Diabetes-fighting gut molecule may help lower insulin resistance

Could a molecule produced by gut bacteria reduce inflammation and increase insulin sensitivity?

• Lifestyle changes, such as dietary interventions, are an effective strategy for managing type 2 diabetes by helping to control blood sugar levels.
• In addition to the type of food a person consumes, the way the food interacts with their gut microbiome may also offer protection against type 2 diabetes.
• Bacteria in the gut may produce beneficial metabolites when breaking down certain foods.
• A study suggests that a microbial molecule could block an immune pathway that triggers inflammation, which could combat insulin resistance and its complications.

Globally, diabetes affects roughly 529 million individualsTrusted Source. In the United States, estimates suggest that more than 30 million peopleTrusted Source are living with type 2 diabetes.

Type 2 diabetes can develop when the body no longer responds correctly to the hormone insulin. This is known as insulin resistance. Inflammation can causeTrusted Source insulin resistance by triggering the immune system to release signals that block insulin’s action.

This resistance can increase blood sugar and insulin levels, which further fuels inflammation, creating a self-perpetuating state that drives metabolic disease such as type 2 diabetes.

The gut microbiome describes microbes living in the intestines that play an important role in overall health. Previous research highlights that the gut microbiome can profoundly influence inflammation and may trigger responses that can lead to the development of inflammatory diseases, such as diabetes.

Now, a study published in NatureTrusted Source highlights the anti-inflammatory properties of a microbial metabolite known as trimethylamine (TMA).

Gut bacteria produce this metabolite from dietary choline, and it may block an immune pathway and help improve blood sugar control.

Choline-derived molecule improves blood sugar control

The authors of the study, consisting of researchers from University of Louvain, in Belgium, and Imperial College London, in the United Kingdom, build on previous researchTrusted Source, noting a link between a high-fat diet, bacterial components, inflammation, and the development of insulin resistance.

The international team observed that TMA can inhibit IRAK4Trusted Source, a protein that under high-fat dietary conditions can trigger inflammation and promote insulin resistance. The gut microbiome can produce this metabolite when breaking down food containing choline, such as eggs, fish, and legumes.

Using human cell models, mouse studies, and molecular-target screening, the researchers found that TMA can directly bind to IRAK4 and block its activity, reducing diet-induced inflammation and restoring insulin sensitivity.

Speaking to Medical News Today, Michelle Routhenstein, MS, RD, CDCES, CDN, a preventive cardiology dietitian and founder of EntirelyNourished, who was not involved in the research, commented:

“The specific mechanism is new, showing that TMA can directly reduce inflammatory signaling and glycemic control, but the overall idea fits with what we already know about the choline–TMA–trimethylamine N-oxide (TMAO) pathway.”

“TMAO has long been linked with cardiovascular risk, so it is noteworthy that TMA may have protective effects when it does not get pushed toward TMAO production. This can help advance the nutrimetabolomics perspective on how gut metabolites affect cardiovascular and metabolic health,” Routhenstein explained.

Crucially, these results indicate a direct link between gut microbial metabolism, immune regulation, and metabolic disease.

They underscore the potential role of nutrition and gut microbes in fighting inflammation and improving metabolic health.

Gut microbiome, nutrition, and diabetes risk

The discovery of TMA’s ability to block this immune pathway reframes the role of the gut microbiome and its influence on immune and metabolic responses.

Identifying TMA’s anti-inflammatory properties could pave the way for new nutritional or drug-based approaches to prevent or treat insulin resistance and diabetes.

Diet remains one of the strongest modulators of gut microbiota composition and function. Previous research has shown that dietary plans rich in fiber, whole plant foods, and prebiotics may cultivate a healthy gut microbiome.

Producing beneficial metabolites, such as short-chain fatty acids (SCFAs), can help regulate glucose metabolism, suppress inflammation, and enhance insulin sensitivity.

Conversely, Western-style diets high in saturated fat and refined sugars but low in fiber are associated with microbial dysbiosis.

