Rapeseed oil, a by-product of ‘rape’ belonging to the Brassica family, has been used as a cooking oil in Asia for many generations. However, its use in Europe and North America has been hampered by its toxicity. There are three health problems concerning rapeseed oil: myocardial lipidosis, myocardial necrosis, and impaired oxidative phosphorylation. The toxicity was thought to be attributed to the erucic acid content, which comprises 40-50% of the total fatty acids in the oil. This has led to the newly developed low erucic acid rapeseed (LEAR) oil (0.4-2.0%). Spanish toxic oil, which resulted in more than 800 deaths consisted, however, mostly of LEAR oils. Prediction of the safety of LEAR oils in man is thus questionable. The LEAR cultivars are high in glucosinolates. A second new type of rapeseed oil, low in both erucic acid and glucosinolates, called canola is now the major rape by-product. This review article discusses the potential factors, which could be potentially responsible for the toxicity of Spanish toxic oil.
This study compares the effects of dietary oleic acid (OA), palmitic acid (PA), and trans fatty acids (TFA) on lipid metabolism in rabbits. Animals were fed semipurified diets in which a fifth of the fat intake (6% total energy) was either OA, PA, or TFA in the presence and absence of dietary cholesterol (0.2% w/w). After 10-12 weeks of feeding the cholesterol-free diets, there were no significant differences in plasma total cholesterol or triacylglycerol concentrations between groups. However, there was an increase in the cholesterol concentration of the lower density lipoproteins in rabbits fed the TFA diet compared with their OA-and PA-fed counterparts. The addition of dietary cholesterol had no effect on plasma lipids, however hepatic cholesterol concentrations were lower in animals fed the PA diet compared with those fed the OA diet (p<0.05), mainly due to a reduction in cholesterol ester concentration (p<0.05). Despite these changes, hepatic low density lipoprotein (LDL)-receptor activity was not affected by diet. Palmitic and linoleic acids comprised similar proportions in the OA and TFA diets, however the proportion of hepatic phospholipid fatty acids as palmitic acid was lower (p<0.0001) while linoleic acid was higher (p<0.01) in animals fed TFA compared with those fed OA. These findings indicate that in rabbits fed dietary cholesterol (0.2%) TFA do not negatively impact on plasma lipids compared with either OA or PA. Also, increased esterification of TFA and linoleic acid to phospholipids at the expense of palmitic acid in animals fed TFA suggests that feeding TFA may result in cellular membranes with altered physical characteristics.
The recent discovery of the positional cloning of the mouse obese (ob) gene has resulted in renewed attention to the scientific study of obesity and body weight regulation. It was further discovered that the ob gene encodes for a circulating hormone, ob protein or leptin, secreted by adipose tissue. In the ob/ob mouse model which becomes very obese, there is a complete leptin deficiency. As such, if leptin is administered to these animals, food intake and body weight decrease significantly. The db/db mouse also becomes obese, but it has high levels of circulating leptin. Thus it is believed that this animal model cannot respond to leptin because of an altered leptin receptor. Because humans appear to have serum leptin levels in proportion to the level of body fat mass it is speculated that “leptin resistance” may also be involved, at least in part, in the development of human obesity. However, it is also proposed that for “normal” body weight regulation, leptin may act like a lipostat in response to changes in energy balance and fat stores and that exogenous leptin could possibly reset the lipostat. Serum leptin levels were measured in three groups of women: those who had lost ≥20% of their body weight and maintained the weight loss; those who lost ≥20% of their body weight and regained it; and weight stable controls who had never dieted. The maintainers and controls had similar leptin levels at 10.2±7.0 and 7.5±3.8ng/ml respectively. Those who had regained the weight had higher leptin levels than the other two groups at 20.8±8.4ng/ml (p<0.05). Body mass index (BMI) was also significantly higher in this group (p<0.001) at 34.1±6.4 compared to 24.0±2.0 in the maintainers and 21.3±2.5 in the controls. Leptin has also been shown to influence resting metabolic rate (RMR). Thus, serum leptin levels were measured in women who were similar in height, weight and age but had a low (≤85% predicted) or high (>100% predicted) RMR. No relationship between leptin and RMR was observed. There appear to be many unanswered questions about the mechanisms of action of leptin in humans.
