Strangled Pancreas

Theory: Type 2 Diabetes is caused by physical pressure to the pancreas, or on arteries leading to the pancreas, and is cured by relieving physical pressure to the pancreas or arteries leading to it.

Challenge: Prove me wrong.

Caveat: I offer no advise to any individual with Diabetes. I am not a doctor or a researcher, just a thinker. What I say here is theory, not accepted fact.

The Big Picture, What Is Known:

While I was lying in bed, daydreaming, an idea occurred to me. It had to do with the role of the first part of the small intestine in diabetes. Since that initial idea, and it being brushed off by a knowledgeable friend, I’ve learned that the pancreas sits in the first fold of the small intestine, and modified my idea. First, some facts:

• (A) Women with fat hips tend not to get diabetes. Women with fat bellies do. Men with fat bellies do (few men gain weight on the hips). (http://esciencenews.com/articles/2008/05/06/not.all.fat.created.equal)
• (B) People with stomach bypass surgery (Roux en Y), which bypasses both the stomach and the first part of the small intestine, who had diabetes, lose their diabetes within a week or two after surgery - before they lose significant weight. (As reported by Leslie Stahl on 60 Minutes, also http://www.cornellsurgery.org/patients/MungoBlobs/777/791/is_type2_diab_operable_rubino.pdf )
• (C) People with bariatric banding (putting a band around the stomach) get diabetes reversal after they lose weight. (Large article in NY Times said this. I can't find it. It is also here: http://www.nationalreviewofmedicine.com/issue/2008/02/5_advances_medicine_2.html)
• (D) Mice with diabetes lose their diabetes when the first part of the small intestine alone is bypassed (bilio pancreatic diversion – BPD). Their stomachs are still in the food path. (60 Minutes)
• (E) Pregnant women sometimes get diabetes. After they deliver the baby, these diabetic pregnant women oftentimes revert to not having diabetes. (http://en.wikipedia.org/wiki/Gestational_diabetes)

If excess fat alone led to diabetes, then people with fat hips would be just as likely to get the disease as people with fat bellies, but they're not (A).

If stomach fat alone led to diabetes, then you would have to wait until its absence for diabetes to be reversed. Although stomach fat dissipation does reverse diabetes (C), people whose stomachs and first part of small intestines are bypassed also have diabetes reversal – before they lose significant belly fat (B). Rats whose first part of small intestine is bypassed also lose their diabetes (D).

Pregnant women, who are not obese, sometimes get diabetes. Many of these women lose their diabetes after delivering the baby (E).

The common denominator is when there is pressure on the first part of the small intestine, and hence the pancreas, due to abdominal fat or baby, diabetes comes about. If the pressure is removed surgically (B, D), by losing weight (C), or by delivering the baby (E), then diabetes is reversed.

Although diabetes is not always reversed in women after they deliver the baby, there may still be pressure on the first part of the small intestine due to weight gain during pregnancy. Or, perhaps, something gets kinked during pregnancy (a vein, a duct, a nerve, something) that stays kinked, for some, after.

How Can Diabetes Reversal Be?

Type 2 Diabetes is supposed to be a degenerative illness. In other words, you can't regenerate (get back) what is lost. Think of an orchard. If one year the birds came and ate half the truck farmer's fruit, nothing the truck farmer could do would bring back the fruit that he or she lost that year. The truck farmer could stop further encroachment by the birds – netting, getting some predatory birds, hiring somebody with a shotgun to stand guard, what have you – but the maximum crop that year would only be what was left on the trees.

Or, think of an ice sculpture. If the weather gets hot, and melts down the ice sculpture, there is nothing you can do to regrow the sculpture. You can slow the melting of the ice sculpture, you can stop the melting of the ice sculpture, but you can't get back the melted spires and edges. In fact, extra effort yields no benefit. Even if you put the ice sculpture in a freezer that maintains a temperature far below zero, you cannot bring the ice sculpture back nor preserve it any better than keeping it at 20 degrees Fahrenheit. You can stop the negative, but you can't go positive. That's what degenerative means.

Diabetes reversal is not supposed to happen. It's a shocker. Type 2 diabetes is supposed to be due to insulin resistance. If the muscles throughout someone's body have become insulin resistant, how can the loss of fat or the loss of something that was being added down in the small intestine (one theory) change that? You'd think that anything that had to do with insulin production would only arrest the decline, not improve it.

