Category: 8. Health

Martha’s rule, which lets NHS patients request a review of their care, is now in operation in every acute hospital in England, health service bosses disclosed on Thursday.

The system has helped hundreds of people receive potentially life-saving improvements to their treatment since its rollout began last year. It has led directly to patients being moved to intensive care or receiving drugs they needed, such as antibiotics, or benefiting from other vital interventions.

It is named after Martha Mills, who died in 2021 at the age of 13 from sepsis after a bicycle accident. A coroner found she would probably have survived if she had been moved to the intensive care unit at King’s College hospital in London when she began deteriorating. Martha would have been 18 on Thursday if she had lived.

Martha’s rule became available in 143 acute hospitals in England last year. But it has also been implemented in the other 67 such sites, which means all 210 acute facilities are covered.

It gives patients, their loved ones and NHS staff the right to ask for a different medical team to examine the care being provided and recommend changes.

NHS England’s national medical director, Prof Meghana Pandit, said it is having “a transformative impact” on how hospitals work with patients and their families when their condition is worsening.

Martha’s rule helplines in hospitals received 4,906 calls between last September and June from patients, relatives or staff who were worried about care. That led to 241 people receiving improvements to their care that may have saved their life.

“It would be Martha’s 18th birthday today, another milestone she has missed as a result of the poor care and hospital errors that led to her unnecessary death,” said her parents, Merope Mills and Paul Laity, who persuaded ministers and NHS bosses to adopt the system of independent review.

“We feel her absence every day. But at least Martha’s rule is already preventing many families from experiencing something similar.

“The figures prove that lives are saved when patients and families are given power to act on their suspicions when they feel doctors might have got it wrong and their voice isn’t being heard.”

They welcomed the adoption of the system named after their daughter by all 210 acute sites in England. “We look forward to a time when every patient in the UK knows about the initiative and has easy access to it,” they added.

Wes Streeting, the health secretary, said Martha’s parents’ “tireless campaigning has created a lasting legacy that is already having a potentially life-saving impact across England”.

Rachel Power, the chief executive of the Patients Association, said the fact that every acute hospital in England now offers Martha’s rule was “a landmark moment for patient safety”.

Almost three-quarters of the 4,096 calls came from parents seeking help, NHS England data showed.

Walsall Manor hospital rolled out Martha’s rule last year across its services for adults and recently extended it to services for children.

Amy Blakemore, a matron in its sepsis and outreach response team, said that showed families and carers “are a vital part of the care and treatment decisions that are made for the children and young people in our hospital”.

“Any concerns in relation to their child’s deteriorating condition that they feel are not being listened to can initiate Martha’s rule and they can get an independent review,” she said.

“Passion, patience, and perseverance are the main skills that are required to work in my lab,” says Professor Angelo Accardo. The scientist is the head of a lab in the Precision and Microsystems Engineering (PME) department of Delft University of Technology (TU Delft)’s Faculty of Mechanical Engineering. Undoubtedly, having all three Ps is essential to researching the most fascinating yet mysterious of the human body: the brain. 

The Accardo lab specializes in creating engineered scaffolds, microenvironments that enable human tissues to grow, just as they do in nature. By analyzing these environments, researchers can gain a deeper understanding of how brain cells function, thereby opening up new possibilities for disease treatment. 

A pioneering brain cancer treatment 

One of the research projects the lab is working on, in collaboration with the Leiden University Medical Center and the Holland Proton Therapy Center, focuses on the use of proton therapy to treat glioblastoma. As the most lethal form of brain cancer, it starts in astrocytes, a type of glial cell in the brain and spinal cord. The tumor cells multiply, spreading into other areas of the nervous system. Like other glial cells, astrocytes play a vital role in ensuring the function of nerve cells. 

Proton therapy is a promising option to treat glioblastoma, being more precise in targeting cancer cells. This technique also reduces collateral damage to healthy tissues compared to conventional X-ray radiotherapy, one of the most commonly used treatment options currently. Accardo’s lab is creating 3D models that enable the formation of networks where brain cancer cells cluster and proliferate in vivo. The models are then treated with proton therapy to assess tissue response to the radiation. 

One way to fabricate these structures is the so-called two-photon polymerization (2PP) technique, which essentially applies laser beams to solidify liquid biomaterials. “By moving a laser beam, we can create 3D microstructures with a resolution that goes down to 200 nanometers, about 1000 times thinner than the diameter of human hair,” explains Accardo. 

These artificial models proved to be close to the natural ones, also significantly outperforming in vitro models—structures replicated on a flat laboratory slide. “We have seen that the DNA damage proton therapy inflicts on our 3D models is lower than that of their 2D counterparts,” underlines Accardo. “This is what we were hoping for, as previous studies on actual brain cancer tumors have shown the same evidence. Therefore, these 3D models reproduce better what is happening in the brain, and we hope to use them as a future benchmark tool for patients.”

Studying the correlation between autism and a rare genetic disease

A dozen people, including PhDs, postdocs, and master’s students, are part of the Accardo lab. Among them is Azza Jacobs, a biomedical engineering master’s student. She developed engineered cell micro-environments in the context of a larger project on brain organoids, autism spectrum disorder, and its possible genetic connection to Tuberous Sclerosis Complex (TSC). A rare genetic disease, TSC causes non-cancerous tumors or lesions in the brain and other parts of the body. Previous research has shown that people with autism spectrum disorder suffer from TSC, making it a potentially early marker to diagnose autism before symptoms arise. 

However, getting a child’s brain tissue is a very invasive operation. “What we do instead is to use induced pluripotent stem cells, obtained originally from reprogrammed skin cells of the patients. Then, we culture them within engineered scaffolds to become brain organoids,” explains Jacobs. Organoids are structures derived from tissue culture. However, the conventional scaffold-free growth of this tissue culture is often uncontrolled and varies from batch to batch. Furthermore, the inner parts of these structures often clump together, lacking vascularization and ultimately dying. 

As a remedy to these functional problems, Jacobs is using micro-digital light processing (µ-DLP), another 3D printing technique, to create scaffolds where these cultures can grow in a controlled manner. These porous hydrogel structures mimic the mechanical properties of brain tissues. “This way the cells can easily grow inside the scaffold, proliferating, and simulating the behavior of human brain cells,” Jacobs underlines. 

