Day: 02/03/2024

World Cancer Day 2024 : How regular exercise shields us from cancer

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Regular workouts can help reduce the risk of cancer by various mechanisms, not least of which is how exercise affects the way each cell in the body breaks down food for energy, the body’s hormonal environment and the benefits of exercise for our immune system

Exercise increases energy metabolism in cells, enhances blood flow, supplies more oxygen to the tissues, and helps remove waste products, including lactate and other metabolites. These changes create a less favourable environment for cancer cells to thrive. (Image: Canva)

Exercise increases energy metabolism in cells, enhances blood flow, supplies more oxygen to the tissues, and helps remove waste products, including lactate and other metabolites. These changes create a less favourable environment for cancer cells to thrive.

Cancer remains one of modern medicine’s most formidable challenges. But amid the complexity of genetic factors and environmental triggers, we have a surprisingly potent ally in our fight against cancer: regular exercise.

In the modern health and wellness dictionary, the virtues of exercise are sung almost universally – a chorus echoing the benefits of improved cardiovascular health, stronger muscles, and enhanced mental well-being.

However, nestled within these well-known melodies is a less discussed yet profoundly significant verse – the role of regular exercise in reducing cancer risk.

To appreciate this relationship, let’s look at the impact of exercise on improving the respiration capabilities of each cell in our body and the beneficial hormonal environment triggered in the body that helps us reduce our risk of developing cancer.

Cellular alchemy of exercise

At its core, cancer is a disease marked by rogue cells that proliferate uncontrollably, a rebellion against the body’s orchestrated systems of controlled growth and programmed cell death known as ‘apoptosis’.

Central to understanding this is the concept of cellular respiration – the process by which cells convert food that we eat into a usable form of energy for the cell known as adenosine triphosphate (ATP).

Cancer cells, as Otto Warburg first observed in the 1920s, exhibit altered metabolic pathways (Chandel, 2014). Normal cells rely heavily on aerobic respiration – or ‘oxidative phosphorylation’ – to produce ATPs. This is a process that occurs in the mitochondria, the powerhouses of every cell, under oxygen-rich conditions in which food is burned for energy using the oxygen we breathe. Cancer cells, on the other hand, preferentially use anaerobic form of respiration known as ‘glycolysis’, a process of converting glucose into the ATP without using oxygen even when it is abundantly available in the cell. This phenomenon, known as the Warburg effect, results in less efficient energy production and an acidic environment conducive to cancer progression and metastasis of tumours (Liberti & Locasale, 2016).

Systemic benefits of exercise

Exercise – a well-choreographed dance of physiological adaptations – can control these cellular processes of energy production. When we exercise, our muscles demand more energy (ATP), accelerating glycolysis and oxidative phosphorylation processes for energy production. Exercise increases energy metabolism in cells, enhances blood flow, supplies more oxygen to the tissues, and helps remove waste products, including lactate and other metabolites. This heightened activity counters lactate production in cancer cells due to perpetual glycolysis and improves its removal. These changes create a less favourable environment for cancer cells to thrive (Høier & Hellsten, 2014).

However, exercise’s benefits extend far beyond these immediate metabolic shifts. Regular physical activity leads to a multitude of long-term adaptations that collectively fortify the body against the threat of cancer. For instance, exercise has been shown to improve the efficiency of mitochondria by accelerating their repair and reproduction rate, thereby improving cellular aerobic respiration and potentially counteracting the Warburg effect observed in cancer cells (Hood, 2011).

Exercise and the reduction of specific cancer risks

The empirical evidence supporting exercise’s protective role against cancer is substantial and growing. Exercise exerts a systemic influence on the body’s hormonal milieu. It lowers levels of inflammatory markers, insulin and insulin-like growth factors, which, at high levels, are associated with increased cancer risk, particularly in colon cancers (Lee, 2003) (Hojman et al., 2018).

Breast cancer, a disease where hormonal factors significantly influence risk, is less prevalent in women who engage in regular physical activity (McTiernan, 2003). This protective effect is partly attributed to exercise-induced reductions in levels of estrogen, a hormone that can fuel certain types of breast cancer.

Moreover, physical activity aids in weight management, which is crucial since obesity is a known risk factor for various cancers, including endometrial and kidney cancers (Lauby-Secretan et al., 2016).

Regular physical activity also boosts the immune system’s efficiency, enhancing its ability to detect and eliminate emerging cancer cells (Pedersen & Saltin, 2015). This bolstered defence is particularly critical in the early stages of cancer development, where the immune system’s ability to curb the growth of aberrant cells can be pivotal.

From a cellular standpoint, exercise induces oxidative stress, paradoxically yielding beneficial effects. This stress activates a cascade of molecular responses that enhance the body’s antioxidant defences and repair mechanisms, fostering resilience against cellular damage that could otherwise lead to cancer (Radak et al., 2005).

In the broader tapestry of cancer prevention, exercise represents a thread interwoven with other lifestyle factors such as diet, smoking cessation, and alcohol moderation. The synergy of these factors creates a robust shield against cancer development.

