How Quitting Smoking Can Quickly Lower Risk Of A-Fib
Smokers who make the decision to quit will experience immediate health benefits, including a rapid reduction in their risk of atrial fibrillation (A-Fib), according to new research published in JACC: Clinical Electrophysiology. The study, conducted by Dr. Gregory Marcus, a cardiologist at the University of California, San Francisco, offers compelling evidence for smokers to quit, showing that it’s never too late to avoid the damaging effects of smoking on heart health.
Dr. Marcus, the senior author of the study, emphasized that A-Fib can be prevented even in individuals who have smoked for years. "The findings provide a compelling new reason to show current smokers that it’s not too late to quit, and that having smoked in the past doesn’t mean you’re ‘destined’ to develop A-Fib," Marcus explained. "Even for the current and longtime smoker, A-Fib can still be avoided."
"There’s strong evidence that smoking increases the risk of A-Fib," Marcus said. "But the benefits of quitting smoking have been less certain." With this in mind, his team sought to determine whether quitting could significantly lower a person’s risk of developing A-Fib, or if the risk would remain the same.
The research team analyzed data from over 146,700 current and former smokers, tracking their smoking habits and health over a 12-year period using data from the UK Biobank database. The results were promising: former smokers had a 13% lower risk of developing A-Fib compared to current smokers, while those who quit during the study saw an 18% reduction in their risk.
"This is likely a testament to the potency of reducing atrial fibrillation risk pretty shortly after quitting," Marcus said in a statement from the American College of Cardiology.
The findings highlight the importance of quitting smoking, not only for general health but specifically for reducing the risk of serious heart conditions like A-Fib.
Quitting smoking is one of the most effective ways to lower the risk of A-Fib and improve overall heart health. While it can be challenging, the benefits of quitting are clear and immediate. Here are some tips to help you quit smoking successfully:
1. Choose a specific date to quit smoking and stick to it. Prepare yourself mentally and physically for this change.
2. Reach out to family, friends, or a support group to help keep you accountable. Sharing your goals with others can provide encouragement.
3. Options like nicotine patches, gum, or lozenges can help ease withdrawal symptoms and reduce cravings.
4. Identify situations that make you want to smoke, such as stress or social gatherings, and find healthy ways to cope with them.
5. Regular exercise can help distract you from cravings and improve your mood during the quitting process.
6. Drinking water can help flush nicotine out of your system faster, reducing cravings.
7. Activities like yoga, meditation, or deep breathing exercises can help manage stress, a common trigger for smoking.
Quitting smoking offers immediate and significant benefits, particularly in reducing the risk of atrial fibrillation. The latest research provides smokers with more motivation to quit, showing that it's never too late to take control of their heart health.
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More American women are starting GLP-1 medications such as Ozempic and Zepbound after giving birth, according to a new study
The findings, published in JAMA, found that the sharpest increases were seen among women with diabetes, obesity or overweight.
Researchers from the University of Southern California Schaeffer Center for Health Policy & Economics analyzed private insurance claims covering just over 1 million births over seven years.
They found that the share of new mothers starting a GLP-1 prescription within six months of childbirth rose from 0.08% in the first half of 2018 to 1.9% by the first quarter of 2025 — a 24-fold increase.
Women with type 2 diabetes had the highest rate of GLP-1 prescriptions. Among them, use increased from 2.3% to 16.9% over the study period — roughly 1 in 6 women.
Prescribing also increased among women who had gestational diabetes, rising from 0.4% in mid-2021 to 2.7% in the first quarter of 2025. Gestational diabetes affects about 5% to 9% of pregnancies and substantially increases the risk of developing type 2 diabetes later.
The fastest relative increase was seen among women diagnosed with obesity or overweight before pregnancy. GLP-1 use in this group rose from 0.4% in the second half of 2021 to 3.9% by the first quarter of 2025.
Since the second half of 2024, women with diagnosed obesity or overweight have accounted for 40% of new postpartum GLP-1 prescriptions.
Another 21% of women had no documented qualifying diagnosis before giving birth. However, most of these women received a diagnosis — usually obesity or overweight — before starting a GLP-1 medication.
Patients are advised to stop using GLP-1 medications during pregnancy. Most postpartum women in the study who started a GLP-1 did so at least three months after giving birth.
“Postpartum is a critical window for addressing metabolic risk after pregnancy, and we're seeing GLP-1 use explode in this population. Because evidence on GLP-1 exposure during breastfeeding remains limited, rising postpartum initiation warrants further study,” said lead author and Schaeffer scholar Sih-Ting Cai.
A 2025 JAMA study found a similar rise in Denmark. Fewer than five GLP-1 prescriptions per 10,000 women were recorded after childbirth in 2018, rising to 173 per 10,000 by 2024 — nearly 2% of new mothers.
GLP-1s are increasingly used for postpartum weight loss, but their safety after childbirth remains poorly studied. According to researchers, little is known about how these drugs affect normal postpartum hormonal changes or maternal recovery.
They also noted that evidence on GLP-1 exposure during breastfeeding remains limited, highlighting the need for further research as postpartum use increases.
“We simply do not know how weight-loss medication interacts with those processes or whether it could affect normal physiological recovery,” Dr. Jonathan Zipursky, a clinical pharmacologist and toxicologist at the University of Toronto, told The New York Times in 2025.
Evidence on GLP-1s during breastfeeding is also limited. A 2024 CMAJ paper suggested low breast-milk exposure, but researchers stressed that infant safety data remain insufficient. Zipursky recommended avoiding GLP-1s while breastfeeding as a precaution.
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A new experimental obesity drug could offer an alternative to GLP-1 medicines for people who struggle with their gastrointestinal side effects.
