SIGNS, SYMPTOMS, AND HELP FOR DRUG PROBLEMS AND SUBSTANCE ABUSE

Some people are able to use recreational or prescription drugs without ever experiencing negative consequences or addiction. For many others, substance use can cause problems at work, home, school, and in relationships, leaving you feeling isolated, helpless, or ashamed.

If you’re worried about your own or a friend or family member’s drug use, it’s important to know that help is available. Learning about the nature of drug abuse and addiction—how it develops, what it looks like, and why it can have such a powerful hold—will give you a better understanding of the problem and how to best deal with it.

Understanding drug use, drug abuse, and addiction

People experiment with drugs for many different reasons. Many first try drugs out of curiosity, to have a good time, because friends are doing it, or in an effort to improve athletic performance or ease another problem, such as stress, anxiety, or depression. Use doesn’t automatically lead to abuse, and there is no specific level at which drug use moves from casual to problematic. It varies by individual. Drug abuse and addiction is less about the amount of substance consumed or the frequency, and more to do with theconsequences of drug use. No matter how often or how little you’re consuming, if your drug use is causing problems in your life—at work, school, home, or in your relationships—you likely have a drug abuse or addiction problem.

Why do some drug users become addicted, while others don’t?

As with many other conditions and diseases, vulnerability to addiction differs from person to person. Your genes, mental health, family and social environment all play a role in addiction. Risk factors that increase your vulnerability include:

  • Family history of addiction
  • Abuse, neglect, or other traumatic experiences in childhood
  • Mental disorders such as depression and anxiety
  • Early use of drugs
  • Method of administration—smoking or injecting a drug may increase its addictive potential

Drug addiction and the brain

Addiction is a complex disorder characterized by compulsive drug use. While each drug produces different physical effects, all abused substances share one thing in common: repeated use can alter the way the brain looks and functions.

  • Taking a recreational drug causes a surge in levels of dopamine in your brain, which trigger feelings of pleasure. Your brain remembers these feelings and wants them repeated.
  • If you become addicted, the substance takes on the same significance as other survival behaviors, such as eating and drinking.
  • Changes in your brain interfere with your ability to think clearly, exercise good judgment, control your behavior, and feel normal without drugs.
  • Whether you’re addicted to inhalants, heroin, Xanax, speed, or Vicodin, the uncontrollable craving to use grows more important than anything else, including family, friends, career, and even your own health and happiness.
  • The urge to use is so strong that your mind finds many ways to deny or rationalize the addiction. You may drastically underestimate the quantity of drugs you’re taking, how much it impacts your life, and the level of control you have over your drug use.

How drug abuse and addiction can develop

 

People who experiment with drugs continue to use them because the substance either makes them feel good, or stops them from feeling bad. In many cases, however, there is a fine line between regular use and drug abuse and addiction. Very few addicts are able to recognize when they have crossed that line. While frequency or the amount of drugs consumed don’t in themselves constitute drug abuse or addiction, they can often be indicators of drug-related problems.

  • Problems can sometimes sneak up on you, as your drug use gradually increases over time. Smoking a joint with friends at the weekend, or taking ecstasy at a rave, or cocaine at an occasional party, for example, can change to using drugs a couple of days a week, then every day. Gradually, getting and using the drug becomes more and more important to you.
  • If the drug fulfills a valuable need, you may find yourself increasingly relying on it. For example, you may take drugs to calm you if you feel anxious or stressed, energize you if you feel depressed, or make you more confident in social situations if you normally feel shy. Or you may have started using prescription drugs to cope with panic attacks or relieve chronic pain, for example. Until you find alternative, healthier methods for overcoming these problems, your drug use will likely continue.
  • Similarly, if you use drugs to fill a void in your life, you’re more at risk of crossing the line from casual use to drug abuse and addiction. To maintain healthy balance in your life, you need to have other positive experiences, to feel good in your life aside from any drug use.
  • As drug abuse takes hold, you may miss or frequently be late for work or school, your job performance may progressively deteriorate, and you start to neglect social or family obligations. Your ability to stop using is eventually compromised. What began as a voluntary choice has turned into a physical and psychological need.

The good news is that with the right treatment and support, you can counteract the disruptive effects of drug use and regain control of your life. The first obstacle is to recognize and admit you have a problem, or listen to loved ones who are often better able to see the negative effects drug use is having on your life.

 

 

5 Myths about Drug Abuse and Addiction

MYTH 1: Overcoming addiction is a simply a matter of willpower. You can stop using drugs if you really want to. Prolonged exposure to drugs alters the brain in ways that result in powerful cravings and a compulsion to use. These brain changes make it extremely difficult to quit by sheer force of will.

MYTH 2: Addiction is a disease; there’s nothing you can do about it. Most experts agree that addiction is a brain disease, but that doesn’t mean you’re a helpless victim. The brain changes associated with addiction can be treated and reversed through therapy, medication, exercise, and other treatments.

MYTH 3: Addicts have to hit rock bottom before they can get better. Recovery can begin at any point in the addiction process—and the earlier, the better. The longer drug abuse continues, the stronger the addiction becomes and the harder it is to treat. Don’t wait to intervene until the addict has lost it all.

