories has been proposed on the fact that an inherited tendency for depression or anxiety can make people more susceptible to alcoholism. Studies have indicated, however, that when children of alcoholic parents raised by parents are not alcoholics, their risk for alcoholism but opportunities remain high for depression or anxiety are greater than those of the general population. Indeed, anxiety and depression are themselves caused by alcoholism can be reduced after the abolition of alcohol. Depression and anxiety can also play a major role in the development of alcoholism in the elderly and others who are subject to undesirable life changes like retirement, loss of a spouse or friend (a) and medical problems.

Physical Effects

Alcohol is not exposed to any process of digestion which mostly goes first to the small intestine before being absorbed by the bloodstream. Only a small portion goes directly into the bloodstream through the stomach lining. In the blood alcohol is metabolized (broken down to be removed or used by the body) through the process of oxidation. That is, it merges with oxygen and breaks down so that its basic elements leave the body in the form of carbon dioxide and water. The first oxidation is the liver, which breaks down approximately 50% of alcohol consumed in one hour. The rest remains in the bloodstream to be removed slowly.

Psychological Effects

Alcohol first affects the central nervous system and excessive and prolonged interference can cause brain damage. Popular belief that alcohol increases the excitement, but actually depresses many brain centers. The feeling of excitement is precisely because the depressed some brain centers reduce tensions and inhibitions and the person experiences feelings of sociability expanded or euphoria. Therefore it is said that alcohol “anesthesia, internal auditing.” However, if the alcohol concentration exceeds certain levels in the blood interferes with higher mental processes so that the distorted visual perception, motor coordination, balance, speech and vision have also suffered heavy damage. Large amounts of alcohol reduce body aches and pains and induce sleep. But continuous use irritates the stomach lining even to develop ulcers. Additionally tends to accumulate fat in the liver, interfering with its operation. In chronic alcoholics are raised serious brain disorders, liver (cirrhosis) and cardiovascular (increased blood pressure and thus the risk of a heart attack.) Even, there is evidence that alcohol increases the level of triglycerides (saturated fat or vegetable in the arteries) and thus also the risk of a heart attacks. Finally, as is well known, alcohol causes physical addiction and psychological dependence.

What damage alcohol causes in the body? At any given time depend on its concentration in the blood which in turn is determined by the following factors: amount ingested over a period of time, presence or absence of food in the stomach to retain the alcohol and reduce its rate of absorption, weight body, liver and efficiency of the person who eats

The first step of alcohol metabolism in the human body is its dehydrogenation into acetaldehyde, a highly toxic substance.

The oxidation of alcohol occurs only in the liver and involves several enzymatic mechanisms.

Alcohol dehydrogenates (ADH)
this enzyme is localized in the cytosol of hepatocytes, liver cells. Its coenzyme nicotinamide adenine dinucleotide or NAD (which is reduced to NADH-H +). This pathway is constantly used but can only deal with moderate amounts of alcohol. Under the action of this enzyme, the alcohol is converted into acetaldehyde.

Aldehyde dehydrogenate (ALDH), is also the coenzyme NAD. It converts acetaldehyde to acetate, a substance much less dangerous for the body. When the possibilities of action of ADH are exceeded, other mechanisms come into action.
The microtonal Ethanol Oxidizing System (MEOS)
This oxidative pathway acts by induction of cytochrome P450 2E1 in macrodomes and can degrade a significant amount of alcohol. It leads also to the formation of acetaldehyde. Its coenzyme NADP.

The way that paroxysmal catalane plays only a minor role in the oxidation of ethanol and requires the presence of hydrogen peroxide. Moreover, this route would allow only limited quantity of alcohol degradation.
The operations of oxidation of alcohol are accompanied by a significant increase in the production of free radicals. Moreover, acetaldehyde interferes with antioxidant defense system of the liver, inhibits the repair of alkylated nucleoproteins, reduces oxygen consumption of mitochondria and induces lipid per oxidation. The radical mechanisms also seem involved in the toxicity of ethanol on various extra hepatic tissues, including the gastric mucosa, central nervous system, heart or testicles.

