University of Michigan

Factors Predicting Long-term Benzodiazepine Use Identified

Posted by

0


Poor-quality sleep, prescribing in an extended manner, and white race are key factors that predict conversion to long-term benzodiazepine use in the elderly, a practice that is strongly tied to poor outcomes, including death.

Dr Lauren Gerlach

 

The results highlight the need to “start with the end in mind” when prescribing a benzodiazepine, author Lauren B. Gerlach, DO, a geriatric psychiatrist and assistant professor in the Department of Psychiatry and the Program for Positive Aging, University of Michigan, Ann Arbor, told Medscape Medical News.

This means “beginning with a short-duration prescription and engaging patients in discussions of when to reevaluate their symptoms and begin tapering the patient off,” she said.

Gerlach said more work is needed to improve access to effective nonpharmacologic treatments, such as cognitive-behavioral therapy, as well as to provide access to education regarding such treatments.

The study was published online September 10 in JAMA Internal Medicine.

A Common Practice

Treatment guidelines recommend that if benzodiazepines are to be used at all, they should be used on a short-term basis. However, research suggests that up to one third of use is long term and that use is most common among older adults.

The investigators point out that the factors that predict extended benzodiazepine use are poorly understood.

To identify these risk factors, the researchers used data from the Supporting Seniors Receiving Treatment and Intervention (SUSTAIN) program, which provides a supplement to a Pennsylvania medication coverage program for low-income older adults.

Program services included detailed interviews to screen for mental health problems, such as anxiety, depression, and sleep problems, as well as pain, and analysis of prescription records and other clinical data.

The investigators examined how many older adults who received a new benzodiazepine prescription from a nonpsychiatric provider went on to long-term use of the medication. They also evaluated patient and clinical characteristics that predicted long-term use.

Long-term use was defined as a medication possession ratio (MPR) greater than 30% in the year following the initial prescription. Gerlach explained that the MPR was calculated by dividing the number of days of medication supplied by 365 days.

The study included 576 older adults (mean age, 78.4 years).

The analysis showed that 1 year after the index prescription, 26.4% of patients met the criteria for long-term use. They were prescribed benzodiazepines for a mean of 232.7 days.

Although treatment guidelines recommend only short-term prescribing, “these long-term patients were prescribed nearly 8 months’ worth of medication after their initial prescription,” said Gerlach.

In adjusted analyses, white race (odds ratio [OR], 4.19; 95% confidence interval [CI] 1.51 – 11.59; P = .006), days supplied in the index prescription (OR, 1.94; 95% CI, 1.52 – 2.47; P < .001), and poor sleep quality (OR for very, very bad vs very good, 4.05; 95% CI, 1.44 – 11.43; P = .008) were factors associated with increased long-term benzodiazepine use.

“Cause for Concern”

It’s a “cause for concern” that nonclinical factors are associated with benzodiazepine prescribing, said Gerlach.

“The decision to prescribe and then continue a benzodiazepine — or any other medical treatment — should be driven by a clinical need,” she said.

Gerlach said it was “particularly striking” that for every 10 additional days of medication prescribed, “a patient’s risk of long-term use nearly doubled over the next year.”

This finding “suggests that providers should pause and think more cautiously when providing a new prescription for benzodiazepines, such as considering a 14-day supply rather than a 30-day supply of medication,” said Gerlach.

Also concerning was the average age of the study participants when they first received a benzodiazepine prescription (78 years), because national guidelines say these drugs “should rarely be given to adults over age 65,” she said.

Of the clinical measures the researchers evaluated, which included depression, anxiety, sleep, and pain, only poor sleep was associated with the likelihood of continued benzodiazepine use.

“This is despite the fact that benzodiazepines are not recommended for long-term use as sleep aids, and may even worsen sleep outcomes the longer they’re used,” said Gerlach.

Because nonpsychiatric clinicians increasingly prescribe psychotropic drugs to older adults, the authors write that it is “critical” to improve access to and education about nonpharmacologic treatments.

The authors note that the study did not account for as-needed medication use, which may have had an effect on the calculation of long-term use. As well, the analysis was limited to low-income older adults from Pennsylvania, which may limit generalizability.

The authors also point out that definitions of long-term benzodiazepine use vary and that it is possible that a different definition of long-term use might have yielded different results. However, the investigators used three alternative definitions, with no significant variation in the findings.

Important Message

Commenting on the article for Medscape Medical News, Peter Yellowlees, MD, professor of psychiatry and vice chair for faculty development, Department of Psychiatry, University of California, Davis, said he was somewhat surprised that not more patients converted to long-term benzodiazepine prescriptions and that whites and not minority groups were more likely to be prescribed these drugs long term.

He said the “single most important message” from the study is that patients should know from the beginning that their benzodiazepine prescription will be short term.

In his own practice, Yellowlees said he “very seldom” prescribes benzodiazepines and “is much more likely” to taper patients off these drugs.

He aims to have patients to take these addictive medicines only three or four times a week — not every day — to avoid “getting hooked on them” and to taper patients off the drugs “extremely slowly” — over 3 to 6 months.

“Most people try to taper patients off in a matter of maybe 2 or 3 weeks; they will go, say, from 10 mg one week, to 5 mg the next, to whatever the next, and honestly, that’s just too hard for many patients,” he said.