I know someone with diabetes who said that the NY Times article about bariatric banding and diabetes reversal was wrong. A nurse, a doctor, and a former diabetes researcher backed her up. It's just too good to be true. The idea of diabetes reversal doesn't fit the theory that diabetes is degenerative. Perhaps the nurse, doctor and researcher were thinking that the researchers who posited diabetes reversal were fooled, that someone had controlled their diet and hence controlled their diabetes. It is possible. If you have Type 2 diabetes, you can eat a high fiber diet, hence release glucogen into your bloodstream slowly, allowing insulin production to catch up, and not have high blood sugar for that day. But this is not what is happening with diabetes reversal. No, these people go back to normal, and can eat normally without high blood sugar. It's incredible!

The Strangled Pancreas

How can diabetes reversal be? How can bypassing of the first part of the small intestine have anything to do with insulin resistance in muscles or decreased insulin production in the pancreas? Guess what sits inside the first loop of the small intestine? The pancreas.

So my theory is this: at some point increased belly fat, or pregnancy in some women, puts pressure on the first loop of the small intestine, which strangles the pancreas nestled inside it (or arteries or nerves leading to the pancreas, or veins leading out of it). The pancreas then malfunctions. It cannot produce insulin when needed, and diabetes kicks in. When pressure on the pancreas is relieved, either through surgery (B, D), or weight loss (C), or by delivering the baby (E), then the pancreas goes back to normal and diabetes ceases.

If you are asking yourself how gastric bypass surgery relieves pressure on the pancreas, look at the drawings of the results of the surgery. In RYGB, most of the stomach and all of the duodenum are surgically removed from the flow of food. Sproing. The loop around the pancreas is loosened. (http://www.riversideonline.com/source/images/image_popup/fn7_gastricbypass.jpg also http://jcem.endojournals.org/cgi/content/full/89/6/2608)
In the duodenal switch operation, the duodenum is severed from the foot of the stomach. Sproing again. The vice is loosened. (http://www.duodenalswitch.com/procedure/procedure.html)
Even vertical sleeve gastrectomy appears to loosen pressure on the pancreas. (http://www.obesityhelp.com/forums/vsg/cmsID,8874/mode,content/a,cms/)

The first part of the small intestine may be what malfunctions due to the fat or baby putting pressure on it and the pancreas. After all, fat or baby that presses on the pancreas also presses on the duodenum (first part of small intestine). So far, bypassing the duodenum has been the only quick fix to Type 2 diabetes. But to have all three factors (fat, baby, bypass) relate to the duodenum, especially in a non-pressure-related way, requires a process that no one has yet proposed. I find it hard to believe. I will talk more about this later.

And Just How, Pray and Tell, Do You Propose Pressure as the Perpetrator?

I have proposed that pressure on the pancreas must be the cause of Type 2 Diabetes, but I will not tie myself down to any one theory as to what the pressure is doing. I offer a few possibilities, one of which is my favorite:

• Inflammation – Oops! Scratch that. Probably not. My scientist, former diabetes researcher, friend asked me what was specifically causing the diabetes if pressure was the culprit – what presses on what to cause what? – and I suggested the pancreas got inflamed and didn't work right. She certainly let me know about that. When the pancreas inflames, it ceases functioning entirely, and if it does not disinflame, the animal who has it will die. Type 2 diabetics live for years and years and show no sign of pancreatic inflammation, which is called "pancreatitis." Inflammation can't be the cause.
o Why not go for "micro inflammation that nobody knows about yet?" Well, never say never, but my scientist friend tells me that pancreases taken from cadavers of people with Type 2 diabetes are as healthy as pancreases taken from cadavers of people without Type 2 diabetes. You'd think they would have detected it.

Let's go back to the drawing board for a second. If pancreases of Type 2 diabetics are just as healthy as pancreases from people who don't have the disease, is there a way that my theory about pressure / strangulation of the pancreas can still be true? I think the answer is yes.

There is an organ in the body that can suffer from a degradation of function but still appear normal. I speak, of course, about the penis. If you have erectile dysfunctionality, this can be caused by a decreased blood flow into the penis, and an increased blood flow out of the penis. Drugs like Viagra act by dilating the blood vessels leading out of the penis, allowing the penis to stay erect even if there is a less than optimal blood flow going into it. The kinking or partial blockage of the artery that leads to the penis, causing the decreased blood flow into it, is thought to occur in the pelvic region somewhere quite far away from the penis. It's not the penis's fault. An examination of the penis itself could not tell you conclusively if its owner was erectiley dysfunctional. The penis appears to be healthy and performs one of its functions, urination, well enough; it just doesn't work right for sex.