Alcohol interferes with the absorption, transport, storage and activation of essential micronutrients such as vitamins. In addition, alcohol metabolism generates free radicals and potentially toxic metabolites, consuming vitamins. Epidemiological surveys confirm the high incidence of vitamin deficiency in people who consume alcohol daily. Foliate, vitamin B1, B6, PP, D and E are the first threat.

The effects of alcohol consumption on plasma micronutrient antioxidants (vitamin E, vitamin C, carotenoids and selenium) and oxidative stress markers such as malondialdehyde and protein Schiff bases were evaluated in 417 control subjects ( 317 consume less than 33g / d of alcohol and 100 more than 33g / d) and 102 alcoholic patients consuming an average of 194 g / d of alcohol. The results showed that alcohol consumption significantly decreased plasma levels of antioxidant micronutrients.

Studies on humans and animals have shown that after chronic alcohol consumption, levels of glutathione, the major natural antioxidant in the liver (see separate PDF file on this site), and were significantly reduced.

SAMe, S-adenosylmethionine plays a particularly important role in the biochemistry of the liver. It is the product of a biochemical reaction between ATP and methionine. Nearly half of the methionine in the body is used in the liver to produce SAMe. Much of the latter is itself transformed into glutathione. Alcohol lowers levels of an enzyme necessary for the transformation of methionine to SAMe. A 1991 study by Spanish researchers has confirmed the ability of SAMe to convert glutathione. It also showed that the absorption of supplements

SAMe helps maintain levels of glutathione, they are absorbed at the same time as alcohol. This has the effect of abrupt decrease glutathione levels. In an alcoholic, a deficiency of SAMe may be predisposed to developing cirrhosis of the liver. The administration of SAMe can restore its levels and reduces hepatic parameters indicators of liver damage induced by ethanol, such as increased circulating transaminases or lesions on the mitochondria. In a study against placebo, 16 patients with liver diseases, alcoholic and non alcoholic received 1200 mg of SAMe, daily for 6 months. Liver biopsies showed a significant increase in levels of glutathione, together with a decrease in oxidized glutathione. In patients with non-alcoholic liver damage, alanine aminotransferase, liver enzyme indicator lesions was reduced. In a study in which 45 patients with alcoholic liver disease received an intravenous injection of SAMe for 15 days, the liver function was significantly improved.

The decrease in phosphatidylethanolamine transferee’s activity is associated with alcoholic liver disease leading to decreased phosphatidylcholine and serious consequences for the integrity of cell membranes. This effect can be offset by supplementation polyénylphosphatidylcholine or PPC.

The PPC is a mixture of polyunsaturated phosphatidylcholines, extracts of bean sprouts. A number of studies on cellular and animals have shown an interest in preventing and treating lesions of alcoholic and non alcoholic liver disease.

Alcohol consumption increases apoptosis (self destruction) of hepatocytes. Enzymes such as P450 E1, used for detoxification of alcohol, become dangerous when they are over-stimulated. They generate large amounts of free radicals and it is then necessary to regulate their activity. It seems that the PPC can do. PPC supplementation reduces apoptosis of hepatocytes induced by alcohol. This effect could explain the mechanism of the protective effect of PPC against liver injury. It could be done in combination with antioxidant action through regulation of induction of cytochrome. PPC supplementation corrects phospholipids depletion induced by alcohol at the same time it opposes oxidative stress. It also deactivates hepatic satellite cells.

A new study confirms the interest of CSF in the treatment of liver diseases. Supplementation with PPC could stop and even reverse liver fibrosis. 18 alcoholic patients received CSF or placebo. Of the nine patients receiving placebo 5 showed an increase of fibrosis two years later. In the 9 patients on CPAP, the disease had remained at the same level or has been slightly improved as the lead researcher, Dr. Charles S. Lieber, Bronx VA Medical Center and Mount Sinai School of Medicine, New York.

