Publisher Health

People who use both cannabis and tobacco show measurable differences in brain activity compared to those who rely solely on cannabis, according to new findings from a McGill University team at the Douglas Research Centre.
These results may help clarify why people who combine the two substances more often experience symptoms such as anxiety and depression, and why attempts to quit cannabis tend to be more difficult for them than for people who avoid tobacco.
“This is the first evidence in humans of a molecular mechanism that may underlie why people who use both cannabis and tobacco experience worse outcomes,” said lead author Rachel Rabin, Associate Professor in McGill’s Department of Psychiatry and researcher at the Douglas.
“Identifying this mechanism is an important step toward finding targets for future medications to treat cannabis use disorder, especially among those that co-use tobacco. Right now, the only available treatments are behavioral therapies such as counseling,” she said.
Co-Use Common Even as Tobacco Use Declines
In Canada, roughly one in 20 people who used cannabis within the past year are considered at risk for cannabis use disorder. Among people who consume cannabis more often, the rate jumps to about one in three.
The researchers note that tobacco use is decreasing overall, yet the majority of cannabis users still report using tobacco as well. Rabin explained that most previous studies focused on each substance separately, leaving a major gap that this early-stage research is beginning to fill.

Changes in the Brain’s “Bliss Molecule” System
PET scans showed that people who used both cannabis and tobacco had elevated levels of FAAH when compared to those using cannabis alone. FAAH is an enzyme that breaks down anandamide, a naturally occurring compound often described as the “bliss molecule” because of its influence on mood and stress responses. Higher FAAH levels mean lower anandamide levels, a pattern that has previously been linked to anxiety, depression and higher relapse rates among people trying to stop using cannabis.
Small Study Offers Early Clues
The analysis involved 13 young adults. Eight used only cannabis, while five used cannabis and smoked cigarettes every day. Cannabis use averaged slightly above one gram per day. Cigarette intake ranged from one to 12 per day.
Because the data was originally gathered for an unrelated project, there was no tobacco-only group for comparison. This means the changes could potentially be caused by tobacco alone, although the researchers believe the results point to a more complex interaction.
“What surprised us was how strong the effect was, and how different it was from those who only used cannabis, compared to those who used both tobacco and cannabis,” said co-author Romina Mizrahi, Professor of Psychiatry and director of the McGill Research Center for Cannabis.

Next Steps in Understanding Tobacco’s Role
The team is now recruiting people who smoke cigarettes and people who vape nicotine for a follow-up project that will explore whether similar brain changes appear in the absence of cannabis.
“A preliminary investigation of tobacco co-use on endocannabinoid activity in people with cannabis use” by Rachel Rabin, Joseph Farrugia, Ranjini Garani and Romina Mizrahi was published in Drug and Alcohol Dependence Reports.
The study received funding from the National Institute of Mental Health.

