There is now ample evidence to suggest that headaches are more common in people with overweight and obesity than in people with normal weight.

Thus, for example in a recent paper by Winter and colleagues from the University of Münster, Germany, published in Cephalalgia, reporting on a cross-sectional study of over 63,000 women, a BMI greater than 35 was associated with a 3-fold increased risk of daily migraine as well as increased risk of phonophobia and photophobia but decreased risk of a unilateral pain and aura.

These findings on obesity and headaches were recently extended to kids, in a paper just published in Headache, Andrew Hershey and colleagues on behalf of the American Headache Society Pediatric Adolescent Section. These investigators reported data in 913 consecutive kids seen at 7 pediatric headache centers in the US. While the prevalence of overweight at initial visit did not significantly differ from the general pediatric population, the higher the BMI percentile, the greater the headache frequency and associated disability. Furthermore, any increase in BMI at 3- and 6-month follow-up was significantly correlated with a further increase in headache frequency.

While the exact reasons for the link between obesity and headaches remains unclear, Marcelo Bigal and colleagues from Albert Einstein College of Medicine, Bronx, NY, USA have previously reviewed some of the putative mechanisms in an article published in Neurology. Firstly, several of the inflammatory mediators that are increased in obese individuals are important in migraine pathophysiology, including interleukins and calcitonin gene-related peptide (CGRP). Obesity is also a state of sympathetic activation, which may contribute to increase in headache frequency. Orexins modulate both pain and metabolism and dysfunction in the orexins pathways appears to be a risk factor for both conditions. Finally, conditions that are comorbid to both states (e.g., depression, sleep apnea) may also promote headaches.

Whatever the exact mechanism, clinicians should be aware of the relationship between headaches and excess weight. Whether headaches promote obesity (i.e. treatment of headaches will prevent obesity) or whether obesity promotes headaches (i.e. treatment of obesity will reduce headaches) remains to be seen.

AMS
Edmonton, Alberta

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Victoria, BC

Last night I gave a talk to General Practitioners at the Medical School in Victoria, BC (hosted by Dr. Brad Amson, General/Bariatric Surgeon).

I spoke about the importance of carefully assessing patients for contributors and barriers to weight management.

As blogged yesterday, pain is one of the most common issues in patients with excess weight and can be both a contributor and barrier to weight gain and severely obese patients appear at particular risk for pain catastrophizing.

But how common is pain and how great is the incident risk in overweight and obese patients?

This issue was addressed in a recent study by Noor Heim and colleagues from the VU University, Amsterdam, The Netherlands, published in OBESITY.

This prospective study investigated the relationship between measured BMI and waist circumference with prevalent and incident pain in 2000 participants of the Longitudinal Aging Study Amsterdam, aged 55-85 years at baseline (1992-1993) and after after 3 years (N = 1,478) and 6 years (N = 1,271) of follow-up.

The overall prevalence of pain was 33% at baseline and increased significantly with higher quartiles of BM. After adjustment for age, education, depression, smoking, physical activity, and chronic diseases, both men and women in the highest quartile of BMI were around twice as likely to present with pain than individuals in the lowest BMI quartile.

Of the participants without pain at baseline, those in the highest quartile of BMI had a  2-fold increased odds for incident pain after 3 years of follow-up and around 2.5-fold after 6 years.

The association with BMI was independent of waist circumference, suggesting that absolute weight rather than weight distribution was important for pain.

This longitudinal study also answers the question whether or not pain in obesity is the chicken or the egg - it appears that obesity increases the risk for incident pain, rather than vice-versa.

But what about weight loss and its effect on pain? This issue, interestingly, has not been widely studied and results have been inconsistent. Apart from the rather dramatic improvement in pain and mobility reported in surgical obesity treatment, the effect of non-pharmacological or pharmacological weight loss on pain incidence or progression is not clear (though my guess is that weight loss can’t hurt - no pun intended).

Given the tendency of obese patients to catastrophize and the high incidence of depression and immobility, pain prevention and management is a key issue in the management of patients challenged by excess weight.

AMS
Victoria, BC

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Pain is one of the most common and debilitating problems in patients challenged by severe obesity. Not just a consequence of mechanical complications of obesity (osteoarthritis, back pain, plantar fasciitis, fibromyalgia, etc.), pain is often a key barrier to physical activity and thus weight management. In fact, excess pain can promote psychological (e.g. depression, anxiety) and behavioural (e.g. binge eating) factors that may further promote weight gain.

