Browsed by
Month: August 2023

Is Alzheimer’s a Genetic (Hereditary) condition?

Is Alzheimer’s a Genetic (Hereditary) condition?

According to some study, having an affected relative may raise a person’s risk of developing Alzheimer’s disease.

Alzheimer’s disease affects memory, thinking, and movement. It is a chronic, progressive condition.

Uncertainty surrounds the condition’s causes. According to recent study, genetics may be one of many variables that contribute to the development of Alzheimer’s.Reliable Source.

The potential connections between genetics and Alzheimer’s disease are evaluated in this article.

Risk genes and deterministic genes are the two components that scientists use to characterise genetic risks for Alzheimer’s disease.

A person has a higher likelihood of developing an illness if they carry risk genes. A disease may emerge as a direct result of deterministic genes.

Numerous deterministic and risk genes for Alzheimer’s have been discovered by scientists.

Risk genes

Alzheimer’s disease is caused by several genes. The apolipoprotein E-E4 gene (APOE-e4) has the strongest connection to the likelihood of developing Alzheimer’s disease (Trusted Source).

The Alzheimer’s Association estimates that 15 to 25 percent of persons who carry this gene may develop Alzheimer’s disease. Additionally, compared to someone who receives the APOE-e4 gene from only one parent, someone who receives the gene from both parents has a higher risk of acquiring Alzheimer’s disease.

A person with the gene may potentially have symptoms earlier in life and be diagnosed sooner.

Although everyone gets an APOE gene in some form, there is no connection between Alzheimer’s disease and the APOE-e3 or APOE-e2 genes. Even against the sickness, APOE-e2 may provide benefits for the brain.

The risk of developing Alzheimer’s disease can also be considerably increased by the trisomy 21 gene.

Deterministic genes

Three distinct deterministic genes that may contribute to Alzheimer’s disease have been found by researchers:

  • amyloid precursor protein (APP)
  • presenilin-1 (PS-1)
  • presenilin-2 (PS-2)

The excessive production of amyloid-beta peptides is caused by these genes. A hazardous protein that collects in the brain is this one. The damage and death of nerve cells brought on by this accumulation are hallmarks of Alzheimer’s disease. These are “dominant genes,” which indicates that if either parent has the ailment, they can convey the gene to their offspring, who will then develop the disorder.

These gene variants are responsible for 5-10% of all early onset dementia cases and 60-70% of familial early onset Alzheimer’s illness cases. Alzheimer’s brought on by deterministic genes often strikes people younger than 65. It occasionally manifests in persons in their 40s and 50s.

But not everyone who has early-onset Alzheimer’s has these genes.

Genes’ role in various forms of dementia

Other genetic abnormalities have been linked to some types of dementia.

For instance, chromosome 4 is altered in Huntington’s disease, which may result in dementia that worsens over time. A dominant genetic disorder, Huntington’s disease.

There may be a hereditary component to Parkinson’s dementia or dementia with Lewy bodies. For instance, SNCA, PARK7, and PRKN are only a few of the genes known to be linked to Parkinson’s disease. However, the underlying causes of these diseases are frequently multifaceted, much like all types of dementia.

Alzheimer’s disease risk factors

Several risk factors for Alzheimer’s disease have been identified by researchers.

These consist of:

Age is the main risk factor for Alzheimer’s disease, according to reliable sources.
Family history: The likelihood of having Alzheimer’s disease is increased if a close relative already has the condition.
People who have experienced serious head trauma in the past may be more susceptible to Alzheimer’s disease.
Cardiovascular health: Alzheimer’s disease risk may be increased by heart or blood vessel conditions. Examples include diabetes, stroke, and high blood pressure.

Alzheimer’s disease signs and prognosis

Memory and brain function are typically gradually lost as a result of Alzheimer’s disease.

Periods of forgetfulness or memory loss may be early indications. A person may gradually become confused or disoriented in familiar environments, including at home. As a result, they might require extra help with daily tasks like tooth brushing, dressing, and food preparation.

Agitation, restlessness, personality withdrawals, and speech difficulties are some possible symptoms.

After the onset of symptoms, an individual with Alzheimer’s disease typically has an 8–10 year survival rate.

Find out more about the progression of Alzheimer’s disease and its prognosis.


Multiple genes are associated with Alzheimer’s disease. The APOE-e4 gene, for example, raises the risk of getting the illness but does not always result in an Alzheimer’s diagnosis.

Some, like the APP gene, are directly responsible for the disease’s onset. However, familial Alzheimer’s is an uncommon form of the illness that affects 5–10% of those with early-onset Alzheimer’s.


For Alzheimer’s medications that have been suggested by doctors worldwide are available here

Can protein predict mental decline before Alzhiemer’s sign?

Can protein predict mental decline before Alzhiemer’s sign?

A protein called NPTX2 that is present in the cerebrospinal fluid may be able to forecast the onset of memory and cognitive issues, according to recent research.

Researchers evaluated people who had initially been in normal mental health but later experienced dementia or mild cognitive impairment (MCI).

According to the study, the quicker start of MCI symptoms was linked to lower levels of NPTX2. The results also demonstrated that NPTX2 levels, like other Alzheimer’s disease-related indicators, appear to fluctuate over time.

Findings from a recent study could be useful for understanding cognitive decline and early Alzheimer’s disease diagnosis.

The levels of a protein called NPTX2 in cerebrospinal fluid (CSF), or more simply put, the fluid surrounding the brain, were evaluated by the researchers in order to better understand the brain changes connected to moderate cognitive impairment and dementia.

Lower levels of NPTX2 were discovered to be associated with a more rapid beginning of cognitive deterioration. Along with other Alzheimer’s disease-related indicators, NPTX2 levels evolved with time.

Alzheimer’s disease indicators in cerebrospinal fluid measurement

The 269 participants in the BIOCARD Study who were initially in good mental health had their brain fluid (CSF) taken by the research team.

These patients were followed for an average of 16.3 years, and their average age at the start of the study was roughly 57.7 years.

Out of these people, 77 subsequently experienced dementia or Moderate cognitive impairment (MCI).

Quantitative parallel reaction monitoring mass spectrometry was used by the researchers to evaluate three similar peptides that make up the NPTX2 protein.

Three other markers—A42/A40, p-tau181, and t-tau—that are frequently linked to Alzheimer’s disease were also measured. These measurements were made using a Lumipulse automated electrochemiluminescence test on the identical CSF samples.

The goal of this data analysis was to help the researchers better understand how these indicators changed over time and whether they might be related to the onset of MCI and dementia in the patients under study.

NPTX2 levels and cognitive issues over time

They discovered that people with lower NPTX2 protein levels in their brain fluid (CSF) exhibited cognitive issues and memory deterioration (MCI) earlier than people with higher NPTX2 protein levels.

Both those who acquired MCI within seven years of the study’s beginning and those who did so later found this link to be substantial.

Even after accounting for other well-known Alzheimer’s disease markers detected in the CSF, the researchers observed that the baseline levels of NPTX2 were able to predict when the symptoms of MCI would manifest.

This implies that the amounts of these markers may be associated with modifications in NPTX2 and may contribute to the emergence of cognitive issues.