Many older Americans shun an identity that could bring helpful accommodations, improve care and provide community.In her house in Ypsilanti, Mich., Barbara Meade said, “there are walkers and wheelchairs and oxygen and cannulas all over the place.”Ms. Meade, 82, has chronic obstructive pulmonary disease, so a portable oxygen tank accompanies her everywhere. Spinal stenosis limits her mobility, necessitating the walkers and wheelchairs and considerable help from her husband, Dennis Meade, who serves as her primary caregiver.“I know I need hearing aids,” Ms. Meade added. “My hearing is horrible.” She acquired a pair a few years ago but rarely uses them.Mr. Meade, 86, is more mobile, despite arthritis pain in one knee, but contends with his own hearing problems. Similarly dissatisfied with the hearing aids he once bought, he said, “I just got to the point where I say, ‘Talk louder.’”But if you ask either of them a question included on a recent University of Michigan survey — “Do you identify as having a disability?” — the Meades answer promptly: No, they don’t.Disability “means you can’t do things,” Mr. Meade said. “As long as you can work with it and it’s not affecting your life that much, you don’t consider yourself disabled.”We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Researchers at Tokyo Metropolitan University have turned to concepts from polymer physics to better understand a central feature of Alzheimer’s disease: the formation of tau protein fibrils. Their work revealed that these fibrils do not appear suddenly. Instead, they emerge after large clusters of tau proteins begin to gather in solution, a process that resembles polymer crystallization. When the scientists disrupted these early clusters, the fibrils failed to form, suggesting a promising direction for new strategies against neurodegenerative conditions.
Alzheimer’s disease (AD) remains one of the most difficult medical challenges, especially as global populations continue to age. Scientists have long focused on pharmacology and traditional biomedical approaches. However, the complexity of AD has driven researchers to explore insights from other scientific fields that may open up new paths for understanding the disease and designing treatments.
How Polymer Behavior Helped Explain Tau Protein Fibrils
Led by Professor Rei Kurita, the research team applied ideas from how polymers organize into crystals. Polymers, which are long chains of repeating molecular units, often do not crystallize by simply adding one chain at a time. Instead, they pass through intermediate precursor structures before forming an ordered crystal. Drawing on this concept, the scientists examined tau proteins in solution and found that fibril formation (fibrillization) is also preceded by a precursor stage. In this case, the precursor is a loose assembly of tau proteins measuring only tens of nanometers. Techniques including small angle X-ray scattering and fluorescence-based analyses confirmed the presence of these structures.
A key discovery was that these precursors are not rigid but instead are soft, temporary clusters. The researchers were able to dissolve them by altering sodium chloride levels in the presence of heparin, a naturally occurring anticoagulant. When the clusters were disrupted or prevented from forming, the solution produced almost no tau fibrils. The team suggested that this effect occurs because increased concentrations of charged ions reduce how strongly tau proteins interact with heparin. According to their explanation, this change enhances electrostatic “screening,” making it more difficult for the molecules to find each other and form clusters.
A New Therapeutic Direction for Alzheimer’s and Beyond
These findings point to a potential shift in how scientists approach AD treatments. Instead of trying to break apart the final fibrils, therapies could aim at stopping the reversible precursor stage before harmful structures develop. This approach could influence not only AD research but also efforts to understand other neurodegenerative diseases, including Parkinson’s disease.
This work was supported by JST SPRING Program Grant Number JPMJSP2156, JSPS KAKENHI Grant Numbers 22K07362, 25K21773, 24H00624, 22H05036, 23K21357, 25K02405, 23H00394, 23KK0133, and 20H01874, JST Moonshot R&D Program Grant Number JPMJMS2024, and AMED Grant Number 24wm0625303 and 25dk0207073.
Tau Protein FibrilsTau protein fibrils are abnormal bundles of tau proteins that assemble inside neurons when tau loses its normal shape and function. Under healthy conditions, tau works like a stabilizing support beam, helping maintain the microtubules that allow nutrients and signals to move through nerve cells. When tau becomes misfolded, it starts clumping together into long, fibrous aggregates known as fibrils. These structures interfere with the cell’s internal transport system and are strongly linked to the cognitive decline seen in Alzheimer’s disease and other neurodegenerative conditions. Because fibrils grow from smaller, early-stage tau clusters, researchers are increasingly focused on blocking these initial steps to prevent downstream damage.

An experimental compound has been found to limit cell death, reduce inflammation, and lessen organ damage associated with diabetes.
A research team at NYU Langone Health reported that, in mouse studies, a drug candidate successfully prevented two proteins from interacting: RAGE and DIAPH1. When these proteins come together, they contribute to heart and kidney injury linked to diabetes and slow the healing of wounds.
Blocking a Key Protein Interaction Boosts Healing
The findings, recently featured as a cover story in Cell Chemical Biology, show that keeping DIAPH1 from attaching to RAGE can ease swelling in diabetic tissues and promote more efficient repair. Tests conducted in human cells and mouse models revealed that the compound significantly reduced both immediate and long-term complications in Type 1 and Type 2 diabetes. The compound, known as RAGE406R, is a small molecule named for the protein it targets.
“There are currently no treatments that address the root causes of diabetic complications, and our work shows that RAGE406R can — not by lowering the high blood sugar, but instead by blocking the intracellular action of RAGE,” said co-senior study author Ann Marie Schmidt, MD, the Dr. Iven Young Professor of Endocrinology at the NYU Grossman School of Medicine. “If confirmed by further testing in human trials, the compound could potentially fill gaps in treatment, including that most current drugs work only against Type 2 diabetes.”
How RAGE and DIAPH1 Contribute to Damage
RAGE is a receptor, a type of protein that responds to signaling molecules known as advanced glycation end products (AGEs). These molecules form when proteins or fats bind to sugars, a process that occurs more frequently in people with diabetes. AGEs accumulate in the bloodstream in individuals with diabetes and obesity, and also naturally increase with age.

