Alzheimer’s, Smoking, Nicotine, and Pesticides: Can The Mystery Be Solved?

There’s something mysterious and, to many people, quite disturbing about the relationship between cigarette smoking and Alzheimer’s Disease development and progression. AD researchers openly admit they can’t explain the puzzling disconnect they see in their data. 

Here’s the conundrum. Smoking cigarettes is strongly associated with Alzheimer’s disease development and progression. There’s no question – cigarette smoking carries a high risk of AD

However, Alzheimer’s research also shows that nicotine – not cigarette smoking, but nicotine itself – offers measurable neuroprotective benefits against Alzheimer’s development and progression. Epidemiological data seem to confirm multiple such lab findings.

Much the same thing is puzzling Parkinson’s Disease researchers, as well as scientists investigating other neurological and endocrinological diseases among smokers. It’s well-established that Nicotine acts as a powerful anti-inflammatory with measurable benefits for people with some neurological diseases.

Nicotine and inflammatory neurological disorders

Nicotine has been shown to alter immune responses by decreasing inflammation, decreasing the antibody-forming cell response of splenocytes, decreasing proliferation of peripheral blood mononuclear cells, regulating lymphocytes, macrophages, DC, and affecting the secretion of cytokines of lymphocytes.

“Although the component in cigarette smoke that confers this apparent neruoprotective action remains to be identified, numerous studies using experimental animal models suggest that nicotine protects against PD through receptor-mediated and non-receptor-mediated pathways as well “

So here’s where the mystery lies. Smoking cigarettes is strongly associated with the development and progression of AD and other neurological diseases, but nicotine itself appears to be at least somewhat neuroprotective against many of these same diseases. 

This potentially significant distinction between the development of AD through smoking cigarettes and some apparent level of protection against AD conferred by exposure to nicotine, can be neatly resolved when you factor in the unrecognized presence of powerful confounding neurologically active variables in cigarette smoke, the insecticides and fungicides that almost universally contaminate tobacco products but that have not ever been accounted for any AD-related smoking and health study I can find, or in any other area of smoking and health research. 

Cigarette smokers inhale and hold in complex combinations of insecticides, fungicides and heavy metals an average of 132 puffs a day – by far the highest incidence of massive population-wide pesticide exposure in society. Despite this, the health impact of this global exposure has never been studied and this (100% preventable) exposure is completely unregulated by any federal or state agency. And I do mean “never studied” and “completely unregulated”.

Unfortunately, it is demonstrable fact that no US government agency, and no private entity claiming to be responsible for public health, has published or funded a single study in the past 50 years on the health effects of pesticides inhaled through smoking. In fact, between CORESTA, the “Kentucky Reference Cigarette” program, and FDA there has been active, very effective, and nearly universal subversion of scientific and medical knowledge, information and data around pesticides, smoking and health.

Here are a few of the dots that suddenly become connected when you factor pesticides into the relationship between smoking cigarettes, Nicotine, and Alzheimer’s.

Smoking and increased Alzheimer’s disease risk: A review of potential mechanisms

Overall, the literature indicates that former/active smoking is related to a significantly increased risk for AD. Cigarette smoke/smoking is associated with AD neuropathology in preclinical models and humans.

Smoking and dementia

Overall, systematic reviews have estimated that smoking confers between a 30-50% increased risk of developing dementia.

There is some evidence that exposure to nicotine, which is one of the components of cigarette smoke, can actually reduce the risk of dementia.

Pesticide exposure and risk of Alzheimer’s disease: a systematic review and meta-analysis

Evidence suggests that lifelong cumulative exposure to pesticides may generate lasting toxic effects on the central nervous system and contribute to the development of Alzheimer’s disease (AD). A number of reports indicate a potential association between long-term/low-dose pesticide exposure and AD, but the results are inconsistent. Therefore, we conducted a meta-analysis to clarify this association.

Subgroup analyses revealed that high-quality studies tended to show significant relationships. The present meta-analysis suggested a positive association between pesticide exposure and AD, confirming the hypothesis that pesticide exposure is a risk factor for AD.

Elevated serum pesticide levels and risk for Alzheimer disease

“Serum levels of DDE were highly correlated with brain levels of DDE (ρ = 0.95). Exposure of human neuroblastoma cells to DDT or DDE increased levels of amyloid precursor protein. Both DDT and DDE increase amyloid precursor protein levels, providing mechanistic plausibility for the association of DDE exposure with AD. Identifying people who have elevated levels of DDE and carry an APOE ε4 allele may lead to early identification of some cases of AD.

Editorial Note: DDT and all the other organochlorine pesticides were heavy contaminants of all cigarette brands from the 1950s through the 1970sthe very age groups of smokers in whom population-wide Alzheimer’s first began showing up in the 1990s. Check this 2022 CDC document showing clear institutional awareness of DDT on Tobacco products.