MYTH 4: You can’t force someone into treatment; they have to want help. Treatment doesn’t have to be voluntary to be successful. People who are pressured into treatment by their family, employer, or the legal system are just as likely to benefit as those who choose to enter treatment on their own. As they sober up and their thinking clears, many formerly resistant addicts decide they want to change.

MYTH 5: Treatment didn’t work before, so there’s no point trying again. Recovery from drug addiction is a long process that often involves setbacks. Relapse doesn’t mean that treatment has failed or that you’re a lost cause. Rather, it’s a signal to get back on track, either by going back to treatment or adjusting the treatment approach.

Signs and symptoms of drug abuse and drug addiction

Although different drugs have different physical effects, the symptoms of addiction are similar. See if you recognize yourself in the following signs and symptoms of substance abuse and addiction. If so, consider talking to someone about your drug use.

Common signs and symptoms of drug abuse

  • You’re neglecting your responsibilities at school, work, or home (e.g. flunking classes, skipping work, neglecting your children) because of your drug use.
  • You’re using drugs under dangerous conditions or taking risks while high, such as driving while on drugs, using dirty needles, or having unprotected sex.
  • Your drug use is getting you into legal trouble, such as arrests for disorderly conduct, driving under the influence, or stealing to support a drug habit.
  • Your drug use is causing problems in your relationships, such as fights with your partner or family members, an unhappy boss, or the loss of old friends.
  • You’ve built up a drug tolerance. You need to use more of the drug to experience the same effects you used to attain with smaller amounts.
  • You take drugs to avoid or relieve withdrawal symptoms. If you go too long without drugs, you experience symptoms such as nausea, restlessness, insomnia, depression, sweating, shaking, and anxiety.
  • You’ve lost control over your drug use. You often do drugs or use more than you planned, even though you told yourself you wouldn’t. You may want to stop using, but you feel powerless.
  • Your life revolves around drug use. You spend a lot of time using and thinking about drugs, figuring out how to get them, and recovering from the drug’s effects.
  • You’ve abandoned activities you used to enjoy, such as hobbies, sports, and socializing, because of your drug use.
  • You continue to use drugs, despite knowing it’s hurting you. It’s causing major problems in your life—blackouts, infections, mood swings, depression, paranoia—but you use anyway.

Common signs and symptoms of drug addiction

Warning signs that a friend or family member is abusing drugs

Drug abusers often try to conceal their symptoms and downplay their problem. If you’re worried that a friend or family member might be abusing drugs, look for the following warning signs:

Physical warning signs of drug abuse

  • Bloodshot eyes, pupils larger or smaller than usual.
  • Changes in appetite or sleep patterns. Sudden weight loss or weight gain.
  • Deterioration of physical appearance, personal grooming habits.
  • Unusual smells on breath, body, or clothing.
  • Tremors, slurred speech, or impaired coordination.
  • Drop in attendance and performance at work or school.
  • Unexplained need for money or financial problems. May borrow or steal to get it.
  • Engaging in secretive or suspicious behaviors.
  • Sudden change in friends, favorite hangouts, and hobbies.
  • Frequently getting into trouble (fights, accidents, illegal activities).
  • Unexplained change in personality or attitude.
  • Sudden mood swings, irritability, or angry outbursts.
  • Periods of unusual hyperactivity, agitation, or giddiness.
  • Lack of motivation; appears lethargic or “spaced out.”
  • Appears fearful, anxious, or paranoid, with no reason.
  • Marijuana: Glassy, red eyes; loud talking, inappropriate laughter followed by sleepiness; loss of interest, motivation; weight gain or loss.
  • Depressants (including Xanax, Valium, GHB): Contracted pupils; drunk-like; difficulty concentrating; clumsiness; poor judgment; slurred speech; sleepiness.
  • Stimulants (including amphetamines, cocaine, crystal meth): Dilated pupils; hyperactivity; euphoria; irritability; anxiety; excessive talking followed by depression or excessive sleeping at odd times; may go long periods of time without eating or sleeping; weight loss; dry mouth and nose.
  • Inhalants (glues, aerosols, vapors):  Watery eyes; impaired vision, memory and thought; secretions from the nose or rashes around the nose and mouth; headaches and nausea; appearance of intoxication; drowsiness; poor muscle control; changes in appetite; anxiety; irritability; lots of cans/aerosols in the trash.
  • Hallucinogens (LSD, PCP): Dilated pupils; bizarre and irrational behavior including paranoia, aggression, hallucinations; mood swings; detachment from people; absorption with self or other objects, slurred speech; confusion.
  • Heroin: Contracted pupils; no response of pupils to light; needle marks; sleeping at unusual times; sweating; vomiting; coughing, sniffling; twitching; loss of appetite.

