Australian the healthiest contry by 2020

The federal government has responded to the National Preventative Taskforce recommendations set out in the document Australia the healthiest country by 2020.

Lots of noise has been made about the tobacco related recommendations some of which the government has agreed to. These are significant tax hikes (as previously blogged about), plain packaging for cigarettes and significant investment in social marketing such as the National Quit Campaign.

The task force also made recommendations on prevention, alcohol, obesity and physical activity. In light of Andrew recent post about bariatric surgery I thought it would be interesting to see what commitment the government has made to fighting the obesity epidemic.

Unfortunately, the government has taken no new action in this area with Nicola Roxon stating there is still no clear evidence of what fights obesity. The Obesity Policy Coalition was very disappointed there were no regulations implemented on junk food marketing to children and also no extra taxes placed on unhealthy foods.

Evidence based policy making is vital but if we know high calorie diets and low levels of physical activity are significant contributors to obesity why are there no new policies aimed at these two areas. Sometimes something is better than nothing.

We know the history with tobacco control with he government being inactive on addressing this problem until 30 years ago. Since then the epidemiological evidence has proven there has been a significant drop in the prevalence of tobacco.

Lets hope mistakes of the past do not come back to haunt us again due to inaction regarding obesity.

Jessica

Does lung cancer cause bad breath?

An interesting Oral Presentation given to us at the TSANZ & ANZSRS Annual Scientific Meeting held in Brisbane in March was a presentation called “Exhaled Breath Analysis Characterises Lung Cancer”. This was a study carried out by the Prince Charles Hospital in Brisbane and the University of Queensland.

They used an electronic nose (Cyranose 320) to measure volatile organic compounds (VOCs) in the exhaled breath of three groups of subjects; those who had lung cancer, smokers with a history of >30 pack years, and healthy non-smokers.

Their aim was to identify an exhaled breath VOC profile (‘smellprint’) in lung cancer subjects that discriminates from healthy non-smokers and smokers, aged 60-74 years.

Subjects performed two exhaled vital capacities (10 minutes apart) into a Tedlar sample bag after breathing tidally through an inspiratory port VOC filter for 5 minutes. The samples were analysed using a Cyranose 320.

Their results were that smellprints from lung cancer (n=8) and smoking subjects (n=13) were separated from normal subjects (n=21) with cross validated accuracy (CVV) of 75.9% (p = 0.006) and 97.1% (p <>

They concluded that VOC profiling of exhaled breath using an eNose distinguished healthy subjects from lung cancer and smoking subjects, and between the lung cancer and smoker group, and therefore that the eNose has the potential to be a diagnostic and screening tool for lung cancer.

Previous studies to support this idea have included Gordon (1985) who identified in the exhaled air of lung cancer patients several volatile organic compounds that appeared to be associated with the disease.

Phillips (2003) found that compared to healthy volunteers, patients with primary lung cancer had abnormal breath test findings that were consistent with the accelerated catabolism of alkanes and monomethylated alkanes. He found that a predictive model employing nine of these VOCs exhibited sufficient sensitivity and specificity to be considered as a screen for lung cancer in a high-risk population such as adult smokers.

Machado (2005) concluded that the exhaled breath of patients with lung cancer has distinct characteristics that can be identified with an electronic nose, and that his results provided feasibility to the concept of using the electronic nose for managing and detecting lung cancer.

Testing with an eNose would be a novel, simple, and non-invasive technique to diagnose lung cancer. I look forward to the results of further research.

Heather

Eosinophilic bronchitis, asthma and bronchoprovocation

Many people are referred to our practice with longstanding symptoms of cough. While our management of such patients is tailored to the individual, and depends very much on the presenting history (characteristics of the cough, sputum production, smoking history, dangerous exposures etc) there are some investigations which we perform very frequently. Of course, spirometry – that first and most basic of investigations – is performed almost universally. It helps pick up people with uncontrolled asthma or chronic obstructive pulmonary disease almost before they come in the door.

Many asthmatic patients will, however, have entirely normal spirometry. In such patients, the diagnosis of asthma will often be made with bronchoprovocation studies.

