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Weight‑loss drugs like Ozempic could work for addiction too – and we finally know how
For many people, the thought of a tasty burger or a cold pint of beer conjures up a vivid mental image and drives behaviour.
This link between thinking and doing serves a clear function – it motivates us to get the necessities for life.
But for some, this process can malfunction. Preoccupation with these rewarding stimuli can lead to disorders of substance overuse, including overeating to the point of obesity and alcohol abuse.
Studies going back to the 1970s have linked vivid mental imagery with drug abuse.
Understanding this link between craving and consuming is central to understanding addiction. This has eluded neuroscience for decades, but the introduction of a new class of drugs for weight loss may have given us just the lever we need to understand it.
These new drugs – including Ozempic and Wegovy – mimic the GLP-1 hormone to stimulate insulin release, slow digestion, and increase feelings of fullness. They are known as GLP-1 agonists and were originally used to treat type 2 diabetes because they help control blood sugar.
As a side effect, people using these drugs also lost a lot of weight, in some cases almost as much as might be expected from bariatric surgery.
But there is another less well publicised effect. Human studies show that GLP-1 agonists reduce alcohol consumption. Preclinical animal studies suggest these drugs also reduce the use of cocaine, amphetamines, opiates and nicotine.
These drugs are changing how we think about the brain’s reward system. They may also open new treatment options for obesity, alcohol dependence and the consumption of other addictive substances.
How the brain regulates reward stimuli
We have a reasonable understanding of the brain’s “reward circuitry” associated with regions that produce the neurotransmitter dopamine.
These brain parts – the ventral tegmental area (VTA) and nucleus accumbens (NAc) – have been the subject of research on reward for decades. They are the obvious candidate regions to look for a mechanism for GLP-1 action in the brain. But they lack significant density of receptors for GLP-1 and are unlikely to be the direct mechanism.
We must, therefore, consider other brain regions to understand the anti-consumption effect of GLP-1 drugs.
One jump “upstream” from the dopamine-producing brain parts is a region called the lateral septum. This brain structure has been historically implicated in emotional regulation.
Back in 1953, pioneering US behavioural researchers Joseph Brady and Walle Nauta coined the term “septal rage” when animals with damage in the lateral septum showed increased aggression, while direct stimulation of this brain region reduced aggression.
Much more recent work has placed the lateral septum at the centre of a neural connectivity network. This has reframed how we think about its function.
While a link between the lateral septum and another region called the hypothalamus is probably responsible for septal rage, the lateral septum links with many other regions with various functions.
The brain’s reward control centre
The lateral septum inherits much of its primary input from a brain region called the hippocampus.
This region is well known as the place that lets us form long-term “episodic memories”. A famous case of hippocampal damage, Henry Molaison (patient HM), was unable to form new memories after his surgery for epilepsy. He effectively lived without a past, in permanent present tense.
The hippocampus also contains the remarkable “place cells” – neurons that fire corresponding to a person’s thoughts about their position in space and, as recent research has shown, time.
This “where and when am I” information gets forwarded to the lateral septum. Key research has recently shown the lateral septum also contains place cells, but these cells strongly respond to rewards. They effectively add “what is good in this place” to the “where and when am I” information from the hippocampus.
Critically, the lateral septum shares this information with the dopamine-producing regions we would normally associate with reward.
Neuroscientists now think of the lateral septum as the brain region that lets us “think about” rewards – our conscious perception of them – and communicates with the machinery in the brain’s reward system that produces dopamine to make us feel good about them.
There is one last reason to suspect the lateral septum as the mechanism behind the anti-consumption effect of GLP-1 agonists. It is absolutely loaded with GLP-1 receptors.
Emerging research points to this as the mechanism. GLP-1 activation directly in the lateral septum has recently been shown to reduce food consumption in mice. Earlier this year, another study showed the same for alcohol consumption.
My own lab has shown this year that GLP-1 drugs reduce a type of activity in the lateral septum that may prevent it communicating so effectively with other brain regions.
These findings are reshaping our understanding of how the brain processes rewards and have put the spotlight firmly on the lateral septum as the home of cravings.![]()
Robert Munn, Senior Lecturer, University of Otago
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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\World’s first AI‑designed vaccine explained
Neil Mabbott, University of Edinburgh
Researchers at the University of Cambridge have developed what they describe as a fundamentally new type of vaccine using artificial intelligence (AI). The vaccine’s key component was designed entirely by AI and has now been tested in people for the first time.
The goal is ambitious: a single vaccine that works not just against all known human coronavirus variants, but against related bat viruses that could jump from animals to humans and cause future pandemics.
