How Does Alcohol Affect Nutrition?

Marko Balašević Author: Marko Balašević Time for reading: ~17 minutes Last Updated: August 09, 2022
How does alcohol affect nutrition?

The relationship between ethanol (alcohol) and nutrition is very complex and controversial. Here's what the experts say.

The relationship between alcohol and nutrition

The relationship between ethanol (alcohol) and nutrition is very complex and controversial.

On the one hand, it gives energy, similar to food, since 1 ml contains 7.11 k cal (29.75 kJ ), and on the other hand, it is a typical poison, which with chronic use of larger quantities leads to to drug addiction and serious damage to health.

For a long time, it was believed that the consumption of alcoholic beverages represents only a load of energy on the body (so-called empty calories), due to the lack of minerals, vitamins and proteins. However, recent studies have shown that when assessing the nutritional value of ethanol, a difference is found between non-alcoholics and alcoholics. In non-alcoholics, the consumption of moderate amounts of alcohol (up to 72 g of absolute alcohol per day) replaces carbohydrates and fats as a source of energy and has the ability, like them, to store nitrogen in the body. Since the energy of alcohol is intermediate between carbohydrates and proteins; on the one hand and fat, on the other when calculating energy intake, nutritionists must always take into account the amount of alcohol consumed. For this purpose, the formula can be used:

 

kcal ethanol=0.568 x alcohol in the drink and in % x consumed cm3

 

The energy from alcohol

However, alcoholics usually consume about 30-60% of their daily energy intake as alcohol. In them, nutritional disorders occur, due to substitution of important nutrients with ethanol, mainly carbohydrates and vitamins. This is especially important for distilled beverages, which practically do not contain vitamins, proteins and mitral substances. Beer and wine are richer in these substances, but also their main nutritional contribution is energy.

The effect of alcohol on the digestive organs

A consequence of the effects of alcohol on the pancreas, liver and small intestine are disturbances in their functions and disturbances in digestion and absorption. Directly or indirectly, ethanol leads to disturbed transport of some vitamins and minerals in the small intestine, disturbed import and deposition of resorbed nutrients in the liver, reduced conversion of nutrients into active metabolites (eg thiamine) and their large losses over time of the anabolic and catabolic phases of liver damage (e.g. zinc, folic acid, etc.).

Today, the toxic effect of alcohol on the human body is undoubted, but as with other toxic substances, its effect depends on the dose, duration of action and many other factors. All organs and systems are affected, but some of them are damaged selectively and more severely. Damage to the liver and digestive system is most common. Alcohol contributes to carcinogenesis.

The absorption of alcohol in the digestive system

Alcohol passes through biological membranes by diffusion, and its amount depends on its concentration gradient and on the coefficient of diffusion for it and the membrane. The reabsorption of alcohol in the digestive system depends on the concentration gradient between the lumen of the relevant organ and the subepithelial capillary and lymphatic vessels. Therefore, blood circulation in the relevant organ is also important for resorption. It is fastest in the duodenum and jejunum, slower in the stomach and colon, and slowest in the mouth.

Up to 20% of the alcohol taken orally is absorbed through the stomach. In pyloric spasm, which occurs frequently in alcoholics, the time for resorption of alcohol varies widely depending on certain conditions. Resorption is greatest at alcohol concentration – 3.25 – 6.51 mol/l (15 – 30 %). At a higher concentration, superficial erosions and hemorrhages develop in the gastric mucosa, paralysis of the smooth muscles and strong secretion of mucus, which slows down resorption. At concentrations lower than 2.17 mal/l (10%), resorption is slower due to the low concentration gradient.

The rate of absorption depends on the type of alcoholic beverages – beer and wine are absorbed more slowly than concentrates. It is determined not only by the different concentration of alcohol in the drinks, but also by the content of other substances in them. Sugar slows down absorption, CO2 and bicarbonates accelerate it. Proteins, some organic acids and their salts, alkaloids and the total buffer capacity are also important.

