digestive system diseases

Life extension and
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Fasting, caloric restriction and diseases of digestive system.

Fasting diet therapy in gastrointestinal tract diseases
Vopr Pitan. 2007; 76(6):33-8. [Article in Russian]
Maksimov VA, Karataev SD, Chernyshev AL, Buntin SE, Panaĭkin VI, Lysov AN, Zelentsov SN, Obukhov IuV, Parkhomenko NA, Mel'nikov VL
The article is devoted to an effective not medicamentous method of therapy--to the medical starvation. Indications and contra-indications to carrying out of medical starvation are given. Own results of use of medical starvation are resulted at diseases of bodies of digestion. Practical recommendations on applications of medical starvation for patients with diseases of bodies of a gastroenteric path are submitted.

Effect of fasting on diarrhoea in collagenous colitis.
Digestion. 2002;65(1):30-4 .
Bohr J, Jarnerot G, Tysk C, Jones I, Eriksson S.
Department of Medicine, Division of Gastroenterology, Orebro University Hospital, Orebro, Sweden.
AIM: Diarrhoea in collagenous colitis has been considered as secretory though the pathophysiology has been studied thoroughly in only a few patients. The result of fasting is one way to distinguish between secretory and osmotic diarrhoea. Our aim was to investigate the effect of fasting on diarrhoea in collagenous colitis.
METHODS: Fourteen patients with collagenous colitis were admitted to the hospital for investigation. All were female. Five of these did not have diarrhoea during admission and were excluded. Stools were examined for weight, electrolytes, pH, fat and osmolality during a period on a normal diet and during fasting.
RESULTS: During the fasting period the faecal weight was significantly reduced from median 757 (440-3,198) to 191 (22- 2,197) g. The faecal sodium concentration was also reduced, though not significantly, during fasting from median 65 (29-85) to 45 (19-88) mmol/l. The osmotic gaps varied according to the method of calculation applied.
CONCLUSIONS: The data indicate that the cause of the diarrhoea in collagenous colitis could be multifactorial. In some patients an osmotic factor dominates and in others a secretory factor, while in some patients a combination of both seems to exist.?

Gallbladder motility and gallstone formation in obese patients following very low calorie diets. Use it (fat) to lose it (well).
Int J Obes Relat Metab Disord 1998 Jun;22(6):592-600
Festi D; Colecchia A; Orsini M; Sangermano A; Sottili S; Simoni P; Mazzella G; Villanova N; Bazzoli F; Lapenna D; Petroni ML; Pavesi S; Neri M; Roda E.
Department of Medicine and Aging, University G D'Annunzio Chieti, Italy.
Dieting obese subjects are at risk of developing gallstones. A gallbladder motor dysfunction could have a pathogenetic role. The principal aim of this study was to evaluate the long term effects of two very low calorie diets differing in fat content on gallbladder emptying and gallstone formation in obese subjects.
DESIGN AND SUBJECTS: Gallbladder emptying in response to meals (breakfast, lunch and dinner) in two different diet regimens (3.0 vs 12.2 g of fat/d) was evaluated by ultrasonography in 32 gallstone-free obese patients on different days, before and during (at 45 d intervals) one or two 6-month weight reduction diets (for the first three months: 2.24 MJ (535.2 kcal), 3.0 g fat/d vs 2.415 MJ (577.0 kcal), 12.2 g fat/d; for the second three months, the same low calorie diet of 4.194 MJ (1002 kcal)/d for both groups). In 10 subjects, bile analysis was also performed.
RESULTS: Twenty-two (69%) subjects concluded the study, eleven in each group, and a significant weight loss was achieved by all subjects. Gallstones (asymptomatic) developed in 6/11 (54.5%) (P < 0.01) of subjects following the lower fat diet, but in none with the higher fat regimen. In the dieters during the first three months (very low calorie phase) the higher fat meals always induced a significantly greater gallbladder emptying than the lower fat meals. The cholesterol saturation index initially increased significantly and then decreased, without difference between the two groups.
CONCLUSION: In the obese during rapid weight loss from a very low calorie diet, a relatively high fat intake could prevent gallstone formation, probably by maintaining an adequate gallbladder emptying, which could counterbalance lithogenic mechanisms acting during weight loss.

