Potential Alzheimer’s Risk with Increased Daytime Napping

Recent research on older adults suggests that excessive daytime napping might be an early indicator of Alzheimer’s disease, particularly when it occurs concurrently with other warning signs like memory loss. Many individuals routinely enjoy afternoon naps. Short naps can refresh one’s energy and enhance productivity, but napping for extended periods often results in feeling lethargic and more tired than before

While there remains ongoing debate regarding the ideal nap length for health benefits, numerous studies advocate for keeping naps under 30 minutes to optimize their positive effects and avoid the drawbacks of longer sleep periods. The research found that longer naps were connected to cognitive deterioration in elderly men, while naps under 30 minutes did not increase the risk of cognitive issues.

The 14-year study involving 1,401 participants revealed that while all adults tended to nap more as they aged, those with progressing Alzheimer’s disease experienced a doubling in both the length and frequency of their daytime naps. While napping by itself is not a direct cause of Alzheimer’s, excessive napping could be a risk factor, potentially increasing the likelihood of developing the condition without necessarily confirming it will occur.

In line with earlier research, it was found that extended naps negatively impacted cognitive function, though the exact cause is unknown. Furthermore, such cognitive decline is frequently seen as a precursor to Alzheimer’s disease.

Daytime sleep patterns in older adults are often overlooked, and there is a lack of consensus on the management of napping in clinical practice. The study’s findings suggest that frequent daytime napping could indicate a higher risk of Alzheimer’s dementia. Additionally, an increase in napping duration each year may signal worsening or more severe progression of the disease.

The study revealed that both the length and frequency of naps increased with age, and there was a reciprocal, long-term link between daytime sleep and Alzheimer’s. Researchers aim to highlight the significance of monitoring changes in daytime sleep habits, as these alterations are crucial for understanding shifts in brain function related to circadian rhythms, cognitive decline, and dementia risk.

To view the original scientific study click below:
Daytime napping and Alzheimer’s dementia: A potential bidirectional relationship

Heartburn Medications and Their Link to Stomach Cancer

A recent review has established a connection between proton pump inhibitors (PPIs), a widely used type of heartburn medication, and an increased risk of stomach cancer. The findings suggest that using PPIs for more than three months significantly raises the risk of developing this cancer, whereas using them for shorter periods seems to present a lower risk.

PPIs effectively reduce stomach acidity by permanently attaching to the proton pumps in the stomach. These pumps are responsible for releasing protons, which are a key part of stomach acid, and the binding action of PPIs inhibits this release.

Proton pump inhibitors (PPIs) are frequently prescribed to manage acid reflux, a condition where stomach acid flows back into the esophagus, leading to heartburn. They are also used to treat gastroesophageal reflux disease (GERD), a chronic variant of acid reflux, as well as stomach and intestinal ulcers. Some PPIs are available as over-the-counter medications.

In their review, the authors analyzed multiple studies examining the association between PPI usage and cancer risks. They discovered a significant relationship between the use of PPIs and the development of stomach cancer and polyps, though they found no evidence linking PPI use to other forms of cancer.

There are multiple potential mechanisms by which PPIs might contribute to cancer development. These medications increase the pH level of stomach contents, which could disrupt the balance of the gut microbiome. Such disruption might diminish the diversity and number of beneficial bacteria, leading to gastrointestinal inflammation. This inflammation may encourage the growth of harmful bacteria that produce carcinogenic substances.

While PPIs are very effective at managing potentially severe stomach ulcers, they can have accumulating negative effects over time. In contrast to antacids and H2 blockers, which are traditionally used for quick relief of heartburn, PPIs take longer to start working but have a more prolonged effect.

Many patients who experience GERD also suffer from underlying inflammatory gut issues that go unaddressed. By improving their diet over a period of 6-12 weeks, these issues can be managed, often leading to a significant resolution or improvement in GERD symptoms. As a result, patients may only need antacids for relief. Interestingly, although heartburn is commonly treated with acid reducers, it can paradoxically stem from low stomach acid, which might be caused by factors such as aging, thyroid disorders, or a specific autoimmune disease affecting the stomach.

To view the original scientific study click below:
Proton Pump Inhibitors and Cancer Risk: A Comprehensive Review of Epidemiological and Mechanistic Evidence

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

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

Molecule Found to Restore Telomerase and Improve Cognition in Mice

Telomeres, which are located at the ends of chromosomes, play a crucial role in protecting DNA from deterioration. The enzyme telomerase helps preserve the length and structural integrity of telomeres, thereby regulating the aging process. Recent studies have identified a novel small molecule that can replenish telomerase levels and reverse signs of aging in senior mice. In preclinical models, significant reductions in aging indicators and symptoms were achieved.

Telomerase reverse transcriptase (TERT) is a critical protein component of telomerase. As people age, the gene responsible for producing TERT tends to deactivate, resulting in lower levels of active telomerase in the body. Numerous laboratories have been working on developing treatments that can reactivate the TERT gene. Sustaining TERT levels in older lab models has shown to lessen cellular aging and inflammation, promote the generation of new neurons enhancing memory, and improve neuromuscular function, thereby boosting strength and coordination.

In recent research, scientists have identified a molecule, referred to as the TERT activator compound (TAC), that achieves this reactivation. They have discovered that activating the TERT gene extends telomeres in cells of tissues that grow and increase rapidly. Additionally, they found that this gene activation improved aging signs in cells that had not produced telomeres, indicating that TERT also plays a role in regulating aging-related genes beyond its conventional function in telomere maintenance.

