Colonics and enemas are similar, but there are some key differences between them. An enema relies on a single infusion of a solution meant to cleanse the lower colon, often ahead of a medical procedure. A colonic, for the purposes of detoxifying the body, reaches more of the colon with multiple infusions.
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Dr. John Harvey Kellogg, founder of the Kellogg cereal company, was an early advocate of colonics and promoted their use in medicine during the early decades of the 1900s. As laxatives grew in popularity, colonics became less popular. The lack of evidence-based science to support colonic therapy added to its decline, though some alternative practitioners recommend colonics.
Bowel cleansing appears to change the bacteria and other elements in your digestive tract. A study of 23 people who used bowel prep solutions found temporary changes returned to normal in two weeks. The authors note that more research is needed on gut microbe effects. Even less is known about the impacts of colonic therapy.
A colonic is meant to remove waste that has accumulated in the colon and prevent or treat constipation. However, colon hydrotherapy might do more harm than good. Colon cleanses have been linked with parasitic infections, abscesses in the digestive tract, rectum and colon perforation, and heart failure.
Colonics, also known as colonic irrigation or colon hydrotherapy, are used to flush out large portions of the bowel system. Colonics are controversial when used for continuous bowel cleanses because of the risks associated with them.
Although health experts say there is no scientific evidence of this, proponents of colonic irrigation believe toxins build up in the gastrointestinal tract and cause a variety of health issues, including arthritis and high blood pressure. But many medical professionals advise against colonics. Not only does the body have its own detoxification system through the kidneys and liver, but there are also several harmful side effects from colonics. They can cause abdominal cramping and pain, dehydration, diarrhea, nausea, vomiting, bowel perforation, and infection. The cleanses also harm the microbiome that exists in the gastrointestinal tract by clearing out beneficial bacteria that are necessary for body health.
Interest has been recently rekindled in short chain fatty acids (SCFAs) with the emergence of prebiotics and probiotics aimed at improving colonic and systemic health. Dietary carbohydrates, specifically resistant starches and dietary fiber, are substrates for fermentation that produce SCFAs, primarily acetate, propionate, and butyrate, as end products. The rate and amount of SCFA production depends on the species and amounts of microflora present in the colon, the substrate source and gut transit time. SCFAs are readily absorbed. Butyrate is the major energy source for colonocytes. Propionate is largely taken up by the liver. Acetate enters the peripheral circulation to be metabolized by peripheral tissues. Specific SCFA may reduce the risk of developing gastrointestinal disorders, cancer, and cardiovascular disease. Acetate is the principal SCFA in the colon, and after absorption it has been shown to increase cholesterol synthesis. However, propionate, a gluconeogenerator, has been shown to inhibit cholesterol synthesis. Therefore, substrates that can decrease the acetate: propionate ratio may reduce serum lipids and possibly cardiovascular disease risk. Butyrate has been studied for its role in nourishing the colonic mucosa and in the prevention of cancer of the colon, by promoting cell differentiation, cell-cycle arrest and apoptosis of transformed colonocytes; inhibiting the enzyme histone deacetylase and decreasing the transformation of primary to secondary bile acids as a result of colonic acidification. Therefore, a greater increase in SCFA production and potentially a greater delivery of SCFA, specifically butyrate, to the distal colon may result in a protective effect. Butyrate irrigation (enema) has also been suggested in the treatment of colitis. More human studies are now needed, especially, given the diverse nature of carbohydrate substrates and the SCFA patterns resulting from their fermentation. Short-term and long-term human studies are particularly required on SCFAs in relation to markers of cancer risk. These studies will be key to the success of dietary recommendations to maximize colonic disease prevention.
Results: No consistent approach to the definition or reporting of ACPO has been developed, which has led to overlapping investigation with other conditions. A vast array of risk factors has been identified, supporting a multifactorial aetiology. The pathophysiological mechanisms remain unclear, but are likely related to altered autonomic regulation of colonic motility, in the setting of other predisposing factors.
Conclusion: Future research should aim to establish a clear and consistent definition of ACPO, and elucidate the pathophysiological mechanisms leading to altered colonic function. An improved understanding of the aetiology of ACPO may facilitate the development of targeted strategies for its prevention and treatment.
