Aligning Eating Schedules with Your Body Clock for Longevity

A recent study on mice has revealed that circadian rhythms, which regulate daily physiological processes, are not solely governed by a central clock in the brain. Instead, they involve a more intricate system where molecular clocks in both the brain and muscle tissue work together to maintain muscle health and function. The research further indicates that adjusting these clocks through changes in meal timing could potentially preserve muscle function in the elderly.

In the study researchers employed a mouse model called Bmal1 knockout (KO), which inhibits the expression of the Bmal1 clock gene in the suprachiasmatic nucleus. This is the region in the brain responsible for regulating circadian rhythms. In this model, however, they were able to restore Bmal1 expression in various tissues, including skeletal muscle. The KO mice exhibited unusual patterns of activity and inactivity, oxygen consumption, energy expenditure, and glucose and lipid oxidation compared to wild-type mice, demonstrating disrupted circadian rhythms due to the absence of the Bmal1 gene.

By 26 weeks, the knockout (KO) mice had experienced a decrease in both weight and muscle mass compared to their condition at 10 weeks, along with evidence of mitochondrial damage in their muscles. However, when the expression of the gene was reinstated in both the muscle and brain of certain mice, their muscle mass and strength were maintained. This led researchers to conclude that interaction between the clocks in the brain and muscle is essential to stave off early muscle aging.

As individuals grow older, their sleep-wake cycles undergo changes, and they also experience a loss of muscle mass. This study proposes that these phenomena are closely linked. Typically, aging leads to an adjustment in sleep patterns, with older adults tending to wake up earlier in the morning and go to bed earlier in the evening. However, for some elderly individuals, especially those suffering from neurodegenerative diseases like Alzheimer’s, sleep patterns may become highly erratic and fragmented.

This research has discovered a potential method to restore the functioning of circadian clocks in both the brain and muscles. By adopting a time-restricted feeding regimen for older adult mice, the scientists were able to revive rhythmic gene expression in the muscle tissue, effectively preventing the decline in muscle function.

These results shed light on potential physiological shifts that occur with aging and how time-restricted eating could potentially counteract these changes. However, confirmation through human trials is necessary before drawing extensive conclusions about the effects of the circadian clock on human aging. It remains unclear whether such dietary strategies could help prevent muscle aging in people. The observation that limiting food intake to the active phase of mice partially reinstated the function of the central clock and bolstered the skeletal clock underscores the significant role that timing of eating plays in supporting circadian rhythms.

To view the original scientific study click below:
Brain-muscle communication prevents muscle aging by maintaining daily physiology

Stem Cells Enhance Memory and Combat Inflammation in Mice

Typically, when discussing potential treatments for Alzheimer’s Disease, the focus tends to be on amyloid proteins and the plaques that form in the brain. Yet, recent studies suggest that the disease is influenced by a broader range of factors, such as neuroinflammation and metabolic imbalances. In a significant breakthrough, a team from Michigan Medicine has demonstrated that transplanting human neural stem cells into a mouse model of Alzheimer’s not only enhances memory but also diminishes neuroinflammation. This research highlights a promising new direction for therapeutic approaches.

The transplantation of human neural stem cells into the brains of mice with Alzheimer’s Disease yielded positive results, even though amyloid plaque levels did not change. This supports the idea that targeting neuroinflammation could be an effective therapeutic approach, separate from strategies focusing on amyloid plaques. Furthermore, the treatment normalized inflammation in the microglia, the brain’s primary immune cells, which become hyperactive in Alzheimer’s Disease. As the disease advances, the inflammatory activity of microglia is believed to play a role in the loss of neurons.

The researchers implanted neural stem cells into the memory-related regions of genetically modified mice that carried mutations linked to familial Alzheimer’s Disease. Eight weeks after the transplantation, both the test group and the control group of mice were subjected to the Morris water maze, a test used to evaluate spatial memory and learning abilities.

