101 Root causes of gallstones include :
“Problems can arise when the gallbladder never receives the signal to squeeze. This leads to a condition known as stasis where bile sits in the gallbladder for long periods of time. If the gallbladder is filled with bile that is laden with high levels of cholesterol, and low levels of phospholipids and bile salts, it can form a supersaturated sludge. This stagnant sludge allows for the perfect environment for crystal-like structures to form that precipitate out of solution”
“These structures are known as gallstones and they can cause irritation in the gallbladder. If the stones are large enough, they may get low”
Research indicates that both gluten and cow’s milk proteins can cause damage in the intestinal tract that leads to gallbladder stasis. Both foods contain proteins that are capable of exciting immune cells in the intestinal tract that can interfere with CCK signaling by disrupting the intestinal lining. If the intestines are damaged, and CCK secretion is interrupted, the gallbladder never fully contracts to squeeze out all of the bile.”
In humans, evacuation of the gallbladder is accomplished by a trigger mechanism which is set off by the presence of fatty foods, meat, and hydragogue cathartics in the duodenum and upper jejunum. Absorption of these substances by the mucous membrane results in the release of cholecystokinin (CCK), a hormone that rapidly circulates in the bloodstream and simultaneously produces contraction of the gallbladder and relaxation of the sphincter of Oddi. The most effective food is egg yolk, which contains certain l-amino acids. Resorption of bile salts by the intestine stimulates the secretion of bile for hours after a meal”
“The lack of endogenous CCK enhances susceptibility to gallstones by impairing gallbladder contractile function and small intestinal motility function. These findings show that celiac disease is an important risk factor for gallstone formation and the gallbladder motility function should be routinely examined by ultrasonography and gallbladder stasis should be prevented in celiac patients”
“Hormones and Neurotransmitters Involved in SO Function. The most important hormone involved in SO function is CCK. CCK released from the enteroendocrine cells in response to a meal exerts direct hormonal effects as well as indirect effects by interacting with neural pathways, leading to gallbladder contraction and pancreatic enzyme secretion. CCK decreases SO basal pressures and inhibits phasic contractions, thereby promoting anterograde flow”
Oh you say diet is key …. ‘No! trust me I’m a Doctor, no other treatment option for gallstones but to rip out your Gallbladder’.
Oh you say a post Gallbladder Surgery complication ( PCS ) is sphincter of Oddi Dysfunction. Which means – ripping out my gallbladder is removing a symptom not treating the root problem
Good doctor – you are a #Fraud. Informed consent requires disclosing all risks and alternative treatment options. And obviously all root causes leading to diagnosis does it not ?
ETHICAL – Violations. The concept of consent arises from the ethical principle of patient autonomy and basic human rights. Patient’s has all the freedom to decide what should or should not happen to his/her body and to gather information before undergoing a test /procedure /surgery. No one else has the right to coerce the patient to act in a particular way.
- Informed Consent: key pieces of information that a physician must disclose:
(1) condition being treated;
- (2) nature and character of the proposed treatment or surgical procedure;
- (3) anticipated results;
- (4) recognized possible alternative forms of treatment; and
- (5) recognized serious possible risks, complications, and anticipated benefits involved in the treatment or surgical procedure, as well as the recognized possible alternative forms of treatment, including non-treatment .
NOT lol funny?
Live Blood Online. http://livebloodonline.com/live-blood-analysis/gall-bladder-gallstones/
Wang, H. H., Liu, M., Portincasa, P., Tso, P., & Wang, D. Q.-H. (2016). Lack of endogenous cholecystokinin promotes cholelithogenesis in mice. Neurogastroenterology and Motility?: The Official Journal of the European Gastrointestinal Motility Society, 28(3), 364–375. http://doi.org/10.1111/nmo.12734 [PMC]
Afghani, E., Lo, S. K., Covington, P. S., Cash, B. D., & Pandol, S. J. (2017). Sphincter of Oddi Function and Risk Factors for Dysfunction. Frontiers in Nutrition, 4, 1. http://doi.org/10.3389/fnut.2017.00001