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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