Limitless X Holdings Inc (LIMX)

$LIMX Sod’s post demonstrates a study that correlates all early onset solid tumors to a particular genetic weakness impacting 60% of all Americans . These people when they consume diet sugars might as well as be eating poison! The other 40% not so. You need to know and low cost genetic dtc testing will be a monster product. It appears this is where LIMX and Jas are going. If so stock is going much higher! I am long and will trade happily as this begins the next leg of its journey!

$LIMX The Hidden Genetic Storm: How a Mitochondrial Weakness Is Fueling the Rise in Early-Onset Disease JD Unfiltered JD Unfiltered 31 Jul 2025 — 4 min read The Hidden Genetic Storm: How a Mitochondrial Weakness Is Fueling the Rise in Early-Onset Disease Over the past two decades, rates of early-onset cancers have climbed at an alarming pace. Young adults under 50 are being diagnosed with colon, pancreatic, breast, and brain cancers at rates not seen in previous generations. While lifestyle changes and processed food consumption are frequently blamed, a growing body of research suggests a more fundamental and underappreciated factor may be driving this crisis: genetic vulnerability to oxidative stress compounded by modern environmental exposures. This article explores a groundbreaking hypothesis: that a specific inherited weakness in mitochondrial antioxidant defense, centered around the SOD2 and GPX1 genes, combined with widespread consumption of artificial sweeteners may explain why early-onset diseases are rising so sharply. And it offers a vision for how this insight could reshape modern medicine. The Genetic Spark: SOD2 and GPX1 Variants At the heart of this new model lies the SOD2 rs4880 polymorphism, a single nucleotide variation that changes the structure and function of superoxide dismutase 2 (SOD2), a crucial mitochondrial enzyme. Individuals who inherit the TT (Val/Val) genotype experience significantly reduced transport of SOD2 from the mitochondria, resulting in lower enzyme activity and an accumulation of reactive oxygen species (ROS). These free radicals cause DNA damage, inflammation, and cellular stress, particularly in high-energy organs like the colon, pancreas, brain, and breast tissue. When SOD2 falters, the GPX1 enzyme, tasked with clearing hydrogen peroxide (H2O2), another form of ROS is forced to compensate. But many people also carry the GPX1 rs1050450 variant, which reduces its effectiveness. This double burden, weakened SOD2 and compromised GPX1, creates an environment where oxidative stress accumulates and overwhelms cellular defenses. Artificial Sweeteners: An Underestimated Catalyst While genetic predispositions create the foundation for vulnerability, modern dietary habits, particularly the rise in artificial sweetener consumption, are rapidly accelerating the problem. Aspartame, sucralose, and other synthetic sweeteners are now ubiquitous in diet sodas, energy drinks, flavored vapes, and countless “sugar-free” products. Emerging research shows these compounds can disrupt gut microbiota, increase inflammatory signaling, and directly generate ROS within cells. In individuals with compromised SOD2 and GPX1 activity, even modest artificial sweetener consumption can trigger a surge of oxidative stress, overwhelming antioxidant defenses and accelerating cellular damage. This means that for genetically predisposed individuals, the daily “zero-calorie” drink or artificially sweetened snack may act as a biochemical storm, pushing already fragile mitochondrial systems toward dysfunction. Finally, as research continues to uncover how genetic predispositions magnify the harm caused by artificial sweeteners, particularly in high‑risk groups, the implications extend beyond public health. These products, long marketed as safe for diabetics and the health‑conscious, may expose companies like Coca‑Cola, Pepsi, and Tate & Lyle to potential class‑action litigation as evidence mounts of their disproportionate impact on genetically vulnerable populations. Glutathione Collapse and the Chain Reaction The antioxidant glutathione (GSH) plays a central role in detoxifying ROS. But the GSH system depends on SOD2 and GPX1 functioning properly. When these enzymes are genetically weakened, glutathione gets used up faster than it can be recycled. This is especially true under stress, whether from artificial sweeteners, poor diet, emotional trauma, or environmental toxins. As glutathione levels collapse, GPX1 becomes ineffective, allowing hydrogen peroxide to accumulate. This further damages mitochondria, impairs cellular function, and sets the stage for chronic inflammation, DNA mutations, and early tumor formation. TKTL1: The Metabolic