The problem is that such a slow tapering approach can be time consuming, and primary care practitioners may have only a 15-minute consult per patient.

Benzodiazepines have been linked to falls and cognitive impairment, said Yellowlees.

“The effects can mimic early dementia. People get confused, and that leads to falling down and not being able to manage at home, with patients then having to go into a nursing home,” he said.

There are also risks of taking these drugs and then driving, said Yellowlees.

In lieu of benzodiazepines, he often uses cognitive-behavioral therapy for patients who have problems sleeping or who have anxiety.

What If You Lose Your Child at an Amusement Park?

Posted by

0


It’s a parent’s worst nightmare: While spending a fun-filled family day at an amusement park, you suddenly lose sight of your child.

As terrifying as that can be, a new survey finds that many American parents don’t talk with their child about what to do if the youngster becomes lost in that setting.

One in five parents said they did not make plans with their children about what to do if they became separated at an amusement park or carnival, according to the survey. It’s the latest C.S. Mott Children’s Hospital National Poll on Children’s Health, at the University of Michigan.

The survey included more than 1,200 parents of children aged 5 to 12.

“As parents prepare for summer trips to the amusement park or local fair, they should keep safety at the top of mind,” poll co-director Dr. Gary Freed said in a university news release. “As we’ve seen in news reports, accidents happen at amusement parks. Consequences range from skinned knees to serious injuries.”

In 2016, U.S. emergency departments dealt with 30,000 injuries linked to amusement parks and carnivals, according to the U.S. Consumer Product Safety Commission.

The poll authors also asked parents what they would do if ride operators did not enforce safety rules or if they suspected the operator of unsafe behavior.

Nine in 10 parents said they would report suspicions that the operator was drunk or on drugs, and 69 percent said they would report failure to enforce safety rules, such as seat belts or height restrictions.

Nearly six in 10 parents believe ride operators should undergo random alcohol and drug testing, with 13 percent supporting weekly testing, 13 percent in favor of monthly testing, and 3 percent backing yearly testing. Eleven percent said checks should only be done if there were suspicions of drug or alcohol use, the survey found.

While most parents said they would report a ride operator who appeared impaired by alcohol or drugs, less than half said they would report a ride operator who used a cellphone while operating a ride.

“Even though cellphone use may seem less harmful, it poses a significant distraction that can increase the risk of accident or injury,” Freed said.

Eighty-seven percent of the parents said it’s the responsibility of both parents and ride operators to make sure kids are safe on rides.

Nearly all the parents said they stayed with their child at all times during visits to amusement parks or carnivals, but it’s important to have a back-up plan in case parents get separated from their child.

“Discussing safety rules, check-in times and meet-up locations should be part of pre-trip planning for families,” Freed advised.

Snoring mothers-to-be linked to low birth weight babies.

Posted by

0


Experts say snoring may be a sign of breathing problems that could deprive an unborn baby of oxygen

A newborn baby. Scientists found that women who snored both before and during pregnancy were more likely to have smaller babies and elective C-sections. Photograph: Christopher Furlong/Getty Images

Mothers-to-be who snore are more likely to give birth to smaller babies, a study has found. Snoring during pregnancy was also linked to higher rates of Caesarean delivery.

Experts said snoring may be a sign of breathing problems that could deprive an unborn baby of oxygen.

Previous research has shown women who start to snore during pregnancy are at risk from high blood pressure and the potentially dangerous pregnancy condition pre-eclampsia.

More than a third of the 1,673 pregnant women recruited for the US study reported habitual snoring.

Scientists found women who snored in their sleep three or more nights a week had a higher risk of poor delivery outcomes, including smaller babies and Caesarean births.

Chronic snorers, who snored both before and during pregnancy, were two-thirds more likely to have a baby whose weight was in the bottom 10%.

They were also more than twice as likely to need an elective Caesarean delivery, or C-section, compared with non-snorers.

Dr Louise O’Brien, from the University of Michigan’s Sleep Disorders Centre, said: “There has been great interest in the implications of snoring during pregnancy and how it affects maternal health but there is little data on how it may impact the health of the baby.

“We’ve found that chronic snoring is associated with both smaller babies and C-sections, even after we accounted for other risk factors. This suggests that we have a window of opportunity to screen pregnant women for breathing problems during sleep that may put them at risk of poor delivery outcomes.”

Women who snored both before and during pregnancy were more likely to have smaller babies and elective C-sections, the researches found. Those who started snoring only during pregnancy had a higher risk of both elective and emergency Caesareans, but not of smaller babies.

Snoring is a key sign of obstructive sleep apnoea, which results in the airway becoming partially blocked, said the researchers, whose findings appear in the journal Sleep.

This can reduce blood oxygen levels during the night and is associated with serious health problems, including high blood pressure and heart attacks.

Sleep apnoea can be treated with CPAP (continuous positive airway pressure), which involves wearing a machine during sleep to keep the airways open.

Dr O’Brien added: “If we can identify risks during pregnancy that can be treated, such as obstructive sleep apnoea, we can reduce the incidence of small babies, C-sections and possibly NICU (neo-natal intensive care unit) admission that not only improve long-term health benefits for newborns but also help keep costs down.”

The Lasting Impacts of Poverty on the Brain.

