L-Nutra, Inc., the world's leading nutrition technology company pioneering the discovery, design, and commercialization of novel nutrition solutions, today announced data in Cell Reports demonstrating the effects of fasting-mimicking diets (FMD) in animal models of Alzheimer's disease and early human safety data. The study reports that FMD cycles reduce cognitive decline and Alzheimer's disease pathology in mouse models. The early clinical data also suggest that FMD cycles are safe and feasible in a small group of Alzheimer's patients.
Alzheimer's disease is a neurodegenerative disease characterized by progressive memory loss and a decline in quality of life and lifespan. An estimated 6.5 million Americans aged 65 and older live with Alzheimer's dementia, and approximately 200,000 under age 65 have early-onset Alzheimer's. The number of people affected globally by dementia is expected to increase to 152.8 million cases in 2050, primarily due to population aging. FDA-approved drugs for Alzheimer's only temporarily improve or slow the deterioration of Alzheimer's symptoms but do not generally affect disease progression.
"L-Nutra is the world's pioneering Nutri-Technology company bringing the revolutionary Fasting-Mimicking Technology (FMT) to transform the paradigm of care in four major chronic illnesses: cancer, diabetes, autoimmune diseases, and Alzheimer's. With this published result, our FMT platform takes another bold step towards turning 'food into medicine.' Leveraging the rigor of the biotech industry, we are the leading nutrition company to have a nutrition solution with the potential to impact human longevity and the course of many chronic health conditions," said Joseph Antoun, M.D., Ph.D., CEO and Chairman of L-Nutra, Inc.
In this newly published paper, the lead author Professor Valter Longo at USC and investigators from other centers* show that cycles of FMT attenuate cognitive decline, reduce Alzheimer's pathology and neuroinflammation, and promote neurogenesis and improve cognition in Alzheimer's mouse models. In a pilot human trial included in the publication, the authors also show that the intervention is safe and feasible in a small group of Alzheimer's patients.
"The patented FMT in previously published studies demonstrated a clear mechanism of action, supported by successful early human trials that showed safety and efficacy in diabetes and various forms of cancer. This exciting result in a neurodegenerative condition extends the finding that the FMT platform as a unique solution has an upstream and overarching systemic impact on the body," said Dr. William Hsu, MD, Chief Medical Officer of L-Nutra, Inc.
L-Nutra plans to evaluate further its FMT platform's impact on driving various chronic conditions into remission or regression. For more information on L-Nutra and its revolutionary approach to targeting a broad spectrum of diseases, visit www.l-nutra.com or contact Dr. William Hsu, Chief Medical Officer, at [email protected].
*Collaborating centers include USC, IFOM, University of Genoa, UCLA, University of Illinois at Chicago, and University of Perugia.
About L-Nutra Inc.
L-Nutra is leading the discovery, design, and commercialization of novel nutri-programs with the mission of adding more life to human life. Current commercial products focus on wellness and healthy aging, including ProLon®, the first and only clinically tested 5-day fasting nutrition program designed to allow your body to enter a fasting state while still allowing you to consume nutrient-dense foods. L-Nutra created the 1-day fasting nutrition kit ProLon Reset™ and ProLon Intermittent Fasting Bar®, the first nutrition bar specifically designed and clinically tested to support intermittent fasting. Nutrition for Longevity® is L-Nutra's science-backed, chef-curated meal program, featuring farm-to-table meals formulated to address the nutritional deficiencies in today's commercially grown produce. For more info, visit https://l-nutra.com/.
Chief Medical Officer
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Original Source: L-Nutra Reports Fasting-Mimicking Diet Cycles Reduce Cognitive Decline and Pathology in Alzheimer's Disease Models