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It’s more difficult to study women than men — women have monthly hormonal cycles, and depending on where they are in their cycle, these hormones can affect the outcome of studies. To get around this, many researchers exclusively study males. The assumption, until recently, was that non-reproductive data gathered about men would also apply to women.

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As cases such as the new Ambien dosage guidelines indicate, this lack of data on female patients can be dangerous. Women were found to be taking up to twice as much of the sleeping drug as was safe, based on data from men.

The bottom line is that men and women have many physiological differences. In order to address these, the National Institutes of Health (NIH) have issued mandates requiring that human studies include women and that preclinical animal studies include female animals.

Now, two new studies explore differences in the way men’s and women’s brains respond to stress and a high-fat diet.

Related News: Men’s and Women’s Brains Are Wired Differently »

Researchers from Duke University Medical Center were already conducting a study on the effects of mental stress on the heart when they decided to take a look at the specific effects of gender, in research published in the Journal of the American College of Cardiology.

The researchers gathered 56 women and 254 men from the parent study. The subjects were asked to perform three tasks that were mentally stressful: a mental math test, a mirror tracing test, and an anger recall test. To compare the effects of mental stress to exercise, the volunteers also completed a treadmill test. At each step in the process, the scientists measured the participants’ heart activity and took blood samples.

The men in the group showed larger increases in blood pressure and heart rate in response to mental stress compared to the women. The women, however, experienced fewer positive emotions and more negative emotions. They also had increased platelet aggregation (which leads to the formation of blood clots), and more frequent signs of cardiac ischemia, or reduced blood flow to the heart.

“Psychosocial stress affects men and women differently; the fact that women had more platelet clumping and cardiac ischemia suggests women may have different mechanisms of low blood flow to the heart,” said Dr. Zainab Samad, an assistant professor of medicine at Duke and the lead author of the study, in an interview with Healthline.

Read More: 10 Ways to Reduce Stress and Protect Your Heart »

Samad believes that mental stress shouldn’t be overlooked when evaluating a patient’s heart disease risk.

“Psychosocial stress is not routinely evaluated when working up patients for heart disease; clearly this is important and needs to be recognized,” she said. “Unlike physical stress, psychosocial stress patients experience is not predictable or controllable. But we can teach patients to be more mindful about being ‘stressed out’ and how to cope with psychosocial stress in healthier ways.”

Another research team looked at gender differences in the way a high-fat diet contributes to heart disease, obesity, and type 2 diabetes. Their results were published in Cell Reports.

The team already knew that heart disease rates are higher among men and postmenopausal women than among premenopausal women. They were also aware that estrogen protects against inflammation, which contributes to these chronic diseases.

The researchers examined the role of palmitic acid in mice. Palmitic acid is a fatty acid that is commonly found in Americans’ diet (and in their bloodstreams).

A diet rich in palmitic acid caused levels of the fatty acid to rise in the brains of male mice, but not in female mice. The high levels of palmitic acid decreased the levels of a compound called PGC-1a, which normally gives a boost to estrogen receptors.

With reduced PGC-1a, the number of estrogen receptors in the male mice decreased. This took away the protective effects of estrogen in the males and increased their inflammation levels.

Specifically, the inflammation occurred in the brain’s hypothalamus, which regulates hunger and metabolism. Inflammation of the hypothalamus is associated with overeating, and also causes insulin resistance, which leads to diabetes.

To confirm this finding, the team manipulated the brains of the male rats to have extra estrogen receptors, thereby making up for the ones lost by the high-fat diet. With the receptors restored, the male rats were protected against brain inflammation once again.

“These data are novel and exciting, and again, remind us that there is so much more we need to learn about,” said Deborah Clegg, a research scientist with the Diabetes and Obesity Research Institute at Cedars-Sinai Medical Center and senior author of the paper, in an interview with Healthline.

“The fact that males and females differ as much as they do really tells us how important sex-based research is. Men and women are not the same, and the more we pay attention to this, the better and more efficacious healthcare can become,” Clegg added.

Samad agrees. “Our knowledge regarding how gender, race, environment, and genes interact to cause disease is evolving currently,” she said. “One day we may be able to fine tune and offer more tailored therapy for individuals. We are not there yet.”

Related Reading: Why Is Multiple Sclerosis More Common in Women than in Men? »

Do you hunker down in an office with a noisy open floor plan? Or do you spend each day in a cubicle? Maybe you labor away in a private office? Your answer to these questions could influence your health.

