1.
Food and Food Products on the Italian Market for Ketogenic Dietary Treatment of Neurological Diseases.
Leone, A, De Amicis, R, Lessa, C, Tagliabue, A, Trentani, C, Ferraris, C, Battezzati, A, Veggiotti, P, Foppiani, A, Ravella, S, et al
Nutrients. 2019;(5)
Abstract
The ketogenic diet (KD) is the first line intervention for glucose transporter 1 deficiency syndrome and pyruvate dehydrogenase deficiency, and is recommended for refractory epilepsy. It is a normo-caloric, high-fat, adequate-protein, and low-carbohydrate diet aimed at switching the brain metabolism from glucose dependence to the utilization of ketone bodies. Several variants of KD are currently available. Depending on the variant, KDs require the almost total exclusion, or a limited consumption of carbohydrates. Thus, there is total avoidance, or a limited consumption of cereal-based foods, and a reduction in fruit and vegetable intake. KDs, especially the more restrictive variants, are characterized by low variability, palatability, and tolerability, as well as by side-effects, like gastrointestinal disorders, nephrolithiasis, growth retardation, hyperlipidemia, and mineral and vitamin deficiency. In recent years, in an effort to improve the quality of life of patients on KDs, food companies have started to develop, and commercialize, several food products specific for such patients. This review summarizes the foods themselves, including sweeteners, and food products currently available for the ketogenic dietary treatment of neurological diseases. It describes the nutritional characteristics and gives indications for the use of the different products, taking into account their metabolic and health effects.
2.
Comorbidities in inflammatory bowel disease: a call for action.
Argollo, M, Gilardi, D, Peyrin-Biroulet, C, Chabot, JF, Peyrin-Biroulet, L, Danese, S
The lancet. Gastroenterology & hepatology. 2019;(8):643-654
Abstract
Inflammatory bowel disease (IBD) is a chronic systemic inflammatory condition. Previously, the focus has been on extraintestinal manifestations of IBD, including arthritis, psoriasis, and uveitis. Although comorbidities have long been the subject of intensive research in other chronic inflammatory diseases such as rheumatoid arthritis, the concept of comorbidities is only beginning to emerge in IBD. Several comorbid conditions have been proposed to be related to IBD, including cardiovascular disease, neuropsychological disorders, and metabolic syndrome. Recognition of these conditions and their treatment could lead to better management of IBD. This Review aims to explore current knowledge regarding classic and emerging comorbidities related to IBD.
3.
Disorders of heavy metals.
Woimant, F, Trocello, JM
Handbook of clinical neurology. 2014;:851-64
Abstract
Heavy metals and trace elements play an important role in relation to the physiology and pathology of the nervous system. Neurologic diseases related to disorders of metabolism of copper and iron are reviewed. Copper disorders are divided into two classes: ATP7A- or ATP7B-related inherited copper transport disorders (Menkes disease, occipital horn syndrome, ATP7A-related distal motor neuropathy, and Wilson disease) and acquired diseases associated with copper deficiency or copper excess. Iron brain disorders are divided into genetic neurodegeneration with brain iron accumulation (NBIA, neuroferritinopathy, and aceruloplasminemia), genetic systemic iron accumulation with neurologic features (hemochromatosis), and acquired diseases associated with iron excess (superficial siderosis) or iron deficiency (restless leg syndrome). The main features of cadmium, lead, aluminum, mercury, and manganese toxicity are summarized.
4.
Peripheral markers of glutamatergic dysfunction in neurological diseases: focus on ex vivo tools.
Tremolizzo, L, Beretta, S, Ferrarese, C
Critical reviews in neurobiology. 2004;(1-2):141-6
Abstract
Since the proposal that excessive glutamatergic stimulation could be responsible for neuronal suffering and death, excitotoxicity and glutamate uptake deficits have been repeatedly confirmed to play a key role in the pathogenesis of different neurological diseases. Therefore, it is conceivable that assessing the glutamatergic system function directly in patients could be extremely useful for early diagnosis, prognostic evaluation, and optimization of the therapy. A possibility is offered by assessing glutamate levels in biological fluid, such as plasma and CSF, where increased levels of this amino acid have been reported in patients affected by stroke, amyotrophic lateral sclerosis (ALS), and AIDS dementia complex. However, the metabolic role of this amino acid acts as a confounding factor, and the possibility of directly assessing glutamatergic functional parameters, such as amino acid reuptake, would probably mirror closely the actual excitotoxic damage operative in each patient. Here we will describe our findings obtained in peripheral ex vivo cells, such as platelets and fibroblasts, both displaying a functional glutamate reuptake system. Consistent with a systemic-impairment assumption, glutamate uptake was shown to be reduced in peripheral cells of Alzheimer's disease, Down syndrome, Parkinson's disease, ALS, and stroke patients. Different systemic factors might be responsible for this phenomenon, including genetic predisposition, oxidative stress, and inflammatory response, raising new, exciting questions about the relevance of their possible interactions for the pathogenesis of neurological disorders.