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Tijdschrift voor Orthomoleculaire Geneeskunde
Multiple Sclerose - TvOG februari 2010 -
updated: 19 January 2010
- Baranzini SE, Oksenberg JR, Hauser SL. J Rehabil Res Dev. 2002 Mar-Apr;39(2):201-9 New insights into the genetics of multiple sclerosis
Tissue injury in multiple sclerosis (MS) results from an abnormal immune response to one or more myelin antigens that develop in genetically susceptible individuals after exposure to a causal agent that is yet undefined.
[Abstract]
- Compston A, Sawcer S. Curr Neurol Neurosci Rep. 2002 May;2(3):259-66. Genetic analysis of multiple sclerosis
The increased recurrence risk within families indicates a role for genetic factors in the etiology of multiple sclerosis. Genes may influence susceptibility to the development of multiple sclerosis and the subsequent course of the disease. [Abstract]
- Kidd PM. Altern Med Rev. 2001 Dec;6(6):540-66 Multiple sclerosis, an autoimmune inflammatory disease: prospects for its integrative management
MS features autoimmune inflammatory attack against the myelin insulation of neurons. Thymus derived (T) cells sensitized against myelin self-antigens secrete tumor necrosis factor, cytokines, prostaglandins, and other inflammatory mediators that strip away the myelin and sometimes destroy the axons.
[Article]
- Dittel BN. Brain Behav Immun. 2008 May;22(4):421-30. CD4 T cells: Balancing the coming and going of autoimmune-mediated inflammation in the CNS
In a T cell-mediated autoimmune response, such as in multiple sclerosis (MS), the CD4 T cell is thought to orchestrate and drive the immune response resulting in inflammation within the central nervous system (CNS).
[Article]
- Bagert BA. Curr Neurol Neurosci Rep. 2009 Sep;9(5):405-10. Epstein-Barr virus in multiple sclerosis
Recent seroepidemiologic and pathologic evidence suggests that prior infection with Epstein-Barr virus (EBV) may be necessary for the development of multiple sclerosis (MS).
[Abstract]
- Farrell RA, Antony D, Wall GR, Clark DA, Fisniku L, Swanton J, Khaleeli Z, Schmierer K, Miller DH, Giovannoni G. Neurology. 2009 Jul 7;73(1):32-8. Humoral immune response to EBV in multiple sclerosis is associated with disease activity on MRI
The correlation between elevated Epstein-Barr virus nuclear antigen 1 (EBNA-1) immunoglobulin G (IgG) and gadolinium-enhancing lesions suggests an association between Epstein-Barr virus (EBV) infection and multiple sclerosis (MS) disease activity.
[Abstract]
- Landtblom AM, Flodin U, Söderfeldt B, Wolfson C, Axelson O. Epidemiology. 1996 Jul;7(4):429-33 Organic solvents and multiple sclerosis: a synthesis of the current evidence
Organic solvents and multiple sclerosis: a synthesis of the current evidence
Our evaluation is consistent with the hypothesis that organic solvents may be a cause of multiple sclerosis
[Abstract]
- Riise T, Moen BE, Kyvik KR. Epidemiology. 2002 Nov;13(6):718-20. Organic solvents and the risk of multiple sclerosis
These results are compatible with the hypothesis of organic solvents being a possible risk factor for MS.
[Abstract]
- Aminzadeh KK, Etminan M. J Public Health Dent. 2007 Winter;67(1):64-6. Dental amalgam and multiple sclerosis: a systematic review and meta-analysis
The pooled OR for the risk of MS among amalgam users was consistent, with a slight, nonstatistically significant increase between amalgam use and risk of MS.
[Abstract]
- Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD. Neuro Endocrinol Lett. 2004 Jun;25(3):211-8. The beneficial effect of amalgam replacement on health in patients with autoimmunity
Mercury-containing amalgam may be an important risk factor for patients with autoimmune diseases.
[Abstract]
- Yamout B, Itani S, Hourany R, Sibaii AM, Yaghi S. J Neurol Sci. 2009 Nov 3The effect of war stress on multiple sclerosis exacerbations and radiological disease activity
Our study shows that exposure to war-related events is likely to lead to an increase in both clinical relapses and MRI disease activity in patients with MS.
[Abstract]
- Mitsonis CI, Potagas C, Zervas I, Sfagos K. Int J Neurosci. 2009;119(3):315-35 The effects of stressful life events on the course of multiple sclerosis: a review
There is growing body of evidence that support an association between stressful life events and an increased risk for Multiple Sclerosis (MS) exacerbations.