Ascorbic acid (AA) is purported to have a preventative role in coronary heart disease (CHD) incidence. Studies in animal models support an interaction of AA in lipid metabolism, while results from epidemiological and supplementation trials conducted in humans are inconsistent. However, AA may mediate its protective action against CHD via its function as an antioxidant, inhibiting lipid peroxidation and regenerating α-tocopherol. Although AA can exert potentially beneficial effects, excessive AA administration can lead to damaging effects via interactions with transition metals, such as iron and copper.
The aim of this study was to examine changes in primary and secondary antioxidant defense system in children with insulin-dependent diabetes mellitus (IDDM). A total of 59 children (age range: 3 months-15 years) living in Cairo, Egypt were recruited. Twenty-four of these subjects had type-I diabetes (IDDM); they were admitted at the Abo-Elrish Hospital, Cairo. Thirty-five healthy well-nourished children were recruited from the local community, and used as controls. The antioxidant status of the study population was determined by measuring copper-zinc superoxide dismutase (Cu-Zn SOD) in red blood cells, glutathione peroxidase (GPX) in whole blood, and total antioxidant status (TAS) as well as ceruloplasmin and albumin in plasma. In addition, the plasma levels of trace elements involving antioxidant activities, such as copper (Cu), zinc (Zn), selenium (Se), and iron (Fe) were determined, along with a select group of vitamins. The latter included ascorbic acid, α-tocopherol and retinol. Plasma levels Se, Zn, and Cu were significantly higher in diabetic patients than in control subjects, while the mean plasma levels of albumin, ceruloplasmin, vitamin E, and vitamin C as well as Cu-Zn SOD activity in red blood cells, were significantly lower in IDDM patients than in their non-diabetic counterparts. No significant differences in plasma concentrations of TAS, vitamin A, retinol binding protein (RBP), and Fe as well as whole blood GPX activity were observed between the diabetic patients and control subjects. The plasma glucose level was inversely correlated with SOD and GPX. Overall, children with IDDM and persistent hyperglycemia are characterized by a decreased antioxidant defense system compared with health controls.
Coenzyme Q10 (CoQ10) deficiency has been observed in apparently healthy subjects as well as in patients with congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, mitral valve prolapse and after coronary revascularization. CoQ10 bolsters the synthesis of ATP and inhibits free radical damage, hence is useful in preventing cellular damage during ischaemia-reperfusion injury. The clinical benefits are mainly due to its ability to improve energy production, antioxidant activity, and membrane stabilizing properties. Several small scale studies indicate that coenzyme Q could be useful in patients with congestive heart failure, angina pectoris, cardiomyopathy, coronary artery disease, acute myocardial infarction and in the preservation of myocardium. CoQ10 may also decrease lipoprotein (a) and plasma insulin. CoQ10 is normally present in the low-density lipoprotein cholesterol fraction and inhibits its oxidation indicating that it can inhibit atherosclerosis. It can also regenerate vitamin E. CoQ10 is known for producing minor gastrointestinal discomfort and elevation in SGOT and LDH when used.
