Use of addictive drugs, such as cocaine, marijuana, and nicotine, affects food and liquid intake behavior, taste preference, and body weight. Changes in specific nutrient status and metabolism can also develop; heroin addiction can cause hyperkalemia and morphine use can result in calcium inhibition. Nutrition-related physiological aspects, such as impaired gastrin release, hypercholesterolemia, hypothermia, and hyperthermia, are also seen with morphine use. Nutrition-related conditions can affect sensitivity to and dependence on drugs and their effects. Diabetes decreases sensitivity to and dependence on morphine, protein deprivation produces preferential fat utilization with low cocaine use, and vitamin D deficiency decelerates morphine dependency. During use and/or withdrawal from nicotine, heroin, marijuana, and cocaine, major changes in food selection and intake occur, which result in weight gain or loss. Detailed human studies are needed to investigate the effects of drug use on the broad spectrum of nutrients and to determine the role of nutrition during drug withdrawal.

Nutritional effects of marijuana, heroin, cocaine, and nicotine

Effects of low- and high-intensity exercise on plasma and cerebrospinal fluid levels of ir-β-endorphin, ACTH, cortisol, norepinephrine and glucose in the conscious dog

Background: Type 2 diabetes is a common disorder that is recognized as a major health problem in Iran. Diabetes is a major cause of morbidity, mortality, and economic burden to the society. Some people believe that smoking opium can reduce serum glucose and lipids in diabetes mellitus. This study was designed to compare blood glucose and lipids in opium addicts with non-addicts among patients with type 2 diabetes. Methods: In this case, control study subjects were chosen from type 2 diabetic patients. Twenty-three males with type 2 diabetes and addicted to opium were selected as the case group, and 46 patients with no addiction to opioid drugs were chosen as control group. Blood Sugar (BS), glycated hemoglobin (HbA1C), lipids and microalbumin in urine were measured in two groups. Results: Our results showed that the mean FBS and 2-hour post prandial were significantly different between two groups. (P =. 04). No significant difference was observed in HbA1C, triglyceride, total cholesterol, LDL, and HDL bet...

Effect of Opium Addiction on Diabetes

Background: Iran is a significant consumer of opium, and, generally, of opioids, in the world. Addiction is one of the important issues of the 21st century and is an imperative issue in Iran. Long-term consumption of opioids affects homeostasis. Objective: To determine the effects of opium and heroin consumption on serum biochemical parameters. Methods: In a cross-sectional study, subjects who had consumed heroin (n = 35) or opium (n = 42) for more than two years and 35 nonaddict volunteers as the control group were compared in regard to various biochemical parameters such as fasting blood sugar (FBS), Na+, K+, Ca2+, blood urea nitrogen (BUN), uric acid (UA), triglyceride (TG), cholesterol, creatinine, and total protein. Chromatography was used to confirm opioid consumption, and the concentration of biochemical parameters was determined by laboratory diagnostic tests on serum. Results: No significant differences were found in Na+, Ca2+, BUN, UA, TG, creatinine, and total protein concentrations among the t...

Opium and Heroin Alter Biochemical Parameters of Human's Serum

Objective—To examine stress-related neurohormonal and metabolic effects of butorphanol, fentanyl, and ketamine administration alone and in combination with medetomidine in dogs. Animals—10 Beagles. Procedure—5 dogs received either butorphanol (0.1 mg/kg), fentanyl (0.01 mg/kg), or ketamine (10 mg/kg) IM in a crossover design. Another 5 dogs received either medetomidine (0.02 mg/kg) and butorphanol (0.1 mg/kg), medetomidine and fentanyl (0.01 mg/kg), medetomidine and ketamine (10 mg/kg), or medetomidine and saline (0.9% NaCl) solution (0.1 mL/kg) in a similar design. Blood samples were obtained for 6 hours following the treatments. Norepinephrine, epinephrine, cortisol, glucose, insulin, and nonesterified fatty acid concentrations were determined in plasma. Results—Administration of butorphanol, fentanyl, and ketamine caused neurohormonal and metabolic changes similar to stress, including increased plasma epinephrine, cortisol, and glucose concentrations. The hyperglycemic effect of butorphanol was not sig...

