Semaglutide (sold as Ozempic, Wegovy and Rybelsus) was initially developed to treat diabetes. It works by stimulating the production of insulin to keep blood sugar levels in check.

This type of drug is increasingly being prescribed for weight loss, despite the fact it was initially approved for another purpose. Recently, there has been growing interest in another possible use: to treat addiction.

Anecdotal reports from patients taking semaglutide for weight loss suggest it reduces their appetite and craving for food, but surprisingly, it also may reduce their desire to drink alcohol, smoke cigarettes or take other drugs.

But does the research evidence back this up?

Animal studies show positive results

Semaglutide works on glucagon-like peptide-1 receptors and is known as a “GLP-1 agonist”.

Animal studies in rodents and monkeys have been overwhelmingly positive. Studies suggest GLP-1 agonists can reduce drug consumption and the rewarding value of drugs, including alcohol, nicotine, cocaine and opioids.

Out team has reviewed the evidence and found more than 30 different pre-clinical studies have been conducted. The majority show positive results in reducing drug and alcohol consumption or cravings. More than half of these studies focus specifically on alcohol use.

However, translating research evidence from animal models to people living with addiction is challenging. Although these results are promising, it’s still too early to tell if it will be safe and effective in humans with alcohol use disorder, nicotine addiction or another drug dependence.

What about research in humans?

Research findings are mixed in human studies.

Only one large randomised controlled trial has been conducted so far on alcohol. This study of 127 people found no difference between exenatide (a GLP-1 agonist) and placebo (a sham treatment) in reducing alcohol use or heavy drinking over 26 weeks.

In fact, everyone in the study reduced their drinking, both people on active medication and in the placebo group.

However, the authors conducted further analyses to examine changes in drinking in relation to weight. They found there was a reduction in drinking for people who had both alcohol use problems and obesity.

For people who started at a normal weight (BMI less than 30), despite initial reductions in drinking, they observed a rebound increase in levels of heavy drinking after four weeks of medication, with an overall increase in heavy drinking days relative to those who took the placebo.

There were no differences between groups for other measures of drinking, such as cravings.

In another 12-week trial, researchers found the GLP-1 agonist dulaglutide did not help to reduce smoking.

However, people receiving GLP-1 agonist dulaglutide drank 29% less alcohol than those on the placebo. Over 90% of people in this study also had obesity.

Smaller studies have looked at GLP-1 agonists short-term for cocaine and opioids, with mixed results.

There are currently many other clinical studies of GLP-1 agonists and alcohol and other addictive disorders underway.

While we await findings from bigger studies, it’s difficult to interpret the conflicting results. These differences in treatment response may come from individual differences that affect addiction, including physical and mental health problems.

Larger studies in broader populations of people will tell us more about whether GLP-1 agonists will work for addiction, and if so, for whom.

How might these drugs work for addiction?

The exact way GLP-1 agonists act are not yet well understood, however in addition to reducing consumption (of food or drugs), they also may reduce cravings.

Animal studies show GLP-1 agonists reduce craving for cocaine and opioids.

This may involve a key are of the brain reward circuit, the ventral striatum, with experimenters showing if they directly administer GLP-1 agonists into this region, rats show reduced “craving” for oxycodone or cocaine, possibly through reducing drug-induced dopamine release.

Using human brain imaging, experimenters can elicit craving by showing images (cues) associated with alcohol. The GLP-1 agonist exenatide reduced brain activity in response to an alcohol cue. Researchers saw reduced brain activity in the ventral striatum and septal areas of the brain, which connect to regions that regulate emotion, like the amygdala.

In studies in humans, it remains unclear whether GLP-1 agonists act directly to reduce cravings for alcohol or other drugs. This needs to be directly assessed in future research, alongside any reductions in use.

Are these drugs safe to use for addiction?

Overall, GLP-1 agonists have been shown to be relatively safe in healthy adults, and in people with diabetes or obesity. However side effects do include nausea, digestive troubles and headaches.

And while some people are OK with losing weight as a side effect, others aren’t. If someone is already underweight, for example, this drug might not be suitable for them.

In addition, very few studies have been conducted in people with addictive disorders. Yet some side effects may be more of an issue in people with addiction. Recent research, for instance, points to a rare risk of pancreatitis associated with GLP-1 agonists, and people with alcohol use problems already have a higher risk of this disorder.

Other drugs treatments are currently available

Although emerging research on GLP-1 agonists for addiction is an exciting development, much more research needs to be done to know the risks and benefits of these GLP-1 agonists for people living with addiction.

In the meantime, existing effective medications for addiction remain under-prescribed. Only about 3% of Australians with alcohol dependence, for example, are prescribed medication treatments such as like naltrexone, acamprosate or disulfiram. We need to ensure current medication treatments are accessible and health providers know how to prescribe them.