Behavioral signs of drug abuse

Psychological warning signs of drug abuse

Warning Signs of Commonly Abused Drugs

Warning signs of teen drug abuse

While experimenting with drugs doesn’t automatically lead to drug abuse, early use is a risk factor for developing more serious drug abuse and addiction. Risk of drug abuse also increases greatly during times of transition, such as changing schools, moving, or divorce. The challenge for parents is to distinguish between the normal, often volatile, ups and downs of the teen years and the red flags of substance abuse. These include:

  • Having bloodshot eyes or dilated pupils; using eye drops to try to mask these signs.
  • Skipping class; declining grades; suddenly getting into trouble at school.
  • Missing money, valuables, or prescriptions.
  • Acting uncharacteristically isolated, withdrawn, angry, or depressed.
  • Dropping one group of friends for another; being secretive about the new peer group.
  • Loss of interest in old hobbies; lying about new interests and activities.
  • Demanding more privacy; locking doors; avoiding eye contact; sneaking around.
  • Visit a Narcotics Anonymous meeting in your area. See below.
  • Call 1-800-662-HELP in the U.S. to reach a free referral helpline from the Substance Abuse and Mental Health Services Administration.

Getting help for drug abuse and drug addiction

Finding help and support for drug addiction

Recognizing that you have a problem is the first step on the road to recovery, one that takes tremendous courage and strength. Facing your addiction without minimizing the problem or making excuses can feel frightening and overwhelming, but recovery is within reach. If you’re ready to make a change and willing to seek help, you can overcome your addiction and build a satisfying, drug-free life for yourself.

Support is essential to addiction recovery

Don’t try to go it alone; it’s all too easy to get discouraged and rationalize “just one more” hit or pill. Whether you choose to go to rehab, rely on self-help programs, get therapy, or take a self-directed treatment approach, support is essential. Recovering from drug addiction is much easier when you have people you can lean on for encouragement, comfort, and guidance.
Support can come from:

  • family members
  • close friends
  • therapists or counselors
  • other recovering addicts
  • healthcare providers
  • people from your faith community

When a loved one has a drug problem

If you suspect that a friend or family member has a drug problem, here are a few things you can do:

  • Speak up. Talk to the person about your concerns, and offer your help and support, without being judgmental. The earlier addiction is treated, the better. Don’t wait for your loved one to hit bottom! Be prepared for excuses and denial by listing specific examples of your loved one’s behavior that has you worried.
  • Take care of yourself. Don’t get so caught up in someone else’s drug problem that you neglect your own needs. Make sure you have people you can talk to and lean on for support. And stay safe. Don’t put yourself in dangerous situations.
  • Avoid self-blame. You can support a person with a substance abuse problem and encourage treatment, but you can’t force an addict to change. You can’t control your loved one’s decisions. Let the person accept responsibility for his or her actions, an essential step along the way to recovery for drug addiction.

 

But Don’t

  • Attempt to punish, threaten, bribe, or preach.
  • Try to be a martyr. Avoid emotional appeals that may only increase feelings of guilt and the compulsion to use drugs.
  • Cover up or make excuses for the drug abuser, or shield them from the negative consequences of their behavior.
  • Take over their responsibilities, leaving them with no sense of importance or dignity.
  • Hide or throw out drugs.
  • Argue with the person when they are high.
  • Take drugs with the drug abuser.
  • Feel guilty or responsible for another’s behavior.

Adapted from: National Clearinghouse for Alcohol & Drug Information

When your teen has a drug problem

Discovering your child uses drugs can generate fear, confusion, and anger in parents. It’s important to remain calm when confronting your teen, and only do so when everyone is sober. Explain your concerns and make it clear that your concern comes from a place of love. It’s important that your teen feels you are supportive.

Five steps parents can take:

  • Lay down rules and consequences. Your teen should understand that using drugs comes with specific consequences. But don’t make hollow threats or set rules that you cannot enforce. Make sure your spouse agrees with the rules and is prepared to enforce them.
  • Monitor your teen’s activity. Know where your teen goes and who he or she hangs out with. It’s also important to routinely check potential hiding places for drugs—in backpacks, between books on a shelf, in DVD cases or make-up cases, for example. Explain to your teen that this lack of privacy is a consequence of him or her having been caught using drugs.
  • Encourage other interests and social activities. Expose your teen to healthy hobbies and activities, such as team sports and afterschool clubs.
  • Talk to your child about underlying issues. Drug use can be the result of other problems. Is your child having trouble fitting in? Has there been a recent major change, like a move or divorce, which is causing stress?
  • Get Help. Teenagers often rebel against their parents but if they hear the same information from a different authority figure, they may be more inclined to listen. Try a sports coach, family doctor, therapist, or drug counselor.

 

Source: Helpguide.org

Fertilizer use responsible for increase in nitrous oxide in atmosphere.


University of California, Berkeley, chemists have found a smoking gun proving that increased fertilizer use over the past 50 years is responsible for a dramatic rise in atmospheric nitrous oxide, which is a major greenhouse gas contributing to global climate change.

Climate scientists have assumed that the cause of the increased nitrous oxide was nitrogen-based fertilizer, which stimulates microbes in the soil to convert nitrogen to nitrous oxide at a faster rate than normal.

The new study, reported in the April issue of the journal Nature Geoscience, uses nitrogen isotope data to identify the unmistakable fingerprint of fertilizer use in archived air samples from Antarctica and Tasmania.

