Alcoholic ketoacidosis (AKA) is a severe disease due to ethanol-based substance use. It is a group of metabolic diseases that involve changes in the metabolism of fatty acids and ketone bodies, resulting in ketoacidosis. Although it has much in common with diabetic ketoacidosis, it still occurs primarily in patients with alcohol-related disorders or sudden alcohol intake.
When taken, alcohol finds its way to the liver, where it undergoes metabolism. However, in cases of acute alcohol consumption, the liver is unable to perform its tasks and consume most of its energy to metabolizing alcohol. It could lead to lowering the glucose levels and increasing ketone level formation.
Ketones are fat-burning byproducts that the body uses to obtain energy when glucose is not available. In AKA, the formation level of ketones goes beyond the body’s capacity to consume them efficiently. Consequently, this leads to the accumulation of ketone in the blood, and the condition of ketoacidosis is attained.
Epidemiology
AKA occurs at any age regardless of the age of the patient since it is caused by alcohol consumption. However, it is more frequent in patients with chronic alcoholism who are 20 to 26 years of age. This age group stands at the highest prevalence because, during this age, there is a high likelihood of indulging in reckless drinking. It occurs in people who have a history of alcohol dependence. Thus, it is most common in alcoholics. It manifests in middle-aged men most of the time; however, it is not impossible to happen in women as well.
Anatomy
Pathophysiology
Alcoholic ketoacidosis is one of the metabolic disorders resulting from alcoholism and inadequate diets. This results in the presence of ketone bodies in the blood and the formation of keto acids, ketoacidosis. Ethanol is primarily toxic to the liver, oxidized to acetaldehyde by alcohol dehydrogenase and then to acetate by acetaldehyde dehydrogenase. This process produces NADH and thus affects the redox state of the liver and suppresses the process of gluconeogenesis. Ethanol pathologic consumption suppresses gluconeogenesis, thus abolishing glucose formation and resulting in hypoglycemia. Malnutrition which is widespread among patients with AKA reduces liver glycogen and fat reserves subsequently receiving fatty acids for oxidation. Ketone bodies are produced from broken fatty acids as a result metabolic acidosis occurs because the blood pH is reduced.
Etiology
Alcoholic ketoacidosis occurs mainly in people who like taking too much alcohol regularly and frequently. It is often linked with chronic alcohol use, however, the quantity and the period, which a person should consume alcohol to develop AKA, differ in some ways. Prolonged use of alcohol affects the individual’s dietary pattern, and there is usually malnutrition. Alcoholics can have poor nutrient diets where some foods that are considered essential for the body such as the vitamins, the minerals, the carbohydrates are scarce. Malnutrition decompensates the liver and in turn hinders the metabolic functions such as gluconeogenesis.
Genetics
Prognostic Factors
The outcomes for alcoholic ketoacidosis are mainly driven by such factors as the degrees of metabolic acidosis, the time at which the treatment begins, and any other co-existing ailments. Early diagnosis of the condition and treatment give a relatively favorable outcome.
The overall mortality rate of alcoholic ketoacidosis has been estimated to arrive at between 2% and as low as 10%. Some of the factors that may predispose the patient to a poor outcome include older age, severe acidosis, other medical conditions, including liver disease or pancreatitis, and a later initiation of proper treatment measures.
Clinical History
Abdominal pain is also a common characteristic seen in persons with AKA when reviewing the case history. The patient may have pain in the epigastric region accompanied by abdominal distension, which may be generalized or localized in the upper central part of the abdomen. This disease is usually accompanied by gastrointestinal symptoms like nausea and vomiting. Eliminating abdominal pain, often present in patients, can worsen the observed reduction in oral intake. Some symptoms that patients may show include irritability, tremor, and confusion.
Age group: Alcoholic ketoacidosis (AKA) mainly affects those who often consume alcohol. This is most observed in adults; those in the working population between the ages of thirty and fifty years are mostly affected.
Physical Examination
Vital signs
Abdominal examination
Skin examination
Neurological examination
Age group
Associated comorbidity
Chronic Alcohol Abuse
Malnutrition
Liver Disease
Pancreatitis
Gastrointestinal Bleeding
Electrolyte Imbalances:
Associated activity
Acuity of presentation
Clinical Presentation:
Some of the clinical presentations may be represented by nausea, vomiting, abdominal pain or discomfort, and altered mental status.
