People struggling with addiction usually deny they have a problem and hesitate to seek treatment. An intervention presents a loved one with a structured opportunity to make changes before things get even worse and can motivate someone to seek or accept help. Signs and symptoms of drug use or intoxication may vary, depending on the type of drug. What do heat waves, homelessness, and the behavioral health crisis have to do with each other?

Triggering and Common Causes of Drug Abuse

But we must ask whether they are necessary components of addiction – or whether addiction would persist even in their absence. Use of hallucinogens can produce different signs and symptoms, depending on the drug. The most common hallucinogens are lysergic acid diethylamide (LSD) and phencyclidine (PCP). Substituted cathinones, also called “bath salts,” are mind-altering (psychoactive) substances similar to amphetamines such as ecstasy (MDMA) and cocaine.

Drugs & Supplements

Family interactions, parenting style, and levels of supervision all play a role in development of coping skills and susceptibility to mental health problems. Studies have linked authoritarian or neglectful parenting, family violence, and divorce to increased likelihood of substance use problems later in life. Growing up with strong ties to and a sense of belonging—to a family, to a belief tradition, developing effective coping skills for substance abuse recovery to a culture—are known to be protective against addiction. Alcohol in some form is widely used for pleasurable purposes and is an important part of the social fabric worldwide, today as in ancient times. Nevertheless, according to the National Institute on Alcohol Abuse and Alcoholism, 14.6 million U.S. adults over the age of 18 have alcohol use disorder, marked by uncontrolled drinking.

1. This might seem puzzling, but it makes sense if the learning rate from negative outcomes is slow.
2. Crooks reportedly also looked up dates of Trump’s public appearances and the upcoming Democratic National Convention.
3. Individuals with fewer than two symptoms are not considered to have a disorder, although they may have had at least one misuse problem.
4. It is a form of group therapy that aims to allow the addict to recognize the social, spiritual, physical, and spiritual effects of their disease.
5. The interactions between one’s genetics and social environment may explain why some people become addicted and some do not (Kreek et al., 2005).
6. While the stigma behind mental health treatment is starting to dissipate, the fact is that there are so many people throughout the world who may go their entire lives without a proper diagnosis for the mental health issues which plague them.

A Look At The Reasons Why We Abuse Drugs And Alcohol

Former peers, speaking to media outlets, painted a portrait of a social outcast who kept a low profile. “Our old coach was a stickler, he trained Navy marksmen, so he knew people. He knew when someone’s not the greatest person,” the classmate said.

This decision is often unwise as it puts them at risk of drug abuse. Painkillers such as opioids carry a strong addiction potential even though they may provide temporary pain relief. But the pleasure derived from opioids like heroin or stimulants like cocaine declines with repeated use. What’s more, some addictive drugs, like nicotine, fail to produce any noticeable euphoria in regular users. Some studies show that genes can account for as much as 50 percent of a person’s risk for addiction, although the degree of genetic influence shifts in importance over time. For example, environmental factors such as family and social relationships are more strongly tied to use of alcohol and nicotine in adolescence than later in life.

For another, they may inherit whatever genetic or biological vulnerabilities laid the groundwork for a parental addiction. Neuroscience research supports the idea that addiction is a habit that becomes deeply entrenched and self-perpetuating, rewiring the circuitry of the brain as it is repeated. The repetition of a highly pleasurable experience—drugs, gambling—alters neurons; they adjust their wiring to become increasingly efficient at the experience. As drug use stops, engaging in other rewarding activities rewires the brain to find interest and pleasure in non-drug pursuits. Adverse childhood experiences (ACEs) such as trauma, especially combined with an unpredictable and chaotic childhood, pose a risk factor for many kinds of maladaptive behaviors and poor health outcomes.

Inpatient treatment is an intensive form of drug addiction treatment that requires living at a treatment facility while receiving treatment, including therapy, support, and constant monitoring by a team of professionals. Even with the unending stream of entertainment available in the world today, many people still complain of boredom. Being bored can play a part in drug abuse, especially in young people.

Most individuals begin taking prescription opioids not for pleasure but rather from a need to manage their pain, often on the recommendation of a doctor. All drugs of abuse trigger a surge of dopamine – a rush of “wanting” – in the brain. With repeated drug use, the “wanting” grows, while our “liking” of the drug appears to stagnate or even decrease, a phenomenon known as tolerance. The best way to prevent an addiction to a drug is not to take the drug at all. If your health care provider prescribes a drug with the potential for addiction, use care when taking the drug and follow instructions. People use cannabis by smoking, eating or inhaling a vaporized form of the drug.

