Category: Asthma Studies

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Why Are Asthma Rates Soaring?

Why Are Asthma Rates Soaring? Researchers once blamed a cleaner world. Now they are not so sure

Research into varying causes of asthma may eventually lead to new ideas on how to manage the condition.

According to an article published in the Scientific American, Asthma rates have been surging around the globe over the past three decades, and for a long time researchers thought they had a good idea of what might be fueling the increase: the world we live in is just a little too clean. According to this notion—known as the hygiene hypothesis—exposure in early childhood to infectious agents programs the immune system to mount differing highly effective defenses against disease-causing viruses, bacteria and parasites. Better sanitary conditions deprive the immune system of this training, so that for reasons that are still unclear, the body pounces on harmless particles—such as dust and ragweed—as if they were deadly threats. The resulting allergic reaction leads to the classic signs of asthma: chronic inflammation or swelling of the airways and acute spasms of those passageways.

Or so the thinking went. Although a lot of data support the hygiene hypothesis for allergies, the same cannot be said for asthma. Contrary to expectations, asthma rates have skyrocketed in urban areas in the U.S. that are not particularly clean. Moreover, the big increase in asthma rates in developed countries did not kick off until the 1980s—well after general sanitary conditions in the richer parts of the world had improved. And some studies are beginning to show that far from protecting children from asthma, respiratory infections in early childhood may actually be a risk factor for it.

The collapse of the hygiene hypothesis as a general explanation for the startling jump in asthma rates has led physicians and scientists to a new realization: asthma is a much more complex condition than anyone had truly appreciated. Indeed, it may not be even be a single disease. Studies now suggest that only half of asthma cases have an allergic component.

The prevention and treatment implications are significant. If, for instance, it is true that allergy is not a fundamental cause of asthma in many people, then an alternative mix of treatments may be more effective for those individuals. To root out asthma’s cause (or causes) and properly treat the burgeoning number of people who are affected—300 million globally at last count—scientists will have to come to grips with the biology of its various forms.

Balancing Act
The hygiene hypothesis was first described in 1989 by David P. Strachan, a British epidemiologist who was studying hay fever. The more children in a family, he noticed, the lower the rates of hay fever and eczema, an allergic skin condition. Children in large families tend to swap colds and other infections more often than children with fewer siblings. Could it be that increased exposure to pathogens from their many siblings was protecting children from large families against allergies?

That same year Erika von Mutius, an epidemiologist at Munich University, was looking into the effect of air pollution on asthma in what was then East and West Germany. Children from dirtier East Germany, she was shocked to find, had dramatically less asthma than their West German counterparts living in cleaner, more modern circumstances. The East German children, unlike their Western counterparts, had spent more time in day care and thus had likely been exposed to many more viruses and bacteria. “That was astonishing,” she recalls, and led to “a major shift” in thinking.

These findings sparked intense debate among scientists. What is it about unhygienic living that might protect against asthma? One of the more popular explanations in the following decades entailed a balance between the immune cells that are involved in the body’s reaction to most viruses and bacteria and those that are involved in the reaction to most parasites and allergens. These two groups of cells produce chemicals that inhibit each other. Early-childhood exposure to bacteria and viruses would cause the infection-related cells to become active, keeping the allergy- and parasite-related cells in check. Without that interplay, the allergy-related cells would later become over­reactive, starting an allergic chain reaction that became chronic and ended in constricted airways, asthmatic spasms and labored breathing.

Inconvenient Facts
There was only one problem. As more data came in, they failed to tell the same story as the hygiene hypothesis. Children in Latin America with high rates of supposedly protective infection have even higher rates of asthma than children in western Europe. Inner-city children in Chicago and New York have quite high rates of asthma, despite unhygienic living. And the rates of asthma varied among countries with very similar histories of cleanliness—indicating that there was more to it than tidiness. For example, by 2004 Sweden’s asthma cases had increased to 10 percent, according to one international study, while the number of cases in the U.K. had soared to 20 percent.