Traditional vaccines train our immune system to recognise one specific virus. The problem is that viruses mutate. When they change enough, the vaccine stops working, which is why we need a new flu shot every year and why COVID vaccines have been updated repeatedly since 2021.
AI offers a way around this. By analysing genetic data from thousands of related viruses, it can identify the parts that stay the same across different strains and that are unlikely to change over time. Target those stable features, and you have a vaccine that should work against the whole family, not just the strain you started with.
This is exactly what the Cambridge team did. They used AI to scan viruses from the sarbecovirus family, which includes the viruses that cause both SARS and COVID, as well as a range of animal coronaviruses – looking for shared features that evolution has left largely untouched. Those features became the basis of the vaccine.
DNA vaccines
While many people are familiar with the mRNA shots used during the pandemic, this new vaccine uses DNA. DNA vaccines are generally more stable than mRNA vaccines, making them easier to store and transport. A significant advantage in lower-income countries where “cold-chain” infrastructure is limited.
They can also be administered without needles. A high-pressure stream of liquid delivers the vaccine through the skin, making administration less painful and easier to scale up during an outbreak.
Could it protect against future pandemics?
These practical advantages matter most if the vaccine itself can do something no existing jab can: protect against viruses we haven’t encountered yet.
Broad-spectrum vaccines could change the way the world responds to emerging infectious diseases. By offering much wider protection than traditional vaccines, they could provide rapid immunity against new and emerging viral threats. This would equip public health officials with tools to stop future outbreaks in their tracks before they have a chance to turn into global pandemics.
They could also transform our approach to more familiar diseases. Influenza is a prime target because it exists in many different strains and evolves so rapidly. Scientists have to predict which strains will dominate each flu season, and they guess wrong, vaccine effectiveness can suffer. A universal flu vaccine that targets features shared across multiple strains could eventually end the annual race to keep up with the virus.
And the Ebola virus shows why this matters right now. The recent outbreak in the Democratic Republic of the Congo and Uganda is driven by the Bundibugyo strain, which bypasses existing vaccines. While researchers rush to create a new vaccine specifically for this strain, local communities remain at high risk. A broad-spectrum vaccine designed to cover an entire virus family could transform that picture.
What the trial found
This is the first human trial of an AI-designed vaccine. The results showed that this DNA vaccine was able to stimulate the immune system to produce antibodies that can recognise different types of sarbecoviruses. The technology was found to be safe and well tolerated.
This is an exciting advance because it demonstrates how AI has the potential to design variant-proof vaccines against future pandemic threats. The needle-free delivery system could also make the vaccine easier to administer and distribute worldwide.
However, there is more work to do. Although the results in this study are encouraging, the immune responses following vaccination were modest. It was also uncertain how long the protection lasts and whether further boosters will be required. Larger trials are also needed to determine whether the vaccine can prevent or reduce virus infections in the real world.
A universal vaccine remains a few years away. And any new vaccine must still pass larger trials to prove it is safe, effective and provides lasting protection. But this study shows the goal is getting closer – and AI may help us get there faster.![]()
Neil Mabbott, Personal Chair of Immunopathology, University of Edinburgh
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Climate change‑related heat increases the risk of premature birth in 13 countries – new study
Dominic Royé, Consejo Superior de Investigaciones Científicas (CSIC); Ana M Vicedo-Cabrera, University of Bern; Aurelio Tobias, Instituto de Diagnóstico Ambiental y Estudios del Agua (IDAEA - CSIC); Carmen Íñiguez, Universitat de València, and Coral Salvador, University of Bern
Picture a sweltering summer’s day. Now imagine enduring the heat while eight months pregnant. Uncomfortable, to say the absolute least.
But in pregnancy, heat is more than just a nuisance, as for many women it can trigger early labour. A premature baby – meaning one born before 37 weeks of gestation – faces a significantly higher risk of mortality, as well as health complications that can affect them for the rest of their lives.
Decades of research has documented the link between exposure to heat and preterm births. However, most studies have been limited to a single city or country, using different methods that yielded results which were difficult to compare.
So how many premature births are actually caused by heat in different parts of the world? Are all pregnant women equally vulnerable? Our new study, published in Environment International, provides the most comprehensive answers to these questions to date.
13 countries, 36 million births
We analysed 36.6 million births that took place during the summer in 250 towns and cities, across 13 countries (Australia, Brazil, Canada, Chile, Ecuador, Estonia, Israel, Italy, Japan, Paraguay, Spain, Switzerland and the United States) between 1979 and 2019. This is the most extensive multi-site analysis conducted on this topic to date.
