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insulin resistance

Manage Blood Sugar Naturally: 7 Hacks from a Diabetologist

by Dr. Michael Lee – Health Editor November 23, 2025

written by Dr. Michael Lee – Health Editor

Diabetologist Shares 7 Natural hacks to ‌Manage Blood Sugar Spikes

Managing blood sugar levels is crucial for individuals with type 2 diabetes, and⁣ incorporating‍ simple ‌lifestyle changes‍ can make a ⁢meaningful difference. A diabetologist ‍recommends seven⁢ natural ‌strategies to help mitigate blood sugar spikes:

1. Chia ‌Seeds: These ‍tiny seeds are‌ packed with fiber,a nutrient ⁤that slows ⁣down digestion and the absorption of sugar. This helps to stabilize blood glucose levels.⁣ Chia seeds are versatile and can be easily added to foods like⁤ oatmeal or ⁢smoothies.

2. Stay Hydrated: Proper hydration plays a⁢ vital role in blood sugar management. Dehydration can contribute to⁣ glucose ‍spikes, so consistent water ⁣intake is essential to support overall⁤ hydration and metabolic processes. Though, moderation is key; excessive water‍ intake can be harmful,‍ notably for individuals with kidney‍ disease, ‍electrolyte imbalances, or heart conditions.

3. Fenugreek Seeds: fenugreek seeds contain soluble fiber, which slows digestion and carbohydrate absorption, leading to improved blood sugar control and reduced fasting glucose ‌levels. Soaking ‌the seeds before consumption ⁤can further‍ enhance their ⁣digestibility and benefits.

4. yoga and Mindful Breathing: Regular practice of yoga and deep breathing⁣ exercises can lower cortisol levels,⁢ a stress⁣ hormone known to impact blood sugar. These‍ practices promote relaxation ⁤and improve glycemic control, helping to mitigate stress-related sugar spikes.

5.Vinegar Before ⁣Meals: Consuming vinegar, especially apple ⁣cider vinegar, can boost insulin sensitivity by⁣ slowing the⁣ rate at which the stomach empties. This can definitely help lower postprandial ⁤(after-meal) glucose ⁢levels, making it a simple ⁣addition to your routine⁣ before⁢ eating. Regular use‌ can provide temporary improvements in glucose control.

6. Add Resistant starch: ⁣Resistant starch functions similarly to soluble fiber,‍ offering numerous health benefits, including ‌improved insulin⁣ sensitivity. ⁤Foods rich in⁣ resistant starch,such as green bananas,legumes,and cooked-then-cooled brown rice,can⁤ contribute to better glycemic control over time.

7. ⁢Magnesium-Rich Foods: Magnesium is essential for glucose metabolism and insulin action. Increasing intake ⁤of magnesium-rich foods like leafy greens and nuts can ‍help ⁤improve⁣ insulin sensitivity, potentially reducing the risk of developing type 2 diabetes.

Disclaimer: This article is for informational purposes only and not a ⁢substitute for professional medical advice. Always seek the advice of your doctor with‍ any questions about‌ a medical condition.

November 23, 2025 0 comments

Health

Diabetes: Insulin Resistance – The Real Cause?

by Dr. Michael Lee – Health Editor November 13, 2025

written by Dr. Michael Lee – Health Editor

Gastro Doctor‌ Challenges Common Beliefs About Diabetes, Points to Insulin Resistance as Key Driver

New Delhi: A leading gastroenterologist, Dr. Pal of‌ Dr. Pal’s NewME, is challenging the ‌widely ⁤held belief that⁣ sugar ⁢is the primary culprit ⁢in the growth of diabetes.‌ Rather,Dr. Pal asserts ⁢that⁢ insulin resistance is the basic issue, triggered by factors beyond ⁢dietary ‍sugar intake. He shared insights on Instagram (@dr.pals_newme) outlining⁣ the‌ real causes of diabetes and early warning signs individuals ‌should ⁤recognize.

While excessive sugar⁣ consumption‍ can exacerbate the problem, Dr. pal⁢ explains that the body’s inability to effectively use‍ insulin – insulin resistance – is the core driver of type 2 diabetes. ‌He emphasizes that focusing solely on sugar reduction ‍may not address the root cause and that other factors play a significant⁢ role in triggering this resistance.