We perform mannitol bronchoprovocation studies frequently in our lab. They are an important part of the evaluation of many patients with chronic cough. For this reason I have been reading with interest the results of a very small study published in Respirology journal in April; a study which looks at the differences between asthma and eosinophilic bronchitis with regards to indirect bronchoprovocation challenges, such as mannitol bronchoprovocation.

First, a brief word about these two diagnoses. I explain to all of our patients with newly diagnosed asthma that there are two important aspects to the pathology of asthma in the airways which need to be understood, and which make sense of why we use the medications we do. Those two are:
- airway inflammation
- airway hyperresponsiveness.

The former is usually mediated by allergic processes in kids, but is more of a mixed bag in adults. ‘Mast cells’ ( a type of white blood cell particularly involved in some allergic reactions) infiltrate the airway lining and muscle. Inhaled steroids help suppress this process. The latter process involves contraction of airway muscles, often experienced as breathlessness and chest tightness. Medications such as salbutamol, an asthma ‘reliever’ help control this process (as do formoterol and salmeterol).

This Journal paper reminds us that eosinophilic bronchitis, estimated to be the cause of cough in up to 15% of chronic cough seen in chest clinics, sees a disconnect between the two processes. That is, mast cell-mediated inflammation occurs in the airways (with lots of ‘eosinophils’ in an induced sputum or bronchoscopy sample) without airway hyperresponsiveness. This is not a new idea. The definition of EB is essentially that there is eosinophilic airway inflammation without abnormal airflow on spirometry and without a drop in lung function on bronchprovocation testing with methacholine. However, airway inflammation in asthma has been demonstrated to be better associated with hyperresponsiveness to mannitol than to methacholine. Likewise, some asthmatics will react to indirect challenges and not to direct challenges. This study was arranged to further test the hypothesis that EB really does exist, I suppose, and to really prove that patients with EB do not have airway hyperresponsiveness to indirect challenges.

This hypothesis was tested in a small number of patients. Patients with diagnoses of EB (all of whom had had previous mannitol bronchoprovocation) and patients with a diagnosis of asthma were compared with each other and with healthy controls. An induced sputum sample was obtained on the day that tests were performed to help confirm the diagnoses. Bronchoprovocation studies were then performed with either AMP or mannitol (both ‘indirect’ challenges that lead to airway hyperresponsiveness in asthma via secondary pathways ) or both.

Now the study was small. There were only 11 healthy and 14 asthmatic patients, with 8 patients suffering from eosinophilic bronchitis. Asthmatic and EB patients had similar levels of eosinophils in their sputum, where healthy controls had none. Asthmatic patients generally reacted to the indirect challenge (7 of 10 asthmatic patients given mannitol had positive responses). None of the healthy controls or EB patients reacted to the mannitol (or to the AMP).

This paper is a good reminder of the diagnosis of eosinophilic bronchitis. I like the idea they put forward that this is a process where the inflammation occurs only in the airway mucosal lining and not in the smooth muscle. I’d like to know for certain, however, that simple treatments like inhaled steroids help. In my experience that’s not necessarily the case, although the disease is supposed to be very responsive to inhaled steroids. The problem at that point is that in asthma we have useful tools such as spirometry and bronchoprovocation studies for objectively monitoring our treatment regimes. In EB, when those tests are normal to begin with, it’s difficult to know how to objectively evaluate treatment effect when symptoms don't settle.

Andrew

World No Tobacco Day

Jessica and I put together the following for a local newsletter on 'World No Tobacco Day':

The World No Tobacco Day, May 31st 2010 theme this year particularly focuses on women and tobacco use. In Australian women, lung cancer passed breast cancer as the most common cause of cancer deaths - back in 2005. Lung cancer accounts for the death of more than 50 Australian women each week.

Locally in the Southern Grampians Shire, across both genders tobacco accounts for 13.69% of deaths, compared to 1.19% for road toll and 2.38% for alcohol related deaths. Of this lung cancer accounts for 30% of the tobacco related deaths. Risk of lung cancer related to cigarette smoking increases for every cigarette smoked. Risk of lung cancer related to cigarette smoking does not reduce, let alone return to normal, after cessation of smoking; it simply stops increasing. To reduce lung cancer risk, early cessation of smoking is imperative.