Continued innovation in addiction treatment is also essential. Our team is leading research towards other individualised and effective medications for alcohol dependence, while others are investigating treatments for nicotine addiction and other drug dependence.

Read the other articles in The Conversation’s Ozempic series here.

Shalini Arunogiri, Addiction Psychiatrist, Associate Professor, Monash University; Leigh Walker, , Florey Institute of Neuroscience and Mental Health, and Roberta Anversa, , The University of Melbourne

This article is republished from The Conversation under a Creative Commons license. Read the original article.

If your summer holiday already feels like a distant memory, you’re not alone. Burnout – a state of emotional, physical and mental exhaustion following prolonged stress – has been described in workplaces since a 5th century monastery in Egypt.

Burnout and depression can look similar and are relatively common conditions. It’s estimated that 30% of the Australian workforce is feeling some level of burnout, while almost 20% of Australians are diagnosed with depression at some point in their lives.

So what’s the difference between burnout and depression?

Burnout is marked by helplessness and depression by hopelessness. They can have different causes and should also be managed differently.

What is burnout?

The World Health Organization defines burnout as an “occupational phenomenon” resulting from excessively demanding workload pressures. While it is typically associated with the workplace, carers of children or elderly parents with demanding needs are also at risk.

Our research created a set of burnout symptoms we captured in the Sydney Burnout Measure to assist self-diagnosis and clinicians undertaking assessments. They include:

• exhaustion as the primary symptom
• brain fog (poor concentration and memory)
• difficulty finding pleasure in anything
• social withdrawal
• an unsettled mood (feeling anxious and irritable)
• impaired work performance (this may be result of other symptoms such as fatigue).

People can develop a “burning out” phase after intense work demands over only a week or two. A “burnout” stage usually follows years of unrelenting work pressure.

What is depression?

A depressive episode involves a drop in self-worth, increase in self-criticism and feelings of wanting to give up. Not everyone with these symptoms will have clinical depression, which requires a diagnosis and has an additional set of symptoms.

Clinically diagnosed depression can vary by mood, how long it lasts and whether it comes back. There are two types of clinical depression:

1. melancholic depression has genetic causes, with episodes largely coming “out of the blue”
2. non-melancholic depression is caused by environmental factors, often triggered by significant life events which cause a drop in self-worth.

When we created our burnout measure, we compared burnout symptoms with these two types of depression.

Burnout shares some features with melancholic depression, but they tend to be general symptoms, such as feeling a loss of pleasure, energy and concentration skills.

We found there were more similarities between burnout and non-melancholic (environmental) depression. This included a lack of motivation and difficulties sleeping or being cheered up, perhaps reflecting the fact both have environmental causes.

Looking for the root cause

The differences between burnout and depression become clearer when we look at why they happen.

Personality comes into play. Our work suggests a trait like perfectionism puts people at a much higher risk of burnout. But they may be less likely to become depressed as they tend to avoid stressful events and keep things under control.

Those with burnout generally feel overwhelmed by demands or deadlines they can’t meet, creating a sense of helplessness.

On the other hand, those with depression report lowered self-esteem. So rather than helpless they feel that they and their future is hopeless.

However it is not uncommon for someone to experience both burnout and depression at once. For example, a boss may place excessive work demands on an employee, putting them at risk of burnout. At the same time, the employer may also humiliate that employee and contribute to an episode of non-melancholic depression.

What can you do?

A principal strategy in managing burnout is identifying the contributing stressors. For many people, this is the workplace. Taking a break, even a short one, or scheduling some time off can help.

Australians now have the right to disconnect, meaning they don’t have to answer work phone calls or emails after hours. Setting boundaries can help separate home and work life.

Burnout can be also be caused by compromised work roles, work insecurity or inequity. More broadly, a dictatorial organisational structure can make employees feel devalued. In the workplace, environmental factors, such as excessive noise, can be a contributor. Addressing these factors can help prevent burnout.

As for managing symptoms, the monks had the right idea. Strenuous exercise, meditation and mindfulness are effective ways to deal with everyday stress.

Deeper contributing factors, including traits such as perfectionism, should be managed by a skilled clinical psychologist.

For melancholic depression, clinicians will often recommend antidepressant medication.

For non-melancholic depression, clinicians will help address and manage triggers that are the root cause. Others will benefit from antidepressants or formal psychotherapy.

While misdiagnosis between depression and burnout can occur, burnout can mimic other medical conditions such as anemia or hypothyroidism.

For the right diagnosis, it’s best to speak to your doctor or clinician who should seek to obtain a sense of “the whole picture”. Only then, once a burnout diagnosis has been affirmed and other possible causes ruled out, should effective support strategies be put in place.

If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.

Correction: This article originally stated that depression is marked by helplessness and burnout by hopelessness, when in fact it is vice versa. This has been amended.

Gordon Parker, Scientia Professor of Psychiatry, UNSW Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.