Septic shock

Patients who present to the emergency department demonstrating clinical signs of circulatory shock constitute a medical emergency, often associated with significant mortality. Severe sepsis, characterized as infection with systemic manifestations and accompanying organ dysfunction or tissue hypoperfusion, can lead to septic shock.Septic shock is defined as severe sepsis plus sepsis-induced hypotension not reversed with adequate fluid resuscitation. Hypotension may be defined by a drop in systolic blood pressure (SBP) to < 90 mm Hg or by at least a 40-mm Hg from baseline. The inadequate perfusion of critical organs (heart, liver, and kidneys) may lead to significant morbidity and mortality.Initial hemodynamic management of patients presenting with hypotension and concern for septic shock should consist of fluid therapy with 10-40 cc/kg of crystalloids, preferably normal saline, or lactated Ringer's solution. Various medications are used in the treatment of patients in circulatory shock.The use of vasopressors is an important component of resuscitation efforts, with the goal of therapy to maintain mean arterial pressure (MAP) at least 65 mm Hg. Dopamine and norepinephrine have generally been considered first-line agents in patients presenting with septic shock; in fact, recent consensus guidelines and expert recommendations have suggested that either agent may be used as a first-choice vasopressor in patients who have septic shock. Epinephrine, vasopressin, and neosynephrine may be useful second-line agents. Inotropic therapy with dobutamine may also be necessary in myocardial dysfunction.Because hypotension may be life-threatening, vasopressors help to maintain adequate blood flow and tissue perfusion despite hypovolemia. Dopamine increases heart rate and stroke volume, leading to an increase in cardiac output and MAP. In contrast, norepinephrine is a vasoconstrictor and thereby increases MAP with little effect on heart rate and stroke volume. While norepinephrine is considered to be more potent and thereby more effective in increasing blood pressure in septic shock, dopamine may be useful in patients with systolic dysfunction, but is also associated with more tachycardia and dysrhythmias. There is also concern regarding adverse effects on the endocrine and immune systems with dopamine. It has also been noted that norepinephrine may potentially decrease cardiac output, oxygen delivery, and blood flow to vulnerable organs despite adequate perfusion pressure.. Meanwhile, vasopressin, an endogenously released peptide hormone, has emerged as an adjunct to catecholamines for patients who have severe septic shock. The rationale for its use is the relative vasopressin deficiency in patients in septic shock and the hypothesis that exogenously administered vasopressin can restore vascular tone and blood pressure, thereby reducing the need for the use of catecholamines. Observational studies involving the use of vasopressin infusion rates below 0.1 units per minute in patients in vasodilatory shock have repeatedly shown improved short-term blood pressure responses.However, vasopressin infusion may also decrease blood flow in the heart, kidneys, and intestine.Interestingly, despite the widespread use of vasopressin in clinical practice, only 2 small randomized trials have evaluated its use in patients in septic shock. Vasopressin increased blood pressure, decreased catecholamine requirements, and improved renal function as compared with a control medication. However, the trials were only powered to evaluate mortality, organ dysfunction, or safety.