Some patients will exhibit symptoms of excessive ethanol consumption and then abstinence from both food and ethanol for a certain period.
They might also present with symptoms of dehydration and postural hypotension.
Differential Diagnoses
Diabetic Ketoacidosis
Uremia
Salicylate Poisoning
Methanol Toxicity
Lactic Acidosis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Treatment paradigm:
Intravenous (IV) fluids: This is crucial of management of AKA as an emergency that requires rapid intervention. IV fluids are used to replenish body fluids and normalize the level of electrolytes.
Thiamine supplementation: Thiamine is administered intravenously to avoid development of Wernicke’s encephalopathy which is neurological complication of thiamine deficiency.
Glucose administration: After the repletion of thiamine, if necessary, glucose may be administered intravenously to facilitate the conversion of fats to glucose in the body.
Electrolyte replacement: Abnormality of potassium, magnesium, and phosphate electrolyte is often noted in AKA, and these require supplementation with IV fluids or phosphate supplements.
Treating alcohol withdrawal syndrome: There might be a necessity to treat non-psychotic drug effects of alcohol dependency, like tremors, anxiety, and seizure.
Diet: After the initial phase of AKA has been managed, the patient should be placed on a diet high in carbohydrates and protein to serve a purpose of glycogen reserves and enhance the general diet. This will help the body to heal and reverse some of the changes that have occurred due to the infection.
Hydration: Crystalloid fluids such as isotonic or moderately hypotonic normal saline and Ringer’s lactate are the mainstay of IV fluids in the management of AKA. It assists in reversal of pathology of dehydration and electrolyte imbalance. On some occasions, rehydration maybe done through oral fluids.
Rest: Sufficient sleep is necessary so that the body could recover from the stress caused by the preceding day’s physical activity.
Supplements: It is often associated with thiamine or vitamin B1 deficiency that is prevalent in alcohol-dependent patients, as well as exacerbates AKA. Thiamine should be administered in the therapy and in the prevention of AKA.
Withdrawal management: Persons with AKA might also be having AW symptoms. These symptoms can be alleviated by medications and other supportive care to prevent the worsening of the condition.
Role of Vitamins in treating alcoholic ketoacidosis
Thiamine (Vitamin B1): Prolonged alcohol consumption results in the depletion of thiamine levels that results in the development of Wernicke’s encephalopathy which is a severe neurological disease. This condition ought to be prevented through the administration of thiamine. The usual schedule in which it is administered is intravenously at the beginning of therapy.
Effectiveness of Electrolytes in treating alcoholic ketoacidosis
Potassium (K+):
Hypokalemia is observed because of poor nutrient intake, vomiting, and renal acidosis, in addition to acute kidney injury.
Special attention should be paid to potassium levels and their maintenance at a proper level. In this case, replacement is normally done through the intravenous (IV) route in the serious cases.
Magnesium (Mg2+):
This one is also prevalent, just as potassium deficiency results from the same causes and can worsen hypokalemia.
Magnesium should be monitored and supplemented if its level is reduced, which is sometimes done while at the same time replacing potassium.
Fluid resuscitation: The treatment of AKA begins and is considered one of the most significant in the entire process of the patient’s recovery. Oral rehydration therapy and intravenous (IV) fluids are given to replace fluid lost because of vomiting and dehydration.
Electrolyte replacement: The patients shown to be affected by AKA have their levels of the following electrolytes low; potassium, magnesium, and phosphate. Such electrolytes are vital to several aspects of the body and need replacement so as not to lead to worse scenarios.
Thiamine supplementation: Another vitamin that is necessary for the proper function of nerves is thiamine or vitamin B1. Patients with alcohol dependency are commonly found with thiamine deficiency and it is asserted that the AKA symptoms deteriorate with the absence of thiamine. Thiamine is given intravenously.
Glucose administration: Once the patient has been ’flushed’ out and their electrolytes balanced, glucose may be administered intravenously to help the body slowly transition from burning fat to fuel its metabolism to burning glucose. This may assist in reducing the concentration of ketones and a further enhancement of acidosis.
Management of alcohol withdrawal: The excess alcohol users also suffer from the AKA and, therefore, are prone to developing AWS. Some drugs may be administered to assist in controlling some of the signs of AWS.
