Medical News Today: Hunger may motivate us more than thirst, fear, or anxiety

Human motivation has been studied for decades, primarily in an attempt to answer one question: what drives us to take one action over another? Researchers shed some light in a new study, after finding hunger is a stronger motivational force than thirst, fear, anxiety, and social needs.
[A girl waiting for food]
Hunger may motivate us more than other driving states, including fear, anxiety, and social needs, researchers suggest.


Senior author Michael J. Krashes, of the National Institutes of Diabetes and Digestive and Kidney Diseases (NIDDK) at the National Institutes of Health (NIH), and colleagues recently published their findings in the journal Neuron.


Put simply, motivation is the reason for acting in a particular way or making a certain choice over another.


In the 1940s, American psychologist Abraham H. Maslow created the “hierarchy of needs” – a set of five “needs” that he believed explained human motivation.


These range from physiological needs – such as food, water, and other requirements for human survival – to self-actualization, the desire for personal growth and success.


Over the years, researchers have either acknowledged, criticized, or amplified Maslow’s theory. With regard to the latter, neurologists have increasingly investigated the role of the human brain in motivation.

Hungry and thirsty mice opted for food over water


According to Krashes and team, most neurological studies of motivation are conducted in tightly controlled conditions and have focused on investigating one motivational state at a time, which has made it difficult to determine if some states are stronger drivers than others and what brain circuits are involved.


With a view to addressing this knowledge gap, the researchers conducted a series of mouse experiments in which they assessed a variety of motivational states, including hunger, fear, anxiety, and social needs.


For the study, the team used optogenetics – a technique that uses light to control cells – to govern nerve cells in the brain known as agouti-related peptide (AgRP) neurons.


AgRP neurons are situated in the brain’s hypothalamus. They are known to regulate appetite and are crucial for survival.


For one experiment, the researchers either deprived mice of food for 24 hours or activated their AgRP neurons in order to make them hungry. These mice were also deprived of water, making them thirsty. A control group was deprived of water but not food.


When presented with food and water, the mice that were both hungry and thirsty opted for food over water, while the control group chose the water. This indicates that hunger is a stronger motivational force than thirst.


“We interpret this as a unique ability of hunger-tuned neurons to anticipate the benefits of searching for food, and then alter behavior accordingly,” says Krashes.

Overcoming fear in the face of hunger


In another experiment, the researchers induced hunger in the mice by activating AgRP neurons, before exposing them to a chamber scented with a chemical produced by foxes – an environment that triggers anxiety and fear for the rodents.


When food was placed in the chamber, the team found that the hungry mice overcame their fear to get food, while control mice that were not hungry chose to stay in the “safe” zones, suggesting that hunger trumps fear and anxiety as a motivational force.


A further experiment revealed hunger is also a greater motivation than social needs; AgRP activation led to socially isolated mice opting for a chamber containing food, rather than a chamber with another mouse. The reverse was true for control mice.


Interestingly, AgRP activity increased when another mouse was close by, which suggests AgRP neurons respond to potential competition for food.


“We think that the presence of another mouse could be viewed as competition for limited resources, increasing the motivation to seek food, which is a finding that no other studies have indicated thus far,” says Krashes.


Overall, Krashes says the team’s findings suggest motivational forces are more deeply connected than previously thought.


“Therefore, studying isolated motivated behaviors may not accurately demonstrate how the big picture nervous system works,” he adds. “Our study is one of the first steps to investigating feeding behavior in a more complicated, naturalistic setting.”


Additionally, the researchers believe the findings shed light on how animals and humans have evolved.

“Our continued existence, among that of other species, has motivated us to pursue an array of behaviors, all governed by our nervous system.


Of course, we can’t pursue all those motivations at once, so we have had to choose which ones were most important during different times of need. Evolutionarily speaking, animals that consistently picked the right motivations over others have survived while other animals have not.”

Michael J. Krashes

Could the findings advance treatments for obesity?


Medical News Today asked Krashes whether their findings might pave the way for new treatments for obesity – for example, by reducing motivation for food.


“It should be stated that we, and others, have demonstrated the necessity of these neurons in regulating feeding and body weight homeostasis,” he replied. “I am of the opinion that no individual study puts us in a position to pave the way in treating obesity, but collectively, as we link and evaluate everyone’s findings, I believe we are on the right track.”




“I do think it’s important to study feeding in a more ethological framework, as we have done here, because the neural circuits underlying food acquisition evolved during a time when we were constantly bombarded with external stimuli and had to make complex decisions regarding our foraging behavior,” he added.


Krashes told MNT that the researchers hope to expand their findings by creating an assay that enables them to study foraging behavior.


“Specifically, we’d like to determine how searching for and eating food is influenced by social structure, distance traveled, predation, thirst etc.,” he explained. “We’re also prioritizing why AgRP neural activity is influenced by the presence of another animal.”


Read about a hunger hormone that interferes with decision-making.

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Medical News Today: Certain NSAIDs may raise the risk of heart failure, study finds

A new study published in The BMJ has uncovered a dose-response relationship between the use of nonsteroidal anti-inflammatory drugs and increased risk of hospital admission for heart failure.
[Bottles of pills in a row]
Researchers have identified certain NSAIDs that may raise the risk of hospital admission for heart failure.


Nonsteroidal anti-inflammatory drugs (NSAIDs) are medications used to alleviate pain and reduce inflammation. They work by blocking the activity of COX-1 and COX-2 – enzymes that produce chemicals called prostaglandins, which promote inflammation.


According to the research team, led by Giovanni Corrao of the University of Milano-Bicocca in Italy, previous research has provided strong evidence that NSAIDs – including COX-2 inhibitors, a new generation of NSAIDs – can raise the risk of heart failure.


As such, clinical guidelines – such as those from the European Society of Cardiology – recommend limiting NSAID use among individuals who are already at increased risk of heart failure, while patients already diagnosed with heart failure should refrain from using NSAIDs completely.


“Nevertheless, there is still limited information on the risk of heart failure associated with the use of individual NSAIDs (both COX-2 inhibitors and traditional NSAIDs) in clinical practice, and especially on their dose-response associations,” the authors note.