My theory is quite simple: physical pressure on the pancreas, or on something that leads to or out of the pancreas (nerves, blood vessels), is causing the pancreas to malfunction, or to function slowly, without actually harming the pancreas. Should the circumstance that is harming or slowing down the pancreas be relieved, the pancreas will again function normally and Type 2 Diabetes will go away. That is my theory.

A few possibilities for pancreatic strangulation:

• The nerve(s) that feed the pancreas is/are pinched.
• The islets of Langerhans or the B cells within them (which make insulin) are pinched.
• Pressure is causing calcium to not enter the B cells (http://en.wikipedia.org/wiki/Insulin_release_oscillations) at the right time in the right levels.
• The flow of blood, and hence insulin, out of the pancreas is diminished due to pressure closing down the capillaries. This would be similar to a probably reason people who smoke are at risk for diabetes. For the smokers, the capillaries would be blocked from within (this is my theory, I know of no proof).
• The flow of blood, and hence insulin, out of the pancreas is diminished due to pressure closing down the portal vein.
• The flow of blood, and hence insulin, out of the pancreas is diminished due to pressure closing down veins other than the portal vein.
• Food (chyme) goes back up into the pancreas through the pancreatic duct and somehow causes B-cell malfunction.
• The flow of blood into the pancreas is diminished, and, as a result, the flow of blood out of the pancreas is diminished. This is my favorite theory. There are 2 arteries that feed the pancreas, the superior pancreaticoduodenal artery and the inferior pancreaticoduodenal artery (http://home.comcast.net/~wnor/pancreas.htm),. If one or both of them are pinched, blood flows through the pancreas at a slower rate, upsetting insulin production (my theory). I suppose, technically, they're not part of the pancreas, so my theory should be the "strangled pancreas-or-things-leading-into-or-out-of-it" theory. For simplicity, I'll stick with "strangled pancreas." More on why slowing blood flow might be the cause later. Also, it may be that these arteries are only partially blocked when food (chyme) is in the duodenum (that would be a fun one to try to get data on). Another thought, along the same lines, is that when the duodenum is under pressure, its half of the arteries "open up" and drain more blood than the pancreas's half. When pressure is released, the disequilibrium in pressure goes away.
• Something within the pancreas I don't know about even to guess at is affected by pressure and causes the organ to malfunction. Perhaps pressure causes chemicals to be released that shouldn't be, or chemicals to be released in the wrong order, in the wrong amount, or at the wrong time, or chemicals not to be released that should be released. Hey, if someone can propose chemicals they propose must exist in abdominal fat, which they propose affect the liver, which they propose must release something not known that then causes insulin resistance, because it seems to fit certain aspects of the data, why not me propose something I don't know about yet that seems to fit the data? If someone can propose chemicals in the duodenum that are "putative," (http://www.cornellsurgery.org/patients/MungoBlobs/777/791/is_type2_diab_operable_rubino.pdf) why can't I proposed something putative?

Proposed Experiments
To show that the problem is the squeezed pancreas, not the malfunctioning duodenum, you would have to leave the duodenum in the food flow. Find a way to free the pancreas from the duodenum while still leaving the duodenum in the food path. Make sure the pancreas is not pressured in its new environment. See if diabetes goes away. Or, find a way to put stiff mesh around the pancreas (or, as my brother suggests, a Budweiser can), making sure not to put pressure on the arteries leading to it or the ducts dumping out of it, so that the duodenum doesn't pressure it; see if diabetes goes away.

The arteries feeding the pancreas and duodenum run along the border between the two organs and branch off into one organ or the other. It will be exceedingly difficult to separate the pancreas from the duodenum while maintaining blood to both organs. It would be much easier to prove the pressure theory by cutting the duodenum away from the stomach, then inserting a tube or piece of cadaver duodenum between the stomach and the duodenum. This would leave the duodenum in the food path while relieving pressure. – Of course, this would be done on test animals first.