Researchers discovered that mice with Alzheimer’s Disease, after receiving stem cell transplants, showed restored learning capabilities that matched those of control mice with normal memory functions. Further analysis using spatial transcriptomics, a technique for mapping gene expression across different brain regions, indicated that over 1,000 genes had their expression normalized in the memory centers of the Alzheimer’s mice post-transplantation.

When examining changes in gene expression within microglia, researchers found that genetic markers associated with Alzheimer’s Disease progression had returned to levels nearly identical to those in control mice. This indicates a decrease in neuroinflammation and a potential slowing of the disease.

The scientists emphasized that the positive results observed following the stem cell transplantation need further exploration in mouse models before progressing to studies in larger animals and, ultimately, human trials. This research is crucial and further reinforces the potential of stem cell therapies in treating neurodegenerative diseases. These preliminary studies are essential initial steps toward developing stem cell treatments.

To view the original scientific study click below:
Human neural stem cells restore spatial memory in a transgenic Alzheimer’s disease mouse model by an immunomodulating mechanism

The Role of Mitochondria Transplants in Muscle Function

Mitochondria, often described as the powerhouses of cells, are crucial for converting nutrients into adenosine triphosphate (ATP), the energy currency of cells. Their existence is fundamental to the survival of complex organisms, including humans. However, as we age, mitochondria sustain damage and become less effective.

The process of energy production inherently generates harmful byproducts known as free radicals. These free radicals can wreak havoc within cells, especially harming mitochondrial DNA. Mitochondria lack the robust DNA repair mechanisms found in the nuclear DNA of cells. Over time, mutations accumulate in mitochondrial DNA, leading to a progressive decline in their ability to function effectively and produce energy. This triggers a downward spiral, further impairing mitochondrial performance. In response, several researchers are exploring therapeutic strategies to address this issue. If these efforts prove successful, they could potentially slow or reverse cellular aging.

It is well-established that mitochondria have the ability to move among cells and be taken up by surrounding cells. This knowledge has led to the idea that transplanting healthy mitochondria into older individuals could be an effective method to rejuvenate them. This concept was put into practice in a recent study, where researchers transferred mitochondria to aged subjects. Interestingly, the mitochondria used in the study were sourced from mice that were the same age, rather than from younger mice.

The mitochondria were isolated from donor tissue and then directly administered to the mice in the test group. This was done through injections into the muscle tissue of the hind legs, which provided a straightforward method of delivery. In comparison to the control group, the mice that received mitochondrial transplants exhibited enhanced mitochondrial and muscle function, as well as increased endurance.

The study revealed notable rises in basal levels of cytochrome c oxidase and citrate synthase activities, along with ATP levels in the transplanted mice compared to those given a placebo. Additionally, there was a significant increase, approximately doubled, in the protein expression of mitochondrial indicators in both oxidative and glycolytic muscle types. These improvements in muscle functionality led to marked gains in exercise endurance for the treated mice.

A significant aspect of this study is that despite the mitochondria being sourced from mice that were the same age, there was still observable improvement. This suggests that the introduction of additional mitochondria might dilute the effects of the damaged ones already present in the recipient. Essentially, the inflow of new mitochondria could be mitigating the impact of the mutated ones. Given these findings, it seems logical to hypothesize that using mitochondria from younger donors could yield even better results. Conducting a follow up research with mitochondria obtained from younger mice would be an excellent next step to test this theory.

To view the original scientific study click below:
Mitochondrial Transplantation as a Novel Therapeutic Strategy for Mitochondrial Diseases

How Bright Light Enhances Cognitive Performance

When you find yourself more alert and focused after basking in bright daylight, science offers an explanation. Recent studies reveal that exposure to increased levels of light can directly influence activity in a vital brain region, the hypothalamus, boosting cognitive performance and promoting wakefulness.

This new study represents a substantial leap forward in understanding the biological effects of light on cognition and neurological well-being. While previous research has shown that light exposure increases alertness, this is one of the first studies to pinpoint how it influences the human brain at the neural level.

