Thursday, 30 April 2026

Ancient DNA Study Reveals Human Evolution Is Happening Faster Than We Thought

By Harvard Medical School, April 28, 2026


A massive ancient-DNA dataset reveals that subtle evolutionary forces have been steadily reshaping human populations since the Ice Age.
 Credit: Stock



New research challenges long-standing assumptions about human evolution, revealing that natural selection has been more active—and more recent—than once believed.

A sweeping analysis of ancient DNA from nearly 16,000 people is reshaping how scientists understand human evolution. By tracking genetic changes across more than 10,000 years in West Eurasia, researchers found that natural selection has been far more active in recent human history than once believed.

For years, evidence for directional selection was surprisingly limited. Only about 21 clear cases had been identified. This process occurs when a specific gene variant provides a survival or reproductive advantage and becomes more common over time, such as the ability to digest milk into adulthood. Because so few examples were known, scientists assumed that this type of evolution played only a minor role after humans spread out of Africa roughly 300,000 years ago.

By analyzing a vastly expanded dataset and applying new statistical tools, researchers uncovered hundreds of gene variants that rose or fell in frequency over time. The findings suggest that human evolution did not slow down in recent millennia. In some ways, it sped up.

Links to Traits and Health

Many of the genetic variants identified in the study are tied to complex traits seen today, including risks for type 2 diabetes and schizophrenia. Exploring how these traits evolved could improve understanding of human biology and disease, and may eventually guide medical research.

At the same time, the authors caution that modern trait definitions do not always apply to ancient populations. For example, measures like household income have no direct equivalent in prehistoric societies, making it difficult to determine why certain variants were originally advantageous.

The study, led by researchers at Harvard University, was published in Nature.

“With these new techniques and large amount of ancient genomic data, we can now watch how selection shaped biology in real time,” said Ali Akbari, the study’s first author. “Instead of searching for the scars natural selection leaves in present-day genomes using simple models and assumptions, we can let the data speak for itself.”

“This work allows us to assign place and time to forces that shaped us,” said senior author David Reich.
10,000 ancient genomes, new computational methods

Since 2010, when scientists first recovered genome-wide data from ancient human remains, the field has transformed our understanding of how populations are related across time and geography.

Still, researchers have struggled to track how natural selection influenced genetic variation over the past 10,000 years, even though DNA from this period is often well preserved.

This study overcame that challenge through two major advances.

First, Reich’s team spent seven years assembling a large and detailed dataset of ancient DNA from West Eurasia, covering present-day Europe and parts of the Middle East. The effort involved more than 250 archaeologists and anthropologists and produced new genetic data from 10,016 ancient individuals. These were combined with 5,820 previously published ancient genomes and 6,438 modern samples.

“If the goal is to uncover changes in the frequency of genetic variants in the last ten millennia that are greater than can be expected by chance, then we need to detect subtle effects, which requires having thousands of genomes spanning that time period,” Reich explained.

“This single paper doubles the size of the ancient human DNA literature,” he added. “It reflects a focused effort to fill in holes that limited the power of previous studies to detect selection.”

The regions from which ancient and recent human DNA samples were studied in this work.
 Credit: Akbari A et al., “Ancient DNA reveals pervasive directional selection across West Eurasia,” Nature (2026)

The second advance was a set of computational methods developed by Akbari to separate true signals of directional selection from other influences on gene frequency, such as migration, population mixing, and random fluctuations in small populations.

“Ali developed a powerful technique that could zoom in on the patterns that actually mattered,” said Reich.

Even with these tools, the signal was faint. The researchers estimate that directional selection explains only about 2 percent of all genetic changes observed.

What has natural selection selected for?

That small percentage still represents a significant portion of the genome. The team identified 479 gene variants, or alleles, that were strongly favored or disfavored in West Eurasian populations.

They also traced when and where some of these variants rose or declined. The results show that selection intensified after farming emerged, likely because new diets, environments, and lifestyles created different evolutionary pressures.

More than 60 percent of the selected variants are linked to traits seen in people today, including

:Light skin tone

Red hair

Risk of celiac disease and Crohn’s disease

Immunity to HIV infection and resistance to leprosy

Lower chance of male-pattern baldness

Lower risk of rheumatoid arthritis and alcoholism

Having the B version of the proteins on red blood cells that confer A, B, and O blood types and influence resistance to infection with bacteria and viruses

In some cases, groups of SNPs were under selection together to influence polygenic traits. Some changes raised the frequency of beneficial traits, including some that are interpreted today as

:“Health span” traits such as faster walking pace

Measures of behavioral and social status or cognitive functions, such as scores on intelligence tests, household income, and years of schooling

Other changes reduced the frequency of harmful traits, such as those that are interpreted today as

:Reduced risk of bipolar disorder and schizophrenia

Lower body fat percentage, waist-to-hip ratio, and body mass index

Less susceptibility to tobacco smoking

Some variants rose in frequency and later declined, reflecting shifting environments. For instance, genes linked to susceptibility to tuberculosis and multiple sclerosis showed changing patterns over time.

Not all results are straightforward. One example is a major genetic risk factor for gluten intolerance that became more common after wheat farming began.

Interpreting the Results

The researchers stress that these associations must be interpreted carefully.

A gene’s link to a modern trait does not mean that trait drove its spread in the past. Traits like education level or income did not exist in ancient societies, so they cannot explain why certain variants were favored.

Some variants affect multiple traits, and current databases may not capture their full effects. In other cases, a variant may have increased in frequency simply because it is located near another gene under selection.

It is also possible that some traits influenced by these variants remain unknown today.

Another key point is that these findings are not limited to West Eurasia. The same methods can be applied to other populations with sufficient ancient DNA data to determine which patterns are shared and which are unique.

Reich expects future work to reveal that some selective pressures acted on common traits across different human groups, even as populations spread and adapted to new environments.

What comes next

The researchers have made their data and methods publicly available to support further studies.