See if an artery leading into or a vein leading out of the pancreas is kinked, occluded, blocked in any way. If it is, put a stent in it to overcome the problem; see if diabetes goes away. Or bypass the artery (superior pancreaticoduodenal artery or inferior pancreaticoduodenal artery) by splicing in a new one across the pinched section. Or shunt in a new artery from another source and splice it in where the superior or inferior pancreaticoduodenal artery enters the pancreas. Or, take a healthy animal, partially clamp or put a pressure-reducing valve in one or both arteries leading to the pancreas or on vein(s) leading out, see if the animal gets diabetes. Remove clamp(s) or pressure-reducing valve(s); see if diabetes goes away (actually, the experiment may have already been performed – I think I read that researchers routinely clamp off the portal vein to induce diabetic symptoms in lab animals. -- Somebody weigh in).

The first experiments that ought to be run should be concentrated on the superior or inferior pancreaticoduodenal arteries (http://home.comcast.net/~wnor/pancreas.htm). Not only are they the most likely culprits, they are the only known potential culprits. – I'd put my money on the inferior pancreaticoduodenal artery, because, from what I can tell, it travels right through the crook in the duodenum, and on the inside of it (http://en.wikipedia.org/wiki/Inferior_pancreaticoduodenal_artery ). I have no access to lab animals, people with diabetes, or cadavers. A researcher must step up!

Extraneous Thought
Have you ever considered that the duodenum hugs the pancreas for a reason? Perhaps chyme flowing through the duodenum massages the pancreas and causes good things to happen. Perhaps the duodenum is supposed to intermittently squeeze off the blood flow to the pancreas, but in diabetics this goes too far. Then again, it may just be that the duodenum is hugging the pancreas so it stays in position to receive the splenic duct and the pancreatic duct. Any thoughts?

Insulin Surge (This is important!)
Take a look at the chart on this website (http://books.google.com/books?id=CRA5N-felmMC&pg=PA91&lpg=PA92&ots=Gp0dy6jmgL&dq=insulin+release+to+portal+vein&sig=ACfU3U1gyWdQxURt7l3-gnkMyCP37S_v0Q#PPA92,M1). It shows page 92 from the book Clinical Diabetes Mellitus: A Problem-oriented Approach by John K. Davidson. Just look at the chart. It shows that there is an insulin pulse coming out of the pancreas just after a person ingests glucose (like, "eats"). During the pulse, a non-diabetic has almost 6 times as much insulin coming out as a diabetic. At other times, the chart shows that the insulin coming out is the same.

Leaving aside what the affect of this difference in insulin pulse mass is, let us ponder what is happening in the pancreas to account for the difference. Something is limiting output. Mightn't it be blood flow?

Analogy: Consider the case of a poor gold processing plant (the pancreas). It has tremendous capacity, works perfectly, and at a magically high rate of speed. In fact, the plant has multiple crushers and smelters (B Cells) inside it. The gold processing plant is fed by trucks bearing ore (glucogen in the blood). The trucks run on an 6-lane one-way highway (artery). Sometimes there are only a few trucks on the road, sometimes hundreds. One day, a landslide (partial arterial blockage) shuts down 5 lanes on the highway. Now, despite the ability of the gold processing plant to refine gold at a high rate of speed, its output is severely limited because it can only refine at the rate the gold ore comes in. At times of the day when traffic is light, the gold processing plant kicks out gold at the same rate as before. When there are a lot of trucks on the road, production only increases a little bit because the amount of ore coming in is limited by the bottleneck in the road.

The B cells in the Islets of Langerhans in the Pancreas make insulin from nutrients in the blood. I'd like to say, "from glucogen" but I've lost the quote. All I can find now is that they make insulin from pro-insulin, and pro-insulin from pre-pro-insulin (http://www.bio.davidson.edu/Courses/Molbio/MolStudents/spring2005/Dresser/My favorite Protein.html). Pre-pro-insulin has the same elements in it as glucogen. But whatever, something traveling in the blood is used by the pancreas to make insulin. Note well: the B cells not only sense an increased level of glucogen in the blood and make insulin, which they would presumably do whether the blood supply was diminished or not, they make insulin from something in the blood. If there is less blood coming in, and hence less raw material available, less insulin can be made in a given time period. A strangled pancreas makes this likely.

My wife, Karen, proposes that there may be a problem with insufficient oxygen getting to the B cells, that that would account for their underperformance. Decreased blood flow is still the main culprit, because of less blood equaling less O2, instead of or in addition to the fact that less blood equals less glucogen. It would be as if the trucks in the analogy above carried fuel as well as ore. Insufficient fuel meant that the factory experienced a brownout and couldn't work at peak levels.