With this in mind, Corrao and team decided to estimate how the use and dose of individual NSAIDs affect the risk of hospital admission for heart failure.

Nine NSAIDs linked to heart failure risk


The researchers assessed data from five population-based healthcare databases across four European countries: Germany, Italy, the Netherlands, and the United Kingdom.


More than 10 million NSAID users were included in the data, and these were matched with more than 8 million controls.


The analysis included a total of 27 NSAIDs, of which four were selective COX-2 inhibitors.


Overall, the researchers found current NSAID users (defined as individuals who had used NSAIDs within the past 14 days) were 19 percent more likely to be admitted to the hospital with heart failure than past users (individuals who had not used NSAIDs for at least 183 days).


After accounting for a number of possible confounding factors, the researchers identified seven widely used NSAIDs (diclofenac, ibuprofen, indomethacin, ketorolac, naproxen, nimesulide, and piroxicam) that raised the risk of hospital admission for heart failure, as well as two COX-2 inhibitors (etoricoxib and rofecoxib).


What is more, the researchers identified a dose-response relationship; at very high doses, diclofenac, etoricoxib, indomethacin, piroxicam, and rofecoxib were associated with double the risk of hospital admission for heart failure.


Corrao and colleagues stress that their study is observational, so they are unable to confirm a causal link between NSAID use and heart failure.


Still, the researchers believe their findings have significant public health implications:

“Our study […] provides evidence that current use of both COX-2 inhibitors and traditional individual NSAIDs are associated with increased risk of heart failure. Furthermore, the magnitude of the association varies between individual NSAIDs and according to the prescribed dose.


Because any potential increased risk could have a considerable impact on public health, the risk effect estimates provided by this study may help inform both clinical practices and regulatory activities.”


Learn more about how NSAIDs work and the conditions they treat.

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Medical News Today: Ultrasmall nanoparticles kill cancer cells in unusual way

Scientists are surprised to find that ultrasmall, fluorescent nanoparticles – originally developed to light up tumors for surgery – can also kill cancer cells by triggering a type of cell death that is not commonly observed.
Human cancer cell
The ultrasmall particles kill cancer cells by taking iron from their environment and delivering it into them. The process – called ferroptosis – ruptures the cell’s membrane.


They report the discovery – and how they tested the nanoparticles in cell cultures and mice – in the journal Nature Nanotechnology.


One of the lead investigators, Ulrich Wiesner, a professor of engineering at Cornell University in Ithaca, NY, says:


“If you had to design a nanoparticle for killing cancer, this would be exactly the way you would do it.”


Nanoparticles are tiny particles with at least one dimension no bigger than 100 nanometers. They have unusual properties compared with the same material on a larger scale, and scientists and engineers are applying them in many fields, including electronics and biomedicine.


The nanoparticles at the center of the new study – called Cornell dots, or C dots – are ultrasmall, fluorescent silica particles, with a diameter of 5 nanometers.


They were originally developed by Prof. Wiesner over 10 years ago as a tool for cancer surgery. They attach to cancer cells and light them up so surgeons can see where to cut.


The particles were also intended to be used for targeted drug delivery and environmental sensing.


‘Intrinsic therapeutic properties’


The new study shows that the cancer-targeting Cornell dots can kill cancer cells without having to carry drugs.


Lead author Michelle Bradbury, director of intraoperative imaging at Memorial Sloan Kettering Cancer Center in New York, NY, remarks:


“In fact, this is the first time we have shown that the particle has intrinsic therapeutic properties.”


“The particle is well tolerated in normally healthy tissue,” Prof. Wiesner explains, “but as soon as you have a tumor, and under very specific conditions, these particles become killers.”


The researchers discovered the cancer-killing properties of the Cornell dots when they were trying to find out how well large concentrations could be tolerated. They carried out several experiments over several years.


Then, to their surprise, they found that when high doses of peptide-coated Cornell dots were incubated with cancer cells – and particularly when the cells were starved of nutrients – the particles took iron from the environment and delivered it into the cancer cells.


Delivering iron into the cells triggers a type of cell death called ferroptosis, which ruptures the cell membrane. This is different to the more commonly observed fragmentation cell death known as apoptosis.


‘Wave of destruction’


Prof. Wiesner says only 24-48 hours after exposure to the Cornell dots, they observed how a “wave of destruction” swept through the entire cancer cell culture.


In further experiments they injected high doses of the coated Cornell dots into mice grafted with melanoma tumors and found they shrank the tumors without causing any adverse reactions.


The authors conclude their findings show “ferroptosis can be targeted by ultrasmall silica nanoparticles and may have therapeutic potential.”


“We’ve found another tool that people have not thought about at all so far. This has changed our way of thinking about nanoparticles and what they could potentially do.”

Prof. Ulrich Wiesner


The researchers now plan to test how the Cornell dots work with other standard therapies in different kinds of cancer tumors.


They want to make them more effective before starting tests in humans. The team will also be exploring ways to tailor the particles to target specific cancer types.




Discover how shutting down fat synthesis in cancer cells stunts tumor growth.



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Medical News Today: Headaches and Menopause: What’s the Connection?

MNT Knowledge Center


When a woman is in the early stages of or fully enters into menopause, it’s normal for her to experience a variety of symptoms. Headaches are among the symptoms some women report during this stage of life.



Like menopause itself, most symptoms are direct or indirect results of the natural changes occurring in a woman’s body. Not all women will experience the same menopausal symptoms or to the same degree, however.






What is menopause?




Briefly defined, menopause is the time when a woman stops menstruating. As her ovaries will stop producing new eggs, a woman will experience hormonal changes that can lead to other symptoms as the body adjusts. Menopause also marks the time in a woman’s life when she can no longer get pregnant.


[Woman looking tired and in pain]
Symptoms of menopause will vary to a degree.



Most women go through menopause between the ages of 40 and 58. The average age a woman has her last menstrual period can vary depending on a number of factors. In developed countries, the average age a woman stops menstruating is 51.4.