Experiments showed that RAGE406R competes for the binding site on RAGE that DIAPH1 normally occupies. DIAPH1 helps form actin filaments, which are part of the cell’s internal structure. The researchers demonstrated that DIAPH1 connects to the inner tail of RAGE, and this pairing increases the formation of actin structures that intensify diabetic complications.
Developing a Safer and More Effective Molecule
Schmidt’s team previously screened a library of more than 58,000 molecules and identified several that interfered with the RAGE-DIAPH1 pathway. Their earlier lead compound, RAGE229, did not pass a standard safety test designed to flag structural features that might alter DNA and raise cancer risk. RAGE406R removes the part of the structure that created this concern.
The team then tested RAGE406R in a widely used model for chronic diabetes complications: delayed wound healing in obese mice with Type 2 diabetes. In both male and female mice, applying RAGE406R directly to the skin accelerated wound closure.
Reducing Misplaced Inflammation to Support Repair
Many of the compound’s benefits stem from its effects on the immune system. The immune response is designed to detect and eliminate harmful invaders such as bacteria and viruses. When activated, it can cause inflammation, which includes swelling triggered by immune cells gathering at an injured area. In diabetes, inflammation often occurs in the wrong places or lasts too long.

RAGE406R lowered the levels of CCL2, a major proinflammatory signaling molecule. Reducing CCL2 activity calmed inflammation in macrophages, a type of immune cell. This shift helped support structural remodeling in tissues, an essential part of the healing process.
“Our findings point to a promising new pathway for treating diabetes in the future,” said co-senior study author Alexander Shekhtman, PhD, a professor in the Department of Chemistry at the State University of New York (SUNY) at Albany. “The current study results serve as a springboard for the development of therapies for both types of diabetes, and for designing markers that can measure how well the new treatment works in live animals.”
Contributors and Funding Support
Along with Schmidt, contributors from the Diabetes Research Program in the Department of Medicine at NYU Langone Health include co-first author Michaele Manigrasso, as well as Gautham Yepuri, Kaamashri Mangar, and Ravichandran Ramasamy. Additional NYU Langone collaborators include Sally Vanegas from the Department of Medicine and Yanan Zhao and Huilin Li from the Division of Biostatistics in the Department of Population Health. Shekhtman’s group at SUNY at Albany includes first author Gregory Theophall, Parastou Nazarian, Aaron Premo, Sergey Reverdatto, and David Burz. Robert DeVita, PhD, from RJD Medicinal Chemistry and Drug Discovery Consulting LLC, also contributed to the research.
This work was funded by U.S. Public Health Service grants 1R24DK103032, 1R01DK122456-01A1, P01HL146367, and 5R01GM085006. The NYU Histology Core receives partial support from the Perlmutter Cancer Center support grant P30CA016087. Additional backing came from the Diabetes Research Program at the NYU Grossman School of Medicine. Drs. Manigrasso, Ramasamy, and Schmidt are listed on patent applications owned by NYU Langone Health related to this research. Their relationship to this intellectual property is being managed in accordance with NYU Langone Health policies. Dr. DeVita, who consults for NYU Technology Opportunities & Ventures’ Therapeutics Alliances and for Intercept Therapeutics, was compensated for his involvement.

Gout is one of the oldest documented human illnesses. It develops when sharp crystals form inside joints, triggering intense swelling and pain, and is considered a type of arthritis. Researchers at Georgia State University believe they may have uncovered a surprisingly ancient way to address it.
A study in Scientific Reports describes how scientists used CRISPR gene-editing tools to restore a gene that disappeared from the human lineage millions of years ago. Bringing this gene back lowered uric acid, the substance responsible for gout and several other health problems.
The long-lost component is uricase, an enzyme that most other animals continue to carry.
Uricase breaks down uric acid, a waste product that routinely forms in the blood. If uric acid levels rise too much, it can crystallize in the joints and kidneys, causing gout, kidney disease and a number of related conditions.
Why Humans Lost Uricase
Humans and other apes shed the uricase gene roughly 20 to 29 million years in the past. Some experts argue this change may have once offered an advantage. According to research cited in Seminars in Nephrology, scientists including Dr. Richard Johnson of the University of Colorado have suggested that elevated uric acid helped early primates convert fruit sugars into fat, providing a survival boost during lean times.
Today, however, that ancient adaptation contributes to a range of modern metabolic issues. This is the challenge that Georgia State biology professor Eric Gaucher and his team aimed to test.