Dr. Pal also listed several early warning signs that blood sugar might be uncontrolled,even with “normal” test reports. These include constant fatigue despite adequate ‍sleep, ⁣cravings for sweets immediately ‍after meals, and experiencing brain fog or ⁣difficulty concentrating. Frequent nighttime⁣ urination,‌ excessive thirst, and restless ‌sleep ‍are also indicators, as the body attempts‌ to eliminate excess glucose.

Furthermore,‌ Dr. Pal highlighted often-overlooked signs like slow wound healing or recurring⁣ skin issues, such⁤ as dark patches on the neck or‌ underarms, as potential indicators⁢ of early insulin resistance.He cautioned⁢ against waiting for elevated HbA1c levels before taking action, stressing that the body ⁣often provides warning signals ‌well before blood test numbers reflect a problem, and early recognition ⁣can be crucial.

November 13, 2025 0 comments

Health

Insulin resistance-related indices, genetic risk, and the risk of cardiovascular disease in individuals with preclinical or clinical obesity: a large prospective cohort study in the UK biobank | Cardiovascular Diabetology

by Dr. Michael Lee – Health Editor October 26, 2025

written by Dr. Michael Lee – Health Editor

Major Study Links Insulin Resistance, Genetic Predisposition‌ to Heightened Cardiovascular Risk in Obesity

A large-scale prospective cohort study utilizing data from the UK Biobank has⁢ revealed a meaningful association between insulin ‌resistance-related indices, genetic risk scores, and an increased risk of cardiovascular disease (CVD) in individuals ⁣with both preclinical and clinical obesity.⁢ Published in cardiovascular Diabetology, the research ⁣underscores the critical need for⁣ early identification and management of⁢ insulin resistance, even before overt obesity develops, to mitigate CVD risk.

The‌ study, involving over 430,000 participants, demonstrates that individuals with higher genetically predicted insulin resistance, coupled ⁢with obesity, face a substantially elevated risk⁢ of coronary artery disease, cerebrovascular disease, and heart failure. ⁣This finding is notably relevant given ‍the global rise in obesity rates and the increasing⁣ prevalence⁤ of insulin ⁢resistance, positioning CVD as a leading ‍cause of morbidity and mortality worldwide. Researchers emphasize that integrating genetic risk assessment with clinical measures ‍of insulin resistance could refine risk stratification and personalize preventative strategies ‌for individuals struggling with weight ⁢issues.

Researchers assessed insulin resistance using several indices – including Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), quantitative ⁣Insulin Sensitivity Check Index⁤ (QUICKI), and the TyG index (Triglyceride-Glucose index) – alongside‌ a polygenic risk score (PRS) for insulin resistance. ‌Participants were categorized based on their body mass index (BMI) into ⁢normal weight, overweight, and obese groups. The study followed participants for a median‌ of 7.2 years, tracking incident CVD events.

The analysis revealed that higher genetically⁣ predicted insulin resistance was associated with a greater risk of CVD across all BMI categories, but the association was most pronounced in individuals with obesity. Specifically, those ⁣in the highest quintile of the insulin⁣ resistance PRS had a 34% increased risk ⁢of coronary artery disease, a 28% increased risk of cerebrovascular disease, and a 41% increased risk of heart failure compared‍ to those in the lowest quintile, when adjusted for various confounding factors.

Further analysis indicated that the association‍ between insulin resistance PRS⁤ and CVD risk was independent of traditional risk factors such as age,sex,smoking⁣ status,and blood pressure. However, the study authors acknowledge potential limitations related to participation bias within the‍ UK Biobank cohort, as highlighted by ⁤Gale et al.‌ (2020) and Schoeler et al.⁢ (2023), which could influence the generalizability of the findings. Gale ‍CR, Kivimäki M, Deary IJ, Bell S. Comparison of risk factor associations in UK biobank⁣ against representative, general population based studies with conventional response rates: prospective cohort study and individual participant meta-analysis. BMJ (clinical ⁣Res ed). 2020;368:m131. Schoeler T, Speed D, Porcu E, Pirastu N, Pingault JB, Kutalik Z. Participation bias in the UK biobank distorts genetic associations and downstream analyses.Nat Hum Behav.2023;7(7):1216-27.