“Our study is the first to show empirically from the data at hand alone that the nitrogen isotope ratio in the atmosphere and how it has changed over time is a fingerprint of fertilizer use,” said study leader Kristie Boering, a UC Berkeley professor of chemistry and of earth and planetary science.

“We are not vilifying fertilizer. We can’t just stop using fertilizer,” she added. “But we hope this study will contribute to changes in fertilizer use andagricultural practices that will help to mitigate the release of nitrous oxide into the atmosphere.”

Since the year 1750, nitrous oxide levels have risen 20 percent – from below 270 parts per billion (ppb) to more than 320 ppb. After carbon dioxide and methane, nitrous oxide (N2O) is the most potent greenhouse gas, trapping heat and contributing to global warming. It also destroys stratospheric ozone, which protects the planet from harmful ultraviolet rays.

Not surprisingly, a steep ramp-up in atmospheric nitrous oxide coincided with the green revolution that increased dramatically in the 1960s, when inexpensive, synthetic fertilizer and other developments boosted food production worldwide, feeding a burgeoning global population.

 

Tracking the origin of nitrous oxide in the atmosphere, however, is difficult because a molecule from a fertilized field looks identical to one from a natural forest or the ocean if you only measure total concentration. But a quirk of microbial metabolism affects the isotope ratio of the nitrogen the N2O microbes give off, producing a telltale fingerprint that can be detected with sensitive techniques.

Archived air from Cape Grim

Boering and her colleagues, including former UC Berkeley graduate students Sunyoung Park and Phillip Croteau, obtained air samples from Antarctic ice, called firn air, dating from 1940 to 2005, and from an atmospheric monitoring station at Cape Grim, Tasmania, which has archived air back to 1978.

Analysis of N2O levels in the Cape Grim air samples revealed a seasonal cycle, which has been known before. But isotopic measurements by a very sensitive isotope ratio mass spectrometer also displayed a seasonal cycle, which had not been observed before. At Cape Grim, the isotopes show that the seasonal cycle is due both to the circulation of air returning from the stratosphere, where N2O is destroyed after an average lifetime of 120 years, and to seasonal changes in the ocean, most likely upwelling that releases more N2O at some times of year than at others.

“The fact that the isotopic composition of N2O shows a coherent signal in space and time is exciting, because now you have a way to differentiate agricultural N2O from natural ocean N2O from Amazon forest emissions from N2O returning from the stratosphere,” Boering said. “In addition, you also now have a way to check whether your international neighbors are abiding by agreements they’ve made to mitigate N2O emissions. It is a tool that, ultimately, we can use to verify whether N2O emissions by agriculture or biofuel production are in line with what they say they are.”

 

Changes in fertilizer use can reduce N2O emissions

 

Limiting nitrous oxide emissions could be part of a first step toward reducing all greenhouse gases and lessening global warming, Boering said, especially since immediately reducing global carbon dioxide emissions is proving difficult from a political standpoint. In particular, reducing nitrous oxide emissions can initially offset more than its fair share of greenhouse gasemissions overall, since N2O traps heat at a different wavelength than CO2 and clogs a “window” that allows Earth to cool off independent of CO2 levels.

“On a pound for pound basis, it is really worthwhile to figure how to limit our emissions of N2O and methane,” she said. “Limiting N2O emissions can buy us a little more time in figuring out how to reduce CO2 emissions.”

One approach, for example, is to time fertilizer application to avoid rain, because wet and happy soil microbes can produce sudden bursts of nitrous oxide. Changes in the way fields are tilled, when they are fertilized and how much is used can reduce N2O production.

Boering’s studies, which involve analyzing the isotopic fingerprints of nitrous oxide from different sources, could help farmers determine which strategies are most effective. It could also help assess the potential negative impacts of growing crops for biofuels, since some feedstocks may require fertilizer that will generate N2O that offsets their carbon neutrality.

“This new evidence of the budget of nitrous oxide allows us to better predict its future changes– and therefore its impacts on climate and stratospheric ozone depletion – for different scenarios of fertilizer use in support of rising populations and increased production for bio-energy,” said coauthor David Etheridge of the Centre for Australian Weather and Climate Research in Aspendale, Victoria.

 

Finding the fingerprint of fertilized microbes

Boering was able to trace the source of N2O because bacteria in a nitrogen rich environment, such as a freshly fertilized field, prefer to incorporate nitrogen-14 (14N), the most common isotope, instead of nitrogen-15 (15N).

“Microbes on a spa weekend can afford to discriminate against nitrogen-15, so the fingerprint of N2O from a fertilized field is a greater proportion of nitrogen-14,” Boering said. “Our study is the first to show empirically from the data at hand alone that the nitrogen isotope ratio in the atmosphere and how it has changed over time is a fingerprint of fertilizer use.”

Just as telling is the isotope ratio of the central nitrogen atom in the N-N-O molecule. By measuring the nitrogen isotope ratio overall, the isotope ratio in the central nitrogen atom, and contrasting these with the oxygen-18/oxygen-16 isotope ratio, which has not changed over the past 65 years, they were able to paint a consistent picture pointing at fertilizer as the major source of increased atmospheric N2O .

