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An estimated 1.5 million people living in the United States alone have RA, an autoimmune disease that causes joint pain, swelling, and eventually damage.

Researchers continue to look for new ways to diagnose RA, especially in its early stages. That is because the earlier a person receives a proper diagnosis of and treatment for RA, the better their chances of good outcomes, such as limiting joint damage and functional loss.

Researchers also remain uncertain as to what exactly causes RA to develop, although it seems to depend on a mix of genetic and environmental factors.

In more recent years, RA researchers have been exploring the link between ERA, people at risk of RA, and the changes in their oral and intestinal microbiota, or community of microbes.

It seems people with ERA and at risk of RA have abnormal levels of certain bacteria in the mucus that lines the mouth and intestines. They also seem to be more likely than other people to have periodontal disease, or gum disease.

What is more, some research indicates RA may begin in the oral cavity.

That is why a team of researchers from the Academic Centre for Dentistry of Amsterdam (ACTA) set out to analyze the microbial populations and periodontal condition of people with ERA, those at risk of RA, and a control group of people without these conditions for comparison.

Their study appears in the journal Arthritis & Rheumatology.

The oral microbiome and RA

Researchers have long speculated that autoimmune diseases, such as RA, are triggered or caused by microorganisms.

For quite some time, researchers have been aware there are links between periodontal disease, changes in the oral and intestinal microbiome, and RA.

Several studies seem to show that oral microbes — in particular anaerobic bacteria, which do not require oxygen — may play a role in the development of RA.

2009 study highlights three types of anaerobic bacteria occurring in the oral cavity that have been identified in joint fluid from people with RA. Several studies show that antibodies for certain types of anaerobic bacteria associated with periodontal disease may play a role in the development of RA.

Some researchers think these bacteria may cause an RA-associated immune response by producing proteins that trigger the formation of anti-citrullinated protein antibodies (ACPAs).

These compounds appear to promote inflammatory responses in different types of cells, including bone cells. Some studies have shown that this response ACPAs promote may be involved in the mediation of bone damage in the joints of people with RA.

For these and other reasons, the detection of ACPAs is now considered the most specific biomarker for RA in serum, which is the fluid component of blood.

The detection of ACPAs in serum also seems to help predict RA development several years before a person has clinical RA or experiences symptoms and receives an RA diagnosis.

That is why several research teams, including the team involved in the current study, have been exploring how changes in the composition and other components of the oral microbiome may relate to the onset of RA.

Oral microbiome changes and RA risk

In the new study, researchers analyzed the oral microbiome and periodontal status of three groups of 50 people.

People in the first group had ERA, and the second group included people at risk of RA (people with serum ACPAs or arthralgia). People in the third group did not have RA and were not at risk, did not have autoimmune conditions, and were generally healthy.

Each participant was examined by a dentist to assess their periodontal condition. Dentists checked whether their gums bled with probing, the inflamed gum surface area, and how deep into the gum line dental tools could probe.

They also examined how many teeth each participant had, how many of their teeth were missing, decayed, or filled, and whether a person wore a removable denture. They also asked each participant about the last time they brushed their teeth and what their regular oral hygiene measures were.

In addition, the scientists collected from each participant samples of the tongue coating or film, saliva, and subgingival dental plaque, which is found below the gum.

After using devices to amplify the DNA present in the samples, they collected, analyzed, and quantified the microbial populations within the samples. They then compared microbial differences between the three groups.

The team identified no difference in periodontal conditions between the groups. There was also no difference in dental plaque samples.

Yet differences did exist between the oral saliva and tongue coating of people with ERA and at risk of RA compared with the control group.

Levels of bacteria belonging to the genera Prevotella and Veillonella were higher in saliva samples from people with ERA and at risk of RA compared with the control group. Veillonella bacterial levels were also higher in the tongue coatings of the RA groups than in those of people in the control group.

According to the authors, these findings suggest that a possible link between the oral microbe and RA may truly exist.

This also suggests that bacteria from these two genera, as well as some others already reported to be involved in RA onset, could help trigger immune responses that influence the development of RA.

The authors explain that these findings correspond to those of previous studies showing that people with new-onset RA and established RA had increased levels of oral Prevotella bacteria. The results also support research that found increased levels of Prevotella bacteria in the gut microbiome of people at risk of RA or with ERA.

The authors write that some strains of Prevotella can cause chronic inflammation, which can trigger immune cells to be released throughout the body. They add that in some cases, microbial dysbiosis, or microbial imbalances, partially resolves with RA treatment.

The wider picture

Medical News Today spoke with Dr. Vanessa L. Kronzer, who cowrote a recent review on the etiology of RA. She said:

“This is an interesting study that, in my mind, achieves two goals. First, it provides further support for the mucosal origin hypothesis for RA. And second, it suggests that dysbiosis occurs even before disease onset and thus may play a role in RA disease pathogenesis.”

Dr. Kronzer believes this research is “an important step in a long path to understanding the etiology of this important disease.”

MNT also contacted Johanna Kroese from ACTA, the corresponding author of the study. She explained:

“Our results indicate a possible role for oral bacteria in triggering the onset of RA. Targeting these bacteria might lower the risk of developing RA. Future research can focus on strategies to target these bacteria and improving oral health, and might eventually lead to the development of measures for RA disease prevention.”

Some limitations

While the study had many strengths, it also had some notable flaws.

People within the ERA group were receiving treatment for RA, while people at risk of RA and those in the control group were not. The researchers also did not collect information on some factors that may influence dental plaque, such as diet.

To confirm their findings, the authors say future studies must collect multiple datasets over longer periods of time, ideally using large groups of people and consistent collection methods.

Nevertheless, these findings may have uncovered yet another stepping stone in the complex, elusive development process of RA. This could be good news for the millions of people living with RA, and the healthcare professionals trying to diagnose and treat them.

