Dr. Sharma's Obesity Notes

There is no doubt that, for severe obesity, bariatric surgery is currently the most effective treatment with well-documented benefits on a wide range of health problems and quality of life.

However, as regular readers will recall, I am also the first to point out that surgery is not a ‘stand-alone’ procedure, but rather, requires intense and probably life-long follow-up to prevent nutritional and psychological complications that may emerge even years after surgery.

This problem is again emphasized by a recent study by McGrice and Porter, from Melbourne, Australia, published in OBESITY SURGERY.

They invited 215 patients to complete validated Food Frequency Questionnaire 12 months following adjustable gastric banding.

Although only bout 25% of patients responded, those who did, reported daily energy intakes ranging between just 270 (???) to over 3000 Calories, with an average of about 1200 Cal/day.

Not surprisingly, many patients failed to meet even the minimum recommendations for macronutrient intake.

The average fibre intake was only 14 g/day (current recommendations are 25 g for women and 30 g for men) and the average diet contained 36% total fat (almost half of which was saturated fat) compared to the recommendations of 20-25%.

From these findings the authors conclude that:

“Patients’ dietary intakes vary significantly 1 year post-laparoscopic adjustable band surgery, with many patients not meeting recommendations. These results suggest that patients decrease their total energy intake; however, eating habits may not improve as they consume a diet high in saturated fat. It is recommended that all patients receive dietary education about diet quality post-laparoscopic adjustable gastric band surgery to assist them in improving their diet quality as well as quantity for optimal health and weight loss.”

Critics will immediately point out the important limitations of this study including the rather low response rate and the rather ‘iffy’ reliability of one-time questionnaires.

But, unless we assume that only people with post-surgical nutritional issues responded to this questionnaire, we must assume that there are severe nutritional issues in a considerable number of patients one year after surgery.

Although this study is limited to patients undergoing gastric banding, we have yet to see data on long-term nutrition intake in patients undergoing other types of bariatric surgery.

Certainly this study (despite its limitations), if nothing else, should serve as a reminder that we need to pay long-term attention to dietary intake with periodic and ongoing assessment of nutritional status in patients undergoing bariatric surgery.

In fact, I would not be surprised if those who lose the most weight (and by surgical standards, would be considered to have the greatest ‘success’), are the ones at highest risk for nutritional problems.

If you have experienced nutritional problems or deficiencies post-surgery, I’d certainly love to hear your story.

AMS
Edmonton, Alberta

McGrice MA, & Porter JA (2012). What are Gastric Banding Patients Eating One Year Post-Surgery? Obesity surgery PMID: 22923340

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Regular readers may recall that in this series, in which every Saturday I talk about a previous study from my lab, I noted how we first described the presence of a renin-angiontensin system in human adipose tissue.

In a paper published in HYPERTENSION in March of 2005, we described the effect of intentional weight loss on this system.

In a first study, we compared plasma levels of angiotensinogen, renin, aldosterone, angiotensin-converting enzyme activity, and angiotensin II between obese and non-obese post-menopausal women. We also looked at the expression of angiotensinogen, renin, renin-receptor, angiotensin-converting enzyme, and angiotensin II type-1 receptor genes in adipose tissue biopsies.

Obese women (n=19) had significantly higher circulating angiotensinogen, renin, aldosterone, and angiotensin-converting enzyme than lean women (n=19), and lower angiotensinogen gene expression in adipose tissue.

We then performed a 13-week weight loss intervention in 17 women, resulting in an average weightloss of about 5% body weight.

This weight loss resulted in a fall in plasma levels of angiotensinogen levels by -27%, renin by -43%, aldosterone by -31%, angiotensin-converting enzyme activity by -12%.

Furthermore, angiotensinogen expression in adipose tissue changed by -20% in adipose tissue.

The plasma angiotensinogen decrease was highly correlated with the waist circumference decline and were accompanied by a -7-mm Hg reduced systolic ambulatory blood pressure.

Thus, we concluded that

“…a 5% reduction in body weight can lead to a meaningfully reduced renin-angiotensin-aldosterone system in plasma and adipose tissue, which may contribute to the reduced blood pressure.”

Since these studies, not only has the fact that there is an adipose tissue renin-angiotensin system become widely accepted but we also understand that this system is affected by changes in body weight and may in turn play a role in obesity related hypertension.

Clinically, the use of agents that block this system (ACE inhibitors, ARBs, Renin Inhibitors) are now widely used in the management of obesity related hypertension.

According to Google Scholar, this paper has 313 citations.

AMS
Edmonton, Alberta

One of the most common clinical findings in patients with obesity is swelling of the lower extremities due to accumulation of fluid.

This is not only cosmetically bothersome to patients but also carries the risk of infection and skin changes.

In the vast majority of cases, this accumulation is benign and can be dealt with by simple physical measures – however, in rare cases it may be the expression of true lymphedema – a more persistent and far more difficult to treat condition.

True lymphedema can be diagnosed by lymphoscinitgraphy, which must show imparied lymphatic function.

In a letter published in the New England Journal of Medicine, Arin Greene and colleagues from Children’s Boston Hospital, describe a series of 15 obese patients presenting with bilateral lower-extremity enlargement (12 women).

