Lean Australian red meat cuts are low in fat and have a ratio of cholesterol-raising saturated fatty acids (SFA) to cis-monounsaturated fatty acids (MUFA) to cis-polyunsaturated fatty acids (PUFA) of around 24:40:14. This is less cholesterol-raising than was earlier estimated, because cuts are now leaner and part of the SFA is stearic acid (that does not raise plasma cholesterol). and there are several other (cholesterol-lowering) PUFA as well as linoleic acid present. Low-fat, predominantly monounsaturated lean meat cuts have been shown to be acceptable in cholesterol-lowering diets. This does not mean that meat eaten with the fat on will not raise plasma cholesterol.Meat is low in sodium, high in potassium and has been shown in human dietary experiments not to raise the blood pressure.Meat is high in protein and contributes to weight reduction by increasing satiety and helping reduce intake in ad-lib weight-reducing diets. Overweight increases the risk of increased plasma cholesterol, increased blood pressure and diabetes.Meat is a good source of bioavailable iron. The hypothesis that people with high iron stores have increased risk of heart disease has not been confirmed in a number of epidemiological studies.Human studies suggest that dietary long-chain omega-3 PUFAs are protective against sudden cardiac death, consistent with lower risk of ventricular fibrillation.
Reducing food intake in lower animals such as the rat decreases body weight, retards many aging processes, delays the onset of most diseases of old age, and prolongs life.A number of clinical trials of food restriction in healthy adult human subjects running over 2-15 years show significant reductions in body weight, blood cholesterol, blood glucose, and blood pressure, which are risk factors for the development of cardiovascular disease and diabetes.Lifestyle interventions that lower energy balance by reducing body weight such as physical exercise can also delay the development of diabetes and cardiovascular disease.In general, clinical trials are suggesting that diets high in calories or fat along with overweight are associated with increased risk for cardiovascular disease, type 2 diabetes, some cancers, and dementia.There is a growing literature indicating that specific dietary constituents are able to influence the development of age-related diseases, including certain fats (trans fatty acids, saturated, and polyunsaturated fats) and cholesterol for cardiovascular disease, glycemic index and fiber for diabetes, fruits and vegetables for cardiovascular disease, and calcium and vitamin D for osteoporosis and bone fracture.In addition, there are dietary compounds from different functional foods, herbs, and neutraceuticals such as ginseng, nuts, grains, and polyphenols that may affect the development of age-related diseases.Long-term prospective clinical trials will be needed to confirm these diet-disease relationships.On the basis of current research, the best diet to delay age-related disease onset is one low in calories and saturated fat and high in wholegrain cereals, legumes, fruits and vegetables, and which maintains a lean body weight.Such a diet should become a key component of healthy aging, delaying agerelated diseases and perhaps intervening in the aging process itself.Furthermore, there are studies suggesting that nutrition in childhood and even in the fetus may influence the later development of aging diseases and lifespan.
This subject was last reviewed at the Chiang Mai Symposium on Protein-Calorie Malnutrition (PCM), which was held in January 1973 and published in 1975 (1). At that time, there had been nearly 20 years of exciting research since Trowell et al. (2) wrote the first comprehensive monograph on kwashiorkor in 1954. This chapter recapitulates what was known about the subject in 1973, brings it up to date with the results of recent research, and speculates on future developments.
AddictionVolume 95, Issue 6 p. 829-832 Australian experience with the Wernicke–Korsakoff syndrome A. Stewart Truswell, A. Stewart TruswellSearch for more papers by this author A. Stewart Truswell, A. Stewart TruswellSearch for more papers by this author First published: 03 May 2002 https://doi.org/10.1046/j.1360-0443.2000.9568291.xCitations: 11AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume95, Issue6June 2000Pages 829-832 RelatedInformation
Medical Journal of AustraliaVolume 168, Issue 11 p. 534-535 Editorial Wernicke's encephalopathy and thiamine fortification of food: time for a new direction? We should be fortifying beer to target the people who develop this disorder Leslie R Drew, Leslie R Drew Senior Lecturer, Department of Psychiatry University of Sydney, Sydney, NSWSearch for more papers by this authorA Stewart Truswell, A Stewart Truswell Professor of Human Nutrition University of Sydney, Sydney, NSWSearch for more papers by this author Leslie R Drew, Leslie R Drew Senior Lecturer, Department of Psychiatry University of Sydney, Sydney, NSWSearch for more papers by this authorA Stewart Truswell, A Stewart Truswell Professor of Human Nutrition University of Sydney, Sydney, NSWSearch for more papers by this author First published: 01 June 1998 https://doi.org/10.5694/j.1326-5377.1998.tb139078.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume168, Issue11June 1998Pages 534-535 RelatedInformation
Abstract Objective: To estimate the incidence of Wernicke's encephalopathy (WE) and Korsakoffs psychosis (KP) before and after the introduction of thiamin enrichment of bread in Australia. Design and subjects: Inpatient records were examined in 17 major public general hospitals in greater Sydney for the 4 years 1993–96 (inclusive) with the International Classification of Diseases (ICD) 9 diagnoses 265.1 (WE), 291.1 and 294.0 (KP). Relevant clinical data were recorded on a specially designed form so that cases could be classified as confirmed or probable WE, confirmed or probable KP, confirmed or probable Wernicke–Korsakoff syndrome (WE + KP) or not WE or KP. The average number of cases of WE + KP was 38 acute (new) cases and 69 total (acute+chronic) cases per annum for all the hospitals combined. Results: This study used the same methods as our earlier retrospective examination of Wernicke–Korsakoff cases in essentially the same hospitals for 1978–93. Records for 1993 were thus pulled twice and, while individual cases (using hospital index number) did not always coincide, the total numbers for 1993 were 69 and 70. For the 5 years after 1991 the number of acute cases of WE and KP in Sydney hospitals was 61% of the number for the 5 years before 1991 (P<0.01). There is, however, no continuing downward trend. Conclusions: These results are consistent with a 40% reduction of the incidence of acute WE and KP since bread has been enriched with thiamin. The disease complex has, however, not been eliminated. To achieve this, further public health action would be needed, such as addition of thiamin to beer.
Plasma glucose and insulin responses to six different meals were determined and compared with values predicted by published glycemic indices of the component foods. The test meals were of different ethnic origins: Indian (lentil curry with rice), Italian (spaghetti bolognaise), Chinese (stir-fried vegetables and chicken with rice), Greek (lentil stew), Western (sirloin chop and vegetables); and Lebanese (sandwich with unleavened bread and hummos). Eight healthy volunteers were given 50 g carbohydrate portions of the above meals after an overnight fast. The glycemic and insulin indices were highest for the Lebanese meal and lowest for the Greek with significant differences among the meals (ANOVA, p less than 0.05). The observed glycemic indices correlated well with the predicted glycemic indices (r = 0.88, p less than 0.01) and insulin responses parallelled the glycemic responses (r = 0.83, p less than 0.05). These results suggest that the glycemic index approach will be useful in planning diets for diabetic people.
The balance of evidence indicates that protein deficiency is more constant than energy deficiency in cases of kwashiorkor. I suggest that well-conducted dietary histories with early home visits would confirm this in South African cases. In areas and groups from which kwashiorkor patients come, a pre-kwashiorkor state has to be detected by laboratory tests, e.g. plasma albumin measurement. Simple anthropometric measurements are not enough. Strategies for prevention must depend on local attitudes and resources, but throughout the world enthusiasm for protein-rich vegetable mixtures has waned. Selective provision of milk powder for sick children in clinics may be a cost-effective measure.