If you work in an office with an open plan, you have the benefit of chatting with your colleagues about new ideas without having to make a trip to a conference room. But you and your colleagues may also need to take more sick days.

According to a new study published in the journal Ergonomics, working in an open floor plan and without individual workstations may negatively affect a worker’s health.

In their study on the effect of office type on sickness absence, Christina Bodin Danielsson and colleagues at Stockholm University evaluated data from 1,852 office workers over two years. The workers toiled in single-room offices; shared-room offices; small, medium-size, and large open-plan offices; flex-offices (with no individual work stations); and combination offices.

Employees who labored in offices with one of the three open floor plans phoned in sick more often. Women who spent their workdays in these environments were particularly likely to be absent for short sick periods. In flex-offices, or open-plan layouts without individual workstations but with some meeting rooms, male workers logged higher rates of short sick leave times and individual days for sickness.

Why all these sick days? People sharing workspace may have a higher infection rate risk, say the researchers. Exposure to noise and the loss of personal control may also be to blame.

Group dynamics also figure in the negative effects tied to traditional open-plan offices, particularly large open-plan offices. But there is some good news for employees who work close to each other: strong group identity and peer control is more likely to be fostered in a smaller group of people, according to the researchers.

Learn How to Stay Healthy on the Job »

In a separate study, published in the Journal of Environmental Psychology, Jungsoo Kim and Richard de Dear studied 42,764 respondents who worked in enclosed private, enclosed shared, and open-plan spaces. The researchers found that in general, people who toiled in enclosed private offices had the highest satisfaction level with their workspace environment.

When comparing people in private offices to those in open-plan spaces, the researchers found a huge discrepancy in their perception of privacy, acoustics, and proxemics. What bugged the people in open plan office layouts most? You guessed it—they were distracted by noise and loss of privacy.

Finally, while you might think that open-plan offices foster better communication between colleagues, the study indicated that people in private offices were the most satisfied about their interactions with others.

What’s more, the degree to which open-plan dwellers were satisfied with their interactions failed to offset the negative impacts of noise and privacy. So even though workers might be satisfied with interactions in open-plan layout, their overall workspace satisfaction will eventually decrease unless a certain level of privacy and acoustical quality is provided, according to the researchers.

Learn How to Create a Healthy Office »

Do you work in a brightly lit office? Or is the lighting so dim that you feel like you are in a dark basement? A study, published in the Journal of Consumer Psychologyshows that bright lights cause a feeling of warmth that intensifies a person’s reactions (positive and negative) and that turning on the lights can affect how people make decisions.

According to the study, lowering the lights during a highly charged meeting may soothe people’s emotions, while maintaining bright lights may help people influence others’ opinions.

The study involved half a dozen experiments that were carried out at Toronto’s Rotman School of Management. There were a total of more than 500 students, with 299 women and 205 men. Study subjects were placed in bright or dim rooms and asked to decide about a variety of issues, such as feelings of warmth, choosing spicy chicken sauces, judging a late worker’s aggressiveness in a script for a fake TV commercial, and rating the attractiveness of several models in print advertisements. They were also asked about their feelings after drinking fruit juices.

Watch: The Best Jobs for People with ADHD »

Study subjects in the bright rooms liked spicier sauces and believed their selections were spicier than those subjects in the dimly lighted room. Brightness also influenced their emotions about aggression and sexiness in other people.

What’s more, bright light enhanced positive feelings about the favored juice, which was orange, and also enhanced negative feelings about vegetable juice, which was the less preferred juice.

Those who smoke marijuana casually are not immune to the structural brain changes that can affect heavy users, according to a study published today in the Journal of Neuroscience.

Researchers from Northwestern University Feinberg School of Medicine, Harvard Medical School, and Massachusetts General Hospital used MRI scans to compare the brains of 20 18- to 25-year-olds who smoked at least once a week to those of 20 individuals who had little or no history of using the drug. Though the low to moderate marijuana users were not addicted to the drug, imaging data showed that their brain anatomy had changed.

Marijuana Legalization: The Experts Weigh In »

The nucleus accumbens, a part of the brain linked to reward processing, was larger and had changed shape in casual smokers compared to non-users. The researchers also found that the amygdala, which helps to regulate emotions, had also changed in shape and density in those who smoked the drug. The more marijuana users said they ingested, the more abnormalities the scientists detected on the brain scans.

