In Coenzyme Q10: A Miracle Vitamin , Dr. Richard A. Kunin extols the benefits of Coenzyme Q10. He also says:

The energy of oxidation in cells depends on CoQ in partnership with niacinamide (vitamin B3), riboflavin (vitamin B2), and minerals such as iron and copper to effect the movement of electrons and hydrogen protons in the power plant of cell, the mitochondrion.
...
Incidentally, tobacco leaf is the champion source, containing 184 mg in a quarter pound.

The natural CoQ10 in Qmelt is made via fermentation in which a microorganism (in the case of CoQ10, a bacterium or yeast) naturally produces CoQ10. The CoQ10 is then extracted from the organism and concentrated. It is termed natural since it is normally and naturally produced by the yeast or bacterium from which it was taken. This is different from synthetic CoQ10 which is made by taking a compound found in tobacco and then mixing it with other chemicals to form a similar structure of CoQ10. While tobacco is natural, CoQ10 is not taken from tobacco in this synthetic process....the only thing taken from the tobacco is a compound which is used as the starting material for chemically creating CoQ10. That is why it is referred to as a synthetic process. Tobacco or plants in general do not contain significant amounts of CoQ10

AN IMPORTANT NOTE: The doctor cited above comments on the importance of CoQ in partnership with other nutrients, including niacinamide, AKA nicotinic acid, niacin and vitamin B3. This is a form of nicotine, which could result from the alteration of nicotine as it is very unstable. Please see Facts about Nicotine.

Neurology. 1999 Sep 22;53(5):1158. Smoking and Parkinson's disease: a dose-response relationship Gorell JM, Rybicki BA, Johnson CC, Peterson EL

Department of Neurology, Henry Ford Health System, National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA.

OBJECTIVE: To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers.

METHODS: Smoking and alcohol consumption were analyzed in 144 PD patients and 464 control subjects, who were frequency matched for sex, race, and age (+/-5 years), in a population-based case-control study of men and women > or =50 years old in the Henry Ford Health System.

RESULTS: With never-smokers as the reference category, there was an inverse association between current light smokers (>0 to 30 pack-years) and PD patients (odds ratio [OR], 0.59; 95% CI, 0.23 to 1.53), and a stronger inverse association of PD with current heavy smokers (>30 pack-years; OR, 0.08; 95% CI, 0.01 to 0.62). When former >30-pack-year smokers were stratified by the interval since quitting, there was an inverse association between those who stopped >20 years ago and PD (OR, 0.86; 95% CI, 0.42 to 1.75), and a greater inverse relationship with those who stopped 1 to 20 years ago (OR, 0.37; 95% CI, 0.19 to 0.72). Alcohol consumption had no independent, significant association with PD, but heavy drinking (>10 drink-years) had a greater effect than light-moderate drinking in reducing but not eliminating the inverse association between smoking and PD.

CONCLUSIONS: The inverse dose-response relationship between PD and smoking and its cessation is unlikely to be due to bias or confounding, as discussed, providing indirect evidence that smoking is biologically protective.

From "Temporal relationship between cigarette smoking and risk of Parkinson disease" (NEUROLOGY 2007;68:764-768):

The lower risk of Parkinson disease among current and former smokers varied with smoking duration, intensity, and recentness. The dependence of this association on the timing of smoking during life is consistent with a biologic effect.

The amount of the enzyme, called monoamine oxidase (MAO), is reduced by 30 to 40 percent in the brains of smokers, compared to nonsmokers or former smokers, the brain scans show. The reduction in brain MAO levels may result in an increase in levels of dopamine, which scientists associate with the reinforcing effects of drugs of abuse.

OBJECTIVE: The authors' goal was to replicate a previous finding that smokers have lower brain monoamine oxidase B (MAO-B) levels than comparison nonsmoking subjects ...RESULTS: Average MAO-B levels in smokers in the present study were similar to those found in the previous study and averaged 39% (SD=17) lower than those found in a comparison group of nonsmokers. Brain MAO-B levels did not differ between baseline levels and 10 minutes after smoking.