As Johanna Kroese explained to MNT, although further research is needed, “improving oral health is relevant for the entire population, and it wouldn’t hurt to already pay attention to oral health in persons at risk of developing RA.”

Kidney cancer is the eighth most common cancer in adults, with just over 10,100 people diagnosed each year.

Signs and symptoms of kidney cancer can include: blood in your urine; a constant pain in your side, just below the ribs; and a lump or swelling in the kidney area (on either side of the body).

See your General Practitioner (GP) as soon as possible if you experience any of these symptoms. They will examine you and may refer you to a specialist clinic for further tests.

In around half of all cases of kidney cancer, there are no symptoms, and the condition is detected during tests for other unrelated conditions.

The kidneys and cancer
The kidneys are two bean-shaped organs located on either side of the body, just underneath the ribcage. Their main role is to filter out waste products from the blood, in addition to producing urine. Only one of the kidneys is usually affected by cancer.

The human body is made up of billions of cells, which normally grow and multiply in an orderly way, with new cells being created only when and where they’re needed. In cancer, this orderly process goes wrong and cells begin to grow and multiply uncontrollably.

Exactly what triggers this growth is unknown; however, there are certain risk factors that can increase the chances of the condition developing, such as smoking and obesity.

Kidney cancer most frequently affects people over 50 years of age and is more common among men.
Treating kidney cancer

The earlier kidney cancer is diagnosed, the easier it is to treat. How it is treated will depend on the size and spread of the cancer. Surgery to remove the cancerous cells is usually the first course of action.

Unlike most other cancers, chemotherapy isn’t very effective at treating kidney cancer. However, non-surgical treatments are available, such as radiotherapy or targeted therapies. These are most commonly used in the more advanced stages of kidney cancer, when the cancer has spread beyond the kidney.

Preventing kidney cancer
As the causes of kidney cancer aren’t fully understood, it is not possible to fully prevent it.

However, leading a healthy lifestyle may reduce the chances of developing the condition. A combination of a healthy diet and regular exercise will help to avoid becoming overweight or obese, which is a significant risk factor for kidney cancer.

If you are overweight or obese, you can lose weight and maintain a healthy weight by combining regular exercise with a calorie-controlled diet.

The unmistakable taste and smell of coffee — not to mention its ability to perk people up in the morning — have made it one of the world’s most popular beverages.

Better still, observational studies indicate that coffee may protect against cardiovascular disease, diabetes, Parkinson’s disease, and certain cancers.

Prospective studies, which follow people over time, have provided evidence that drinking this beverage is safe for most people and is associated with lower mortality rates.

However, a new study suggests that some of the supposed health benefits of coffee for cardiovascular health may have been overblown. The research was limited to white British participants.

As a result of the caffeine that coffee contains, excessive consumption can cause unpleasant symptoms such as tachycardia (a fast resting heart rate) and palpitations.

Drinking coffee can also lead to a moderate, temporary increase in blood pressure.

So it may come as a surprise that regular coffee drinkers either have normal or reduced blood pressure compared with people who do not drink coffee.

One explanation may be that coffee drinkers develop a physiological tolerance for the effects of caffeine.

But a new study suggests that people with a high genetic risk of cardiovascular disease unconsciously reduce how much they drink to avoid unpleasant cardiovascular symptoms.

The research found that individuals with high blood pressure, angina, or arrhythmia drank less caffeinated coffee and were more likely to drink decaffeinated coffee.

Crucially, there was strong evidence that their genetic vulnerability to cardiovascular disease led to their reduced consumption of coffee.

This rules out the alternative explanation that consuming less coffee made them more vulnerable to cardiovascular disease.

Researchers at the University of South Australia in Adelaide conducted the study, which appears in The American Journal of Clinical NutritionTrusted Source.

Guided by genetics

“Whether we drink a lot of coffee, a little, or avoid caffeine altogether, this study shows that genetics are guiding our decisions to protect our cardio health,” Professor Elina Hyppönen, who led the research and directs the Australian Centre for Precision Health at the university.

“If your body is telling you not to drink that extra cup of coffee, there’s likely a reason why,” she adds. “Listen to your body — it’s more in tune with your health than you may think.”

In observational studies, this effect could give the false impression that coffee prevents high blood pressure and protects the heart.

In reality, people vulnerable to high blood pressure may simply avoid drinking coffee because, for them, the caffeine is more likely to cause unpleasant symptoms.

The scientists drew on information about 390,435 white British participants aged 39–73 years who are part of a medical and genetic database called UK Biobank.

On recruitment, participants reported their regular coffee consumption. Researchers also measured their blood pressure and heart rate and noted any cardiovascular symptoms.

Participants with high blood pressure, angina, or arrhythmia consumed less caffeinated coffee compared with those without these symptoms.

To determine whether regular coffee consumption caused the symptoms, or whether the symptoms triggered a reduction in coffee consumption, the researchers used a statistical technique called Mendelian randomization.

This technique exploits the random inheritance of genetic variants that increase a person’s risk of a particular outcome later in life — in this case, the association between blood pressure and heart rate with habitual coffee consumption.

Because factors, such as lifestyle or diet, cannot change a person’s genetic sequence, any associations that the researchers discovered must be due to the gene variants rather than any other factors.

When they analyzed the data, it showed that having a particular genetic variant determined how much coffee a person drank.

“What this means is that someone who drinks a lot of coffee is likely more genetically tolerant of caffeine, as compared to someone who drinks very little,” says Prof. Hyppönen.

“Conversely, a noncoffee drinker, or someone who drinks decaffeinated coffee, is more likely prone to the adverse effects of caffeine and more susceptible to high blood pressure,” she adds.

Psychological effects

Medical News Today asked Prof. Hyppönen whether the psychological effects that some people experience when they drink a lot of coffee, such as anxiety and agitation, could also play a role.

“This is not something that we looked at in our study, but any unpleasant sensation that an individual feels in response to coffee consumption is likely to reduce their wish to drink coffee,” said Prof. Hyppönen.

