The Maimonides Model for a Regimen of Health: A Comparison with the Contemporary Scenario.

Rabbi Moses Ben Maimon, known as Maimonides, or The "Rambam" (a Hebrew acronym for his name), was one of the greatest arbiters of all times on matters of Jewish law, one of the greatest philosophers of the Middle Ages, a scientist, and a researcher. In addition, he was a court physician to the Egyptian Sultan. In addition to his monumental work on Jewish law and ethics, his writings on medicine have been considered classics over the generations. The aim of this paper is to assess Maimonides' health regimen and to compare his dietary recommendations with contemporary dietary regimens. To this end, Maimonides' recommendations were compared to the modern guidelines of the United States, the Netherlands, and the World Health Organization (WHO), as well as to the Mediterranean diet, which is popular worldwide. Both marked similarities and contrasts were noted between Maimonides' and modern recommendations. Most of Maimonides' medical recommendations remain relevant more than 800 years later.

Insights into the development of alcoholic chronic pancreatitis at Soweto, South Africa: a controlled cross-sectional study.

OBJECTIVE: We asked why so few working-class Africans of Soweto have chronic pancreatitis (CP) when alcoholism is the norm. METHODS: Twenty-one alcoholics with acute psychosis but normal pancreas were investigated for lifestyle, micronutrient status, electrophilic stress, and iron overload. RESULTS: Alcoholics consumed more ethanol daily than did 14 previously studied patients with CP (P = 0.003); cigarette usage was similar; both groups had even poorer vitamin C status than 14 healthy controls, and no participant had iron overload. The CP group had higher scores for exposure to occupational xenobiotics than did alcoholics (P < 0.05), with lower plasma glutathione (P = 0.047) and urinary inorganic sulfate (P = 0.009). Further analysis identified hyperhomocysteinemia in the alcoholic set, with lower vitamin B12 (P < 0.001), higher folic acid (P = 0.003), and similar vitamin B6 levels compared with controls. CONCLUSIONS: The transition from alcoholism to CP in Soweto is associated with occupational exposure to xenobiotics. Among detoxification systems that are strained thereby, glutathione and inorganic sulfate depend on methionine intake, which is ample in Sowetans, whereas vitamin C, which exerts a glutathione-sparing effect, is deficient. Hence, a daily tablet of vitamin C may enable community prophylaxis against the disease--but homocysteine status would need monitoring.

Duodenal ulcer in South Africa: home-pounded versus milled maize.

BACKGROUND: In South Africa there is suggestive evidence that home-pounded maize protects against duodenal ulceration. Therefore the purpose of the present paper was to test, in an animal model, whether oil from home-pounded maize gives protection against ulceration and whether this effect is present in commercially prepared maize oil. METHODS: Gastric ulceration was induced in rats with topical ethanol 1 h after giving oil prepared either from fresh-pounded or from commercially treated maize. The lengths of the linear ulcers produced were measured with a planimeter and summed in each rat. Control observations were made using arachis oil (which is known not to be ulceroprotective) and horse gram lipid (which is known to be strongly ulceroprotective). Statistical comparisons were performed mainly with the Mann-Whitney U-test, but also with reference to the normal distribution. Thin-layer chromatography (TLC) was performed on the oil from fresh maize, and the fractions similarly investigated for ulceroprotective activity. RESULTS: Fresh maize oil was strongly ulceroprotective (P = 0.0039), commercial maize oil was not (P = 0.2864). The active ingredient in the fresh maize oil was located in the fraction near the solvent front. CONCLUSION: These findings support the hypothesis that home-pounded maize protects against duodenal ulceration.

Recent advances in biological therapy for inflammatory bowel disease.

Immune system is a major determinant of pathophysiology of inflammatory bowel disease (IBD), and cytokines are well known mediators of immune system. Recently, informations on pro-inflammatory cytokines and their role in IBD have led to development of potential therapeutic approach to manipulate these cytokines and there by inhibiting inflammation in IBD. These therapeutic approaches include inhibitors of the tumour necrosis factor (TNF)-alpha lymphocyte trafficking, type 1 T helper (Th1) cell polarization and nuclear factor type beta; immunoregulatory cytokines and various growth factors. Studies on these therapies have documented variable results and the outcomes of many clinical trials are awaited. However, these potential therapies, if become real may revolutionise approach in patients with IBD. Analysis of the inflammed mucosa from patients with Crohn disease (CD) and ulcerative colitis (UC) have shown increased expression of certain proinflammatory cytokines such as interleukin-1 (IL-1), interleukin 6 (IL-6) and TNF-alpha. The latter is important in the recruitment of neutrophils into inflammed tissue, a process which results from three physiological steps: (i) rolling, (ii) adhesion, and (iii) transendothelial migration. Understanding of the biology of chronic inflammation has expanded the therapies available for IBD and particularly CD. At present, the biological therapies that are being used in clinical practice or investigated for the treatment of IBD are predominantly proteins, usually delivered intravenously or subcutaneously. The therapies used include: 1. TNF-alpha inhibitors: infliximab, CDP 571, etanercept, onercept, CNI- 1493 and thalidomide. 2. Inhibitors of lymphocyte trafficking: natalizumab, LPD-02 and ICAM-1. 3. Inhibitors of Th1 polarization: monoclonal antibodies for IL-12, interferon (IFN)-gamma and anti IFN-gamma. 4. Immunoregulatory cytokines: IL-10 and IL-11. 5. Inhibitors of nuclear factor kappa (beta NF-kbeta.) 6. Growth factors: epidermal growth factor (EGF) and Keratinocyte growth factor (KGF).

