No abstract

Neurodegenerative diseases (NDD) are a group of illness with diverse clinical importance and etiologies. NDD include motor neuron disease such as amyotrophic lateral sclerosis (ALS), cerebellar disorders, Parkinson's disease (PD), Huntington's disease (HD), cortical destructive Alzheimer's disease (AD) and Schizophrenia. Numerous epidemiological and experimental studies provide many risk factors such as advanced age, genetic defects, abnormalities of antioxidant enzymes, excitotoxicity, cytoskeletal abnormalities, autoimmunity, mineral deficiencies, oxidative stress, metabolic toxicity, hypertension and other vascular disorders. Growing body of evidence implicates free radical toxicity, radical induced mutations and oxidative enzyme impairment and mitochondrial dysfunction due to congenital genetic defects in clinical manifestations of NDD. Accumulation of oxidative damage in neurons either primarily or secondarily may account for the increased incidence of NDD such as AD, ALS and stroke in aged populations. The molecular mechanisms of neuronal degeneration remain largely unknown and effective therapies are not currently available. Recent interest has focused on antioxidants such as carotenoids and in particular lycopene, a potent antioxidant in tomatoes and tomato products, flavonoids and vitamins as potentially useful agents in the management of human NDD. The pathobiology of neurodegenerative disorders with emphasis on genetic origin and its correlation with oxidative stress of neurodegenerative disorders will be reviewed and the reasons as to why brain constitutes a vulnerable site of oxidative damage will be discussed. The article will also discuss the potential free radical scavenger, mechanism of antioxidant action of lycopene and the need for the use of antioxidants in the prevention of NDD.

clinicaltrials.gov Identifier: NCT00438425.

OBJECTIVEFat intake, especially monounsaturated fatty acid (MUFA), has been liberalized in diabetic diets to preserve HDL cholesterol and improve glycemic control, yet the exact sources have not been clearly defined. Therefore, we assessed the effect of mixed nut consumption as a source of vegetable fat on serum lipids and HbA1c in type 2 diabetes.RESEARCH DESIGN AND METHODSA total of 117 type 2 diabetic subjects were randomized to one of three treatments for 3 months. Supplements were provided at 475 kcal per 2,000-kcal diet as mixed nuts (75 g/day), muffins, or half portions of both. The primary outcome was change in HbA1c.RESULTSThe relative increase in MUFAs was 8.7% energy on the full-nut dose compared with muffins. Using an intention-to-treat analysis (n = 117), full-nut dose (mean intake 73 g/day) reduced HbA1c (−0.21% absolute HbA1c units, 95% CI −0.30 to −0.11, P < 0.001) with no change after half-nut dose or muffin. Full-nut dose was significantly different from half-nut dose (P = 0.004) and muffin (P = 0.001), but no difference was seen between half-nut dose and muffins. LDL cholesterol also decreased significantly after full-nut dose compared with muffin. The LDL cholesterol reduction after half-nut dose was intermediate and not significantly different from the other treatments. Apolipoprotein (apo) B and the apoB:apoA1 ratio behaved similarly. Nut intake related negatively to changes in HbA1c (r = −0.20, P = 0.033) and LDL cholesterol (r = −0.24, P = 0.011).CONCLUSIONSTwo ounces of nuts daily as a replacement for carbohydrate foods improved both glycemic control and serum lipids in type 2 diabetes.