“Without uricase, humans are left vulnerable,” said Gaucher, a co-author of the study. “We wanted to see what would happen if we reactivated the broken gene.”
Reintroducing an Ancient Gene With CRISPR
Working with postdoctoral researcher Lais de Lima Balico, Gaucher relied on CRISPR-Cas9, often referred to as molecular scissors, to insert a reconstructed version of the ancient uricase gene into human liver cells. This allowed the team to observe how the enzyme functioned in a modern biological environment.
The results surprised them. Uric acid levels fell sharply, and liver cells no longer accumulated fat when exposed to fructose. Because experiments in individual cells cannot always predict what will occur in more complex systems, the researchers advanced to a more sophisticated model.
They tested the gene in 3D liver spheroids, which are small, lab-grown structures that more closely resemble actual organ function. The reintroduced uricase gene again reduced uric acid. The enzyme also moved into peroxisomes, the cellular compartments where uricase naturally operates, suggesting the therapy might behave safely and appropriately in living organisms.
“By reactivating uricase in human liver cells, we lowered uric acid and stopped the cells from turning excess fructose into triglycerides — the fats that build up in the liver,” Gaucher said.

The Wider Impact of High Uric Acid
The findings extend well beyond gout. High uric acid, known as hyperuricemia, is associated with many modern health disorders. Research highlighted in the journal Hypertension has linked elevated uric acid to hypertension and cardiovascular disease, and the risks have been compared to those of high cholesterol.
These concerns are reflected in patient statistics. Between one-quarter and one-half of people with high blood pressure also have high uric acid, and in newly diagnosed hypertension, that overlap rises to 90 percent, according to the study.
“Hyperuricemia is a dangerous condition,” Gaucher said. “By lowering uric acid, we could potentially prevent multiple diseases at once.”
Toward Future Therapies
Current treatments for gout are not effective for everyone, and some individuals experience adverse reactions to existing uricase-based medications. A CRISPR method that restores uricase directly in liver cells could avoid these issues.
“Our genome-editing approach could allow patients to live gout-free lives and potentially prevent fatty liver disease,” Gaucher said.
Animal studies are the next step, followed by human trials if early results hold up. Potential delivery methods include direct injections, returning modified liver cells to patients, or using lipid nanoparticles (the same technology employed in some COVID-19 vaccines).
If the strategy proves safe, Gaucher believes it could reshape the way gout and related metabolic disorders are treated. However, several challenges still need to be addressed.
“Genome-editing still faces substantial safety concerns,” he said. “Once those are addressed, society will be faced with contentious ethical discussions about who should and should not have access.”

Serious injury to short-term kidney function, known as acute kidney injury (AKI), can be life-threatening and also raise the likelihood of developing permanent chronic kidney disease. AKI can occur after major stressors such as sepsis or heart surgery, and more than half of all intensive care patients experience it. No approved medications currently exist to treat this condition.
Researchers at University of Utah Health (U of U Health) have discovered that fatty molecules called ceramides initiate AKI by damaging the mitochondria that supply energy to kidney cells. By using a backup drug candidate designed to alter how ceramides are processed, the team protected mitochondrial structure and prevented kidney injury in mice.
“We completely reversed the pathology of acute kidney injury by inactivating ceramides,” says Scott Summers, PhD, distinguished professor and Chair of the Department of Nutrition and Integrative Physiology in the University of Utah College of Health and senior author on the study. “We were stunned — not only did kidney function stay normal, but the mitochondria were unscathed,” Summers says. “It was truly remarkable.”
The results are published in Cell Metabolism.
Ceramide spikes may serve as an early warning
Earlier studies from the Summers lab showed that ceramides can harm organs such as the heart and liver. When the researchers measured ceramides in AKI models, they found a strong connection: levels rose sharply after injury in both mice and in human urine samples.
“Ceramide levels are very elevated in kidney injury,” says Rebekah Nicholson, PhD, first author on the work, who completed the research as a graduate student in nutrition and integrative physiology at U of U Health and is now a postdoctoral fellow at the Arc Institute. “They go up quickly after damage to the kidneys, and they go up in relation to the severity of the injury. The worse the kidney injury is, the higher the ceramide levels will be.”
These findings indicate that urinary ceramides could act as an early biomarker for AKI, giving clinicians a tool to identify vulnerable patients, including those preparing for heart surgery, before symptoms begin. “If patients are undergoing a procedure that we know puts them at high risk of AKI, then we can better predict whether or not they’re actually going to have one,” Nicholson says.

