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Comment by Dr. Krishna Kumari Challa on July 1, 2026 at 11:27am

Growing evidence shows sugar substitutes disrupt gut health and metabolism

Since the first introduction of saccharin, an array of artificial and other non-nutritive (i.e., low-calorie or calorie-free) sweeteners have become ubiquitous in the food supply. However, a growing body of research suggests that these compounds are not inert in the body and may be disrupting metabolism.
A new review and meta-analysis by researchers, published in Current Atherosclerosis Reports, pulls together the best available evidence on how non-nutritive sweeteners affect health. Across 21 randomized clinical trials in adults, researchers observed that artificial and other low-calorie sweeteners, compared with noncaloric controls such as water or placebo, raised fasting insulin and HbA1c, a marker of long-term blood sugar control, and showed a trend toward worsening insulin sensitivity.

Non-nutritive sweeteners, compared with noncaloric controls, increase fasting insulin and HbA1c and tend to worsen insulin sensitivity, indicating adverse metabolic effects. Evidence suggests they alter gut microbiome composition and function and are associated with higher cardiometabolic disease risk in observational data. Heterogeneity among sweeteners and labelling gaps limit precise risk assessment.

One explanation based on the current evidence, the researchers say, involves the gut microbiome. Non-nutritive sweeteners generally pass through the gut and come into direct contact with these microbes. In one trial they reviewed that used detailed microbiome profiling along with experiments transferring microbes from humans to mice, certain low-calorie sweeteners were shown to alter both the composition and the function of the gut microbiota.
In addition to randomized trials, the researchers reviewed large observational studies, which generally found that consuming non-nutritive sweeteners is linked to a higher risk of developing cardiometabolic diseases. The team notes that these studies have limitations, as people already at risk for these conditions may be more likely to choose these products. Different sweeteners may also have different health effects, so grouping them together may obscure the full picture. Taken together with the clinical trial findings, however, the researchers say the overall body of evidence raises concern.

Meng Wang et al, Artificial and Other Non-Nutritive Sweeteners, the Microbiome, and Cardiometabolic Health, Current Atherosclerosis Reports (2026). DOI: 10.1007/s11883-026-01429-9

Comment by Dr. Krishna Kumari Challa on July 1, 2026 at 11:18am

Chain reaction in cells may be driving low energy in ME/CFS patients

Researchers have identified a key immune cell dysfunction in people with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), offering new clues about the condition.
The study addressed a critical question: Are the mitochondrial deficits reported by other researchers a downstream consequence of the ion-channel and calcium abnormalities previously identified?
Researchers used advanced live-cell imaging to observe TRPM3-dependent calcium movement into mitochondria in real time.

The paper "Deficient TRPM3-linked mitochondrial Ca2+ influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome" has been published in BMC Immunology.

Symptoms included profound, persistent exhaustion; post-exertional malaise; pain; cognitive difficulties; dizziness; temperature instability; and sensory sensitivity, which could severely restrict day-to-day functioning, education, employment and social participation.
The researchers found a significant TRPM3-calcium pathway dysfunction in ME/CFS, resulting in impaired calcium entry into mitochondria, a region of the cell responsible for energy production.
It explains how reduced calcium entry into mitochondria may impair immune cell function and energy production, effectively triggering a chain reaction in the body.

Chandi Tabeth Magawa et al, Deficient TRPM3-linked mitochondrial Ca²⁺ influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome, BMC Immunology (2026). DOI: 10.1186/s12865-026-00849-1

Comment by Dr. Krishna Kumari Challa on July 1, 2026 at 11:12am

Improving growth outcomes for children living with dwarfism

Achondroplasia occurs in 1 out of every 26,000 to 40,000 children and is caused by genetic changes that affect bone growth, proportionality, and differences in the shape of the spine and limbs. Children with the condition often have disproportionately short stature and may experience health challenges involving the spine, legs, ears, nose and throat.

New findings from a trial conducted at Children's Hospital Coloradodemonstrate significantly increased growth rates in children with achondroplasia, the most common form of dwarfism.
The children who received oral therapy experienced a statistically significant increase in height—an observed improvement of 2.10 centimeters per year compared with those who received the placebo. Furthermore, proportionality improved among children ages 3 to less than 8 years, an age range in which changes in body proportions are most evident.
A phase 3 randomized, placebo-controlled trial of the oral FGFR1–3 inhibitor infigratinib in 114 children with achondroplasia showed a statistically significant additional annual height gain of 2.10 cm versus placebo over 52 weeks, with improved body proportionality in children aged 3 to <8 years. Adverse events were mainly mild to moderate, with no treatment-related serious events or deaths; long-term effects remain under investigation.

Ravi Savarirayan et al, Phase 3 Trial of Oral Infigratinib in Children with Achondroplasia, New England Journal of Medicine (2026). DOI: 10.1056/nejmoa2604565

Comment by Dr. Krishna Kumari Challa on July 1, 2026 at 10:12am

The report also provides fundamental insights for pharmaceutical research: In the case of the active pharmaceutical ingredients examined, which have a known mechanism of action, the PFAS content is not responsible for the intended medical effect. Per- and polyfluorination are used in pharmacology to improve the stability and distribution of active ingredients within the body.

