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New omega-3 could Prevent Visual Decline from Alzheimer’s.

New omega-3 could Prevent Visual Decline from Alzheimer’s.

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The region of the eye known as the retina is impacted by some of the main causes of vision loss.

Docosahexaenoic acid, or DHA, is a specific type of omega fatty acid that can be supplemented to lessen the risk of retinal disease. However, because of the retina-blood barrier, raising DHA levels in the retina is difficult.

Now, a team of scientists has demonstrated that a particular kind of DHA they created can permeate the retinal tissue—at least in mice. The supplement may be used to lower risk and perhaps even treat various retinal illnesses if the same outcome is shown in humans.

According to the World Health Organization, the annual global cost of losing one’s sight is estimated to be $411 billion. This cost includes missed wages and productivity as well as medical and care expenses.

The majority of persons who lose their sight are over 50, and the following are the main reasons for vision loss worldwide:

  • mature macular degeneration with ageing
  • cataract
  • retinopathy in diabetics
  • glaucoma
  • mistakes in refractive correction.

Both diabetic retinopathy and age-related macular degeneration have an impact on the retina, which is located at the back of the eye and is home to numerous light-sensitive cells that enable vision.

Data

The macula, a portion of the retina, is impacted by age-related macular degeneration, which causes blurry central vision. In the meanwhile, diabetic retinopathy, which affects people with both type 1 and type 2 diabetes, is brought on by high blood sugar levels that disrupt the retina’s blood flow and, if left untreated, can result in blindness.

The concentration of docosahexaenoic acid, or DHA, an omega-3 fatty acid, is highest in the brain and retina among all bodily tissues. Given that the body can only produce modest amounts of this fatty acid, it must be consumed through diet or supplementation.

Although epidemiological studies have demonstrated the positive effects of DHA supplementation on lowering the risk of developing retinal illness, it is considerably more difficult to deliver this molecule to the retina and sustain normal functioning. This is despite the fact that the relevance of omega-3 fatty acids in the diet is well established.

This is due to the difficulty in obtaining DHA supplements that not only permeate the blood-retinal barrier but also DHA in a form that can pass through the intestinal barrier.

Once scientists developed a novel form of DHA that can enter the retina of the eye, new research offers a ray of hope for treating and possibly preventing visual losses linked to Alzheimer’s disease, diabetes, and other conditions. A research grant from the Alzheimer’s Association paid for the study (AARG).

DHA: New form

The study’s authors, from the University of Illinois at Chicago, presented their findings at the American Society for Biochemistry and Molecular Biology’s annual meeting, which took place March 25–28 in Seattle.

They demonstrated that a newly created version of DHA may be employed to penetrate both the intestinal and retinal blood barriers.

The scientists developed a fresh lysophospholipid version of DHA, called LPC-DHA, to achieve this. During six months, they gave mice a low dose of this supplement, which corresponds to 250 to 500 mg of omega-3 fatty acids daily for people.

DHA levels in their retinas increased by 100% as a result of this. LPC-DHA was found to be superior when researchers compared the effects of supplementation to those of fish oil and krill oil, two alternative sources of DHA.

New DHA and eyesight

DHA is primarily located in the retina of healthy eyes. Photoreceptors—cells that transform light into signals that are delivered to the brain—are maintained with the aid of this.

The findings imply that this supplement may aid in preventing visual problems in people with Alzheimer’s disease and other conditions that share a common DHA shortage and vision impairment.

One issue with existing supplements is that DHA must first enter the bloodstream through the intestines before reaching the retina. Up until today, there has been no way to raise the DHA levels in the retina. The brand-new vitamin gets past blood-retinal and digestive barriers.

Further research is required to prove the safety and efficacy of DHA supplements in people.

It’s always a fascinating issue, says Benjamin Bert, MD, an ophthalmologist at MemorialCare Orange Coast Medical Center in Fountain Valley, California, to investigate dietary supplementation’s potential to halt the advancement of diseases. In this instance, the researchers are examining a novel version of DHA called LPC-DHA, which they believe will be more readily absorbed by the body than the DHA formulations already on the market. We still have a lot to learn because this study is one of the first to use this supplement.

Vision problems in Alzheimer’s people

According to Howard R. Krauss, MD, surgical neuro-ophthalmologist and director of Pacific Neuroscience Institute’s Eye, Ear & Skull Base Center at Providence Saint John’s Health Center in Santa Monica, California, “Visual impairment is a significant component of Alzheimer’s disease, but while there are indeed degenerative retinal changes in association with Alzheimer’s disease, most of the visual impairment is secondary to brain dysfunction rather than retinal dysfunction.”

Krauss stated, “Yet, one may consider the retina as both an extension of the brain and a window into the brain. “Thus, therapeutic approaches that may show promise for improving retinal health may also do so for improving brain health.”

According to the Alzheimer’s Foundation of America, vision issues in those with Alzheimer’s disease may result from the brain’s inability to absorb the information that the eyes send to it. The individual may experience the following issues:

  • Loss of peripheral pitch
  • sensitivity to contrast being lost
  • Inability to accurately perceive depth
  • difficulties with glare

According to Bert, specific layers of the retina gradually become weaker in people with Alzheimer’s disease. “With a supplement like the one disclosed here, the hope is that this process will slow down or halt entirely.”

Note on omega-3 fatty acids

You need omega-3 fatty acids for good health. Your body does not, however, make them. You must therefore consume them through your diet.

The following are typical foods rich in omega-3 fatty acids:

  • Fatty fish, such as salmon, tuna, mackerel, and sardines
  • Fish oil
  • Flax seeds
  • Chia seeds
  • Soybean oil
  • Walnuts

Omega-3 fatty acids are added as a supplement to some diets. For those who don’t typically eat these foods, there are supplements available, like fish oil or algal oil.

According to the National Institutes of Health, your body’s cell membranes contain essential components called omega-3 fatty acids. One of the most important types of omega-3 fatty acids is docosahexaenoic acid (DHA). Your retina normally has high DHA levels.

The conclusion

Scientific research always includes mouse experiments. Yet, they occasionally reveal whether a therapy approach is secure and efficient in people. This research is in its early stages.

The “takeaways” from this study, in Krauss’s opinion, show that additional investigation is necessary before people should start using omega-3 supplements.

Even though some people may benefit from taking supplements, the purity and concentration of over-the-counter vitamins varies. Certain supplements, especially when used in excess, may pose a risk to some individuals. Anyone thinking about using supplements should talk to their primary care physician about it.

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Wound-healing and Anti-aging found in an invasive weed.

Wound-healing and Anti-aging found in an invasive weed.

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Many people are expressing a desire for skin care products made from natural ingredients. Fruit from the cocklebur plant contains antioxidant and anti-inflammatory characteristics. This may make it effective as a skin protectant, according to researchers presenting at Discover BMB.

In 3D tissue models, researchers discovered that cocklebur extracts sped up wound healing and decreased UVB damage. More and more individuals are looking for substances that are naturally derived when it comes to skin care. According to previous customer polls, many women prefer all-natural skin care products.

According to recent studies, the fruit of the cocklebur plant, a noxious weed, possesses anti-inflammatory and antioxidant qualities that may not only make it beneficial as a skin protectant but also aid reduce UVB damage and speed wound healing.

The research is presented at Discover BMB, the American Society for Biochemistry and Molecular Biology’s annual meeting, March 25–28 in Seattle, Washington.

What is the cocklebur plant?

