Drug - Nutrient Interactions
Prescription drugs may interfere with nutrient absorption, digestion, metabolism, utilization, or excretion. Similarly, both nutritional status and diet can affect the action of drugs by altering their metabolism and function, and various dietary components can have pharmacologic activity under certain circumstances.
Drugs may act centrally or peripherally to decrease appetite or may reduce appetite as a result of side effects. Drugs that act centrally include catecholaminergics, dopaminergics such as levodopa for Parkinson's disease, serotoninergics, and endorphin modulators such as naloxone. Peripherally acting agents include those that inhibit gastric emptying, and bulking agents.
The emetic centre, located in the brain stem, is easily stimulated by the action of many drugs. Almost all drugs have the potential to alter gastrointestinal function, causing nausea, vomiting, diarrhoea, and constipation. Any drug causing nausea, especially alcohol, can decrease appetite. For instance, it has been well documented that digitalis toxicity leads to anorexia, nausea, weight loss, and wasting. Narcotics, analgesics, and clofibrate are also commonly associated with nausea and vomiting. Cancer chemotherapeutic drugs such as methotrexate have a strong anoretic effect and can cause gastroenterologic toxicity.
In addition, drugs may alter nutritional status, which in turn can result in anorexia and weight loss. High doses of aluminum or magnesium hydroxide antacids can cause phosphate depletion, leading to muscle weakness, anorexia, and even congestive heart failure. Thiazide and furosemide diuretics can cause sodium, potassium, and magnesium depletion, resulting in anorexia and muscle weakness. Commonly used folate antagonists include methotrexate, a cancer chemotherapeutic agent; triamterene, a diuretic; trimethoprim, an antibacterial agent; phenytoin, an anticonvulsant; and sulphasalazine, an anti-inflammatory agent. Sulphasalazine and phenytoin are competitive inhibitors of folate transport in addition to being folate antagonists. Folate deficiency can lead to weight loss and anorexia. Penicillamine induces zinc depletion, which may cause a loss of taste acuity and possibly decreased food intake. Alcohol abuse also commonly results in deficiencies of thiamin, folate, vitamin B6, vitamin A, and zinc. [Fischer, J., and Johnson, M.A. Department of Foods and Nutrition, College of Family and Consumer Sciences, University of Georgia, Athens, Georgia.]
About a billion dollars is spent each year in the United States on antacids, making these products among the most popular over-the-counter (OTC) drugs. These tablets and liquids are gulped down for the relief of heartburn, sour stomach, and indigestion. Antacids may also be prescribed to treat stomach ulcers.
Although many consumers take antacids almost casually, these drugs are not as harmless as they may seem. Antacids can effect the way other drugs behave in the body. They can speed the absorption of some prescription drugs, possibly causing an overdose, or slow it for others, thus reducing their effectiveness.
Because of concerns about known interactions between antacids and other prescription drugs, FDA is proposing to change that label warnings read:
"Antacids may interact with certain prescription drugs. If you are presently taking a prescription drug, do not take this product without checking with your physician."
Dietary factors can decrease, delay or enhance the absorption of drugs, primarily by altering their availability, their solubility, or the amount of time they spend in the stomach or intestine. Calcium, for example, can bind tetracycline antibiotics and form a complex that renders both the drug and nutrient unavailable. The acidity of the gastrointestinal tract also affects drug disposition. A more acidic environment reduces the bioavailability of penicillin and isoniazid but increases the absorption of tetracyclines. Food decreases, delays, or enhances the absorption of certain antibiotics.
Instructions to take drugs with or between meals, or the coating of drugs to prevent dissolution, attempt to take advantage of these gastric properties, but it is uncertain how well patients adhere to such instructions.
The effects of drugs are modulated by their rates of metabolism by the liver and other tissues. Drugs are metabolized by two basic processes. The first (Phase I) metabolic step is usually an oxidation reaction that alters a functional group in the drug. This alteration may either activate the drug or deactivate it. The second step (Phase II) conjugates the oxidized drug to an inactive, water-soluble form that can be readily excreted.
The rate of drug metabolism by mixed-function oxidase systems can be accelerated by the drugs themselves as well as by a variety of dietary factors. Such factors include protein, cruciferous vegetables (broccoli or cabbage), and charcoal-broiled meats.
