For all my Canadian readers (and any international readers planning to attend), here just a quick reminder that the deadline for early bird discount registration for the upcoming 4th Canadian Obesity Summit in Toronto, April 28 – May 2, ends March 3rd.
To anyone who has been at a previous Canadian Summit, attending is certainly a “no-brainer” – for anyone, who hasn’t been, check out these workshops that are only part of the 5-day scientific program – there are also countless plenary sessions and poster presentations – check out the full program here.
To register – click here.
During my current visit to speak at the Icelandic Medical Association Annual Conference and meet with policy makers, my hosts are doing a wonderful job of introducing me to their “Nordic” fare consisting largely of fish, rye bread and other local produce.
Reason enough to post on this recent article by Marjukka Kolehmainen and her team of Scandinavian colleagues, published in the American Journal of Clinical Nutrition, which examines the effects of a Nordic diet on the expression of inflammatory markers in adipose tissue of individuals with the metabolic syndrome.
Participants in this 18-24 week study were randomised to either a Nordic or control diet in the SYSDIET study, whereby participants for this “substudy” were selected from centres in Kuopio, Lund and Oulo. Importantly, subjects chosen for this analysis were relatively weight stable, having lost or gained less than 5% of their body weight during the course of the study.
In accordance with recommendations for a healthy Nordic diet, subjects in the intervention group were counselled to increase their consumption of whole-grain products, berries, fruits and vegetables, rapeseed oil, have three fish meals per week, and chose low-fat dairy products, while avoiding sugar-sweetened products. In contrast, the control group was advised to consume low-fiber cereal products and dairy fat–based spreads while limiting their fish intake to that generally consumed by the average Nordic population.
Gene expression studies were performed in biopsies from subcutaneous fat tissue and showed differential expression of about 130 genes between the two dietary groups – most of which were related to pathways involved in immune and inflammatory response, including genes involved in leukocyte trafficking and macrophage recruitment (e.g., interferon regulatory factor 1, CD97), adaptive immune response (interleukin32, interleukin 6 receptor), and reactive oxygen species (neutrophil cytosolic factor 1).
Together, the analyses showed a significant reduction in many of these markers consistent with an “anti-inflammatory” effect of the Nordic diet.
As the authors point out, these beneficial effects were seen with very little or no weight loss, suggesting that they are indeed attributable to the changes in dietary intake.
These findings may well have implications for us here in Canada, where eating a “Nordic” diet with local ingredients, may well be a far better alternative than trying to emulate a “Mediterranean” diet, the green house impact of which would be anything but healthy.
While preparing for this new venture included working with professional comedians, taking improv classes, and, yes, impromptu appearances at local “open-stages”, I have also delved into the (sometimes rather serious) literature on the science of comedy and laughter.
Indeed, as one may suspect, there is indeed a rather large and growing body of scientific literature on humor, comedy and laughter – including its physiological and psychological effects, its therapeutic use (in everything from depression and chronic pain to cancer and obesity), and as a communication tool for health professionals.
Anyone interested in this topic, may wish to refer to a recent article by Dexter Louie and colleagues from the University of California, Harvard Medical School and the Joslin Diabetes Centre on laughter as a tool for lifestyle medicine that recently appeared in the American Journal of Lifestyle Medicine (btw – a term that I really don’t like).
The article begins with a brief discussion of the three preeminent theories (out of over 100 competing ideas) of why we laugh, which are summarized as follows (the examples are mine):
1. Release theory, which argues that laughter is the physical manifestation of repressed desires and motivations (which explains potty jokes).
2. Superiority theory, which posits that laughter is a means of increasing one’s self-esteem at the expense of others (which is probably why most people laugh at fat jokes).
3. Incongruity theory, which states that humor is created by a sense of incongruity between two or more objects within a joke (e.g. an obesity doctor making jokes about obesity doctors).
The article then goes on to briefly review the physiological effects of laughter, whereby it makes a clear distinction between spontaneous and and self-induced laughter:
“The former refers to “genuine” or unforced laughter, often in response to a stimulus, whereas the latter describes laughter that is simulated de novo. Spontaneous laughter is often associated with positive mood, whereas simulated laughter is primarily physical and is not necessarily associated with positive emotions or feelings. Neuroimaging suggests that different neural pathways are used in these 2 forms of laughter.”
The researchers review a range of studies documenting the positive effects of spontaneous laughter on stress hormones, endorphins, immune response, pain tolerance, anxiety as well as studies showing that the cardiovascular response to a good laugh are virtually identical to those elicited by a bout of physical exercise (exercise physiologists take note!).
Despite these promising findings, the authors are also quick to point out that,
“There is great potential for future research in laughter. Randomized controlled large-scale trials are needed to further elucidate the physiologic effects of laughter.”
In the second part of the article, the authors discuss whether or not physicians should use humor as a tool to induce therapeutic laughter?
“Of course, health is a serious and often grave matter, and humor delivered at inappropriate times can be devastating, insensitive, and crass……Within the bounds of appropriateness, however, both humor and laughter can be beneficial. For one, laughter shared between the provider and patient conveys a measure of trust and light-heartedness. Furthermore, humor can improve communication, as a joke can signal a transition in the conversation from the serious to more benign topics.”
