How Quitting Smoking Can Quickly Lower Risk Of A-Fib

Updated Sep 14, 2024 | 02:00 AM IST

SummaryNew research reveals that quitting smoking quickly reduces the risk of atrial fibrillation (A-Fib). Former smokers have a significantly lower risk compared to current smokers, emphasizing the health benefits of quitting.
How Quitting Smoking Can Quickly Lower Risk Of A-Fib

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."

What is Atrial Fibrillation (A-Fib)?

A-Fib is a heart condition that affects the upper chambers of the heart, known as the atria. When these chambers beat irregularly, blood can pool and form clots, increasing the risk of stroke. Stroke is one of the most serious complications associated with A-Fib, and smoking is known to exacerbate this risk.

"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.

Tips for Quitting Smoking

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.

End of Article

AI Creates 16 Viruses To Kill Drug-Resistant E. coli, Raises Biosafety Concerns

Updated Aug 8, 2026 | 12:07 AM IST

SummaryThe researchers believe the same AI-driven approach could eventually be used to develop phages against other drug-resistant bacteria, including:tuberculosis, superbug MRSA, and Pseudomonas aeruginosa, a leading cause of antibiotic-resistant hospital-acquired infections.
AI Creates 16 Viruses To Kill Drug-Resistant E. coli, Raises Biosafety Concerns

Credit: iStock

In a major scientific breakthrough, researchers at Stanford University have used artificial intelligence (AI) to design entirely new viruses that do not exist in nature.

The AI-generated viruses successfully killed Escherichia coli (E. coli) bacteria that had become resistant to naturally occurring bacteriophages (phages)—viruses that infect and destroy bacteria—offering new hope for tackling antibiotic-resistant infections.

The study, published in the journal Science, also raises important biosafety concerns, as the same technology could potentially be misused to design harmful pathogens.

How AI Created the Viruses?

Chemical engineer Brian Hie and bioengineering graduate student Samuel King developed Evo 2, a generative AI model capable of writing complete DNA sequences and designing entirely new genomes.

The researchers focused on bacteriophages, viruses that infect bacteria and are already being explored as alternatives to antibiotics for treating difficult bacterial infections.

Using genomes designed by Evo 2, the team synthesized nearly 300 novel phages and tested them against E. coli. From these, they identified 16 highly effective phages that successfully killed bacteria resistant to naturally occurring phages.

The researchers believe the ability to rapidly design customized phages could transform phage therapy and expand the arsenal against antibiotic-resistant bacteria.

The team redesigned bacteriophage ΦX174, one of the simplest known viruses. Despite its small size, ΦX174 efficiently infects and kills bacteria, making it a valuable model for developing new phage therapies.

A New Weapon Against Antibiotic Resistance

One of the biggest challenges in infectious disease treatment is that bacteria eventually develop resistance to antibiotics—and even to individual phages. To overcome this, the researchers designed a genetically diverse cocktail of 16 AI-created phages.

"If the bacteria gain resistance to a single phage, it's game over for the medication," Hie said. "But if you have multiple genetically distinct phages in a mixture, it would be harder for the bacteria to develop resistance to the entire cocktail."

The team showed that the phage cocktail successfully eliminated E. coli strains that had become resistant to the natural ΦX174 virus.

"We have a proof of concept in the paper, where we show that this cocktail of 16 phages rapidly overcomes resistance in E. coli that is immune to native ΦX174," Hie said.

Potential Beyond E. coli

Researchers believe the same AI-driven approach could eventually be used to develop phages against other drug-resistant bacteria, including:

  • Mycobacterium tuberculosis (tuberculosis)
  • Methicillin-resistant Staphylococcus aureus (MRSA)
  • Pseudomonas aeruginosa, a leading cause of antibiotic-resistant hospital-acquired infections

If successful, AI-designed phage cocktails could provide a powerful alternative to conventional antibiotics, whose effectiveness continues to decline because of antimicrobial resistance.

Biosafety Concerns Grow

The researchers have made Evo 2 freely available as open-source software, allowing scientists around the world to design and study new genomes.

While this could accelerate advances in medicine and biotechnology, experts say it also highlights the urgent need for stronger oversight.

"The ability to compose viral genomes using generative AI now exists; the governance to safely steer it does not," wrote Prof. Tom Inglesby and Dr. Moritz Hanke of the Center for Health Security at Johns Hopkins University in an accompanying Science commentary.

Tom Ellis, Professor of Synthetic Genome Engineering at Imperial College London, described the research as impressive but cautioned that AI could theoretically be used to design harmful viruses if trained on the genetic code of dangerous pathogens, The Guardian reported.

However, he said safeguards—such as restricting access to sensitive genetic data and screening synthetic genomes before they are manufactured—could help reduce those risks.

End of Article

Donald Trump Mulls Order Targeting Childhood Vaccines And Autism

Updated Aug 7, 2026 | 09:58 PM IST

SummaryTrump has repeatedly suggested there may be a connection between vaccines and autism, despite overwhelming scientific evidence disproving the claim. ​He has also argued that the US childhood vaccination schedule should be reduced, raising concerns among public health experts.
Donald Trump Mulls Order Targeting Childhood Vaccines And Autism

Credit: AP Photo

The Donald Trump administration is reportedly considering an executive order focused on the US childhood vaccination schedule and autism research, despite decades of scientific evidence showing no link between vaccines and autism.

According to a Washington Post report citing official sources, the proposed order would examine the childhood immunization schedule and autism research. However, its scope and timing have not been finalized and could still change.

The move comes even as some of Trump's political advisers have reportedly warned that elevating the issue could hurt Republican candidates ahead of the November midterm elections.

