While much of our body ceases to grow after a certain age, our brains are a remarkable exception. They constantly evolve, giving birth to new cells through neurogenesis and building and rearranging their flexible cellular connections, known as synaptic plasticity. Recent advances in neuroscience have increasingly focused on understanding how our brain's growth and development shift with age and what proactive steps we can take to ensure optimal cognitive health. In this Research Review article, we aim to provide a more comprehensive and in-depth overview of the changes in our brains as we age. Additionally, we will explore the intriguing role of diet in maintaining brain health, illuminating how our food choices directly impact neurogenesis and synaptic plasticity in adulthood. This discussion offers insightful perspectives on potential dietary strategies to combat the aging process in the brain.

In the field of Neuroscience, recent research has focused on the potential role that the gut microbiome may play in the development of age-related neurological disorders such as Parkinson's Disease. Recent research has found that the development of Parkinson’s may have a surprising connection to the gut microbiome, a complex community of microorganisms living in our digestive tract. In this Research Review Article, we will explore how our gut changes with age and how these changes affect the development of diseases like Parkinson's. Additionally, we will uncover compelling strategies that can slow down aging and potentially ease Parkinson’s challenges by targeting the gut microbiome.

As the scientific community grapples with neurodegenerative disorders, the study of mTOR signaling provides a glimmer of optimism. But what's the connection between mTOR and debilitating conditions like Alzheimer's or Parkinson's? And how can we leverage this knowledge to stave off cognitive decline? In this article, we dive deep into the molecular intricacies of mTOR pathways and their potentially profound implications in neurodegenerative diseases. Moreover, we delve into the therapeutic promise of rapamycin, a molecule that may herald a paradigm shift in neurodegenerative disease management and prophylaxis.

The incidence of cancer increases exponentially as we age. One link between age-related cancer and degeneration could be an inflammatory tissue environment driven by MTOR in senescent cells. In her pivotal 2010 research paper, "The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression," Dr. Judith Campisi delves into how senescent cells create to a cellular 'microenvironment' favorable for cancer progression. In this article, we review Campisi's important insights and explore the potential of rapamycin to mitigate the cancer-promoting tendencies of these dysfunctional senescent cells.

If you have diabetes or know someone who does, it is likely that you are familiar with metformin—a first-line medication universally used in the treatment and prevention of type 2 diabetes (T2DM). In recent years, numerous studies have provided evidence that its benefits extend beyond blood sugar control, suggesting that metformin is capable of taming the detrimental effects of aging by reducing both inflammation and oxidative stress, and promoting autophagy. The positive health effects commonly observed in individuals with T2DM who use metformin, along with insights gained from studies in animals like worms and mice, have raised a compelling question: could metformin potentially serve as an anti-aging medication, capable of extending healthspan?

In this research review, we analyze the intricacies of telomere biology and its implications for human health and longevity. Telomeres, the 'timers' of cell life, gradually shorten with each division, leading to cellular senescence—making telomeres pivotal biomarkers in the study of aging. The focus of recent scientific inquiry has shifted to telomerase, the enzyme responsible for adding length to telomeres, thus offering a countermeasure to the aging process. However, the resurgence of telomerase activity is a double-edged sword; while it may hold the key to prolonged cell vitality and improved tissue regeneration, its aberrant activity is closely linked to cancer development, highlighting the complex role of telomerase in human biology. This article assesses the current landscape of telomerase research, acknowledging the enzyme's dualistic nature. We probe the intricate challenges that scientists face in leveraging telomerase for therapeutic benefits, emphasizing the need for caution and the profound implications of this research for the future of medicine.

Even though more than 1.8 million individuals worldwide are diagnosed with Multiple Sclerosis, the exact cause of the disease remains unclear, with scientists believing that it arises from a complex interplay of genetic, environmental, and immunological factors. Recent studies have cast the spotlight on the mammalian target of rapamycin (mTOR) pathway, which is believed to play a significant role in MS pathophysiology. The heightened activity of mTOR is gaining recognition for its potential to influence the course of MS, presenting new therapeutic opportunities to modulate this pathway. A recent narrative review paper by Dr. Aigli Vakrakou from the University of Athens provides a comprehensive analysis of emerging approaches to the treatment of Multiple Sclerosis. The review provides a thoughtful analysis of mTOR's role within the cellular framework and its impact on the progression and symptoms of MS. In our comprehensive Research Review, we delve into the pivotal role of mTOR inhibition in MS. We present findings on how this inhibition can bolster autophagy, potentially leading to improved clinical outcomes for MS sufferers. Moreover, we examine the influence of mTOR regulation on T cells and the ensuing impact on immune system equilibrium, with the aim of decreasing MS-related symptoms.