One next step is to investigate more than 7,600 additional genetic locations that may represent cases of directional selection. Akbari said these sites have better than a 50 percent chance of “being real examples of directional selection” and deserve closer examination.

Applying the methods to other regions and older time periods is another priority.

“To what extent will we see similar patterns in East Asia or East Africa or Native Americans in Mesoamerica and the central Andes?” Reich asked. “If we can’t use ancient DNA to study the most important period in human evolution 1 million to 2 million years ago, then at least we can study selective pressure on human genomes during more recent periods of change and learn broader principles.”

Further laboratory studies will also be needed to understand how these genetic changes affect health.

The findings could help identify new factors involved in disease, improving risk prediction and treatment. They may also inform gene therapy research. For example, targeting a gene that has been strongly favored by evolution could carry risks.

“You could speculate that if the variant someone wants to knock out was strongly selected for, it’s probably not the best idea,” he said.

Scientists could also use the new methods to study natural selection in other species. Such work could uncover alleles that have made cattle or chickens well-suited to domestication, Akbari suggested, or that have helped animals adapt to changes in climate.

The possibilities are enticing for deepening our appreciation of human diversity, history, and health, Reich said.

“This paper shows how complex selection can be and provides an opportunity to consider the richness of variation in human populations,” he said.


The Life of Earth
https://chuckincardinal.blogspot.com/

Common Food Compound Shows Surprising Power Against Superbugs

By Higher Education Press, April 28, 2026

A plant-based food additive was found to suppress bacterial gene exchange in lab and animal models. Its ability to act without noticeable toxicity highlights its potential for controlling resistance spread. 
Credit: Stock

A familiar compound found in everyday foods may hold unexpected potential in the fight against antibiotic resistance.

A compound found in everyday foods may offer a new way to slow one of the most urgent threats to modern medicine. Researchers report in Engineering that cinnamic acid, a natural substance present in cinnamon and widely used as a food additive, can interfere with how bacteria share antibiotic resistance.

Antibiotic resistance is a growing global crisis. The World Health Organization has warned that common infections are becoming harder to treat as bacteria evolve defenses against widely used drugs. In the United States alone, antibiotic-resistant infections cause more than 2.8 million illnesses and over 35,000 deaths each year. A major reason for this rapid spread is not just mutation, but the ability of bacteria to exchange genetic material directly.

This exchange often happens through plasmid conjugation, a process in which bacteria pass small DNA molecules, known as plasmids, to one another. These plasmids can carry powerful resistance genes such as mcr‑1, blaNDM‑1, and tet(X4), allowing even unrelated bacterial species to quickly acquire drug resistance. Efforts to block this process have been limited, as many candidate compounds are either toxic or fail to work effectively in living systems.

To address this gap, researchers investigated cinnamic acid. This plant-derived compound is part of the human diet and is produced naturally as a defense molecule in many species. The team tested its effects in controlled lab settings, simulated gut environments, and live animals, focusing on several plasmids commonly linked to clinical infections.

Blocking Gene Transfer Without Harming Growth

Rather than killing bacteria outright, cinnamic acid appears to disrupt their ability to share genetic information. The results showed that CA lowered the transfer rate of multiple resistance plasmids in a concentration-dependent manner. Importantly, it did not significantly affect bacterial growth within the tested range.

A fluorescence-labeled plasmid tracking system confirmed that CA reduces plasmid transfer within gut microbial communities ex vivo. In mouse experiments, oral doses of CA also decreased conjugation frequency in vivo in a dose-dependent pattern, indicating that the compound remains active under real biological conditions.

Further analysis revealed how CA produces these effects. Transcriptomic data showed that it disrupts the tricarboxylic acid cycle, which weakens the electron transport chain and reduces proton motive force. As a result, intracellular ATP levels drop, limiting the energy needed for conjugation. CA also suppresses genes involved in mating pair formation, DNA transfer, and replication, while slightly increasing the permeability of the donor cell outer membrane.

Safety and Biological Compatibility

Safety testing in mice showed no clear harmful effects after CA treatment. Body weight remained stable, and there were no noticeable changes in the structure of major organs.

The composition and diversity of gut microbiota also remained unchanged, supporting the compound’s strong safety profile for in vivo use.

Overall, the findings identify cinnamic acid as a broad-spectrum inhibitor of plasmid conjugation that works by disrupting bacterial energy metabolism. Because it is already widely consumed and considered safe, CA could serve as a practical addition to current strategies aimed at slowing the spread of antibiotic resistance. The results also encourage further research into natural compounds that target metabolism to control gene transfer in medical, agricultural, and environmental settings.


The Life of Earth
https://chuckincardinal.blogspot.com/

Scientists Just Discovered Light Can Actually Slow Plant Growth

By Osaka Metropolitan U., April 29, 2026

Cells exposed to light showed a different fluorescence pattern, consistent with the accumulation of large amounts of p-coumaric acid, a compound that strengthens cell walls. 
Credit: Osaka Metropolitan University

Light doesn’t just help plants grow, it also strengthens their internal structure by tightening the connection between tissues. This added rigidity can actually slow growth, revealing a hidden balance between strength and expansion.

Light is widely recognized as a key factor in plant growth, but scientists are still uncovering the details of how it works. Researchers at Osaka Metropolitan University have now identified a previously unknown process that helps explain how light influences plant development.

Light Increases Adhesion Between Plant Tissues

The study, led by Professor Kouichi Soga from the Graduate School of Science, focused on young pea stems. The team developed a specialized technique to measure how strongly the epidermal (the outermost layer) is connected to the inner tissues. Their experiments showed a clear difference depending on whether the plants were grown in light or darkness.

Plants exposed to light had significantly stronger adhesion between these layers compared to those grown in the dark.

“Compared with plants grown in the dark, the epidermal and inner tissues of plants grown in the light are more tightly bound together,” Professor Soga said. “This phenomenon has never been reported before, making it a particularly interesting finding.”

p-Coumaric Acid Strengthens Plant Cell Walls

To investigate the cause of this effect, the researchers examined the plant cells using a fluorescence microscope. They observed that stems grown in light produced signals indicating higher levels of a phenolic acid known as p-coumaric acid.

