As requested by several members, here is a little info on the health benefits of smoking. My intent is not to prove tobacco is healthy/unhealthy but just to show that there is a lot of research that shows there are benefits to smoking. Life is all about trade-offs (benefits to risks). The nature of this subject would best be explained in a very large book but due to the nature of forums I have to limit myself to brevity. I have included just a few research papers showing the possible benefits of consuming tobacco. There are many, many such studies.
1. Tobacco improves memory
J Psychopharmacol. 2014 Oct; 28(10): 915–922.
Published online 2014 Aug 13. doi: 10.1177/0269881114543721
PMCID: PMC4305443
NIHMSID: NIHMS657005
Effects of Tobacco Smoke Constituents, Anabasine and Anatabine, on Memory and Attention in Female Rats
Edward D. Levin, Ian Hao, Dennis Burke, Marty Cauley, Brandon J. Hall, and Amir H. Rezvani
Author information ► Copyright and License information ►
Abstract
Nicotine has been well characterized to improve memory and attention. Nicotine is the primary, but not only neuroactive compound in tobacco. Other tobacco constituents such as anabasine and anatabine also have agonist actions on nicotinic receptors. The current study investigated the effects of anabasine and anatabine on memory and attention. Adult female Sprague-Dawley rats were trained on a win-shift spatial working and reference memory task in the 16-arm radial maze or a visual signal detection operant task to test attention. Acute dose-effect functions of anabasine and anatabine over two orders of magnitude were evaluated for both tasks. In the radial-arm maze memory test, anabasine but not anatabine significantly reduced the memory impairment caused by the NMDA antagonist dizocilpine (MK-801).
2. Prevents Alzheimer's ( there is a lot of evidence for this)
Anatabine lowers Alzheimer's Aβ production in vitro and in vivo.
Paris D1, Beaulieu-Abdelahad D, Bachmeier C, Reed J, Ait-Ghezala G, Bishop A, Chao J, Mathura V, Crawford F, Mullan M.
Abstract
Brain Aβ accumulation represents a key pathological hallmark in Alzheimer's disease. In this study, we investigated the impact of anatabine, a minor alkaloid present in plants of the Solanacea family on Aβ production in vitro using a cell line overexpressing the human amyloid precursor protein (APP) and in vivo using a transgenic mouse model of Alzheimer's disease. In vitro, anatabine lowers Aβ₁₋₄₀ and Aβ₁₋₄₂ levels in a dose dependent manner and reduces sAPPβ production without impacting sAPPα levels suggesting that anatabine lowers Aβ production by mainly impacting the β-cleavage of APP. Additionally, we show that anatabine lowers NFκB activation at doses that inhibit Aβ production in vitro. Since NFκB is known to regulate BACE-1 expression (the rate limiting enzyme responsible for Aβ production), we determined the impact of anatabine on BACE-1 transcription. We show that anatabine inhibits BACE-1 transcription and reduces BACE-1 protein levels in human neuronal like SHSY-5Y cells suggesting that the Aβ lowering properties of anatabine are mediated via a regulation of BACE-1 expression. In vivo, we show that an acute treatment with anatabine for four days significantly lowers brain soluble Aβ₁₋₄₀ and Aβ₁₋₄₂ levels in a transgenic mouse model of Alzheimer's disease. Altogether our data suggest that anatabine may represent an interesting compound for regulating brain Aβ accumulation.
3. Prevents Parkinson's
Neurotoxicology. 2004 Jan;25(1-2):279-91.
Tobacco leaf, smoke and smoking, MAO inhibitors, Parkinson's disease and neuroprotection; are there links?
Castagnoli K1, Murugesan T.
Abstract
The potential neuroprotective properties of monoamine oxidase B (MAO-B) inhibitors have been of interest in part because of the role that this enzyme plays in the bioactivation of the parkinsonian inducing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Interestingly, tobacco smokers have lowered levels of brain and blood platelet MAO-B activity and a well documented lowered incidence of Parkinson's disease (PD) compared to non-smokers. This correlation has led to the intriguing question of whether there are possible relationships between smoking, MAO-B activity and PD.
I have noticed that with each passing year tobacco becomes more and more vilified so much so that it is now considered completely evil. Researchers back through the 80's all knew of tobacco's effect on lowering AD and PD as well as MS and improving brain function ( as evidenced by their many research papers). Now it is hard to find any current research paper that talks of the benefits. Studies are typically designed to prove that tobacco is bad, not to truly investigate the good and bad aspects.
If you want to conduct your own research you have to figure out how to get by the dishonest science that is posted. If you were to do a search for "Smoking and Alzheimer's" you would probably get 10,000 hits, all telling you how smoking causes AD. To get to the truth you need to know how to ask the question.
So(a). Alzheimer's Disease (AD). In a nut shell the hallmarks of AD are the destruction of Acetylcholine receptors and the build up of A-beta protein. Smoking upregulates acetylcholine receptors (increases the quantity) and reduces A-beta. Its interesting to note that there are only 2 kinds of acetylcholine receptors. Muscarinic and Nicotinicacetylcholine. Interesting how the medical field always leaves off the "nicotine" portion of the word when talking of AD. (b) One of the hallmarks of Parkinson's Disease (PD) is the loss of Dopamine receptors in the substantia nigra of the brain. The loss is due to an enzyme the rises as we age. It is: Monoamine Oxidase (MAO). Tobacco is a natural MOA inhibitor which probably accounts for long time smokers having an 80% reduction in PD.
