Showing posts with label obesity. Show all posts
Showing posts with label obesity. Show all posts

Tuesday, June 8, 2010

Asthma and obesity

I am enjoying having opportunity this week to catch up on some of the talks from the American Thoracic Society conference, which was held in New Orleans just over two weeks ago. I’m impressed that they are available online already.

One symposium looked at the interaction between obesity and respiratory / critical care medicine. I’ll probably blog more about this as I work through the talks.

Dr Stephanie Shore, PhD, from the Harvard School of Public Health, gave an excellent lecture on obesity and asthma at that session. The following is a summary of what I got out of that talk.

Firstly, we do know that asthma and obesity interact in the following ways:
- there is an increased prevalence of asthma amongst obese individuals;
- as people become more obese, the likelihood of new asthma developing increases;
- obesity leads to reduced control of asthma;
- obesity leads to increased severity of asthma;
- weight loss helps improve asthma control;
- and obese mice…..

What have mice got to do with it? Well, many data relevant to human health were initially derived from mice, so it turns out that obese mice have something to teach us. And obese mice have a tendency to develop asthma. But more of that later.

Why is there more asthma amongst people who are obese? Is this a new sort of asthma? Does obesity give some people asthma? Or is it the same old sort of asthma, with obese individuals simply predisposed.

It looks more like the former suggestion – ie obese individuals with asthma have a particular sort of asthma. Obese individuals with asthma have less eosinophils in bronchoalveolar lavage fluid (fluid that is washed through the smallest airways at bronchoscopy). They also are less sensitive to the impact of corticosteroid. All of this suggests that they do not have ‘allergic asthma’ of the sort that occurs almost universally in children with asthma, but less frequently in older asthmatics.

What’s going on there? There is ‘more thought than data’ when it comes to how obesity may contribute to asthma development. The ideas include the suggestions that there may be:
1. Common aetiologies. The same processes that contribute to the development of obesity may contribute to the development of asthma. These may be congenital / in-utero issues; dietary factors; genetic abnormalities or acquired exposures
2. Co-morbid problems. People with obesity suffer from more lipid abnormalities, gastro-oesophargeal reflux, obstructive sleep apnoea, diabetes and hypertension. Do these associated problems contribute to the development of asthma. GORD and OSA have been shown to. The others, maybe.
3. Obesity impacts on lung mechanics, leading to reduced functional residual capacity and reduced tidal volume. Either of these mechanisms may lead to airway hyperresponsiveness – and asthma.
4. Systemic inflammation or other systemic consequences of obesity may contribute to development of asthma.

With regards to this last issue, in particular, Dr Shore embarked on a little tutorial on adiponectin. I didn’t know too much about this hormone, so was helped by the tute. Like leptin, adiponectin is produced in fat cells (adipocytes) and circulates in several different forms in the blood stream. Its levels are reduced in obesity. It sensitizes to the effect of insulin (so low levels contribute to insulin resistance) and it has anti-inflammatory properties (so low levels in obesity can lead to more inflammation). Dr Shore’s lab had researched the impact of this compound in the lungs of mice. In mice given adiponectin, allergen –induced airway hyperresponsiveness (AHR) and inflammation is reduced. In adiponectin deficient mice there is increased allergen induced AHR and inflammation. Transgenic mice that overexpress adiponectin demonstrate reduced airway inflammation. The suggestion (idea rather than data) is that adiponectin may be a mediator of airway inflammation in people who are obese – not just in mice – contributing to the development of asthma.

The important clinical information for now is that weight loss helps. There have been, in the last 10 years, 10 studies looking at patients with bariatric-surgery – induced weight loss and 4 looking at patients with dietary weight loss, with regards to the impact of weight loss on asthma control. They have demonstrated:
- improved lung function parameters;
- reduced medication use;
- reduced symptoms;
- improved asthma control;
- improved asthma-related quality of life;
- reduced severity of asthma and reduced frequency of hopitalisation ….

….as a consequence of weight loss in people with asthma.

So, there is evidence that obese patients with poorly controlled asthma should be encouraged to lose weight. It will help bring their asthma under control.

Andrew

Thursday, May 6, 2010

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