Culturing and comparing both healthy and TSC-affected brain cells takes several weeks to grow a mature structure. The goal is to study their behavior, morphology, and gene expression, ultimately paving the way for potential treatment options. This project was conducted in collaboration with the Amsterdam University Medical Center. 

Bone tissue culture

Another interest of the Accardo lab is the application of these techniques to bone tissue culture. Drawing full inspiration from nature, a significant difference between bone tissues and brain tissues is the higher stiffness of bone tissues, which is approximately six orders of magnitude more rigid than that of neural tissues. There is no shortage of ambition in this strand of research either. 

“For instance, we are working in collaboration with the Department of Biomechanical Engineering on meta-biomaterials designs for bone tissue engineering. Particularly, scaffolds with such properties can have a direct effect on the mechanobiology of bone cells. This aspect plays a fundamental role in prospective use as implants, such as total hip replacement, where the contact between the host tissue and the implant must be optimized to prevent infections,” explains the professor. 

Serving patients

The three Ps are certainly shaping the vibe of the research group, with Accardo being proud of the work done by his group and by the continuous influx of ideas and projects. Ultimately, the goal is to deliver the results of all these efforts to those who need them most: patients. 

“What I dream of is that, in ten years, we can utilize our approach to treat glioblastoma to perform minimally invasive biopsies in a patient’s tumor. Take those cells, culture them in our environment, assess the dose of proton therapy that yields the best results, and use this as a benchmark tool to apply directly to the patient,” he concludes. 

• Togo launches R21 malaria vaccine nationwide
• 269,000 children targeted across all 39 health districts
• Togo is the 22nd African nation to adopt R21 vaccine

Togo has launched the R21/Matrix-M malaria vaccine into its national immunization program, the Health Ministry announced in a press conference on Tuesday. The initiative, which began on September 1, 2025, aims to protect approximately 269,000 children in its initial phase, covering all 39 of the country’s health districts simultaneously.

The decision is a significant step in the nation’s fight against malaria, a major health challenge, particularly for children under five. Health and Public Hygiene Minister Tchin Darré stated that the move reflects the government’s goal to “liberate communities and families from the burden of malaria by 2030 so they can contribute effectively to the country’s development,” according to a statement from the World Health Organization (WHO).

This program is a collaborative effort involving the Togolese government, the WHO, UNICEF, Gavi, the Vaccine Alliance, and other technical and financial partners.

Malaria remains endemic across all regions of Togo, with cases surging during the rainy season due to the proliferation of mosquitoes. In 2022, children under five accounted for 64% of confirmed malaria cases, 32% of outpatient consultations, and 53% of hospitalizations in Togo. Hospital mortality for this age group was 65%, making them the primary target of this vaccination campaign.

The Togolese government has invested significantly in malaria control, including a $271.7 million budget for the National Malaria Control Plan. With this introduction, Togo becomes the 22nd country in Africa to incorporate the R21/Matrix-M vaccine into its national immunization schedule.

Ingrid Haffiny (Intern)

Adapted in English by Mouka Mezonlin

Scientists have found that the diabetes/weight loss drug Semaglutide, sold commercially under brand names like Ozempic and Wegovy, significantly reduces cocaine-seeking behaviour in rats. This work needs to be confirmed in humans, but it suggests that Semaglutide is a candidate to be developed as a treatment for cocaine dependency; at the moment there is no effective pharmacological treatment for cocaine dependency. The work is published in the September edition of the peer-reviewed journal European Neuropsychopharmacology.

Cocaine is the second most popular illegal drug used in Europe. The European Drug Agency reports that around 2.7 million young adults (between the age of 15-34) use cocaine regularly, representing around 2.5% of the population in that age group. Cocaine use in the UK is the second highest in the world, with around 2.7% of adults using the drug (see notes). There is, to date, no effective pharmacological treatment for problematic cocaine use.

Scientists from the University of Gothenburg in Sweden and the University of Pennsylvania, led by Professor Elisabet Jerlhag (University of Gothenburg), gave male rats access to directly-injected cocaine, which they could dispense by pressing a lever in the cage. Then an experimental group of 10 of these animals were treated with semaglutide before being given access to the cocaine dispenser.

Elisabet Jerlhag said:

“We found that in comparison to the control animals, self-administration of cocaine use dropped by 26% in those animals which had been given semaglutide. Previous results, both from our group and from other groups, have found that semaglutide can reduce alcohol consumption and craving in both humans and animals, and this work on cocaine seems to reflect these previous findings on alcohol use. This is the first trial showing Semaglutide’s potential as a drug for cocaine dependence.

Importantly, we also found that after a period of abstinence, there was a 62% drop in cocaine seeking in those animals which had taken semaglutide and the motivation (work undertaken to attain the drug) was lowered by 52%.

This is animal work, so at the moment, we can’t say that we have anywhere near a viable treatment for human cocaine dependency. We need a bigger study to confirm these results, and then we need to see if the findings also apply to humans. However, these results are very promising, underlining the need for human studies, especially since there are no existing pharmacological treatments for cocaine dependency”.

Semaglutide belongs to a class of drugs called GLP-1 inhibitors. These drugs (along with the similar drug Mounjaro) have revolutionised the treatment of excess weight, and are now showing promise in the treatment of mental health problems.

Commenting, Professor Christian Hendershot (of the Institute for Addiction at the Keck School of Medicine, University of Southern California, Los Angeles) said:

“This is a carefully conducted study that provides additional evidence that GLP-1 receptor agonists can reduce cocaine reinforcement. These findings have clinical implications given the challenges identifying medications for stimulant use disorder, and the increasing clinical use of semaglutide in many areas of the world. These findings should encourage clinical trials of GLP-1 receptor agonists for stimulant use disorder”.

Professor Hendershot was not involved in this research; this is an independent comment. Professor Hendershot was lead researcher on the first randomized, placebo-controlled clinical trial of semaglutide’s effects on alcohol craving in adults.

