Arteries

(This is a work in progress.  When I'm done, I'll remove this paragraph.)

My wife has asked some very interesting questions over time.  Think of the following topics as being preceded by "If the reduced blood flow theory is correct, that how do you account for..."

Growth
As a child grows to become an adult, he or she increases size.  His or her chest expands.  Why don't all children, then, get diabetes?  Wouldn't this normal expansion of the chest cause the same problem that visceral fat expanding the chest causes in the chest?  --  Well visceral fat may actually press on arteries as well, but if we just go with the stomach yanked to one side and duodenum yanked to the other, this is a valid question.  The answer, I propose, is that the arteries in children also grow, but that the adult body loses the ability to grow.  Therefore, an increase in chest diameter for an adult is a big problem, but it is not for a child.

• I'd like to propose a possible explanation for juvenile onset diabetes.  In rare cases, a child experiences a growth spurt and suddenly gets diabetes.  Perhaps the arteries of such children have been forced into adult, non-growing mode before the rest of their bodies are forced into that mode, and they suffer reduced blood flow to the pancreas as a result.  (It could also have something to do with congenitally short ligament of treitz.)  -- This is just a theory, folks.  

How Does Blood Get To Fat Cells?

Turns out that stem cells still exist in the body and that new miniature arteries needed to feed fat cells can grow even in adults.  It's just the larger, preexisting arteries that can no longer grow.

How Can Arteries Work After Being Nearly Collapsed?

If you tie a string to a small tree's top, and pull the string over to the side, the tree will bend.  If you leave the tree like that for long enough, when you remove the string, the tree will stay bent.  This is one of the techniques of bonsai.  So why don't arteries stay tweaked if they are being pulled on, even if the pressure is released?  There are two answers:  First, those arteries don't grow into position.  They're done growing.

So why don't arteries just stay collapsed, as a pipe stays collapsed if you dent it?  Arteries have muscle cell walls.  That's why you get a pulse, because the muscle cells fire off and help the blood flow.  These muscle cells are resilient.  There is something called the "elastic limit."  If you do not force a piece of metal to its elastic limit, you can bend it many times and it will spring back to where it was.  Metal that is used in such a manner is, in fact, called a spring.  There are leaf springs and coiled springs.  I propose that the arteries leading to the B cells in the pancreas are forced out of shape, but they are not stressed to their elastic limits, and therefore they spring back to where they need to be when the pressure is released.

Two Plausible Theories

I'm going to cobble these thoughts together over the course of days.  When I'm done, I'll remove this paragraph.  Please bear with me.

Gestational Diabetes

I read an article that said they had discovered the reason for gestational diabetes in mice.  If mommy mouse got sufficient serotonin during her first trimester, then she developed an increase in B cells.  If she did not, then when the baby mice got big during the third trimester, the extra demand for insulin forced her to develop gestational diabetes.  Once the babies were delivered, her need for insulin returned to normal and she no longer had diabetes.

The Role of Sugar

Mark Bittman wrote an editorial in the New York Times relating the work of a group of scientists who had done statistical research on sugar and diabetes.  They found a correlation between sugar-of-any-kind (corn syrup or just plain sugar) and diabetes.  The incidence of diabetes rose within a data group (country) in direct proportion to per capita sugar intake.  This was the same kind of correlation used by scientists to show the link between cigarette smoking and lung cancer.

Another article I found explains that sugar is processed slightly differently in the body than other carbohydrates.  It turns to the kind of fat that produces triglycerides.  The presence of triglycerides in the blood causes muscle cells to become more insulin resistant.

Correlating This Gestational Theory With This Sugar Theory

Clearly, these two theories don't correlate.  In fact, (and I have to look this up), doesn't eating sugar produce serotonin?  Doesn't it give you a serotonin high?  (I think that eating fat produces dopamine and sugar or carbs in general serotonin, but I have to reconfirm - post a reply if you have any thoughts).