According to the study’s first author, Anja Soldan, Ph.D., an associate professor of neurology at Johns Hopkins University, “our study shows that low levels of the protein ‘neuropentraxin 2’ (or NPTX2) measured in the cerebrospinal fluid among cognitively healthy middle-aged and older adults may predict later onset of mild cognitive impairment (MCI).”

[NPTX2] has been connected to learning and memory in mice in the past. Our findings add to the mounting evidence that low levels of this protein in individuals could signal MCI years before symptoms manifest. Notably, our results demonstrate that low levels of the protein enhance the prediction of cognitive impairment even when traditional Alzheimer’s disease biomarkers (such as those linked to amyloid plaques and tau tangles) and well-established genetic risk factors for late-onset Alzheimer’s disease are taken into account,” according to Dr. Anja Soldan.

According to Dr. Soldan, NPTX2 is “predictive of subsequent symptoms of MCI both within and beyond seven years before symptoms occurred.”


The study does have a few drawbacks.

Namely that the majority of the participants were white, educated people with a history of dementia in their families. Therefore, it is uncertain whether the results apply to other populations, according to Dr. Soldan.

Without taking part in the study, Santosh Kesari, Ph.D., a neurologist at Providence Saint John’s Health Centre in Santa Monica, California, and the regional medical director for the Research Clinical Institute of Providence Southern California, told that “identifying blood or CSF biomarkers that predict developing dementia is critical to intervene earlier by preventative approaches or treat at the earliest onset of cognitive issues or even before when patients are aware they have dementia.”

Could this indicate new Alzheimer’s medications?

There is now just one FDA-approved treatment on the market that is known to even slightly reduce the signs of Alzheimer’s disease in its early stages, and there are no known therapies or strategies to avoid the disease, according to Dr. Soldan.

Our research demonstrates that reduced NPTX2 levels exist for many years before MCI or dementia brought on by Alzheimer’s disease, which increases the prospect of creating therapies that specifically target NPTX2.

Additionally, Dr. Soldan added, “Our findings may be relevant to other neurodegenerative diseases since this protein does not appear to be a specific marker for Alzheimer’s disease.”

Although significant work is being done to create sensitive methods of testing NPTX2 in blood rather than cerebrospinal fluid, we are not yet able to routinely measure brain levels of the substance in clinic settings. Another crucial area of research, according to Dr. Anja Soldan, is the factors that affect the levels of NPTX2 in the brain. However, we know very little about these factors.

Dr. Kesari concurred, stating that “NPTX2 may turn out to be a good target of drug development to prevent cognitive decline and will need to be further tested and validated in future studies.”

Future research will examine NPTX2 in more detail. In the end, additional study is required.


For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here

How does eating too much fructose cause obesity?

How does eating too much fructose cause obesity?

In the United States, more than 40% of adults are obese, with approximately 10% having extreme obesity.

Obesity increases the chance of developing a variety of ailments, such as type 2 diabetes, heart disease, and several malignancies.

An energy imbalance between calories consumed and calories burned is the primary cause of obesity.

Obesity, however, may result from more than just calorie intake—it may also result from the calories.

According to recent studies, the simple sugar fructose, which is present in many foods, may be the cause of obesity and other related health issues.

Around 13% of persons globally, according to the World Health Organisation (WHO), are obese. Although obesity rates are rising in low-income nations, the majority are in wealthy nations.

According to National Institutes of Health (NIH) data, 42.4% of adults and 19.3% of children and adolescents in the United States were obese in 2017–18. Additionally, these figures are rising.

Obesity raises the risk of a number of illnesses. It is linked to a poor diet and an unbalanced energy intake, but it may also have a genetic component. These are listed by the NIH as follows:

What connection exists between fructose and obesity?

According to recent study, obesity may not just be caused by an energy imbalance; rather, the source of that energy may be what causes the illness.

According to the study, which was published in Philosophical Transactions of the Royal Society B, fructose may be the cause of obesity because of an evolutionary “survival switch” that makes people store energy from fructose rather than utilize it.

The study’s results were discussed by Dr. Eamon Laird, a postdoctoral research fellow at the University of Limerick in Ireland who was not engaged in the study, he observed:

This is a highly intriguing theory, even though it is only a narrative overview and not a systematic meta-analysis of the available data. It is conceivable that our present energy-dense diets have altered an evolutionary pathway that was advantageous millions of years ago.

Fructose converts to energy reserves.

According to the study, metabolic diseases like obesity may have arisen as a result of overstimulation of an evolutionary-based biological reaction called the “survival switch,” which is meant to safeguard animals before a crisis like hibernation.

Contrary to glucose, which is used as immediate fuel, the researchers contend that fructose causes the body to conserve energy.

This is better for an animal going into long-term hibernation than for a person who has constant access to high-sugar diets.

This “survival switch” may be more detrimental than beneficial in areas where people have easy access to food. People develop fat reserves as a result of the constant availability of high-fructose foods, which causes obesity and related health issues.

Metabolic effects of fructose

What causes fructose to make the body store energy rather than use it?

Adenosine triphosphate, or ATP, is often utilised and swiftly replaced from nutritional intake or fat storage. ATP is the chemical that supplies energy to power all cell operations.

Fructose, on the other hand, lowers the amount of ATP present in cells and hinders the production of ATP.

A chain of chemical processes that stop the mitochondria of the cell from making more ATP and put them under oxidative stress are triggered when ATP levels fall low enough.

Fructose consumption increases appetite in addition to lowering ATP levels. Once deposited as fat, these extra calories. The ATP levels eventually rise once more, but the fat reserves are still there.

Repeated exposure to oxidative stress causes mitochondrial dysfunction to become persistent over time. The body of a mammal that is hibernating adjusts to the low ATP levels by lowering the resting metabolic rate.

Without reducing calorie consumption, this lower energy usage leads to weight increase in persons who still have access to plenty of food.

Dr. Laird concurred that this theory could help to explain the rise in obesity.

He said, “I agree it could be one component. But obesity and metabolic syndrome are complex conditions; there is seldom just one contributing cause. Lack of exercise, unhealthy eating habits, vitamin deficiencies, socioeconomic causes, and even risk factors related to one’s race and ethnicity are all significant risk factors.”

Therefore, even if fructose did affect obesity, it would only have a minor impact overall, he continued.

Dietary sources of fructose

Although fruit naturally includes fructose, which gives it its sweetness, a normal Western diet also contains a variety of additional sources of fructose.

The majority comes from table sugar, high fructose corn syrup (HFCS), a sweetener manufactured from cornflour, and sucrose, a molecule composed of glucose and fructose chemically bound together.

Fructose can make up to 55% of HFCS. To transform the glucose in corn syrup into the sweeter-tasting fructose, manufacturers must add enzymes.

Since the fructose in HFCS is present as free molecules, it is absorbed more quickly than it is in table sugar.

HFCS is included in practically all processed foods and many other foods. They consist of:

  • sodas
  • fruit juices with added sugar
  • crackers
  • ready-made meals
  • salad dressings and condiments
  • a few pastries and bread.

According to the scientists, the growth in sugar consumption, particularly that found in processed foods, fructose-sweetened beverages, and carbohydrates with a high glycemic index (GI), is related to the global epidemics of obesity and diabetes.

Must you stay away from foods high in fructose?