Pathway to cancer prevention

So, how much exercise is needed to harness these protective benefits? The American Cancer Society recommends at least 150 minutes of moderate-intensity or 75 minutes of high-intensity exercise each week (Rock et al., 2012). However, the magic of exercise is not in its complexity but in its accessibility. From brisk walking to structured gym workouts, the spectrum of physical activity that can confer these benefits is vast, offering a plethora of choices adaptable to different ages, preferences, and lifestyles. Each step taken, each pedal turned, is not just a physical act but a declaration of resilience against a formidable foe.

The narrative of exercise as a cancer prevention tool is as compelling as it is scientifically grounded. As we navigate through the complexities of cancer, let us not underestimate the power of putting our bodies in motion. By delving into the intricate dance of cellular respiration and the systemic physiological adaptations invoked by physical activity, we uncover a powerful ally in the fight against cancer. This understanding empowers us to take proactive steps to reduce our cancer risk, and sheds light on potential avenues for scientific research and public health policies.

As we continue to unravel the mysteries of cancer, the role of exercise in this saga remains a beacon of hope and a testament to the human body’s resilience. Finally, in the words of Siddhartha Mukherjee, Pulitzer Prize winner and a leading researcher in cancer, we are “the agents of our destiny.” Through exercise, we wield a powerful tool in shaping that destiny away from cancer.

First functional human brain tissue produced through 3D printing

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A team of researchers has created the first functional 3D-printed brain tissue to examine the brain’s function and study various neurological disorders. 

Representational image of signal transmitting neurons.

Representational image of signal transmitting neurons.

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The first functional 3D-printed brain tissue has been developed to examine the human brain’s function and study various neurological disorders. 

According to experts at the University of Wisconsin-Madison, printed tissue can “grow and function like typical brain tissue.”

This 3D-printed brain model might be useful in studying various neurological and neurodevelopmental problems, including Alzheimer’s and Parkinson’s disease.

“This could be a hugely powerful model to help us understand how brain cells and parts of the brain communicate in humans,” said Su-Chun Zhang, professor of neuroscience and neurology at UW–Madison’s Waisman Center.

“It could change the way we look at stem cell biology, neuroscience, and the pathogenesis of many neurological and psychiatric disorders,” added Zhang in the release. 

Use of horizontal 3D printing approach

Instead of using the conventional vertical layer stacking method, the researchers followed an innovative horizontal 3D printing approach in this development.

Neurons produced from induced pluripotent stem cells were carefully put in layers utilizing a softer bio-ink gel, creating a more favorable environment for growth.

“The tissue still has enough structure to hold together but it is soft enough to allow the neurons to grow into each other and start talking to each other,” Zhang said. 

First functional human brain tissue produced through 3D printing
Functional network model.

The developers mention that they deliberately maintained the tissue’s thinness to ensure optimal oxygen and nutrient intake for the neurons from the surrounding growth media.

The multilayer printing allowed the cells to form connections, resulting in networks similar to those observed in human brains.

Within these networks, neurons appeared to actively communicate by sending signals to one another. This communication occurs via neurotransmitters, chemical messengers that aid in passing signals between neurons.

“We printed the cerebral cortex and the striatum, and what we found was quite striking. Even when we printed different cells belonging to different parts of the brain, they could still talk to each other in a very special and specific way,” said Zhang in the press release.

The authors highlight that this method provides precision, allowing for control over cell types and arrangement. This feature is absent in brain organoids, which are miniature lab-grown organs created for brain research. 

This 3D print approach to emulate sophisticated communication and network development found in human brain tissue has great potential to provide insights into brain function and its disorders. 

The findings were published in the journal Cell Stem Cell.

Study abstract:

Probing how human neural networks operate is hindered by the lack of reliable human neural tissues amenable to the dynamic functional assessment of neural circuits. We developed a 3D bioprinting platform to assemble tissues with defined human neural cell types in a desired dimension using a commercial bioprinter. The printed neuronal progenitors differentiate into neurons and form functional neural circuits within and between tissue layers with specificity within weeks, evidenced by the cortical-to-striatal projection, spontaneous synaptic currents, and synaptic response to neuronal excitation. Printed astrocyte progenitors develop into mature astrocytes with elaborated processes and form functional neuron-astrocyte networks, indicated by calcium flux and glutamate uptake in response to neuronal excitation under physiological and pathological conditions. These designed human neural tissues will likely be useful for understanding the wiring of human neural networks, modeling pathological processes, and serving as platforms for drug testing.

Studies Shed Light on Contributors to Sudden Infant Death Syndrome

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Researchers have discovered that seizures and brain infections may be two contributors, and some believe SIDS could be a rare adverse vaccination event.

Two papers were recently published consecutively, discussing the possible disease cause for sudden infant death syndrome (SIDS).

Researchers have discovered that seizures and brain infections may be two contributors. Additionally, as infants are widely vaccinated, some researchers suggest that SIDS could be a rare adverse event of vaccination, as established in previous studies.

SIDS is the sudden and unexplained death of a healthy baby under the age of 1 who dies while sleeping. According to the U.S. Centers for Disease Control and Prevention (CDC), SIDS is the third leading cause of overall infant mortality in the United States, with most deaths occurring in infants less than 6 months old.

Currently, there is no established mechanism for the cause of SIDS, though there has been extensive public health messaging linking SIDS with sleeping positions. Scientists are continuously looking for other causes.

The most recent report published in JAMA Neurology on Jan. 29 points to the human parechovirus 3 (HPeV3) as potentially tied to the death of one child in the study.

