Showing posts with label immune system. Show all posts
Showing posts with label immune system. Show all posts

Sunday, November 30, 2014

Why students need to get enough sleep

This article explains why it is so important for young adults, especially students, need to get enough sleep.

Humans need sleep. Young adults especially need it, and more  of it if possible. While growth spurts may be over, teenaged brains are still developing, and they will not fully mature until a person’s mid-20s, at the least. While students are in school trying to expand their minds, the very structure of their brains is expanding at the same time. Young adults need to balance academics with their sleep, which actually aids in learning and development. It may often seem like these two activities are at odds with each other, but their correlation is important.
Young adults have odd sleeping schedules, and it is not completely their fault. Developing brains of adolescents are wired to go to sleep later. When combined with heavy collegiate workloads, freedom from parental restrictions and the atmosphere of the city that never sleeps, it is no wonder that NYU students often go to sleep extremely late. While late bedtimes alone can be troubling, affecting everything from throwing off our circadian rhythms to our immune systems, this issue is compounded during the winter time. Moreover, students from warmer regions with longer days and shorter nights may not be aware of the effects the winter can have on one’s system. By going to bed late, young adults exacerbate these effects, which can lead to medical issues.
Seasonal affective disorder — a form of depression caused by changes in seasons — is among the potential complications. It can be triggered by a variety of factors, including an unnatural sleep schedule and decreased exposure to light. Symptoms of seasonal affective disorder usually manifest during fall and winter, and deficient sleep during this period can make individuals more vulnerable to depression. Research indicates that going to bed late when the sun sets later is not necessarily problematic. An 11 a.m. wake-up time gives one plenty of sunlight to maintain proper Vitamin D levels and circadian rhythm. Going to bed late when the sun goes down early is a recipe for disaster, however, because an 11 a.m. wake-up time means five hours of sunlight at the most. Students should be wary of seasonal affective disorder and take sleep seriously. Depression in the middle of a semester can jeopardize both academics and social life.
In college, personal well-being is seldom prioritized. This should not be the case — sleep is an essential tool for physical and mental health. Sleeping in late for Palladium brunch rather than waking up to an early breakfast may seem preferable, but a balanced sleep schedule can literally make winter much brighter. Suspend late-night study sessions, close Netflix and go to sleep — your mind and body will be grateful.
Read more here

Friday, June 06, 2014

What causes poor sleep, and how do I get better sleep?

This article discusses health conditions that cause a person to get poor sleep, and discusses things everyone can do to get better sleep.