MNT asked Dr. Edo Paz, a doctor atdigital primary care platform K Health, about the effects of drinking too much coffee.

He responded:

“[D]rinking too much coffee can result in headache, anxiety, tremors, and difficulty sleeping. With regards to the heart, in particular, excess coffee intake can result in palpitations and may trigger events in the heart, such as abnormal heart rhythms, in susceptible individuals.”

The problem of reverse causation

The findings of the new research suggest that observational studies that found an association between coffee consumption and better health may have fallen prey to “reverse causation.”

In other words, heart health issues led people to drink less coffee, rather than the other way round.

Prof. Hyppönen said Mendelian randomization studies had cast doubt on other apparent protective effects.

For example, epidemiological studies have led people to infer that moderate alcohol consumption protects against cardiovascular disease, and that having excess weight reduces mortality compared with moderate weight.

“According to [Mendelian randomization] studies, there does not appear to be any benefit for having [excess weight] versus [slim or moderate] weight, with the possible exception for smokers,” she said.

Smoking reduces appetite and hence weight, but it also has links with a wide range of negative effects on health.

“Also for alcohol, [the] evidence suggests linear increases in blood pressure and stroke risk, with no benefit for light alcohol consumption,” she added.

While further studies are necessary using a more diverse population, this study suggests using a considered, personalized approach when promoting high coffee intakes.

There have been numerous investigations into a possible role for vitamin D in preventing both SARS-CoV-2 infections and COVID-19 complications.

These studies have drawn conflicting conclusions. Now, a study from researchers in Brazil provides a more robust answer to at least one key question: can vitamin D help prevent COVID-19 complications in particularly ill hospitalized patients? According to the results, the answer appears to be no.

The study found that high doses of vitamin D administered to hospital patients with moderate or severe COVID-19 did not affect the course of the disease.

“In vitro studies or trials with animals had previously shown that in certain situations, vitamin D and its metabolites could have anti-inflammatory and antimicrobial effects, as well as modulating the immune response,” explains Rosa Pereira, principal investigator for the study.

“We decided to investigate whether a high dose of the substance could have a protective effect in the context of an acute viral infection, reducing either the inflammation or the viral load.”

Based on the study’s results, says Pereira, “So far, we can say there’s no indication to administer vitamin D to patients who come to the hospital with severe COVID-19.”

The research appears in JAMA.

COVID-19 and vitamin D

Scientists at the University of São Paulo’s Medical School (FM-USP) in São Paulo, Brazil, conducted the randomized, double-blind, and placebo-controlled clinical trial. The researchers say this study is the first of its kind.

The team tracked the experiences of 240 volunteers receiving treatment for COVID-19 symptoms at FM-USP’s Hospital das Clínicas and the Ibirapuera Park field hospital in São Paulo City, from June to August 2020. All participants had tested positive for SARS-CoV-2 using a polymerase chain reaction test or via antibody testing.

All of them received treatment with standard COVID-19 protocols that include antibiotic and anti-inflammatory medications. The researchers then divided them into two equal groups at random.

The scientists gave participants in the first group a single 200,000-unit dose of vitamin D3 dissolved in peanut oil. They gave those in the second group unaltered peanut-oil placebos.

The design of the study was to discover whether a high dose of vitamin D was associated with a shorter hospitalization — the researchers found that it was not.

The investigation also found no evidence that vitamin D made a person less likely to be admitted to the intensive care unit or less likely to need intubation.

Vitamin D also seemed to have no effect on mortality, although Pereira cautions that a larger study with more participants is required before researchers can draw final conclusions.

More vitamin D studies needed

The study conclusively rules out vitamin D as a “magic bullet” for treating COVID-19.

Co-author Bruno Gualano, a researcher at FM-USP, says, “But that does not mean continuous use of vitamin D cannot have beneficial effects of some kind.”

Having suggested that a single high dose of vitamin D is not a solution to severe COVID-19, Pereira is now leading a new study to determine whether a vitamin D deficiency has any effect on a person’s ability to overcome SARS-CoV-2.

Pereira is also looking to establish the amount of vitamin D a person should have in their bloodstream to promote good health. This threshold will vary depending on an individual’s characteristics. Younger, generally healthy people should have at least 20 nanograms per milliliter of blood (ng/ml). Whereas for older people, for example, and those with osteoporosis, the minimum is 30 ng/ml.

Pereira says, “The ideal approach is case-by-case analysis, if necessary dosing the substance periodically by means of blood work, with supplementation if a deficiency is detected.”

If you are looking for the best natural skin care treatment, Moringa Oleifera, the plant native to India and now grown in more than 80 countries is your best option. Moringa oil is extracted from the nuts of the Moringa plant to make the most trustworthy natural skincare products.

We Asked Mr Amrit Walia, Co-Founder of Pioneer Sustainable Agriculture here in Nigeria who also produces one of the best premium cold-pressed oil ( Puro moringa oil ) coming straight from organic moringa farms, to know more about Moringa oil and why it is highly coveted in the cosmetic and lubricating industry, and this is what we got, enjoy reading.

In cosmetics, Moringa oil is a primary ingredient in the manufacture of expensive, natural fragrances and perfumes. The oil is also included in skin scrubs, soaps, and shampoos, lip balm, lotions and is the foremost ingredient in the manufacture of blended massage oil.

As an agent to beauty, Moringa oil is used for a manicure, pedicure, and in making beauty soap which utilizes its skin cleansing and moisturizing properties. Moringa oil can sometimes be used to dress vegetables, salads, and various green dishes. In cooking, the amazing oil can be used for deep frying and sautéing.