To estimate the relationship between temperature and the risk of preterm birth, we used cutting edge statistical models that allowed us to see the delayed and non-linear effects of heat exposure in the days leading up to delivery.
The findings are clear: the risk of preterm birth increases linearly as temperatures rise. On days of moderate heat, this risk increases by 2.8%. On days of extreme heat, the increase reaches 3.8%.
855 extra premature births per million
Translating these risks into specific figures provides a clearer picture of the scale of the problem. We estimate that 1.41% of all premature births occurring during the summer are attributable to heat. In absolute terms, this equates to 855 extra premature births per million births.
The magnitude is comparable to that of other well-established factors. For example, it far exceeds the contribution of maternal smoking in low and middle-income countries, and is on a par with that of malaria. And heat is already a major environmental risk factor for reproductive health.
The differences between countries are also revealing. Paraguay has the highest rate, with 1,347 preterm births per million, while Switzerland has the lowest, with 628. Spain falls in the upper-middle range, with 1,080 per million. This variability suggests that climate, the level of socio-economic development, and each country’s capacity to adapt significantly influence the vulnerability of pregnant women.
Not all pregnancies have the same risk
One of our study’s most significant findings suggests that heat may not affect all women equally. Young single mothers with lower levels of education who are in a vulnerable socio-economic situation may be at greater risk of heat-induced preterm birth.
Female foetuses also appear to be more susceptible than male foetuses. However, most of these subgroup analyses were not statistically significant, so further research is needed to confirm them.
There are specific mechanisms behind these differences. People who are economically disadvantaged are more likely to live in particularly hot areas due to the urban heat island effect. They are also more likely to work outdoors, and to lack access to air conditioning or other means of protection against the heat. Social inequality and climate inequality overlap, and the most vulnerable pregnant women pay the highest price.
Heat also speeds up births at term
Perhaps the most surprising finding of our research is that the effect of heat is not limited to preterm births. We have also observed a significant increase in the risk of delivery in pregnancies that would be considered clinically normal, between weeks 37 and 42. Specifically, extreme heat increases the risk of delivery in weeks 37-38 by 3.66%, and in pregnancies of 39 weeks or more by 2.97%.
This means that heat can act as a trigger for labour in foetuses that, under other circumstances, would have continued to develop normally. The most sensitive gestational window is from week 31 to week 40, spanning late preterm and early term births.
Root causes
There are many biological mechanisms at play here. Heat can raise body temperature and trigger uterine contractions. The dehydration caused by heat also disrupts the electrolyte balance and reduces blood flow to the placenta. Furthermore, heat triggers inflammatory processes and oxidative stress, which can compromise foetal development and accelerate cervical ripening.
Pregnant women are particularly vulnerable because their bodies generate more heat than usual due to foetal growth, while also having a reduced ability to dissipate that heat because of weight gain.
Global warming
These findings are particularly worrying in light of climate change. Over the coming decades, heatwaves will become more frequent, more intense, and will last longer. If we fail to act, the burden of preterm births attributable to high temperatures will only increase, undermining decades of progress in neonatal and child health.
A proper response requires action on several fronts. In the clinical setting, health systems must incorporate heat as a risk factor in antenatal care, particularly for socially vulnerable women. In the urban sphere, it is urgent to develop adaptation strategies – green spaces, climate shelters, early warning systems – that protect pregnant women during episodes of extreme heat. And at the policy level, these findings must be translated into ambitious emissions reduction targets.
Extreme heat is no longer just a matter of comfort. It is a question of public health, social equity and climate justice. And pregnant women are on the front line.![]()
Dominic Royé, Investigador Ramon y Cajal, Consejo Superior de Investigaciones Científicas (CSIC); Ana M Vicedo-Cabrera, Head Climate Change & Health research group, University of Bern; Aurelio Tobias, Associate professor, Instituto de Diagnóstico Ambiental y Estudios del Agua (IDAEA - CSIC); Carmen Íñiguez, Profesora en el Departamento de Estadística e Investigación Operativa, Universitat de València, and Coral Salvador, Senior Research Assistant, University of Bern
This article is republished from The Conversation under a Creative Commons license. Read the original article.
First video of immune cells eating live skin cancer in real time
Macrophages (green) engulfing melanoma cells (purple). Keith et al. / Garvan Institute, CC BY-SA
Yuki Keith, Garvan Institute and Tri Phan, Garvan InstituteFor the past 15 years or so, a class of drugs called immune checkpoint inhibitors have been used to treat melanoma – the most dangerous kind of skin cancer.
For many patients, they produce remarkable results. For others, they do nothing.
