Lees !!! Het staat allemaal op internet.
While Science Sleeps© W. Monte
The Etiology of Multiple Sclerosis – Follow the Methanol Every Disease has a Beginning, a First Performance – Just How Old is MS?
When an individual is suffering from the early stages of MS, it could easily be mistaken for many other diseases; however, the ultimate symptoms and unusual gate of the full-blown disease are unique, unmistakable, and so tragic as to still bring a tear even to my trained eye. Nevertheless, medical texts from the Middle Ages contain no descriptions of any disease which would be recognizable as MS.[#230] The fact that this obvious severe symptomology is completely absent from any historical or even biblical literature is telling. Wolfgram even noted during his plea for the search of a small solvent as the cause of MS that “there is a curious lack of reference to the obvious symptoms of MS in the medical literature prior to the middle of the nineteenth century.”[#151] This is all proof that MS is indeed a disease of modern civilized man.
We hebben het eerder over gehad, maar m.s bestaat pas vanaf ongeveer 1860.
Ook dit boek is gratis te downloaden op internet; wel weer erg veel, maar erg duidelijk. Over methanol.
Jossi
Methanol - m.s. als moderne ziekte.
-
Sebastiaan
Gewoon niet waar. De Heilige Lidwina wordt door sommigen gezien als een van de eerste personen die symptomen van MS vertoonde. In de 14e eeuw dus.
Dat wil zeker niet zeggen dat Lidwina ook MS had (zullen we nooit zeker weten), maar haalt wel de stelling uit het boek onderuit dat er geen enkel geval bekend is.
Methanol als oorzaak wordt vrijwel altijd in verband gebracht met aspartaam of andere voedseladditieven. Dat verklaart dan weer niet de MS-gevallen uit de 19e eeuw, beschreven door bijvoorbeeld Charcot.
Dat wil zeker niet zeggen dat Lidwina ook MS had (zullen we nooit zeker weten), maar haalt wel de stelling uit het boek onderuit dat er geen enkel geval bekend is.
Methanol als oorzaak wordt vrijwel altijd in verband gebracht met aspartaam of andere voedseladditieven. Dat verklaart dan weer niet de MS-gevallen uit de 19e eeuw, beschreven door bijvoorbeeld Charcot.
-
Robbie
ahum
ahum
[quote]1421 First documented case of MS; St. Lidwina of Schiedam
1860-70 First studies of myelin and glial cells in brain tissue
1868 First correlation of MS clinical symptoms with central nervous system pathology; disease named "Sclerose en plaques" by Jean Martin Charcot
1869 First attempts to treat MS with gold chloride, zinc, sulfate, silver nitrate, strychnine and electrical stimulation (by Charcot)
1928 Discovery that myelin is produced by oligodendrocyte glial cells
1933 Acute experimental allergic encephalomyelitis (EAE) developed as model for MS
1936 Discovery that lymphocytes are involved in immune function
1943 First detailed description of the composition of myelin
1950 First studies of prevalence of MS in the US
1954-55 First well defined MS diagnostic criteria (clinical and laboratory) and development of quantitative disability scoring techniques
1963 First understanding of familial susceptibility to MS
1969 Completion of first controlled clinical trial for intramuscular ACTH in acute attacks of MS; shows more rapid recovery from attacks than would happen without ACTH