Over the past several years, rapamycin has captivated the scientific and medical communities with its promising potential as an anti-aging compound. Pioneering studies suggest that this molecule could play a pivotal role in delaying the onset of age-related diseases and possibly extending lifespan. However, as with many groundbreaking discoveries, its use in the realm of longevity is still shrouded in questions and uncertainty. The optimal dosage, long-term impacts, and the full scope of its therapeutic benefits remain areas of active research and exploration. In this review, we will delve deeper into rapamycin's intricacies, and highlight how new clinical trials are inching us closer to understanding its transformative impact on age-related health and longevity.

The mTOR pathway has emerged as a focal point in the realm of longevity science. When mTORC1's signals are controlled, it potentially paves the way for a longer, healthier existence. Contrastingly, mTORC2 reveals a more complex tale, with its suppression leading to metabolic complications and decreased survival rates in mice. Rapamycin, a compound frequently highlighted in our previous research reviews, targets this pivotal pathway. The intrigue around rapamycin is rooted in its dual nature: it might extend lifespan and counteract age-related ailments, but it also walks a fine line between the benefits of inhibiting mTORC1 and the risks tied to inadvertently suppressing mTORC2. In this comprehensive analysis, we delve deep into the latest research on rapamycin to elucidate its potential and influence on the most critical markers of longevity and healthspan—highlighting the vital nuances of how dosing influences its potential benefits and side effect profile.

In our previous research review articles, we explored the intricate factors contributing to the aging process, with a specific focus on molecular pathways and underlying mechanisms. In this week's research review, we delve into the intriguing and paradoxical role played by DNA Damage Response (DDR) programming, which is crucial for maintaining DNA stability. However, with advancing age, the constant activation of this system can pose significant challenges to cellular health, leading to phenomena such as senescence, inflammation, and the onset of age-related diseases. We spotlight the research conducted by Qian, Zhou, Tanaka, and Takahashi, who have undertaken a comprehensive examination of the intricate interplay between protective responses and their paradoxical contribution to accelerated aging in later stages of life.

In past articles, we delved deeply into the impact of cellular dysfunction on aging and the associated tissue degeneration. We focused on the role of senescent cells that accelerate age-related decline in tissue function. We have discussed in detail how the dysfunction of these damaged cells is characterized by toxic overactivity and growth, which compromises overall tissue function and accelerates aging. In this segment, we'll pivot to a detailed exploration of metabolic health, particularly the signaling pathways responsible for nurturing or inhibiting these dysfunctional cells. As we age, the cellular mechanisms that detect nutrient levels and gauge the energy status of cells start to falter. This article aims to shed light on the consequences of this metabolic decline and its interplay with aging.

It is well-established that calorie restriction can improve metabolic health in multiple preclinical models, as well as delay or at least slow down the rate of biological aging by reducing the incidence of developing age-related pathologies. Other dietary manipulations, such as complete fasting and/or time-restricted feeding, have also gathered attention as alternative approaches to improve metabolic flexibility and lifespan. Yet, what is the actual impact of these dietary approaches, and how do they fare in real-world applications? A groundbreaking study published in Nature Metabolism by Professor Dudley Lamming’s research team seeks to decipher the mysteries surrounding these diets. We delve into the intriguing findings of this study, exploring the pros and cons of different calorie restriction models and their implications for human health and longevity, offering you a concise overview and critical insights into translating these dietary manipulations to everyday life.

In this week’s edition of Healthspan Research Review, we delve deep into the latest research surrounding taurine and its correlation with aging. We investigate the diminishing levels of taurine as we age and dissect the intricate biochemical processes that determine the boundaries of taurine supplementation in restoring these levels.

When the National Institute for Aging tested over a dozen longevity molecules, acarbose was one of five molecules shown to increase lifespan. The intrigue around acarbose stems from its dual function: it influences metabolic health and reshapes our gut microbiota. But how does this alteration in microbial balance translate to enhanced healthspan? This article probes the notion that the healthspan-promoting benefits of acarbose are intrinsically linked to its role in diversifying the gut microbiome and amplifying the production of short-chain fatty acids.