This compound plays a role in reinforcing plant cell walls, which helps increase the strength of the connection between tissues.

“This provided strong evidence that the accumulation of p-coumaric acid was a key factor in strengthening the adhesion between the epidermal and the inner tissues,” said Yuma Shimizu, a graduate student and first author of the study.

Stronger Adhesion Can Limit Plant Growth

The findings reveal that this increased adhesion has a direct impact on growth. While stronger connections improve structural integrity, they also make it harder for the inner tissues to expand.

As a result, overall stem growth is reduced. This suggests that light not only supports plant development but can also restrict it by tightening internal structures.

Implications for Plant Growth and Crop Resilience

The researchers believe this mechanism could be part of a broader pattern in how plants regulate growth. By continuing to measure adhesion under different conditions, they aim to determine whether this process applies widely across plant species.

“By measuring the adhesion between the epidermal and the inner tissues as stem growth changes in response to various factors, we expect to determine whether growth regulation mediated by changes in adhesion is a universal mechanism,” Professor Soga concluded. “These findings could be highly significant for plant cultivation. If we can control adhesion, it may be possible to breed plants with improved tolerance to environmental stress.”


The Life of Earth
https://chuckincardinal.blogspot.com/

Wednesday, 29 April 2026

2.8 Days to Disaster: Scientists Warn Low Earth Orbit Could Suddenly Collapse

BY SCITECHDAILY.COM, APRIL 28, 2026

A new study suggests that modern satellite networks may be far more fragile than they appear, with the risk of orbital collisions rising sharply if control systems are disrupted. 
Credit: Shutterstock

A new study warns that if satellite operators suddenly lose control during a major disruption, a catastrophic collision in orbit could happen in as little as 2.8 days.

A major solar storm does not need to smash satellites apart directly to create a crisis in orbit. It may only need to interrupt the tracking, commands, and avoidance maneuvers that keep today’s crowded satellite environment under control.

That risk is growing as low Earth orbit fills with mega constellations, large networks of satellites launched and replaced in rapid cycles. These spacecraft support internet access, communications, weather monitoring, navigation, and other services. However, they also add congestion to an orbital region where objects travel at roughly 17,000 miles per hour (27,000 kilometers per hour).

A new paper led by Sarah Thiele, who began the work as a PhD student at the University of British Columbia and is now at Princeton, attempts to measure how fragile this system has become. The study introduces a metric called the Collision Realization And Significant Harm (CRASH) Clock, which estimates how long it could take for a serious collision to occur if satellites could no longer maneuver or if operators lost reliable awareness of where objects were.

The result is alarming. Using satellite catalog data from June 2025, the researchers calculated that if operators lost the ability to send commands for avoidance maneuvers, a catastrophic collision could occur in around 2.8 days. A broader version of the CRASH Clock, based on all resident space object interactions, was 5.5 days. Back in 2018, before the rapid expansion of mega constellations, that value was 164 days.

Solar storms as a systemic threat

Satellites in low Earth orbit do not simply coast along fixed paths. They depend on station keeping, tracking updates, and collision avoidance maneuvers. According to SpaceX’s most recent biannual report cited in the study, Starlink satellites performed 144,404 collision avoidance maneuvers between December 1, 2024, and May 31, 2025. That averages 41 maneuvers per satellite per year, or one avoidance maneuver every 1.8 minutes across the Starlink network.

Paths of Starlink satellites as of Feb 2024. 
Credit: NASA Scientific Visualization Studio

During a major solar storm, this carefully managed system can become harder to control. Solar storms heat Earth’s upper atmosphere, causing it to expand. That increases drag on satellites, pulls spacecraft away from predicted paths, forces operators to use fuel to maintain altitude, and makes orbit forecasts less reliable.

The May 2024 “Gannon Storm” showed how disruptive this can be. Nearly half of all active satellites in low Earth orbit maneuvered because of increased atmospheric drag. The study notes that widespread repositioning, combined with unpredictable drag, made collision assessment during and after the storm much harder.

The danger grows if a storm also disrupts navigation, communications, or ground control. In that case, satellites may be harder to track just as they become less able to respond.

Why one collision matters

Kessler syndrome is the most well-known version of this kind of catastrophe, where cascading collisions fill orbit with debris and eventually make it extremely difficult to safely launch or operate spacecraft. But that runaway scenario would take years or decades to fully unfold.

To highlight the much more immediate danger, the researchers introduced a new metric called the Collision Realization and Significant Harm (CRASH) Clock, which estimates how quickly a major, debris-generating collision could become possible if active satellite control and coordination were disrupted.

Even one high-speed impact can have lasting consequences. A collision between large objects can create thousands of fragments, each becoming another hazard. Today’s debris environment is still shaped by China’s 2007 anti-satellite test involving Fengyun 1C and the 2009 collision between Iridium 33 and Kosmos 2251.

The new study finds that the densest parts of today’s satellite networks are now especially concerning. Starlink’s main shell, around 550 kilometers (342 miles) above Earth, reaches densities more than an order of magnitude higher than the peak in tracked debris near 800 kilometers (497 miles).

A shrinking margin for error

The researchers estimate that across all of low Earth orbit, close approaches within 1 kilometer (0.62 miles) occur every 36 seconds. Encounters involving at least one satellite occur about every 41 seconds, while those involving Starlink and another resident space object occur about every 47 seconds.

A close approach is not the same as a collision. Operators weigh distance, uncertainty, object size, and collision probability before deciding whether to move a satellite. Still, the frequency of these encounters shows how dependent orbit has become on fast, accurate, coordinated control.

Major solar storms are rare, but they are not hypothetical. The May 2024 Gannon Storm was the strongest geomagnetic storm in decades. The Carrington Event of September 1859 was at least twice as intense, according to the paper, and included two strong storms within a few days.