It's not a slam dunk. Maybe something is wrong in the pancreas itself, not in blood flow. Numerous possibilities are mentioned in Mr. Davidson's book. Only further experiments will show what that is. The point I would make is this: researchers should take into account the fact that diabetes goes away when the duodenum is bypassed. If some aspect of pressure is not causing the problem, then what is?

For now, rhetorically, I'd put it this way:

• Which is more likely, that the duodenum releases chemicals (not yet known) into the food path, blood stream, or pancreas itself – that cause the pancreas to malfunction only when it would otherwise produce an insulin pulse
or
• that the post prandial insulin pulse dampening in Type 2 diabetics is caused by decreased blood flow?

You've got to admit, the second option is a lot easier to visualize. It should be a lot easier to test for, too. How are you going to test for chemicals you don't know exist?

Why Do Some Fat People, and Most Pregnant Women, Not Get Diabetes?
Consider the case of two men I know, a generation older than myself. Both grew up on a farm. One left the farm for a desk job. His farm boy appetite did not leave him, however. He had a fat belly. He could grab parts of his belly and perform a hula dance of sorts with them. I was there, I saw it, I laughed, I don't want to see it again. The other stayed on the farm. His belly extended quite far. You would have called it a beer gut. But his gut was made of iron, you could punch it and your hand would just bounce back. The office guy developed diabetes; the farmer did not. One had a muscular frame for his fat to take residence in; the other did not. The one with less muscles had diabetes. – This story is what's known as anecdotal evidence.

Now look at a study of fat teenage boys (http://www.sciencedaily.com/releases/2006/07/060727101521.htm). The ones who were given weight training either did not get diabetes or delayed the onset of diabetes compared to the control group. The weight lifters ended up with just as much fat as the non-weight lifters. Was it that they had more muscles, and therefore mysteriously didn't have "insulin resistance," as the author of the study suggests, or was it that their pancreases weren't strangled?

Most pregnant women don't get diabetes. Why not? Is it because their fetuses don't send forth chemical signals to cause insulin resistance, which would free more glucogen for the fetus, or is it that their bodies stretch out and accommodate the baby more readily and don't end up strangling the pancreas? Why is it that obese women are more likely to get gestational diabetes than fit women? It seems obvious to me that they've already got a head start on pancreatic strangulation. There's only so far a person can expand, and if the space is already partially taken, extra pressure ensues. Else, what is your theory? Is it that the fat produces unknown chemical B7, which doesn't cause diabetes in itself unless in conjunction with a chemical produced by the fetus, unknown chemical B8, which doesn't cause diabetes by itself, but in combination with B7 does cause diabetes, and only in some women? Science is about prediction, about disprovable theorems. Find me these chemicals, and write me guidelines that can predict which women when pregnant will get diabetes. Find me these chemicals, tell me the proportion and concentration already present in diabetics, and we will inject non-pregnant, non-obese, non-diabetic test animals with just the right amount of them and see if they get diabetes.

Other Theories: Vague, Narrowly Focused, Hormonal

Chemicals From Belly Fat Cause Diabetes
From the Los Angeles Times(http://articles.latimes.com/2006/apr/24/health/he-fat24):

"Visceral fat cells make another beneficial hormone, adiponectin, which helps insulin pull sugar from the bloodstream into cells to be used for energy or stored. This also declines as visceral fat levels go up. That can lead to insulin resistance, a condition in which cells no longer respond properly to insulin and which can lead to diabetes.

(paragraphs skipped…inflammatory chemicals discussed…)

"Visceral fat may be worse than fat in the hips or buttocks not just because of the substances it makes – but because of its location. It sits near the portal vein, a major vessel that carries blood from the abdominal organs. “Visceral fat dumps its products into this vein that goes right into the liver,” Bergman says.

"These substances include free fatty acids – fat that circulates in the bloodstream – which appear to make the liver produce too much sugar, upsetting the body’s ability to produce the right amount of insulin. This sets up the body for insulin resistance and possibly Type 2 diabetes."

Oh Yeah?
Yes, the portal vein dumps into the liver. So what? Blood from all over the body eventually makes its way to the liver. Wouldn't free fatty acids from hip fat make their way to the liver, too? And just how is it that someone with a Roux En Y bypass has his or her diabetes resolved before he or she loses belly fat? Doesn't he or she still have less adiponectin than optimal? Doesn't he or she still have visceral fat dumping to the portal vein? What about those weight lifters who had plenty of belly fat but didn't get diabetes (http://www.sciencedaily.com/releases/2006/07/060727101521.htm)? Why doesn't their belly fat "appear to make the liver produce too much sugar, upsetting the body’s ability to produce the right amount of insulin?"