With any illness, injury or sniffle, you'll hear one common suggestion: Get plenty of rest. Whether we're nursing a broken bone or trying to recover from the flu, we are led to believe that adequate sleep will put us right on the path to recovery. But just how important is sleep, and what about those of us who can't seem to get quality sleep?
Lack of sleep is linked to several health concerns:
Colds, flu, viruses and infections. One of the first systems to be adversely affected by lack of quality sleep is immune function. When you're tired, you feel worn down -– and that's not just a feeling. Your body is using all energy reserves to fight off the viruses and exposure to germs that might not affect a person with a thriving immune system. Also, if you receive vaccines, the sleep-deprived are slow to respond to the immunity the vaccines are designed to build.
Heart disease. According to Donna Arand, clinical director of the Kettering Sleep Disorder Centers in Dayton, Ohio, lack of sleep causes an inflammatory response to the cardiovascular system. Rises in C-reactive protein due to impaired sleep are warning signs that the body is responding to a perceived injury, infection or disease. In this case, lack of sleep is that perceived threat that results in inflammation. Poor sleep also causes the body to produce more stress hormones, which may contribute to cardiovascular disease. Chronic stress coupled with lack of quality sleep causes double trouble for the heart, arteries and ventricles.
Diabetes. In the past decade, there has been growing evidence that too little sleep can affect hormones and metabolism in ways that promote diabetes. According to a study published in the Lancet in 1999, healthy men with a week of impaired sleep –- only four hours a night –- showed dramatic changes in glucose tolerance. They also had higher-than-normal glucose levels after just one week. This study involved healthy people with no previous record of insulin resistance or history of diabetes.
For those already diagnosed with diabetes, sleep deprivation leads to extremely poor blood sugar control. These studies do not include control factors of the snowball effect that often starts with losing a night's sleep. Sleepy people don't usually reach for healthy foods as snacks and meals. They don't usually choose to walk during their lunch break -– or head to the weight room after work. Tight glucose control involves nutrition and exercise parameters, and both of those are adversely affected by just one night of impaired sleep.
How Can We Improve Our Sleeping Patterns? 
1. Keep the bedroom for sleep and sex. Don't let the bedroom become the home office. Keep the clutter and distraction of that quickly approaching timeline out of the bedroom. Keep a cool temperature, and design the room for its purpose. Walking into your bedroom should be a clear change from the rest of the house.
2. Put down the screens. An hour or more before bedtime, put down the computer, smartphone and TV. Dim the lights throughout the house, and start getting your mind ready to wind down. Some people use blackout shades in the bedroom during the summer months. Before electricity, people stayed awake two or three hours past dusk with candlelight, and their natural circadian rhythms prompted them to sleep. There's a lot of research that links artificial light –- including blue-light from screens -– with interrupted sleep patterns. If we're staying up six or more hours past dusk with fluorescent light glowing, our bodies don't know when it’s time to sleep.
3. Pay attention to what you eat and drink before bedtime. Try not to go to bed ravenous or stuffed. Be aware that a glass of wine might help calm the nerves, but metabolizing alcohol keeps the body in an alert mode while the mind is trying to snooze. Have that glass of wine earlier in the evening. And yes, eating bad pizza right before bed can cause nightmares. So can stuffing yourself with any food minutes before trying to sleep. Your body is trying to do two things: metabolize food and sleep. The food is going to win, and that's a cause for dreams and other disruptions to quality sleep.
4. Move your body. There is substantial evidence that exercise helps you sleep. Even moderate exercise like a daily walk promotes better sleep -– in terms of quality and quantity. Be careful with your exercise timing, so you're not too energized with endorphins to sleep. There's also a direct link between exercise and stress, and stress is a big factor in sleep-deprived people. Move your body. Manage your stress. Get quality sleep.
Read more here

Monday, May 19, 2014

Children with autism have deifcits in their mitochondrial DNA

Research showed that children with autism have deficits in their mitochondrial DNA. These deficits can make it harder for the body to fight off infection.

Children with autism experience deficits in a type of immune cell that protects the body from infection. Called granulocytes, the cells exhibit one-third the capacity to fight infection and protect the body from invasion compared with the same cells in children who are developing normally.
The cells, which circulate in the bloodstream, are less able to deliver crucial infection-fighting oxidative responses to combat invading pathogens because of dysfunction in their tiny energy-generating organelles, the mitochondria.
The study is published online in the journalPediatrics.
"Granulocytes fight cellular invaders like bacteria and viruses by producing highly reactive oxidants, toxic chemicals that kill microorganisms. Our findings show that in children with severe autism the level of that response was both lower and slower," said Eleonora Napoli, lead study author and project scientist in the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine. "The granulocytes generated less highly reactive oxidants and took longer to produce them."
The researchers also found that the mitochondria in the granulocytes of children with autism consumed far less oxygen than those of the typically developing children -- another sign of decreased mitochondrial function.
Mitochondria are the main intracellular source of oxygen free radicals, which are very reactive and can harm cellular structures and DNA. Cells can repair typical levels of oxidative damage. However, in the children with autism the cells produced more free radicals and were less able to repair the damage, and as a result experienced more oxidative stress. The free radical levels in the blood cells of children with autism were 1 ½ times greater than those without the disorder.
The study was conducted using blood samples of children enrolled in the Childhood Risk of Autism and the Environment (CHARGE) Study and included 10 children with severe autism age 2 to 5 and 10 age-, race- and sex-matched children who were developing typically.
In an earlier study the research team found decreased mitochondrial fortitude in another type of immune cell, the lymphocytes. Together, the findings suggest that deficiencies in the cells' ability to fuel brain neurons might lead to some of the cognitive impairments associated with autism. Higher levels of free radicals also might contribute to autism severity.
"The response found among granulocytes mirrors earlier results obtained with lymphocytes from children with severe autism, underscoring the cross-talk between energy metabolism and response to oxidative damage," said Cecilia Giulivi, professor in the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine and the study's senior author.
"It also suggests that the immune response seems to be modulated by a nuclear factor named NRF2," that controls antioxidant response to environmental factors and may hold clues to the gene-environment interaction in autism, Giulivi said.
Read more here

