Wie helpt me aan de volgende wetenschappelijke artikelen?
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Bij voorkeur niet dus!!!!
Hé DR P, wederom bedankt voor het compleet maken van mijn verlanglijstje.
Kan ik weer braaf verder met deze meuk doorlezen.............
Isdatzo, ben jij nog bezig met b-vitamins/methylaters en diseases/mortaliteit?
Recente study:
Cancer incidence and mortality after treatment with folic acid and vitamin B12.
CONTEXT: Recently, concern has been raised about the safety of folic acid, particularly in relation to cancer risk. OBJECTIVE: To evaluate effects of treatment with B vitamins on cancer outcomes and all-cause mortality in 2 randomized controlled trials. DESIGN, SETTING, AND PARTICIPANTS: Combined analysis and extended follow-up of participants from 2 randomized, double-blind, placebo-controlled clinical trials (Norwegian Vitamin Trial and Western Norway B Vitamin Intervention Trial). A total of 6837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005, and were followed up through December 31, 2007. INTERVENTIONS: Oral treatment with folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) and vitamin B(6) (40 mg/d) (n = 1708); folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) (n = 1703); vitamin B(6) alone (40 mg/d) (n = 1705); or placebo (n = 1721). MAIN OUTCOME MEASURES: Cancer incidence, cancer mortality, and all-cause mortality. RESULTS: During study treatment, median serum folate concentration increased more than 6-fold among participants given folic acid. After a median 39 months of treatment and an additional 38 months of posttrial observational follow-up, 341 participants (10.0%) who received folic acid plus vitamin B(12) vs 288 participants (8.4%) who did not receive such treatment were diagnosed with cancer (hazard ratio
, 1.21; 95% confidence interval [CI], 1.03-1.41; P = .02). A total of 136 (4.0%) who received folic acid plus vitamin B(12) vs 100 (2.9%) who did not receive such treatment died from cancer (HR, 1.38; 95% CI, 1.07-1.79; P = .01). A total of 548 patients (16.1%) who received folic acid plus vitamin B(12) vs 473 (13.8%) who did not receive such treatment died from any cause (HR, 1.18; 95% CI, 1.04-1.33; P = .01). Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B(12). Vitamin B(6) treatment was not associated with any significant effects. CONCLUSION: Treatment with folic acid plus vitamin B(12) was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway, where there is no folic acid fortification of foods. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00671346.
PMID: 19920236 [PubMed - in process]
Commentaar erop:
BERGEN, Norway—Treatment with folic acid plus vitamin B12 was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease, according to a recent Norwegian study (JAMA 2009;302(19):2119-2126); however, nutrition scientists questioned the validity of the combined analysis protocol and results. The study used a combined analysis and extended follow-up of participants from two randomized, double blind, placebo-controlled clinical trials (Norwegian Vitamin Trial (NAT) and Western Norway B Vitamin Intervention Trial (NORVIT)). A total of 6,837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005, and were followed up through Dec. 31, 2007.Oral treatment administered 0.8 mg/d of folic acid plus 0.4 mg/d of vitamin B12 and 40 mg/d of vitamin B6 (n=1708); 0.8 mg/d of folic acid plus 0.4 mg/d of vitamin B12 (n=1703); 40 mg/d of vitamin B6 alone (n=1705); or placebo (n=1721).
During study treatment, median serum folate concentration increased more than six-fold among participants given folic acid. After a median 39 months of treatment and an additional 38 months of post-trial observational follow-up, 341 participants (10.0 percent) who received folic acid plus vitamin B12 versus 288 participants (8.4 percent) who did not receive such treatment were diagnosed with cancer. A total of 136 (4.0 percent) who received folic acid plus vitamin B12 versus 100 (2.9 percent) who did not receive such treatment died from cancer. A total of 548 patients (16.1 percent) who received folic acid plus vitamin B12 versus 473 (13.8 percent) who did not receive such treatment died from any cause. Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B12. Vitamin B6 treatment was not associated with any significant effects.
Andrew Shao, Ph.D., vice president, scientific and regulatory affairs at the Council for Responsible Nutrition (CRN) commented on the study results, stating: ““The real headline of this study should be that smoking increases the risk of lung cancer—the study found 94 percent of the subjects who developed lung cancer were either current or former smokers. It is puzzling why patients who were given high-doses of folic acid were more likely to develop lung cancer than those subjects in the control group; however, it is important to point out that these results are inconsistent with the larger body of data and that this effect has not been observed previously. In fact, as the authors themselves point out, ‘Epidemiological studies have demonstrated no associations between intakes of folate or folic acid and lung cancer risk.’”