[Abstract]
- Butcher J. N Z Med J. 1976 Jun 23;83(566):427-30 The distribution of multiple sclerosis in relation to the dairy industry and milk consumption
This report emphasises the striking correlation between the world distribution of dairy production and consumption and the incidence of multiple sclerosis.
[Abstract]
- Lucchinetti CF, Brück W, Rodriguez M, Lassmann H. Brain Pathol. 1996 Jul;6(3):259-74 Distinct patterns of multiple sclerosis pathology indicates heterogeneity on pathogenesis
Our data indicate, that the demyelinated plaques of multiple sclerosis may reflect a common pathological end point of a variety of different immunological mechanisms of myelin destruction in this disease
[Abstract]
- Edlich R, Mason SS, Chase ME, Fisher AL, Gubler K, Long WB 3rd, Newkirk AT. J Environ Pathol Toxicol Oncol. 2009;28(2):143-52 Revolutionary advances in the prevention of demyelinating diseases
In general, the rate of MS increases with latitude. Clinical studies have pointed out that vitamin D deficiency may exacerbate the development of MS. Because vitamin D3 is an inhibitor of MS, providing supplemental D3 for individuals at risk for MS should be mandatory.
[Abstract]
- Niino M, Fukazawa T, Kikuchi S, Sasaki H. Curr Med Chem. 2008;15(5):499-505. Therapeutic potential of vitamin D for multiple sclerosis
Multiple sclerosis (MS) is a major inflammatory and demyelinating disease of the central nervous system and has an increasing prevalence in populations residing at higher latitudes. This observation may indicate a protective effect of sunlight exposure, which is reduced at higher latitudes and may contribute to insufficient levels of vitamin D in the MS population
[Abstract]
- Hayes CE, Cantorna MT, DeLuca HF. Proc Soc Exp Biol Med. 1997 Oct;216(1):21-7. Vitamin D and multiple sclerosis
Recently, it has been clearly demonstrated that exogenous 1,25-dihydroxyvitamin D3, the hormonal form of vitamin D3, can completely prevent experimental autoimmune encephalomyelitis (EAE), a widely accepted mouse model of human multiple sclerosis (MS).
This theory can explain the striking geographic distribution of MS, which is nearly zero in equatorial regions and increases dramatically with latitude in both hemispheres. It can also explain two peculiar geographic anomalies, one in Switzerland with high MS rates at low altitudes and low MS rates at high altitudes, and one in Norway with a high MS prevalence inland and a lower MS prevalence along the coast. Ultraviolet (UV) light intensity is higher at high altitudes, resulting in a greater vitamin D3 synthetic rate, thereby accounting for low MS rates at higher altitudes. On the Norwegian coast, fish is consumed at high rates and fish oils are rich in vitamin D3.
Although genetic traits certainly contribute to MS susceptibility, an environmental factor is also clearly involved.
[Abstract]
- Pierrot-Deseilligny C. J Neurol. 2009 Sep;256(9):1468-79 Clinical implications of a possible role of vitamin D in multiple sclerosis
Hypovitaminosis D is currently one of the most studied environmental risk factors for multiple sclerosis (MS) and is potentially the most promising in terms of new clinical implications. Clinically, most MS patients have low serum levels of vitamin D and are in a state of insufficiency or even deficiency compared to the international norm, which has been established on a metabolic basis.
In animal studies, vitamin D prevents and improves experimental autoimmune encephalomyelitis.
[Article]
- Smolders J, Peelen E, Thewissen M, Menheere P, Cohen Tervaert JW, Hupperts R, Damoiseaux J. Autoimmun Rev. 2009 Jun;8(7):621-6The relevance of vitamin D receptor gene polymorphisms for vitamin D research in multiple sclerosis
A poor vitamin D status has been associated with several autoimmune diseases, including multiple sclerosis (MS).
[Abstract]
- Mark BL, Carson JA. J Am Diet Assoc. 2006 Mar;106(3):418-24Vitamin D and autoimmune disease--implications for practice from the multiple sclerosis literature
Recent studies and commentaries link vitamin D with several autoimmune diseases, including multiple sclerosis (MS).
Adequate vitamin D intake reduces inflammatory cytokines through control of gene expression, thus inadequate vitamin D intake is suggested as a mechanism that could contribute to inflammation and, consequently, development of MS.