This describes reduced microbial diversity, lower levels of beneficial bacteria, and fewer protective metabolites, which may contribute to diabetes through inflammation and insulin resistance.

These findings may broaden the scope for nutritional interventions, highlighting that it is not just a person’s dietary pattern, but how their gut microbiome metabolizes those nutrients.

One of the study’s lead authors, Marc-Emmanuel Dumas, FRSB, FRSC, Chair in Systems Medicine and Head of the Division of Systems Medicine in the Department of Metabolism, Digestion and Reproduction at Imperial College London, noted in a press release that:

“This flips the narrative. We’ve shown that a molecule from our gut microbes can actually protect against the harmful effects of a poor diet through a new mechanism. It’s a new way of thinking about how the microbiome influences our health.”

Potential therapeutic opportunities

The research team also observed that genetically deleting IRAK4 or blocking it pharmacologically produced the same beneficial effects as TMA.

This may offer a novel approach to combating insulin resistance and its complications by designing drugs to block this enzyme or boost TMA production.

Other evidence notes that IRAK4 inhibitors could be a useful therapeutic strategy against inflammatory diseases, autoimmune disorders, and cancer.

How to manage and prevent diabetes through diet

While the results of this study are promising, more human research is necessary to confirm whether increasing dietary choline and TMA from gut bacteria can improve glucose control and have no unintended effects.

Routhenstein noted that these findings could open the door for future nutritional approaches that encourage targeted probiotics, postbiotics, or personalized choline intake based on someone’s microbiome.

“For now, it supports aiming for adequate choline from whole foods while continuing to follow a high fiber, minimally processed, plant-forward eating pattern for diabetes management,” Routhenstein concluded.

At present, health experts typically recommend certain eating plans that may help manage type 2 diabetes.

For example, a meta-analysis presented at the 2025 Annual Meeting of the European Association for the Study of Diabetes (EASD) found that the AHEI, Mediterranean, and DASH diet could help reduce the risk of developing type 2 diabetes.

All three dietary plans focus on incorporating healthy fats, plant-based foods like vegetables and fruits, and reducing processed foods and those high in sugar or with added sugars.

Furthermore, a 2025 review also suggests that the DASH diet may be one of the most effective ways to reduce the risk of diabetes complications. The authors propose that his dietary plan can improve the biological pathways that drive diabetes complications.

https://www.medicalnewstoday.com/articles/diabetes-fighting-gut-molecule-may-help-lower-insulin-resistance#How-to-manage-and-prevent-diabetes-through-diet

Alzheimer's Breakthrough: How Green Tea Nanoparticles Target Brain Plaques and Memory Loss

Researchers at INST Mohali have pioneered a new multifunctional therapy for Alzheimer's. Their approach uses specially designed nanoparticles that combine compounds from green tea, a neurotransmitter, and an amino acid. This innovative treatment simultaneously tackles four major pathological features of the disease. Early results from models show it can break down toxic plaques and even improve memory function.

Novel therapy integrates green tea antioxidant, dopamine, and tryptophan into a single nanoparticle

Targets amyloid plaques, oxidative stress, inflammation, and neuron loss simultaneously

Functionalized with BDNF protein to clear toxic clumps and promote neural regeneration

Shows promise in lab and mouse models by improving memory and disassembling harmful fibrils

INST researchers develop new nanoparticle-based multifunctional therapy for Alzheimer's

INST Mohali researchers create a novel nanoparticle therapy using green tea antioxidants to combat Alzheimer's by targeting plaques, inflammation, and boosting neuron growth.

"This is a rare approach in Alzheimer’s therapeutics which uniquely combines antioxidant, anti-amyloid, and neurotrophic actions for the therapy. - Dr. Jiban Jyoti Panda's research team"

Researchers at the Institute of Nano Science and Technology (INST), Mohali, have identified a new pathway involving nanoparticles to treat Alzheimer’s Disease (AD), said the Ministry of Science & Technology on Tuesday.

Conventional Alzheimer’s therapies often target only a single pathological feature, such as amyloid aggregation or oxidative stress, yielding limited clinical benefit.