Factors like a woman’s race or ethnicity, health history, and lifestyle also play a role.



A 2011 article published in Obstetrics and Gynecological Clinics of North America notes that some studies show that African-American and Latina women experience natural menopause about 2 years earlier than white women. Asian women tend to go through menopause at similar ages to Caucasian women.



The same article also mentions that social and economic factors can affect when a woman enters menopause. Numerous studies have found that lower social class is linked to an earlier age for natural menopause.



One common mistake people make about menopause is that it happens as one clearly defined event. Menopause usually happens in three transitional periods, usually over multiple years. These stages and what to expect during them are as follows:



1. Perimenopause




This is the stage of menopause when a woman first begins to experience changes. Perimenopause can begin 8 to 10 years before a woman’s last menstrual period. It will last for about 4 years, according to the Cleveland Clinic.



Perimenopause usually begins when a woman is in her 40s. Menstruation is still ongoing but may become irregular. It’s important to remember that women can still get pregnant during perimenopause.



During this time, the body’s production of estrogen and progesterone begins to change, which can lead to experiencing menopausal symptoms, such as:




  • Breast tenderness

  • Worsening of premenstrual syndrome

  • Heavier or lighter than usual periods

  • Headaches

2. Menopause



This is the stage when a woman completely stops menstruating. The ovaries are no longer producing eggs, and the body is producing less estrogen and progesterone.



This is the stage most often associated with menopause. It’s common to experience a number of symptoms, such as:



[Woman with headache]
Women have often reported headaches during menopause.



  • Hot flashes

  • Night sweats

  • Cold flashes

  • Vaginal dryness

  • Pain or discomfort during sex

  • Difficulty sleeping

  • The need to urinate more frequently or urgently and urine leakage

  • Mood swings, anxiety, or depression

  • Joint aches and pains

  • Headaches

  • Skin flushing

  • Weight gain or loss

3. Postmenopause



This is the stage after a woman has stopped having her period for at least 1 year and can no longer get pregnant. The years after are called postmenopause.



Some symptoms, like hot flashes, should get better during this time. This is also when a woman’s risk for health issues like brittle bones and heart disease increases because of the lower amounts of estrogen in her body.



Medication or lifestyle changes can help to reduce this risk, so it’s important to speak to a doctor.




Menopause and headaches



Although headaches aren’t usually the first symptom one might associate with menopause, women have often reported them during this time.



A 2014 study from the University of Cincinnati’s Headache and Facial Program confirmed that women tend to experience more migraine headaches in the early years of menopause due to the fluctuating hormone levels.



“In the past physicians had not really recognized the effect of hormones on migraines,” Dr. Vincent Martin, co-director of the program and lead author of the study was quoted saying in a Los Angeles Times article:



“Headaches do increase during this time period. It’s what women have been telling us for years. Perimenopause and early menopause are very turbulent times for women with migraines.”



For some women, migraines will get better once their periods stop, but tension headaches will get worse. Women who are taking hormonal replacement therapy during perimenopause or menopause may find that their migraines get better or worse. Some will not feel any different.



Given the recent research linking headaches and menopause, headaches could signal early menopause for older women who don’t usually suffer from them. As only 10 percent of headaches have a known cause, however, it’s difficult to say that they are a clear sign of menopause.


When to see a doctor



Most headaches can be treated with over-the-counter pain relievers. If the pain persists or worsens, it’s a good idea for people to see a doctor. If headaches disrupt someone’s ability to do everyday activities, they should seek medical attention.



Headaches can also be a sign of another, more serious issue. If someone notices any of the other following warning signs, they should see a doctor immediately:



  • Headaches after they’ve hit or injured their head

  • Headaches paired with a painful red eye

  • Headaches that get worse with coughing or movement

  • Headaches that are paired with fever, stiff neck, confusion, decreased alertness or memory

  • Headaches that are paired with nerve-related symptoms such as vision changes, slurred speech, weakness, numbness, or seizures

  • Headaches after receiving hormonal therapy treatments

  • Headaches that come on severely and abruptly

Treatment and prevention


[Woman doing Yoga]
Yoga and meditation are a good way to treat menopausal headaches.



Acetaminophen, aspirin, ibuprofen, and naproxen are commonly used nonprescription pain relievers that help with headaches.



Stress-relieving activities like yoga and meditation can also work. For some, a cool washcloth or an ice pack are effective in relieving the pain. Other people simply need to eat or properly rehydrate.



A doctor may prescribe medication for persistent or worsening headaches that don’t get better with these forms of treatment.



For women taking hormonal treatment therapy, their doctor may reduce the estrogen dose or switch them to an estrogen skin patch with a lesser dose.



What are headaches?



A headache is defined as any pain in the head. The pain can be on one or both sides of the head, be in one place only, or even move from one place to another.



The types of pain people experience with headaches also vary, and sometimes because of what is causing them. Some headaches may be paired with sharp pains, some may have dull pains, and others may come with throbbing pains.



The National Headache Foundation list more than 15 different types of headaches. These range from allergy headaches and menstrual migraines to hangover headaches and sinus headaches.



Some headaches are caused by internal factors, like with changing hormone levels during menstruation and menopause. Others are the results of external factors, like eyestrain or bright sunlight.






What headaches are most common?




About 95 percent of headaches are caused by things people deal with every day, according to Harvard Health Publications. These include things like stress, tiredness, weather changes, and caffeine withdrawal.



The most common headaches are:



  • Tension headaches

  • Sinus headaches

  • Migraines


The symptoms, severity, risk factors, and complications can vary for each type of headache. Some can be prevented with lifestyle changes or medication, while others cannot be prevented as simply.


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Medical News Today: Exercise does not reduce multiple sclerosis risk

Some researchers have theorized that regular physical activity reduces the risk of developing multiple sclerosis. A new analysis demonstrates that, as a preventative measure, exercise does not appear to have the desired effect.
[Multiple sclerosis on a computer screen]
Recent research clears up the debate about physical exercise and MS risk.



Although the exact number of people with multiple sclerosis (MS) in America is not known, there are estimated to be 2.3 million people affected worldwide.