In addition, research showed that the relation between asthma and allergy is not at all straightforward. Some cases of asthma are indeed triggered by allergies, although the consensus among researchers over the past decade is that the connection is probably not as clear-cut as the hygiene hypothesis would suggest. Still other layers of immune regulation must be involved. Maria Yazdanbakhsh, a parasitologist at Leiden University in the Netherlands, has shown that people infected with parasitic worms have very high levels of the allergy-related immune cells but very low rates of asthma, disproving a direct connection between allergy and asthma in these cases at least.

What is more, a landmark review of asthma studies in 1999 by Neil Pearce, now at the London School of Hygiene and Tropical Medicine, demonstrated that at least half of asthma cases in the general population have no connection to allergic reactions at all. These could never be explained by the hygiene hypothesis.

In fact, the same factors that the hygiene hypothesis suggests protect people from developing allergic asthma may cause them to develop nonallergic asthma. “We think that dirt protects against allergic asthma, as foretold by the hygiene hypothesis, but increases the risk of having a nonallergic form,” says Laura Rodrigues of the London School of Hygiene and Tropical Medicine, who studies asthma in Latin America. Pollutants in the air can irritate the airways and cause inflammation that leads to constricted breathing. Childhood colds, which the hygiene hypothesis suggested might help prevent development of asthma, can actually be a risk factor for asthma, especially if severe, says James E. Gern, a pediatrician who studies colds and asthma at the University of Wisconsin–Madison. “Early-life infections are an indicator of asthma risk rather than protective in any way,” he says.

Besides the hygiene hypothesis, what can explain the increase in asthma rates? Other suggested causes include a rise in sedentary lifestyle, which could affect lung strength, and the rise in obesity, which increases inflammation throughout the body. A reworking of the hygiene hypothesis that focuses on changes in the normal nondisease-causing bacteria that live inside and on the body (in the intestines or the airways or on the skin) has promise. Studies by von Mutius and others have shown that children who live on farms where cows or pigs are raised and where they drink raw milk almost never have asthma, allergic or otherwise. Presumably because the children drank unpasteurized milk and handled livestock, they have different strains of normal bacteria in their airways that are somehow more protective than those found in city kids.

But the short answer to the question of why asthma has increased, according to Pearce, von Mutius, Rodrigues and many others, is, “We don’t know.” Pearce, in particular, wonders whether modernization in general or westernization in particular may play a role. “There is something about westernization that means people’s immune systems function in a different way,” he says. “But we don’t know what the mechanism is.”

Getting at the true underlying cause of the climb will require better ways of distinguishing among various possible types of asthma. Major asthma research networks supported by the National Institutes of Health have begun recording the details of thousands of individuals’ symptoms and treatments. As the results are gathered and analyzed, researchers hope to identify clusters of asthma cases that have different causes and respond to different treatments. The hope is that “if you come in with these characteristics in asthma, we can anticipate what the prognosis is going to be and what the most effective treatment for you is going to be,” says William W. Busse of the University of Wisconsin School of Medicine and Public Health, who is part of one such network.
It will take years to understand fully whether microbial exposure, lifestyle changes or the obesity epidemic is more important in explaining the continuing increase in asthma rates. But one thing is clear: the hygiene hypothesis was just the beginning.

To subscribe to the Scientific American and for more information about the Asthma article visit http://www.scientificamerican.com/article.cfm?id=why-are-asthma-rates-soaring&page=3

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New Asthma Medicines Show Promise

New Asthma Medicines Show Promise Says Scientists

ANAHEIM, — In what they described as the opening of a new era in the development of potentially life-saving new drugs, scientists today reported discovery of a way to tone down an overactive gene involved in colon cancer and block a key protein involved in asthma attacks. Those targets long had ranked among hundreds of thousands that many scientists considered to be “undruggable,” meaning that efforts to reach them with conventional medicines were doomed to fail.

“These substances represent an entirely new class of potential drugs,” study leader Gregory Verdine, Ph.D., told the 241st National Meeting & Exposition of the American Chemical Society, being held here this week. “They herald a new era in the drug-discovery world.”