This suggested to many in the scientific community that these areas were the brain’s pleasure centers and that dopamine was our own internal pleasure neurotransmitter. The brain does have pleasure centers, but they are not modulated by dopamine. This is not to say that pleasure, habits or withdrawal are not involved in addiction.

The vast majority of children whose parents abuse alcohol or drugs do not grow up to do the same. However, they are at some increased risk for doing so, and there esgic butalbital acetaminophen and caffeine capsules are a number of reasons why. For one, they are exposed to those substances, and exposure during early adolescence may especially influence substance use.

But with continued use, a person’s ability to exert self-control can become seriously impaired. Outside the venue at that time, Greg Smith says he tried desperately to get the attention of police. He told the BBC that he and his friends saw a man crawling along a roof overlooking the rally. Other witnesses said they also saw a man atop the American Glass Research building outside the official event security perimeter, well within the range of a 5.56 rifle bullet. In a call with reporters Sunday night, the FBI special agent in charge, Kevin Rojek, said there was “no indication of any mental health issues” regarding the shooter. In short what determines whether or not drug use escalates into addiction, and the prognosis once it has, is less to do with the power of the drug and more to do with the social, personal and economic circumstances of the user.

Studies show that having multiple ACEs puts children at risk of poor school performance, unemployment, and high-risk health behaviors including smoking and drug use. How the body metabolizes, or breaks down and eliminates, foreign substances such as drugs or alcohol is heavily dependent on the presence of various enzymes, and they may vary significantly between individuals and even between ethnic groups. However, there are a number of personality traits, each of which is partly genetically influenced, alcohol use disorder symptoms and causes that contribute to the risk of addiction. These include impulsiveness, frustration tolerance, and sensitivity to rejection. Impulsivity is thought to play its strongest role in the early stages of addiction, driving the motivation for seeking drugs. Brain imaging studies of people with addiction show physical changes in areas of the brain that are critical to judgment, decision-making, learning and memory, and behavior control.12 These changes help explain the compulsive nature of addiction.

Therefore, education and outreach are key in helping people understand the possible risks of drug use. Teachers, parents, and health care providers have crucial roles in educating young people and preventing drug use and addiction. A full drug addiction is characterized by a chronic disease state whereby symptoms of physical withdrawal begin. With an addiction, the person physically cannot live without drugs and may eventually die as a result. Drug use, no matter what initially led to it, can eventually turn into an addiction for some people. As people begin to rely more and more on substances to accomplish their psychological, physical, or emotional needs, it increases the risk of developing an addiction.

Studies show that those who are high in the trait of neuroticism—they are prone to experiencing negative emotions—are overwhelmed by minor frustrations and interpret ordinary situations as stressful. Neuroticism is linked to a wide array of mental health problems, including anxiety, depression, and eating disorders as well as substance abuse. Neuroticism is also linked to a diminished quality of life, another factor that could increase the allure of substance use. Prevention science has concluded that there are three important points regarding vulnerability. First, no single personal or environmental factor determines whether an individual will have a substance misuse problem or disorder. Second, most risk and protective factors can be modified through preventive policies and programs to reduce vulnerability.

An activated neuron sends chemical signaling molecules called neurotransmitters through the neural circuit which bind to specific molecules called the receptors. Depending upon the circuit involved, the binding of these neurotransmitters may cause excitatory or inhibitory signals to be passed further along the circuit. Recent advances in the study of alcoholism have thrown light on the involvement of various neurotransmitters in the phenomenon of alcohol addiction. Various neurotransmitters have been implicated in alcohol addiction due to their imbalance in the brain, which could be either due to their excess activity or inhibition. This review paper aims to consolidate and to summarize some of the recent papers which have been published in this regard. The review paper will give an overview of the neurobiology of alcohol addiction, followed by detailed reviews of some of the recent papers published in the context of the genetics of alcohol addiction.