“While I don’t think anyone has directly contrasted recreational with dependent users, it is pretty clear from our data that the more you use, the more the brain is impacted,” said Anne Blood, Ph.D., who leads the Laboratory for Mood and Movement Disorders at Massachusetts General Hospital.

“This study raises a strong challenge to the idea that casual marijuana use isn’t associated with bad consequences,” added Dr. Hans Breiter, a professor of psychiatry and behavioral sciences at Northwestern University, who was also involved with the study.

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Blood said that any brain changes have the potential to cause behavioral and neurological changes as well. The parts of the brain where they detected structural differences are “powerhouses of function.”

“These are not brain regions that you want to alter,” she said, calling for more studies that target recreational marijuana users. “There is no doubt that we will find these structural changes have some impact on these individuals’ neurological or psychiatric and behavioral function.”

According to data from the National Survey on Drug Use and Mental Health (NSDUH), 18.9 million Americans say they’ve recently used marijuana. The drug is commonly linked to problems with attention, learning, and motivation. Previous studies involving animal exposure to tetrahydrocannabinol (THC)—the main psychoactive ingredient in the drug—have shown that repeated exposure can alter the brain. Until now, there was little research on low-level exposure to THC.

“This study suggests that even light to moderate recreational marijuana use can cause changes in brain anatomy,” Carl Lupica, Ph.D., who studies drug addiction at the National Institute on Drug Abuse, and who was not involved with this study, said in a statement. “These observations are particularly interesting because previous studies have focused primarily on the brains of heavy marijuana smokers, and have largely ignored the brains of casual users.”

Can One Pill Reduce the ‘Haze’ of Medical Marijuana Use? »

People who feel extremely nervous at parties or when speaking in public may soon be able to calm themselves down by squirting a new drug in their noses, researchers say.

“It may represent a way of helping people with social anxiety disorder on an as-needed basis when they encounter a stressful situation,” said the lead researcher, Michael Liebowitz, a clinical psychiatry professor at Columbia University in New York.

Liebowitz and his colleagues reported the finding in the American Journal of Psychiatry.

Calm Down: 7 Unnecessary Causes of Stress (and How to Avoid Them) »

The drug is not on the market yet. It’s so experimental that researchers are still calling it by its chemical name, 3b-androsta-4,16-dien-3-ol, or PH94B for short.

It works by mimicking pheromones, the chemicals that animals use to communicate alarm, sexual readiness, and other messages to each other.

Researchers peering into human noses long ago noticed an organ—the vomeronasal organ—similar to the ones animals use for detecting pheromones.

But many scientists thought it was a useless relic from an earlier time in human evolution. This is the first time anyone has shown that a drug might influence human behavior by stimulating the organ.

There are already several drugs that can be used to calm social fears, but they may take a long time to act or cause side effects.

Learn More: How Stress Affects Your Health »

To test PH94B, the researchers randomly divided 91 women diagnosed with social anxiety into two groups. One group got a placebo; the other group got the real thing. 

The women then prepared and delivered a speech to a group of strangers.

All the women rated their anxiety on a scale of 0-100. The average anxiety score of the group taking the fake drug went from a 50.22 before the speech to 66.68 when they were giving the speech. The average score of the PH94B group went from 46.22 to 52.55.

A few people reported side effects like irritation in their noses, but these effects were not serious, and they weren’t significantly different between the two groups.

The experiment impressed Carol Bernstein, a past president of the American Psychiatric Association. “I think it’s worth further study,” she said. But she wondered whether the effects of PH94B are really different from drugs already prescribed for social anxiety. And she emphasized that the drug needed to be tested in a larger group of people over a longer period of time before it is released to the public.

Leave it to researchers in Denmark, home of long, dark winters, to find the cause of seasonal affective disorder, or the aptly named SAD.

In a study presented earlier this month at a European College of Neuropsychopharmacology meeting in Berlin, researchers from the University of Copenhagen confirmed why, come winter, some people are hit with seasonal blues.

SAD is a condition that can result in depression and is normally tied to seasonal change. About 5 percent of the population suffers from SAD. If you have ever lived in a northern region where the days shrink come November and you don’t feel the heat of the sun until March, chances are you’ve met someone with SAD. The most popular treatment for SAD is exposure to ultraviolet light. 

