Kategori: Sober living

The biological weakening of decision-making areas in the brain suggests why addicts pursue and consume drugs even in the face of negative consequences or the knowledge of positive outcomes that might come from quitting the drugs. It’s hard to nail down what that means, but it does rightly suggest that there is an involuntary takeover of the brain that compromises decision-making and diminishes freedom of choice, making quitting difficult even in the face of desire to do so. What happens in addiction is that, through completely natural processes involved in all learning, the brain prunes nerve pathways of attention and motivation to preferentially notice, focus on, desire, and seek the substance. In 1956, the American Medical Association (AMA) declared that alcoholism was a disease—not a moral failing, weakness, or character defect as so many people previously thought and still may think. In 2011, the American Society of Addiction Medicine (ASAM) officially defined addiction as a chronic disease of motivation, memory, and related circuitry.

• Therefore, an investigation of the neurobiological processes that underlie recovery and contribute to improvements in social, educational, and professional functioning is necessary.
• This was later also found to be the case for heroin [103], methamphetamine [104] and alcohol [105].
• Dose-dependent neurotoxicity of alcohol use is also observed in other neurocognitive domains that were previously discussed, including attention and impulsive choice (Squeglia et al., 2009b; Jones et al., 2017).
• Addiction to drugs while pregnant can lead to serious outcomes for both mother and child.

Indeed, preliminary imaging data showing that mindfulness activated the amygdala, striatum, ACC, PFC, and insula, which are regions that modulate emotion, self-regulation, and interoception, highlight its potential promise in addiction treatment (319). TDCS is an alternative noninvasive brain modulation technique with therapeutic potential whereby some (hard to assess) portion of the current penetrates through the scalp affecting cortical excitability. Six of seven tDCS studies found significant reductions in alcohol-related craving or consumption after the treatment, whereas five of eight studies found significant reductions in nicotine cravings and/or consumption (reviewed in Ref. 70). Only two proof of principle studies investigated PFC targeting tDCS for reducing cocaine (18, 80) and while results were positive, the sample sizes were too small (11 and 17 subjects, respectively) and replication is needed.

Traumatic Brain Injury

Longitudinal studies on the effects of combined substance use on psychiatric morbidity are warranted to understand the directionality of this relationship. Nicotine and alcohol also have additive effects on the risk for future substance use in that concurrent use predicts a greater risk of future substance abuse. A U.S. national survey on alcohol users aged 12–20 found that 14 Reasons Being Sober Makes Your Life Better subjects with a past-year smoking status drank more alcohol on average and had a higher risk for AUD than those that drank equal amounts without smoking (Grucza and Bierut, 2006). In line with these findings, a longitudinal study found similar results, showing that by age 15, alcohol users that smoked tobacco consumed more alcohol and cannabis (Schmid et al., 2007).

When someone continues to use drugs, their health can deteriorate both psychologically and neurologically. If left untreated drug addiction can lead to serious, life-altering effects on the body. Pulses to the brain may help loss-of-control eating, offering new hope for those with eating disorders.

Box 1 What’s in a name? Differentiating hazardous use, substance use disorder, and addiction

Nevertheless, even after controlling for these variables, the association between earlier alcohol use and poorer neurocognitive performance remained across both studies. The variability in confounding influences and the different neuropsychological measures taken across studies highlight the need for high-quality, long-term prospective cohort studies with standardized measures to better understand the lasting consequences of adolescent drinking. https://g-markets.net/sober-living/is-there-a-connection-between-narcissism-and-2/ The rising popularity of next-generation e-cigarette devices are concerning due to their ability to deliver higher nicotine concentrations in the form of nicotine salts (Boykan et al., 2019). One study suggests that urinary levels of cotinine, a metabolite of nicotine, are higher in adolescent e-cigarette users, relative to levels observed in another study of those who consume combustibles (Benowitz et al., 2018; Goniewicz et al., 2019).

Melis et al. (2013) examined sex differences in dopamine neuronal properties and activity of the cannabinoid system in the ventral tegmental area (VTA) in the rat and found that females displayed larger depolarization-induced suppression of inhibition (DSI) than male rats via tonic 2-arachidonoylglycerol signaling. These findings highlight sex-specific differences in VTA endocannabinoid activity that may regulate responses to aversive intrinsic properties to cannabinoids and contribute to differences in cannabinoid consumption. McCall et al. (2013) utilized a mouse model of selective deletion of the neuropeptide Y 2 (Y2) receptor in GABA neurons to examine sex differences in the role of Y2 receptor on anxiety and drinking. Females displayed greater basal anxiety, higher levels of ethanol consumption, and faster fear conditioning than males, and Y2 knockout mice exhibited enhanced depressive-like behavior in the forced swim test. This study extends work on sex differences in ethanol consumption and highlights the importance of Y2R function in GABAergic systems in the expression of depressive-like behavior.