Mice treated with TAC exhibited numerous anti-aging benefits compared to the control group mice. These included decreased cellular aging and neuritis, along with an increased production of new neurons in the hippocampus. Elderly mice, which began receiving TAC injections at about 20 months of age, which would be equivalent to a senior adult, showed enhanced cognitive performance after 6 months. Additionally, one test revealed improved grip strength in these mice, indicating that the compound also boosted muscle function.

The study emphasizes the considerable potential for regenerating aging organ systems and the possibility of therapeutically adjusting indicators of aging in the natural aging process. These initial findings are promising due to TAC’s effective absorption across various tissues, including the brain. Nonetheless, further investigations are crucial to fully determine its safety and efficacy in prolonged treatment scenarios.

To view the original scientific study click below:
TERT activation targets DNA methylation and multiple aging hallmarks

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

The Association Between Belly Fat and Cognitive Decline

More than 60 million people globally are currently affected by Alzheimer’s disease, and projections suggest this number could rise to 78 million in the next seven years. Given these figures, it’s crucial to allocate resources towards mitigating the disease. Recent insights suggest that addressing belly fat could be a key strategy in reducing Alzheimer’s risk.

The human body contains two types of fat: subcutaneous and visceral. Subcutaneous fat accounts for 90% of body fat and is the layer you can pinch with your fingers. Visceral fat, on the other hand, is hidden deep within the abdomen, encasing the internal organs and is not pinchable. Experts consider visceral fat to be the more hazardous of the two, as its accumulation is linked to a higher risk of various health problems, including diabetes and potentially Alzheimer’s disease.

Recently, researchers focused on investigating the connection between visceral fat and Alzheimer’s disease. Unlike previous studies that correlated BMI with brain degeneration and a heightened dementia risk, this new study is the first to connect a specific type of fat to Alzheimer’s disease proteins in individuals who are cognitively normal. The analysis included 54 adults that were cognitively health and aged between 40 and 60, with a BMI that averaged 32. The researchers measured several health indicators, as well as levels of subcutaneous and visceral fat.

According to the results published in the journal Aging and Disease, the study found that excess visceral fat correlated with increased levels of amyloid, an abnormal protein, in areas of the brain that are among the first affected by Alzheimer’s disease. Additionally, the research uncovered a relationship between higher amounts of visceral fat and the shrinkage of gray matter in regions of the brain crucial for memory, a process known as brain atrophy. This observation is critical as brain atrophy serves as another significant biomarker for Alzheimer’s disease.

The study revealed that individuals with greater amounts of visceral fat typically exhibited more inflammation in extensive white matter tracts within the brain. White matter is essential for creating connections between brain cells and the rest of the nervous system, and any interference can impair the brain’s communication with other areas and the body. Additionally, the researchers observed that male participants showed a stronger correlation between belly fat and amyloid levels, likely due to their higher visceral fat compared to women.

Given that Alzheimer’s disease can begin to develop in the brain two decades before symptoms first emerge, the researchers intend to investigate the long-term effects of visceral fat by conducting follow-up studies with the participants. This approach underscores the necessity for further research to validate their initial findings.

To view the original scientific study click below:
Alzheimer Disease Pathology and Neurodegeneration in Midlife Obesity: A Pilot Study

Consistent Lack of Sleep Can Damage Immune Stem Cells

A new study by the Icahn School of Medicine at Mount Sinai has uncovered a connection between poor sleep quality and serious health risks. People who consistently miss out on an hour and a half of sleep per night are more susceptible to inflammatory disorders, cardiovascular disease, as well as weakened immunity levels.

Our immune system works hard to keep us protected from infection. This study is the first to show that sleep disruption alters our DNA structure in stem cells responsible for producing white blood cells. Its effects on inflammation may be long-lasting. Even catching up on some lost shut-eye won’t necessarily protect us against these dangers.

Researchers studied the effects that insufficient sleep can have on our immune systems. They had 14 healthy adults track their regular 8-hour sleeping patterns for 6 weeks, then reduce this time by 90 minutes each night over another 6 week period. They monitored any changes in blood samples and hematopoietic cells afterwards. Astonishingly, it was found that inadequate sleep led to an increased number of these cells as well as structural alterations to elemental DNA strands – indicating a negative impact from not getting enough rest.

Research into the effects of sleep on immune health took a novel direction with an innovative study utilizing mouse models. Mice were subjected to disruptions in their normal sleep patterns as well from 16 weeks of uninterrupted recovery. During this time investigators collected and analyzed both stem cells and other immune cells from each group. Results indicated that fragmented sleep induced dramatic changes in the mice’s immunity. It showed increased numbers of individual cellular components along with evidence suggesting some level reprogramming or rewiring had occurred, which was also consistent among human participants. This study reveals the powerful connection between sleep and immune system health. In humans and mice, not getting enough rest can cause a decrease in protective immunological effects which leave us more prone to infection, even months later.

Insufficient sleep patterns can have far-reaching effects on our health. The findings show that even weeks of recovery rest are not always enough to reverse the damage, creating a molecular imprint in our immune stem cells. Unexpectedly, this imprint affects some cell clusters differently than others – with some pools growing larger and other becoming smaller over time. The reduction resulting from changes in diversity and aging poses serious risks for cardiovascular diseases as well as inflammation problems.

These findings explicitly state why it is so important for adults of all ages to get 7-8 hours of quality sleep every night. This helps keep inflammation at bay while also protecting those with medical conditions against potential disease risks.

To view the original scientific study click below:
Sleep exerts lasting effects on hematopoietic stem cell function and diversity

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

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