The isotope ratios also revealed that fertilizer use has caused a shift in the way soil microbes produce N2O. The relative output of bacteria that produce N2O by nitrification grew from 13 to 23 percent worldwide, while the relative output of bacteria that produce N2O by denitrification – typically in the absence of oxygen – dropped from 87 to 77 percent. Although the numbers themselves are uncertain, these are the first numerical estimates of these global trends over time, made possible by the unique archived air dataset of this study.

Source: University of California.

 

Biosecurity Board Recommends Publication of Mutant-Flu Studies.


Decision comes one day after release of new guidelines for dual-use research.

 

The U.S. National Science Advisory Board for Biosecurity (NSABB) on March 30 recommended the publication of two controversial avian flu papers.

In December 2011, the board said that experimental details of the two studies should be redacted from any publications because of concerns that the information could be used in a bioterror attack. The board also feared that publishing the details would prompt more laboratories to work on the viruses, making an accidental release more likely.

On March 30, after a two-day meeting, the board decided to revise its earlier decision. The NSABB unanimously recommended full publication of one of the two disputed papers, a manuscript submitted to Nature by Yoshihiro Kawaoka of the University of Wisconsin, Madison, and his colleagues. “We at Nature are delighted,” said editor-in-chief Philip Campbell. “Subject to any outstanding regulatory or legal issues, we intend to proceed with publication as soon as possible.” (Scientific American is part of Nature Publishing Group.)

But in a 12-to-6 vote, the board advised only the publication of the data, methods and conclusions of a second manuscript, submitted to Science by Ron Fouchier of Erasmus Medical Center in Rotterdam, the Netherlands.

Kawaoka says he believes that the board’s revised decision was influenced by a better understanding of the public-health implications of the work, which described the changes in a key viral protein called hemagglutinin that could make avian flu more transmissible among mammals. “We were able to explain that very few mutations are needed for the hemagglutinin of the currently circulating H5N1 viruses to become a hemagglutinin that supports respiratory droplet transmission in ferrets,” he says.

The revised NSABB opinion brings the board closer in line with the World Health Organization, which last month advised full publication of both papers. The NSABB is only an independent advisory board, and the U.S. government has yet to weigh in with any official decision on the new NSABB recommendations. Publication of the manuscripts may also be affected by export controls in various countries. Such controls can be used to regulate the dissemination of restricted information.

Ultimately, the NSABB’s revised decision was a practical one, says Richard Ebright, a molecular biologist and biodefense expert at Rutgers University in Piscataway, N.J., who has argued that the research should not have been funded in the first place. Much of the information was already in the public domain, and the remainder, he says, was likely to be leaked online: “Information that’s not born classified can’t be reborn as classified.”

The NSABB said that its decision was informed by a new government policy that could facilitate earlier review of “dual-use” research that can both benefit the public and be misused to threaten public health, agriculture or the environment. The policy, released on March 29, makes it compulsory for the first time for all U.S. federal research agencies to assess research proposals for their dual-use risk in cases where the research involves one of a list of dangerous pathogens specified by the policy.

Under the new guidelines, research judged to be of risk would then be subject to mitigation measures such as modifications to the proposed research, tougher biosecurity or biosafety precautions, and determinations of how the research should be communicated, and to whom. If federal department and agencies consider that mitigation measures do not rule out serious risks of the research, they would have the authority to request voluntary redaction of results, classify the research and withhold or withdraw research funding.

The new rules are “a tremendous step forward,” says Ebright, who says the obligation for prior review of research proposals is “critically important” and should prevent cases such as the two H5N1 studies, whose potential biosecurity and biosafety implications were raised only on the eve of publication of their results.

But the rule’s Achilles’ heel, he adds, is that although research funders will have to inform their parent government departments of the outcomes of reviews and any mitigation measure taken, there seems no mechanism to allow independent oversight of these. That is a “a very big weakness,” he says, and could result in what appears to be a comprehensive scheme not being applied effectively in practice.

The dual-use rules come into force immediately, and agencies will have 90 days to report existing projects of dual-use risk to their parent agencies. Anthony Fauci, the director of the U.S. National Institute of Allergy and Infectious Diseases in Bethesda, Md, told the Associated Press that the National Institutes of Health had already completed its review, and “found fewer than ten projects that met the criteria for further risk management.”

This article is reproduced with permission from the magazine Nature. The article was first published on March 30 2012.

 

Source: Scientific American.

 

 

 

Supermassive Black Holes in the Center of most Galaxies.


A study led by a University of Utah astrophysicist found a new explanation for the growth of supermassive black holes in the center of most galaxies: they repeatedly capture and swallow single stars from pairs of stars that wander too close.

 

Using new calculations and previous observations of our own Milky Way and other galaxies, “we found black holes grow enormously as a result of sucking in captured binary star partners,” says physics and astronomy Professor Ben Bromley, lead author of the study, which is set for online publication April 2 inAstrophysical Journal Letters.

