Headphones (Credit: Canva)
Can't leave your house without your earphones, airpods or headphones? Well, you aren't alone. There are millions of others who feel the same. However, do not be surprised if I tell you that it may lead to memory loss and dementia. According to the National Library of Medicine, the auditory nerve, which carries sound signals to the brain, when constantly bombarded with loud noises, starts transmitting weaker signals. This forces the brain to work harder to interpret the sound, leading to cognitive overload. Prolonged cognitive strain can eventually pave the way for dementia and memory loss.
Long-term headphone use also affects brain function directly. High decibel levels of noise can damage the insulation of nerve fibres that carry auditory signals to the brain, disrupting the flow of information. Moreover, the electromagnetic waves produced by headphones have been linked to problems like headaches, fatigue, and, in some cases, neurological discomfort.
Beyond The Brain, Headphones Can Make You Deaf
Empirical evidence shows that nearly one billion young people are at risk of hearing loss due to excessive exposure to loud music through headphones. For the uninitiated, sound intensity is measured in decibels. Prolonged exposure to noise above 85 decibels can be harmful to hearing. Music listened to at maximum volume using headphones often falls in the range of 85 to 120 decibels, a level capable of causing significant hearing damage over time.
Studies Show The Ill Effects
According to a recent survey in the UK, a staggering 65% of students admitted to listening to music at maximum volume through their headphones. A similar study revealed that adolescents exposed to high noise levels via headphones in noisy environments experienced a hearing loss prevalence of 22.6%. Those who used earphones for 80 minutes or more per day had a hearing loss prevalence of 22.3%. These figures are alarming, especially given how ingrained headphone use has become in daily life.
The ramifications of early-onset hearing loss go far beyond damaged ears. It can also jeopardize your mental health. Hearing loss in youth can set off a chain reaction, leading to social isolation and depression. Over time, it can also escalate and jeopardise your relationships. Ill-fitting headphones add to the woes, causing pain that extends from the inner ear to the jaws and top of the head. They can also lead to ear infections, which eventually hamper cognitive functions.
Protecting hearing and brain health requires a shift in listening habits. Experts recommend keeping the volume below 60 per cent and limiting usage to 60 minutes per day. Investing in noise-cancelling headphones can also help reduce the need to crank up the volume in noisy environments.
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It has been long suspected that Western diets could contribute to the risk of colorectal cancer. The theory may finally have a clearer scientific explanation.
A new study suggests that gut bacteria can convert compounds produced by high-fat, low-fibre diets into cancer-causing chemicals. The research sheds light on how unhealthy eating habits may lead to cancerous tumour growth in colon in the long term.
Published in the journal Gut, the research was led by Dr. Annika Osswald (first author) and Dr. Soeren Ocvirk (corresponding author), along with a large team of international scientists.
The collaboration included researchers from Technical University of Munich (TUM), Germany, German Institute of Human Nutrition (DIfE), RWTH Aachen University, Freie Universität Berlin, University Hospital of Regensburg, and other institutions.
Researchers found that a western-style diet, which is commonly high in red and processed meat, saturated fats, refined carbohydrates and ultra-processed foods, significantly changes the composition of the gut microbiome.
These altered bacteria then modify bile acids in ways that promote inflammation and create an environment that accommodates the development of colorectal cancer tumours.
According to the researchers, diet alone is not the only factor. The trillions of microbes living in the intestine determine how food is processed, producing metabolites that can either protect the gut or damage it.
The study found that specific bacterial groups transformed bile acids into compounds that stimulated tumour growth in the colon.
This provides one of the strongestt explanations yet for why western dietary patterns have consistently been associated with higher risk of colorectal cancer.
"Our findings highlight the critical interaction between diet, gut microbes and cancer biology," the researchers noted, adding that targeting the microbiome could become a future strategy for preventing colorectal cancer.
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A western diet typically includes:
Previous research has repeatedly linked this eating pattern with obesity, diabetes, heart disease and colorectal cancer, but scientists have long found it challenging to explain the exact cause until now.
The human gut is home to trillions of bacteria that help digest food, regulate immunity and produce beneficial compounds like fatty acids.
A fibre-rich diet supports good bacteria that reduce inflammation, whereas diets high in fat and processed foods can cause microbial imbalance.
The new findings suggest this imbalance changes how bile acids are metabolised, increasing the production of molecules capable of damaging the colon and supporting cancer growth in the long run.
Also read: WHO Cancer Agency Flags 3 Common Medicines As Carcinogenic: What It Means For Millions Of Patients
Earlier research has linked harmful gut bacteria, including toxin-producing E. coli, with DNA damage that may begin early in life and contribute to the rise of colorectal cancer among younger people.
However, the latest findings do not prove diet alone causes cancer. Genetics, obesity, physical inactivity, sedentary life, smoking and alcohol consumption also influence risk.
