Flavoured nicotine pouches are being promoted to young people on social media platforms such as TikTok and Instagram.

Although some viral videos have been taken down following a series of reports in The Guardian, clips featuring Australian influencers have claimed nicotine pouches are a safe and effective way to quit vaping. A number of the videos have included links to websites selling these products.

With the rapid rise in youth vaping and the subsequent implementation of several reforms to restrict access to vaping products, it’s not entirely surprising the tobacco industry is introducing more products to maintain its future revenue stream.

The major trans-national tobacco companies, including Philip Morris International and British American Tobacco, all manufacture nicotine pouches. British American Tobacco’s brand of nicotine pouches, Velo, is a leading sponsor of the McLaren Formula 1 team.

But what are nicotine pouches, and are they even legal in Australia?

Like snus, but different

Nicotine pouches are available in many countries around the world, and their sales are increasing rapidly, especially among young people.

Nicotine pouches look a bit like small tea bags and are placed between the lip and gum. They’re typically sold in small, colourful tins of about 15 to 20 pouches. While the pouches don’t contain tobacco, they do contain nicotine that is either extracted from tobacco plants or made synthetically. The pouches come in a wide range of strengths.

As well as nicotine, the pouches commonly contain plant fibres (in place of tobacco, plant fibres serve as a filler and give the pouches shape), sweeteners and flavours. Just like for vaping products, there’s a vast array of pouch flavours available including different varieties of fruit, confectionery, spices and drinks.

The range of appealing flavours, as well as the fact they can be used discreetly, may make nicotine pouches particularity attractive to young people.

Users absorb the nicotine in their mouths and simply replace the pouch when all the nicotine has been absorbed. Tobacco-free nicotine pouches are a relatively recent product, but similar style products that do contain tobacco, known as snus, have been popular in Scandinavian countries, particularly Sweden, for decades.

Snus and nicotine pouches are however different products. And given snus contains tobacco and nicotine pouches don’t, the products are subject to quite different regulations in Australia.

What does the law say?

Pouches that contain tobacco, like snus, have been banned in Australia since 1991, as part of a consumer product ban on all forms of smokeless tobacco products. This means other smokeless tobacco products such as chewing tobacco, snuff, and dissolvable tobacco sticks or tablets, are also banned from sale in Australia.

Tobacco-free nicotine pouches cannot legally be sold by general retailers, like tobacconists and convenience stores, in Australia either. But the reasons for this are more complex.

In Australia, under the Poisons Standard, nicotine is a prescription-only medicine, with two exceptions. Nicotine can be used in tobacco prepared and packed for smoking, such as cigarettes, roll-your-own tobacco, and cigars, as well as in preparations for therapeutic use as a smoking cessation aid, such as nicotine patches, gum, mouth spray and lozenges.

If a nicotine-containing product does not meet either of these two exceptions, it cannot be legally sold by general retailers. No nicotine pouches have currently been approved by the Therapeutic Goods Administration as a therapeutic aid in smoking cessation, so in short they’re not legal to sell in Australia.

However, nicotine pouches can be legally imported for personal use only if users have a prescription from a medical professional who can assess if the product is appropriate for individual use.

We only have anecdotal reports of nicotine pouch use, not hard data, as these products are very new in Australia. But we do know authorities are increasingly seizing these products from retailers. It’s highly unlikely any young people using nicotine pouches are accessing them through legal channels.

Health concerns

Nicotine exposure may induce effects including dizziness, headache, nausea and abdominal cramps, especially among people who don’t normally smoke or vape.

Although we don’t yet have much evidence on the long term health effects of nicotine pouches, we know nicotine is addictive and harmful to health. For example, it can cause problems in the cardiovascular system (such as heart arrhythmia), particularly at high doses. It may also have negative effects on adolescent brain development.

The nicotine contents of some of the nicotine pouches on the market is alarmingly high. Certain brands offer pouches containing more than 10mg of nicotine, which is similar to a cigarette. According to a World Health Organization (WHO) report, pouches deliver enough nicotine to induce and sustain nicotine addiction.

Pouches are also being marketed as a product to use when it’s not possible to vape or smoke, such as on a plane. So instead of helping a person quit they may be used in addition to smoking and vaping. And importantly, there’s no clear evidence pouches are an effective smoking or vaping cessation aid.

Further, some nicotine pouches, despite being tobacco-free, still contain tobacco-specific nitrosamines. These compounds can damage DNA, and with long term exposure, can cause cancer.

Overall, there’s limited data on the harms of nicotine pouches because they’ve been on the market for only a short time. But the WHO recommends a cautious approach given their similarities to smokeless tobacco products.

For anyone wanting advice and support to quit smoking or vaping, it’s best to talk to your doctor or pharmacist, or access trusted sources such as Quitline or the iCanQuit website.

Becky Freeman, Associate Professor, School of Public Health, University of Sydney

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

We’re all time-poor, so multi-tasking is seen as a necessity of modern living. We answer work emails while watching TV, make shopping lists in meetings and listen to podcasts when doing the dishes. We attempt to split our attention countless times a day when juggling both mundane and important tasks.

But doing two things at the same time isn’t always as productive or safe as focusing on one thing at a time.