HPeV3 is known to cause both mild respiratory infections and severe nervous system infections

“Our findings demonstrate proof of concept that undetected infections may contribute to risk of SIDS and that increased surveillance of HPeV3 in particular may be warranted,” study co-author Ben Okaty, a geneticist at Harvard Medical School, told Live Science.

However, the virus cannot be definitively confirmed to be the cause of the infant’s death. The study evaluated 64 cases overall, and no conclusive findings were reported on the other infants.

“It is likely that there might be other similar cases,” specifically involving the HPeV3 virus, said Dr. Avindra Nath, clinical director of the National Institute of Neurological Disorders and Stroke, who was not involved in the study, told Live Science. “Patients should be investigated for that possibility.”

In 1994, Drs. James Filiano and Hannah Kinney conceptualized that SIDS involved an intersection of the following three risks:

  1. Infant vulnerability.
  2. The infant is in a critical development period, such as the first year of life.
  3. An exogenous stressor.

Most SIDS research has gone into identifying the external stressor, which could then be linked to a potential disease process.

Premature birth, low birth weight, and exposure to tobacco smoke may all put an infant at risk of sudden death.

In the case of the JAMA Neurology study, the authors considered HPeV3 infection a possible stressor that may have caused changes in the brainstem, which exacerbated an underlying vulnerability.

Vaccines may also be considered a stressor.

Another Recent Study

Some studies have considered convulsive seizures as a potential cause of SIDS.

Most recently, seven deaths in young toddlers were linked to convulsive seizures after analyzing videos from baby monitors. The seven cases made up 301 deaths registered in the New York University Sudden Unexplained Death in Childhood Registry and Research Collaborative. Around 250 deaths occurred in children under 5 years of age.

“Audio-visual recordings in 7 toddlers with unexplained sudden deaths strongly implicate that deaths were related to convulsive seizures, suggesting that many unexplained sleep-related deaths may result from seizures,” the study authors wrote. Four of the seven toddlers had illnesses up to three days before their time of death.

Furthermore, the authors found that among the children who died before 5, 29.4 percent had a history of febrile seizures, and 22 percent of toddlers who died due to infections or accidents also experienced febrile seizures.

Vaccines Contributing to SIDS

With COVID-19 vaccines and boosters being approved for pregnant mothers and anyone aged 6 months or older, interest in the link between vaccines and potential SIDS has been renewed.

“I was very interested in sudden infant death syndrome. … There is a relationship with vaccines,” Dr. Paul Byrne, a retired neonatologist and one of the founders of neonatal and perinatal medicine, said in an informal 2017 interview.

“One of the things that we identified was magnesium deficiency,” Dr. Byrne said.

Magnesium is an essential nutrient for a baby’s development. Studies have linked magnesium deficiency to SIDS. Vaccinations may also contribute to magnesium deficiency since activation of the immune system causes the body to use up nutrients like magnesium.

While this temporary magnesium depletion may be relatively harmless in a well-adjusted adult, babies are far more sensitive to such changes.

Furthermore, early magnesium deficiencies may not be detected through common laboratory tests, Dr. Byrne explained in the interview.

The most common tests for magnesium are blood tests, but they may not give the full picture of a baby’s nutritional status since the cells may become nutrient deficient before this is ever indicated in the blood.

Dr. Byrne said a good way to detect magnesium deficiency is to give babies magnesium and see if they excrete it in their urine. If all the magnesium is retained, it indicates the baby is deficient, whereas if magnesium is excreted, the baby is sufficient in it.

Some case studies involving SIDS have also ruled that vaccines could be a contributor.

A 2019 study in Japan evaluated 57 cases of sudden death in children 2 years or younger. Among these children, 32 were vaccinated.

The authors identified three infants who died within three days of getting the hepatitis B vaccine alongside other vaccines. All three cases had pneumonia and upper respiratory tract infection as contributors to their deaths, and all three had inflammation in the same organs.

“Judgment of the disorders as truly related to vaccination is difficult, but suspicious cases do exist. Forensic pathologists must devote more attention to vaccination in sudden infant death cases,” the authors wrote.

In his review of the CDC’s vaccine adverse event reporting system (VAERS) on SIDS, investigative medical journalist and director of the Institute of Medical and Scientific Inquiry Neil Miller found that between 1999 and 2019, 58 percent of SIDS occurred within three days of vaccination, while over 78 percent occurred within seven days, forming a strong temporal association.

A major limitation of his study is that there is a chance of reporting bias since doctors and parents may have been more likely to report SIDS to VAERS if it happened in close temporal proximity to the vaccination than if it had happened several days or weeks later, he reasoned.

However, he found that a smaller proportion of total infant deaths were reported on the day of vaccination than on the day afterward, and this fits in with neuropathologist Dr. Douglas Miller’s hypothesis that the physiological effects of vaccines occur over time, activating various immune messengers over one to two days after the vaccination.

Mr. Neil Miller’s review discussed that before the introduction of organized vaccination programs in the 1960s, crib deaths or SIDS was a very rare phenomenon that had no clinical term to describe it.

The national immunization campaigns were expanded during this time, and new vaccines were introduced. For the first time, most U.S. infants were required to receive several doses of diphtheria-pertussis-tetanus (DPT), polio, and measles vaccines.