A protein particle hidden within the SARS-CoV-2 virus could lead to longer-lasting, more protective vaccines for COVID-19. 

Scientists from La Trobe University and Kumamoto University in Japan have discovered that the body’s immune system strongly reacts to an internal protein from SARS-CoV-2, the virus that causes COVID-19, which mutates less frequently than the surface-spike protein currently targeted by vaccines.

New research published in Nature Communications shows that these protein particles, known as peptides, appear on the surface of infected cells via an immune molecule called HLA-C, which killer T cells then use to identify and eliminate infection. 

La Trobe University lead researcher Distinguished Professor Stephanie Gras, Deputy Director of the La Trobe Institute for Molecular Science (LIMS), said the discovery could open the way for the development of new vaccines and treatments that offered protection across multiple strains of the SARS-CoV-2 virus.

“Currently, vaccines target the spike proteins that decorate the surface of the virus – but they mutate frequently as they are constantly under pressure by our immune cells, which means we might need a new vaccine for each new variant,” Professor Gras said. 

“We found that the killer T cells, which also fight infection, can be activated by a protein that forms a part of the shell that protects the virus’s genetic material, like the yolk of an egg. 

“Because this protein is inside the virus, it mutates much less frequently – knowledge which could guide the development of vaccines and therapeutics that are still effective as the virus evolves.” 

Professor Gras said the development of a longer-lasting vaccine could mean that people would need fewer booster vaccines to fight COVID, and help protect against the development of Long COVID.

“The more people get vaccinated, the more we’re protecting the population, which helps to reduce the virus’s death toll and the impact of the infection itself,” Professor Gras said. 

“But there is more than just COVID – we now know that about 10 per cent of the population is impacted by Long COVID and the more you catch the virus, the more likely you can develop Long COVID.”

Professor Gras, Dr Demetra Chatzileontiadou, Dr Janesha Maddumage, and PhD candidate You Min Ahn led the research team at LIMS and La Trobe University’s School of Biomedicine, Agriculture and Environment (SABE).

It was funded through Professor Gras’s National Health and Medical Research Centre (NHMRC) Leadership Investigator Grant (L2) and her Medical Research Future Fund (MRFF) grant to investigate COVID. 

The research was done in collaboration with Associate Professor Chihiro Motozono and Yoshihiko Goto from the Joint Research Center for Human Retrovirus Infection at Kumamoto University in Japan, with data collection by the Australian Synchrotron. 

Professor Gras will also lead a new research centre at La Trobe University which aims to uncover the cause of Long COVID and other life-limiting post-viral infections such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Multiple Sclerosis (MS). 

The Post-Acute Viral Infection diseases Group (PAVING) Centre of Research Excellence has received $3 million in Federal funding from the National Health and Medical Research Council (NHMRC).

Breakfast is one of the most unique meals of the day because it’s consumed after a long fast. (Hence the name “break” “fast.”) If you have diabetes, you may want to know what time you should eat breakfast. Right after waking up? Post-coffee? Wait a little bit?

The real answer to this question is that everyone’s needs are unique. Individualization runs deep when it comes to managing diabetes because a variety of factors, including your pre-meal blood sugar, hormones, medication and schedule all play into your choice. In short: What works for you may not work for someone else. 

To dive deeper into this discussion, we asked diabetes care and education specialists (CDCES) living with diabetes about breakfast timing, meal composition and factors that can influence when and what they eat for breakfast. Here’s more about how to time your breakfast right.

When To Eat Your First Meal of the Day

When it comes to diabetes, you need to put yourself first because there’s no right or wrong way to break your fast. What matters is that you find the pattern that works for you.

“I don’t recommend a specific time for eating breakfast because the best time is very individualized and differs for every person,” says Mary Lechner, RN, CDCES, who has lived with type 1 diabetes for over 25 years. “For me personally, I eat breakfast based on whether I am hungry and what my blood glucose level is. I do not force myself to eat breakfast if I am not hungry,” she explains. 

Lauren Plunkett, RDN, CDCES, who lives with type 1 diabetes, agrees with not providing blanket recommendations because there are so many factors that can affect your levels. “Blood glucose can be especially reactive in the early morning due to physiological factors. It’s constantly affected by hormones, nutrition, stress and exercise, and this influence varies individually and is often unpredictable,” she explains. 

To help take these factors into account, test your blood sugar often. “One of my best strategies is to check your blood glucose levels before eating and two hours after to be able to know if your breakfast plan worked well,” says Smithson. If you notice that your blood sugar is above goal, you may need to make changes to your breakfast meal, exercise regimen or medications, she says. For example, walking after a meal is a powerful tool to help manage your blood glucose levels. It’s something you can incorporate into your routine if your breakfast unexpectedly causes a rise in blood sugar.

Why Breakfast Matters for Blood Sugar

What you eat for breakfast matters for your health. It plays a role in metabolism, provides sustainable energy and delivers important nutrients for your well-being. In addition, breakfast can be protective against chronic inflammation and the disease risks that go with it.

“There are several truths behind the adage, ‘Start your day with breakfast,’” says Toby Smithson, M.S., RDN, CDCES, who has been managing diabetes for more than five decades. “Consuming breakfast may help manage blood sugar by disrupting a spike in glucose levels throughout the day, [which] allows for our intake of carbohydrates to be spread out throughout the day, offers an opportunity to obtain nutrition (it’s hard to get all our nutrition squeezed into two meals) and helps us feel fuller until lunchtime,” she explains.

How to Build a Balanced Morning Meal

Breakfast does not have to mean juice, eggs, bacon or cereal and milk, says Plunkett. “Beans, vegetables, fruit and greens can be eaten, and regular intake of whole plant foods contribute to long-term insulin sensitivity,” she says. These types of whole plant foods are low in saturated fat and rich in fiber. Fiber can help keep us full, contributes to gut health and regulates blood sugar. 

When planning a meal, including breakfast, Smithson uses the American Diabetes Association’s Diabetes Plate Method. Half of the plate is filled with non-starchy vegetables, one-quarter is lean protein and one-quarter is a quality carbohydrate. “Building a healthy breakfast revolves around combining a source of lean protein and a source of quality carbohydrate to keep blood glucose steady,” she says.

