Efficacy of Vagal Blockade For Obesity Treatment Remains Vague

Efficacy of Vagal Blockade For Obesity Treatment Remains Vague


Efficacy of Vagal Blockade For Obesity Treatment Remains Vague

Posted: 18 Sep 2014 05:00 AM PDT

VBLOC

VBLOC

Regular readers may recall past posts on the use of intermittent electrical blockade of the vagus nerves (VBLOC) as a means of reducing food intake to promote weight loss.

Now a large randomised controlled study of vagal blocakade, published by Sayeed Ikramuddin and colleagues, published in JAMA, reports on rather disappointing outcomes with this treatment.

In this study (ReCharge), conducted  at one of 10 sites in the United States and Australia between May and December 2011, 239 participants with a BMI greater than 40 (or greater than 35 with at least one comorbidity), were randomised to receiving an active vagal nerve block device (EnteroMedics’ Maestro® Rechargeable (RC) System, n=162) or a sham device (n=77).

Over the 12-month blinded portion of the 5-year study (completed in January 2013), the vagal nerve block group lost about 9% or their initial body weight compared to only 6% in the sham group.

In addition to this rather modest difference in weight loss between the groups (about 3%), participants in the active treatment group also experienced a number of clinically relevant adverse effects (heartburn or dyspepsia and abdominal pain).

Thus, overall these rather disappointing results are in line with the previously disappointing observations in the smaller MAESTRO trial.

Based on these findings, it seems that intermittent electrical blockade of the vagal nerve may not hold its promise of a safe and effective long-term treatment for severe obesity after all.

@DrSharma
Edmonton, AB

ResearchBlogging.orgIkramuddin S, Blackstone RP, Brancatisano A, Toouli J, Shah SN, Wolfe BM, Fujioka K, Maher JW, Swain J, Que FG, Morton JM, Leslie DB, Brancatisano R, Kow L, O’Rourke RW, Deveney C, Takata M, Miller CJ, Knudson MB, Tweden KS, Shikora SA, Sarr MG, & Billington CJ (2014). Effect of reversible intermittent intra-abdominal vagal nerve blockade on morbid obesity: the ReCharge randomized clinical trial. JAMA, 312 (9), 915-22 PMID: 25182100

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Is Food Addiction Better Described As Eating Addiction?

Is Food Addiction Better Described As Eating Addiction?


Is Food Addiction Better Described As Eating Addiction?

Posted: 16 Sep 2014 05:00 AM PDT

sharma-obesity-addiction-typesThe term “food addiction” has found its way into both the scientific and popular literature.

Now, a thoughtful paper by Johannes Hebebrand and colleagues, published in Neuroscience & Biobehavioral Reviews, argues that there is in fact little evidence for addiction to “food” per se (as you would see in addiction to a specific substance) and that therefore, it may be better to describe the addiction-like overconsumption of food as a behavioural addiction, in this case, an addiction to eating.

Eating is intrinsically rewarding and reinforcing, and food consumption is well-known to activate the reward system in the brain; this applies particularly in the physiological state of hunger. It is easy to see that the rewarding properties of food and their activation of the reward pathway might lead intuitively to the idea that food substances may have addictive properties. However, just because eating behavior engages these reward systems, it does not necessarily follow that specific nutrients (substances) are able to evoke a substance addiction. Instead, the complex activation of the reward system as the initial step of the process ending in addiction can be viewed as being dependent on eating (subjectively) palatable foods irrespective of their nutritional/chemical composition.”

Per se, foods are nutritionally complex and there is hardly any evidence to suggest that under normal physiological circumstances humans crave specific foods in order to ingest a specific 'substance'. Instead, the diet of subjects who overeat typically contains a broad range of different, subjectively palatable foods. It can be argued that access to a diversity of foods, especially a diverse range of palatable foods, may be a pre-requisite for the development of addictive-like eating behavior.”