1. Moringa Oil as a Skin Care Agent
This oil is rich in fatty acids like Oleic acid which automatically restores the skin’s natural barrier and in keeping the skin hydrated.
Moringa has antibacterial, antioxidant, and antifungal properties that can do the following concerning skincare:

  • The unique combination of fatty acids in the oil is essential for maintaining cell membranes. The fatty acids also possess lubricant, and anti-inflammatory properties that restore the lost natural oils and protect the skin from damage in a hostile environment.
  • Moringa’s phytochemical profile can defend the skin from ongoing pollution which adversely affects the epidermis of the skin. The rich content of Oleic acid also keeps the skin hydrated despite exposure to pollution.
  • Moringa works as an anti-aging oil. By fighting the activity of free radicals, it slows down the process of aging, prevents sagging of facial skin, and clears wrinkles.
  • Moringa oil regulates oil secretion and purifies the skin from the harmful effects of pollution thus revealing the natural glow.
  • It is a super antiseptic containing antimicrobial properties capable of curing acne and dark spots. It also regulates the production of excess sebum and removes dirt and bacteria clogged on the pores of the skin.
  • Moringa oil is an amazing deep skin cleanser and skin detoxifier. It contains sulfur which helps in building natural keratin for youthful skin.

2. Moringa Oil in Health Care
Moringa tree oil has 90 different types of nutrients, 46 antioxidant proteins, and 36 anti-inflammatory agents.

This comes along with many health benefits including, but is not limited to the following:

  • Soothing the nervous system
  • Protecting bones
  • Optimal gum and oral health
  • Management of hysteria
  • Fights stomach disorders
  • Fights asthma
  • Fights arthritic pain
  • Softens and heals cracked heels
  • Heals insomnia
  • Treats sunburns
  • Provides stronger hair
  • Acts as a rheumatic oil
  • Cures hypertension

There are still more uses of Moringa oil, which truly reveals how beneficial this oil is to your overall health.

Moringa oil can also be applied effectively in the management of hysteria, fighting asthma, management of arthritic pain, treatment of stomach disorders, softening and healing cracked heels, in the treatment of sunburns, and in the treatment of hypertension, insomnia, and many other conditions.

You can try this natural extract and start enjoying most of its health benefits today.

According to the World Health Organization (WHO), cancer accounted for 10 million deaths worldwide in 2020. Globally, it is a leading cause of death.

In the United States, an estimated 39.5% of people will receive a cancer diagnosis within their lifetime.

Myths tend to develop around particularly prevalent conditions. It is no surprise, therefore, that people often misunderstand cancer.

“Cancer” is a generic term for a group of diseases that can affect any part of the body. This variety adds fuel to the fire of confusion.

In this article, we hope to dispel some myths and clarify this common and varied group of diseases.

1. Cancer is a death sentence

Cancer is not a death sentence. Despite the sobering statistics quoted above, cancer is not always terminal.

As scientists understand cancer better and develop improved treatments, recovery rates continue to improve.

For instance, in January 2019, an estimated 16.9 million cancer survivors were living in the United States. In the United Kingdom, survival rates have doubled in the last 40 years.

It is also worth noting that survival rates vary significantly depending on the type of cancer. For instance, in the U.K., survival rates for testicular cancer are 98%, whereas survival rates for pancreatic cancer are just 1%.

According to the National Cancer Institute:

“In the United States, the likelihood of dying from cancer has dropped steadily since the 1990s. Now, 5-year survival rates for some cancers, such as breast, prostate, and thyroid cancers, are 90% or better. The 5-year survival rate for all cancers combined is currently about 67%.”

Overall, cancer death rates are slowly declining, although the survival rates of some cancers are increasing more than others. An annual report on the status of cancer in the U.S., which appears in Cancer in 2020, concludes:

“[C]ancer death rates decreased 1.5% on average per year during 2001 through 2017.”

2. Cancer is contagious

This is a myth. Cancer is not contagious. Someone with cancer cannot spread it to others.

However, some sexually transmitted diseases, including human papillomavirus (HPV) and hepatitis B and C, can cause cancers in the cervix and the liver. In these cases, an infectious agent causes the cancer, but the cancer itself is not contagious.

As an interesting aside, scientists have documented that cancers in some animals, including Tasmanian devils and dogs, can cause fatal transmissible cancers: devil facial tumor disease and canine transmissible venereal tumor, respectively.

3. Cell phones cause cancer

To date, there is no evidence that cell phones cause cancer. One of the reasons this myth developed is that these devices emit radiofrequency radiation (radio waves), a form of non-ionizing radiation. The body absorbs this radiation.

Scientists know that exposure to ionizing radiation, for instance, X-rays, increases the risk of cancer. However, radiofrequency radiation is non-ionizing radiation, which does not increase cancer risk. The National Cancer Institute writes:

“[A]lthough many studies have examined the potential health effects of non-ionizing radiation from radar, microwave ovens, cell phones, and other sources, there is currently no consistent evidence that non-ionizing radiation increases cancer risk in humans.”

4. Power lines cause cancer

This is also a myth. The extremely low frequency (ELF) magnetic fields produced by power lines are non-ionizing and, therefore, do not cause cancer.

The American Cancer Society writes:

“Several large studies have looked at the possible effects of ELF magnetic fields on cancer in rats and mice. These studies expose the animals to magnetic fields much stronger than what people are normally exposed to at home […]. Most of these studies have found no increase in the risk of any type of cancer. In fact, the risk of some types of cancer was actually lower in the animals exposed to the ELF radiation.”

However, the American Cancer Society also explains that some studies have found a slight increase in leukemia risk for children who live close to power lines. However, the reasons for this remain unclear.

Medical News Today spoke with Dr. Joel Newman, a consultant hematologist and specialty lead for pathology at East Sussex Healthcare Trust in the U.K. He puts the risk into perspective:

“We don’t have any real evidence that cell phones or power lines cause cancer, and there are many other things that we do daily that put us at a much greater risk than these ever could, including smoking and alcohol consumption.”

5. Artificial sweeteners cause cancer

To date, there is no good evidence that artificial sweeteners increase the risk of developing cancer.

The National Cancer Institute explains why this myth may have arisen:

“Questions about artificial sweeteners and cancer arose when early studies showed that cyclamate in combination with saccharin caused bladder cancer in laboratory animals.”