Altering ceramide production protects kidney function
The team nearly eliminated kidney injury in a mouse model by modifying the genetic program that controls ceramide production. This change produced “super mice” that did not develop AKI even under conditions that typically cause severe damage.
The researchers then tested a ceramide-lowering drug candidate created by Centaurus Therapeutics, a company co-founded by Summers. Mice treated ahead of time avoided kidney injury, maintained normal kidney function, remained active, and had kidneys that appeared close to normal under the microscope. Nicholson notes that their model places extreme stress on the kidneys, making it “really remarkable that mice were protected from the injury.”
“These mice looked incredible,” Summers adds.
The team found that ceramides harm mitochondria, the parts of the cell responsible for energy production. Damaged mitochondria in kidney cells become distorted and function poorly. Adjusting ceramide production, whether genetically or with the drug, kept mitochondria intact and working even under strain.
Potential for future therapies targeting mitochondrial health
Summers explains that the compound used in this study is closely related to, but not identical to, the ceramide-lowering drug that has entered human clinical testing. He emphasizes that mouse results do not always predict human outcomes and that further research is needed to confirm safety.

“We’re thrilled by how protective this backup compound was, but it’s still preclinical,” Summers says. “We need to be cautious and do our due diligence to make sure this approach is truly safe before moving it into patients.”
Even so, the researchers are encouraged by the findings. If the results extend to people, the drug could potentially be administered ahead of time to individuals who face a high risk of AKI, including patients undergoing heart surgery, where about one quarter experience the condition.
Because the drug appears to work by maintaining mitochondrial health, the team believes that the approach may have relevance for other disorders linked to mitochondrial dysfunction.
“Mitochondrial problems show up in so many diseases — heart failure, diabetes, fatty liver disease,” Summers says. “So if we can truly restore mitochondrial health, the implications could be enormous.”
The results are published in Cell Metabolism as “Therapeutic Remodeling of the Ceramide Backbone Prevents Kidney Injury.”
Funding and disclosures
This work was supported by a NCRR Shared Instrument Grant, the Kidney Precision Medicine Project, and several branches of the National Institutes of Health, including the National Cancer Institute (P30CA042014, CA272529), the National Institute of Diabetes and Digestive and Kidney Diseases (DK115824, DK116888, DK116450, DK130296, DK108833, DK112826, 1F31DK134088 and 5T32DK091317), and the National Institute of General Medical Sciences (3R35GM131854 and 3R35GM131854-04S1). Additional support came from the Juvenile Diabetes Research Foundation (JDRF 3-SRA-2019-768-A-B and JDRF 3-SRA-2019-768-A-B to WLH), the Burroughs Wellcome Fund Postdoctoral Diversity Enrichment Program (1058616), the American Diabetes Association, the American Heart Association, the Margolis Foundation, and the University of Utah Diabetes and Metabolism Research Center. The authors state that the content is their responsibility and does not necessarily reflect the views of the National Institutes of Health.
Scott Summers and Jeremy Blitzer are co-founders and shareholders of Centaurus Therapeutics. Liping Wang is also a shareholder. DN and Blitzer are listed as inventors on US Patents 1177684, 11597715, and 11135207 licensed to Centaurus Therapeutics, Inc.