The incidence of autoimmune diabetes in the BB diabetic-prone (BBdp) rat can be substantially delayed or prevented by replacing cereal-based mixed ingredient (chow) rodent diets with semi-purified (SP) diets differing in protein sources. Replacing a chow diet with a casein-based SP diet early in life reduces the incidence of BB rat diabetes. Feeding soy-based SP diets results in lower diabetes rates than chow but higher than casein. The following study was conducted to determine the effect of early feeding of chow to casein and soy-based SP diets on the development of the immune system in the BB rat. BBdp and non-diabetes prone (BBn) rats were fed a defined chow (NIH) or one of a casein or soy SP diet, to the dams at least one week prior to birth and to the pups of 21-30 days of age. Pups were killed at 15 and 30 days of age and effects of early diet on several immune parameters were determined. At 30 days of age, all chow fed rats were heavier (p<0.05) than the rats of both SP diets. Although the BBdp rats in the chow and soy diet groups were significantly heavier (p<0.05) than BBn rats of the same diet groups, the body weights of casein-fed BBdp and BBn rats were similar. The BBdp animals had a lower (p<0.05) proportion of T cells than BBn rats at 30 days of age. However, the proportion of CD4 and CDS cells did not differ significantly from BBn for the casein-fed rats. The BBdp animals had poor proliferative responses and their production of IL-2 was unchanged by diet, but the natural killer (NK) activity of the casein-fed rats was reduced (p<0.05) to a level not different from the BBn rats. Diet also altered the immune response of the BBn rats. Feeding a soy-based as compared to a casein-based diet reduced (p<0.05) T cell responses (proliferation and IL-2 production) but increased (p<0.05) parameters of the innate immune system (nitric oxide production and NK cell activity). The findings of this study have important implications in identifying an immune mechanism for dietary effects on the incidence of diabetes in the BB rat and are of potential interest in defining the role of dietary protein source on the development of the immune system.
The role of nutrition and food in the prevention and treatment of malignancy is a complex one and is currently characterized by intense research efforts to further our understanding of the relationship. The best preventive and safest policy that can be recommended with a certain degree of confidence at present is to exert moderation, maintain an appropriate body weight and eat a variety of foods. This article provides an insight to the relationships between select group of nutrients and certain forms of cancer.
Diabetes mellitus is a chronic, systemic, metabolic disease defined by hyperglycemia and characterized by alterations in the metabolism of carbohydrate, protein, and lipid. The cumulative effects of these metabolic derangements lead to cell damage, circulatory changes, and eventually to cardiovascular disorders, including increased plasma lipoproteins, atherosclerosis, hypertension, and cardiomyopathy. Other clinical consequences of diabetes include nephropathy, neuropathy, and retinopathy. The latter can reach a proliferative phase associated with neovascularization of retinal vessels, vitreous hemorrhage and retinal detachment; this, in fact, is the leading cause of visual impairment and blindness in adults. Visual defects are also known to be a clinical consequence of vitamin A deficiency. Evidence to date point to the fact that diabetes is associated with an impaired metabolic availability of the vitamin. This paper delineates the link between insulin-dependent diabetes mellitus (IDDM) (Type I) and the biochemical evidence of vitamin A deficiency.
The Asian Indian population is the fastest growing group of Asian immigrants in the USA, however, there is no documentation of their food choices and dietary intakes, especially for the women. The objective of this study was to compare dietary profiles of Caucasian women (CIA) and Asian Indian women in the USA (AIA) with that of Asian Indian women in India (AII). Dietary assessments were carried out using a modified Block Health Habits and History Questionnaire and 4-day food diaries, as well as selected biochemical indices. The total caloric intake was highest in the AII followed by the CIA and lowest in the AIA who bordered on being deficient. Fat intake of Asian Indian women was consistently lower than that of Caucasian women and so was the consumption of sugar, fiber and alcohol. The women of the AIA group are moving up to the levels of Caucasian women in the USA in fat intake which is supported by their higher serum triglycerides compared to the AII. On the other hand, their serum cholesterol remained lower than their counterpart in India. Dietary intakes and serum concentrations of antioxidant vitamins were lower in the Asian Indian women than in the Caucasian women with the exception of ascorbic acid. The increasing fat and low antioxidants in the AIA are predisposing factors to many chronic diseases and should be monitored as these are likely to become threatening as the acculturation of this group of women attains maturation.