By 1969, a surge in unexplained infant deaths had prompted researchers to coin a new medical term: sudden infant death syndrome (SIDS). By 1972, SIDS had become the leading cause of post-neonatal mortality in the United States.

Considering the rarity of SIDS prior to organized vaccination programs, Mr. Miller informed The Epoch Times that he believes a significant portion of SIDS cases may be linked to vaccination.

One challenge in establishing a connection between vaccines and potential infant deaths stems from the fact that updated International Classification of Diseases (ICD) codes haven’t included “prophylactic inoculation and vaccination” as a category of death since 1979.

As a result, Mr. Miller suspects that coroners may now be categorizing infant deaths under SIDS.

What is an orgasm headache?

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An orgasm headache is a sudden, intense headache before or during an orgasm. It is also called a primary headache associated with sexual activity. The exact cause is unclear, but some medications may help.

If a person regularly experiences headaches during sex. It is best to contact a doctor for advice. Headaches can sometimes signal an underlying condition.

Read on to learn more about what orgasm headaches feel like, when they can occur, and possible risk factors. This article also discusses treatment options, when to contact a doctor, and more.

A note about sex and gender

Sex and gender exist on spectrums. This article will use the terms “male,” “female,” or both to refer to sex assigned at birth. Click here to learn more.

Two people are in bed.

An orgasm headache is a primary headache. A primary headache is a condition itself, not a symptom of another health issue.

A person may experience an orgasm headache just before or during sexual climax. These headaches can happen during masturbation or partnered sex.

Orgasm headaches are one of two types of primary sex headaches. The other type is a sexual benign headache, which doctors also call a pre-orgasm headache.

Learn more about the relationship between sex and headaches.

What do orgasm headaches feel like?

People typically experience orgasm headaches just before or during an orgasm.

The pain may feel:

  • intense
  • explosive
  • throbbing

An orgasm headache may beTrusted Source painful behind or around the eye area.

The condition can often cause pain on both sides of the head. Moving around may make the pain worse.

The pain can occur abruptly, and after it diminishes a person may feel a throbbing in their head, which can sometimes last for several hours or even days.

Unlike migraine headaches, orgasm headaches do not usually occur with nausea or sensitivity to light or sound.

What causes orgasm headaches?

Doctors do not know what causes orgasm headaches, but they may beTrusted Source a type of vascular headache. These result from blood vessels swelling in the brain.

When a person has an orgasm, their blood pressure increases rapidly. This surge in pressure causes blood vessels in the head to dilate quickly, which can trigger sudden, intense headaches in some people.

What are the risk factors for orgasm headaches?

Anyone can experience orgasm headaches. However, males are up to four timesTrusted Source more likely to experience primary headaches associated with sexual activity than females.

The mean age of onset is 39.2 years, though they can begin earlier or later.

People with a history of migraine headaches, exertional headaches, or cough headaches may be more likely to get orgasm headaches.

What are the treatments for orgasm headaches?

According to the International Headache Society, studies indicate that up to 40% of people with primary headaches associated with sexual activity experience them for over a year.

If a person experiences orgasm headaches, it is best to contact a doctor to discuss how best to manage them.

Treatment options for orgasm headaches can include prescription medications such as triptans. Taking triptans before sexual intercourse may prevent orgasm headaches in up to 50%Trusted Source of cases.

A doctor may also recommend topiramate and beta-blockers such as propranolol.

If a person does not respond well to beta-blockers, a doctor may recommend indomethacin, which is a prescription nonsteroidal anti-inflammatory drug (NSAID). Some calcium channel blockers may also be beneficial. These include:

  • verapamil
  • flunarizine
  • nimodipine

Headaches during sex can sometimes result from another condition. In this case, they are secondary headaches. Treating the underlying issue can help reduce or prevent these headaches.

When should a person contact a doctor?

People who regularly experience headaches during sex should contact a doctor. The doctor can help determine if they are primary or secondary headaches.

Orgasm headaches are primary headaches. A secondary headache occurs as a result of an underlying condition. Some serious conditions that can cause secondary headaches during sex include:

Secondary sex headaches with a serious cause are likely to occur alongside other symptoms, such as:

  • nausea
  • vomiting
  • a stiff neck
  • loss of consciousness

People who experience these symptoms should seek immediate medical attention.

Summary

An orgasm headache is a type of primary headache that occurs during sexual activity.

Orgasm headaches may result from a rapid expansion of blood vessels in the brain. This occurs when a person’s blood pressure rises before and during orgasms.

It is best for anybody who experiences orgasm headaches to contact their doctor for an evaluation. The doctor can recommend medications to help treat or prevent headaches.

Disease risk rises for health care workers exposed to radiation on the job

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Health care professionals who have been exposed to radiation over the long term face a higher risk of disease, according to a study published Tuesday in the journal Circulation.

Why it matters:

Radiation has long been recognized as a cancer risk. This study suggests health care professionals who work in labs that use radiation for procedures such as coronary angiography and angioplasty face an elevated risk of a number of health problems beyond cancer.

