Anyone who has drunk alcohol will be familiar with how easily it can lower your social inhibitions and let you do things you wouldn’t normally do.

But you may not be aware that mixing certain medicines with alcohol can increase the effects and put you at risk.

When you mix alcohol with medicines, whether prescription or over-the-counter, the medicines can increase the effects of the alcohol or the alcohol can increase the side-effects of the drug. Sometimes it can also result in all new side-effects.

How alcohol and medicines interact

The chemicals in your brain maintain a delicate balance between excitation and inhibition. Too much excitation can lead to convulsions. Too much inhibition and you will experience effects like sedation and depression.

Alcohol works by increasing the amount of inhibition in the brain. You might recognise this as a sense of relaxation and a lowering of social inhibitions when you’ve had a couple of alcoholic drinks.

With even more alcohol, you will notice you can’t coordinate your muscles as well, you might slur your speech, become dizzy, forget things that have happened, and even fall asleep.

Medications can interact with alcohol to produce different or increased effects. Alcohol can interfere with the way a medicine works in the body, or it can interfere with the way a medicine is absorbed from the stomach. If your medicine has similar side-effects as being drunk, those effects can be compounded.

Not all the side-effects need to be alcohol-like. Mixing alcohol with the ADHD medicine ritalin, for example, can increase the drug’s effect on the heart, increasing your heart rate and the risk of a heart attack.

Combining alcohol with ibuprofen can lead to a higher risk of stomach upsets and stomach bleeds.

Alcohol can increase the break-down of certain medicines, such as opioids, cannabis, seizures, and even ritalin. This can make the medicine less effective. Alcohol can also alter the pathway of how a medicine is broken down, potentially creating toxic chemicals that can cause serious liver complications. This is a particular problem with paracetamol.

At its worst, the consequences of mixing alcohol and medicines can be fatal. Combining a medicine that acts on the brain with alcohol may make driving a car or operating heavy machinery difficult and lead to a serious accident.

Who is at most risk?

The effects of mixing alcohol and medicine are not the same for everyone. Those most at risk of an interaction are older people, women and people with a smaller body size.

Older people do not break down medicines as quickly as younger people, and are often on more than one medication.

Older people also are more sensitive to the effects of medications acting on the brain and will experience more side-effects, such as dizziness and falls.

Women and people with smaller body size tend to have a higher blood alcohol concentration when they consume the same amount of alcohol as someone larger. This is because there is less water in their bodies that can mix with the alcohol.

What drugs can’t you mix with alcohol?

You’ll know if you can’t take alcohol because there will be a prominent warning on the box. Your pharmacist should also counsel you on your medicine when you pick up your script.

The most common alcohol-interacting prescription medicines are benzodiazepines (for anxiety, insomnia, or seizures), opioids for pain, antidepressants, antipsychotics, and some antibiotics, like metronidazole and tinidazole.

It’s not just prescription medicines that shouldn’t be mixed with alcohol. Some over-the-counter medicines that you shouldn’t combine with alcohol include medicines for sleeping, travel sickness, cold and flu, allergy, and pain.

Next time you pick up a medicine from your pharmacist or buy one from the local supermarket, check the packaging and ask for advice about whether you can consume alcohol while taking it.

If you do want to drink alcohol while being on medication, discuss it with your doctor or pharmacist first.

Nial Wheate, Associate Professor of the School of Pharmacy, University of Sydney; Jasmine Lee, Pharmacist and PhD Candidate, University of Sydney; Kellie Charles, Associate Professor in Pharmacology, University of Sydney, and Tina Hinton, Associate Professor of Pharmacology, University of Sydney

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

Globally, one in eight people are living with obesity. This is an issue because excess fat increases the risk of type 2 diabetes, heart disease and certain cancers.

Modifying your diet is important for managing obesity and preventing weight gain. This might include reducing your calorie intake, changing your eating patterns and prioritising healthy food.