The cocklebur plant, or Xanthium strumarium as it is named in science, is a summer-growing weed. The weed has both male and female heads as it grows. Its maximum height at maturity is six feet.

With burs, the weed produces blooms. The “fruit” of the plant is found inside these burs. The burs can attach to an individual and disseminate to other locations when a person or animal rubs up against the plant.

Plants called cocklebur are indigenous to parts of China, Central Asia, and Southern Europe. The United States is one of the places in the globe where they are presently, nevertheless.

From ancient times, the cocklebur has been utilised in traditional Chinese medicine, most frequently to relieve headaches and rhinitis. More recently, researchers have investigated using the cocklebur plant to treat cancer, diabetes, and rheumatoid arthritis.

Cocklebur extract and skin protection

In this work, scientists examined how the molecular characteristics of cocklebur fruit extracts can impact collagen synthesis, wound healing, and UVB radiation damage using cell cultures and a 3D tissue model resembling human skin.

Upon examination, researchers discovered that the cocklebur fruit extracts accelerated the healing of wounds and boosted both the creation and breakdown of collagen. It had a protective effect against UVB radiation at lesser doses as well, but at the highest measured dose, it reduced the ability of the cell to react to UVB.

Eunsu Song, a PhD student at Myongji University in South Korea and the study’s principal author, told that there have been numerous published studies that describe the chemical makeup of cocklebur fruit.

The identification of bioactive substances in natural goods is greatly helped by solvents. In the majority of published studies, solvents were extracted using methanol, which may not be suitable for usage as food or cosmetic additives. The initial step in our research, according to Song, was the ethanol extraction and examination of the cocklebur fruit’s bioactive component.

As a result, the primary phenolic ingredient in cocklebur was the antioxidant chlorogenic acid, she said. Additionally, the predominant phytosterol in cocklebur was ß-sitosterol. Both bioactive substances have been investigated because of their antioxidant, skin-allergenic, and wound-healing properties.

Potential toxicity of cocklebur in high doses

Although the research team’s findings are encouraging, they also issued a warning that cocklebur fruit extract taken in large dosages may be dangerous. To ascertain the safe limits for cosmetic and pharmaceutical purposes, more study must be done.

According to Song, the carboxyatractyloside found in the burs of cocklebur is what gives it its toxic properties. That can be one of the causes of the poisonous effects in the high cockleburs concentration. At high amounts, additional substances than carboxyatractyloside can also be hazardous. As a result, it is crucial to determine the optimum dose using acute toxicity studies.

It hasn’t been clear up until now whether cocklebur actually promotes collagen formation and wound healing, two processes that are crucial to the molecular health of the skin. We need to identify any potential molecular mechanisms before moving on to the next phase. Following that, we’ll test cocklebur using additional non-animal methods.

Intriguing anti-aging, healing potential

Dermatologist Dr. Alexis L. Young, clinical assistant professor in the department of internal medicine at the Hackensack Meridian School of Medicine, provided the following commentary on this study:

According to her, the field of cosmeceuticals as well as wound healing could be greatly impacted by this new study, which she called “extremely exciting.” “The key principles of anti-aging products include promoting collagen synthesis, preventing collagen degradation, using antioxidants to ward off DNA damage and the ageing effects of free radicals, and boosting the skin’s elasticity and volume. This plant could be able to do those tasks in cell and tissue culture.

Hyaluronic acid (HA) is a temporary addition to the skin that briefly plumpens the skin for around 15 minutes before disappearing, according to Dr. Young. “A topical agent that can genuinely boost collagen and HA formation would be new. Presently available retinols, which promote collagen synthesis and prevent its deterioration, can be quite irritating to the skin. We’re constantly looking for skin-care products that are more tolerable yet still effective.

This study, according to Dr. Lamb, is interesting since it reveals a novel development that may be employed as both an antioxidant and a skin protectant: “Naturally derived goods are currently popular, and this is a fresh one that can be quickly added to the arsenal.”

The main concern will be whether or whether something similar can induce allergic contact dermatitis, as the plant itself can. Whilst the research is encouraging, we must wait to see if we should put it on the skin because it actually seems to be quite irritating. If it can do more harm than good, we should avoid using it.

The conclusion

Compounds found in the cocklebur’s fruit, according to South Korean researchers, may aid in skin protection. These substances accelerated wound healing, lowered UVB exposure damage, and boosted collagen formation in tests employing cells and tissues. But more research is still required.

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How coffee helps lower type 2 diabetes risk?

How coffee helps lower type 2 diabetes risk?

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A significant new study investigates the mechanisms underlying the well-established link between coffee drinking and a decreased risk of type 2 diabetes.

According to the study, coffee’s anti-inflammatory characteristics may account for a major portion of its positive effects. Pro-inflammatory biomarkers seem to decrease with coffee consumption while anti-inflammatory biomarkers rise.

Coffee consumption has been associated to a decreased risk of type 2 diabetes. According to a recent study, the connection is well-established, although the exact mechanism is still unknown.

Another study contends that through reducing subclinical inflammation, coffee consumption may reduce the incidence of type 2 diabetes. The advantage was greatest in espresso or filtered ground coffee consumers and non-smokers or never-smokers.

Data set on coffee and type 2 diabetes

The authors of the study examined a sizable data set from participants in two population-based studies: the Rotterdam Study in the Netherlands and the UK Biobank.

The 502,536 participants in the UK Biobank cohort were from England, Scotland, and Wales and enrolled in the study between April 2006 and December 2010. They ranged in age from 37 to 73. Follow-up information on these people became accessible in 2017.

The Rotterdam Study, which started in 1990 and will eventually include 14,929 people, is still ongoing. In 2015, follow-up information was revealed. Researchers found alterations in the levels of type 2 diabetes-associated biomarkers connected to inflammation in the study.

Researchers found that those who increased their daily intake of coffee by just one cup had a 4% lower risk of type 2 diabetes and insulin resistance. This reduction in risk was most likely brought about by decreased inflammation, the study’s authors speculate.

The current study’s “main strength is the large number of individuals included in the cohorts, the long follow-up time, and the comprehensive assessment of inflammatory markers,” according to Dr. Angélica Amato, associate professor in the Faculty of Health Sciences at the University of Brasil who was not involved in it.

Effects of coffee on inflammation

The Rotterdam Project and the UK Biobank provided the researchers with the 152,479 participants’ health records for evaluation. They examined the daily coffee consumption of the participants, which ranged from 0 to about 6 cups, as well as the prevalence of type 2 diabetes across a 13-year period.

By the use of fasting blood samples, the team also assessed levels of inflammatory markers such as C-reactive protein (CRP), leptin, and adiponectin as well as indicators of insulin resistance.

The researchers discovered that drinking an extra cup of coffee each day was linked to a 4–6% decreased chance of developing diabetes.

Greater levels of interleukin-13 and adiponectin concentrations, which have anti-inflammatory effects, were linked to higher levels of coffee consumption instead of lower levels of CRP and leptin, pro-inflammatory markers. Blood glucose levels can be lowered by adiponectin’s ability to make people more sensitive to insulin.

Researchers believe that drinking coffee can help lower inflammatory biomarkers, which are known to rise in the body when there is inflammation, as is the situation with type 2 diabetes.

The researchers also think that the type of coffee is important because espresso or filtered coffee was more closely related to risk reduction.

According to Andrew Odegaard, PhD, an associate professor of epidemiology and biostatistics at the University of California, Irvine, the results are consistent with earlier research that found a relationship between higher levels of coffee consumption and a decreased risk of type 2 diabetes across various populations and demographics.