Although he was not involved in the study, Dr. Mir Ali, a bariatric surgeon and medical director of the MemorialCare Surgical Weight Loss Centre at Orange Coast Medical Centre in Fountain Valley, California, stated that for people who are overweight or obese, “any source of sugar, including non-processed sugars, such as those found in fruits, can have a similar effect on the body.”

We advise our patients to minimize all sources of sugar, including fruits,” the doctor added.

However, Dr. Laird cautioned that most people should not worry excessively about fruit’s sugar content: Most of us don’t consume enough fruits, despite the fact that doing so would benefit our overall health by providing fibre, vitamins, and minerals. The modest amounts of fruit we do consume would probably not amount to much.

However, he continued, “The main risk probably arises when the fructose is highly concentrated and added to other foods (these foods often contain high fat, high sugar, and low nutrition), which could result in an increased risk of obesity.”

So maybe avoid that processed snack since it’s probably laden with fructose to help lower your risk of becoming obese.


For Type 2 Diabetes medications that have been suggested by doctors worldwide are available here

Breast cancer: Can a wearable device help to detect it?

Breast cancer: Can a wearable device help to detect it?

To screen for breast cancer at home, researchers created a wearable gadget.

Initial testing reveal that it is capable of detecting tiny cysts that are comparable in size to early-stage breast tumours. To confirm the effectiveness of the gadget, clinical trials are required.

One day, a cutting-edge piece of wearable technology that can be fastened to a bra might enable individuals to identify breast cancer symptoms while lounging at home.

With approximately 1 in 6 cancer-related deaths among women, breast cancer is the most common cancer in the world. Women make up the great majority of breast cancer patients. Men experience 0.5% to 1% of cases, though.

If discovered when the cancer has not yet moved outside of the breast, breast cancer has a 5-year relative survival rate of up to 99%. The 5-year survival rate drops to 30% if discovered later, such as when cancer has spread to distant bodily areas like the lungs, liver, or bones.

Currently, the most popular approach for detecting breast cancer is a mammography, an X-ray imaging procedure.

Mammograms must be performed in an imaging center even though they are typically efficient at detecting 87% of malignancies. This limits access for many people, especially those with low incomes, who could postpone screening as a result of the high associated expenses and challenges in organizing transportation.

The health outcomes for those diagnosed with the condition globally could be improved by initiatives to increase accessibility and lower the cost of breast cancer screening.

Researchers recently created a wearable ultrasound breast patch that could enable patients to scan for breast cancer at home.

Bard-certified doctor Dr. Kamila Seilhan, stated: “This wearable ultrasound device may help patients at high risk of breast cancer in the interim between routine mammograms by enabling early tumor detection.”

A breast-attached wearable breast cancer detector

The same ultrasound technology that imaging centres utilise is the foundation of the device. However, because of the piezoelectric materials used, it can be made smaller to function as a portable ultrasound scanner. Through a mechanism called piezoelectricity, crystals transform mechanical energy into electrical energy, which in this instance can be used to interpret ultrasound measurements.

The device sends sound waves into the breast tissue, and as it moves across the breast, it produces high-quality images identifying cysts that may need to be investigated by a breast cancer specialist,” said Dr. Jennifer Tseng, F.A.C.S., medical director of breast surgery and a double board-certified surgical oncologist specializing in breast cancer at City of Hope Orange County Lennar Foundation Cancer Centre in Irvine, California, who was not involved in the research.

To make the device wearable, the researchers created a flexible, 3D-printed patch with honeycomb-like holes. The patch fastens to a bra with holes so it may touch the skin and scan breast tissue there.

The entire breast may be imaged thanks to the scanner’s six various positioning options. In order to capture photographs from various perspectives, it can also be rotated.

The scanner has already been tested on a 71-year-old woman who has a history of breast cysts. They were able to identify cysts with the gadget that were as small as early-stage tumours, or 0.3 centimetres in diameter. According to their findings, the images produced had an 80mm depth and a resolution comparable to that of conventional ultrasounds.

Senior author of the study Canan Dagdeviren, Ph.D., Associate Professor of Media Arts and Science at Massachusetts Institute of Technology (MIT), stated that the technology makes it simple to repeatedly take pictures from the same location.

Increased screening availability for breast cancer

Dr. Dagdeviren stated that the ultimate purpose of the device is to reach underrepresented women, including those living in less economically developed nations, and to make breast cancer screening more accessible and affordable.

Dr. Seilhan remarked that if successful, the device could be especially helpful in isolated locations without simple access to medical facilities.

Healthcare facilities and organizations with limited funds can purchase the device more easily because of its low cost,” she said.

She continued by saying that while the gadget is simple to operate, it might be useful in settings where medical personnel have limited technical expertise.

Dr. Tseng pointed out, however, that in order for patients in less developed nations to benefit fully from diagnostic technologies, it is equally critical for them to have better access to those tools.

However, she added, “patients still need to have the data reviewed by an expert who can recommend what to do next.” This device may assist patients identify potential problem areas that they were unable to identify before.

When will the breast cancer wearable device be obtainable?

According to Dr. Dagdeviren, the device might be usable for 4-5 years. She is starting a business to achieve this goal and is looking for partners and investors. For mass production and FDA certification, she stated, “we will need about $40 million.”

In spite of the fact that the device now needs a “bulky computer interface” to process photographs, the author continued, her team is currently working on a more portable design and will soon release an iPhone-size image processor.

The researchers are also creating a workflow that will enable artificial intelligence to examine data and produce diagnostic evaluations that might be more precise than those made by a radiologist comparing photos that were obtained over some time.

Experts spoke with Dr. Richard Reitherman, Ph.D., a board-certified radiologist and medical director of breast imaging at MemorialCare Breast Centre at Orange Coast Medical Centre in Fountain Valley, California, who was not involved in the study to learn more about potential future uses for the device.

This kind of product will be a welcomed supplemental addition to women’s health care,” the doctor said. “If it can be demonstrated to be on par with mammography and dedicated breast ultrasound for breast cancer screening, it will be a welcome alternative.”

However, he pointed out that one of the biggest obstacles for any new gadget is completing successful clinical trials, which will probably require collaboration with the American College of Radiology.

This is a complex and difficult proposition,” he said. “The jump from translational science to clinical efficacy remains to be seen.”

What are the limitations of the study?

Its limits stem from the fact that the technology is still in its early stages of development.

The University of Kansas Cancer Centre breast radiologist Dr. Onalisa Winblad, who was not part of the study, stated that she does not currently support its use because it “does not have scientific data to prove utility.”

The linked article’s photographs are of low quality when compared to those from our normal breast ultrasound. In patients with dense breast tissue, ultrasonography is a tool that is beneficial in addition to mammography.

Dr. Tseng concurred that although ultrasonography is a useful tool for breast cancer screening, it cannot take the place of mammography and other types of preventive treatment provided by a breast cancer specialist.

Different technologies are more effective than others at detecting various breast alterations. For instance, while some calcifications cannot be seen with ultrasonography, others can be seen with mammography, she noted.

She stated that two of the most crucial elements in how effectively the tool performs as a breast cancer screening tool are “the device’s ability to find true positive cases and avoid fake positive cases.

She continued by saying that even while the tool might be simple to use, how well it works may still rely on the user. Also, she added that because the human breast varies from person to person and even among individuals, large-area and deep-tissue imaging can be challenging.

