I returned to Greece (where I spend half the year) yesterday, in a state of some exhaustion after a really busy time teaching in the UK and Europe.
On Saturday I lectured for 90 minutes at a one day symposium held at the University of Westminster, London, on the topic of leptin (see below for more on this) and its link to the obesity problem that most developed countries are facing.
I was the 4th of 4 speakers, and because a number of the earlier talks had actually covered elements that I had wanted to speak on – I was obliged to think laterally, trying to identify areas of interest that had not already been explored – sometimes several times!
Three thoughts emerged:
One was to address the biomechanical issues that emerge from being grossly overweight – but because the audience comprised (mainly) nutritionists, this had to be presented in broad terms. I was able to pull up an image (see above) showing an example. The basic message was that the illustrated individual would (apart from the cardiovascular and other health implications of obesity):
- a/ be likely to develop a range of musculoskeletal symptoms
- b/ would have difficulty in breathing normally
- c/ would be almost certain to suffer from pelvic floor issues – and possible incontinence
- d/ would have such highly stressed abdominal organs that the chance of these functioning normally would be close to zero.
The second lateral thought that I introduced in relation to obesity was an expansion of the point (b) above – as to the inability of the person involved to be able to breathe normally. The drag of the abdominal contents on the diaphragm and lower rib cage, together with the obvious bilateral shortness of psoas muscles (the fibers of which merge with the diaphragm) would make normal breathing function nigh on impossible. I was hoping that this information would help the nutritionally oriented delegates to appreciate that the biochemistry of upper chest breathing would probably lead to respiratory alkalosis, with repurcussions associated with poor oxygenation of all bodily tissues, as well as smooth muscle constriction – which would impact negatively on digestive function. [Chaitow et al 2002]
And finally my thought was to link this last issue (breathing dysfunction) with the huge problem of engaging anyone to alter built in habits — whether these relate to poor posture, imbalanced breathing — or undesirable eating patterns.
For more on breathing pattern disorders visit my website <www.leonchaitow.com> which has freely down-loadable articles on the topic [go to the “Research & Articles” section]- as well details of my coauthored book on the subject, “Multidisciplinary Approaches to Breathing Pattern Disorders”
To change any of these habit that might be having harmful effects on the body – I believe there are at least 4 essentials:
- Understanding the processes – the person affected needs to gain a cognitive, intellectual awareness of the mechanisms and issues involved in whatever the habit involves – whether breathing, posture, eating, or anything else.
- Retraining exercises or behaviors, including aspects that operate subcortically, allowing replacement of currently habituated patterns with more appropriate ones
- Biomechanical structural modifications that remove obstacles to desirable and necessary functional changes – in eating pattern disorders this might involve efforts to enhance the stressed gut status as illustrated above.
- Time for these elements to merge and become incorporated into moment-to-moment use patterns
Leptin and ghrelin are two hormones with major influences on health. [Klok 2007]
Leptin which is released by WAT (white adipose tissue) mediates long-term regulation of energy balance, suppressing food intake and so inducing weight loss. Put simply leptin is supposed to tell you when you have eaten enough. The problem is that over time – for complex reasons this post hasn’t time to address – the body stops recognising the signals.
Ghrelin is a fast-acting hormone, that plays a role in meal initiation. It tells you that you need to eat – and unfortunately we tend to listen to this signal more keenly than that from Leptin!
With obesity incidence rising dramatically, understanding the mechanisms by which these (and other) substances influence energy balance has been a subject of intensive research
In obesity, circulating level of the leptin (satiety) hormone is increased, whereas surprisingly, the level of ghrelin (appetite inducing) is decreased. ….but weight gain continues.
As mentioned, it is now established that most obese patients are leptin-resistant.
How this happens seems to relate to lifestyle (e.g. exercise & sleep patterns), as well as to food choices, and the timing of meals – and I’ll return to these topics in a later blog posting if there is sufficient interest.
The main external indicator of the evolution of leptin resistance involves weight gain in the abdominal region (obesity is defined as a waist circumference of 40 inches (101.6 cms) or greater in men and 35 inches (88.9 cms) or greater in women [Elliott 2008]). This where we accumulate WAT, which releases leptin. Abdominal dimensions are not only associated with leptin imbalance, but also with high risks of developing cardiovascular disease, type 2 diabetes and other morbidities collectively known as Syndrome-X.
Measuring waist circumference half way between the lower ribs and the crest of the pelvis
If there is further interest in this topic – and only be sending messages will this become clear to me – I will explore it further another time.