Odegaard noted that more information is required to fully grasp the potential pathways, but that “the mediating estimates of inflammation provide evidence on a major postulated mechanism.”

Enjoy coffee but avoid relying on it

Tan would not necessarily recommend it to individuals wanting to protect themselves. Tan says persons with diabetes and those at risk for the condition should feel comfortable consuming black coffee or espresso.

There are alternative strategies that have been more thoroughly researched to lower the risk of diabetes, cardiovascular disease, obesity, and general health, according to Tan.

Tan advises increasing physical exercise, reducing inactive time, abstaining from alcohol and tobacco, having a balanced diet, and, if at all feasible, avoiding specific drugs that can worsen hyperglycemia in order to reduce one’s chance of developing diabetes.

She exhorts them to consider the kind of coffee they consume. Moreover, Tan remarked, “I would like to caution patients that the study indicated the most benefit from filtered coffee or espresso rather than from coffee beverages that can include very high amounts of sugar and fat.”

Why inflammation matters in diabetes?

Dr. Amato expressed his concern that a longitudinal study like this one could not be used to conclusively prove causality. She did, however, add that “it is most likely that the association between coffee use and reduced type 2 diabetes risk is due to decreased insulin resistance, one of the physiopathological pathways underpinning the development of type 2 diabetes.”

Insulin produced by the pancreas cannot regulate blood sugar levels in persons with type 2 diabetes. These levels are able to escalate dangerously out of control due to such insulin resistance.

According to Dr. Amato, subclinical inflammation, which is reportedly reduced by coffee drinking, has a significant role in insulin resistance.

Dr. Kausel continued, “Adipokine released by adipocytes has anti-inflammatory benefits in addition to making patients more sensitive to insulin. Further enhancing insulin sensitivity and lowering systemic inflammation are coffee’s polyphenol components.

Dr. Ochoa-Rosales advised patients worried about preventing type 2 diabetes to take a stance against inflammation by consuming a diet high in polyphenols from fruits and vegetables.

Smokers don’t get the same coffee benefits

The researchers also discovered that among people who smoke, coffee’s health benefits were less pronounced.

According to Dr. Ochoa-Rosales, “there is a correlation between smoking and higher coffee consumption – heavy coffee consumers are often smokers,” therefore the researchers first considered smoking a confounding factor in their analysis.

Nevertheless, when they investigated the impact of coffee consumption on diabetes risk among smokers, non-smokers, and never-smokers, they discovered that the effect of coffee’s positive relationship with decreased C-reactive protein and type 2 diabetes risk was only present among former- and never-smokers.

Treating and avoiding type 2 diabetes

Although the link between inflammatory markers and cardiovascular disease has been researched, Dr. Kausel pointed out that the new study offers a “fresh perspective.”

However finding increasing your coffee intake won’t likely prevent type 2 diabetes, “anything that lowers these inflammation indicators can be acquired as a daily routine, and since most people consume coffee, it’s a good thing to know,” she continued.

Dr. Ochoa-Rosales noted that there is already increased interest in treatments that target inflammatory indicators as a result of the substantial body of information linking systemic inflammation to the onset of type 2 diabetes.

Dr. Amato acknowledged this and suggested that the biomarkers identified in the study could serve as “promising targets” for therapeutic treatment of type 2 diabetes:

“Exploring the precise mechanisms by which the bioactive components of coffee function to elucidate potential targets and pathways that may be addressed to treat or prevent the disease” is another fascinating option.

No matter what new pharmacological targets are discovered as a result of research like this one, Dr. Kausel emphasised that “if individuals don’t start thinking about healthy practises, it will be impossible to avoid the disease.”

Dr. Kausel underlined that eating a good diet is the major component in preventing diabetes.

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Healthy effects of walnut on heart and gut.

Healthy effects of walnut on heart and gut.

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Researchers from Texas Tech University and Juniata College undertook a study to examine the effect walnuts have on the gut flora because they offer advantages for heart health. The possibility that walnuts’ heart-healthy properties originate in the gut intrigued the researchers.

Three groups of participants, including one that consumed whole walnuts, were given different diets by the researchers. Following this, biological samples from each person were examined.

According to their research, those who ate a diet high in walnuts had higher levels of the amino acid L-homoarginine in their intestines. This finding suggested that dietary changes that affect the gut may be able to improve heart health since people with lower homoarginine levels are more likely to develop cardiovascular disease.

There are still numerous unanswered concerns regarding how particular diets affect heart health and what other foods may reduce cardiovascular risk, despite the fact that experts are aware of this.

Researchers from Juniata College in Huntingdon, Pennsylvania, and Texas Tech University in Lubbock were interested in finding out whether walnuts’ potential heart health benefits stem from the digestive system.

They carried out their research by examining the microorganisms’ genomic expression in subjects who either consumed or did not consume a diet high in walnuts. The American Society of Biochemistry and Molecular Biology’s annual meeting, Discover DMB, is where the study’s findings were presented.

Quick facts of Heart health

The greatest cause of death for adults in the United States, according to the Centers for Disease Control and Prevention (CDC), is heart disease. Heart disease claims the lives of up to 700,000 individuals annually.

One significant component that affects heart health is nutrition. Individuals who consume a lot of fat and cholesterol in their diets are more likely to experience problems that could ultimately result in heart disease.

People can adopt diets that are low in fat, include lean meats, and are low in sugar and salt to help lower their risk of heart disease. Additionally helpful is avoiding processed foods and foods high in trans fats.

The following are some heart-healthy foods that the National Institutes of Health (NIH) advises consumers to eat:

  • vegetables
  • fruits
  • whole grains
  • lean meats and seafood
  • nuts

Several studies have demonstrated that walnuts in particular help lower a person’s risk profile for cardiovascular disease.

Role of the gut microbiome

For optimum health, a balanced gut microbiota is essential. A collection of microbes that inhabit the gastrointestinal tract is known as the gut microbiota. According to some estimates, the human gastrointestinal tract contains 1,013 bacteria, or nearly the same number of cells as an adult human body.

Bad bacteria may occasionally outnumber good bacteria in the gut microbiome as a result of sickness or lifestyle decisions.

“The gut microbiome plays a crucial role in human health and influences the development of chronic diseases ranging from metabolic disease to gastrointestinal disorders and colorectal cancer,” the NIH state.

Using probiotic pills to balance the gut microbiota is one strategy to promote gut health. Yogurt, pickled veggies, and kombucha are a few foods people can take to aid with this.

New study

The current study’s authors were particularly interested in the effects of walnuts on gastrointestinal and cardiovascular health. Walnuts contain more alpha-linolenic acid (ALA), which is important since ALA may have an effect on cardiovascular and neurological health.

For this study, the researchers examined data from 42 people. All of the patients had a high risk of developing cardiovascular disease. At first, each participant took part in a conventional Western diet for two weeks. The researchers determined that their diet consisted of 34% lipids, 16% protein, and 50% carbohydrates.

After analysing the participants’ gut microbiomes with stool samples, the researchers divided the subjects into three groups.

Participants who consumed 57–99 grammes (g), or about 1 cup, of walnuts per day made up the first group, which was referred to as the “walnut diet group.” Without eating walnuts, the second group consumed the same amounts of the omega-3 fatty acid alpha-linolenic acid. This diet was used as the “matched walnut control diet.”

The third group, known as the “oleic acid replaces ALA in diet without walnuts group,” was instructed to replace their ALA intake with oleic acid while avoiding walnuts. To “explore the makeup and functionality of the gut microbiota,” the researchers took faeces samples from the subjects at the conclusion of the six-week diet periods. They then used metatranscriptomics to examine the samples.