General anesthetics

General anesthetics are administered to approximately 50 million patients each year in the United States. Anesthetic vapors and gases are also widely used in dentists' offices, veterinary clinics, and laboratories for animal research. All the volatile anesthetics that are currently used are halogenated compounds destructive to the ozone layer. These halogenated anesthetics could have potential significant impact on global warming. The widely used anesthetic gas nitrous oxide is a known greenhouse gas as well as an important ozone-depleting gas. These anesthetic gases and vapors are primarily eliminated through exhalation without being metabolized in the body, and most anesthesia systems transfer these gases as waste directly and unchanged into the atmosphere. Little consideration has been given to the ecotoxicological properties of gaseous general anesthetics. Our estimation using the most recent consumption data indicates that the anesthetic use of nitrous oxide contributes 3.0% of the total emissions in the United States. Studies suggest that the influence of halogenated anesthetics on global warming will be of increasing relative importance given the decreasing level of chlorofluorocarbons globally. Despite these nonnegligible pollutant effects of the anesthetics, no data on the production or emission of these gases and vapors are publicly available.. Since Fox et al. first published their warning in 1975, concern has been repeatedly expressed about the potential harm that the release of halogenated general anesthetic gases poses to the global environment.All the volatile anesthetics that are currently used (halothane, isoflurane, enflurane, sevoflurane, and desflurane) are halogenated compounds potentially destructive to the ozone layer. The widely used anesthetic gas nitrous oxide (N2O) is an established greenhouse gas.A recent report suggests that N2O is also an important ozone-depleting gasAs the world population continues to grow and as modern anesthesia becomes available to more regions of the world, the global use of volatile anesthetics and N2O will rapidly grow. General anesthetics were administered to approximately 50 million patients in the United States in 2006, according to data released by the National Center for Health Statistics Anesthetic vapors and gases are also widely used in dentists' offices, veterinary clinics, and laboratories for animal research. A key attribute that differentiates all of these anesthetic gases from other medical drugs is that they are substantially eliminated through exhalation, without being metabolized in the body. At present, most anesthesia systems transfer these waste gases directly and unchanged into the atmosphere. Although the introduction of scavenging systems has significantly reduced spillage of general anesthetics into the operating room, they are still exhausted into the environment. Little consideration has been given to the ecotoxicological properties of gaseous general anesthetics. Chemically, halogenated volatile anesthetics are closely related to the chlorofluorocarbons (CFCs), which play major roles in ozone depletion. The effect of a volatile anesthetic on ozone depletion will depend on its molecular weight, the number and type of halogen atoms, and its atmospheric lifetime (defined as the time taken to remove or transform 1/e, or 63%, of an emitted gas). The atmospheric lifetime of these trace gases depends on their removal by chemical reaction with radicals, photolysis, and dry or wet deposition, such as “rainout.” Those species with a tropospheri lifetime of more than 2 years are then believed to reach the stratosphere in significant quantities. The tropospheric lifetime of halogenated anesthetics is much shorter than that of CFCs, because hydrogen atoms of the anesthetic molecules are susceptible to attack by hydroxyl radicals in the troposphere, making them less likely to reach the stratosphere. However, a concern has been raised about very short-lived compounds (with a lifetime of a few months or less) and their potentially significant contribution to ozone destruction. Once anesthetics reach the stratosphere, chlorine-containing anesthetics such as halothane, isoflurane, and enflurane may be more destructive to the ozone layer than are newer drugs, such as sevoflurane and desflurane, which are halogenated entirely with fluorine. By measuring the rate of reaction with hydroxyl radicals, Brown et al. have calculated that the tropospheric lifetimes of halothane, enflurane, and isoflurane are 2, 6, and 5 years, respectively. A more recent evaluation of the lifetimes of halogenated volatile anesthetics and their potential contribution to ozone depletion has been reported by Langbein et al.Using measurements of hydroxyl radical reaction kinetics and ultraviolet absorption spectra of anesthetics, we estimated the total atmospheric lifetimes of these anesthetics at 4.0 to 21.4 years. Contributions to total stratospheric ozone depletion were reported as approximately 1% for halothane and 0.02% for enflurane and isoflurane, suggesting that these anesthetics can play important roles in ozone depletion. The global warming potential (GWP) of halogenated anesthetics is reported to range from 1230 (isoflurane) to 3714 (desflurane) times the GWP of carbon dioxide (CO2) . Recently, Ryan and Nielsen reported on the impact of halogenated volatile anesthetics on global warming within the framework of common clinical practice, an approach that has not been taken before. Their study suggests that all the anesthetics (isoflurane, sevoflurane, and desflurane) can have a significant influence on global warming with the greatest impact produced by atmospheric desflurane.With an atmospheric lifetime of approximately 120 years, N2O is a remarkably stable gas.N2O traps thermal radiation escaping from the Earth's surface, contributing to what is known as the “greenhouse effect”. The GWP of N2O is approximately 300 times more than that of CO2. N2O, along with CO2 and methane, are the most influential long-lived greenhouse gases among all gases encompassed by the Kyoto Protocol. N2O is produced by human sources including agriculture (nitrogen-based fertilizers) and the use of fossil fuels, as well as natural sources in soil and water, such as microbial action in moist tropical forests. The N2O concentration is reported to be steadily increasing at a rate of 0.7 to 0.8 parts per billion (ppb) per year in past decades, and N2O currently contributes about 6% of the total radiative forcing (difference between incoming and outgoing radiation energy within the Earth's atmosphere). In addition, N2O is a primary source of stratospheric nitrogen oxides, referring specifically to NO and NO2. Both destroy ozone. Although the ozone depleting potential (ODP) of N2O (0.017) is lower than that of CFCs (only 10% of N2O is converted to nitrogen oxides), N2O emission is reported to be the single largest ODP-weighted emission and is expected to remain the largest for the rest of this centurySherman and Cullen first reported in 1988 that N2O, the most popular anesthetic gas, could contribute to global warming, and estimated that approximately 1% of total N2O production was used for clinical anesthesia on the basis of the number of surgical procedures in the United States, approximately 21 million cases at that time. They estimated the worldwide annual use of N2O for anesthesia to be 0.5 to 1.0 × 109 moles (2.2 to 4.4 × 104 tons). Although the precise quantities manufactured for medical use are unavailable to the public, we can estimate the most recent consumption of N2O for anesthetic purposes. Our institution consumed 20.2 tons of N2O for anesthetic use in 2006 for approximately 40,000 procedures that were performed with an anesthesiologist present. In the United States, approximately 70 million procedures were performed in 2006 with an anesthesia provider (all types of anesthesia included), according to data from the National Center for Health Statistics. Extrapolating from these figures, we estimate that approximately 3.5 × 104 tons of N2O were used for anesthetic purposes for 70 million patients in 2006 in the United States. The latest inventory of greenhouse gas emissions by the United States Environmental Protection Agency reports that total United States emissions of N2O were 1.187 × 106 tons in 2006, a reduction of 8% from 1996 levels. The anesthetic use of N2O is therefore estimated to be 3.0% of total 2006 N2O emissions in the United States. These numbers are provided only as an example of the volume of N2O liberated by 1 country, because there seems to be a declining trend in the use of N2O in European countries. However, the data on the worldwide anesthetic use of N2O, including all developed and developing countries, are not available. Until those data are obtained, a warning that the medical use of N2O can be a significant contributor to overall greenhouse gas emissions should be maintained. The use of volatile anesthetics could be reduced by up to 80% to 90% if closed circuit anesthesia were widely used for all patients, and to a lesser degree if “low-flow” anesthesia were routinely used. Although closed-circuit anesthesia is not a difficult technique with modern anesthesia systems for well-trained anesthesiologists, continuous accurate gas monitoring is required to prevent inadequate oxygenation or volatile anesthetic concentration. Shifting to total IV anesthesia would eliminate the use of anesthetic gases. Nevertheless, many anesthesiologists may still prefer volatile anesthetics and N2O, and their use is almost always required for anesthesia in infants and children. Modifying our practice towards more conservation of anesthetic gases can usually be done without compromising patient care if appropriate monitoring is used, and these techniques should be available to most anesthesiologists in developed countries. Doyle et al. have shown that silica zeolite (Deltazite™) was effective at completely removing isoflurane (1% in exhaled gases) in the scavenging line for a period of 8 hours. The trapped halogenated agents could then be reprocessed by steam extraction or fractional distillation for reuse. Reprocessing techniques are essential to reducing the amount of the anesthetics released into the atmosphere because disposal does not change the eventual fate of the anesthetics. A technique for conserving halogenated anesthetic vapors using a zeolite filter at the Y-piece connector has been proposed by Thomasson et al and the principles of this technique have been used to develop an anesthetic conserving device (ACD). The system is closed to volatile anesthetics, but it is open to oxygen; volatile anesthetics are supplied to the ACD through a syringe pump. This system has been shown to successfully reduce the total amount of volatile anesthetics released by 40%–75%, suggesting that the ACD may provide an alternative to low-flow systems. First reported >50 years ago, the anesthetic property of xenon has been revisited. Xenon is a naturally occurring atmospheric trace gas, existing at 0.08 parts per million (ppm), with no known detrimental ecotoxicological effect. The pharmacokinetic benefits of xenon include profound analgesia, neuroprotection, and hemodynamic stability. Xenon also has an extremely low blood–gas partition coefficient, which lends itself to rapid induction and emergence. However, clinical use of xenon has been limited mostly by its high cost of manufacture, which involves fractional distillation of liquid air. Furthermore, the production of xenon consumes enormous amounts of energy (220 W/h per 1 L of xenon gas), significantly more energy than that required for N2O production. Routine use of xenon for clinical anesthesia would only be economically possible with a closed-circuit system that recycles the rare gas.An ideal inhaled anesthetic should be safe, effective, and environmentally benign. This third characteristic has received insufficient consideration in part because of uncertainties on the environmental effects of gaseous anesthetics. Key criteria that will determine the global environmental impact of alternatives to halogenated anesthetics and N2O are their atmospheric lifetime, GWP, and ODP. These characteristics should be determined for existing anesthetics, and for any new anesthetic gases before widespread clinical use. Novel anesthetic gases should be adopted only if the clinical benefits outweigh any adverse environmental consequences. Although anesthetic gases are considered medically essential, an appreciable change is occurring in medical society. CFC propellants were previously considered medically essential for metered dose inhalers, but these have now been replaced with hydrofluoroalkane propellants. Current evidence may be insufficient for determining whether the contribution of waste anesthetics to the global climate change is significant. However, it is likely that anesthetic gas contributions, calculated in full carbon equivalents, will become an important part of efforts to limit the production of greenhouse and ozone-depleting gases. In summary, the use of N2O in medicine contributes to both global warming and ozone depletion. The use of halogenated anesthetics is a concern for producing global warming. In addition, the influence of halogenated anesthetics on ozone depletion will be of increasing relative importance, given the decreasing level of CFC usage globally. Furthermore, it should be recognized that other uses of anesthetic gases, including the use of N2O in dental offices and anesthetic gases in veterinary clinics and animal laboratories, may make significant additional contributions to adverse environmental change. It is essential to collect primary information on the quantities of N2O and halogenated volatile anesthetics manufactured or used, especially in consideration of serious international efforts to successfully reduce the emissions of ozone-depleting substances and greenhouse gases. We should develop tools for monitoring the use of ecotoxic gases, and initiate an international dialogue on these medically useful pollutants.
References