When challenged about the device’s limits, Dr. Reitherman stated that in order to maintain good quality metrics, the scanner must be operated under medical supervision, such as through “virtual supervision by a radiologist.”

Therefore, the existing medical community and physicians that would be interpreting and recommending actions based on this device’s information would need to be on board,” he said.


For Breast Cancer medications that have been suggested by doctors worldwide are avalaible here (

Can a new Alzheimer’s vaccine cure or prevent the illness?

Can a new Alzheimer’s vaccine cure or prevent the illness?

Finding a cure for Alzheimer’s disease has proven difficult and contentious. A vaccination has been created for a new target, a protein present in blood vessels and aging brain cells.

It has been tested on mice, and it enhances behavior while lowering levels of a protein precursor to amyloid-beta.

What molecules should be the focus of Alzheimer’s disease therapeutic research is still up for debate.

The development of amyloid beta protein plaques in the brain, which are defining symptoms of the disease, has been the focus of much of the research into treating Alzheimer’s disease. Using a mouse model, scientists have now created a novel vaccination that specifically targets a particular protein present in aging brain cells and blood vessels.

Recent years have seen debate concerning the history of the amyloid beta model and its application as a therapy target. For instance, there was debate about the efficacy and adverse effects of lecanemab (Leqembi) when the Food and Drug Administration (FDA) gave fast approval for its use in treating persons with early Alzheimer’s disease in January 2023. Particularly when the FDA did not, as anticipated, approve donanemab, an Alzheimer’s medicine made by the pharmaceutical corporation Eli Lilly because additional evidence was required to establish its efficacy.

When you think that finding a treatment target for Alzheimer’s disease is potentially big business for pharmaceutical companies, this explosive year for Alzheimer’s science may not have come as a surprise. There are presently 6 million cases in the United States alone, and it is predicted that number would increase to 13 million by the year 2050.

Importants facts about Alzhiemer’s disease

  • Alzheimer’s disease is a persistent, chronic (long-term) illness. It is not a normal ageing symptom.
  • Dementia and Alzheimer’s disease are not the same thing. A form of dementia is Alzheimer’s disease.
  • Its symptoms appear gradually, and its degenerative effects on the brain result in a steady decline.
  • Alzheimer’s disease can affect anyone, but some people are more susceptible to it than others. People over 65 and those with a family history of the illness are included in this.
  • Alzheimer’s patients cannot be predicted to have a particular outcome. While some persons experience a slower onset of symptoms and a faster rate of disease progression, others experience lengthy lifespans with minor cognitive impairment.

A vaccination for Alzheimer’s disease may also target atherosclerosis.

Inflammation is one of the other pathways known to contribute to the development of Alzheimer’s disease. There is some disagreement as to whether or not atherosclerosis and inflammation are related diseases. Inflammation also underlies other disorders.

Vasculature and inflammation are involved in both disorders. People with specific APOE gene variations are known to be predisposed to both disorders.

For around ten years, mouse models have been used in the research and development of potential treatments for both disorders.

Researchers in Tokyo found that senescence-associated glycoprotein (SAGP-protein) was elevated in immunological and vascular endothelial cells in animal models with atherosclerosis as one recent example of this. In animal models with mutations on the APOE gene, greater expression of this protein has been connected to an increased risk of atherosclerosis and Alzheimer’s disease. Around the immune cells called microglia in the brain, SAGP-protein is also present.

The team’s prior research has demonstrated that decreasing the expression of this protein reduces atherosclerotic plaques in the aorta of mice with APOE gene variations and improves glucose metabolism in obese animals.

They also disclosed that they had created a vaccination that specifically targeted older cells with high levels of SAGP-protein expression.

The same research recently revealed they had found this vaccine may also lessen levels of inflammatory chemicals and amyloid-beta peptide, which is a precursor to amyloid beta protein and affects how Alzheimer’s disease behaves in mice models.

These preliminary research findings were presented at the Basic Cardiovascular Sciences Scientific Sessions of the American Heart Association in Boston in 2023.

A new Alzheimer’s vaccine may change the game.

In an email, the study’s lead author, Dr. Chieh-Lun Hsiao, stated: “Unfortunately, how we generate vaccine is not allowed to expose, but the design of the vaccine is to eliminate or reduce the cells which contain an abundance of our target, SAGP.”

How the vaccination functions are described by Dr Hsiao as follows:

The immune system is trained through vaccination to recognize a particular foreign substance, such as an antigen or peptide. In our theory, we would say that we hypothesize that the pathogenic/abnormal cells with elevated SAGP expression.

Therefore, following vaccination, individuals would have the immunity necessary to recognize SAGP-HIGH expressed signal and then remove/destroy the cells that contain SAGP-HIGH expressed signal.

The study’s authors concluded that Alzheimer’s disease might someday be treated with their vaccine.

In the future, we’d probably switch to different animal models for more in-depth research on vaccination effectiveness, according to researcher Dr Hsiao. We are also interested in how different cell types’ phenotypes alter in response to immunisation. As we move forward, we’ll pay greater attention to the mechanisms.

Potential drawbacks and effects of the new vaccine

There needs to be more research on the potential negative consequences of this target, according to Kath Intson, CEO of the Canadian business Variant that specialises in precision medicine and a PhD candidate at the University of Toronto.

In an email, Intson stated:

At best, there is a low likelihood that a medication like this will be used prophylactically, or like a vaccination, to prevent AD. One of the targets is microglia, which function similarly to immune cells in the brain. I’m interested in learning more about the percentage of SAGP-enriched, highly enriched microglia that were removed. As you might expect, eliminating a significant portion of the brain’s immune system has negative effects.”

She also questioned whether Alzheimer’s disease treatments should focus on preventing the accumulation of amyloid-beta peptide (APP), the precursor of amyloid beta-protein: “One point – we must cease thinking of APP accumulation as a fundamentally abnormal physiological process.”

Previous research has shown that APP acts as a protective factor in the brain after acute lesions like strokes or traumatic brain injuries. In response to these assaults, APP overexpression increases brain cell survival in the near term. Any suggestion of mass vaccination campaigns with APP-elimination goals has my utmost scepticism. It would have effects on the health of healthy people about other brain-damaging disorders to remove this necessary and typical function.


For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here

Does Alzhiemer’s symptoms worsen due to light sensitivity?

Does Alzhiemer’s symptoms worsen due to light sensitivity?

The late afternoon and evening are when sundowning, a characteristic of Alzheimer’s disease, typically manifests. Increased agitation, anxiety, and mood fluctuations are some of its defining characteristics.

The impact of Alzheimer’s disease on the brain has been suggested as one of the causes, however the exact mechanisms remain unclear.

Increased light sensitivity was shown in recent studies using Alzheimer’s disease mice models, which is a result of retinal alterations.

Sundowning is a crippling symptom of Alzheimer’s disease that makes people’s dementia symptoms get worse in the late afternoon and evening.

Some researchers hypothesised that this symptom was caused by brain abnormalities, and a recent study confirmed that immune cells in the brains of Alzheimer’s patients may experience circadian disruptions that increase the accumulation of amyloid beta.