Petrelintide, a once-weekly injectable drug that works on the hormone amylin, helped people with obesity lose more than 10% of their body weight in a Phase 2 trial.
Published in The Lancet Diabetes & Endocrinology, the drug showed a relatively low rate of gastrointestinal side effects.
The study, however, did not directly compare petrelintide with drugs like semaglutide or tirzepatide.
So, while the results suggest it may be better tolerated, researchers cannot yet say that it causes fewer side effects than GLP-1 drugs.
Petrelintide is a long-acting amylin analogue. Amylin is a hormone produced by the pancreas alongside insulin and helps control appetite and food intake.
A yet-to-be approved drug, unlike Ozempic and Wegovy, which target the GLP-1 hormone, petrelintide focuses on amylin.
It is being developed by Danish drugmaker Zealand Pharma with Roche.
Also read: CSIR-CCMB Scientists Find Flu & COVID Viruses May Affect A Protein Linked To Parkinson’s Disease
The Phase 2 ZUPREME-1 trial included 485 people who received at least one dose of petrelintide or placebo, with everyone also receiving lifestyle advice.
After 42 weeks, average weight loss ranged from 8.7% to 10.7%, depending on the petrelintide dose.
The group receiving placebo lost about 1.7% of their body weight. The 5 mg dose produced the largest average reduction, at 10.7%.
At 28 weeks, weight loss across the petrelintide groups ranged from about 7.9% to 9.8%, compared with 1.7% with placebo.
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This is perhaps one of the biggest attractions of petrelintide. Nausea was the most common side effect, affecting 20% of people compared to 6% in the placebo group.
However, vomiting was uncommon, occurring in 3% of the petrelintide group compared with 6% of the placebo group. Diarrhoea occurred in 7% and constipation in 7% of those receiving petrelintide. Researchers also reported that most gastrointestinal side effects were mild.
This is a well-tolerated medication," lead investigator Dr. Timothy Garvey of the University of Alabama at Birmingham told HCPLive . Approved GLP-1 drugs have produced larger average weight loss in their own trials, but Garvey said "This current level of 10-15% is sufficient to treat a large number of patients who have obesity.
Three serious adverse events were considered related to petrelintide, including two cases of gallstones and one case of obstructive pancreatitis, according to an independent expert assessment of the study.
One may be inclined to compare petrelintide's side-effects with that of GLP-1 drugs like Ozempic, Wegovy, Zepbound and Mounjaro, but the trial was designed to compare petrelintide with placebo, not with semaglutide or tirzepatide.
Dr Marie Spreckley of the University of Cambridge cautioned that the comparison with GLP-1 medicines is too strong because “the trial did not test petrelintide against any of those medicines, so we cannot say from these results that it causes fewer side effects.”
That means more investigation will be needed to compare petrelintide’s tolerability and existing obesity treatments.
However, the results have prompted further development of petrelintide, with Phase 3 trials planned. Researchers are particularly interested in whether the drug can provide sustained weight loss while allowing people to remain on treatment without gastrointestinal symptoms.
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Repeated viral infections may play a key role in shaping Parkinson’s disease risk. A new study by researchers at CSIR-Centre for Cellular and Molecular Biology (CCMB), Hyderabad, has found that RNA viruses like influenza and even SARS-CoV-2 can interact with a protein called alpha-synuclein, accelerating the formation of abnormal protein clumps associated with Parkinson’s.
Published in Cell Reports, the study, which was led by Dr Swasti Raychaudhuri’s laboratory at CCMB, also identified a cellular protein that appears to act as a defense against this process.
Alpha-synuclein is a protein that is naturally found in nerve cells. In Parkinson’s disease, the protein can accumulate into abnormal clumps called amyloid aggregates.
These aggregates are a characteristic feature of Parkinson’s and can interfere with the normal functioning of neurons.
The new study looked at what happens to alpha-synuclein when a cell is infected by an RNA virus.
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Flu and COVID viruses contain RNA, which is their genetic material. The researchers found that parts of this viral RNA can fold into unusual shapes called RNA G-quadruplexes (rG4s).
These RNA structures can interact with a protein called alpha-synuclein. Alpha-synuclein normally exists in brain cells, but in Parkinson’s disease it can clump together and form abnormal deposits.
The researchers found that viral RNA structures may encourage alpha-synuclein to clump together more easily.
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The researchers also identified a protein called DDX39A, which counters both viral multiplication and alpha-synuclein aggregation.
Normally found inside the cell nucleus, DDX39A moves into the cytoplasm during an RNA viral infection. There, it can interact with both viral RNA structures and alpha-synuclein.
DDX39A acts as an RNA “unwinding” protein. It breaks apart the rG4 structures in viral RNA, making it harder for the virus to replicate. At the same time, this process appears to slow the formation of alpha-synuclein amyloids.
Study first author Aanchal said, “The virus fails to replicate with its RNA structures dismantled, and thus, the viral load in the cells decreases. At the same time, the unwinding of viral RNA’s secondary structure effectively slows down α-Synuclein amyloid formation.”
The researchers caution against making that conclusion. Not every viral infection will increase amyloid formation, and not everyone who gets influenza or COVID-19 will develop Parkinson’s.
The study suggests that the outcome depends on a complex balance between the virus, viral RNA, alpha-synuclein, and the cell’s defence mechanisms.
There have been previous studies reporting an association between certain viral infections and an increased risk of neurodegenerative diseases. But the biological mechanism behind such associations has remained unclear.
The CCMB researchers are now investigating what happens to these molecular interactions over longer periods.
The concern is that repeated exposure to viral infections could alter the balance between protective cellular mechanisms and protein aggregation. However, this remains an area of investigation and cannot currently be used to predict an individual's Parkinson’s risk.
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