http://www.sciencedaily.com/releases/2007/04/070409164849.htm
In families affected by Parkinson's disease, the people who smoked cigarettes and drank a lot of coffee were less likely to develop the disease, say researchers at Duke University Medical Center.
The findings suggest that both genetic and environmental factors may influence the development of Parkinson's, a progressive neurodegenerative disease marked by trembling of the arms and legs, stiffness and rigidity of the muscles and slowness of movement.
Previous studies have suggested that smokers and coffee drinkers have a lower risk of developing Parkinson's disease. However, this is the first study to look specifically at cigarette smoking and caffeine consumption within families affected by the disease, the researchers said.
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Disclaimer:
To make a long story short, I don't take any responsibility for anything I post here. It's not news, it's not truth, it's not serious. It's parody. It's satire. It's bitter. It's angsty. Your mother's a *****. You like to jack off dogs. That's right, you heard me. You like to grab that dog by the bone and rub it like a ski pole. Your dad? Gay. Your priest? Straight. **** off and let me post. It's not true, it's all in good fun. Now go away.
To make a long story short, I don't take any responsibility for anything I post here. It's not news, it's not truth, it's not serious. It's parody. It's satire. It's bitter. It's angsty. Your mother's a *****. You like to jack off dogs. That's right, you heard me. You like to grab that dog by the bone and rub it like a ski pole. Your dad? Gay. Your priest? Straight. **** off and let me post. It's not true, it's all in good fun. Now go away.
Second-hand smoke should be subsidized.
Jophiel wrote:
I managed to be both retarded and entertaining.
Smoking also decreases the likelihood I'll die of old-age. Wonders never cease.
The odd thing is...
While watching the film "Thank you for Smoking", Nick Nayler says
Recent studies show that cigarettes can offset Parkinson's.
Who knew they used actual science to be the punchline of a joke?
I often wonder how many "strange" things there are that can do things such as what is stated above.
Can Boston Cream donuts cure cancer too smash? I prefer those over jelly ><
While watching the film "Thank you for Smoking", Nick Nayler says
Recent studies show that cigarettes can offset Parkinson's.
Who knew they used actual science to be the punchline of a joke?
I often wonder how many "strange" things there are that can do things such as what is stated above.
Can Boston Cream donuts cure cancer too smash? I prefer those over jelly ><
Quote:
people who smoked cigarettes and drank a lot of coffee were less likely to live long enough to develop the disease,
FTFY
"If you have selfish, ignorant citizens, you're gonna get selfish, ignorant leaders". Carlin.
Why would someone die/develop from those diseases when lung cancer and emphysema will surely do them in before hand? 
Edited, Apr 10th 2007 1:45am by Rimesume
Edited, Apr 10th 2007 1:45am by Rimesume
Wow, I had no idea the anti-smoking brainwashing had reached such a level. Sure, it's bad for you, but really, it's not nearly THAT bad for you.
This myth that somehow smoking guarantees you health problems is a little disturbing, frankly.
This myth that somehow smoking guarantees you health problems is a little disturbing, frankly.
Disclaimer:
To make a long story short, I don't take any responsibility for anything I post here. It's not news, it's not truth, it's not serious. It's parody. It's satire. It's bitter. It's angsty. Your mother's a *****. You like to jack off dogs. That's right, you heard me. You like to grab that dog by the bone and rub it like a ski pole. Your dad? Gay. Your priest? Straight. **** off and let me post. It's not true, it's all in good fun. Now go away.
To make a long story short, I don't take any responsibility for anything I post here. It's not news, it's not truth, it's not serious. It's parody. It's satire. It's bitter. It's angsty. Your mother's a *****. You like to jack off dogs. That's right, you heard me. You like to grab that dog by the bone and rub it like a ski pole. Your dad? Gay. Your priest? Straight. **** off and let me post. It's not true, it's all in good fun. Now go away.
Smasharoo wrote:
Wow, I had no idea the anti-smoking brainwashing had reached such a level. Sure, it's bad for you, but really, it's not nearly THAT bad for you.
This myth that somehow smoking guarantees you health problems is a little disturbing, frankly.
This myth that somehow smoking guarantees you health problems is a little disturbing, frankly.
Smash I wasn't being serious.
Oh it DOES guarantee you health problems. It's just that if you are lucky, you won't even be aware of the health problems, because they'll be subtle. You don't pay attention to them because you don't know what you'd be like if you'd never smoked.