Walnuts, heart health, and the gut

The researchers took stools samples from each group and then performed a genetic analysis on the gut microbiota from each group. They were able to identify which germs were present in higher or lower concentrations.

In the walnut diet group, the researchers discovered increased concentrations of Gordonibacter bacteria. This bacterium is in charge of metabolizing plant-based substances. In this group, the researchers also observed greater levels of gene expression in pathways involving the amino acid L-homoarginine.

This is relevant because those with low homoarginine levels are at a higher risk for heart disease. Also, they discovered that after following their diets for 6 weeks, the individuals’ dysbiosis index values—which measure the proportion of harmful to beneficial bacteria—improved.

Despite the study’s modest sample size, the findings point to the possibility of reducing cardiovascular disease risk through dietary modifications that have an impact on the gut.

In an interview, Mansi Chandra, an undergraduate researcher at Juniata College who will present the study, discussed it.

What do the experts advice?

The results were discussed with MNT by Dr. John Higgins, a professor of cardiovascular medicine at McGovern Medical School at UTHealth Houston who was not involved in the study.

“Walnuts are an excellent source of omega-3 fatty acids, particularly alpha-linolenic acid, and they are helpful for enhancing cardiovascular health. According to Dr. Higgins, they lower blood pressure, lessen blood clotting, lower inflammation, and lower the chance of developing metabolic syndrome and cardiovascular disease.

Dr. Higgins explained the significance of such findings by pointing out “how various organ systems are interrelated.” Dr. Higgins stated that “in this circumstance, the gastrointestinal system and the heart [are related]”. “A healthy heart is a result of a healthy gut!”

“Our research implies that by altering diet and modulating intestinal microbiota composition and metabolism — for example, starting to eat a cup of walnuts each day — we may be able to better support cardiovascular disease prevention,” he added, while he cautioned that “[m]ore research is needed.”

Another speaker about the study was Dr. Ernst von Schwarz, a cardiologist and professor at UCLA who was not involved in it.

He asserts that “the study also supports the concept of a Mediterranean-style diet as the most heart-healthy diet, which in some studies has [been] shown to result in a regression of atherosclerosis (calcification/hardening) of the blood vessels in the heart, the brain, and even in the sexual organs.

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Insufficient sleep tied to increased risk of stroke.

Insufficient sleep tied to increased risk of stroke.

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Peripheral artery disease (PAD), which affects more than 200 million people worldwide and results in blocked arteries in the legs and raises the risk of stroke and heart attack, is a condition that causes blocked arteries, and new research published in the European Heart Journal has shown a strong correlation between sleep habits and the development of PAD.

Researchers discovered that compared to people who sleep 7 to 8 hours each night, those who sleep less than 5 hours have a 74% increased risk of developing PAD. The study stresses the need of getting enough sleep for preserving vascular health and delaying the onset of PAD.

A recent study that was just published in the European Heart Journal found a strong connection between getting too little sleep and an elevated risk of peripheral artery disease (PAD).

In comparison to people who follow a healthy sleep schedule of 7 to 8 hours per night, the research showed that people who sleep fewer than 5 hours each night have a 74% higher risk of developing PAD.

Both excessive daytime naps and insufficient sleep at night have previously been associated with an increased risk of coronary artery disease, which, like PAD, is brought on by blocked arteries. With the goal of filling in the knowledge gap about how sleep habits affect PAD and how they affect it the other way around, this study sought to provide insightful information.

Using genetic data to study PAD risk

Almost 650,000 people participated in the survey, which was conducted in two phases. The first thing the researchers did was look at how napping during the day and how much sleep an individual gets at night correlated with their chance of developing PAD.

They next performed a Mendelian randomization analysis utilising genetic data to see whether these relationships were indeed responsible for the elevated risk of PAD.

Mendelian randomization is a research technique that examines whether there is a cause-and-effect link between specific factors and a specific outcome using genetic data. In layman’s terms, it is comparable to a natural experiment that makes use of the randomness with which our genes are passed along.

Stronger evidence for probable causal ties is produced by this strategy, which assists researchers in distinguishing between real cause-and-effect correlations and merely associational relationships.

The possibility of reverse causality is one of the drawbacks of observational research, making it difficult to determine whether sleep habits caused PAD or if having PAD affected them when a link between them and the condition is found.

Mendelian randomization is a trustworthy method for determining causality, increasing the confidence in the results.

Link between short sleep duration and PAD

Sleeping less than 5 hours each night compared to sleeping 7 to 8 hours significantly quadrupled the risk of PAD in observational research involving 53,416 adults. This result was confirmed by other analyses involving 156,582 and 452,028 individuals.

In the causative investigations, not only was short sleep associated with an increased risk of PAD, but PAD was also associated with an increased risk of short sleep.

These findings imply that insufficient nighttime sleep increases the risk of PAD development and that PAD itself increases the risk of insufficient nighttime sleep.

An observational study of 53,416 adults indicated that sleeping for more than eight hours per night was linked to a 24% higher risk of PAD than sleeping for seven to eight hours.

Analyses in two larger groups of 156,582 and 452,028 people provided support for this observation. However, no cause-and-effect relationship was observed between extended sleep and PAD.

Similar results were reported for daytime napping, when nappers had a 32% higher risk of PAD than non-nappers, although no causative links were found.

“This is a well-put-together study that better examines the link of sleep length with PAD,” said Dr. Rigved Tadwalkar, a board-certified cardiologist at Pacific Heart Institute in Santa Monica, California, who was not involved in the study.

According to Dr. Tadwalkar, “The study is of high value because earlier studies addressing this link have been limited because of less reliable study design and lower statistical power.”

Study implications

Dr. Tadwalkar told that the American Heart Association released a document titled “Life’s Essential” last year, adding that the consequences for patients and the general public are enormous.

It aims to enhance public health by offering recommendations for lifestyle modifications that can lower the risk of cardiovascular disease. The paper is an update of “Life’s Easy.” The most recent update includes an eighth element that emphasises sleep length.

According to other studies, “Life’s Essential 8” makes it clear that getting between 7-9 hours of sleep each night is ideal from a cardiovascular standpoint.

What do the experts think?

In order for people to improve their health results, Dr. Tadwalkar also emphasised the need for “increased understanding of the importance of high-quality sleep for individuals.”

This study “adds to the growing body of data demonstrating strong and consistent links between sleep quality and risk of developing cardiovascular disease,” according to Dr. Devin W. Kehl, a cardiologist at Providence Saint John’s Health Center in Santa Monica, California who was not involved in the current study.

The majority of people are aware of how crucial it is to maintain a balanced diet and engage in regular exercise to reduce one’s chance of developing heart disease. Now, with studies like these and others, it is becoming more and more obvious that we also need to think of sufficient sleep duration and sleep quality in the same category as an important lifestyle habit, according to Dr. Devin Kehl.

Although not engaged in the study, board-certified physician Dr. Collin Johnston stated: “In my years of practising medicine, I have always believed that the western medical model must strive and focus more on the prevention of disease rather than merely the treatment of sickness.”

Dr. Johnston continued, “Unfortunately, during my medical school and residency training, a relatively small portion of time was spent learning the importance of basic health principles such as well-balanced nutrition, regular and frequent physical activity, and the integral role that quality “sleep hygiene” practises can play in helping prevent the onset of chronic health conditions.