One of the distinguishing features of Alzheimer’s disease is the accumulation of this protein. A psychiatrist from the Rehab Clinics Group named Dr. Alexander Lapa stated in an email:

Both the affected person and their carers may find sunseting upsetting. Increased care requirements and potential major disruptions to daily routines can result from the increase in bewilderment and agitation. Sundowning in some circumstances could endanger the patient’s safety or the safety of those around them.

He continued by saying that many doctors advise individuals with Alzheimer’s disease to follow a daily regimen that includes predictable timings, relaxing hobbies, reducing noise, and making sure there is enough illumination at night.

Increased light sensitivity in Alzheimer’s mice models

The aetiology of sundowning is unknown, despite the incapacitating nature of this symptom of Alzheimer’s disease. Given that it manifests in the middle and late phases of the disease, it may coexist with a number of other symptoms that have all been connected to sundowning, including sleep disturbances, forgetting to eat or drink, and adverse drug reactions.

A group of researchers from the University of Virginia, Charlottesville, Virginia, chose to further explore this connection because sleep disturbance has previously been closely linked to Alzheimer’s disease. Their research was published most recently in Frontiers to Ageing Neuroscience.

It had been thought that sleep disturbance might also result from damage to the brain brought on by the buildup of tau protein and amyloid beta protein, two signs of Alzheimer’s disease.

According to the main author Dr. Heather Ferris, an assistant professor of medicine at the University of Virginia, “We were interested in why sleep and circadian rhythms are disrupted in Alzheimer’s disease.”

After ruling out a number of potential causes in the brain, she stated, “We turned our attention to the retina because we thought the problem would be occurring in the brain.”

According to Dr. Ferris, the retina contains specialized cells known as inherently photosensitive retinal ganglion cells. Although these cells are sensitive to light, they are not used for vision. Instead, these cells are employed to inform the brain that it is daytime.

We discovered that we could activate these cells in Alzheimer’s disease model mice with much less light and that the retina contained a greater number of these cells, she said.

Looking for the cause of the sundowning

Researchers first employed mice models with genetic alterations that resembled Alzheimer’s disease, along with controls, to learn this. To simulate jet lag, they first gave 13-month-old female mice a 6-hour change in their exposure to sunshine before going back to a regular 24-hour schedule.

They discovered that Alzheimer’s disease-affected mouse models retrained to a 24-hour clock pattern more quickly than control mice.

The initial theory put forth by researchers was that this difference resulted from a higher concentration of microglia, a kind of immune cell present in the brain that surrounds amyloid beta plaques and works to eliminate them.

However, fewer microglia in the Alzheimer’s disease mouse models did not result in a quicker recovery to a typical 24-hour cycle after jet lag.

Researchers then found that mouse models of Alzheimer’s disease were more likely than wild-type mice to behave differently in response to changes in lighting, indicating that they were more sensitive to light reception.

The researchers came to the conclusion that Alzheimer’s disease affects the retina rather than the brain as a result of this discovery.

The retina contains the photosensitive cells that control circadian rhythms. The light-sensitive protein that they produce, called melanopsin, is located in the retina and is what we saw in Alzheimer’s disease mice, according to Dr. Ferris, even though they travel through the optic nerve to interact with the brain.

How to possibly handle sundowning?

This hypothesis is supported by prior research, which has shown that amyloid and tau proteins can be found in the retina of people with Alzheimer’s disease and that this condition also causes the retinal blood barrier to break down.

The discovery that the retina in a mouse model of Alzheimer’s disease may be impacted in a way that increases light sensitivity may point to novel strategies for coping with dusk.

In the future, Dr. Ferris stated she hoped to test this notion. To maintain rhythms as close to normal as possible, she added, doctors currently advise keeping persons with Alzheimer’s disease on a rigorous schedule for eating, sleeping, and light exposure.

She suggested that light treatment might provide the solution.

According to our findings, these efforts might be thwarted by lower levels of light than might be anticipated. To increase the effectiveness of these therapies, we plan to examine next whether we can reduce exposure to light at particular periods or alter its wavelength to prevent some behavioral changes.

Beyond maintaining a regular schedule, she continued, “It makes sense to try to reduce evening exposure to blue light (screens) as this type of light is most likely to trigger melanopsin and disrupt sleep and circadian rhythms — whether you have Alzheimer’s disease or not.”


For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here

Type 2 Diabetes: Can kombucha help to manage blood sugar?

Type 2 Diabetes: Can kombucha help to manage blood sugar?

A fermented tea called kombucha offers advantages including enhancing gut health. Researchers carried up a study on persons with type 2 diabetes because they were interested in whether the probiotic beverage may be useful in decreasing blood sugar.

After four weeks, the researchers evaluated the blood sugar levels of two groups of individuals with type 2 diabetes who had either received kombucha or a placebo beverage that tasted similar. They switched the groups after a break, then assessed the participants again after another 4 weeks.

In contrast to a placebo, the results showed that drinking kombucha for four weeks dramatically reduced fasting blood glucose levels in comparison to baseline.

The researchers claim that this is the first investigation of kombucha’s effects on persons with type 2 diabetes.

In type 2 diabetes, the body has trouble producing or properly controlling insulin. According to the Centres for Disease Control and Prevention (CDC), diabetes affects millions of people in the United States and is the eighth largest cause of mortality in the nation.

Scientists are interested in discovering new ways to lower blood sugar, especially through dietary choices, as the prevalence of type 2 diabetes rises.

The School of Health at Georgetown University in Washington, D.C., conducted research to see whether the Chinese tea known as kombucha, which is fermented with bacteria and yeasts, could lower blood sugar levels.

They discovered that merely 4 weeks of consuming kombucha reduced fasting blood sugar levels prior to meals from an average of 164 to 116 milligrammes per deciliters (mg/dL) after comparing blood sugar averages between drinking kombucha versus a placebo.

In contrast, according to the American Diabetes Association, normal fasting glucose levels are between 80 to 130 mg/dL before meals.

Tracking fasting blood sugar

The authors highlight that the study’s participants were drawn from the General Internal Medicine Clinic at MedStar Georgetown University Hospital, which has “a strong interest in diabetes care.”

They recruited 12 individuals with type 2 diabetes for the trial. They had to consent to consume the designated beverage on a regular basis as well as test their fasting glucose at various intervals at home.

The individuals were also told by the researchers to stick to their regular meals. They did not want dietary modifications to have an impact on prospective blood sugar drops.

The participants were split into two groups, and each group was given an 8-ounce beverage to consume everyday with dinner for a period of 4 weeks. Some participants received kombucha, while others received a placebo beverage that, according to the authors, tasted like kombucha.

The recipients of the kombucha were switched around during the study’s second phase. The individuals had to wait eight weeks before starting back up on their drinking routine so that the researchers could account for any lasting effects of the kombucha.

The subjects experienced further 4 weeks of consuming their assigned beverage after the 8-week “washout period” ended. In the initial phase of the study, participants who consumed kombucha also consumed a placebo beverage, whereas the others consumed kombucha.

The researchers next examined the information the subjects supplied regarding their fasting glucose, which they assessed at the following intervals:

  • their starting point before starting the drinking program
  • after the first week
  • towards the conclusion of week four
  • following the washout time
  • end of the first week of the second round.
  • following the fourth week of the second round.

Drinkers of kombucha had reduced blood sugar.