Posted by

0


Poverty shapes people in some hard-wired ways that we’re only now beginning to understand. Back in August, we wrote about some provocative new research that found that poverty imposes a kind of tax on the brain. It sucks up so much mental bandwidth – capacity spent wrestling with financial trade-offs, scarce resources, the gap between bills and income – that the poor have fewer cognitive resources left over to succeed at parenting, education, or work. Experiencing poverty is like knocking 13 points off your IQ as you try to navigate everything else. That’s like living, perpetually, on a missed night of sleep.

That finding offered a glimpse of what poverty does to a person during a moment in time. Picture a mother trying to accomplish a single task (making dinner) while preoccupied with another (paying the rent on time). But scientists also suspect that poverty’s disadvantages – and these moments – accumulate across time. Live in poverty for years, or even generations, and its effects grow more insidious. Live in poverty as a child, and it affects you as an adult, too.

Some new research about the long-term arc of poverty, particularly on the brain, was recently published in theProceedings of the National Academy of Sciences, and these findings offer a useful complement to the earlier study. In this new paper, researchers from the University of Illinois at Chicago, Cornell, the University of Michigan, and the University of Denver followed children from the age of 9 through their early 20s.

The Lasting Impacts of Poverty on the Brain

Those who grew up poor later had impaired brain function as adults—a disadvantage researchers could literally see in the activity of the amygdala and prefrontal cortex on an fMRI scan. Children who were poor at age 9 had greater activity in the amygdala and less activity in the prefrontal cortex at age 24 during an experiment when they were asked to manage their emotions while looking at a series of negative photos. This is significant because the two regions of the brain play a critical role in how we detect threats and manage stress and emotions.

Poor children, in effect, had more problems regulating their emotions as adults (regardless of what their income status was at 24). These same patterns of “dysregulation” in the brain have been observed in people with depression, anxiety disorders, aggression and post-traumatic stress disorders.

Over the course of the longitudinal study – which included 49 rural, white children of varying incomes – these same poor children were also exposed to chronic sources of stress like violence and family turmoil, or crowded and low-quality housing. Those kinds of stressors, the researchers theorize, may help explain the link between income status in childhood and how well the brain functions later on. That theory, they write, is consistent with the idea that “early experiences of poverty become embedded within the organism, setting individuals on lifelong trajectories.”

To add some of these findings together: Poverty taxes the ability of parents to do all kinds of things, including care for their children. And the developmental challenges that children face in a home full of stressed adults may well influence the adults that they, themselves, become.

Probiotics may save patients from deadly chemotherapy.

Posted by

0


If you or someone you love is facing the possibility of cancer or chemotherapy, make sure they read this story. Breakthrough new science conducted at the University of Michigan and about to be published in the journal Nature reveals that intestinal health is the key to surviving chemotherapy.

 

The study itself is very difficult for laypeople to parse, however, so I’m going to translate into everyday language while also offering additional interpretations of the research that the original study author is likely unable to state due to the nutritional censorship of medical journals and universities, both of which have an anti-nutrition bias.

The upshot is this: A clinical study gave mice lethal injections of chemotherapy that would, pound for pound, kill most adult human beings, too. The study authors openly admit: “All tumors from different tissues and organs can be killed by high doses of chemotherapy and radiation, but the current challenge for treating the later-staged metastasized cancer is that you actually kill the [patient] before you kill the tumor.” (See sources below.)

Chemotherapy is deadly. It is the No. 1 cause of death for cancer patients in America, and the No. 1 side effect of chemo is more cancer. But certain mice in the study managed to survive the lethal doses of chemo. How did they do that? They were injected with a molecule that your own body produces naturally. It’s production is engineered right into your genes, and given the right gene expression in an environment of good nutrition (meaning the cellular environment), you can generate this substance all by yourself, 24 hours a day.

The substance is called “Rspo1″ or “R-spondon1.” It activates stem cell production within your own intestinal walls, and these stem cells are like super tissue regeneration machines that rebuild damaged tissues faster than the chemotherapy can destroy them, thereby allowing the patient to survive an otherwise deadly does of chemo poison.

As the study showed, 50 – 75 percent of the mice who were given R-spondon1 survived the fatal chemotherapy dose!

The cancer industry needs to find a way to stop killing all their customers

The problem with the cancer industry today is that all the conventional cancer treatments keep killing the patients. This is bad for business. So the purpose of research like the R-spondon1 research mentioned here — which was funded by a government grant — is to find ways to keep giving patients deadly doses of high-profit chemotherapy without actually killing them. You slap a patient with a dose of R-spondon1 (sold at $50,000 a dose as a patented “drug,” of course), dose ‘em up with a fatal injection of chemotherapy, and then thanks to the R-spondon1 you get a repeat cancer customers instead of a corpse.

That’s called “good business practices” in the cancer industry, which is so far best known for turning patients into body bags rather than actually curing cancer.

(Yes, there is a reason why most oncologists would never undergo chemotherapy themselves. They know it doesn’t work on 98% of all cancers.)

Probiotics are likely the key to generating your own R-spondon1

Before I discuss why these findings are so important for followers of natural health and nutrition, let me first offer a disclaimer. The research mentioned here was conducted on mice, not humans, so it isn’t full proof that the same mechanism works in humans. Nevertheless, the reason mice are used for such research is because they are nearly identical to humans in terms of biology, gene expression, endocrine system function and more.