Sarcopenia, commonly associated with the frailty of advanced age, goes beyond mere muscle weakness—it holds potential implications for our cognitive faculties. But what links the muscle's decline to the brain's? The answer, it seems, could lie in the realm of myokines—specific chemicals our muscles dispatch during exercise, intricately connected to brain health. Factor in disturbances like insulin imbalances, protein metabolism anomalies, compromised mitochondrial functions, mounting inflammation, and a portrait of cognitive erosion emerges. In their recent review, Oudbier et al. dissect these connections. In this research review, we dive into their analysis, revealing the biochemical and physiological connections between skeletal muscle and the brain, and the pathophysiological mechanisms underlying cognitive decline.

The persistent battle against chronic inflammatory ailments highlights an unyielding hyperactivity of our immune system. But could the answer lie in LDN, a promising anti-inflammatory agent? In this comprehensive review, we dive deep into the mechanisms by which LDN modulates our immune response, revealing not just its interaction with opioid receptors, but its profound influence on endorphin levels and inflammation. Delving further, we scrutinize LDN's effects on three prominent chronic inflammatory diseases: Multiple Sclerosis, Fibromyalgia, and Inflammatory Bowel Disease (IBD).

Aging, that inevitable march towards senescence, has puzzled and intrigued scientists for centuries. Traditionally, our understanding of aging has centered on wear and tear, with the belief that our cells and tissues break down over time due to accumulated damage. However, a fresh perspective by Dr. João Pedro de Magalhães challenges this narrative, suggesting that the very processes responsible for our growth and development might also be driving our decline after we hit our reproductive prime.

As we age, our bodies exhibit a reduced capacity to construct new muscle protein, even in the presence of anabolic stimuli like resistance exercise or protein intake. This perplexing state has captivated scientists for decades, yet the molecular mechanisms behind anabolic resistance have remained ambiguous. Emerging evidence from the pioneering lab of Dr. David J. Glass, MD, sheds light on a potential player in this enigma: the dysregulation of a signaling pathway known as mTOR. By delving into the intricacies of mTOR signaling, Dr. Glass and his team have begun to unravel the mysteries of anabolic resistance, providing insights into the cellular processes that underlie this physiological phenomenon.

As longevity science uncovers surprising connections between seemingly unrelated drugs and health outcomes, the curious case of Low-Dose Naltrexone (LDN) has captured researchers' attention. Originally designed as a treatment for addiction, LDN's impact on our biological systems has revealed unexpected benefits in modulating the immune response and fighting chronic inflammatory diseases. Through subtle increases in endorphin production and a cascade of anti-inflammatory responses, LDN presents an intriguing opportunity for enhancing overall well-being. In this article, we explore the multifaceted potential of LDN in extending healthspan, delve deeper into its proposed mechanisms of action, and examine its therapeutic applications in conditions like Multiple Sclerosis, Fibromyalgia, and Inflammatory Bowel Disease (IBD)—highlighting an unlikely candidate turned powerful ally in the pursuit of longevity and health.

Mikhail Blagosklonny's theory of cellular hyperfunction has shifted our understanding of aging by proposing that it's not a result of cellular decline or damage accumulation but rather an overactive state of cellular metabolism. One of the most infamous examples of this is cancer. In a recent research perspective article, Blagosklonny outlined the role of rapamycin in slowing both the progression and delaying the onset of cancer. In this week’s research review, Jacob Rose, from the Buck Institute for Aging Research, discusses the multiple mechanisms of rapamycin that impede cancer development and formation.

In a recent episode of the Wise Athletes Podcast, Healthspan's founder and CEO, Daniel, shared his story. He talked about how his research on mTOR-driven aging and his wife's lymphoma relapse led him to create Healthspan. Daniel also explained the scientific research that informs the rapamycin protocol offered by Healthspan.

In this installment of the Science Literacy Series, Jacob Rose, from the Buck Institute on Aging, dives into the fascinating world of microscopy, charting its evolution from a simple tool for viewing thin tissue sections to a powerful instrument capable of illuminating complex cellular interactions. He explores how innovative staining techniques and fluorescence microscopy are revolutionizing our understanding of diseases, particularly cancer, and guiding the development of targeted treatments. This article aims to simplify the understanding of these advanced microscopy techniques and highlight their critical role in diagnosing diseases and conducting research.

The recent rise in interest around cold exposure therapy has not only gripped the health-conscious circles on social media, but has also sparked crucial conversations among experts. But what underlies the health benefits of cold exposure therapy? In this review, Dr. Ryan Marshall, from the Metabolic & Molecular Physiology Research Group at the University of Birmingham, explores the latest research findings on cold exposure to shed light on the science behind the benefits and the underlying mechanisms that make this therapy effective.