1970 Discovery of different classes of T-lymphocytes: T-helper cells, T-suppressor cells, etc.
1972 Negative results from attempts to find specific viruses in MS brain, cerebrospinal fluid and blood
1978 First use of monoclonal antibodies to identify specific T-lymphocyte sub-types
1981 Identification of oligodendrocytes in MS brain with capability for regeneration of myelin
1981 Consensus on the essential role of double-blind, placebo controlled clinical trials for new therapeutic agents in MS
1982 First use of MRI to image lesions in living patients
1983 First report of temporary control of chronic- progressive MS with the immunosuppressive drug, Cytoxan (widely disputed throughout decade)
1984 First modern documentation of cognitive problems in MS
1985 First association of HTLV-I retroviruses with MS (later disproved)
1988 First demonstration, using MRI, that there is significant lesion activity in MS brain, even when the disease is clinically quiescent
1988 First quality studies identifying possible prognostic factors for MS disability early in disease
1988 Protection from EAE by monoclonal antibodies against T-cell sub-types
1989 Increased knowledge of genetic factors that control T-cell function and T-cell receptor structure
1989 Initiation of pilot clinical studies of specific monoclonal antibodies against T-cell sub-types in chronic progressive MS
1980's-1990's Undertaking of many well designed clinical trials, in 1980-1990's pilot or definitive studies: copolymer I pilot study for relapsing/remitting disease (possible efficacy seen); copolymer I studies for chronic progressive disease (no efficacy); cyclosporine A (slight efficacy with significant toxicity); alpha and beta interferons (possible efficacy; continuing studies underway); 4 Aminopyridine and 3,4 Diaminopyridine (possible efficacy for symptomatic improvement); use of oral myelin to initiate tolerance (possible efficacy); and others
1990-91 Successful transplantation of myelin-making oligodendrocytes into myelin deficient mice, resulting in production of new myelin
1990-92 Development of techniques to identify specific T-cell receptor usage in MS brain and blood that may lead to disease; application of this knowledge to specific treatment approaches using specific peptides[/quote]
en
[QUOTE][LEFT][B]1838[/B]: doctors’ autopsy drawings show changes in brain tissues, but MS is not yet identified[/LEFT]
[LEFT][B]1868[/B]: A French neurologist, Dr. Jean Martin Charcot, tracks several patients with neurological symptoms such as tremors, slurred speech, walking difficulties, and muscle spasms. He examines one particular patient’s brain after her death and discovers multiple sclerosis “plaques” or scarring along nerve pathways.[/LEFT]
[/QUOTE]
Volgens mij is rond 1860 MS als aandoening gedefinieerd, daarvoor werd je gewoon als ' gek' beschouwd.
Dus, vroeger was je gek, nu noemen we het ms:haha::haha::haha:
[quote]1421 First documented case of MS; St. Lidwina of Schiedam
1860-70 First studies of myelin and glial cells in brain tissue
1868 First correlation of MS clinical symptoms with central nervous system pathology; disease named "Sclerose en plaques" by Jean Martin Charcot
1869 First attempts to treat MS with gold chloride, zinc, sulfate, silver nitrate, strychnine and electrical stimulation (by Charcot)
1928 Discovery that myelin is produced by oligodendrocyte glial cells
1933 Acute experimental allergic encephalomyelitis (EAE) developed as model for MS
1936 Discovery that lymphocytes are involved in immune function
1943 First detailed description of the composition of myelin
1950 First studies of prevalence of MS in the US
1954-55 First well defined MS diagnostic criteria (clinical and laboratory) and development of quantitative disability scoring techniques
1963 First understanding of familial susceptibility to MS
1969 Completion of first controlled clinical trial for intramuscular ACTH in acute attacks of MS; shows more rapid recovery from attacks than would happen without ACTH