MS is a varied condition that affects the brain and/or spinal cord.


It can cause a wide range of symptoms including difficulties with the movement of limbs, changes in vision, and problems with balance and sensation.



Although there is no cure, scientists have demonstrated that, for individuals with mild to moderate disability, exercise can improve the severity of certain symptoms.


Exercise has been shown to increase muscular strength and aerobic capacity and improve the individual’s sense of wellness. Additionally, there is some evidence that exercise might help slow the progression of MS, although the data is conflicting.


How exercise reduces the symptoms of MS is not known, but researchers believe that it could be due to the modulation of immune factors or stress hormones, or perhaps by altering the expression of neuronal growth factors.

Risk factors for MS


A number of MS risk factors are known; for instance, the condition is more prevalent in women than men, and it seems to have links with certain infections, including Epstein-Barr. White people and those who live in temperate climates are also more likely to develop MS. However, the full list of risks is yet to be uncovered.


One potential risk factor that has received some attention from scientists is the level of exercise an individual is involved in prior to the onset of MS. It is commonly believed that a higher level of physical activity reduces the risk of MS; however, this is still very much up for debate.


Findings are contradictory or unclear; for instance, some studies have shown that individuals who develop MS tend to be more physically active before onset; others showed no difference in pre-onset activity.


However, earlier studies did not use detailed, validated questionnaires to assess physical activity levels. There is also a confounding variable that makes some of the results difficult to interpret. Two of the early symptoms of MS are weakness and fatigue. So, did the lack of physical exercise promote the onset of MS, or was the lack of exercise a sign of the onset of MS?


A team of scientists from Harvard T.H. Chan School of Public Health in Boston, MA, recently set out to investigate whether physical activity has an effect on MS risk once and for all. Their results are published this week in the journal Neurology.

Fitness level and the onset of MS


The team took data from more than 193,000 women who participated in the Nurses’ Health Study and Nurses’ Health Study II; these individuals were followed up for 20 years, starting in 1976. Each woman completed detailed questionnaires about their current levels of physical activity and also their activity levels as teens and young girls. Over the course of 20 years, 341 women developed MS.


Once the data were collated, the researchers calculated the hours of exercise each individual carried out per week and what types of exercise they did. The group adjusted the results for ethnicity, age, smoking, place of residence at the age of 15, BMI at 18, and vitamin D supplement intake.


After the analysis had been completed, the data showed that, contrary to expectation, exercise was not correlated in any way to the appearance of MS.

“Overall, there was no consistent association of exercise at any age and MS. Exercise has been shown to be beneficial to people with the disease, but it seems unlikely that exercise protects against the risk of developing MS.”

Kassandra Munger, study author


When Medical News Today asked Munger whether the results had come as a surprise, she said:


“Given the overall health benefits of physical activity, in addition to recent studies suggesting that physical activity in persons with MS may provide some benefit, our working hypothesis was that physical activity would be associated with a reduced MS risk.”


Although the team has no further MS studies planned at this stage, in a perfect future, Munger told MNT that she would “spend time and money on better understanding the role for physical activity in promoting wellness and improving quality of life among MS patients.”


We still have much to learn about MS and the risk factors involved. No doubt further research will steadily provide the vital details necessary to prevent this debilitating condition.


Learn about a new MS drug that promises to reduce progression.

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Medical News Today: Hormonal contraceptives may raise depression risk

The risk of depression and antidepressant use might be increased for women and teenage girls who use hormonal contraceptives – such as birth control pills or implants – according to new research.
[Packets of birth control pills]
The risk of depression and first-time antidepressant use was higher for subjects who used hormonal contraceptives, researchers found.


Study co-author Dr. Oevind Lidegaard, of the University of Copenhagen in Denmark, and colleagues report their findings in JAMA Psychiatry.


According to the most recent data from the Centers for Disease Control and Prevention (CDC), in the United States, more than 61 percent of women of reproductive age currently use some form of contraception.


Oral contraceptives – or birth control pills – remain the most common form of contraception, currently used by around 16 percent of women aged 15-44 in the U.S.


Combined oral contraceptives contain the hormones estrogen and progestin; progestin may refer to synthetic forms of the hormone progesterone or progesterone itself. These contraceptives work by preventing ovulation and making it harder for sperm to reach the egg, thereby preventing pregnancy.


The progestin-only pill – also known as the “mini-pill” – primarily prevents pregnancy by stopping sperm from reaching the egg, and it may sometimes suppress ovulation.


Other forms of hormonal contraception include the birth control implant, injection, patch, and the vaginal contraception ring – all of which release estrogen, progestin, or both as a way of preventing pregnancy.

Limited data on how hormonal contraception influences depression


Dr. Lidegaard and team note that previous research has suggested that changes in estrogen and progesterone levels – particularly the latter – may play a role in depression. However, they say few studies have investigated whether the use of hormonal contraceptives influences depression risk.


“The aim of this study was to assess the influence of specific types of hormonal contraceptives on the risk for first use of antidepressants and first diagnosis of depression as an inpatient or an outpatient at a psychiatric hospital,” say the authors.


To reach their findings, the team analyzed 1995-2013 data from the Danish National Prescription Register and the Psychiatric Central Research Register, including more than 1 million women aged 15-34.


Over an average follow-up period of 6.4 years, the researchers assessed participants’ use of hormonal contraception and tracked first diagnoses of depression and first-time antidepressant use. None of the participants had a history of depression or antidepressant use at study baseline, the researchers report.


During follow-up, 55.5 percent of the subjects were current or recent users of hormonal contraceptives, and there were 23,077 first depression diagnoses and 133,178 first-time antidepressant prescriptions.

Depression risk greater for teens who use hormonal contraceptives


Overall, compared with nonusers of hormonal contraceptives, participants who were current or recent users of hormonal contraceptives were found to be at greater risk for depression and antidepressant use.


As an example, women aged 20-34 who used combined oral contraceptives or the progestin-only pill were at 1.23 and 1.34 times greater relative risk of first-time antidepressant use, respectively, and similar or slightly lower estimates were found for the risk of depression diagnosis.