The research team selected 26 young adults to undertake cognitive tasks within an MRI scanner while experiencing different degrees of light, ranging from total darkness to exceptionally bright illumination. The auditory tasks assessed executive functions such as working memory and emotional processing. Employing a 7 Tesla functional MRI with high resolution, a method offering improved brain imaging, the researchers investigated the impact of light level alterations on activity within distinct regions of the hypothalamus during the tasks. Their discoveries unveiled a noteworthy pattern.

The researchers observed that as light levels heightened, activity in the posterior part of the hypothalamus intensified. Conversely, activity in the inferior and anterior hypothalamus decreased with greater exposure to light. In essence, various segments of this compact brain area, no larger than an almond, responded differently based on the brightness level.

Upon analyzing the participants’ scores on the executive functioning task, the researchers uncovered a distinct correlation: heightened light levels correlated with enhanced performance on cognitive tasks. Interestingly, this improvement was associated with reduced activity in the posterior hypothalamus. The researchers suggest that this indicates the activity in the posterior hypothalamus is not directly linked to light’s beneficial impact on cognitive performance. Instead, it suggests the involvement of other brain regions.

Under conditions of high light levels, specific brain cells might be enlisted to enhance performance on certain cognitive tasks. The authors underscore the need for further research to examine how light affects entire brain networks and their interaction with the cortex, the outer layer of the brain responsible for higher cognition, in order to comprehensively understand these effects.

The present discoveries offer promising prospects. By illuminating the neurological pathways connecting light exposure to cognitive function, this research unveils opportunities for the development of light therapy interventions. Such treatments could offer assistance to individuals grappling with sleep disturbances and alertness issues, while potentially enhancing mood and cognitive performance throughout the day.

To view the original scientific study click below:
Regional response to light illuminance across the human hypothalamus

Young Extracellular Vesicles’ Role in Extending Life

For centuries, the mythic qualities of young blood as a source of rejuvenation captivated human imagination. These beliefs, though rooted in delusion and cruelty, contain a kernel of scientific truth. Studies in heterochronic parabiosis, where the blood systems of young and old animals are connected, have demonstrated that this process can rejuvenate the older participant and accelerate aging in the younger. The exact mechanisms remain unclear. However, recent research has identified extracellular vesicles in the blood as key agents driving many rejuvenating effects.

Extracellular vesicles are small vesicles composed of a lipid bilayer similar to that of cell membranes. Secreted by cells, these vesicles carry diverse molecular cargoes, such as proteins and microRNAs, facilitating intercellular communication. Research has demonstrated that EVs sourced from young blood can confer benefits to older organisms, but the complexity of the molecular interactions involved means that research into the precise mechanisms is still actively underway.

Researchers concentrated on small EVs measuring 200 nanometers or less. To assess their rejuvenating effects, older male mice were given weekly injections of these small EVs sourced from either humans or young mice. The treatment began when the mice were 20 months old and continued until their death. For comparison, control groups of both young and the old mice received equivalent doses of phosphate-buffered saline. The results were notable: the treated mice experienced an increase in median lifespan of 34.4 vs 30.6 months, a significant extension considering the age at which treatment commenced. Additionally, the treatment enhanced various indicators of health span, including reduced frailty and better hair retention.

Further exploration into the treatment’s impact revealed that even a short, two-week regimen significantly reduced the presence of senescent cells and lowered levels of reactive oxygen species across various tissues, aligning them with those found in young control subjects. Similar decreases were noted in the levels of advanced glycation end products and lipofuscin, of which both are deleterious compounds linked to aging characteristics. Proteomic analysis across multiple tissues showed that the small extracellular vesicles had a broad impact, primarily addressing issues like epigenetic changes, mitochondrial dysfunction, and genomic instability, which are recognized as key aging markers. Notably, in muscle tissues and the hippocampus, the treatment effectively rejuvenated markers of mitochondrial health, such as DNA content, ATP production, and mitochondrial structure and quantity.

According to the researchers, since the biological activity of small EVs shows minimal species specificity, they experimented with injecting old mice with small EVs taken from the blood of young humans. This approach replicated many of the positive outcomes seen in earlier experiments. If benefits are reciprocal, this could potentially address the issue of sourcing sufficient quantities of EVs for human therapies.