Switch That Fuels Disease One of the most fascinating downstream effects of this oxidative storm is the dysregulation of TKTL1, a gene that governs an alternative route in the pentose phosphate pathway (PPP). Under normal conditions, the PPP helps produce nucleotides and maintain redox balance. But when oxidative stress is chronic, TKTL1 becomes overexpressed. This metabolic shift rewires the cell’s energy production to favor glycolysis (the Warburg effect), allowing cells to survive and proliferate in a high-ROS environment. Unfortunately, this adaptation also promotes cancer growth, immune evasion, and metabolic dysfunction. TKTL1 is overexpressed in colon, pancreatic, breast, and brain cancers—all of which are rising in younger adults. The “Stress Threshold” Model: A New Lens on Vulnerability The implications of this genetic-environmental cascade are profound. Individuals with the TT (and to a lesser extent TC) genotype of SOD2 are fundamentally more vulnerable to environmental and emotional stress. Even modest exposures, like artificial sweeteners, a high-sugar drink, an intense workout, or a traumatic event, can tip the redox system into dysfunction. By contrast, individuals with the CC genotype have more robust mitochondrial defenses and can tolerate much higher levels of stress before cellular damage occurs. This "stress threshold" model offers a powerful framework for understanding why certain people experience early-onset disease despite seemingly moderate exposures. Rethinking Healthcare: From Reaction to Precision Prevention If this genetic mechanism holds true, it calls for a complete reimagining of how we approach health and disease. Instead of waiting for cancer to appear, we could screen for SOD2 and GPX1 variants early in life and offer targeted interventions to those at greatest risk. A mitochondrial resilience protocol might include: NAC (N-acetylcysteine) and liposomal glutathione to replenish antioxidant defenses CoQ10 and alpha-lipoic acid to support mitochondrial energy and redox balance Selenium, vitamin C, and vitamin E to cofactor antioxidant enzyme systems Niacinamide and spirulina to boost NADPH and pentose phosphate pathway support Polyphenols (EGCG, quercetin, pterostilbene) to regulate TKTL1 and reduce inflammation Vitamin D and melatonin to enhance antioxidant gene expression Combined with lifestyle modifications such as plant-forward diets, reduced exposure to artificial sweeteners and processed foods, regular movement, and stress reduction, these strategies could delay or prevent disease onset in genetically susceptible individuals. Testing, Research, and Equity We are at the cusp of a healthcare revolution. Affordable genetic testing now makes it possible to identify SOD2 and GPX1 risk profiles in infancy. Public health systems could integrate this screening into pediatric care, allowing for lifelong risk management. Research must now focus on: Mapping disease risk by genotype across diverse populations Testing antioxidant protocols in high-risk groups Studying TKTL1 modulation as a therapeutic target Investigating the cumulative effects of artificial sweetener consumption in genetically predisposed populations Creating clinical decision-support tools that incorporate genotype, stress load, and metabolic health Ethically, this model also demands attention to disparities. Populations with higher TT genotype prevalence—such as East Asians and individuals of African ancestry—may need tailored prevention strategies and increased awareness. Healing Begins in the Mitochondria The rise in early-onset cancers is not just a coincidence or consequence of poor lifestyle. For millions of people, it may reflect an inherited fragility in the mitochondrial antioxidant system, magnified by environmental exposures, most notably artificial sweeteners, that modern life is uniquely equipped to exploit. By recognizing and addressing this vulnerability, we can finally shift from a reactive sick-care model to a precision health system rooted in prevention, resilience, and personalized care. The future of medicine is mitochondrial, and the time to act is now. READ MORE Genetics, Diet, and Oxidative Stress: Why Some Ethnicities Face a Higher Risk of Fatty Liver Disease Genetics, Diet, and Oxidative Stress: Why Some Ethnicities Face a Higher Risk of Fatty Liver Disease Non‑alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) have emerged as silent epidemics in the United States, affecting tens of millions of people, often without symptoms until advanced stages. These conditions do not develop in a vacuum. Instead, they are driven by a complex interplay between genetics, By JD Unfiltered 29 Jul 2025 The Roaring 2020s: 3 More Years of