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Faulty regulation of copper levels in tissues plays a major role in a wide range of illnesses, including Alzheimer’s disease, Parkinson’s disease, and motor neuron disease. An investigation of molecules that carry copper in the bloodstream has provided new leads for diagnosis and treatment.

The metal copper is crucial for a healthy metabolism, and yet, scientists know surprisingly little about how the body transports it and maintains optimum levels in tissues.

Bonded to protein molecules, copper is a vital component of numerous enzymes that catalyze key metabolic reactions.

“Biochemists have known about the importance of copper in the human body for a long time, but even they do not know, for example, how this element reaches from our food to the right destinations, i.e., various copper enzymes,” says Prof. Peep Palumaa, head of the Research Group of Metalloproteomics at Tallinn University of Technology in Estonia.

Copper is present in trace amounts throughout the body. The highest concentrations occur in areas of the body that have extremely high activity, such as the liver, brain, heart, kidneys, and skeletal muscle.

Multiple roles

Among its many roles, the metal is vital for producing energy during cell respiration, making red blood cells, mounting immune responses, and maintaining nerve cells.

In excess, however, it can trigger the production of destructive free radicals and contribute to inflammation.

Research has linked the faulty regulation of copper levels to several neurodegenerative illnesses, including Menkes syndrome, motor neuron disease, Parkinson’s disease, and Alzheimer’s disease.

A study that Medical News Today reported on in 2013, for example, found that when copper accumulates in the brain, it promotes the development of the beta-amyloid plaques that are the hallmark of Alzheimer’s disease.

The study found that copper not only inhibits the removal of soluble beta-amyloid molecules from the brain but also encourages them to clump together to form insoluble plaques.

Biochemists have been trying to get a better grasp of how the body maintains optimum levels of copper in its tissues and what happens when this homeostatic process goes awry.

The knowledge could help them develop new ways to diagnose, monitor, and treat diseases that involve the breakdown of copper homeostasis.

As part of this endeavor, Prof. Palumaa and his colleagues wanted to find out how copper is transported around the body in the bloodstream.

Unusually for science, they discovered that the process was less complicated than they had expected. Previously, biochemists believed that three proteins play a role in transporting copper, but, according to the new study, only one is a major player.

Their results appear in Scientific Reports.

Affinity for copper

To measure each protein’s affinity for copper — meaning how tightly it binds to copper ions — the researchers developed a new and innovative approach called liquid chromatography and ICP-MS (inductively coupled plasma mass spectrometry). These biochemical techniques separate and identify molecules that are present in trace amounts in a biological fluid, such as blood or cerebrospinal fluid.

The scientists found that in the blood, about 75% of copper ions are bound to an enzyme called ceruloplasmin, while about 25% are bound to an enzyme called albumin.

However, ceruloplasmin binds to copper so tightly that it is unlikely to play a role in transporting the metal to where it is needed. The enzyme’s main job appears to be helping another protein transport iron in the blood.

Albumin, on the other hand, binds to copper much less strongly and is likely to be the principal copper transporter.

The researchers found that a tiny proportion of copper in the blood (about 0.2%) also binds to an amino acid called histidine. They speculate that histidine acts as a catalyst, helping release copper from albumin when it reaches a destination such as the liver.

Biochemists had assumed that a further protein, called alpha-2 macroglobulin, also transports copper. However, Prof. Palumaa and his colleagues report that in their experiments, it did not bind to copper in blood plasma in significant quantities.

Regulating copper levels

The research is a product of collaboration between scientists at Tallinn University of Technology and the Swedish pharmaceutical company Wilson Therapeutics AB.

Wilson Therapeutics AB’s lead product is Decuprate, which is a promising therapeutic agent to treat Wilson’s disease, a rare genetic disorder that causes copper to accumulate in toxic quantities in the liver, brain, and other tissues.

By binding to copper, Decuprate promotes its excretion from the body.

In their paper, Prof. Palumaa and his colleagues say that their findings could make it possible to detect the disturbances in copper metabolism that characterize diseases such as Wilson’s and Alzheimer’s.

Their research could also provide new ways to monitor the effectiveness of drugs such as Decuprate in regulating copper levels.

“[Our] research findings can be used for various applications. First, they help to understand the normal copper metabolism in the body, which has a direct diagnostic value. Second, these results also help to identify disturbances in the body’s copper metabolism. The latter occur in several genetic diseases, such as Wilson’s and Menkes disease, as well as the most common neurodegenerative disease — Alzheimer’s disease.”

– Prof. Peep Palumaa

He continues, “In addition to specific diagnoses, the effect of pharmaceuticals normalizing copper metabolism that are used for the treatment of the abovementioned diseases can also be monitored through copper equilibrium in blood.”

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Photo Taken In Oradea, Romania

A new study has identified how ketamine can combat difficult-to-treat depression.

New research has revealed the specific parts of the brain that ketamine affects when doctors use it to treat people with difficult-to-treat depression.

The study, which appears in the journal Translational Psychiatry, may open the door to new therapies in the treatment of depression.

According to the Centers for Disease Control and Prevention (CDC), in the United States, about 7.6% of people over the age of 12 have depression during any 2-week period. The CDC describe depression as a sad mood that extends for a long period and affects a person’s ability to live a normal life.