Fox JW, Fox EJ, Villanueva R . Letter: Stratospheric ozone destruction and halogenated anaesthetics. Lancet 1975;1:864
Brown AC, Canosa-Mas CE, Parr AD, Pierce JM, Wayne RP . Tropospheric lifetimes of halogenated anaesthetics. Nature 1989;341:635–7
Byrick R, Doyle DJ . Volatile anaesthetics and the atmosphere: an end to ‘scavenging'? Br J Anaesth 2001;86:595–6
Langbein T, Sonntag H, Trapp D, Hoffmann A, Malms W, Roth EP, Mors V, Zellner R . Volatile anaesthetics and the atmosphere: atmospheric lifetimes and atmospheric effects of halothane, enflurane, isoflurane, desflurane and sevoflurane. Br J Anaesth 1999;82:66–73
Logan M, Farmer JG . Anaesthesia and the ozone layer. Br J Anaesth 1989;63:645–7
McCulloch A . Volatile anaesthetics and the atmosphere: atmospheric lifetimes and atmospheric effects of halothane, enflurane, isoflurane, desflurane and sevoflurane. Br J Anaesth 2000;84:534–6
Pierce JMT, Linter SPK . Anesthetic agents and the ozone layer. Lancet 1989;333:1011–2
Rogers RC, Ross JAS . Anaesthetic agents and the ozone layer. Lancet 1989;333:1209–10
Sherman SJ, Cullen BF . Nitrous oxide and the greenhouse effect. Anesthesiology 1988;68:816–7