The risks were higher for adolescents aged 15-19, the team found; use of combined oral contraceptives or progestin-only pills among this age group was associated with a 1.8 and 2.2 times greater relative risk of first-time antidepressant use, respectively, and those who used non-oral hormonal contraceptives were at three times greater risk.


Again, similar or marginally lower estimates arose for adolescent girls when it came to the risk of depression diagnosis.


“Our data indicate that adolescent girls are more sensitive than older women to the influence of hormonal contraceptive use on the risk for first use of antidepressants or first diagnosis of depression,” the authors note. “This finding could be influenced by attrition of susceptibility, but also that adolescent girls are more vulnerable to risk factors for depression.”


Overall, the researchers conclude that their findings suggest the use of hormonal contraceptives may raise the risk of depression and antidepressant use for teenage girls and women.

“In this study, use of all types of hormonal contraceptives was positively associated with a subsequent use of antidepressants and a diagnosis of depression.


That finding complies with the theory of progesterone involvement in the etiology of depression, because progestin dominates combined and progestin-only contraceptive.”




‘It is important for women to be aware of potential risk’


Talking to Medical News Today, Dr. Lidegaard said it is no surprise that hormonal contraceptives might raise the risk of depression.


“Generally estrogen improves mood and progestogens worsen mood. As hormonal contraception generally is dominated by progestogens, it is not very surprising that mood generally has a tendency to be changed in direction for depression,” he said.


Still, despite their findings, Dr. Lidegaard told MNT he does not recommend that women of reproductive age turn to non-hormonal forms of contraception.


“But I think it is important that women, especially young women, are aware of this potential risk with use of hormonal contraception, including oral contraceptives,” he added.


The team now plans to investigate whether the use of hormonal contraceptives is associated with increased risk of suicide or suicidal attempts.


Learn more about what types of contraception are available.

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Medical News Today: What is hyperbaric oxygen therapy good for?

In hyperbaric oxygen therapy, a patient breathes almost pure oxygen in a pressurized room or tube. By bringing more oxygen into the bloodstream, the treatment is thought to enhance healing for people with a number of conditions.
[diver]
A diver who ascends too quickly to the surface can end up in the decompression chamber.



As long ago as 1662, a British clergyman and physician called Henshaw built the first hyperbaric chamber, a sealed room with a series of bellows and valves. He believed that using pressure could help in treating certain respiratory diseases.


Since the 1940s, hyperbaric oxygen treatment (HBOT) has been standard treatment for military divers in the United States.


Divers who surface too quickly are at risk of decompression sickness (DCS), sometimes called “the bends,” or of an air gas embolism (AGE). Jointly, these are known as decompression illness (DCI), and they both relate to problems with air in the body. Consequences can be severe. HBOT is the primary treatment for both.


Treatment involves early administration of oxygen, and, if necessary, time spent in a decompression chamber. The diver must return to the pressure, or “depth,” at which they were diving, followed by gradual decompression. The pressure reduces the volume of the bubbles.


DCI affects around 1,000 American divers each year, but the uses of HBOT go beyond the diving community.


HBOT has been shown to benefit people with infections, embolism, or air bubbles in the blood vessels, and some wounds that do not respond to other treatment.


More recently, it has been promoted as an alternative therapy for various conditions, from Alzheimer’s disease to infertility.


To meet the growing demand, HBOT chambers have sprung up across a range of facilities, from hospital outpatient departments to spas. There are even chambers for home use. Some call it a “miracle cure.”


While research suggests that some of these claims may be true, not all of the suggested uses are approved by the U.S. Food and Drug Administration (FDA). Concerns have been raised about the risks associated with “off-label” use of HBOT.

How does hyperbaric oxygen therapy work?


The Undersea and Hyperbaric Medical Society (UHMS) – an international organization set up in 1967 to encourage cooperation on diving and undersea medicine – defines HBOT as:

“An intervention in which an individual breathes near 100 percent oxygen intermittently while inside a hyperbaric chamber that is pressurized to greater than sea level pressure (1 atmosphere absolute, or ATA). For clinical purposes, the pressure must equal or exceed 1.4 ATA [atmosphere absolute] while breathing near 100 percent oxygen.”


The body’s tissues need oxygen to work. Additional oxygen can help damaged tissue to heal. Oxygen at high pressure can enhance tissue function and fight infection, under certain conditions.


At 1.4 ATA, the ambient pressure is three times higher than the air pressure we normally breathe. Breathing almost pure oxygen at this pressure triples the concentration of oxygen available to the lungs.

What are the benefits of HBOT?


Apart from DCI, HBOT is the primary treatment for carbon monoxide poisoning, and it supports a number of other therapies.


Working with the UHMS, the FDA have approved 13 uses of HBOT. Evidence has shown that they are safe and effective. Insurance companies or Medicare will normally cover the cost of treatment.


The approved uses are:

[diabetic foot wound]
HBOT is approved in the treatment of certain wounds that do not respond to conventional treatment.

  • Decompression sickness, experienced by divers and pilots
  • Acute traumatic ischemia – for example, crush injury
  • Air or gas embolism
  • Arterial insufficiencies
  • Anemia due to severe blood loss
  • Thermal burns
  • Carbon monoxide poisoning
  • Some brain and sinus infections
  • Intracranial abscess
  • Gas gangrene
  • Necrotizing soft tissue infections
  • Radiation injury – for example, as a result of cancer therapy
  • Skin grafts.


Wounds and infections that have not responded to other treatment, such as bone infections and diabetic foot ulcers, have been shown to respond to HBOT. HBOT has been found to reduce the risk of amputation in people with diabetic foot ulcers.

How is HBOT delivered?


HBOT is normally provided in an outpatient setting. The number of visits will depend on the condition.

[HBOT chamber]
A large HBOT chamber can accommodate many people at one time.


According to the Mayo Clinic, a person with carbon monoxide poisoning may need three sessions, while a person with a non-healing diabetic wound may need 20-40 sessions. An acute condition, such as DCI, may need only one longer session.


A chamber can hold one or many people, and the patient will probably wear a mask or hood that delivers oxygen.