Detection of a putative novel Wolinella species in patients with squamous cell carcinoma of the esophagus.

BACKGROUND: Certain regions of South Africa exhibit an extraordinarily high incidence of esophageal carcinoma that develops via an esophagitis-dysplasia-carcinoma sequence. Bacteria belonging to the family Helicobacteraceae are candidates for involvement in the initiation of the esophagitis. We investigated patients with esophageal carcinoma for the occurrence of Helicobacter-related species. METHODS: Biopsies from tumor and nonlesional tissue of the esophagus from nine patients with squamous cell carcinoma were investigated for Helicobacteraceae using a PCR-based method targeting the 16S rRNA gene. RESULTS: Four out of nine patients tested negative, while samples from the other five patients revealed an infection by different Helicobacter species. Sequence analysis of the PCR fragments led to the identification of a hitherto unknown bacterium in three of these patients. Phylogenetically, this bacterium was assigned to the genus Wolinella within the family of Helicobacteraceae. Helicobacter pylori was identified in three patients, and one revealed a coinfection with the novel Wolinella species. CONCLUSIONS: Helicobacteraceae were detected in approximately 50% of South African patients with esophageal carcinoma. Furthermore, a novel bacterium was identified that might be linked to the enhanced incidence of esophagitis and subsequent malignant disease in South Africa.

Physiological small bowel malabsorption of carbohydrates protects against large bowel diseases in Africans.

In African black people there is a paucity of 'developed society' large bowel diseases such as diverticular disease, colorectal adenomas and carcinomas, ulcerative colitis and Crohn's disease. Appendicitis has an incidence of about 5-10% of the number likely to be observed in a white population. The conundrum is that the disparity exists despite many Africans having adopted an urbanized lifestyle with major changes in their dietary pattern. Dietary fiber intake, which was previously 30-35 g, has decreased to 12-14 g daily. Studies on small bowel function in black people have shown that physiological malabsorption of lactose, fructose, sucrose and maize (the staple food) occurs. It is hypothesized that the increased concentration of substrate available for fermentation in the colon compensates for the low dietary fiber intake, is protective to the large bowel and is a factor in the prevention of 'developed society' large bowel diseases in the African population.

Acute pancreatitis in Soweto, South Africa: relationship between trypsinogen load, trypsinogen activation, and fibrinolysis.

OBJECTIVE: It is not known why acute pancreatitis in Soweto, South Africa, pursues an aggressive course. We sought clues from circulating trypsinogen load at admission as marker of initial acinar injury, trypsinogen activation using the carboxypeptidase B activation peptide as surrogate, proteinase inhibitors, the coagulation-fibrinolysis axis, indicators of inflammation, oxidative stress markers, and antioxidant status. This article reports on the first four aspects. METHODS: The study involved 24 consecutive patients with a first attack. All of them were admitted within 24 h, and 22 were alcoholic. Urine was analyzed for anionic trypsinogen and the carboxypeptidase B activation peptide. Serum was tested for anionic and cationic trypsinogen, alpha1 proteinase inhibitor and alpha2 macroglobulin. Plasma from a subset was assayed for soluble fibrin, cross-linked fibrin degradation products (surrogates for thrombin and plasmin activity, respectively), and tissue-type plasminogen activator and inhibitor. RESULTS: Soweto controls had higher serum anionic trypsinogen (p = 0.004) and plasminogen activator:inhibitor ratio (p = 0.047) than U.K. controls. The outcome of acute pancreatitis was mild in 17 but severe in seven with three deaths, two on day 2. In mild pancreatitis, intense plasmin activity (p < 0.001) accompanied the surge in trypsinogen, especially anionic (p < 0.001), but without increased thrombin activity and in five patients without trypsinogen activation. In severe pancreatitis, further significant increments in plasmin activity and trypsinogens were accompanied by increased thrombin activity (p = 0.013) and trypsinogen activation (p = 0.046). There was no correlation between surrogates of plasmin and thrombin activity, or between either and the carboxypeptidase B activation peptide, which showed a curvilinear relationship to total serum trypsinogen. CONCLUSIONS: The aggressive nature of alcoholic acute pancreatitis in Soweto seems to reflect early profound fibrinolysis, which precedes coagulation and is initially independent of trypsin. Subclinical acinar-cell injury and a profibrinolytic diathesis in outwardly healthy Sowetans may predispose to this problem.