Verdine cited estimates that conventional medicines, most of which belong to a family termed “small molecules,” cannot have any effect on 80-90 percent of the proteins in the body known to be key players in disease. Throwing up their hands in frustration, scientists had even begun to term these prime targets for battling disease as “untouchables” and “undruggable.”

The new substances are not small molecules, but “stapled peptides,” named because they consist of protein fragments termed peptides outfitted with chemical braces or “staples.” The stapling gives peptides a stronger, more stable architecture and the ability to work in ways useful in fighting disease.

“Our new stapled peptides can overcome the shortcomings of drugs of the past and target proteins in the body that were once thought to be undruggable,” Verdine said. “They are a genuinely new frontier in medicine.”

In one advance, Verdine and colleagues at Harvard University described development of the first stapled peptides that target colon cancer and asthma attacks. The colon cancer stapled peptides inhibit activity of a protein called beta-catenin that, when present in a hyperactive form, causes cells to grow in an aggressive and uncontrolled way. That protein normally helps keep certain cells, including those lining the colon, in good health. But the abnormal protein has been directly linked with an increased risk of colon cancer and other types of cancer, including those of the skin, brain, and ovaries.

When added to human colon cancer cells growing in laboratory cultures, the stapled peptides reduced the activity of beta-catenin by 50 percent. In patients, that level of reduction could be sufficient to have a beneficial impact on the disease, Verdine suggested.

Verdine also reported development of the first stapled cytokines, which show promise for fighting asthma. Cytokines are hormone-like proteins secreted by cells of the immune system and other body systems that help orchestrate the exchange of signals between cells. The stapled cytokines moderate the activity of a cytokine called interleukin-13, which asthma patients produce in abnormally large amounts that contribute to asthma attacks.

Current asthma drugs, he noted, tend to treat the underlying symptoms of asthma, particularly inflammation. By contrast, stapled cytokines could treat the underlying causes of the disease. Verdine’s team is collaborating with a pharmaceutical firm on efforts to further develop the stapled peptides.

The American Chemical Society is a nonprofit organization chartered by the U.S. Congress. With more than 163,000 members, ACS is the world’s largest scientific society and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.M

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Asthma diagnosis breakthrough

Simple blood test to detect respiratory disease says news study

In a world-first study, Hunter researchers have found that respiratory diseases could soon be diagnosed through a simple blood test.

Currently, people suspected of suffering asthma or chronic obstructive pulmonary disease (COPD), are diagnosed by undertaking a series of clinical tests to assess their lung function and response to medication.

The study, to be published in the American Thoracic Society’s American Journal of Respiratory and Critical Care Medicine, has identified four novel blood-based biomarkers that can tell whether a person is suffering asthma, COPD or if they have a healthy lung function.

Lead researcher Professor Peter Gibson said that correct diagnosis of asthma or COPD was vital in managing and treating the conditions.

“Asthma and COPD have similar characteristics such as coughing and wheezing, but they are two very different conditions in terms of disease onset, frequency of symptoms and treatment.

“To date, some studies have attempted to identify biomarkers of COPD or asthma, but no one had investigated whether blood-based diagnosis was possible.”

Professor Peter Gibson and his team relied on the proteomics approach – an emerging field of science that focuses on the structure and functions of an organism’s proteins.

Using clinical trials they found that when used in combination, four blood-based biomarkers were able to discriminate between a clinical diagnosis of asthma, COPD and a control group.

Professor Gibson said that identifying the biomarker involved in the development of airway diseases may allow clinicians to diagnose the diseases in their earlier, more treatable stages.

“Since these biomarkers can be detected in blood, which is readily obtainable from patients, this panel of biomarkers has the potential to become an extremely useful addition to the clinical diagnosis and management of respiratory disease.

“Combined with well-defined clinical groups and advanced statistical analyses, we have shown that proteomics is a powerful tool for the identification of novel disease biomarkers. The study is a good example of how high-quality biological science can be translated effectively to a useful result for people with asthma and COPD.”

Professor Peter Gibson is a senior staff specialist at Hunter New England Local Health Network and a Conjoint Professor at the University of Newcastle.