According to Dr. Lieber, the current prognosis of these patients is very poor, effective treatment is needed. In patients over 60 years with cirrhosis of the liver, a mortality of 50% is achieved in a year.

The first mechanism to neutralize acetaldehyde using sulfur-based antioxidants. The two most important are cysteine, an essential amino acid, and glutathione, a polymer with three amino acids. Cysteine and glutathione act effectively against acetaldehyde because they contain a reduced form of sulfur called sulfhydryl group with a sulfur atom bound to an atom of hydrogen. This powerful mechanism of detoxification of acetaldehyde is easily overwhelmed by relatively large amounts of alcohol as that typically consumed in alcoholic beverages. Fortunately, the sulfur-based antioxidants can be easily enhanced by nutritional supplementation.

The N-acetyl-cysteine provides protection as effective as cysteine, vitamin C is necessary to maintain the cysteine in a reduced state capable of acting effectively against acetaldehyde. Vitamin B1 or thiamine and alpha-lipoic acid are also involved in the detoxification of acetaldehyde. Their levels are also reduced by the consumption of alcohol. A team of researchers evaluated the effect of vitamin B1 and brought it showed a protective effect against the toxicity of acetaldehyde when combined with vitamin C and cysteine. Alcoholics are often deficient in vitamin B1. It is unclear however, whether such failure is due to a decrease in intestinal absorption caused by alcohol or by destruction of thiamine by acetaldehyde. In its reduced form, alpha-lipoic acid is powerful antioxidant based sulfur. Alpha lipoic acid and acetaldehyde can interact in cells of the liver. The liver metabolizes large quantities of alcohol ingested and the levels of acetaldehyde can be relatively high in liver cells. Acetaldehyde can bind to the lipoamide reduced, the active factor alpha lipoic acid, making it harmless. For the action of alpha-lipoic acid is possible, it must absorb several hours before and after consumption of alcohol. The standardized extract of silymarin (see below on the site) is a powerful antioxidant, widely used in Europe to treat liver diseases. It protects the liver from damage induced by alcohol ingestion, including reduced levels of glutathione in the liver. A month of silymarin supplementation can increase levels of hepatic glutathione by 35%. A proper combination of antioxidants, including without limitation, vitamins E, C, B1, cysteine, selenium, N-acetyl-cysteine, taken when alcohol is consumed or until the person intoxicated goes down, can effectively prevent some of the adverse effects of alcohol as cell damage or “hangover”. The primary use of silymarin is the treatment of liver damage related to the ingestion of alcohol. A first double-blind study examined 66 patients with liver disease induced by alcohol (Fintelmann and Albert, 1980). In 31 patients receiving 420 mg / d of silymarin levels of serum gamma-GT and transaminases (AST, ALT) have returned to normal faster than in 35 placebo patients. Another double-blind study with 36 patients with liver disease related to alcohol, found that pathological parameters (AST, ALT, GGT and bilirubin) were significantly reduced after 6 months of treatment, in patients receiving silymarin compared to the placebo group (Feher and others. 1990). In another randomized, controlled trial was performed to determine the effect of silymarin in the treatment of 170 patients with cirrhosis alcoholic and nonalcoholic (Ferenci and others., 1989). 87 patients received 420 mg / d of silymarin, 83 placebo. The survival rate at four years was 58% in patients receiving silymarin against 39% in patients receiving placebo.

Several epidemiological studies indicate a clear relationship between alcohol consumption and liver disease. It has also shown a close correlation between alcoholic cirrhosis mortality per capita per year.

Despite the direct relationship between the amount of alcohol ingested and the risk of liver damage, cirrhosis occurs in only a small proportion of cases. Of all the people who abuse alcohol, about 40 – 50% liver and presents 15 to 20% have cirrhosis.

Alcohol can trigger various clinical in the liver, among which we highlight.

Fatty liver and alcohol

it is the accumulation of fat inside liver cells (hepatocytes). It is the most frequent abnormality observed in most alcoholics. It occurs as a result of changes in fat metabolism induced by alcohol. In some cases produces no clinical manifestations, but in others, causing specific symptoms such as nausea, vomiting, abdominal discomfort and weight loss.