Additionally, Daniel Fabricant, Ph.D., vice president of scientific and regulatory affairs for the Natural Products Association (NPA), commented: “This is an analysis of two studies—the NORVIT and WENBIT. Despite the authors’ justification for the analysis, previous review has indicated the NORVIT might not have been adequately powered and the factorial design might have been too complex, thus rendering the trial incapable of isolating the effect of folate per se. Being combined with the WENBIT, which was terminated early, and which wasn’t without its design flaws, either, creates a scenario in which two flawed studies are combined to yield one larger flawed study. This does not seem to be in the best interest of medical science or public health.”
Ik heb niet echt in het onderwerp verdiept, en ik hou al helemaal niet in epidemiology, dus ik heb niet echt een goed overzicht van de stand van zaken. Jij, iemand anders?
Ander recent onderzoek, wat zegt oa dat methione restrictie leven verlengt bij een hoog calorie diet en dat het mogelijk het mechanisme is achter het effect van CR op levensverlening, wat een HUGE impact zou hebben op wat we weten:
Amino-acid imbalance explains extension of lifespan by dietary restriction in Drosophila.
[1] Institute of Healthy Ageing, Department of Genetics Evolution and Environment, University College London, Gower St, London WC1E 6BT, UK [2] These authors contributed equally to this work.
Dietary restriction extends healthy lifespan in diverse organisms and reduces fecundity. It is widely assumed to induce adaptive reallocation of nutrients from reproduction to somatic maintenance, aiding survival of food shortages in nature. If this were the case, long life under dietary restriction and high fecundity under full feeding would be mutually exclusive, through competition for the same limiting nutrients. Here we report a test of this idea in which we identified the nutrients producing the responses of lifespan and fecundity to dietary restriction in Drosophila. Adding essential amino acids to the dietary restriction condition increased fecundity and decreased lifespan, similar to the effects of full feeding, with other nutrients having little or no effect. However, methionine alone was necessary and sufficient to increase fecundity as much as did full feeding, but without reducing lifespan. Reallocation of nutrients therefore does not explain the responses to dietary restriction. Lifespan was decreased by the addition of amino acids, with an interaction between methionine and other essential amino acids having a key role. Hence, an imbalance in dietary amino acids away from the ratio optimal for reproduction shortens lifespan during full feeding and limits fecundity during dietary restriction. Reduced activity of the insulin/insulin-like growth factor signalling pathway extends lifespan in diverse organisms, and we find that it also protects against the shortening of lifespan with full feeding. In other organisms, including mammals, it may be possible to obtain the benefits to lifespan of dietary restriction without incurring a reduction in fecundity, through a suitable balance of nutrients in the diet.
PMID: 19956092 [PubMed - as supplied by publisher]
Dus de vraag is, hoe zou dit effect tot stand komen? Een mogelijkheid is het effect van methiodine op homocysteine:
Effect of methionine loading on 5-methyltetrahydrofolate, S-adenosylmethionine and S-adenosylhomocysteine in plasma of healthy humans.
Metabolic Unit, University Children's Hospital Basel, Switzerland.
1. Elevated plasma homocysteine concentration, either in the fasting state or after methionine loading, is an independent risk factor for vascular disease in man. Methionine loading has been used to investigate impaired methionine metabolism, especially of the trans-sulphuration pathway, but most studies have focused on changes in homocysteine. 2. We investigated the effect of methionine excess on total plasma homocysteine, 5-methyltetrahydrofolate (which is the active form of folate in the remethylation of homocysteine to methionine), S-adenosyl-methionine (the first metabolite of methionine) and S-adenosylmethionine) (the demethylated product of S-adenosylmethionine) over 24h in 12 healthy subjects. 3. As well as the expected increase in homocysteine (from 8.0 +/- 1.3 to 32.6 +/- 10.3 mumol/l, mean +/- SD, P < 0.001), S-adenosylmethionine showed a significant transient increase (from 37.9 +/- 25.0 to 240.3 +/- 109.2 nmol/l, P < 0.001), which correlated well with homocysteine (r2 = 0.92, P < 0.001). 5-Methyltetrahydrofolate values decreased significantly (from 23.2 +/- 7.2 to 13.1 +/- 2.9 nmol/l, P < 0.01), and gradually returned to baseline levels after 24h. No significant change over the time of measurement was found for S-adenosylhomocysteine. 4. The sequence of metabolic changes observed in this study strongly suggests that a change in either homocysteine or S-adenosylmethionine may cause a reduction in 5-methyltetrahydrofolate. This must be considered in evaluating the relationship between folate and homocysteine in vascular disease. The metabolic relationships illustrated in this study should be evaluated in the search for pathogenetic mechanisms of mild hyperhomocysteinaemia and vascular disease.
