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

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

Here’s the issue. 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 offers measurable neuroprotective benefits against Alzheimer’s development and progression. Epidemiological data confirms the lab findings.

Much the same thing is puzzling Parkinson’s Disease researchers, as well as those investigating other neurological and endocrinological diseases among smokers. Nicotine is a powerful anti-inflammatory with measurable benefits for people with different neurological diseases. I’ll link you to the validating research below.

Of course, this association doesn’t apply to non-smokers who are not exposed to nicotine, but a distinctly disproportionate % of smokers develop AD compared with non-smokers, so the association is very strong.

Here’s where the mystery lies. Smoking cigarettes is strongly associated with the development and progression of AD and other neurological diseases, but nicotine appears to be neuroprotective against these diseases. 

This conundrum between the development of AD and the prevention of AD can be neatly resolved when you factor in the unrecognized presence of powerful confounding variables, the insecticides and fungicides that almost universally contaminate tobacco products, but that are not accounted for in AD smoking and health studies, or in any other field of smoking and health research. 

It is demonstrable fact that no US government agency, and no private research entity 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 very effective and nearly universal subversion of scientific and medical knowledge, information and data around pesticides, smoking and health.

Here’s a few of the dots that are connected by understanding the presence of pesticides in cigarettes. More dots will be connected later in this post.

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.”

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.

Here’s the problem.

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

My 2018 “Smoke No Evil” pesticide laboratory research, since validated by a 2022 Saudi government research publication (link below graphic), demonstrates this near-universal and highly variable pesticide contamination of tobacco products.

However, along with an almost complete absence of contemporary published research on the presence of pesticide residues in tobacco products, there is an even more disturbing absence of research on the health effects of chronic exposure to these pesticides through inhalation by smokers. 

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.

Knowing how difficult it is to quit smoking, and acknowledging the potential benefits of nicotine, what would be the effect of a cohort of smokers 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.

American Spirit organic brand is a widely available USDA certified, 100% leaf tobacco cigarette, as shown in the comparative data above.

The reduced health risks of organic tobacco cannot be advertised by the manufacturer due to FDA legal action overtly designed to counter the natural (and correct) public assumption that organic tobacco without pesticides is safer to smoke than other cigarettes with pesticides. There has been no published research on the relative health benefits of organic tobacco, which means that there has been no RFP or funding offered, ever. 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 a few more of the many examples of how some of the dots connect within just one area of this matrix that includes every one of the co-morbidities currently labelled ‘smoking related’ diseases that may in reality be ‘inhaled pesticide-related’ diseases, and that may not be ‘tobacco smoking-related’ diseases at all: 

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 see of the research on key markers of the inflammation that is “a common dysregulated pathway shared by most of the comorbidities associated with AD”.

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? I propose that it may be sufficient 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 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 also arises 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?

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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