The nitty gritty:

Researchers in Italy surveyed more than 700 health care workers, scientists, and engineers and collected information about their work, lifestyles, and health, including over 400 who worked in catheterization labs, which use radiation. After controlling for age, gender, and smoking, the researchers found that cath lab workers had higher rates of disease: They were 2.8 times more likely to have skin lesions, 6.3 times more likely to have cataracts, and 7.1 times more likely to have back, neck, and knee problems. Researchers also reported higher rates of thyroid disease, anxiety, depression, high blood pressure, and high cholesterol. This risk was especially pronounced in workers with longer duration of radiation exposure over their careers.

You’ll want to know:

The study highlighted a “graded relationship” in the prevalence of disease, explained Dr. Sripal Bangalore, an interventional cardiologist at New York University’s Langone Medical Center who wasn’t involved in the research. There was a higher prevalence of disease in those workers who stood closest to the source of radiation: Physicians were more at risk than than nurses, who in turn were more at risk than techs.

But keep in mind:

The study was based on self-reported data, which has limitations. Studies that measure actual radiation exposure, rather than self-reports, would provide more precise data, said Dr. Sunil Rao, an associate professor of medicine at Duke who wasn’t involved in the study.

What they’re saying:

“Unfortunately I don’t think this is going to engender any kind of cultural change,”  Rao said. “Procedural-related medicine tends to have this macho culture where people don’t necessarily pay attention to their own health.”

Other experts noted that workers may not use protective gear because of time constraints.

Protective measures like leaded aprons, thyroid collars, leaded glasses, and overhead radiation shields can be used to reduce workers’ radiation exposure, but “unfortunately, in many catheterization laboratories, these measures do not exist or are not employed routinely,” said lead investigator Maria Grazia Andreassi of the Italian National Research Council.

The bottom line:

Education and awareness are key, said Andreassi. Health care workers should understand the risks they’re exposed to in catheterization labs and other settings, and take protective measures.

Lead aprons offer little protection during X-rays. Why do so many clinicians keep using them?

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Think back to the last time you had an X-ray: The radiologic technologist probably placed a lead apron over part of your body to protect it from radiation. That’s now an outdated practice: The American Association of Physicists in Medicine no longer supports shielding patients’ reproductive organs and fetuses during imaging studies that use radiation, such as X-rays and CT scans.

Changing this practice has been a near impossible feat.

While the association’s statement rocks the boat of convention, it’s based on mounting evidence that shielding is not as helpful as once thought, and it might even have negative consequences.

One of the downsides is that shielding can obscure the imaging field, leading to an unusable X-ray or CT scan, requiring the patient to have another. That increases his or her radiation exposure. One study found that shields were misplaced half of the time during pelvic X-rays and often obscured important bony landmarks.

Another concern is that most imaging machines that use radiation automatically determine the dose of radiation required to produce a successful image. If the machine senses a shield, it increases the dose in an effort to image through the shield, leading to an increase in radiation exposure.

There are few positive effects to shielding. The chance of radiation exposure outside the beam’s scope is already minimal. If reproductive organs or a fetus are outside the beam’s path, there is no reason to shield. A Mayo Clinic study found that shielding the abdomen or pelvis during chest CT scans didn’t actually reduce the dose of radiation enough to justify the risk of artifacts in the imaging field.

There are two important exceptions to changing the practice of shielding. First, it still applies to providers. “Health care professionals who regularly use radiation, such as radiologic technologists or surgeons, have a higher rate of exposure day in and day out than a single patient undergoing an imaging study,” says Jennifer O’Riorden, director of health physics and radiation safety officer at Lahey Medical Center in Burlington, Mass. “These providers should continue to wear the appropriate protective apparel.”

Second, shielding should be used if or when it offers patients a psychological benefit. Some patients may be nervous if their provider doesn’t automatically shield them during an X-ray or CT or nuclear imaging scan. Rebecca Marsh, a medical physicist and author of the journal article that served as the framework for the American Association of Physicists in Medicine statement, suggests that providers should talk with their patients about the risks of shielding but still make the professional decision to shield if the comfort it provides outweighs the risks.

Given the evidence and the current guidelines, why is it so hard to change the status quo?

First, radiation is a very real fear for many people, partly because of past disasters. Chernobyl, Hiroshima, and Fukushima are very public demonstrations of the power of radiation gone wrong. In the clinical setting, the fear of radiation is also likely due to a lack of education and understanding of exposure and risk.

A survey of patients in an emergency department found that most do not accurately understand the radiation dose associated with various imaging studies: Standard X-rays use a negligible amount of radiation; CT scans and nuclear imaging use the most. Only 14% of those surveyed said that CT scans use more radiation than chest X-rays. Less than one-quarter accurately said that MRIs do not use radiation at all. A separate survey found that even medical providers do not always fully understand radiation exposure and risk.

Another reason it is hard to move away from shielding is that it is a deeply engrained practice for both patients and providers. “Provider education has always been based on the ALARA principle — as low as reasonably achievable — using time, distance, and shielding to minimize the radiation dose,” says O’Riorden. Patients have come to expect it, too.

Shielding reproductive organs and fetuses became the norm in the mid-1900s because experts worried that radiation-induced genetic mutations in sperm or eggs could be passed on to a patient’s future children. It’s worth noting that hereditary mutations due to radiation exposure have never been clinically documented. The federal government issued regulations in the 1970s recommending shielding, solidifying the practice. (The Food and Drug Administration is considering revising these regulations later this year.)