Nutritional support: After stabilizing the patient, it will be essential to encourage the patient to eat to refill the glycogen storage and enhance their diet intake.
Alcoholic ketoacidosis (AKA) is a severe disease due to ethanol-based substance use. It is a group of metabolic diseases that involve changes in the metabolism of fatty acids and ketone bodies, resulting in ketoacidosis. Although it has much in common with diabetic ketoacidosis, it still occurs primarily in patients with alcohol-related disorders or sudden alcohol intake.
When taken, alcohol finds its way to the liver, where it undergoes metabolism. However, in cases of acute alcohol consumption, the liver is unable to perform its tasks and consume most of its energy to metabolizing alcohol. It could lead to lowering the glucose levels and increasing ketone level formation.
Ketones are fat-burning byproducts that the body uses to obtain energy when glucose is not available. In AKA, the formation level of ketones goes beyond the body’s capacity to consume them efficiently. Consequently, this leads to the accumulation of ketone in the blood, and the condition of ketoacidosis is attained.
AKA occurs at any age regardless of the age of the patient since it is caused by alcohol consumption. However, it is more frequent in patients with chronic alcoholism who are 20 to 26 years of age. This age group stands at the highest prevalence because, during this age, there is a high likelihood of indulging in reckless drinking. It occurs in people who have a history of alcohol dependence. Thus, it is most common in alcoholics. It manifests in middle-aged men most of the time; however, it is not impossible to happen in women as well.
Alcoholic ketoacidosis is one of the metabolic disorders resulting from alcoholism and inadequate diets. This results in the presence of ketone bodies in the blood and the formation of keto acids, ketoacidosis. Ethanol is primarily toxic to the liver, oxidized to acetaldehyde by alcohol dehydrogenase and then to acetate by acetaldehyde dehydrogenase. This process produces NADH and thus affects the redox state of the liver and suppresses the process of gluconeogenesis. Ethanol pathologic consumption suppresses gluconeogenesis, thus abolishing glucose formation and resulting in hypoglycemia. Malnutrition which is widespread among patients with AKA reduces liver glycogen and fat reserves subsequently receiving fatty acids for oxidation. Ketone bodies are produced from broken fatty acids as a result metabolic acidosis occurs because the blood pH is reduced.
Alcoholic ketoacidosis occurs mainly in people who like taking too much alcohol regularly and frequently. It is often linked with chronic alcohol use, however, the quantity and the period, which a person should consume alcohol to develop AKA, differ in some ways. Prolonged use of alcohol affects the individual’s dietary pattern, and there is usually malnutrition. Alcoholics can have poor nutrient diets where some foods that are considered essential for the body such as the vitamins, the minerals, the carbohydrates are scarce. Malnutrition decompensates the liver and in turn hinders the metabolic functions such as gluconeogenesis.
The outcomes for alcoholic ketoacidosis are mainly driven by such factors as the degrees of metabolic acidosis, the time at which the treatment begins, and any other co-existing ailments. Early diagnosis of the condition and treatment give a relatively favorable outcome.
The overall mortality rate of alcoholic ketoacidosis has been estimated to arrive at between 2% and as low as 10%. Some of the factors that may predispose the patient to a poor outcome include older age, severe acidosis, other medical conditions, including liver disease or pancreatitis, and a later initiation of proper treatment measures.
Abdominal pain is also a common characteristic seen in persons with AKA when reviewing the case history. The patient may have pain in the epigastric region accompanied by abdominal distension, which may be generalized or localized in the upper central part of the abdomen. This disease is usually accompanied by gastrointestinal symptoms like nausea and vomiting. Eliminating abdominal pain, often present in patients, can worsen the observed reduction in oral intake. Some symptoms that patients may show include irritability, tremor, and confusion.
Age group: Alcoholic ketoacidosis (AKA) mainly affects those who often consume alcohol. This is most observed in adults; those in the working population between the ages of thirty and fifty years are mostly affected.
Vital signs
Abdominal examination
Skin examination
Neurological examination
Chronic Alcohol Abuse
Malnutrition
Liver Disease
Pancreatitis
Gastrointestinal Bleeding
Electrolyte Imbalances:
Clinical Presentation:
Some of the clinical presentations may be represented by nausea, vomiting, abdominal pain or discomfort, and altered mental status.