When severe, depression can have a serious negative effect on a person’s life, sometimes leading to suicidal thoughts.

Experts do not fully understand why some people experience depression, although the National Institute of Mental Health suggest that genetic, environmental, biological, and psychological factors may play a role. It is treatable with medication, psychological therapy, or a combination of the two.

Previous research has made it clear that the drug ketamine can be an effective antidepressant, and some scientists have proposed it as a treatment in cases of depression that do not respond to conventional treatments.

However, precisely how and why ketamine functions as an antidepressant is less clear. As a consequence, the authors of the present study wanted to identify precisely what effects ketamine has on the brain of a person who is not responding to conventional treatments. They hope that this research may lead to better treatment options for these individuals.

Suicide prevention

If you know someone at immediate risk of self-harm, suicide, or hurting another person:

  • Ask the tough question: “Are you considering suicide?”
  • Listen to the person without judgment.
  • Call 911 or the local emergency number, or text TALK to 741741 to communicate with a trained crisis counselor.
  • Stay with the person until professional help arrives.
  • Try to remove any weapons, medications, or other potentially harmful objects.

If you or someone you know is having thoughts of suicide, a prevention hotline can help. The National Suicide Prevention Lifeline is available 24 hours per day at 800-273-8255. During a crisis, people who are hard of hearing can call 800-799-4889.

Looking at ketamine’s effect in the brain

To do this, the researchers gave participants doses of ketamine that were low enough not to have an anesthetic effect and then took images of their brains using a positron emission tomography (PET) camera.

According to the study’s first author, Dr. Mikael Tiger, a researcher at the Department of Clinical Neuroscience at the Karolinska Institutet in Solna, Sweden, “In this, the largest PET study of its kind in the world, we wanted to look at not only the magnitude of the effect but also if ketamine acts via serotonin 1B receptors.”

“We and another research team were previously able to show a low density of serotonin 1B receptors in the brains of people with depression.”

By using a radioactive marker that binds to a person’s serotonin receptors, the PET images could highlight what effects ketamine was having on these receptors, which play a crucial role in depression by modulating the amount of serotonin that a person receives. Experts believe that low levels of serotonin correlate to more severe experiences of depression.

The authors of the study recruited people through internet advertising. After receiving 832 volunteers, the authors reduced this number to 30 to make sure that the participants were as relevant to the study as possible.

Other than having major depressive disorder (MDD), the participants were healthy. They had not responded to previous treatment for MDD.

The researchers split the participants into two groups, treating 20 people with ketamine and the other 10 with a placebo.

The study was a randomized, double-blind, placebo-controlled study, meaning that neither the doctors nor the participants initially knew to which group each participant belonged.

Prior to the treatment, the researchers took a baseline scan of the participants’ brains. They took a second scan in the days following the treatment.

For the second phase of the study, 29 of the participants agreed to take ketamine twice a week for 2 weeks.

Serotonin reduced, dopamine increased

Using a rating scale for depression, the researchers found that 70% of the participants in the second phase of the study responded to the ketamine.

Furthermore, after analyzing the PET images, the authors found that the ketamine was affecting the participants’ brains in a previously unidentified manner, reducing the output of serotonin but increasing the output of dopamine, which is also important for mood regulation.

According to the last author of the study, Dr. Johan Lundberg, research group leader at the Department of Clinical Neuroscience, Karolinska Institutet, “We show for the first time that ketamine treatment increases the number of serotonin 1B receptors.”

“Ketamine has the advantage of being very rapid-acting, but at the same time, it is a narcotic-classed drug that can lead to addiction. So it’ll be interesting to examine in future studies if this receptor can be a target for new, effective drugs that don’t have the adverse effects of ketamine.”

– Dr. Johan Lundberg

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According to a new study analyzing the data of thousands of people, an excessive intake of a certain kind of amino acid — present in protein-rich foods — is associated with a higher cardiometabolic risk.

person slicing meat
A new study in humans adds to the evidence that protein-rich foods, such as meat, may have a negative effect on heart health.

Many people follow diets that are high in protein, which can help with weight loss and building muscle mass.

However, increasingly, researchers are starting to question whether protein-rich foods provide enough benefits to offset the potential risks.

For the most part, various recent studies have suggested that high protein foods may affect the health of the heart and the cardiovascular system.

For example, a study in animal models that Medical News Today covered last week found that diets that are high in protein may be directly responsible for cardiovascular problems, such as atherosclerosis.

Now, hot on its heels, a new study in humans points out a link between eating foods with a high sulfur amino acid content — typically high protein foods — and an increased cardiometabolic risk.

The research — the findings of which appear in EClinicalMedicine — comes from Pennsylvania (Penn) State University in State College.

Proteins comprise tiny compounds called amino acids, which vary in their components. Some contain atoms of the element sulfur, which gives them their name: sulfur amino acids.

Cardiometabolic risk and diet

Two sulfur amino acids occur in protein-rich food. These are methionine, an essential amino acid, and cysteine, a semi-essential amino acid.