Chronic illness due to smoking related conditions such as chronic obstructive pulmonary disease (COPD) is also prevalent, greatly reducing the quality of life of many people.

COPD should be considered in any smoker or ex-smoker over the age of 35 with breathlessness, chronic cough and / or sputum production. A spirometry assessment should be performed in such patients to pursue this diagnosis. Spirometry is highly recommended in any smoker over the age of 45 regardless of clinical symptoms, as COPD is often asymptomatic in its early stages. Cessation of cigarette smoking does not lead to reversal of damage in COPD; it only stops getting worse. In COPD, early cessation of cigarette smoking is imperative

Cessation of smoking is the first, and most important, step in treatment of COPD.

For help trying to quit please see your local GP, call the quit line on 137848 or enroll in a local quit course.

Andrew

Cardiopulmonary exercise testing

A big thank you to Julian above for agreeing to appear in our blog.
Most lung function tests assess lung function using maximum expiratory/inspiratory manoeuvres at rest, but, although providing very useful information, the procedures are unnatural. More often than not, patients complain of dyspnoea during exercise. A number of tests to assess the patient’s performance while exercising have been developed. There are three main reasons for performing an exercise test:
• to identify a cardiac or respiratory cause for exercise limitation
• to quantify functional disability
• to assess the response to treatment
Exercise tests can fall into two categories:
• Simple tests of exercise capacity such as the six-minute walk test or shuttle test
• Sophisticated, progressive multistage exercise tests, usually to maximal effort, during which a wide variety of cardiac and pulmonary variables are measured continuously to assess the pattern of cardio respiratory limitation on exercise
When ordering an exercise test, it is essential to have a clearly formulated clinical question you wish the test to answer, and order the correct test for that clinical indication or question. The results of progressive exercise tests are often not clear-cut and so must always be interpreted within the patient’s clinical situation.
Two methods of varying exercise workload are commonly used; the treadmill and the cycle ergometer. Each device has advantages and disadvantages. In our lab we have chosen to use the cycle ergometer. One of the chief advantages of the cycle ergometer is that the workload is independent of the weight of the patient and VO2 (target oxygen uptake) can be reasonably estimated if the pedaling speed and resistance are carefully measured and better stability of the patient for blood pressure and oxygen saturation monitoring. Patients of different weight, walking on a treadmill at the same speed and slope perform different work and different walking patterns, or stride length, may also affect the actual amount of work being done. Patients who grip the handrails of the treadmill may use their arms to reduce the amount of work being performed. For these reasons estimating VO2 from a patient’s weight and the speed and slope of the treadmill may produce erroneous results. VO2max (maximal oxygen uptake) has been shown to be measured slightly higher (approximately 7% - 10%) on a treadmill compared to a cycle ergometer.
In the exercise test we perform the patient is asked to carry out progressively increasing workloads of exercise while their respiration is monitored breath by breath, their cardiovascular responses are also observed by recording their heart rate and ECG continuously during the exercise period and into recovery.
The exercise is a test of the three components involved in heavy physical exercise:
1. respiration
2. the cardiovascular system (both the heart and peripheral circulation)
3. the condition of the peripheral musculature.
4. It is important to note that the results of exercise testing may indicate the organ system limiting exercise capacity, but will not provide a diagnosis. In many patients there may be a combination of factors (such as skeletal muscle deconditioning in patients with advanced cardiac disease).
We calculate the following variables for each breath and provide a running average over a set number of breaths for tidal volume, oxygen consumption and carbon dioxide production as well as continuously monitoring heart rate and oxygen saturation. The responses of these variables are usually compared to workload and compared with a predicted range of normal values.
In health, exercise tolerance is limited by the ability of the cardiovascular system to supply oxygen to the musculature. When the ability to supply oxygen to the muscles is exceeded, any additional work is generated by anaerobic metabolism, producing lactic acid. In order to compensate for this metabolic acidosis, ventilation increases and carbon dioxide is eliminated at a greater rate than would be expected with respect to oxygen uptake referred to as anaerobic threshold. Anaerobic exercise is difficult to maintain causing the person to stop exercising due to fatigue. In health this usually occurs at 60-70% of the VO2max.
In order to interpret a study appropriately it is important to look at the responses throughout exercise as well as the maximal values achieved. They should be interpreted in the context of the clinical presentation. It is also important to bear in mind the reason for test cessation – was this really a maximum exercise test?