However, it is precisely these properties that mean these substances are difficult or impossible to break down in nature and, once excreted by humans, place a burden on ecosystems. There, they may accumulate in living organisms and break down into problematic, persistent transformation products such as trifluoroacetic acid (TFA). TFA does not degrade in the environment, is carried by the water cycle and is considered toxic to reproduction. According to the expert report, more than 80% of the PFAS active ingredients examined have the potential to break down into TFA.
There is no immediate risk to patients from medicines containing PFAS, as these are thoroughly tested for potential risks to human health before they are authorized.
Doctors can use these new findings to prioritize prescribing PFAS-free medicines—particularly when starting new patients on treatment—provided this is appropriate from a therapeutic point of view.

Johanna Greinke et al, Per- and polyfluorinated active pharmaceutical ingredients: Overview and alternatives, Sustainable Chemistry and Pharmacy (2026). DOI: 10.1016/j.scp.2026.102416

Part 2

Comment by Dr. Krishna Kumari Challa on July 1, 2026 at 10:11am

PFAS in most medicines can be replaced with alternatives
Analysis of 139 PFAS-containing active ingredients shows that 87% of human and 65% of veterinary medicines have PFAS-free alternatives, and alternatives are in development for most remaining human drugs. PFAS structures are not required for pharmacological action but drive environmental persistence and TFA formation. Findings support preferential prescription and development of PFAS-free medicines.
Certain medicines contain per- and polyfluorinated alkyl compounds, known as PFAS, which are causing increasing environmental harm because of their long-lasting effects. A study published in Sustainable Chemistry and Pharmacy shows that many PFAS-based active ingredients used in medicines can be replaced by alternative active ingredients. Based on the report's findings, doctors will in the future be able to give preference to prescribing PFAS-free medicines, where this is appropriate from a therapeutic point of view.
Researchers have shown that, for 87% of the identified human medicines and 65% of the veterinary medicines containing PFAS structures, active ingredients without PFAS properties already exist for the same applications.

The study examined 111 active pharmaceutical ingredients for human medicines and 28 for veterinary medicines that are classified as PFAS according to the definition of the Organization for Economic Co-operation and Development (OECD). Furthermore, the researchers were able to demonstrate that PFAS-free alternatives are already in development for almost all the remaining human medicines.

"The fact that PFAS-free alternatives already exist for almost all indications is a clear indication that, from a pharmacological point of view, per- or polyfluorination is not strictly necessary.
Part 1

Comment by Dr. Krishna Kumari Challa on July 1, 2026 at 9:59am

Rising summer heat linked to higher youth suicide rates, especially ages 15 to 24

From India to the U.S. and across Europe, millions are enduring an intense heat wave as temperatures soar to an unbearable range. Summers over the past few years have been extremely hot in these regions because of the combined effects of climate change and persistent weather patterns that amplify these sweltering conditions.
As temperatures climb, so do the risks of a range of mental health disorders, including suicide.

Heat exposure doesn't affect everyone equally. It hits harder on people who work outdoors, people facing housing instability in neighborhoods with fewer resources, and those without air conditioning. Young people are also particularly vulnerable.

Children and adolescents have a higher surface-area-to-mass ratio and sweat less efficiently than adults, causing their bodies to absorb heat more quickly and making it harder to cool down. Studies also suggest that young adults adapt to prolonged summer heat less effectively than older adults.
A recent study found that higher summer temperatures were strongly associated with increased suicide rates among youth, with the connection appearing specifically in summer. During those months, every 1°C (1.8°F) rise in average monthly temperature was associated with a 2.68% increase in the suicide rate. The summer heat effect was strongest among older teens and young adults ages 15 to 24.
Across the full year, for every 1°C rise in average monthly temperature, youth suicide rates increased by 0.75%, about the same as what was seen in the general population. That pattern changed considerably when the team looked at each season individually.

The link between heat and suicide turned out to be statistically significant only in summer (July–September), when rates jumped 2.68% for every 1°C increase, more than 3.5 times higher than the average for the rest of the year.

They also found that heat had a stronger effect on females, raising their rate by 5.20% per 1°C compared with 2.37% for males. They observed the summer effect across most regions of the country, though it weakened, moving from east to west.
As temperatures rise because of global warming and climate patterns such as El Niño, protecting the mental health of young people will require not only better science but also structural interventions.

Pranav Jayaraman et al, Deadly Heat: The Association Between Ambient Temperature and Suicide in Young People in the United States, American Journal of Psychiatry (2026). DOI: 10.1176/appi.ajp.20250096

Comment by Dr. Krishna Kumari Challa on June 30, 2026 at 7:19am

The brain's physical shape guides its internal wiring
A new study by researchers has shed light on the factors shaping the intricate wiring of our brains. The research, published in the journal Cell, reveals that the brain's complex wiring diagram, known as the cortical connectome, does not form at random. Instead, a new mathematical model shows that connections preferentially form between locations that support natural, shape-driven "resonant patterns."
Just as the physical shape of a bell or a drum determines its vibrations and the music that it produces, the physical geometry of the brain constrains the patterns of neural activity it can support.
By testing their mathematical formula against publicly available datasets, the research team showed that this geometric rule holds true across various species, from mice to humans.