PMID: 8774264 [PubMed - indexed for MEDLINE]
Een andere of bijkomende optie kan de rol van methiodine in DNA methylation zijn:
Assessing the effects of high methionine intake on DNA methylation.
Methylation of DNA occurs at cytosines within CpG (cytosine-guanine) dinucleotides and is 1 of several epigenetic mechanisms that serve to establish and maintain tissue-specific patterns of gene expression. The methyl groups transferred in mammalian DNA methylation reactions are ultimately derived from methionine. High dietary methionine intake might therefore be expected to increase DNA methylation. Because of the circular nature of the methionine cycle, however, methionine excess may actually impair DNA methylation by inhibiting remethylation of homocysteine. Although little is known regarding the effect of dietary methionine supplementation on mammalian DNA methylation, the available data suggest that methionine supplementation can induce hypermethylation of DNA in specific genomic regions. Because locus-specific DNA hypomethylation is implicated in the etiology of various cancers and developmental syndromes, clinical trials of "promethylation" dietary supplements are already under way. However, aberrant hypermethylation of DNA could be deleterious. It is therefore important to determine whether dietary supplementation with methionine can effectively support therapeutic maintenance of DNA methylation without causing excessive and potentially adverse locus-specific hypermethylation. In the viable yellow agouti (Avy) mouse, maternal diet affects the coat color distribution of offspring by perturbing the establishment of methylation at the Avy metastable epiallele. Hence, the Avy mouse can be employed as a sensitive epigenetic biosensor to assess the effects of dietary methionine supplementation on locus-specific DNA methylation. Recent developments in epigenomic approaches that survey locus-specific DNA methylation on a genome-wide scale offer broader opportunities to assess the effects of high methionine intake on mammalian epigenomes.
PMID: 16702343 [PubMed - indexed for MEDLINE]
Aangezien methione deel uitmaakt van het methylation patyway, zou dit wel eens gelinkt kunnen zijn met de effecten van b-vitamines/methylators:
[Afbeelding niet meer beschikbaar]
Dit is niet echt mijn pakkie aan, maar dit kan wel eens het belangrijkste (voedings)onderzoek zijn van .....eeuwig(?), als het een praktische manier oplevert waarop alle levensduur en/of kwaliteitverbeterd kan worden.
Recente study:
Cancer incidence and mortality after treatment with folic acid and vitamin B12.
CONTEXT: Recently, concern has been raised about the safety of folic acid, particularly in relation to cancer risk. OBJECTIVE: To evaluate effects of treatment with B vitamins on cancer outcomes and all-cause mortality in 2 randomized controlled trials. DESIGN, SETTING, AND PARTICIPANTS: Combined analysis and extended follow-up of participants from 2 randomized, double-blind, placebo-controlled clinical trials (Norwegian Vitamin Trial and Western Norway B Vitamin Intervention Trial). A total of 6837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005, and were followed up through December 31, 2007. INTERVENTIONS: Oral treatment with folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) and vitamin B(6) (40 mg/d) (n = 1708); folic acid (0.8 mg/d) plus vitamin B(12) (0.4 mg/d) (n = 1703); vitamin B(6) alone (40 mg/d) (n = 1705); or placebo (n = 1721). MAIN OUTCOME MEASURES: Cancer incidence, cancer mortality, and all-cause mortality. RESULTS: During study treatment, median serum folate concentration increased more than 6-fold among participants given folic acid. After a median 39 months of treatment and an additional 38 months of posttrial observational follow-up, 341 participants (10.0%) who received folic acid plus vitamin B(12) vs 288 participants (8.4%) who did not receive such treatment were diagnosed with cancer (hazard ratio
, 1.21; 95% confidence interval [CI], 1.03-1.41; P = .02). A total of 136 (4.0%) who received folic acid plus vitamin B(12) vs 100 (2.9%) who did not receive such treatment died from cancer (HR, 1.38; 95% CI, 1.07-1.79; P = .01). A total of 548 patients (16.1%) who received folic acid plus vitamin B(12) vs 473 (13.8%) who did not receive such treatment died from any cause (HR, 1.18; 95% CI, 1.04-1.33; P = .01). Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B(12). Vitamin B(6) treatment was not associated with any significant effects. CONCLUSION: Treatment with folic acid plus vitamin B(12) was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease in Norway, where there is no folic acid fortification of foods. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00671346.