However, they explain that further studies “have not provided clear evidence of an association with cancer in humans. Similarly, studies of other [Food and Drug Administration (FDA)]-approved sweeteners have not demonstrated clear evidence of an association with cancer in humans.”

Similarly, a study investigating aspartame and cancer, which included data from more than half a million participants, found no links between “aspartame consumption and lymphoma, leukemia, or brain cancer.”

6. Cancer surgery causes cancer to spread

This is only a partial myth. It is true that cancer surgery can cause the cancer to spread, but this is rare. As the American Cancer Society explains:

“Advances in equipment used during surgery and more detailed imaging tests have helped make this risk very low.”

A related myth indicates that a tumor will grow faster or spread to other parts of the body when exposed to the air. This is untrue.

7. Herbal medicines can cure cancer

There is no evidence that any herbal medicines can cure or treat cancer.

However, some people find certain alternative therapies, such as acupuncture, meditation, and yoga, help with the psychological stress associated with cancer and some of the side effects of cancer treatment.

As the National Cancer points out, just because something is “natural” does not mean it is safe. In some circumstances, herbal supplements can harm a person’s health; they provide a couple of examples:

“[S]ome studies have shown that kava kava, a herb that some people use to help with stress and anxiety, may cause liver damage. And St. John’s wort, which some people use for depression, may cause certain cancer drugs not to work as well as they should.”

It is important that people with cancer speak with a doctor about supplements and vitamins before taking them.

8. Cancer runs in families

Although some cancers are passed on genetically through families, they are the minority of cases: an estimated 3–10% of cancers result from mutations inherited from parents.

Because people are more likely to develop cancer as they age, and people today live longer lives, it is not uncommon for people to have some relatives who develop cancer. This might help explain why this myth persists.

Most cases of cancer are due to a buildup of mutations in genes that accumulate over time. As the American Cancer Society explains:

“Some types of cancer run in certain families, but most cancers are not clearly linked to the genes we inherit from our parents. Gene changes that start in a single cell over the course of a person’s life cause most cancers.”

9. Cancer always comes back

To address this question, MNT spoke with Dr. Collin Vu, a medical oncologist and hematologist at MemorialCare Cancer Institute at Orange Coast Medical Center in Fountain Valley, CA. He said:

“Fortunately for all of us, this statement is a myth and entirely not true. The current therapies for cancers are improving to the point where the cure of cancer — that is, treatments that will kill cancer completely — are improving continuously.”

However, he explains that the subject is complicated because “different cancer types have a markedly different ability to be cured, and different cancer types also have different time frames for which a cancer may typically recur. [This] makes it very difficult for patients to know when they may be truly ‘cured’ or when they still have a high risk of cancer recurrence.”

Dr. Vu has great hopes for the future of cancer treatment; he told MNT:

“In the future, with current scientific progress in better treatments for cancer, and improved population awareness of cancer risks and diagnosis, the statement that ‘cancer always comes back’ may become even more of a myth.”

10. There is no cure for cancer

Thankfully, this is also a myth. As medical science delves deeper into the mechanisms behind cancer, treatments steadily grow more effective.

According to Dr. Vu, some cancers, such as testicular and thyroid cancer, have a 60% cure rate. Dr. Vu defines the cure rate as “the population of cancer patients that has the same life expectancy as the general population.”

Breast, prostate, and bladder also have cure rates of around 50%. Dr. Vu concludes:

“As can be seen by the above data, some cancers can be eradicated, but, unfortunately, not all cancers can be cured completely. There is ongoing optimism that cure rates are increasing given the ongoing focus on screening and better treatments for cancer.”

MNT also spoke with Dr. Anton Bilchik, Ph.D., a surgical oncologist, professor of surgery, chief of gastrointestinal research, and chief of medicine at Saint John’s Cancer Institute at Providence Saint John’s Health Center in Santa Monica, CA. He also leads with a message of hope:

“It is imperative that patients who are diagnosed with cancer, even at an advanced stage, do not lose hope: there are many effective, novel therapies, as well as more effective surgical techniques. A good example is with the use of modern immunotherapy, up to 40% of patients with stage 4 melanoma are curable, and 50% of patients with stage 4 colon cancer metastatic to the liver can be cured with a combination of chemotherapy and surgery.”

In short: although the battle with cancer is ongoing, science is making significant headway.

Schizophrenia is a psychiatric condition that is characterized by “positive” symptoms, such as hallucinations and delusions, and “negative” symptoms, such as social withdrawal and apathy.

For almost a century, scientists have speculated about a possible link between the immune system and schizophrenia.

Several lines of evidence suggest that the inflammation provoked by a viral infection, either before birth or during childhood, could trigger the condition in adulthood.

Some studies have also found changes in the blood-brain barriers of people with schizophrenia.

The blood-brain barrier comprises the tightly packed layer of cells that line the blood vessels in the brain and spinal cord. It prevents blood-borne immune cells from gaining entry to the central nervous system.

This is sometimes known as conferring “immune privilege” on the brain — in other words, protecting it from harmful inflammation.

Researchers at the University of Pennsylvania’s School of Veterinary Medicine in Philadelphia wondered whether a compromised blood-brain barrier in people with a rare genetic disorder known as DiGeorge syndrome or 22qDS, a genetic deletion syndrome, could be responsible for their increased risk of schizophrenia.

People born with the condition have a 1 in 4 risk of developing schizophrenia later in life. This is compared with an overall risk of schizophrenia of around 1 in 100 in the wider adult population.

People with 22qDS have a small section of DNA missing from chromosome 22 of their genome.

Leaky barrier

To test their hypothesis, the researchers isolated cells from people with DiGeorge syndrome and schizophrenia and from healthy matched controls. They then turned these cells into pluripotent stem cells, which can develop into any type of cell in the body.