The human body needs these amino acids to function well, and it must obtain them from a food source. The body cannot synthesize essential amino acids, and it cannot make enough of the semi-essential ones.

However, as with many other nutrients, if they are present in excessive quantities, amino acids can end up doing more harm than good.

This is what Penn State researchers noticed when they looked at the diets and health status of 11,576 individuals, whose data they accessed via the third National Health and Nutrition Examination Survey (NHANES III), which the Centers for Disease Control and Prevention (CDC) conducted.

The researchers came up with a composite cardiometabolic disease risk score assessing each participant’s risk of developing cardiometabolic problems, such as heart disease, stroke, and diabetes.

To do this, they measured the levels of tell-tale biomarkers — including cholesterol, triglycerides, glucose (sugar), and insulin — in the participants’ blood following a 10–16 hour fast.

“These biomarkers are indicative of an individual’s risk for disease, just as high cholesterol levels are a risk factor for cardiovascular disease,” explains study co-author Prof. John Richie.

“Many of these levels can be impacted by a person’s longer-term dietary habits leading up to the test,” Prof. Richie adds.

The researchers also analyzed information about the participants’ dietary habits, which included nutrient intake calculations. They excluded from the study any individuals who reported having an overly low intake of sulfur amino acids.

‘First epidemiologic evidence’

The team’s final analysis, which accounted for body weight measurements, revealed that the participants had an average intake of sulfur amino acids that was almost 2.5 times higher than the estimated average requirement of 15 milligrams per kilogram of body weight per day.

“Many people in the U.S. consume a diet rich in meat and dairy products, and the estimated average requirement is only expected to meet the needs of half of healthy individuals,” points out study co-author Xiang Gao.

“Therefore, it is not surprising that many are surpassing the average requirement when considering these foods contain higher amounts of sulfur amino acids,” says Gao.

Moreover, the investigators found that participants with higher sulfur amino acid intakes also tended to have higher composite cardiometabolic risk scores.

This association remained in place even after the researchers accounted for confounding factors, including age, biological sex, and a history of health conditions such as hypertension and diabetes.

As for the source of the sulfur amino acids, the team said that they were present in almost all foods, excluding grains, fruit, and vegetables.

“Meats and other high protein foods are generally higher in sulfur amino acid content,” notes lead author Zhen Dong, Ph.D.

“People who eat lots of plant-based products like fruits and vegetables will consume lower amounts of sulfur amino acids. These results support some of the beneficial health effects observed in those who eat vegan or other plant-based diets,” Dong adds.

The researchers caution that the current findings are, so far, only observational, pointing to an association rather than verifying causality.

“A longitudinal study would allow us to analyze whether people who eat a certain way do end up developing the diseases these biomarkers indicate a risk for,” notes Prof. Richie.

Nevertheless, he stresses that the recent study shows that researchers should pay more attention to the possible risks associated with dietary amino acids.

“For decades, it has been understood that diets restricting sulfur amino acids were beneficial for longevity in animals. This study provides the first epidemiologic evidence that excessive dietary intake of sulfur amino acids may be related to chronic disease outcomes in humans.”

– Prof. John Richie

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New research uses high quality data to find that the type 2 diabetes drug rosiglitazone raises the risk of adverse cardiovascular events by 33%.

Rosiglitazone is a drug originally developed to treat type 2 diabetes. The United States Food and Drug Administration (FDA) approved it in 1999 under the name Avandia.

Although Europe suspended the drug due to concerns about its adverse effects on heart health, and the United States restricted its use, the research on its safety has so far yielded mixed results.

Now, a new study, appearing in the journal The BMJ has used more reliable data to investigate the effects of this drug on cardiovascular health.

Joshua D. Wallach, who is an assistant professor in the Department of Environmental Health Sciences at Yale School of Public Health in New Haven, CT, is the lead author of the new paper.

The need for more accurate data

The FDA approved rosiglitazone in 1999, a year ahead of Europe, note Wallach and colleagues in their paper.

Regulatory bodies warned about its potential effects on heart failure as early as 2006, and a meta-analysis of several trials pointed to a 43% higher risk of heart attack in 2007.

As a result, by 2010, the drug was pulled off European markets because it raised the risk of heart attack and stroke.

In the U.S., the drug is still available, although it features warnings on its packaging, and the FDA restricted its availability in 2010-2011.

The fact that the drug is still available is primarily due to the mixed results yielded by the investigation into the drug’s cardiovascular effects.

However, the new research suggests that these mixed results are due to the poor quality of the data that these previous studies used.

Namely, these previous papers did not have access to “individual patient data (IPD),” that is, raw data, such as the medical records of patients, instead of summary-level data, which are the final results of clinical trials, for example.

Studying rosiglitazone and heart health

To rectify this methodological problem, Wallach and colleagues set out to analyze over 130 clinical trials; the researchers had access to IPD for 33 of these trials. This totaled 48,000 adult patient data, of which researchers had IPD for 21,156.

The clinical trials were randomized, controlled, phase II-IV trials that had studied and compared the effects of rosiglitazone with any other control for at least 24 weeks.

“The control group was defined as patients who received any drug regimen other than rosiglitazone, including placebo,” explain the researchers.