But is one formula for weight loss more likely to result in success than another? Our new research compared three weight-loss methods, to see if one delivered more weight loss than the others:

• altering calorie distribution – eating more calories earlier rather than later in the day
• eating fewer meals
• intermittent fasting.

We analysed data from 29 clinical trials involving almost 2,500 people.

We found that over 12 weeks or more, the three methods resulted in similar weight loss: 1.4–1.8kg.

So if you do want to lose weight, choose a method that works best for you and your lifestyle.

Eating earlier in the day

When our metabolism isn’t functioning properly, our body can’t respond to the hormone insulin properly. This can lead to weight gain, fatigue and can increase the risk of a number of chronic diseases such as diabetes.

Eating later in the day – with a heavy dinner and late-night snacking – seems to lead to worse metabolic function. This means the body becomes less efficient at converting food into energy, managing blood sugar and regulating fat storage.

In contrast, consuming calories earlier in the day appears to improve metabolic function.

However, this might not be the case for everyone. Some people naturally have an evening “chronotype”, meaning they wake up and stay up later.

People with this chronotype appear to have less success losing weight, no matter the method. This is due to a combination of factors including genes, an increased likelihood to have a poorer diet overall and higher levels of hunger hormones.

Eating fewer meals

Skipping breakfast is common, but does it hinder weight loss? Or is a larger breakfast and smaller dinner ideal?

While frequent meals may reduce disease risk, recent studies suggest that compared to eating one to two meals a day, eating six times a day might increase weight loss success.

However, this doesn’t reflect the broader research, which tends to show consuming fewer meals can lead to greater weight loss. Our research suggests three meals a day is better than six. The easiest way to do this is by cutting out snacks and keeping breakfast, lunch and dinner.

Most studies compare three versus six meals, with limited evidence on whether two meals is better than three.

However, front-loading your calories (consuming most of your calories between breakfast and lunch) appears to be better for weight loss and may also help reduce hunger across the day. But more studies with a longer duration are needed.

Fasting, or time-restricted eating

Many of us eat over a period of more than 14 hours a day.

Eating late at night can throw off your body’s natural rhythm and alter how your organs function. Over time, this can increase your risk of type 2 diabetes and other chronic diseases, particularly among shift workers.

Time-restricted eating, a form of intermittent fasting, means eating all your calories within a six- to ten-hour window during the day when you’re most active. It’s not about changing what or how much you eat, but when you eat it.

Animal studies suggest time-restricted eating can lead to weight loss and improved metabolism. But the evidence in humans is still limited, especially about the long-term benefits.

It’s also unclear if the benefits of time-restricted eating are due to the timing itself or because people are eating less overall. When we looked at studies where participants ate freely (with no intentional calorie limits) but followed an eight-hour daily eating window, they naturally consumed about 200 fewer calories per day.

What will work for you?

In the past, clinicians have thought about weight loss and avoiding weight gain as a simile equation of calories in and out. But factors such as how we distribute our calories across the day, how often we eat and whether we eat late at night may also impact our metabolism, weight and health.

There are no easy ways to lose weight. So choose a method, or combination of methods, that suits you best. You might consider

• aiming to eat in an eight-hour window
• consuming your calories earlier, by focusing on breakfast and lunch
• opting for three meals a day, instead of six.

The average adult gains 0.4 to 0.7 kg per year. Improving the quality of your diet is important to prevent this weight gain and the strategies above might also help.

Finally, there’s still a lot we don’t know about these eating patterns. Many existing studies are short-term, with small sample sizes and varied methods, making it hard to make direct comparisons.

More research is underway, including well-controlled trials with larger samples, diverse populations and consistent methods. So hopefully future research will help us better understand how altering our eating patterns can result in better health.

Hayley O’Neill, Assistant Professor, Faculty of Health Sciences and Medicine, Bond University and Loai Albarqouni, Assistant Professor | NHMRC Emerging Leadership Fellow, Bond University

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

The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.