The study was funded by the Australian government as part of its Cooperative Research Centre for Asthma and Airways program. The findings were published online ahead of the print edition of the American Thoracic Society’s American Journal of Respiratory and Critical Care Medicine.

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Asthma and Food Allergies

Asthma and Food Allergies: Children, Males and Blacks are at increased risk for Food Allergies says new NIH Study

A new study estimates that 2.5 percent of the United States population, or about 7.6 million Americans, have food allergies. Food allergy rates were found to be higher for children, non-Hispanic blacks, and males, according to the researchers. The odds of male black children having food allergies were 4.4 times higher than others in the general population.

The research, which was funded by the National Institutes of Health and appears in the Journal of Allergy and Clinical Immunology, is the first to use a nationally representative sample, as well as specific immunoglobulin E (IgE) or antibody levels to quantify allergic sensitization to common foods, including peanuts, milk, eggs, and shrimp. The hallmark of food allergy is production of IgE antibodies to a specific food protein. Once IgE antibody is made, further exposure to the food triggers an allergic response. IgE levels are often high in people with allergies.

“This study is very comprehensive in its scope. It is the first study to use specific blood serum levels and look at food allergies across the whole life spectrum, from young children aged 1 to 5, to adults 60 and older,” said Darryl Zeldin, M.D., acting clinical director at the NIH’s National Institute of Environmental Health Sciences (NIEHS) and senior author on the paper. “This research has helped us identify some high risk populations for food allergies.” In addition to the identification of race, ethnicity, gender, and age as risk factors for food allergies, the researchers also found an association between food allergy and severe asthma.

Food allergy rates were highest (4.2 percent) for children 1 to 5 years. The lowest rates (1.3 percent) were found in adults over the age of 60. The prevalence of peanut allergies in children aged 1 to 5 was 1.8 percent and in children aged 6 to19, it was 2.7 percent. In adults, the rate was 0.3 percent.

The odds of patients with asthma and food allergies experiencing a severe asthma attack were 6.9 times higher than those without clinically defined food allergies.

“This study provides further credence that food allergies may be contributing to severe asthma episodes, and suggests that people with a food allergy and asthma should closely monitor both conditions and be aware that they might be related,” said Andrew Liu, M.D., of National Jewish Health and the University of Colorado School of Medicine, Denver, and lead author on the paper.

The data used for the study comes from the National Health and Nutrition Examination Survey (NHANES) 2005-2006. NHANES is a large nationally representative survey conducted by the National Center for Health Statistics, a part of the Centers for Disease Control and Prevention.

Zeldin and Liu note more research is needed to understand why certain groups are at increased risk for food allergy. The authors comment in the paper that food allergies may be under-recognized in blacks, males, and children, because previous studies relied on self-reporting and not food-specific serum IgE levels.

“Having an accurate estimate of the prevalence of food allergies is helpful to public health policy makers, schools and day care facilities, and other care providers as they plan and allocate resources to recognize and treat food allergies,” said Linda Birnbaum, Ph.D., NIEHS director.

The National Institutes of Health (NIH) — The Nation’s Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases.

Reference: Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, Massing M, Cohn RD, Zeldin DC. National prevalence and risk factors for food allergy and relationship to asthma: Results from the National Health and Nutrition Examination Survey 2005-2006. J Allergy Clin Immunol. DOI: 10.1016/j.jaci.2010.07.026.

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Asthma and Stress

Asthma and Stress Related Says Survey

People who regularly feel stressed out by their jobs may have a higher risk of developing asthma than those with a more-relaxed work atmosphere, a new study suggests.

High on-the-job stress has been linked to a number of health consequences, including heightened risks of heart disease, diabetes and depression.

The new findings, published in the journal Allergy, are the first to show an association between work stress and later asthma risk, according to the researchers.

The investigators found that among more than 5,100 adults they followed for nearly a decade, those who reported high job stress at the outset were twice as likely as those with low levels of work stress to develop asthma.