P/T depletion effects on frontolimbic FC

Given the relevance of dopamine in the chronic phase of alcohol use and in the development of alcohol dependence, there is considerable interest in evaluating medications that can specifically modify dopamine, thereby serving as potential pharmacotherapies to treat alcohol dependence. Dopamine has also been implicated in schizophrenia and ADHD; the brain systems underlying these conditions (as well as substance abuse disorder) are complex. The activity of the dopamine system depends on the state of one’s dopamine receptors, and in people with these conditions, the chemical interacts with other factors in ways that have yet to be explained. By jacking up dopamine levels in your brain, alcohol tricks you into thinking that it’s actually making you feel great (or maybe just better, if you are drinking to get over something emotionally difficult). The effect is that you keep drinking to get more dopamine release, but at the same time you’re altering other brain chemicals that are enhancing feelings of depression.

Choose a Treatment Model That Works

However, in this study, the behavioral tasks were performed after the resting-state scan; future work pairing event-related fMRI AB tasks with the P/T depletion procedure may provide additional insight into the dopamine response to alcohol or non-drug reward cues. A series of experiments in outbred rats show that the dopamine stabilizer OSU6162 attenuates several alcohol‐mediated behaviours including voluntary alcohol intake, alcohol withdrawal symptoms and cue/priming‐induced reinstatement of alcohol seeking in long‐term drinking rats [196]. Furthermore, OSU6162 blunted alcohol‐induced dopamine output in the NAc of alcohol‐naïve rats [196], indicating that OSU6162 has the ability to attenuate the rewarding effects of alcohol.

Alcohol’s Actions as a Reinforcer: Dopamine’s Role

There’s also more of an effect on your brain and its development if you’re younger — one that can have a lasting impact. As BAC ascends, drinkers report increases in elation, excitement, and extroversion, with simultaneous decreases in fatigue, restlessness, depression, and tension. Conversely, a descending BAC corresponds to a decrease in vigor and an increase in fatigue, relaxation, confusion, and depression. I would like to acknowledge https://sober-home.org/ my faculty at Amity Institute of Biotechnology, Dr. Manju Pathak for her unwavering support and encouragement in writing this review paper. She single-handedly inspired me to undertake this task and the work would not have borne fruition without her support and guidance. Thanks are also due to my mother, Dr. Sharmila Banerjee, without whose support and editorial help, I could not have had the will to complete this work.

1. The brain reward system: the mesocorticolimbic dopamine system

For example, different subpopulations of neurons in the striatum carry different dopamine receptors on their surfaces (Le Moine et al. 1990, 1991; Gerfen 1992). Dopamine binding to D1 receptors enhances the excitatory effects that result from glutamate’s interaction with a specific glutamate receptor subtype (i.e., the NMDA receptor4). Conversely, activation of D2 receptors inhibits the effects induced by glutamate’s binding to another glutamate-receptor subtype (i.e., the AMPA receptor5) (Cepeda et al. 1993).

2. Atypical dopamine D2 receptor antagonists

1. Furthermore, a genome-wide association study identified PDE4B as a risk factor in elevated alcohol consumption [6,7].
2. Overall, the results from studies evaluating olanzapine as a potential medication for alcohol dependence have provided evidence of a marginal effect restricted to a sub population of patients (with the longer dopamine D4 receptor allele).
3. Finally, preclinical and clinical studies evaluating the potential of available dopaminergic agents as well as indirect dopamine modulators as novel medications for alcohol dependence are discussed.

A gatekeeper, the cell membrane’s job is to regulate what goes in and out of a cell. We hear many different things about how alcohol affects the brain and body, most notably that it is a depressant. Alcohol is a depressant, but it’s also an indirect stimulant, and plays a few other roles that might surprise you. Beyond this, by definition, consuming enough alcohol to cause a “brownout,” “blackout,” hangover, or other overt brain symptomatology is evidence that the alcohol you’ve consumed is creating problems in your brain. It has been linked to a higher risk for dementia, especially early-onset dementia in a study of 262,000 adults, as well as to smaller brain size. Alcohol addiction and dependence of late has been shown to be affected by the influence of genes.

Thus, an alcohol-induced increase in adenosine levels might be responsible for part of alcohol’s sedative actions. Studies about the relationship of D1 receptors and affinity for alcohol have had inconsistent results. While drinking initially boosts a person’s dopamine levels, the brain adapts to the dopamine overload with continued alcohol use. It produces less of the neurotransmitter, reducing the number of dopamine receptors in the body and increasing dopamine transporters, which carry away the excess dopamine. Researchers are investigating whether drugs that normalize dopamine levels in the brain might be effective in reducing alcohol cravings and treating alcoholism.