PMID: 19920236 [PubMed - in process]
Commentaar erop:
BERGEN, Norway—Treatment with folic acid plus vitamin B12 was associated with increased cancer outcomes and all-cause mortality in patients with ischemic heart disease, according to a recent Norwegian study (JAMA 2009;302(19):2119-2126); however, nutrition scientists questioned the validity of the combined analysis protocol and results. The study used a combined analysis and extended follow-up of participants from two randomized, double blind, placebo-controlled clinical trials (Norwegian Vitamin Trial (NAT) and Western Norway B Vitamin Intervention Trial (NORVIT)). A total of 6,837 patients with ischemic heart disease were treated with B vitamins or placebo between 1998 and 2005, and were followed up through Dec. 31, 2007.Oral treatment administered 0.8 mg/d of folic acid plus 0.4 mg/d of vitamin B12 and 40 mg/d of vitamin B6 (n=1708); 0.8 mg/d of folic acid plus 0.4 mg/d of vitamin B12 (n=1703); 40 mg/d of vitamin B6 alone (n=1705); or placebo (n=1721).
During study treatment, median serum folate concentration increased more than six-fold among participants given folic acid. After a median 39 months of treatment and an additional 38 months of post-trial observational follow-up, 341 participants (10.0 percent) who received folic acid plus vitamin B12 versus 288 participants (8.4 percent) who did not receive such treatment were diagnosed with cancer. A total of 136 (4.0 percent) who received folic acid plus vitamin B12 versus 100 (2.9 percent) who did not receive such treatment died from cancer. A total of 548 patients (16.1 percent) who received folic acid plus vitamin B12 versus 473 (13.8 percent) who did not receive such treatment died from any cause. Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B12. Vitamin B6 treatment was not associated with any significant effects.
Andrew Shao, Ph.D., vice president, scientific and regulatory affairs at the Council for Responsible Nutrition (CRN) commented on the study results, stating: ““The real headline of this study should be that smoking increases the risk of lung cancer—the study found 94 percent of the subjects who developed lung cancer were either current or former smokers. It is puzzling why patients who were given high-doses of folic acid were more likely to develop lung cancer than those subjects in the control group; however, it is important to point out that these results are inconsistent with the larger body of data and that this effect has not been observed previously. In fact, as the authors themselves point out, ‘Epidemiological studies have demonstrated no associations between intakes of folate or folic acid and lung cancer risk.’”
Additionally, Daniel Fabricant, Ph.D., vice president of scientific and regulatory affairs for the Natural Products Association (NPA), commented: “This is an analysis of two studies—the NORVIT and WENBIT. Despite the authors’ justification for the analysis, previous review has indicated the NORVIT might not have been adequately powered and the factorial design might have been too complex, thus rendering the trial incapable of isolating the effect of folate per se. Being combined with the WENBIT, which was terminated early, and which wasn’t without its design flaws, either, creates a scenario in which two flawed studies are combined to yield one larger flawed study. This does not seem to be in the best interest of medical science or public health.”
Ik heb niet echt in het onderwerp verdiept, en ik hou al helemaal niet in epidemiology, dus ik heb niet echt een goed overzicht van de stand van zaken. Jij, iemand anders?
Ander recent onderzoek, wat zegt oa dat methione restrictie leven verlengt bij een hoog calorie diet en dat het mogelijk het mechanisme is achter het effect van CR op levensverlening, wat een HUGE impact zou hebben op wat we weten:
Amino-acid imbalance explains extension of lifespan by dietary restriction in Drosophila.