On the other hand, low-protein, high-carbohydrate diets and deficiencies of several vitamins and minerals reduce levels of drug-metabolizing enzymes and consequently the rate of drug metabolism, so that the drug concentrations may decline slowly. thus, in many cases the net effect of nutritional deficiency is to increase drug potency.
Certain drugs can interfere with specific nutrients or non-nutrient components in foods to cause acute adverse reactions. Such reactions can be prevented by avoiding the foods when taking the medication. Examples include interactions between monoamineoxidase inhibitors and foods containing tyramine, and between alcohol and disulphiram, hypoglycaemic agents, and many other drugs.
Nutrients are sometimes used in unusually high doses for their pharmacologic effect. Niacin, for example is used pharmacologically to reduce blood cholesterol levels. Retinoid derivatives of vitamin A have been used successfully to treat severe acne and other conditions.
All pharmacologic therapies induce side effects, and high-dose nutritional therapies are no exception. Although excess water-soluble vitamins are excreted and usually cause little difficulty, side effects have been reported in cases of excessively high doses.
High dose niacin induces flushing, and neurologic symptoms have been reported from excessive intake of vitamin B6. Excessive intake of fat-soluble vitamins or their derivatives is well known to induce toxic symptoms. Excess vitamin A, for example, causes birth defects in animals, and possibly, in humans. Caution has been urged in its use for women who are pregnant or likely to become pregnant.
Individuals who are born without the genes to produce key functional enzymes may require amounts of certain nutrients greatly in excess of those required by most people. Such inborn metabolic errors have been identified for enzymes necessary for absorption, metabolism, or storage of nearly all of the vitamins.
In some cases, higher than normal intake of the vitamin will restore activity. A classic example of such a vitamin-responsive syndrome is pernicious anaemia, a condition of impaired absorption of vitamin B12. Patients with this condition must have exceedingly high doses of the vitamin from food supplements, or lower doses by injection.
In other conditions, certain metabolic products cannot be degraded and, therefore, accumulate to toxic levels. In some cases, such disorders can be treated with carefully designed dietary preparations having a very low content of the poorly metabolized nutrient. An example of this type of condition is phenylketonuria, a genetic lack of the enzyme that converts the amino acid phenylalanine to tyrosine. Patients with phenylketonuria accumulate phenylalanine and other metabolites that at high levels, are toxic and cause mental retardation and other neurologic damage. Dietary treatment is designed to reduce the phenylalanine content of the diet to levels below those that cause symptoms.
It is the position of the American Dietetic Association that nutrition intervention, planned and provided by a qualifiednutrition professional, is an essential component of the treatment and recovery from chemical dependency.
Figures are for estimated retail sales through retail outlets.
*Excludes sales through health-food stores, door-to-door, or by mail.
(Source: Frost and Sullivan, Inc., FDA consumer, Pg 5, October, 1986.)
American consumers tend to be surprisingly conservative in their responses to common illnesses. More than a third do not treat their ailments at all, but they are becoming more knowledgeable about the effects of Over-the Counter remedies.
The severity of malnutrition and the need for nutrition therapy in addiction vary. Mind altering substances (eg. alcohol) are toxic to the body, causing physical adaption, damage, and malnutrition.
Abuse of drugs accelerates nutrition needs beyond normal, so that even a well-balanced diet may be inadequate. Nutritional problems are also caused by an increased nutrient requirement to detoxify and metabolize drugs, inactivation of vitamins and coenzymes needed to metabolize energy, inadequate nutrient storage in the liver, malabsorption, poor utilization of nutrients, breakdown of organs, and increased loss of nutrients through diuresis and diarrhoea.
Nutrition care is defined to include an elevation of the addict's nutritional status at detoxification, supervision of nutritional rehabilitation through delivery of palatable, nourishing meals and supplements that encourage normal eating patterns, and provision of nutritional counselling to help the addict develop an eating plan supportive of stable recovery.
Chemical dependence is a bio-psychosocial disease. Patients with a compromised liver function have a narrow therapeutic window for iron or fat-soluble vitamin supplements and may even be in a condition of iron overload. Therefore the use of high-potency vitamin or mineral supplements should be discouraged unless clinical evidence of nutritional deficiency is present.