Sleep and Heart Health During Pregnancy

The heart is put under greater stress during pregnancy, and some women experience cardiovascular issues at this time. For instance, high blood pressure can develop or get worse during pregnancy, which could have negative effects on both the mother and the unborn child.

Several pregnant women struggle with insomnia, sleep apnea, and other sleep disorders, and research has linked these concerns to an increased risk of cardiovascular diseases both during and after pregnancy. With the aim of lowering hypertension and other cardiovascular problems, ongoing research investigations are attempting to determine how to make pregnancy sleep better.

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Gout due to deficiency of a protein found in joint fluid.

Gout due to deficiency of a protein found in joint fluid.

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A multinational research team discovered a novel molecular route that is thought to be the origin of gout and the path it takes to joint tissue disintegration.

A protein called lubricin, which is present in joint fluid, may represent a unique therapeutic target for the prevention and treatment of gout, according to researchers.

The discovery was made, in part, through research on a lady who had urate crystal formations and joint degradation but low blood urate levels.

Gout, a common kind of inflammatory arthritis, can make joints extremely painful, swollen, and stiff. A punishment for those Gout has often affected one joint at a time since ancient times. Frequently the joint at the base of the big toe.

According to the American College of Rheumatology, the illness affects more than 3 million people in the US. Men. Also, postmenopausal women and persons with kidney problems are more prone to the condition.

An innovative molecular mechanism that causes gout and leads to the erosion of joint tissue has been discovered by an international research team headed by the University of California San Diego School of Medicine. The journal Arthritis & Rheumatology reported the researchers’ findings.

What is Gout?

An extremely painful, swollen, and stiffening form of arthritis known as gout generates these symptoms in the joints. The metatarsophalangeal joint, which is located at the base of the big toe, is typically affected. The body having too much uric acid is its main cause.

More than 3 million Americans suffer from gout, which is the most prevalent kind of inflammatory arthritis in men. Additionally, females are more prone to get gout after menopause despite the fact that disease is generally less likely to harm them.

Gout episodes can start suddenly and may continue to happen over time. This persistent recurrence can be quite painful and gradually destroy the tissue surrounding the inflammation. Obesity, cardiovascular disease, and hypertension are gout risk factors.

Unusual case study on gout

Purines, which are present in the body, meat, and some beverages, are broken down by the body to produce uric acid.

Uric acid crystals may grow inside a joint as a result of hyperuricemia. This is a high quantity of uric acid in the blood and promotes inflammation.

High uric acid levels are also frequently found in the joint fluid of gout sufferers. Although not invariably, gout can be caused by hyperuricemia. Up to 21% of the population may have asymptomatic hyperuricemia, according to one study.

Dr. Robert Terkeltaub is a professor at the University of California San Diego School of Medicine. He is section chief of rheumatology at the Veterans Affairs San Diego Healthcare System. Also, he is the study’s senior author, stated: “There are factors well beyond having a high serum rate to determine who gets gout, who doesn’t get gout.”

Factors that can cause gout

The researchers’ investigation of a 22-year-old lady with an atypical case of gout was included in their report. She had urate crystal formations and joint degradation, but her blood tests did not reveal elevated urate levels.

Researchers employed RNA-sequencing, a technology that gives a quantitative analysis of messenger RNA molecules in a biological sample, and whole genome sequencing, an investigation of an organism’s entire DNA composition, for their study.

In order to pinpoint a molecular route underlying the patient’s condition. They also used quantitative proteomic techniques, a method that enables a thorough examination of proteins. They examined samples from the young woman, her parents, and unrelated individuals.

Finally, scientists discovered a chemical route that had been damaged in the young woman. Their research focused on lubricin, a protein that lubricates joints.

Researchers found that the woman’s joint fluid had many proteins that were lower than those of her parents’ joint fluid. Also, lower than the combined results from four healthy controls.

“We searched for something that would either be tenfold decreased in the sick… related to the mother or father and the control or tenfold increased in the patient relative to the mother or father and the healthy control,” the researcher explained. And we discovered that the patient had roughly a dozen proteins that had significantly lower levels, Terkeltaub added.

Lubricin was one of those proteins. The following analysis focused on 18 individuals who had uncontrolled hyperuricemia and common gout. Five of them also showed low lubricin levels.

Lubricin inhibits inflammation

In a different section of the investigation, scientists employed mice with and without lubricin. Interleukin-1β, an inflammatory cytokine, was administered into the animals’ knee joints.

The main enzyme that really produces uric acid, xanthine oxidase, was enriched in the cells known as macrophages in the joint lining of the mice that didn’t produce lubricin, according to Terkeltaub.

According to the experiment, lubricin prevents urate from crystallising in joints and inhibits the release of xanthine oxidase and urate via stimulating white blood cells.

Dr. Puja Paul Khanna, an associate professor in the department of Internal Medicine at the University of Michigan Medical School. He stated that the study suggests lubricin may function as a biomarker for gout.

“With the mice models, they are observing that even if you did not have a high level of uric acid, but you are already experiencing damage from those small little, you know, monosodium urate crystals. We have identified lubricin as the cause, so we could block that pathway, Khanna added. “The [monosodium urate] crystals have a higher possibility of accumulating and harming that joint if the mice are deficient, meaning [they] lack lubricin. Right? More research on the same is required in people.

Terkeltaub emphasised that the findings demonstrates that lubricin’s function extends beyond just lubricating joint tissues.

In addition to inhibiting the inflammation brought on by the crystals and limiting the formation of new crystals, lubricin is something that is “actually involved in what we term the homeostasis of uric acid in the joint,” according to the expert.

Terkeltaub noted that the individual’s lubricin and other molecule-controlling lubricin gene variations may have an impact on whether or not a person with hyperuricemia develops gout.

The development of gout

This study shows that more can be learned about the pathophysiology of gout, according to Dr. Theodore Fields, a rheumatologist from Weill Cornell Medicine and Hospital for Special Surgery in New York who was not involved in the study.

He stated, “We continue to have big information gaps about why some patients get gout and some don’t, even if both have the same level of serum urate. It makes perfect sense that factors like lubricin deficiency play a role in certain patients.

Further studies by Terkeltaub will focus on lubricin’s potential as a novel therapeutic target for the prevention and treatment of gout as well as gout biomarkers and biomarkers for other inflammatory diseases.

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How Bone Density May Be Linked to Dementia Risk?

How Bone Density May Be Linked to Dementia Risk?

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According to researchers, a decline in bone density may be associated with a higher risk of dementia.

Low bone density and dementia tend to develop at later age, but the researchers caution that they are unsure of why there may be a connection.

A nutritious diet and regular exercise, according to experts, are two strategies to enhance overall bone health.

A study was published in Neurology, the official journal of the American Academy of Neurology. People with low bone density may be more likely to develop dementia. 3,651 individuals with an average age of 72 whose medical histories and X-rays were examined by Dutch researchers.

Everybody underwent physical exams, including X-rays and dementia screenings, as well as interviews every four to five years.

Prior to the trial, none of the subjects had dementia. Among the conclusions were:

  • Dementia affected 688 people (19%) over an average of 11 years.
  • 90 of the 1,211 individuals with the lowest bone density who lived the longest had dementia.
  • During a decade, 57 of the 1,211 individuals with the highest bone density had dementia.

The researchers found that those with lower bone density were 42% more likely to develop dementia than those with higher bone density. Even after controlling for age, sex, education, other illnesses, medicinal use, and family history of dementia.

The study only demonstrates a connection, not cause and effect, the researchers noted.