[1] Institute of Healthy Ageing, Department of Genetics Evolution and Environment, University College London, Gower St, London WC1E 6BT, UK [2] These authors contributed equally to this work.
Dietary restriction extends healthy lifespan in diverse organisms and reduces fecundity. It is widely assumed to induce adaptive reallocation of nutrients from reproduction to somatic maintenance, aiding survival of food shortages in nature. If this were the case, long life under dietary restriction and high fecundity under full feeding would be mutually exclusive, through competition for the same limiting nutrients. Here we report a test of this idea in which we identified the nutrients producing the responses of lifespan and fecundity to dietary restriction in Drosophila. Adding essential amino acids to the dietary restriction condition increased fecundity and decreased lifespan, similar to the effects of full feeding, with other nutrients having little or no effect. However, methionine alone was necessary and sufficient to increase fecundity as much as did full feeding, but without reducing lifespan. Reallocation of nutrients therefore does not explain the responses to dietary restriction. Lifespan was decreased by the addition of amino acids, with an interaction between methionine and other essential amino acids having a key role. Hence, an imbalance in dietary amino acids away from the ratio optimal for reproduction shortens lifespan during full feeding and limits fecundity during dietary restriction. Reduced activity of the insulin/insulin-like growth factor signalling pathway extends lifespan in diverse organisms, and we find that it also protects against the shortening of lifespan with full feeding. In other organisms, including mammals, it may be possible to obtain the benefits to lifespan of dietary restriction without incurring a reduction in fecundity, through a suitable balance of nutrients in the diet.
PMID: 19956092 [PubMed - as supplied by publisher]
Dus de vraag is, hoe zou dit effect tot stand komen? Een mogelijkheid is het effect van methiodine op homocysteine:
Effect of methionine loading on 5-methyltetrahydrofolate, S-adenosylmethionine and S-adenosylhomocysteine in plasma of healthy humans.
Metabolic Unit, University Children's Hospital Basel, Switzerland.
1. Elevated plasma homocysteine concentration, either in the fasting state or after methionine loading, is an independent risk factor for vascular disease in man. Methionine loading has been used to investigate impaired methionine metabolism, especially of the trans-sulphuration pathway, but most studies have focused on changes in homocysteine. 2. We investigated the effect of methionine excess on total plasma homocysteine, 5-methyltetrahydrofolate (which is the active form of folate in the remethylation of homocysteine to methionine), S-adenosyl-methionine (the first metabolite of methionine) and S-adenosylmethionine) (the demethylated product of S-adenosylmethionine) over 24h in 12 healthy subjects. 3. As well as the expected increase in homocysteine (from 8.0 +/- 1.3 to 32.6 +/- 10.3 mumol/l, mean +/- SD, P < 0.001), S-adenosylmethionine showed a significant transient increase (from 37.9 +/- 25.0 to 240.3 +/- 109.2 nmol/l, P < 0.001), which correlated well with homocysteine (r2 = 0.92, P < 0.001). 5-Methyltetrahydrofolate values decreased significantly (from 23.2 +/- 7.2 to 13.1 +/- 2.9 nmol/l, P < 0.01), and gradually returned to baseline levels after 24h. No significant change over the time of measurement was found for S-adenosylhomocysteine. 4. The sequence of metabolic changes observed in this study strongly suggests that a change in either homocysteine or S-adenosylmethionine may cause a reduction in 5-methyltetrahydrofolate. This must be considered in evaluating the relationship between folate and homocysteine in vascular disease. The metabolic relationships illustrated in this study should be evaluated in the search for pathogenetic mechanisms of mild hyperhomocysteinaemia and vascular disease.
PMID: 8774264 [PubMed - indexed for MEDLINE]
Een andere of bijkomende optie kan de rol van methiodine in DNA methylation zijn:
Assessing the effects of high methionine intake on DNA methylation.