In addition, Smithson says she has been eating high-fiber oatmeal combined with protein powder and an egg white wrap filled with bell peppers and onions. These are foods that she prefers and that nourish her body. She makes adjustments based on her blood glucose and activity level. 

Knowing what foods work for you is advantageous to maintaining energy and managing blood glucose levels. Alternatively, knowing which foods don’t work well for you can be equally important. 

For example, Lechner points out that her blood sugars rise more quickly (and her hunger is not satisfied) if she eats cereal with milk compared to nut butter spread on toast.

Our Expert Take

If you have diabetes, the best time to eat breakfast will depend on a variety of factors. Professionals living with diabetes say that the time and type of breakfast they eat varies depending on what their blood sugar is, what they are in the mood for, if they are going to exercise and more. These are all things you can consider when deciding when the best time is for you to eat breakfast.

Foods that are higher in fiber and protein can help you manage your appetite and blood sugar while hitting your nutrient needs. Choosing foods like fruits, vegetables, whole grains, lean proteins and legumes might be a good place to start. For personalized nutrition information, reach out to a registered dietitian or certified diabetes care and education specialist.

Kirsten Smith was 16 when a boy from school injected her with morphine, 18 when she and a date Googled how to crush up and inject themselves with oxycodone, and 19 when she first shot up heroin. Living in Knoxville, Tennessee and modelling herself on Pulp Fiction’s freewheeling Mia Wallace, Smith spent her days experimenting with alcohol, cannabis, ecstasy, mushrooms, LSD and benzodiazepines. She read Kurt Vonnegut and the Beats, and wrote poems on an actual typewriter while listening to the Velvet Underground. For Smith, as for thousands of Americans who came of age in the early 2000s, drug use was a seemingly harmless lifestyle choice.

That is, until she ran out of money. After Smith dropped out of high school and started regularly using heroin, she was caught stealing credit cards and chequebooks from a boyfriend’s wealthy parents, from a family friend at church and from her grandmother. On probation for two years, and forced by her parents into a month-long stay at an addiction treatment facility, Smith felt, for the first time, ashamed.

Returning to school was supposed to be Smith’s lifeline. She went to community college and got a job as a waiter at Charlie’s, a local restaurant chain. Then, in the summer of 2004, she met Brad Renfro, who had starred as a child actor in Hollywood films such as The Client and Sleepers. He introduced her to smoking crack cocaine and the best heroin she had ever known. After three months together, Smith began to wonder whether she would be a junkie for the rest of her life.

One day, standing in the living room of Renfro’s downtown boarding house, Smith watched him struggle to find a vein. Blood ran down his arm as he plugged in the dregs of his cocaine supply, a residue shot that Smith called a “low sad point in an addict’s life”. For her, Renfro had crossed a line into the shadowlands of compulsion. It was over between them. (Smith didn’t hear of Renfro again until he died of an overdose in 2008.)

While waiting on tables at Charlie’s, Smith met a young man named Michael, who had grown up in the same suburb as her. Michael was quiet and kept mostly to himself. His buzz cut and angular features contrasted with his sweet smile and blue eyes. The two clicked when Smith revealed that she had sent a fan letter to the author of Fight Club, Chuck Palahniuk, and had received a written response. Michael didn’t believe her until Smith brought the letter to work, dusty and charred by a house fire Smith had started when she was 15.

In 2005, Smith and Michael rented a one-bedroom apartment in an old building downtown. They also did drugs together, shoplifting to subsidise their lifestyle, which Smith described as a “romanticised junkiedom”. Through their network of white suburban addicts, Michael and Smith became hooked on expensive black tar heroin shipped in by a drug cartel that they referred to as “the Mexicans”. Despite their addictions, Smith and Michael maintained a stable, domestic existence. They wrote stories, paid their bills and owned two cats.

Later that year, Smith and Michael were both admitted to the University of Tennessee. This was Smith’s cue to get sober, but treatments for substance-use disorders and the torturous symptoms of withdrawal were limited. Relatively few medications were approved, and although behavioural and community-based treatments existed, when Smith, 23, tried to return to rehab, her stepfather’s insurance company rebuffed her.

The couple attended meetings at Narcotics Anonymous (NA), a 12-step programme, where they were told that recovery was only possible with total abstinence and strict adherence to a set of rules. To them, it seemed as if they were being made to feel helpless in the grip of their addictions, which were thought of as a lifelong disease. The concept, pervasive in treatment, that addiction is a disease, emphasises the power of compulsions to overwhelm the individual. The problem, Smith told me, was that no one asked or cared about what her desires were. “When I was young and wanted to be a heroin addict, my behaviours were in line with my desires. Was that addiction?”

After she was accepted to university, Smith continued to use heroin. This was less of a personal failure, in her view, and more of a series of decisions she made to try to pursue both drugs and education at the same time. As long as Smith had access to drugs and wanted to use, she was not going to choose abstinence. On one occasion, Smith and Michael flung their unused needles and syringes down a garbage chute, desperate to begin their fresh start. Within hours, they dived into a skip to get them back.

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After she was caught nodding out in front of customers, Smith was fired from her job, and later, so was Michael. Broke and withdrawing, they lay in bed until sunrise, racking their brains for fast money schemes to pay for heroin. Smith remembered hearing about an unsolved bank robbery near her parents’ home. The bank was a small redbrick building in an ideal location, abutting the entrance of the expressway, and it would be open at 8am.

While Michael slept, Smith collected her supplies: an Airsoft gun her stepfather had bought her for Christmas, the bright orange tip painted black; supermarket bags, a scarf to wrap around her head, and a pair of Jackie O sunglasses.

When she walked up to the front desk of the SunTrust bank and pointed her toy gun at the teller, Smith said: “You have 60 seconds to put money in these bags.” When the teller returned the plastic bags, Smith apologised and said: “Thank you.”

As her Volkswagen sped down Northshore Drive, a pack of dye in one of the bags detonated, staining the bills red and filling the car with scarlet smoke. On the expressway, Smith got out, tore the duct tape off her licence plate, and barrelled home. Stumbling into her apartment, Smith woke Michael up. After soaking the bills in their bathtub with water and bleach, they salvaged about $11,000, enough for two months of rent, food, and heroin.