1970 Discovery of different classes of T-lymphocytes: T-helper cells, T-suppressor cells, etc.
1972 Negative results from attempts to find specific viruses in MS brain, cerebrospinal fluid and blood
1978 First use of monoclonal antibodies to identify specific T-lymphocyte sub-types
1981 Identification of oligodendrocytes in MS brain with capability for regeneration of myelin
1981 Consensus on the essential role of double-blind, placebo controlled clinical trials for new therapeutic agents in MS
1982 First use of MRI to image lesions in living patients
1983 First report of temporary control of chronic- progressive MS with the immunosuppressive drug, Cytoxan (widely disputed throughout decade)
1984 First modern documentation of cognitive problems in MS
1985 First association of HTLV-I retroviruses with MS (later disproved)
1988 First demonstration, using MRI, that there is significant lesion activity in MS brain, even when the disease is clinically quiescent
1988 First quality studies identifying possible prognostic factors for MS disability early in disease
1988 Protection from EAE by monoclonal antibodies against T-cell sub-types
1989 Increased knowledge of genetic factors that control T-cell function and T-cell receptor structure
1989 Initiation of pilot clinical studies of specific monoclonal antibodies against T-cell sub-types in chronic progressive MS
1980's-1990's Undertaking of many well designed clinical trials, in 1980-1990's pilot or definitive studies: copolymer I pilot study for relapsing/remitting disease (possible efficacy seen); copolymer I studies for chronic progressive disease (no efficacy); cyclosporine A (slight efficacy with significant toxicity); alpha and beta interferons (possible efficacy; continuing studies underway); 4 Aminopyridine and 3,4 Diaminopyridine (possible efficacy for symptomatic improvement); use of oral myelin to initiate tolerance (possible efficacy); and others
1990-91 Successful transplantation of myelin-making oligodendrocytes into myelin deficient mice, resulting in production of new myelin
1990-92 Development of techniques to identify specific T-cell receptor usage in MS brain and blood that may lead to disease; application of this knowledge to specific treatment approaches using specific peptides[/quote]
en
[QUOTE][LEFT][B]1838[/B]: doctors’ autopsy drawings show changes in brain tissues, but MS is not yet identified[/LEFT]
[LEFT][B]1868[/B]: A French neurologist, Dr. Jean Martin Charcot, tracks several patients with neurological symptoms such as tremors, slurred speech, walking difficulties, and muscle spasms. He examines one particular patient’s brain after her death and discovers multiple sclerosis “plaques” or scarring along nerve pathways.[/LEFT]
[/QUOTE]
Volgens mij is rond 1860 MS als aandoening gedefinieerd, daarvoor werd je gewoon als ' gek' beschouwd.
Dus, vroeger was je gek, nu noemen we het ms:haha::haha::haha:
-
Robbie
historie met de vasculaire-relatie
[QUOTE][B]1839, Cruveilhier
[/B]
According to Putnam1, who pioneered experiments linking vascular abnormalities to MS in 1936, the first observations related to abnormal vasculature were documented by French anatomist Cruveilhier2 in 1839. Cruveilhier compared areas of sclerosis with the results of embolism.
[B]1863, Rindfleisch and Charcot
[/B]
In 1863, Rindfleisch3 microscopically observed autopsy specimens of MS brains and noted an engorged blood vessel in the center of each plaque. In the same year Charcot4 described vascular obstruction in MS.
[B]1934-1953, Putnam
[/B]
Putnam studied the effects of obstructed venous flow in the cerebral veins of dogs. These animals developed a number of abnormalities similar to encephalitis or multiple sclerosis. His comment was as follows5:
[I]"The similarity between such lesions and many of those seen in cases of multiple sclerosis in man is so striking that the conclusion appears almost inevitable that venular obstruction is the essential immediate antecedent to the formation of typical sclerotic plaques."[/I]
Putnam and his colleagues in the neurology department at Boston City Hospital, Harvard University, and Columbia University continued to investigate damage caused to the brain and central nervous system resulting from disruption of blood flow well into the 1950's.
[B]1942, Dow and Berglund
[/B]
Dr. Robert Dow and Dr. George Berglund continued Dr. Putnam's research, finding further venous connections to MS lesions. The authors note that Ribbert6 earlier maintained that the demyelinated areas were related to a primary disseminated thrombosis. He described a congested central vessel in all the sclerotic patches.
[B]1950, Zimmermann and Netsky
[/B]
Drs. Zimmerman and Netsky furthered Dow and Berglund's research. They noted that the lesions were indeed venous in nature, but not caused by small thrombosis as Putnam had surmised7.
[B]1963, Fog
[/B]
Dr. Torben Fog, a Danish professor, noted that MS lesions were predominantly found around the small veins. Fog summarized his results from a series of cadaver brain studies8 stating "30 plaques showed that they definitely followed the course of the veins, so that course and dimensions of the veins determine the shape, course and dimension of the plaques."
[B]1973-1981, Schelling[/B]
In 1973, at the University of Innsbruck, F. Alfons Schelling, M.D. began investigations into the enormous individual differences in the widths of the venous outlets of the human skull. The results of this study appeared in 1978 in "Anatomischer Anzeiger"9, from the German-speaking Anatomical Societies.