You just put them down to "getting older".
Like, 25 year olds have less energy than 18 year olds, and 30 year olds have less energy than 25 year olds, and 35 years olds have less energy than 30 year olds, right? Right?
You just put them down to "getting older".
Like, 25 year olds have less energy than 18 year olds, and 30 year olds have less energy than 25 year olds, and 35 years olds have less energy than 30 year olds, right? Right?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=DisplayFiltered&DB=pubmed
Look around the 7-13 level on the reviews tab - this is somewhat old news (to the point that geneticists are saying - whoop de doo a sib-pair study).
In the lab I worked in, first summer as an undergrad, we had a MD who was working on his PhD who smoked and if anyone gave him hell about it he'd pull out all the papers on parkinsons and smoking and say he was just protecting himself. Granted this same guy claimed women couldn't be in high positions because they just weren't as good as men and yet was ok working in the lab of a female PI.
Look around the 7-13 level on the reviews tab - this is somewhat old news (to the point that geneticists are saying - whoop de doo a sib-pair study).
In the lab I worked in, first summer as an undergrad, we had a MD who was working on his PhD who smoked and if anyone gave him hell about it he'd pull out all the papers on parkinsons and smoking and say he was just protecting himself. Granted this same guy claimed women couldn't be in high positions because they just weren't as good as men and yet was ok working in the lab of a female PI.
Quote:
Smoking cigarettes and consuming copious amounts of caffeine carry their own risks and should not be taken up in an attempt to avoid developing Parkinson's disease, cautions study investigator Burton L. Scott, M.D., Ph.D., associate professor of medicine.
Quote:
Sure, it's bad for you, but really, it's not nearly THAT bad for you.
Sure, it's only one of the leading causes of death.
Smasharoo wrote:
This myth that somehow smoking guarantees you health problems is a little disturbing, frankly.
If you die an earlier death due to A, then by deduction, you are less likely to die because of B. This does not mean A prevents B. In other breaking news: herion addiction prevents death due to old age as no herion addicts could be found who lived long enough to die of old age.
You all keep talking as though A) only old people get Parkinson's; and B) the study didn't correct for age.
Granted, the article doesn't mention age, and doesn't give details about the study itself. /shrug
Granted, the article doesn't mention age, and doesn't give details about the study itself. /shrug
In a time of universal deceit, telling the truth is a revolutionary act.
At the risk of being called pedantic, and I will say that certain points made are still valid, people don't die directly of old age. Being old is more of a risk factor.
The results section of the actual article:
Six-hundred seventy-three individuals from 375 families were analyzed. Cases (n = 356) included 338 probands, 8 siblings, 7 extended relatives, 2 children, and 1 parent. Controls (n = 317) included 289 siblings, 10 parents, 10 spouses or other unrelated controls, 6 extended relatives, and 2 children. Two hundred thirty-five case subjects (66.0%) were male, whereas 139 controls (43.9%) were male. The mean ± SD AAE was 66.1 ± 10.7 years in cases and 63.7 ± 12.3 years in controls. Cases had a mean ± SD age at onset of 58.1 ± 11.6 years and a mean disease duration of 8.0 years. Because individuals with PD were more likely than unaffected relatives to be male and older at examination, sex and AAE were considered important confounders in our analyses.
Exposure histories were not obtained for 8.0% of participants for smoking, 5.9% for caffeine, and 5.3% for NSAIDs. Data from individuals with a missing exposure history were excluded from analyses for the relevant factor. Reported exposure histories were correlated as follows: smoking and caffeine, r = 0.19; smoking and NSAIDs, r = 0.05; and caffeine and NSAIDs, r = 0.10. Given these modest correlations, models with multiple exposures were valid.
Results from models examining associations of smoking while controlling for AAE and sex are shown in Table 1. Individuals with PD were 0.56 times as likely to report ever smoking and 0.30 times as likely to report current smoking compared with unaffected relatives. Dosage, duration, and intensity presented ORs indicative of inverse relationships between PD and smoking with significance at most exposure levels. Dose-response associations were detected with increasing status, dosage, duration, and intensity (P<.005). Patterns remained significant after truncating exposure at 10 and 20 years before the reference age (Table 1) and adjusting for caffeine and NSAIDs (data not shown). Even after applying the conservative Bonferroni correction for multiple testing, most associations and trends in ORs for smoking remained significant.