The majority of abusers have suppressed immune status, which is compounded by an inadequate diet. Abusers exposed to the human immunodeficiency virus (HIV) are thus at greater risk for contracting HIV infection. Unless rectified, a poor diet may be one factor in stimulating propagation of the virus toward more severe stages of HIV infection.
If AIDS is diagnosed in the patient in treatment, nutrition monitoring is essential. Adequate-calorie, nutrient-dense diets, with supportive or aggressive supplementation if indicated, are essential.
Nutritional recovery is a component of the physical foundation for rehabilitation that precedes healthy mental, emotional, and spiritual recovery. Patients need to eat regularly and prudently. An eating pattern that emphasizes complex carbohydrates, moderate amounts of protein, and conservative quantities of dietary fats and emphasizes balance, variety, caloric appropriateness, and regularity will be conducive to progress in recovery. A high-protein, high-fat diet has been reported to increase the incidence of drinking. [Yung, L., Gordis, E., and Holt, J.: Dietary choices and likelihood of abstinence among alcoholic patients in an outpatient clinic. Drug Alcohol Dependence 12:355, 1983.]
The menu planner should recognize that the stay of the average addict in treatment is lengthy. Food offerings should be designed to maximize attractive appearance and palatability to stimulate appetite and willingness to eat regular meals as well as to support general morale. The patient should be encouraged to choose foods freely in a cafeteria or family-style setting. Social interaction during mealtime facilitates treatment goals of resocialization without drugs.
Substance substitution, such as the replacement of sugar, caffeine, or nicotine for the drug of choice, often occurs during recovery. Substance substitution compromises the quality of nutritional rehabilitation and perpetuates the behavioural aspect of addiction. The recovering addict needs to learn how to cope with substitution patterns.
Irregular meals, snacking, and consequent blood sugar fluctuations, along with a stressful environment, may stimulate cravings that make the recovering addict susceptible to relapsing. Addicts have been reported to believe that consumption of sweets helped them maintain sobriety.
Eating disorders are common in chemically dependant women. Current theories of addiction suggest that compulsive eating, like alcoholism, is rooted in similar issues of codependency that form the addictive personality. Eating disorders may involve an addiction that occurred long before alcohol or other drugs were abused. However, as chemical dependency develops, the eating disorder may go into remission, only to reappear during abstinent recovery. In other patients the abuse of alcohol and drugs suchas amphetamine and cocaine alters normal appetite, digestion, and metabolic regulatory systems, stimulating the development of an eating disorder.
Nutrition counselling should include specific food-related emotional issues. Self-esteem, responsibility, and socialization skills should be addressed to change eating habits. Because the family is intimately involved in the success of recovery, the family member involved with meal preparation should also receive counselling to prevent the use of food as a weapon of sabotage.
Besides the usual presentation of nutritional consequences of drug abuse and food sources for nutrient needs, the dietitian should discuss practical ways to handle stress and cravings, how to integrate healthy life-style choices into daily recovery principals, weight management and eating disorder risks, and avoidance of substance substitutions such as sugar, caffeine, and nicotine. The dietitian should also counter nutrition myths touted in the popular literature and circulated among people.
Many debilitating nutritional consequences result from drug and alcohol abuse. Chronic nutrition impairment causes serious damage to the liver and the brain, which reinforces the craving for more drugs and alcohol, and perpetuates the phycological aspect of addiction. During treatment efforts are concentrated on physical recovery, which prepares individuals to function at a higher level in treatment - cognitivaly, mentally, and socially.
Improved nutritional status can make treatment more effective, while reducing drug and alcohol craving, thereby preventing relapse. Nutrition professionals should take aggressive action to ensure involvement in treatment and recovery programs. In addition they are encouraged to participate in nutrition research activities to strengthen the knowledge base in this area. [Position of The American Dietetic Association: Nutrition intervention in the treatment and recovery from chemical dependency. Journal of Amer Dietetic Assoc, 90:1274-1277, 1990.]
Prescription drugs may interfere with nutrient absorption, digestion, metabolism, utilization, or excretion. Similarly, both nutritional status and diet can affect the action of drugs by altering their metabolism and function, and various dietary components can have pharmacologic activity under certain circumstances.
Drugs may act centrally or peripherally to decrease appetite or may reduce appetite as a result of side effects. Drugs that act centrally include catecholaminergics, dopaminergics such as levodopa for Parkinson's disease, serotoninergics, and endorphin modulators such as naloxone. Peripherally acting agents include those that inhibit gastric emptying, and bulking agents.