Sorry for the long post. I feel I should add more studies and go into greater details of the beneficial pharmacological effects of tobacco but a forum isn't the best place for this.
1. Tobacco improves memory
J Psychopharmacol. 2014 Oct; 28(10): 915–922.
Published online 2014 Aug 13. doi: 10.1177/0269881114543721
PMCID: PMC4305443
NIHMSID: NIHMS657005
Effects of Tobacco Smoke Constituents, Anabasine and Anatabine, on Memory and Attention in Female Rats
Edward D. Levin, Ian Hao, Dennis Burke, Marty Cauley, Brandon J. Hall, and Amir H. Rezvani
Author information ► Copyright and License information ►
Abstract
Nicotine has been well characterized to improve memory and attention. Nicotine is the primary, but not only neuroactive compound in tobacco. Other tobacco constituents such as anabasine and anatabine also have agonist actions on nicotinic receptors. The current study investigated the effects of anabasine and anatabine on memory and attention. Adult female Sprague-Dawley rats were trained on a win-shift spatial working and reference memory task in the 16-arm radial maze or a visual signal detection operant task to test attention. Acute dose-effect functions of anabasine and anatabine over two orders of magnitude were evaluated for both tasks. In the radial-arm maze memory test, anabasine but not anatabine significantly reduced the memory impairment caused by the NMDA antagonist dizocilpine (MK-801).
2. Prevents Alzheimer's ( there is a lot of evidence for this)
Anatabine lowers Alzheimer's Aβ production in vitro and in vivo.
Paris D1, Beaulieu-Abdelahad D, Bachmeier C, Reed J, Ait-Ghezala G, Bishop A, Chao J, Mathura V, Crawford F, Mullan M.
Abstract
Brain Aβ accumulation represents a key pathological hallmark in Alzheimer's disease. In this study, we investigated the impact of anatabine, a minor alkaloid present in plants of the Solanacea family on Aβ production in vitro using a cell line overexpressing the human amyloid precursor protein (APP) and in vivo using a transgenic mouse model of Alzheimer's disease. In vitro, anatabine lowers Aβ₁₋₄₀ and Aβ₁₋₄₂ levels in a dose dependent manner and reduces sAPPβ production without impacting sAPPα levels suggesting that anatabine lowers Aβ production by mainly impacting the β-cleavage of APP. Additionally, we show that anatabine lowers NFκB activation at doses that inhibit Aβ production in vitro. Since NFκB is known to regulate BACE-1 expression (the rate limiting enzyme responsible for Aβ production), we determined the impact of anatabine on BACE-1 transcription. We show that anatabine inhibits BACE-1 transcription and reduces BACE-1 protein levels in human neuronal like SHSY-5Y cells suggesting that the Aβ lowering properties of anatabine are mediated via a regulation of BACE-1 expression. In vivo, we show that an acute treatment with anatabine for four days significantly lowers brain soluble Aβ₁₋₄₀ and Aβ₁₋₄₂ levels in a transgenic mouse model of Alzheimer's disease. Altogether our data suggest that anatabine may represent an interesting compound for regulating brain Aβ accumulation.
3. Prevents Parkinson's
Neurotoxicology. 2004 Jan;25(1-2):279-91.
Tobacco leaf, smoke and smoking, MAO inhibitors, Parkinson's disease and neuroprotection; are there links?
Castagnoli K1, Murugesan T.
Abstract
The potential neuroprotective properties of monoamine oxidase B (MAO-B) inhibitors have been of interest in part because of the role that this enzyme plays in the bioactivation of the parkinsonian inducing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Interestingly, tobacco smokers have lowered levels of brain and blood platelet MAO-B activity and a well documented lowered incidence of Parkinson's disease (PD) compared to non-smokers. This correlation has led to the intriguing question of whether there are possible relationships between smoking, MAO-B activity and PD.
I have noticed that with each passing year tobacco becomes more and more vilified so much so that it is now considered completely evil. Researchers back through the 80's all knew of tobacco's effect on lowering AD and PD as well as MS and improving brain function ( as evidenced by their many research papers). Now it is hard to find any current research paper that talks of the benefits. Studies are typically designed to prove that tobacco is bad, not to truly investigate the good and bad aspects.
If you want to conduct your own research you have to figure out how to get by the dishonest science that is posted. If you were to do a search for "Smoking and Alzheimer's" you would probably get 10,000 hits, all telling you how smoking causes AD. To get to the truth you need to know how to ask the question.
So(a). Alzheimer's Disease (AD). In a nut shell the hallmarks of AD are the destruction of Acetylcholine receptors and the build up of A-beta protein. Smoking upregulates acetylcholine receptors (increases the quantity) and reduces A-beta. Its interesting to note that there are only 2 kinds of acetylcholine receptors. Muscarinic and Nicotinicacetylcholine. Interesting how the medical field always leaves off the "nicotine" portion of the word when talking of AD. (b) One of the hallmarks of Parkinson's Disease (PD) is the loss of Dopamine receptors in the substantia nigra of the brain. The loss is due to an enzyme the rises as we age. It is: Monoamine Oxidase (MAO). Tobacco is a natural MOA inhibitor which probably accounts for long time smokers having an 80% reduction in PD.
Sorry for the long post. I feel I should add more studies and go into greater details of the beneficial pharmacological effects of tobacco but a forum isn't the best place for this.