Despite these limitations, the study provides compelling evidence for a causal link between insulin resistance,⁣ genetic predisposition, and CVD risk in ⁣the context of obesity. The findings suggest ⁢that interventions targeting insulin ⁢resistance, alongside weight management strategies, may be crucial for preventing cardiovascular complications in at-risk individuals. Future research should ⁢focus on validating these findings in more diverse populations and⁣ exploring the potential of targeted therapies to improve⁢ insulin sensitivity and ‍reduce CVD burden.

October 26, 2025 0 comments

Health

Enzyme Discovery Offers Potential Treatment for Obesity and Metabolic Diseases

by Dr. Michael Lee – Health Editor September 24, 2025

written by Dr. Michael Lee – Health Editor

Enzyme Targeted in Immune Cells Prevents Diet-Induced⁤ Obesity in Mice, Offering Potential New therapeutic avenue

MELBOURNE, AUSTRALIA – Researchers at Monash University have ‍discovered that inhibiting a specific enzyme, CAMKK2, within immune cells can ‍protect against diet-induced obesity and related metabolic disorders in ⁣mice. The study, published in Molecular Metabolism, reveals a surprising link‍ between CAMKK2 activity in macrophages and the body’s ability to burn fat, reduce inflammation, and improve metabolic health.

The team‌ found that mice genetically engineered to‍ lack the CAMKK2⁢ gene in macrophages exhibited an anti-inflammatory profile and demonstrated increased fat oxidation‌ and improved mitochondrial‌ function. This metabolic ‍shift‍ led to increased energy production and efficiency at the cellular ‌level. Notably, fat tissue in these mice displayed ⁢a “beiging” effect, activating genes that promote fat burning and heat generation.

“Our findings show that when the CAMKK2 gene is removed from certain ‍immune ‌cells ⁢(in this case, macrophages), fat tissue shifts its activity‍ in a ⁤healthier direction,” explained researcher⁢ Scott. ”The ⁤genes in the fat start working in ways ‍that support better metabolism⁢ and reduce harmful inflammation.”

The research suggests CAMKK2⁣ directly regulates both immune cell and whole-body metabolism, ⁢positioning it as a potential therapeutic target for obesity and associated conditions like insulin resistance and fatty liver disease. Furthermore, ‍given the role of macrophage-driven inflammation in atherosclerosis, infections, and certain cancers, inhibiting CAMKK2 could offer broader ⁤health benefits.

While promising, the study acknowledges limitations.Results from mouse models may ⁢not fully translate to humans, and direct confirmation ⁤of increased fat burning within live animals requires further examination. Existing compounds like STO-609, ⁣used to inhibit CAMKK2, lack the specificity and drug-like properties needed for‍ clinical application. However, researchers ⁢beleive these challenges‌ can be addressed in future studies, paving the way‌ for⁤ the advancement of targeted therapies.

September 24, 2025 0 comments

Technology

Peroxisomes: New Key to Boosting Brown Fat and Metabolic Health

by Rachel Kim – Technology Editor September 17, 2025

written by Rachel Kim – Technology Editor

Peroxisomes Show Promise as Backup heat Generators, Possibly Aiding Metabolism

St. Louis, MO – Researchers at Washington University in St. Louis have identified peroxisomes as a potential alternative pathway for heat production in brown fat, offering a possible compensatory mechanism if mitochondria – the cell’s primary heat-producing organelles – become impaired. The findings, published September 17, 2025, in Nature, suggest a novel approach to combating obesity and improving metabolic health.

The study, led by Dr. Imran J. Lodhi and colleagues, centers on acyl-CoA oxidase 2 (ACOX2), a key protein within peroxisomes. Experiments with mice revealed that ACOX2 plays a critical role in consuming fuel and generating heat. Mice lacking ACOX2 in their brown fat exhibited reduced cold tolerance, displaying lower body temperatures when exposed to cold environments compared to control mice. These mice also demonstrated impaired insulin sensitivity and a greater susceptibility to obesity when fed a high-fat diet.

Conversely, mice genetically engineered to produce elevated levels of ACOX2 in brown fat showed increased heat production, improved cold tolerance, and enhanced insulin sensitivity, alongside better weight control on the same high-fat diet. Researchers utilized a newly developed fluorescent heat sensor and infrared thermal imaging to confirm these findings, demonstrating that ACOX2 metabolism of specific fatty acids directly correlates with increased heat within brown fat cells, and that ACOX2-deficient mice generated less heat.

