It’s taking time, but I am working my way through a study, an article and a commentary surrounding some recent work by Dr. Katarina Borer and colleagues on endocrine, appetite and exercise.
I believe I mentioned that Dr. Borer contacted me in response to my Open Letter to Weight Management Scientists. I may have also mentioned that she said my postings were, ahem, interesting and remarkably well informed for a person who is not actively engaged in research. I am digging deep to find my inner objective scientist who would not be moved by such flattery.
I am working my way through these pieces simultaneously because they are based on the same trials, but they present two sets of conclusions. The first set may be found in the study itself, entitled Appetite Responds to Changes in Meal Content, Whereas Ghrelin, Leptin and Insulin Track Changes in Energy Availability and was published in July 2009 in The Journal of Clinical Endocrinology and Metabolism. To give credit where due, her co-scientists are Elizabeth Wuorinen, Kimberly Ku and Charles Burant, not that those names are meaningful to me. Actually, very few of the names in this line of research are meaningful to me . . . yet.
The way I read a study or article is to turn first to the footnotes to get an idea of the bricks that form the foundation for the work or thought at hand. I screen through the lens of my own evaluation system to determine what biases are present. Mostly, in the past, I have read studies that are solely obesity focused, and, whether they admit to it or not, most scientists in this area come with one or more biases. Some feel that obesity is a medical and social ill that must be reversed or cured, and their research is colored by that view – it may prevent them from seeing certain options. Some of these scientists have accepted support from commercial interests – diet companies, foundations associated with pharmaceutical companies, and the like, and that makes their work horribly suspect. Others who publish in this realm are testing the “Health at Every Size” paradigm, or, more accurately, are Hell bent on proving the efficacy of that model, and that limits their view. In any event, I often can see a study or article’s self-imposed limitations in its footnotes. Certain names pop up together over and over, and they indicate a point of view.
I don’t have a grasp of such biases and limitations in the world of endocrine and exercise. In this world, obesity and weight loss are sometimes the focus, but often just confounding factors. With the exception of Cummings et. al., who produced a Ghrelin study that I happened upon by accident, I recognized no one. I am, therefore, trusting that these are all sterling people, and none is a “scientist for sale.” Feel free to correct me if I’m wrong.
In addition to the study, I’m reading a follow-up article that Dr. Borer wrote, that was accepted by Exercise and Sports Sciences Review for publication in April 2010, Nonhomeostatic Control of Human Appetite and Physical Activity in Regulation of Energy Balance and a commentary on that article by Dr. Barry Braun, Why Doesn’t Weight Gain Blunt Appetite and Increase Movement? Nonhomeostatic Responses to Energy Surplus in Humans. (I apologize for not getting you beyond the abstracts.) This follow-up is not merely reinforcing or selling her prior research, but viewing it through an entirely different lens, one that acknowledges that homeostasis (or set point) is a misunderstood player in the regulation of energy balance and inconsistently affects fat storage. We have discussed in these pages that dicey creature, homeostasis. I look forward to synthesizing this scientist’s findings, and I applaud her for being able to look at her own work from different angles.
Next week, I hope to present my thoughts on what she said, and I hope you will have had time to read her writings too, but here I will summarize, sans most scientific jargon, my understanding of what she did, or her methodology, which is enough for today.
The subjects were nine post-menopausal women who submitted themselves for testing on five different days. When you see what they went through, you will acknowledge that they are saints, regardless of how much they were paid. Testing ran from 6 am to 5 pm. They were fed at 6 am and 1:00 pm. Meal content was 60% carbohydrate, 25% fat and 15% protein. Subjects had to consume all of their breakfast meals, but were allowed to eat their 1 pm meals to their own satisfaction (to evaluate for homeostatic energy compensation. Pardon the jargon.). Hourly, subjects were asked to evaluate their hunger, except from 10 am to 1 pm, when they gave evaluations every half hour. Blood was collected hourly and at 15- and 30-min intervals at the start of meals and exercise. Blood panels were evaluated for ghrelin, leptin, insulin and glucose insulinotropic peptide (GIP), and sent for additional analysis of plasma glucose, nonesterified fatty acid (FFA) and a substance I am positive that I am mentally mispronouncing – Beta-hydroxybutyrate? Here are the variables manipulated on each of the five days, presented to subjects in a random order:
1. A small meal (100 kcal) + saline infusion + rest
2. A small meal + intravenous nutrient replacement (TPN) of 364 kcal — the same macronutrient content as the meal + rest
3. A small meal + TPN calorie replacement + exercise (administered over a two-hour period and tailored to the individual based on pre-testing in order to burn roughly 550 kcal)
4. A large (500 kcal.) sized meal + exercise
5. A control day where they were simply given a nice 500 kcal breakfast and allowed to rest
All of this testing resulted in multitudinous graphs that will test my brain to its capacity, and I look forward to talking about them.
Not to ruin the outcome, but there are sentences and paragraphs in the early narrative that I have already marked with special stars. They give me comfort. For example, in the introductory remarks in the study itself, she tell us (using three citations for support) that “Hunger stimulus is less clearly defined (than satiation), with the stomach hormone ghrelin a potential mediator. Ghrelin and satiation hormones communicate with the hindbrain through the afferent vagus.” Is it my imagination, or is that a nice way to say that my “eat impulses” are REAL!? Leptin and pancreatic insulin are much more vulgar in how they communicate with us, reaching “the hypothalamic arcuate nucleus through the circulation.” Seems to me, this probably creates a wholly different sensation.
Meanwhile, people bemoan weight regain in women’s magazines and blame themselves, because they’re sure they’re too emotional. The Jillian Michaels of the world bark at them that they have “NO excuses.” Maybe. But maybe not. Perhaps some of them aren’t so emotional as they are hormone imbalanced. Maybe when they are weight reduced, a 24% elevation in ghrelin is quietly pickling their hindbrain (by way of their afferent vagus, of course) and compelling them to eat.
I also put a star next to this footnoted sentence, because of its practical applications for those of us who are maintainers: “Exercise does not affect appetite at low intensities and volumes but suppresses it as both increase.” Yeah, baby. That’s why 90% of maintainers on the National Weight Control Registry, are exercising fairly intensely for one hour a day. It’s suppressing our appetites!!!!
Speaking of appetites, I hope this post has whetted yours. Over the weekend, I will try valiantly to understand and translate these interesting words of Dr. Borer et. al. into a less technical jargon. Someday, I may also have to read some of the articles that serve as foundation bricks in the footnotes. There are many interesting titles there.
Eventually, I will also respond to Dr. Jay Olshansky, who last week jumped into the comments of my March 5th post on whether obesity is lowering life expectancy for our children. He thinks I have misinterpreted his article. I owe his work a second look for paying me the respect of a comment, but I am not optimistic. Maybe he was more careful in his language than I recall or gave him credit for, and if I owe him an apology, I should extend it. But one thing I know is that his article is continually used to inflame fat phobia and push forward the “war on obesity” agenda (translation: war on fat people or, in this case, war on parents of fat children). In that regard, Bacon and Aphramor got it right. Perhaps I have missed those times he has jumped in and corrected people who have overblown his findings, but, again, I am not optimistic. I should also look at Olshansky’s more recent work, as well. He is kind hearted for taking me seriously and visiting this blog.