Methylation of DNA occurs at cytosines within CpG (cytosine-guanine) dinucleotides and is 1 of several epigenetic mechanisms that serve to establish and maintain tissue-specific patterns of gene expression. The methyl groups transferred in mammalian DNA methylation reactions are ultimately derived from methionine. High dietary methionine intake might therefore be expected to increase DNA methylation. Because of the circular nature of the methionine cycle, however, methionine excess may actually impair DNA methylation by inhibiting remethylation of homocysteine. Although little is known regarding the effect of dietary methionine supplementation on mammalian DNA methylation, the available data suggest that methionine supplementation can induce hypermethylation of DNA in specific genomic regions. Because locus-specific DNA hypomethylation is implicated in the etiology of various cancers and developmental syndromes, clinical trials of "promethylation" dietary supplements are already under way. However, aberrant hypermethylation of DNA could be deleterious. It is therefore important to determine whether dietary supplementation with methionine can effectively support therapeutic maintenance of DNA methylation without causing excessive and potentially adverse locus-specific hypermethylation. In the viable yellow agouti (Avy) mouse, maternal diet affects the coat color distribution of offspring by perturbing the establishment of methylation at the Avy metastable epiallele. Hence, the Avy mouse can be employed as a sensitive epigenetic biosensor to assess the effects of dietary methionine supplementation on locus-specific DNA methylation. Recent developments in epigenomic approaches that survey locus-specific DNA methylation on a genome-wide scale offer broader opportunities to assess the effects of high methionine intake on mammalian epigenomes.
PMID: 16702343 [PubMed - indexed for MEDLINE]
Aangezien methione deel uitmaakt van het methylation patyway, zou dit wel eens gelinkt kunnen zijn met de effecten van b-vitamines/methylators:
[Afbeelding niet meer beschikbaar]
Dit is niet echt mijn pakkie aan, maar dit kan wel eens het belangrijkste (voedings)onderzoek zijn van .....eeuwig(?), als het een praktische manier oplevert waarop alle levensduur en/of kwaliteitverbeterd kan worden.
Topic van Amerikaans board waarin dit onderwerp ook besproken wordt:
http://forum.bodybuilding.com/showthread.php?t=120408531
en
http://scholar.google.com/scholar?rlz=1C1GGLS_enUS326US326&sourceid=chrome&q=methionine restriction
http://forum.bodybuilding.com/showthread.php?t=120408531
en
http://scholar.google.com/scholar?rlz=1C1GGLS_enUS326US326&sourceid=chrome&q=methionine restriction
isdatzo
Advanced Bodybuilder
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Nope. Heb in het verleden wel discussies gehad over effecten van bepaalde B vitamines op de gezondheid. Ook op dit forum. Hier kwam o.a. uit dat foliumzuur blijkbaar geen effect heeft op hart- en vaatziekten en overlijden:
http://forum.dutchbodybuilding.com/...slik-doen-mijn-gezondheid-109178/#post1904984
Dat effect wordt ook niet tegengesproken door de resultaten van het onderzoek waar je naar verwijst, en wat ook op mijn site staat.
Er staat ook in de abstract dat het om de specifieke combinatie van deze 2 B-vitamines ging. Dan moet je je maar afvragen wat het effect zal zijn indien hieraan weer andere vitamines worden toegevoegd, zoals ook wordt gesteld door de toevoeging van vitamine B6.
Dit vind ik een bijzonder vreemd commentaar van iemand in zijn functie. Tenminste, zolang hij dit niet onderbouwt. Hij heeft pas een punt indien hij laat zien dat de gevonden effecten daadwerkelijk werden beïnvloedt door roken. Dat lijkt niet aannemelijk aangezien het om gerandomiseerd onderzoek gaat. Natuurlijk is dit niet uitgesloten, maar voor dit soort uitspraken, moet je de rauwe gegevens van het onderzoek hebben en hier je theoriën op loslaten. Zolang je dat niet hebt gedaan, heb je naar mijn mening geen recht van spreken.
Hiermee suggereert hij dat hij inderdaad zijn theoriën niet heeft kunnen staven door ze te toetsen aan de realiteit (het onderzoek waar hij kritiek op heeft). Stellen dat een onderzoek onzin is doordat vorige onderzoeken andere resultaten laten zien vind ik nogal onwetenschappelijk.
Daarbij ben ik zelf nog nooit een onderzoek tegengekomen naar de gecombineerde effecten van foliumzuur + vitamine B12.
Geen idee of deze er wel zijn...............
Niet zo vreemd dat deze man bij voorbaat de resultaten probeert te ontzenuwen: President van de Natural Products Association --> [Link niet meer beschikbaar]
Maar even inhoudelijk reageren: Hij stelt dat het misschien zou kunnen dat er zwakheden in de studie zitten. Dat zal best kunnen, maar dit betekent nog niet dat de resultaten anders zouden zijn indien deze mogelijke zwakheden niet zouden bestaan. In principe blijven resultaten van gerandomiseerde onderzoeken het meest betrouwbaar. Natuurlijk kun je hier niet zomaar conclusies uit trekken en behoeven de resultaten bevestiging door meerdere gerandomiseerde onderzoeken.