Combining food and alcohol

It has long been known that alcohol is better tolerated when consumed with food. This effect is explained by delaying the emptying of the stomach, and thus the resorption of alcohol in the small intestine. The type of food - protein, carbohydrate or with more fat, does not matter much. However, mixed food is thought to have the most pronounced effect, especially if consumed before, at the same time or shortly after alcohol. Accelerated absorption has also been observed in some individuals with the consumption of very high-fat foods, possibly due to induced nausea and accelerated gastric emptying.

Many other physiological and pharmacological factors can affect the rate of alcohol absorption through changes in gastrointestinal motility and circulation. Drinking water before consuming alcohol, increasing body temperature, cholinergic drugs, insulin, etc. speed up resorption. Strong mental and physical tension, the drop in body temperature, 0.90 mol/l (10%) solution of CaCl 2 or 0.83 mol/l (10%) MgSo 4, sympathomimetic and anticholinergic agents, aspirin, pyramidone, etc. delay resorption.

Absorbed alcohol is distributed in the total amount of water in the body, therefore its concentration in the blood, tissues and body secretions is determined by their water content. Many people are drunk with a blood concentration above 32.55 mmol/l(150 mg %), which is the borderline forensic-medical value for the presence of intoxication. Equalization of the concentration of alcohol between the blood and the liver occurs only after its complete resorption. After that, a linear decrease in the level of alcohol in the blood began, which is due to its oxidation to acetaldehyde and its emission from the kidneys, lungs, etc. Oxidation occurs almost exclusively in the liver and only 10-15% is oxidized in other tissues. Knowledge of alcohol metabolism in the liver is important for understanding the energy requirements and nutritional status of alcoholics.

 

 

The limiting factor in alcohol oxidation is the activity of alcohol dehydrogenase, which in the presence of NAD oxidizes 75-80% of alcohol to acetaldehyde. The rest is oxidized by the microsomal ethanol-oxidizing system (MEOS) in the presence of NADPH. Catalase plays a minor role. The energy that is released in the first phase of the oxidation of alcohol (to acetaldehyde) is only a part of the total energy of oxidation to CO2 through the Krebs cycle. It should be emphasized that ADH and MEOS reach their maximum activity at different concentrations of alcohol in the blood. K m of ADH is 2 mmol ethanol, which corresponds to 9 mg % of alcohol in the blood. Such are the values ​​for "household" drinkers. The Km of MEOS is 8.6 mmol, corresponding to 40 mg = ethanol in the blood, and therefore the activity of the enzyme is greater at higher concentrations, which are reached in chronic alcoholics. It should also be kept in mind that MEOS needs NADP and oxygen for its activity and releases only heat without energy conservation. ADH, conversely, restores NADH and provides hydrogen equivalents to the electron transport system to form ATP. Therefore, the degradation of alcohol by MEOS is "energy wasteful". Experimental studies of Pirola and Liber confirmed these data, showing that in rats receiving 36 percent of daily food energy as ethanol for 3–4 weeks, hepatic MEOS activity and oxygen consumption increased, and growth decreased. The ratios are similar in humans – when replacing 50% of the energy intake with ethanol, a decrease in body weight is observed. If alcoholics were given an additional 2000 kcal (8368 kJ ) to their daily ration either as enatol or as chocolate, a relative reduction in weight was found in those receiving alcohol.

These data strongly suggest that, taken in small amounts, alcohol is a rich source of easily digestible energy. Taking into account the disturbances in fat metabolism in the second phase of its degradation, it becomes clear the significant role that alcohol plays in the development of obesity, one of the most common diseases of modern society. With high alcohol consumption, the metabolic mechanism through MEOS is activated, which leads to energy loss and conditions are created for cellular damage to the various organs.

