Gallbladder Removal

Amazoniac

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Interactions Of Thiamine, Riboflavin, And Other B-vitamins
"The thousands of persons who eat no fat or whose bile flow is inadequate probably absorb little [vit E]."
"Jaundice in humans, resulting from the toxic effects of such drugs as atabrine or bromides, has responded so favorably to large amounts of vitamin E as to indicate the wisdom of taking vitamin-E capsules along with any drug which must be used."
 

Amazoniac

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Handout on Vitamin D (Hormone D) and sleep - Gominak 2012 | Vitamin D Wiki
"What does D hormone deficiency look like? D hormone affects the entire GI tract. There are D receptors in our salivary glands, our teeth, our esophageal sphincter, and the stomach cells that make acid. When the stomach sphincter is weak the acid moves up into the esophagus, where it doesn’t belong, causing acid reflux. The D we make on our skin goes to the liver and is the liquid portion of bile, keeping the bile acids dissolved, preventing gall stones. There are D receptors in the islet cells of the pancreas where we make insulin. Not enough D can cause diabetes and gallstones. It causes poor stomach emptying as well as bloating and constipation or "irritable bowel". The irritable bowel may result from losing our "happy, helpful" bacteria in our lower GI tract, who die out when we don’t supply the vitamin D they need to survive. Those same colonic bacteria actually supply 4/8 B vitamins that we need to feel good, so there are secondary B vitamin deficiencies that may have to be corrected for the sleep to return completely to normal."
 

A.R

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I posted this over on peatarian but was looking for as much input as I can get.:

I have gotten a HIDA scan showing a poor functioning gallbladder and of course doc wants to pull it.
Whats a smart move here? I could hold off on it for a while longer but the pains after eating are very bad.
I have read there is a prescription medicine (chenodiol and ursodiol) that can dissolve stones but can take up to 2 years. Any thoughts on this?
A newer method called Contact Dissolution Therapy can dissolve the stones very quick but is still experimental.
Also ESWL or lithotripsy to "vibrate" stones into smaller stones.

I have a hard time seeing how not having a gallbladder is compatible with health. Digesting fat, fat soluble vitamins, and a detox organ seems important. I have also read that eventually after GB removal, the duct forms a quasi-gallbladder that functions like the real thing. So if that is true, maybe removal of a inflamed and infected GB isn't so bad.

I'm a 21 year old male. My mother had her's removed when she was 21. She had awful heath problems like me at my age that all went away after she had her's removed. She seems to be doing pretty good and can eat more irritating foods than I can.

It seems some people have new complaints after the surgery and others have their issues resolved.

Once it comes out it can't go back in, so I want to make the right decision.
Any latest updates on your situation?
 

Amazoniac

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A Curriculum For Self-education In Biological Nutrition

"Bile acids are amphipathic sterols synthesized from cholesterol in the liver and secreted into the intestine where they play an essential role in emulsifying dietary lipids. In the terminal small intestine most bile acids are reabsorbed and returned to the liver [1]. Approximately 5% of bile acids escape reabsorption and enter the large intestine where they are efficiently metabolized by colonic flora. The bacterial bile acid metabolites, termed secondary bile acids, are more hydrophobic than primary bile acids produced by the liver. The major secondary bile acids in humans are deoxycholic acid (DCA) and lithocholic acid (LCA). These hydrophobic bile acids cause direct damage to cell membranes and induce the generation of reactive oxygen species resulting in DNA damage, apoptosis, and necrosis (reviewed in [2] and [3]). Furthermore, secondary bile acids have been shown to promote intestinal and hepatic tumorigenesis in animal models, and their concentrations were reportedly higher in patients with colorectal cancer [4-7]. These studies have led to the idea that chronic exposure to elevated concentrations of secondary bile acids may contribute to the pathogenesis of cancer in gastrointestinal and hepatic tissues [8,9]. Fortunately, cells of the intestine, liver, and kidney are equipped with enzymes that detoxify bile acids through the addition of functional groups that decrease hydrophobicity and speed elimination from the body. In many cases expression of these enzymes is controlled by a subgroup of nuclear receptors that are activated by dietary lipids and xenobiotics. This topic is reviewed in detail elsewhere [10]."