Learn More: What Is SAD? »

SAD most commonly affects women, teens, and young adults. It turns out that the brain chemical serotonin and the serotonin transporter (SERT) protein may be to blame.

Serotonin is a neurotransmitter made in the brain and in the gut that is thought to affect mood, social behavior, sleep, appetite, memory, sexual desire, and more. Serotonin levels are associated with depression, but whether low serotonin levels cause depression or vice versa is still unclear. Medications like selective serotonin reuptake inhibitors (SSRIs) are prescribed as antidepressants to help maintain serotonin levels in a person’s brain.

Researchers speculate that lack of exposure to sunlight is the cause of SAD, but this study may help pin down why SAD is so tied to the changing seasons. Using PET brain scans, researchers studied 11 people with SAD and 23 without. “We found that healthy individuals with no [SAD] actually have lower SERT in winter,” said lead researcher Dr. Brenda Mc Mahon.

While shorter days and cold weather are enough to make anyone stay inside with a cup of hot cocoa, for some, SAD is much more than just a couple days of feeling down. What Mc Mahon and her team found is that for people affected by SAD, compared to the general population, SERT levels are significantly higher.

During the winter, the SAD population experiences an uptick in SERT, which carries serotonin into nerve cells where it is inactive. So, the more SERT, the less active serotonin in the brain.

10 Foods Tips to Help Ease Winter Blues »

Mc Mahon and her team focused on SERT because previous studies have shown that SERT levels fluctuate in healthy subjects.

“We would like to see if the SERT is susceptible to light changes in a controlled setting using … bright light therapy,” Mc Mahon said. “Genetic studies of the gene 5-HTTLPR that codes for the SERT are implicated in regulating the response to bright light therapy.”

These findings point to a genetic reason why some people are affected by SAD and some aren’t, as well as why some people respond to UV light therapy while others don’t.

However, there is still the chicken-and-egg issue of whether changes in SERT levels cause SAD or are simply a side effect of the condition. “We would like to investigate if these SERT changes are the primary event or a secondary compensatory mechanism,” Mc Mahon said.

Learn to Shine a Light on Depression with Light Therapy »

At this point, the research is still in its infancy. Before these findings can be applied, researchers need to determine how SERT can be used to diagnose and treat SAD.

“This is basic research, aimed [at explaining the] neurobiological underpinnings of SAD,” Mc Mahon said. “Future research must clarify how this can be used.”

For those living in colder climates under a thick blanket of SAD, there may be a bright light at the end of a long winter tunnel.

For some people, stress is a motivator to focus, work harder, and endure difficult circumstances until the stress ends. For others, stress quickly becomes overwhelming and spirals into paralyzing anxiety and depression.

A team of scientists at Cold Spring Harbor Laboratory have pinpointed a region of the brain that seems to control who will sink and who will swim. It’s called the medial prefrontal cortex (mPFC), and it has been previously associated with depression. The region is part of the default mode network, the circuitry responsible for self-awareness and introspection.

“Brain scans of depressed people have revealed significant hyperactivation of the mPFC,” said associate professor Bo Li, a principal investigator of this research, in an interview with Healthline. “The region is required for effective coping with stress, and its function has been implicated in a wide variety of mood and anxiety disorders. But we have never been able to move beyond correlation in humans.”

Check Out 2014’s Best Meditation Apps for iPhone and Android »

To model the effects of stress, Li’s team employed a well-known theory called learned helplessness. They subjected mice to a series of uncontrollable, inescapable, randomly timed electric shocks over the course of an hour. The mice quickly learned that there was nothing they could do to make the pain stop.

The researchers then tested the mice to see how they responded to this stress. They placed the mice into a box, half of which was lined with an electric grid. Then they shone a light to signal to the mice that they were about to send an electric shock into the grid. If the mice fled to the other half of the box when they saw the light, or left quickly once the shock started, they were considered to be resilient. Despite their stressful conditioning, these mice still took action to protect themselves against further injury.

“Resilience is defined as ‘an ability to come back quickly after difficulty,’” said Li. “The majority will quickly avoid [the shocks]. But a subset of the mice, about 20 percent, will passively endure the shock. This helpless behavior is quite similar to what clinicians see in depressed individuals: an inability to take action to avoid or correct a difficult situation.”