Alcoholic hepatitis by alcohol

generally they are chronic alcoholics, following a high intake, present a picture of loss of appetite, tiredness, nausea and vomiting. After several days, there is pain in the upper right abdomen, fever and yellowing of the skin and mucous membranes. Alcoholic hepatitis is the step immediately prior to cirrhosis, favoring the continued development of alcohol consumption, especially in women.

Alcoholic liver cirrhosis by alcohol

Cirrhosis is a disease characterized by an alteration in liver architecture and the presence of regenerative nodules surrounded by fibrous tissue. In this type of cirrhosis was reported the same clinical manifestations as those produced by any other cause. But they are more obvious pictures of malnutrition, vitamin deficiency, disorders and delusional tables.

Gastritis is an inflammation of the gastric mucosa. It may be accidental and strong (acute), due to ingestion of poison (usually alcohol, abuse of coffee, exciting or snuff), and chronic, caused by the slow action of the gastric juices. It results in difficulty to digest properly.

Acute gastritis, stomach upset also affects the head, general malaise. It disappears just as aggression. Almost always caused by overeating and drinking. There is also an acute gastritis drug, usually analgesics or anti-inflammatory.

Chronic gastritis, occurs either after the recurrence of acute or especially, by age. It’s like gastric weakening its ability to digest. There is also a chronic atrophic gastritis, compatible with age, which prevents the absorption of B vitamins another type of gastritis prevents absorption of iron deficiency anemia and creates. That is why the elderly are advised to eat a varied diet and digestible.

Some diabetics should not drink because alcohol can worsen their conditions. For example, diabetics with high triglycerides (a type of blood fat) should not consume alcohol because it affects the liver’s ability to remove fat from the bloodstream.

Some studies have reported that consumption of low or moderate alcohol may have a mild protective effect against developing type 2 diabetes. Moreover, studies suggest that for some people with type 2 diabetes even moderate alcohol consumption can induce low blood sugar.

Alcoholic drinks are mostly sugar and high in carbohydrates, depending on the natural compound that is extracted and further handling. Among the highest glycemic index are the beer (for its high-maltose) and fruit liqueurs.

Moreover ethanol itself (not the entire alcoholic beverage) has high power hypoglycemic, by several mechanisms: it prevents gluconeogenesis (formation of new glucose molecules) in the liver, this leads to hypoglycemia especially when glycogen stores are being depleted, for example after intense exercise or prolonged fasting, decreases the response of hormones contrainsulares therefore aggravate hypoglycemia caused by insulin or oral hypoglycemic agents and finally, increases pancreatic insulin secretion after ingestion sugar (this of course in no diabetic patients).

However, it may once again the main danger for the diabetic is its ability to mask these hypos.

A high fever may be accompanied by a delusional state is in spoken, seen or lived, no memory, different situations. The toxic products that act directly on the CNS (Central Nervous System) are those which arise more frequently delusions. Almost all drugs are produced, although some, such as hallucinogens, are characterized precisely by that.

But let’s focus on those produced by alcohol, and which is characterized by varying degrees. The specialists come to distinguish sub acute, sharp, and state of hallucination, delusions and hallucinatory psychosis Jealous. The damage that the alcohol produced in the brain causes these changes and some others, leading to alcoholic dementia.

Encephalosis sub acute or sub acute alcoholic. Appears in alcoholics between 30-40 years. Start with nightmares that disrupt sleep, repeating several nights to be continuous. Sweating profusely, is agitated, speaking in broken phrases and ask for help. He gives orders; relive scenes from their regular work. There vision of animals (zoopsia). Temperature normal or slightly elevated. The difference with the delirium tremens is one of degree.