“I believe this has got to be the dominant method for growing supermassive black holes,” he adds. “There are two ways to grow a supermassive black hole: with gas clouds and with stars. Sometimes there’s gas and sometimes there is not. We know that from observations of other galaxies. But there are always stars.”

“Our mechanism is an efficient way to bring a star to a black hole,” Bromley says. “It’s really hard to target a single star at a black hole. It’s a lot easier to throw a binary at it,” just as it’s more difficult to hit a target using a slingshot, which hurls a single stone, than with a bola, which hurls two weights connected by a cord.

A binary pair of stars orbiting each other “is essentially a single object much bigger than the size of the individual stars, so it is going to interact with the black hole more efficiently,” he explains. “The binary doesn’t have to get nearly as close for one of the stars to get ripped away and captured.”

 

But to prove the theory will require more powerful telescopes to find three key signs: large numbers of small stars captured near supermassive black holes, more observations of stars being “shredded” by gravity from black holes, and large numbers of “hypervelocity stars” that are flung from galaxies at more than 1 million mph when their binary partners are captured.

Bromley, a University of Utah astrophysicist, did the study with astronomers Scott Kenyon, Margaret Geller and Warren Brown, all of the Smithsonian Astrophysical Observatory in Cambridge, Mass. The study was funded by both institutions.

 

What Does a Supermassive Black Hole Eat: Gas or Stars?

 

Black holes are objects in space so dense that not even light can escape their gravity, although powerful jets of light and energy can be emitted from a black hole’s vicinity as gas and stars are sucked into it.

Small black holes result from the collapse of individual stars. But the centers of most galaxies, including our own Milky Way, are occupied by what are popularly known as “supermassive” black holes that contain mass ranging from 1 million to 10 billion stars the size of our sun.

Astrophysicists long have debated how supermassive black holes grew during the 14 billion years since the universe began in a great expansion of matter and energy named the Big Bang. One side believes black holes grow larger mainly by sucking in vast amounts of gas; the other side says they grow primarily by capturing and sucking in stars.

Just last month, other researchers published a theory that a black hole sucks in “food” by tipping its “plates” – two tilted gas disks colliding as they orbit the black hole – in a way that makes the speeding gas slow down so the black hole can swallow it.

Bromley says that theory overcomes a key problem: gas flows into black holes inefficiently. “But are misaligned gas disks common enough to be important for black hole growth?” he asks. “It’s fair to say that gas contributes to the growth of black holes, but it is still uncertain how.”

The new theory about binary stars – a pair of stars that orbit each other – arose from Bromley’s earlier research to explain hypervelocity stars, which have been observed leaving our Milky Way galaxy at speeds ranging from 1.1 million to 1.8 million mph, compared with the roughly 350,000 mph speed of most stars.

 

Munching Binaries: One is Captured, One Speeds Away

“The hypervelocity stars we see come from binary stars that stray close to the galaxy’s massive black hole,” he says. “The hole peels off one binary partner, while the other partner – the hypervelocity star – gets flung out in a gravitational slingshot.”

“We put the numbers together for observed hypervelocity stars and other evidence, and found that the rate of binary encounters [with our galaxy’s supermassive black hole] would mean most of the mass of the galaxy’s black hole came from binary stars,” Bromley says. “We estimated these interactions for supermassive black holes in other galaxies and found that they too can grow to billions of solar masses in this way.”

As many as half of all stars are in binary pairs, so they are plentiful in theMilky Way and other galaxies, he adds. But the study assumed conservatively that only 10 percent of stars exist in binary pairs.

The new study looked at each step in the process of a supermassive black hole eating binary stars, and calculated what would be required for the process to work in terms of the rates at which hypervelocity stars are produced, binary partners are captured, the captured stars are bound to the black hole in elongated orbits and then sucked into it.

The scientists then compared the results with actual observations of supermassive black holes, stars clustering near them and “tidal disruption events” in which black holes in other galaxies are seen to shred stars while pulling them into the hole.

“It fits together, and it works,” Bromley says. “When we look at observations of how stars are accumulating in our galactic center, it’s clear that much of the mass of the black hole likely came from binary stars that were torn apart.”

He refers to the process of a supermassive black hole capturing stars from binary pairs as “filling the bathtub.” Once the tub – the area near the black hole – is occupied by a cluster of captured stars, they go “down the drain” into the black hole over millions of years. His study shows the “tub” fills at about the same rate it drains, meaning stars captured by a supermassive black hole eventually are swallowed.

 

The study’s key conclusions:

— The theory accurately predicts the rate (one every 1,000 to 100,000 years) at which hypervelocity stars are observed leaving our galaxy and at which stars are captured into the star cluster seen near our galaxy’s supermassive black hole.

— The rate of “tidal disruption events,” which are stars being shredded and pulled into supermassive black holes in other galaxies, also matches what the theory predicts, based on the limited number seen since they first were observed in the early 2000s. That rate also is one every 1,000 to 100,000 years.

— The calculations show how the theory’s rate of binary capture and consumption can explain how the Milky Way’s supermassive black hole has at least doubled to quadrupled in mass during the past 5 billion to 10 billion years.

