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Comment by Dr. Krishna Kumari Challa on March 10, 2026 at 10:18am

Daily multivitamins may slow biological aging, two-year trial suggests

A two-year randomized trial in older adults found that daily multivitamin use slowed biological aging, as measured by five epigenetic clocks, by approximately four months compared to placebo. The effect was more pronounced in participants with accelerated biological age at baseline. These findings suggest multivitamins may modestly slow cellular aging, particularly in those aging faster biologically.
An analysis by investigators found slower aging in older adults after two years of a daily multivitamin, with greater benefits for those who began the trial with accelerated biological age.
How quickly our bodies age on a cellular level, our "biological age," can differ from how old we actually are in years. Using data from a large randomized clinical trial of older adults, researchers evaluated the effects of taking a daily multivitamin over the course of two years on five measures of biological aging and found a slowing equivalent to about four months of aging.

The benefits were increased in those who were biologically older than their actual age at the start of the trial. Their results are published in Nature Medicine.
Epigenetic clocks estimate biological aging based on tiny changes in our DNA. These clocks look at specific sites in our DNA that regulate gene expression (known as DNA methylation) and change naturally as we get older, helping track mortality and the pace of aging.

This study, which uses data from the well-established COcoa Supplement Multivitamins Outcomes Study (COSMOS), analyzed DNA methylation data from blood samples of 958 randomly selected healthy participants with an average chronological age of 70.

The study participants were randomized to take a daily cocoa extract and multivitamin; daily cocoa extract and placebo; placebo and multivitamin; or placebos only. Samples were analyzed for changes in five epigenetic clocks from the start of the trial and at the end of the first and second years.
Compared to the placebo-only group, people in the multivitamin group had slowing in all five epigenetic clocks, including statistically significant slowing seen in the two clocks that are predictive of mortality. The changes equated to about four months less biological aging over the course of two years. Additionally, people who were biologically older than their actual age at the start of the trial benefitted the most.

Howard Sesso, Effects of daily multivitamin–multimineral and cocoa extract supplementation on epigenetic aging clocks in the COSMOS randomized clinical trial, Nature Medicine (2026). DOI: 10.1038/s41591-026-04239-3. www.nature.com/articles/s41591-026-04239-3

Comment by Dr. Krishna Kumari Challa on March 10, 2026 at 10:11am

This doesn't mean lab accidents don't happen. But it does mean that if a virus had been extensively passaged in a lab before an outbreak, we would expect to see it in the evolutionary record. In nearly all pandemics we've studied, that signal simply isn't there.

Looking ahead, the researchers see potential applications in outbreak forensics, viral surveillance and pandemic preparedness.

Jennifer L. Havens et al, Dynamics of natural selection preceding human viral epidemics and pandemics, Cell (2026). DOI: 10.1016/j.cell.2026.02.006

Part 2

Comment by Dr. Krishna Kumari Challa on March 10, 2026 at 10:09am

Recent pandemic viruses jumped to humans without prior adaptation, study finds

A new  study published in Cell challenges a long-standing assumption about how animal viruses become capable of sparking human epidemics and pandemics. Using a phylogenetic, genome-wide analysis across multiple viral families, researchers report that most zoonotic viruses—infectious pathogens that spread from animals to humans, including the cause of COVID-19—do not show evidence of special evolutionary adaptation before spilling over into humans.

From an evolutionary perspective, researchers find no evidence that SARS-CoV-2 was shaped by selection in a laboratory or prolonged evolution in an intermediate host prior to its emergence. That absence of evidence is exactly what we would expect from a natural zoonotic event—and it represents another nail in the coffin for theories invoking laboratory manipulation.

The prevailing model of zoonotic emergence has often assumed that viruses must first acquire adaptive mutations before they can sustain human-to-human spread. To test that assumption, the research team analyzed viral genomes from outbreaks caused by influenza A virus, Ebola virus, Marburg virus, mpox virus, SARS-CoV and SARS-CoV-2. They focused on the evolutionary period immediately preceding human outbreaks, where any substantial pre-spillover adaptation should leave a detectable imprint.

Across these diverse viruses, the investigators found a strikingly consistent pattern: selection pressures before zoonotic emergence were indistinguishable from those acting during routine circulation in animal reservoirs. In other words, there was no evolutionary signal suggesting that these viruses were being "pre-adapted" for humans prior to their outbreaks. Instead, measurable changes in selection typically appeared only after sustained transmission began in people.

These findings challenge the idea that pandemic viruses are evolutionarily special before they reach humans.

Rather than requiring rare, finely tuned adaptations in animals, many viruses may already possess the basic capacity to infect and transmit between humans. What matters most is human exposure to a diverse array of animal viruses.

