On the Herbal hall mailing list, Dec96,
>This is an energetic process, something that goes far beyond the world of biochemistry, known and accepted western psycho-physiology, light years beyond the world of standardized extracts. It is the essence of wonder and magic that is part of the potential of the art of herbalism.
For years, not presuming to understand very well the TCM model, I have laboriously separated such things as Spleen (Anatomy and Physiology) from "Spleen" (TCM energetic) and Gall Bladder (A & P) from "Gall Bladder (TCM).
I have tended to view such thing as TCM Gall Bladder as an archetype or an urtype...not to EVER be confused with the actual organ. (Always figgered it was sloppy translation by some early German writer)
Still...having my own personal examples of food binges, food obsession and all-around oralism to view others with, and finding a constant stream of intestinal tract - emotional disorders in my clients, I took it upon myself to find if there were any excepted physiologic explanations...I am always looking to physiology to help me find patterns, since I am TCM-impaired.
It turns out there are at LEAST 6 direct GI-CNS hormonal cascade links, and hints of more.
I no longer view gallbladder (A&P) as separate from gallbladder (TCM).
Maybe there WASN'T some mis-translation after all.
Primary Intestinal Tract Endocrine Hormones
- Endocrine hormone, secreted by G-cells in antrum stomach mucosa
- Stimulates secretion of gastric acids, lowers pH
- Stimulates growth of gastric mucosa (cell-proliferative)
- Exists in glycine-bound precursor in intercellular fluid (progastrin), the probable growth-stimulating factor
- Stimulates pancreatic, gallbladder and small intestinal secretions
- Diminished gastric acid, increased serum gastrin
- Increased gastric acidity, decreased serum gastrin
- Too much gastrin, stomach mucosa hyperplasia
- enterochromaffin-like cells (ECL, found only in the acid-secreting stomach) proliferate in diminished acidity, dangerously so when inhibited by H2 blockers...even anticholinergics.
- Infection with Helicobacter pylori causes hypergastrinemia, often causing gastric ulcer
- Yeast metabolites (such as in beer or bread) stimulate gastrin
- Normal gastrin response stimulates acquired immunity in gut
- Diminished OR excessive levels impair normal resistance
- Endocrine hormone, secreted by cells in upper small-intestinal mucosa
- Stimulates stomach enzymes, water and alkali secretions from pancreas and liver: SUPPRESSES gastric acids
- Complex meals stimulate the most; fluids and sugars the least
- Paracrine/endocrine hormone (in the intestinal tract)
- Made by D-cells in gastric mucosa
- Suppresses gastric secretions; Gastrin rises, until suppressed by a combination of luminal acids and somatostatin
- Infection with Helicobacter pylori causes somatostatin suppression, usually causing duodenal ulcer
- Somatostatin also produced in small intestines and large intestines.
- Somatostatin also produced in brain, and released by myenteric plexus cells
- It inhibits motility and tone of stomach and small intestines and gall bladder, and inhibits formation of liver bile, but NOT bilirubin
- It STIMULATES motility and tone of esophagus
- It is elevated in blood and cerebrospinal fluids of obsessive-compulsives
- It inhibits the release of ALL known GI hormones
- It inhibits saliva, gastric, pacreatic, small intestinal and liver secretions
- It inhibits splanchnic blood flow
- It inhibits intestinal absorption
- In the brain it inhibits somatotropin release by the hypothalamic/pituitary axis.
- It is also secreted into the bloodstream by the hypothalamus, where it acts on the primary target tissues in the gut.
- Like epinephrine, it is made LOCALLY (paracrine), and secreted SYSTEMICALLY (endocrine)
- A paracrine hormone in brain, it moderates blood flow (somehow)
- It is an endocrine hormone, secreted from cells in the duodenum and jejunum.
- It stimulates gastric ACID and pancreatic ENZYMES.
- It stimulates contractions of the gall bladder and the biliary duct
- It relaxes the common duct and sphincter of Oppy (see: Garfield)
- It strongly stimulates acquired immunity and antibody response in biliary apparatus AND duodenum/jejunum
- It helps trigger Cholecystokinin release
- It is a vasoconstrictor to breast arteries (??)
- An endocrine hormone secreted by cells in the mucosa of the duodenum the jejunum, also (natch) by the hypothalamus
- Meals stimulate CCK secretions by BOTH the gut and CNS simultaneously
- It stimulates gall bladder contractions and pancreatic enzymes
- Release of CCK GENERALLY satiates the appetite for more food.
- Coincidentally, it is also the LAST major gut hormone secreted in a food cycle
- A secondary rise of CCK (following the initial release) inhibits stomach motility and emptying, but NOT peristaltic action.
- CCK can slow colon transit (unpredictable)
- CCK has no effect on small intestinal transit.
- CCK is secreted MORE with unsaturated dietary fats than with saturated fats, and least of all with butterfats.
- Coffee (intact or decaffeinated) increases intestinal CCK secretions.
- Secretion stimulated by phenylalanine
- It is part of the "antianalgesia response" in the spinal chord, following endorphin or opiate activity.
- It is directly involved in opiate tolerance
- CCK-4 (CCK-tetrapeptide) is associated, and may induce, panic states
- CCK-8 (CNS) stimulates and modifies appetite for food
- CCK-8 is VERY low in those with anorexia and/or bulimia
- Anorectic/bulimics produce less gut CCK (usually CCK-4)
- CCK is also a gut immuno-stimulant, but less active than gastrin and Bombesin (the most active)