To view the original scientific study click below:
Small extracellular vesicles from young plasma reverse age-related functional declines by improving mitochondrial energy metabolism

New Study Suggests Acetaminophen May Influence Heart Function

New research conducted on mice indicates that acetaminophen, a common pain relief medication and the active ingredient in Tylenol, may interfere with heart pathways involved in energy production, antioxidants, and protein breakdown. The study reveals that even standard adult dosages of acetaminophen, previously deemed safe, could lead to detrimental changes in heart tissue. These findings contribute to the increasing scrutiny regarding the broad spectrum of potential side effects associated with this widely used drug.

In the study with mice, researchers supplied water containing acetaminophen at a dosage corresponding to 500 mgs daily for a typical adult. Within a week, notable alterations were detected in the protein levels linked to key biochemical pathways essential for cardiac function. These pathways are involved in energy generation, antioxidant processes, and the degradation of impaired proteins.

The findings indicate that acetaminophen, even at doses generally deemed safe for humans, can interfere with multiple signaling pathways in the heart. While researchers anticipated alterations in two to three pathways, the study revealed that more than 20 different pathways were impacted. Previously, acetaminophen was considered to have a low risk of adverse side effects when used according to guidelines.

The extended use of acetaminophen at medium to high doses may cause cardiac problems due to oxidative stress or toxin buildup from the drug’s breakdown, potentially overloading the body’s detox systems. The observed alterations in the study suggest increased stress and mitochondrial dysfunction in the hearts of mice treated with acetaminophen.

This research contributes to our knowledge of acetaminophen’s effects, which are known to include risks of gastrointestinal issues, elevated blood pressure, and liver toxicity with high dosages. The study emphasizes the significance of monitoring both the dosage and duration of use, as long-term consumption at medium to high levels could present more severe risks compared to occasional or low-dose use.

To view the original scientific study click below:
Acetaminophen May Be Less Heart-safe than Previously Thought

Health Concerns Linked to Plant-Based Vegan Meats

Recent research has shown that numerous plant-based meat products, often included in vegan diets, are heavily processed and contain high levels of salt, additives, and saturated fats. According to a recent peer-reviewed study, these plant-based meat alternatives, such as vegan sausages and burgers designed to replicate the taste and texture of meat, do not offer any significant cardiometabolic health advantages over diets that incorporate animal meats. The study specifically examined the impact of these plant-based meat analogues (PBMA) on aspects of cardiometabolic health.

The study consisted of dividing 82 participants into two groups. One group replaced their usual protein sources with six commonly used plant-based meat alternatives (PBMAs), while the other group continued with animal-based protein foods. The study assessed various cardiometabolic health indicators of the participants both before and after the trial period. These indicators included cholesterol levels and the body’s capacity to manage blood pressure and blood sugar levels.

The study determined that over an 8-week period, a diet consisting of plant-based meats did not demonstrate significant cardiometabolic health benefits when compared to a mixed diet that includes both plant and animal foods. The available plant-based meat alternatives on the market today do not provide the same health benefits as a traditional plant-based diet, which typically features whole foods like whole grains, fruits, legumes, and vegetables.

Currently, the manufacture of plant-based meat alternatives (PBMAs) typically requires significant processing, and the final products often contain high levels of saturated fats, salts and additives to replicate the taste and texture and other qualities of actual meat. Despite the meticulous selection of ingredients, recipes, and improvements in processing methods aimed at achieving meat-like textures and flavors, there are still notable differences in the nutritional profiles between PBMAs and traditional animal-based meats. It was noted that the high levels of phytates can interfere with the body’s ability to absorb minerals.

Simply being plant-based does not guarantee a healthier product. Therefore, it is crucial to keep an eye on how frequently these products are consumed by the population and to track the health impacts associated with plant-based meat alternatives.