Schelling's 1981 discovery, at the Hospital for Nervous Diseases in Salzburg, of a striking anomolies of the main venous passageways through the skulls in victims of multiple sclerosis were to occupy the author's thoughts through the following decades of his career. A crucial observation was the venous involvement in MS7 and lesion genesis. Predating Dr. Zamboni’s similar (but more detailed) CCSVI hypothesis, Dr. Schelling suggested that MS may be at least partially a result of venous ‘back-jets’ (reflux) into the CNS. While Dr. Schelling’s early hypothesis now appears strikingly relevant, when Schelling went public with his research at the time, he was ridiculed, dismissed, or simply ignored.
[B]1981 Allen et al.[/B]
Further evidence of the vascular mechanical effect comes from the observations of I.V. Allen, who noticed the wide vascular beds around veins and the central widening of the venous tree indicative of intermittent increases in cerebral pressure10.
[B]1987, Adams et al. [/B]
C. W. M. Adams, who specialized in microscopic tissue studies of MS plaque development (“histopathology”), lead a series of experiments in the 1980s which confirmed the fundamental vascular nature of MS plaque development 11.
[B]1990, Kermode et al.[/B]
In a seminal publication, “Breakdown of the Blood Brain Barrier Precedes Symptoms and Other MRI Signs of New Lesions in Multiple Sclerosis,”12 Kermode et al. demonstrated via four meticulously documented cases studies that breach of the BBB (Blood Brain Barrier) occurred before MS symptom onset. Kermode concludes that “This supports the view that a defect in the blood brain barrier, and therefore inflammation, is an early and possibly crucial event in the pathogenesis of the new lesion in MS.” Kermode also notes that “Such perivascular inflammation [inflammation around veins] has also been seen in the normally appearing white matter… leading to the conclusion that perivascular inflammation in MS can occur in the absence of myelin breakdown, and the suggestion that a vascular event is a necessary preliminary to the development of structural damage.”
[B]1994, Kwon & Prineas[/B]
Validating Kermode’s findings, Kwon and Prineas’ histological studies corroborated that BBB permeability appears prior to demyelination13.
[B]1998, Juurlink[/B]
In a hypothetical presentation14, B.H.J. Juurlink of the Cameco MS & Neuroscience Research Center in Saskatoon, Canada, tied together a wide body of research linking MS with white blood cell infiltration of the CNS via abnormal vascular permeability. Juurlink’s work, which stressed the role of hypoperfusion (decreased blood flow), built a compelling case for endothelial breakdown as a key component of BBB breach that is often considered a hallmark of MS.
[B]Zamboni; Zamboni et al., 2006; 2009[/B]
In 200615, prior to proposing CCSVI, Dr. Zamboni presented a paper noting the remarkable similarity between Chronic Venous Disease (CVD), and MS, including similar liaisons and iron/fibrinogen deposition. In 200916, Dr. Zamboni used duplex ultrasonography to demonstrate a strong correlation between CCSVI and MS.
[B]2008, Ge et al. 2008[/B]
Ge, Zohrabian, and Grossman used state-of-the-art ultra-high resolution imaging techniques available to “describe the perivenous relationship of MS lesions”17. Producing images with detail never before seen, Ge et al. note that of the 80 lesions studied in RRMS patients, “all lesions showed a strict perivascular distribution, following the form, orientation, and course of the vessels". They note that “these findings, which have never been shown on conventional field of MRI, not only allow for direct evidence of vascular pathogenesis in MS [I]in vivo[/I], but have important implications for monitoring lesion activity and therapeutic response.”
[B]McQuaid, 2009[/B]
McQuaid, Kirk, et al. in Ireland have spent a decade researching MS plaque development and MS pathogenesis. Summarizing their work, McQuad et al. (2009)18 confirms that “Dysfunction of the BBB is a major hallmark of MS.” Additionally, they note that abnormal fibrinogen leakage (as hypothesized by Zamboni, 2006, above) is “one of the earliest events associated with MS lesion formation,” noting finally that “fibrinogen could function to mediate the initial activation of resting microglia leading to increased phagocytosis” (in other words, fibrinogen that has migrated across the BBB due to endothelial dysfunction can effect (regulate) native CNS cells and accompanying immune activity).
