Bariatric surgery can
fail. No one wants to talk about that, especially when we’re filled with hope
about what bariatric surgery can do for us. Why does weight loss surgery fail,
and what does that mean for each of us?
In the bariatric
community, we spend a lot of time debating about which WLS is the best – that
is, which one yields the best outcome (my own definition of that is optimal
weight loss with minimal complications). I think we can all agree that there’s
no such thing as a perfect or one-size-fits-all bariatric surgery. If we’ve all
fought weight battles long and hard enough to need or choose WLS, we can surely
agree that obesity is tough to overcome. And that is, I think, the grounds for
further agreement, about why WLS fails.
Here’s my premise:
weight loss surgery fails because of obesity. If you’re thinking you need not
read further because you already knew that, please wait until I explain a bit
more. And those of you snickering in the back of the room, simmer down. I’m a
natural blonde (duh) as well as an old fogey who needs time to make her point,
but like Ellen DeGeneres, I do have a
point.
OK, let’s continue. Some
disappointment or failure can be attributed to the inadequacy of a bariatric medical
device or surgical procedure or surgeon or patient, but underlying all that is
the basic reality of obesity: it’s a chronic and currently incurable disease,
caused by a mixture (unique to each patient) of genetics, behavior, environment
and biology. Weight loss surgery may address some aspects of those factors, but
not enough to cure obesity. So it fails because of obesity.
In the past, I’ve
given a lot of thought to how genetics, behavior, and environment have
contributed to my own case, but no more than a passing glance at the biology of
it. I’m the daughter of a gifted scientist who passed on not one single gene of
scientific aptitude to me (instead, I got his nose and the name McMillan).
I realize that saying
that WLS fails because of obesity is like saying the ocean is wet because it
contains water, but as with many obvious facts of life, it’s easily overlooked.
We go into WLS believing or at least hoping that surgery will fix enough of
what’s wrong in us to help us lose weight and maintain that weight loss, but we
need to remember that no WLS will cure our obesity. We need to remember that
our obesity is at least partly caused by factors that are invisible to us.
Those factors were
invisible to me until a few months ago, when I was asked to write a magazine
article about some recent research studies that found a link between obesity
and fibromyalgia. I’m uniquely qualified to write that article because I’m a
veteran of both wars.
When I began
researching the article, I was astounded by the dense mountain of information:
scientific data, theories, probabilities and conjectures that I’d heard little
or nothing of before despite my exalted status as the World’s Greatest Living
Expert on the Adjustable Gastric Band. I’ve had WLS, talked to dozens of
bariatric medical professionals, attended three bariatric conferences, read
countless books, articles, blogs and reports, but suddenly I felt like a babe
in the bariatric woods. Why hadn’t either of my bariatric surgeons (never mind
my primary care physician) mentioned any of this to me? Are they unaware of it?
Are they hiding it from me and the rest of their patients? Is there a
conspiracy afoot?
This information is
of enormous importance if only because it knocks a big hole in the old-school
blame-the-patient approach. The paranoid in me wonders if the information is
hidden to protect an industry or to further a political cause, but I put those
thoughts aside and instead considered the very real possibility that bariatric
surgeons are well aware of the obesity mountain but are practicing a form of
medicine that circumvents it. They don’t climb the mountain and they don’t hike
around it. They cut right through the middle of it.
THE OBESITY OCTOPUS
To explain myself
now, I’ll have to resort to another simile. In a sense, bariatric surgeons
treat obesity by stuffing a many-armed octopus in a sack and bludgeoning it
with an axe. I’m not criticizing the surgeons. Surgery of any kind requires a
breathtaking degree of confidence, skill, and audacity. Although surgery
doesn’t address every waving octopus arm, it is the only effective long-term
treatment for obesity available in the United States today, and I’m very
grateful that I was able to have WLS and lose my excess weight as a result of
it. At the same time, I sometimes worry about the future. This spring, treatment
of a medical problem required removal of my band. I’ll soon have vertical
sleeve gastrectomy surgery, but what if obesity takes over my life again in
spite of my band and all my hard-won lifestyle changes? Are researchers working
on an obesity cure now that can help me with that in the future?
WHAT CAUSES OBESITY?
It turns out that
researchers have indeed been busy searching out the causes of obesity in the
hope of finding a better way (or ways) to treat it, prevent it, and/or cure it.
As I mentioned above,
several studies have reported a link between obesity and fibromyalgia. It’s
easy to get caught up in a chicken & egg debate about that – does one
disease cause the other? I don’t want to go down that road right now. Instead I
want to talk about some factors that are associated with (and may be contributing
to) both conditions. They are:
Non-restorative sleep – Sleep affects the production of
hormones (leptin, grehlin, cortisol) that are key to the experience of hunger,
appetite, and satiety. Poor sleep tends to decrease leptin (satiety hormone)
production and increase grehlin (hunger hormone) production. It also seems to
increase sensitivity to pain. If you have sleep apnea or another type of sleep
disorder, or even subclinical sleep disturbance, it’s likely that your physical
hunger is increased and your sense of satiety is decreased. The adjustable
gastric band can intervene on your behalf, but it doesn’t correct the hormone
production problem.