Caffeinated coffee associations with PD relative to never consuming it were assessed while controlling for AAE and sex. When truncating exposure at the reference age, a significant dose response for intensity (trend P = .05) was observed. When truncating exposure at 10 years before the reference age, high dosage (>2.0 cups/d) was significantly inversely associated with PD (OR = 0.64; 95% confidence interval, 0.42-0.99), and increasing dosage showed a significant trend in ORs (P = .05). No significant associations were observed after truncating exposure at 20 years before the reference age or adjusting for smoking and NSAIDs (data not shown).
Overall caffeine associations with PD compared with never consuming it were also assessed while controlling for AAE and sex. These results are presented in Table 2. Case subjects were neither more nor less likely than controls to report ever consuming caffeine. However, a significant inverse association with PD at high dosage and significant inverse gradients for dosage and intensity were detected. The significant inverse gradient for dosage persisted after truncating exposure at 10 and 20 years before the reference age. The trends in ORs for dosage and intensity were nearly significant after adjusting for AAE, sex, smoking, and NSAIDs (trend P = .06 for both), but the significant trends shown in Table 2 did not withstand the conservative Bonferroni correction (trend P = .08 for dosage and trend P = .09 for intensity after Bonferroni correction).
Most users of NSAIDs reported a current exposure of relatively short duration, so assessment of status and exposure truncation before the reference age was not possible. No significant associations between NSAIDs and PD were detected (Table 3). There were also no significant associations between nonaspirin NSAIDs and PD (data not shown). Adjustment for smoking and caffeine did not change these results (data not shown).
Title and authors - this was in Archives of Neurology
Smoking, Caffeine, and Nonsteroidal Anti-inflammatory Drugs in Families With Parkinson Disease
Dana B. Hancock, BS; Eden R. Martin, PhD; Jeffrey M. Stajich, PA-C; Rita Jewett, RN; Mark A. Stacy, MD; Burton L. Scott, PhD, MD; Jeffery M. Vance, PhD, MD; William K. Scott, PhD
Arch Neurol. 2007;64:576-580.
For what its worth they use a statistical method of evaluation that I'm not too familiar with (GEE - Population-averaged generalized estimating equations) so I'm really not qualified to comment on the accuracy of the P-values here, but the results are in the same direction as pretty much all other research with regard to smoking (as they note in the section I quoted NSAIDs were not found to be significant with goes against some previous articles).
As a general rule, sample selection is done in such a way as to exclude those people who are dying from other diseases prior to onset, especially in this sort of age related (sporadic PD tends to be later onset, the earlier onset PD tends to be a matter of mendelian type mutations) disease there's exclusion criteria in sample selection (no co-morbidities or other diseases that would mask or otherwise interfere with the disease of interest).
Bottom line (for me) - it fits with previous studies, its a genetic test that should be done, but all in all its not surprising or all that novel. But just like the studies that show drinking lots of red wine is good for resviritrol (anti-oxidant polyphenol) drinking the amount of red wine that would give you a noticable effect will increase your risk for other diseeases.
Quote:
Six-hundred seventy-three individuals from 375 families were analyzed. Cases (n = 356) included 338 probands, 8 siblings, 7 extended relatives, 2 children, and 1 parent. Controls (n = 317) included 289 siblings, 10 parents, 10 spouses or other unrelated controls, 6 extended relatives, and 2 children. Two hundred thirty-five case subjects (66.0%) were male, whereas 139 controls (43.9%) were male. The mean ± SD AAE was 66.1 ± 10.7 years in cases and 63.7 ± 12.3 years in controls. Cases had a mean ± SD age at onset of 58.1 ± 11.6 years and a mean disease duration of 8.0 years. Because individuals with PD were more likely than unaffected relatives to be male and older at examination, sex and AAE were considered important confounders in our analyses.
Exposure histories were not obtained for 8.0% of participants for smoking, 5.9% for caffeine, and 5.3% for NSAIDs. Data from individuals with a missing exposure history were excluded from analyses for the relevant factor. Reported exposure histories were correlated as follows: smoking and caffeine, r = 0.19; smoking and NSAIDs, r = 0.05; and caffeine and NSAIDs, r = 0.10. Given these modest correlations, models with multiple exposures were valid.