If a Carrington-scale storm occurred today, it would hit a world that relies heavily on satellites for communications, timing, Earth observation, weather forecasting, military operations, disaster response, finance, and navigation. It would also strike an orbital environment far more crowded than it was even a decade ago.

Beyond collision risk, mega constellations also contribute to debris, reentry hazards, interference with astronomy, and atmospheric pollution.

The study does not call for eliminating satellites, but it highlights a critical vulnerability. Low Earth orbit now relies on constant, precise control, and if that control is disrupted, the window to prevent a major collision could be just days.




The birth of modern Man
https://chuckincardinal.blogspot.com/

Natural Compound Shows Powerful Potential Against Rheumatoid Arthritis

By Higher Education Press, April 28, 2026

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which the immune system attacks the joints, causing inflammation, pain, swelling, and progressive damage. It can also affect other organs, making it a systemic condition, and often requires long-term treatment to manage symptoms and slow its progression. 
Credit: Stock

A new study links fatty acid metabolism to rheumatoid arthritis treatment, revealing a natural compound that disrupts inflammation by targeting a previously overlooked enzyme.

A compound derived from a traditional medicinal plant may offer a new way to treat rheumatoid arthritis by targeting how the body processes fats rather than simply suppressing the immune system.

In a study published in Engineering, researchers examined obakulactone (OL), a natural molecule from Phellodendri cortex. They found that OL promotes the breakdown of acyl coenzyme A thioesterase 1 (ACOT1), a protein involved in fatty acid metabolism. This process occurs through the ubiquitin‒proteasome system and helps restore balance in unsaturated fatty acids, which are closely linked to inflammation.

Rheumatoid arthritis is not only driven by immune dysfunction but also by metabolic changes, including disruptions in lipid pathways. Targeting these pathways offers an alternative direction for treatment.

Experimental Model and Treatment Effects

The researchers tested OL in rats with rheumatoid arthritis induced by complete Freund’s adjuvant. The animals received daily doses of OL at low, medium, and high levels for 21 days.

Treated rats showed reduced joint swelling and improved cartilage and synovial tissue structure. The thymus and spleen, which are involved in immune regulation, also showed signs of recovery.

(a) OL makes the ACOT1 protein break down faster, meaning it controls ACOT1 after it is made.
(b) Blocking the cell’s protein disposal system prevents this effect, confirming OL works through that pathway.
(c) OL reduces ACOT1 by marking it for destruction via the ubiquitin–proteasome system.
(d) By lowering ACOT1, OL reduces harmful fatty acids and inflammation signals, slows abnormal joint cell growth, and helps relieve joint damage in rheumatoid arthritis.
 Credit: Hongda Liu, Le Yang et al.

OL reduced the presence of inflammatory immune cells in joint tissue. It shifted macrophages from the proinflammatory M1 (CD86) type to the anti-inflammatory M2 (CD206) type and limited the formation of Th17 cells from CD4⁺ T cells.

Blood levels of inflammatory molecules, including IL-1β, IL-6, IL-17, and TNF-α, decreased. RA-related markers such as RF, CCP-Ab, CRP, and MMP-3 were also reduced, with stronger effects at higher doses.
Multiomics Insights and Cellular Mechanisms

Multiomics analyses showed that OL corrected abnormalities in key unsaturated fatty acids, including arachidonic acid, linoleic acid, and α-linolenic acid. These molecules influence inflammation through their role in signaling pathways.

In lab experiments, OL slowed the growth of synovial fibroblasts, triggered their programmed cell death, and reduced their release of inflammatory signals.

Binding studies confirmed that OL directly targets ACOT1, with a dissociation constant (Kd) of (6.18 ± 0.26) μmol·L⁻¹ (analyzed by microscale thermophoresis (MST)) and (6.34 ± 0.38) μmol·L⁻¹ (analyzed by surface plasmon resonance (SPR)). OL promotes the degradation of ACOT1, which lowers levels of stearoyl-CoA desaturase-1 (SCD1).

This effect disrupts signaling pathways that drive disease progression, including Janus kinase (JAK)–signal transducer and activator of transcription (STAT) and phosphoinositide 3-kinase (PI3K)–protein kinase B (AKT). As a result, inflammation and fibrosis in synovial fibroblasts are reduced.
Therapeutic Implications for Rheumatoid Arthritis

Additional experiments confirmed that ACOT1 is central to OL’s anti-inflammatory, antiproliferative, and proapoptotic effects, linking fatty acid regulation to immune signaling pathways.

Rheumatoid arthritis affects about 1% of the global population, and current treatments can have limited effectiveness and significant side effects.

These findings suggest that targeting ACOT1 and fatty acid metabolism could lead to more precise treatment strategies that address underlying disease mechanisms.


The Life of Earth
https://chuckincardinal.blogspot.com/

Scientists Uncover How Serotonin May Trigger Tinnitus

BY OREGON HEALTH & SCIENCE U., APRIL 28, 2026

Scientists have identified a brain circuit that directly connects serotonin signaling to the auditory system, offering new insight into how tinnitus may arise. 
Credit: Stock

A widely used neurotransmitter for treating mental health conditions may have unintended consequences for auditory perception.

New research published in the Proceedings of the National Academy of Sciences suggests that a neurotransmitter widely used to treat depression and anxiety may also worsen a frustrating condition known as tinnitus.

Tinnitus causes a persistent ringing or buzzing in the ears. For some people it is a minor nuisance, but for others it can lead to significant distress and anxiety. The condition is common worldwide, affecting up to 14% of the population, with many cases considered severe.

Scientists at Oregon Health & Science University and Anhui University in China used a mouse model to study the effects of serotonin in the brain. They found that higher serotonin levels were linked to stronger behavioral signs associated with tinnitus.

Co-senior author Laurence Trussell, Ph.D., a professor of otolaryngology at the OHSU School of Medicine and a researcher at the OHSU Vollum Institute and Oregon Hearing Research Center, said the results could be important for millions of people living with tinnitus.