However, they say maintaining a fibre-rich diet with fruits, vegetables, legumes and whole grains may help preserve a healthier gut microbiome and lower long-term colorectal cancer risk.
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Could air pollution may do more than harm the lungs and heart? A new study has found that exposure to polluted air could trigger painful flare-ups in people living with rheumatoid arthritis (RA).
The study comes when evidence is mounting that environmental factors contribute significantly to autoimmune diseases.
The study, published in the Annals of the Rheumatic Diseases, found that excessive exposure to air pollutants, particularly fine particulate matter (PM2.5), was associated with increased rheumatoid arthritis activity and a greater risk of flare ups.
Researchers say the findings suggest that improving air quality should become an important part of managing the chronic condition, alongside treatment, medications and lifestyle changes.
"Our findings highlight that environmental exposure, especially air pollution, may significantly influence rheumatoid arthritis disease activity and flare risk," the researchers said, noting that patients and clinicians should consider air quality as a modifiable risk factor.
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Rheumatoid arthritis is an autoimmune disease in which the immune system attacks healthy joints, causing pain, swelling, stiffness and, over time, permanent joint damage.
While genetics, smoking and infections have been recognised as risk factors, scientists are investigating how environmental pollutants may worsen the disease.
The latest findings are particularly relevant for countries such as India, where millions are exposed to unhealthy air for large parts of the year. Previous reports have already linked poor air quality in cities like Delhi to rising concerns over autoimmune diseases.
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A flare is a period when rheumatoid arthritis symptoms suddenly worsen. During this time, people may experience:
Flares can last from a few days to several weeks and are often triggered by infections, stress, missed medications or other environmental factors.
Researchers believe tiny airborne particles like PM2.5 can enter the lungs and bloodstream, triggering inflammation throughout the body.
This inflammatory response may overstimulate the immune system, making rheumatoid arthritis symptoms worse and increasing the likelihood of painful flare-ups.
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The researchers emphasised that the study shows an association rather than proving that air pollution directly causes rheumatoid arthritis flares.
However, the consistent link suggests reducing exposure to polluted air may help lower the chances of flare-ups in high-risk individuals.
Experts advise patients to continue prescribed medications, constantly monitor local air quality, avoid outdoor activities during periods of severe pollution when possible, and discuss symptom changes with their rheumatologist.
The findings add to a growing body of research linking air pollution with autoimmune diseases.
Earlier studies have suggested that long-term exposure to pollutants may increase the risk of developing rheumatoid arthritis, while the new research indicates polluted air may also worsen symptoms in people already living with the disease.
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Commonly prescribed medicines for high blood pressure and heart disease could also help antidepressants work better, according to a new study by researchers at the All India Institute of Medical Sciences (AIIMS).
The research offers hope for people with depression whose condition is not adequately managed with standard antidepressants.
The study found that certain cardiovascular medications, when taken along with antidepressants, may improve the brain's response to treatment, potentially making clinical depression treatments more effective.
The findings establish a foundation for repurposing common medicines to improve mental health treatment. The researchers stress that larger clinical trials are needed to validate the study before it can be included in standard depression treatments.
"Our findings suggest that some drugs already being used to treat hypertension and heart disease may have the potential to act as adjuncts to antidepressant therapy," the AIIMS research team said.
They also said that the strategy could particularly benefit patients who do not respond to antidepressants well.
Even though depression affects hundreds of millions of people worldwide, almost one-third of patients do not receive adequate relief from their first antidepressant.
Even when medications work, they often take several weeks to show results. This has led researchers to explore more ways to improve treatment outcomes, especially for mental health issues.
Repurposing existing medicines is considered an attractive strategy because their safety profiles are already well understood, potentially reducing the time and cost needed to bring new treatment options into clinical practice.
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Antidepressants, including selective serotonin reuptake inhibitors (SSRIs), are among the most commonly prescribed medicines for moderate to severe depression. They work by changing the levels of neurotransmitters like serotonin in the brain, helping regulate mood over time.
However, individual responses may vary widely, and many patients end up needing multiple treatment approaches before achieving any relief.
While the exact biological mechanisms are still under investigation, researchers believe that some cardiovascular drugs may have an effect on pathways associated with inflammation, blood flow to the brain, or nerve signaling, all of which are increasingly play a role in depression treatment.
The researchers noted that these medicines are not intended to replace antidepressants. Instead, they could eventually be used alongside standard treatment to improve its effectiveness in some patients.
Experts caution that patients should not start or stop blood pressure or heart medications in the hope of treating depression without clinical supervision.
More clinical studies are required to identify which cardiovascular drugs offer the greatest benefit, which patients are most likely to respond, and whether the combination remains safe over long-term use.
The AIIMS study could pave the way for a cost-effective strategy to improve depression treatment by giving a new role to medicines that are already widely available.
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