This benefit of inhibiting MAO-B was known as long ago as 1987. From Irreversible inhibition of monoamine oxidase by some components of cigarette smoke, Life Science (1987 Aug 10;41(6):675-82), "Inhibitory activity towards monoamine oxidase has been found in a solution of cigarette smoke. The inhibition was irreversible."

Smoking is associated with increased telomerase activity in short-term cultures of human bronchial epithelial cells, Cancer Letters 2007 Feb 8;246(1-2):24-33. Epub 2006 Mar 6--from the Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.

The epithelial cells on the alveolar surface of the human lower respiratory tract are vulnerable to toxic oxidants derived from inhaled pollutants or inflammatory cells. Although these lung cells have intracellular antioxidants, these defenses may be insufficient to protect the epithelial surface against oxidants present at the alveolar surface. This study demonstrates that the epithelial lining fluid (ELF) of the lower respiratory tract contains large amounts of the sulfhydryl-containing antioxidant glutathione (GSH). The total glutathione (the reduced form GSH and the disulfide GSSG) concentration of normal ELF was 140-fold higher than that in plasma of the same individuals, and 96% of the glutathione in ELF was in the reduced form. Compared with nonsmokers, cigarette smokers had 80% higher levels of ELF total glutathione, 98% of which was in the reduced form. Studies of cultured lung epithelial cells and fibroblasts demonstrated that these concentrations of reduced glutathione were sufficient to protect these cells against the burden of H2O2 in the range released by alveolar macrophages removed from the lower respiratory tract of nonsmokers and smokers, respectively, suggesting that the glutathione present in the alveolar ELF of normal individuals likely contributes to the protective screen against oxidants in the extracellular milieu of the lower respiratory tract.

From CO-RMs: Therapeutic Carbon Monoxide Releasing Molecules (Monday, October 22, 2007; medGadget, Internet journal of Medical Technologies):

Carbon monoxide (CO), a silent and powerful poison gas, might actually lend itself for a variety of promising clinical applications, according to the researchers from Sheffield University in the UK. Professor Brian Mann and colleagues from the University's Department of Chemistry and hemoCORM Ltd, a spinout company, are working on water-soluble molecules that can deliver CO to tissues to "reduce inflammation, widen blood vessels, increase blood flow, prevent unwanted blood clotting and even suppress the activity of cells and macrophages which attack transplanted organs," according to the university's press release.

Relation of age and smoking to serum levels of total testosterone and dehydroepiandrosterone sulfate in aged men in Geriatrics & Gerontology International (Volume 6 Issue 1 Page 49-52, March 2006), which found these results, "Serum T did not decrease with age, and was significantly higher in smokers than for non-smokers. Serum DHEA decreased with age more sharply in non-smokers than for smokers."

From Signals from the reproductive system regulate the lifespan of C. elegans (Nature. 1999 May 27;399(6734):308-9), "Mutants with reduced activity of the insulin/IGF-1-receptor homologue DAF-2 have been shown to live twice as long as normal". From Dietary and Lifestyle Correlates of Plasma Insulin-Like Growth Factor-I (IGF-I) and IGF Binding Protein-3 (IGFBP-3): The Multiethnic Cohort (Cancer Epidemiology Biomarkers & Prevention, Vol. 13, 1444-1451, September 2004), "In addition, we observed associations between current smoking and low IGF-I levels..."--and, on p. 1449, table 3 shows that smoking had strongest reduction effect on IGF-1 in males!

Hmmmmm.... So, IGF-1 is reduced in people who smoke and animals bred to have reduced IGF-1 have a tendency to double their life spans. That goes a long way toward explaining the reason that the people who have lived longest on this earth are all smokers!

