Nine people died and 8,500 more recently were hospitalized with severe asthma in Australia in a single week of thunderstorms. Said storms occurred during the peak of rye grass pollen season. The rain caused the pollen to become saturated, and the electrical discharges caused fragmentation of the pollen grains into tiny particles. More typically, pollen grains are filtered out by the nose/sinus area, leading to hay fever symptoms. But tiny fragments created by the storms were able to slip right through the upper airways, landing in the lungs, precipitating sudden, severe allergic asthma. In addition, many of the victims had no prior history of asthma, just allergic hay fever.
Dear Dr. K: Dear Dr. K.: My husband and I both have allergies and we are both triathletes. When we exercise my husband’s nasal congestion always improves, while mine seems to get worse. What’s going on?
The answer to your question is statistics.
Your husband is on the good side of statistics and you are on the bad side. What I mean is that in the majority of people with allergies exercise helps open the nasal passages. It does this by two main mechanisms: neurologic and chemical. In most persons, exercise increases preferentially the sympathetic nerves that control blood vessel size, constricting these blood vessels, and thus, improving nasal patency (being open or expanded).
Exercise also releases “adrenal-like” chemicals that exert the same effect on the nasal blood vessels.
In a small number of people, exercise preferentially stimulates the parasympathetic nerves, which dilate nasal blood vessels and cause congestion. This phenomenon is called exercise-induced rhinitis. It is similar to a related phenomenon in asthmatics called exercise-induced-bronchospasm.
One predisposing factor to exercise-induced-rhinitis is deviation of the nasal septum. Apparently, people with septal deviation have a chronic disparity in air flow through the two nostrils. For some reason, this makes the parasympathetic nerves more sensitive, and thus their adverse response to exercise.
An amazing 96 percent of patients with lung conditions attending a “Singing for Breathing” program in the United Kingdom (UK) report improvement.
Research done by UK scientists has shown that singing therapy can improve lung function in a variety of conditions including asthma, COPD and cystic fibrosis.
The program consists of six weeks of twice-weekly voice lessons, followed by once-a-week maintenance classes. It is sponsored by the British Lung Foundation and is held at 55 clinics across Great Britain.
The British scientists feel that singing improves lung function in a variety of ways:
First of all, it strengthens the muscles of respiration: the diaphragm, the intercostal muscles and the chest wall muscles. Secondly, it helps dilate the airways by substantial exhalation and greater air movement. Thirdly, training the laryngeal muscles helps prevent laryngospasm that often occurs in asthmatics and COPD patients. Fourthly, the positive effects associated with singing help both airway patency (openness) and chest wall muscle function. Finally, participants were trained to try singing a sustained note as a mechanism to stop a coughing/wheezing attack prior to reaching for a rescue inhaler. More often than not, the sustained note was therapeutic.
Asthma worse? Being female and a list of other factors might be the cause — based on Columbia University’s recently published data on research about women and asthma. They found that a number of factors led to greater difficulty with asthma including: hormones, obesity, stress, depression and PTSD (Post Traumatic Stress Disorder).
The researchers note that hormone levels (especially estrogen) impact the Th-2/ Th-1 balance that has been previously discussed in this newsletter. High estrogen leads to Th-2 predominance, which promotes allergy. Increased estrogen can come from the normal wax and wane of the menstrual cycle, pregnancy, hormone replacement or oral contraceptives.
Obesity is also pro-inflammatory via the Th-2 mechanism. Columbia found that as little as a 15pound weight loss by obese women asthmatics resulted in 20 percent improvement in their asthma.
The issue of stress and depression is a double bind. In general, women experience depression more frequently than men. The asthmatic condition itself can cause life stress and depression, but the opposite is also true: stress and depression cause worsening of asthma. The Columbia group found that upwards of 15 percent of women with poorly controlled asthma had unresolved issues from childhood sexual trauma. They consider this a form of PTSD.
Interestingly, they found strong correlation of PTSD and worsening asthma in military women who had service-related traumas. Stress, depression and PTSD all lead to a number of stress hormone changes by way of the adrenal glands, along with production of inflammatory molecules such as interleukins, substance-P, and natural killer-cell function.