We still don’t really know why. But in new research published in the Journal of Experimental Medicine, we observed immune cells called macrophages attacking melanoma cells in real time – which may offer clues about how we can make those therapies work for all patients, not just some.
Tumours, hot and cold
One of us (Yuki) treated patients with melanoma in Japan as a dermatologist. The other (Tri Phan) runs a lab at the Garvan Institute in Sydney, where his team specialises in observing the cells of the immune system in real time.
When Yuki wanted to understand why immune checkpoint inhibitors were failing for many patients, she joined Tri Phan’s lab to continue her research.
The treatment fails in what oncologists call “cold” tumours, where the cancer’s environment actively prevents a kind of immune cell called a T cell attacking it. One of our lab’s aims is trying to work out how to make the tumours “hot”, allowing T cells to penetrate and destroy the cancer cells.
Our new findings suggest a different kind of immune cell, called macrophages, may hold the key.
Macrophages (green) engulfing melanoma cells (purple). Yuki Keith, CC BYThe housekeepers we’ve been ignoring
In 1908, Russian zoologist Ilya Mechnikov was awarded a Nobel Prize for the discovery of phagocytosis (“cell eating”) in the immune system, which is carried out by cells he called macrophages (from the Greek for “big eaters”).
These cells engulf and clear away the debris caused by tissue damage and cell death. They are often regarded as the body’s silent, no-fuss housekeepers.
However, their role in cancer has often been overlooked. Unlike other immune cells that move through the blood and patrol the whole body, macrophages are “tissue-resident” and stay in one place.
A microscopic view of a melanoma tumour growing in the skin shows CD169 macrophages in green and yellow forming a biological boundary wall around the tumour. Keith et al. / Garvan Institute, CC BYEarlier studies of the role of macrophages in cancer assumed these housekeepers were all the same. But when we looked closely in the skin, it became clear that there were many different kinds of macrophages living in different layers.
One particular kind of macrophages (recognised by a protein called CD169) lives in a deeper part of the skin, called the hypodermis.
We found that these macrophages arranged themselves around the edges of a melanoma tumour, as if they were trying to wall it off. When we depleted the macrophages, the melanomas grew bigger, suggesting they were constraining the growth of the tumours.
Watching cancer cells being eaten alive
To understand what these CD169-positive macrophages were actually doing, we used an advanced imaging technique called intravital two-photon microscopy. This allows us to watch biological processes unfold in living tissue in real time.
What we saw was surprising: the macrophages were “nibbling” and actively engulfing live melanoma cells. While we had seen macrophages eat dead cells in our lab before, we had never seen them eat a live melanoma cell in a model organism.
What was even more surprising was that this immune attack was happening without the need for T cells, or antibodies made by another kind of immune cell called B cells – the immune players most commonly credited with fighting cancer.
We also confirmed this is not something that just happens in the lab. Our colleagues at the Melanoma Institute Australia analysed samples from human melanoma patients and found similar populations of CD169-expressing macrophages on the edges of the tumour, suggesting they may play a similar protective role there.
Calling in the cavalry – implications for therapies
Macrophages don’t just clear away debris. They can also alert the immune system to danger. After they have digested the debris, they can display it like a biological “red flag” to direct T cells to find and kill the cancer cells.
What makes a macrophage decide whether to silently dispose of debris without alerting the immune system, or wave the red flags to activate the immune system, is still unclear. Because the CD169-expressing macrophages are strategically positioned around the tumours, we suspect they may hold the key.
Macrophages are widespread in most solid tumours – including glioblastoma, breast cancer and many others. This is an army already in place waiting to be mobilised.
Our next step is to understand precisely how these macrophages eat live cancer cells and how they can communicate the danger to T cells, so we can harness this population with new treatments.![]()
Yuki Keith, Postdoctoral Researcher, Immunology, Garvan Institute and Tri Phan, Program Director – Precision Immunology / Laboratory Head, Garvan Institute
This article is republished from The Conversation under a Creative Commons license. Read the original article.
New AI Glasses for Dementia ‘Sees’ Objects With Labels Projected on Lenses to ‘Significantly’ Improve Lives
Carole Grieg testing the CrossSense AI glasses – SWNS
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Artist’s illustration of tuberculosis bacteria (TB) – credit, US CDCAI-powered digital stethoscopes show promise in bridging screening gaps
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Masaya at the Liverpool Vet. Hospital where she underwent surgery – credit, Chester Zoo via SWNSCouples share 30% of their gut bacteria. Here’s how that may affect health
Conor Meehan, Nottingham Trent University and Janelle Mwerinde, Nottingham Trent University
When living with a partner, you might be sharing more than just the same home, lifestyle and interests. You might also share various microscopic organisms residing on and in you.