The second robbery was more carefully planned. This time, Smith waited in the car while Michael went inside. But someone saw him leave the bank, and before they could get away, Smith and Michael were arrested.

Awaiting trial under house arrest at the home of her mum and stepfather, Smith handwrote letters to Michael, who was also under house arrest just a couple of blocks away. She told him about the cocktail of medications she was given, which included Xanax and Focalin, a stimulant used to treat ADHD that enabled her to write poetry, a “countdown to prison” journal and a 450-page novel, all in a week.

Smith also drank heavily during this time. One night, with an ankle monitor on, she drove off drunk in her stepfather’s new car. Within two miles, she crashed into a tree and ended up in an emergency room downtown. With blood all over her face and wires holding her teeth together, Smith looked down and saw that she still had her bag, containing her syringe. She remembers that the first thing she thought was: “I still have time to buy heroin.”

In December 2007, at Smith’s sentencing hearing, her stepfather testified that he hoped she would get the treatment she needed to overcome her problems. “She is a smart person who has made some mistakes,” he said. “Made them willingly.”

Was Smith a patient simply in need of the right medications or a criminal who deserved punishment for actively choosing to harm others – or both? Before the hearing, in a character letter sent to the judge, Thomas Varlan, Smith chose to take responsibility for her crimes. “I wasn’t abused or molested as a child,” she wrote. “I didn’t grow up on the ‘wrong’ side of town. I wasn’t raised by wolves but by a mother and stepfather who love me and gave me countless opportunities to succeed.”

Smith was steadfast in her belief that her actions were volitional from the start. Her drug use and crimes were not the products of an immoral character or a faulty brain incapable of change, but rather of an environment where heroin was accessible and desirable. This outlook determined her experiences in prison and beyond, ultimately leading her to dedicate her life to challenging predominant medical models of addiction with her research. Today, she is an assistant professor of psychiatry and behavioural sciences at Johns Hopkins University in Baltimore, Maryland.

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In light of the non-violent nature of their crimes and their youth, Judge Varlan sentenced Smith to 47 months in custody and Michael to 46 months, the minimum duration for their charges. Smith’s first destination, Blount county jail, was a concrete bunker or, as she put it, a “hell”. She went into drug withdrawal without a doctor to manage her symptoms. Without medical care, she had to remove the wires in her mouth with a fork.

Locked down 23 hours a day for two weeks with a wide-eyed stranger who rocked back and forth while withdrawing from cocaine, Smith, for the first time in her adult life, had no access to drugs or the outside world. The only reading material she had in the tiny room was a pocket-sized copy of the Gospels of the New Testament that community volunteers placed through a slot in the jail cell door. Smith read the words repeatedly to fall asleep; when she woke up, she started reading them again. After nine months, she was shipped to federal prison in Florida.

In Smith’s account of her story, no amount of psychiatric diagnoses or personal reflection helped her quit heroin. The only things that did were incarceration and forced abstinence, followed by her return to education. In prison, it occurred to Smith that there were only two things people could not take away from her: “my tattoos and my education”. After she was released, at the age of 27, she got a job serving sandwiches at a deli that hired former convicts – including Michael, although their romantic relationship was over. Smith stayed sober and was eventually accepted by the University of Kentucky, which – unlike some other institutions – did not require students to disclose past criminal charges. She excelled, and after four years of college went on to graduate school with the hope of becoming an addiction therapist.

Doing shifts at a rehab facility in 2015 while completing her master’s, Smith had a formative encounter with a man in his 20s who was detoxing from opioids. The patient mentioned to her that he had been drinking “a tea from Vietnam” called kratom. He said it soothed his anxiety and helped with his cravings for opioids. Although kratom is described by organisations such as the CDC as a stimulant, the patient said it did not make him feel high. However, the rehab facility enforced an abstinence-only approach to treating addiction, and Smith was required to report the young man. After he was kicked out of rehab, he stayed in contact with her, and told her about his commitment to achieving abstinence through the 12 steps. Two weeks later, he tried heroin and died from an overdose.

In an essay titled Disease and Decision, published in 2022 in the Journal of Substance Abuse Treatment, Smith wrote about how, disillusioned by medical systems with no individualised or evidence-based care, she decided to change careers and turn her ambitions towards research. Often, Smith argued, people with substance-use disorders are actively discouraged from vocalising what they want from the recovery process. “If they try, they are told that they are selfish; that their character defects and thinking were what got them into trouble; and that thinking for themselves is dangerous.”

For Smith, free will is a spectrum, and yet many volitional behaviours get jumbled together under the label “addiction”, as if people with substance-use disorders have permanently lost control over their actions. She believes that although her desires, intentions and choices were constrained by factors that developed from continued drug taking – such as a lack of access to medical care, running out of money, being locked out of the university system – she maintains her behaviour was always the result of conscious decisions. For the same reason, she emphasises that lifelong cravings and relapses are not inevitable. Like everyone else, people who use drugs are “complex systems that can change”, and she believes that they should be held responsible for enacting that change.

Smith is thin and pale, with green eyes and dark curly hair. Her arms are covered in tattoos. On her right forearm, sealing the spot where she used to inject most frequently, are the words “Room 101”, the location in George Orwell’s Nineteen Eighty-Four where Winston Smith betrays his lover to escape his greatest fear. When she was incarcerated, relapsing became Smith’s greatest fear. “That’s the betrayal,” she told me. “I would have broken my mother’s heart, and broken the people who invested love and hope in me.”

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The idea that addiction is a bodily disease was articulated in 1884 by the Scottish physician Norman Kerr. In his inaugural address to the Society for the Study and Cure of Inebriety, he said that addiction to alcohol is “for the most part the issue of certain physical conditions”. He continued: “Whatever else it may be, in a host of cases it is a true disease, as unmistakably a disease as is gout, or epilepsy, or insanity.”