The emetic centre, located in the brain stem, is easily stimulated by the action of many drugs. Almost all drugs have the potential to alter gastrointestinal function, causing nausea, vomiting, diarrhoea, and constipation. Any drug causing nausea, especially alcohol, can decrease appetite. For instance, it has been well documented that digitalis toxicity leads to anorexia, nausea, weight loss, and wasting. Narcotics, analgesics, and clofibrate are also commonly associated with nausea and vomiting. Cancer chemotherapeutic drugs such as methotrexate have a strong anoretic effect and can cause gastroenterologic toxicity.
In addition, drugs may alter nutritional status, which in turn can result in anorexia and weight loss. High doses of aluminum or magnesium hydroxide antacids can cause phosphate depletion, leading to muscle weakness, anorexia, and even congestive heart failure. Thiazide and furosemide diuretics can cause sodium, potassium, and magnesium depletion, resulting in anorexia and muscle weakness. Commonly used folate antagonists include methotrexate, a cancer chemotherapeutic agent; triamterene, a diuretic; trimethoprim, an antibacterial agent; phenytoin, an anticonvulsant; and sulphasalazine, an anti-inflammatory agent. Sulphasalazine and phenytoin are competitive inhibitors of folate transport in addition to being folate antagonists. Folate deficiency can lead to weight loss and anorexia. Penicillamine induces zinc depletion, which may cause a loss of taste acuity and possibly decreased food intake. Alcohol abuse also commonly results in deficiencies of thiamin, folate, vitamin B6, vitamin A, and zinc. [Fischer, J., and Johnson, M.A. Department of Foods and Nutrition, College of Family and Consumer Sciences, University of Georgia, Athens, Georgia.]
Antacids
About a billion dollars is spent each year in the United States on antacids, making these products among the most popular over-the-counter (OTC) drugs. These tablets and liquids are gulped down for the relief of heartburn, sour stomach, and indigestion. Antacids may also be prescribed to treat stomach ulcers.
Although many consumers take antacids almost casually, these drugs are not as harmless as they may seem. Antacids can effect the way other drugs behave in the body. They can speed the absorption of some prescription drugs, possibly causing an overdose, or slow it for others, thus reducing their effectiveness.
Because of concerns about known interactions between antacids and other prescription drugs, FDA is proposing to change that label warnings read:
"Antacids may interact with certain prescription drugs. If you are presently taking a prescription drug, do not take this product without checking with your physician."
Effects of Diet on Drug Metabolism
Dietary factors can decrease, delay or enhance the absorption of drugs, primarily by altering their availability, their solubility, or the amount of time they spend in the stomach or intestine. Calcium, for example, can bind tetracycline antibiotics and form a complex that renders both the drug and nutrient unavailable. The acidity of the gastrointestinal tract also affects drug disposition. A more acidic environment reduces the bioavailability of penicillin and isoniazid but increases the absorption of tetracyclines. Food decreases, delays, or enhances the absorption of certain antibiotics.
Instructions to take drugs with or between meals, or the coating of drugs to prevent dissolution, attempt to take advantage of these gastric properties, but it is uncertain how well patients adhere to such instructions.
The effects of drugs are modulated by their rates of metabolism by the liver and other tissues. Drugs are metabolized by two basic processes. The first (Phase I) metabolic step is usually an oxidation reaction that alters a functional group in the drug. This alteration may either activate the drug or deactivate it. The second step (Phase II) conjugates the oxidized drug to an inactive, water-soluble form that can be readily excreted.
The rate of drug metabolism by mixed-function oxidase systems can be accelerated by the drugs themselves as well as by a variety of dietary factors. Such factors include protein, cruciferous vegetables (broccoli or cabbage), and charcoal-broiled meats.
On the other hand, low-protein, high-carbohydrate diets and deficiencies of several vitamins and minerals reduce levels of drug-metabolizing enzymes and consequently the rate of drug metabolism, so that the drug concentrations may decline slowly. thus, in many cases the net effect of nutritional deficiency is to increase drug potency.
Certain drugs can interfere with specific nutrients or non-nutrient components in foods to cause acute adverse reactions. Such reactions can be prevented by avoiding the foods when taking the medication. Examples include interactions between monoamineoxidase inhibitors and foods containing tyramine, and between alcohol and disulphiram, hypoglycaemic agents, and many other drugs.
