The Effects of Alcohol-Based Mouthwash on Oral Health

The oral microbiome consists of bacteria residing in the mouth, which aid in food digestion and maintain oral health. Alterations in the composition of this bacterial community have been associated with periodontal diseases and certain types of cancer. According to a study in the Journal of Medical Microbiology the findings suggest that alcohol-based mouthwash could affect the levels of bacteria in the mouth.

Alcohol-based mouthwashes are commonly used by the public for daily oral hygiene, such as combating bad breath or preventing periodontitis. However, it’s important to be informed about the potential risks of their use.

Researchers have discovered that daily use of alcohol-based mouthwash significantly increases the abundance of two aggressive bacterial species in the mouth. These bacteria are associated with various diseases, including gum disease, and cancers of the esophagus and colon. It was also observed a reduction in a group of bacteria known as Actinobacteria, which play a key role in regulating blood pressure.

Many mouthwashes sold include alcohol, which may cause a short-lived burning feeling, a bad taste, and dryness in the mouth. This alcohol not only kills harmful bacteria but also the beneficial ones. On the other hand, mouthwashes without alcohol don’t eliminate all bacteria but rather help establish an alternative balance with the bacteria in the mouth.

It’s crucial to note that mouthwash use does not directly cause cancer. Alcohol-containing mouthwash might contribute to increased risk when combined with other factors such as smoking, heavy alcohol use, or poor diet, but research does not indicate that it is a sole cause of cancer. Although studies show that daily use of alcohol-based mouthwash can alter the oral microbiome, researchers are cautious about drawing definitive conclusions from these findings.

Alcohol-based mouthwash may be safe to use for short periods, but based on the findings and other types of evidence, long-term use is not recommended.

To view the original scientific study click below:
The effect of daily usage of Listerine Cool Mint mouthwash on the oropharyngeal microbiome: a substudy of the PReGo trial

Aging Reversed / ABC News

Now researchers have found a way not just to stop, but, reverse the aging process. The key is something called a telomere. We all have them. They are the tips or caps of your chromosomes. They are long and stable in young adults, but, as we age they become shorter, damaged and frayed. When they stop working we start aging and experience things like hearing and memory loss.

In a recent study published in the peer reviewed journal Nature scientists took mice that were prematurely aged to the equivalent of 80-year-old humans, added an enzyme and essentially turned their telomeres back on. After the treatment they were the physiological equivalent of young adults. You can see the before and after pictures in the videos above. Brain function improved, their fertility was restored it was a remarkable reversal of the aging process. In the top video the untreated mouse shows bad skin, gray hair and it is balding. The mouse with it’s telomeres switched back on has a dark coat color, the hair is restored and the coat has a nice healthy sheen to it. Even more dramatic is the change in brain size. Before treatment the aged mice had 75% of a normal size brain like a patient with severe Alzheimers. After the telomeres were reactivated the brain returned to normal size. As for humans while it is just one factor scientists say the longer the telomeres the better the chances for a more graceful aging.

The formal study Telomere dysfunction induces metabolic and mitochondrial compromise was published in Nature.

Additional information published by Harvard can be found in the following articles.

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

While scientists are not yet able to accomplish the same results in humans we believe we have developed a nutraceutical to help prolong youth and possibly extend life until age reversal therapy for humans becomes available.

Stem Cell Secret’s of 115 Year Old Woman

New evidence that adult stem cells are critical to human aging has recently been published on a study done on a super-centenarian woman that lived to be 115 years. At death, her circulating stem cell pool had declined to just two active stem cells from stem cell counts that are typically more than a thousand in younger adults. Super-centenarians have survived all the normal diseases that kill 99.9% of us before 100 years of age, so it has been a mystery as to what actually kills these hardy individuals. This recent data suggest that stem cell decline may be the main contributor to aging. If so, stabilizing stem cells may be the best thing one can do to slow your rate of aging.

There are many theories of aging that have been proposed. For example, damage to cells and tissues from oxidative stress has been one of the most popular fundamental theories of aging for more than half a century. Yet antioxidant substances or genes that code antioxidant enzymes have proven largely ineffective in slowing aging when tested in model animals. Thus, interest by scientists has shifted to other hypotheses that might provide a better explanation for the slow declines in function with age.