“People with tinnitus should work with their prescribing physician to find a drug regimen that gives them a balance between relief of psychiatric symptoms like depression and anxiety, while minimizing the experience of tinnitus,” Trussell said. “This study highlights the importance of clinicians recognizing and validating patient reports of medication-associated increases in tinnitus.”

Antidepressants and Auditory Effects

The medications involved include selective serotonin reuptake inhibitors, or SSRIs, a widely used class of antidepressants. These drugs treat moderate to severe depression and anxiety by increasing serotonin levels in the brain.

“We’ve suspected that serotonin was involved in tinnitus, but we didn’t really understand how,” said co-author Zheng-Quan Tang, Ph.D., of Anhui University in China. “Now, using mice, we’ve found a specific brain circuit involving serotonin that goes straight to the auditory system, and found that it can induce tinnitus-like effects. When we turned that circuit off, we were able to ameliorate the tinnitus significantly.

“This gives us a much clearer picture of what’s going on in the brain — and points toward new possibilities for treatment.”

Tang began this work as a postdoctoral researcher in Trussell’s lab.
‘A delicate balance’

The study builds on earlier research published in 2017 and provides new details about how tinnitus may develop.

Researchers used optogenetics, a technique that uses fiber optics to deliver light into the brain, allowing them to activate serotonin-producing neurons with precision. They then measured how the mice responded using a modified auditory startle test.

“When you stimulate these serotonergic neurons, we can see that it stimulates activity in the auditory region in the brain,” Trussell said. “We also saw that animals then behaved as if they were hearing tinnitus. In other words, it’s producing symptoms that we would expect to be experienced as tinnitus in humans.”

These results match reports from some patients who notice that tinnitus worsens when taking medications that increase serotonin, including SSRIs.

“Our study suggests a delicate balance,” he said. “It may be possible to develop cell- or brain region-specific drugs that steer the elevation of serotonin in some brain regions but not others. In that way, it may be possible to separate the beneficial and important effects of the antidepressant from the potentially harmful effects on hearing.”


The Life of Earth
https://chuckincardinal.blogspot.com/


Tuesday, 28 April 2026

 Michael Button History,  26 Apr 2026

For most of human history, survival demanded something from us. Memory. Awareness. Social intelligence. The ability to think under pressure. If you lost those skills… you didn’t make it. 

But today, we don’t need them anymore. We’ve outsourced memory to devices. Navigation to GPS. Even thinking is starting to be handed over to algorithms and AI. So what happens when the very skills that built civilisation… are no longer required? 

In this video, we compare two humans separated by thousands of years - and the result is uncomfortable. Because this isn’t just about the past. It’s about what we’re becoming.

https://www.youtube.com/watch?v=y_Q-o0z8zfw


The birth of modern Man
https://chuckincardinal.blogspot.com/


Common Food Preservative Linked to Rising Suicide Deaths Among Young People

By BMJ Group, April 28, 2026


A widely used food preservative is increasingly linked to suicide deaths in the UK, particularly among younger individuals and men, according to a multi-year forensic analysis. 
Credit: Shutterstock



Sodium nitrite-related suicides are increasing in the UK, especially among young people, prompting calls for regulation and better safeguards.

A widely available food preservative is emerging as a disturbing factor in a growing number of suicide deaths in the UK — particularly among young people. Researchers analyzing cases from the past five years have identified a sharp rise in incidents involving sodium nitrite, a common curing agent, raising urgent questions about how easily it can be accessed and misused.

The trend is especially pronounced among boys and young men, who account for the majority of cases. The findings, published in BMJ Public Health, suggest that what was once considered a routine household or industrial chemical is now playing a troubling role in preventable deaths.

Researchers say there is an urgent need for public health officials to reassess the unrestricted availability of this substance to prevent further avoidable deaths.

Although suicide rates in the UK have generally declined since the early 1990s, recent data suggest a reversal of this trend. This increase appears to coincide with growing reports worldwide of suicides involving sodium nitrite poisoning.

Investigating Sodium Nitrite Poisoning Cases

To examine whether sodium nitrite is contributing to suicide deaths in the UK, researchers reviewed case records submitted by coroners, forensic pathologists, and police between March 2019 and August 2024. These cases were analyzed by the main UK laboratory responsible for measuring nitrite and its oxidized form, nitrate, in postmortem samples.

During this period, the lab processed 274 samples linked to 201 suspected cases of intentional or accidental poisoning across the UK, Ireland, and Gibraltar.

Most cases were reported in Greater London, South East England, Ireland, and the Midlands. However, the researchers caution that this distribution may reflect differences in reporting awareness rather than actual regional rates.


Sodium nitrite is a chemical compound commonly used as a food preservative, particularly in processed meats, where it helps prevent bacterial growth and maintains color and flavor.
 Credit: Shutterstock



Increase in Cases and Data Scope

Case numbers rose sharply after 2019, which was the first year testing for nitrite and nitrate became available.

The final dataset included only cases approved by coroners, representing 82% (164) of all cases received during the study period.

The average age of individuals was 28. Ages ranged from 14 to 74 among males and 17 to 82 among females. Nearly three-quarters (71%) of cases involved younger groups, including Gen Z (33%; born 1981-96) and Millennials (38%; born 1997-2012, though counted only up to 2005 to separate minors, who made up 4% of cases).
Demographics and Gender Patterns

Men accounted for the majority of cases, with 109 compared to 52 women. In nearly every age group, more than half of the cases involved men. The only exception was the oldest group (Silent generation, born 1928-45), which included a single case involving a woman.

In 87% of cases, blood levels of nitrite and nitrate were about 100 times higher than normal physiological levels, strongly suggesting intentional ingestion.

The researchers also note important limitations. Testing for nitrite and nitrate is not routinely required in all suspected suicide cases, making it difficult to determine the true number of deaths linked to this substance.