A Very Important Experiment
Check this out: http://wholehealthsource.blogspot.com/2008/03/visceral-fat.html .
"Rats that had their VF (visceral fat) surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well."

What does it mean? If you're just looking at this one experiment, it could mean that visceral fat does something to the liver. But if you look at it in conjunction with other experiments and surgeries, it means something altogether different. To me, it supports my thesis that pressure on the pancreas causes diabetes, not "total fat mass." Both (1) providing a frame via weightlifting for the fat to expand into and (2) removing belly fat – produce the same result. You can factor out the extra muscle gained by weightlifting because the mice did not have extra muscle; neither did the RYGB patients. The common denominator is pressure.

Hormones Block Insulin To Provide More Glucose To Help The Baby
From the Bupa.co.uk website: http://hcd2.bupa.co.uk/fact_sheets/html/diabetes_in_pregnancy.html

"During pregnancy, various hormones block the usual action of insulin. This helps to make sure your growing baby gets enough glucose. Your body needs to produce more insulin to cope with these changes. Gestational diabetes develops when your body can't meet the extra insulin demands of the pregnancy."

Oh Yeah?
Even though later in the same webpage it says that the causes of gestational diabetes are not known, let's just look at this statement. Most pregnant women don't get gestational diabetes. So, even though "various hormones block the usual action of insulin," pregnancy doesn't cause diabetes in them. Wouldn't it be logical to conclude that these various hormones are not the culprit in gestational diabetes? At least you could say that they aggravated something else that caused the diabetes. Whatever you say, doesn't it seem that the doctors are telling us that gestational diabetes is entirely different than other kinds of diabetes, even though the effects are the same? If it is not different, not caused by entirely different hormones for instance, then what does gestational diabetes have in common with diabetes milletus? Is it fat? Not really, though that contributes. It must be … pressure.

Bypassing the Duodenum Allows More Incretins Into The System, Which Facilitate Insulin Production and Usage
From the 2004 article in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism, "Gastric Bypass for Obesity: Mechanisms of Weight Loss and Diabetes Resolution: http://jcem.endojournals.org/cgi/content/full/89/6/2608

"The incretin hormone, GIP, produced primarily by the foregut, is stimulated by ingested nutrients and promotes insulin secretion. Bypass of the foregut should, theoretically, decrease GIP levels…

Oh Yeah?
Actually, the sentence above continues, "and there is little consensus on the actual effect of intestinal bypass operations on this hormone; various reports claim decreased, unchanged, or increased postoperative levels." So, we can pretty much toss out GIP out of hand. – I'm putting this in to show that the scientists are working hard to narrow things down.

Hindgut Hypothesis: "bariatric operations that expedite delivery of ingested nutrients to the hindgut promote weight loss by accentuating the ileal brake."

Oh Yeah?
The ileal brake is the mechanism whereby the second part of the small intestine, the ileum, slows down food progression through the guts (http://www.current-reports.com/article.cfm?PubID=GR01-5-1-05&KeyWords=&Type=Abstract&CFID=15970866&CFTOKEN=98234989). Aside from the fact that it is hard to see how keeping food in the intestines so that it can be absorbed better can "promote weight loss," this is still problematic. We already know that diabetes goes away before significant weight is lost in the RYGB operation, so any positive weight-reducing affect of the hindgut can't be cause the diabetes remission.

Bypassing the Duodenum Disallows Anit-incretins Into The System. Without Those Nasty Anti-incretins, Insulin Goes Back To Normal, Health Is Restored, And Cinderella Lived Happily Ever After
From the 2004 article in The Endocrine Society's ournal of Clinical Endocrinology & Metabolism, "Gastric Bypass for Obesity: Mechanisms of Weight Loss and Diabetes Resolution: http://jcem.endojournals.org/cgi/content/full/89/6/2608

"The GJB (gastric jejunal bypass) resulted in better glycemic control than did either rosiglitazone therapy or substantial weight loss from food restriction. The implication of these findings is that bypss of the intestinal foregut (e.g. as accomplished by RYBG and BPD) can ameliorate type 2 DM independently of weight loss, through mechanisms that remain unclear. The authors hypothesize alternation in gut hormones, but candidate molecules are not obvious."