As immune function declines with age, a ripple effect ensues that accelerates aging. In an attempt to improve immune function, Dr. Joan Mannick's research has led her to examine the effect of mTOR inhibition on improving the aging immune system’s function. Mannick's trials have shown that the use of very low doses or intermittent doses of mTOR inhibitors actually enhances immune function. Despite this, the paradoxical nature of rapamycin's effects raises fascinating questions about the intricate relationship between immunity and aging. In this article, we explore the profound implications of Mannick's findings and delve deeper into the curious case of rapamycin—an immunosuppressant turned ally in enhancing immunity.

In the second part of our Hallmarks of Aging series, we explore the "Antagonistic Hallmarks," which include Cellular Senescence, Mitochondrial Dysfunction, Deregulated Nutrient Sensing, Dysbiosis, Chronic Inflammation, Altered Cellular Communication, and Stem Cell Exhaustion. We uncover how these processes intricately shape our aging trajectory. Additionally, we'll explore interventions that have shown promise in reducing the harm caused by these hallmarks, paving the way for a better understanding of potential strategies to slow down the aging process.

The "Hallmarks of Aging" represent a crucial turning point in the scientific understanding of the aging process. These hallmarks, first articulated in a landmark 2013 paper and recently expanded, capture the key physiological and molecular shifts that occur as we age. In this two-part article, we'll delve into these revised hallmarks, focusing first on the 'Primary Hallmarks,' and the age-related pathways they affect. To begin, we will start with the “Primary Hallmarks” of aging: Telomere Attrition, Genomic Instability, Epigenetic Alterations, Loss of Proteostasis, and Disabled Macroautophagy.

Since GLP-1 was first discovered in the 1970s its role in human physiology remained largely unexplored for decades. However, in early 2005, the development of GLP-1 receptor agonists took the world by storm. Recent studies have shown their potential to significantly reduce body mass, particularly body fat in patients with obesity and type II diabetes. Despite this, Dr. Peter Attia has raised concerns about possible adverse effects on muscle mass. We explore Dr. Attia's perspective and delve into the relationship between GLP-1 and muscle mass in this piece.

Science and discovery are typically slow and painstaking processes, particularly when the goal is to produce factual results. The human tendency to seek swift solutions, especially in confronting mortality and disease, can lead to hasty conclusions. One example of this phenomenon was the pervasive belief in sirtuins as conserved longevity drugs—a viewpoint that has resulted in the considerable expenditure of time and resources. It's a cautionary tale for the scientific community—reminding us that the pursuit of knowledge should prioritize accuracy over expediency.

Among the several benefits of rapamycin to human health, recent research has begun to demonstrate that rapamycin may have significant benefits for women's health, particularly in preserving ovarian function, extending fertility, and delaying menopause. How does rapamycin work to promote ovarian function? In this article, Dr. Ryan Marshall from the Metabolic & Molecular Physiology Research Group at the University of Birmingham reviews these latest findings and how rapamycin may be utilized to enhance reproductive health and longevity in women.

A common belief is that a high-protein diet will facilitate an increase in muscle mass, strength, and function across the lifespan. However, is a high-protein diet still beneficial in the absence of any resistance-type exercise? Recent evidence from the world-leading laboratory of Professor Dudley Lamming at the University of Wisconsin-Madison has shown a high-protein diet, without any exercise, causes insulin resistance and an accumulation of white adipose tissue in as little as 18 weeks, even when matched for caloric intake. Here we discuss these provocative findings, their mechanisms, and how to prevent them.

A recent study investigated the potential of rapamycin to slow down skin senescence when applied topically as a cream. The results were striking—patients who underwent the treatment exhibited a significant reduction in senescence markers and an overall younger skin phenotype. But how does it work? The study found that the treatment either prevented cells from entering senescence or increased the clearance of senescent cells. These findings could have far-reaching implications for the broader quest to deaccelerate the aging process across the body.

Although inflammation represents a hallmark of aging, to grasp the underlying mechanisms of aging, we must delve deeper into the cellular state of senescence and the evolutionary pathways that culminate in a dysfunctional state. Indeed, the story of aging is fraught with paradoxes - the same cellular programming that once safeguarded us is ultimately responsible for driving us toward a state of dysfunction.