Poor vitamin D status has been associated with increased risk for development of MS, and patients with MS may suffer consequences of vitamin D deficiency, such as bone loss.
[Abstract]
- Hayes CE. Proc Nutr Soc. 2000 Nov;59(4):531-5. Vitamin D: a natural inhibitor of multiple sclerosis
Inheriting genetic risk factors for multiple sclerosis (MS) is not sufficient to cause this demyelinating disease of the central nervous system; exposure to environmental risk factors is also required. MS may be preventable if these unidentified environmental factors can be avoided
However, the clearest evidence that vitamin D may be a natural inhibitor of MS comes from experiments with experimental autoimmune encephalomyelitis (EAE), a model of MS. Treatment of mice with 1,25-(OH)2D3 completely inhibited EAE induction and progression.
The hormone stimulated the synthesis of two anti-encephalitogenic cytokines, interleukin 4 and transforming growth factor beta-1, and influenced inflammatory cell trafficking or apoptosis.
[Article]
- VanAmerongen BM, Dijkstra CD, Lips P, Polman CH. Eur J Clin Nutr. 2004 Aug;58(8):1095-109 Multiple sclerosis and vitamin D: an update
The prevalence of MS is highest where environmental supplies of vitamin D are lowest.
[Article]
- Smolders J, Menheere P, Kessels A, Damoiseaux J, Hupperts R. Mult Scler. 2008 Nov;14(9):1220- Association of vitamin D metabolite levels with relapse rate and disability in multiple sclerosis
Serum levels of 25(OH)D were associated with both relapse rate and disability in MS patients. These results are suggestive for a disease modulating effect of the serum concentrations of 25(OH)D on MS.
[Abstract]
- Gezondheidsraad September 2008 Naar een toereikende inname van vitamine D
Vitamine D-tekort komt onder alle lagen van de bevolking voor
[Article]
- Smolders J, Damoiseaux J, Menheere P, Hupperts R. J Neuroimmunol. 2008 Feb;194(1-2):7-17 Vitamin D as an immune modulator in multiple sclerosis, a review
The evidence obtained from these studies strongly supports a model in which vitamin D mediates a shift to a more anti-inflammatory immune response, and in particular to enhanced regulatory T cell functionality.
[Abstract]
- Vieth R. Am J Clin Nutr. 1999 May;69(5):842-56 Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety
Total-body sun exposure easily provides the equivalent of 250 microg (10000 IU) vitamin D/d, suggesting that this is a physiologic limit.
The assembled data from many vitamin D supplementation studies reveal a curve for vitamin D dose versus serum 25-hydroxyvitamin D [25(OH)D] response that is surprisingly flat up to 250 microg (10000 IU) vitamin D/d. To ensure that serum 25(OH)D concentrations exceed 100 nmol/L, a total vitamin D supply of 100 microg (4000 IU)/d is required.
Except in those with conditions causing hypersensitivity, there is no evidence of adverse effects with serum 25(OH)D concentrations <140 nmol/L, which require a total vitamin D supply of 250 µg (10000 IU)/d to attain
[Article]
- Vieth R. J Nutr. 2006 Apr;136(4):1117-22 Critique of the considerations for establishing the tolerable upper intake level for vitamin D: critical need for revision upwards
Exposure of skin to sunshine can safely provide an adult with vitamin D in an amount equivalent to an oral dose of 250 mcg/d.
The incremental consumption of 1 mcg/d of vitamin D3 raises serum 25-hydroxyvitamin D [25(OH)D ] by approximately 1 nmol/L (0.4 microg/L).
Published reports suggest toxicity may occur with 25(OH)D concentrations beyond 500 nmol/L (200 microg/L).
[Article]
- Vieth R. J Bone Miner Res. 2007 Dec;22 Suppl 2:V64-8Vitamin D toxicity, policy, and science
However, because sunshine can provide an adult with vitamin D in an amount equivalent to daily oral consumption of 250 mug (10,000 IU)/d, this is intuitively a safe dose.
The incremental consumption of 1 mug (40 IU)/day of vitamin D(3) raises serum 25(OH)D by approximately 1 nM (0.4 ng/ml).