Effects of Pharmacologic Doses of Nutrients
Nutrients are sometimes used in unusually high doses for their pharmacologic effect. Niacin, for example is used pharmacologically to reduce blood cholesterol levels. Retinoid derivatives of vitamin A have been used successfully to treat severe acne and other conditions.
All pharmacologic therapies induce side effects, and high-dose nutritional therapies are no exception. Although excess water-soluble vitamins are excreted and usually cause little difficulty, side effects have been reported in cases of excessively high doses.
High dose niacin induces flushing, and neurologic symptoms have been reported from excessive intake of vitamin B6. Excessive intake of fat-soluble vitamins or their derivatives is well known to induce toxic symptoms. Excess vitamin A, for example, causes birth defects in animals, and possibly, in humans. Caution has been urged in its use for women who are pregnant or likely to become pregnant.
Individuals who are born without the genes to produce key functional enzymes may require amounts of certain nutrients greatly in excess of those required by most people. Such inborn metabolic errors have been identified for enzymes necessary for absorption, metabolism, or storage of nearly all of the vitamins.
In some cases, higher than normal intake of the vitamin will restore activity. A classic example of such a vitamin-responsive syndrome is pernicious anaemia, a condition of impaired absorption of vitamin B12. Patients with this condition must have exceedingly high doses of the vitamin from food supplements, or lower doses by injection.
In other conditions, certain metabolic products cannot be degraded and, therefore, accumulate to toxic levels. In some cases, such disorders can be treated with carefully designed dietary preparations having a very low content of the poorly metabolized nutrient. An example of this type of condition is phenylketonuria, a genetic lack of the enzyme that converts the amino acid phenylalanine to tyrosine. Patients with phenylketonuria accumulate phenylalanine and other metabolites that at high levels, are toxic and cause mental retardation and other neurologic damage. Dietary treatment is designed to reduce the phenylalanine content of the diet to levels below those that cause symptoms.
Treatment and recovery from chemical dependency
It is the position of the American Dietetic Association that nutrition intervention, planned and provided by a qualifiednutrition professional, is an essential component of the treatment and recovery from chemical dependency.
Table 2.12 Estimated Sales of Over-the-Counter Internal Medications (Millions of dollars)
Category of Medications | 1982 | 1985 | 1990 |
|---|---|---|---|
Analgesics Cough, cold, allergy, sinus Digestive aids Motion sickness Sleep aids/sedatives Appetite suppressants* Vitamins and minerals* | 1484 1269 1228 25 41 229 1031 | 1844 1659 1393 33 50 280 1509 | 2490 2241 1654 43 66 350 2176 |
$5307 | $6768 | $9020 |
Figures are for estimated retail sales through retail outlets.
*Excludes sales through health-food stores, door-to-door, or by mail.
(Source: Frost and Sullivan, Inc., FDA consumer, Pg 5, October, 1986.)
American consumers tend to be surprisingly conservative in their responses to common illnesses. More than a third do not treat their ailments at all, but they are becoming more knowledgeable about the effects of Over-the Counter remedies.
The severity of malnutrition and the need for nutrition therapy in addiction vary. Mind altering substances (eg. alcohol) are toxic to the body, causing physical adaption, damage, and malnutrition.
Abuse of drugs accelerates nutrition needs beyond normal, so that even a well-balanced diet may be inadequate. Nutritional problems are also caused by an increased nutrient requirement to detoxify and metabolize drugs, inactivation of vitamins and coenzymes needed to metabolize energy, inadequate nutrient storage in the liver, malabsorption, poor utilization of nutrients, breakdown of organs, and increased loss of nutrients through diuresis and diarrhoea.
Nutrition care is defined to include an elevation of the addict's nutritional status at detoxification, supervision of nutritional rehabilitation through delivery of palatable, nourishing meals and supplements that encourage normal eating patterns, and provision of nutritional counselling to help the addict develop an eating plan supportive of stable recovery.
Chemical dependence is a bio-psychosocial disease. Patients with a compromised liver function have a narrow therapeutic window for iron or fat-soluble vitamin supplements and may even be in a condition of iron overload. Therefore the use of high-potency vitamin or mineral supplements should be discouraged unless clinical evidence of nutritional deficiency is present.