In a chamber for one person, the patient usually lies on a table that slides into a clear plastic tube.


Nowadays, HBOT chambers encourage patients to be comfortable. They can relax by listening to music or watching TV.


A session can last from 30 minutes to 2 hours, after which the chamber is slowly decompressed.

What has HBOT not been approved for?


The FDA have expressed concern that HBOT is being used to treat conditions for which its safety and effectiveness have not been confirmed.


“Patients may incorrectly believe that these devices have been proven safe and effective for uses not cleared by FDA, which may cause them to delay or forgo proven medical therapies. In doing so, they may experience a lack of improvement and/or worsening of their existing condition(s).”

Nayan Patel, senior lead reviewer and Intercenter Consult team leader at the FDA


Diseases and conditions that the FDA believe people may wrongly seek HBOT for include HIV and AIDS, Alzheimer’s and Parkinson’s diseases, asthma, Bell’s palsy, cerebral palsy, depression, heart disease, hepatitis, migraine, multiple sclerosis, sports injury, stroke, brain injury, and spinal cord injury.


In 2013, responding to a number of complaints, the FDA insisted that certain conditions should not be treated with HBOT. The Alliance for Natural Health (ANH) called the announcement a “deceptive statement.”

[stressed veteran]
There are suggestions that HBOT could help people with PTSD, and veterans in particular.


Those who support the use of HBOT for a wider range of conditions point out that pressure and additional oxygen can benefit various bodily functions. They cite a number of studies supporting their claims.


There are calls for HBOT to be approved as an alternative therapy for autism, attention deficit hyperactivity disorder (ADHD), cerebral palsy, and post-traumatic stress disorder (PTSD). There is strong support in certain circles for its use in helping improve the quality of life of veterans.


Clinical trials have been investigating the effect of HBOT on traumatic brain injury (TBI).


It is believed that HBOT can help to heal brain injury by improving the way dormant neurons function and stimulating the growth of axons. A meta-analysis published in May 2016 suggests that HBOT can enhance a patient’s score on the Glasgow Coma Scale, but no significant change was seen in the PTSD score.


Dr. Paul Harch, hyperbaric medicine, diving, and emergency medicine physician, and coauthor of the book The Oxygen Revolution calls for wider approval of the uses of HBOT, and especially for TBI and neurological disorders.


Dr. Harch told Medical News Today:

“It was found that diseases and disorders with similar disease processes responded similarly to HBOT. In Russia nearly 100 diagnoses are treated and nearly 70 in China. We have been much more restricted in the U.S. based on reimbursement considerations.”


The UHMA note that “meticulous scrutiny” is needed before new applications of HBOT can be approved for use in treating a condition. Each case involves a stringent review of a wide range of research by an interdisciplinary team.


More research is needed before the requested new uses can be implemented, say the FDA and the UHMA.

What are the risks of HBOT?


High atmospheric pressure can damage the ear. Middle ear barotrauma affected 2 percent of 1,446 participants in one study. A higher incidence of Eustachian tube dysfunction, up to 45 percent, has been detected using sensitive testing equipment.


Sinus pain can affect people with upper respiratory tract infections or allergic rhinitis. People who have recently had a cold or fever should not undergo HBOT.


People with certain lung diseases or an airway obstruction may be at risk of pulmonary barotrauma and damage to the lungs as a result of air becoming trapped during decompression. The result could be a collapsed lung or an air embolism. Long-term treatment could compromise lung function.


Those with existing cardiovascular problems should be monitored for acute pulmonary edema or an embolism. Symptoms include joint pain and paralysis.


Some patients may experience confinement anxiety, or claustrophobia, during treatment. Myopia has been reported following HBOT.


Overexposure to oxygen at high pressure can lead to oxygen poisoning. When a person uses oxygen, highly reactive byproducts are released. At high pressure, these build up, saturating tissues and possibly leading to convulsions and other adverse effects.


Dr. Harch told MNT that some people, for example, those with seizure disorders should be treated by “medical professionals who have knowledge, experience, and hopefully training in the field.”

“The more underlying medical problems one has (e.g., diabetes, high blood pressure, lung disease, etc.) the more you want to be evaluated and treated by medical professionals.”

Dr. Paul G. Harch


HBOT is not recommended for people who have undergone recent surgery or trauma.

A growing trend brings growing concerns


In January 2015, the Wall Street Journal reported that growing numbers of people are seeking out HBOT as a solution to problems that conventional medicine seems unable to resolve. In 2010, 20,000 Medicare beneficiaries had FDA-approved treatments using HBOT, up 24 percent from 2008.


Johns Hopkins Medicine urge caution in the choice of treatment setting. HBOT should only be carried out in a hospital, they say, with trained medical staff.


If Medicare and insurance do not cover the treatment, it may be because it has not yet been approved as safe and effective.


The WSJ point out that since not all the claims for HBOT are conclusively supported by evidence, people who seek unapproved treatments from small clinics and spas may be wasting their money. It is important for people to understand that HBOT is not a “magic bullet.”




Non-hospital use may include “soft” or “mild” chambers that cannot sustain the necessary pressure, or guarantee the purity of the oxygen. As a result, the patient may undergo many treatments without seeing any benefit.


If the power is disrupted, the chamber could deflate, leading to suffocation. These chambers are not considered appropriate by many hyperbaric practitioners.


Since pure oxygen is highly explosive and flammable, a number of explosions have been reported, especially when used at home or without appropriate supervision.


HBOT may yet turn out to be a miracle cure. But, as with all health choices, it pays to be cautious.

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Medical News Today: Cell reprogramming discovery may lead to treatments for eye diseases

Using cell reprogramming techniques, scientists have managed to induce support cells in the retina to become stem cells capable of making new neurons. They suggest the technique could lead to new treatments for glaucoma, macular degeneration, and other eye diseases where retinal neurons are lost.
age related macular degeneration
The researchers hope their study will help develop new treatments for progressive diseases that damage the retina, such as age-related macular degeneration.


The researchers, led by Bo Chen, an associate professor of ophthalmology at Yale University School of Medicine in New Haven, CT, report their work in the journal Cell Reports.