[Article]
- Hathcock JN, Shao A, Vieth R, Heaney R. Am J Clin Nutr. 2007 Jan;85(1):6-18. Risk assessment for vitamin D
The present a risk assessment based on relevant, well-designed human clinical trials of vitamin D. Collectively, the absence of toxicity in trials conducted in healthy adults that used vitamin D dose > or = 250 microg/d (10,000 IU vitamin D3) supports the confident selection of this value as the UL.
[Article]
- 1. http://www.ajcn.org/cgi/content/full/85/1/6
Kimball SM, Ursell MR, O'Connor P, Vieth R. Am J Clin Nutr. 2007 Sep;86(3):645-51 Safety of vitamin D3 in adults with multiple sclerosis
In a 28-wk protocol, 12 patients in an active phase of multiple sclerosis were given 1200 mg elemental Ca/d along with progressively increasing doses of vitamin D3: from 700 to 7000 microg/wk (from 28 000 to 280 000 IU/wk). Patients' serum 25(OH)D concentrations reached twice the top of the physiologic range without eliciting hypercalcemia or hypercalciuria. The data support the feasibility of pharmacologic doses of vitamin D3 for clinical research, and they provide objective evidence that vitamin D intake beyond the current upper limit is safe by a large margin.
[Article]
- Mirshafiey A, Mohsenzadegan M. Immunopharmacol Immunotoxicol. 2009;31(1):13-29Antioxidant therapy in multiple sclerosis
Reactive oxygen species (ROS) play an important role in various events underlying multiple sclerosis pathology. In the initial phase of lesion formation, ROS are known to mediate the transendothelial migration of monocytes and induce a dysfunction in the blood-brain barrier.
[Abstract]
- Schreibelt G, van Horssen J, van Rossum S, Dijkstra CD, Drukarch B, de Vries HE. Brain Res Rev. 2007 Dec;56(2):322-30Therapeutic potential and biological role of endogenous antioxidant enzymes in multiple sclerosis pathology
We propose that antioxidants may inhibit the development and progression of MS lesions and may therefore represent an attractive therapeutic target for the treatment of MS and other oxidative stress-related neurological diseases
[Abstract]
- Ghafourifar P, Mousavizadeh K, Parihar MS, Nazarewicz RR, Parihar A, Zenebe WJ. Front Biosci. 2008 Jan. Mitochondria in multiple sclerosis
Mitochondria are one of the main cellular sources of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and play a pivotal role in many neuro-pathological conditions. Mitochondrial dysfunction leading to excessive production of ROS and RNS plays a significant role in the pathogenesis of MS, particularly in loss of myelin/oligodendrocyte complex
[Abstract]
- Schreibelt G, Musters RJ, Reijerkerk A, de Groot LR, van der Pol SM, Hendrikx EM, Döpp ED, Dijkstra CD, Drukarch B, de Vries HE. J Immunol. 2006 Aug 15;177(4):2630-7. Lipoic acid affects cellular migration into the central nervous system and stabilizes blood-brain barrier integrity
Reactive oxygen species (ROS) play an important role in various events underlying multiple sclerosis (MS) pathology.
In conclusion, we show that LA has a protective effect on EAE development not only by affecting the migratory capacity of monocytes, but also by stabilization of the BBB, making LA an attractive therapeutic agent for the treatment of MS.
[Article]
- Mirshafiey A, Mohsenzadegan M. Immunopharmacol Immunotoxicol. 2009;31(1):13-29. Antioxidant therapy in multiple sclerosis
Reactive oxygen species (ROS) play an important role in various events underlying multiple sclerosis pathology. In the initial phase of lesion formation, ROS are known to mediate the transendothelial migration of monocytes and induce a dysfunction in the blood-brain barrier
Antioxidant therapy may therefore represent an attractive treatment of MS. Several studies have shown that antioxidant therapy is beneficial in vitro and in vivo in animal models for MS.
[Abstract]
- Salinthone S, Yadav V, Bourdette DN, Carr DW. Endocr Metab Immune Disord Drug Targets. 2008 Jun;8(2):132-42 Lipoic acid: a novel therapeutic approach for multiple sclerosis and other chronic inflammatory diseases of the CNS
LA reduces and recycles cellular antioxidants such as glutathione, and chelates zinc, copper and other transition metal ions in addition to heavy metals. LA can also act as a scavenger of reactive oxygen and nitrogen species.