To view the original scientific study click below:
Plant-Based Meat Analogs and Their Effects on Cardiometabolic Health: An 8-Week Randomized Controlled Trial Comparing Plant-Based Meat Analogs With Their Corresponding Animal-Based Foods

Why You Should Avoid Tap Water in Your Neti Pot

As spring unfolds, bringing vibrant blooms, millions prepare to face the challenges of allergy season, marked by sneezing, wheezing, and unyielding nasal congestion. Many people seek relief through the use of neti pots, which provide a drug-free solution by flushing out pollen and mucus with a saline rinse. However, studies indicate that tap water, when used in neti pots, may harbor organisms capable of causing rare, yet frequently fatal infections if not used correctly for nasal rinsing.

Neti pots are devices intended to clear out mucus and debris from the nasal passages using water. They are commonly used to relieve symptoms from nasal allergies, sinus problems, irritation from dry air, or colds. However, recent studies by the U.S. Centers for Disease Control and Prevention (CDC) have highlighted that using tap water in these pots for nasal rinsing can heighten the risk of acquiring rare yet severe infections caused by Acanthamoeba, tiny organisms that are prevalent in soil, water, and air.

These single-celled creatures can lead to various symptoms and are fatal in 82% of cases, although infections are uncommon, impacting only 3-12 people in the United States each year. Despite widespread exposure to Acanthamoeba, the number of people who actually fall ill remains low.

Acanthamoeba is responsible for several serious health conditions, including:
Acanthamoeba keratitis- an eye infection that threatens permanent vision loss, particularly in individuals who wear contact lenses.
Granulomatous amebic encephalitis- a severe infection of the brain and spinal cord that occurs in immunocompromised patients.
Disseminated infection- a pervasive infection that affects the skin, sinuses, lungs, and other organs, predominantly found in those with weakened immune systems.

The research focused on 10 immunocompromised patients with conditions such as HIV/AIDS, cancer or kidney disease, who had utilized neti pots and later developed Acanthamoeba infections. Seven of these patients survived, likely aided by the early intervention for concurrent sinus infections. Infections by Acanthamoeba, particularly those impacting the brain or central nervous system, are challenging to treat effectively. Unfortunately, most cases involving brain infections typically lead to death.

Nasal irrigation tools like neti pots, squeeze bottles, bulb syringes, and battery-operated water devices are deemed safe and effective when correctly maintained and used. However, the agency advises against using tap water for nasal rinsing, even though it’s safe for drinking. This is because stomach acid can neutralize microorganisms such as bacteria, amoebas and protozoa found in low quantities in tap water, but these can survive in the nasal passages and lead to severe infections. For nasal irrigation, it is recommended to use distilled or sterile water, boiling tap water for 3-5 minutes then cooled, or water filtered through a device capable of removing infectious organisms.

To minimize the risk of waterborne infections, it is essential to use uncontaminated water and also to maintain good hygiene practices. This includes washing your hands thoroughly, keeping the neti pot clean and dry, and adhering to the manufacturer’s guidelines for use.

To view the original scientific study click below:
Acanthamoeba Infection and Nasal Rinsing, United States, 1994–2022

Study Reveals Household Chemicals Damage Crucial Brain Cells

Is it possible that items meant to ensure our safety are instead compromising our neurological well-being? Recent findings indicate that typical household chemicals, including those in flame retardants and disinfectants, may be to blame. Scientists have examined thousands of chemicals considered potentially dangerous, identifying two particular types as detrimental to brain cells. With neurological disorders impacting millions, and the incidence rate climbing, genetic reasons account for only a small portion of these cases. Thus, hinting at the significant role environmental influences play in their prevalence.

Recent research has pinpointed two detrimental groups of chemicals: organophosphate flame retardants, present in plastics and dyes, and quaternary ammonium compounds (QAC’s), ingredients in disinfectants. Flame retardants are frequently found in items such as furniture, foam items, construction materials, and electronic devices. Meanwhile, QACs are ingredients in products like surface cleaning agents, hand sanitizers, shampoos, soaps, conditioners, and fabric conditioners.

