smoking diseases wiki
smoking diseases wiki
Was Bernie Mac a smoker? He died today at 50. In Bad Santa, he played a character that smoked a lot.
I have a feeling his disease was caused from cigarette smoking or breathing in second hand smoke when he was on the comedy club circuit.
http://en.wikipedia.org/wiki/Bernie_Mac
No Bernie had a lung disease called sarcoidosis. Its an inflammatory disease that can affect any organ in the body. The disease he had was hereditary. It didnt come from smoking It causes heightened immunity, which means that a person’s immune system, which normally protects the body from infection and disease, overreacts, resulting in damage to the body’s own tissues. The classic feature of sarcoidosis is the formation of granulomas, microscopic clumps of inflammatory cells that group together (and look like granules, hence the name). When too many of these clumps form in an organ they can interfere with how that organ functions.
smoking diseases wiki
Is Oxidative Stress Affecting Your Dna?
Many people today are becoming more aware of using antioxidants (from specific foods or supplements) to combat oxidative stress. When asked why antioxidant strategies are taken, many say they fear oxidative damage to their DNA (deoxyribonucleic acid), a molecule containing genetic instructions for building cells.
These fears may be justified. The fact is, the resulting mutation from oxidized DNA may trigger pathological outcomes, including cancer, neurological degeneration and organ failure. Other oxidation targets include proteins, cell membranes, lysosomes, mitochondria, blood and tissue lipids, polyunsaturated fatty acids, and vitamins or antioxidant molecules themselves. So, how does oxidative stress begin and what attacks the DNA?
Oxidative Stress on our DNA
Our bodies use oxygen to create energy as fuel for our cells, forming by-products in the process. Carbon dioxide and water are two such by-products, but others include reactive oxygen species (ROS), which have both beneficial and potentially dangerous roles in human physiology.
ROS are reactive species because they lack an electron. This electron deficiency then forces the reactive species to aggressively seek a new one from any source, including cell membranes and DNA. Usually, the ROS are neutralized by antioxidants our bodies form (endogenous antioxidants, e.g., glutathione) and by antioxidants provided from food (dietary antioxidants, e.g., phenolics).
Reactive Oxygen Species-the good side, the bad side
The beneficial roles of ROS include antibacterial and antiviral actions, cell-to-cell signaling (such as by nitric oxide and hydrogen peroxide), stimulation of enzyme functions, and regulation of cells controlling release of hormones. That’s the good. However, when your body produces more ROS than needed to perform these useful functions, and when you body doesn’t have enough antioxidant reserves, this creates a positive-ROS state, or oxidative stress.
How to possibly prevent an oxidative attack
Even during healthy and normal metabolism – but worsened by exposure to added environmental pathogens such as ultraviolet radiation, smoke or other pollutants – the ROS (which are formed continuously) are attacking each cell in our bodies thousands of times per minute or more than a million times per day!
When counterbalancing antioxidant mechanisms are insufficient, DNA lesions occur, including loss or oxidation of base material and breaks of DNA strands. The good news is that not all DNA lesions become pathogenic, as our cells (hard-workers, indeed) also contain mending functions for correcting the DNA injury, called base excision repair (BER).
While it works to repair most of the time, BER may not fully correct all injuries to DNA, leading to mutated DNA, as found in carcinogenesis, aging or age-related diseases.
Give your body a “metabolic tune-up”
For 20 years, Dr. Bruce N. Ames of the University of California-Berkeley has analyzed ROS-initiated DNA lesions, aging onset and disease progression, and has advocated nutritional remedies as protection, including dietary supplementation with lipoic acid, acetylcarnitine, folic acid, biotin, vitamins C, E, B6 (pyridoxine) and -12 (cyanocobalamin), iron and zinc. Together, these nutrients provide what Dr. Ames has coined a “metabolic tune-up.”