Euphoria Before the Hangover The Roaring 2020s: 3 More Years of Euphoria Before the Hangover In February, I wrote that 2025 would rhyme with 1926, the year when a volatile, skeptical market finally launched into the vertical phase of one of history’s greatest bull runs. By mid-year, that forecast has held: the spring correction shook out the weak hands, and U.S. equities have By JD Unfiltered 24 Jul 2025 The Breast Cancer Surge: Genetics, Demographics, and the Role of SOD Sciences The Breast Cancer Surge: Genetics, Demographics, and the Role of SOD Sciences Over the past two decades, breast cancer has surged in unexpected ways—particularly among young Asian American women. Once considered a lower-risk group, Asian American and Pacific Islander (AAPI) women are now seeing some of the fastest increases in breast cancer incidence in the United States. According to recent data, By JD Unfiltered 22 Jul 2025 The Global Rise of Early-Onset Colon Cancer and the Hidden Threat of Artificial Sweeteners The Global Rise

$LIMX Today, Jas is on a mission to remind every resilient youngster chasing success that every human’s greatest asset is their health and it is best when you invest in health young. His wellness platform reflects his own hard-learned truth: real success isn’t measured in money, but in energy, confidence, and self-mastery. Talking about his transformation journey, Jas Mathur said, “If there’s one thing my journey taught me, it’s that you can chase all the success in the world, but none of it matters if your body and mind are breaking down. I had built businesses, but I had also built habits that nearly cost me everything. It wasn’t until I took control of my health that I realized what being Limitless really means.” Jas Mathur’s story is more than a transformation — it’s a call to action for every ambitious dreamer: Prioritise Your Health, Invest in It Early, and Never Forget That Your Greatest Asset Isn’t What You Build — It’s How Well You Can Live and Lead

$LIMX From 450 Pounds To Global Wellness Mentor: Jas Mathur’s Incredible Transformation Zoom TV Digital Zoom TV Digital Updated Jul 29, 2025, 02:31 PM IST Jas Mathur’s story is more than a transformation — it’s a call to action for every ambitious dreamer Join Us Jas Mathur Jas Mathur It is right when they say that no amount of success can outrun poor health. Jas Mathur, the Indian-origin entrepreneur, transformation coach, and founder of Limitless X , made headlines early in life for making his first million by the age of 16 and building his tech empire by the age of 25. But behind the story of boardroom triumphs and multi-million-dollar ventures was a more personal, deeply challenging battle; a wake-up call for every young person chasing success at the cost of their health. Born in India & raised in Montreal, Quebec, Canada, Jas was always ahead of the curve — building successful ventures in satellite technology, entertainment, and wellness. But behind the applause, he was trapped in a body that didn’t match his ambitions. Years of neglect, stress, and unhealthy habits pushed his health to the edge — at his peak, he weighed over 450 pounds. With that came isolation, frustration, and a hard truth: success means nothing if your health is failing. That realisation sparked one of the most remarkable transformation journeys. Through discipline, structured fitness, and a complete lifestyle overhaul, Jas lost over 250 pounds and rediscovered his true purpose. In today’s world, young people are grinding harder than ever — chasing money, status, recognition — but they’re sacrificing their health in the process, often without even realizing it. Jas’s transformation has become a powerful reminder to the youth that you shouldn’t have to reach a breaking point to understand that real success starts with your health — because no ambition, no achievement is worth it if your body and mind can’t keep up. Ads By Google Ad will close in 24 Skip Ad READ FULL ARTICLE

$LIMX The prior posts shows where LIMX intends to go with HealthMD. The want to head into genetic testing for a reason! I am long and willing to trade around