In the laboratory, they transformed the stem cells into the type of cells that line the blood vessels in the brain. These are the cells that together function as the blood-brain barrier.

The researchers found that the cells derived from people with DiGeorge syndrome and schizophenia created a less effective, more “leaky” barrier than those derived from the healthy controls.

In addition, the cells produced more of a type of molecule that promotes inflammation. This allowed more immune cells to penetrate the barrier.

The researchers obtained similar results when they investigated the integrity of the blood-brain barrier in a mouse model of DiGeorge syndrome.

Finally, they performed the same tests in postmortem brain tissue from three people who had DiGeorge syndrome and from three age-matched healthy controls.

They found evidence that the effectiveness of the actual blood-brain barrier of these people had indeed been compromised.

The research, which doctoral student Alexis Crockett led, now appears in the journal Brain.

Other brain disorders

The study authors speculate that a compromised blood-brain barrier may interact with environmental or other genetic risk factors to increase the likelihood not only of psychosis but also of other brain disorders in the case of people with DiGeorge syndrome.

“[W]e think these findings could also be used to understand how the blood-brain barrier and neurological processes impact not only schizophrenia but mental disorders at large,” says senior study author Prof. Jorge Iván Alvarez, from the School of Veterinary Medicine.

In 2019, Medical News Today reported on a study that suggested that a faulty blood-brain barrier in aging mice triggered brain inflammation and cognitive impairment in the animals.

Prof. Alvarez speculates that further research into the link between inflammation and neuropsychiatric disease could lead to new therapies for these conditions.

Anti-inflammatory and immunotherapy drugs have already shown some promise as treatments for schizophrenia, alongside standard treatments.

Schizophrenia is multifactorial

It is worth noting that schizophrenia is a “multifactorial” condition. This means that there is no single, clear cause. Rather, a wealth of different genetic and environmental influences interact to increase or decrease an individual’s risk of developing it.

Prof. Alvarez told MNT that people with the DiGeorge syndrome “phenotype” — that is, the characteristics arising from interactions between genetics and environment — will respond negatively to particular environmental challenges.

“These might include prenatal infection in the mother, or an infection in childhood.”

This “second hit” would worsen their condition in distinctive ways. “In terms of a ‘second hit,’” he said, “we believe that such environmental challenges will exacerbate the phenotype described under [steady] conditions.”

In their paper, Prof. Alvarez and colleagues also report some limitations of their study.

For example, their experiments did not prove that everyone with DiGeorge syndrome has a compromised blood-brain barrier. There remains a possibility that the changes are only present in those who develop schizophrenia.

To test this possibility, Prof. Alvarez said that he and his team would repeat the experiments using pluripotent stem cells from people who have this particular genetic deletion syndrome but have not developed schizophrenia.

“[W]e are planning to run these experiments using deleted non-schizophrenia [stem cells],” he said.

The Johnson & Johnson COVID-19 vaccine, also called Ad26.COV2.S, was developed by Janssen Pharmaceuticals of Johnson & Johnson.

It is a single-dose vaccine, which differentiates it from two-dose COVID-19 vaccines, such as the ones from Pfizer and Moderna.

In early 2021, the Food and Drug Administration (FDA) and, after a recommendation from the European Medicines Agency (EMA), the European Commission issued emergency and conditional authorization for the Johnson & Johnson vaccine for individuals aged 18 years and older. The vaccine has been approved for emergency use in 40 countries.

However, the FDA recommended a pause in the vaccine’s use, as a precautionary measure following a small number of rare blood clot incidents. At the same time, Johnson & Johnson delayed the distribution of the vaccine in Europe while the EMA conducted its own review.

On April 20, the company announced it would resume distribution of its vaccine in the European Union but with a safety warning, after the EMA concluded that the vaccine’s benefits continue to outweigh its risks.

After halting vaccination in the United States a few weeks ago, the FDA and the CDC recently recommended that vaccinations resume. They noted, however, that women under the age of 50 should be aware of the risk of rare blood clots.

Moreover, both agencies want women to know that alternative COVID-19 vaccines are available, for which there are currently no reports of rare blood clots.

The World Health Organization (WHO) has stated that, while it continues to monitor the safety responses from regulatory agencies, the vaccine is safe and effective against the severe risks of COVID-19.

How does the vaccine work?

The vaccine is categorized as a viral vector vaccine.

This vaccine form utilizes a different, harmless virus to deliver the genetic instructions for making the SARS-CoV-2 virus’ surface spike protein, which triggers the body’s immune response to produce antibodies. The vaccine does not contain the SARS-CoV-2 virus and cannot cause COVID-19.

The Johnson & Johnson vaccine has a 66% efficacy rate. While this is lower than the efficacy rates of the Pfizer or Moderna vaccines, it should be noted that the clinical trials of the Johnson & Johnson vaccine took place in different contexts — globally in regions where variants were more prevalent, and in the U.S. during a period of significant increase in COVID-19 cases.

The vaccine is around 85% effective at preventing severe disease from COVID-19, including hospitalization and death.

Common side effects

According to the FDA’s vaccine fact sheetTrusted Source, possible side effects include:

Allergies and anaphylaxis

As with other COVID-19 vaccines, the Johnson & Johnson vaccine has a low but potential risk of causing an allergic reaction.

A non-severe allergic reaction may include symptoms such as hives, swelling, rash, and respiratory problems.

A more severe, anaphylaxis response is much rarer. According to the FDA, a severe reaction can be characterized by:

An ingredient that has raised particular concerns about allergic response is polysorbate 80, a chemical that is structurally related to polyethylene glycol (PEG), found in Pfizer’s and Moderna’s mRNA vaccines, both of which have prompted similar worries.

While knowledge about the mechanisms of this allergy is limited, PEG and polysorbate allergies are extremely rare. For the Pfizer vaccine, an analysis of one patient who experienced PEG-related anaphylaxis showed that they had a history of allergic reactions to PEG-containing products.