In order to determine if kombucha increased glucose levels, researchers averaged baseline data from subjects, data from each 4-week round of kombucha consumption, and data from placebo consumption.

Following 4 weeks of kombucha consumption, the subjects’ average baseline blood sugar level fell to 116 mg/dL from 164 mg/dL. This represents a decline for the kombucha group of almost 30%.

In contrast, after consuming the placebo beverage, the subjects’ baseline blood glucose levels barely changed. The authors report that there was no statistically significant difference between the placebo and the average fasting blood glucose levels.

A larger investigation, according to the researchers, is required due to the study’s drawback of a limited sample size.

According to a press statement from the study’s lead author, Dr. Chagai Mendelson, “We were able to provide preliminary evidence that a common drink could affect diabetes.”

We hope that a much larger trial, using the lessons we learned in this trial, could be undertaken to give a more definitive answer to the effectiveness of kombucha in reducing blood glucose levels, and hence prevent or help treat type 2 diabetes,” he continued.

A residency program is being completed by Dr. Mendelson at MedStar Georgetown University Hospital Medical School.

Experts discuss the advantages of kombucha

The outcomes of the study were discussed by Alyssa Wilson, a registered dietitian and metabolic health coach with the California-based company Signos.

Wilson stated that there is “some encouraging data” supporting the inclusion of kombucha in a nutrition care strategy.

For those seeking a healthy alternative to sugary drinks, she said kombucha is a “great option” and may help “reduce hunger and prevent sugar cravings.”

Wilson noted that further research is required to support the findings even though she thinks the study to be promising.

More research is needed in a larger follow-up study to determine the effectiveness of kombucha in reducing blood glucose levels, but the findings are promising and exciting for this patient population,” she said.

The work was also discussed by endocrinologist Dr. Florence Comite, who founded the Comite Centre for Precision Medicine and Health in New York City.

Dr. Comite pointed out that more research is indicating a link between conditions like type 2 diabetes and the composition of the gut microbiome, which is changed by probiotics like kombucha.

The metabolism, inflammation, and immunological response all seem to be substantially influenced by the microbiome. Managing glucose management will be impacted by improving the proportion of beneficial bacteria to harmful bacteria in the stomach, according to Dr. Florence Comite.

She expressed her need for more research in this area, stating that “a causal association between kombucha and lowering blood glucose deserves further study. It is unclear whether diabetes affects the gut or if an unhealthy microbiome contributes to the disease.”

Additional information on kombucha

Depending on how much you consume, kombucha has around the same amount of caffeine as a cup of regular tea.

Due to its high caffeine and low alcohol level, kombucha is not advised for children or pregnant or nursing women.

It’s recommended to buy kombucha rather than attempt to create it at home if you decide to start drinking it (after consulting with your healthcare professional).

Start out with a little quantity of kombucha.

Always check your blood sugar levels to see whether they have an effect on how you control your blood sugar in general. (Each individual is affected differently.)


For Type 2 diabetes medications that have been suggested by doctors worldwide are available here

Brain Bleeding: Can daily low-dose aspirin increases risk?

Brain Bleeding: Can daily low-dose aspirin increases risk?

Researchers looked into how low-dose aspirin affected older person’s risk of stroke. They discovered that low-dose aspirin increased the risk of cerebral bleeding by 38% but did not significantly reduce the risk of stroke.

Before administering aspirin to prevent stroke, doctors should examine patients for cardiovascular and head injury risks.

An ischemic stroke, also known as a blocked blood vessel in the brain, or a hemorrhagic stroke, often known as an unexpected burst of bleeding in the brain, both constitute strokes.

Every year, more than 795,000 people in the US experience a stroke. Stroke is a factor in about 1 in 6 deaths from cardiovascular diseases.

The incidence of stroke must be decreased through preventive measures. Aspirin, a common pain reliever, is currently used extensively to prevent the condition.

The risk of intracranial and intracerebral haemorrhages, or bleeding in the skull and brain, may increase even if meta-analyses suggest that low-dose aspirin may lower the risk of stroke.

Due to the fragility of their small blood vessels and their higher risk of injury from incidents like falling, older people are particularly vulnerable to haemorrhaging. These elements could change how aspirin’s risks and benefits balance out.

Stroke prevention measures may be influenced by knowing how low-dose aspirin impacts older person’s risk for stroke and hemorrhage.

Recent studies looked into how low-dose aspirin affected older persons’ risk for stroke and haemorrhage. Low-dose aspirin increased the incidence of cerebral haemorrhage by 38% while having no effect on stroke risk.

Low-dose aspirin’s effects on stroke risk

The average age of the 19,114 persons whose data were analysed for the study was 74. None of the participants, who made up about 56% of the total, had a history of cardiovascular diseases like:

  • stroke
  • AFib, or atrial fibrillation
  • chest pain

The individuals were divided into two groups at random and given a daily dose of 100 mg of aspirin or a placebo. They were monitored for 4.7 years on average.

Low-dose aspirin use was discovered to be associated with marginal, clinically inconsequential decreases in the incidence of ischemic stroke.

Stroke occurred in 1.5% of those who received aspirin (146 people), whereas it happened in 1.7% of the placebo group (166 people). Additionally, there was no statistically significant decrease in hemorrhagic strokes after using aspirin.

A hemorrhagic stroke occurred in 0.5% of aspirin-assigned participants (49 people), although 0.4% of placebo-assigned participants (37 people) also experienced one. The researchers also discovered that aspirin users had a markedly increased risk of cerebral hemorrhage compared to those taking a placebo.

Intracranial hemorrhage occurred in 1.1% of aspirin-taking participants (108 people), compared to 0.8% of placebo-taking participants (79 people). Dr. Arun Manmadhan, an assistant professor of medicine at Columbia University’s Vagelos College of Physicians and Surgeons who was not engaged in the study, provided the following information to us:

This study adds to the growing body of evidence showing that routine aspirin usage to prevent first-time cardiovascular events in the general adult population has minimal benefits and may even be harmful due to increased bleeding, especially in older persons. This study supports previous recommendations from the U.S. Preventive Services Task Force that persons over 60 should not regularly take aspirin to prevent cardiovascular disease.

Although aspirin is a blood thinner, low doses may cause more brain bleeding.

Experts discussed how aspirin may lower the risk of stroke with Dr. Hardik P. Amin, associate professor of neurology at Yale School of Medicine who was not involved in the study.

He claimed that individuals at risk for cardiovascular diseases may develop little clusters of blood platelets, a type of blood cell that facilitates clotting, inside their blood arteries.

Aspirin stops platelets from aggregating inside blood arteries, which results in its blood-thinning action and lowers the chance of a heart attack or stroke, according to Dr. Amin.

Experts also enquired about how aspirin might raise the risk of cerebral hemorrhage Dr Walavan Sivakumar, a board-certified neurosurgeon and the director of neurosurgery at Pacific Neuroscience Institute-South Bay in Torrance, California was not involved in the study.

Aspirin may enhance the risk of brain haemorrhage in the same manner that it lowers the likelihood of blood clots developing and travelling to the brain, according to Dr. Sivakumar.

One of the ways that the body stops bleeding is by forming blood clots. As a result, aspirin also makes it harder for the body to stop bleeding once it starts,” the doctor explained.