Li examined the mice’s brains and found the expected: their mPFCs were more active if they were “depressed,” and less active if they were resilient. But this correlation wasn’t enough to prove cause and effect on its own.

Li’s team took the next step. Using a technique called chemical genetics, they took resilient mice and engineered them to have an overactive mPFC.

“We find that hyperactivation of the neurons in this region actually causes helplessness,” said Li. “We were able to convert once resilient mice into helpless ones. That makes these neurons an excellent target for treatment [of depression].”

So why does hyperactivity of the mPFC cause depression?

When the default mode network is active, it decreases activity in its opposite half: the task-positive network, which is responsible for interacting with (and enjoying) the outside world. Normally, switching between the two networks allows people to shift between introspecting and paying attention to what’s around them. But when mPFC-fueled introspection gets too strong and reward gets too weak, the result is two hallmark symptoms of depression: rumination (the tendency to get lost in thought) and anhedonia (the inability to enjoy things).

Li’s research will add to knowledge available to scientists who are targeting the mPFC to treat depression. A few experimental techniques currently exist, including using electricity to stimulate the brain through the scalp, and implanting nets of electrodes deep into the brain to stimulate it directly.

The latter is more effective but also dangerous, since it requires brain surgery. “We have very little understanding about why it works,” said Li. “Our study sheds some light on one path that it might use to treat depression—it may be weakening neurons in the mPFC.”

Learn How to Beat Depression Naturally »

Li plans to take future research in this direction. “Beyond looking at how neurons in the mPFC become hyperactive, we are interested in trying to find ways to control the activity of the mPFC,” he said. “Our research may help to find less invasive treatments for depression.”

He added, “Complex neural mechanisms underlie the development of resilience or depression in the face of stress. With the advent of new techniques, scientists in the field are starting to unveil these mechanisms, which ultimately will lead to a better understanding of depression and better treatments.”

8 Ways Stress Is More Dangerous Than You Think »

A new study confirms that older adults who don’t get enough of the essential nutrient vitamin D could double their risk of dementia or Alzheimer’s disease.

The study, published in Neurology, examined blood tests from 1,658 people over the age of 65. None of the volunteers had dementia. After about six years, 171 of them developed dementia and 102 were diagnosed with Alzheimer’s disease.

“We expected to find an association between low vitamin D levels and the risk of dementia and Alzheimer’s disease, but the results were surprising — we actually found that the association was twice as strong as we anticipated,” study author David J. Llewellyn of the University of Exeter Medical School in the U.K. said in a press statement.

Compared to people with normal levels of vitamin D, those with low levels had a 53 percent increased risk for dementia and were 70 percent more likely to develop Alzheimer’s. Those who were severely deficient in vitamin D had a 125 percent greater risk for dementia and were more than 120 percent more likely to get Alzheimer’s.

The results were the same after the researchers adjusted their numbers to take other risk factors like smoking, alcohol consumption, and education level into account.

Read More: This Common Beverage Improves Memory — and a New Study Shows How »

Llewellyn said more clinical trials should be conducted to test whether eating foods high in vitamin D or taking vitamin D supplements could delay or even prevent dementia and Alzheimer’s.

“Given that there are currently no disease modifying treatments for dementia this is an important area for future research,” said Llewellyn, who explained that the research is at an early stage and does not demonstrate that low vitamin D levels cause dementia — it just links the two conditions. “Even if a small number of people could benefit, this would have enormous public health implications given the devastating and costly nature of dementia,” he said.

Llewellyn said it’s too early to know if boosting vitamin D levels could delay or prevent dementia, but past trials have shown that it is effective for other health issues, such as preventing bone fractures.

“People should eat a balanced diet including oily fish and regularly venture outdoors as part of an active lifestyle, which includes moderate intensity exercise such as brisk walking,” he said.

Related News: Apathy in Seniors Could Be a Sign of a Shrinking Brain, Says New Study »

A new study from Rush University Medical Center, also published in Neurology, found that people with depression have a greater risk of developing dementia as well.

Researchers studied 1,764 people for about eight years. The volunteers had no memory problems at the start of the study. The researchers found that people who were later diagnosed with dementia or mild cognitive impairment — often an early sign of Alzheimer’s disease — were more likely to have had higher levels of depression before their diagnosis. The researchers also linked higher levels of depression to a faster decline in memory.