Some patients will exhibit symptoms of excessive ethanol consumption and then abstinence from both food and ethanol for a certain period.
They might also present with symptoms of dehydration and postural hypotension.
Diabetic Ketoacidosis
Uremia
Salicylate Poisoning
Methanol Toxicity
Lactic Acidosis
Treatment paradigm:
Intravenous (IV) fluids: This is crucial of management of AKA as an emergency that requires rapid intervention. IV fluids are used to replenish body fluids and normalize the level of electrolytes.
Thiamine supplementation: Thiamine is administered intravenously to avoid development of Wernicke’s encephalopathy which is neurological complication of thiamine deficiency.
Glucose administration: After the repletion of thiamine, if necessary, glucose may be administered intravenously to facilitate the conversion of fats to glucose in the body.
Electrolyte replacement: Abnormality of potassium, magnesium, and phosphate electrolyte is often noted in AKA, and these require supplementation with IV fluids or phosphate supplements.
Treating alcohol withdrawal syndrome: There might be a necessity to treat non-psychotic drug effects of alcohol dependency, like tremors, anxiety, and seizure.
Endocrinology, Metabolism
Diet: After the initial phase of AKA has been managed, the patient should be placed on a diet high in carbohydrates and protein to serve a purpose of glycogen reserves and enhance the general diet. This will help the body to heal and reverse some of the changes that have occurred due to the infection.
Hydration: Crystalloid fluids such as isotonic or moderately hypotonic normal saline and Ringer’s lactate are the mainstay of IV fluids in the management of AKA. It assists in reversal of pathology of dehydration and electrolyte imbalance. On some occasions, rehydration maybe done through oral fluids.
Rest: Sufficient sleep is necessary so that the body could recover from the stress caused by the preceding day’s physical activity.
Supplements: It is often associated with thiamine or vitamin B1 deficiency that is prevalent in alcohol-dependent patients, as well as exacerbates AKA. Thiamine should be administered in the therapy and in the prevention of AKA.
Withdrawal management: Persons with AKA might also be having AW symptoms. These symptoms can be alleviated by medications and other supportive care to prevent the worsening of the condition.
Endocrinology, Metabolism
Thiamine (Vitamin B1): Prolonged alcohol consumption results in the depletion of thiamine levels that results in the development of Wernicke’s encephalopathy which is a severe neurological disease. This condition ought to be prevented through the administration of thiamine. The usual schedule in which it is administered is intravenously at the beginning of therapy.
Endocrinology, Metabolism
Potassium (K+):
Hypokalemia is observed because of poor nutrient intake, vomiting, and renal acidosis, in addition to acute kidney injury.
Special attention should be paid to potassium levels and their maintenance at a proper level. In this case, replacement is normally done through the intravenous (IV) route in the serious cases.
Magnesium (Mg2+):
This one is also prevalent, just as potassium deficiency results from the same causes and can worsen hypokalemia.
Magnesium should be monitored and supplemented if its level is reduced, which is sometimes done while at the same time replacing potassium.
Endocrinology, Metabolism
Fluid resuscitation: The treatment of AKA begins and is considered one of the most significant in the entire process of the patient’s recovery. Oral rehydration therapy and intravenous (IV) fluids are given to replace fluid lost because of vomiting and dehydration.
Electrolyte replacement: The patients shown to be affected by AKA have their levels of the following electrolytes low; potassium, magnesium, and phosphate. Such electrolytes are vital to several aspects of the body and need replacement so as not to lead to worse scenarios.
Thiamine supplementation: Another vitamin that is necessary for the proper function of nerves is thiamine or vitamin B1. Patients with alcohol dependency are commonly found with thiamine deficiency and it is asserted that the AKA symptoms deteriorate with the absence of thiamine. Thiamine is given intravenously.
Glucose administration: Once the patient has been ’flushed’ out and their electrolytes balanced, glucose may be administered intravenously to help the body slowly transition from burning fat to fuel its metabolism to burning glucose. This may assist in reducing the concentration of ketones and a further enhancement of acidosis.
Management of alcohol withdrawal: The excess alcohol users also suffer from the AKA and, therefore, are prone to developing AWS. Some drugs may be administered to assist in controlling some of the signs of AWS.