Concomitantly, adaptations in glutamatergic, GABAergic, and dopamine transmission occur [15] and greater or continued amounts of alcohol can result in allostatic changes to preserve normal brain function. This allostasis is characterized by aberrant glutamate, GABA, and opioid signaling, as well as, a dysfunction in nigrostriatal and mesolimbic dopamine transmission [16, 17]. The mechanisms underlying this dysregulation of dopamine transmission are not well understood, particularly in a primate brain. Therefore, in the current study, we used fast-scan cyclic voltammetry (FSCV) to study dopamine release dynamics in striatal slices from long-term alcohol drinking and control rhesus macaques.

The following text introduces some of the neural circuits relevant to AD, categorized by neurotransmitter systems. These neural circuits include the dopaminergic, serotoninergic, glutamatergic and GABAergic neural circuits. Dopamine’s effects on neuronal function depend on the specific dopamine-receptor subtype that is activated on the postsynaptic cell.

When alcohol consumption is abruptly reduced or discontinued, a withdrawal syndrome may follow, characterized by seizures, tremor, hallucinations, insomnia, agitation, and confusion (Metten and Crabbe 1995). Scientists postulate that this syndrome represents the hyperactivity of neural adaptive mechanisms no longer balanced by the inhibitory effects of alcohol (see figure). Researchers are focusing much of their attention on other inhibitory neurotransmitters. Alcohol has been shown to increase the function of glycine receptors in laboratory preparations (Valenzuela and Harris 1997). Alcohol’s actions on inhibitory neurotransmission in this lower area of the central nervous system may cause some of alcohol’s behavioral effects.

The effects of SSRI’s and other serotonergic medications on alcohol abuse will be difficult to disentangle from their effects on co-occurring mental disorders. Nevertheless, the information currently available clearly indicates that serotonergic signal transmission plays an important role in alcohol abuse and therefore may yet be a target for therapies to reduce alcohol consumption. More research is needed to determine how and under what drinking conditions alcohol consumption is affected by different serotonin receptor antagonists.

Studies in animal models provide initial hints to possible contributors to these differences. Furthermore, rats undergoing intermittent access to 20% alcohol in 2 bottle choice paradigm exhibit distinct profiles of intake ranging from low alcohol consumers to rats that exhibit slow or rapid escalation of excessive drinking [125]. The kinase mTOR in complex 1 (mTORC1) plays a crucial role in synaptic plasticity, learning and memory by orchestrating the translation of several dendritic proteins [39]. MTORC1 is activated by alcohol in discrete brain regions resulting in the translation of synaptic proteins such as Collapsin response-mediated protein 2 (CRMP2) [40] and ProSap-interacting protein 1 (Prosapip1) [41], as well as Homer1 and PSD-95, GluA2 and Arc [40,42,43]. Through the translation of these transcripts and others, mTORC1 contributes to mechanisms underlying alcohol seeking and drinking as well as reconsolidation of alcohol reward memories and habit [44–46].

Your brain adapts to the sudden increase in the neurotransmitter by producing less dopamine, but because of the link to pleasure, it doesn’t want you to stop after a few drinks — even when your dopamine levels start to deplete. Dopamine levels fall, and the euphoric buzz goes with it, but your brain is looking to regain the feeling caused by the increased level of dopamine. Eventually, you rely fully on alcohol to generate dopamine release, and without it, you experience withdrawal symptoms. Alcohol-induced epigenetic alterations are often mediated by altered expression or activity of epigenetic enzymes, which thus represent a promising new avenue for targeted therapeutic interventions. For example, increased enrichment of DNA methylation in the mPFC was linked to enhanced DNA methyltransferase (Dnmt) activity [23]. Inhibition of Dnmt rescued the methylation and transcriptional changes and prevented the escalation of alcohol intake [23].

These alleles are of 9 base pair repeats, 10 base pair repeats as well as 12 base pair repeats. The 9 base pair repeat is extremely rare and in statistical studies, often clubbed with the 10 base pair repeat. Recently mutations in the SERT gene, commonly known as 5’- hydroxtryptamine transporter linked polymorphic region (5’-HTTLPR), has been implicated in cases of alcoholism.

