Alcohol and Endorphins in The Sinclair Method
To understand how Naltrexone is used in The Sinclair Method (TSM) for Alcohol Dependence, it is important to understand how the body’s opioid system works.
When people hear the word opiate, they usually think of heroin or prescription pain medications such as morphine, hydrocodone, codeine, or Vicodin. These drugs target the opioid system in our bodies, causing pain relief, euphoria, cough suppression, and constipation.
The wide-ranging effects occur because the opioid system is not limited to various parts of the brain, but is also found in the gastrointestinal tract and spinal cord.
In addition to the drugs that target our opioid receptors, we also have naturally occurring opioids in our bodies called Endorphins. Endo means “from within” and Orphin is a shortened form of morphine. The endorphins function in part as the body’s First Responder, because they are released in response to high levels of pain when when injure ourselves. If you were to fracture your arm, your brain would release endorphins to reduce your pain. The effect would be similar to ingesting a prescription opiate.
Alcohol Causes a Release of Endorphins
It is also well established that drinking alcohol also causes a release of endorphins, resulting in the pleasurable experience known as a “buzz”. This pleasurable sensation is distinguished from alcohol’s other intoxicating effects such as slurred speech, dis-inhibition, respiratory depression, decreased motor coordination, and sleepiness. This distinction is important:
The buzz and the impairment from alcohol are two different effects, and they operate through different physiological pathways.
It is the pleasure that drinkers seek, not the slurred speech and the loss of balance. If a beer simply made people unable to walk in a straight line–but caused no pleasure–it would not be a popular drink.
Alcoholism Treatment with Naltrexone
This is where Naltrexone enters the picture. Naltrexone is a prescription drug that is FDA-approved for alcohol treatment that blocks opioid receptors from being activated when you drink. This means that heroin, morphine, and hydrocodone do not have effects if naltrexone is present, but it also means that naturally occurring opiates that are released when alcohol is consumed are blocked if naltrexone is present.
If you have taken naltrexone before drinking, you will become impaired, but you will not enjoy it, because no opiates have been released in your brain.
Each and every time you’ve had a drink, you’ve received a powerful reward in the form of endorphins (see Operant Conditioning). With naltrexone treatment and the Sinclair Method, however, your brain will no longer receive the reward you’ve trained it to seek.
When the behavior of drinking alcohol is no longer rewarded, your brain will lose interest in alcohol, a process known as pharmacological extinction. When extinction has occurred with naltrexone treatment, it is accurate to call it a cure for alcoholism, because you will have control over if and how much you drink.
Alcohol Appears to Affect Endogenous Opioid Receptors Differently in Alcoholics
Initial stages of research into human behaviors usually begins with animals, and this is the case for investigations of the relationships among alcohol, endorphins, and naltrexone. This 1996 study Implications of Endogenous Opioids and Dopamine in Alcoholism describes many of the available animal studies, which will be summarized below.
One interesting feature of these studies is that the rodents they used were selectively bred to be Alcoholic Rodents or Alcoholic-averse Rodents. If nothing else, this demonstrates the large genetic component involved in the development of alcoholism.
- Mice bred to prefer alcohol had higher levels of hypothalamic endorphin release than alcohol-avoiding mice under normal conditions.
- Mice bred to prefer alcohol had greater release of hypothalamic endorphin release in terms of magnitude and duration after exposure to alcohol.
- Mice bred to prefer alcohol had a higher density of delta-opioid receptors than the alcohol-avoidant mice.
- Mice bred to avoid alcohol had a higher density of mu-opioid receptors than than the alcohol-preferring mice.
The researchers take a moment to note that the variations were “genetically determined.”
Endogenous Opioids and Alcohol in Humans
In the same study, human subjects between the ages of 20-30 who were not currently heavy drinkers were divided into a high-risk group (HR) and a low-risk group (LR) for the development of alcoholism, based on their family history. The participants were given varying amounts of alcohol or a placebo (that smelled and tasted like alcohol). The results were:
- LR subjects had higher baseline levels of endorphins in their blood plasma.
- Alcohol released more endorphins in the HR subjects (there was no difference in the blood-alcohol content over time between the two groups).
The researchers speculated that, “It appears that the pituitary B-endorphin system of the HR subjects is more sensitive to ethanol than that of LR subjects.”
There was a more pronounced release of endorphins to the presence of alcohol in the HR human group and the mice bred to prefer alcohol. This increased release may explain the increased reinforcement and excessive drinking seen in alcoholism.
However, the basal endorphin levels in plasma were lower in the HR human group and the basal endorphin levels in the hypothalamus were higher in the alcohol-preferring mice. The reason that these baseline levels might vary between the blood and the hypothalamus were not explained. The researchers hypothesize that is the sensitivity of the endogenous opioid system, rather than baseline levels of endorphins that determine risk for high alcohol consumption.
“What is most important for mediating the reinforcing effects of ethanol and maintaining a high level of alcohol consumption is the ability of ethanol to stimulate the activity of the endogenous opioid system.”