This community of microorganisms, which consists of mainly bacteria, viruses and fungi, is known collectively as the human microbiome. The various microbiomes found throughout the body all play an important role in health.
From birth, the human microbiome is shaped by our interactions with our mother, who introduces diverse microorganisms that build our immune and digestive systems. As we get older, social interactions with our close community continue influencing this delicate ecosystem.
The people we live with have huge influence on what microbes we have in our microbiome. In fact, it’s thought that partners share around 30% of their resident microbes in the gut alone.
But it isn’t just the microbes in your gut that may be similar to your partner. The microbes in many other parts of the body may also be shared with your loved one – and this could potentially affect your health.
Gut microbiome
Diet and lifestyle are thought to have the greatest influence on the gut microbiome’s make-up. But studies on couples have found that living with your partner can also influence the microbiome.
Couples living together may share 13% to 30% of their gut bacteria. This was true even when diet (which many couples share) was factored out. Research also shows that couples who live together have greater microbial diversity compared to people who live alone.
This is good news for couples who co-habitate, as a more diverse gut microbiome is correlated with lower risk of irritable bowel syndrome, cardiovascular diseases and potentially high blood sugar.
But it might not all be good news. Research shows that some of the bacterial species couples share can have varying effects on health.
Take the bacteria from the Ruminococcus family. While some species of Ruminoccocus benefit health, others have been linked to negative health outcomes, including diabetes and irritable bowel syndrome.
So these bacteria may not always offer the same benefits in different demographics. This highlights the complexity of resident gut bacteria and their health impacts.
Oral microbiome
Sharing an oral microbiome with our partners might seem obvious considering we regularly exchange saliva when we kiss. A ten-second kiss alone can exchange up to 80 million bacteria. The more kisses a couple shares, the more shared salivary bacteria they will have.
Although most of these bacteria will quickly pass through our mouth and into our gut when we swallow saliva, research show that couples actually share many of the same longer-term tongue microbes that form the foundation of the oral microbiome. Research even suggests that 38% of the oral microbiome is shared in couples living together – compared to only 3% in couples who don’t live together.
Sharing this proportion of your oral microbiome could have many potential health effects.
A healthy oral microbiome is important for protecting against tooth decay and it has anti-inflammatory properties. Some researchers also suggest the oral microbiome’s health effects may extend as far as the gut and nervous system.
But some of the bacteria that couples tend to share may also have potentially harmful health effects.
Couples are more likely to have similar numbers of the bacteria Neisseria in their gut compared to single people. Neisseria can reside in the mouth for long periods of without causing disease.
So while you may want to avoid kissing someone when they’re poorly for obvious reasons, it turns out that a kiss even when you’re healthy can transfer all sorts of bacteria between the two of you.
More research is needed to really understand what overall effect sharing these bacteria with your partner has on health.
Skin microbiome
The skin microbiome is the most unique and personalised microbiome, tailored to each person. It’s even sometimes referred to as our microbial fingerprint.
Being the most exposed microbiome, the skin microbiome has evolved to be adaptable to external factors such as the climate and cosmetic products. No matter what, these bacteria work hard to remain at an equilibrium.
Close contact with our partners – and even pets – has a huge influence on what bacteria live on our skin. After comparing the gut and oral microbiome, researchers found the skin microbiome to be the most similar among couples.
It isn’t just the bacteria on your arms or hands that are shared, either. Research shows that couples shared 35% of the bacteria living on their feet, and around 17.5% of the bacteria on their eyelids.
You may not even need to touch your partner to have the same skin bacteria as them. Factors such as sleeping in the same bed and walking on similar surfaces are thought to explain why such a large proportion of our skin microbiome is similar.
This is because humans naturally shed bacteria in a similar way as dogs shed fur. We leave traces of our bacteria on everything we touch – and we also easily pick up bacteria from our environments.
The shared effect of living together on the skin microbiome is so great that researchers were able to use computer models to accurately predict 86% of cohabiting couples based off of their individual bacterial samples alone.
But while it’s clear that couples share much of the same skin microbiome, the health effect that this has is not currently known.
While sharing bacteria with your partner may sound alarming, there’s often no cause for concern. Bacteria teach our bodies how to fight infections, they help us digest foods and even produce key nutrients. The bacteria we share with our partners are often harmless and sometimes benefit our health rather than hindering it.![]()
Conor Meehan, Associate Professor of Microbial Bioinformatics, Nottingham Trent University and Janelle Mwerinde, PhD Candidate, Skin Microbiology, Nottingham Trent University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