Bone density and dementia

According to the researchers, bone density loss may occur in the early stages of dementia and, if it does, may be a sign of risk.

With that information, healthcare providers may focus on providing earlier and more regular screenings. Also, a better care to those who have bone loss.

The researchers also stated that little was known about a potential connection in the years preceding dementia and that inactivity and poor nutrition. Both of which are present in dementia patients, both cause bone loss, which is accelerated by inactivity.

The majority of the individuals in the study were Europeans over the age of 70. They poses a drawback in that the findings may not be generalizable to other races, ethnicities, and age groups.

Dr. Joel Salinas, is a behavioural neurologist, researcher at NYU Langone Health and the chief medical officer at Isaac Health in New York. He stated that he always believes that additional research is necessary to determine why there may be a relationship.

According to Salinas, “In this scenario, there could be a few reasons why there is an association between dementia and bone loss.”

He listed a few potential explanations:

  • These two illnesses have a strong connection to ageing.
  • Both disorders may be influenced by inflammation in some way.
  • nutrition, diet, and way of life.

Salinas continued, “Improving lifestyle factors like nutrition and activity levels can never be too late. Even if there are already symptoms of cognitive deterioration, putting out a conscious effort in these areas can help prevent the progression of dementia.

Common Bed Partners

In the elderly population, Low bone mineral density (BMD) and dementia frequently co-occur, with bone loss accelerating in dementia patients as a result of inactivity and poor nutrition. It’s unknown, though, how much bone loss already exists before dementia manifests.

The new findings are based on 3651 seniors (mean age 72 years, 58% women). These were dementia-free between 2002 and 2005 and participated in the Rotterdam Study.

Dual-energy radiography absorptiometry (DXA) was used to measure BMD at the femoral neck, lumbar spine, and overall body at that time. The trabecular bone score, which provides additional information like bone microarchitecture, was also calculated. Up to January 1st, 2020, participants were monitored.

Age, sex, education, physical activity, smoking status, body mass index, blood pressure, cholesterol, history of comorbidities (stroke and diabetes), and apolipoprotein E genotype were all taken into account while doing the analyses.

In the 688 people who underwent follow-up who got dementia, the majority (77%), had Alzheimer’s disease.

Preventing bone loss

Dr. Nahid Rianon, a professor of general medicine at McGovern Medical School at UTHealth Houston who was not involved in the study, responded to Medical News Today when asked what would account for the connection between poor bone density and dementia risk:

Although this is a very useful study, it is impossible to determine if low bone density causes dementia, whether dementia causes low bone density, or whether low bone density and dementia share a risk factor.

The findings are significant because each of the three hypotheses has a critical role to play. To prevent both fatal diseases, it is imperative to find out if they share a common cause.

According to Rivadeneyra, “Dementia and bone health are two typical diseases we all struggle with to some extent as we age, so it’s no surprise there would be a correlation.” “We are aware that smoking increases the risk of dementia, low bone density, and cardiorespiratory problems. As we age, alcohol misuse is also linked to weak bones and dementia. Many of these ‘age-related’ diseases we frequently see are caused by heart disease, prolonged pharmaceutical usage (for some medications), injuries and trauma, metabolic issues like thyroid disease or diabetes, and a strong family history (genetics).

Consuming a diet high in calcium and vitamin D is also essential.

Osteoporosis and women

Osteoporosis is a prominent factor in broken bones in older men and postmenopausal women. Although each bone in the body has the potential to fracture, hip, vertebral, and wrist fractures are the most common in older people.

According to Dr. Gayatri Devi, a neurologist at Lenox Hill Hospital in New York, “women have a higher risk of osteoporosis and dementia, which could be related to decrease of oestrogen after menopause.”

According to Devi, those who engage in less physical activity—often older adults due to conditions like heart disease, diabetes, and stroke—have lower bone density and, thus, are at a greater risk for dementia.

The crucial conclusion, she continued, is that treating low bone density can lower the risk of dementia, fractures, and hospitalisation. “I think that everyone over the age of 50 should get a baseline bone density test because there is a good treatment, either through medication or exercise.”

Study limitations and implications

Dr. Wiggins noted that although other studies have described such relationships, since the majority of the patients in this study were in their 70s and of European heritage, they might not apply to other populations.

We must be careful not to conclude that lower bone density directly causes dementia, he cautioned, since this study merely found a link between bone and brain health.

Board-certified neuropsychologist Dr. Karen D. Sullivan, who runs the Pinehurst, North Carolina-based practise I CARE FOR YOUR BRAIN and was not engaged in the study, said:

The results of this study suggest that dementia may be more likely to strike those with inadequate bone density. According to Dr. Sullivan, this study “adds to the persuasive body of literature that demonstrates that maintaining bone health integrity is a crucial component of successful ageing.

“Evidence-based techniques for enhancing bone health after age 50 include putting a premium on high-quality animal/plant protein, polyunsaturated fatty acids, fruits and vegetables high in potassium, fibre, and foods high in calcium and vitamin D having the greatest study backing. In order to maintain strong, healthy bones as we age, frequent weight-loading and resistance exercises are also necessary, the expert concluded.

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New combination could reduce the risk of Prostate cancer.

New combination could reduce the risk of Prostate cancer.

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The effectiveness of talazoparib plus enzalutamide in treating metastatic castration-resistant prostate cancer in adult males was investigated in the TALAPRO-2 international phase 3 clinical trial.

Comparing talazoparib and enzalutamide therapy to placebo and enzalutamide therapy, a 37% lower risk of cancer progression or death was observed.

In 2023, the Food and Drug Administration (FDA) is anticipated to make a decision on the use of this combination therapy to treat men with metastatic castration-resistant prostate cancer.

Prostate cancer affects one in eight men in the United States and is the second most frequent cancer in males after skin cancer, according to the American Cancer Society.

Male hormones called androgens, such testosterone, promote the growth of prostate cancer cells. Even when blood testosterone levels are controlled, prostate cancer occasionally still progresses. Castration-resistant prostate cancer is the term for this.

Metastatic castration-resistant prostate cancer is the term used to describe a type of cancer that has migrated from the prostate gland to other bodily tissues like the lymph nodes and bones.

Treatment for metastatic castration-resistant prostate cancer has greatly advanced in recent years. Despite these advancements, cancer might recur after therapy because existing medicines only have a temporary impact.

Pfizer researchers have combined the drugs talazoparib (Talzenna) and enzalutamide to create a breakthrough treatment for metastatic castration-resistant prostate cancer (Xtandi). In the phase 3 trial of TALAPRO-2, they evaluated the effectiveness and safety of this combination medication.

Dr. Neeraj Agarwal, professor of oncology and Presidential Endowed Chair of Cancer Research at Huntsman Cancer Institute, University of Utah, and principal investigator for TALAPRO-2, delivered the trial’s findings at the 2023 ASCO Genitourinary Cancers Conference.

Why this combination therapy?

Enzalutamide is a type of hormone therapy that has been approved for the treatment of prostate cancer in males. It functions by preventing testosterone from growing prostate cancer cells. Even after they have migrated to other parts of the body, without which they cannot proliferate.

The group of cancer medications known as poly-ADP ribose polymerase (PARP) inhibitors includes talazoparib. An enzyme (protein) called PARP is present in all cells and aids in the self-healing of injured cells. The repair activity of PARP in cancer cells is blocked by PARP inhibitors, which leads to the death of the cancer cells.

The FDA has authorised the PARP inhibitor talazoparib to treat germline (inherited) HER2-negative advanced breast cancer. However, has not yet licenced it to treat prostate cancer.