Yet throughout most of the 20th century, a different model of addiction predominated in popular culture. The “moral model” sees addiction not as a disease of the body but of the will. Partly as a result, numerous countries adopted a penal approach to drug use that, particularly in the US, led to vast numbers of people being imprisoned for substance abuse.

A turning point came in 1997, when the then-director of the National Institute on Drug Abuse (Nida), psychologist Alan Leshner, published an article in the respected journal Science, in which he argued that addiction should be treated not as a moral failing but primarily as a chronic, relapsing disease of the brain. Addiction, according to Leshner, starts with voluntary consumption of drugs but over time the addictive qualities of the drug hijack the individual’s decision-making with uncontrollable cravings and compulsions.

When I spoke to Leshner earlier this year, he explained how he sought to change addiction from a criminal issue into a public health problem that could be treated with medication instead of incarceration. He had been inspired by how advances in neuroscience had shifted cultural assumptions about people with schizophrenia, who had come to be viewed in a far more humane manner: as people with neurological diseases who deserved medical care. “It became clear to me,” Leshner said, “that a core difference between addicted and non-addicted people was the same as the core difference between individuals with and without schizophrenia – which is that they have changes in their brains.”

Leshner stands by his 1997 article, in which he recognised the importance of environmental and socioeconomic factors on persistent drug use but argued that over-emphasising social and spiritual solutions to addiction only worsened “the tremendous stigma attached to being a drug user or, worse, an addict”. (By overturning the moralistic attitude towards drug use, Leshner also sought to justify putting medications such as buprenorphine – a weak opioid restricted because of its potential for abuse – into doctors’ offices and prisons.)

Leshner’s approach, known as the brain disease model of addiction or BDMA, became the model for teaching addiction in medical schools in the US and beyond, as well as shaping drug education campaigns in schools. However, this approach has itself come under attack. Critics of BDMA, such as Smith, believe that downplaying the role of free will in addiction can dampen the belief that full recovery is possible. Smith does not deny that brains change from drug use – the impact of addictive substances on the brain’s reward pathways is well established – but claims that a perception of people with substance-use disorders as “recovering” but never “recovered” does little to improve the general understanding of addiction and can destroy any shred of hope that they may hold. Smith argues that terms such as “chronic” and even “disease” can push people with substance-use disorders and the people around them to see relapse as “an inevitable outcome”.

Similarly, Eric Strain, an addiction psychiatrist who has helped mentor Smith at Johns Hopkins University, argues that the BDMA oversimplifies our understanding of addiction. The BDMA, according to Strain, says doctors know what people with substance-use disorders need. “It implies: ‘Just take Suboxone, everything will get better’,” Strain explained to me, referring to a commonly prescribed medication. But things are not always so simple. “Look at the treatment dropout rates,” he said. “They’re abysmally high.”

The label of “disease” has trailed Smith for most of her adult life. After she obtained her PhD, which studied the treatment of substance-use disorders in incarcerated women, Smith went on to complete a four-year research fellowship at Nida, the centre of American addiction research. But her postdoctoral position came with conditions: she was forbidden from handling any of the money used to pay research participants or the drugs being tested in the labs. The issue of trust, and the assumptions people made about her capacity to function and resist relapsing, would not go away.

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Smith belongs to a new generation of addiction scientists who are using their personal experiences to inform their research. Their focus is on helping people with substance-use disorders to identify the environmental factors that lead them to use drugs, and encouraging them to take action to change those factors.

In Smith’s own research at Johns Hopkins, which includes clinical trials and lab-based pharmacological studies, she interviews people with substance-use disorders about their experience of self-medication with unregulated substances like kratom. Instead of asking how the medical system can best force people into sobriety, Smith’s research asks how people with substance-use disorders have learned to manage their addictions themselves.

Justin Strickland, a behavioural pharmacologist who worked with Smith on models of addiction that emphasise environmental triggers, told me that there is actually more agreement than disagreement between supporters and detractors of the BDMA. “We all know that addiction is affected by neurobiology, genetics and childhood trauma,” he said. “The differences are in what is emphasised.” As the psychiatrist Carl Erik Fisher, who had an alcohol-use disorder during his medical training, wrote in his recent book about addiction, The Urge: “It is not that addiction is or is not a brain disease, or a social malady, or a universal response to suffering – it’s all of these things and none of them at the same time, because each level has something to add but cannot possibly tell the whole story.”

In the past five years, organisations such as Nida and the National Institutes of Health (NIH) have increasingly supported research into psychosocial approaches to addiction, harm reduction and methadone clinics, as well as community-based services that emphasise continuity of care. Meanwhile, some addiction scientists with histories of substance-use disorders think that the BDMA debate is still worth having. Noel Vest, a friend of Smith’s who is now an academic, began to use methamphetamines at the age of 21 and became addicted to alcohol. By 25, he had lost his business, his car and his house. After seven years in prison for multiple offences including identity theft, Vest became a drug and alcohol counsellor, which he abandoned when he realised his work was merely an extension of the criminal justice system he had just left. Treatment failure and missed appointments were an inherent part of recovery, and he refused to punish people for what he saw as the natural course of addiction. While on parole, Vest attended a local university and went on to complete a PhD in experimental psychology.

For Vest, the problem is not the BDMA itself but how early the concept of disease and the necessity of treatment is forced on to people with substance-use disorders. “If you tell someone early on in addiction – someone who can’t even tie their shoes because they can’t put a thought together – that they have this lifelong condition that will never get better, that’s a huge leap most are not ready for.”

In many of my conversations with scientists both for and against the BDMA, one idea kept coming up: indeterminism. In an indeterministic model of addiction, any outcome, whether that be relapse or recovery, is neither predestined, nor fully within our control. The structure of the brain and one’s environment, as well as the influence of one’s past, are dynamic processes that we can study and attempt to shape, either through policy, treatments or personal choices. Hope and courage can coexist with chaos and chance.

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In our conversations, Smith always maintained that her drug taking was a choice, and that she was saved from hitting rock bottom by her upbringing, which she frequently described as perfect. “I wasn’t abused,” she told me. “I practised violin. I had a lot of protective factors. A lot of people in prison do not have those things.”