There is currently no evidence that single nutritional substances can elicit a Substance Use Disorder in humans according to DSM 5 criteria. In light of the lack of clinical studies that have aimed to detect addictions to specific nutrients, it cannot as yet be ruled out that a predisposed subgroup does indeed develop such a substance based addiction, which in theory may be substantially weaker than in the case of addictions based on well-known exogenous substances such as alcohol, cannabis, nicotine or opiates. The fact, that clinical case studies do not abound on an addiction like intake of specific nutrients or even specific foods, would suggest that such cases are rare, if they exist at all. Alternatively, the addiction is so weak that it is not adequately perceived and reported as such. This leads to the question as to the boundaries between excessive consumption and the beginning of a true addiction.”

Thus,

“…there is very little evidence to indicate that humans can develop a "Glucose/Sucrose/Fructose Use Disorder" as a diagnosis within the DSM-5 category Substance Use Disorders. We do, however, view both rodent and human data as consistent with the existence of addictive eating behavior. The novel DSM-5 (APA, 2013) currently does not allow the classification of an "Overeating Disorder" or an "Addictive Eating Disorder" within the diagnostic category Substance-Related and Addictive Disorders; indeed, the current knowledge of addictive eating behaviors does not warrant such a diagnosis. However, efforts should be made to operationalize the diagnostic criteria for such a disorder and to test its reliability and validity. It needs to be determined if such a disorder can occur distinct from other mental disorders.”

Overall I believe that reframing the perceived loss of control over food intake often reported by my patients as a “behavioural” rather than a “substance” addiction may be helpful in approaching this rather complex topic and may well open the path to novel therapeutic approaches more consistent with our current understanding of behavioural addictions.

@DrSharma
Vienna, Austria

ResearchBlogging.orgHebebrand J, Albayrak O, Adan R, Antel J, Dieguez C, de Jong J, Leng G, Menzies J, Mercer JG, Murphy M, van der Plasse G, & Dickson SL (2014). “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior. Neuroscience and biobehavioral reviews PMID: 25205078

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Update on New Medications for Obesity

Update on New Medications for Obesity


Update on New Medications for Obesity

Posted: 15 Sep 2014 05:00 AM PDT

sharma-obesity-fda4Last week, while I was off on a brief holiday, two important events took place in the US with regard to obesity medications.

On September 10, the US-FDA granted approval for Contrave, a fixed combination of bupropion and naltrexone, two centrally active compounds, also used in the treatment of addictions.

Then, on September 11, an advisory panel appointed by the FDA, voted strongly in favour of approving the GLP-1 agonist liraglutide at the 3.mg dose for the treatment of obesity.

These two new entities would bring the currently approved prescription medications for the treatment of obesity in the US to six – a dramatic change from just a couple of years ago.

This is still a long shot away from the many effective treatments we have for treating other common conditions (e.g. there are more than 20 prescription medications approved for treating diabetes and almost 100 compounds for the treatment of hypertension).

Why would we need this many different medications for obesity? For the simple reason that not everyone will respond favourably or tolerate all of these compounds.

Given that obesity is a remarkably heterogeneous disorder and that these drugs have distinctly different modes of action, I would not expect all of these medications to work in all individuals.

It is also important to note that all of these drugs work best when combined with intense behaviour modification – no pill will ever serve as a substitute for a healthy diet and a daily dose of moderate to vigorous physical activity. But we also know that the latter alone, will rarely produce sustainable weight loss in the long-term.

Obviously, given the chronic nature of obesity, medications for obesity will need to be used long-term in the same manner that we use medications to treat other chronic conditions (e.g. diabetes, hypertension, etc.).

This means that we will need more long-term data on the efficacy and safety of these compounds.

Nevertheless, there is reason to hope that for many people with obesity related health problems, these new obesity medications will provide much-needed therapeutic options.

@DrSharma
Vienna, Austria

Disclaimer: I have served as a paid consultant and/or speaker for the makers of Contrave and liraglutide.

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