Need for larger investigations on the dangers of aspirin at low doses

Dr. Maria Parekh, an expert on stroke and an assistant professor of neurology at McGovern Medical School at UTHealth Houston who was not involved in the study, was consulted by experts regarding its limitations.

She pointed out that because there weren’t many episodes of cerebral hemorrhage and stroke in the study overall, the conclusions could have been tainted by random and intentional mistakes.

Aspirin is also known to help those who have experienced an ischemic stroke, in which the blood supply to the brain is halted or diminished, as it prevents blood clots from developing that could cause another stroke, Dr. Parekh continued. She stated that this is referred to as “secondary prevention.”

However, this research focused on the use of aspirin as “primary stroke prevention,” specifically in healthy older persons “free of overt cardiovascular disease,” to prevent first-time ischemic stroke. As a result, it excludes those who would most likely benefit from taking low dose aspirin, Dr. Maria Parekh pointed out.

Dr. Ziad Hage, a cerebrovascular and endovascular neurosurgeon at Novant Health in Charlotte, North Carolina, who is board-certified and fellowship-trained, was also questioned by experts about the study.

He said that groups at high risk of stroke or secondary stroke prevention may not be affected by the findings. He cautioned that the results might not apply to more varied demographics because the study’s participants were mostly older, white, and had easy access to blood pressure and lipid-lowering drugs.

Do you need to quit using low-dose aspirin?

These results indicate that advocating aspirin use can hurt patients who are healthy and have no cardiovascular risk factors, according to Dr. Sivakumar.

“At that point, patients may choose to make more conservative lifestyle changes, such as eating a healthy diet and exercising frequently.”

Dr. Hage concurred that individuals who had a higher risk of developing cardiovascular diseases like stroke should take aspirin. He said that unless required, aspirin should also be avoided by individuals who have a higher risk of falling.

In conclusion, it’s critical that the public comprehend that aspirin can be helpful in some circumstances, thus speaking with an expert on the subject is of the utmost importance. Stroke symptoms include sudden onset, facial, arm, or leg weakness, speech slurring or difficulty speaking, sudden loss of vision in one eye, and sudden loss of balance, among other symptoms. Dr. Ziad Hage, a cerebrovascular and endovascular neurosurgeon, advised patients to get medical attention if they experience any of these symptoms.


For Brain bleeding medications that have been suggested by doctors worldwide are available here

Cancer: physical activity a day could lower your risk.

Cancer: physical activity a day could lower your risk.

In a recent study, the impact of vigorous intermittent lifestyle physical activity (VILPA) on the risk of developing cancer was examined.

Using information from wrist-worn accelerometers, researchers followed 22,398 non-exercisers’ health records for cancer for nearly 7 years while also tracking their daily intense activity.

When compared to not participating in VIPLA, 4.5 minutes of VILPA per day, divided into 1-minute bursts, was linked to a 32% lower chance of developing cancer.

Power walking, lugging groceries, and climbing stairs are just a few examples of the many possibilities that exist in daily life for strenuous physical activity.

The importance of physical activity to overall health and wellbeing cannot be overstated. According to research, regular exercise can reduce the risk of developing chronic diseases like cancer, diabetes, and cardiovascular disease.

In fact, the World Health Organisation (WHO) reports that those who are not adequately active have a death risk that is 20–30% higher than those who are.

Even though the benefits of physical activity are obvious, only about 1 in 3 women and 1 in 4 men globally adhere to the guidelines for 75 minutes of strenuous exercise or at least 150 minutes of moderate exercise per week.

Good news has arrived from a recent study for those who dislike or are unable to engage in structured, intense exercise.

Just 4.5 minutes per day of vigorous-intensity physical exercise undertaken in 1-minute bursts was related with an up to 32% decreased risk of cancer, according to wrist-worn accelerometer data taken from 22,398 non-exercising people collected from the UK Biobank.

VILPA: What is it?

Short bursts of physical activity that are a regular component of our lifestyle (daily living) are referred to as vigorous intermittent lifestyle physical activity (VILPA) by Dr. Stamatakis and his colleagues.

VILPA examples include, but are not restricted to:

  • climbing hills
  • ascending stairs
  • power walking, also known as maximising walking pace for a short distance (like 100–200 metres) to reach intense intensity, involves carrying children or groceries for 50–100 metres.
  • intense housework.
  • VILPA differs from conventional intense physical activity in that it is intermittent and transient, lasting up to two minutes at a time, as opposed to continuous and planned.

Effects of VILPA and cancer risk

The study was a prospective cohort study of adults, aged 40 to 69, who provided the UK Biobank with their data.

The research team led by Dr. Stamatakis only included participants from the accelerometer-wearing group who reported not exercising in their free time and taking one or fewer leisurely walks per week in their analysis of the association between VILPA and cancer incidence.

The study removed participants who provided incomplete information, had a history of cancer, or improperly wore the activity monitor.

22,398 participants made up the study population, and their average age was 62. 54.8% of these were female, and 96% of them were white.

The researchers found 2,356 new cancer occurrences throughout a mean follow-up period of 6.7 years, including cancer registration, hospitalisation for cancer, or death from any malignancy.

The researchers utilised a machine-learning method known as “random forest” to categorise accelerometer-recorded physical activity based on intensity — vigorous, moderate, and light.

VILPA reduces cancer risk by just a few minutes every day.

The majority of VILPA incidents took place in spurts of up to one or two minutes. People participated in VILPA for a maximum of 16 minutes, or about 4.5 minutes per day on average.

According to statistical assessments, the association between VILPA and cancer risk is almost linear, meaning that a person’s risk of developing cancer decreases as they engage in more VILPA.

People who engaged in VILPA for an average of 4.5 minutes per day, in short bursts of up to 1 or 2 minutes, had a 20% lower chance of developing cancer than those who did not engage in any VILPA (6.2% of study participants).

Previous studies have demonstrated a link between insufficient physical activity and several cancer forms. These consist of:

  • liver
  • lung
  • kidney
  • gastric cardia (a type of stomach cancer)
  • endometrial
  • Leukaemia myeloid
  • myeloma
  • colorectal
  • neck and head
  • bladder
  • mammary cancer
  • esophageal adenocarcinoma (esophageal cancer)

This study demonstrates that those who engaged in 4.5 minutes of VILPA daily have a 31% lower risk of developing certain physical activity-related malignancies.

The least amount of VILPA necessary to significantly lower the chance of developing cancer was also determined by the researchers. They discovered that 3.4 minutes of VILPA per day can reduce the risk of cancer overall by 17% and 3.6 minutes of VILPA per day can reduce the risk of cancer linked to physical activity by 18%.

More study is required to determine how VILPA affects cancer.

A relatively small quantity of strenuous lifestyle activity can have such a large link with decreased cancer risk, according to the “high-quality study,” according to Dr. David Raichlen, professor of biological sciences and anthropology at the University of Southern California.

According to him, “the authors used a novel machine learning-based method to identify behaviours and this study moves the field forward, allowing us to better understand the benefits of this form of physical activity on [the] risk of developing cancer.”

Because of the study’s methodology, Dr. Raichlen advised that causality could not be established; however, “this work certainly suggests that future intervention studies using VILPA are warranted.”