The majority of abusers have suppressed immune status, which is compounded by an inadequate diet. Abusers exposed to the human immunodeficiency virus (HIV) are thus at greater risk for contracting HIV infection. Unless rectified, a poor diet may be one factor in stimulating propagation of the virus toward more severe stages of HIV infection.
If AIDS is diagnosed in the patient in treatment, nutrition monitoring is essential. Adequate-calorie, nutrient-dense diets, with supportive or aggressive supplementation if indicated, are essential.
Nutritional recovery is a component of the physical foundation for rehabilitation that precedes healthy mental, emotional, and spiritual recovery. Patients need to eat regularly and prudently. An eating pattern that emphasizes complex carbohydrates, moderate amounts of protein, and conservative quantities of dietary fats and emphasizes balance, variety, caloric appropriateness, and regularity will be conducive to progress in recovery. A high-protein, high-fat diet has been reported to increase the incidence of drinking. [Yung, L., Gordis, E., and Holt, J.: Dietary choices and likelihood of abstinence among alcoholic patients in an outpatient clinic. Drug Alcohol Dependence 12:355, 1983.]
The menu planner should recognize that the stay of the average addict in treatment is lengthy. Food offerings should be designed to maximize attractive appearance and palatability to stimulate appetite and willingness to eat regular meals as well as to support general morale. The patient should be encouraged to choose foods freely in a cafeteria or family-style setting. Social interaction during mealtime facilitates treatment goals of resocialization without drugs.
Substance substitution, such as the replacement of sugar, caffeine, or nicotine for the drug of choice, often occurs during recovery. Substance substitution compromises the quality of nutritional rehabilitation and perpetuates the behavioural aspect of addiction. The recovering addict needs to learn how to cope with substitution patterns.
Irregular meals, snacking, and consequent blood sugar fluctuations, along with a stressful environment, may stimulate cravings that make the recovering addict susceptible to relapsing. Addicts have been reported to believe that consumption of sweets helped them maintain sobriety.
Eating disorders are common in chemically dependant women. Current theories of addiction suggest that compulsive eating, like alcoholism, is rooted in similar issues of codependency that form the addictive personality. Eating disorders may involve an addiction that occurred long before alcohol or other drugs were abused. However, as chemical dependency develops, the eating disorder may go into remission, only to reappear during abstinent recovery. In other patients the abuse of alcohol and drugs suchas amphetamine and cocaine alters normal appetite, digestion, and metabolic regulatory systems, stimulating the development of an eating disorder.
Nutrition counselling should include specific food-related emotional issues. Self-esteem, responsibility, and socialization skills should be addressed to change eating habits. Because the family is intimately involved in the success of recovery, the family member involved with meal preparation should also receive counselling to prevent the use of food as a weapon of sabotage.
Besides the usual presentation of nutritional consequences of drug abuse and food sources for nutrient needs, the dietitian should discuss practical ways to handle stress and cravings, how to integrate healthy life-style choices into daily recovery principals, weight management and eating disorder risks, and avoidance of substance substitutions such as sugar, caffeine, and nicotine. The dietitian should also counter nutrition myths touted in the popular literature and circulated among people.
Many debilitating nutritional consequences result from drug and alcohol abuse. Chronic nutrition impairment causes serious damage to the liver and the brain, which reinforces the craving for more drugs and alcohol, and perpetuates the phycological aspect of addiction. During treatment efforts are concentrated on physical recovery, which prepares individuals to function at a higher level in treatment - cognitivaly, mentally, and socially.
Improved nutritional status can make treatment more effective, while reducing drug and alcohol craving, thereby preventing relapse. Nutrition professionals should take aggressive action to ensure involvement in treatment and recovery programs. In addition they are encouraged to participate in nutrition research activities to strengthen the knowledge base in this area. [Position of The American Dietetic Association: Nutrition intervention in the treatment and recovery from chemical dependency. Journal of Amer Dietetic Assoc, 90:1274-1277, 1990.]
Table 2.13 Biological, psychological, and social factors of chemical dependence disease.
Biological | Brain and liver dysfunction caused by chronic alcohol and drug poisoning. |
Psychological | Personality disorganization created by progressive brain dysfunction (often alluded to as the addictive personality). |
Social | Secondary relationship problems that interfere with the functioning and support systems at home, on the job, and with friends. |
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