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Try out PMC Labs and tell us what you think. Learn More. Opioid dependence poses ificant public health risks arising from associated morbidity and mortality caused by accidents, infectious disease, and social ramifications of crime and unemployment, among other complications.
Opioid use, acute and chronic, is also associated with weight gain, glycemic dysregulation, and dental pathology. The literature supporting the connection Why do heroin addicts drink milk opiate use and development of preference for sweet tastes is reviewed, and further association with dental pathology, weight gain, and loss of glycemic control are considered.
We discuss the impact of sweet tastes on the endogenous opioid system as well as clinical implications for analgesia and treating the opiate-dependent patient. Opioid dependence is ificant public health concern. It is estimated that 1 million Americans are currently addicted to heroin in the United States 1. Morbidity and mortality are associated with intravenous administration HIV, Hepatitis Cintoxication accidents, overdoseand chronic use dependence of opiates.
Research has demonstrated associations between opioid consumption and sugar intake and metabolism in human and nonhuman subjects. The following article will review will explore some clinical implications of these relationships on the morbidity of opioid users, including those related to dental pathology, weight gain, and glycemic control.
Literature describing the analgesic properties of sugar, and possible associations to the endogenous opioid system, will also be examined. Evidence from both preclinical Why do heroin addicts drink milk clinical studies demonstrates that chronic opioid exposure is associated with increased sugar intake. Preclinical research has attempted to refine the potential pathways and mechanisms of action through which opiates may regulate sugar intake, and how sugar consumption may affect the endogenous opiate system. Preclinical animal studies suggest that direct action of mu agonists at the nucleus accumbens shell, hypothalamus, and paraventricular nucleus is associated with development of sweet preference 2 — 7.
This process possibly involves GABA-b activity in the ventral tegmental area 6.
Consumption of palatable foods, especially on intermittent schedules, is associated with acute binding of the endogenous opiate B-endorphin in the hypothalamus, accumbens shell, cingulated, hippocampus, and locus ceruleus of rats 28. Furthermore, in rats, intermittent access to sucrose le to decreased enkephalin MRNA production 9. Methadone-maintained patients assessed at entry to treatment, 9 months and 4 years into treatment demonstrate increased consumption of sugary food, fewer complex carbohydrates, less fruits, vegetables and fats from fish or vegetables It was noted that female methadone patients consumed fewer total calories, but maintained similar BMI to the national average BMI Clinical literature demonstrates that chronic exposure to mu-opiate agonists le to heightened taste preference for high-sugar foods 12 — Yet human subjects chronically exposed to opiates maintain their ability to distinguish various tastes compared with control subjects 15indicating that taste preferences associated with opiate exposure are not related to an impaired taste sense.
Further, studies of mu-opiate antagonists naloxone and naltrexone in non-human opiate-dependent subjects, as well as clinical trials of binge eaters without opiate dependence, demonstrate decreased preference for high-sugar foods, with decreased caloric Why do heroin addicts drink milk from those types of foods 3 — 616 — It has been found that the novelty of the diet may alter the effect of an opiate antagonist.
With naltrexone, rats decreased both fat and carbohydrate intake from an established diet, but selectively decreased either fat or carbohydrate from a novel diet In a study of Why do heroin addicts drink milk human subjects who were administered a single 2. Buprenorphine, a partial mu-opiate agonist, appears to decrease saccharine consumption in non-opiate-dependent male Sprawg-Dawley rats, behaving like an opiate antagonist However, this effect of buprenorphine becomes extinguished during chronic administration In rats receiving their normal complement of food, while chronically administered buprenorphine, decreased sucrose intake in reward situations was noted; however, the rats would generally consume their overall expected quantity of food The preference for sugary foods resulting from opiate administration may lead to increased consumption of such foods, and possibly accumulation of excess body fat and weight gain.
Heroin addicts who initiated methadone maintenance treatment typically demonstrated ificant weight gain, possibly related to their expressed strong cravings for sweets during protracted abstinence The rats in acute opiate withdrawal also express a similar increased craving for sweets A recent study of methadone-maintained patients found higher BMI, and increased liking of sweet foods, over Why do heroin addicts drink milk Taken together, these findings suggest that opiate-dependent patients on methadone maintenance appear to develop increased BMI, with a greater proportion of them overweight and pre-obese than the average drug user.
Reviews of the preclinical and clinical literature demonstrate a trend of increased eating following opiate agonist intake, with decreased eating after opiate antagonist intake in animals under acute food deprivation or stress, but not those that are chronically food deprived 28 — An earlier review concluded that mu agonists generally stimulate food intake, and may or may not be associated with increased BMI in humans Conversely, intravenous administration of the mu antagonist naloxone, a drug with a relatively short half life, was associated with short-term single-meal decreased oral intake in lean and obese humans.
However, the daily oral administration of naltrexone, an opioid agonist with a relatively longer half life, was associated with zero to minimal weight loss in humans Further studies are needed to explore whether long-term opioid antagonist maintenance is indeed a weight-neutral treatment strategy.
There are links between obesity and the mu-opiate receptor system in the absence of substance use pathology. When IV naloxone and methylnatrexone were administered to genetically obese mice over a day period, food consumption and weight gain decreased compared to control obese mice Clinical investigations have demonstrated that B-endorphin appears in higher concentrations in the cerebrospinal fluid of obese adults and adolescents compared to lean human subjects There are emerging neurochemical similarities between regulation of substance use and food intake.