“These findings are exciting because they suggest depression truly is a risk factor for dementia, and if we can target and prevent or treat depression and causes of stress we may have the potential to help people maintain their thinking and memory abilities into old age,” lead researcher Robert S. Wilson, a neuropsychologist at the Rush Alzheimer’s Disease Center, said in a press statement.

Learn More: New Blood Test Can Predict Alzheimer’s Disease »

Although philosophers and scientists have written about dreams for centuries, science is only just beginning to understand how dreams work in the brain. Lucid dreaming (LD), in which the dreamer is aware that he or she is dreaming and is able to manipulate the dream, is even less well understood.

“Often during a LD, you can control dream events voluntarily, for example flying, or you can gain access to waking cognitive abilities that are not normally available, such as remembering events from the previous day,” explained Tore Nielsen, the director of the Dream and Nightmare Laboratory at Montreal’s Sacre-Coeur (Sacred Heart) Hospital and a professor of psychiatry at the University of Montreal, in an interview with Healthline. “In regular dreaming, you are not aware that you are dreaming, you are not usually in voluntary control of dream events, and you don’t usually have access to all your waking cognitive abilities.”

Learn More About Sleep: Healthy Sleep 101 »

This dream control might be able to help people with post-traumatic stress disorder (PTSD) overcome nightmares. These can be frightening and overwhelming for anyone, but for people with PTSD, nightmares can be a way of reliving the events that first traumatized them. Every dream seems dangerous, and sleep becomes an ordeal rather than a refuge.

“Nightmares are terrifying experiences because during regular nightmares (like regular dreams) we are unable to produce a rational judgment about its bizarreness, thus we strongly believe that what is happening during the nightmare is real,” said Dr. Sérgio Mota-Rolim, Ph.D., of the Federal University of Rio Grande do Norte in Brazil, told Healthline.

Mota-Rolim hopes that lucid dreaming might be able to help. He explained, “Psychotherapies based on inducing LD could be an effective way of treating recurrent nightmares of PTSD patients, because they—being lucid during the nightmare—would be able to: one, naturally lose their fear by realizing the absence of real threats, i.e. the lack of reality of the perceptual experience; two, simply try to wake up during the nightmare; and, three, change dream context, in a way of transforming the nightmare into a neutral or even a pleasant dream.”

There’s evidence to support this idea. One set of case studies showed that people with recurring nightmares saw their bad dreams go away after they learned lucid dreaming.

Another study co-authored by Victor Spoormaker, Ph.D., found that lucid dreaming reduced the frequency and intensity of nightmares, but didn’t do anything to treat the sleep disturbance, anxiety, and depression that often accompany PTSD. “We found that LD was effective in reducing nightmare frequency, but there are a few ‘but’s in there,” said Spoormaker, a staff scientist at Max Planck Institute of Psychiatry in Munich, in an interview with Healthline. “One is that not everyone could learn. It is a complex treatment, one for which there are easier treatments available.”

Spoormaker recommends an alternative treatment for nightmares. “Imagery rehearsal therapy is a treatment in which the people with nightmares write down their nightmares and at some point, they will write a new ending, make a change in the nightmare itself,” he said. “Then they will rehearse this new nightmare. By imagining the new nightmare, the nightmare has a lower frequency afterwards. There’s some promising research in several PTSD populations. It is much more effective in the data than lucid dreaming treatment.”

Read More: What Causes Nightmares? »

Lucid dreaming can be difficult to master. But if you’re wondering if there’s a shortcut, Ursula Voss, a professor at J.W. Goethe-University in Frankfurt, Germany, may have found a way. In a study published earlier this month, Voss’s team discovered how to create lucid dreams by applying an electrical current to the brains of study participants while they slept.

Earlier research had identified a type of brain activity called gamma waves as being important for lucid dreaming, especially in the frontal and temporal lobes of the brain. “Gamma is usually strongly reduced in normal REM sleep dreaming. It is strongly increased in lucid dreaming,” said Voss in an interview with Healthline. “It goes along with higher-order consciousness that enables us to be self-reflective, to plan ahead and to make logical decisions.”