Agency for Toxic Substances and Disease Registry (ATSDR). 2022. Toxicological Profile for DDT, DDE, DDD . Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service.

Toxicological Profile for DDT, DDE, and DDD

“Djordjevic et al. (1995) assessed the chlorinated pesticide residues in U.S. and foreign cigarettes manufactured from the 1960s to the 1990s. Since 1970, the concentration of DDT analogues decreased by >98%. Concentration ranges of DDT-related compounds in samples of cigarettes manufactured between 1961 and 1979 and between 1983 and 1994 were: 


(1961–1979 levels) 1,540–30,100 ng/g (Ed. note: 30,100 ng/g is approximately equal to 30.1 ppm.)

(1983–1994 levels) 12.6–99.7 ng/g; 


(1961–1979 levels) 396–7,150 ng/g, 

(1983–1994 levels) ND-19.0 ng/g; 


(1961–1979 levels) 720–13,390 ng/g, (Ed. note: 13,390 ng/g is approximately equal to 13.99 ppm)

(1983–1994 levels) 19.7–145 ng/g; 


(1961–1979 levels) 105–1,940 ng/g; 

(1983–1994 levels) ND-88 ng/g; 


(1961–1979 levels) 58– 959 ng/g, 

(1983–1994 levels) 6.6–15.8 ng/g; 

p,p’-DDMU (1-chloro-2,2-bis(p-chlorophenyl)ethylene)

(1961–1979 levels) 92.7–2,110 ng/g, 

(1983–1994 levels) ND–27.5 ng/g. 

“The transfer rate from tobacco into mainstream smoke amounts to 22% for DDD, 19% for DDT, and 27% for DDE.” (p. 332)

“Until 1970, tobacco smoke contributed significantly to the intake of DDT by humans, but since then, the amount of DDT in tobacco has dropped markedly and today, cigarette smoke is a minor source of human exposure (Djordjevic et al. 1995).” (p 385)

Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease

“In the past 5 years, the link between pesticide exposure and AD has been considerably strengthened, while basic understanding of pesticide-associated neuropathology has improved.”

Pesticides and Development of Alzheimer’s Disease — New Evidence

Although further research is warranted, the mechanistic explanation of why pesticide exposure (DDT/DDE) would increase AD risk is rooted in their propensity to increase amyloid precursor protein.

Here’s the problem.

Researchers looking at the association of smoking with neurological and endocrinological diseases like AD have been operating without any knowledge at all of this powerful set of confounding variables. AD researchers, clinicians and smokers have literally no knowledge of these confounding variables that are potential sources of many of the pathological consequences of smoking that all can observe. 

Put simply, I propose that it may be that chronic pesticide exposure, and not tobacco or nicotine, are responsible for the undeniably strong association between smoking cigarettes and AD, as well as other “smoking-related diseases”.

My 2018 “Smoke No Evil” pesticide laboratory research, since validated by a 2022 Saudi government research publication (link below graphic), demonstrates the extent of the pesticide contamination of tobacco products.

Here’s a graphic summary of the 2022 Saudi Health Ministry findings with a link to the full study

Aside from this 2022 published research, there has been no published data on pesticides in cigarettes and other ‘tobacco’ products for many years. Along with this, there is an even more disturbing absence of research on the health effects of chronic exposure to these pesticides through inhalation by smokers. 

Pesticide hazard information is never obtained during registration by EPA, or by FDA, USDA, or any other agency, using exposure regimens even remotely resembling the cigarette smoking scenario for inhalation exposure.

Which leads to the question – if you eliminate the pesticides in the tobacco being smoked and change nothing else, what will happen? Since these confounding variables are not properties of tobacco itself, their impact on the development and progression of AD could then be isolated, verified and measured. The experimental design would be simple, inexpensive, and ethical. A group of smokers with early-stage AD could be divided by a volunteering process into those who continue smoking their preferred brand and those who begin smoking readily available USDA organic tobacco cigarettes. Then follow the smokers and note any differences.

Knowing how difficult it is to quit smoking, and acknowledging the potential benefits of nicotine, what would be the effect to smokers of switching to pesticide-free, tobacco-only cigarettes, perhaps as an intermediate step in a quit-smoking program? The impact of withdrawal from chronic pesticide exposure would be clinically and experientially verifiable within a very short time – weeks.

There is also the tantalizing possibility that since Nicotine appears to be protective against neurological disease, and since pesticides are known neurotoxic agents, if a pesticide-free tobacco smoking option were available, smokers with any neurological (or endocrinological) disease might be able to benefit in terms of slowed disease progression in the very short term without having to give up smoking first.

It might also be possible that the tobacco in cigarettes is somewhat neuroprotective against the impact of the pesticides. In other words, if that same concentration of pesticides were being inhaled 132 times a day by smoking a non-tobacco material like the synthetic smoking materials used by Tobacco Cartel manufacturers, they might have a more deleterious effect on the smoker who would otherwise be partially protected by tobacco. Who knows?