The team examined the outcomes of “acute myocardial infarction, heart failure, cardiovascular-related death, and noncardiovascular-related death” in their analysis of trials for which they had IPD.

For the other trials, the researchers examined myocardial infarction and cardiovascular-related death only, using summary-level data.

A 33% higher risk of cardiovascular disease

The analysis revealed a 33% higher risk of heart attack, heart failure, cardiovascular deaths, and noncardiovascular-related deaths combined for people who were taking the drug compared with people who were taking another control substance, including placebo.

Wallach and colleagues conclude:

“The results suggest that rosiglitazone is associated with an increased cardiovascular risk, especially for heart failure events.”

The findings also serve to emphasize the importance of using raw data to accurately assess the safety of a drug, say the authors.

“Our study suggests that when evaluating drug safety and performing meta-analyses focused on safety, IPD might be necessary to accurately classify all adverse events,” they write.

“By including this data in research, patients, clinicians, and researchers would be able to make more informed decisions about the safety of interventions.”

“Our study highlights the need for independent evidence assessment to promote transparency and ensure confidence in approved therapeutics, and postmarket surveillance that tracks known and unknown risks and benefits.”

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Experts know that processed red meats are likely to raise the risk of cardiovascular disease and death. But are unprocessed meats, fish, and poultry less harmful? New research investigates.

Several studies have established a link between consuming processed meat — such as bacon, hot dogs, sausages, and other similar meats — and an increased risk of cardiovascular disease (CVD) and death.

The higher amount of saturated fats in these foods, along with a higher level of salt and preservatives, might explain these associations. Newer research has suggested that even a low amount of these foods is enough to jeopardize health.

But what about other meats, such as unprocessed red meat, poultry, or fish? Do these foods affect cardiovascular risk and longevity in the same way?

Here, the research is more mixed. The results of several studies vary partly because the methods were different and partly because the existing prospective cohort studies had their limitations.

So, to fill this gap in the research, a group of scientists led by Victor W. Zhong, Ph.D., of Cornell University in Ithaca, New York, set out to conduct a new meta-analysis of 6 existing studies.

The pooled analysis appears in the journal JAMA Internal Medicine.

Studying intake of meat, poultry, and fish

Zhong and the team looked at prospective cohort studies that had been carried out across the United States, totaling 29,682 U.S. adults who did not have CVD at baseline.

Of the participants, 44% were men, and almost 31% were non-white.

Researchers had recorded the participants’ dietary data between 1985–2002 and clinically followed them for 30 years, until August 31, 2016.

Over a median follow-up period of 19 years, 6,963 adverse cardiovascular events and 8,875 all-cause deaths occurred.

Of the cardiovascular events, 38.6% were cases of coronary heart disease, 25% were stroke events, and 34.0% involved heart failure.

To define what constitutes 1 serving of meat and assess the participants’ diet, the researchers used the Willett Food Frequency Questionnaire.

“1 serving was equivalent to 4 [ounces] of unprocessed red meat or poultry or 3 [ounces] of fish. For processed meat, 1 serving consisted of 2 slices of bacon, 2 small links of sausage, or 1 hot dog,” explain the authors.

The median consumption in terms of servings of meat, poultry, and fish per week was 1.5 for processed meat, 3 for unprocessed red meat, 2 for poultry, and 1.6 for fish.

“Compared with participants with lower total intake of these four food types, participants with higher total intake,” write the authors, were more likely to:

  • be younger and male
  • be non-Hispanic black
  • be smokers, have diabetes, a higher body mass index (BMI), higher non-high-density lipoprotein (HDL) cholesterol levels, and consume more alcohol
  • have lower HDL cholesterol levels and eat a lower diet quality diet
  • have a higher incidence of CVD and death from any cause

The main outcome that the scientists looked for was the relative risk of CVD and all-cause mortality over the 30 years between people who consumed these different foods, as well as the difference in absolute risk over the same period.

They calculated the risks for each additional intake of 2 servings per week.

Up to 7% higher relative risk of death, CVD

Zhong and the team summarize the findings: the “intake of processed meat, unprocessed red meat, or poultry was significantly associated with incident cardiovascular disease, but fish intake was not.”

More specifically, the increased relative risks of CVD and all-cause mortality ranged from about 3% to 7%. “The increased absolute risks were less than 2% over the 30 years of follow-up,” add the authors.

More in-depth detail shows that for every 2 additional servings of processed meat per week, the relative risk of all-cause mortality rose by 3% compared with those who did not eat processed meat.

The same was true for each additional 2 servings of unprocessed meat.

The relative risk of CVD rose by 7% for every 2 servings of processed meat per week. For unprocessed red meat, this risk was 3%.

An increase of 2 weekly servings of poultry correlated with a 4% higher relative risk, whereas fish was not associated with CVD risk.

“People who consume more servings per week would have greater risks,” add the researchers.

Study of ‘critical public health’ importance

The authors deem the findings of “critical public health” importance. They also note that more research is necessary to strengthen the findings.

As it stands, the current study has some limitations, such as the self-reported nature of dietary data. This may have resulted in over or underestimation of the association.