However, the new therapy involves nanoparticles that integrate polyphenol with antioxidant properties found in green tea, a neurotransmitter, and an amino acid.

It has the potential to treat Alzheimer’s Disease by changing the path of the progression of the disease, slowing it, improving memory, and supporting thinking skills, said the researchers in the paper, published in the journal Small.

The therapy works by integrating epigallocatechin-3-gallate (EGCG) -- an antioxidant found in green tea --, dopamine -- a neurotransmitter important for mood -- and tryptophan -- an amino acid involved in many cellular functions -- into a nanoparticle called EGCG-dopamine-tryptophan nanoparticles (EDTNPs).

This enables it to simultaneously target amyloid aggregation, oxidative stress, inflammation, and neuronal degeneration -- four key pathological hallmarks of Alzheimer’s.

“Incorporation of Brain-Derived Neurotrophic Factor (BDNF) -- a protein crucial for the survival, growth, and function of neurons onto EDTNPs (B-EDTNPs) creates a dual-action nanoplatform that not only clears neurotoxic Amyloid Beta aggregates (protein clumps that disrupt neural function and drive Alzheimer’s disease pathology) but also enhances neuronal regeneration,” said the team led by Dr. Jiban Jyoti Panda from INST, an autonomous institute of the Department of Science and Technology (DST).

“This is a rare approach in Alzheimer’s therapeutics which uniquely combines antioxidant, anti-amyloid, and neurotrophic actions for the therapy,” they added.

The research, conducted with support from Dr. Ashok Kumar Datusalia (NIPER Raebareli) and Dr Nisha Singh (Gujarat Biotechnology University), involves the synthesis of EDTNPs using biocompatible assembly techniques like pressure-assisted hydrothermal and electrostatic-based co-incubation methods to combine antioxidant, neurotransmitter, and amino acid components.

These nanoparticles were then functionalised with BDNF, producing B-EDTNPs with enhanced neuroprotective potential.

In lab experiments and mouse models, these nanoparticles disassembled toxic plaques, reduced inflammation, restored balance inside brain cells, and even improved memory and learning. Computer simulations further confirmed that the nanoparticles latch onto harmful Amyloid beta fibrils and pull them apart at the molecular level.

“The research could help people with Alzheimer’s disease by offering a treatment that works on multiple levels. The nanoparticles not only remove harmful protein plaques but also reduce brain stress, inflammation, and help nerve cells grow through BDNF,” said the researchers.

https://www.newkerala.com/news/o/inst-researchers-develop-new-nanoparticle-basedmultifunctional-therapy-alzheimers-173

Low confidence, inability to cope with problems among six signs of later dementia risk

Six depressive symptoms in midlife such as not being able to cope with problems and losing confidence in oneself might predict risk of dementia two decades later, according to a new study.

Feeling nervous and tensed most of the time, not feeling warmth and affection for others and difficulties concentrating were among the six symptoms contributing towards dementia, according to the findings published in The Lancet Psychiatry journal.

Researchers led by those at the University College London said the cluster of specific symptoms, rather than depression overall, could indicate the relationship between midlife depression and dementia risk in later life.

Lead author Philipp Frank from University College London’s division of psychiatry, said, “Our findings show that dementia risk is linked to a handful of depressive symptoms rather than depression as a whole. This symptom-level approach gives us a much clearer picture of who may be more vulnerable decades before dementia develops. Everyday symptoms that many people experience in midlife appear to carry important information about long-term brain health. Paying attention to these patterns could open new opportunities for early prevention,” Frank said.

Data from 5,811 middle-aged adults who participated in the UK’s Whitehall II study, a long-term research that started in 1985 looking into social inequalities in health, was analysed.

Midlife depressive symptoms were assessed during 1997-1999, when the participants were dementia-free and middle-aged (45-69 years) through questionnaires covering 30 common depressive symptoms. The participants were followed up for 25 years through national health registries, 10.1 per cent of whom developed dementia.

Those reporting five or more depressive symptoms in the questionnaire were found to have a 27 per cent higher risk of developing dementia.

