Comment

Vitamins to prevent cancer: supplementary problems

Inflammatory bowel disease (IBD) patients have an increased risk of developing colitis-associated colon cancer (CAC); however, the basis for inflammation-induced genetic damage requisite for neoplasia is unclear. Several studies have shown that IBD patients have signs of increased oxidative damage, which could be a result of genetic and environmental factors such as an excess in oxidant molecules released during chronic inflammation, mitochondrial dysfunction, a failure in antioxidant capacity, or oxidant promoting diets. It has been suggested that chronic oxidative environment in the intestine leads to the DNA lesions that precipitate colon carcinogenesis in IBD patients. Indeed, several preclinical and clinical studies show that different endogenous and exogenous antioxidant molecules are effective at reducing oxidation in the intestine. However, most clinical studies have focused on the short-term effects of antioxidants in IBD patients but not in CAC. This review article examines the role of oxidative DNA damage as a possible precipitating event in CAC in the context of chronic intestinal inflammation and the potential role of exogenous antioxidants to prevent these cancers.

Atherosclerotic cardiovascular disease (CVD) and diabetic vascular disease have been associated with an increase in oxidative stress. Mechanistic studies in vitro and in animals have demonstrated a direct role for oxidatively modified protein and lipid molecules in the pathophysiology of these diseases. As a result of this oxidation hypothesis numerous studies have been carried out over the past 5–10 years testing the ability of antioxidant vitamins to decrease the incidence of these diseases. The general consensus from these studies, involving over 200,000 individuals, has been that antioxidant vitamins do not provide any vascular protection. Moreover, several of these studies have demonstrated that antioxidant supplementation may be associated with an increased incidence of disease and mortality. One reason why these antioxidant vitamins may have failed to demonstrate benefit may have been due to inappropriate patient selection. In this review we provide supporting clinical evidence and a mechanistic basis for utilizing a genetic marker, the haptoglobin (Hp) genotype, in determining whether antioxidant vitamin therapy may or may not be beneficial for a given patient with diabetes.

Micronutrients play a central role in metabolism and in the maintenance of tissue function, but effects in preventing or treating disease which is not due to micronutrient deficiency cannot be expected from increasing the intake. There is a highly integrated system to control the flux of micronutrients in illness, and this demonstrates just how important the body perceives the micronutrients to be. An adequate intake therefore is necessary to sustain metabolism and tissue function, but provision of excess supplements to individuals who do not need them may be harmful. Clinical benefit is most likely in those individuals who are severely depleted and at risk of complications, and is unlikely if this is not the case. Much more research is needed to characterise better markers of micronutrient status both in terms of metabolic effects and antioxidant effects, so that at-risk patients can be identified and supplementation modified accordingly. Large-scale trials of different doses of micronutrients are required with precise outcome markers to optimise intakes in different groups of patients as well as in the general population.

El cáncer es la segunda causa de muerte en los países desarrollados. Su incidencia aumenta con la edad y la dieta es la causante en al menos un 30% de los casos. El riesgo es menor en poblaciones con un alto consumo de alimentos de origen vegetal. Es importante que reconozcamos que el cáncer, como otras enfermedades crónicas, se puede prevenir para reducir los años potenciales de vida perdidos y las tasas de incapacidad. Para conseguirlo disponemos de las guías alimentarias. Cuando la enfermedad se presenta podemos indicar modificaciones dietéticas para mejorar el estado nutricional del paciente, y en la fase terminal debemos respetar su opinión.

Cancer is the second cause of death in the developed world. Its incidence increases with age and diet is responsible for at least 30% of cases. The risk is lower in populations with a high consumption of foods of vegetable origin. To reduce the number of potential years of life lost and disability rates, it is important that we recognise that cancer, like other chronic diseases, can be prevented. To achieve this, dietary recommendations are available. When the disease develops, dietary modifications to improve the patient's nutritional status can be indicated. In the terminal phase of the disease, the patient's opinion should be respected.

Clefts of the lip and palate are generally divided into two groups, isolated cleft palate and cleft lip with or without cleft palate, representing a heterogeneous group of disorders affecting the lips and oral cavity. These defects arise in about 1·7 per 1000 liveborn babies, with ethnic and geographic variation. Effects on speech, hearing, appearance, and psychology can lead to longlasting adverse outcomes for health and social integration. Typically, children with these disorders need multidisciplinary care from birth to adulthood and have higher morbidity and mortality throughout life than do unaffected individuals. This Seminar describes embryological developmental processes, epidemiology, known environmental and genetic risk factors, and their interaction. Although access to care has increased in recent years, especially in developing countries, quality of care still varies substantially. Prevention is the ultimate objective for clefts of the lip and palate, and a prerequisite of this aim is to elucidate causes of the disorders. Technological advances and international collaborations have yielded some successes.