Stem cells provide one such promising mechanism of aging. Of course, we all know that babies are young and vigorous, independent of the age of their parents. This is because adults have embryonic stem cells that can generate young new cells needed to form a complete young baby. Indeed, these embryonic stem cells are the product of continuously evolving stem cell populations that go back to the beginning of life on earth over 3.5 billion years ago!

In adults, the mostly immortal embryonic stem cells give rise to mortal adult stem cells in all the tissues of the body. These adult stem cells can regenerate your cells and tissues as they wear out and need replacement. Unfortunate, adult stem cells also age, which leads to fewer cells and/or loss of function in cell replacement. As functional stem cells decline, skin and organs decline with age.

Blood from world’s oldest woman suggests life limit

Time Magazine: Long-Life Secrets From The 115-Year-Old Woman

Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis

Abstract
The somatic mutation burden in healthy white blood cells (WBCs) is not well known. Based on deep whole-genome sequencing, we estimate that approximately 450 somatic mutations accumulated in the nonrepetitive genome within the healthy blood compartment of a 115-yr-old woman. The detected mutations appear to have been harmless passenger mutations: They were enriched in noncoding, AT-rich regions that are not evolutionarily conserved, and they were depleted for genomic elements where mutations might have favorable or adverse effects on cellular fitness, such as regions with actively transcribed genes. The distribution of variant allele frequencies of these mutations suggests that the majority of the peripheral white blood cells were offspring of two related hematopoietic stem cell (HSC) clones. Moreover, telomere lengths of the WBCs were significantly shorter than telomere lengths from other tissues. Together, this suggests that the finite lifespan of HSCs, rather than somatic mutation effects, may lead to hematopoietic clonal evolution at extreme ages.

Connection Between Tattoos and Lymphoma

A recent observational study from Sweden has linked tattoos with a 21% higher risk of developing lymphoma, a form of blood cancer. Conducted by researchers at Lund University, the study utilized Sweden’s comprehensive medical records to investigate the issue further. Although the carcinogenic potential of certain tattoo inks was previously known, the extent of their impact on cancer risk remained unclear, leading researchers to initiate this study.

Tattoos have gained popularity as a form of self-expression, likely influenced by a decrease in societal taboos. The inks used in tattoos typically contain chemicals that have been identified as carcinogenic in other settings, such as among workers with occupational exposure. Additionally, it is known that the body’s immune system moves the ink away from the skin in an effort to eliminate the particles it identifies as foreign substances, a process that results in the permanent storage of the pigment in the lymph nodes.

Researchers focused on individuals aged 20 to 60 who were diagnosed between 2007 and 2017. They reached out to the affected individuals with three controls for each, inviting them to participate in the study. Ultimately, the study comprised 1,398 lymphoma patients and 4,193 controls. The team then explored the relationship between tattooing and lymphoma incidence. Lymphoma, a cancer of the lymphatic system, affects many young people, though it is among the less lethal types of cancer.

The study took into account various lifestyle factors, such as smoking and socioeconomic status, during its analysis. Although tattoos were identified as a risk factor for lymphoma, the lifestyle habits commonly associated with tattooed individuals, such as smoking and substance use, might also play a role in the heightened risk.

The researchers found no relationship between the size of the tattooed area and the incidence of lymphoma, which was unexpected. They suggested that this could be due to the time period between evaluating tattoo status and diagnosing lymphoma, during which some participants may have gotten additional tattoos, potentially causing misclassification. However, another explanation could be that any tattoo, regardless of its size, might induce a low-grade inflammation in the body, potentially leading to cancer.

This study is the most thorough so far in examining the potential link between tattoos and lymphoma, yet its conclusions are not conclusive. The results of the study highlight the necessity for additional research to explore the relationship. Nonetheless, it is generally considered safer to avoid getting tattoos than to have them.

To view the original scientific study click below:
Tattoos as a risk factor for malignant lymphoma: a population-based case–control study

The Effects of Ketogenic Eating on Cellular Lifespan

Ketogenic diets have been a very popular diet in the last few years but not without controversy and there have been no major studies on how the diet affects a person’s health. Some people use the diet to lose weight but it is also known to help manage childhood epilepsy, prohibiting neurodegenerative diseases and supporting cancer treatment. Many individuals also report feeling more energetic while experiencing other beneficial effects on the diet, although more comprehensive human studies are needed to confirm these claims.