When combined with medications that restrict testosterone, PARP inhibitors may be beneficial for the treatment of advanced prostate cancer, according to earlier research.

This inspired Pfizer researchers to create a combination therapy that combines the testosterone-blocking drug enzalutamide with the PARP inhibitor talazoparib.

Study

Adult men from 26 different countries who had metastatic castration-resistant prostate cancer were included in the trial in December 2017.

At random, the participants were given one of the following:

  • Enzalutamide 160 mg once daily and talazoparib 0.5 mg were given to 402 individuals.
  • Or, for 403 individuals, a placebo and enzalutamide 160 mg once daily.

The TALAPRO-2 trial’s main goal was to determine whether adding talazoparib to enzalutamide extends radiographic progression-free survival (rPFS)—the period of time patients remain cancer-free—in comparison to placebo plus enzalutamide.

To see if any study participants had defective DNA repair genes, the researchers also analysed the DNA from the cancer cells of all study participants.

Drug combo lowers cancer progression risk

The median follow-up period for the combination therapy group was 24.9 months. However, the group receiving placebo + enzalutamide experienced a median follow-up period of 24.6 months.

According to the findings, talazoparib plus enzalutamide significantly decreased the risk of disease progression or mortality compared to placebo and enzalutamide by 37%. This was true whether “homologous recombination repair,” or DNA repair gene mutations, were present or not (HRR).

Dr. Andrew J. noted that TALAPRO-2, which joins the PROPEL research, is the second randomised phase 3 trial to show a benefit with combination [androgen receptor] plus PARP inhibition in delaying rPFS in the first line [metastatic castration-resistant prostate cancer] context.

According to Dr. Armstronf, “the delays in rPFS range from > 50% relative improvements in HRR+ patients to 30-40% improvements in HRR-undetected individuals.

The results of TALAPRO-2 “differ from what was seen in the MAGNITUDE study with niraparib and abiraterone. Those without HRR deficiency (biomarker negative) group were stopped early due to lack of efficacy,” added Dr. Cora N. Sternberg, a genitourinary cancer specialist at Weill Cornell Medicine who was not involved in the study.

Data on overall survival were “immature” when the trial findings were announced. This indicates that more research is required to evaluate whether combination therapy with talazoparib and enzalutamide extends patient survival when compared to placebo and enzalutamide.

Is the combination therapy safe?

The study assessed any negative effects that men may have had from combination therapy.

The most frequent negative consequences were:

  • (65.8%) Anemia
  • reduction in neutrophil count (35.7%)
  • exhaustion (33.7%)
  • reduction in platelet count (24.6%)
  • Leukocyte count dropped (22.1%).
  • a backache (22.1%)
  • loss of appetite (21.6%
  • sickness (20.6%).

According to Dr. Zorko, the severe anaemia and neutropenia in the combination therapy group are not surprising given what is known about the side effects of PARP inhibitors.

Also, he advised that “before beginning combination therapy, consideration should be given to the necessity for transfusions and dose cessation. Particularly since 49% of patients had anaemia previous to therapy.”

The time toxicity required to obtain transfusions and supportive care in the clinic may further lessen patients’ enthusiasm for this oral combo therapy, the doctor added.

According to Dr. Armstrong, “there is higher toxicity and cost to patients getting combination [treatment], but these are tolerable for most patients and do not seem to impede quality of life in the long run in most patients with [dose] changes and side effect control.”

Study limitations and next steps

The primary limitations of this trial, according to Dr. Scott T. Tagawa, professor of medicine and urology at Weill Cornell Medicine who was not involved in it, include “early data for overall survival as well as [unknown] long-term adverse events.”

Dr. Zorko added: “In the trial, only 5.2% of patients had received abiraterone treatment in the past. We will see more patients in this area as they become castration-resistant as [triple therapy with] androgen-deprivation therapy, docetaxel, abiraterone/prednisone is used more frequently in the metastatic hormone-sensitive prostate cancer setting, but whether this specific subgroup benefits will be interesting to see.

The final stage of medication development was the phase 3 clinical trial. The FDA must now analyse the results of the clinical trials and make a determination regarding the applicability of this therapy to patients with metastatic castration-resistant prostate cancer. In 2023, the FDA is anticipated to make a decision regarding the clinical application.

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Common sweetener in high doses may suppress immune system.

Common sweetener in high doses may suppress immune system.

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According to a recent study, sucralose, an artificial sweetener, lowers immunological responses in mice when given in large amounts. In particular, it lessens their T cells’ level of activation. Researchers emphasise that sucralose ingestion by humans in usual amounts is unlikely to be detrimental.

Researchers plan to investigate if this popular sweetener could be utilised to calm down overactive immune systems in the future in high doses.

Sucralose, which goes by the brand name Splenda, is one of several artificial sweeteners that have been given the go-ahead for usage in the US. The sugar substitute has 600 times more sweetness than regular sugar.

Sucralose was given the go-ahead by the US Food and Drug Administration in 1999 to be used as a general-purpose sweetener for food.

In order to better understand how nutrition affects disease, Dr. Karen Vousden’s team at the Francis Crick Institute in London decided to study sucralose. She is a specialist in cancer biology.

“Sweetener consumption is rising quickly around the world, and comprehensive research by numerous regulatory bodies have demonstrated that they are safe at levels of usual consumption,” she said.

There have been reports in recent years suggesting that sweeteners may have more impacts than previously believed, including an impact on the gut flora. Hence, we conducted a study to examine these sweeteners’ impact on mice. Karen Vousden, Ph.D.

They recently had a publication about their study appear in Nature. It indicates the scientists discovered that sucralose lowers mice’s immune systems when taken in large dosages.

Recommended sucralose consumption

Sucralose has an acceptable daily intake (ADI) of 5 milligrammes per kilogramme of body weight per day, as set by the FDA. It has an ADI set by the European Food Safety Authority (EFSA) of 15 mg per kg of body weight per day.

Sucralose amounts to 12 milligrammes every packet of Splenda. In the United States, a person weighing 150 pounds can consume 340 mg of sucralose per day and still meet the ADI.

The researchers provided mice with access to water that was comparable to the ADI suggested by the EFSA (.72 mg) and the FDA for rodents for the experiments they conducted for their study (.17 mg).

Higher doses of sucralose

In order to examine the potential impact of sucralose on the immune system, the researchers conducted a number of laboratory tests on the T cells, a subset of white blood cells, of mice and people.

In one experiment, scientists fed mice either 0.17 or 0.72 mg of sucralose or sodium saccharin, a chemically unrelated sweetener (NaS). For several cell types, neither the amount of sucralose nor the presence of NaS had any discernible impact.

Another experiment assessed the homeostatic expansion of donor T cells in mice that were given sucrose but were unable to develop mature T cells or B cells. The growth of vital adaptive immune system cells was only prevented by sucralose.

Overall, results from numerous studies indicated that high sucralose exposure reduces T cell proliferation and differentiation.

Dr. Vousden, the senior author of the study, told that the team was shocked that “the effect was so evident across several mice models” due to sucralose’s poor absorption.

Sucralose did not appear to affect the activity of other immune cells, which shocked her team as well. “We were also startled to discover such a particular effect of sucralose on T-cells — none of the other sweeteners had this effect,” she said.

Effects of sucralose

Sucralose or NaS administration to mice for up to 12 weeks did not influence their dietary habits or body weight, according to the research. It also had no discernible impact on the mice’s fasting insulin levels or glucose tolerance.