African-American women seemed more prone to depression and PTSD than their Caucasian, Asian and Hispanic sisters. In yet another fallout from racial discrimination, Columbia found a strong correlation between African-American asthmatics who had experienced significant racial bias versus women who had not, in terms of severity of asthma and frequency of exacerbation.
The researchers’ take-home message is that both patients and doctors should be aware of the interplay and dynamic force of stress/depression and asthma.
Mayo Clinic researchers have found that having asthma increases the risk for developing shingles almost two-fold. This is true both in children and adults.
For quite some time it has been known that calcium plays a major role in muscle contraction. A number of calcium-altering medicines are used to help heart problems and hypertension by relaxing the smooth muscle found in the heart and arteries. Now there may be an application to asthma.
Smooth muscle is also found in our bronchial tubes; constriction of this muscle that occurs through proteins called calcium-sensing receptors causes asthma.
A recent British study examined the use of a class of drugs used to treat osteoporosis called calcilytics. These drugs were administered to asthmatic mice with dramatic results: the drugs blocked the action of calcium-sensing receptors and thus, prevented the smooth muscle constriction.
The scientists are now starting human studies. This research is very compelling as it offers a mechanism to control asthma that has never before been available.
A recent Canadian study on obese asthmatics found marked improvement in airway function associated with weight loss. The degree of improvement seemed to track with the amount of weight shed, but notable improvement was found with as little as an eight-pound loss.
A “pay attention” article was recently published in the Journal of Allergy and Clinical Immunology cautioning adults with asthma to be more aware that aspirin may aggravate their condition.
The authors pointed out that while some adult asthmatics with Aspirin Exacerbated Respiratory Disease (AERD) are cognizant of the negative effects aspirin can have on their health, most are not.
Studies have shown that AERD is more likely to occur if adult asthmatics also have chronic sinus problems and/or nasal polyps. Overall, seven percent of asthmatics have AERD, but 15 percent with severe asthma have it.
Unfortunately there is no simple blood or skin test to diagnose Aspirin Exacerbated Respiratory Disease. Right now, only two ways are available for these patients to become aware of the possibility: 1.) Monitoring their breathing symptoms after ingesting aspirin or other NSAIDS (non-steroid anti-inflammatories). 2.) Doing an aspirin challenge in a doctor’s office by measuring baseline pulmonary function tests and then incrementally increasing doses of aspirin, while repeating the pulmonary tests.
Research on a very exciting new medicine for asthma was featured several weeks ago in The New England Journal of Medicine. This drug — the first ever to work on both the acute and late phases of allergic response — is an enzyme that inactivates GATA-3 messenger RNA, and is being called SB010.
GATA-3 is a signal that favors T-helper cells to follow the TH-2 pathway, which promotes allergy. TH-1 eliminates allergy. Or, to use a Star Wars analogy: TH-1 is the Force, while TH-2 is the Dark Side of the Force.
All allergic reactions, including asthma, are bimodal; that is, after exposure to the allergen there is an immediate response occurring right away and lasting minutes to a few hours, but also a delayed response that builds gradually and lasts for many days. This late phase accounts for the chronic nature of allergies and asthma.
SB010 blocks both responses. In research done at Hannover Medical Center in Germany, patients received SB010 once a day via nebulizer. The results were immediate and dramatic, with most asthmatics experiencing dramatic reduction in their symptoms — even if they were purposely exposed to their causative allergen, such as cat dander.
Also, the medication was very well tolerated with minimal or no side effects. Other medical centers are also completing research on SB010. Hopefully, this will lead to it soon becoming clinically available.
Tough news reported in research results recently published in The Journal of the American Medical Association that persons with asthma were twice as likely to develop sleep apnea as non-asthmatics.
The study was done at the University of Wisconsin and involved thousands of people over a 25-year period. Sleep studies were done every four years in order to observe the frequency with which sleep apnea developed.
The striking outcome was compelling because asthma itself is a frequent cause of disturbed sleep. Hence, if the asthma gets blamed as the sole cause for nighttime wakening, the sleep apnea will go undetected and therefore, untreated.
The Wisconsin researchers suggested greater awareness of this possibility in asthmatics, their families and their doctors. If family members report snoring or apneic episodes, or if the patient has daytime somnolence, a sleep study should be considered.