Biology of Lupus

Researchers think they may have discovered the mechanism that drives the body’s attack on its own cells and tissues in the autoimmune disease lupus.
Two new studies published in the journal Science Translational Medicine point to a cycle of cell death and chronic inflammation involving blood cells called neutrophils, versatile soldiers of the immune system that race to the site of infection to destroy invaders, as a key engine in the disease.
The discoveries come during a week when the FDA is expected to announce its decision on the biologic drug Benlysta, which could be the first drug approved to treat lupus in nearly 50 years.
According to the Lupus Foundation of America, lupus affects about 1.5 million Americans, many of them younger women.
The disease can affect many different parts of the body, including the skin, joints, lungs, heart, blood, and kidneys, which often makes it a challenge for doctors to diagnose.
One of the hallmarks of lupus is that patients make antibodies to their own DNA, called anti-nuclear antibodies, or ANAs. Blood tests for ANAs are sometimes helpful as an initial step in diagnosing lupus.
Researchers had long wondered how that happens since DNA was thought to be protected inside cells. Then, in 2004, a team of researchers discovered that neutrophils can die in an explosive way, shooting strings of cellular material studded with proteins and bits of nuclear DNA out like webs to entangle harmful bacteria, viruses, or fungi.
These neutrophil extracellular traps, or NETs, get slung outside the cell.
“They’re called NETs because they really look like a net, like a spider web,” says study researcher Michel Gilliet, MD, a dermatologist at University Hospital Lausanne, in Switzerland. The cells, he says, “shoot them out.”
In healthy people, once these NETs enter the liquid space between cells, the bits of nuclear DNA degrade quickly and probably don’t cause any problems, but Gilliet and his team found that patients with lupus have antimicrobial proteins called LL37 and HNP that appear to protect these bits of DNA from being broken down by the body.
Together, these proteins and DNA can trigger another type of immune cell, a kind of chemical factory called a plasmacytoid dendritic cell, which pumps out proteins that stoke the immune response.
One of those proteins, called type 1 interferon, is often present in high amounts in patients that have lupus, which has largely been another mystery of the disease.
Type 1 interferon, it turns out, triggers neutrophils to release more NETs, setting up an apparently self-perpetuating disease process.
“What this suggests is that there is a vicious cycle between the production of interferon, the way the neurtrophils die and the increase in the production of auto-antibodies, so this is a very, very efficient pathogenic loop that amplifies itself,” says study researcher Virginia Pascual, MD, an instructor of medicine at Baylor Institute of Immunology Research in Dallas.
Gilliet and his team are already testing the blood of lupus patients to see if one of these proteins may turn out to be a more specific marker for the disease, and thus useful in diagnosis.
That’s important because right now, doctors have to rely on a set of 11 criteria, which can overlap with many other diseases, to try to make a diagnosis.
“It is one of the most complex clinical diagnoses,” says Pascual, who is also a practicing pediatric rheumatologist.
“It might lead to better diagnostic tests, but we don’t know that yet,” Pascual says. Other experts say the discoveries will most certainly lead to new drug targets.
“It really provides a model for understanding why interferon is released, and that’s important because the more we understand why this very inflammatory cytokine is released, the more we can think about therapeutic options to block its production,” says Joseph E. Craft, MD, a rheumatologist and immunologist at Yale University in New Haven, Conn., who wrote a perspective article on the discoveries.