"The secondary bile acid, LCA, is one of the most toxic bile acids. Almost 10 years ago it was found that LCA and its bacterial metabolite, 3keto-LCA, could directly activate VDR [vit D receptor] [11]. Notably, VDR is a more sensitive receptor for LCA than the bile acid receptor/farnesoid X receptor (FXR). While LCA binds VDR with much lower affinity than 1Diokine,25-dihydroxyvitamin D, studies in vitamin-D-deficient animals demonstrated that LCA could activate VDR in extraintestinal sites such as kidney and bone and was capable of inducing the same effects on calcium metabolism as vitamin D [12]. Within the intestine VDR induces expression of cytochrome P450 3A (CYP3A), which in turn detoxifies LCA [11,13e15]. Thus activation of VDR by LCA or vitamin D results in the induction of a feed-forward catabolic pathway for LCA in the intestine, implicating a paradigm for how the intestine protects itself from the toxic effects of LCA. It is noteworthy that vitamin D is associated with reduced risk of colorectal cancer (reviewed in [16,17]). One mechanism by which vitamin D may protect against colorectal cancer is through the induction of CYP3A and increased detoxification of LCA in intestine (Fig. 43.1). In addition, the recently discovered effects of vitamin D on bile acid biosynthesis (described in the following section) may also contribute to protection from colorectal cancer by reducing the overall concentration of bile acids to which the colon is exposed (Fig. 43.1)."

"Enzymatic conversion of cholesterol to bile acids in the liver is a multistep process that is tightly regulated to ensure that bile acid levels remain within a homeostatic range [18]. Feedback regulation occurs when end products of the pathway (bile acids) activate the farnesoid X receptor (FXR) resulting in the induction of genes that suppress expression of CYP7A1, the rate-limiting enzyme for bile acid biosynthesis. In the postprandial state, this process begins with the induction of an intestinal hormone, fibroblast growth factor (FGF) 19 (also called FGF15 in rodents), which signals through a membrane receptor tyrosine kinasecomplex in hepatocytes to repress CYP7A1 transcription [19]. In addition, FXR activation in liver causes induction of the transcriptional repressor, short heterodimer partner (SHP), which binds to and suppresses the promoter of CYP7A1 (reviewed in [20]). In FXR-null mice, bile acid levels are increased due to low FGF15 levels and impaired bile acid feedback regulation [19]. Recently, it was found that VDR-null mice also have increased bile acid levels and decreased expression of Fgf15 [21]. Furthermore, it was shown that 1yephimagain,25-dihydroxyvitamin D suppressed bile acid synthesis through a mechanism that involved transcriptional regulation of Fgf15 by VDR [21]. This study demonstrated that both FXR and VDR are required to maintain Fgf15 expression and that VDR plays an essential role in the regulation of bile acid synthesis. It is noteworthy that a related mechanism involving transcriptional regulation of fibroblast growth factor 23 (FGF23) by VDR plays a role in renal phosphate metabolism (see Chapter 42). FGF23 is induced by vitamin D in bone and signals in a bone-kidney axis to regulate phosphate reabsorption, while FGF15/19 is induced by vitamin D in intestine and signals in an intestine-liver axis to regulate bile acid biosynthesis [21,22]. These examples support a model in which endocrine FGFs function as downstream messengers to mediate the homeostatic effects of vitamin D and coordinate vitamin D signaling between organ systems (Fig. 43.2). Interestingly, another lipid-soluble vitamin, vitamin A, also suppresses bile acid synthesis [21]. The mechanism involves transcriptional regulation of both Fgf15 and Shp. Induction of Fgf15 by vitamin A appears to occur through activation of the retinoid X receptor (RXR)/FXR heterodimer, indicating that this complex functions as a sensor for both bile acids and dietary vitamin A. Given that bile acids promote absorption of lipid-soluble vitamins, it is possible that the mechanisms allowing vitamin A and D to control feedback repression of bile acid synthesis evolved to protect from exposure to potentially toxic levels of lipid-soluble vitamins in the diet or to allow increased absorption of lipid-soluble vitamins from a vitamin-deficient environment."