These recommendations and conversations leave out an important stakeholder: dentists. About half of the X-rays completed in the U.S. each year are done in dentists’ offices, not doctors’ offices. Shielding is less likely to interfere with a dental X-ray, or even be necessary for it. It seems logical that dentists would be willing to adopt new guidelines about shielding, but they were left out of the push to change the status quo. That was a huge oversight. (In the United Kingdom, dentists have been asked to cease “the widespread practice of applying patient contact shielding.”) If U.S. dentists continue to shield their patients while doctors don’t, there is potential for considerable confusion among patients.

Radiation exposure is an example of the risk/benefit trade-off we make with every decision. When imaging studies that use radiation are clinically appropriate, the benefits far outweigh the risks and shielding does little to mitigate those risks. “When it comes to patient safety and radiation risk, it is very important — yet difficult — to not let emotions and fear overrule an unbiased evaluation of available data,” says Marsh.

Fear and tradition are powerful forces that often work against change. Aligning current guidelines with the growing evidence that suggests shielding is not protective will take buy-in from both providers and patients. But to earn that, we must focus first on conversations that address the engrained fear of medical radiation and misunderstanding about it.

Lead aprons not necessary for patients during X-rays, says largest U.S. dental group

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Since the 1920s, lead vests and aprons have served as trusted shields against the harmful effects of X-rays for radiologists, technicians, and patients. But new safety guidelines from the American Dental Association (ADA) call for discontinuing their use among patients, both because X-ray technology has evolved significantly over the years, and because there are better ways to reduce patients’ exposure to radiation, such as using digital as opposed to conventional X-ray film.

Other medical organizations have been making similar points for some time. In 2019, the American Associations of Physicists in Medicine concluded that the use of patient lead aprons should be discontinued as they were both unnecessary for safety and had the potential to jeopardize the quality of images. In 2021, the American College of Radiology also recommended discontinuing lead shielding.

Lead aprons and other lead shields provide “no additional benefit to the patient except for some psychological comfort,” said Mahadevappa Mahesh, a professor of radiology and cardiology at Johns Hopkins University and the chair of the American College of Radiology Commission on Medical Physics. It’s still recommended that doctors and technicians wear lead garments if they’re working in rooms where X-rays are delivered.

But safety practices can linger even after technological advances render them outdated — so it’s reasonable to think that some patients and practitioners may be reluctant to let lead armor go. Mahesh said it will take time to educate dentists and convince them to discontinue use of the shields, as has been the case with other medical professionals.

“This is a legacy practice,” he said. X-ray technicians and radiologists were trained to have patients wear lead shields for their protection, and it takes time to learn to do things differently. “There seem to be pockets of resistance … so I foresee the same type of resistance [among dentists] also.”

Letting go of lead armor

Lead vests and other shields, such as thyroid collars, are meant to protect patients against scattered radiations. But modern X-ray machines are designed to restrict the beam so it only hits the area that needs the imaging, without potentially dangerous secondary rays.

The dose of radiation delivered by the machines is also much smaller than it used to be, so the risk of secondary radiation for the patient is essentially nonexistent. X-rays nowadays are considered safe for patients irrespective of age and health conditions, including pregnancy.

Moreover, lead shields can even be counterproductive, as awkward or incorrect positioning may end up blocking some necessary X-rays, which leads to repeat imaging and exposure to additional unnecessary radiation.

Clues from mice could help explain why women face a higher risk of autoimmune disorders

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Researchers have long known that women are more likely to develop autoimmune disorders than men, though they’ve struggled to fully understand why. Now a new study in mice suggests a key part of the answer may be that an RNA molecule that’s indispensable for female survival steers the body toward immune friendly fire.

A team led by Stanford scientists found that Xist, a molecule that teams up with proteins to keep female cells from activating a double (and deadly) dose of X chromosome genes, can trigger antibodies that latch onto complexes of the RNA and its protein partners.

Xist isn’t normally expressed in male cells, but to show that these complexes help drive autoimmunity, the authors created male mice that made Xist on demand. These animals were likely to show signs of autoimmune disease roughly as severe as in female mice.

It’s too early to tell for certain if the findings, published on Thursday in the journal Cell, will hold up in people. But the study’s authors found an encouraging hint. When they examined blood samples from healthy adults and patients with autoimmune diseases that mainly affect females, they found that the latter group was more likely to have antibodies that recognized Xist-protein complexes. That raises the possibility that the findings could be used to devise new and better ways to diagnose autoimmune diseases and to monitor whether treatments are working.

“This is like a completely different and novel explanation for female bias in immune disease,” said Howard Chang, a Stanford physician-scientist and the study’s senior author. “What our study really showed was that it’s not just the second X chromosome, it’s actually a very special RNA that comes from that second X chromosome, and just that RNA perhaps plays a major role.”

While many individual autoimmune disorders are rare, they’re together the third most common disease category after cancer and heart disease and affect about 8% of the population. The sex bias for these diseases is stark; four out of every five patients are female. In some cases, the imbalance is even more lopsided; 90 percent of lupus patients and 95% of those with Sjögren’s syndrome are female.

By comparison, males are generally more susceptible to infectious disease. Case in point: Men are more likely to die of Covid-19, while women have been more likely to develop long Covid, which experts say mimics aspects of autoimmune disorders.