Lung power

Lung power is the number-one predictor of how long you’ll live. How well you breathe determines how long you’ll stay active and healthy.
The medical journal Chest did a 29-year follow up to the Buffalo Health Study, which followed over 1,100 people up to age 89. They found that the better your lungs work, the less likely you are to die of any cause. The correlation was even stronger for heart disease.
This makes me wonder about all those workout “gurus.” They keep telling you to do “cardio” which only wears down your heart and lungs. The studies prove that lungpower – not wearing down your heart with hours of aerobics – will keep you going.
Most doctors aren’t aware of this, either. They don’t bother to measure your lungpower during a doctor visit. Yet it’s easy to do, and I measure it at my clinic.
The best way to tell how powerful your lungs are is a measurement called VO2 max.
That’s because VO2 max measures the amount of oxygen your lungs can use while you’re exercising at your maximum capacity. And the more oxygen you can get to your body, the better your body works.
VO2 max is usually written in milliliters of volume per kilograms of body weight (ml/kg) because oxygen and energy needs are different depending on how big you are.
VO2 max typically declines with age.

The American Journal of Epidemiology looked at respondents from the famous Harvard Health study, which followed over 13,000 people for 15 years. They found that people live longer if they do vigorous exercises, but not if they only do light or moderate workouts.
And the risk of death kept getting lower and lower not for those who expended energy for the longest time, but who expended the most energy. In other words, intensity is the key to lowering the likelihood of death.

Neck pain

Exercises you can do to relieve your neck pain:
1. Side Neck Stretch with Resistance – Reach one hand over the opposite side of your head, and hold with your fingers just above the ear. Gently pull your head toward your raised arm until you feel a stretch in your neck muscles. To strengthen, push back with your head as you pull with your hand. Hold for 15-30 seconds and repeat 3 times.

2. Chin Tuck – Stand or lie down with both hands by your sides. With your head in a neutral position, push slowly forward and down, trying to press your chin into your chest. Hold the stretch for 15 seconds. If you’re standing, slowly lifting your head back to neutral will strengthen the muscles at the same time you stretch them.

3. Head Retraction – This is designed to improve the strength of muscles at the base of the neck. Glide your head straight back, lifting your chin, and hold for 15 seconds. Repeat 3-5 times. Lifting slowly will give those muscles more strength as well.

4. Neck Press with Resistance – For a little more rigorous exercise, clasp your fingers behind your head, elbows out to the sides. Slowly pull forward on your head, while resisting with your neck. Do this for 10 seconds at a time, and repeat up to three