Oh Yeah?
Savor the beauty of this: "mechanisms that remain unclear…candidate molecules are not obvious." Give them credit for humility, honesty. Actually this is a wonderful thing… But look at the mountain they have to climb here. They have to find a molecule or two that they did not know about before, after studying the endocrine system for decades, and these molecules have to be so powerful that they cause diabetes. They have to show not only what the molecule(s) are but what they do – to the liver, the pancreas, the muscle cells.

We know that the duodenum only releases these putative mysterious chemicals when food is present, because the duodenum/bile duct/pancreatic duct, although cut off from food (chyme), is allowed to drain further down into the small intestine in these bypass operations. And the duodenum is healthy, so far as we know, so it's improbable that it's doing something that it wasn't designed to do. It almost defies nature. Why would the mammals evolve in such a way that, in the course of its natural functioning, a part of every mammal's intestines could cause diabetes? Perhaps there is a positive effect from these chemicals. Look at ghrelin. It impedes the action of insulin, but it has a positive effect: it makes you hungry. They've already ruled out ghrelin, though. So, what positive effect could these awful unknown molecules have that would allow the process of natural selection to retain them? (And if you don't believe in evolution, it's even worse. What was God thinking?) Why is food processed satisfactorily when the duodenum is bypassed, if there is a positive effect to these unknown hormones? … Or, perhaps these putative chemicals don't exist and something else is causing diabetes?

Actually, the theory of the mysterious anti-incretins is the only one that, like my theory of pressure, goes across all Type 2 diabetic categories. That is, although I have not seen wherein the proponents of the anti-incretins out of the duodenum theory say so, this theory could apply to all diabetic categories. It can only apply to them, though, if you factor in pressure. Pressure causes the duodenum to spectacularly malfunction and release an unknown hormone that in some mysterious way causes diabetes. Their theory is that once either the duodenum is bypassed or pressure is released by weight loss or delivering the baby, the duodenum no longer produces such hormones, at least not in sufficient quantity, and everything goes back to swank.

Problems With The Strangled Pancreas Theory

Some Diabetic Rats Are Not Fat and Bypass Operations Still Work On Them
From the Annals of Surgery, 2004 January; 239(1): 1-11 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1356185): "A gastrojejunal bypass (GJB) with preservation of an intact gastric volume was performed in 10- to 12-week-old Goto-Kakizaki rats, a spontaneous nonobese model of type 2 diabetes." It worked. They no longer had diabetes after the operation. The authors, Doctors Rubino and Marescaux, conclude, "These findings suggest a potential role of the proximal gut in the pathogenesis (of) the disease…"

Oh Yeah?
It could still be that the reason those rats had diabetes was that they had strangled pancreases, or strangled arteries leading to their pancreases, from the get-go. Perhaps their arteries were congenitally weak and prone to partial collapse, or their pancreases were congenitally prone to malfunction due to pressure, or their duodenums were congenitally constrictive or extra thick and strangely. If such is the case, these rats don't need fat or baby to cause pressure and cause diabetes; they will get diabetes anyway. Release of duodenal pressure would still relieve the cause of diabetes.

Yes, these Goto-Kakizaki rats are a counter indicator to the pressure theory. But so many other factors, already mentioned, point to pressure being the culprit. Let's not give up on pressure without running a few more experiments. I'm begging you.

Plastic Tubes In the Duodenum Do The Same Thing as Bypass Surgery
From a web entry by "ISDAMan," published April 20, 2008, called, "Diabetes Cured? – the Surgery that Stops Diabetes" (http://www.associatedcontent.com/article/723751/diabetes_cured_the_surgery_that_stops.html?cat=5):
"Dr. Steven Garner also notes that some doctors are bypassing the first foot of the small intestine by inserting a plastic tube by way of a patient's throat. This practice is a creative non-surgical option providing the same prevention of nutrient interaction with the duodenum and jejunum. However, some treatable vomiting may result as a side effect."

Oh Yeah?
This does seem to be bad news for the strangled pancreas theory. Unless such plastic tubes stretch out the duodenum, thus releasing pressure on the pancreas or arteries leading to it, diabetes resolution from the tube operation pretty much knocks the pressure theory out of the water. However, I have been unable to locate any data on this method of bypassing the duodenum. Does it actually work? If the pressure theory is correct, and if the tube doesn't stretch things out, it won't.