The study relies on a sophisticated phylogenetic framework that measures changes in the intensity of natural selection across entire viral genomes. By comparing rates of different types of mutations, the researchers were able to detect whether natural selection was intensified, relaxed or unchanged across key evolutionary transitions. Importantly, the team validated their approach using known examples of artificially selected viruses propagated in cell culture or in laboratory animals, which produced clear and reproducible evolutionary signatures distinct from natural transmission.

Part 1

Comment by Dr. Krishna Kumari Challa on March 8, 2026 at 10:45am

Microplastics May Be Fueling Parkinson's Disease, Scientists Warn

Plastic pollution is seeping into the Earth, into wildlife, and into our bodies, and a new research review suggests tiny microplastics and nanoplastics could be disrupting some of the brain processes associated with Parkinson's.

While Parkinson's disease is associated with a wide range of risk factors, the rise we're seeing in the number of people being diagnosed – its prevalence has doubled in the last 25 years – could be at least partly down to a rise in pollutants in the environment.
For this recent review, a team of researchers referenced more than 100 previous studies, including animal studies, laboratory experiments, and computational models, to build a compelling case linking plastics to Parkinson's.
While it's not yet clear that microplastics are directly responsible, the researchers are calling for the association to be investigated further: more data is badly needed on how these ubiquitous particles may accumulate in the body and harm human health.

"With the intensification of global plastic pollution, the potential threats posed by micro- and nanoplastics (MPs/NPs) to human health have become a major concern," write the researchers in their published paper.
MPs/NPs enter the organism through ingestion, inhalation, and skin contact, subsequently accumulating in multiple organs – particularly the brain."
Microplastics are defined as fragments smaller than 5 millimeters, while nanoplastics are smaller than a micrometer – a thousandth of a millimeter. They enter the environment in numerous ways, including dissentegration of plastic waste and the release of water used to wash synthetic clothing.
Connecting findings from previous studies, the review states we ingest plastics through our food and drink, breathe them in through the air, and even absorb them through our skin.
From there, microscopic plastic fragments make their way into our brain by crossing the blood-brain barrier or entering the nerve cells lining of our nasal cavity.
To speculate on what the plastic might do when it's in the brain, the researchers point to studies showing microplastics and nanoplastics encouraging the formation of toxic alpha-synuclein protein clumps typical of brains with Parkinson's.
The review presents evidence that plastic fragments may drive neuroinflammation, disrupt communications between the brain and the gut, and carry damaging metals into the brain – a process known as ferroptosis.
All of these types of damage have been connected to Parkinson's disease in the past.

https://www.nature.com/articles/s41531-026-01272-4

Comment by Dr. Krishna Kumari Challa on March 8, 2026 at 10:39am

Tinnitus may be linked to sleep. Here's how.

Comment by Dr. Krishna Kumari Challa on March 8, 2026 at 10:35am

Scientists Cut Amyloid Plaques by 50% in Mice With Engineered Cells

A new kind of cellular immunotherapy shows promise in preventing Alzheimer's-associated plaques from forming in the brain – and even removing some when given in advanced cases.
Working with mice, scientists at Washington University developed a specially engineered virus that genetically alters cells into "super cleaners" that remove harmful proteins in the brain.
The study's authors have shown that a single injection of their new gene therapy seemed to prevent amyloid plaque development when administered before plaques had begun to form.
Even in mice with existing amyloid plaques, one injection of the gene therapy was associated with a roughly 50 percent reduction in plaques, the researchers report.
The new method borrows from a type of cancer treatment known as chimeric antigen receptor (CAR) T cell therapy, in which scientists can genetically modify the immune system's T cells to attack cancer cells.
In the new study, researchers focused on star-shaped brain cells called astrocytes, which they engineered to hunt down the amyloid beta proteins associated with cognitive decline in Alzheimer's.
This study marks the first successful attempt at engineering astrocytes to specifically target and remove amyloid beta plaques in the brains of mice with Alzheimer's disease.

https://www.science.org/doi/10.1126/science.ads3972

Comment by Dr. Krishna Kumari Challa on March 7, 2026 at 10:18am

Smart combinations of antibiotics can slow down resistance

When a bacterium becomes resistant to one antibiotic, it may sometimes become more sensitive to another. This biological side-effect offers an unexpected opportunity in the fight against antibiotic resistance.

Analysis of extensive clinical data reveals that resistance to one antibiotic can coincide with increased sensitivity to another, a phenomenon known as collateral sensitivity. This effect is observed across multiple bacterial species and suggests that strategic combinations or sequencing of antibiotics could help slow the development of resistance, offering new avenues for treatment optimization.
By switching wisely between antibiotics or combining them, you can use this biological effect—known as collateral sensitivity—to reduce the chance that bacteria become resistant, and prevent treatments from failing.