Limitations and Underreporting Concerns

“It is therefore likely that the cases included here represent a substantial underestimate of the actual incidence. Secondly, the interval between death and sample receipt varied considerably, introducing the possibility that delays may have affected the accuracy of the biochemical measurements,” they say.

Despite these limitations, the increase in cases among younger individuals, who are often highly familiar with digital tools, is troubling.

“Intentional poisoning has contributed to these recent increases, and at least in the USA, this rise has been partly attributed to the use (and availability) of sodium nitrite,” they point out.

Online Access and Emerging Risks

“This trend has emerged alongside freely accessible online information detailing how sodium nitrite can be obtained and used, disseminated both under the guise of providing mental health support and for more explicitly harmful purposes,” they explain.

The findings point to the need for immediate action. “Collectively, these findings establish unequivocally that use of sodium nitrite in the UK as a method of suicide is both substantial and concerning,” they write.

“Our data provide strong support for the suggestion that the improved digital literacy of younger people enables access to illicit online material promoting suicide practices and lends further support for calls for tighter legislation to prevent availability of such information in online forums,” they add.

Prevention Measures and Policy Recommendations

Meanwhile, the researchers suggest practical steps to reduce harm. Providing an antidote (methylthioninium chloride kits) in ambulances could offer “a simple and cost-effective timely method to prevent the devastating consequences of ingestion,” they point out.

Lead researcher Professor Amrita Ahluwalia adds, “This is an extremely difficult subject to talk about, and we appreciate the impact that this might have on all those affected by suicide.

“What our research shows is deeply upsetting. But it makes clear why urgent steps are needed to regulate access to this chemical and to reduce the spread of harmful information about it online.”


The birth of modern Man
https://chuckincardinal.blogspot.com/

Your Pleasant Memories Can Vanish For a Surprisingly Simple Reason

28 April 2026, ByM. Spear, The Conversation

(Agung Pandit Wiguna/Pexels)

My husband was recently describing something that happened on a past holiday. It wasn't a significant event, but it sounded pleasant. I, however, had no recollection of what he was telling me.

He couldn't quite believe it.

We know that "recollections may differ", but how can they be so different? And why do I not have this memory? I'm busy at work – have I simply run out of space?

It's a tempting explanation. We talk about "full heads", "information overload", and "too much to take in" as though the brain were a container that eventually reaches capacity. But the brain does not fill up. Instead, it filters.

At any given moment, far more information is available to us than we could ever realistically store. The sights, sounds, and conversations of even a single day would overwhelm any system that attempted to record them in full.

Instead, the brain relies on selection. Attention determines what is noticed. Emotion helps determine what matters. Then, structures such as the hippocampus decide what is worth committing to longer-term memory.

If your attention is elsewhere, the process falters at the first step.

On that holiday, my husband may have paused long enough to register the moment. I may have been thinking about where we were going next, checking timings, or simply moving through the day without stopping to take it in.

The difference is subtle, but it matters.

Without focused attention, experiences are only weakly encoded, if at all. In that sense, the memory was not lost. It was never fully formed.


The sights, sounds, and conversations of even a single day would overwhelm any system that attempted to record them in full.
 (Asia-Pacific Images Studio/Getty Images)



Even when memories are successfully encoded, they are not stored as fixed records. Each time we recall an event, we reconstruct it, drawing on fragments of sensory detail, prior knowledge, and expectation.

With repetition – through conversation, reflection, or retelling – those reconstructions become stronger and more coherent.

Over time, they can feel increasingly vivid and certain.

This helps explain why shared experiences can diverge so dramatically. We assume that living through the same moment should produce the same memory, but the brain does not work that way. It does not passively record experience. It actively selects, prioritizes, and, just as importantly, discards.

The feeling that our brains are "full" arises not because we have run out of storage, but because we have reached the limits of what we can process at once. Attention is finite. Working memory – the small amount of information we can actively hold in mind – is even more limited.

When these systems are saturated, new information struggles to gain a foothold. This is the mental equivalent of too many tabs open: nothing has been permanently lost, but everything becomes harder to manage.

Computing analogies are useful up to a point. If working memory resembles RAM – fast, temporary, limited – then long-term memory is often compared to a hard drive.


Working memory is a bit like RAM. 
(ภาพของWodthikorn Phutthasatchathum/Canva)



But this is where the parallel breaks down. A hard drive stores files in fixed locations, retrievable in exactly the same form in which they were saved.


The brain does not work this way.

Memories are not stored as discrete files. They are distributed across networks of neurons, overlapping, reshaped, and reassembled each time they are recalled.

New experiences do not simply add to what is already there – they interact with it, altering both the new and the old.

Attempts have been made to estimate how much the brain could theoretically hold.

One widely cited figure from the Salk Institute puts it at around a petabyte – roughly equivalent to hundreds of years of continuous video. It is an impressive number, but also a somewhat misleading one.

It implies a storage system that fills up over time, when in reality, the brain is constantly reorganizing itself. Capacity is not fixed, and information is not stored in isolation. It is integrated, modified, and, when no longer useful, allowed to fade.

Which raises a slightly uncomfortable question: what happens to the memories we would like to keep?

Some of them will fade – not because the brain has run out of space, but because they are not continually reinforced. Memory is not preserved simply because it matters to us. It is preserved when it is revisited, retold, or reconnected to other experiences.

Without that reinforcement, even meaningful moments can become harder to access over time.

What is lost, in most cases, is not the memory itself but our ability to retrieve it. A familiar smell, a piece of music, or an unexpected detail can bring something back that seemed entirely gone.

The trace remains, but it has slipped out of reach.

And the absence of a memory is rarely evidence of a system at capacity – more often, it is the trace of a moment that was never fully stored, or one that has simply not been called upon.