Furthermore, even though this study used an injection of R-spondon1 as the “activator” of gene expression in endothelial cells of the intestinal lining, in truth your cells already possess the blueprint to produce R-spondon1 on their own. In fact, human intestines are coated with a layer of epithelial cells that are regenerated every 4-5 days in a healthy person. This is only possible through the activation and continued operation of intestinal stem cells, a normal function for a healthy human.

And what determines the health of those stem cells more than anything else? Their local environment which is predominantly determined by gut bacteria. If your gut bacteria are in balance, the gene expression of your epithelial cells is normal and healthy. If your gut bacteria are out of whack, so to speak, the gene expression of your epithelial cells will be suppressed, thereby slowing or halting the regenerative potential of your intestinal cells. This is why people who have imbalanced intestinal flora also suffer from inflammatory intestinal conditions such as Crohn’s, IBS and so on.

Thus, probiotics are a key determining factor in the ability of your intestines to maintain the appropriate gene expression for the very kind of rapid cellular regeneration that can help your body survive a fatal dose of chemotherapy.

Meat and dairy cause devastating gut flora imbalances that may increase susceptibility to chemotherapy drugs

This may also explain why people who eat large quantities of processed meat, cheese and dead, pasteurized dairy products — especially when combined with starchy carbohydrates and processed sugars — are far more likely to die from chemotherapy than people who eat more plant-based diets. (There isn’t yet a source to substantiate this claim, but it’s something I’ve noted from considerable personal observation. You may have noticed it too among your own family members who have undergone chemotherapy treatments. Those with the worst diets seem to have far higher fatality rates.)

Those who consume processed meat and dead dairy have their intestines filled with fiber-less, difficult-to-digest proteins that are putrefied and sit in the intestines for 2 – 5 days, typically. Dietary sugars and carbohydrates then feed the bacteria fermentation process, resulting in the rapid growth and replication of sugar-feeding bacteria that displace the kind of healthy flora which best protect intestinal wall cells.

This imbalance, I suggest, increases susceptibility to chemotherapy toxicity while simultaneously impairing the ability of the patient to absorb key nutrients that protect healthy cells from the toxicity of chemo drugs. This may explain why patients who heavily consume meat, cheese and dairy diets tend to die so easily when exposed to chemotherapy.

But there’s something even more alarming about all this that everyone needs to know…

Antibiotics may also set you up to be killed by chemo

Although the research did not directly address this question, its findings seem to indicate that the kind of gut bacteria “wipeout” caused by antibiotics could prove fatal to a chemotherapy patient.

This is especially worrisome because many cancer patients are simultaneously prescribed antibiotics as they undergo chemotherapy. This could be a death sentence in disguise. While neither the antibiotics nor the chemo directly kill the patient, the combination of sterilized gut bacteria and highly-toxic chemotherapy drugs could multiply the toxicity and prove fatal. The death certificate, however, will say the patient died from “cancer,” not from the chemotherapy which is usually the actual cause of death.

And yet, every single day in America, patients who are taking antibiotics are subjected to multiple courses of chemotherapy. This may quite literally be a death sentence for those patients.

There’s also a self-fulfilling death spiral at work in all this: following the first round of chemotherapy, many patients suffer from weakened immune system that result in symptomatic infections. Physicians respond to this by prescribing antibiotics, resulting in the patient undergoing subsequent rounds of chemotherapy with “wiped out” gut flora. So the chemo causes the problem in the first place, and then the response to the problem by western doctors makes the next round of chemo fatal. This is a self-fulfilling death spiral of failed medicine.

Oncologists seem to have no awareness whatsoever of the importance of gut bacteria in allowing patients to protect their own healthy cells from the devastating effects of chemotherapy drugs. Many oncologists, in fact, actively discourage their patients from taking any sort of supplements during chemotherapy out of an irrational, anti-scientific fear that such supplements may “interfere” with the chemo and make the treatment fail.

This is one of the many ways in which oncologists get cancer patients killed.

Takeaway points from this article:

• New research shows that a substance generated by intestinal stem cells allows subjects to survive an otherwise fatal dose of toxic chemotherapy.

• Healthy gene expression of intestinal cells allows them to naturally produce protective molecules that support and boost cell regeneration.

• Probiotics may protect and support the intestinal stem cells that help cancer patients survive toxic chemotherapy. (More studies needed to explore this and document the impact.)

• Antibiotics may be a death sentence when followed by chemotherapy.

• Oncologists need to consider the risks and benefits of postponing chemotherapy in patients who are simultaneously taking antibiotics. The combination may be deadly. Conversely, they need to consider the benefits of encouraging chemotherapy patients to take probiotic supplements before beginning chemotherapy treatment.

Source: naturalnews.com

Facebook Use Predicts Declines in Subjective Well-Being in Young Adults.

Posted by

0


Abstract

Over 500 million people interact daily with Facebook. Yet, whether Facebook use influences subjective well-being over time is unknown. We addressed this issue using experience-sampling, the most reliable method for measuring in-vivo behavior and psychological experience. We text-messaged people five times per day for two-weeks to examine how Facebook use influences the two components of subjective well-being: how people feel moment-to-moment and how satisfied they are with their lives. Our results indicate that Facebook use predicts negative shifts on both of these variables over time. The more people used Facebook at one time point, the worse they felt the next time we text-messaged them; the more they used Facebook over two-weeks, the more their life satisfaction levels declined over time. Interacting with other people “directly” did not predict these negative outcomes. They were also not moderated by the size of people’s Facebook networks, their perceived supportiveness, motivation for using Facebook, gender, loneliness, self-esteem, or depression. On the surface, Facebook provides an invaluable resource for fulfilling the basic human need for social connection. Rather than enhancing well-being, however, these findings suggest that Facebook may undermine it.