[I][COLOR=#1c3e95]Summary[/COLOR][/I]
From the very first observations of MS lesions over 150 years ago up to the most current state-of-the-art histological and Magnetic Resonance Imaging and studies, the clear link between MS and the vascular system has been apparent. Recent findings that vascular dysfunction, whatever its cause, may precede both T-cell and B-Cell activation and demyelination advances our understanding of the complex interplay between the immune and vascular components of MS. It is hoped that the groundbreaking research summarized above, research conducted across four continents and over 150 years, will contribute to creative new approaches for managing, ameliorating, and avoiding MS onset and progression. [/QUOTE]
[QUOTE][B]1839, Cruveilhier
[/B]
According to Putnam1, who pioneered experiments linking vascular abnormalities to MS in 1936, the first observations related to abnormal vasculature were documented by French anatomist Cruveilhier2 in 1839. Cruveilhier compared areas of sclerosis with the results of embolism.
[B]1863, Rindfleisch and Charcot
[/B]
In 1863, Rindfleisch3 microscopically observed autopsy specimens of MS brains and noted an engorged blood vessel in the center of each plaque. In the same year Charcot4 described vascular obstruction in MS.
[B]1934-1953, Putnam
[/B]
Putnam studied the effects of obstructed venous flow in the cerebral veins of dogs. These animals developed a number of abnormalities similar to encephalitis or multiple sclerosis. His comment was as follows5:
[I]"The similarity between such lesions and many of those seen in cases of multiple sclerosis in man is so striking that the conclusion appears almost inevitable that venular obstruction is the essential immediate antecedent to the formation of typical sclerotic plaques."[/I]
Putnam and his colleagues in the neurology department at Boston City Hospital, Harvard University, and Columbia University continued to investigate damage caused to the brain and central nervous system resulting from disruption of blood flow well into the 1950's.
[B]1942, Dow and Berglund
[/B]
Dr. Robert Dow and Dr. George Berglund continued Dr. Putnam's research, finding further venous connections to MS lesions. The authors note that Ribbert6 earlier maintained that the demyelinated areas were related to a primary disseminated thrombosis. He described a congested central vessel in all the sclerotic patches.
[B]1950, Zimmermann and Netsky
[/B]
Drs. Zimmerman and Netsky furthered Dow and Berglund's research. They noted that the lesions were indeed venous in nature, but not caused by small thrombosis as Putnam had surmised7.
[B]1963, Fog
[/B]
Dr. Torben Fog, a Danish professor, noted that MS lesions were predominantly found around the small veins. Fog summarized his results from a series of cadaver brain studies8 stating "30 plaques showed that they definitely followed the course of the veins, so that course and dimensions of the veins determine the shape, course and dimension of the plaques."
[B]1973-1981, Schelling[/B]
In 1973, at the University of Innsbruck, F. Alfons Schelling, M.D. began investigations into the enormous individual differences in the widths of the venous outlets of the human skull. The results of this study appeared in 1978 in "Anatomischer Anzeiger"9, from the German-speaking Anatomical Societies.
Schelling's 1981 discovery, at the Hospital for Nervous Diseases in Salzburg, of a striking anomolies of the main venous passageways through the skulls in victims of multiple sclerosis were to occupy the author's thoughts through the following decades of his career. A crucial observation was the venous involvement in MS7 and lesion genesis. Predating Dr. Zamboni’s similar (but more detailed) CCSVI hypothesis, Dr. Schelling suggested that MS may be at least partially a result of venous ‘back-jets’ (reflux) into the CNS. While Dr. Schelling’s early hypothesis now appears strikingly relevant, when Schelling went public with his research at the time, he was ridiculed, dismissed, or simply ignored.
[B]1981 Allen et al.[/B]
Further evidence of the vascular mechanical effect comes from the observations of I.V. Allen, who noticed the wide vascular beds around veins and the central widening of the venous tree indicative of intermittent increases in cerebral pressure10.
[B]1987, Adams et al. [/B]
C. W. M. Adams, who specialized in microscopic tissue studies of MS plaque development (“histopathology”), lead a series of experiments in the 1980s which confirmed the fundamental vascular nature of MS plaque development 11.
