I have a gut feeling about the pathology of Type 2 Diabetes (T2). A radical new treatment, gastric bypass surgery, suggests we might have had it all wrong. Maybe it is not just about visceral fat and a burnt out pancreas. Can surgery cure diabetes? As the medical establishment stands scalpel in hand preparing to separate us from our small intestine … and $15-35,000 … I hope you do not think me too impertinent for asking, “So, what’s wrong with the small intestine they want to cut out?”
I was told that the disease that plagues me was caused by the genes from my parents and my own gluttony and sloth. We all know it is principally a disease of insulin resistance associated with upper body obesity, right? So, I lost weight and greatly reduced the carb load in my insulin resistant body. I was pretty happy and healthy as I drifted along in the flow of conventional wisdom, but then some troublesome contradictions began to ripple the surface of my understanding of D. As I dove into some of the latest research, I have found myself struggling to keep my head above water in confounding cross currents of new ideas.
Maybe my family lacks intestinal fortitude. My cousin had serious problems related to morbid obesity, and diabetes was one of them. Just short of her 60th birthday, she had gastric bypass surgery. Conventional wisdom holds that fat people are insulin resistant and would predict that massive weight-loss would greatly improve diabetes, but that’s not my cousin’s story. Apparently, her diabetes was reversed shortly after her surgery before she had lost any significant weight.
It’s not the weight-loss, it’s the rerouting the small intestine that seems to be behind the cure. My second cousin to undergo the weight-loss surgery sent me a University of Minnesota study of 8000 diabetics who had undergone such surgery where most reported a reversal of their diabetes. According to the study, “More than 95 percent of patients reported no diabetes symptoms after a duodenal switch, a more complicated procedure that shrinks the size of the stomach and bypasses the duodenum, or first segment of the small intestine.”
Sensing a new medical opportunity, some doctors are now expanding their gastric bypass surgery practice to include other diabetics, even if they are not morbidly obese. Writing in American Diabetes Association (ADA) publications, Dr. Francesco Rubino has put forward “The Anti-Incretin Theory” to justify surgical interventions. Before we explore the mysteries of the anti-incretin, first a word about incretins.
Incretins are peptides in the human body that signal the pancreas to produce insulin. There are two – GIP, which is produced in the lining of the upper small intestine, and GLP-1, which is produced in the small and large intestine. Both GLP-1 and GIP have a very short half-life in the body because the substance DPP-4 shuts them down shortly after they are produced in the intestine. Please underline intestine as we will be winding back to this point shortly.
Pharmaceutical companies are all over the incretins business now. With billion buck drugs like the statins about ready to go off patent, they need a new hit. Diabetes is booming and drugs to mimic and control incretins to better regulate glucose metabolism could be big. Synthetic GLP-1’s, like Byetta and Victoza, have been developed to have a longer half-life than endogenous GLP-1. Another approach is drugs like Januvia and Galvus which inhibit DPP-4 from deactivating the incretins.
The “anti-incretin” theory put forth by the bariatric surgery club has no relevance to the pharmaceutical industry’s plans which to develop and commercialize more incretin drugs. Unproven theories are not needed to recognize that T2s have virtually zero first phase insulin response and any drug that can stimulate better insulin signaling can be a best seller. These new incretin drugs do not attempt to heal the underlying pathology. Like insulin injections, artificial incretins try to balance the hormonal disorder. The results are mixed. many T2s are helped by incretin drugs, but not most. The side effects have been significant and the results imperfect.
So, back to cutting out the mysterious anti-incretin. After reading Dr. Rubino’s writings, I still do not really understand his “The Anti-incretin Theory.” It seems like the anti-incretin is simply DPP-4 which inactivates incretins and other peptides, but no, it is not that simple. Dr. Rubino has not actually discovered his anti-incretin yet, but he believes “it is reasonable to postulate the existence of a counterregulatory mechanism stimulated by the same passage of nutrients. Such an anti-incretin system would have opposite actions to those of incretins” and Dr. Rubino is convinced it originates in the small intestine. He writes that his “findings suggest that a proximal intestinal bypass could be considered for diabetes treatment and that potentially undiscovered factors from the proximal bowel might contribute to the pathophysiology of type 2 diabetes.” Although these “undiscovered factors” remain elusive, the doctors, now joined by ADA prepare to exorcise the demon “anti-incretin” declaring it to be the source of “insulin resistance, diminished insulin secretion, and β-cell depletion—in other words, type 2 diabetes.”
Excuse me, but before you begin cutting your theoretical anti-incretin out of me and my diabetic buddies, may I ask a question. What’s wrong with my diabetic small intestine anyway? As it turns out, this is a rather impertinent question. There is no good medical research yet explaining what the malfunction is in the small intestine. I feel like I am pulling back the curtain in the presence of the Great and Powerful Oz, and peering beyond the current reach of medical science. So, as long as I am in the realm of non-science, allow me some more uneducated speculation.