$LIMX Genetics, Diet, and Oxidative Stress: Why Some Ethnicities Face a Higher Risk of Fatty Liver Disease JD Unfiltered JD Unfiltered 29 Jul 2025 — 4 min read Genetics, Diet, and Oxidative Stress: Why Some Ethnicities Face a Higher Risk of Fatty Liver Disease Non‑alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) have emerged as silent epidemics in the United States, affecting tens of millions of people, often without symptoms until advanced stages. These conditions do not develop in a vacuum. Instead, they are driven by a complex interplay between genetics, oxidative stress, and modern dietary patterns, with some populations bearing a disproportionate burden of risk. Understanding who is most at risk and why, is essential for developing effective prevention and treatment strategies. This is where SOD Sciences Inc., a leader in genetic and antioxidant profiling, is reshaping how physicians can assess and manage these conditions. By offering advanced panels for key oxidative‑stress genes and antioxidant levels, SOD Sciences is helping clinicians move beyond one‑size‑fits‑all care to personalized, data‑driven interventions. Ethnic Disparities in Fatty Liver Disease NAFLD affects nearly 25–30% of U.S. adults, but the risk is not evenly distributed. Latino Americans, especially those of Mexican origin, have the highest prevalence, with studies reporting rates exceeding 60% in some subgroups. Genetics play a major role here, particularly the PNPLA3 I148M variant, which is more common in this population. East Asian populations (Japanese, Korean, and Filipino Americans) also face elevated risks, but for different reasons. Many experience “lean NAFLD,” developing fatty liver at much lower BMI thresholds than White or Black Americans. In these groups, subtle changes in metabolism, oxidative‑stress pathways, and diet can have outsized effects on liver health. South Asians, including Indian Americans, also carry unique susceptibility patterns, driven by high rates of insulin resistance and distinct genetic risk factors. By contrast, Non‑Latino Black populations consistently show the lowest prevalence of NAFLD but tend to experience more aggressive fibrosis progression once the disease develops. These disparities underscore the need for ethnicity‑specific approaches to screening and management—a challenge standard guidelines often fail to meet. The Genetic Puzzle: SOD2, GPX1, APOE4, and TKTL1 Fatty liver disease is more than fat accumulation, it is an oxidative‑stress‑driven condition, and several key genes dictate how the body responds to that stress. SOD2 (rs4880 Ala16Val): This gene encodes a mitochondrial antioxidant enzyme, superoxide dismutase 2. The T allele (Val/Val), which is highly prevalent in East Asians (~77% homozygous), reduces mitochondrial import efficiency and antioxidant capacity, leaving cells vulnerable to reactive oxygen species (ROS). GPX1 (rs1050450 Pro198Leu): This gene codes for glutathione peroxidase, another antioxidant defense enzyme. While the riskier T allele (Leu/Leu) is relatively rare in East Asians (~1%), it is more frequent in Europeans and Latinos. When combined with SOD2 dysfunction, this can compound oxidative injury. APOE4 (rs429358): Unlike its well‑known association with Alzheimer’s disease, APOE4 actually appears protective against fatty liver, shifting fat storage away from the liver and improving lipid handling. This protective effect has been observed across ethnic groups, though frequencies vary. TKTL1: While not as well studied in humans, this gene affects the pentose phosphate pathway, influencing glutathione recycling and de novo lipogenesis. Overexpression may contribute to steatosis and impaired redox balance. The interaction of these genes helps explain why some individuals develop NAFLD or ALD despite appearing metabolically healthy, and why others progress to fibrosis more rapidly. Glutathione Depletion: A Core Feature of Fatty Liver The liver is the body’s glutathione reservoir, storing roughly 25% of total GSH, a master antioxidant critical for neutralizing ROS. In both NAFLD and ALD, glutathione levels are 20–40% lower than in healthy livers, correlating with disease severity. This depletion reflects a vicious cycle, where SOD2 dysfunction (TT genotype) increases ROS leakage. GPX1 is forced to compensate, further depleting glutathione stores. And TKTL1 dysregulation disrupts NADPH production, impairing glutathione recycling. The end result is an exhausted antioxidant defense system, leaving the liver vulnerable to fibrosis and cirrhosis. This is where measuring both genetic risk and antioxidant status, as done by SOD Sciences Inc., can provide actionable insights for clinicians. The Western Diet Effect: A Perfect Storm for At‑Risk Populations The rise of NAFLD parallels the adoption of the Western diet, high in processed sugars, saturated fats, and red meats, and low in antioxidant‑rich fruits, vegetables, and whole grains. For Asian Americans and younger East Asians, this dietary shift is particularly damaging. Populations with a high prevalence of the SOD2 TT genotype are less equipped to buffer the ROS overload generated by these foods, accelerating oxidative stress and depleting glutathione reserves. Similarly, Latino Americans face a double burden: a high prevalence of