Discussion

Within a relatively short timespan, Facebook has revolutionized the way people interact. Yet, whether using Facebook predicts changes in subjective well-being over time is unknown. We addressed this issue by performing lagged analyses on experience sampled data, an approach that allowed us to take advantage of the relative timing of participants’ naturally occurring behaviors and psychological states to draw inferences about their likely causal sequence [17], [18]. These analyses indicated that Facebook use predicts declines in the two components of subjective well-being: how people feel moment to moment and how satisfied they are with their lives.

Critically, we found no evidence to support two plausible alternative interpretations of these results. First, interacting with other people “directly” did not predict declines in well-being. In fact, direct social network interactions led people to feel better over time. This suggests that Facebook use may constitute a unique form of social network interaction that predicts impoverished well-being. Second, multiple types of evidence indicated that it was not the case that Facebook use led to declines in well-being because people are more likely to use Facebook when they feel bad—neither affect nor worry predicted Facebook use and Facebook use continued to predict significant declines in well-being when controlling for loneliness (which did predict increases in Facebook use and reductions in emotional well-being).

Would engaging in any solitary activity similarly predict declines in well-being? We suspect that they would not because people often derive pleasure from engaging in some solitary activities (e.g., exercising, reading). Supporting this view, a number of recent studies indicate that people’sperceptions of social isolation (i.e., how lonely they feel)—a variable that we assessed in this study, which did not influence our results—are a more powerful determinant of well-being than objectivesocial isolation [25]. A related question concerns whether engaging in any Internet activity (e.g., email, web surfing) would likewise predict well-being declines. Here too prior research suggests that it would not. A number of studies indicate that whether interacting with the Internet predicts changes in well-being depends on how you use it (i.e., what sites you visit) and who you interact with [26].

Future research

Although these findings raise numerous future research questions, four stand out as most pressing. First, do these findings generalize? We concentrated on young adults in this study because they represent a core Facebook user demographic. However, examining whether these findings generalize to additional age groups is important. Future research should also examine whether these findings generalize to other online social networks. As a recent review of the Facebook literature indicated [2] “[different online social networks] have varied histories and are associated with different patterns of use, user characteristics, and social functions (p. 205).” Therefore, it is possible that the current findings may not neatly generalize to other online social networks.

Second, what mechanisms underlie the deleterious effects of Facebook usage on well-being? Some researchers have speculated that online social networking may interfere with physical activity, which has cognitive and emotional replenishing effects [27] or trigger damaging social comparisons[8], [28]. The latter idea is particularly interesting in light of the significant interaction we observed between direct social contact and Facebook use in this study—i.e., the more people interacted with other people directly, the more strongly Facebook use predicted declines in their affective well-being. If harmful social comparisons explain how Facebook use predicts declines in affective well-being, it is possible that interacting with other people directly either enhances the frequency of such comparisons or magnifies their emotional impact. Examining whether these or other mechanisms explain the relationship between Facebook usage and well-being is important both from a basic science and practical perspective.

Finally, although the analytic approach we used in this study is useful for drawing inferences about the likely causal ordering of associations between naturally occurring variables, experiments that manipulate Facebook use in daily life are needed to corroborate these findings and establish definitive causal relations. Though potentially challenging to perform—Facebook use prevalence, its centrality to young adult daily social interactions, and addictive properties may make it a difficult intervention target—such studies are important for extending this work and informing future interventions.

Caveats

Two caveats are in order before concluding. First, although we observed statistically significant associations between Facebook usage and well-being, the sizes of these effects were relatively “small.” This should not, however, undermine their practical significance [29]. Subjective well-being is a multiply determined outcome—it is unrealistic to expect any single factor to powerfully influence it. Moreover, in addition to being consequential in its own right, subjective well-being predicts an array of mental and physical health consequences. Therefore, identifying any factor that systematically influences it is important, especially when that factor is likely to accumulate over time among large numbers of people. Facebook usage would seem to fit both of these criteria.

Second, some research suggests that asking people to indicate how good or bad they feel using a single bipolar scale, as we did in this study, can obscure interesting differences regarding whether a variable leads people to feel less positive, more negative or both less positive and more negative. Future research should administer two unipolar affect questions to assess positive and negative affect separately to address this issue.

Concluding Comment

The human need for social connection is well established, as are the benefits that people derive from such connections . On the surface, Facebook provides an invaluable resource for fulfilling such needs by allowing people to instantly connect. Rather than enhancing well-being, as frequent interactions with supportive “offline” social networks powerfully do, the current findings demonstrate that interacting with Facebook may predict the opposite result for young adults—it may undermine it.

Source: PLOS one

 

 

 

 

 

Studies Show That These Prescriptions Make Your Brain Stop Working.

Posted by

0


Drugs commonly taken for a variety of common medical conditions negatively affect your brain, causing long term cognitive impairment. These drugs, called anticholinergics, block acetylcholine, a nervous system neurotransmitter.
They include such common over-the-counter brands as Benadryl, Dramamine, Excedrin PM, Nytol, Sominex, Tylenol PM, and Unisom.