We all know that diabetes is often an inflammatory disease as evidenced by high C-reactive protein (CRP) numbers. Where does the inflammation come from? Conventional wisdom again implicates our plump bodies and believes the adipose tissue is the origin of the inflammation. And why are we fat? Genetics and poor lifestyle, right? Maybe, but how does that genetic part work? What is the actual mechanism? Two views: Old view is that we get fat like our relatives which creates inflammation which leads to insulin resistance and eventually burns out our pancreases. Revisionist view is that we suffer inflammation first and then insulin resistance, obesity and the whole parade that leads to diabetes.
So, I find myself exploring the inflammation part of the diabetes equation. Where does the inflammation come from? Before, I might look in the mirror and point to my T2 belly, but now the medical establishment is pointing a scalpel at my small intestine. Could gut inflammation be the root cause of much T2 diabetes?
Alternative medicine has long blamed imbalanced diet as the cause of most chronic disease. My blog talks about how foods like simple carbohydrates (especially fructose), bad fats (omega-6, trans-fats, arachidonic acid, etc.) and some allergenic foods (wheat, corn, soy, etc.) might exacerbate inflammation. The Huffington Post’s alternative MD, Dr. Mark Hymann explains the theory.
The typical American diet promotes the growth of bad bugs in the gut. These bugs damage the gut lining and produce toxins that your system absorbs. When your gut is leaky, partially digested food particles can enter your bloodstream, where your immune system reacts, creating inflammation. Inflammation triggers insulin resistance - which makes you gain weight.
When your gut is damaged, it becomes leaky and food particles become exposed to its immune system. The result? A full-body immune response that triggers inflammation, which in turn leads to insulin resistance. And insulin resistance leads to belly fat (and leads to T2).
We often read that T1 diabetes, unlike T2, is an autoimmune disease. While T1 is obviously caused by an autoimmune attack on the beta cells of the pancreas, T2 also has several characteristics of an autoimmune disease with high levels of tissue inflammation being the most obvious. Many T2s also suffer from other autoimmune diseases like hypothyroidism, Celiac, rheumatoid arthritis, fibromyalgia, allergies, asthma, lupus, etc. What if T2 is similar to Crohn’s disease where the lining of the intestine is inflamed? If the lining of the small intestine was inflamed, it would impair our ability to produce incretins resulting in poor insulin signaling, and a leaky gut might spread the inflammation resulting in greater insulin resistance.
So, should we cut it out? Well, maybe we could first explore a kinder and gentler approach. I am appalled at how quickly the medical establishment and the ADA has jumped to the conclusion that gastric bypass surgery is the cure for T2 diabetes. Why don’t we first diagnose the disease and see if we can heal it before we begin cutting. Let’s exhaust all lifestyle interventions before we go to surgery.
Because of the close association between insulin resistance and inflammation, most of things we do to manage our blood glucose (BG) levels will also address the inflammation issue … but not all. Injecting insulin is the clear example of a powerful BG management tool that will not address inflammation as a causal factor. A restricted carbohydrate diet, on the other hand, is an example of a practice that will dramatically lower BG and greatly lower CRP.
If gut inflammation is the root cause of T2, what would happen if the small intestine was completely empty? My most dramatic personal experiment was a seven-day water fast at the end of 2009. From Day 2-7 of my fast, my BGs (tested frequently) were all in the non-diabetic range and my CRP plummeted … and I required no diabetic medications. Specifically, BGs ranged from 74-98 and averaged 86. My CRP dropped from an elevated 8 to a normal 2. Talk about a diabetic cure!
No, I am not advocating the complete cessation of eating, but there is an important lesson. Frankly, fasting is not pleasant. The fasting gurus will tell you that after the initial discomfort, you will feel wonderful. I had a few lucid moments, but generally I felt exhausted, irritable and achy. I believed that this zero carb zero calorie diet would definitely lower BG, but I was sure that, based on how terrible my body was feeling, my CRP would be elevated. My lower back was very sore and my head was throbbing when I went to the lab to get tested. I can only attribute my 75% reduction in general inflammation as measured by CRP to my empty intestine.
In the month of January 2010, I continued my experiment. I did intermittent fasting where I fasted for 24 hour periods every 2-3 days. Results? All my morning BGs were under 100 and my post pradial BGs were also in the non-diabetic range. My morning BGs were good even when I was eating or the mornings after the days I ate. As I lost no significant weight through intermittent fasting, we cannot attribute improved CRP and BGs to weight-loss. Here I must agree with the fasting gurus who say that allowing your intestine periods of healing improves health.
I continue to experiment with lifestyle interventions to reduce inflammation and normalize my BGs including choice of foods, timing and quantities of eating, nutritional supplements and exercise. It’s hard. I understand why doctors are more comfortable with pharmaceuticals and surgery. Lifestyle interventions are extremely difficult to sustain. They only work when discipline can withstand errant hormonal signaling, emotion-based unhealthy behavior, and a whole lot of societal pressure to do the wrong thing. But, when they work, it’s all good.
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