Leptin, a protein produced by adipose tissue and associated with food satiety, appears to decrease heroin relapse in food-restricted rats when infused into the hypothalamus 33 — Melanocortin is another protein involved in brain aling related to appetite.
Melanocortin agonists have been associated with inhibition Why do heroin addicts drink milk food intake in obese animal models, as well as decreased alcohol and food intake in alcohol dependent mice 35 — In light of the growing body of evidence linking the opioid system to food intake and risk of obesity, clinicians should reinforce proper exercise and dietary habits with opioid-dependent patients.
Opiate antagonists, like naltrexone, appear to be at least weight neutral, and possibly weight reducing, by decreasing preference for sweet foods. Further study and clinical use of these agents for treatment of opiate dependence may be warranted in overweight patients, those at risk of gaining excessive weight, and those with extant cardiac risk factors, such as hypertension and elevated lipids. There is compelling evidence that chronic administration of mu-opiate agonists is associated with pathology clinically similar to non-insulin dependent diabetes mellitus.
It has been demonstrated that use of heroin in humans is associated with increased resting insulin levels, as well as delayed and increased insulin response to glucose lo Similarly, methadone-maintained patients have clinically evident delayed insulin response to food ingestion with associated mild hyperglycemia Furthermore, increased fasting insulin levels have been noted in both heroin addicts and methadone patients An earlier study in healthy adults given a single dose of IV morphine 0. The authors concluded that morphine has no direct impact on insulin activity, but rather the slowing of gastric motility associated with mu-agonists causes delayed absorption of glucose, and therefore a delayed insulin response Inhibited gastric motility and delayed gastric emptying, with associated ileus and constipation, are known sequelae of mu-opiate administration Several other studies demonstrate a likely association between opioids and glycemic control that extends beyond mu-opiate agonist effects on gastric motility and emptying.
In a preclinical study rats administered daily methadone over a day period demonstrated increased resting serum glucose and impaired oral glucose tolerance tests during methadone exposure, as expected. However, the rats also demonstrated impairment in Why do heroin addicts drink milk enzymes related to glucose metabolism: the glycolytic activity of hexokinase and phosphofructokinase-1 activity was diminished, leading to less breakdown of plasma glucose.
Meanwhile, the gluconeogenic activity of glucosephosphatase and fructose-1,6-biphosphatase was increased, leading to augmented production of plasma glucose The authors concluded that methadone maintenance produces a metabolic state similar to non-insulin-dependent diabetes.
However, the finding that opioid addicts, in addition to elevation of plasma glycosylated hemoglobin A1 and delayed insulin response to IV glucose lo, also demonstrated normal insulin responses to arginine, a hallmark of functional pancreatic beta cell function, implies pathology more similar to non-insulin-dependent diabetes mellitus There may be ificant clinical implications inherent in the potential derangement of glycemic control in opioid-dependent patients. A retrospective chart review of 91 methadone maintained patients in the Atlanta Veterans Medical Center system revealed an odds ratio of The authors noted that while the 9.
The hyperglycemia in these cases was noted to exceed what would have been expected from merely the ingestion of the syrup in which he methadone had been dissolved And buprenorphine in the post-op period has shown divergent effects on glucose metabolism. In a study of patients receiving total hip replacements, an immediate post-operative dose of IV 0. However, a sublingual buprenorphine 4mg dose administered 3 hours post-op was associated with an acute decrease in plasma glucose This difference may suggest that with respect to effects on glycemic control, buprenorphine acts similarly to mu-agonists at low initial doses, and more like an antagonist at higher or later doses.
Further research would need to be conducted to clarify the dose-response curve of buprenorphine regarding these effects. Consumption of palatable foods is associated Why do heroin addicts drink milk acute binding of the endogenous opiate B-endorphin in the brain 28and decreased enkephalin MRNA production 9 which may be a consequence of mu opiate receptor down-regulation associated with increased mu-opiate receptor agonism There is some evidence that mu-opiate agonism associated with palatable food ingestion may have clinically relevant analgesic properties.
Preclinical studies demonstrate ificant increased pain tolerance in rats receiving oral sucrose compared to rats receiving water 47an effect reversible by the Why do heroin addicts drink milk antagonist naloxone Sweet and palatable food intake has been associated with clinically ificant analgesia in humans. Clinically, sucrose is often administered to preterm infants in neonatal ICUs to provide analgesia for routine heel sticks for blood sampling This practice is grounded in evidence that orally administered sucrose solutions 49 and artificial sweeteners 50 decrease crying and heart rate in infants subjected to heel pricks.
Sucrose administered via nasogastric tube does not appear to reduce pain response in infants It is postulated that the sweet taste of the sucrose or sweetener, not the substance itself, causes the analgesia Further evidence this effect of sweeteners occurs through the opiate system is that infants born to methadone-dependent mothers did not have the expected analgesic response The authors surmise this is likely because these infants are born with tolerance to mu-opiates because of chronic transplacental exposure to methadone Contrary to the theory that sweet-tasting solution le to central mu-agonism in infants, resulting in analgesia, one study was not able to detect elevated levels of plasma B-endorphins in infants within 5 minutes of receiving a heel prick for drawing blood, during oral sucrose administrationWhy do heroin addicts drink milk
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The relationship between opioid and sugar intake: Review of evidence and clinical applications