Other anticholinergic drugs, such as Paxil, Detrol, Demerol and Elavil are available only by prescription.

Physorg reports:

“Researchers … conducted a six-year observational study, evaluating 1,652 Indianapolis area African-Americans over the age of 70 who had normal cognitive function when the study began … ‘[T]aking one anticholinergic significantly increased an individual’s risk of developing mild cognitive impairment and taking two of these drugs doubled this risk.’”

Many view over-the-counter (OTC) drugs as safe because they don’t require a prescription. Well nothing could be further from the truth.

In fact, many OTC drugs were previously carefully monitored prescription drugs. Many people are not aware that while I was in college in the 1970s, I worked as a full time pharmacy apprentice and helped sell drugs to patients all day long.

Motrin was the first non-salicylate prescription NSAID. Now it is a popular OTC ibuprofen option. Similarly, anti-ulcer drugs like Tagamet, Zantec, and Prilosec used to be carefully controlled. Now they can all be easily purchased in a smaller “OTC strength” that nearly doubles the number of pills required to equal the prescription dose.

Just because a drug is available without a prescription does not make it any less dangerous. It is still a chemical, which in no way, shape, or form treats the cause of the problem and can lead to complications that can seriously injure, if not kill, you or someone you love.

So this is clearly important information that can help you or someone you love reduce your risk of dementia as you get older. Based on the findings of this study, I would strongly recommend that seniors in particular avoid all anticholinergic drugs, like Benadryl (generic is diphenhydramine) which is a pervasive and commonly used in virtually all of the OTC sleeping pills.

Researchers will continue studying the matter to see whether anticholinergic-induced cognitive impairment can be reversed, but don’t hold your breath. Avoidance is really the best solution.

What are Anticholinergic Drugs?Anticholinergic drugs block a nervous system neurotransmitter called acetylcholine. Those suffering from Alzheimer’s disease typically have a marked shortage of acetylcholine.

Anticholinergic drugs are available both over-the-counter and by prescription, as medications used for a variety of symptoms can have this effect. Examples include night-time pain relievers, antihistamines, and other sleep aids, such as:

Excedrin PM
Tylenol PM
Nytol
Sominex
Unisom
Benadryl
Dramamine

Prescription drugs with anticholinergic effects include certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Examples of prescription meds in these categories include:

Paxil
Detrol
Demerol
Elavil

A Special Note for Aspartame ‘Reactors’

Many of the drugs listed here, as well as a long list of additional ones, contain diphenhydramine. As an important side note, you need to beware that chewable tablets and rapidly disintegrating tablets that contain diphenhydramine may be sweetened with aspartame

If you have the genetic disease phenylketonuria (PKU), you must be particularly careful to avoid these types of drugs and all other types of aspartame-sweetened foods and beverages in order to prevent mental retardation.

But many other people also suffer detrimental health effects from aspartame, so you should know that this is yet another potential source of this toxic sweetener.

Anticholinergic Drugs Increases Dementia in the Elderly

I’ve previously written about the health dangers of many of these individual drugs. Paxil, for example, is an addictive antidepressant that is well known to increase the risk of suicide in children and teens. It is also known to increase violent behavior.

Benadryl and Sominex have previously been found to cause hallucinations in the elderly, and a number of the drugs on the list also promote dental decay.

The results of this study indicate that drugs with anticholinergic effects may be yet another piece of the puzzle that might explain the sharp rise in dementia and cognitive decline.

According to the University of Michigan, dementia strikes about 50 percent of people who reach the age of 85. Of those, about 60 percent go on to develop Alzheimer’s disease.

In this study, the researchers tracked the intake of anticholinergic drugs and monitored the cognitive abilities of 1,652 African-American seniors, aged 70 and older, for six years. All of the participants had normal cognitive function at the outset of the study.

Fifty-three percent of the participants used a ‘possible anticholinergic,’ and 11 percent used a ‘definitive anticholinergic’ drug.

They found that those who took drugs classified as ‘definite anticholinergics’ had a four times higher incidence of cognitive impairment.

In those who were not carriers of the specific gene, APOE ε4 allele, the risk was over seven times higher. (The APOE ε4 gene is known to influence many neurological diseases, and is considered a high risk factor for Alzheimer’s.)

Taking two of these drugs further increased the risk of cognitive impairment.

PhysOrg reports:

“Simply put, we have confirmed that anticholinergics, something as seemingly benign as a medication for inability to get a good night’s sleep or for motion sickness, can cause or worsen cognitive impairment, specifically long-term mild cognitive impairment which involves gradual memory loss.

As a geriatrician I tell my Wishard Healthy Aging Brain Center patients not to take these drugs and I encourage all older adults to talk with their physicians about each and every one of the medications they take,” said Malaz Boustani, M.D., IU School of Medicine associate professor of medicine, Regenstrief Institute investigator and IU Center for Aging Research center scientist.”
Even More Reasons to Ditch the Sleep Meds

In 2008, Americans filled more than 56 million prescriptions for sleeping pills and spent more than $600 million on over-the-counter sleep aids. But anticholinergic sleep medications in particular may be causing far more harm than good, especially long term, without providing any benefit at all.