It is controversial in the respect that in can increase levels of LDL cholesterol, which could lead to heart disease. It has also been reported to cause bone fractures and kidney stones in adults with epilepsy. The long-term effects of this diet are not known and gives reason to reconsider this diet. A new study has investigated the diet’s effects on cellular senescence in mice using two different keto diets with interesting results.

A keto diet is high in fats, whether saturated or unsaturated. The two diets used in the study had different amounts of these fats but largely had the same results. One diet consisted of no carbohydrates, 10% protein and 90% from fats. The other diet was balanced with most of the calories from carbohydrates and some from protein and fat. The mice all consumed the same amount of calories and no substantial weight gain was noted until after 21 days, where there was a slight increase.

What was noted at the end of 21 days was an elevation of senescent cells in the heart of 15-20%. Also, there was a marked increase on cellular senescence in liver and kidney tissue. The mice displayed signs of metabolic dysregulation with higher levels of triglycerides, and LDL and HDL cholesterol. Significant levels of pro-inflammatory molecules, which can affect surrounding cells were also found.

The effects on the mice after 90 days on the keto diet were insignificant, but after 180 days showed a marked increase. This leads one to wonder what the long-term effects might be of this diet. When the mice were put back on a regular diet their senescence cells returned to normal, suggesting the damage could be reversible for a certain time period. The effects of the keto diet occurred in both younger and older mice, therefore, the diet affects all age groups the same.

The study results contend that the keto diet is intricate, manifesting both advantages and drawbacks that are influenced by a range of elements. Items as diet timing, its makeup, and the individual’s genetic profile, hormonal influences, and health status need to all be taken into consideration. Therefore, it is suggested that the starting a ketogenic diet should be evaluated and assessed to decide who might or might not see improvements from this nutritional strategy.

To view the original scientific study click below:
Ketogenic diet induces p53-dependent cellular senescence in multiple organs

Why Chronic Pain is More Common in Older Adults

As we age, our senses, particularly sight and hearing, gradually deteriorate. Similarly, our ability to perceive touch-related sensations like cold, heat, movement, and vibration also declines. However, the sensation of pain does not diminish in the same way. In fact, aging is commonly associated with an increase in chronic pain, which can often be linked to conditions such as arthritis. Additionally, research focused on the primary somatosensory cortex (S1), a crucial area of the brain involved in pain signal processing, indicates that pathways responsible for inhibiting pain are less effective as we age.

Previous studies have revealed that PGC-1a, a key player in mitochondrial development and operation, also impacts neuronal functions, particularly in neurons that process pain signals. Nonetheless, the interplay among PGC-1a, the S1 pain sensation, and aging has not been thoroughly investigated.

This study involved two groups of wild-type Black 6 mice, one group aged 4 weeks and the other 18 weeks. It was found that the younger mice exhibited almost three times as much PGC-1a expression compared to the older group. The mice underwent an injury involving constriction of the sciatic nerves to their hind legs. Recovery was slower in the older mice, who displayed increased sensitivity to touch and for an extended duration. The researchers describe this phenomenon as ‘aging-associated pain chronification.’

In a subsequent experiment, the researchers developed a group of mice with only one functional allele of PGC-1a, as opposed to normal mice that possess two. At 4 weeks old, both groups were subjected to the same type of injury as in the previous study. The mice with diminished PGC-1a expression suffered more severely than the older mice, with none fully recovering within 7 weeks. This effect was consistent across both male and female mice.

Following leg injuries, the brain activity of both younger and older mice was analyzed. On day 7, activity levels in the S1 excitation neurons were similar across both age groups. By day 35, however, the increased activity had subsided in the younger mice, whereas it remained significantly higher in the older mice. Activity in interneurons, which link the S1 to other parts of the brain, was reduced in both groups on day 7, but by day 35, it had only returned to normal in the younger mice. Subsequent testing with highly targeted drugs revealed that increased interneuron activity correlated with behaviors indicative of reduced chronic pain.