[B]1990, Kermode et al.[/B]
In a seminal publication, “Breakdown of the Blood Brain Barrier Precedes Symptoms and Other MRI Signs of New Lesions in Multiple Sclerosis,”12 Kermode et al. demonstrated via four meticulously documented cases studies that breach of the BBB (Blood Brain Barrier) occurred before MS symptom onset. Kermode concludes that “This supports the view that a defect in the blood brain barrier, and therefore inflammation, is an early and possibly crucial event in the pathogenesis of the new lesion in MS.” Kermode also notes that “Such perivascular inflammation [inflammation around veins] has also been seen in the normally appearing white matter… leading to the conclusion that perivascular inflammation in MS can occur in the absence of myelin breakdown, and the suggestion that a vascular event is a necessary preliminary to the development of structural damage.”
[B]1994, Kwon & Prineas[/B]
Validating Kermode’s findings, Kwon and Prineas’ histological studies corroborated that BBB permeability appears prior to demyelination13.
[B]1998, Juurlink[/B]
In a hypothetical presentation14, B.H.J. Juurlink of the Cameco MS & Neuroscience Research Center in Saskatoon, Canada, tied together a wide body of research linking MS with white blood cell infiltration of the CNS via abnormal vascular permeability. Juurlink’s work, which stressed the role of hypoperfusion (decreased blood flow), built a compelling case for endothelial breakdown as a key component of BBB breach that is often considered a hallmark of MS.
[B]Zamboni; Zamboni et al., 2006; 2009[/B]
In 200615, prior to proposing CCSVI, Dr. Zamboni presented a paper noting the remarkable similarity between Chronic Venous Disease (CVD), and MS, including similar liaisons and iron/fibrinogen deposition. In 200916, Dr. Zamboni used duplex ultrasonography to demonstrate a strong correlation between CCSVI and MS.
[B]2008, Ge et al. 2008[/B]
Ge, Zohrabian, and Grossman used state-of-the-art ultra-high resolution imaging techniques available to “describe the perivenous relationship of MS lesions”17. Producing images with detail never before seen, Ge et al. note that of the 80 lesions studied in RRMS patients, “all lesions showed a strict perivascular distribution, following the form, orientation, and course of the vessels". They note that “these findings, which have never been shown on conventional field of MRI, not only allow for direct evidence of vascular pathogenesis in MS [I]in vivo[/I], but have important implications for monitoring lesion activity and therapeutic response.”
[B]McQuaid, 2009[/B]
McQuaid, Kirk, et al. in Ireland have spent a decade researching MS plaque development and MS pathogenesis. Summarizing their work, McQuad et al. (2009)18 confirms that “Dysfunction of the BBB is a major hallmark of MS.” Additionally, they note that abnormal fibrinogen leakage (as hypothesized by Zamboni, 2006, above) is “one of the earliest events associated with MS lesion formation,” noting finally that “fibrinogen could function to mediate the initial activation of resting microglia leading to increased phagocytosis” (in other words, fibrinogen that has migrated across the BBB due to endothelial dysfunction can effect (regulate) native CNS cells and accompanying immune activity).
[I][COLOR=#1c3e95]Summary[/COLOR][/I]
From the very first observations of MS lesions over 150 years ago up to the most current state-of-the-art histological and Magnetic Resonance Imaging and studies, the clear link between MS and the vascular system has been apparent. Recent findings that vascular dysfunction, whatever its cause, may precede both T-cell and B-Cell activation and demyelination advances our understanding of the complex interplay between the immune and vascular components of MS. It is hoped that the groundbreaking research summarized above, research conducted across four continents and over 150 years, will contribute to creative new approaches for managing, ameliorating, and avoiding MS onset and progression. [/QUOTE]
-
jossi
Sebastiaan, zowel het artikel van W. Monte, evenals het artikel van Herald D. Foster aangaande voedsel als waarschijnlijke oorzaak van m.s., is van dusdanig hoog wetenschappelijk gehalte en zo ontzettend veel en uitgebreid, dat ik van jou of anderen niet kan en mag verwachten dat hier een zinnige respons/commentaar op kan worden verwacht.