Secondly, the scientists did not have any data on the method of food preparation. Whether the meat was fried or non-fried may have impacted the health outcomes.

Thirdly, the study only used one dietary measurement at the beginning of the study, but the dietary habits of the participants may have changed over time.

Finally, residual confounding, the observational nature of the study, and the fact that the data may only be limited to U.S. adults are further shortcomings of this research. Still, Zhong and team conclude:

“The findings of this study appear to have critical public health implications given that dietary behaviors are modifiable, and most people consume these four food types on a daily or weekly basis.”

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Assortment of fresh vegetables and fruit

A recent review and meta-analysis have investigated whether a plant pigment called quercetin could reduce the risk of cardiovascular disease. In particular, the authors identified that quercetin reduced blood pressure.

Chopped red onion
A compound that occurs naturally in a range of fruits and vegetables, including red onion, may help reduce blood pressure.

Globally, cardiovascular disease is responsible for about 17.3 million deaths each year. As the population’s average age increases, experts expect cardiovascular disease to rise in step.

Researchers have identified a range of lifestyle factors that increase the risk of cardiovascular disease, such as poor diet, low physical activity, smoking, and consuming alcohol. Certain biological markers, including high blood pressure, raised serum lipids, and high blood glucose levels, also predict cardiovascular disease.

Although lifestyle and medical interventions benefit most individuals, they do not work for everyone. For this reason, some researchers are focused on identifying novel ways to reduce cardiovascular risk.

Introducing quercetin

Researchers from Dongguan Shilong People’s Hospital of Southern Medical University in China are interested in quercetin. Quercetin is a flavonoid that naturally occurs in a range of foods, including vegetables, fruits, wine, nuts, red onions, kale, and black tea.

According to the authors of the recent review, “Accumulating evidence indicates that quercetin possesses protective anti-inflammatory as well as antioxidant effects and may be useful in treating a myriad of chronic conditions.”

However, despite some encouraging results, human studies — rather than animal studies or experiments on tissues — have produced inconsistent results. To date, researchers have carried out few meta-analyses to examine the pooled findings of these studies.

To address this issue, the authors of the current paper analyzed studies that investigated quercetin’s influence over a range of cardiovascular risk factors, including blood pressure, lipid profiles, and glucose levels. They published their findings in the journal Nutrition Reviews.

Reanalyzing recent studies

In their analysis, the scientists only included research papers that met certain criteria. All of the studies were randomized placebo-controlled clinical trials that had investigated the effect of quercetin for 2 weeks or more and had involved adults.

The scientists identified 17 relevant papers, which involved a total of 896 participants. The studies took place in six countries: Iran, United States, United Kingdom, Germany, Italy, and Korea.

Overall, they identified no significant effect of quercetin on glucose levels or lipid profiles. However, when they only analyzed data from trials that used a parallel design and lasted 8 weeks or longer, quercetin did appear to improve levels of high-density lipoprotein (HDL or “good”) cholesterol and triglycerides.

A study with a parallel design is one in which researchers compare two or more treatments; for instance, comparing the effects of quercetin against those of a control.

The greatest benefit of quercetin, however, was its effect on blood pressure. The findings showed that quercetin lowered both systolic and diastolic blood pressure. The authors write:

“The main conclusion was that dietary intake of quercetin significantly lowered [blood pressure].”

Benefits for blood pressure

Systolic blood pressure is the pressure in the arteries as the heart contracts, and diastolic blood pressure is the blood pressure when the heart is resting between beats. As an example, if someone’s blood pressure is 120/80 millimeters of mercury (mm Hg), the first number refers to systolic pressure, and the second number denotes diastolic pressure.

On average, quercetin reduced systolic blood pressure by 3.09 mm Hg and diastolic blood pressure by 2.86 mm Hg.

The authors explain that “a reduction in [blood pressure] of more than 10 mm Hg lowers cardiovascular risk by 50% for heart failure, by 35–40% for stroke, and by approximately 20–25% for myocardial infarction.”

The authors believe that “[t]he favorable effects of quercetin on [blood pressure] found in the current investigation support the use of quercetin as an adjunctive therapy in patients with hypertension.”

In other words, quercetin might enhance the benefits of taking hypertension medication and making lifestyle changes, thus helping reduce cardiovascular risk.

Limitations and holes

As the authors explain, the results are not yet conclusive, and many questions remain. They note that the changes in blood pressure varied depending on the type of quercetin formulation and how long the trials lasted.

The authors also noticed substantial differences among the findings of the studies. These differences might be, in part, due to the size of the trials in the analysis: Four of the 17 trials included fewer than 30 participants.

There were also differences in the design of the studies and the age, sex, and body mass index (BMI) of the participants. These differences make it difficult to generalize and compare among experiments.

Overall, the results are promising, but scientists need to conduct larger, longer-term clinical trials before they can confirm the full benefits of quercetin. If the compound eventually proves to reduce cardiovascular risk, it could benefit vast swathes of the population.

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Walnuts may not just be a tasty snack, they may also promote good-for-your-gut bacteria. New research suggests that these “good” bacteria could be contributing to the heart-health benefits of walnuts. In a randomized, controlled trial, researchers found that eating walnuts daily as part of a healthy diet was associated with increases in certain bacteria that can help promote health. Additionally, those changes in gut bacteria were associated with improvements in some risk factors for heart disease.