All underwent lymphoscintigraphy, which revealed pathological findings consistent with lymphedema in 5 patients – the other 10 had normal results.

Interestingly, the average BMI of those with true lymphedema was around 70 compared to the average BMI of those with normal findings. All patients with lymphedema had a BMI greater than 59 whereas all patients with a BMI less than 54 had normal findings.

This strongly suggests that severe obesity is likely to be an important risk factor for lymphedema and that, as the authors discuss, there may be a threshold of BMI above which lymphatic flow becomes impaired. This could be either due to a change in lymph production (load) or lymphatic function (clearance) – the latter may result from dysfunctional lymphatics due to either local compression through fat mass or inflammation. On the other hand, increased lymph production from an expanding limb may overwhelm lymphatic capacity.

Whatever the cause, the question is whether or not this process can be reversed by weight loss – surprisingly enough the medical literature appears to be rather sparse on this issue.

I wonder if any of my readers have noted reversal of true lymphedema following significant weight loss – surgically or otherwise.

AMS
Edmonton, Alberta

Greene AK, Grant FD, & Slavin SA (2012). Lower-extremity lymphedema and elevated body-mass index. The New England journal of medicine, 366 (22), 2136-7 PMID: 22646649

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Univ.-Prof. Dr. med. Jürgen E. Scholze, Charité, Berlin

Together with my colleagues Pischon, Engeli, and Juergen Scholze, we argued that some classes of antihypertensive agents may have potentially unwanted effects on some of the metabolic and haemodynamic abnormalities that link obesity and hypertension and noted that most hypertension guidelines fail to provide specific advice on the pharmacological management of obese patients, perhaps not surprising, as we failed to find even a single study examining the efficacy of specific antihypertensive agents in reducing mortality in obese hypertensive patients.

We nevertheless, discussed the theoretical reasons for the differential use of the major classes of antihypertensive agents in the pharmacological management of obesity related hypertension and also considers the potential role of anti-obesity agents.

Since then, many hypertension studies have included sub analyses of their outcomes in obese participants and given the increasing use of fixed combination agents, some of our discussion points raised in this paper may be considered moot. At the time, however, there was clearly a gap in the literature on this issue.

According to Google Scholar, this paper has been cited 63 times

AMS
Lake Louise, Alberta

No doubt obesity is associated with a wide range of health problems affecting almost every organ system.

But acute earache is perhaps not a health problem that immediately comes to mind when we consider the health risks of excess weight.

According to a paper by Stefan Kuhle and colleagues from University of Alberta, School of Public Health, published in the latest issue of Pediatric Obesity, acute middle ear infections (otitis media) may be far more common in obese than in normal weight kids.

This prospective cohort study, linked data from a population-based survey of Grade 5 students (aged 10-11 years) in the Canadian province of Nova Scotia in 2003 with Nova Scotia administrative health data via Health Card numbers.

Relative to normal weight children, obese children had twice as many healthcare provider contacts for severe purative otitis media (ICD9: 382; ICD10: H65-66), incurred more costs per otitis media-related visit ($47 vs. $24) and were two-and-a-half times more likely to have repeated otitis media infections.

There was a significant dose-risk effect with overweight kids fitting nicely between normal weight and obese kids in terms of increased risk.

This risk was independent of a range of socioeconomic factors, history of breastfeeding, presence of an allergic disorder or chronic adenoid/tonsil disorders.

Although, association does not prove causality, it is worth noting that this finding has considerable biological face value.

Thus, the authors provide the following possible explanation for this relationship:

“…obesity has been linked with low-grade systemic inflammation, which may produce a milieu that increases the risk of otitis media or lead to chronic otitis media. Alternatively, gastroesophageal reflux, which is seen more frequently in individuals with higher BMI may enter the middle ear through the Eustachian tube and cause otitis media. Finally, in obese individuals fatty tissue may accumulate around the Eustachian tube thereby compromising ventilation of the middle ear.”

As the authors also point out, this finding may have considerable public health implications:

“Acute otitis media is the second most common reason for visits to a family physician, accounting for 10– 15% of all childhood visits. Recurrent otitis media may result in long-term sequelae such as learning disability, impaired linguistic development or hearing disorder, or sleep apnoea because of the development of chronic adenoid/tonsil disorder.”

But the cost implications are also worth noting:

“We were able to show that the per capita physician costs for otitis media between 2001 and 2006 were 92% higher ($47 vs. $24) in obese children compared with normal weight children. This cost differential is second only to that of chronic adenoid/tonsil disorder (230%) out of the 10 childhood disorders examined”

While the study does not provide any insights into whether reducing childhood obesity would reduce ear infections or whether or not obese kids need to adopt any other precautions to avoid earaches, it certainly points to an under appreciated risk factor for this common and excruciatingly painful condition.

AMS
Edmonton, Alberta

Kuhle S, Kirk SF, Ohinmaa A, Urschitz MS, & Veugelers PJ (2012). The association between childhood overweight and obesity and otitis media. Pediatric obesity, 7 (2), 151-7 PMID: 22434755

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