The Life of Earth
https://chuckincardinal.blogspot.com/

Monday, 27 April 2026

Common Pregnancy Medications Linked to Higher Autism Risk in Massive U.S. Study

By U. of Nebraska Medical Center, April 27, 2026
https://scitechdaily.com/common-pregnancy-medications-linked-to-higher-autism-risk-in-massive-u-s-study/

A large-scale national study analyzing millions of U.S. births has uncovered a potential link between prenatal exposure to certain widely prescribed medications and increased rates of autism spectrum disorder. 
Credit: Shutterstock



Prenatal use of certain common medications may raise autism risk, especially when multiple drugs are combined. Findings highlight the need for caution and further research.

A major study led by researchers at the University of Nebraska Medical Center (UNMC) and published in Molecular Psychiatry reports a strong link between medications commonly prescribed during pregnancy and an increased risk of autism spectrum disorder (ASD) in children.

The researchers reviewed 6.14 million maternal-child health records from the Epic Cosmos database, which covers nearly one-third of all U.S. births between 2014 and 2023. They found that drugs known to disrupt the body’s cholesterol production pathway were consistently tied to higher rates of ASD in children.

Cholesterol Pathway–Inhibiting Drugs Identified

Instead of grouping medications by their intended use, as earlier research has done, the UNMC team classified drugs based on their shared impact on sterol biosynthesis, including both direct effects and side effects.

This group of sterol biosynthesis-inhibiting medications (SBIMs) includes certain antidepressants, antipsychotics, anxiolytics, beta-blockers, and statins. 

The 15 drugs examined were aripiprazole, atorvastatin, bupropion, buspirone, fluoxetine, haloperidol, metoprolol, nebivolol, pravastatin, propranolol, rosuvastatin, sertraline, simvastatin, cariprazine, and trazodone. Many of these are widely prescribed in the United States, with more than 400 million prescriptions filled each year.

Key FindingsPregnant individuals who were prescribed at least one SBIM had a 1.47 times higher likelihood of having a child diagnosed with ASD. The risk rose with greater exposure. Each additional SBIM increased the risk by 1.33 times, reaching a 2.33 times higher risk when four or more were used at the same time.

Of the 234,971 children in the study diagnosed with ASD, 15% had been exposed to SBIMs before birth.
Use of these medications during pregnancy has also increased significantly, from 4.6% of pregnancies in 2014 to 16.8% in 2023.

Importance of Cholesterol in Fetal Development

Cholesterol plays a critical role in fetal development, particularly for the brain, which contains more cholesterol than any other organ. The fetal brain begins producing its own sterols at about 19–20 weeks of gestation. Disruptions in this pathway can lead to serious developmental conditions such as Smith-Lemli-Opitz syndrome (SLOS), in which up to 75% of affected children meet criteria for ASD.

Many commonly used medications can interfere with this biological process. This study is the first nationwide effort to examine how prenatal exposure to this class of drugs may influence neurodevelopmental outcomes.

Expert Caution and Medical Guidance

“Our findings do not suggest that these medications are unsafe for adults,” said corresponding author Karoly Mirnics, MD, PhD, dean and director of the UNMC Munroe-Meyer Institute. “But they raise important questions about their use during pregnancy, a period when even small biochemical disruptions may have outsized effects on fetal brain development.”

The researchers emphasize that pregnant patients should not stop or change medications without guidance from a healthcare provider, since many SBIMs are necessary and can be life-saving. Instead, the findings highlight the need to reassess prescribing practices and develop safer options for use during pregnancy.

Recommendations for Safer Prescribing Practices

The team recommends several steps to improve medication safety for pregnant patients:

Develop a comprehensive list of drugs that affect sterol pathways.

Screen all new medications for unintended interference with cholesterol synthesis.

Improve provider awareness of how medications may disrupt sterol processes during pregnancy.

Consider safer alternatives when stopping treatment is not an option.

Limit the use of multiple SBIMs during pregnancy when possible.

Identify patients with genetic risks affecting sterol metabolism, who may be more vulnerable.

Support further research to better understand these mechanisms and reduce risk.



The birth of modern Man
https://chuckincardinal.blogspot.com/

Scientists Discover a Surprising Reason Intermittent Fasting Extends Life

By UT Southwestern Medical Center, April 26, 2026

Intermittent fasting has long been linked to longer life, but new research points to an unexpected driver behind its benefits. 
Credit: Stock

How the body efficiently shifts metabolism after fasting may be key to improving health, UTSW-led research suggests.

Cutting calorie intake has long been linked to longer life, and intermittent fasting often appears to work better than maintaining a constant diet. Even so, scientists have struggled to explain exactly why this happens.

New research from UT Southwestern Medical Center, published in Nature Communications, suggests that the key factor is not the fasting period itself, but how the body adjusts its metabolism when food is reintroduced. The experiments were carried out in Caenorhabditis elegans, a type of roundworm commonly used in laboratory studies, and the findings could eventually inform approaches to improving human health.

“Our discoveries shift the focus toward a neglected side of the metabolic coin – the refeeding phase. Our data suggest that the health-promoting effects of intermittent fasting are not merely a product of the fast itself, but are dependent on how the metabolic machinery recalibrates during the subsequent transition back to a fed state,” said study leader Peter Douglas, Ph.D., Associate Professor of Molecular Biology and a member of the Hamon Center for Regenerative Science and Medicine at UT Southwestern. Dr. Douglas co-led the study with Lexus Tatge, Ph.D., a former member of the Douglas Lab.


Peter Douglas, Ph.D., is Associate Professor of Molecular Biology and a member of the Hamon Center for Regenerative Science and Medicine at UT Southwestern. 
Credit: UT Southwestern Medical Center



Metabolic switch drives fasting benefits

During fasting, cells quickly use up limited glucose supplies and then switch to breaking down stored lipids for energy. This shift, known as catabolism, is controlled by a protein called NHR-49. When glucose levels drop, NHR-49 activates and triggers lipid breakdown. Once food is available again, NHR-49 turns off, allowing cells to stop breaking down fats and begin restoring their energy reserves. Earlier work published in 2022 by Dr. Douglas and colleagues showed that NHR-49 also monitors lipid levels inside cells and helps prevent starvation when those reserves run low.