When the researchers considered the number of stars near the Milky Way’s center, their speed and the odds they will encounter the supermassive black hole, they estimated that one binary star will be torn apart every 1,000 years by the hole’s gravity.

 

During the last 10 billion years, that would mean the Milky Way’s supermassive black hole ate 10 million solar masses – more than enough to account for the hole’s actual size of 4 million solar masses.

“We found a wide range of black hole masses can be explained by this process,” Bromley says.

Confirmation of the theory must await more powerful orbiting and ground-based telescopes. To confirm the theory, such telescopes should find many more stars in the cluster near the Milky Way’s supermassive black hole (we now see only the brightest ones), a certain rate of hypervelocity stars in southern skies, and more observations of stars being shredded in other galaxies.

Source:University of Utah 

 

Smoking Cessation Counseling Beliefs and Behaviors of Outpatient Oncology Providers.


Many cancer patients continue to smoke after diagnosis, increasing their risk for treatment complications, reduced treatment efficacy, secondary cancers, and reduced survival. Outpatient oncology providers may not be using the “teachable moment” of cancer diagnosis to provide smoking cessation assistance.

Providers and Methods. Physicians and midlevel providers (n = 74) who provide outpatient oncology services completed an online survey regarding smoking cessation counseling behaviors, beliefs, and perceived barriers. Outpatient medical records for 120 breast, lung, head and neck, colon, prostate, and acute leukemia cancer patients were reviewed to assess current smoking cessation assessment and intervention documentation practices.

Results. Providers reported commonly assessing smoking in new patients (82.4% frequently or always), but rates declined at subsequent visits for both current smokers and recent quitters. Rates of advising patients to quit smoking were also high (86.5% frequently or always), but <30% of providers reported frequently or always providing intervention to smoking patients (e.g., nicotine replacement therapy or other medications, self-help materials, and/or referrals). Only 30% of providers reported that they frequently or always followed up with patients to assess progress with quitting. Few providers (18.1%) reported high levels of confidence in their ability to counsel smoking patients. Patients’ lack of motivation was identified as the most important barrier to smoking cessation.

Conclusions. Although beliefs about providing cessation services to smoking patients were generally positive, few providers reported commonly providing interventions beyond advice to quit. Additional training and clinic-based interventions may improve adherence to tobacco cessation practice guidelines in the outpatient oncology setting.

Source: The Oncologist.

 

 

A Prospective Study of the Factors Shaping Antibody Responses to the AS03-Adjuvanted Influenza A/H1N1 Vaccine in Cancer Outpatients.


To identify the determinants of antibody responses to adjuvanted influenza A/H1N1/09 vaccines in a cohort of cancer outpatients.

Patients and Methods. Patients with cancer and controls were enrolled in a prospective single-center field study. Two doses of AS03-adjuvanted pandemic influenza vaccine were administered to patients and one dose was administered to controls. Antibody responses were measured using hemagglutination inhibition and confirmed by microneutralization. Geometric mean titers (GMTs) and seroprotection rates (defined as GMTs ≥40) were compared.

Results. Immunizations were safe and well tolerated in 197 cancer patients (lymphoma, 57; glioma, 26; lung or head and neck, 37; gastrointestinal, 41; breast, 36) and 138 controls. Similar seroprotection rates (82.3% versus 87%) and GMTs (336.9 versus 329.9) were achieved after two doses of adjuvanted vaccine in cancer patients and one dose in controls. Univariate analyses identified older age, prior immunization against seasonal influenza, lymphoma, CD4 count, active chemotherapy, and rituximab and steroid treatments as being associated with weaker antibody responses. However, only age and chemotherapy plus rituximab remained independent determinants of vaccine responses in multivariate analyses.

Conclusions. Two doses of AS03-adjuvanted influenza vaccine elicited potent antibody responses in most cancer patients despite ongoing chemotherapy, with the exception of rituximab-induced B-cell depletion. Oncology patients treated in an outpatient setting benefit from preventive vaccination against influenza with adjuvanted vaccines.

Source: The Oncologist.

Outpatient Use of Low Molecular Weight Heparin Monotherapy for First-Line Treatment of Venous Thromboembolism in Advanced Cancer.


Evidence-based treatment guidelines recommend low molecular weight heparin (LMWH) monotherapy for cancer-associated venous thromboembolism (VTE). This analysis assessed the first-line treatment strategies for VTE in patients with advanced solid tumors.

Methods. Using administrative data from advanced lung, prostate, colon, or breast cancer patients diagnosed between January 2000 and December 2007 at four HMOs with integrated delivery systems, patients with an inpatient or outpatient VTE diagnosed within 2 years after cancer diagnosis and an outpatient purchase of warfarin, LMWH, and/or fondaparinux anticoagulant within 7 days of the VTE diagnosis were identified. First-line outpatient VTE pharmacological treatment and factors independently associated with receipt/non-receipt of LMWH monotherapy were assessed.

