Friday, 24 July 2015
Burdock, dandelion, Diabetes and gut bacteria - how my brain chews on a mystery
(Originally published 21 October, 2014 here )
There are two types of Diabetes;
Type 1, sometimes erroneously called Juvenile Diabetes, in which the pancreas simply stops producing insulin. Blood sugar levels, left unchecked, rise, causing kidney, circulation and heart problems. It is now thought to be auto-immune in origin, meaning the body does not recognise the difference between self and not self, and for some reason attacks and destroys the beta cells within the insulin producing islets in the pancreas.
Type 2, sometimes erroneously called Adult Onset Diabetes, where-in the pancreas produces insulin, but the body is "resistant" to this insulin and the blood sugar rises, causing kidney, circulation and heart problems. In this case, it is thought to be induced by a diet high in sugar, simple carbohydrates and fats. (Although some people are re-visiting this)
Now, I can wrap my head around auto-immunity (strangely enough) but I don't understand "insulin resistance".
So, off I go to Wikipedia, where I find it explained : (please note the bit I've italicized)
"Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue. In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood. The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion."
The liver! Hmmm. Why is it that no one ever mentions this involvement of the liver? This is exciting!
So what do I not know about the auto-immune form? Back to Wiki .. you know, I have a love/hate relationship with Wiki. As anyone and their uncle can add to an article, it's often filled with contradictions and you really have to know how to read, rather than skim. So, after plowing through what I know to be already outdated material (grrr), I find these interesting tid-bits (again, please note the italicized portion):
"The pathophysiology in diabetes type 1 is a destruction of beta cells in the pancreas, regardless of which risk factors or causative entities have been present.
Individual risk factors can have separate pathophysiological processes to, in turn, cause this beta cell destruction. Still, a process that appears to be common to most risk factors is an autoimmune response towards beta cells, involving an expansion of autoreactive CD4+ T helper cells and CD8+ T cells, autoantibody-producing B cells and activation of the innate immune system.
After starting treatment with insulin a persons own insulin levels may temporarily improve. This is believed to be due to altered immunity and is known as the "honeymoon phase"."
T-cells! Of course!
But wait, on reread of the next paragraph (and now, even my eyes are glazing over, I pity the reader trying to follow along!)
"Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system. However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also required."
"Incretin"?? What's that?
Here we go again ... and EUREKA
"Incretins are a group of gastrointestinal hormones that stimulate a decrease in blood glucose levels."
"In 1970, GIP was isolated and sequenced from intestinal mucosa (JC Brown)."
Okay, lets review -
Type 2 - Gastrointestinal hormones. Intestinal mucosa. = gut bacteria involvement.
Insulin resistance = liver
Type 1 - Autoreactive CD4+ T helper cells. CD8+ T cells. = gut bacteria involvement
Now why is all this so interesting to me?
Because in all the herbal lore and literature, there's reference to Burdock and Dandelion being "good for diabetics". There is rarely, if ever anything else said about this, except a vague reference to something called inulin. which they both contain in their roots (and to an extent, leaves). Not insulin, and if I see one more amateur blogger get the two mixed up, I will launch an attack in their comment section they won't soon forget
Inulin is a pre-biotic, a form of starch that is not digestible by the body, but it is digestible by certain gut bacteria.
Gut bacteria are responsible for our immune and autoimmune activity as well as the maintenance of the intestinal mucosa. Could it be, then, that it is the relatively recent lack of inulin in the Western diet is starving out these regulators, and so leading to a prevalence of diabetes in both forms? That the reason these two herbs, burdock and dandelion are "good" for diabetics is that they feed and so help to replenish the bacteria?
Maybe - of course no one knew about gut bacteria a couple hundred years ago - but they knew these plants helped diabetics.
There is more, (of course), that is helpful about these plants. Each of them, but especially in tandem, are are excellent tonics for the liver (glucose regulation, remember?) and the kidneys (vulnerable in diabetes, remember?).
So all the more reason that these detested weeds should be seen as the treasured medicine plants they are.
And that, my friends, is the sort of thing I love to play with. The marriage of traditional wisdom and the new science of the microbiome.
(By the way, onions and garlic are excellent sources of inulin.)