Opioid peptide antagonists act primarily on a brain area where dopaminergic neurons that extend to the NAc originate. These observations indicate that alcohol stimulates the activity of endogenous opioid peptides, leading indirectly to the activation of dopaminergic neurons. Opioid peptide antagonists would interfere with this process, thereby reducing dopamine release. Dopaminergic neurons that relay information to the NAc shell are extremely sensitive to alcohol.

Inhibitory neurotransmitters transiently decrease the responsiveness of other neurons to further stimuli, whereas excitatory neurotransmitters produce the opposite effect. Some neurotransmitters produce longer lasting changes, contributing to processes such as learning and memory. In addition, https://sober-home.org/family-involvement-in-treatment-and-recovery-for/ one of the latest studies on this pathway found an association between a polymorphism in the promoter of a glutamate receptor subunit gene and alcoholism. The study was conducted by[68] and the study found that short alleles were significantly less frequent among AD subjects.

Here we quantified AB toward alcohol and non-drug, reward-conditioned cues and their neural underpinnings after acute dopamine precursor depletion across a broad spectrum of alcohol users. P/T depletion significantly reduced AB across three different tasks, particularly in individuals who reported heavier drinking. P/T depletion altered FC between prefrontal and subcortical brain regions involved in reward processing and motivation, and these alterations predicted changes in AB. A one-factor ANOVA with Tukey’s post hoc test was used to compare the average lifetime alcohol intake between cohorts. Two-factor ANOVAs (stimulation intensity and treatment group) were used for the input–output curve experiments examining dopamine release. For the dopamine uptake rate (Vmax) data, two-factor ANOVAs (treatment and brain region) were used.

Other drugs that affect serotonergic signal transmission also alter alcohol consumption in animals (LeMarquand et al. 1994b). For example, antagonists of the 5-HT3 and 5-HT1A receptors reduced alcohol ingestion in rodents (Litten et al. 1996; Pettinati 1996; DeVry 1995). However, the 5-HT1A receptor antagonists also altered food and water intake, suggesting that this receptor may modulate general consummatory behavior rather than specifically reduce the desire to drink alcohol. In humans, the 5-HT3 receptor antagonist ondansetron reduced total alcohol consumption and the desire to drink in alcoholics; as with the SSRI’s, however, this effect was relatively modest (Johnson et al. 1993; Pettinati 1996; Sellers et al. 1994).

Many addicts experience substantial weight gain during this period as their metabolism slows and their caloric intake increases greatly. With time, most addicts’ metabolism return to pre-use levels and their appetite catches up and returns to normal as well. Still, there’s no doubt that a little exercise can help many addicts in early recovery steer their bodies back on track. If snorting the drug in crystal meth form, the high will come on in three to five minutes; if swallowing methamphetamine, it can take 15 to 20 minutes. The drug’s effects can last anywhere from six to 12 hours, which can lead people to continue using to keep the high going. Users who binge on crystal meth can stay awake for as long as 10 days, often subsisting with very little food or drink.

Treatment options

Some people call it Tina when out in public, because it sounds like they’re talking about a person rather than a drug. The drug has devastating effects on those who become addicted to it. According to MethProject.org, the meth addiction factor is extreme—it’s “one of the most addictive substances” out there today. The National Institute on Drug Abuse states that meth withdrawal symptoms can alter a person’s emotions.

Meth paraphernalia and other signs of use include:

1. Of course, the aim is to clear the last molecule of the drug from the body.
2. You may also feel a lot more confident, social, and energetic.
3. Therapy like CBT (Cognitive-behavioral therapy) helps teach new ways to cope with cravings and what might trigger meth use.
4. You may continue to use meth because of uncomfortable withdrawal symptoms that come once the drug leaves your system.
5. Practicing relapse prevention and management techniques can help improve your chances of recovery in the long term.

In some cases, a nonthreatening conversation is a better option. The first step is to recognize any misconceptions you might have about substance use and addiction. It’s important to remember that ongoing drug use changes the brain’s structure and chemistry.

How to Recognize and Treat Meth Addiction

Meanwhile, regular users’ withdrawal symptoms can last up to 3 years. It doesn’t matter whether it was used regularly or occasionally. People can experience withdrawal symptoms when they stop using it. These can range from fatigue and depression to intense cravings. Although most withdrawal symptoms may resolve after a few weeks, some may continue for much longer.