Kristina Petersen, assistant research professor at Penn State, said the study — recently published in the Journal of Nutrition — suggests walnuts may be a heart- and gut-healthy snack.

“Replacing your usual snack — especially if it’s an unhealthy snack — with walnuts is a small change you can make to improve your diet,” Petersen said. “Substantial evidence shows that small improvements in diet greatly benefit health. Eating two to three ounces of walnuts a day as part of a healthy diet could be a good way to improve gut health and reduce the risk of heart disease.”Previous research has shown that walnuts, when combined with a diet low in saturated fats, may have heart-healthy benefits. For example, previous work demonstrated that eating whole walnuts daily lowers cholesterol levels and blood pressure.

According to the researchers, other research has found that changes to the bacteria in the gastrointestinal tract — also known as the gut microbiome — may help explain the cardiovascular benefits of walnuts.“There’s a lot of work being done on gut health and how it affects overall health,” said Penny Kris-Etherton, distinguished professor of nutrition at Penn State. “So, in addition to looking at factors like lipids and lipoproteins, we wanted to look at gut health. We also wanted to see if changes in gut health with walnut consumption were related to improvements in risk factors for heart disease.”

For the study, the researchers recruited 42 participants with overweight or obesity who were between the ages of 30 and 65. Before the study began, participants were placed on an average American diet for two weeks. After this “run-in” diet, the participants were randomly assigned to one of three study diets, all of which included less saturated fat than the run-in diet. The diets included one that incorporated whole walnuts, one that included the same amount of alpha-linolenic acid (ALA) and polyunsaturated fatty acids without walnuts, and one that partially substituted oleic acid (another fatty acid) for the same amount of ALA found in walnuts, without any walnuts.

In all three diets, walnuts or vegetable oils replaced saturated fat, and all participants followed each diet for six weeks with a break between diet periods. To analyze the bacteria in the gastrointestinal tract, the researchers collected fecal samples 72 hours before the participants finished the run-in diet and each of the three study diet periods. “The walnut diet enriched a number of gut bacteria that have been associated with health benefits in the past,” Petersen said. “One of those is Roseburia, which has been associated with protection of the gut lining. We also saw enrichment in Eubacteria eligens and Butyricicoccus.”

The researchers also found that after the walnut diet, there were significant associations between changes in gut bacteria and risk factors for heart disease. Eubacterium eligens was inversely associated with changes in several different measures of blood pressure, suggesting that greater numbers of Eubacterium eligens was associated with greater reductions in those risk factors.

Additionally, greater numbers of Lachnospiraceae were associated with greater reductions in blood pressure, total cholesterol, and non-High Density Lipo-protein (HDL) cholesterol. There were no significant correlations between enriched bacteria and heart-disease risk factors after the other two diets.

Regina Lamendella, associate professor of biology at Juniata College, said the findings are an example of how people can feed the gut microbiome in a positive way. “Foods like whole walnuts provide a diverse array of substrates — like fatty acids, fiber and bioactive compounds — for our gut microbiomes to feed on,” Lamendella said. “In turn, this can help generate beneficial metabolites and other products for our bodies.” Kris-Etherton added that future research can continue to investigate how walnuts affect the microbiome and other elements of health.

“The findings add to what we know about the health benefits of walnuts, this time moving toward their effects on gut health,” Kris-Etherton said. “The study gives us clues that nuts may change gut health, and now we’re interested in expanding that and looking into how it may affect blood sugar levels.”

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A team at George Mason University, Fairfax, VA, has uncovered another electronic cigarette health concern. This time, it relates to stroke risk.

In recent years, the popularity of e-cigarettes has soared.

A 2016 study found that 10.8 million adults in the United States were current e-cigarette users. It is common for people to switch from traditional cigarettes to the e-variety because they think they are a healthier option.

But newly issued health warnings have pointed to the potential risks of smoking e-cigarettes. In June 2019, the U.S. saw an outbreak of lung injuries associated with e-cigarettes.

Experts believe that vitamin E acetate — an ingredient found in some e-cigarettes containing THC — may be the link.

In December 2019, the Centers for Disease Control and Prevention (CDC) reported that more than 2,500 individuals from the U.S., Puerto Rico, and the U.S. Virgin Islands were hospitalized or died as a result of using vapes, e-cigarettes, or associated products.

Recent studies, albeit small-scale, have found both benefits and risks to e-cigarettes.

One study that appears in PNAS found that nicotine from e-cigarette smoke caused lung cancer in mice as well as precancerous growth in the bladder.

However, a second study, appearing in the Journal of the American College of Cardiology, noted a significant improvement in vascular health within a month of a traditional smoker switching to e-cigarettes.

A trend among the young

Despite their nicotine content, the variety of e-cigarette flavors available has led to the products becoming a trend among young adults. There is also a concern this habit could lead to conventional cigarette smoking.

Equally worrying findings have come from a new study that appears in the American Journal of Preventive Medicine. The study found that young adults smoking both traditional and e-cigarettes face a significantly higher risk of stroke.