The dilemma with multi-tasking is that when tasks become complex or energy-demanding, like driving a car while talking on the phone, our performance often drops on one or both.

Here’s why – and how our ability to multi-task changes as we age.

Doing more things, but less effectively

The issue with multi-tasking at a brain level, is that two tasks performed at the same time often compete for common neural pathways – like two intersecting streams of traffic on a road.

In particular, the brain’s planning centres in the frontal cortex (and connections to parieto-cerebellar system, among others) are needed for both motor and cognitive tasks. The more tasks rely on the same sensory system, like vision, the greater the interference.

This is why multi-tasking, such as talking on the phone, while driving can be risky. It takes longer to react to critical events, such as a car braking suddenly, and you have a higher risk of missing critical signals, such as a red light.

The more involved the phone conversation, the higher the accident risk, even when talking “hands-free”.

Generally, the more skilled you are on a primary motor task, the better able you are to juggle another task at the same time. Skilled surgeons, for example, can multitask more effectively than residents, which is reassuring in a busy operating suite.

Highly automated skills and efficient brain processes mean greater flexibility when multi-tasking.

Adults are better at multi-tasking than kids

Both brain capacity and experience endow adults with a greater capacity for multi-tasking compared with children.

You may have noticed that when you start thinking about a problem, you walk more slowly, and sometimes to a standstill if deep in thought. The ability to walk and think at the same time gets better over childhood and adolescence, as do other types of multi-tasking.

When children do these two things at once, their walking speed and smoothness both wane, particularly when also doing a memory task (like recalling a sequence of numbers), verbal fluency task (like naming animals) or a fine-motor task (like buttoning up a shirt). Alternately, outside the lab, the cognitive task might fall by wayside as the motor goal takes precedence.

Brain maturation has a lot to do with these age differences. A larger prefrontal cortex helps share cognitive resources between tasks, thereby reducing the costs. This means better capacity to maintain performance at or near single-task levels.

The white matter tract that connects our two hemispheres (the corpus callosum) also takes a long time to fully mature, placing limits on how well children can walk around and do manual tasks (like texting on a phone) together.

For a child or adult with motor skill difficulties, or developmental coordination disorder, multi-tastking errors are more common. Simply standing still while solving a visual task (like judging which of two lines is longer) is hard. When walking, it takes much longer to complete a path if it also involves cognitive effort along the way. So you can imagine how difficult walking to school could be.

What about as we approach older age?

Older adults are more prone to multi-tasking errors. When walking, for example, adding another task generally means older adults walk much slower and with less fluid movement than younger adults.

These age differences are even more pronounced when obstacles must be avoided or the path is winding or uneven.

Older adults tend to enlist more of their prefrontal cortex when walking and, especially, when multi-tasking. This creates more interference when the same brain networks are also enlisted to perform a cognitive task.

These age differences in performance of multi-tasking might be more “compensatory” than anything else, allowing older adults more time and safety when negotiating events around them.

Older people can practise and improve

Testing multi-tasking capabilities can tell clinicians about an older patient’s risk of future falls better than an assessment of walking alone, even for healthy people living in the community.

Testing can be as simple as asking someone to walk a path while either mentally subtracting by sevens, carrying a cup and saucer, or balancing a ball on a tray.

Patients can then practise and improve these abilities by, for example, pedalling an exercise bike or walking on a treadmill while composing a poem, making a shopping list, or playing a word game.

The goal is for patients to be able to divide their attention more efficiently across two tasks and to ignore distractions, improving speed and balance.

There are times when we do think better when moving

Let’s not forget that a good walk can help unclutter our mind and promote creative thought. And, some research shows walking can improve our ability to search and respond to visual events in the environment.

But often, it’s better to focus on one thing at a time

We often overlook the emotional and energy costs of multi-tasking when time-pressured. In many areas of life – home, work and school – we think it will save us time and energy. But the reality can be different.

Multi-tasking can sometimes sap our reserves and create stress, raising our cortisol levels, especially when we’re time-pressured. If such performance is sustained over long periods, it can leave you feeling fatigued or just plain empty.

Deep thinking is energy demanding by itself and so caution is sometimes warranted when acting at the same time – such as being immersed in deep thought while crossing a busy road, descending steep stairs, using power tools, or climbing a ladder.

So, pick a good time to ask someone a vexed question – perhaps not while they’re cutting vegetables with a sharp knife. Sometimes, it’s better to focus on one thing at a time.

Peter Wilson, Professor of Developmental Psychology, Australian Catholic University

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

An article published this week in the prestigious journal Nature Medicine documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person.

The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.

Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s.

The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.

What’s CJD got to do with Alzehimer’s?

CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.

Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.

Human growth hormone used to come from donated organs

Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.

But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around 16,000 donated glands.

An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people.

hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.

What are the latest findings about Alzheimer’s disease?

The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission.

The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease.

They considered other explanations for the findings but concluded donated hGH was the likely cause.

Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease.

Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.

However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.

When was this process used in Australia?

In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.

More than 2,000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.

The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.

Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for around 5% of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution.

The risk is very low – and you can’t ‘catch’ it like a virus

The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.

Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.

The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.

Steve Macfarlane, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, Monash University

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