De opzet van een studie wordt vaak aangevallen indien de resultaten niet zijn zoals men verwacht. Kijk maar naar de vleesindustrie die het rapport van het WCRF onterecht aanviel toen bleek dat je van sommige vleesproducten darmkanker zou kunnen krijgen.
Nog niet. Heb het veel te druk met de huidige shit op mijn sites. Kan wel een paar jaar duren voor ik hier aan toe kom. Als ik dan nog zin heb........
Ik heb niet zoveel met onderzoek bij fruitvliegjes. Heb ook geen verstand van deze schattige beestjes.
Ik begrijp niet helemaal wat ze hiermee suggereren, maar volgens mij hoeft een effect op homocysteine nog niet te betekenen dat er ook een effect wordt gevonden op hart- en vaatziekten/overlijden:
Zelf vind ik het pas interessant om te weten hóe een effect wordt bewerkstelligd zodra er overtuigend bewijs is dat er ook daadwerkelijk een effect is gevonden. Mijn kennis op het gebied van theoretische modellen schiet dan ook tekort.
Ik probeer mezelf zoveel mogelijk te beperken tot de meest-relevante start- en end points.
De "methylation patyway" is dan ook weer niet mijn pakkie aan. Doordat er duizenden gerandomiseerde en prospective onderzoeken zijn gedaan naar interessante shit voor mensen, heb ik helaas geen tijd om mezelf te verdiepen in de theorie. Hoe interessant deze ook is. Maar zodra je iets concreets weet hoor ik het graag
isdatzo
Advanced Bodybuilder
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Sorry voor de kleine bump, maar ik heb weer een paar artikelen nodig. Kan zo niet verder met mijn "huiswerk". Ik verwacht dat niemand aan alle studies kan komen (nr. 2 helemaal niet), maar je weet nooit.
Op het verlanglijstje staan:
Gartside PS. Relationship of dietary intake to hospital admission for coronary heart and vascular disease: the NHANES II national probability study. J Am Coll Nutr. 1993 Dec;12(6):676-84.
Link: http://www.ncbi.nlm.nih.gov/pubmed/8294723
Seino F. Dietary lipids and incidence of cerebral infarction in a Japanese rural community. J Nutr Sci Vitaminol (Tokyo). 1997 Feb;43(1):83-99.
Link: http://www.ncbi.nlm.nih.gov/pubmed/9151243
Egeland GM. Cod liver oil consumption, smoking, and coronary heart disease mortality: three counties, Norway. Int J Circumpolar Health. 2001 Apr;60(2):143-9.
Link: http://www.ncbi.nlm.nih.gov/pubmed/11507963
De Goede J. Marine (n-3) fatty acids, fish consumption, and the 10-year risk of fatal and nonfatal coronary heart disease in a large population of Dutch adults with low fish intake. J Nutr. May;140(5):1023-8.
Link: http://www.ncbi.nlm.nih.gov/pubmed/20335635
Op het verlanglijstje staan:
Gartside PS. Relationship of dietary intake to hospital admission for coronary heart and vascular disease: the NHANES II national probability study. J Am Coll Nutr. 1993 Dec;12(6):676-84.
Link: http://www.ncbi.nlm.nih.gov/pubmed/8294723
Seino F. Dietary lipids and incidence of cerebral infarction in a Japanese rural community. J Nutr Sci Vitaminol (Tokyo). 1997 Feb;43(1):83-99.
Link: http://www.ncbi.nlm.nih.gov/pubmed/9151243
Egeland GM. Cod liver oil consumption, smoking, and coronary heart disease mortality: three counties, Norway. Int J Circumpolar Health. 2001 Apr;60(2):143-9.
Link: http://www.ncbi.nlm.nih.gov/pubmed/11507963
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isdatzo
Advanced Bodybuilder
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Erg bedankt weer!
Ik had ook niet echt verwacht dat iemand aan de overige 3 artikelen zou kunnen komen.
Balen alleen dat je altijd 2-3 maanden moet wachten voordat je een buitenland aanvraag binnenkrijgt.
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