In a recent article, CBC News reported that the U.S. Food and Drug Administration has had data for 15 years which shows that over-the-counter sleep aids like Tylenol PM and Excedrin PM do not offer any significant benefit to patients.

There’s no explanation for why the FDA took 15 years to evaluate the industry’s research, but upon final analysis “the data suggests the combination products are statistically better than a placebo but not by much,” CBC News reported.

I guess it can be chalked up as yet another vibrant example of how industry research frequently amounts to little more than corporate wishes and good PR fodder.

Another analysis of sleeping pill studies from 2007 (financed by the National Institutes of Health) found that sleeping pills like Ambien, Lunesta, and Sonata reduced the average time to go to sleep by just under 13 minutes compared with fake pills — hardly a major improvement.

Yet, the participants believed they had slept longer, by up to one hour, when taking the pills.

This may actually be a sign of a condition called anterograde amnesia, which causes trouble with forming memories. When people wake up after taking sleeping pills, they may, in fact, simply forget that they had been unable to sleep!

You would be far better off putting your money toward authentic solutions to help you sleep than on sleeping pills, as it’s now clear that they do next to nothing to help you sleep – in fact, they may actually make it more difficult for you to get a good night’s rest naturally – and may significantly increase your risk of dementia.

Sleeping Pills are NOT a Safe Solution for Sleepless Nights

Understand that resorting to sleep medications is risky business, and that these pills do not address the underlying reasons why you’re having trouble sleeping in the first place.

In addition to the long-term problems already discussed, there are other serious, not to mention bizarre, risks involved.

For starters, these pills are notorious for being addictive, which means that once you want to stop taking them, you’ll likely suffer withdrawal symptoms that could be worse than your initial insomnia. Some, such as Ambien, may also become less effective when taken for longer than two weeks, which means you may find yourself needing ever higher dosages.

Ambien may also make you want to eat while you’re asleep — and I don’t mean sneaking down to grab a piece of fruit. The sleep eating can include bizarre foods such as buttered cigarettes, salt sandwiches, and raw bacon.

Sleeping pills, and again Ambien in particular, are also known to increase your risk of getting into a traffic accident. Ambien actually ranks among the top 10 drugs found in the bloodstreams of impaired drivers, according to some state toxicology labs.

Among the elderly, using sleeping pills may increase the risk of nighttime falls and injuries, and anyone who takes them may find they wake up feeling drowsy if the effects of the drug have not worn off yet.

You’re far better of finding safe and natural solutions that will actually address the underlying causes of your sleepless nights instead of just cover up the resulting symptoms.

Source: Raw For Beauty

 

Brief Emergency Department Intervention to Reduce Teen Dating Violence.

Posted by

0


Among teens with a history of dating violence, effectiveness of the intervention depended on the baseline level of violence.
Investigators evaluated the effectiveness of the SafERteens intervention for reducing dating violence among adolescents presenting to an emergency department (ED). The 35-minute bedside intervention involves goal setting, feedback, decision-balancing exercises, and role-playing scenarios. In the SafERteens study, 726 patients aged 14 to 18 years with a history of aggression or violence and alcohol use in the previous year were randomized to one of three groups: intervention delivered by computer, intervention delivered by a therapist with computer assistance, or a standard brochure about resources (control). Participants were followed up with self-assessments 3, 6, and 12 months after the ED visit.

This secondary analysis included 397 adolescents (36% male) with a history of dating violence. The computer-only group, compared to controls, had a reduction in moderate dating violence (e.g., slapped, hair pulled, shoved) at 3 months and 6 months, but not at 12 months. Neither intervention had an effect on severe dating violence (e.g., punched, choked, knife or gun used). Adolescents with a baseline moderate level and high frequency (>8 times per year) of dating violence had a decrease in moderate dating violence at 6 and 12 months; those with a baseline severe level and high frequency had a decrease in severe violence at 3 months.

COMMENT

Emergency physicians are in a unique position to capitalize on many “teachable moments.” While much remains to be learned as to the best interventions for reducing teen dating violence, we should not miss these opportunities — such as when caring for a beaten teen — to help our patients make wiser choices.

Source: NEJM

What does Tamiflu do, and how will we know?

Posted by

0


Jonathan Nguyen-Van-Tam, virologist and researcher from the University of Nottingham, told a group of triallists and virologists last week “we must remember why we’re here—because of the controversies. The clinical world doesn’t believe that Tamiflu works. We should assess whether the regulatory approval/product insert for Tamiflu is valid.”

That group, the MUltiparty Group for Advice on Science (MUGAS) was at a workshop in Brussels on 18 June organised by the European Scientific Working group on Influenza (ESWI) and supported by an unrestricted grant from Roche. Led by several of the original Tamiflu regulatory triallists, the workshop heard plenty of evidence to challenge current claims about Tamiflu’s effects. MUGAS decided to plan and conduct individual participant data (IPD) meta-analyses of the randomised trial data—and observational data. That’s quite a remarkable turnaround, given the strength of claims made by some of the same people over the past decade.

BMJ readers will already be very familiar with growing concerns about oseltamivir’s effectiveness. Earlier this year Professor Harlan Krumholz and co-authors concluded in an editorial in the BMJ that “Despite government claims, we should acknowledge the uncertainty surrounding oseltamivir’s effectiveness and the gaps in publicly available evidence. On the basis of the available data, at best the drug shortens symptoms by about a day when used within the first two days of symptoms, but it has no effect on hospital admissions. In addition, trial data from which to draw conclusions about complications and transmission of flu are lacking.”

