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orka med alla dessa cancerartiklar… går ju fram och tillbaka med vad som är farligt och vad som inte är det hela tiden så jag har slutat bry mig
King Grub wrote:Själva slutsatsen i översättning:”Resultaten av detta megaexperiment indikerar att aspartam är en multipotentiell carcinogen, även vid ett dagligt intag på 20/mg/kg kroppsvikt, en mycket lägre dos än dagens acceptabla dagliga intag. Baserat på på dessa resultat är en omvärdering av nuvarande riktlinjer vad gäller bruk och intag av aspartam brådskande och får inte fördröjas.”
Jag väger 69 kg. Det innebär enligt studien att 120 mg är cancerogent för mig? Dock säger det mig inte så mycket. Hur mycket aspartam fanns det i en 1,5 l Coca Cola Light tidigare? Hur mycket strör man på gröten på morgonen?
En vuxen person som väger 60 kilo skulle nå 20 mg/kg genom att dricka runt 2.4 liter lightläsk med ”normal” aspartammängd.
Simon Persson wrote:Hmm, Nina: 20 mg * 69 = 1380 mg :nerd:Hahahaha. Jag är usel. Till saken hör att jag har räknat det med XP:s lilla miniräknare. Som synes har hjärnan på intet sett varit inkopplad.
CMG wrote:Fan va bra att man inte dricker en massa läsk mer isåfall. Det finns också aspartam i tuggumi.Hur fan kan de sätta in sånt här i våra produkter när det är så farligt… sjukt.
tja det verkar inte vara så värst svårt för dem. Läskindustrin har länge vetat om att vissa ämnen i läsken reagerar med varandra och bildar bensen. Inte heller så trevligt för oss.
Hur är det egentligen med Sackarin som bland annat Hermesetas består av?
Det enda jag hittat är att det i vissa länder är begränsat förbud mot medlet på grund av misstankar om toxiska effekter. Annars verkar det harmlöst men jag har inte hittat någon undersökning.smurfpucko wrote:Hur är det egentligen med Sackarin som bland annat Hermesetas består av?
Det enda jag hittat är att det i vissa länder är begränsat förbud mot medlet på grund av misstankar om toxiska effekter. Annars verkar det harmlöst men jag har inte hittat någon undersökning.Sackarin och cyklamat är sötningsmedel jag inte till något pris vill ha i mig.
Något som bevisat ger råttor urinblåsecancer och som ger apor lymfom, tumörer , fettlever och levercystor håller jag mig borta från.
”The National Toxicology Program’s advisory panel on the federal government’s Report on Carcinogens today recommended the continued listing of saccharin in the ninth edition of this official report of cancer-causing substances.”
Urinblåsecancer:
National Institute of Environmental Health Sciences, Oct 31, 1997
Natl Cancer Inst. 1998 Jan 7;90(1):19-25. Long-term feeding of sodium saccharin to nonhuman primates: implications for urinary tract cancer.
I det allmänt tillgängliga abstraktet står det:
”Twenty monkeys of three species (six African green, seven rhesus, six cynomolgus, and one hybrid [of rhesus male and cynomolgus female parentage]) were treated with sodium saccharin (25 mg in the diet/kg body weight daily for 5 days a week) beginning within 24 hours after birth and continuing for up to 24 years. Sixteen monkeys (seven rhesus and nine cynomolgus) served as controls.
Sodium saccharin treatment had no effect on the urine or urothelium in any of these monkeys. There was no evidence of increased urothelial cell proliferation, and there was no evidence of formation of solid material in the urine. Although the dose of sodium saccharin administered to these monkeys was only five to 10 times the allowable daily intake for humans, the results provide additional evidence that sodium saccharin is without a carcinogenic effect on the primate urinary tract.”
Låter ju bra.
Vad står det i fullängdsstudien? Jo:
”When the 12 remaining saccharin-treated monkeys were euthanized in
1995, three of them had gross evidence of tumors. Histologic
examination revealed a thyroid lymphoma in the first monkey,
leiomyoma of the uterus in the second monkey, and a papillary
cystadenoma of the ovary and leiomyoma of the stomach in the
third monkey. In addition to the tumors, three of the 12 monkeys had myocardial fibrosis and three had myocardial fatty degeneration. In seven of
these 12 monkeys, fatty degeneration of the liver was noted, and
one animal had a liver cyst.”Kontrollgruppen, som inte fick sackarin, hade inga tumörer…
Återigen en apstudie, fast på cyklamat, där man kommit fram till att det inte är cancerframkallande. Ändå står det i studien:
”In 1994, two of the 24-year-old monkeys in the 500 mg/kg dose group were diagnosed with advanced cancer; a female (801J) with metastatic adenocarcinoma of the colon and a male (787J) with metastatic hepatocellular carcinoma. The third cancer case was a minute (3 x 3 mm) well-differentiated papillary adenocarcinoma of the prostate that was found during necropsy of an animal (774J) dosed at 100 mg/kg. Benign neoplasms were found during necropsy of two females in the 100 mg/kg cyclamate group and one in the 500 mg/kg group; one was an adenoma of the thyroid (791J) and two were leiomyomas of the uterus (772J and 801J). No neoplasms were detected in the control animals.