The fatty acids utilized by ACOX2 are naturally produced by the human body, but are also present in dairy products, human breast milk, and are synthesized by certain gut microbes.This discovery opens the door to potential dietary interventions – including foods, probiotics, or “nutraceuticals” – designed to boost this heat-production pathway. Dr. Lodhi also noted that his team is exploring drug compounds that could directly activate ACOX2.

“While our studies are in mice, there is evidence to suggest this pathway is relevant in people,” Lodhi said. “Prior studies have found that individuals with higher levels of these fatty acids tend to have lower body mass indices.” He emphasized that while a correlation exists, further research is needed to establish causation. “Our long-term goal is to test whether dietary or other therapeutic interventions that increase levels of these fatty acids or that increase activity of ACOX2 could be helpful in dialing up this heat production pathway in peroxisomes and helping people lose weight and improve their metabolic health.”

The research was supported by grants from the National Institutes of Health (NIH), including R01DK133344, R01DK115867, R01DK132239, GM103422, T32DK007120, S10 OD032315, DK020579 and DK056341, as well as funding from the FP7 funded European Infrafrontier-I3 project.Lodhi and co-author Xiaowei liu have filed a provisional patent application related to targeting ACOX2 activation as a treatment for obesity and related metabolic diseases.

Source: Liu, X., et al. (2025) Peroxisomal metabolism of branched fatty acids regulates energy homeostasis. Nature. doi.org/10.1038/s41586-025-09517-7

September 17, 2025 0 comments

Health

Gut microbial metabolites restore hormone-producing cells in obesity

by Dr. Michael Lee – Health Editor July 29, 2025

written by Dr. Michael Lee – Health Editor

Gut Microbe Byproducts Boost Metabolism-Regulating Cells

New research identifies a pathway to potentially combat obesity’s metabolic effects.

Scientists have discovered that byproducts from gut bacteria may offer a new therapeutic approach for metabolic issues linked to obesity. The research centers on restoring crucial hormone-producing cells within the intestine.

Restoring Gut Hormone Production

The study, published in the *International Journal of Molecular Sciences*, highlights enteroendocrine cells (EECs). These specialized intestinal cells are vital for metabolic control, releasing hormones like GLP-1, which aids insulin secretion and appetite suppression. Obesity is known to reduce the number and function of these essential cells, contributing to insulin resistance.

Researchers explored how indole, a metabolite derived from dietary tryptophan (an amino acid in protein-rich foods), could help regenerate EECs. Using “mini-gut” organoids and rat models, they found that obesity caused a roughly 60% decrease in these hormone-producing cells.

Intriguingly, treating human gut organoids with indole or a probiotic’s growth medium significantly increased EECs, more than doubling their numbers. This effect was dependent on a cell receptor known as the aryl hydrocarbon receptor (AhR), indicating its key role in the process.

“Our findings suggest that microbial metabolites derived from dietary tryptophan can reverse obesity-associated reductions in hormone-secreting gut cells. This points to a potential therapeutic strategy that leverages the gut microbes to improve metabolic outcomes in obesity.”

—Alip Borthakur, Ph.D., Assistant Professor of Biomedical Sciences at Marshall University Joan C. Edwards School of Medicine

This research provides foundational evidence for developing interventions targeting the gut microbiota. Such strategies, including probiotics or dietary changes, could enhance incretin hormone production, thereby improving glucose metabolism and appetite regulation in individuals with obesity.

Student Collaboration and Future Potential

The study benefited from the work of several students, including undergraduate Morrison Chicko and graduate students James Hart and Hassan Mansour, as well as doctoral student Harshal Sawant. Faculty members Subha Arthur, Ph.D., and Jennifer Haynes, Ph.D., also contributed.

“It has been exciting to mentor four enthusiastic, intelligent, curious and dedicated Marshall students at different times of the study,” stated Borthakur. “They were thrilled to use the ‘mini gut’ model, a 3D human intestinal organoid model that truly represents the architecture and compositional complexity of the native human gut.”

The study received support from the National Institutes of Health through grants from the National Institute of Allergy and Infectious Diseases (NIAID) and the National Institute of General Medical Sciences (NIGMS).

The potential for gut microbiome modulation in treating metabolic disorders is significant. For example, studies have shown that interventions like fecal microbiota transplantation can improve insulin sensitivity in individuals with metabolic syndrome (Source: Frontiers in Endocrinology, 2023).

July 29, 2025 0 comments

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