Friday, March 28, 2014

Sleep necessary for mental health and well-being

This article discusses how crucial good sleep is for a person's mental health and well-being, and the consequences of not having good quality sleep.
Having a good quality and restorative sleep is essential for one to be able to function well throughout the day. Failure to do so will lead to numerous impacts to health, both long- and short-term.
According to the Sleep Disorder Society Malaysia (SDSM) president Dr Muhammad Muhsin Ahmad Zahari, some of the short-term negative impacts include short attention span, memory recall and learning; while its long-term effects have long been associated with hypertension, ischaemic heart disease, stroke, obesity, diabetes, weakened immune system, and cancer.
Dr Muhammad Muhsin added that sleep disorder can also increase the risk of accidents.
"People who suffer from insomnia are seven times more likely to become involved in an accident which then resulted in death or serious injury," he said at the launch of the `World Sleep Day Celebration and Sleep 2014 Conference' at Cititel Hotel, here, today.
He revealed that sleep disorder actually constitute a global epidemic that threatens health and quality of life for up to 45% of the world's population, thus it is essential for everyone to have a better understanding of sleep conditions.
"Sleep is a basic human need and it is crucial not only to our health and well-being, it also plays an important role in the metabolic regulation in children," said Dr Muhammad adding that SDSM is working closely with the relevant authorities, associations and organisations in improving the quality of service of sleep medicine.
"With regards to the quality service in sleep medicine, facilities such as sleep laboratory are vital. As our population grows, there is definitely a need to increase the number of sleep laboratory in public hospitals to cater to the need of the people." he added.
Read more here

Monday, January 13, 2014

Study shows that narcolepsy is an autoimmune disorder

A study claims that narcolepsy is actually an autoimmune disorder which has important impacts for treatment options.

