Search Results for "addiction"
Yesterday, I posted on the recent Senate Committee call on the FDA to ease the path to approval of new obesity, which it described as “a significant unmet medical need.” In my commentary, I suggested that one solution to better balancing risk and benefit would be to subcategorize obesity into meaningful subtypes, ideally based on an objective aetiological framework. In a paper just published in Appetite, Caroline Davis and colleagues from Toronto’s York University provide evidence suggesting that ‘food addiction’ (FA) may be a valid clinical sub-phenotype of obesity. The researchers examined the validity of the Yale Food Addiction Scale (YFAS) – the first tool developed to identify individuals with addictive tendencies towards food – in a sample of obese adults (aged 25-45 years) and non-obese controls. The YFAS is available here – the instruction sheet for interpreting the test is available here. In their analysis, the researchers focused on three domains relevant to the characterization of conventional substance-dependence disorders: clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance. Not only were their results strongly supportive of the ‘food addiction’ construct demonstrated validity of the YFAS, in addition, those who met the diagnostic criteria for food addiction had a significantly greater co-morbidity with Binge Eating Disorder, depression, and attention-deficit/hyperactivity disorder compared to their age- and weight-equivalent counterparts. Those with FA were also more impulsive and displayed greater emotional reactivity than non-FA obese controls. They also displayed greater food cravings and the tendency to ‘self-soothe’ with food. As the authors conclude: “These findings advance the quest to identify clinically relevant subtypes of obesity that may possess different vulnerabilities to environmental risk factors, and thereby could inform more personalized treatment approaches for those who struggle with overeating and weight gain.” From a treatment perspective, these would be the patients, who would perhaps be most responsive to behavioural and pharmacological treatments aligned with an addiction paradigm. In contrast, non-food addicted obese individuals will likely be far less responsive to these approaches. Thus, while it may make sense to expose individuals with food addiction to drugs like buproprion, naltrexone, or rimonabant, non-addictive obese individuals may neither respond well nor warrant the risk of these drugs for treating their obesity. As long as we continue on the path to developing obesity treatments using an outdated and simplistic ‘let’s-get-anyone-with-a-BMI-higher-than-X-to-lose-weight’ approach, we will never get a good handle on risk benefit ratios, let alone,… Read More »
Have you ever wondered why it is almost impossible to only eat one potatoe chip or French fry? Regular readers may recall a previous post on the discovery that we have specific oral sensory receptors that allow us to sense the ‘fattiness’ of food – a function that makes a lot of sense, given that dietary fat provides the densest source of caloric intake. Now, Nicholas DiPatrizio and colleagues from the University of California, Irvine, have discovered that these oral dietary fat sensors activate a powerful ‘addiction-type’ mechanism in your gut that serves to promote further fat intake – their study is published in a recent issue of the Proceedings of the US National Academy of Science. For their studies, the researchers used a well established ‘sham feeding’ model in the rat, where liquid diets eaten by the animal can be drained from the stomach via a chronically implanted gastric cannula, thereby preventing them from reaching the small intestines. Using this model, the researchers showed that ‘sham feeding’ of a high-fat diet resulted in the potent activation of endocannabinoids in the early part of the small intestine by altering enzymatic activities that control endocannabinoid metabolism. The endocannbinoids (cannabis-like compounds produced in the body) are well known to play an important role in regulating ‘rewarding’ feeding behaviours. This effect was abolished by surgical transection of the vagus nerve showing that the stimulation of these changes in the gut is driven through a centrally mediated neuronal pathway. Furthermore, the local application of cannabinoid type 1 receptors blockers (e.g. rimonabant) in the small gut, reduced increased sham fat ingestion. In other words, this study shows that oral sensing of fat sends a signal to the brain, which in turn sends a signal to the gut leading to formation of endocannabinoids, which in turn re-enforce fat eating. This is probably why, just eating one piece of fatty food (say one potatoe chip or French fry) is so hard – simply eating one makes you want to continue eating till the whole bag or plate is empty. Unfortunately, the drug rimonabant, used to effectively block this effect in this study, is no longer available for obesity management (it was withdrawn due to its negative impact on mood), but it may well be that other CB-1 inhibitors that do not enter the brain may prove to be effective to reduce fat intake. Or, in the words… Read More »
Ok, this post is not about comparing overeating to smoking. It is also not about borrowing obesity prevention or management policies from tobacco. And it is most definitely not about even suggesting for a moment that obesity solutions are even remotely related to the way we have dealt with with smoking by making it socially unacceptable, inconvenient, or unaffordable. This post is about something very different. It is about how, in my experience, many “obesity deniers” often use the very same strategies and arguments used by ‘Big Tobacco’ to discredit even the suggestion that there may be an obesity epidemic out there and that, even if it did exist, it has any impact on population health. These strategies, that could have been directly gleaned from Big Tobacco, include the following: 1) All scientific studies are flawed and inconclusive – associations do not prove causality. This is a very common strategy used by interest groups to discredit any unwelcome research findings. Thus, despite experimental proof of carcinogenicity (biologic plausibility) and overwhelmingly consistent associations between smoking and health risks (coherence of data), critics and activists argue away all such evidence with the following tactics: a) findings in animal studies or cell culture cannot be extrapolated to humans. b) smokers have poor health not because they smoke but because they also don’t exercise, eat poorly, lead stressful lives, are risk takers, have lower socioeconomic status, etc, etc, etc. Indeed, anyone even suggesting that tobacco may be unhealthy and smoking cessation may be a good idea is accused of not understanding the literature, jumping to conclusions, ulterior motives, promoting the nanny state, inability to see the big picture, being a ‘health nazi’, and countless other ‘personal’ accusations (if you can’t discredit the science, you can always discredit the scientist). 