By employing an adeno-associated virus (AAV) to enhance PGC-1a production in older animals, researchers were able to reduce their chronic pain post-injury to levels comparable to those observed in younger animals. Additionally, similar to the younger animals, there was a decrease in excitation neuron activity and an increase in interneuron activity observed on day 35 after the injury.

These findings indicate that chronic pain in older adults is not solely due to conditions like arthritis but can also stem from a decline in vital brain functions related to aging. Consequently, future treatments that aim to restore these brain functions could play an essential role in alleviating such pain.

To view the original scientific study click below:
Aging-associated decrease of PGC-1a promotes pain chronification

The Secret Behind Stem Cells’ Remarkable Longevity

Hematopoietic stem cells (HSCs) have a remarkable longevity compared to other cells in the body. These are the cells responsible for forming blood. They produce progenitor cells that rapidly divide and generate hundreds of billions of cells each day. These cells are essential for meeting the body’s daily needs, from oxygen-transporting red blood cells and immune-defending white blood cells to clot-producing platelets.

Typically inactive within the bone marrow, hematopoietic stem cells (HSCs) can spring into action to continuously regenerate blood cells, helping to maintain their youthful function over an organism’s lifespan. What is the key to their longevity? Researchers have discovered that cyclophilin A, an enzyme produced in high levels by HSCs, plays a critical role in preserving their ability to regenerate and resist the aging process.

A major factor in cellular aging is the buildup of proteins that are no longer functional. As cells age, proteins are prone to misfolding, aggregating, and accumulating within the cell, creating toxic stress that impairs cell function. Cells that divide regularly, such as progenitor cells, can mitigate this buildup by diluting protein aggregates during cell division. However, long-lived hematopoietic stem cells (HSCs), which seldom divide, encounter the challenge of accumulated misfolded proteins and the resulting toxic stress. Despite this, HSCs continue to resist the effects of aging.

In their study with mice, researchers initially analyzed the protein composition of hematopoietic stem cells (HSCs) and identified cyclophilin A as a common chaperone protein. They found that the levels of cyclophilin A were notably reduced in older HSCs. When cyclophilin A was genetically removed, it led to accelerated aging in the stem cell population. Conversely, reintroducing cyclophilin A into older HSCs improved their functionality. These results underscore the crucial role of cyclophilin A in maintaining the longevity of HSCs.

Following this, the researchers examined the proteins that interact with cyclophilin A, focusing on how it helps maintain their stability. They discovered that proteins featuring intrinsically disordered regions, which can shift their three-dimensional shapes to bind with various proteins, nucleic acids, or molecules, are often stabilized by cyclophilin A. These intrinsically disordered proteins play a crucial role in regulating cellular processes by facilitating targeted interactions between molecules.

The study indicates that cyclophilin A engages with intrinsically disordered proteins right from their synthesis, ensuring they adopt the correct shapes and are present in adequate amounts. Removing cyclophilin A genetically leads to a noticeable deficiency of intrinsically disordered proteins in stem cells. This research reveals for the first time that the production of disordered proteins and the preservation of their structural variety within cells are critical factors in the aging of hematopoietic stem cells (HSCs).

To view the original scientific study click below:
Cyclophilin A supports translation of intrinsically disordered proteins and affects haematopoietic stem cell ageing

Exploring the Health Risks of Modern Earphone Use

An earphone user reported that after using AirPods for some time, he developed a persistent high-pitched tone in his ears. He has always taken great care to protect his hearing, avoiding loud noises and carrying earplugs to shield himself from potential harmful sounds. Despite these precautions, his condition worsened. He noticed that even when he inserts his AirPods and doesn’t play any audio, they emit a high-pitched tone that closely mimics his tinnitus. This experience has led him to believe that the AirPods might have caused his tinnitus.

AirPods and similar earphones are the most popular choices among teenagers today. The rise of wireless earphones has significantly influenced how different generations use these devices, with younger people adopting them more widely than older ones. However, the core issue isn’t the type of earphones used but rather a widespread problem: irresponsible usage. The allure of convenient features like wireless connectivity, noise cancellation, and improved sound quality has led to increased overuse, exacerbating the problem.