A recent study confirms long-held suspicions that the sleep disorder narcolepsy -- a condition where a person feels uncontrollably sleepy during the daytime and can experience muscle weakness -- is actually an autoimmune disorder. The findings also help to explain why narcolepsy was linked to the Pandemrix H1N1 flu vaccine.
Nearly all people with narcolepsy have a specific genetic signature -- called the HLA signature, where HLA stands for human leukocyte antigens -- but not everyone with this genetic signature goes on to develop narcolepsy (20 percent of the general population is thought to possess this signature). A type of immune cell, called the CD4+ T cell, is associated with this HLA signature; immune cells, like this type of T cell, are responsible for recognizing and eradicating foreign invaders in the body.
Previously, researchers had found evidence to suggest that the immune system was responsible for narcolepsy by attacking neurons that produce a neurotransmitter called hypocretin, which promotes wakefulness. (People with narcolepsy are known to have low levels of hypocretin).
In the new study, published in December in the journal Science Translational Medicine, researchers found that only people with narcolepsy have these CD4+ T cells that react to portions of the hypocretin protein, while people without narcolepsy do not have these T cells. WebMD reported that this discovery was based on examinationof 39 people with narcolepsy, and 35 people without the sleep disorder.
However, Nature News also pointed out that the study did not prove that these T cells themselves kill neurons that produce hypocretin -- there could be something else that's going on causing the death of these neurons.
The researchers also found that CD4+ T cells react strongly to a portion of the H1N1 hemagglutinin protein because it strongly resembles that of two portions of hypocretin -- which could help to explain the link between narcolepsy and the H1N1 Pandemrix vaccine, which actually contained parts of viral protein.
Reuters reported that 900 cases of narcolepsy, if not more, were linked with the Pandemrix vaccine, which was administered in the 2009/2010 flu pandemic in Europe but not the United States. (It is no longer being administered in Europe.)
"The relationship between H1N1 infection, vaccination and narcolepsygave us some very interesting insight into possible causes of the condition," study researcher Dr. Emmanuel Mignot, M.D., Ph.D., a professor of psychiatry and behavioral sciences at Stanford University School of Medicine, as well as director of the Stanford Center for Sleep Sciences and Medicine, said in a statement. "In particular, it strongly suggested to us that T cells of the immune system primed to attack H1N1 can occasionally also cross-react with hypocretin and somehow cause the destruction of hypocretin-producing neurons."
The new findings mean that researchers now have a target to set their sights on -- finding ways to stop the loss of brain cells by the body's own immune system.
"By giving us a new way to think about how neurons in these patients die, it alsosuggests new therapeutic approaches that we would not have considered if we hadn’t learned that this is an autoimmune disease," study researcher Dr. Elizabeth Mellins, M.D., an immunology researcher at Stanford, said in the statement.
Read more here

Thursday, December 26, 2013

Inflammation can be caused by anti-epilepsy drugs

A report claims that anti-epilepsy drugs can cause inflammation and thus may have roots in the immune system.

Physicians at the Ruhr-Universität Bochum (RUB) have been investigating if established anti-epilepsy drugs have anti-inflammatory or pro-inflammatory properties -- an effect for which these pharmaceutical agents are not usually tested. One of the substances tested caused stronger inflammations, while another one inhibited them. As inflammatory reactions in the brain may be the underlying cause for epileptic disorders, it is vital to take the trigger for the disorder under consideration when selecting drugs for treatment, as the researchers concluded. They published their report in the journal Epilepsia.
Glial cells play a crucial role in the nervous system
Hannes Dambach from the Department for Neuroanatomy and Molecular Brain Research, together with a team of colleagues, studied how anti-epilepsy drugs affect the survival of glial cells in cultures. Glial cells are the largest cell group in the brain; they are crucial for supplying neurons with nutrients and affect immune and inflammatory responses. The question of how glial cells are affected by anti-epilepsy drugs had previously not been studied in depth. The RUB work group Clinical Neuroanatomy, headed by Prof Dr Pedro Faustmann, analysed four substances: valproic acid, gabapentin, phenytoin and carbamazepine.
Four anti-epilepsy drugs affect glial cells in different ways
Glial cells treated by the researchers with valproic adic and gabapentin had better survival chances than those treated with phenytoin and carbamazepine. However, carbamazepine had a positive effect, too: it reduced inflammatory responses. Valproic acid, on the other hand, turned out to be pro-inflammatory. In how far the anti-epilepsy drugs affected inflammations was also determined by the applied dose. Consequently, different drugs affected glial cells -- and hence indirectly the neurons -- in different ways.
Inflammatory responses should be taken under consideration in clinical studies
"Clinical studies should focus not only on the question in how far anti-epilepsy drugs affect the severity and frequency of epileptic seizures," says Pedro Faustmann. "It is also necessary to test them with regard to the role they play in inflammatory responses in the central nervous system." Thus, doctors could take the underlying inflammatory condition under consideration when selecting the right anti-epilepsy drug.
Epilepsy may have different causes
In Germany, between 0.5 and 1 percent of the population suffer from epilepsy that requires drug treatment. The disease may have many causes: genetic predisposition, disorders of the central nervous system after meningitis, traumatic brain injury and stroke. Inflammatory responses may also be caused by damage to the brain.
Read more here

Study: Narcolepsy could be caused by the immune system

According to a recent study, narcolepsy might be caused by an immune system attack, meaning it could be tested for by a blood test, and treatment may center around the immune system.