[Abstract]
- Chaudhary P, Marracci GH, Bourdette DN. J Neuroimmunol. 2006 Jun;175(1-2):87-96. Lipoic acid inhibits expression of ICAM-1 and VCAM-1 by CNS endothelial cells and T cell migration into the spinal cord in experimental autoimmune encephalomyelitis
Spinal cords from mice receiving LA had significantly reduced inflammation (decreased CD4 and CD11b staining) as compared to EAE mice that received saline. Overall, our data suggest that the anti-inflammatory effects of LA in EAE may be partly due to inhibition of ICAM-1 and VCAM-1 expression by central nervous system (CNS) endothelial cells.
[Abstract]
- Marracci GH, Marquardt WE, Strehlow A, McKeon GP, Gross J, Buck DC, Kozell LB, Bourdette DN. Biochem Biophys Res Commun. 2006 Jun 9;344(3):963-71 Lipoic acid downmodulates CD4 from human T lymphocytes by dissociation of p56(Lck)
Lipoic acid is an antioxidant that suppresses and treats a model of multiple sclerosis, experimental autoimmune encephalomyelitis. We now demonstrate that treatment of human PBMC and T cell lines with LA downmodulated CD4 expression in a concentration-dependent manner.
[Abstract]
- Morini M, Roccatagliata L, Dell'Eva R, Pedemonte E, Furlan R, Minghelli S, Giunti D, Pfeffer U, Marchese M, Noonan D, Mancardi G, Albini A, Uccelli A. J Neuroimmunol. 2004 Mar;148(1-2):146-53 Alpha-lipoic acid is effective in prevention and treatment of experimental autoimmune encephalomyelitis
Daily oral administration of alpha-LA, starting at the time of immunization, significantly prevented EAE progression as compared to control mice. This was associated with a reduction of CNS infiltrating T cells and macrophages as well as decreased demyelination.
[Abstract]
- Yadav V, Marracci G, Lovera J, Woodward W, Bogardus K, Marquardt W, Shinto L, Morris C, Bourdette D. Mult Scler. 2005 Apr;11(2):159-65 Lipoic acid in multiple sclerosis: a pilot study
Thirty-seven MS subjects were randomly assigned to one of four groups: placebo, LA 600 mg twice a day, LA 1200 mg once a day and LA 1200 mg twice a day.
We conclude that oral LA is generally well tolerated and appears capable of reducing serum MMP-9 and sICAM-1 levels. LA may prove useful in treating MS by inhibiting MMP-9 activity and interfering with T-cell migration into the CNS.
[Abstract]
- Kocer B, Engur S, Ak F, Yilmaz M. J Clin Neurosci. 2009 Mar;16(3):399-403. Serum vitamin B12, folate, and homocysteine levels and their association with clinical and electrophysiological parameters in multiple sclerosis
Patients with multiple sclerosis (MS) may have low serum vitamin B12 and folate levels and high levels of homocysteine.
Thus, we found a significant relationship between MS and vitamin B12 deficiency, and also demonstrated a relationship between vitamin B12 deficiency, VEP and posterior tibial SEP in MS.
[Abstract]
- Reynolds EH. J Neuroimmunol. 1992 Oct;40(2-3):225-30. Multiple sclerosis and vitamin B12 metabolism
Multiple sclerosis (MS) is occasionally associated with vitamin B12 deficiency. Recent studies have shown an increased risk of macrocytosis, low serum and/or CSF vitamin B12 levels, raised plasma homocysteine and raised unsaturated R-binder capacity in MS.
[Abstract]
- Sandyk R, Awerbuch GI. Int J Neurosci. 1993 Jul-Aug;71(1-4):93-9. Vitamin B12 and its relationship to age of onset of multiple sclerosis
Attention has been focused recently on the association between vitamin B12 metabolism and the pathogenesis of multiple sclerosis (MS). Several recent reports have documented vitamin B12 deficiency in patients with MS.
In addition, since vitamin B12 is required for the formation of myelin and for immune mechanisms, we propose that its deficiency in MS is of critical pathogenetic significance.