The odds of any study participant being newly diagnosed with asthma were low, however. Among those with high job stress, 2.4 percent developed asthma during the study period, compared with 1.3 percent of men and women who reported little on-the-job stress.

The findings do not prove that work stress, itself, is the reason for the relatively higher asthma rate.

But the findings build on other evidence that chronic stress may contribute to asthma development in some people, write Dr. Adrian Loerbroks and colleagues at Heidelberg University in Germany.

Other studies, they note, have linked distressing life events and stress-related personality traits, for example, to heightened asthma risk.

For their study, Loerbroks and his colleagues used data from 5,114 adults, aged 40 to 65 years, who completed questionnaires on their health, lifestyle and jobs, and then were followed for 8.5 years.

Work stress was measured by a questionnaire that asked participants to rate how much strain they felt at work, and how often, at the end of the workday, they thought about work or felt exhausted or unable to cope with their job demands.

Overall, participants with high scores on the work-stress measure tended to have higher asthma rates at the outset. Moreover, among men and women who were asthma-free, those with high job stress were twice as likely to develop the lung condition over the follow-up period.

That higher risk was seen even with a number of other variables taken into account, including body weight, exercise habits, smoking, and family history of asthma.

It is not fully clear why work stress, itself, might affect asthma risk in some people.

Less-healthy lifestyle did not appear to account for the relationship, the researchers note, so it’s possible that there are direct effects of chronic stress on the hormonal and immune systems that contribute to asthma development — by, for example, making the airways more prone to inflammation in response to an environmental trigger.

The researchers point out, however, that even if work stress does raise asthma risk in some people, the absolute risk to any one worker would be small — given that only 2 percent of all study participants developed asthma over 8.5 years.

And from a public-health standpoint, the researchers write, curbing on-the-job stress would prevent only a small number of asthma cases.

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Inhaled Steroids May Increase Diabetes Risk

Inhaled Corticosteroids Increase Diabetes Mellitus Risk According to New Study published in the American Journal of Medicine

Inhaled corticosteroids are widely used in the treatment of asthma and chronic obstructive pulmonary disease (COPD). However, these drugs may be associated with diabetes development and progression. In a study published in the most recent issue of The American Journal of Medicine, researchers found that inhaled corticosteroids were associated with a 34% increase in the rate of diabetes onset and in the rate of diabetes progression. At the highest inhaled doses the risk increased by 64% in diabetes onset and 54% in diabetes progression.

Although inhaled corticosteroids are recommended only for patients with the most severe COPD, current practice has led to their use in less severe cases. In fact, over 70% of all patients with COPD are using inhaled corticosteroids. Since COPD and diabetes tend to increase with age, it is particularly important to assess any possible interaction between inhaled corticosteroid use and deterioration in glycemic control.

Investigators from McGill University and the Lady Davis Institute of the Jewish General Hospital, Montreal, Quebec, used data from over 380,000 patients treated for respiratory diseases identified in the Quebec health insurance databases. 30,167 patients developed diabetes during 5 ½ years of follow-up and another 2099 who progressed from oral hypoglycemic treatment to insulin.

Lead investigator Samy Suissa, PhD, Center for Clinical Epidemiology, Lady Davis Research Institute, Jewish General Hospital, Montreal, Quebec, Canada, and the Department of Epidemiology and Biostatistics and Department of Medicine, McGill University, observed that “high doses of inhaled corticosteroids commonly used in patients with COPD are associated with an increase in the risk of requiring treatment for diabetes and of having to intensify therapy to include insulin. Therefore, patients instituting therapy with high doses of inhaled corticosteroids should be assessed for possible hyperglycemia and treatment with high doses of inhaled corticosteroids limited to situations where the benefit is clear.”

This large cohort allowed the accurate estimation of relative risk. There have been other major randomized trials that have not shown a significant association of inhaled corticosteroids and diabetes onset. In this study, the authors found an incidence of diabetes onset of 14.2 per 1000 patients per year. At that rate, previous studies may not have had sufficient data to detect the excess risk. “These are not insubstantial numbers,” commented Dr. Suissa. “Over a large population the absolute numbers of affected people are significant.”