An evaluation of vaccine allergies with PEG and polysorbate skin testing concluded that the usefulness of skin testing in predicting potential allergic responses remains unclear.

The CDC advises that anyone with a known allergy to any of the vaccine’s ingredients, including polysorbate 80, seek advice from a healthcare professional before receiving the COVID-19 vaccine.

People who have had a severe allergic reaction to any of the vaccine’s ingredients should not receiveTrusted Source this particular shot.

Controversy regarding blood clots

Similar to the AstraZeneca COVID-19 vaccine — Vaxzevria — the Johnson & Johnson vaccine was put on hold after eight cases of a rare blood clotting disorder, in combination with low blood platelet counts, were found in the vaccine recipients.

Most of these cases of thrombosis with thrombocytopenia were extremely rare types, including cerebral venous sinus thrombosis (CVST), which occurs in the brain.

All eight cases occurred within 21 days of vaccination in people under the age of 60. Also, the majority of the eight vaccine recipients who experienced these side effects were women.

The EMA’s safety assessment committee concluded on April 20 that the vaccine’s label should include blood clots as a potential rare side effect and state that the benefits of the vaccine outweigh these risks.

Authorities are uncertain what causes these cases of blood clotting. They suggest that it may be a triggered immune response similar to a rare condition of thrombocytopenia induced by heparin, which is a blood thinner.

CVST is rare in the general population, occurring at a rate of around 5 in 1 million people annually. Reports indicate that there have been eight cases among more than 7 million people who have received the Johnson & Johnson vaccine.

The benefits of receiving the vaccine outweigh the risk of blood clots and the risk of the complications that can come with COVID-19.

However, the pause is likely to have caused some hesitancy toward the vaccine and has slowed rollout.

“There is no doubt in my mind that there are groups for whom this vaccine is of benefit,” Dr. Paul Offit, director of the Vaccine Education Center at Children’s Hospital of Philadelphia, told The New York Times, “meaning that they’re more likely to get this vaccine than the other vaccines, whether it’s because of where they live, or because they’re homebound, or it’s hard to get a second dose.”

Dr. Offit warns that any vaccine hesitancy caused by this controversy would have “elevated a rare risk above a much more common risk,” that of developing COVID-19, which could place many people’s health in danger.

Researchers know that HDL, or good, cholesterol reduces inflammation. At healthy levels, HDL can also reduce the risk of stroke and heart attack.

So far, intervention trials using medications to improve or increase HDL levels have been unsuccessful. Also, some genetic research indicates that lifelong high or low levels of HDL do not seem to relate to cardiovascular outcomes, as expected.

That is why some cardiovascular risk prevention researchers are shifting their focus from circulating HDL levels to the actual functional ability of HDL.

Indeed, a research team from the Netherlands has studied the relationship between HDL’s ability to reduce inflammation and the risk of experiencing a first cardiovascular event.

“HDL are very complex particles with anti-atherosclerotic functions that are not reflected by measuring just the cholesterol quantity,” says senior study author Dr. Uwe J. F. Tietge, Ph.D., a professor and head of the Division of Clinical Chemistry at the Karolinska Institute in Stockholm, Sweden.

“Atherosclerosis [plaque buildup in the arteries] underlying cardiovascular disease is increasingly recognized as a disease with a strong inflammatory component, and a central biological function of HDL is to decrease inflammation.”

By analyzing data from 680 adults, the team found evidence to suggest that HDL’s ability to reduce inflammation is associated with a reduced risk of a cardiovascular event.

In the study, people who did not experience a cardiovascular event demonstrated higher anti-inflammatory HDL levels than participants who did experience a cardiovascular event.

“By using a novel research tool, our results provide strong support for the concept that plaque buildup in the arteries has an inflammatory component and that the biological properties of HDL particles have clinical relevance to cardiovascular disease risk prediction.” – Dr. Uwe J. F. Tietge, Ph.D.

The study appears in the journal Circulation, which is the American Heart Association’s (AHA) flagship journal. It received funding from the Netherlands Organization for Scientific Research and the Swedish Heart-Lung Foundation.

HDL: A natural anti-inflammatory

HDL is called good cholesterol because it picks up excess cholesterol in the blood and takes it back to the liver, which breaks it down and helps remove it from the body.

HDL can also reduce inflammation in the cells lining blood vessels. This occurs because HDL removes cholesterol stored in macrophage foam cells in atherosclerotic plaques and carries it to the liver.

Atherosclerosis occurs when plaque accumulates on the inner walls of arteries. Plaque is a substance made of cholesterol, calcium, fat, and other molecules.

As plaque deposits grow, they can gradually narrow the blood vessel, reducing blood flow and oxygen delivery to parts of the body or organs.

If atherosclerosis is severe enough, it can lead to major health concerns, including stroke, heart attack, and death.

When HDL removes cholesterol from foam cells in plaques, it helps reduce the size of the plaque. By reducing its size, it also reduces the amount of inflammation associated with the plaque.

Because of these factors, healthcare professionals typically include circulating HDL levels in many cardiovascular risk assessment tools.

HDL’s anti-inflammatory capacity

In the new study, the researchers included participants from a larger study: the PREVEND (Prevention of Renal and Vascular End Stage Disease) Study.

The PREVEND Study began in 1998 and is investigating the relationship between cardiovascular disease and kidney damage. The study has about 40,856 participants, all of whom are adults living in the city of Groningen in Northern Netherlands.

From this massive participant pool, the researchers behind the new study selected 680 participants. They excluded people who had experienced a cardiovascular event before the program tracking period.

The researchers used these 680 participants to create 340 case-control pairs of individuals. This meant that there were two groups: an experimental group of 340 people who experienced an initial cardiovascular event during the PREVEND tracking period and 340 people who did not.

The term “case-control pairs” refers to the fact that individuals from the experimental group were matched with someone from the control group who had the same sex, the same smoking status, and similar HDL levels. Each person in a pair had an age within 5 years of the other.