Je hebt hiervoor vele dagen/weken nodig om het door te lezen, en dat is wat teveel van het goede.
Wel jammer zoals zoveel, maar ja.
Jossi
Je hebt hiervoor vele dagen/weken nodig om het door te lezen, en dat is wat teveel van het goede.
Wel jammer zoals zoveel, maar ja.
Jossi
-
Jolande
[QUOTE=jossi;902644]Sebastiaan, zowel het artikel van W. Monte, evenals het artikel van Herald D. Foster aangaande voedsel als waarschijnlijke oorzaak van m.s., is van dusdanig hoog wetenschappelijk gehalte en zo ontzettend veel en uitgebreid, dat ik van jou of anderen niet kan en mag verwachten dat hier een zinnige respons/commentaar op kan worden verwacht.
Je hebt hiervoor vele dagen/weken nodig om het door te lezen, en dat is wat teveel van het goede.
Wel jammer zoals zoveel, maar ja.
Jossi[/QUOTE]
Beste Jossi,
Hoog wetenschappelijk gehalte, veel en uitgebreid?
Dus er zijn hier geen mensen die behalve jij dat niveau aankunnen?
Ik heb wel eens vaker van je gelezen dat als iets maar veel is je al onder de indruk bent.
Vind het wel jammer dat je zonder je medemens te kennen zo neerbuigend over ze oordeelt.
Ben je zelf wetenschapper? Of wat brengt jou in de verleiding zoiets te beweren?
Je hebt hiervoor vele dagen/weken nodig om het door te lezen, en dat is wat teveel van het goede.
Wel jammer zoals zoveel, maar ja.
Jossi[/QUOTE]
Beste Jossi,
Hoog wetenschappelijk gehalte, veel en uitgebreid?
Dus er zijn hier geen mensen die behalve jij dat niveau aankunnen?
Ik heb wel eens vaker van je gelezen dat als iets maar veel is je al onder de indruk bent.
Vind het wel jammer dat je zonder je medemens te kennen zo neerbuigend over ze oordeelt.
Ben je zelf wetenschapper? Of wat brengt jou in de verleiding zoiets te beweren?
-
Sebastiaan
[QUOTE=jossi;902644]Sebastiaan, zowel het artikel van W. Monte, evenals het artikel van Herald D. Foster aangaande voedsel als waarschijnlijke oorzaak van m.s., is van dusdanig hoog wetenschappelijk gehalte en zo ontzettend veel en uitgebreid, dat ik van jou of anderen niet kan en mag verwachten dat hier een zinnige respons/commentaar op kan worden verwacht.
Je hebt hiervoor vele dagen/weken nodig om het door te lezen, en dat is wat teveel van het goede.
Wel jammer zoals zoveel, maar ja.
Jossi[/QUOTE]
Beetje kort door de bocht, Jossi. Toen ik zeven jaar geleden begon met mijn werk bij de MSVN was de DVD van Monte een van de eerste dingen die ik op mijn bureau kreeg. Er is toen door de redactie heel veel gelezen en uitgezocht, ook door mij.
Monte heeft een hoop werk verzet, maar een aantal aannames kloppen gewoonweg niet. Zoals de bewering dat er geen MS voorkwam voor de 19e eeuw. Zie bovenstaande commentaren voor het tegendeel. Monte koppelt dat aan het ontstaan van methanol in ingeblikt voedsel. Die link is verder door niemand aangetoond.
Verder nemen mensen al eeuwen methanol tot zich. Bij het distilleren van alcohol ontstaat methanol als bijproduct en het duurde tot de 19e eeuw voor het mogelijk was die methanol (de zogenaamde "voorloop") te scheiden van het minder giftige ethanol. Ook nu bevat de meeste sterke drank nog sporen van ethanol. Een verband tussen alcoholgebruik (of misbruik) en MS heeft nog niemand gevonden tot op heden.