Neuroendocrine dysfunction – the nervous system (neuro) and endocrine system (glands) control all
physiologic processes in the human body. The nervous system works by sending
messages through nerves, as if it’s a hard-wired telephone system. Nervous
control is electrochemical in nature and is rapid. The endocrine system sends
messages by the secretion of hormones into the blood and extracellular fluids.
Like a radio broadcast, it requires a receiver to get the message. To receive
endocrine messages, a cell must bear a receptor (a receiver) for the hormone
being sent in order to respond to it. If the cell doesn’t have a receptor, it
doesn’t “hear” or react to the message.
Researchers studying neuroendocrine interactions discovered (among other
things) that in fibromyalgia and obesity patients, certain cells have damaged
or malfunctioning receptors for the leptin, the satiety hormone. It’s the one
that tells your brain you’ve had enough to eat. So one of the reasons you
rarely feel satisfied by a reasonable amount of food (or in my case, an
infinite amount of food) may be that satiety messages are going astray because
your cells’ in-boxes are locked or absent.
Dysregulated HPA is a factor contributing to both obesity and fibromyalgia. HPA stands
for hypothalamus-pituitary-adrenal, three glands (part of the endocrine system)
that are crucial to healthy functioning of many bodily processes. The HPA axis
is a grouping of responses to stress. When you experience stress (whether it’s
physical, like an injury or illness, or mental, like a fight with your spouse),
your body produces a biomarker (messenger cell) that stimulates your HPA axis.
Your hypothalamus (in your brain) then sends a message to your pituitary gland
(also in your brain), where it triggers the release of ACTH
(adrenocorticotrophic hormone) into your bloodstream and causes the adrenal
glands (on your kidneys) to release the stress hormones, particularly cortisol.
Cortisol increases the availability of the body's fuel supply (carbohydrate,
fat, and glucose), which is needed to respond to stress. However, prolonged
elevation of cortisol levels can cause havoc: muscle breaks down, your body’s
inflammatory response is compromised, and your immune system is suppressed. If
you’ve ever taken a corticosteroids medication like Prednisone to treat an
inflammatory problem (like an allergic reaction) or disease (like lupus),
you’ve probably learned the hard that it can turn you into a bad-tempered
eating machine.
Inflammation, as mentioned above, is another culprit in both chronic pain and
obesity. A European study of showed that obese rats have chronic low-grade
systemic inflammation that sensitizes them to pain. Immunological vulnerability
is common to obese and chronic pain patients and contributes to pain, fatigue,
sleep disturbance, and depression. All of those are factors that can prevent us
from exercising and are associated with the neuroendocrine dysfunction
described above.
Mitchondrial dysfunction may also play a role in both chronic pain and obesity. According to
Karl Krantz, D.C., “mitochondria are the power house of the cell. If energy is
not being produced, logically it can lead to or contribute to chronic fatigue
and pain.” A Finnish study of identical twins (each pair including a normal
weight and an obese twin) found that the fat cells of the obese twins contained
fewer copies of the DNA that’s located in mitochondria. This DNA contains
instructions for energy use by the cell. The lead researcher of the study says,
“If one were to compare this cellular power plant with a car engine, it could
be said that the engine of the fat individual is less efficient.” So it’s no
wonder that obese people are not able to burn or use all the calories they
consume. Some medical professionals believe that chemical toxins (such as the
preservative sodium benzoate, used in many soft drinks) and biotoxins (such as
mold) can damage the mitochondria, increase inflammation, and aggravate both
obesity and chronic pain.
WHERE DO WE GO FROM HERE?
Your own brain may in
overload now after working its way through all the biological business I’ve
ineptly but earnestly tried to explain. Even if nothing else is clear, I hope
you’ve grasped the message that the causes of and factors in obesity are
extremely complicated and well beyond the means of any currently existing
medical device or surgical procedure to cure. I also hope you can see that
blaming yourself for your obesity doesn’t go very far in treating it. You are
not in conscious control of your neuroendocrine system. But neither are you entirely helpless. You have, or will soon have,
a bariatric tool that when carefully used, can bring your appetite under better
control and increase your sense of satiety. You can learn as much as possible
about the factors that can improve your overall health and counteract the
misbehavior of your nerves, hormones, and immune system. For example, I know
for a fact that regular exercise helps me manage not just my weight but my
depression and pain. You may feel defeated by the very idea of that, but
according to an article in the July-August 2011 issue of IDEA Fitness Journal,
as little as 5 to 15 minutes of exercise a day can yield health benefits and
also increase your self-control when it comes to food choices.
At the end of the day, I
still suffer from obesity and fibromyalgia, both puzzling and difficult to
treat, but I try not to think of myself as a victim of those diseases. I can
curl up in a chair with a box of chocolates and weep about my situation, or I
can go on learning about my medical conditions and experimenting with ways to
improve my health and quality of life. The author of one of the
obesity-fibromyalgia studies, Akiko Okifuji, recommends that patients adopt
healthier lifestyles and take more positive attitudes toward symptom
management. That may sound condescending, but as Dr. Krantz wryly pointed out,
“every person in America would benefit from that approach.” I know that’s
easier said than done, but I’m willing to try it…are you?