For more information about alcohol and brain health, please visit the Alcohol and the Brain topic page.

It has prompted the development of pharmaceuticals that can ease withdrawal symptoms. The disease model of addiction, studies show, also fosters more compassionate attitudes towards those who are addicted and more human treatment. Addiction is also viewed as a disease in order to facilitate insurance coverage of any treatment. It stimulates the nucleus accumbens, and overactivity of the nucleus accumbens progressively weakens its connectivity to the prefrontal cortex, seat of executive functioning. One result is impaired judgment, decision-making, and impulse control, a hallmark of addiction. Aside from potential smoking-induced deficits in attentional and inhibitory processes, there is some evidence that adolescent smoking alters intelligence.

• In turn, HPA axis activation influences brain circuits involved in drug reward and the acquisition of drug-seeking behavior.
• These effects account for the euphoric or intensely pleasurable feelings that people experience during their initial use of alcohol or other substances, and these feelings motivate people to use those substances again and again, despite the risks for significant harms.
• In fact, as shown by the studies correlating dopamine receptors with social experience, imaging is capable of capturing the impact of the social environment on brain function.
• Alcohol makes it harder for the brain areas controlling balance, memory, speech, and judgment to do their jobs, resulting in a higher likelihood of injuries and other negative outcomes.
• Addressing these critiques requires a very different perspective, and is the objective of our paper.
• Some of these behavioral characteristics, in turn, contribute to a greater likelihood of initiating substance use (Lisdahl et al., 2018).

It originates from within the scientific community itself, and asserts that this conceptualization is neither supported by data, nor helpful for people with substance use problems [4,5,6,7,8]. Addressing these critiques requires a very different perspective, and is the objective of our paper. We readily acknowledge that in some cases, recent critiques of the notion of addiction as a brain disease as postulated originally have merit, and that those critiques require the postulates to be re-assessed and refined.

Help Someone With Drug Addiction

Additionally, mRNA-based therapies can specifically change which genes are expressed to treat diseases like cancer. In the future, we may discover similar therapies for alcohol and substance use disorder. These treatments could potentially target important signaling pathways linked to addiction, altering how brain circuits function and how alcohol and drugs affect them.

Similarly, a recent study reported that cue-induced reinstatement was intensified by either activating D1R-MSNs or reducing the activity of D2R-MSNs (151). Using optical imaging in transgenic mice, we showed that in the dorsal striatum of naive mice, acute cocaine led to fast [Ca2+] increase in D1R-MSNs and to progressive [Ca2+] decreases in D2R-MSNs, consistent with DA stimulating D1R-MSNs and inhibiting D2R-MSNs (213). In contrast, in mice chronically exposed to cocaine, the [Ca2+] responses to acute cocaine were blunted but to a significantly greater extent in D2R-MSNs than in D1R-MSNs, unbalancing the relative signaling towards a predominance of D1R-MSNs over D2R-MSNs (251). However, studies are needed to assess if similar changes occur in NAc and their association with compulsive drug taking, particularly since there is evidence that in the NAc there is coexpression of D1R and D2R and of projections of both D1R-MSNs and D2R-MSNs into ventral pallidum. Despite these advances, we still do not fully understand why some people develop an addiction to drugs or how drugs change the brain to foster compulsive drug use. This booklet aims to fill that knowledge gap by providing scientific information about the disorder of drug addiction, including the many harmful consequences of drug use and the basic approaches that have been developed to prevent and treat substance use disorders.

In the most severe cases of alcohol intoxication, they may even fall into a coma. Due to this, it is really important to get someone emergency help if their condition is deteriorating. Depending on the severity of someone’s alcohol use disorder, they may choose to seek inpatient or an outpatient treatment. Withdrawal symptoms from alcohol can be extremely painful and sometimes life-threatening, so if detox is needed, it is recommended to undergo treatment in a facility providing around-the-clock medical supervision. But what does being ‘blackout’ really mean in terms of brain processing, memory formation, and how someone acts – and how common is it, particularly among young people?