Parkinson's disease

Ibuprofen was associated with a 38% lower risk of Parkinson's disease, but we didn't find any significant protective effects for other NSAIDs [nonsteroidal anti-inflammatory drugs], for example, aspirin or acetaminophen," lead study author Xiang Gao, MD, PhD, from the Channing Laboratory at the Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, said in an interview.
Their results were supported by those of a separate meta-analysis of other such trials included in this report. The findings were presented last year at the American Academy of Neurology 62nd Annual Meeting in Toronto, Ontario, Canada.
Neuroinflammation may contribute to the pathology of Parkinson's disease, the study authors note, and use of NSAIDs in general, and ibuprofen in particular, has previously been linked to reduced risk for the disease.
Dr. Gao and colleagues published a previous report in 2003 using data from NHS and HPFS showing a reduced risk for PD with NSAIDs but not aspirin (Arch Neurol. 2003;60:1059-1064). A subsequent article by Dr. Gao's Harvard School of Public Health colleagues, using data from the American Cancer Society's Cancer Prevention Study II Nutrition Cohort, showed that ibuprofen, but not other NSAIDs, was associated with a reduction in PD risk of about 35% (Ann Neurol. 2005;58:963-967).
In the present study, the study authors analyzed data on 136,197 men and women included in the prospective cohorts of the NHS and the HPFS who were free of PD and other diseases at baseline in 1998 for the NHS and 2000 for the HPFS. The use of NSAIDs was assessed by questionnaire. For this analysis, they included only new incident cases since their previous report.
During 6 years of follow-up, there were 291 incident cases of PD. The study authors report that users of ibuprofen had a significantly lower risk of developing PD than nonusers and, further, that there was a dose-response relationship between the number of tablets taken per week and PD risk (P for trend = .01).
Further adjustment for self-reported gout, use of other types of analgesics, sleep duration, bowel movement, and use of antidepressants "did not materially change these results," they write.
They also performed an additional meta-analysis combining 5 published prospective studies, Dr. Gao added. "We found similar results," he said. "The use of ibuprofen is associated with around 30% lower risk of PD in this meta-analysis."
The mechanism of an apparent advantage for ibuprofen is not clear, but ibuprofen can activate the PPARγ pathway, Dr. Gao noted. "That's a very important pathway for Parkinson's disease because it inhibits apoptosis, suppresses oxidative damage, and moderates inflammation in the brain," he said. "So we thought that is a potential mechanism why ibuprofen but not other NSAIDs are associated with a lower risk of Parkinson's disease but this is just a hypothesis."
If it's confirmed in a future clinical trial, ibuprofen could be a very useful and inexpensive new treatment for Parkinson's disease.
An important next step is to see whether use of ibuprofen can slow disease progression among PD patients, Dr. Gao said. "I hope in the future we'll have the opportunity to look at this potential effect of ibuprofen. If it's confirmed in a future clinical trial, ibuprofen could be a very useful and inexpensive new treatment for Parkinson's disease."
In an editorial accompanying the publication, James H. Bower, MD, MSc, from the Department of Neurology at Mayo Clinic, Rochester, Minnesota, and Beate Ritz, MD, PhD, from the Department of Epidemiology at the University of California, Los Angeles. School of Public Health, are cautious in their assessment of the relationship between ibuprofen use and PD.
Although these observational studies are well-conducted and analyzed and have "excellent" participation rates that would minimize selection bias, short follow-up of 6 years could miss PD cases that can take up to 20 years to manifest, they suggest.
In addition, they ask, "Could gastrointestinal symptoms cause a patient with preclinical PD to be less likely to take ibuprofen regularly, thus explaining the association? The 2-year lag they employed and the long-term 'ibuprofen' use sensitivity analysis would not suffice to refute this alternative hypothesis."
Still, they are intrigued by the possible biological explanation suggested by the study authors that ibuprofen may act as a ligand for PPARγ, an inhibitor of apoptosis and oxidative damage.
"Are we ready to tell our patients with PD that they should start taking ibuprofen? Absolutely not," they conclude. "Nor should we tell them to start smoking, drinking coffee, and eating liver pâté in hopes of developing gout."
However, "just as prior epidemiologic associations have inspired the development of clinical trials for transdermal nicotine (smoking), istradefylline (coffee), and inosine (uric acid), a clinical trial for ibuprofen, or perhaps a safer PPARγ antagonist, may be warranted."
The study was supported by a grant from the National Institutes of Health (NIH)/National Institute of Neurological Disorders and Stroke (NINDS) and in part by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences. Dr. Gao reports he has received research support from NIH/NINDS. Disclosures for other coauthors appear in the article. Dr. Bower reports research support from the NIH. Dr. Ritz reports receiving research support from the NIH, the US Department of Defense, Environmental Protection Agency, Health Resources and Services Administration, and the Foundation for Psychocultural Research.