The authors even have suggestions on how to address the issue of laughter in clinical practice:
“Providers can ask, “What has made you laugh recently?” or “How often do you laugh?” Inquiring about laughter opens the door to light heartedness and also could lead to counseling on laughter and sharing the latest research with the patient. More important, it allows the provider to determine what the patient finds funny, thereby allowing the provider to tailor recommendations to better fit the patient’s needs and preferences. This also contains the potential to deepen the therapeutic relationship between patient and provider. Put together with a more structured approach, the health care provider could consider prescribing laughter to patients.”
And here is what a laughter prescription could look like (directly borrowed from exercise prescriptions):
(F) Frequency: once a week
(I) Intensity: belly laughing
(T) Time: 30 minutes
(T) Type: your favorite sit-com
While much remains to be studied in terms of the therapeutic use of laughter (e.g. spontaneous vs. self-induced, individual vs. group laughter, dose-response relationships, laughter yoga, etc.), as the authors point out, there is an increasing body of evidence pointing to potential benefits for health and well-being.
Or, as the authors put it,
“With no downsides, side-effects, or risks, perhaps it is time to consider laughter seriously.”
This happened last week, when Stephanie Simonds and an international group of researchers, in a paper published in Cell, present a rather elegant and sophisticated range of studies clearly demonstrating that the adipocyte-derived hormone leptin is a key mediator of hypertension in diet-induced (and probably other types of) obesity.
The reason I thought that this question had already long been put to rest was due to a series of rather convincing animal and human studies published in the early 2000s (some of which I was directly involved in) that nicely demonstrated a) that obesity in hypertension is largely mediated by an increase in (renal) sympathetic activity; b) that leptin stimulates sympathetic activity and sodium retention; c) in dogs and humans leptin concentrations are closely correlated with sympathetic nerve activity and blood pressure. We’ve also known that obese mice lacking leptin or its receptor do not develop hypertension despite considerable weight gain.
If anyone should have any remaining questions, these are now answered in the paper by Simonds and colleagues which uses an array of experiments involving animals deficient in leptin or leptin receptors, humans with loss-of-function mutations in leptin and the LepR and show that leptin’s effects on blood pressure are mediated by neuronal circuits in the dorsomedial hypothalamus (DMH), an effect that is prevented or reversed by blocking leptin with a specific antibody, antagonist, or inhibition of the activity of LepR-expressing neurons in the DMH.
All of this is interesting and highlights the fact that adipose tissue is far more than a simple storage organ for fat but rather a tissue that plays an active role in the regulation of a wide range of bodily functions.
Leptin alone, just one of the many hormones secreted by fat cells (often collectively referred to as adipokines), has been shown to play an important role in appetite and energy regulation, immune function and bone development.
As for bringing us a step closer to obesity treatments, the study suggests that it may not be easily possible to harness leptin as a treatment for weight loss, as one expected side effect would be an increase in blood pressure and heart rate – effects that have limited the clinical tolerability of other “sympathomimetic” drugs.
This fallacy is based on the rathe simplistic notion that because 7 x 500 arithmetically happens to equal 3,500 Cal, which just happens to be approximately the caloric content of 1 lb of fat tissue, a reduction in weekly energy intake of 3,500 calories should lead to a 1 lb weight loss.
Thus, a recent rather unfortunate “Patient Information” page published in JAMA, states that,
“A total of 3500 calories equals 1 pound of body weight. This means if you decrease (or increase) your intake by 500 calories daily, you will lose (or gain) 1 pound per week. (500 calories per day × 7 days = 3500 calories.)”
Nothing could be further from the truth!
Now David Allison and colleagues, in a letter to the JAMA editors, points out just how nonsensical this “rule” actually is:
“For example, if a 5′6″, 30-year-old woman weighing 180 lb and consuming 2622 calories daily reduced her intake by 500 calories per day, the 3500-calorie rule would estimate her weight loss at 1 year to be almost 52 lb. At 10 years, the 3500-calorie rule would yield a negative body weight..”
Or, as I tell my patients, no one will continue losing weight till they disappear.
As regular reader of these page will appreciate, the simple reason why the 3500 Cal rule is wrong, is because the relationship between changes in caloric intake and weight loss is anything but linear. Rather, as daily caloric consumption decreases (or increases), metabolic demands adapt to compensate for this decrease (or increase), thereby limiting what happens to body weight.
This “dynamic” model of weight loss is nicely illustrated in the many validated predictors of weight loss available online (click here for an example).
Thus, based on such a model, in the above case, the actual expected weight loss at 1 year would only be around 12 lb with stabilization of a a 31-lb loss after 3 years.
Incidentally, these number, which in the above case correspond to about a 7% weight loss at one year and a 16% weight loss at 3 years are well in excess of what can generally be achieved with diet and exercise alone (those numbers being closer to 3-5% at 12-24 months).
As Allison and colleagues rightly point out, such inaccuracies (especially when propagated by reputable journals such as JAMA) mislead both health professionals and the public and do little more than promote unrealistic expectations about weight loss.
It is high time we abandoned simplistic “energy-in energy-out” models of obesity or weight management.