Sucralose has been demonstrated to have an impact on the gut microbiota in certain studies, including one from 2008. But, in this most recent publication, researchers found “no consistent alteration in the bacterial species” in the mice given sucralose-treated stools.

The researchers also opted to investigate the medicinal potential of sucralose in the management of autoimmune diseases. They did this by administering sucralose to NOD (nonobese diabetic) mice.

According to Vousden, sucrose does not necessarily have a detrimental impact on the immune system. The findings suggest that the sweetener might one day be utilised therapeutically to treat autoimmune diseases, according to her.

The researchers treated mice that were engineered to be predisposed to type 1 diabetes, an autoimmune disorder that induces T cells to assault pancreatic cells, excessive dosages of the sweetener to test this notion in animals. Just approximately a third of the mice given the sweetener acquired diabetes after about 30 weeks; in contrast, all of the animals given simply water got the disease.

In the event that human studies reveal a similar outcome, according to Zani, he could imagine the sweetener being used in conjunction with more traditional immunosuppressive medications. As a result, doctors might be able to reduce the dosages of these medications. Walther believes that this line of enquiry is promising, particularly in light of the fact that sucralose is inexpensive to produce and would have less negative side effects.

long-term use of sucralose

In a 2018 study, Dr. Fabio Cominelli of Case Western Reserve University School of Medicine in Ohio discovered that sucralose consumption by mice may negatively affect the intestinal flora. Dr. Cominelli is the director of the Digestive Health Research Institute.

Dr. Cominelli, who was not involved in the current study, stated that he was unsure of the reason why the microbiome did not undergo significant changes as reported by the researchers.

He did, however, draw MNT’s attention to the fact that the rodent testing relied on doses of the sweetener that are far greater than what humans generally ingest, meaning that the article may not be relevant to scientists interested in the long-term effects of sucralose on humans.

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Focused ultrasound can improve Parkinson’s symptoms?

Focused ultrasound can improve Parkinson’s symptoms?

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In a recent study, a novel, non-invasive method of using focused ultrasound to lessen Parkinson’s disease symptoms was presented. In order to disrupt the neural network that causes uncontrolled movement and motor dysfunction, the approach entails deleting a tiny neuron cluster.

Twice as many research participants received the new treatment than those who received sham care, and these improvements in symptoms frequently sustained for at least a year.

An innovative, noninvasive strategy for lowering dyskinesia, or uncontrollable movements, and motor impairment in Parkinson’s disease patients is presented in a recent study. Focused ultrasound is used in the novel technique.

When compared to trial participants who underwent a sham, or placebo, therapy, twice as many people reported improvement in dyskinesia and motor impairment three months after undergoing the incision-less procedure.

In 77% of individuals who responded to the medication, the gains persisted for up to a year. Patients who receive focused ultrasound therapy often return home the same day.

Gait issues, speaking difficulty, and eye disruption were among the infrequently reported negative effects by the researchers. The group that received the treatment experienced more severe adverse effects than the group that received a placebo.

Focused ultrasound

Focused ultrasound is a minimally invasive, non-surgical technique that causes an ablation in a region that reduces Parkinson’s and tremor symptoms. To produce a clear thermal lesion deep into the brain without harming nearby structures, we use focused ultrasonic waves. The basal ganglia are what we are primarily aiming for. A set of brain regions are involved in the coordination and control of movement. We employ a thermal imaging equipment for magnetic radiofrequency imaging (MRI) during the procedure. This gauges alterations in the skull’s temperature and enables us to guarantee the patient’s security.

The treatment is fantastic because it allows us to work on really delicate places securely, effectively, and with very minimal adverse effects.

Dopamine and L-DOPA

Parkinson’s disease is caused by low levels of the neurotransmitter dopamine in the substantia nigra of the brain. This is brought on by the death of neurons that produce dopamine.

The predominant idea holds that autophagy, the brain’s housekeeping mechanism, has failed, causing an accumulation of waste that impairs brain function.

Dopamine synchronises various brain regions so that they are communicating with one another at the same frequency, according to Dr. Jean-Philippe Langevin, director of the Pacific Neuroscience Institute’s Restorative Neurosurgery and Deep Brain Stimulation Program, who was not involved in the study.

“Consider all these parts of the brain as walkie-talkies or phones trying to communicate, but the frequency at which they’re trying to communicate is off,” said Dr. Langevin. Movements become stiff, hesitant, and tremble as a result, and are no longer flowing.

Dr. Langevin stated that the absence of dopamine causes the motor system of the brain, which regulates movement, to be “quite noisy.” Researchers can actually recognise electrical noise as this “noise.” According to recent research, Parkinson’s disease actually causes some neuronal frequencies to rise.

Levodopa, also known as L-DOPA, which replenishes dopamine in the brain, is the most widely used medication for the illness.

Yet, for many people, the dyskinesia and motor dysfunction they encounter are genuine side effects of L-DOPA therapy. Over time, the medication’s effectiveness deteriorates as well.

New treatment

The novel method examined in the trial is based on an essential tremor medication that was previously authorised in 2016.

A small group of neurons in the globus pallidus area of the brain are removed or ablate during focused ultrasound therapy. By leaving scarring on the tissue, ablation causes tissue destruction.

Dr. Howard M. Eisenberg, co-author of the study and professor of neurosurgery at the University of Maryland Medical System, with the following explanation of how a little more than 1,000 sound energy beams ablate the target tissue:

“Like light, sound can be concentrated. Imagine you had a magnifying glass when you were a child. If you focused the sun’s rays on a piece of paper, you would receive a tiny dot of light that would then transform into heat and burn a hole in the paper. With sound, we may achieve the same results.

When the beams are concentrated and the intensity is strong enough, “you can burn a little hole in the brain” precisely at the target location without harming surrounding tissue, he told us.

In essence, Dr. Eisenberg said, “that’s how it works: Back to the future, similar to ablation that was done years ago for essential tremor, but using different technology.”

According to Dr. Eisenberg, the dyskinesia and motor dysfunction are not always brought on by the ablated neurons. Instead, “it’s a system of targets that are interconnected nuclei, and you’re interrupting that system,” he said.

Motives for excitement

If the procedure enables Parkinson’s patients to take less L-DOPA medication, then there are many reasons to be optimistic, according to Dr. Langevin.

According to Dr. Eisenberg, based on prior experience with essential tremor ablation, we can anticipate benefits in roughly 80% of patients, and they might last at least five years.

However, not every participant in the research benefited from this treatment. A few participants, according to Dr. Eisenberg, might have skulls that are less effective at transmitting acoustic energy.

The reason for this is that the skull is made up of two hard layers of bone sandwiched by a softer layer, “like an Oreo biscuit,” rather than being one solid piece of bone.

Focused ultrasound vs. DBS

Dr. Eisenberg pointed out that deep brain stimulation is thought to be more successful for treating essential tremors than ablation (DBS). DBS stimulates tissue rather than destroying it. Furthermore, Parkinson’s dyskinesia and motor disability are treatable by DBS.

DBS, however, necessitates creating one or more tiny holes in the skull through which a wire is placed and directed to the desired location in the brain. The wire is then attached to a tiny neurostimulator that has been inserted into the chest.

“They won’t consider it even though we always explain that deep brain stimulation has advantages over focused ultrasound,” Dr. Eisenberg said of individuals who would prefer it instead. Hence, it’s beneficial for individuals who simply don’t want deep brain stimulation, which is understandable.

Yet, he added, the advantages provided by the new focused ultrasound approach are still potent enough to be life-altering.

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