The article is “Inhaled Corticosteroids and the Risks of Diabetes Onset and Progression” by Samy Suissa, PhD, Abbas Kezouh, PhD, Pierre Ernst, MD, MSc. It appears in The American Journal of Medicine, Volume 123, Issue 11 (November 2010) published by Elsevier.

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Asthma Study Shows How Flu Infections May Prevent Asthma

Activating the right immune cells in infants could lead to new vaccine strategies

In a paper that suggests a new strategy to prevent asthma, scientists at Children’s Hospital Boston and their colleagues report that the influenza virus infection in young mice protected the mice as adults against the development of allergic asthma. The same protective effect was achieved by treating young mice with compound isolated from the bacterium Helicobacter pylori (H. pylori), a bacterium that colonizes the stomach and is best known for causing ulcers and increasing the risk of gastric cancers.

The findings, published online December 13 in the Journal of Clinical Investigation, provide a potential immunological mechanism in support of the “hygiene hypothesis,” an idea that attributes the increasing rate of asthma and allergies to the successful reduction of childhood infections with vaccines and antibiotics. The hygiene hypothesis is also supported by epidemiological studies associating certain childhood infections, such as respiratory viral infections or gastrointestinal infection with H. pylori, with a lower risk of developing asthma.

“Some infections appear to result in important protective effects against asthma,” says Dale Umetsu, MD, Ph.D., of Children’s Division of Immunology, a senior author of the paper, and Professor of Pediatrics at Harvard Medical School. “But we certainly don’t want to give people dangerous infections to prevent asthma. So if we can understand how infections prevent asthma, we may be able to replicate the good parts and avoid the bad parts of infection and develop new treatments for children to prevent asthma.”

In mice, influenza A infection appeared to confer its benefits by expanding an immature cell type in the lung known as natural killer T (NKT) cells, part of the innate immune system. The same beneficial NKT cells in the lung could be expanded by several NKT-stimulating molecules known as glycolipids, including one isolated from H. pylori.

The active infectious agents protected against asthma only if the mice were exposed when very young (2 weeks). “Flu infection in adult mice makes the allergic reaction worse,” says Ya–Jen Chang, Ph.D., first author and a postdoctoral fellow in Umetsu’s lab.

Previous studies examining the hygiene hypothesis have focused on the adaptive immune system, which features immune cells that are slow to respond but are able to develop long-term memory, such as those stimulated by each year’s flu vaccine or those involved in seasonal allergies.

In contrast, the new paper examines the innate immune system, which responds rapidly to infections and shapes adaptive immune responses. This study specifically focuses on NKT cells, one of the first responders to many infections. Previous work by Umetsu’s team implicated NKT cells as a cause of asthma. http://www.childrenshospital.org/newsroom/Site1339/mainpageS1339P1sublevel194.html. In contrast, the latest study reports on a new subset of inhibitory NKT cells that seem to prevent allergic reactions in the airways — if stimulated at the right time by the right infectious agents or the right glycolipid.

“In the absence of influenza A or the H. pylori compound, we see an expansion of NKT cells that cause asthma and allergies,” says Umetsu. “We’re now trying to understand how to specifically activate the inhibitory subset of NKT cells. Treatments focused on specifically expanding this inhibitory subset of cells in children might prevent the development of asthma.”

The researchers want to explore the therapeutic applications of the H. pylori glycolipid compound, synthesized by British lipid biochemist Petr Illarionov, Ph.D. “It might be a good candidate for an asthma vaccine,” says Chang. Umetsu wants to test the next generation of glycolipid compounds, and to illuminate their specific mechanism of action, with a more detailed characterization of the inhibitory NKT cells.

Funding: US National Institutes of Health, including stimulus funding from the 2009 Recovery Act; Bunning Food Allergy Project; and Ministry of Education, Culture, Sports, Science, and Technology of Japan.

Disclosure: Children’s Hospital Boston has filed for a provisional patent on the glycolipid compound formula to treat or prevent inflammatory disease.