Researchers have identified many potential explanations. Autoimmunity typically kicks in after puberty, suggesting that sex hormones play an important role, a theory supported by past research. The X chromosome itself is another potential culprit, as females carry two copies while males have one — well, most of the time. People with Klinefelter’s syndrome have two X’s and one Y, and, while they are biologically male, have an increased risk of autoimmunity compared to XY males.

That observation suggested to Chang and others that something on the X chromosome contributes to autoimmunity. That’s why his team zeroed in on Xist, an RNA molecule coded for by the X chromosome. Cells with two X’s can’t survive if both are active, as they’d produce a deadly double dose of proteins. Xist helps shut down one of the two X’s in each female cell by coating the chromosome in a way that looks a bit like a cloud of cotton candy spooled around a cone at a county fair.

If you’ve ever seen a calico cat, you’ve seen X inactivation. The gene that codes for fur pigment is on the X, and the orange and black patches on these cats reflect areas where one X chromosome was inactivated versus the other. And since X inactivation doesn’t happen in males, nearly all calico cats are female.

Chang’s lab had previously found that Xist associates with scores of proteins that help with X inactivation, and he’d noticed that these RNA-protein complexes resemble known targets of autoantibodies, antibodies often linked to autoimmunity that recognize the body’s own proteins rather than pieces of a pathogen. That led the team to wonder if Xist-protein complexes might play an important role in driving the sex bias seen in autoimmunity.

But the researchers wanted to separate the role of Xist from that of the rest of the X chromosome and from the effects of female sex hormones, so they went looking for clues in an unlikely place: male mice. The scientists genetically engineered male mice to carry Xist on one of their chromosomes and to produce the RNA molecule any time the animals were injected with doxycycline, an antibiotic. And they modified Xist so that it wouldn’t silence the chromosome but would simply cling to it.

The authors then tried to trigger lupus in the animals by injecting them with pristane, an oil known to induce inflammation and autoimmunity in mice. They found that most of the male mice producing Xist developed the same sort of multi-organ autoimmunity typically seen in females, but only if the mice came from a strain known to be susceptible to developing autoimmunity. Other experiments showed that switching on Xist in male mice caused their T cells to activate genes in ways that more closely resembled females.

To see if their findings matched what was happening in people, researchers analyzed blood samples from healthy donors and from patients with dermatomyositis, lupus, and systemic sclerosis. They found that autoimmune patients, about 86% of whom were female, had higher levels of autoantibodies against proteins associated with Xist than healthy donors. Some of these autoantibody responses were largely disease-specific while others were shared across all three conditions.

Chang says the findings suggest that, in women genetically predisposed to autoimmunity, a bit of inflammation or tissue damage might expose Xist-protein complexes that are usually cloistered in a cell’s nucleus, and that this exposure could trigger autoantibodies and increase their risk of developing disease. He adds that his team is now exploring whether they can use their findings to develop better ways to spot autoimmune disease and monitor treatment effectiveness, as a drop in autoantibodies to Xist-associated proteins might be an encouraging sign a therapy is working.

But it’s too early to say for sure that the autoantibodies the authors focused on are a key driver of autoimmunity, cautioned Montserrat Anguera, a researcher at the University of Pennsylvania who was not involved in the study. Anguera, who studies X inactivation and sex biases in autoimmunity, notes that it would be helpful to know if researchers find autoantibodies to Xist-linked proteins in autoimmune diseases that don’t have a sex bias. And she adds that Xist likely contributes to autoimmunity in many ways, citing recent evidence that the molecule itself can directly trigger inflammation.

“I don’t think the data is there yet to say that it’s the most important [factor] right now, because it’s sort of the first observation that this is possible,” she said of the Stanford team’s findings. “It just really highlights the fact that it’s not one pathway that involves the inactive X chromosome; there’s different ways that the inactive X can contribute to female bias in autoimmune disease.”

18 Secrets for a Longer Life.

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Protect Your DNA

Protect Your DNA

1/18

As you age, the ends of your chromosomes become shorter. This makes you more likely to get sick. But lifestyle changes can boost an enzyme that makes them longer. Plus, studies show diet and exercise can help protect them. The bottom line: Healthy habits may slow aging at the cellular level.

Play to Win

Play to Win

2/18

An 80-year study found people who are conscientious — meaning they pay attention to detail, think things through, and try to do what’s right — live longer. They do more for their health and make choices that lead to stronger relationships and better careers. 

Make Friends

Make Friends

3/18

Here’s another reason to be grateful for your friends: They might help you live longer. Dozens of studies show a clear link between strong social ties and a longer life. So make the time to keep in touch.

Choose Friends Wisely

Choose Friends Wisely

4/18

Your friends’ habits rub off on you, so look for buddies with healthy lifestyles. Your chances of becoming obese go up if you have a friend who adds extra pounds. Smoking also spreads through social ties, but quitting is also contagious.

Quit Smoking

Quit Smoking

5/18

We know giving up cigarettes can lengthen your life, but by how much may surprise you. A 50-year British study shows that quitting at age 30 could give you an entire decade. Kicking the habit at age 40, 50, or 60 can add 9, 6, or 3 years to your life, respectively.  

Embrace the Art of the Nap

Embrace the Art of the Nap

6/18

A siesta is standard in many parts of the world, and now there’s scientific evidence that napping may help you live longer. One study showed that those who had a regular snooze were 37% less likely to die from heart disease than those who rarely steal a few winks. Researchers think naps might help your heart by keeping stress hormones down.