However, the increased risk of dementia was driven entirely by the six specific symptoms in adults under 60 -- loss of self-confidence and difficulty coping with problems were each associated with a roughly 50 per cent increased risk of dementia, the researchers found.

“A distinct set of midlife depressive symptoms was associated with an increased risk of dementia, suggesting that these symptoms might be early markers of underlying neurodegenerative processes,” the authors wrote.

“These findings could inform earlier identification and more targeted interventions for individuals with depression who are at risk of dementia,” they said.

Symptoms such as loss of self-confidence, difficulty coping with problems, and poor concentration can lead to reduced social engagement and fewer cognitively stimulating experiences, both of which are important for maintaining cognitive reserve, the team noted.

They explained cognitive reserve as the brain’s ability to cope with damage or disease, allowing one to maintain normal thinking and function even when the brain is physically affected.

An August 2024 study found that lacking a purpose in life and perceiving fewer opportunities for personal growth could be a very early sign of dementia.

Findings published in the Journal of Neurology Neurosurgery and Psychiatry suggested that the aspects of psychological wellbeing noticeably declined among older adults three to six years before being diagnosed with mild cognitive impairment that usually precedes dementia and where memory and thought processes are impacted, yet does not interfere with daily functioning.

https://www.tribuneindia.com/news/health/low-confidence-inability-to-cope-with-problems-among-six-signs-of-later-dementia-risk/

Study finds normalising blood glucose with lifestyle could halve heart disease risk in prediabetics

Fasting blood glucose value of under 97 milligrams per decilitre proves to be a marker for a persistently lower risk of heart disease

Bringing blood glucose to normal range through lifestyle changes could halve the risk of heart attack, heart failure and premature death among prediabetics, according to a study.

Findings published in ‘The Lancet Diabetes and Endocrinology’ journal show that remission of prediabetes — achieving normal blood glucose levels — may establish a new, measurable target for clinical guidelines, according to researchers.

A fasting blood glucose value of under 97 milligrams per decilitre proved to be a simple marker for a persistently lower risk of heart disease, regardless of age, weight, or ethnic background, the researchers said.

This threshold could be applied in primary care practices worldwide, making prevention more tangible, they added.

“Our results suggest that remission of prediabetes not only delays or prevents the onset of type 2 diabetes, as already known, but also protects people from serious cardiovascular diseases in the long term, over the span of decades,” author Dr Andreas Birkenfeld, a board member of the German Center for Diabetes Research and medical director of the department of medicine at University Hospital Tübingen, said.

The team, including researchers from the US and China, analysed long-term data from more than 2,400 people with prediabetes. The participants’ risk of cardiovascular death reduced by roughly 50 per cent, with a significant lowering of overall mortality.

The US study followed its participants for 20 years, while the China one tracked participants for 30.

Cardiovascular prevention has so far rested on three pillars — blood pressure control, lowering LDL cholesterol, and smoking cessation. With the new findings, a fourth pillar could be added — a sustained normalisation of blood glucose in prediabetes, the team said.

“Reaching prediabetes remission is linked to a decades-long benefit, halving the risk of cardiovascular death or hospitalisation for heart failure in diverse populations. Targeting remission might represent a new approach to cardiovascular prevention,” the authors wrote.

Birkenfeld said, “We see a clear therapeutic window: If glucose levels are normalised already at the prediabetes stage, the long-term risk of heart attack, heart failure and premature death can be markedly reduced.”

“Our data support explicitly anchoring remission as a primary treatment goal in guidelines for the prevention of diabetes and cardiovascular disease,” the author said.

https://www.tribuneindia.com/news/health/study-finds-normalising-blood-glucose-with-lifestyle-could-halve-heart-disease-risk-in-prediabetics/

When mind is alerted to danger: nail biting, procrastination, and other forms of self-sabotage

Why the brain sometimes turns against itself: The neuroscience of self-sabotage and survival

Neurons in the brain can make us believe in things that do not exist, anticipate our decisions, activate selectively in response to visual stimuli, and interact with one another to store the information that forms our memory.