Or acute delirium tremens. Arguably, it is the same as above, but more pronounced in every way. It has a more abrupt initiation and more serious. Sweating, trembling and shaking, total sleep loss and high fever. The rise of fever is a symptom of poor prognosis, as there may be hyperthermic coma. Those who have been affected by this psychosis later give the highest percentage of abstinence. The patient suffers a lot, have real anxiety and fear with zoopsia. Go and live like the animals they eat you invade or physically.

Alcoholic hallucinosis. Are the insults, harassment and threats those excessive drinkers and can hear and believe. They produced a situation so desperate that during psychiatric treatment is recommended for extreme vigilance what causes them agony of which neither knows nor can they defend themselves.

Jealous delusions. It is a fit of jealousy motivated exclusively by alcohol. It is the individual alcoholic who accuses his innocent wife of having affairs. The reactions of aggression and violence against alleged infidelity and towards their children are scary. As guilty even includes his in-laws. Often the killing.

Hallucinatory psychosis. It is very similar to the “acute alcohol hallucinosis. It is less abrupt and usually occurs in demented patients with delusional themes unclear.

Delirium by alcohol withdrawal or delirium tremens, usually begins between 48 and 72 hours after the last intake, and precedes the first signs and symptoms of abstinence, although these symptoms can be masked or delayed by associated diseases or taking medication.

Signs of sympathetic hyperactivity (such as tachycardia, hypertension, fever and diaphoresis or excessive sweating), are hallmarks of alcohol withdrawal delirium, and often profound. The mortality rate is estimated between 1% and 5%, but increases if diagnosis is delayed, if done improperly treat, or concurrent medical conditions.

Incoming search terms for the article:

• Acute Delirium

As to the causes, any excuse seems sufficient to trigger the pain, but actually the origin lies mostly in a dilation of the arteries and vessels of the “dura”, one of the layers covering the brain. That explains one of the most common manifestations of headache, throbbing character, i.e. a succession of “beats” that sometimes give us the impression of being real hammering. It seems that the heart has been moved to the brain. Do not forget that stress adversely affects blood circulation.

And although it seems a paradox, sometimes the headache arises precisely when we are relaxed or want to be. What happens is that the accumulated stress is expected at time of quiet to blame us. Should be subsumed under these vascular headaches that occur as a reflection of situations that disturb, ultimately, normal circulation, such as hypertension or the abundance of toxins in the blood (coffee, snuff, alcohol, are substances taken in high doses, “flooding” the blood of toxic elements).

Apart from toxins, alcohol itself is a factor. There are spirits that have more power than others to trigger the headache. It has been found, for example, wine or liquor with higher content of “histamine” easily produces headaches.

It is the accumulation of fat inside liver cells (hepatocytes). It is the most frequent abnormality observed in most alcoholics. It occurs as a result of changes in fat metabolism induced by alcohol. In some cases produces no clinical manifestations, but in others, causing specific symptoms such as nausea, vomiting, abdominal discomfort and weight loss.

Alcoholic hepatitis by alcohol

Generally they are chronic alcoholics, following a high intake, present a picture of loss of appetite, tiredness, nausea and vomiting. After several days, there is pain in the upper right abdomen, fever and yellowing of the skin and mucous membranes. Alcoholic hepatitis is the step immediately prior to cirrhosis, favoring the continued development of alcohol consumption, especially in women.

Alcoholic liver cirrhosis by alcohol

Cirrhosis is a disease characterized by an alteration in liver architecture and the presence of regenerative nodules surrounded by fibrous tissue. In this type of cirrhosis was reported the same clinical manifestations as those produced by any other cause. But they are more obvious pictures of malnutrition, vitamin deficiency, disorders and delusional tables.

Several epidemiological studies indicate a clear relationship between alcohol consumption and liver disease. It has also shown a close correlation between alcoholic cirrhosis mortality per capita per year.

Despite the direct relationship between the amount of alcohol ingested and the risk of liver damage, cirrhosis occurs in only a small proportion of cases. Of all the people who abuse alcohol, about 40 – 50% liver and presents 15 to 20% have cirrhosis.

Alcohol can trigger various clinical in the liver, among which we highlight.