Using data from the 2016-17 Behavior Risk Factor Surveillance System (BRFSS), the study examined smoking-related responses from a total of 161,529 people aged between 18 and 44.

Just over half of the respondents were female, with 50.6% identifying as white and just under a quarter identifying as Hispanic.

The team calculated the adjusted odds ratios for strokes among those who currently smoked, former smokers who now used e-cigarettes, and people who used both.

“It’s long been known that smoking cigarettes is among the most significant risk factors for stroke,” says lead investigator Tarang Parekh from George Mason University.

“Our study shows that young smokers who also use e-cigarettes put themselves at an even greater risk.”

Tarang Parekh

An important message and a ‘wake-up call’

The study identified that young adults who smoked both traditional and e-cigarettes were almost twice as likely to have a stroke compared with conventional cigarette smokers.

This risk rose to almost three times as likely when compared with non-smokers. Results also showed there was no clear advantage to switching from traditional cigarettes to e-cigarettes.

However, people using e-cigarettes who had never smoked before did not display an increased stroke risk. This may be down to factors including young age and normal heart health.

This study relied on self-reported data, which is a limitation. However, the findings prove the need for large-scale, long-term studies to confirm which detrimental health effects e-cigarettes are causing and which ingredients are responsible.

“This is an important message for young smokers who perceive e-cigarettes as less harmful and consider them a safer alternative,” Parekh states.

According to Parekh, the results are “a wake-up call” for policymakers to urgently regulate e-cigarette products “to avoid economic and population health consequences.”

“We have begun understanding the health impact of e-cigarettes and concomitant cigarette smoking, and it’s not good.”

Tarang Parekh

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Researchers have found that living in polluted cities may cause the bones to be weaker and easier to break.

The researchers also found that city-dwellers exposed to toxic air have weaker hips and spines and are more prone to fractures

The Spanish researchers believe that bones are weakened because tiny pollutants seep into the blood when inhaled and speed up the ageing process.

A study carried out India of nearly 4,000 people found that those exposed to toxic particles had less bone density in their lower back and those who inhaled more toxic airborne particles had less bone mass in their spines and hips.

Meanwhile, previous studies have linked pollution to low levels of parathyroid hormone, which regulates calcium production, leading to more fragile bones.

Researchers found that smog-filled towns and cities have been linked to an increased risk of stroke, heart disease, lung cancer, acute respiratory diseases such as asthma and even dementia.

Although, there have only been a few studies into the effect of toxic airborne particles on bone health, the results have so far been inconclusive.

Researchers from the Barcelona Institute for Global Health in their latest paper, looked at 3,700 people who were all residents from 28 villages outside the city of Hyderabad in southern India between 2009 and 2012.

The researchers took measurements of PM2.5 and black carbon in the atmosphere in each village.

PM2.5 is the finest type of particulate matter, while black carbon is a larger toxin. Both come mainly from petrol and diesel vehicle exhausts.

Their analysis revealed average PM2.5 exposure was 33 micrograms per metre cubed (ug/m3) – far above the maximum 10ug/m3 levels recommended by the World Health Organisation.

By comparison, the average level is 13ug/m3 in London, 12ug/m3 in New York and 10ug/m3 in Sydney.

The researchers also cross-referenced pollution levels with X-rays measuring bone mass in participants’ lower back, known as the lumbar spine, and hip.

The results showed that exposure to air pollution was associated with lower levels of bone mass.

For every 3ug/m3 increase in fine particulate matter, there was a decrease of -0.57g of bone mass in the spine and -0.13g in the hip, while an increase of 1ug/m3 of carbon saw bone density shrink by -1.13g in the spine and -0.35g in the hip.

The study lead author, Otavio Ranzani said: “This study contributes to the limited and inconclusive literature on air pollution and bone health.

“Inhalation of polluting particles could lead to bone mass loss through the oxidative stress and inflammation caused by air pollution.’ The findings were published in the journal Jama Network Open.

However, a 2017 study by Columbia University of more than nine million people was the first to find a link between traffic fumes and fractures caused by osteoporosis.

Osteoporosis is a health condition that weakens bones, making them fragile and more likely to break.

The study linked pollution exposure to low levels of parathyroid hormone, which regulates calcium production, leading to weaker bones and more hospitalisations for fractures.

The study found hospital admissions for bone fractures were higher in communities with elevated levels of PM2.5, as more than 80 per cent of the world’s urban population is breathing unsafe levels of air pollution.

Described as an invisible killer, it causes an estimated seven million premature deaths yearly worldwide, according to the World Health Organisation (WHO).

However, health experts fear that pollution is also fuelling increases in degenerative diseases such as Alzheimer’s and other forms of dementia.

Previous studies found that air pollution has a negative impact on students’ cognitive abilities.

Many pollutants are thought to directly affect brain chemistry in a variety of ways.

For instance, particulate matter from traffic and industry can carry toxins through small passageways and directly enter the brain.

Culled from www.dailymail.co.uk

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Lung cancer is the second most common type of cancer in adults in the United States. It is also the leading cause of death from cancer.