Sebastian T Tandar et al, Clinical prevalence of collateral sensitivity: a systematic exploration of multicentre antimicrobial surveillance data, The Lancet Microbe (2026). DOI: 10.1016/j.lanmic.2025.101274

Comment by Dr. Krishna Kumari Challa on March 7, 2026 at 10:15am

Cancer has a unique nuclear metabolic fingerprint: New discovery

More than 200 metabolic enzymes, many of which are normally tasked with producing energy in the mitochondria, are also found sitting directly on top of human DNA, according to a study published in Nature Communications. The research shows that different cell types, tissues and even cancers each have a unique pattern of metabolic enzymes compartmentalized inside the nucleus and interacting with DNA. It's the first evidence of human cells having what the authors of the study call a "nuclear metabolic fingerprint."

Though further work needs to be done to clarify whether the enzymes are catalyzing reactions, turning genes on or off or simply providing structural support, the research provides new clues for how different types of tumors grow, adapt or resist treatment.

Many of these enzymes synthesize essential building blocks of life, and their nuclear localization is associated with DNA repair. Their presence in the nucleus may therefore directly shape how cancer cells respond to genotoxic stress, a hallmark of many chemotherapeutic treatments. It's an entirely new world to explore, say the researchers of this new work.

The absence, presence and abundance of the enzymes differed by cancer type. For example, oxidative phosphorylation enzymes were common in breast cancer cells but largely absent in lung cancer cells. When they examined tumor samples from patients, the authors of the study saw a similar pattern, demonstrating the tissue and disease-specific nature of nuclear metabolism.

Scientists have been treating metabolism and genome regulation as two separate universes till now, but  this work suggests they're talking to each other, and cancer cells might be exploiting these conversations to survive.

The researchers carried out experiments to figure out what some of the metabolic enzymes are doing. They studied one group of enzymes which provide building blocks for DNA synthesis and repair and found they gather around chromatin when DNA is damaged, helping repair the genome.

During these experiments they discovered that location matters. The enzyme IMPDH2 showed completely different behavior depending on where it was. When the researchers forced it to stay only in the nucleus, it helped maintain genome stability, but when confined to the cytoplasm, it affected other pathways instead.

The discovery raises new questions about how cancer treatments work. Some drugs target a cancer's metabolic activity, while others target its DNA repair mechanisms. If the two systems are more closely linked than previously thought, it has important implications for cancer research.

It could help explain why tumors of different origins, even when carrying the same mutations, often respond very differently to chemotherapy, radiotherapy, or targeted inhibitors.

According to the authors of the study, their research is the first global evidence that the nucleus is crowded with metabolic enzymes. In the long run, mapping the location and function of the enzymes could help identify new biomarkers for diagnosis or new vulnerabilities that anti-cancer drugs could exploit.

Nature Communications (2026). DOI: 10.1038/s41467-026-69217-2

Comment by Dr. Krishna Kumari Challa on March 7, 2026 at 9:51am

Toxic evolution: wasps and frogs mimic pain molecules to deter predators

Certain species of wasps and frogs share a pain and inflammation peptide similar to one found in vertebrates to help defend against predators—a discovery that contributes to a shifting view of how evolution works, say researchers.

Wasps and frogs independently evolved bradykinin-like peptides, structurally similar to vertebrate bradykinin, as a defense against predators. These peptides originate from toxin gene families, not from the vertebrate kininogen gene, and effectively trigger pain in predators. The findings highlight convergent evolution as a significant and predictable evolutionary process.
In vertebrates, bradykinin plays a role in wound healing and pain signaling. The research demonstrated the bradykinin‑like peptides in wasps and frogs are derived from toxin gene families, not from the vertebrate kininogen gene that produces bradykinin.

Each lineage across multiple wasp and frog families evolved these molecules separately, often multiple times, to deter predators.

Naiqi Shi et al, Repeated convergent evolution of bradykinin mimics as defensive toxins, Science (2026). DOI: 10.1126/science.adx0452

Comment by Dr. Krishna Kumari Challa on March 7, 2026 at 9:45am

Tracking the toxic metals left behind by wildfires

Wildfire heat can convert benign chromium-3 in soil to toxic chromium-6 at around 600oC, but this reverts to the safer form at higher temperatures typical of wildfires (800–1200oC). Iron in soil influences these transformations, suggesting post-fire monitoring of iron content could help assess chromium toxicity risks efficiently.

Alireza Namayandeh et al, Nonlinear Redox Transformations of Chromium in Soil during Wildfire Heating: The Critical Role of Iron Mineralogy, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c10407

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