In the study, the researchers defined a cardiovascular event as experiencing a non-fatal or fatal heart attack, receiving a diagnosis of ischemic heart disease, or having surgery to open clogged coronary arteries.

The researchers extracted HDL from participant blood samples and assessed how much it was able to reduce inflammatory responses in endothelial cells, which line blood vessels.

They also measured levels of the participants’ C-reactive protein, which is a substance that increases in response to body-wide inflammation.

The researchers also assessed the participants’ cholesterol efflux capacity. This refers to how effectively their HDL removes cholesterol from cells similar to those in plaque.

After their analysis, the researchers found that HDL anti-inflammatory capacity was higher in people who did not experience cardiovascular events (31.6%) than in people who did (27%) during the follow-up period (1997–2009). For every 22% increase in HDL anti-inflammatory capacity, the risk of experiencing a heart event during the next 10 years reduced by 23%.

The participants’ HDL anti-inflammatory capacities were not related to circulating HDL cholesterol levels, cholesterol efflux efficiency, or C-reactive protein levels. The protective effect of increased HDL anti-inflammatory capacity was more powerful in women than men.

Improving cardiovascular risk prediction

Importantly, the team was also able to improve cardiovascular risk prediction by factoring HDL anti-inflammatory capacity into the Framingham Risk Score or replacing HDL levels with HDL anti-inflammatory capacity in the formula.

The Framingham Risk Score is a common tool that healthcare professionals use to assess the risk of developing coronary artery disease (CAD) during the next 10 years. It accounts for six CAD risk factors:

  • age
  • sex
  • total cholesterol levels
  • HDL levels
  • systolic blood pressure
  • smoking habits

The researchers write that their findings could have major clinical implications by providing healthcare professionals with more information to assess CAD risk.

If HDL inflammation capacity impacts CAD risk more than HDL levels, they could also help make currently used risk assessment tools more accurate.

Their findings could also encourage researchers to find medications to target or improve HDL inflammation capacity. This could offer healthcare professionals, and people at risk of CAD, a whole new avenue of preventive treatments.

Study limitations

Limitations in the study mean that scientists must now reproduce these findings in a much larger and far more diverse group of individuals.

The study included almost exclusively white participants. Just under 240 of the 340 case-control pairs in the study were male. The researchers also did not include information about stroke incidence in the study.

Furthermore, the study participants were genetically similar, coming from the same relatively small region of the world.

There are also no standardized methods of how to isolate HDL from plasma or how to test HDL functional abilities.

Still, despite these study drawbacks, the researchers are optimistic about their findings and what they could mean for millions of people going forward.

“The HDL cholesterol level is a good, established, simple, and cost efficient [cardiovascular disease] risk biomarker,” says Dr. Tietge.

“Our results, however, demonstrate that the anti-inflammatory capacity or assays looking at HDL function in general have the potential to provide clinically relevant information beyond the static HDL cholesterol measurements that are currently used.”

In a mouse study, scientists have shown that motor and non-motor symptoms of Parkinson’s disease are associated with two specific neural pathways.

The study paper, published in the journal Nature Neuroscience, opens the door to future research that may help develop interventions to treat the disease and its symptoms.

Parkinson’s disease

According to the National Institute on Aging (NIA), Parkinson’s disease is a progressive neurological condition that typically occurs in people aged 60 and older.

Parkinson’s primarily affects a person’s motor functions, that is, their ability to move their body in a coordinated manner. However, it can also have an impact on a person’s cognition and behavior, leading to mental health issues and problems with memory and attention.

According to the NIA, Parkinson’s occurs when neurons, or brain cells, die or become damaged. Cognitive and motor functions are affected by specific brain cells, and it is damage to these cells in particular that results in the symptoms of Parkinson’s.

Scientists do not know exactly why some people develop Parkinson’s. Research suggests it is likely to be due to a combination of hereditary and environmental factors, as well as the process of aging.

There is no known cure for Parkinson’s disease. As a consequence, treatments usually focus on relieving the symptoms caused by the condition.

To manage these symptoms, it is important to understand the structure of the parts of the brain that may be involved in the key symptoms of the disease.

However, the relationship between different neural circuits and the effects of Parkinson’s disease is still being explored.

Parkinson’s in the brain

In the present study, a team led by researchers from the University of California San Diego (UC San Diego) in La Jolla wanted to contribute to this knowledge.

They conducted a study in mice to understand the relationship between neural circuits in the brain and some of the functions that are typically affected by Parkinson’s disease, such as cognitive and motor abilities.

They looked in particular at the external globus pallidus (GPe) in the brains of mice, which previous research has linked to the motor symptoms of Parkinson’s.

The researchers used multiple methods to give a more detailed overview of this region of the mice’s brains, including electrophysiology, viral tracing, and behavioral experiments.

Importance for Parkinson’s therapy

The researchers identified two areas of the GPe and were able to relate these areas to motor skills and cognitive skills in the mice.

By manipulating neurons in these two parts of the brain, the scientists improved the mice’s locomotion and their reversal learning.

Dr. Byungkook Lim is an associate professor in the Neurobiology Section of the Division of Biological Sciences at UC San Diego and corresponding author of the study.

He explains, “our work demonstrates that the distinct neural circuitries in the basal ganglia are differentially involved in the motor and non-motor symptoms of Parkinsonian-like behaviors that occur at different stages of the disease.”

“This suggests that evaluation of the detailed circuit mechanisms is needed to fully understand the changes in [the] brain during the progression of [Parkinson’s disease] and could provide better therapeutic strategies for the treatment of [Parkinson’s disease].” – Dr. Byungkook Lim

The fact that specific neurons could be linked to particular changes in the brain regions of the mice means that it may be possible to develop new treatments for the symptoms of Parkinson’s.

In Dr. Lim’s words, “[s]elective manipulation of specific changes can rescue one type of symptom — without affecting other symptoms — of Parkinson’s disease.”