Vanessa

SAD

It is that time of year again when the cold weather reminds us that the change of season is upon us. It has prompted me to reassess my winter wardrobe (which is sadly lacking) and I am finding it just that bit harder to get out of bed in the morning. But then again I have children who take care of that. My mood has altered somewhat and I also find myself hoping that we will be blessed with just a few more lovely sunny days.....

As I understand it, all these feelings are normal. For some people however, there is a very real winter related disorder called Seasonal Affective Disorder or SAD for short. It is also commonly confused with the winter blues or winter depression but the two are in fact different. There has been much written on this topic since it was first defined in an article published in a Psychiatry paper in the early eighties.

The American Psychiatric Association recognizes SAD as a sub type of a major depressive disorder.

Symptoms of SAD include lack of energy, difficulty getting up in the mornings, overeating, craving carbohydrates (and weight gain), difficulty concentrating and completing tasks, withdrawal from usual social activities and friends/family. Of course this leads to depression. Symptoms typically begin in autumn, peak in winter and usually disappear in spring and summer. These people are known to experience normal mental health throughout the rest of the year.

There are four major criteria as set out by the American Psychiatric association DSM -IV which must be met in order to diagnose SAD:

Depressive episodes at a particular time of year

Remissions or mania/hypomania also at characteristic time of year

These patterns must have lasted two years with no nonseasonal major depressive episodes during that same period and

These seasonal depressive episodes outnumber other depressive episodes throughout the patient’s lifetime.

Winter blues is considered to be much more mild than SAD. Symptoms still include feeling sad and a lack of energy but the key difference is that these people can still function. People diagnosed with SAD, typically find it difficult to perform normal activities of daily living.

Apparently many more women are affected by SAD than men. While it is far more common in the Northern Hemisphere than Australia, it has been estimated that one in three hundred Australians are affected.

It is also worth noting that there are a small number of people who display depressive symptoms such as insomnia, decreased appetite, weight loss, irritability, anxiety, and decreased sex drive in the SPRING and SUMMER months (Summer SAD). These people may also have short bouts of mania/hypomania behaviour at this time of year.

Classic major depression often (but not always) presents with decreased appetite (weight loss) and decreased sleep patterns.

Research shows that it is the lack of light during the winter months which leads to SAD. The brain does not produce enough serotonin which has been found to lead to depression. Serotonin is a neurotransmitter which is produced by the brain and relays messages from one part of the brain to other parts. It has a major influence on mood, and our serotonin levels are lowest in winter. Put simply, serotonin stimulates us during the day time but it is another hormone, melatonin whose job it is to promote sleep.

In the evening the body (or more accurately the pineal gland) responds to decreased light by making melatonin. Usually the secretion of melatonin peaks in the middle of the night when we are in our deepest sleep but is switched off by the pineal gland in response to light exposure in the mornings.

During winter, people affected by SAD commonly have higher levels of melatonin during the day which leads to many of the previously discussed symptoms associated with SAD. The body’s internal body clock is out of “synch”.

Light therapy, either bright white light/blue light has been used to effectively treat SAD by suppressing melatonin and stimulating serotonin production. It helps to reset the body’s natural sleep/wake cycle. Other treatments such as taking melatonin or other antidepressants used in conjunction with light therapy have proven to be effective. Or one could just head outside for a natural dose of light – great in the summer months but harder to use effectively in the colder winter months.

During my research I was also surprised to learn that it has been estimated that up to 20% of people with SAD already have/ go on to develop bipolar disorder. Interestingly, some studies have indicated that people with dark coloured eyes react differently to light than those with light coloured eyes. Also that genetic differences in photoreceptors and glucose metabolism also play a role.