To explore whether NHR-49 is responsible for the lifespan benefits of fasting, Dr. Douglas and colleagues removed the gene for this protein in C. elegans and then subjected the worms to a 24-hour fast. The outcome was unexpected. The absence of NHR-49 did not reduce the lifespan benefit. The fasted worms still lived about 41 percent longer on average and showed more youthful behavior, including increased movement, similar to worms with normal NHR-49 function.

These images show how three Caenorhabditis elegans roundworms use and restore fat (green) during feeding, fasting, and refeeding: full when fed (left), reduced during fasting (middle), and rebuilt after refeeding (right). UT Southwestern researchers found that short fasting cycles can extend lifespan by over 60%, supporting longer, healthier life. Credit: UT Southwestern Medical Center

Refeeding response determines longevity

The researchers then turned their attention to what happens after fasting ends, when NHR-49 is normally switched off.

Vincent Tagliabracci, Ph.D., is Associate Professor of Molecular Biology at UT Southwestern and a Howard Hughes Medical Institute Investigator. 
Credit: UT Southwestern Medical Center



To understand this process, they examined how NHR-49 is naturally inactivated. Experiments led by Vincent Tagliabracci, Ph.D., Associate Professor of Molecular Biology at UTSW and a Howard Hughes Medical Institute Investigator, along with Victor Lopez, Ph.D., a postdoctoral researcher in the Tagliabracci Lab, showed that an enzyme called protein kinase CK1 alpha 1 (KIN-19) modifies NHR-49 through phosphorylation. When Dr. Douglas and colleagues altered this system so that NHR-49 remained active even after feeding resumed, lipid breakdown continued, and the lifespan-extending effects of fasting disappeared.

Targeting metabolism could extend life

Taken together, the findings indicate that the ability to properly shut down NHR-49 after fasting is critical for extending lifespan through calorie restriction. Adjusting this process may offer a way to gain the benefits of fasting without needing to follow strict dietary regimens.

“Our findings bridge a gap between lipid metabolism and aging research,” Dr. Douglas said. “By targeting aging, the single greatest risk factor for human disease, we move beyond treating isolated conditions toward a preventive model of medicine that enhances quality of life for all individuals.”



The Life of Earth
https://chuckincardinal.blogspot.com/

Pomegranate Compound Could Help Protect Against Heart Disease

By Cardiff U., April 27, 2026

Urolithin A appears to protect the arteries by targeting the underlying biology of plaque formation rather than simply lowering cholesterol. It reduces oxidative stress and inflammation, limits the movement of immune cells into vessel walls, and decreases the buildup of cholesterol inside macrophages, which are key drivers of plaque growth. 
Credit: Shutterstock

A compound produced by gut bacteria from pomegranate-derived molecules may play a critical role in protecting the cardiovascular system.

A compound created by gut bacteria from pomegranate-derived nutrients may help protect the arteries by reducing plaque buildup, easing inflammation, and making plaques less likely to rupture, according to researchers at Cardiff University.

In a study published in Antioxidants, scientists identified urolithin A as a key factor behind these effects. This molecule forms when gut microbes break down pomegranate polyphenols and shows strong cardiovascular benefits in preclinical models of atherosclerosis, the condition responsible for most heart attacks and strokes.

Pomegranates contain high levels of punicalagin, a polyphenol often associated with heart health. However, the body absorbs very little of this compound directly. Instead, gut bacteria convert it into smaller molecules called urolithins, which can circulate in the bloodstream and interact with tissues.

“Our findings show that the real biological effects come from what gut bacteria make from pomegranate compounds, rather than from the compounds in the fruit itself,” said Professor Dipak Ramji, senior author of the study and Professor of Cardiovascular Science at Cardiff University.

Cellular Evidence of Protective Effects

Researchers tested punicalagin, its intermediate form ellagic acid, and several urolithins in human immune and blood vessel cells grown in the lab. Urolithin A stood out, consistently reducing oxidative stress, lowering inflammatory gene activity, limiting immune cell movement, and decreasing cholesterol uptake by macrophages. These processes are central to the formation and growth of arterial plaques.

The team then evaluated urolithin A in LDL receptor-deficient mice fed a high-fat diet, a widely used model that resembles human atherosclerosis. After twelve weeks, treated mice developed smaller plaques with fewer inflammatory cells.

Plaques in these mice also showed higher levels of smooth muscle cells and collagen, both linked to stronger, more stable plaques that are less likely to rupture. Plaque rupture is the leading cause of heart attacks and strokes.

“What was striking is that these benefits occurred without lowering blood cholesterol levels,” Professor Ramji said. “This suggests urolithin A works by suppressing inflammation and stabilizing plaques, rather than by changing lipid levels.”

Broader Effects on Immunity and the Microbiome

The effects extended beyond the arteries. Mice given urolithin A had lower levels of circulating inflammatory monocytes and granulocytes, which are known to worsen atherosclerosis. At the same time, levels of beneficial short-chain fatty acids rose in blood and feces, suggesting positive shifts in gut microbial activity.

Further analysis using RNA-sequencing showed that urolithin A influenced hundreds of genes involved in inflammation, oxidative stress, and metabolism. Harmful pathways linked to atherosclerosis were reduced, while protective antioxidant and metabolic pathways became more active.

“These results help explain why diets rich in fruits like pomegranates are associated with cardiovascular benefits, but also why responses can vary between individuals,” Professor Ramji said. “Not everyone’s gut microbiome produces urolithin A efficiently.”

The researchers note that studies in humans are still needed to confirm these findings. If similar effects are seen, urolithin A could support existing heart disease treatments by targeting inflammation and improving plaque stability.

“This study opens the door to the use of urolithin A and microbiome‑driven strategies for cardiovascular disease prevention,” Professor Ramji said.



The Life of Earth
https://chuckincardinal.blogspot.com/