Lung cancer treatment is much more effective when the disease is in its earlier stages. However, most people with lung cancer do not experience symptoms until the disease has spread.

Some people experience subtle symptoms of early stage lung cancer, but these symptoms more often stem from other health issues or factors such as smoking.

Below, we describe early symptoms of lung cancer, as well as risk factors and when to see a doctor.

Possible signs and symptoms of early stage lung cancer

According to the American Cancer Society (ACS), most types of lung cancer do not cause symptoms until they have spread to other areas.

However, some people experience subtle symptoms during the earlier stages of the disease.

The early lung cancer symptoms that we describe below usually result from some other cause. However, people who experience these symptoms should consider visiting their doctors as a precautionary measure.

Sudden weight loss

The American Society of Clinical Oncology report that weight loss is often the first noticeable sign of cancer.

They estimate that 40% of people who receive a cancer diagnosis experience unexplained weight loss during that time.

Cancer can cause weight loss for many reasons, including:

  • changes to immune function
  • changes to metabolism
  • changes to hormones
  • a sudden loss of appetite
  • difficulty swallowing

Shortness of breath

Shortness of breath and wheezing can also be early symptoms of lung cancer.

Some people may experience a slight cough in addition to shortness of breath. Others may have difficulty catching their breath but have no cough.

Cough

A slight cough that does not go away can indicate early stage lung cancer. Some people assume that this cough is only a result of smoking.

A person who regularly coughs because of another lung condition may notice changes in their cough, and these can likewise indicate lung cancer.

Also, a cough that produces blood may result from lung cancer or another issue with the lungs. Anyone who experiences this symptom should see a doctor.

General fatigue

Lung cancer can cause the number of red blood cells in the body to drop. The medical term for this issue is anemia.

Because red blood cells carry oxygen, a person with anemia may not take in enough oxygen to support their body’s needs. This can result in tiredness and fatigue. Severe fatigue can make it difficult to function on a day-to-day level.

Shoulder, chest, or back pain

Most people with lung cancer do not feel pain or other symptoms during the early stages. This is because there are very few nerve endings in the lungs.

However, pain can occur when lung cancer invades the chest wall, ribs, vertebrae, or certain nerves. For example, Pancoast tumors, which form at the very top of the lungs, often invade nearby tissues, causing shoulder pain.

As a tumor develops, a person may begin to feel pain in their:

  • arms
  • chest
  • back

Hoarse voice

A person with lung cancer or another respiratory disease may develop a hoarse, raspy voice.

This can happen if a tumor presses on the laryngeal nerve, which is located within the chest. When the nerve is compressed, it can paralyze a vocal cord, causing the voice to change.

Risks

According to the Centers for Disease Control and Prevention (CDC), cigarette smoking is still the biggest risk factor for lung cancer, accounting for 80–90% of lung cancer-related deaths.

Other risk factors for lung cancer include:

  • using other tobacco products, such as cigars or pipe tobacco
  • inhaling secondhand smoke
  • being exposed to radon gas, possibly from materials within the home
  • working with dangerous chemicals, such as asbestos, arsenic, or diesel
  • living in a highly polluted area
  • having other lung conditions, such as chronic obstructive pulmonary disease
  • having a family history of lung cancer

When describing risk, organizations and experts sometimes use the term “pack-year.” A pack-year refers to the number of cigarettes smoked per day each year. So a person with a 30 pack-year smoking history may have:

  • smoked one pack per day for 30 years
  • smoked two packs per day for 15 years

The ACS recommend yearly lung cancer screenings for people aged 55–74 who:

  • currently smoke or have quit smoking in the past 15 years
  • have at least a 30 pack-year smoking history
  • currently smoke and are receiving counseling to help them quit
  • are aware of the potential benefits and harms of screening
  • have access to a facility that has experience with lung cancer screening and treatment

Screening cannot detect every instance of lung cancer, but it does lower a person’s chance of dying from the disease.

Smokers vs. nonsmokers

According to the CDC, people who smoke are 15–30 times more likely to die from lung cancer than people who do not.

Meanwhile, according to statistics from 2013–2014, about 1 in 4 people who do not smoke, including children, are exposed to secondhand smoke. This increases their risk of developing the disease.

Quitting smoking at any age can lower the risk of lung cancer.

When to see a doctor

The symptoms above usually result from issues other than lung cancer. However, anyone who experiences any of the following issues should visit a doctor:

  • a cough that lasts longer than 2–3 weeks
  • a persistent cough that worsens
  • a cough that produces blood
  • aches or pains when breathing or coughing
  • persistent shortness of breath
  • persistent tiredness or fatigue
  • recurrent chest infections
  • unexplained weight loss

Summary

Lung cancer is the second most common form of cancer. It can affect anyone but is particularly prevalent among people who smoke.

Usually, lung cancer does not cause symptoms until it has spread. As a result, it is not always possible to detect lung cancer in its earliest stages.

Nonetheless, some people experience subtle symptoms during the initial stages. It is important to recognize these because treatment is typically more effective when a person receives it early.

Anyone who experiences early symptoms of lung cancer should see a doctor. In many cases, something other than cancer is the cause. Still, it is best to seek medical advice as a precaution.

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