Naar aspartaam is keer op keer onderzoek gedaan, vaak met het doel om het middel in diskrediet te brengen. Oorzaak: financiering van het onderzoek door de suikerindustrie, die niet blij was met deze concurrent. Eenzelfde truc hebben ze nu uitgehaald met Stevia, waarvan het gebruik aan allerlei richtlijnen gebonden is.
Je hebt hiervoor vele dagen/weken nodig om het door te lezen, en dat is wat teveel van het goede.
Wel jammer zoals zoveel, maar ja.
Jossi[/QUOTE]
Beetje kort door de bocht, Jossi. Toen ik zeven jaar geleden begon met mijn werk bij de MSVN was de DVD van Monte een van de eerste dingen die ik op mijn bureau kreeg. Er is toen door de redactie heel veel gelezen en uitgezocht, ook door mij.
Monte heeft een hoop werk verzet, maar een aantal aannames kloppen gewoonweg niet. Zoals de bewering dat er geen MS voorkwam voor de 19e eeuw. Zie bovenstaande commentaren voor het tegendeel. Monte koppelt dat aan het ontstaan van methanol in ingeblikt voedsel. Die link is verder door niemand aangetoond.
Verder nemen mensen al eeuwen methanol tot zich. Bij het distilleren van alcohol ontstaat methanol als bijproduct en het duurde tot de 19e eeuw voor het mogelijk was die methanol (de zogenaamde "voorloop") te scheiden van het minder giftige ethanol. Ook nu bevat de meeste sterke drank nog sporen van ethanol. Een verband tussen alcoholgebruik (of misbruik) en MS heeft nog niemand gevonden tot op heden.
Naar aspartaam is keer op keer onderzoek gedaan, vaak met het doel om het middel in diskrediet te brengen. Oorzaak: financiering van het onderzoek door de suikerindustrie, die niet blij was met deze concurrent. Eenzelfde truc hebben ze nu uitgehaald met Stevia, waarvan het gebruik aan allerlei richtlijnen gebonden is.
-
jossi
Methanol vooral in sigaretten. Apparatuur voor automatisch oprollen van sigaretten was erg belangrijk.
Vergeet niet, dat niet bij iedereen dezelfde invloed van schadelijke stoffen dezelfde symptomen geven. Je kan roken zonder longkanker te krijgen etc. Synergie is van groot belang, evenals de epigenetica.
We zijn het gewoon fundamenteel oneens over de meeste zaken.
Van elkaar vinden we dat we een bord voor ons kop hebben.
P.s.: ik ga - zoals zovelen die met voeding bezig zijn - VOORUIT. Geweldig. Heb ik dan niet een beetje gelijk ?!
Jossi
Vergeet niet, dat niet bij iedereen dezelfde invloed van schadelijke stoffen dezelfde symptomen geven. Je kan roken zonder longkanker te krijgen etc. Synergie is van groot belang, evenals de epigenetica.
We zijn het gewoon fundamenteel oneens over de meeste zaken.
Van elkaar vinden we dat we een bord voor ons kop hebben.
P.s.: ik ga - zoals zovelen die met voeding bezig zijn - VOORUIT. Geweldig. Heb ik dan niet een beetje gelijk ?!
Jossi
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Jolande
[QUOTE=jossi;902668]P.s.: ik ga - zoals zovelen die met voeding bezig zijn - VOORUIT. Geweldig. Heb ik dan niet een beetje gelijk?![/QUOTE]
Nee, daarmee heb je zeker niet een beetje gelijk. Je trekt volstrekt voorbarige en ongefundeerde conclusies.
Er zijn legio mssers die zich aan geen enkel dieet houden en opzienbarende oplevingen kennen :cool:
Ik snap wel dat je een verklaring zoekt en je vooruit graag wilt toekennen aan datgene wat je doet en er voor laat maar zo simpel is het allemaal niet helaas
Nee, daarmee heb je zeker niet een beetje gelijk. Je trekt volstrekt voorbarige en ongefundeerde conclusies.
Er zijn legio mssers die zich aan geen enkel dieet houden en opzienbarende oplevingen kennen :cool:
Ik snap wel dat je een verklaring zoekt en je vooruit graag wilt toekennen aan datgene wat je doet en er voor laat maar zo simpel is het allemaal niet helaas