Still, Smith’s childhood was not always straightforward. She describes her mother as a “good stay-at-home mother”, but she was also eccentric and volatile. When she divorced Smith’s father after 12 years of marriage, she plunged into a depression that she never fully rose out of. (“I had two people, whom I trusted and loved, telling me that the other person was evil,” said Smith, who was six when their drawn-out custody battle began.) While Smith was under house arrest, her mother attempted suicide for the first time. Returning home from prison years later, Smith found that her mother’s place was now packed with clutter. Her mother slept in the middle of the day, heavily medicated and not able to leave the house. In 2024, her mother died from complications with her medication regimen after a long struggle with mental illness. Months later, Smith’s stepfather also died.

It was in the period after her mother and stepfather’s deaths that Smith was hired as an assistant professor at Johns Hopkins. Last year, the district court in Knoxville invited Smith to speak at a graduation ceremony for a programme called Full Circle that allowed people in prison with substance-use disorders to leave federal probation early after a year of working with a mentor.

At the ceremony, Smith met the judge who had sentenced her all those years ago. The memory of that day, probably the bleakest of her existence, was a blur. “I remember looking up at this thing that was clearly a judge,” she recalled. “But I was crying so hard when I addressed him that I only remember sobbing.”

It was difficult to look him in the eyes. Judge Varlan was a head taller than Smith, with a wiry frame and a clean-shaven face. She was surprised how quiet he was. His cadence was slow, his demeanour laconic, but his smile was warm and fatherly. To the judge’s wife, Smith expressed how nervous she was to meet them. Mrs Varlan smiled with tears in her eyes, and reassured Smith that the judge had been looking forward to her visit.

In her speech, Smith told the graduates: “Most of us in this room are likely hard-headed and stubborn. Turning that stubbornness in the right direction can be a powerful thing.”

Shoulder to shoulder with Judge Varlan, Smith watched a dozen or so ex-inmates walk across the stage, many starting over at an older age than she had. It sank in how rare “full circle” moments were for people like her. She had willed it into existence by remaining, as the judge and his wife, and Smith’s mother and stepfather had been, stubborn about her ability to change.

Published on
04/09/2025 – 6:00 GMT+2

Loneliness is a common problem – and it’s expensive to health systems, according to a new analysis from the United Kingdom.

People who are often lonely cost the UK’s National Health Service (NHS) up to £885 (€1,024) more annually than their more sociable peers, according to the estimates, which were published in the journal PLOS One.

Researchers surveyed more than 23,000 Britons on their levels of loneliness, well-being, and health care visits from 2021 to 2023, and used the figures to estimate their health costs.

They found that eight per cent of people often experienced loneliness and another 32 per cent were lonely some of the time.

Loneliness was tied to mental distress, worse mental well-being, poorer physical health, and lower quality of life, the study found. Lonely people were also more likely to visit their general practitioner (GP) or the hospital than people who were not lonely.

“Our findings highlight the importance of recognising loneliness as both a public health issue and an NHS priority,” Antonieta Medina-Lara, one of the study’s authors and a professor of public health economics at the University of Exeter, said in a statement.

“Too often overlooked, loneliness carries substantial personal and societal costs,” she added.

The UK is far from the only country grappling with loneliness. The World Health Organization (WHO) estimates that loneliness affects 16 per cent of people worldwide, and views social disconnection as a “serious threat to global health”.

Social isolation and loneliness are linked to a higher risk of heart disease, type 2 diabetes, depression, and anxiety, according to the WHO.

Several countries, including the UK, have launched national plans to combat loneliness in recent years, to foster both in-person and online connections between people who may be at risk of loneliness or social isolation, such as older adults.

The latest study indicates that age also plays a role in the health spending gap. Lonely young people and seniors incurred much higher costs than their non-lonely peers, a disparity that narrowed for people in midlife.

The researchers said they hope that more awareness of loneliness’s complex personal and societal consequences will lead to more concrete steps to address it.

“By making these visible, we hope to encourage new approaches to help people build connections, improve well-being, and ultimately reduce the burden on health services,” Medina-Lara said.

A broad swath of neuropsychiatric conditions, including autism, depression and schizophrenia, share genetic underpinnings. But individual variants can have strikingly different effects on clinical diagnoses: A variant that increases the likelihood of one condition may reduce that of another, according to two new preprints.

“When you delete and duplicate genes, you get very different, often diametrically opposed, outcomes,” says Jonathan Sebat, professor of psychiatry and cellular biology at the University of California, San Diego and co-principal investigator of the studies. He and his colleagues analyzed whole-genome sequencing data from 574,965 people, collected at dozens of institutions as part of the Psychiatric Genomics Consortium, a massive international project aimed at finding common variants in psychiatric conditions.

The work, posted on medRxiv in July, revealed nearly three dozen links between copy number variants (CNVs)—deletions or duplications of small segments of DNA—and any of six different neuropsychiatric conditions: autism, attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder, post-traumatic stress disorder (PTSD) and schizophrenia.

Nearly all of these rare variants are tied to more than one diagnosis, one of the studies shows. But duplications and deletions can have different and sometimes opposite effects: If a deletion raises a condition’s likelihood, the corresponding duplication may lower it, and vice versa.

Autism was unique in that no deletions or duplications decreased autism probability, whereas some variants lowered the chances of having schizophrenia or one of the other conditions, Sebat says.

“What was surprising is that sometimes a gene duplication can be protective,” says Hyejung Won, associate professor of genetics at the University of North Carolina School of Medicine, who did not contribute to the studies. “That provides a lot of food for thought. How does excessive expression of a gene protect you from another disorder?”

The six neuropsychiatric conditions analyzed in the first study converge on a common set of molecular pathways but are associated with distinct cell types, brain regions and gene dosages, according to the other study.

“The overlapping biology of these disorders might not be quite as overlapping as we would have thought,” says Jason Lerch, professor of neuroscience at the University of Oxford, who did not contribute to the research. “This is important stuff.”

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ecause the list of thousands of genes linked to neuropsychiatric conditions doesn’t say much about how those genes affect psychiatric traits, Sebat and his colleagues turned to deletions and duplications, which predictably alter gene dosage—an approach akin to studying gain- or loss-of-function variants, he says.