American Spirit organic brand is a widely available USDA certified, 100% leaf tobacco cigarette, as shown in the comparative data above. American Spirit organic tobacco cigarettes are an anomaly in the Tobacco Cartel’s universe, but their profitability and popularity demonstrate that producing organic, pesticide-free tobacco products is a viable business. The Tobacco Cartel has other reasons for using pesticides as they do, and for suppressing all discussion of the associated severe health risks.

The reduced health risks of organic tobacco cannot be advertised for the American Spirit organic brand due to FDA legal action overtly designed to counter the intuitively correct public assumption that organic tobacco without pesticides is safer to smoke than other cigarettes with pesticides. The FDA did this knowing that the hazards of inhaling pesticides in tobacco product smoke have never been considered, much less evaluated. There has been zero published research on the relative health benefits of organic tobacco, although organic tobacco cigarettes have been on the market for decades. I have not been able to find any RFPs on this simple question in the Federal Register, nor from any university, non-profit organization, or institution. However, in spite of the blackout, could this option represent a path to better health for current smokers at any stage of AD or any other neurological disease development? That’s a question that I hope others will finally begin to ask and answer.

Here are some more examples of how the inhaled pesticide dots connect.

Inflammation, Pesticides, Smoking & Alzheimer’s

Notably, inflammation is a common dysregulated pathway shared by most of the comorbidities associated with AD.” (from) The Impact of Disease Comorbidities in Alzheimer’s Disease

Here are links to some current research on key markers of the inflammation that is “a common dysregulated pathway shared by most of the comorbidities associated with AD”. You’ll be connecting dots pretty quickly as you browse.

The Aggregate Index Of Systemic Inflammation (AISI)

Pesticide AISI

Smoking AISI

Alzheimer’s AISI

The Monocyte-To-Lymphocyte Ratio (MLR)

Pesticide MLR

Smoking MLR

Alzheimer’s MLR

The Neutrophil-To-Lymphocyte Platelet Ratio (NLPR)

Pesticide NLPR

Smoking NLPR

Alzheimer’s NLPR

The Systemic Inflammation Response Index (SIRI)

Pesticide SIRI

Smoking SIRI

Alzheimer’s SIRI

Testing the validity of the assumptions made here, based on assembled science and breakthrough data, would not be costly or difficult especially when compared with the typically high costs of Alzheimer’s Disease research. Further, participation in such a study would not impose the burden of quitting smoking on participants, with obvious benefits for their long-term retention, and would be a strong financial incentive by replacing an expensive burden with study-supplied organic tobacco cigarettes. 

The research could consist of answering a single question: 

Once daily, repetitive pesticide exposure by inhalation is removed, with no other changes, what improvements in health status, if any, are experienced by cigarette smokers with diagnosed early-stage AD? 

That might be all it would take to begin to let in the light.


So what about people who have never smoked cigarettes or ever been seriously exposed to pesticides who develop Alzheimer’s disease? There are many people who develop AD who have never smoked – how could cigarette pesticides be involved? Well, what if they were born after 1950 and their mother smoked cigarettes?

It’s pretty well-established that the children of mothers who have been exposed to pesticides while the child is still in the womb have significantly increased risk of developing a range of neurological and endocrinological diseases like Diabetes and Obesity, as well as some cancers like Breast Cancer. This increased risk is due to epigenetic changes caused by pesticides that cross the placental barrier and target the genetic components of the embryonic neurological and endocrinological systems at the molecular level, pre-disposing the child to early and adult development of these diseases.

This fetal exposure to pesticides and its consequences have never once been associated with inhaled pesticides from cigarettes. All the studies on pesticide exposure and epigenetic changes in the fetus have focused on environmental exposure. Again, there has been no knowledge among researchers that cigarette smoking equals chronic pesticide exposure. No FDA studies, no “Smoke-Free Kids” studies, no “Truth Initiative” studies, no WHO studies – nada. No wonder the dots haven’t been connected.

However, now that it is an established fact that smoking equals inhaling pesticides that are, by themselves, known to cause specific epigenetic changes in the embryo or fetus, and since these epigenetic changes influence the development and growth of pathways leading to these diseases, isn’t it possible or even likely that, similarly, Alzheimer’s could also arise due to epigenetic changes caused by pesticides inhaled in cigarette smoke by the mother? Isn’t is possible that, unlike childhood diabetes and obesity that develop early in life – both diseases associated with pesticide-exposed fetal epigenetic changes – Alzheimer’s simply takes longer to develop to a detectable level? Could this bear on the increasing appearance of mid-life AD in today’s world?

I think it’s time, to the extent possible, to look at the mothers of AD patients and others, like those with PD and Dementia, who were born any time after 1950 and who have never smoked cigarettes but whose mother (or grandmother) did. The results might be enlightening.

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