In their effort to pinpoint these hazardous substances, researchers concentrated on chemicals that negatively impact oligodendrocytes. These are key nerve cells responsible for forming the protective myelin sheath around nerve fibers in the brain and spinal cord, which is essential for efficient signal transmission. By studying the impact of more than 1,800 chemicals on the development of mouse oligodendrocytes in laboratory cell cultures, the scientists discovered 292 chemicals that are lethal to these cells and another 49 that impede their development.

The goal of this study is to deepen the understanding of how environmental chemicals might affect neurological health. Through extensive laboratory testing, the research demonstrated that certain chemicals, at particular concentrations, can damage brain cells. Notably, the findings revealed that these chemicals primarily affect not the nerve cells themselves but other types of cells within the brain.

The researchers highlighted that specific chemicals found in everyday products pose a direct threat to cells that produce myelin, unveiling a novel risk factor for neurologic conditions that had not been identified before.

These substances are present in various household products, serving critical functions. It’s essential to determine safe exposure levels versus those that may impact neurological health. This study sets the stage for subsequent research to pinpoint dangerous exposure thresholds, aiming to guide better practices and policy-making. This is an initial step, suggesting caution rather than an immediate ban on these chemicals.

To view the original scientific study click below:
Pervasive environmental chemicals impair oligodendrocyte development

The Role of Protein in the Progression of Atherosclerosis

Recent research featured in Nature Metabolism indicates that dietary protein, especially a specific amino acid, significantly contributes to atherosclerosis. This disease leads to the buildup of plaques along the walls of arteries, triggering heart attacks and strokes, and accounts for a quarter of all fatalities worldwide.

Protein intake from our diet is essential for our body’s ability to synthesize its own proteins, yet the optimal quantity of dietary protein is still debated. Evidence from animal studies shows that limiting protein intake can significantly increase lifespan, with some human epidemiological research suggesting similar outcomes. Conversely, protein plays a crucial role in muscle development, crucial for preventing sarcopenia, a condition characterized by muscle loss.

A 2020 investigation by the same researchers found that in a mouse model of atherosclerosis, consuming high amounts of protein worsened the condition by triggering the activity of mTORC1 protein in macrophages. These immune cells are attracted to emerging lesions on artery walls, where they play a healing role by clearing away dangerous debris and LDL cholesterol. Unfortunately, these macrophages can sometimes consume excessively, transforming into engorged foam cells that become lodged within the atherosclerotic plaque, thereby exacerbating its expansion.

The mTORC1 protein facilitates the synthesis of additional proteins in the presence of abundant nutrients and hinders autophagy, the cellular process for eliminating internal waste. When nutrient levels drop, mTORC1 activity diminishes, leading cells to enter a state focused on maintenance and conservation. This shift from growth to repair mode is believed to be a key factor behind the lifespan extension observed with caloric restriction and the use of rapamycin, an effective mTORC1 blocker, in animal studies. The 2020 research indicated that excessive protein intake impairs the efficiency of macrophages by stimulating mTORC1 and reducing autophagy.

Leucine, which is plentiful in animal-based proteins, may explain why some studies find plant-based proteins to be healthier. These findings highlight that protein consumption implications extend beyond muscle mass, crucial as it is. Focusing on the intake of specific amino acids seems to be a prudent approach, as demonstrated by studies where limiting methionine and isoleucine has been linked to enhanced healthspan and lifespan in animals.

The research has identified a process where elevated protein consumption leads to an increase in blood leucine levels, which in turn activates mTORC1. This activation suppresses the autophagic capabilities of monocytes and macrophages, leading to the development of atherosclerosis. Given the widespread acceptance of protein intake levels exceeding the minimum daily recommendation of 0.8 gr per kg of body weight as safe and beneficial, these findings hold significant implications for clinical practices and public health policies. Thus, increasing protein consumption with the aim of improving metabolic health might not be a cure-all strategy and could potentially harm your arterial health.

To view the original scientific study click below:
Identification of a leucine-mediated threshold effect governing macrophage mTOR signalling and cardiovascular risk

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