An excerpt from a 2002 publication in the Annals of the NY Academy of Science (partly edited)
In feeding studies in old rats, these mitochondrial metabolites and antioxidants furnish several benefits that include :
1) arresting the age-associated decline of ambulatory activity and memory,
2) partially restoring mitochondrial structure and function,
3) inhibiting age-associated increase of oxidative damage to lipids, proteins, and nucleic acids,
4) elevating levels of antioxidants,
5) restoring activity and substrate binding affinity of a key mitochondrial enzyme, carnitine acetyltransferase.
These mitochondrial metabolites and antioxidants:
1) protect neuronal cells from neurotoxin- and oxidant-induced toxicity and oxidative damage;
2) delay the normal aging of human fibroblast cells,
3) inhibit oxidant-induced acceleration of aging.
These results suggest a plausible mechanism: with age, increased oxidative damage to proteins and lipid membranes, particularly in mitochondria, causes a) a deformation of enzyme structure, with b) a consequent decrease of enzyme activity as well as c) substrate binding affinity for their substrates. An increased level of substrate restores the velocity of the reaction and restores mitochondrial function, thus delaying mitochondrial decay and aging.
So, if you want fight reactive oxygen radicals, eat the right antioxidant foods.
References and Reading
* Liu J, Atamna H, Kuratsune H, Ames BN. Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites. Ann N Y Acad Sci. 2002 Apr;959:133-66.
* Ames BN. A role for supplements in optimizing health: the metabolic tune-up. Arch Biochem Biophys. 2004 Mar 1;423(1):227-34.
* PubMed, online database of the US National Library of Medicine, http://pubmed.org
* Wikipedia, the free encyclopedia, Oxidative Stress, http://en.wikipedia.org/wiki/Oxidative_stress
Reading and References
* Nutrient Data Laboratory, Agricultural Research Service, US Department of Agriculture, http://www.nal.usda.gov/fnic/foodcomp/contact.html
* Phytochemical database of the USDA, Agricultural Research Service, http://www.pl.barc.usda.gov/usda_chem/achem_home.cfm
* Wikipedia, the free encyclopedia, http://www.wikipedia.com
Copyright 2006 Berry Health Inc.
About the Author
Dr. Paul Gross is a scientist and expert on cardiovascular and brain physiology. Gross is founder of Berry Health Inc, a developer of nutritional, berry-based supplements. For more information, visit
http://www.berrywiseonline.com
If the oldest woman in the world smokes and drinks….?
Jeanne Calment is 122+ and she has always smoked and drunk red wine…..so could it be that the 2 habits even each other out medically speaking?
Why does it seem that people who give up smoking get disease whilst those who NEVER quit seem to stay fairly healthy? Just looking at the oldest people on earth and most of them seem to be smokers…..
http://en.wikipedia.org/wiki/Jeanne_Calment
I once heard that 20% people are genetically immune to the lung cancer caused by tobacco. And reversely, some people (I do not know the statistics for that case) are so extremely susceptible to lung cancer that a very low exposure, for exemple to second-hand smoke, will do it.
Genetics plays a very important role in life expectancy. In the case of people living exceptionnally long lives (over 100), you can make pretty a safe bet that their ancestors, on the maternal side (you can check research on mitochondrial DNA for the reason for that, very interesting), also lived long lives, barring accidents.
But lifestyle is also very determinant in life expectancy. Smoking tobacco does shorten most smokers lives from lung cancer and heart disease. Not everybody has won the genetic lottery. And I doubt very much that red wine has any ‘reversing effect’ on the damage caused to the lungs by tobacco. Sure, if you have an otherwise healthy lifestyle, and you are not an habituated smoker (not a-pack-a-day person), it probably makes your risks not significantly higher that a non-smoker, if, and only if, you do not have a hightened genetic susceptibility.
But I know very few non-habituated, occasionnal smokers… And nothing tells you you do not have a genetic weakness for heart disease or lung cancer… So why take chances ?
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