A new study has uncovered evidence that most cases of narcolepsy are caused by a misguided immune system attack -- something that has been long suspected but unproven.
Experts said the finding, reported Dec. 18 in Science Translational Medicine, could lead to a blood test for the sleep disorder, which can be difficult to diagnose.
It also lays out the possibility that treatments that focus on the immune system could be used against the disease.
"That would be a long way out," said Thomas Roth, director of the Sleep Disorders and Research Center at Henry Ford Hospital, in Detroit.
"If you're a narcolepsy patient now, this isn't going to change your clinical care tomorrow," added Roth, who was not involved in the study.
Still, he said, the findings are "exciting," and advance the understanding of narcolepsy.
Narcolepsy causes a range of symptoms, the most common being excessive sleepiness during the day. But it may be best known for triggering potentially dangerous "sleep attacks." In these, people fall asleep without warning, for anywhere from a few seconds to a few minutes.
About 70 percent of people with narcolepsy have a symptom called cataplexy -- sudden bouts of muscle weakness. That's known as type 1 narcolepsy, and it affects roughly one in 3,000 people, according to the U.S. National Institute of Neurological Disorders and Stroke.
Research shows that those people have low levels of a brain chemical called hypocretin, which helps you stay awake. And experts have believed the deficiency is probably caused by an abnormal immune system attack on the brain cells that produce hypocretin.
"Narcolepsy has been suspected of being an autoimmune disease," said Dr. Elizabeth Mellins, a senior author of the study and an immunology researcher at Stanford University School of Medicine, in California.
"But," she said, "there's never really been proof of immune system activity that's any different from normal activity."
Mellins thinks her team has uncovered "very strong evidence" of just such an underlying problem.
The researchers found that people with narcolepsy have a subgroup of T cells in their blood that react to particular portions of the hypocretin protein -- but narcolepsy-free people do not. T cells are a key part of immune system defenses against infection.
That finding was based on 39 people with type 1 narcolepsy, and 35 people without the disorder -- including four sets of twins in which one twin was affected and the other was not.
It's known that genetic susceptibility plays a role in narcolepsy. And the theory, Mellins explained, is that in people with that inherent risk, certain environmental triggers may cause an autoimmune reaction against the body's own hypocretin.
Infections are the main culprit, and there is already evidence that the H1N1 "swine" flu is one trigger. In China, Mellins noted, there was an upswing in childhood narcolepsy cases after the H1N1 flu pandemic of 2009.
And in 2010, a cluster of narcolepsy cases in Europe was linked to a particular H1N1 vaccine that contained an "adjuvant" designed to induce a stronger immune system response. That vaccine, called Pandemrix, is no longer in use.
All of that led experts to speculate that in some genetically vulnerable people, the H1N1 virus could cause T cells to mistakenly attack hypocretin-producing brain cells.
And in the current study, Mellins's team found that segments of the H1N1 virus were similar to portions of the hypocretin protein -- the same portions that activated narcolepsy patients' T cells. They say that supports the idea that certain infections confuse T cells into attacking hypocretin-producing cells.
An expert on sleep welcomed the new study.
"They're providing more-compelling evidence that this is an autoimmune disease," said Dr. Nathaniel Watson, an associate professor of neurology at the University of Washington in Seattle, and a member of the board of directors for the American Academy of Sleep Medicine.