The retina at the back of the eye contains many types of cell, including the retinal neurons that process visual images and help us to see, and support cells called glial cells.


The most common type of glial cell in the eye of mammals is the Müller glial (MG) cell. These cells give structural support and also help keep the chemical environment of retinal neurons stable.


MG cells have the capacity to become stem cells, proliferate, and turn into new neurons. However, the researchers explain how recent studies suggest that, in mammals, this ability is only switched on through injury, otherwise it remains dormant.



In cold-blooded creatures such as zebrafish, this is not the case. Their MG cells act as a source of retinal stem cells to replenish lost retinal neurons.


Researchers are keen to find a way to activate MG cells in the mammalian eye so they behave more like the ones in zebrafish. Previous studies have shown that trying to induce retinal injury through neurotoxins is a counterproductive approach as it results in death of neurons.


Thus, as Prof. Chen and colleagues note, “An injury-free strategy that would not necessitate inflicting further damage to a diseased retina is highly desirable.”


Activating Wnt signaling induced MG proliferation


For their investigation, the team focused on a Wnt signaling pathway that is activated by injury in MG cells.


By inserting genes into adult mouse retinas, they found they could reprogram MG cells to activate Wnt signaling and induce MG proliferation without retinal injury.


The authors also describe how – by inserting and deleting particular genes – they could manipulate signaling upstream and downstream of this pathway to influence effects on MG proliferation.


They note: “Deletion of GSK3β resulted in β-catenin stabilization and MG proliferation without retinal injury,” and that, “Intriguingly, after gene transfer of β-catenin or Lin28, a subset of cell-cycle-reactivated MGs express markers for amacrine cells, a type of retinal interneurons.”


They conclude their results show that a particular pathway – called Wnt-Lin28-let7 miRNA signaling – plays a key role in “regulating proliferation and neurogenic potential of MGs in the adult mammalian retina.”


“In the future we are hoping to manipulate these cells to replenish any lost retinal neurons, either in diseased or physically damaged retinas. Potentially, it’s a therapy to treat many different retinal degenerative diseases.”

Prof. Bo Chen


One of the diseases the researchers hope their discovery will help with is macular degeneration, often called age-related macular degeneration (AMD), a disorder that results in progressive damage to the central part of the retina – the macula.


AMD is the leading cause of permanent impairment of reading and fine or close-up vision among people aged 65 years and older in the United States.



Estimates from the Centers for Disease Control and Prevention (CDC) suggest around 1.8 million Americans aged 40 and over are affected by AMD, and another 7.3 million are at risk of AMD because of a condition called “large drusen.” Drusen are tiny yellow or white deposits under the retina.


Learn how scientists restored key parts of vision in blind mice for the first time.



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Medical News Today: Cancer and Genetics: What’s the Connection?

MNT Knowledge Center


Genes control the way cells work, and in particular how they grow and divide. When something goes wrong with one or more of the genes in a cell, changes occur that can lead to cancer.



Such changes are commonly referred to as faults or mutations. Although cancer is mainly the result of life choices and not related to family gene pools, it can also be caused by these faults or mutations.



As a result, cancer can be inherited from parents and grandparents and passed on to future generations.










How do genetic changes lead to cancer?


[cancerous cells graphic image]
A higher risk of some forms of cancer can be inherited from parents and grandparents.



A cell must typically contain six or more faults to become cancerous. Such faults can cause the cell to stop functioning normally, become cancerous, and grow and divide uncontrollably.



This may happen as people get older as a result of random mistakes when a cell is dividing. Changes can also occur due to exposure to substances that can cause cancer called carcinogens. These include cigarette smoke or sunlight.



Though potentially cancerous, these gene changes don’t affect all body cells, are not inherited, and cannot be passed on to children.



Cancer is such a common disease that many families have several members who have had cancer. Certain types of cancer seem to run in some families, but only a small portion of all cancers are inherited.


How is cancer risk passed on?



Faulty genes that increase the risk of cancer can be passed on from parent to child. Such genes are called inherited cancer genes. They occur when there is a mistake or a fault in the genes contained in an egg or sperm cell.



Genes that increase the risk of cancer are known as cancer susceptibility genes. Their normal job is to correct DNA damage that naturally occurs when cells divide, protecting people against cancer.



Inheriting a faulty copy of one these genes means that it is unable to repair damaged DNA in cells. As a consequence, the cells may become cancerous.



People inherit genes from both parents. If a gene fault occurs in each parent, a child has a 1 in 2 chance of inheriting it. While some children will have the faulty gene and an increased risk of developing cancer, others won’t.





What forms of cancer are hereditary?



Cancers caused by inherited faulty genes are much less common than cancers caused by gene changes due to aging or other factors.



Most cancers develop through a combination of chance and the environment rather than inheriting a specific cancer gene. However, about 5 to 10 percent of all cancer cases occur in people who have inherited genetic mutations that raise the risk of cancer.



Mutations and syndromes that can increase the risk of cancer include:



  • BRCA1 and BRCA2 genetic mutations – raised risk of breast, ovarian, and prostate cancer

  • Cowden syndrome – raised risk of developing breast, uterine, and thyroid cancer

  • Familial adenomatous polyposis – raised risk of colorectal cancer, and soft tissue and brain tumors

  • Li-Fraumeni syndrome – raised risk of developing many different types of cancer

  • Lynch syndrome – raised risk of colorectal cancer, some skin cancers, and brain tumors

  • Multiple endocrine neoplasia – raised risk of endocrine cancers

  • Von Hippel-Lindau disease – raised risk of kidney and other cancers

Genetic testing for cancer



Tests are currently available for gene faults that increase the risk of breast, bowel, ovarian, womb, and prostate cancer. Tests are also available for rare gene faults that can increase the risk of kidney, skin, and thyroid cancer, and even a type of eye cancer called retinoblastoma.


[DNA graphic]
Tests are available for some rare gene faults that lead to certain types of cancer.



Tests are not presently available for other types of cancer genes. Research is always being conducted, however, with tests being developed for more and more gene faults.