Lisa

Crouch St, South

Having our own rooms in Mount Gambier is working wonderfully. Above is a picture of the street entrance to the rooms. Patients have been full of praise commenting on how neat and tidy they are. We always appreciate to hear feedback about our service. There is car parking available around the back of the practice or there is ample parking on the street. A google map is on the website for the Crouch St, South rooms.

From June 15 2010 Dr. Bradbeer will be consulting in Mount Gambier on Tuesdays. The office is open from 9.45am-4.00pm on these days.

We are working hard to secure another full time physician to the practice and when this comes to fruition we will be able to offer two consulting days per week in Mount Gambier. Fingers crossed, that I will have some good news pertaining to this within the month.

Spriometry, gas transfer and bronchial provocation tests are also available on consulting days in Mount Gambier.

Jessica

More bariatric surgery

It’s not rocket science.

Evaluation of patients prior to bariatric surgery is largely a matter of common sense. The goal is to identify any problems that are able to be modified with non-surgical intervention, and to introduce treatment to reduce risk. As I explain to patients, the fitter they are prior to surgery the less likely they are to get really crook if they encounter unforeseen complications, and the better they will do afterwards when it comes to getting on their feet and losing weight. However, for most patients the good stuff really happens post-operatively. Diabetes resolves, hypertension improves, sleep apnoea is cured…. For that reason, we really want to identify and treat only those problems which will significantly increase the risks of surgery. All other problems should be addressed after surgery. For example, diabetic control preoperatively does not need to made perfect, as it almost universally improves dramatically after surgery.

Guidelines as to whom we should consider suitable for bariatric surgery were introduced nearly 20 years ago – and have not altered since. Now there’s a situation that has to change with the times! In any case, the National Institutes of Health in the US came up with the following recommendations:

Bariatric surgery should be considered in individuals with:
- BMI of 40kg/m2 or greater
- BMI of 35 to 39kg/m2 with severe comorbid conditions such as life- threatening cardiopulmonary problems or diabetes.
- BMI of 35 to 39kg/m2 with obesity-induced physical problems interfering with lifestyle (e.g joint disease which is treatable but for the obesity)
- No underlying endocrine abnormality that can contribute to obesity, ongoing substance abuse or uncontrolled psychiatric disturbance
- An ability to understand the surgery and its consequences and comply with post-operative dietary modification
- No illness that greatly reduces life expectancy


In our clinical evaluation of patients preoperatively we want to ensure that there is no undiagnosed cardiac, respiratory or endocrine disease that will significantly increase the risk of perioperative complications. The population of patients undergoing bariatric surgery is at particular risk of coronary artery disease, cardiomyopathy, uncontrolled hypertension, hypothyroidism, obstructive sleep apnoea or obesity hypoventilation syndrome, asthma or chronic obstructive pulmonary disease or undiagnosed diabetes. Not every patient will require the same specific workup. However, investigation which we frequently request include exercise testing, echocardiography, lung function tests and diagnostic sleep studies. Everybody has blood tests, including coagulation studies, iron studies, blood glucose and thyroid function, lipid studies and full blood count as well as an ECG. (Most of our patients have had these investigations requested by their general practitioners).

In 2007, a useful clinical risk-stratification tool was suggested by DeMaria and colleagues in a paper published in the journal of Surgery for Obesity Related Disease. This score reminds us that mortality rates are generally very low for bariatric surgery, but are significant in some patient groups.

The score takes into account the following variables:
- BMI >50
- Male gender
- History of hypertension
- Increased risk for pulmonary embolism ( variable included previous PE, inferior vena cava filter, right heart failure, obesity hypoventilation syndrome)
- Age 45 years of more

One point is awarded for each variable, with mortality rates as follows:
- score 0-1, mortality rate 0.31%
- score 2-3, mortality rate 1.90%
- score 4-5, mortality rate 7.56%

This scoring system was, however, created from one particular retrospective analysis in one institution and validated in another institution. The PE risk variable is not straight forward, and less than 1% of patients scored all 5 points. The operation involved was gastric bypass, which is a much more complicated procedure than gastric banding or vertical gastroplasty, which are the major procedures performed in Hamilton.