This issue is of even more importance in patients who display the now well-described phenomenon of pain catastrophizing, or the maladaptive responses to pain (tendency to focus on and magnify pain sensations with an intense sense of unbearable suffering and helplessness) that plays an extremely important role in how pain is perceived and processed. Pain catastrophizing now accounts for a substantial proportion of pain-related disability.

Studies in patients with fibromyalgia show that pain catastrophizing is associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala) and motor control. Thus, catastrophizing influences pain perception through altering attention and anticipation, and heightening emotional responses to pain.

In another recent study by Tamara Somers and colleagues from Duke University, morbidly obese patients with osteoarthritis (OA) reported higher levels of pain catastrophizing than OA patients in the overweight and obese category. The severely obese patients who engaged in a high level of pain catastrophizing reported having much more intense and unpleasant pain, higher levels of binge eating, lower self-efficacy for controlling their eating and lower weight-related quality of life.

The relationship between pain catastrophizing and eating behaviour is of particular interest, as high-fat and high-sucrose foods have been shown to increase pain tolerance. Thus, binging on highly-palatable foods may be a compensatory response to emotional distress and pain. It is not difficult to see how patients can enter into a vicious cycle of pain, increased eating, weight gain, more pain, more eating, and so on.

In routine practice, pain catastrophizing can be easily and reliably assessed with questionnaires like this one, which can be scored like this.

Fortunately, pain catastrophizing is responsive to cognitive behavioural therapy, with clinically relevant improvements in upto 50% of individuals.

I would have little doubt that failure to recognize and address pain catastrophizing increases the likelihood of further weight gain and disability in patients with severe obesity.

AMS
Edmonton, Alberta

Yesterday, I came across a recent article on osteoarthirits by Simon Juang from the University of British Columbia, published in the latest issue of Parkhurst Exchange.

Given that osteoarthritis (OA) is probably the most common cause of pain and disability in patients with obesity, as a non-expert, I found the article most informative and relevant.

The following are some of the key pieces of information I gleaned from this overview:

First of all, I was surprised to learn that OA is not always painful, but on the other hand, that not all joint pain, simply because there may be radiological signs of OA, is actually due to OA. In fact, quite often the pain may result from the structures around the joint, i.e. the muslces, ligaments, tendons, bursae, osteophytes, injury, etc. As the course of treatment may well be different, proper diagnosis of the actual source of pain is essential.

The 4 pillars of OA management include:
- patient education
- non-pharmacological interventions
- drug therapy
- appropriate referral

The 4 goals of treatment are:
- reducing pain
- maintaining range and strength
- preserving function
- dercreasing the rate of progression

As expected, the basic joint health program starts with “optimal weight”, whereby however, Huang automatically assumes that this can be fixed by “proper diet”, best achieved by referral to a dietitian (readers of these pages will likely appreciate that if obesity management was indeed that simple, we would probably not have a crisis).

Other aspects of the joint program involve physiotherapists (exercises, heating pads, nerve stimulation, etc.), occupational therapists (activities of daily living), but also orthoticists, or podiatrists.

The article also lists a number of useful resources for patients, which I list here:

- The Athritis Society
- Arthritis Resource Guide for BC
- OASIS (OsteoArthritis Service Integrated System, Vancouver Coastal Health)
- Joint Health, Arthritis Consumer Experts
- Alberta Bone and Joint Institute
- Canadian Orthopedic Foundation

Remember, while managing pain and increasing mobility will not automatically result in weight loss, impaired mobility is certainly a major barrier to any weight management program.

AMS
Edmonton, Alberta

Based on the number of patient who have told me that their orthopedic surgeons require them to lose unrealistic amounts of weight before they will be considered for knee surgery, I would assume that surgical outcomes in patients with severe obesity are so miserable that few surgeons are willing to risk surgery.

But is this really true?

This question was addressed by Rajgopal and colleagues from Western University, London, Ontario just out in the Journal of Arthroplasty.

This study evaluated the 1-year outcomes in 550 patients who underwent primary total knee arthroplasty between 1987 and 2004 with a primary diagnosis of osteoarthritis. Outcomes were measured using the Western Ontario and McMaster Osteoarthritis Index [WOMAC].

Although 1-year outcomes were indeed slightly worse for patients with a BMI >40, compared to patients with lower BMIs, it was the severely obese patients that actually showed greater improvement in function compared with normal weight or less obese patients.

This data is quite consistent with previous reports that obesity per se should neither be a contraindication for joint replacement surgery nor is it a predictor of less satisfaction or pain relief in these patients, despite somewhat less mobility.

Denying patients joint replacements because of their weight or expecting them to lose unrealistic amounts of weight prior to surgery is not evidence-based medicine.

AMS
Toronto, Ontario