There’s no question about it in my mind. Obesity is, in large measure, for most of us, a condition of genetic susceptibility. I have to qualify this because I want to address in particular NOT the very small number of people who have a rare genetic disorder (e.g.: Prader-Willi syndrome). I want to address the one-third of us, and I certainly include myself, which I suppose gives me a bias, who will gain weight eating the same foods in the same amounts that the other two-thirds do who do not gain weight. We did, at one time, eat the same foods and amounts without gaining weight, but then something changed, and that something is not simply behavioral (although it lead to ‘behavioral’ change), nor is it less physical activity.
My bias, while it has to be accounted for, is also an advantage. I am simply amazed by several respected authors in the health and nutrition field, whom I will not bash here, who just don’t get it. It’s too bad, but I think you just have to be in our shoes to understand – to know, actually, how the body responds to carbohydrates once your metabolism becomes disregulated – deranged, really, by insulin resistance and the resulting intolerance for carbohydrates of any stripe.
Anyway, I do not seek sympathy. I would hope for understanding of the science, based on emerging (and long forgotten or ignored) knowledge. That would enable empathy, I suppose, but more importantly, an interest in furthering 1) the science, for those who endeavor in that field, and 2) acceptance by the medical and public health establishments of the evidence presented by those serious researchers. Unfortunately, both the medical and public health establishments today are thoroughly corrupted by Agribusiness and Big Pharma. So, only independent researchers and writers, most of them younger and unencumbered by conflicts of interest or conscience, can make a difference. I am but a speck in this firmament, but I power on, seeking the truth, and “broadcasting it” to a small (but rapidly growing) following. Thank you for reading.
My bias is generally informed by the 3-time award winning science writer, Gary Taubes. His seminal tome, “Good Calories – Bad Calories,” is a foundation document. My column #5, “Gary Taubes and the Alternative Hypothesis,” has his “10 certain conclusions” which lay down the basis for my, and many others’, understanding of the science of obesity.
And in #120, “Nutrigenomics -- an Emerging New Science,” quoting from Wikipedia, I wrote: “It is hoped that by building up knowledge in this area, nutrigenomics will promote an increased understanding of how nutrition influences metabolic pathways and homeostatic control, which will then be used to prevent the development of chronic diet related diseases such as obesity and type two diabetes.” Obesity, then, by this definition, clearly is a condition of genetic susceptibility.
Recently, in this piece by Patti Neighmond, broadcast on NPR, Dr. Lee Kaplan, an obesity specialist and director of the Mass. General Hospital Weight Center, said, “We’re all wired in slightly different ways,” adding that “those subtle differences are reflected in how the body deals with energy stores and fat.” The piece continues, “There are thousands of genes in the body, and Kaplan says about 100 of them are involved in making some people more susceptible to weight gain.”
Dr. Osama Hamdy, who directs the Obesity Clinical Program at the Joslin Diabetes Center in Boston, then said: “The reality is, if you have that genetic susceptibility to gain weight, you will gain weight easily, no matter what. Genetic susceptibility has to do with hormones and chemical systems in the body that direct appetite, metabolism and the absorption of nutrients and fat. One of those hormones is leptin. It's produced by fat cells and tells the body when it's eaten enough.”
Hamdy says the majority of people who are obese are resistant to leptin. "The brain is shielded from the information on how much fat you have in your body. The brain is under the assumption all the time that you need more fat." Other hormones make some people get hungry more often than others. Then there's another system of brain chemicals, the endocannabinoid system. When it malfunctions, it fails to tell the body to stop eating appealing foods. For example, if you've always loved the sugary taste of ice cream, you may end up eating way too much of it simply because an enzyme in your brain fails to halt the chemical signal to eat as much of the beloved food as you can.
A 2009 study on the genetic susceptibility of weight gain found that when 12 pairs of identical twins were overfed 1,000 calories a day for about three months, each set of twins gained a different amount of weight. Some only gained about 8 pounds, while others gained nearly thirty pounds. But within the pairs of twins themselves, the weight gain was the same.
Another piece, by Bruno Waterfield, in a British newspaper, The Telegraph, recently reported that Paul van der Velpen, the head of Amsterdam’s health service, said, “Just like alcohol and tobacco, sugar is actually a drug.” Van der Velpen claims that sugar, unlike fat or other foods, interferes with the body’s appetite creating an insatiable desire to carry on eating, an effect he accuses the food industry of using to increase consumption of their products, Waterfield said. “Sugar upsets that mechanism. Whoever uses sugar wants more and more, even when they are no longer hungry. Give someone eggs and he’ll stop eating at any given time. Give him cookies and he eats on even though his stomach is painful,” van der Velpen argued. I can relate to that. I wonder if I am being objective. I wonder if van der Velpen is fat too, or does he just “get it.” I wonder…Postscript: Here’s a video (Part 1 of 3) about Dr. Jay Wortman’s diet experiment with First Nation people in British Columbia, produced by the CBC: http://www.youtube.com/watch?v=bjTmdvFH3gQ. I made a related post in The Nutrition Debate #61, “Steffansson and ‘the Eskimo Diet,’ over a year ago and will return to the subject in #150, “Homage to Vilhjalmur Steffansson by his wife Evelyn,” next week.
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