According to Prof. Markus Gruber, chair of Training and Movement Science and director of the University Konstanz’s Human Performance Research Centre, the study supports the long-held belief in exercise science that “intensity matters.”

Prof. Gruber made the same observation as Dr. Raichlen, namely that although the study’s data, methods, and analysis are sound, the study is cross-sectional and can only report relationships between VILPA and cancer incidence.

When challenged about the connection between VILPA and cancer incidence, Prof. Gruber responded that there are a number of plausible “explanations for the results that need to be tested.”

He claims that VILPA may either directly lower the risk of cancer, boost physical fitness, or show superior physical fitness, which is linked to a lower risk of cancer. Additionally, VILPA may reduce the effects of aging-related fitness decreases and reduce cancer risk by doing so.

Overall, according to Prof. Gruber, VILPA is a promising substitute for duration-based advice on physical activity, “especially for people who don’t like to exercise.”


For Cancer disease medications that have been suggested by doctors worldwide are available here

MIND diet: Can it assist in improving cognitive ability?

MIND diet: Can it assist in improving cognitive ability?

People may start to notice a minor slowdown in processing speed and sporadic memory lapses as a result of ageing or an age-related illness like dementia.

Although these results have not been replicated in clinical trials, diet may provide protective advantages against cognitive deterioration.

An older person’s cognition may be improved by reducing daily caloric consumption by a small amount, according to a recent study.

Improvements in cognition were similar for those on the MIND diet and those on any minor calorie restriction, with no significant differences between the two groups.

As we age, cognitive change is typical. Even in your 20s and 30s, you may notice a modest reduction in memory and processing speed, however this is typically accompanied by advances in accumulated knowledge well into old age.

Observational studies imply that the Mediterranean diet may have positive effects on cognition, despite the fact that no specific vitamin has been found to stop cognitive decline.

The MIND diet, a combination of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets, and mild calorie restriction have now been examined for their impact on cognition.

Both diets had a somewhat positive impact on cognition, according to the study, but neither was noticeably superior to the other.

This study results point to mild caloric restriction and an average weight loss of 5.5% as lifestyle factors that may support cognition in older adults,” said Molly Rapozo, a registered dietitian nutritionist and senior nutrition and health educator at the Pacific Neuroscience Institute in Santa Monica, California.

The MIND diet: what is it?

The acronym “MIND” refers to “Mediterranean-DASH Intervention for Neurodegenerative Delay.”

The MIND diet seeks to lessen dementia and the deterioration of brain health that frequently happens as people age. It combines elements of the Mediterranean diet with the Dietary Approaches to Stop Hypertension (DASH) diet, two highly well-known eating plans.

The DASH diet and the Mediterranean diet are two of the healthiest diets, according to many experts. They can lower blood pressure and lower the risk of heart disease, diabetes, and a number of other ailments, according to research.

However, scientists sought to develop a diet designed particularly to support better brain health and guard against dementia.

They mixed foods from the DASH and Mediterranean diets, which have been demonstrated to improve brain function, to achieve this.

For illustration, both the DASH diet and the Mediterranean diet advise consuming lots of fruit. Berries in particular have the greatest supporting data, although eating fruit in general has been related to increased brain function.

So, while the MIND diet does not emphasize fruit consumption in general, it does advocate eating berries.

As of right now, there are no fixed rules for adopting the MIND diet. You can easily increase your consumption of the 10 items that the diet suggests and decrease your consumption of the 5 foods that it advises you to limit.

Cutting calories may benefit the brain.

A total of 604 participants were enlisted in the study by the researchers. Despite eating poorly and reporting a family history of Alzheimer’s, none of the participants tested negatively for cognitive deterioration. Body mass index (BMI) > 25 (overweight) was present in each individual.

The participants were randomized into two groups at random: 301 individuals were assigned to the MIND diet, and the remaining 303 individuals continued to follow their regular dietary regimen.

Additionally, as one of the study’s objectives was to reduce body mass by 3-5%, the researchers decreased everyone’s daily calorie consumption by 250 calories.

For three years, the participants were instructed to stick to their diet, and throughout that period, they received frequent dietary counselling over the phone and in person. To make sure both groups were getting the right amount of calories, advice was given about portion size. The MIND diet participants also received instructions on which new meals to incorporate and which ones they should avoid.

Four times over the three years, the researchers checked in with the individuals to evaluate their mental functioning, blood pressure, diet, level of physical activity, and usage of medications.

Participants had a variety of cognitive tests administered by researchers who were not aware of which diet group they were in after six months, then at 12, 24, and 36 months. To detect any abnormalities in the brain, some also had magnetic resonance imaging (MRI) scans.

Inflammation and oxidative stress are reduced by the MIND diet?

The particular mechanisms by which the MIND diet operates are yet unknown, according to the available research. However, researchers believe that it might function by decreasing inflammation and oxidative stress.

Free radicals, which are unstable chemicals, build up significantly in the body and cause oxidative stress. Cells are typically harmed by this. Particularly susceptible to this kind of harm is the brain.

Your body naturally responds to injury and infection with inflammation. However, inflammation can also be damaging and a factor in many chronic diseases if it is not well controlled.

Inflammation and oxidative stress can both hurt your brain. They have been the focus of some recent Alzheimer’s disease prevention and treatment initiatives.

Lower levels of oxidative stress and inflammation have been linked to following the DASH and Mediterranean diets.

The MIND diet is a combination of these two diets, thus the foods that make up the MIND diet likely also have antioxidant and anti-inflammatory benefits.

By shielding the brain from oxidative stress, antioxidants in berries and vitamin E in olive oil, green leafy vegetables, and almonds are thought to improve brain function.

Omega-3 fatty acids, which are present in fatty fish, are also well known for their capacity to reduce brain inflammation and have been linked to a slower loss of cognitive function.

The dangerous beta-amyloid proteins may be reduced by the MIND diet.

Researchers think that by lowering potentially hazardous beta-amyloid proteins, the MIND diet may also benefit the brain.

Protein fragments called beta-amyloid proteins can be found in the body naturally. However, they can assemble into plaques that develop in the brain, obstructing neural connections and ultimately resulting in the death of brain cells.

In fact, a lot of scientists think that these plaques are one of the main reasons why Alzheimer’s occurs.

Studies on animals and in cells indicate that the antioxidants found in several MIND diet items may aid in preventing the development of beta-amyloid plaques in the brain.

The Summary

The MIND diet was developed to decrease the deterioration of brain function that can occur with ageing and prevent dementia. The diet promotes the consumption of fruits, vegetables, whole grains, olive oil, fish, chicken, beans, and wine.

These meals provide a variety of nutrients that support healthy brain function, perhaps by lowering oxidative stress, inflammation, and beta-amyloid plaque development.

According to preliminary study, strictly adhering to the MIND diet is linked to a lower risk of Alzheimer’s disease and a slower decline in brain function over time. To fully comprehend the consequences of the diet, more research is required.

Future study revealing that the MIND diet provides additional health advantages linked to the Mediterranean and DASH diets won’t come as a surprise because it is a combo of these two diets.

But for now, the MIND diet is a terrific and easy-to-follow method if you’re seeking for a way of eating that focuses on maintaining brain function as you age.


For Mental disease medications that have been suggested by doctors worldwide are available here