These ideas are explored in several books by neurobiologist and science communicator Rodrigo Quian Quiroga, a researcher at the Catalan Institute for Research and Advanced Studies (ICREA) at the Hospital del Mar Research Institute in Barcelona.The enormous capacity of the central nervous system to process information, particularly visual input - allows us to predict the consequences of events around us and make decisions accordingly. This ability is considered a distinctly human trait and is essential for survival.

Self-sabotage as a warning sign

When we are nervous, we may find ourselves biting our nails, cracking our knuckles, scratching a pimple, or even lightly hitting ourselves with a pen or another object. Even when faced with an important task where much is at stake, we might procrastinate until time runs out.

According to clinical psychologist Charlie Heriot-Maitland, these behaviours stem from our survival instinct. In his book Controlled Explosions in Mental Health, he explains how the brain sometimes inflicts minor, controlled harm as a protective measure to avoid greater damage.

In essence, the brain prefers the certainty of a known, manageable threat over the risk of an unknown and potentially greater one.

Different forms of damage control

Procrastination - delaying a report, project, or crucial decision until the last moment, can function as a defence against failure, rejection, and the depression that may follow.

Perfectionism, by contrast, operates through hyper-concentration and excessive attention to detail. While this may help avoid mistakes, it exposes individuals to stress and burnout, which can ultimately lead to failure.

The same applies to extreme self-criticism, which creates a false sense of control and independence. All these behaviours arise from the brain’s need for a predictable, controllable world - one free from surprises. Situations that lack control are poorly tolerated.

An evolutionary defence mechanism

The geneticist Theodosius Dobzhansky famously stated that “nothing in biology makes sense except in the light of evolution.” This principle applies to neuronal function as well.

Humans are diurnal organisms with few physical defences. Our greatest weapon against predators has always been intelligence - the ability to analyse danger, anticipate outcomes, confront threats, or avoid them altogether. As a result, the brain has evolved to detect danger everywhere, even in situations where no real threat exists.

Our alert and threat systems, including fear, trigger neural processes that assess situations and predict outcomes. Neurotransmitters such as norepinephrine, dopamine and glutamate heighten sensory perception and neuronal activity, enabling rapid responses aimed at survival.

The cost of constant alertness

One of the major problems with self-sabotaging behaviours is that they can become self-fulfilling prophecies. Overconfidence may lead us to underperform, while fear of failure can cause us to avoid challenges we are capable of handling.

Both extremes limit growth and reinforce the very outcomes we seek to avoid.

Self-harm and adolescence

Self-harm among adolescents is more common than is often acknowledged. This includes behaviours such as cutting and other forms of non-suicidal self-injury (NSSI), typically occurring during periods of intense stress, anxiety or depression.

Such actions can be viewed as the brain accepting minor harm to avoid more overwhelming emotional pain. These painful circumstances may include sexual abuse, bullying, trauma, substance abuse, parental separation, depression, anxiety, or social isolation.

The release of endogenous opioids, such as beta-endorphins, following minor self-inflicted injury can temporarily reduce symptoms of anxiety and depression.

Autism spectrum disorder and self-harm

Children and individuals with autism spectrum disorder (ASD) represent a distinct case. Autism is considered a risk factor for self-harming behaviours, which may include head-hitting, cutting, strangulation, biting, scratching, or hair-pulling.

As with adolescents, self-harm in some people with ASD may help regulate anxiety, cope with sensory overload (such as noise, light or smells), or manage situations that are confusing or overwhelming. In this sense, it functions as a biological coping mechanism to avoid more intense distress.

Heriot-Maitland advocates psychological therapies that reduce the need for self-harm while helping individuals face reality with less anguish and stress. Understanding the evolutionary and neurological roots of these behaviours is essential to addressing them, particularly when the problem is deeply embedded in our instinct for survival.

https://www.tribuneindia.com/news/health/when-mind-is-alerted-to-danger-nail-biting-procrastination-and-other-forms-of-self-sabotage/