Effect of alcohol on metabolism

Chronic alcohol use leads to profound changes in a number of metabolic processes in the body. Some of them are related to nutrition, which on the one hand affects their degree and frequency, and they, on the other hand, affect the nutrition of chronic alcoholics. There is a nutritional deficiency, the reasons for which are complex:

  1. imbalanced or unbalanced intake of food - taking in a large amount of energy without the other necessary nutrients;

  2. poor absorption in the small intestine as a result of alcohol damage or due to a lack of essential food ingredients;

  3. reduced absorption or deposition of resorbed nutrients by the damaged liver;

  4. inability of the damaged liver to convert nutrients into their metabolically active products;

  5. increased loss of nutrients with urine in the catabolic phase of liver damage;

  6. a combination of each of these factors.

It should be noted the indisputable tendency in almost all countries to reduce the prevalence of these nutritional deficiencies after the Second World War. The reasons for this are the improved material well-being of the population, the better supply of food products and, last but not least, the change in the stereotype of chronic alcoholics, the majority of whom drink intermittently. Food intake in the free intervals is usually sufficient to prevent them from developing a marked nutritional deficiency.

 

PREMIUM CHAPTERS ▼

Nutritional deficiency (PREMIUM)

Protein deficiency. The problem of the role of protein deficiency in the development of the clinical picture of chronic alcoholism and in particular of alcoholic liver damage is one of the most discussed. Some authors believe that the cause is primarily the nutritional imbalance, and not the direct toxic effect of alcohol. The importance of the import of proteins and satisfaction with lipotropic factors (choline, methionine) etc. is emphasized. When feeding rats for 19 months. with a liquid diet containing 35.5 energy percent alcohol and 25 energy percent protein, very slight changes in nigral nuclei were found—swelling of mitochondria in some cells with increased deposition of triglycerides and a slight increase in collagen. However, the majority of authors advocate the opposite opinion.

Undoubtedly, the chronic consumption of large quantities of alcoholic beverages, combined with a low-protein diet, leads to the development of protein deficiency in chronic alcoholics. Clinically, it is demonstrated with steatosis of the liver, edema, normocytic anemia, hypoalbuminemia, and hypocholesterolemia. The changes are significantly less pronounced than with kwashiorkor in children, because the needs of essential amino acids and total nitrogen in adults are smaller. In a number of cases, this syndrome is observed in isolation without accompanying liver damage. In most cases, they are found at the same time and it is possible to distinguish them.

A number of other factors are also involved in the development of hepatic steatosis, which during the stage of alcoholic hepatitis ends with liver cirrhosis. In addition to the protein deficiency and the duration of alcohol consumption, other factors are also important. nutritional and genetic factors. Correcting the diet in terms of protein intake, giving lipotropic substances and stopping alcohol consumption do not always lead to a complete cure. It has been experimentally proven that the higher the fat content in food (over 25 energy percent), the more pronounced hepatic steatosis is when taking 36 energy percent alcohol with a liquid diet.

Deficiency of vitamins (PREMIUM)

Vitamin deficiency is often observed in chronic alcoholics with or without liver damage. The reasons are complex, but the most important is the reduced import with food, with which up to 2499 kcal (10,041.6 kJ   ) at the expense of alcohol with an almost complete lack of vitamins in alcoholic beverages. As fat-soluble vitamins are absorbed, deposited and stored better in the body, alcoholics develop a deficiency of water-soluble vitamins more often, sometimes with clinical signs of the corresponding avitaminosis. Despite the unsaturation of vitamin C, scurvy occurs rarely. In alcoholics with liver damage, resorption of vitamin B1 and B6 and folate is reduced, while vitamin B2 and pantothenates are better absorbed. Because of this, a deficiency of B group vitamins – thiamin, folic acid, riboflavin, niacin and pyridoxine – prevails.

Vitamin B1 deficiency is the most common. It manifests clinically in different forms depending on its degree, affecting the muscular and nervous systems. The picture in Wernicke 's syndrome is the most severe - ophthalmoplegia, nystagmus, paralysis of the VI cranial nerve, ptosis, ataxia, state of confusion and coma. Sometimes it is also accompanied by peripheral neuropathy and heart failure. This form is very severe. Vigorous treatment with high doses of vitamins is necessary. Sometimes it ends in death or passes into Korsakov's pychosis.  