Given this long history, it may surprise you that experts don’t agree about what depression is, how to define it or what causes it.

But many experts do agree that depression is not one thing. It’s a large family of illnesses with different causes and mechanisms. This makes choosing the best treatment for each person challenging.

Reactive vs endogenous depression

One strategy is to search for sub-types of depression and see whether they might do better with different kinds of treatments. One example is contrasting “reactive” depression with “endogenous” depression.

Reactive depression (also thought of as social or psychological depression) is presented as being triggered by exposure to stressful life events. These might be being assaulted or losing a loved one – an understandable reaction to an outside trigger.

Endogenous depression (also thought of as biological or genetic depression) is proposed to be caused by something inside, such as genes or brain chemistry.

Many people working clinically in mental health accept this sub-typing. You might have read about this online.

But we think this approach is way too simple.

While stressful life events and genes may, individually, contribute to causing depression, they also interact to increase the risk of someone developing depression. And evidence shows that there is a genetic component to being exposed to stressors. Some genes affect things such as personality. Some affect how we interact with our environments.

What we did and what we found

Our team set out to look at the role of genes and stressors to see if classifying depression as reactive or endogenous was valid.

In the Australian Genetics of Depression Study, people with depression answered surveys about exposure to stressful life events. We analysed DNA from their saliva samples to calculate their genetic risk for mental disorders.

Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?

You may be wondering why we bothered calculating the genetic risk for mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, some less. Even people who already have depression might have a low genetic risk for it. These people may have developed their particular depression from some other constellation of causes.

We looked at the genetic risk of conditions other than depression for a couple of reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. So we wanted to cast a wide net to look at a wider spectrum of genetic variants linked to mental disorders.

If reactive and endogenous depression sub-types are valid, we’d expect people with a lower genetic component to their depression (the reactive group) would report more stressful life events. And we’d expect those with a higher genetic component (the endogenous group) would report fewer stressful life events.

But after studying more than 14,000 people with depression we found the opposite.

We found people at higher genetic risk for depression, anxiety, ADHD or schizophrenia say they’ve been exposed to more stressors.

Assault with a weapon, sexual assault, accidents, legal and financial troubles, and childhood abuse and neglect, were all more common in people with a higher genetic risk of depression, anxiety, ADHD or schizophrenia.

These associations were not strongly influenced by people’s age, sex or relationships with family. We didn’t look at other factors that may influence these associations, such as socioeconomic status. We also relied on people’s memory of past events, which may not be accurate.

How do genes play a role?

Genetic risk for mental disorders changes people’s sensitivity to the environment.

Imagine two people, one with a high genetic risk for depression, one with a low risk. They both lose their jobs. The genetically vulnerable person experiences the job loss as a threat to their self-worth and social status. There is a sense of shame and despair. They can’t bring themselves to look for another job for fear of losing it too. For the other, the job loss feels less about them and more about the company. These two people internalise the event differently and remember it differently.

Genetic risk for mental disorders also might make it more likely people find themselves in environments where bad things happen. For example, a higher genetic risk for depression might affect self-worth, making people more likely to get into dysfunctional relationships which then go badly.

What does our study mean for depression?

First, it confirms genes and environments are not independent. Genes influence the environments we end up in, and what then happens. Genes also influence how we react to those events.

Second, our study doesn’t support a distinction between reactive and endogenous depression. Genes and environments have a complex interplay. Most cases of depression are a mix of genetics, biology and stressors.

Third, people with depression who appear to have a stronger genetic component to their depression report their lives are punctuated by more serious stressors.

So clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their chance of developing depression in the first place. It might also help some people with depression reduce their ongoing exposure to stressors.

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

Jacob Crouse, Research Fellow in Youth Mental Health, Brain and Mind Centre, University of Sydney and Ian Hickie, Co-Director, Health and Policy, Brain and Mind Centre, University of Sydney

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