Nutritional support: After stabilizing the patient, it will be essential to encourage the patient to eat to refill the glycogen storage and enhance their diet intake.
Alcoholic ketoacidosis (AKA) is a severe disease due to ethanol-based substance use. It is a group of metabolic diseases that involve changes in the metabolism of fatty acids and ketone bodies, resulting in ketoacidosis. Although it has much in common with diabetic ketoacidosis, it still occurs primarily in patients with alcohol-related disorders or sudden alcohol intake.
When taken, alcohol finds its way to the liver, where it undergoes metabolism. However, in cases of acute alcohol consumption, the liver is unable to perform its tasks and consume most of its energy to metabolizing alcohol. It could lead to lowering the glucose levels and increasing ketone level formation.
Ketones are fat-burning byproducts that the body uses to obtain energy when glucose is not available. In AKA, the formation level of ketones goes beyond the body’s capacity to consume them efficiently. Consequently, this leads to the accumulation of ketone in the blood, and the condition of ketoacidosis is attained.
AKA occurs at any age regardless of the age of the patient since it is caused by alcohol consumption. However, it is more frequent in patients with chronic alcoholism who are 20 to 26 years of age. This age group stands at the highest prevalence because, during this age, there is a high likelihood of indulging in reckless drinking. It occurs in people who have a history of alcohol dependence. Thus, it is most common in alcoholics. It manifests in middle-aged men most of the time; however, it is not impossible to happen in women as well.
Alcoholic ketoacidosis is one of the metabolic disorders resulting from alcoholism and inadequate diets. This results in the presence of ketone bodies in the blood and the formation of keto acids, ketoacidosis. Ethanol is primarily toxic to the liver, oxidized to acetaldehyde by alcohol dehydrogenase and then to acetate by acetaldehyde dehydrogenase. This process produces NADH and thus affects the redox state of the liver and suppresses the process of gluconeogenesis. Ethanol pathologic consumption suppresses gluconeogenesis, thus abolishing glucose formation and resulting in hypoglycemia. Malnutrition which is widespread among patients with AKA reduces liver glycogen and fat reserves subsequently receiving fatty acids for oxidation. Ketone bodies are produced from broken fatty acids as a result metabolic acidosis occurs because the blood pH is reduced.
Alcoholic ketoacidosis occurs mainly in people who like taking too much alcohol regularly and frequently. It is often linked with chronic alcohol use, however, the quantity and the period, which a person should consume alcohol to develop AKA, differ in some ways. Prolonged use of alcohol affects the individual’s dietary pattern, and there is usually malnutrition. Alcoholics can have poor nutrient diets where some foods that are considered essential for the body such as the vitamins, the minerals, the carbohydrates are scarce. Malnutrition decompensates the liver and in turn hinders the metabolic functions such as gluconeogenesis.
The outcomes for alcoholic ketoacidosis are mainly driven by such factors as the degrees of metabolic acidosis, the time at which the treatment begins, and any other co-existing ailments. Early diagnosis of the condition and treatment give a relatively favorable outcome.
The overall mortality rate of alcoholic ketoacidosis has been estimated to arrive at between 2% and as low as 10%. Some of the factors that may predispose the patient to a poor outcome include older age, severe acidosis, other medical conditions, including liver disease or pancreatitis, and a later initiation of proper treatment measures.
Abdominal pain is also a common characteristic seen in persons with AKA when reviewing the case history. The patient may have pain in the epigastric region accompanied by abdominal distension, which may be generalized or localized in the upper central part of the abdomen. This disease is usually accompanied by gastrointestinal symptoms like nausea and vomiting. Eliminating abdominal pain, often present in patients, can worsen the observed reduction in oral intake. Some symptoms that patients may show include irritability, tremor, and confusion.
Age group: Alcoholic ketoacidosis (AKA) mainly affects those who often consume alcohol. This is most observed in adults; those in the working population between the ages of thirty and fifty years are mostly affected.
Vital signs
Abdominal examination
Skin examination
Neurological examination
Chronic Alcohol Abuse
Malnutrition
Liver Disease
Pancreatitis
Gastrointestinal Bleeding
Electrolyte Imbalances:
Clinical Presentation:
Some of the clinical presentations may be represented by nausea, vomiting, abdominal pain or discomfort, and altered mental status.
Some patients will exhibit symptoms of excessive ethanol consumption and then abstinence from both food and ethanol for a certain period.