Follow a Mediterranean Diet

Follow a Mediterranean Diet

7/18

It’s rich in fruits, vegetables, whole grains, olive oil, and fish. The plan can also put a serious dent in your chances of getting metabolic syndrome — a mix of obesity, high blood sugar, high blood pressure, and other things that make you more likely to get heart disease and diabetes.

Eat Like an Okinawan

Eat Like an Okinawan

8/18

The people of Okinawa, Japan, once lived longer than any other group on Earth. The region’s traditional diet is why. It’s high in green and yellow vegetables and low in calories. Plus, some Okinawans made a habit of eating only 80% of the food on their plate. Younger generations have dropped the old ways and aren’t living as long.

Get Hitched

Get Hitched

9/18

Married people tend to outlive their single friends. Researchers say it’s due to the social and economic support that wedded bliss provides. While a current union offers the greatest benefit, people who are divorced or widowed have lower death rates than those who’ve never tied the knot.

Lose Weight

Lose Weight

10/18

If you’re overweight, slimming down can protect against diabetes, heart disease, and other conditions that take years off your life. Belly fat is bad for you, so focus on deflating that spare tire. Eat more fiber and exercise regularly to whittle your middle.

Keep Moving

Keep Moving

11/18

The evidence is clear. People who exercise live longer on average than those who don’t. Regular physical activity lowers your chances of getting heart disease, stroke, diabetes, some forms of cancer, and depression. It may even help you stay mentally sharp into old age. Ten-minute spurts are fine, as long as they add up to about 2.5 hours of moderate exercise per week.

Drink in Moderation

Drink in Moderation

12/18

Heart disease is less common in people who drink in moderation than in people who don’t drink at all. On the other hand, too much alcohol pads the belly, boosts blood pressure, and can cause a host of other health problems. If you don’t drink, don’t start now!  The risks outweigh the benefits when it comes to alcohol. If you do drink alcohol limit yourself according to limits set by national guidelines (from the National Institute on Alcohol Abuse and Alcoholism-NIAAA). The limits are based on your sex and age: 

Get Spiritual

Get Spiritual

13/18

People who attend religious services tend to live longer than those who don’t. In a 12-year study of people over age 65, those who went more than once a week had higher levels of a key immune system protein than their peers who didn’t. The strong social network that develops among people who worship together may boost your health.

Forgive

Forgive

14/18

Letting go of grudges has surprising physical health benefits. Chronic anger is linked to heart disease, stroke, poorer lung health, and other problems. Forgiveness will reduce anxiety, lower blood pressure, and help you breathe more easily. The rewards tend to go up as you get older.

Use Safety Gear

Use Safety Gear

15/18

Accidents are the third most common cause of death in the U.S. and the top cause for people ages 1 to 24. Wearing safety gear is an easy way to boost your odds of a long life. Seatbelts reduce the chances of death in a car wreck by 50%. Most fatalities from bike accidents are caused by head injuries, so always wear a helmet.

Make Sleep a Priority

Make Sleep a Priority

16/18

Getting enough quality sleep can lower your risk of obesity, diabetes, heart disease, and mood disorders. It’ll also help you recover from illness faster. Burning the midnight oil, on the other hand, is bad for you. Snooze for less than 5 hours a night and you might boost your chances of dying early, so make sleep a priority.

Manage Stress

Manage Stress

17/18

You’ll never completely avoid stress, but you can learn ways to control it. Try yoga, meditation, or deep breathing. Even a few minutes a day can make a difference.

Keep a Sense of Purpose

Keep a Sense of Purpose

18/18

Hobbies and activities that have meaning for you may lengthen your life. Japanese researchers found men with a strong sense of purpose were less likely to die from stroke, heart disease, or other causes over a 13-year period than those who were less sure of themselves. Being clear about what you’re doing and why can also lower your chances of getting Alzheimer’s disease.

Hepatitis Delta Virus Clinical Practice Guidelines

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European Association for the Study of the Liver

These are some of the highlights of the guidelines without analysis or commentary. For more information, go directly to the guidelines by clicking the link in the reference.

New clinical practice guidelines for hepatitis delta virus (HDV) were published in August 2023 by the European Association for the Study of the Liver in Journal of Hepatology.[1]

Screen all HBsAg-positive individuals for anti-HDV antibodies with a validated assay at least once. Retest for anti-HDV antibodies in HBsAg-positive persons whenever clinically indicated (eg, during aminotransferase flares or acute decompensation of chronic liver disease); testing may be performed yearly in patients who remain at risk for infection.

Test for HDV RNA in all anti-HDV-positive patients using a standardized and sensitive reverse transcription PCR assay to identify active HDV infection.

Perform liver biopsy during and/or after antiviral treatment, whenever it may add to the patient’s management or for grading and staging of liver disease when clinical signs or indirect evidence (by imaging techniques) of cirrhosis are lacking.

Noninvasive tests may be used to evaluate advanced liver disease, but specific cut-off values are poorly established.

All patients with CHD and compensated liver disease, irrespective of whether they have cirrhosis or not, should be considered for treatment with pegylated interferon-α (pegIFNα) for 48 weeks as the preferred treatment schedule.