This article is part of Overlooked, a series of obituaries about remarkable people whose deaths, beginning in 1851, went unreported in The Times.Sigmund Freud, Carl Jung — and Sabina Spielrein. As the field of psychoanalysis was emerging in the early 1900s, those scientists were linked in a triangular dialogue that included letters, scholarly articles and debates. Yet for decades, Spielrein’s contributions were overshadowed by the two men. Only recently has her role begun to be fully acknowledged.In 1911, Spielrein presented a bold theory before the Vienna Psychoanalytic Society at an event hosted by Freud.During her talk, she proposed that the same inner forces that drive people to love, desire and create can also make them want to destroy — even themselves — a notion that became the focus of her 1912 paper “Destruction as the Cause of Becoming.”When Freud published his essay “Beyond the Pleasure Principle” (1920), he gave a label to the urge — Thanatos, or the death drive — that acted in opposition to the sex drive, which he called Eros.He cited Spielrein in a footnote and, for many decades since, she remained just that, despite publishing more than 35 papers in three languages and making significant contributions to the fields of psychoanalysis and child psychology.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Under the plan, the company will dissolve and its owners, members of the Sackler family, will pay as much as $7 billion of their personal fortune to states, localities, tribes and others harmed in the opioid crisis.The drugmaker Purdue Pharma, which along with its owners came to symbolize greedy indifference to surging opioid overdose deaths, will soon cease to exist, after a bankruptcy judge said Friday that he would give final approval to a plan to settle thousands of lawsuits against the company.The agreement comes more than two decades after the first legal actions were filed against Purdue over its aggressive sales tactics and promotion of the opioid painkiller OxyContin as largely nonaddictive. It requires members of the billionaire Sackler family to relinquish ownership of the company and pay as much as $7 billion over 15 years to states, communities, tribes and others harmed in what became a decades-long national opioid addiction crisis.“I will tell you now that I’m going to confirm the plan,” Judge Sean H. Lane of the United States Bankruptcy Court for the Southern District of New York said Friday afternoon at the conclusion of three days of testimony. He said he would issue a formal ruling on Tuesday.Purdue will immediately contribute $900 million and then be dissolved. It will be reborn as a public benefit company called Knoa Pharma, which will manufacture limited quantities of opioid painkillers and also opioid overdose-reversal medications. Profits will go to programs to remediate the continuing devastation related to opioids.Over the many years of the national opioid litigation, this plan, which the company says is worth $7.4 billion with potential to grow larger, represents the biggest settlement with a single pharmaceutical company. It will bring long-sought payments to states, municipalities, hospitals and school districts, plus nearly 150,000 personal injury victims and families of babies born with symptoms of opioid withdrawal. (On a separate track, the company and the Sacklers are expected to pay $175 million to federally recognized tribes.)At a hearing Friday on the plan in bankruptcy court in Lower Manhattan, lawyers for Purdue said payments could possibly begin in March or April.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

3 days agoShareSaveShareSaveGetty ImagesScotland’s abortion laws are “not fit for purpose” according to an expert group, which has called for legal recognition for a woman’s right to choose.Currently, an abortion is only legal before 24 weeks when two doctors agree that certain grounds have been met – such as a risk to the mother’s physical or mental health. An independent report recommends that these grounds are dropped, and doctors’ agreement should only be required for late-term abortions after 24 weeks.The Scottish government said it would carefully consider the proposals and women would continue to be supported to access “safe and timely” services.The Abortion Law Expert Group, chaired by Prof Anna Glasier, was commissioned by the Scottish government to review existing law.It said the current system requiring approval from two doctors was “anachronistic, paternalistic and failed to reflect best modern practice”. It stated: “The group agreed unanimously that current Scottish abortion law is not fit for purpose and that alternative models should be considered. “Legal recognition should be given to the woman’s right to make their own decision regarding whether to continue or to end a pregnancy, and that abortion should become available on request, at least within gestational limits.”After 24 weeks, an abortion is only possible in very limited circumstances, such as to save the life of the mother or if there is a fatal anomaly with the foetus.The group said it considered clinical practice, international examples, academic research and a range of views from across Scotland.Prof Glasier said: “The group worked incredibly hard, and benefited greatly from the input and expertise of a wide range of stakeholders, to develop evidence-based, balanced recommendations.”The report demonstrates the group’s view that it is time for an abortion law that reflects the reality of current clinical practice where abortions are safely provided in the best interests of women.”‘Women are supported’Christian campaign group, Care for Scotland, urged ministers to reject the “extreme proposals” in the report.Director of advocacy and policy, Caroline Ansell, said: “If enacted, we believe they would have heartbreaking consequences for women and babies, including exposing more women to the dangers and harms of late-term abortions.”The Scottish government said it would begin its own period of evidence-gathering and “engagement with a range of stakeholders”. Scotland’s minister for public health, Jenni Minto, said: “It is right that we continue to ensure that abortion is treated as a healthcare matter and that women are supported to access safe and timely abortion services.”The recommendations within the report represent the views of the expert group – it is only one part of this review process.”We will take time to carefully consider all the findings and respond in due course.”This is a significant report which could pave the way for a major change in the way abortion is viewed and administered in Scotland. But that change is unlikely to be happening any time soon, given how close we are to the end of the parliamentary term.Scottish ministers have a fairly clear view on the issue – they pointedly talk about abortion as a healthcare issue, not a criminal one.However, they are also going to take time to do their own evidence-gathering, and any changes would require primary legislation which would take months to get through parliament.We shall see if their promised response materialises before Holyrood breaks up for the election – which oddly enough is 24 weeks away.But really what will tell us the most about the future of abortion care is what makes it into party manifestos for that poll – because it will be MSPs in the next Scottish Parliament who ultimately end up making the decision.