How to find a treatment center

Addiction Resource is not a healthcare provider, nor does it claim to offer sound medical advice to anyone. Addiction Resource does not favor or support any specific recovery center, nor do we claim to ensure the quality, validity, or effectiveness of any particular treatment center. No one should assume the information provided on Addiction Resource as authoritative and should always defer to the advice and care provided by a medical doctor. Meth withdrawal symptoms are both physical and mental in nature. In fact, the intensity of the symptoms on the body and mental health varies, depending on the amount and the duration of the drug abuse. Furthermore, if a Methamphetamine addict used other drugs with Meth, withdrawal symptoms could be extreme.

Addiction Treatment Programs

Common physical effects of “coming down” from the drug use include body aches, heartburn and feeling extremely lethargic, nauseous and confused. When meth wears off, dopamine and serotonin are both depleted, resulting in anxiety and depression. Learn more about the risks and side effects of substance use disorders, living with an alcoholic: what you need to know including the signs of intoxication or overdose. Look into treatment options to suggest to your loved one. Overcoming crystal meth addiction requires a comprehensive approach, combining medical intervention with psychological support. Some individuals may experience prolonged withdrawal symptoms, known as PAWS.

This is reflected in current number of methamphetamine addicts in United States, which are estimated to be approximately 1.4 million individuals. With amphetamine placed under federal control, illegal alcohol use and cancer american cancer society drug suppliers found that ephedrine, used in over-the-counter cold medicine, produces methamphetamine, according to Frontline. It didn’t take long for crystal meth to become “discovered” in the 1980s.

Withdrawal from crystal meth is a challenging but crucial step towards recovery. Remember, recovery is a journey, and it’s never too late to start. Some detox or rehab programs may cost $250 to $800 a day.

There’s no one right way to talk to someone about potential substance use, but you’ll want to avoid a few things along the way. But sometimes letting them know you’re short & long-term effects of heroin use willing to listen without judgment can help them feel safe enough to talk. Choose a time when it’s just the two of you and they seem like they’re in a decent mood.

Your loved one might deny having a problem at all or refuse to seek help. If that happens, consider seeking out additional resources or find a support group for family members or friends of people living with addiction. Although an intervention may motivate your loved one to seek treatment for an addiction, it could also have the opposite effect. Confrontation-style interventions can sometimes lead to shame, anger, or social withdrawal.

Or maybe you’re not even sure it’s your place to broach the subject. Medically, methamphetamine is a Schedule II stimulant with a high potential for abuse. Medical methamphetamine is used to treat narcolepsy and ADHD. Medical methamphetamine is prescribed at a far lower dose than the street version.

To make matters worse, the long-term meth use has caused a decrease in the number of dopamine receptors available which means there’s not only less dopamine, but fewer receptors to activate. It’s not a surprise then that people who quit meth find themselves in a state of anhedonia, or an inability to feel pleasure. Once again, unlike the heroin withdrawal symptoms, anhedonia doesn’t make you throw up and sweat, but it’s a pretty horrible state to be in. Things that bring a smile to a normal person’s face just don’t work on most crystal-meth addicts who are new to recovery.

Methamphetamine affects one’s mental health and triggers changes in the central nervous system (CNS) and brain. Additionally, as the user’s system continually absorbs Meth, it becomes reliant on the substance. As a result, the user is unable to function without it properly.

Those who choose to stop using the drug cold turkey without medical supervision may not know how to alleviate painful withdrawal symptoms. Attending rehab for detox is much safer because patients have access to immediate medical care. Withdrawal from methamphetamine occurs when a regular meth user suddenly stops taking the substance. When this happens, the person may experience a range of distressing physical and psychological health problems.

Usually, people who use crystal meth smoke it with a small glass pipe, but they may also swallow it, snort it, or inject it into a vein. People say they have a quick rush of euphoria shortly after using crystal meth, but it’s dangerous. It can damage your body and cause severe psychological problems. Our writers and reviewers are experienced professionals in medicine, addiction treatment, and healthcare. AddictionResource fact-checks all the information before publishing and uses only credible and trusted sources when citing any medical data. Addiction Resource does not offer medical diagnosis, treatment, or advice.