Depression in Men

Tough economic times and profound societal change currently under way may mean rates of depression among men from Western nations are likely to increase, predict the authors of a commentary published in the March issue of the British Journal of Psychiatry.
It's well known that women are nearly twice as likely as men to develop major depressive disorder in their lifetime, but this difference may well change in the coming decades, argue Boadie W. Dunlop, MD, director of the Mood and Anxiety Disorders Program at Emory University School of Medicine in Atlanta, Georgia, and his Emory colleague and coauthor Tanja Mletzko, MA.
Western economies are undergoing a "profound restructuring," they point out, with traditional male jobs in manufacturing, construction, and other physical-labor jobs being outsourced to low- and middle-income nations or becoming obsolete due to technological advances.
The current economic downturn has hit men particularly hard, Dr. Dunlop and Ms. Mletzko note in their article. They point to research showing that roughly 75% of jobs lost in the United States since the beginning of the recession in 2007 were held by men, leading some to dub this recession the "Mancession."
And the odds that traditional male jobs will return in significant numbers with economic recovery are slim. "Western men, particularly those with low education, will face a difficult road in the 21st century," Dr. Dunlop and Ms. Mletzko write.
Aaron Rochlen, PhD, a psychologist and associate professor in counseling psychology at the University of Texas at Austin, said he wouldn't be surprised if the occupations traditionally held by a high percentage of men continue to be those most affected by layoffs.
"Of course, it's very difficult to 'link' this with depression, but it's not uncommon for men to struggle with a range of mental health consequences when faced with unexpected layoffs. Therefore, I think men need to prepare themselves and 'diversify' their work and personal portfolios,"said Dr. Rochlen .
In their commentary, Dr. Dunlop and Ms. Mletzko also note that women are increasingly becoming the primary household breadwinners, with 22% of wives earning more than their husbands in 2007 vs only 4% in 1970. Compared with women, men attach greater importance to their roles as providers and protectors of their families, and men’s failure to fulfill the role of breadwinner may contribute to depression and marital conflict.
Men who suddenly find themselves in the homemaker/childrearing role may need help adjusting, Dr. Dunlop said. "There could be increased rates of life dissatisfaction and substance abuse. Some men who do better in this role are the older siblings in a family who already have had the experience when younger of taking care of younger siblings, but the youngest men in the family, or last born, may have the hardest time with this," he noted.
To get the conversation going, Dr. Dunlop encourages clinicians to ask "simple, nonthreatening general questions, for example, How is work going? How is life at home? How are you guys getting by with how the economy is doing?"
In shifting economic times, said Dr. Rochlen, it is important that men consider how to "redefine themselves and their conceptualizations of masculinity.
"There's at least some evidence," he said, "that men are expanding the ways they think of themselves. And I'd say, in many ways, this is a good thing."
"For example," he said, "we are seeing more active and involved fathers, including men as primary care providers for their children. I do think the idea of male as 'provider' is expanding. And while there are some growing pains with this, I'd argue that it's needed and a positive thing in the long run." Dr. Rochlen's research interests include men’s gender role socialization, help-seeking behaviors, and the lives of men in nontraditional work/family roles.
Dr. Dunlop receives research support from the National Institutes of Health and various pharmaceutical companies, including AstraZeneca, Evotec, Forest, GlaxoSmithKline, Novartis, Pfizer, and Wyeth, and has served as a consultant to Imedex, MedAvante, and Pfizer. Dr. Rochlen has disclosed no relevant financial relationships.

The "silent killer"

An alarming one in three American adults has high blood pressure. Known medically as hypertension, many people don't even know they have it, because high blood pressure has no symptoms or warning signs. But when elevated blood pressure is accompanied by abnormal cholesterol and blood sugar levels, the damage to your arteries, kidneys, and heart accelerates exponentially. Fortunately, high blood pressure is easy to detect and treat. Sometimes people can keep blood pressure in a healthy range simply by making lifestyle changes, such as losing weight, increasing activity, and eating more healthfully. This report details those changes, including a Special Section that features numerous ways to cut excess salt from your diet — a policy strongly recommended by new federal guidelines. This report also includes tips on how to use a home blood pressure monitor, as well as advice on choosing a drug treatment strategy based your age and any other existing medical issues you may have.

Muscle strength

A study from the University of Pittsburgh followed nearly 2,300 people for five years. It found that low quadriceps muscle strength made you 51 percent more likely to die.
Two other studies found that leg strength offsets the risk of death for people with certain illnesses.
In the first study, the only two things that predicted death were age and quadriceps muscle strength.
The second found that for people who had congestive heart problems, the ones with the weakest quadriceps muscles were 13 times more likely to die within two years.
Your muscles are made up of different kinds of fibers that you use for different purposes.
Traditional cardio or aerobic exercise uses the smaller muscle fibers because they are more oxygen efficient, and don’t tire as easily as large muscle fibers.
If you continue to do moderate aerobic workouts, your body will ignore the larger fibers, leaving them weak.
One study even found that long-duration running makes your leg muscles deteriorate.
Take a look at this new study that followed endurance runners during the Trans-Europe Foot Race in 2009.
They had a mobile MRI machine scan these endurance athletes every day. When the race was over, instead of the runners’ muscles getting stronger, their leg muscles had degenerated.
They had lost 7 percent of their muscle mass.4
This is why doing aerobics and running for hours on end is not a good idea.
The solution to building stronger muscles that will keep you going for years to come is PACE program (PACE stands for Progressively Accelerating Cardiopulmonary Exertion ). With PACE, you challenge your cardiopulmonary peak a little bit at a time. Your body will then respond with added lung, heart and especially muscle strength while you rest.
It draws on those larger muscle fibers, which generate more power. By exercising the larger fibers, you get stronger muscles that can handle heavy-duty demands.
Strengthening your muscles this way is the most important thing you can do to keep your mobility and independence as you get older.
The first is a warm-up set that lasts from 4-6 minutes. The second is a ramp-up set that should last for 4 minutes. You exert yourself to the point where you could still talk, but you’re out of breath.
The third is for peak exertion. It should only last from 2-4 minutes, and you should be pumping hard enough by the end that you could only grunt a word or two if you had to.
Challenging your peak this way – a little bit each time, followed by periods of rest – is what causes your body to adapt by adding muscle mass and cardiopulmonary capacity.
In between sets, you want to recover so that your heart rate is about 30 beats per minute above your resting rate. It will take only 30 seconds for some, and longer for others. But don’t worry how long it takes at first. Your body will progress as you get more fit.
This is one of the things that makes PACE different. You don’t time your recovery in strict intervals. You recover fully, and then challenge yourself again during the next exertion period.

