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?