A much bigger study of qualified surgeons in the US, which was published in the New England Journal of Medicine last year and which included gastric bands, showed very low mortality rates, as per the attached table. In that study, only very high BMI, history of pulmonary embolism, and perhaps history of OSA, were associated with increased risk of mortality.

A study published in the NEJM in 2007 suggested that long-term mortality in very obese patients was reduced by 40% in patients who had gastric-bypass surgery. The slightly – increased risk of dieing post-operatively should, perhaps, be considered in light of that sobering, dramatic statistic.

Andrew

I’ve been reading about obesity. More specifically, I have been reading about bariatric surgery.

As I have the privilege of reviewing many of the patients who undergo bariatric surgery locally (either laparoscopic adjustable gastric band insertion or vertical banded gastroplasty), I was invited to speak to some of the local medicos last week on the preparation of patients for these surgical procedures.

It’s not intuitive that obesity is a problem which warrants drastic intervention. It probably needs to be reiterated that the following medical problems, which no-one really wants to suffer from, are associated with obesity, and can be a major cause of suffering in our community, as well as an increasing burden on our health-care infrastructure:
- coronary artery disease
- insulin resistance and type two diabetes
- cancer (endometrial, breast and colon)
- hypertension
- dyslipidaemia
- stroke
- liver and gall bladder diseae
- obstructive sleep apnoea and respiratory disorders
- osteoarthritis
- gynaecological problems (infertility, polycystic ovarian syndrome, menstrual irregularity)
- pseudotumour cerebri



One might also wonder what all of the fuss is about. How much of a problem is this, really? I think the accompanying graph speaks for itself. (The measurement tool that we most commonly use to assess weight / obesity is the body mass index. While this tool may be, to some extent, flawed it is pretty standard. BMI over 30 defines obesity, with BMI over 40 being labelled 'morbidly obese'. It is the tool used in collection of the data that go into compiling a graph such as this).

My professional exposure to people who struggle with obesity, and my reading around the topic, has caused me to become less and less optimistic that lasting control of weight problems can be achieved with non-surgical measures (ie diet and exercise). Professor Joe Proietto, from Melbourne, spoke at the recent World Congress of Internal Medicine in Melbourne (I wasn’t there but got the DVD!) and at the Australasian Sleep Association meeting last year. Wow, if you want to hear someone who presents a scientific basis for the failure of non-surgical weight loss and the inevitability of continued increase of the obesity epidemic in our society, then Joe is the man!

He explained that the hypothalamus, the part of the brain where appetite is ‘controlled’, seems to be programmed to hunt for food. There is only one hormone (chemical messenger) which we know of which circulates in the blood stream and is designed to stimulate appetite. It is called Ghrelin, and is secreted mainly from cells in the stomach. There is a number (around nine) of hormones that suppress appetite. The two we probably know most about are Leptin (secreted by adiopose tissue) and cholecystokinin (made and secreted in the small bowel in response to ingestion of food). Prof Joe P has convincing experimental data that demonstrate how prolonged low-calorie diet is accompanied by weight loss (no surprises there) and a reduction in secretion of leptin and CCK (ie less suppression of appetite). At the end of a prolonged period of low calorie diet, experimental subjects have their appetites unleashed and choose to eat high protein and high fat foods. In real life, this is called “Yo-yo dieting”. Seems it’s not just a matter of willpower.

Current thinking is that bariatric surgery impacts on the secretion of the above hormones, and others involved in suppression of appetite, in ways that are sustained. This facilitates long term dietary modification. It also contributes to the rapid resolution of complications of obesity, and in particular diabetes, following bariatric surgery. To my disappointment a recent review article in Nutrition journal found no good studies to date testing this hypothesis.

Bariatric surgery certainly is, however, the only intervention which regularly results in sustained weight loss. I used to be hesitant to refer patients for these procedures. Now it is often an issue discussed at the initial consultation.

Next post: What are the indications for bariatric surgery? What are the risks? What does a pre-operative evaluation entail?

Andrew