2) Present anecdotal evidence and personal stories and testimonials: These arguments fall along the lines of pointing to people who smoked all their lives and died after falling out of bed at age 104 or the fact that most people who die of heart attacks, strokes or cancer never smoked a cigarette in their lives. I have heard the quote, “you only have to look at me to see that smoking does not kill people”. 3) The need for nicotine is a ‘natural’ condition Here the argument is that some people (not everyone, but many) are genetically (or otherwise) predisposed to addictions and that for… Read More »
As my regular readers know, this week, I am attending a Scientific Symposium called “Recovery From Addiction“, organised as part of the Alberta Family Wellness Initiative of the Norlien Foundation. Anyone familiar with addictions is well aware of the discussions in this field about harm reduction (or controlled use) versus abstinence. In people where obesity is a consequence of an addiction, abstinence of course is not an option. Thus, the default in weight management is harm reduction. Obviously, this does not make obesity management any easier. In alcohol dependence, abstinence is an option – no one would try to manage their alcohol addiction with a “drinking plan”. But in “food-addiction”, clients are often presented with and are expected to follow “diet plans”. When they fail to stick with these “plans”, they are simply labelled as non-compliant and often discharged from these programs. In addition, it appear to me that “compulsive overeating” is perhaps as often a “process” addiction as it can be a “substance” addiction. Readers may be aware that a process addiction is an addiction to an activity or process, such as eating, spending money, gambling, or working too much rather than an identifiable agent or substance. Unfortunately, these addictive behaviors can be as debilitating as those associated with substance addictions. However, while with substance addictions, clients can be expected to simply give up or reduce use of the substance and can be monitored for compliance, process addictions provide much of their reward from the behaviour itself. Sometimes, these behavioural patterns of process addictions can be transferred to other seeminlyg unrelated activities. Thus, as one speaker presented at this conference, people with gambling addictions, can get the same “reward” from running a yellow light, people with shopping addictions, an get hooked on the simple act of trying to find bargains or comparing prices. Thus, “eating addicts” can get “addicted” to the process of fantasizing about, finding, buying, preparing, and eating food – it may not be one food that they are addicted to, because their addiction it to the processes around acquiring food and eating it and not to a particular food or food group. This adds a level of complexity to applying an addiction model to obesity, that may not be quite appreciated by the people who pass out the well-meant but useless “eat-less-move-more” (ELMM) mantra. Indeed, it appears that applying an addiction model to obesity requires a level of sophistication that… Read More »
This week, I am attending a Scientific Symposium called “Recovery From Addiction“, organised as part of the Alberta Family Wellness Initiative of the Norlien Foundation. My interest in this meeting (where, for once, I am not a speaker on the program), comes from the close links between mental health, addictions and obesity that I regularly note in my patients. As someone with no formal training in diagnosing or treating addiction disorders, this symposium is turning out to be most interesting. Yesterday, much of the program focussed on the link between trauma and addictions; on how addictive behaviours (including food addictions) can result from a wide range of traumatic experiences. I was particularly interested in the presentation by Stephanie Covington from the Institute for Relational Development at the Center for Gender and Justice, La Jolla, CA, who talked about the important differences in both the nature and behavioural impact of trauma between genders. Some of these differences are profound and should be noted by anyone dealing with trauma in men and women. For example, while much of the mental, physical or sexual trauma in men is often inflicted by strangers, women often experience these traumas from very people they love and want to be close to. Perhaps not surprisingly, women often have a history of domestic violence, something men are far less likely to have experienced. This perhaps explains the very different responses that men and women have to trauma: while men tend to respond to trauma with destructive actions (aggression, violence, rages), women tend to respond more often with retreat (isolation, dissociation, depression, anxiety). Interestingly, both genders can respond with self-destructive action (substance abuse, eating disorder, deliberate self-harm, suicidal actions). Overall it appears that women are more likely to respond to trauma with depression than with classical PTSD as defined in DSM IV. While men will use addictive behaviours to escape and distance themselves from the realities of their lives, women will often manifest addictive behaviours in order to maintain a relationship, to fill a void of what is missing in a relationship, or to self-medicate the pain of abuse or betrayal. These important differences have a direct relevance for addressing addictions (or obesity) in group settings, which is why Covington made a strong case for running separate groups for men and women. Overall, Covington made a strong case for using a trauma-informed gender-responsive intervention for women in addiction treatments. Thus,… Read More »