By Jen Christensen, CNNThe inventor of the electronic cigarette, Hon Lik smokes his invention in Beiijng on May 25, 2009.E-cigarettes don't have cancer-causing toxins, but still deliver nicotineNicotine exposure hurts heart cells, new research showsCellular degradation due to nicotine exposure may lead to atherosclerosisThe nicotine delivered by cigarettes -- even the electronic versions -- may still contribute to heart disease, a new study suggests.A new paper delivered at the
annual meeting in New Orleans on Sunday suggests that nicotine can cause direct harm to cells in the heart.
Nicotine is an highly addictive substance found in tobacco and is also found in vegetables in the nightshade family like eggplant and tomatoes.
The substance itself has a powerful impact on the body. It elevates your mood, suppresses your appetite and st however, it also speeds up your heart rate and blood pressure.Just Watched 04:41PLAY VIDEOJust Watched 04:56PLAY VIDEOJust Watched 04:57PLAY VIDEOE-cigarettes satisfy a smoker's craving for nicotine and mimic the physical movements of smoking, but were viewed as a healthier alternative by some since they don't contain the cancer-causing toxins of regular cigarettes.
Previous studies, such as
published in the journal The Lancet in September, have suggested e-cigarettes may be a
way for smokers to quit than nicotine patches or the "cold turkey" method. In 2007, the
concluded, "If nicotine could be provided in a form that is acceptable and effective as a cigarette substitute, millions of lives could be saved."
is the leading preventable cause of premature death, according to the.For years, doctors have also known that smokers often develop
in addition to lung problems.
Smoking increases a person's risk of developing , a disease in which plaque, a waxy substance, builds up in the arteries, narrowing and hardening them over time and limiting blood flow.Atherosclerosis can cause , , and can even lead to death.
The connection between
has been unclear, but scientist
may have discovered the root cause of the problem in the new study.
The molecular pharmacology professor at
exposed cells found in the heart to nicotine.
After only six hours, a kind of cellular drill, called
formed and ate through tissue. When this happens in the which are in the middle layer of the arterial wall to the inner layer, this can cause plaque to form in atherosclerosis.
This happened when Hai exposed human and rat cells to nicotine. What that means is that the nicotine is acting like "a kind of cancer of the blood vessel which is waking up these cells and breaking them away from their surrounding matric and then migrating having an effect like it is almost like digging a hole through the wall," Hai said. "I think this is potentially very interesting and significant."
It also means that the nicotine substitute of an e-cigarette may reduce a person's chance of having lung cancer, but it does not mean that their risk of heart disease will go away.
Research is still in the very early stages, Hai said, but he believes it would be a good area for the government to invest in to better understand the connection between smoking and heart disease.
"We have certain pillars in this data that shows something significant is going on here and we need to understand it better," Hai said.Dissecting the signaling pathway of nicotine-mediated neuroprotection in a mouse Alzheimer disease model.
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):61-73. Epub
2006 Nov 29.Dissecting the signaling pathway of nicotine-mediated neuroprotection in a mouse Alzheimer disease model.1, , , , , .1State Key laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Academia Sinica, Beijing, China.AbstractNicotine has a therapeutic benefit in treating Alzheimer's disease (AD). In the present study we show that nicotine decreases accumulation of beta-amyloid (Abeta) in the cortex and hippocampus of APP (V717I) transgenic mice. Nicotine prevents activation of NF-kappaB and c-Myc by inhibiting the activation of MAP kinases (MAPKs). As a result, the activity of inducible NOS and the production of NO are down-regulated. RNA interference experiments show that the above nicotine-mediated process requires alpha7 nAChR. Nicotine decreases Abeta via the activation of alpha7nAChRs through MAPK, NF-kappaB, and c-myc pathways. Nicotine also inhibits apoptosis and cell cycle progression in this mouse line. The dissected signaling pathway of nicotine-mediated neuroprotection in the present study provides a mechanistic basis for the potential development of drug targets for treating AD.PMID:
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2008 Apr 3;452(. doi: 10.1038/nature06846.A variant associated with nicotine dependence, lung cancer and peripheral arterial disease.1, , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , .1deCODE Genetics, 101 Reykjavik, Iceland. thorgeir@decode.isAbstractSmoking is a leading cause of preventable death, causing about 5 million premature deaths worldwide each year. Evidence for genetic influence on smoking behaviour and nicotine dependence (ND) has prompted a search for susceptibility genes. Furthermore, assessing the impact of sequence variants on smoking-related diseases is important to public health. Smoking is the major risk factor for lung cancer (LC) and is one of the main risk factors for peripheral arterial disease (PAD). Here we identify a common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent. The variant has an effect on the number of cigarettes smoked per day in our sample of smokers. The same variant was associated with ND in a previous genome-wide association study that used low-quantity smokers as controls, and with a similar approach we observe a highly significant association with ND. A comparison of cases of LC and PAD with population controls each showed that the variant confers risk of LC and PAD. The findings provide a case study of a gene-environment interaction, highlighting the role of nicotine addiction in the pathology of other serious diseases.Comment inPMID:
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2008 Apr 3;452(. doi: 10.1038/nature06846.A variant associated with nicotine dependence, lung cancer and peripheral arterial disease.1, , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , .1deCODE Genetics, 101 Reykjavik, Iceland. thorgeir@decode.isAbstractSmoking is a leading cause of preventable death, causing about 5 million premature deaths worldwide each year. Evidence for genetic influence on smoking behaviour and nicotine dependence (ND) has prompted a search for susceptibility genes. Furthermore, assessing the impact of sequence variants on smoking-related diseases is important to public health. Smoking is the major risk factor for lung cancer (LC) and is one of the main risk factors for peripheral arterial disease (PAD). Here we identify a common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent. The variant has an effect on the number of cigarettes smoked per day in our sample of smokers. The same variant was associated with ND in a previous genome-wide association study that used low-quantity smokers as controls, and with a similar approach we observe a highly significant association with ND. A comparison of cases of LC and PAD with population controls each showed that the variant confers risk of LC and PAD. The findings provide a case study of a gene-environment interaction, highlighting the role of nicotine addiction in the pathology of other serious diseases.Comment inPMID:
[PubMed - indexed for MEDLINE]
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