Another severe form of vitamin B1 deficiency in alcoholics is similar in its clinical picture to classic beriberi. It manifests itself mainly with disturbances in the neuromuscular apparatus of the limbs and with disturbances in the metabolism of the heart muscle, with heart failure.

The mildest form is manifested by polyneuropathy of the lower limbs - suppression of tendon reflexes, muscle cramps, paresthesias, etc.

Biochemical criteria for proving vitamin deficiency depend on its degree. In Wernicke 's syndrome, pyruvate in the blood is increased, and the activity of transketolase in erythrocytes is decreased; in alcoholic polyneuropathy, the values ​​of vitamin B1 are reduced - below 103/884 mmol creatinine in the urine (below 30 µg/g ).   

Pellagra - what is it and how does it affect the body? (PREMIUM)

Pellagra occurs with vitamin B3 deficiency. The main symptoms of pellagra are: dermatitis, diarrhea and dementia.

It is due to a lack of nicotinic acid or tryptophan, which is the starting product for its formation in the body. It is observed very rarely under the current conditions of nutrition, because conditions for its development can hardly be realized even with the nutritional imbalance of chronic alcoholics. It is clinically manifested by photosensitive dermatitis, which must be differentiated from photosensitive skin changes in porphyria cutanea tarda symptomatic , inflammatory changes on the mucous membranes of the organs of the gastro-intestinal tract, encephalopathy and peripheral neuropathy. Manifestations of encephalopathy in pellagra often mimic other mental illnesses. For making the correct diagnosis, an essential criterion is the emission of less than 7.4 µmol/24 h (1 mg/24 h )     N -methylnicotinamide in urine – the norm for adults is 36.5 – 146 µmol/24 h (5 – 20 mg/24 h ).   

Vitamin B2 deficiency. It is usually combined with alcoholic pellagra and accounts for part of the clinical picture. It is proven by establishing values ​​lower than 133 µmol/24 h (50 mg/24 h ) in the urine.   

Vitamin B6 deficiency. Pyridoxine deficiency is characterized by excitability, insomnia, nervousness, mild ataxia, and skin changes similar to those seen in riboflavin deficiency. In alcoholics, it is combined with the withdrawal syndrome and causes convulsions. Laboratory findings show a decrease in pyridoxine acid below 0.546 µmol/24 h (0.1 mg/24 h ) - a norm above 3.276 µmol/24 h (0.6 mg/24 h ), and an increase in xanthurenic acid in the urine - about 122 µmol/24 h (25 mg/24 h ).         

Folic acid deficiency (PREMIUM)

It is the most common cause of macrocytic anemia in alcoholics. The minimum daily oral dose to cover the needs of the body is 113 mmol/24 h (50 µg /24 h), and serum values ​​below 68 pmol/l (3 ng % ) are considered reduced. In alcoholics with folic acid deficiency anemia, feeding food containing 226 nmol/24 h (100 µg/24 h ) of folic acid induced a reticulocyte crisis only when alcohol consumption was stopped. It took the administration of much higher doses of folic acid to produce a reticulocyte crisis, but without a complete return of megaloblastic hematopoiesis to normoblastic before alcohol withdrawal.        

Deficiency of mineral substances (PREMIUM)

The long-term use of large quantities of alcoholic beverages in alcoholics leads to a deficiency of mineral substances - sodium, chlorides, potassium, magnesium, zinc, etc. It is often accompanied by general dehydration of the body, a decrease in alkalinity with the development of acidosis. It's going very hard.

Magnesium deficiency (PREMIUM)

Alcohol increases the excretion of magnesium in the urine. When a diet poor in magnesium salts is added to it, magnesium deficiency manifests itself in alcoholics. It is found in about 25% of them and is more pronounced in severe forms of alcoholism. The notion that delirium tremens is etiologically related to hypomagnesemia has not been confirmed, although parenteral therapy with MgSO 4 has a beneficial effect on tremor.   