…
In conclusion, the findings of this study showed that long-term feeding of nonhuman primates with high doses of cyclamate did not affect the general health of most of these animals.”
Hur kan man dra den slutsatsen, när djuren som fått cyklamat utvecklade cancer, men inte dom som inte fick det?
Takayama S, Renwick AG, Johansson SL et al. Long-term toxicity and carcinogenicity study of cyclamate in nonhuman primates. Toxicol Sci 2000; 53: 33–39.
King Grub wrote:Sackarin och cyklamat är sötningsmedel jag inte till något pris vill ha i mig.Något som bevisat ger råttor urinblåsecancer och som ger apor lymfom, tumörer , fettlever och levercystor håller jag mig borta från.
”The National Toxicology Program’s advisory panel on the federal government’s Report on Carcinogens today recommended the continued listing of saccharin in the ninth edition of this official report of cancer-causing substances.”
Urinblåsecancer:
National Institute of Environmental Health Sciences, Oct 31, 1997
Natl Cancer Inst. 1998 Jan 7;90(1):19-25. Long-term feeding of sodium saccharin to nonhuman primates: implications for urinary tract cancer.
I det allmänt tillgängliga abstraktet står det:
”Twenty monkeys of three species (six African green, seven rhesus, six cynomolgus, and one hybrid [of rhesus male and cynomolgus female parentage]) were treated with sodium saccharin (25 mg in the diet/kg body weight daily for 5 days a week) beginning within 24 hours after birth and continuing for up to 24 years. Sixteen monkeys (seven rhesus and nine cynomolgus) served as controls.
Sodium saccharin treatment had no effect on the urine or urothelium in any of these monkeys. There was no evidence of increased urothelial cell proliferation, and there was no evidence of formation of solid material in the urine. Although the dose of sodium saccharin administered to these monkeys was only five to 10 times the allowable daily intake for humans, the results provide additional evidence that sodium saccharin is without a carcinogenic effect on the primate urinary tract.”
Låter ju bra.
Vad står det i fullängdsstudien? Jo:
”When the 12 remaining saccharin-treated monkeys were euthanized in
1995, three of them had gross evidence of tumors. Histologic
examination revealed a thyroid lymphoma in the first monkey,
leiomyoma of the uterus in the second monkey, and a papillary
cystadenoma of the ovary and leiomyoma of the stomach in the
third monkey. In addition to the tumors, three of the 12 monkeys had myocardial fibrosis and three had myocardial fatty degeneration. In seven of
these 12 monkeys, fatty degeneration of the liver was noted, and
one animal had a liver cyst.”Kontrollgruppen, som inte fick sackarin, hade inga tumörer…
Återigen en apstudie, fast på cyklamat, där man kommit fram till att det inte är cancerframkallande. Ändå står det i studien:
”In 1994, two of the 24-year-old monkeys in the 500 mg/kg dose group were diagnosed with advanced cancer; a female (801J) with metastatic adenocarcinoma of the colon and a male (787J) with metastatic hepatocellular carcinoma. The third cancer case was a minute (3 x 3 mm) well-differentiated papillary adenocarcinoma of the prostate that was found during necropsy of an animal (774J) dosed at 100 mg/kg. Benign neoplasms were found during necropsy of two females in the 100 mg/kg cyclamate group and one in the 500 mg/kg group; one was an adenoma of the thyroid (791J) and two were leiomyomas of the uterus (772J and 801J). No neoplasms were detected in the control animals.
…
In conclusion, the findings of this study showed that long-term feeding of nonhuman primates with high doses of cyclamate did not affect the general health of most of these animals.”
Hur kan man dra den slutsatsen, när djuren som fått cyklamat utvecklade cancer, men inte dom som inte fick det?
Takayama S, Renwick AG, Johansson SL et al. Long-term toxicity and carcinogenicity study of cyclamate in nonhuman primates. Toxicol Sci 2000; 53: 33–39.
vad för produkter finns det i?
King Grub wrote:Tror du man ger människor massiva doser med ämnen man misstänker kan vara cancerframkallande och ser vad som händer?Alla gränsvärden bygger på djurstudier. Dessa är ofta mycket applicerbara på människa. Om något ämne ger råttor cancer… brukar man inte tillåta detta i produkter avsedda för mänsklig konsumtion.
En studie på människa, som gav cancer? eller hade de fått cancer ändå?