WHO made particularly firm claims about oseltamivir in August 2009 during the swine flu (H1N1) pandemic. WHO then stated that, “The guidelines represent the consensus reached by an international panel of experts who reviewed all available studies on the safety and effectiveness of these drugs…Evidence reviewed by the panel indicates that oseltamivir, when properly prescribed, can significantly reduce the risk of pneumonia (a leading cause of death for both pandemic and seasonal influenza) and the need for hospitalization.”

That expert panel advising WHO was anonymous: all its members had signed a confidentiality agreement. But at least one member was identified later as Professor Arnold Monto of the University of Michigan, who coauthored several trials of neuraminidase inhibitors back in the 1990s. The same Professor Monto is one of the four convenors of MUGAS, along with Professor Ab Osterhaus (of Erasmus MC University in Rotterdam, a scientific advisor to Roche, another oseltamivir triallist), Professor Menno de Jong (of Academic Medical Center Amsterdam, virologist and researcher) and Professor Rich Whitley (of University of Alabama at Birmingham, professor of pediatric infectious diseases and an adviser on flu to the Obama administration).

Barry Clinch, Principal Clinical Scientist at F. Hoffmann-La Roche, presented at the MUGAS workshop an overview of all studies in the company’s oseltamivir research programme. His slides showed that in all, 18,928 patients had taken part in trials, observational studies of treatment, and studies of prophylaxis; around 11,500 of them treated with oral oseltamivir. Randomised controlled trials (RCTs) had included 4799 adults and 1368 children and, along with some open label studies, a total of 8078 patients had taken part. All but one of the 12 RCTs took place in the late 1990s. Roche’s lab researchers had also done experimental flu studies and clinical pharmacology studies.

Clinch confirmed that investigators were told to always report admissions to hospital during the Roche trials, but warned that “caution should be exercised in interpreting results on hospitalisation.” This is because there were such low event rates: for example in trial WV15671 just 1 of 201 participants was hospitalised. The main intention to treat analyses in the 12 Roche RCTs (for all patients enrolled with flu-like illness and who had at least 1 dose of trial medication) failed to find statistically significant evidence that hospitalisation rates were reduced by oseltamivir when compared against placebo. For the ITTI population (the subset with flu confirmed by culture or >4 fold rise in antibody titre) the overall P value was 0.06 but this was grossly underpowered.

Presenting the key oseltamivir trials that yielded data on flu complications, Clinch explained that a standard case report form was used to collected data on “Secondary illness.” “We didn’t ask physicians to actively look for complications,” he said. “They simply reported them if they thought patients had, for example, sinusitis, otitis media, bronchitis, pneumonia or other chest infections.” Clinicians could also say if patients needed antibiotics or X rays—thereby implying that there might be some secondary illness—but there was no requirement to confirm diagnoses without anything more than a clinical diagnosis. “To be honest, we weren’t that stringent at the time,” acknowledged Clinch. (And, of course, at that time Roche was testing oseltamivir primarily as another antiviral for seasonal flu, not as a lifesaver in a pandemic.) Only two trial protocols required reporting of clinically diagnosed complications (coded as bronchitis, pneumonia, lower respiratory tract complication, or antibiotic prescription occurring >48h after start of treatment with oseltamivir) as a formal secondary endpoint: those among older and at risk participants. Statistical analyses of these outcomes were exploratory, said Clinch.

The ensuing questions and discussion among the MUGAS review board members (some of whom co-authored some of the trials in question) confirmed that “secondary illness” was indeed only a clinical diagnosis, that in most of the trials its reporting was ad hoc, and that Roche does not know the extent of any missing data. Decisions to give antibiotics were made for nonspecified clinical reasons, and, as someone pointed out, antibiotic usage rates will have varied a lot from site to site because of geographical variations in prescribing behaviour.

However, some of the MUGAS virologists said we know from Roche’s original observational studies and from subsequent case series from the H1N1 pandemic that oseltamivir does reduce complications. Do we? Not yet, although Professor Van Tam’s group has conducted a systematic review and IPD meta-analysis of published andunpublished observational study data during the H1N1 pandemic that will be submitted soon for publication. This study was sponsored by Roche but Professor Van Tam said the data agreement gives Roche no access to the data. The authors plan, however, to share the data with other investigators on request.

When asked what proportion of the original Roche oseltamivir research programme had results in the public domain, Clinch said “about 90% in one form or another.” Virologist Fred Hayden, co-author of several Roche trials, asked: “the contentious area is the 8-10 unpublished trials done some time ago. Are there any plans to publish those?” Clinch replied “it’s a good question…we’d like MUGAS to discuss that. Roche has no objection to that.” Professor Osterhaus said that MUGAS wants to analyse the IPD from those trials and to publish the resulting papers in peer reviewed journals.

So, of course, does the Cochrane Acute Respiratory Infections Group, which has been struggling for years to get the unpublished trial data from Roche. That data release has now begun, and the Cochrane group is poring over the partly redacted Clinical Study Reports right now.

So it’s from famine to feast, with two different groups working towards meta-analyses of the unpublished patient-level data on the effects of oseltamivir in flu. Will they come to the same conclusions?

Source: BMJ