Predictive genetic testing refers to the type of testing done on genes that increase the risk of cancer. They do not usually give precise answers about inherited diseases. The tests will only show if there is a specific gene mutation, not whether cancer is present.



A positive result means there is a raised risk of developing cancer but does not mean that cancer is present or will develop. For example, a particular gene mutation may be found through testing, but it might not be clear if this raises the risk of cancer.



In short, the test can show what might happen, but it cannot show what will happen. A negative result does not mean there is no risk of getting cancer. The risk can change over time due to non-genetic reasons, such lifestyle choices or simply getting older.



Genetic tests may be flawed, and test results can be interpreted wrongly. Although this is not common, different labs may have different ways of interpreting changes because genetic testing is not tightly regulated.



The makers of tests often advertise and promote their tests to doctors and the public. In doing so, they can make the test sound more helpful and decisive than it actually is. This can be misleading as decisions about testing may be made on incomplete or wrong information.



Reputable genetics counselors should, however, be able to help people know what to expect from test results.



Who should get genetic testing?


[Cancer patient consulting doctor]
Genetic tests may be flawed, and results can be interpreted incorrectly.



If a person has a strong family history of cancer and the genetic specialist thinks they could have inherited a faulty gene, they will offer that person a genetic test.



According to Cancer Research UK, the following scenarios signal what is considered to be a strong family history of cancer:



  • If more than two close relatives on the same side of the family have had cancer

  • The relatives have had the same cancer or different cancers that can be caused by the same gene fault

  • The cancers appeared when the relatives were below the age of 50

  • One relative has had a gene fault found by genetic tests


What to do if you think you may have a hereditary risk of cancer



People are advised to talk to their family doctor if they think that they may have a strong family history of cancer. Specialists will ask about their family in order to determine how many members have been diagnosed with cancer. If they think that a person has an increased risk, they will refer them to a genetics clinic for testing.



According to the American Cancer Society, the most effective ways of reducing the risk of cancer are simple things, such as:



  • Eating a healthy well-balanced diet

  • Not smoking

  • Exercising regularly

  • Keeping to a healthy weight

  • Staying safe in the sun

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Medical News Today: Economic hardships pave the way to cognitive aging

The negative implications of poverty on health have received a wealth of research over recent years. A new study, published this week, charts the cognitive impact of poverty on people aged 18-30 across a 25-year period.
[Man counting change]
Poverty’s negative impact on cognitive abilities strikes at a younger age than previously thought.



Due to a steady rise in socioeconomic inequality, many Americans are likely to experience poverty.


According to an Associated Press survey, a staggering 4 out of every 5 United States citizens will live near the poverty line at least once in their lives.


In 2015, an estimated 19.7 percent of American children under the age of 18 fell below the poverty line.


A problem of such size must be examined from every angle. The politics are, of course, a minefield, but the associated health issues are only slowly coming to light.


Earlier research has shown that exposure to poor socioeconomic environments in childhood, adulthood, or both, is associated with cognitive deficits later in life.


However, previous findings have come from studies focusing predominantly on older individuals. Little information has been gleaned about the effects of poverty on younger people’s mental acuity.


Researchers from the Division of Epidemiology, Department of Public Health Sciences at the University of Miami set out to fill this gap in current understanding. Their results are published this week in the American Journal of Preventive Medicine.

“Income is dynamic and individuals are likely to experience income changes and mobility especially between young adulthood and midlife. Monitoring changes in income and financial difficulty over an extended period of time and how these influence cognitive health is of great public health interest.”

Lead investigator Adina Zeki Al Hazzouri, Ph.D.


Studying poverty and the mind


With poverty at such a high rate, understanding all of its implications is vital for the successful management of public health today, and in the future. As Al Hazzouri says: “Maintaining cognitive abilities is a key component of health.”


To answer questions about the cognitive effects of socioeconomic hardships, Al Hazzouri took data from an ongoing study – the Coronary Artery Risk Development in Young Adults (CARDIA) prospective cohort study.


The team used data from 3,400 black and white men and women. The participants were aged 18-30 at the start of the study in 1985-86. Information regarding household income was taken from the cohort six times between 1985-2010.


Poverty level was defined as the percentage of time that each participant’s household income was under 200 percent of the federal poverty level; these annual income cut-offs amounted to:

  • $26,718 in 1990
  • $28,670 in 1992
  • $31,138 in 1995
  • $35,206 in 2000
  • $39,942 in 2005
  • $44,630 in 2010.


Participants were then split into four groups: never in poverty; in poverty less than one third of the time; from one third to 100 percent of the time, and always in poverty.

Cognitive testing uncovers deficits


In 2010, participants completed three psychological tests to assess their cognitive abilities. The tests were all standard psychological measures and considered reliable assessors of cognitive aging.


The Digit Symbol Substitution Test involves matching symbols to numbers; it tests memory and speed of mental processing. The Rey Auditory-Verbal Learning Test measures short-term auditory-verbal memory, rate of learning, and memory attention, among other skills. The Stroop Test assesses a number of cognitive skills including processing speed and selective attention.


Once the data was analyzed, a clear pattern emerged. There was a strong and graded association between time spent enduring economic hardship and a decline in cognitive function. Although the deficit was measured across all three test types, it was particularly pronounced in processing speed.


Even after adjusting for factors such as sex, race, marital status, smoking, and cholesterol levels, the effect remained. Participants in the “100 percent poverty” group performed significantly worse than those from the “no poverty” group. The researchers conclude that perceived hardship and poverty are contributors to cognitive aging.


This is the first time that such cognitive deficits have been measured in a younger population.

“Findings among this relatively young cohort place economic hardship as being on the pathway to cognitive aging and as an important contributor to premature aging among economically disadvantaged populations.


It is important to monitor how trends in income and other social and economic parameters influence health outcomes.”

Adina Zeki Al Hazzouri, Ph.D.


The results are clear, as the authors conclude: “Sustained economic hardship over 20 years was associated with worse cognitive function among middle-aged adults.”


Learn how childhood poverty is linked to brain changes related to depression.

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