Ischemic Stroke

Ischemic Stroke
There is a rising risk for stroke among young people, including children and teens, warn analysts from the US Centers for Disease Control and Prevention (CDC).
Presenting new numbers here at the American Stroke Association International Stroke Conference, researchers showed more hospitalizations for acute ischemic stroke among young people age 5 to 44 years at the same time rates were declining among the middle-aged and elderly.
"Acute ischemic stroke is currently considered something that mostly happens to older people," Xin Tong, MPH, a health statistician with the CDC's Division for Heart Disease and Stroke Prevention in Atlanta, Georgia, told reporters attending a news conference. "But awareness of rising rates in the young is important or else tissue plasminogen activator and other important stroke treatment may be unnecessarily delayed in younger patients."
"I think this is a very important use of epidemiological data," Lee Schwamm, MD, director of telestroke and acute stroke services at Massachusetts General Hospital in Boston, told reporters. "These are important findings about the frequency of diagnosis in young and very young patients who have typically been understudied."
Largest Inpatient Database
Using the Nationwide Inpatient Sample, the analysts tracked trends in hospitalizations from 1994 to 2007. This is the largest all-payer inpatient care database in the United States.
Tong showed increasing stroke-related hospitalizations in young patients age 5 to 44 years (P for linear trends < .01).
Increasing Stroke Hospitalizations in Patients Age 5 to 44 Years
Ischemic Stroke Patients Increase (%)
Males age 5 - 14 (31%)
Females age 5 - 14 (36%)
Males age 15 - 34 (51%)
Females age 15 - 34 (17%)
Males age 35 - 44 (47%)
Females age 35 - 44 (36%)
Conversely, they found a decline in stroke hospitalizations for older and younger age groups. The decline in hospitalizations for babies and toddlers exceeded that of middle-aged and elderly patients (P for linear trends < .01).
Decreasing Stroke Hospitalizations by Age Group
Ischemic Stroke Patients Decrease (%)
Males age 0 - 4 (31%)
Females age 0 - 4 (51%)
Males age 45 - 64 (12%)
Females age 45 - 64 (13%)
Males age 65 and older (25%)
Females age 65 and older (28%)
"We cannot link anything in particular to the trend in younger patients, but I believe the role of obesity and hypertension will prompt a big discussion," Tong said. "Unfortunately, right now we can't speculate on the causes."
We cannot link anything in particular to the trend in younger patients, but I believe the role of obesity and hypertension will prompt a big discussion.
Dr. Schwamm pointed out the decline in hospitalizations for stroke among older people is consistent with other reports and suggests that this confirms improvements in primary and secondary prevention and controlling traditional risk factors.
"Among children, the story is more complicated," Dr. Schwamm said. "It seems unlikely the increases in hospitalizations are due to traditional risk factors — particularly in patients aged 5 to15. Although in people aged 15 to 35, it also seems unlikely," he noted.
Dr. Schwamm explained that although risk factors such as obesity, hypertension, and diabetes in a child are likely to contribute to cardiovascular disease and atherosclerosis later in life, they probably won't trigger events such as stroke right away.
Better Detection?
Dr. Schwamm suggests the increase in hospitalizations may be related to better detection rather than true incidence or rate of new strokes. He questions whether more widespread use of magnetic resonance imaging is identifying more cases.
"It may also be because it's more cost-effective or leads to greater reimbursement when young adults or children are evaluated in a hospital setting," he said. "This may reflect a shift from outpatient to inpatient care."
Still, he points out, percentage increases can be somewhat misleading. "Hospitalizations for stroke might be very rare but twice as common. Raw rates are different from percentage increases," he said. "The distribution of stroke over decades is important to keep in mind."
. "Stroke in children is rare, but it does exist," lead author Franz Babl, MD, from the Royal Children's Hospital and Murdoch Children's Research Institute in Melbourne, Australia, said in a news release.
"Stroke patients in our study had previously been generally healthy, unlike their adult counterparts. Because pediatric stroke is so rare, it's not the first thing we look for," Dr. Babl said. "Stroke symptoms in children are frequently attributed to other, more common problems, such as migraine, seizures, or encephalitis."
This study was funded by the Agency for Healthcare Research and Quality. The researchers have disclosed no relevant financial relationships.