As researchers continue to search for a cure for osteoarthritis, recent studies have uncovered a fascinating link between hypertrophic and senescent chondrocytes - the cells that make up our cartilage - and the progression of the disease. But what causes this degenerative condition, and how can we stop it in its tracks? In this article, we delve into the science behind these cranky chondrocytes and explore their pivotal role in this debilitating condition. We also explore the exciting potential of microparticle rapamycin therapy, which delivers the drug directly to the affected joints and encourages a shift towards greater joint health and improved mobility.

Mikhail Blagosklonny's theory of cellular hyperfunction has shifted our understanding of aging by proposing that it's not a result of cellular decline or damage accumulation, but rather an overactive state of cellular metabolism. This idea challenges conventional wisdom and suggests that aging is a reversible phenomenon that can potentially be slowed down or even reversed. This shift in understanding has significant implications for how we approach the aging process.

New research reveals a surprising link between mTOR inhibition and the prevention of obesity and metabolic dysfunction. This complex story of mTOR's involvement in metabolic disorders unlocks new insights into the link between mTOR and obesity, and raises the potential for mTOR inhibitors like rapamycin to play a crucial role in preventing and treating these conditions.

As researchers delved into the promising role of rapamycin in promoting bone growth, they sought to unravel the underlying mechanisms at play. The story of rapamycin as a bone growth molecule and treatment for osteoporosis centers around its capacity to subtly adjust bone cell activity, encouraging a shift toward greater bone formation and improved skeletal health.

Dr. Rhonda Patrick proposes a mechanism for the phospholipid form of DHA to play a role in the prevention of APOE4-associated Alzheimer's Disease.

When the NIA tested over a dozen longevity molecules, acarbose was one of five molecules shown to increase lifespan, but how does it work? The story of acarbose as a longevity molecule lies at the intersection of its ability to augment our metabolic health and remodel our gut microbiota.

We'll be covering how you can reduce senescent cell burden with respect to aging and disease.

The fourth installment of our Rapamycin for Longevity series where we explore rapamycin and its effect on human longevity. In series 4 we go over the paper "Effect of rapamycin on aging and age-related diseases - past and future" written by Ramasamy Selvarani, Sabira Mohammed, and Arlan Richardson

The fourth installment of our Rapamycin for Longevity series where we explore rapamycin and its effect on human longevity. In series 4 we go over the paper "Effect of rapamycin on aging and age-related diseases - past and future" written by Ramasamy Selvarani, Sabira Mohammed, and Arlan Richardson

Pharmaceutical interventions with regards to aging requires targeting multiple pathways, thus there is rationale to test combinations of drugs that target different but overlapping processes. A multifaceted  approach to treatment of aging in order to determine if combining drugs shown to extend lifespan and healthy aging in mice would have greater impact than any individual drug.

A continuation of our Rapamycin for Longevity series exploring rapamycin and its effect on human longevity. Part 1 of 2.

Part 2 of our second series on Rapamycin for Longevity, where we explore rapamycin and its effect on human longevity. Part 2 of 2.

A continuation of our Rapamycin for Longevity series, where we explore rapamycin and its effect on human longevity. A brief explanation and overview of Harrison et al’s groundbreaking rapamycin study, aptly titled “Rapamycin fed late in life extends lifespan in genetically heterogeneous mice.”

Learn about cellular senescence and the hyperfunction theory of aging and how rapamycin treatment ties into these subjects.

Sleep is incredibly important for the human body as a whole as well as on the cellular level. What causes alterations in the quantity and quality of sleep and what are the consequences of these changes are quite important questions. What changes exacerbate aging and a more dysfunctional physiology and what changes are caused by aging that are detrimental to your health as well. We will cover the characterization of related changes in sleep structure on both the macro and micro scale and cover the differences between men and women when it comes to sleep and age.

Rapamycin Added to Diet in Late Mid-Life Delays Age-Related Hearing Loss in UMHET4 Mice

The first of our Rapamycin for Longevity series where we explore rapamycin and its effect on human longevity.

As the lexicon of health, longevity, and anti-aging enthusiasts continues to evolve, one term - 'autophagy' - has solidified its place within the discourse. Nonetheless, a relatively lesser-known offshoot, 'mitophagy,' or mitochondrial-specific autophagy, remains more obscure despite its critical significance. Recent evidence has begun to show how critical this process is in maintaining proteostasis within a cell or tissue and how dysregulation of this process can result in the accumulation of damaged mitochondria.