Review: low caloric intake and gall-bladder motor function.
Aliment Pharmacol Ther 2000 May;14 Suppl 2:51-3
Festi D; Colecchia A; Larocca A; Villanova N; Mazzella G; Petroni ML; Romano F; Roda E.
Department of Medicine and Aging, University G. d'Annunzio, St Annunziata Hospital, Chieti, Italy
Cholelithiasis is the primary expression of obesity in the hepatobiliary system. In obese subjects the risk of developing gallstones is increased due to a higher cholesterol saturation of gall-bladder bile. During weight reduction with very low calorie diets (VLCD) the incidence of gallstones increases, but the mechanism for gallstone formation is not completely understood and several pathogenetic mechanisms have been suggested: increased saturation of bile, increased gall-bladder secretion of mucin and calcium, increased presence of prostaglandins and arachidonic acid. Alterations in gall-bladder motility may contribute to gallstone formation, but few studies have addressed the issue of gall-bladder motility during rapid weight loss and its possible role in gallstone formation. VLCD have been associated with a gall-bladder stasis, as a consequence of reduced gall-bladder stimulation by low fat content of the diets. A threshold quantity of fat (10 g) has been documented to obtain efficient gall-bladder emptying. Ursodeoxycholic acid administered during VLCD seems to have a protective role in developing a biliary cholesterol crystals. Gall-bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as during the VLCD. This may account the possibility of an adaptative response of the gall-bladder motility to a given diet regimen. Adequate fat content of the VLCD may prevent gallstone formation, maintaining adequate gall-bladder motility and may be more economic and physiologically acceptable
than administration of a pharmacological agent.

Gallstone formation in obese women treated by a low-calorie diet.
Int J Obes Relat Metab Disord. 1995 Aug;19(8):593-5?
Spirt BA, Graves LW, Weinstock R, Bartlett SJ, Wadden TA.
State University of New York Health Science Center (Syracuse, NY), Department of Radiology, USA.
This study assessed the incidence of gallstone formation in 47 obese women who consumed a low-calorie diet (LCD) for the first 16 weeks of a 26-week weight loss program. The LCD consisted of four daily servings of a liquid diet combined with an evening meal of a pre-packaged dinner entree and provided approximately 925 kcal/d. Six of the 47 patients (12.8%) displayed gallstones at week 17, as determined by sonography. Five patients were asymptomatic when followed for up to 48 weeks. The sixth, however, reported severe abdominal pain 30 weeks after beginning treatment and required a cholecystectomy. Patients who developed gallstones, as compared with those who did not, had significantly higher baseline triglyceride and total cholesterol levels and had a significantly greater rate of weight loss. Results of this study indicate that an increased risk of gallstones is not limited to very-low-calorie diets and that the incidence of this complication should be assessed in persons who consume popular over-the-counter meal replacement plans.

Gastro-intestinal tract [Naturopathic dietary treatment in functional disorders]
MMW Fortschr Med. 2006 Feb 16;148(7):34-6.
Stange R. Komm. Chefarzt, Abt. fur Naturheilkunde, Charite - Universitatsmedizin Berlin.

Fasting prevents experimental murine colitis produced by dextran sulfate sodium and decreases interleukin-1 beta and insulin-like growth factor I messenger ribonucleic acid.
Endocrinology. 1997 Feb;138(2):734-40
Savendahl L, Underwood LE, Haldeman KM, Ulshen MH, Lund PK.
Department of Pediatrics, University of North Carolina, Chapel Hill 27599, USA.is, gastr


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