[Abstract]
- Miller A, Korem M, Almog R, Galboiz Y. J Neurol Sci. 2005 Jun 15;233(1-2):93-7. Vitamin B12, demyelination, remyelination and repair in multiple sclerosis
Multiple Sclerosis (MS) and vitamin B12 deficiency share common inflammatory and neurodegenerative pathophysiological characteristics
Additionally, low or decreased levels of vitamin B12 have been demonstrated in MS patients. Moreover, recent studies suggest that vitamin B12, in addition to its known role as a co-factor in myelin formation, has important immunomodulatory and neurotrophic effects
[Abstract]
- Saposnik G, Ray JG, Sheridan P, McQueen M, Lonn E; Heart Outcomes Prevention Evaluation 2 Investigators. Stroke. 2009 Apr;40(4):1365-72 Homocysteine-lowering therapy and stroke risk, severity, and disability: additional findings from the HOPE 2 trial
We analyzed stroke outcomes among participants of the Heart Outcomes Prevention Evaluation 2 (HOPE 2) trial that randomized 5522 adults with known cardiovascular disease to a daily combination of 2.5 mg of folic acid, 50 mg of vitamin B6, and 1 mg of vitamin B12, or matching placebo, for 5 years.
[Article]
- van Rensburg SJ, Kotze MJ, Hon D, Haug P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT. Metab Brain Dis. 2006 Sep;21(2-3):121-37. Iron and the folate-vitamin B12-methylation pathway in multiple sclerosis
Some subjects with multiple sclerosis (MS) present with low blood iron parameters. Anecdotal reports and a single patient study suggest that iron supplementation may be beneficial in these subjects. Myelin is regenerated continually, but prerequisites for this process are iron and a functional folate-vitamin B12-methylation pathway.
[Abstract]
- Simopoulos AP. J Am Coll Nutr. 2002 Dec;21(6):495-505 Omega-3 fatty acids in inflammation and autoimmune diseases
Among the fatty acids, it is the omega-3 polyunsaturated fatty acids (PUFA) which possess the most potent immunomodulatory activities, and among the omega-3 PUFA, those from fish oil—eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—are more biologically potent than -linolenic acid (ALA).
There have been a number of clinical trials assessing the benefits of dietary supplementation with fish oils in several inflammatory and autoimmune diseases in humans, including rheumatoid arthritis, Crohn's disease, ulcerative colitis, psoriasis, lupus erythematosus, multiple sclerosis and migraine headaches. Many of the placebo-controlled trials of fish oil in chronic inflammatory diseases reveal significant benefit, including decreased disease activity and a lowered use of anti-inflammatory drugs.
[Article]
- Mehta LR, Dworkin RH, Schwid SR. Nat Clin Pract Neurol. 2009 Feb;5(2):82-92 Polyunsaturated fatty acids and their potential therapeutic role in multiple sclerosis
Considerable interest has been shown in the potential anti-inflammatory effects of polyunsaturated fatty acids (PUFAs) in multiple sclerosis (MS) and other autoimmune inflammatory disorders. Studies suggest a modest association between consumption of low levels of unsaturated fat and an increased incidence of MS.
We propose that the potential role of PUFAs as disease-modifying, anti-inflammatory treatments for MS should be revisited in proof-of-concept trials that use accepted MRI outcome measures.
[Article]
- Liuzzi GM, Latronico T, Rossano R, Viggiani S, Fasano A, Riccio P. Neurochem Res. 2007 Dec;32(12):2184-93. Inhibitory effect of polyunsaturated fatty acids on MMP-9 release from microglial cells--implications for complementary multiple sclerosis treatment
microglial cells--implications for complementary multiple sclerosis treatment
Our results suggest that a low fat diet supplemented with omega-3 PUFA may become recommended for the well being of MS patients under therapy.
[Abstract]
- Swank RL, Dugan BB. Lancet. 1990 Jul 7;336(8706):37-9 Effect of low saturated fat diet in early and late cases of multiple sclerosis
144 multiple sclerosis patients took a low-fat diet for 34 years. For each of three categories of neurological disability (minimum, moderate, severe) patients who adhered to the prescribed diet (less than or equal to 20 g fat/day) showed significantly less deterioration and much lower death rates than did those who consumed more fat than prescribed (greater than 20 g fat/day). The greatest benefit was seen in those with minimum disability at the start of the trial; in this group, when those who died from non-MS diseases were excluded from the analysis, 95% survived and remained physically active.
[Abstract]
- Schwarz S, Leweling H. Mult Scler. 2005 Feb;11(1):24-32 Multiple sclerosis and nutrition
There is some evidence that a high intake of saturated fat increases the incidence of MS.
[Abstract]
- Mollao?lu M, Ustün E. J Clin Nurs. 2009 May;18(9):1231-8. Fatigue in multiple sclerosis patients
Fatigue is the most common symptom and has the greatest effect on multiple sclerosis patients' activities of daily living.