50 minutes agoShareSaveNick TriggleHealth correspondentShareSavePA MediaNHS bosses are aiming to keep nearly all services running as resident doctors begin a five-day walkout in England.The strike – the 13th by British Medical Association members in the long-running pay dispute – began at 07:00 GMT and lasts until 07:00 Wednesday.Resident doctors – the new name for junior doctors – will walk out of both emergency and non-urgent care.Hospitals will come under the most strain, with resident doctors making up about half the medical workforce. But NHS England said patients should still attend appointments unless advised otherwise.It said it wanted to keep 95% of non-urgent work, such as hip and knee operations, going.The NHS aims to do this by re-deploying and offering overtime to consultants and and other senior doctors as well as relying on those not striking – around a third of resident doctors are not BMA members.But this will come at significant cost with the NHS estimating the five-day walkout is costing £240m to cover.’I’m furious’OtherDespite the attempt to keep services going, patients like Colette Houlihan, 68, have still had to face postponements.She was due to have a pre-surgery appointment on Monday, but this has now been pushed back to late December.Ms Houlihan, from Cambridgeshire, who is waiting for a benign tumour in her neck to be removed, said she had had to put up with two cancellations already, but could understand those as she was told patients who were higher priorities needed to be seen.”They could have had cancer. I didn’t mind that, but this is different.”I am furious. By striking they ignore the Hippocratic Oath – first and foremost do no harm.”Striking causes harm by way of delaying procedures, taking senior doctors from their posts and causing chaos within the system,” she said.ChallengingNHS England medical director Prof Meghana Pandit said it was frustrating and disappointing that there was another round of industrial action at a challenging time for the NHS, with flu cases rising earlier than usual.”Despite this, staff across the NHS are working extremely hard to maintain care and limit disruption,” he added.But BMA leader Dr Tom Dolphin said keeping most services running would be “challenging”.He said doctors had a legal right to strike and should not be “bullied or coerced” into working.And he warned his members would only leave the picket line if there was a major emergency – such as a mass casualty event.The latest walkout comes after Health Secretary Wes Streeting launched arguably his strongest attack on the BMA.Addressing a conference of health managers this week, he called the union “morally reprehensible” and accused it of acting like a cartel, attempting to hold the public and government to ransom.He said doctors had received generous pay rises over the past three years – worth nearly 30%, bringing average basic salaries to just over £54,000.Talks between him and the union broke down last week after the BMA turned down a fresh offer to end the dispute.Streeting has maintained throughout the year that he could not negotiate on pay, but he proposed a deal that would see out-of-pocket expenses like exam fees and membership fees covered, along with a boost in speciality training places.But the BMA has argued that, despite the pay rises, resident doctors’ pay is still a fifth lower than it was in 2008, once inflation is taken into account.The union has also warned doctors are struggling to find jobs at a key stage of their training – between years two and three when they start speciality training.This year there were more than 30,000 applicants for 10,000 jobs at this stage, although some will have been doctors from abroad.”We need a solution for the jobs crisis, that bottleneck for doctors who are out of permanent work or out of consistent work,” Dr Emma Runswick, deputy chair of the BMA Council, told the BBC.”Then we need to be able to retain those doctors throughout their careers by paying them appropriately, and that means restoration of pay.”