Results from models examining associations of smoking while controlling for AAE and sex are shown in Table 1. Individuals with PD were 0.56 times as likely to report ever smoking and 0.30 times as likely to report current smoking compared with unaffected relatives. Dosage, duration, and intensity presented ORs indicative of inverse relationships between PD and smoking with significance at most exposure levels. Dose-response associations were detected with increasing status, dosage, duration, and intensity (P<.005). Patterns remained significant after truncating exposure at 10 and 20 years before the reference age (Table 1) and adjusting for caffeine and NSAIDs (data not shown). Even after applying the conservative Bonferroni correction for multiple testing, most associations and trends in ORs for smoking remained significant.
Caffeinated coffee associations with PD relative to never consuming it were assessed while controlling for AAE and sex. When truncating exposure at the reference age, a significant dose response for intensity (trend P = .05) was observed. When truncating exposure at 10 years before the reference age, high dosage (>2.0 cups/d) was significantly inversely associated with PD (OR = 0.64; 95% confidence interval, 0.42-0.99), and increasing dosage showed a significant trend in ORs (P = .05). No significant associations were observed after truncating exposure at 20 years before the reference age or adjusting for smoking and NSAIDs (data not shown).
Overall caffeine associations with PD compared with never consuming it were also assessed while controlling for AAE and sex. These results are presented in Table 2. Case subjects were neither more nor less likely than controls to report ever consuming caffeine. However, a significant inverse association with PD at high dosage and significant inverse gradients for dosage and intensity were detected. The significant inverse gradient for dosage persisted after truncating exposure at 10 and 20 years before the reference age. The trends in ORs for dosage and intensity were nearly significant after adjusting for AAE, sex, smoking, and NSAIDs (trend P = .06 for both), but the significant trends shown in Table 2 did not withstand the conservative Bonferroni correction (trend P = .08 for dosage and trend P = .09 for intensity after Bonferroni correction).
Most users of NSAIDs reported a current exposure of relatively short duration, so assessment of status and exposure truncation before the reference age was not possible. No significant associations between NSAIDs and PD were detected (Table 3). There were also no significant associations between nonaspirin NSAIDs and PD (data not shown). Adjustment for smoking and caffeine did not change these results (data not shown).
Title and authors - this was in Archives of Neurology
Quote:
Smoking, Caffeine, and Nonsteroidal Anti-inflammatory Drugs in Families With Parkinson Disease
Dana B. Hancock, BS; Eden R. Martin, PhD; Jeffrey M. Stajich, PA-C; Rita Jewett, RN; Mark A. Stacy, MD; Burton L. Scott, PhD, MD; Jeffery M. Vance, PhD, MD; William K. Scott, PhD
Arch Neurol. 2007;64:576-580.
For what its worth they use a statistical method of evaluation that I'm not too familiar with (GEE - Population-averaged generalized estimating equations) so I'm really not qualified to comment on the accuracy of the P-values here, but the results are in the same direction as pretty much all other research with regard to smoking (as they note in the section I quoted NSAIDs were not found to be significant with goes against some previous articles).
As a general rule, sample selection is done in such a way as to exclude those people who are dying from other diseases prior to onset, especially in this sort of age related (sporadic PD tends to be later onset, the earlier onset PD tends to be a matter of mendelian type mutations) disease there's exclusion criteria in sample selection (no co-morbidities or other diseases that would mask or otherwise interfere with the disease of interest).
Bottom line (for me) - it fits with previous studies, its a genetic test that should be done, but all in all its not surprising or all that novel. But just like the studies that show drinking lots of red wine is good for resviritrol (anti-oxidant polyphenol) drinking the amount of red wine that would give you a noticable effect will increase your risk for other diseeases.
Right, so the average age at onset was 58 years. Hardly old.
Maybe I should take up smoking. I need a new hobby.
Maybe I should take up smoking. I need a new hobby.
In a time of universal deceit, telling the truth is a revolutionary act.
As I recall, you can take up the crossword puzzle and get a similar result. I have no idea if the magnitude of the effect is the same or not. I'm just waiting for the study to link sex/****/************ to lesser risk of Parkinson's.
Wait, wait, wait.
I can smoke crossword puzzles?
I can smoke crossword puzzles?
In a time of universal deceit, telling the truth is a revolutionary act.
If this study tells me that I can start smoking again, I'm all for it.
I've just finished second lunch.
Nexa
I've just finished second lunch.
Nexa
“It has always been the prerogative of children and half-wits to point out that the emperor has no clothes. But a half-wit remains a half-wit, and the emperor remains an emperor.â€
― Neil Gaiman, The Sandman, Vol. 9: The Kindly Ones
― Neil Gaiman, The Sandman, Vol. 9: The Kindly Ones
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