http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119708/?report=classic Go to: 1. Introduction The influence of nutrition and dietary supplements on the course of neurodegenerative diseases (ND) has been recently studied, particularly, the effects of nutritional factors, such as polyunsaturated fatty acids, vitamins, milk proteins, gluten, and probiotics, on the development, relapse rate, and progression of multiple sclerosis (MS) [1]. Recently malnutrition at the time of diagnosis has been associated with a shorter duration of disease in amyotrophic lateral sclerosis (ALS) [2]. Nutritional approaches have been proposed to reduce the risk and improve the management of Alzheimer's disease (AD) [3]. Cell damage due to both oxidative stress and depletion of endogenous antioxidants could be considered mechanisms of injury for ND. Indeed, the use of antioxidants seems to help prevent the formation of reactive species and counteract the damage to DNA, lipids, proteins, and other biomolecules [4]. For example, serum nitric oxide and peroxynitrite levels have been shown to be higher in patients affected by Parkinson's disease (PD) [5] than in controls, establishing a relationship between serum levels of these oxidants and the severity of the disease. In this context, other studies have demonstrated the usefulness of phenolic compounds and N-acetylcysteine as antioxidants in ND and PD, respectively [6, 7]. Mitochondrial dysfunction is considered to be the basis of the development and progression of several neurologic diseases with different aetiologies, including ND [8]. Therefore, mitochondria have become an interesting target of drug therapy [9]. Particularly, as reported by Mao et al.'s study, mitoQ, a mitochondria-targeted antioxidant, can delay disease progression and alleviate pathogenesis in an experimental autoimmune encephalomyelitis mouse model of MS [10]. We had previously shown how helpful antioxidant compound Cellfood was in improving mitochondrial respiratory metabolism of endothelial cells and inhibiting hypoxia-induced reactive oxygen species (ROS) generation in vitro [11]. In this prospective study we evaluated the influence of Cellfood treatment on blood parameters in patients affected by ND and subjected to chelation therapy with the chelating agent calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA or EDTA), administered intravenously. Two groups of subjects were studied: 39 patients affected and 11 subjects unaffected by ND (controls). All subjects were affected by chronic body burden of heavy metals and were treated with EDTA to remove metal intoxication [12–14]. The subjects were also daily treated with antioxidant therapy to help the detoxification process: some of them received Cellfood and some other antioxidants [15]. Oxidative status represents the result of the balance between ROS generation and antioxidant capacity of the organism. Blood parameters could possibly highlight oxidative stress conditions. In this study serum concentrations of ROS, total antioxidant capacity (TAC), oxidized LDL (oxLDL), cholesterol profile (total cholesterol (TC); HDL; and LDL), and the blood GSH/GSSG red-ox couple were assessed. The latter is mostly responsible for maintaining homeostasis of cell red-ox state [16]. Homocysteinemia and metabolically related vitamins (vitamin B12, active vitamin B12, serum, and erythrocyte folate) were also determined. In fact, if vitamin levels are inadequate, hyperhomocysteinemia can have a prooxidant effect causing or promoting oxidation. The aim of this prospective pilot study was to evaluate the influence of Cellfood treatment during chelation therapy and to compare it with that of other antioxidants. Go to: 2. Materials and Methods 2.1. Patient Recruitment Out of 80 consecutive subjects who had undergone a medical checkup in an outpatient medical center, only 50 were selected and enrolled for this study due to their compliance in following the protocol, for example, receiving chelation therapy once a week by personal choice and taking daily antioxidants. Antioxidants were distributed at random. Twenty patients were affected by MS; fifteen of them had been previously treated with conventional drugs against MS (e.g., immunosuppressant agents, such as mitoxantrone and azathioprine, broad-spectrum immunomodulatory agents, such as glatiramer acetate and interferon β, monoclonal antibodies, such as rituximab and natalizumab, and the recently discovered fingolimod, a sphingosine-1-phosphate-receptor modulator) [17, 18]. However, all these patients had interrupted previous therapies almost 2 months before starting chelation treatment. Five of these MS patients had never been previously treated with drugs. Nineteen patients affected by ND were also recruited as well as 11 subjects not affected by any known disease but previously exposed to environmental or occupational heavy metals, who decided to start chelation therapy and acted as controls. Subjects' age ranged from 18 to 75. All subjects provided written informed consent to participate in this study. Declaration of Helsinki and all procedures involving human participants were approved by the Milan University's Ethical Advisory Committee (number 64/14). 2.2. Study Design All subjects (ND and controls) underwent chelation therapy for 3 months. EDTA is endowed with antioxidant properties; in fact, without any added vitamin C, it can decrease oxidative DNA damage and lipid peroxidation [19]. However, since its administration occurred once a week, the subjects were treated daily with antioxidants. At the beginning (basal values) and at the end of the treatments (after 3 months), blood lipid panel, homocysteine metabolism, and some oxidative stress parameters were evaluated. 