PNPLA3 variants coupled with Westernized dietary patterns that worsen metabolic dysfunction. How SOD Sciences Inc. Is Helping SOD Sciences Inc. is addressing these challenges head‑on by providing advanced genetic and antioxidant testing solutions for physicians and healthcare systems. Their offerings include: Genetic risk panels for key variants (SOD2, GPX1, APOE, and others) linked to oxidative stress and liver disease progression. Antioxidant profiling, including glutathione status and superoxide dismutase activity levels. Clinical decision support tools, helping physicians integrate these findings into patient‑specific care plans. For clinicians, these tools offer a way to identify high‑risk patients earlier, personalize dietary and pharmacologic interventions, and track therapeutic responses over time. Clinical & Public Health Implications With NAFLD now projected to affect more than half of U.S. adults by 2040, the need for targeted, personalized strategies is urgent. For clinicians: Integrating genetic and antioxidant testing could refine risk stratification and guide antioxidant therapy or lifestyle interventions. For policymakers: Expanding coverage for advanced biomarker testing, like the panels offered by SOD Sciences Inc., can help identify and manage at‑risk populations before irreversible damage occurs. For patients: Understanding their genetic and oxidative‑stress profiles empowers them to make informed decisions about diet, supplements, and medical care. Conclusion Fatty liver disease isn’t just about calories or alcohol, it’s a biological story of oxidative stress, genetic vulnerability, and environmental pressures. For at‑risk groups, this story often unfolds faster and more aggressively. By combining genetic risk assessment with antioxidant profiling, companies like SOD Sciences Inc. are giving clinicians the tools to intervene earlier and more effectively paving the way for personalized, precision‑based liver care. READ MORE The Roaring 2020s: 3 More Years of Euphoria Before the Hangover The Roaring 2020s: 3 More Years of Euphoria Before the Hangover In February, I wrote that 2025 would rhyme with 1926, the year when a volatile, skeptical market finally launched into the vertical phase of one of history’s greatest bull runs. By mid-year, that forecast has held: the spring correction shook out the weak hands, and U.S. equities have By JD Unfiltered 24 Jul 2025 The Breast Cancer Surge: Genetics, Demographics, and the Role of SOD Sciences The Breast Cancer Surge: Genetics, Demographics, and the Role of SOD Sciences Over the past two decades, breast cancer has surged in unexpected ways—particularly among young Asian American women. Once considered a lower-risk group, Asian American and Pacific Islander (AAPI) women are now seeing some of the fastest increases in breast cancer incidence in the United States. According to recent data, By JD Unfiltered 22 Jul 2025 The Global Rise of Early-Onset Colon Cancer and the Hidden Threat of Artificial Sweeteners The Global Rise of Early-Onset Colon Cancer and the Hidden Threat of Artificial Sweeteners Over the past 15 years, early-onset colorectal cancer (EOCRC), once a medical rarity, has exploded into a global public health crisis. Rates are climbing across nearly every major country, particularly among individuals aged 15 to 40. In fact, colorectal cancer is now on track to become the most diagnosed cancer By JD Unfiltered 15 Jul 2025 Rewiring Healthcare: How Genetics, AI, and Nutrition Could Save Trillions Rewiring Healthcare: How Genetics, AI, and Nutrition Could Save Trillions U.S. healthcare spending is on track to hit $7.7 trillion by 2032, a staggering and unsustainable figure. Yet emerging technologies in genetic stratification, remote biomarker monitoring, artificial intelligence, and targeted nutrition offer a potential paradigm shift. These tools offer a blueprint for cutting healthcare costs by as much

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$LIMX SOD2 really posted a great article. We r early but Jas will be the face of personalized medicine! Doctors now work for us!

$LIMX Trend to Al for med aid Forget Dr. Google. Americans are turning to artificial intelligence for health needs. According to a survey of 2,000 US adults, a little more than a third (35%) already use Al to learn about and manage aspects of their health and wellness. Top uses for this tech in-clude: to get insight into specific medical conditions or issues (31%), to help with weekly meals and recipes (25%, to learn about new exercise routines (23%) and for emotional or therapeutic support and advice (20%). About a quarter of current users (24%) even use Al to fact-check health and wellness information.