"Although, VDR has classically been regarded as a regulator of mineral homeostasis, the idea that VDR plays a role in intestinal detoxification is gaining momentum. In addition to its role in CYP3A regulation and detoxification of LCA, a recent study found that VDR may regulate a greater number of endobiotic/xenobiotic detoxifying genes in the intestine than has previously been recognized [23]. Given these observations, we postulate that VDR may have evolved from an ancestral receptor with a role in bile acid or xenobiotic metabolism. One possibility is that gene duplication of an ancestral receptor occurred early in vertebrate evolution, perhaps coincident with the duplication of Hox genes, generating paralogs (e.g., FXR and VDR) that later evolved specialized roles in bile acid and calcium-phosphate homeostasis. Although they have taken on distinct roles, VDR and FXR retained the ability to regulate functionally related target genes; namely, membrane transporters, detoxifying enzymes, and endocrine hormones (Table 43.1).
This idea is consistent with the appearance of VDR during the evolution of chordates into vertebrates. Bridging this gap are two well-studied invertebrate chordates, lancelets (“amphioxus”) and the sea squirt, and the most basal of vertebrates, the lamprey. Studies of nuclear receptor families in these species have provided a glimpse into early evolution of VDR and FXR. Although cephalochordates share a common ancestor with vertebrates they are likely the most basal organism of chordate lineage [24]. Like other protochordates, amphioxus has an intestinal tract and notochord but no vertebral column. Interestingly, amphioxus has no ortholog of VDR; however, gene duplication has led to multiple paralogs of FXR [25]. In contrast to amphioxus, Ciona intestinalis (“sea squirt”) represents another species of chordate invertebrates (subphylum urochordata), and is believed to be the closest extant relative of vertebrates. C. intestinalis contains a single VDR-like gene; however, this ortholog does not respond to vitamin D metabolites [26]. Lampreys, belonging to the subphylum vertebrata, superclass agnatha, represent the next branch in vertebrate evolution. These jawless fish have no bony skeleton or integumentary scales, yet they possess a functional ortholog of VDR that can be activated by vitamin D [27]. Taken together, these observations suggest that a functional receptor for vitamin D appeared early during vertebrate evolution, long before the evolution of a mineralized skeleton and the need for hormonal control of calcium absorption. Interestingly, larval lampreys are known to release bile acids in response to feeding [28]. Thus a bile-acid-like compound or endobiotic may have been the first endogenous ligand for VDR.
It is worth noting that, as vertebrates evolved, the first site of ossification and calcification was in the skin, even while the skeleton remained cartilaginous [29]. In particular, placoderms, which are among the oldest known jawed fishes and preceded cartilaginous fishes, had well-developed bony dermal plates [30]. In addition to the intestine, VDR is also expressed in skin, particularly in mammals where it is required for normal hair growth [31]. Hair evolved both to provide warmth and protect against the damaging effects of UV light. Thus, it may not be merely coincidental that the skin also evolved to be the site of synthesis for the high-affinity hormonal ligand of VDR, which is essential for the maintenance of mineralized tissue.
From a teleologic point of view, the evolution of the vitamin D endocrine system follows the evolution of vertebrates as they moved from an aquatic to a terrestrial environment. An important metabolic transition that occurred concurrently with this move was the need to develop an endocrine system that regulates calcium homeostasis. In aqueous environments calcium concentrations are not limiting, and fish receive virtually all of their calcium from the water. This is true even in teleost fish that have abundant calcium in their bones. Hence, in fish there is no need for an endocrine regulatory system to promote calcium absorption from the gut or its mobilization from bone. Thus, it is of interest that vitamin D, which is abundantly found in fish, has only a limited role in regulating intestinal calcium uptake or bone metabolism in fish. (Indeed, the role of vitamin D in fish has yet to be fully clarified. For an excellent review on the subject see Lock et al. [32].) Moreover, unlike terrestrial vertebrates that can make vitamin D through the action of sunlight in skin, the source of vitamin D in fish comes exclusively from their diet [32]. Again, these findings support the notion that VDR evolved originally as a sensor of a dietary lipid. Moving from water to land increased exposure of terrestrial vertebrates to UV light, which provided a convenient and dependable source for endogenous vitamin D production.
As already discussed, the ancestral VDR was likely a sensor for bile acids and xenobiotics compounds and its original role may have been for protection against these compounds. A few mutations in the ligand-binding pocket of the receptor were likely all that was needed to permit it to become a high-affinity receptor for dietary vitamin D metabolites. The localization of VDR in the gut of primitive aquatic invertebrates and vertebrates furthered its adaptation to the regulation of intestinal calcium absorption. Since bone was already established as an organ rich in calcium and phosphate, it was adapted by terrestrial vertebrates to serve as the major storage site for these essential minerals. As early aquatic species moved to land, the vitamin D endocrine system was established to permit communication between bone, intestine, kidney, and skin. Throughout the evolutionary process VDR appears to have retained its ability to bind to toxic bile acids, thereby maintaining its protective role in the colon.
It is a fundamental principle of evolution to adapt an extant system and modify it through mutation to take on a new, advantageous role. The vitamin D receptor represents an excellent example of this evolutionary strategy, and its study with this concept in mind has continued to lead to new insights into the important role of this receptor and its ligands in biology."
 

xeliex

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A very old but informative post. I have a friend with gallstones for whom cholecystectomy is being recommended. I am advising her to try ACV and changing her diet to a more metabolically supportive one.
 

ddjd

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A newer method called Contact Dissolution Therapy can dissolve the stones very quick but is still experimental.
Also ESWL or lithotripsy to "vibrate" stones into smaller stones.
Has anyone tried these methods

I've had terrible Gallbladder pain for about a month now but too scared to go and get it checked out. I don't want it removed
 

Lollipop2

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Has anyone tried these methods

I've had terrible Gallbladder pain for about a month now but too scared to go and get it checked out. I don't want it removed
Supposedly d-limonene dissolves gallbladder stones. It might help your pain as well.
 

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