They might also present with symptoms of dehydration and postural hypotension.
Diabetic Ketoacidosis
Uremia
Salicylate Poisoning
Methanol Toxicity
Lactic Acidosis
Treatment paradigm:
Intravenous (IV) fluids: This is crucial of management of AKA as an emergency that requires rapid intervention. IV fluids are used to replenish body fluids and normalize the level of electrolytes.
Thiamine supplementation: Thiamine is administered intravenously to avoid development of Wernicke’s encephalopathy which is neurological complication of thiamine deficiency.
Glucose administration: After the repletion of thiamine, if necessary, glucose may be administered intravenously to facilitate the conversion of fats to glucose in the body.
Electrolyte replacement: Abnormality of potassium, magnesium, and phosphate electrolyte is often noted in AKA, and these require supplementation with IV fluids or phosphate supplements.
Treating alcohol withdrawal syndrome: There might be a necessity to treat non-psychotic drug effects of alcohol dependency, like tremors, anxiety, and seizure.
Endocrinology, Metabolism
Diet: After the initial phase of AKA has been managed, the patient should be placed on a diet high in carbohydrates and protein to serve a purpose of glycogen reserves and enhance the general diet. This will help the body to heal and reverse some of the changes that have occurred due to the infection.
Hydration: Crystalloid fluids such as isotonic or moderately hypotonic normal saline and Ringer’s lactate are the mainstay of IV fluids in the management of AKA. It assists in reversal of pathology of dehydration and electrolyte imbalance. On some occasions, rehydration maybe done through oral fluids.
Rest: Sufficient sleep is necessary so that the body could recover from the stress caused by the preceding day’s physical activity.
Supplements: It is often associated with thiamine or vitamin B1 deficiency that is prevalent in alcohol-dependent patients, as well as exacerbates AKA. Thiamine should be administered in the therapy and in the prevention of AKA.
Withdrawal management: Persons with AKA might also be having AW symptoms. These symptoms can be alleviated by medications and other supportive care to prevent the worsening of the condition.
Endocrinology, Metabolism
Thiamine (Vitamin B1): Prolonged alcohol consumption results in the depletion of thiamine levels that results in the development of Wernicke’s encephalopathy which is a severe neurological disease. This condition ought to be prevented through the administration of thiamine. The usual schedule in which it is administered is intravenously at the beginning of therapy.
Endocrinology, Metabolism
Potassium (K+):
Hypokalemia is observed because of poor nutrient intake, vomiting, and renal acidosis, in addition to acute kidney injury.
Special attention should be paid to potassium levels and their maintenance at a proper level. In this case, replacement is normally done through the intravenous (IV) route in the serious cases.
Magnesium (Mg2+):
This one is also prevalent, just as potassium deficiency results from the same causes and can worsen hypokalemia.
Magnesium should be monitored and supplemented if its level is reduced, which is sometimes done while at the same time replacing potassium.
Endocrinology, Metabolism
Fluid resuscitation: The treatment of AKA begins and is considered one of the most significant in the entire process of the patient’s recovery. Oral rehydration therapy and intravenous (IV) fluids are given to replace fluid lost because of vomiting and dehydration.
Electrolyte replacement: The patients shown to be affected by AKA have their levels of the following electrolytes low; potassium, magnesium, and phosphate. Such electrolytes are vital to several aspects of the body and need replacement so as not to lead to worse scenarios.
Thiamine supplementation: Another vitamin that is necessary for the proper function of nerves is thiamine or vitamin B1. Patients with alcohol dependency are commonly found with thiamine deficiency and it is asserted that the AKA symptoms deteriorate with the absence of thiamine. Thiamine is given intravenously.
Glucose administration: Once the patient has been ’flushed’ out and their electrolytes balanced, glucose may be administered intravenously to help the body slowly transition from burning fat to fuel its metabolism to burning glucose. This may assist in reducing the concentration of ketones and a further enhancement of acidosis.
Management of alcohol withdrawal: The excess alcohol users also suffer from the AKA and, therefore, are prone to developing AWS. Some drugs may be administered to assist in controlling some of the signs of AWS.
Nutritional support: After stabilizing the patient, it will be essential to encourage the patient to eat to refill the glycogen storage and enhance their diet intake.
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