Children’s Hospital Boston is home to the world’s largest research enterprise based at a pediatric medical center, where its discoveries have benefited both children and adults since 1869. More than 1,100 scientists, including nine members of the National Academy of Sciences, 12 members of the Institute of Medicine and 13 members of the Howard Hughes Medical Institute comprise Children’s research community. Founded as a 20-bed hospital for children, Children’s Hospital Boston today is a 392-bed comprehensive center for pediatric and adolescent health care grounded in the values of excellence in patient care and sensitivity to the complex needs and diversity of children and families. Children’s also is the primary pediatric teaching affiliate of Harvard Medical School. For more information about the hospital and its research visit: www.childrenshospital.org/newsroom.

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Asthma study: Spiriva as good as Serevent

Asthma study: Spiriva as good as Serevent Says Press Reports

According to press reports published in the USATODAY, researchers say they’ve found a possible new treatment for adults with hard-to-control asthma. Their discovery, however, came at a price.

Scientists of a U.S. government-funded asthma study had to spend nearly $1 million of taxpayers’ money after British drugmaker GlaxoSmithKline PLC declined to donate its asthma drug and look-alike dummy medicine for the study, which compared two other treatments.

Editors of the New England Journal of Medicine, which published the study, chastised Glaxo, saying its actions made the research harder and more expensive to do. Drug companies aren’t required to supply their medicines for study, but they often do.

“In the end, the study results provided the truth” — the drug, Spiriva, was as good as Glaxo’s Serevent, they wrote. The study was published online Sunday to coincide with a presentation at a medical meeting in Barcelona, Spain.

About 300 million people worldwide suffer from asthma. In the U.S., 22 million Americans have asthma, which kills about 4,000 a year. For people who can’t control their asthma with inhaled steroid medicine, current guidelines call for doubling the dose or adding a different drug that relaxes the muscles to help patients breathe.

Researchers tested three inhaled treatments: doubling the steroid dose, adding Glaxo’s Serevent or adding Boehringer Ingelheim’s Spiriva, which is approved for emphysema and other chronic lung conditions, but not asthma.

The study involved 210 people whose asthma was not well controlled. They took each drug for 14 weeks with two-week breaks in between treatment.

Researchers found Spiriva worked better than a double steroid dose and was as effective as Serevent. When the study first began, patients on average had 77 asthma-free days a year — days in which they had no symptoms and did not have to use their rescue inhaler.

Doubling the steroid medicine gave patients an extra 19 asthma-free days; taking Spiriva gave them an additional 48 days with no symptoms, and taking Serevent gave them an extra 51 days.

Spiriva is a promising alternative asthma treatment and some doctors are already using it in people who don’t respond to steroid medicine, but more study on drug safety is needed, Dr. Lewis Smith of Northwestern University wrote in an accompanying editorial.

Two years ago, safety concerns were raised with Spiriva inhalers. But the Food and Drug Administration earlier this year said recent data do not show a connection between the inhaler and previously reported risks of stroke, heart attack and death.

The $5.3 million study was funded by the National Heart, Lung and Blood Institute. Teva Pharmaceutical Industries supplied the inhaled steroid medicine and Boehringer Ingelheim provided Spiriva. Both companies also donated matching placebos. Researchers bought Glaxo’s Serevent.

Glaxo declined to participate because Spiriva is not approved for treating asthma. The company also “lacked adequate information in this case to understand what the impact would be on patients in the trial,” said company spokeswoman Mary Anne Rhyne.

The study’s leader, Dr. Stephen Peters of Wake Forest University Baptist Medical Center in North Carolina, said that since his team did not have access to Glaxo’s drug, they bought it from a third-party supplier and hired another company to make the placebo — at a cost of $900,000.

Peters said it’s harder to get drug companies to donate their medicine for research compared with a decade ago.

“Now more drug companies are more likely to ponder whether a trial could help them in the marketplace” and decline to provide their products for studies, Peter said.

Peters has received lecture fees from Teva. Several other researchers on the team reported ties with Glaxo and other drug companies.