2.3. Chelation Test All ND patients and controls had been subjected to “chelation test” in order to verify their possible burden by toxic metals. Generally, for the “chelation test,” EDTA (2g), diluted in 500mL physiological saline (Farmax srl, Brescia, Italy), is slowly (in about 2 hours) administered intravenously in subjects who are invited to collect urine samples before and after the first intravenous EDTA treatment. Urine collection following chelation treatment lasted 12 hours. Urine samples are accurately enveloped in sterile vials and sent to the Laboratory of Toxicology (Doctor's Data Inc., St. Charles, IL, USA) to be analysed, as previously reported [12]. Briefly, samples are acid-digested with certified metal-free acids (digestion takes place in a closed-vessel microwave digestion system), diluted with ultrapure water, and carried out via inductively coupled plasma with mass spectrometry (ICP-MS) utilizing collision/reaction cell methods coupled with ion-molecule chemistry, a reliable new method for reducing interference. Urine standards, both certified and in-house, are used for quality control and validation of data. To avoid the potentially great margin of error due to fluid intake and sample volume, results were reported in micrograms (μg) per g of creatinine. When the first “chelation test” showed intoxication by heavy metals, our subjects started chelation therapy once a week. 2.4. Antioxidant Supplementation 2.4.1. Cellfood Treatment Cellfood (Eurodream, La Spezia, Italy) is an antioxidant nutritional supplement containing 78 ionic/colloidal trace elements and minerals combined with 34 enzymes and 17 amino acids, all suspended in a solution of deuterium sulphate, efficient in protecting against oxidative damage in vitro [20]. A gradually increasing concentration of Cellfood was administered daily to subjects (22 ND patients and 6 controls) according to the following scheme: the first, second, and third day 1 drop in mineral water three times a day, the fourth, fifth, and sixth day 2 drops, the seventh and eighth day 3 drops three times a day, that is, 1 drop more three times a day, and finally 20 drops altogether were given three times a day. The treatment lasted three months. 2.4.2. Other Antioxidant Treatments Twenty-two patients (17 ND and 5 controls) took daily other antioxidants, instead of Cellfood. Particularly, 10 of them (6 ND and 4 controls) took α-lipoic acid (400mg/day), the other 10 glutathione (Ultrathione, 500mg/day), alone or together with multivitamin complexes, aminoacid and mineral mixtures, or probiotics. Also these treatments lasted three months. 2.5. Evaluation of Blood Parameters 2.5.1. Sample Collection Biochemical parameters were measured in blood drawn from patients before starting therapy with EDTA and antioxidants (basal values) and after three months. Peripheral blood samples were collected after overnight fasting into preevacuated and light-protected tubes, with no additive or with EDTA, in order to evaluate oxidative status (ROS; TAC; oxLDL) and glutathione and homocysteine metabolism (homocysteine, Hcy; holotranscobalamin, active B12; serum folate, s-Fol; erythrocyte folate, ery-Fol). Serum aliquots were used to measure ROS, TAC, oxLDL, active B12, and s-Fol concentrations while EDTA whole blood was used for glutathione and ery-Fol levels determination. The remaining EDTA whole blood sample was centrifuged within 30 minutes to obtain plasma for total Hcy determination. All the aliquots, except for the one used for blood counting, were immediately frozen and stored at −80°C ready for assay. A 12-hour urine sample was used for the “chelation test,” as previously described. 2.5.2. Oxidative Status Serum ROS expressed as Carratelli Units (UCarr), oxLDL concentrations, and TAC were measured by using a commercial enzyme-linked immunoabsorbent assay (ELISA, Mercodia, Uppsala, Sweden) on the EASIA reader (Medgenix Diagnostics, Fleurus, Belgium) and by using spectrophotometric commercial kits (dROMs test, Diacron International, Grosseto, Italy; OXY-adsorbent test, Diacron International, Grosseto, Italy) on F.R.E.E. analyzer (Free Radical Elective Evaluator analyzer, Diacron International, Grosseto Italy) (Diacron), respectively. Total and free glutathione concentrations were assessed by HPLC method followed by fluorescent detection using a commercially available kit (Chromsystems Instruments & Chemicals, Munich, Germany). Total glutathione is the sum of oxidized (GSSG) and free (GSH) glutathione existing in the sample prior to reduction. Briefly, since chromatography can only determine GSH, GSSG present in the sample was converted into GSH by using a reduction reagent which reduced one GSSG molecule to 2 GSH molecules obtaining total glutathione. GSSG concentration was calculated by subtracting the GSH amount from the total glutathione. GSH/GSSG ratio was also calculated and used as an oxidative stress marker. 2.5.3. Homocysteine Metabolism Plasma Hcy levels were measured using homocysteine liquid enzymatic assay (Sentinel Diagnostics, Milan, Italy) on Modular P analyser (Roche Diagnostics, Indianapolis, IN, USA). Serum active B12, s-Fol, and ery-Fol concentrations were determined using the relevant Abbott Microparticle Enzyme Immunoassay (MEIA) kits (Holotranscobalamin-Active-B12 and Architect Folate, Abbott Laboratories, Abbott Park, IL, USA) on Architect analyser (Abbott). 2.5.4. Lipid Panel Serum total cholesterol (TC), high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) cholesterol concentrations were determined using the routine tests on Modular P analyser. Total/HDL cholesterol and LDL/HDL cholesterol ratios were calculated together with oxLDL/HDL and oxLDL/LDL ratios. 2.6. Statistical Analysis Data were analyzed by analysis of variance (ANOVA) with the solution type as main factor. Post hoc comparisons were made using Tukey's honestly significant difference test (HSD). Go to: 3. Results 3.1. Patients' Characteristics As shown in Figure 1, eleven of these subjects were classified as controls (C) because they were not affected by ND or other known diseases. Six of them took Cellfood and five took other antioxidants. Thirty-nine patients were classified as ND: 20 MS, 5 ALS, 9 PD, and 5 AD. Twenty-two of them took Cellfood while the other seventeen received other antioxidants. The subjects of these two groups were matched for age, sex, disease duration, and previous drug treatments. Mean age of each group was 43±5. Subjects' basal values were obtained before the beginning of each treatment. more on the link
Hahahaha sure.... The medical study is using Cellfood with normal treatment for Neurodegenerative Diseases like MS, Alzheimers, and Amyyotrophic Lateral Sclerosis. The studies were positive, with Cellfood acting like a chelating agent to deliver the necessary chelates to the body necessary to neuro repair.