Voss used a method called transcranial alternating current stimulation (tACS), which can alter brainwaves without producing any side effects of stimulating the brain, such as muscle twitches or seeing bursts of color. Her team took a group of subjects with no training in lucid dreaming and then waited for them to enter REM sleep, the stage of sleep where dreaming typically occurs. Once they were in REM, the researchers applied tACS to create gamma waves in the frontal and temporal lobes of the brain. The result? Most of the subjects in the study experienced lucid dreams. The sweet spot for tACS appeared to be electric current at 25 and 40 Hz.

Related News: The FDA Cuts Starting Dose of Sleep Aid Drug Lunesta in Half, Citing Impairment the Next Day »

Montreal’s Nielsen hopes that Voss’s work will lead the way to more effective lucid dreaming therapies. “With refinements, the approach might be developed into a method that would allow scientists to explore dreaming more quickly, effectively and reliably,” he said. “If nightmare sufferers can gain some amount of control over their negative dream content, this might be therapeutically effective.”

Mota-Rolim appreciates Voss’s work but has his doubts. He points out that other research that used a similar type of brain simulation had only a weak effect on lucid dreaming, and worked only in experienced lucid dreamers. As for the gamma wave activity? It might be the result of the rapid eye movement that gives REM sleep its name.

His own research instead points to alpha waves in a different region of the brain, the occipital lobe. “What we found is that during LD, the occipital alpha activity reaches an intermediate level between non-lucid dreaming and waking, as if LD were a phase transition between regular dreaming and waking,” he said. “We found that for most of the people, LD is an unstable experience that usually lasts a short time, since people tend to wake up as soon as they become lucid.”

They all agree that more research is needed to understand just how lucid dreaming works. And for now? “Don’t try this at home!” warns Nielsen. “Using the wrong placement of electrodes or incorrect amounts or types of electrical current could have disastrous consequences. Imagery Rehearsal Therapy is a much better option for treating nightmares at this point.”

“It’s interesting to become lucid in a dream,” said Spoormaker. “It can help to become lucid in a nightmare and then change it. But if you’re suffering from post-traumatic stress disorder, it’s better to search for an alternative treatment: image rehearsal therapy.” 

Most psychiatrists believe that depression is caused by low levels of the chemical serotonin. This is why the treatment for depression is often selective serotonin reuptake inhibitors (SSRIs), which boost serotonin levels in the brain.

But a new study suggests that there are at least five biotypes of clinical depression. William J. Walsh, Ph.D., president of the Walsh Research Institute, and his team looked at about 300,000 blood and urine chemistry test results and 200,000 medical history factors from approximately 2,800 patients diagnosed with depression. They found that five major depression biotypes represented about 95 percent of the patients.

Upon close examination, Walsh and his team discovered that three of these forms of depression are not caused by fluctuating serotonin levels.

Learn How Depression Treatment Could Be Good for the Heart »

The five defined depression biotypes are:

Undermethylated Depression

This type of depression was found in 38 percent of patients in the study. The problem in these cases is low activity at serotonin receptors, apparently due to rapid reabsorbtion after serotonin is released into a synapse. 

“It’s not serotonin deficiency, but an inability to keep serotonin in the synapse long enough. Most of these patients report excellent response to SSRI antidepressants, although they may experience nasty side effects,” Walsh said.

Pyrrole Depression

This type was found in 17 percent of the patients studied, and most of these patients also said that SSRI antidepressants helped them. These patients exhibited a combination of impaired serotonin production and extreme oxidative stress.

Copper Overload

Accounting for 15 percent of cases in the study, these patients cannot properly metabolize metals. Most of these people say that SSRIs do not have much of an effect—positive or negative—on them, but they report benefits from normalizing their copper levels through nutrient therapy. Most of these patients are women who are also estrogen intolerant. 

“For them, it’s not a serotonin issue, but extreme blood and brain levels of copper that result in dopamine deficiency and norepinephrine overload,” Walsh explained. “This may be the primary cause of postpartum depression.”

Low-Folate Depression

These patients account for 20 percent of the cases studied, and many of them say that SSRIs worsened their symptoms, while folic acid and vitamin B12 supplements helped. Benzodiazepine medications may also help people with low-folate depression.

Walsh said that a study of 50 school shootings over the past five decades showed that most shooters probably had this type of depression, as SSRIs can cause suicidal or homicidal ideation in these patients.

Toxic Depression 

This type of depression is caused by toxic-metal overload—usually lead poisoning. Over the years, this type accounted for 5 percent of depressed patients, but removing lead from gasoline and paint has lowered the frequency of these cases.