This demonstrates that the physical shape of the brain has served as a blueprint in guiding its internal wiring for at least 90 million years of mammalian evolution.
The researchers also showed that the formula successfully predicts both how the brain is wired—its "topology"—and where the wires physically go—its "topography"—important properties that previous theories have failed to predict.
Their new model suggests the brain wires itself in an energy-efficient way to support these resonant patterns, strongly favouring low-frequency patterns, resembling a deep, low hum rather than a high-pitched chirp. These broad, brain-wide patterns require far less energy to sustain.
The fact that a single mathematical formula can accurately predict brain networks in both a tiny mouse and a human reveals just how powerful physical geometry is in shaping brain connectivity.

Francis Normand et al, Geometric constraints on the architecture of mammalian cortical connectomes, Cell (2026). DOI: 10.1016/j.cell.2026.05.048

Comment by Dr. Krishna Kumari Challa on June 30, 2026 at 7:13am

What fights an itch depends on its cause and there's a need for better treatments. For now, antihistamines and certain other drugs for hives can tamp down some itchiness triggered by mast cells. Drug companies are experimenting with other approaches called MRGPRX2 blockers that target the pathway the team linked to scratching.
For the summer itchiness of bug bites, poison ivy and other types of contact dermatitis, dermatologists recommend anti-itch balms such as hydrocortisone cream, calamine lotion or oatmeal baths.

Another trick : Menthol-containing creams can temporarily fool the skin into sensing cold instead of itch, just long enough that "if you don't scratch, then you break that itch-scratch cycle" . "It's like a cheat code."
- Dematologists!

Part 2

Comment by Dr. Krishna Kumari Challa on June 30, 2026 at 7:10am

Scratching that bug bite might feel good at first but science explains why it's a bad idea
Scratching itch-inducing skin lesions amplifies inflammation by mechanically triggering pain fibers that release substance P, which activates mast cells via a non-allergen pathway, increasing swelling and itch. Mouse “cone” experiments show preventing scratching markedly reduces inflammatory cells and edema. Although scratching can modestly reduce skin bacteria, the net effect is detrimental, and topical anti-itch therapies are recommended to break the itch-scratch cycle.

A lot of things can cause itchiness, sometimes serious diseases. Whatever the cause, doctors have long warned that scratching too much can damage the skin. Now researchers better understand why even a mildly annoying itch could put you on an itch-and-scratch cycle if you give in.
They also gained insight into why a good scratch at least at first brings a sigh of relief. After all, not just people and other mammals scratch, even fish do. The commonality suggests there must be some evolutionary reason and the mouse experiment hints at a little germ protection—but still not a reason to scratch.

Evidence matches people's everyday experiences that scratching really can make things worse.

Ignore a mosquito bite and the itch is "gone in five or 10 minutes for most people. But if you start scratching it, it's your friend for a week, getting itchier and more inflamed.
To understand what was happening in the skin, researchers took a deeper look at mast cells, among the immune system's first responders. When called into action, they release compounds that can help fight germs or toxins—or, through a compound called histamine, trigger itchy allergic reactions.

Scientists have long known that allergens can activate mast cells. But other signals can summon mast cells, too, including pain. And when we scratch, we tend to scratch until it starts to hurt.
Pain-sensing nerve cells release a chemical messenger called substance P. In findings published last year, the same team reported that substance P can activate mast cells through a different molecular pathway than allergens do—a double whammy that explains why scratching further inflames itchy rashes or bites.
If we experience pain like touching a hot stove, we'll learn not to do that again. Yet relief from a good scratch, in evolutionary terms, is positive feedback. Why?

One long-held theory is that it may help creatures slough off parasites like fleas or mites.

"Ultimately, scratching is deleterious," the researchers stressed. "You should avoid scratching, although it's "easier said than done."
Part 1

Comment by Dr. Krishna Kumari Challa on June 30, 2026 at 6:59am

Scientists uncover how ovarian cancer resists chemotherapy—and how to reverse it
Ovarian cancer cells acquire cisplatin and carboplatin resistance by stabilizing microtubules via elevated TPPP3, altering the tubulin “code” beyond DNA repair mechanisms. High TPPP3 correlates with poorer survival, while TPPP3 loss restores cisplatin sensitivity in models, suggesting TPPP3 as a therapeutic target and potential biomarker for platinum resistance and treatment optimization.

Sachi Horibata et al, Cisplatin resistance in an ovarian cancer model is mediated by microtubule dynamics regulator TPPP3 in synergy with tubulin code rewiring, Cell Reports (2026). DOI: 10.1016/j.celrep.2026.117414

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