Influence of medetomidine on stress-related neurohormonal and metabolic effects caused by butorphanol, fentanyl, and ketamine administration in dogs.

This study was designed to assess the effects of morphine sulfate on glucose kinetics and on glucoregulatory hormones in conscious overnight fasted dogs. One group of experiments established a dose-response range. We studied the mechanisms of morphine-induced hyperglycemia in a second group. We also examined the effect of low dose morphine on glucose kinetics independent of changes in the endocrine pancreas by the use of somatostatin plus intraportal replacement of basal insulin and glucagon. In the dose-response group, morphine at 2 mg/h did not change plasma glucose, while morphine at 8 and 16 mg/h caused a hyperglycemic response. In the second group of experiments, morphine (16 mg/h) caused an increase in plasma glucose from a basal 99 +/- 3 to 154 +/- 13 mg/dl (P less than 0.05). Glucose production peaked at 3.9 +/- 0.7 vs. 2.5 +/- 0.2 mg/kg per min basally, while glucose clearance declined to 1.7 +/- 0.2 from 2.5 +/- 0.1 ml/kg per min (both P less than 0.05). Morphine increased epinephrine (1400 +/- 300 vs. 62 +/- 8 pg/ml), norepinephrine (335 +/- 66 vs. 113 +/- 10 pg/ml), glucagon (242 +/- 53 vs. 74 +/- 14 pg/ml), insulin (30 +/- 9 vs. 10 +/- 2 microU/ml), cortisol (11.1 +/- 3.3 vs. 0.9 +/- 0.2 micrograms/dl), and plasma beta-endorphin (88 +/- 27 vs. 23 +/- 6 pg/ml); all values P less than 0.05 compared with basal. These results show that morphine-induced hyperglycemia results from both stimulation of glucose production as well as inhibition of glucose clearance. These changes can be explained by rises in epinephrine, glucagon, and cortisol. These in turn are part of a widespread catabolic response initiated by high dose morphine that involves activation of the sympathetic nervous system, the endocrine pancreas, and the pituitary-adrenal axis. Also, we report the effect of a 2 mg/h infusion of morphine on glucose kinetics when the endocrine pancreas is clamped at basal levels. Under these conditions, morphine exerts a hypoglycemic effect (25% fall in plasma glucose, P less than 0.05) that is due to inhibition of glucose production (by 25-43%, P less than 0.05). The hypoglycemia was independent of detectable changes in insulin, glucagon, epinephrine and cortisol, and was not reversed by concurrent infusion of a slight molar excess of naloxone. Therefore, we postulate that the hypoglycemic effect of morphine results from the interaction of the opiate with non-mu receptors either in the liver or the central nervous system.

/pdf/effects-of-morphine-on-glucose-homeostasis-in-the-conscious-39g8vm2nzb.pdf

Effects of morphine on glucose homeostasis in the conscious dog.

The effect of human beta-endorphin (h beta E) infusion (0.2 mg/h) on glucose homeostasis was studied in 10 conscious overnight fasted dogs in which endocrine pancreatic function was fixed at basal levels with somatostatin plus intraportal replacement of basal insulin and glucagon. h beta E caused a fall in plasma glucose from 107 +/- 5 to 76 +/- 6 mg/dl by 3 h (P less than 0.01). This was due to a 25% fall in tracer-determined glucose production (Ra; P less than 0.01). A significantly larger fall in Ra was observed in four dogs in which hypoglycemia was prevented by use of an exogenous glucose infusion (45 vs. 25%, P less than 0.05). These changes occurred in the absence of changes in circulating levels of insulin, glucagon, epinephrine, norepinephrine, and cortisol. We conclude that the naturally occurring opioid peptide, beta-endorphin, inhibits glucose production by the liver in vivo. This appears to be a direct effect of the opioid on the liver, since the inhibition took place in the absence of changes in the other hormones measured. These results suggest that endorphins act on glucose homeostasis in a complex way, both by affecting other glucoregulatory hormones as demonstrated elsewhere, and by directly modulating hepatic glucose production as shown here.

/pdf/beta-endorphin-inhibits-glucose-production-in-the-conscious-7ucp3geelq.pdf

J R McRae

Papers

Effects of morphine on glucose homeostasis in the conscious dog.

Beta-endorphin inhibits glucose production in the conscious dog.