(Other reading has shown me that bypass operations in the distant past that did not allow the duodenum to drain caused many severe and painful conditions. I sure hope these plastic tubes have holes in them that allow the bile duct and pancreatic duct to drain.)

… Doctor Garner seems to be a radiologist, not a diabetes expert. I will attempt to contact him. – Those of you who know something about this, respond to the blog and tell me what's up. Does the plastic tube resolve diabetes? Does it resolve diabetes as fast as RYGB? Does it not resolve diabetes right away, but impede food intake and resolve diabetes after fat loss?

I can see a way where the pressure theory is correct and a plastic tube in the duodenum could still resolve diabetes. Since the superior and inferior pancreaticoduodenal arteries serve both the pancreas and the duodenum, if the duodenum were to require much less blood, then more blood would flow to the pancreas. My hunch is that this would be insufficient to make up for a squeezed artery, but I wouldn't want to rule it out.

Why It Matters
Since we already know that a bypassed duodenum, or sufficient weight loss after gastric banding, or delivering the baby, reverses diabetes, what difference does it make whether the problem lay in the duodenum or in the squeezing of the pancreas or whether millions of tiny leprechauns approve of bypass operations and go about making everything right after they are performed just because they can?

First of all, is bypassing the duodenum the best way to defeat diabetes? If the problem is pressure on the pancreas or on a vein coming out of it or an artery leading into it, might there be some other approach that brings about a faster recovery, does less damage to the digestive system, or has less surgical trauma?

Secondly, is there a cheaper way that is sufficiently successful? What about removal of visceral fat, or just the right section of visceral fat? What about an arterial or veinal stent? What about an arterial bypass (where I'd go first)? What about dis-attaching the side of the pancreas away from the stomach from the duodenum to release pressure from the far side, but still leaving the duodenum in the food path?

Thirdly, time's a wastin'. There are 2 reasons for this:

Reason #1
Currently, almost every researcher I've come across is looking for a hormone that causes diabetes. This is understandable because everything else in their world is regulated by hormones. Insulin itself is a hormone. They're looking for a hormone so they can find a drug to counteract it. So long as their minds are set on such a course, they will be reluctant to recommend surgery to alleviate the problem. They'll be chasing the grail until kingdom come.

Personal Pitch: Look, I'm not saying that hormones have nothing to do with it. Consider one of those scales you see at the gym or doctor's offices, the ones with the sliding counter weights. There's the big weight and the small weight. If you weigh 165 or so, you put the big weight on 150, then slide the small weight to 15 or thereabouts. My theory is that the strangled pancreas, or strangled nerve or artery leading to it or vein or veins coming out of it, is the big weight.

Reasons #2
Drug companies don't have a financial interest in a surgery that reverses diabetes; they're making a fortune off of diabetics as it is. Insurance companies may not have a financial interest in a surgical cure either, if they would have to cover and pay for the surgery but don't cover and pay for the drugs. So there is a huge incentive for "experts" to look for a drug that cures diabetes, and to put off surgery until such a drug is found. There is an incentive for them to say "we don't know enough yet," "we don't really know what's going on so we'd better go slow." If researchers really nail down what's going on, the excuses will be unviable; the doctors will have to do the surgeries. The people, through their governments, will insist on it.

It's clear to me that even knowing what they know now, they should be doing these surgeries. I wish it were clear to the powers that be. The high glucogen levels in the blood of Type 2 diabetics can destroy the B cells that produce insulin. When that happens, the human in question gets Type 1 diabetes, which, at present, is not reversible.

Fourthly, a clear determination of cause for Type 2 diabetes may yield insight into Type 1 diabetes. If dimished blood flow to the pancreas is the cause for Type 2 diabeties, for instance, might it not also be a factor in the B cell death that Type 1 diabetics see? Could early intervention help in some way? -- This is wild speculation, folks. Even if this is the case, I find it hard to see how it would help people who already have Type 1 diabetes. It might help somebody in the future, though. I'm just throwing it out there. The point is, somebody with a lab needs to do some experiments attempting to disprove pressure is a culprit in Type 2 diabetes.

And Me
If I am proven right, I'd like a little cred and a little mon. A Genius Award or the Nobel Prize would be just fine. It's the little things that mean so much. Or you could invite me to speak for a fee. I won't have much to say, but I'll appreciate the gesture. If I am wrong, just point me toward the research that shows it. I'll take down the blog and that will be that.

- Matthew Kenney. August 14, 2008.