Do the theories have to correlate?  Do Gestational Diabetes and regular Type 2 Diabetes have to be caused by the same thing in all cases?  No. It could be like "leg pain," which could be caused by sore muscles, a bullet, a nerve in the back being pinched, cancer, etc.  However, the Reduced Blood Flow Theory could be the holy grail of diabetes, something that isn't obvious that actually does explain both gestational and regular Type 2 Diabetes.

How The REDUCED BLOOD FLOW THEORY Could Still Be True

Gestational:  Just because gestational diabetes can be caused in mice by messing with serotonin in the first trimester doesn't mean that that is actually what is causing it in mice or humans.  It could be that most mice and human mothers do increase their B cells during the first trimester, and a reduced blood flow during their third trimesters prevents an insulin surge.  It could be there is a combination of these factors.  The "you need an increase in B cells" theory does not explain why some women retain their diabetes after delivering the baby.  The Decreased Blood Flow Theory does explain it:  the arteries remain tweaked, most likely because of added visceral fat.

Sugar:  More than one factor is going on in diabetes.  Since the factors are related, it is an oversimplification to break the phenomenon down into distinct, separate factors.  However, for the sake of understanding, I am going to do just that for now.  In Type 2 Diabetes, there's what's happening up at the muscles, and there's what's happening down at the pancreas.  There's insulin resistance and there's insulin.  Clearly, all this information about how bad sugar is, and what triglycerides do, relates to why muscles become insulin resistant, but says nothing about pancreas.

Sugar(2):  It could well be that both sugar and reduced blood flow conspire to cause diabetes.  Sugar use makes you need more insulin in a timely manner, and reduced blood flow insures that you're not going to get it.  The sugar use theory does not explain why diabetics lack an insulin surge, except in the leprechaun sense.  You could say, "Somehow the triglycerides prevent an insulin surge as well.  We're still working on the how."  Also, the sugar use theory leaves unanswered why bypass surgeries relieve diabetes.  The Reduced Blood Flow Theory explains why bypass surgery relieves diabetes.

Sugar(3):  The Reduced Blood Flow Theory is a theory that entirely places the development of diabetes down at the pancreas.  It is my idea that any muscle cell in any body would develop insulin resistance given an environment of high blood sugar, or an environment of high triglycerides.  I propose that muscle cells would go back to normal if that environment was the only factor.  Unfortunately, people with diabetes can eat healthily for days, then eat normally and have high blood sugar/diabetes.  I propose that the reason they do not go back to truly normal is a reduced blood flow, not a continuation of triglyceride being released into the blood from their fat cells.  I propose that if triglyceride from the fat cells was causing diabetes, bypass patients would continue to have diabetes until they lost fat, not immediately after surgery.

Sugar(4):  Epedimiological (I have to look up this word) studies, such as the one that shows heart disease rises with smoking, are very useful.  Over time, however, a cause for the effect ought to become clear.  With smoking what we have learned is that smoke enters the blood stream, causes inflammation in the arterial walls, and the inflammation is fought off by the body in a way that produces swelling.  The swelling diminishes or shuts off blood flow and all kinds of problems ensue from that:  heart problems, strokes, legs not getting enough blood.  To date, the step by step link between sugar intake and diabetes has been hinted at on the insulin resistance end, but remains completely unproved on the insulin side of the equation.  Perhaps it will eventually come to light what the link is.  Perhaps the link doesn't exist.

Funny Explanation

This blog is getting unwieldy.  Please refer to my new blog for a coherent presentation.  I will keep this blog for interesting sideshows such as this one.

Overview of This Entry
I will present what somebody said about why duodenal switch resolves diabetes.  I will then mock that.  I will thereafter explain more academically why I think the explanation is either wrong or severely limited, and what it would take to prove it was right.

Someone Else's Explanation of Why Duodenal Switch Works

This article attempts to explain the diabetes reversal effect of duodenal bypass surgery in the following way.  Dr. John Husted is quoted.