It is estimated that 20% of teenagers are at risk of experiencing hearing loss, partly because of their frequent use of headphones and earphones. A review revealed that between 6-60% of earphone users exhibit signs of hearing loss, such as difficulty hearing and tinnitus. Meanwhile, the use of earphones among young people is on the rise. A poll conducted in February involving parents of children aged 5 to 12 found that two-thirds of them reported their children regularly use headphones and earphones.

It’s commonly understood that loud noises can harm hearing. However, even listening at low volumes for prolonged periods can be detrimental. Many people use their earphones throughout the day, while working, at home, and even during sleep. Although the volume may not always be high, wearing earphones for extended hours can still strain the ears.

The cochlea, situated behind the eardrum within our ears, is crucial for converting sound waves into electrical signals that are sent to the brain. Extended earphone use can stress and damage the cells in the cochlea, potentially leading to hearing loss if some cells die. Continuously wearing earphones in the ear canals creates a humid and congested environment, increasing the risk of ear infections. Additionally, in-ear earphones generate more pressure inside the ear compared to over-ear headphones.

Research indicates a strong connection between chronic tinnitus, hearing loss, and increased brain activity. The majority of those with tinnitus have some degree of hearing impairment, where the brain lacks sound input at specific frequencies. Individuals with mild tinnitus might not always perceive the phantom noises when ambient sounds in their surroundings help mask the tinnitus. However, the high-pitched noises become more apparent in quiet settings, when wearing ear protection, or while using noise-canceling earphones.

It is advised that earphones be used at a maximum volume of 85 decibels, similar to the noise level of a food blender or heavy city traffic, to avoid hearing damage. Additionally, it’s recommended to take breaks from earphones every two hours, even at lower volumes, to prevent ear fatigue. People who suffer from hearing loss and tinnitus can still enjoy earphones by limiting their usage. For those concerned about ear infections, over-ear headsets are a safer option. Earphones, which are positioned close to the eardrums, can create more pressure in the ear canal than headphones, potentially worsening hearing loss and contributing to headaches.

To view the original scientific study click below:
Associations between adolescents’ earphone usage in noisy environments, hearing loss, and self-reported hearing problems in a nationally representative sample of South Korean middle and high school students

New Study Reveals Unexpected Sleep Functions

For many years, the prevailing theory was that sleep helped the brain eliminate harmful molecules. However, recent preliminary research on mice suggests this might not be the case. A new study aims to delve deeper into the reasons we need sleep, potentially challenging our initial assumptions. Findings now indicate that physical activity could be more effective than sleep in aiding the brain’s detoxification process.

The scientific community has long emphasized the notion that sleep aids in clearing toxins as a primary reason for sleep, so it was quite surprising to observe contrary results. The research team mentioned that their findings, which were published in the journal Nature Neuroscience, require validation in human studies to confirm these unexpected results.

Previously, it was believed that the brain’s glymphatic system played a crucial role in waste removal during sleep. Yet, a study involving the tracking of fluid movement in mouse brains with a fluorescent dye revealed surprising results. Their findings showed a diminished capacity for toxin removal during sleep and under anesthesia. Specifically, sleeping mice were 30% less efficient at clearing the dye compared to their awake counterparts, and the clearance rate for anesthetized mice dropped by 50%.

The researchers noted that the molecule size might influence the speed at which toxins are transported through the brain, with some substances being eliminated via alternate systems. Currently, it remains unclear why states such as sleep or anesthesia slow down the brain’s molecular clearance. The next phase of their research will focus on understanding the reasons behind this phenomenon. Additionally, the team plans to investigate whether these findings are consistent in human subjects.

Disrupted sleep frequently affects those with dementia, yet it remains uncertain whether this is a result of the disease or a contributing factor to its progression. It is possible that quality sleep plays a role in reducing the risk of dementia for reasons beyond toxin clearance.

Another aspect of the study demonstrates that toxin clearance in the brain is highly efficient during wakefulness. Generally, being awake, active, and engaging in exercise may enhance the brain’s ability to rid itself of toxins more effectively.

To view the original scientific study click below:
Brain clearance is reduced during sleep and anesthesia

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