Results. Overall, 25% of the 1,089 eligible patients received LMWH monotherapy as primary VTE treatment. The percentage increased steadily over time from 18% among patients diagnosed in 2000 to 31% among those diagnosed in 2007. Factors associated with LMWH monotherapy included VTE diagnosis year, chemotherapy within 60 days prior to VTE diagnosis, history of VTE prior to cancer diagnosis, and invasive surgery in the 90 days following VTE diagnosis. Colorectal and prostate cancer patients versus lung cancer patients and stage III versus stage IV patients were less likely to be treated with LMWH monotherapy.

Conclusions. Adoption of LMWH monotherapy as initial treatment for cancer-associated VTE was low but increased steadily over the study period. Future studies should explore reasons underlying the underutilization of this preferred evidence-based treatment as well as the comparative effectiveness of LMWH versus warfarin-based anticoagulation in real-world cancer patients with VTE.

Source: The Oncologist.

Radiation-Induced Sarcoma of the Breast: A Systematic Review.


Radiation-induced sarcoma (RIS) is a rare, aggressive malignancy. Breast cancer survivors treated with radiotherapy constitute a large fraction of RIS patients. To evaluate evidenced-based practices for RIS treatment, we performed a systematic review of the published English-language literature.

Methods. We performed a systematic keyword search of PubMed for original research articles pertaining to RIS of the breast. We classified and evaluated the articles based on hierarchal levels of scientific evidence.

Results. We identified 124 original articles available for analysis, which included 1,831 patients. No randomized controlled trials involving RIS patients were found. We present the best available evidence for the etiology, comparative biology to primary sarcoma, prognostic factors, and treatment options for RIS of the breast.

Conclusion. Although the evidence to guide clinical practice is limited to single institutional cohort studies, registry studies, case–control studies, and case reports, we applied the available evidence to address clinically relevant questions related to best practice in patient management. Surgery with widely negative margins remains the primary treatment of RIS. Unfortunately, the role of adjuvant and neoadjuvant chemotherapy remains uncertain. This systematic review highlights the need for additional well-designed studies to inform the management of RIS.

Source: The Oncologist.

 

Adult Brainstem Gliomas.


Brainstem gliomas are uncommon in adults and account for only 1%–2% of intracranial gliomas. They represent a heterogeneous group of tumors that differ from those found in their pediatric counterparts. In adults, a low-grade phenotype predominates, which is a feature that likely explains their better prognosis compared to that in children. Because biopsies are rarely performed, classifications based on the radiological aspect of magnetic resonance imaging results have been proposed to establish treatment strategies and to determine outcomes: (a) diffuse intrinsic low-grade, (b) enhancing malignant glioma, (c) focal tectal gliomas, and (d) exophytic gliomas. Despite significant advances in neuroradiology techniques, a purely radiological classification remains imperfect in the absence of a histological diagnosis. Whereas a biopsy may often be reasonably avoided in the diffuse nonenhancing forms, obtaining histological proof seems necessary in many contrast-enhanced brainstem lesions because of the wide variety of differential diagnoses in adults. Conventional radiotherapy is the standard treatment for diffuse intrinsic low-grade brainstem gliomas in adults (the median survival is 5 years). In malignant brainstem gliomas, radiotherapy is the standard treatment. However, the possible benefit of combined radiotherapy and chemotherapy (temozolomide or other agents) has not been thoroughly evaluated in adults. The role of anti-angiogenic therapies in brainstem gliomas remains to be defined. A better understanding of the biology of these tumors is of primary importance for identifying homogeneous subgroups and for improving therapy options and outcomes.

Source: The Oncologist.

 

 

Transarterial Chemoembolization Plus Sorafenib: A Sequential Therapeutic Scheme for HCV-Related Intermediate-Stage Hepatocellular Carcinoma: A Randomized Clinical Trial.


Recurrence of hepatocellular carcinoma (HCC) is a major problem after surgical or ablative treatments. The aim of this prospective, single-center, placebo-controlled, randomized, double-blind clinical study was to evaluate the effectiveness of transarterial chemoembolization (TACE) combined with sorafenib as a sequential treatment regimen in delaying time to progression (TTP) of intermediate-stage HCC in patients with chronic hepatitis C virus (HCV) infection.

Material and Methods. Between October, 2007 and January, 2011, 80 HCV-infected patients with Barcelona Clinic Liver Cancer stage B HCC underwent the TACE procedure. All had Child-Pugh class A disease. They were randomized 1:1 to receive sorafenib at a dose of 400 mg twice daily or placebo. Endpoints were the TTP and the rates of adverse events and toxicity.

Results. Sixty-two of 80 patients (77%), 31 in the sorafenib group and 31 in the control group, completed the study. The median TTP was 9.2 months in the sorafenib group and 4.9 months in the placebo group (hazard ratio, 2.5; 95% confidence interval, 1.66–7.56; p < .001). Metachronous, multicentric HCC progression occurred less frequently in sorafenib-treated patients (p < .05). Adverse reactions to sorafenib caused withdrawal from the study of 9 (22%) patients.

Conclusion. A conventional TACE procedure followed by sorafenib treatment resulted in a significantly longer TTP in patients with intermediate-stage HCV-related HCC, with no unexpected side effects.

Source: The Oncologist.