He and Mellins both said the results could have practical use, too. For one, researchers may be able to develop a blood test to help objectively diagnose narcolepsy.
Right now, Watson said, narcolepsy can be difficult to pinpoint, because the most common symptom -- daytime sleepiness -- has far more common causes. The most common, he noted, is simple: Not going to bed early enough.
So to diagnose narcolepsy, people may have to spend 24 hours in a sleep lab or, in some cases, have a lumbar puncture (spinal tap) to measure hypocretin in the spinal fluid.
Mellins said that if an autoimmune reaction is the cause of type 1 narcolepsy, it might be possible to treat with an immune-suppressing therapy.
The problem, though, is that once people develop full-blown symptoms, their hypocretin-producing cells have already been knocked off.
"We'd need some kind of pre-clinical marker of the disease to be able to intervene," said Watson at the University of Seattle.
Roth of Henry Ford Hospital agreed. "The big challenge is, how will you identify the people to treat?"
Three of the study authors reported they are inventors on a patent to use the hypocretin protein segments to diagnose narcolepsy. Stanford owns the intellectual property rights for this use.
Read more here

Wednesday, October 09, 2013

Study: No link found between autism and celiac disease

A study claims there is no link between autism and celiac disease.

There's no link between celiac disease and autism spectrum disorders, a nationwide study from Sweden says.
People who were diagnosed with an autism spectrum disorder (ASD) in the study were no more likely to be diagnosed with celiac disease than people without an ASD.
Dr. Jonas Ludvigsson, the study's lead author, said the finding offers one less thing to worry about for people with either celiac or ASDs.
"To them, this is good news," Ludvigsson, of Sweden's Karolinska Institute, said.
Some researchers have reported on single cases of people who were diagnosed with an ASD and who were then diagnosed with celiac disease.
In celiac disease, which is estimated to affect about one percent of Americans, an individual's own immune system attacks the small intestines if they eat gluten, a protein in wheat and certain other grains.
Other studies have found that switching those people to gluten-free diets appeared to also reduce ASD symptoms, but larger trials have not shown any link between the two conditions.
For the new study Ludvigsson and his colleagues connected several Swedish databases to compare the celiac disease diagnoses among people with ASDs to a group of people without the developmental disorders.
The researchers had information on more than 250,000 people and they found no difference in the rate of ASD diagnoses among people with celiac disease compared to those without the condition.
About 44 people per 100,000 were diagnosed with an ASD before they were diagnosed with celiac disease. That compared to about 48 people per 100,000 who were diagnosed with an ASD but not with celiac disease.
There was, however, a link between ASDs and a positive blood test for celiac disease, which alone is not enough to diagnose someone with the condition. A celiac disease diagnosis requires both a positive blood test and evidence of damage to the small intestine.
"It's very interesting in my mind, because it points to some relationship to gluten that's separate from celiac disease," Dr. Peter Green, professor of medicine and director of the Celiac Disease Center at Columbia University Medical Center and a gastroenterologist at NewYork-Presbyterian/Columbia.
But Ludvigsson cautioned that the link between ASDs and a positive celiac blood test is based on a small number of cases. There could be a real relationship between the two or it could be a result of doctors overtesting people with ASDs, he said.
"I want to underline that the positive association we found in this small group could be by chance," Ludvigsson said.
The study also does not shed any light on whether a gluten-free diet improves ASD symptoms, he added.
"I think the next step would be for someone to carry out a well-performed study on a gluten-free diet in autism," Ludvigsson said. "There are several such studies, but my understanding is that they haven't been large enough in size."
Green, who was not involved in the new report, agreed that people can't draw any conclusions on gluten-free diets for autism.
"This (study) provides some evidence that there may be a role, but it may also help to find those who would possibly benefit from this therapy," he said.
Ludvigsson, who published his findings in JAMA Psychiatry, said it's also important to examine possible relationships between celiac disease and other "neurocognitive" disorders.
"Our study is definitive when it comes to refuting an association between celiac disease and autism, however, we can't rule out that autism is related to other intestinal conditions that do not fulfill the traditional criteria of celiac disease," he added.

Wednesday, July 24, 2013

Study claims poor sleep during pregnancy can cause birth complications

Not getting enough quality sleep during pregnancy can lead to birth complications such as low birth weight. It is important to treat sleep issues during pregnancy early.