The instruction of the immune system to be tolerant of self, thereby preventing autoimmunity, is facilitated by the education of T cells in a specialized organ, the thymus, in which self-reactive cells are either eliminated or differentiated into tolerogenic Foxp3(+) regulatory T (T(reg)) cells. However, it is unknown whether T cells are also educated to be tolerant of foreign antigens, such as those from commensal bacteria, to prevent immunopathology such as inflammatory bowel disease. Here we show that encounter with commensal microbiota results in the peripheral generation of T(reg) cells rather than pathogenic effectors. We observed that colonic T(reg) cells used T-cell antigen receptors (TCRs) different from those used by T(reg) cells in other locations, implying an important role for local antigens in shaping the colonic T(reg)-cell population. Many of the local antigens seemed to be derived from commensal bacteria, on the basis of the in vitro reactivity of common colon T(reg) TCRs. These TCRs did not facilitate thymic T(reg)-cell development, implying that many colonic T(reg) cells arise instead by means of antigen-driven peripheral T(reg)-cell development. Further analysis of two of these TCRs by the creation of retroviral bone marrow chimaeras and a TCR transgenic line revealed that microbiota indigenous to our mouse colony was required for the generation of colonic T(reg) cells from otherwise naive T cells. If T cells expressing these TCRs fail to undergo T(reg)-cell development and instead become effector cells, they have the potential to induce colitis, as evidenced by adoptive transfer studies. These results suggest that the efficient peripheral generation of antigen-specific populations of T(reg) cells in response to an individual's microbiota provides important post-thymic education of the immune system to foreign antigens, thereby providing tolerance to commensal microbiota.
Microbes in the colon produce compounds, normally excreted by the kidneys, which are potential uremic toxins. Although p-cresol sulfate and indoxyl sulfate are well studied examples, few other compounds are known. Here, we compared plasma from hemodialysis patients with and without colons to identify and further characterize colon-derived uremic solutes. HPLC confirmed the colonic origin of p-cresol sulfate and indoxyl sulfate, but levels of hippurate, methylamine, and dimethylamine were not significantly lower in patients without colons. High-resolution mass spectrometry detected more than 1000 features in predialysis plasma samples. Hierarchical clustering based on these features clearly separated dialysis patients with and without colons. Compared with patients with colons, we identified more than 30 individual features in patients without colons that were either absent or present in lower concentration. Almost all of these features were more prominent in plasma from dialysis patients than normal subjects, suggesting that they represented uremic solutes. We used a panel of indole and phenyl standards to identify five colon-derived uremic solutes: α-phenylacetyl-l-glutamine, 5-hydroxyindole, indoxyl glucuronide, p-cresol sulfate, and indoxyl sulfate. However, compounds with accurate mass values matching most of the colon-derived solutes could not be found in standard metabolomic databases. These results suggest that colonic microbes may produce an important portion of uremic solutes, most of which remain unidentified.
According to the most frequently performed diagnostic study, radiopaque markers transit, colonic inertia patients have been classified as: (1) having a delayed transit with markers scattered throughout the viscus[16-20], with exclusion of obstructed defecation on manometry or defecography[21,22]; (2) synonymous of STC (without specification of markers' distribution)[23-34]; (3) presenting markers' delay in the ascending[35] or the right colon[36]; (4) showing a delayed transit only in the left colon, or in both the left and right colon[37]; or (5) displaying a delayed right and left colonic transit, but with normal transit in the sigmoid colon and rectum[38].
As regards colonic inertia patients defined by scintigraphic transit, they have been classified as: (1) with delay limited to the transverse colon and the splenic flexure[39]; (2) with delay limited to the cecum, ascending colon, hepatic flexure, and transverse colon[40]; and (3) with delay in the whole colon[41]. Once again, it may be noted that colonic inertia is differently defined by different authors, and the patients under investigation do not represent a homogeneous entity.
Things are not better when colonic inertia patients are classified on the basis of instrumental evaluations, which include: (1) a generic "decrease" of colonic motility[42]; (2) disturbance of colonic motility, defined by severe constipation and abdominal pain, abnormal transit study, and normal anorectal manometry[43]; (3) refractory constipation and motility abnormalities only of the lower gastrointestinal tract[44]; and (4) complete or almost complete absence of colonic motility, documented by manometry or electromyography[45-48]. Again, the great variability of definitions makes likely confusion between entities, as some of the patients in groups 1-3 could easily fit criteria for the irritable bowel syndrome. 2ff7e9595c
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