• People with diabetes should be sure to pay attention to any potential warnings.
• However, Lin and colleagues (1995) reported that the LDL cholesterol in alcoholics exhibits altered biological functions and may more readily cause cardiovascular disease.
• Ketoacidosis typically occurs in patients with type 1 diabetes who completely lack insulin.
• In rare cases, however, the condition also may affect people with type 2 diabetes.

The National Institute of Neurological Disorders and Stroke estimate that 70% of people with epilepsy can control their symptoms by taking medication or undergoing surgery. A doctor may prescribe fludrocortisone to reduce blackouts in people who experience neurally mediated syncope. Take our free, 5-minute alcohol abuse self-assessment below if you think you or someone you love might be struggling with alcohol abuse. The evaluation consists of 11 yes-or-no questions that are intended to be used as an informational tool to assess the severity and probability of an alcohol use disorder. The test is free and confidential, and no personal information is needed to receive the results. Generally, eating a meal with your drinks is critical, and ideally, that meal would contain a few carbohydrates, too.

Is Blacking Out a Sign of an Alcohol Use Disorder?

Ketoacidosis typically occurs in patients with type 1 diabetes who completely lack insulin. In rare cases, however, the condition also may affect people with type 2 diabetes. In a milder form, ketoacidosis may even occur in people who are fasting. In those people, insulin levels are diminished, because the fasting has considerably lowered their blood sugar levels, thereby depriving the pancreas of its stimulus to produce and secrete insulin. Glycogen is a large molecule that consists of numerous glucose molecules and serves as a storage form of glucose in the tissues, particularly the liver.

The frontal lobe also plays a role in short-term and long-term memory formation and recall. Drinking too much alcohol can cause diabetes by causing chronic inflammation of the pancreas (pancreatitis), impairing its ability to release insulin. Diabetes and alcohol use may also co-occur because alcohol is can diabetics get drunk “empty calories,” meaning it has no nutritional value. Consuming alcohol can contribute to unhealthy eating patterns, weight gain, and obesity, which is a major risk factor for diabetes. Alcohol can also interfere with the body’s sensitivity to insulin, which can affect the onset of type 2 diabetes.

Recognizing the risks

Alcohol can worsen diabetes by blocking the production of glucose in the liver, which can result in very low blood sugar levels. The symptoms of low blood sugar (hypoglycemia) are usually similar to the side effects of alcohol, making it difficult to differentiate the two. Low blood sugar and alcohol can both cause symptoms like blurred vision, slurred speech, sedation, and impaired coordination. Accordingly, more studies are needed to determine whether the beneficial effects of daily moderate alcohol consumption outweigh the deleterious effects. Diabetics clearly should avoid heavy drinking (i.e., more than 10 to 12 drinks per day), because it can cause ketoacidosis and hypertriglyceridemia.

The prevalence of alcohol consumption among adults with chronic medical conditions in the U.S. is ∼31% (19). In our study of an ethnically diverse population of patients with type 2 diabetes, the level of alcohol consumption was similar. A 2006 study found that temporary memory loss caused by a fall in blood pressure (syncope) is a more likely cause of nonalcoholic-induced blackouts. Another complicating factor for research on blackouts is the potential use of other drugs (illicit or prescription) that might also contribute to memory loss. Although several research studies statistically control for or exclude individuals who report co-occurring illicit drug use, research clearly indicates that some individuals who report blackouts also report other drug use (Baldwin et al., 2011; Haas et al., 2015). Thus, researchers must be cautious and account for factors other than alcohol that might contribute to blackouts.

Diabetic Shock And Insulin Reactions

Elevated levels of those compounds can cause nausea, vomiting, impaired mental functioning, coma, and even death. Ketoacidosis is caused by complete or near-complete lack of insulin and by excessive glucagon levels. Among their many functions, insulin and glucagon regulate the conversion of fat molecules (i.e., fatty acids) into larger molecules (i.e., triglycerides), which are stored in the fat tissue. In the absence of insulin, the triglycerides are broken down into free fatty acids, which are secreted into the bloodstream and delivered to the liver.

Contact us today to find an alcohol treatment program for yourself or a loved one with diabetes. The most effective way to overcome alcohol use and addiction as a diabetic is to seek professional treatment. While feeling a bit dizzy or drowsy after drinking does not always signal harm for a non-diabetic, for diabetics this can signal larger problems.

A blackout is not the same as “passing out,” which means either falling asleep or losing consciousness from drinking too much. Many symptoms of hyperglycemia and hypoglycemia are similar to those of being drunk. Alcohol slows down activity in the brain and throughout the body and can cause numerous effects from a feeling of relaxation to drowsiness and decreased coordination.