Poor sleep quality and quantity during pregnancy can disrupt normal immune processes and lead to lower birth weights and other complications, finds a University of Pittsburgh School of Medicine study published today in the journalPsychosomatic Medicine. Women with depression also are more likely than non-depressed women to suffer from disturbed sleep and to experience immune system disruption and adverse pregnancy outcomes.
"Our results highlight the importance of identifying sleep problems in early pregnancy, especially in women experiencing depression, since sleep is a modifiable behavior," said Michele Okun, Ph.D., assistant professor of psychiatry at Pitt's School of Medicine and lead author of the report. "The earlier that sleep problems are identified, the sooner physicians can work with pregnant women to implement solutions."
Adequate and high-quality sleep, both in pregnant and non-pregnant women as well as men, is essential for a healthy immune system. Pregnancy often is associated with changes in sleep patterns, including shortened sleep, insomnia symptoms and poor sleep quality. These disturbances can exacerbate the body's inflammatory responses and cause an overproduction of cytokines, which act as signal molecules that communicate among immune cells.
"There is a dynamic relationship between sleep and immunity, and this study is the first to examine this relationship during pregnancy as opposed to postpartum," added Dr. Okun.
While cytokines are important for numerous pregnancy-related processes, excess cytokines can attack and destroy healthy cells and cause destruction of tissue in pregnant women, thereby inhibiting the ability to ward off disease. For expectant mothers, excess cytokines also can disrupt spinal arteries leading to the placenta, cause vascular disease, lead to depression and cause pre-term birth.
Previous studies conducted postpartum have shown higher inflammatory cytokine concentrations among women who experienced adverse pregnancy outcomes such as preeclampsia and pre-term birth. While infection accounts for half of these adverse outcomes, researchers discovered that behavioral processes such as disturbed sleep also may play a role, given the relationship between sleep disturbance and immune function.
Furthermore, higher concentrations of inflammatory cytokines also are found in depressed individuals.
The study is the first to evaluate all factors -- inflammatory cytokines, depression and insomnia -- and their possible combined effect on pregnant women. The study examined nearly 170 women, both depressed and not depressed, at 20 weeks of pregnancy and analyzed their sleep patterns and cytokine production levels over the course of 10 weeks (pregnancy-related physiological adaptations are in flux prior to 20 weeks).
The findings reveal:
  • Women with depression and poor sleep are at greatest risk for adverse birth-related outcomes. Cytokine levels may be one biological pathway through which this is accomplished, particularly with regard to preterm birth.
  • Any shift in immunity, such as poor sleep and/or depression, could set the stage for increased risk for adverse outcomes.
  • At 20 weeks, depressed pregnant women have higher levels of inflammatory cytokines compared to non-depressed women.
  • At 30 weeks of pregnancy, differences in cytokines among depressed and non-depressed women were negligible, likely because as pregnancy progresses, levels of cytokines normally increase.
Read more here

Saturday, March 30, 2013

CDC study shows Autism is not caused by too many vaccines

The idea that 'too many vaccines too soon' causes autism has been proven false by research done by the Centers for Disease Control and Prevention.

Although scientific evidence suggests that vaccines do not cause autism, approximately one-third of parents continue to express concern that they do; nearly 1 in 10 parents refuse or delay vaccinations because they believe it is safer than following the Centers for Disease Control and Prevention's (CDC) schedule. A primary concern is the number of vaccines administered, both on a single day and cumulatively over the first 2 years of life. In a new study scheduled for publication in The Journal of Pediatrics, researchers concluded that there is no association between receiving "too many vaccines too soon" and autism.