Cigarette Smoking and the Risk of Colorectal Cancer in Women (Journal of the National Cancer Institute, Vol. 80, No. 16, 1329-1333, October 19, 1988) states, "Colorectal cancer incidence rates for smokers, nonsmokers living with smokers (i.e., passive smokers), and non-smokers in smoke-free households were compared in a 12-year prospective study of 25, 369 women who participated in a private census conducted in Washington County, MD, in 1963. Women who smoked had a decreased relative risk of colorectal cancer compared with the risk for nonsmokers (age-adjusted relative risk, 0.76; 95% confidence interval, 0.52-1.10). The risk for passive smokers was similar to that for smokers. The relative risks were significantly reduced for older women; relative risks were 0.42 for smokers and 0.66 for passive smokers over age 65. The data suggest that older women who smoke have a lower risk of colorectal cancer than non-smokers. The effect may be mediated by an antiestrogenic effect of smoking." More evidence can be found in this scanned document

From "Investigating the Association Between Cigarette Smoking and Schizophrenia in a Cohort Study," Am J Psychiatry (160:2216-2221, December 2003):

Cigarette smoking may be an independent protective factor for developing schizophrenia. These results are consistent with animal models showing both neuroprotective effects of nicotine and differential release of prefrontal dopamine in response to nicotine.

The incidence of cancer in patients diagnosed with schizophrenia was compared with the incidence in the general population. The results showed that the cancer standardized incidence ratios (SIRs) for all sites were significantly lower among men and women with schizophrenia, 0.86 [95% confidence interval (CI) 0.80-0.93] and 0.91 (95% CI 0.85-0.97), respectively. This reduced overall risk was clearest for those born in Europe-America, both men (SIR 0.85, 95% CI 0.74-0.97) and women (SIR 0.86, 95% CI 0.77-0.94).

From The Straight Dope Classics:

"A statistically significant inverse association between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption" (International Journal of Epidemiology, 1991)

"The risk of Alzheimer's disease decreased with increasing daily number of cigarettes smoked before onset of disease. . . . In six families in which the disease was apparently inherited . . . the mean age of onset was 4.17 years later in smoking patients than in non-smoking patients from the same family" (British Medical Journal, June 22, 1991)

"Although more data are needed . . . [an analysis of 19 studies suggests] nicotine protects against AD" (Neuroepidemiology, 1994)

Nicotine injections significantly improved certain types of mental functioning in Alzheimer's patients (Psychopharmacology, 1992).

One theory: nicotine improves the responsiveness of Alzheimer's patients to acetylcholine, an important brain chemical.

"When chronically taken, nicotine may result in: (1) positive reinforcement [it makes you feel good], (2) negative reinforcement [it may keep you from feeling bad], (3) reduction of body weight [by reducing appetite and increasing metabolic rate], (4) enhancement of performance, and protection against: (5) Parkinson's disease, (6) Tourette's disease [tics], (7) Alzheimer's disease, (8) ulcerative colitis and (9) sleep apnea. The reliability of these effects varies greatly but justifies the search for more therapeutic applications for this interesting compound." ("Beneficial Effects of Nicotine," Jarvik, British Journal of Addiction, 1991)

Prepublished from the American Journal of Epidemiology (Sep 2007). From the abstract of pubmed's Alcohol Drinking, Tobacco Smoking, and Anthropometric Characteristics as Risk Factors for Thyroid Cancer: A Countrywide Case-Control Study in New Caledonia. (Unité 754, INSERM, Villejuif, France) by Guignard R, Truong T, Rougier Y, Baron-Dubourdieu D, Guénel P., quote (emphasis added):

Exceptionally high incidence rates of thyroid cancer are observed in New Caledonia, particularly in Melanesian women. To investigate further the etiology of thyroid cancer and to clarify the reasons of this elevated incidence, the authors conducted a countrywide population-based case-control study in this multiethnic population. The study included 332 cases with histologically verified papillary or follicular carcinoma (293 women and 39 men) diagnosed in 1993-1999 and 412 population controls (354 women and 58 men) frequency matched by gender and 5-year age group. Thyroid cancer was negatively associated with tobacco smoking and alcohol drinking, but no inverse dose-response relation was observed. Height was positively associated with thyroid cancer, particularly in men. Strong positive associations with weight and body mass index were observed in Melanesian women aged 50 years or more, with an odds ratio of 5.5 (95% confidence interval: 1.5, 20.3) for a body mass index of 35 kg/m(2) or greater compared with normal-weight women, and there was a clear dose-response trend. This study clarifies the role of overweight for thyroid cancer in postmenopausal women. Because of the high prevalence of obesity among Melanesian women of New Caledonia, this finding may explain in part the exceptionally elevated incidence of thyroid cancer in this group.