White House Pushes Greater Scrutiny of Vaccines

According to The Wall Street Journal, Trump wants "alleviating autism" to become part of his presidential legacy and has privately expressed frustration that US Health and Human Services (HHS) Secretary Robert F. Kennedy Jr. has not gone far enough in reducing the recommended childhood vaccination schedule. The report also said Trump believes that reducing the number of recommended childhood vaccines could lower autism rates.

In recent months, Trump has urged senior administration officials, including Kennedy Jr., to increase scrutiny of childhood vaccines.

Last year, Kennedy had cancelled roughly $500 million in mRNA vaccine research grants and replaced every member of a federal immunization advisory panel. However, he has been relatively quiet on vaccine policy this year after White House aides reportedly advised that vaccine skepticism was unpopular with many voters.

Scientists Reject Vaccine-Autism Link

Medical experts continue to emphasize that extensive research has found no evidence that vaccines cause autism.

"Donald Trump has been anti-vaccine at least since 2015," Dr. Paul Offit, Director of the Vaccine Education Center and an infectious disease specialist at Children's Hospital of Philadelphia, was quoted as saying by CNN.

During the 2015 Republican primary debate, Trump claimed autism had gotten "totally out of control" and suggested vaccines should be administered in "smaller doses over a longer period of time."

Trump Repeats Claims on Childhood Vaccines

Trump has repeatedly suggested there may be a connection between vaccines and autism, despite overwhelming scientific evidence disproving the claim. He has also argued that the US childhood vaccination schedule should be reduced, raising concerns among public health experts.

"I believe in vaccines, but I don't believe that, you know, you have to have a mandate for all of them," Trump said in a May interview with journalist Sharyl Attkisson. "I really feel that vaccines, if they were given in smaller quantities—they want to cut some out, and that's good, too. I agree with that."

Scientific Consensus Remains Unchanged

Multiple large-scale studies conducted over the past two decades have consistently found no causal link between childhood vaccines—including the MMR vaccine—and autism spectrum disorder.

Major health organizations, including the World Health Organization (WHO) and the US Centers for Disease Control and Prevention (CDC), continue to recommend routine childhood immunization as one of the safest and most effective ways to prevent infectious diseases.

End of Article

Alex Hughes: Former Manchester United Star’s Son Dies of Sudden Adult Death Syndrome

Updated Aug 7, 2026 | 08:55 PM IST

SummarySADS refers to a sudden, unexpected death caused by an abnormal heart rhythm in people whose hearts appear structurally normal after death. ​The condition is most commonly linked to inherited disorders that affect the heart's electrical system.
Alex Hughes: Former Manchester United Star’s Son Dies of Sudden Adult Death Syndrome

Credit: Grimsby Town FC

Alex Hughes, the son of former Wales and Manchester United footballer Mark Hughes, has died at the age of 38 from Sudden Arrhythmic Death Syndrome (SADS), also known as Sudden Adult Death Syndrome.

Alex Hughes, who served as Grimsby Town's Head of Player Recruitment, was found collapsed on the bedroom floor of his Cheshire home by his two sons at around 7 a.m. on June 19, an inquest at Cheshire Coroner's Court heard.

According to the hearing, Alex's eldest son immediately began CPR before paramedics arrived. Despite prolonged resuscitation efforts, emergency responders were unable to revive him.

Area Coroner Victoria Davies concluded that Hughes died from Sudden Arrhythmic Death Syndrome (SADS), a condition in which a fatal heart rhythm abnormality causes sudden cardiac arrest even though the heart appears structurally normal during a post-mortem examination.

Following his death, Mark Hughes and his wife, Jill, said they were "totally heartbroken by the sudden and unexpected loss of our beloved son."

What Is Sudden Arrhythmic Death Syndrome (SADS)?

SADS refers to a sudden, unexpected death caused by an abnormal heart rhythm in people whose hearts appear structurally normal after death. The condition is most commonly linked to inherited disorders that affect the heart's electrical system, triggering life-threatening irregular heart rhythms (arrhythmias) that can lead to sudden cardiac arrest.

According to the British Heart Foundation, around 500 people die from SADS each year in the UK, with young adults—particularly men—being most commonly affected.

What Causes SADS?

Most cases of SADS are caused by inherited genetic conditions that interfere with the heart's electrical signals. Because these disorders often cause few or no symptoms, many people remain unaware they have them until a cardiac arrest occurs.

Early diagnosis through cardiac evaluation and family screening can help identify those at risk and prevent sudden deaths.

Inherited Conditions Linked to SADS

Several inherited heart rhythm disorders are associated with SADS, including:

  • Brugada syndrome: Causes dangerous abnormal rhythms in the heart's lower chambers (ventricles).
  • Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT): Triggers dangerously fast heart rhythms during exercise or emotional stress.
  • Long QT syndrome (LQTS): Delays the heart's electrical recovery between beats, increasing the risk of life-threatening arrhythmias.
  • Short QT syndrome (SQTS): Causes the heart to recharge too quickly, raising the risk of atrial fibrillation and ventricular arrhythmias.
  • Timothy syndrome: A rare form of Long QT syndrome associated with severe heart rhythm abnormalities.
  • Wolff-Parkinson-White (WPW) syndrome: An extra electrical pathway in the heart causes episodes of rapid heartbeat.

Symptoms That May Signal SADS

Many people with inherited heart rhythm disorders experience no warning signs. However, symptoms that warrant medical evaluation include:

  • Fainting or seizures, particularly during exercise, excitement or emotional stress.
  • Chest pain during physical activity.
  • Shortness of breath while exercising.
  • Episodes of rapid or irregular heartbeat (palpitations).
  • A family history of unexplained sudden cardiac death.

End of Article