Dr. Frank DeStefano and colleagues from the CDC and Abt Associates, Inc. analyzed data from 256 children with autism spectrum disorder (ASD) and 752 children without ASD (born from 1994-1999) from 3 managed care organizations. They looked at each child's cumulative exposure to antigens, the substances in vaccines that cause the body's immune system to produce antibodies to fight disease, and the maximum number of antigens each child received in a single day of vaccination.
The researchers determined the total antigen numbers by adding the number of different antigens in all vaccines each child received in one day, as well as all vaccines each child received up to 2 years of age. The authors found that the total antigens from vaccines received by age 2 years, or the maximum number received on a single day, was the same between children with and without ASD. Furthermore, when comparing antigen numbers, no relationship was found when they evaluated the sub-categories of autistic disorder and ASD with regression.
Although the current routine childhood vaccine schedule contains more vaccines than the schedule in the late 1990s, the maximum number of antigens that a child could be exposed to by 2 years of age in 2013 is 315, compared with several thousand in the late 1990s. Because different types of vaccines contain varying amounts of antigens, this research acknowledged that merely counting the number of vaccines received does not adequately account for how different vaccines and vaccine combinations stimulate the immune system. For example, the older whole cell pertussis vaccine causes the production of about 3000 different antibodies, whereas the newer acellular pertussis vaccine causes the production of 6 or fewer different antibodies.
An infant's immune system is capable of responding to a large amount of immunologic stimuli and, from time of birth, infants are exposed to hundreds of viruses and countless antigens outside of vaccination. According to the authors, "The possibility that immunological stimulation from vaccines during the first 1 or 2 years of life could be related to the development of ASD is not well-supported by what is known about the neurobiology of ASDs." In 2004, a comprehensive review by the Institute of Medicine concluded that there is not a causal relationship between certain vaccine types and autism, and this study supports that conclusion.
Read more here

Monday, February 20, 2012

Irregular Sleep Could Weaken Your Immune System


I frequently see one symptom of disrupted sleep as frequent colds...JR


We have all heard about just how important sleep is for our bodies. Not only is it necessary for us to function, but it also plays an important role on our weight and metabolism, our mood, our cardiovascular health, and disease . The frightening side effects of sleep deprivation are only compounded by the fact that a many Americans are sleep deprived. According to the National Sleep Foundation (NSF), 40 million Americans suffer from some type of sleeping disorder, with 60% of adults saying that they do have sleep problems a few nights a week, if not more.
But do we do anything to help cure our insomnia or our sleep problems? Not really.
Perhaps the newest study to come out of the journalImmunity this week will have people taking their sleep a whole lot more seriously than they have before. Now we’ve all heard about our circadian rhythm and we’re aware that our body functions on a 24 hour cycle. While it’s been proven that this rhythm and how we follow it does affect things like our metabolism and memory, researchers at the Yale School of Medicine in the United States have now been able to prove that sleep – or lack thereof – can influence our vulnerability to disease.
Lab mice were used to conduct the study. Dr Erol Fikrig, a professor of epidemiology and microbial pathogenesis at Yale, along with his colleagues, found that the circadian clock in mice was controlled by the “Toll-like receptor 9” (or TLR-9). This gene is incredibly important for our immune system as it reacts any presence of DNA from harmful bacteria and viruses.
What was discovered was that the mice had the strongest response to vaccinations, and the highest ability to resist any infection, when their expression levels of TLR-9 were also at their highest point. And in order for the TLR-9 to be at its highest point, the mice needed to have a decent amount of sleep.
This has raised a lot of questions about how sleep deprivation and sleep problems may affect human health. One observation that researchers find to be significant is the fact that septic human patients are most likely to die between 2 and 6am, possibly when their sleep is disturbed. Fikrig made the comment that the “… sleeping patterns of patients in intensive care are often disrupted because of the noise and prolonged exposure to artificial light… it will be important to investigate how these actors influence immune system response.”
The study could have very important implications on how we both prevent and treat diseases. Rather than reach for a pill, perhaps a darkened, quiet room that allows one to ease into sleep would be better treatment. Maybe sleep plays a far larger role on our immunity than we even realize. The study has unveiled a new, direct molecular link between the body clock and our immunity, thus opening up a pathway to explore all new therapies that could help treat and even cure disease.