(undigested food enters the non-bypassed part of the stomach and therefore) ...secretion of GLP-1 is enhanced. Enteroglucogan (GLP-1) has the effect of suppressing the secretion of insulin in response to a carbohydrate meal, resulting in a lesser amount of ingested carbohydrates being converted to body fat.

The portion of intestine that is bypassed holds an important role as well. Enterogastrone is a hormone that is secreted by the upstream small intestine when food passes through it. This hormone has the effect of converting food to fat. When the upstream portion of the intestine is bypassed - as is the case with Duodenal Switch - enterogastrone secretion is suppressed. The effect of this bypass is that the patient's body after Duodenal Switch has less of a tendency to convert food to fat. 

Not quoting Dr. Husted now, the article then states:  "The metabolic effect of Duodenal Switch surgery... explains why there is a 99% cure rate for type 2 diabetes following the Duodenal Switch procedure."

I Mock This Explanation

Are you telling me that an increase in something that suppresses the secretion of insulin can help cure diabetes?  What about the insulin spike needed to shut down the liver and get the whole business of muscles absorbing gluocogan going?  Did that just go out the window?  You're saying that what diabetics have needed all along was a way to suppress insulin release, not increase it?  Are you mad?

I have read that one of the horrible realities of diabetes is that muscle requires insulin to absorb glucogan, but fat doesn't.  Therefore, when there is insulin resistance in the muscle cells, fat cells just gobble up a lot of the glucogan - they 'convert food to fat.'  Now you're telling me that that isn't exactly true, that fat cells need insulin to ingest glucogan just as muscle cells do.  Ok, fine, whatever.  So now, you're telling me that duodenal switch surgery decreases insulin (thus stopping fat cells from absorbing glucogan as quickly as they would) and it also decreases the fat cells' ability to absorb food by suppressing enterogastrone secretion.  By two ways fat cells just aren't going to take as much of the glucogan that is out there as they would otherwise.  Fine.  How exactly does that help the muscle cells?  Wouldn't that mean that there'd be even more glucose in the blood even longer, because fat cells weren't absorbing glucogan, and because there'd be less insulin for the muscle cells?  Wouldn't that, in the short term, create even greater hyperglycemia, and all the damage resulting therefrom?

Keep in mind that duodenal switch surgery resolves diabetes nearly immediately - before fat is lost.  The longterm goal of fat reduction, albeit noble, ought not to come into consideration when trying to understand why duodenal switch bypass resolves diabetes in the near term.  Dr. Husted's explanation might help explain longterm fat decrease, but what's happening in the blood, in the muscle and fat, before fat is lost is the more relevant concern.  So, really, after all the jargon slinging, absolutely nothing is proposed to explain the diabetes reversal.  Some explanation!

A Slightly More Academic Response

O.k, o.k., I'll try to be calm.  Clearly what we are presented with is a great, mysterious truth:  duodenal switch surgery resolves diabetes.  It is wonderful.  But why?  Well, let's look at what the bypassed parts do.  That's a good place to start.  Bypassed Part #1 absorbs proteins and sugars.  Bypassed Part #2 makes enterogastrone.  So, maybe the presence of more proteins and sugars, and less enterogastrone, explains diabetes reversal.  But does it?  Where are the follow-up experiments that prove it?  Let's say you bypass part of the stomach in a diabetic rat without bypassing the duodenum - just the stomach.  Does that resolve diabetes?  

I think that the part of the "upstream small intestine" that releases enterogastrone is not the duodenum, but the jejunum.  Let's say you bypass part of the jejunum after the duodenum, without bypassing either the stomach or duodenum.  Does that resolve diabetes?  Show me!

Perhaps I am wrong.  Perhaps enhanced enteroglucogan (GLP-1) and decreased enterogastrone, through a series of as-yet unexplained steps, resolve diabetes.  Until that is conclusively shown, however, I'm sticking with the Reduced Blood Flow Theory.