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Journal of the National Cancer Institute, Vol. 88, No. 21, 1560-1570, November 6, 1996
© 1996 Oxford University Press
{alpha}-Tocopherol and beta-Carotene Supplements and Lung Cancer Incidence in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study: Effects of Base-line Characteristics and Study Compliance
Demetrius Albanes, Olli P. Heinonen, Philip R. Taylor, Jarmo Virtamo, Brenda K. Edwards, Matti Rautalahti, Anne M. Hartman, Juni Palmgren, Laurence S. Freedman, Jaason Haapakoski, Michael J. Barrett, Pirjo Pietinen, Nea Malila, Eero Tala, Kari Liippo, Eija-Riitta Salomaa, Joseph A. Tangrea, Lyly Teppo, Frederic B. Askin, Eero Taskinen, Yener Erozan, Peter Greenwald, Jussi K. HuttunenDivision of Cancer Prevention and Control, National Cancer Institute Bethesda, MD
Department of Public Health, University of Helsinki Finland
National Public Health Institute Helsinki, Finland
Information Management Services, Inc. Silver Spring, MD
Department of Diseases of the Chest, Turku University Hospital Finland
Finnish Cancer Registry Helsinki
Department of Pathology, The Johns Hopkins School of Medicine Baltimore, MD
University of Helsinki School of Medicine Baltimore. MDDemetrius Albanes, M.D., National Institutes of Health, Executive Plaza North, Rm. 211, Bethesda. MD 20892-7326.
Background: Experimental and epidemiologic investigations suggest that {alpha}-tocopherol (the most prevalent chemical form of vitamin E found in vegetable oils, seeds, grains, nuts, and other foods) and beta-carotene (a plant pigment and major precursor of vitamin A found in many yellow, orange, and dark-green, leafy vegetables and some fruit) might reduce the risk of cancer, particularly lung cancer. The initial findings of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) indicated, however, that lung cancer incidence was increased among participants who received beta-carotene as a supplement. Similar results were recently reported by the Beta-Carotene and Retinol Efficacy Trial (CARET), which tested a combination of beta-carotene and vitamin A. Purpose: We examined the effects of {alpha}-tocopherol and beta-carotene supplementation on the incidence of lung cancer across subgroups of participants in the ATBC Study defined by base-line characteristics (e.g., age, number of cigarettes smoked, dietary or serum vitamin status, and alcohol consumption), by study compliance, and in relation to clinical factors, such as disease stage and histologic type. Our primary purpose was to determine whether the pattern of intervention effects across subgroups could facilitate further interpretation of the main ATBC Study results and shed light on potential mechanisms of action and relevance to other populations. Methods: A total of 29 133 men aged 50–69 years who smoked five or more cigarettes daily were randomly assigned to receive {alpha}-tocopherol (50 mg), beta-carotene (20 mg), {alpha}-tocopherol and beta-carotene, or a placebo daily for 5–8 years (median, 6.1 years). Data regarding smoking and other risk factors for lung cancer and dietary factors were obtained at study entry, along with measurements of serum levels of {alpha}-tocopherol and beta-carotene. Incident cases of lung cancer (n = 894) were identified through the Finnish Cancer Registry and death certificates. Each lung cancer diagnosis was independently confirmed, and histology or cytology was available for 94% of the cases. Intervention effects were evaluated by use of survival analysis and proportional hazards models. All P values were derived from two-sided statistical tests. Results: No overall effect was observed for lung cancer from {alpha}-tocopherol supplementation (relative risk [RR] = 0.99; 95% confidence interval [CI] = 0.87–1.13; P =.86, logrank test). beta-Carotene supplementation was associated with increased lung cancer risk (RR = 1.16; 95% CI = 1.02–1.33; P =.02, logrank test). The beta-carotene effect appeared stronger, but not substantially different, in participants who smoked at least 20 cigarettes daily (RR = 1.25; 95% CI = 1.07–1.46) compared with those who smoked five to 19 cigarettes daily (RR = 0.97; 95% CI = 0.76–1.23) and in those with a higher alcohol intake (≥11 g of ethanol/day [just under one drink per day]; RR = 1.35; 95% CI = 1.01–1.81) compared with those with a lower intake (RR = 1.03; 95% CI = 0.85–1.24). Conclusions: Supplementation with {alpha}-tocopherol or beta-carotene does not prevent lung cancer in older men who smoke. beta-Carotene supplementation at pharmacologic levels may modestly increase lung cancer incidence in cigarette smokers, and this effect may be associated with heavier smoking and higher alcohol intake. Implications: While the most direct way to reduce lung cancer risk is not to smoke tobacco, smokers should avoid high-dose beta-carotene supplementation. [J Natl Cancer Inst 1996; 88: 1560–70]
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