Genome-wide association studies involving participants grouped according to six psychiatric diagnoses revealed a total of 35 associations between rare CNVs and least one of the conditions. In the case of schizophrenia, for example, deletions in the 22q11.21 A-D chromosomal region significantly increase likelihood, whereas duplications decrease it. And the effect sizes of schizophrenia-linked reciprocal deletions and duplications are inversely correlated, indicating a linear dose-dependent relationship between gene copy number and a person’s chances of having schizophrenia.

A similar pattern held for other chromosomal regions and diagnostic categories, but not all.  Autism was a notable exception because no CNV decreased the likelihood of having the condition—perhaps because autism encompasses a particularly broad spectrum of traits, Sebat says.

The second study identified gene sets based on the genes’ roles in molecular pathways, along with cell types, brain regions and gene dosage (duplication or deletion), and then determined which genes sets correlated with which psychiatric conditions by way of a gene-set burden analysis.

All of the 35 CNVs flagged in the first study act on a small set of molecular pathways, such as MAPK signaling, synaptic transmission or chromatin regulation, the second study showed. “All of the same 19 canonical pathways are involved in all disorders,” Sebat says. And separating these pathways by cell type and brain region in addition to gene dosage showed further distinctions among conditions, he says.

This multidimensional analysis provided three unique factors, or signatures, that captured the neurobiological processes involved in each condition. Schizophrenia, for example, is strongly associated with factor 1, a set of genes involved in chromatin regulation and MAPK signaling, specifically in postnatal excitatory neurons, microglia and vascular cells. And it is linked primarily to duplications in cell signaling and metabolic pathways in postnatal excitatory neurons and neurovascular cells, as well as to deletions in inhibitory interneurons.

This pattern supports the hypothesis that schizophrenia is associated with an imbalance in excitation and inhibition, Sebat says.

Autism is also strongly correlated with factor 1—a finding that aligns with past studies that point to microglia and postnatal excitatory neurons, as well as chromatin remodeling. But both duplications and deletions linked to autism act on the same pathways and cell types in most cases. In addition, deletions that increased autism likelihood were linked to a decrease in schizophrenia risk, the study showed.

Factor 2, which is associated with mood disorders, isn’t strongly tied to specific pathways and involves changes in non-neuronal cells. Factor 3 separates conditions by brain region: In bipolar disorder, for instance, deletions are concentrated in frontotemporal regions, whereas in ADHD, depression and schizophrenia, they are more common in sensory regions.

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he directional effects of duplications and deletions are interesting, says Mark Gerstein, professor of biomedical informatics at Yale University, who was not involved in the research. But duplications and deletions do not lead only to increases or decreases in protein expression, he says. In practice, both can also lead to novel protein functions or disruptions that weren’t captured in the study’s analysis.

Sebat contends that the general equivalence between gene copy number and protein expression holds, but he adds that deletions and duplications can both disrupt gene functions in unpredictable ways. “There’s still a lot we don’t know,” he says.

Ultimately, the findings could one day help clinicians distinguish different clinical presentations of heterogeneous diagnoses such as autism, Sebat says.

Won agrees. If this line of study can identify “some disease specificity,” she says, “we can diagnose individuals with better genetic etiology and find tailored therapeutic options.”

A new study reveals the profound emotional and physical toll of extreme morning sickness, with more than half of affected women reporting they considered terminating their pregnancy, and 9 in 10 saying they had thought about not having more children.

The national survey, published in PLOS ONE, is one of the most comprehensive investigations into the lived experience of hyperemesis gravidarum (HG)-a severe form of nausea and vomiting in pregnancy – in Australia.

It highlights not only the debilitating nature of the condition but also the inconsistent effectiveness of commonly prescribed treatments.

Lead author Associate Professor Luke Grzeskowiak, a pharmacist and researcher from Flinders University, says that the findings underscore the urgent need for more compassionate, evidence-based care for pregnant women experiencing HG.

“Hyperemesis gravidarum is not just morning sickness-it’s a serious condition that can have devastating consequences for women’s mental health, relationships, and decisions about future pregnancies,” says Associate Professor Grzeskowiak.

“Our study shows that many women are not getting the support or relief they need, and that’s something we must urgently address.”

The survey of 289 Australian women found that 54% had considered terminating a pregnancy due to HG symptoms, while 90% had considered not having more children.

The condition was also linked to high rates of anxiety and depression, with 62% of respondents reporting they ‘often’ or ‘always’ experienced these feelings during pregnancy.

Despite the severity of symptoms, only half of the women surveyed rated commonly used treatments as effective.

Ondansetron, doxylamine and corticosteroids were perceived as the most effective medications, yet many women reported significant side effects, including constipation, sedation, and impaired cognition.

Metoclopramide, another frequently used drug, was discontinued by nearly one-third of users due to adverse effects.

“Women are often prescribed multiple medications in an attempt to manage their symptoms, but the reality is that many of these treatments come with their own burdens,” says Associate Professor Grzeskowiak.

“We need better evidence to guide treatment decisions and ensure women are supported to make informed choices.”

Beyond the physical symptoms, the study paints a dismal picture of the broader impact of HG on women’s lives.

More than half of respondents reported major disruptions to their ability to work, care for children, maintain relationships, and perform daily tasks. Thirty-seven per cent requested early induction of labour to end their pregnancy sooner due to the severity of their symptoms.

Caitlin Kay-Smith, founder of consumer organisation Hyperemesis Australia and co-author on the study, says the findings should prompt a shift in how HG is understood and managed in clinical settings.

“Too often, women’s symptoms are dismissed as a normal part of pregnancy, when in fact they are experiencing a condition that can be life-altering,” she says.

“We need to move away from a one-size-fits-all approach and toward personalised care that recognises the full impact of HG.”

The study was co-designed with Hyperemesis Australia and supported by the Robinson Research Institute at the University of Adelaide. It calls for further research into the long-term effects of HG and its treatments, as well as greater investment in support services for affected women.

Associate Professor Luke Grzeskowiak says the message from women was clear: “They want to be heard, believed, and treated with dignity.”