[Abstract]
- Shah A. Phys Med Rehabil Clin N Am. 2009 May;20(2):363-72. Fatigue in multiple sclerosis
In summary, MS-related fatigue can be a severe problem causing interference with home and vocational activities
[Abstract]
- Johnson SL. J Neurosci Nurs. 2008 Apr;40(2):72-7. The concept of fatigue in multiple sclerosis
Fatigue is one of the most common symptoms of multiple sclerosis (MS), and it can have a major impact on health-related quality of life. Therefore, it is imperative that healthcare practitioners regularly assess fatigue in their patients with MS
[Abstract]
- Kos D, Kerckhofs E, Nagels G, D'hooghe MB, Ilsbroukx S. Neurorehabil Neural Repair. 2008 Jan-Feb;22(1):91-100. Origin of fatigue in multiple sclerosis: review of the literature
Primary fatigue may be the result of inflammation, demyelination, or axonal loss. A suggested functional cortical reorganization may result in a higher energy demand in certain brain areas, culminating in an increase of fatigue perception. Higher
Fatigue may be secondary to sleep problems, which are frequently present in MS and in their turn result from urinary problems, spasms, pain, or anxiety.
[Abstract]
- Lebrun C, Alchaar H, Candito M, Bourg V, Chatel M. Mult Scler. 2006 Jun;12(3):321-4. Levocarnitine administration in multiple sclerosis patients with immunosuppressive therapy-induced fatigue
Deficiency of carnitine may play a role by reducing energy production through fatty acid oxidation and numerous MS therapies can induce fatigue syndrome.
Treatment consisted of oral levocarnitine, 3-6 g daily. All patients achieved normal plasma carnitine levels. For 63% of patients treated with immunosuppressive or immunomodulatory therapies, oral levocarnitine adjunction decreased fatigue intensity, especially in patients treated with cyclophosphamide and interferon beta.
[Abstract]
- Tomassini V, Pozzilli C, Onesti E, Pasqualetti P, Marinelli F, Pisani A, Fieschi C. J Neurol Sci. 2004 Mar 15;218(1-2):103-8 Comparison of the effects of acetyl L-carnitine and amantadine for the treatment of fatigue in multiple sclerosis: results of a pilot, randomised, double-blind, crossover trial
Statistical analysis showed significant effects of ALCAR compared with amantadine for the Fatigue Severity Scale (p = 0.039).
The results of this study show that ALCAR is better tolerated and more effective than amantadine for the treatment of MS-related fatigue.
[Abstract]
- Giovannoni G, Heales SJ, Land JM, Thompson EJ. Mult Scler. 1998 Jun;4(3):212-6 The potential role of nitric oxide in multiple sclerosis
Nitric oxide (.NO) and its reactive derivative peroxynitrite (ONOO-) have been implicated in the pathogenesis of multiple sclerosis (MS). They are cytotoxic to oligodendrocytes and neurones in culture by inhibiting the mitochondrial respiratory chain (complexes II/III and IV) and inhibiting certain key intracellular enzymes.
[Abstract]
- Heales SJ, Bolaños JP, Stewart VC, Brookes PS, Land JM, Clark JB. Biochim Biophys Acta. 1999 Feb 9;1410(2):215-28Nitric oxide, mitochondria and neurological disease
Damage to the mitochondrial electron transport chain has been suggested to be an important factor in the pathogenesis of a range of neurological disorders, such as Parkinson's disease, Alzheimer's disease, multiple sclerosis, stroke and amyotrophic lateral sclerosis. There is also a growing body of evidence to implicate excessive or inappropriate generation of nitric oxide (NO) in these disorders. It is now well documented that NO and its toxic metabolite, peroxynitrite (ONOO-), can inhibit components of the mitochondrial respiratory chain leading, if damage is severe enough, to a cellular energy deficiency state.
[Abstract]
- Calabrese V, Scapagnini G, Ravagna A, Bella R, Butterfield DA, Calvani M, Pennisi G, Giuffrida Stella AM. Neurochem Res. 2003 Sep;28(9):1321-8 Disruption of thiol homeostasis and nitrosative stress in the cerebrospinal fluid of patients with active multiple sclerosis: evidence for a protective role of acetylcarnitine
Our data sustain the hypothesis that nitrosative stress is a major consequence of NO produced in MS-affected CNS and implicate a possible important role for acetylcarnitine in protecting brain against nitrosative stress, which may underlie the pathogenesis of MS.
[Abstract]
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