Potassium and sodium deficiency (PREMIUM)

It goes astray in about 1/3 of alcoholics and is due to insufficient dietary intake, poor absorption in the gastrointestinal tract and especially increased urinary loss. The severity of the clinical picture and biochemical changes show considerable diversity. Clinical manifestations are usually absent, but in severe cases, the picture of electrolyte coma may develop. In milder cases, mild hypokalemia with hypernatremia and hyperchloremia is found in the serum, and as the changes deepen, sodium and chloride also decrease. In the most severe forms, changes also develop intracellularly. In such cases, only an emergency infusion of electrolytes can protect the patient from complications and death.

A particular form of hyponatremia is seen in beer drinkers. They often consume large quantities - 3 - 10 l/day. This leads to a strong increase in diuresis with increased sodium emission and from there to hyponatremia. The same changes develop with large amounts of water, but in this case the alcohol contained in beer worsens the situation even more because it is an antagonist of the antidiuretic hormone. To its action should be added the reduced intake of sodium with food and the increased loss due to frequent diarrhea. Clinically, there is a clouding of consciousness, which ends in a severe coma. The clinical picture must be well known. When neurological symptoms appear in beer drinkers, it is necessary to examine the ionogram. Prognosis is good with prompt sodium infusion and water restriction.

Zinc deficiency (PREMIUM)

Urinary zinc excretion is known to be increased in alcoholics with or without marked liver damage. It is highest in patients with alcoholic liver cirrhosis and ascites or jaundice. The pathogenesis of these changes in zinc metabolism is explained not so much by the influence of nutritional factors as by the evolution of liver damage under the influence of alcohol. Since the molecule of alcohol dehydrogenase contains 4 atoms of zinc, the increased excretion in the urine and the decrease of zinc in the liver tissue are associated with the reduced activity of the enzyme in the liver in advanced damage and lead to changes in alcohol metabolism. According to our unpublished studies on 60 chronic alcoholics, zinc in serum and urine did not differ significantly from a healthy control group.

Influence of some trace elements (PREMIUM)

Alcoholic beverages contain trace elements, the amount of which under certain conditions may exceed the accepted limits. In these cases, their impact on chronic alcoholics should be evaluated. Such trace elements are primarily iron and copper. The essential question is to what extent their resorption in the digestive tract increases and to what extent their deposition in the liver increases. And in healthy people, alcohol increases the resorption of ferric ions, probably by stimulating the secretion of hydrochloric acid. Concomitant alcoholic pancreatitis also contributes to iron overload, and folic acid deficiency contributes to elevated serum iron due to reduced utilization of heme synthesis. In experimental alcohol intoxication in humans, a significant hardening of serum iron was induced.

Therapeutic nutrition in chronic alcoholism. Regardless of the fact that in recent years the severity of nutritional deficiency among alcoholics is significantly less, along with their hospital treatment, intensive therapeutic nutrition should also be carried out. In patients with acute psychosis and withdrawal syndrome, parenteral therapy is administered to correct water, electrolyte and vitamin deficiency and hypoglycemia. Then a diet with sufficient energy, electrolytes and vitamins, more often foods that stimulate the appetite, are included.

 

 

 

In ambulatory patients, regular meals at the same time (preferably in a family setting) should be insisted upon, which aids post-treatment socialization. In treatment-resistant alcoholics, maintaining a regular and nutritious diet reduces complications due to nutritional deficiency. In alcoholics, it is a principle to avoid overfeeding, as well as the parenteral administration of electrolytes and vitamins without a proven deficiency. The old notions that the development of alcoholism is predisposed by the very high requirements of B vitamins in some individuals, and that the administration of high doses of B vitamins may prevent a resumption of heavy drinking, are now rejected.

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