We know that the organophosphates in pesticides and herbicides can cause Parkinson’s.
It’s an open secret, but many researchers don’t speak out for fear of retribution.
Whistleblower Jonathan Lundgren saw his research dollars dry up.
And GMO researcher, Arpad Pusztai, lost not just his funding, but his job.
So researchers aren’t just paranoid, they know what can happen.
A large segment of biochemical research is either directly or indirectly dependent on the big chemical companies.
Profits from companies like Monsanto, Dow, BASF, and DuPont fund most of the research.
So when studies show very high correlations between their chemicals and Parkinson’s, they do their best to ignore them.
And so, these studies get little attention outside of academia.
For example, this study showed very high correlations between insecticides and Parkinson’s Disease.
PD was positively associated with insecticide exposure (OR = 5.75), past residency in a fumigated house (OR = 5.25), herbicide exposure (OR = 3.22).
The findings aren’t much of a surprise — the very thing about them that kills bugs also caused these results.
The very way they work against insects is how they work against us.
Organophosphates diffuse into the space where nerves meet the muscles.
The fancy scientific name for that place is a neuromuscular junction.
But it’s here that the chemicals bind to the enzyme that breaks down acetylcholine.
Acetylcholine is a neurotransmitter molecule in muscle tissue.
When the enzyme can’t do its job, acetylcholine builds up — leading to toxic levels.
This toxicity leads to damage and uncontrollable movements.
And uncontrollable movements are the hallmark symptom of Parkinson’s.
But interestingly, they found that smoking helped in the prevention of Parkinson’s.
PD was inversely associated with cigarette smoking at 5 years (OR = 0.50), 10 years (OR = 0.43), and 15 years (OR = 0.37) before diagnosis.
A five-year smoker had EXACTLY HALF the rate as nonsmokers (.50).
And smoking for 15 years was enough to decrease the incidence to nearly one-third of nonsmokers (.37).
They showed that one of the benefits of smoking cigarettes is lower risk of Parkinson’s!
It’s an odd finding — or it would be if other studies didn’t show the same results.
In the article: Lifestyle-related risk factors for Parkinson’s disease: a population-based study, we read:
Heavy smoking was inversely related to PD. […] and pesticide-use license (OR = 3.7) kept their significant correlation with the disease.
The article showed that just having a pesticide use license increases Parkinson’s risk by 370%!
And it also detailed how smoking protects against Parkinson’s.
In fact, smoking’s role in protecting against Parkinson’s became so well-known that researchers started remarking on it.
They even started adjusting the data to account for this.
From another article: The risk of Parkinson’s disease with exposure to pesticides, farming, well water, and rural living.
When adjusted for these variables and smoking status, there was a significant association of occupational exposure to herbicides (OR, 4.10) and insecticides (OR, 3.55) with PD.
And a more recent study published in the British Medical Journal reports more of the same.
Cigarette smoking and caffeine consumption histories were also included as confounders given significant inverse associations between these environmental factors and PD [Parkinson’s] in this dataset.
It’s so protective that they needed to analyze the smokers and nonsmokers independently.
Or they compensated for this effect mathematically.
This idea may sound unusual to some people, but nicotine is heavily involved in the neuromuscular junction.
There is even a receptor named after it: the nicotinic acetylcholine receptor.
This receptor responds to both the body’s acetylcholine as well as nicotine.
Nicotine couples with the receptor and prevents acetylcholine levels from becoming toxic.
In another study, researchers pre-treated cells with nicotine.
They tested the treated cells against other muscle toxins.
When glutamate reaches toxic levels, it causes the muscles to hold onto too much calcium.
This treatment reduced that calcium influx by 41%.
Several studies have identified biochemical responses to nicotine that might contribute to its neuroprotective effects, including increased levels of neuronal growth factors, decreased nitric oxide generation, decreased arachidonic acid release.
As far back as 1994, research showed that nicotine prevents toxic levels of the neurotoxin, N-methyl-D-aspartate (NMDA).
This an archetypal neurotoxin, so it’s a “big bad.”
And once researchers dove deeper into the research to study the chemical effects, they found more proof.
And then, even further confirming this phenomenon, we have postmortem investigations in humans.
Research shows conclusively that for people with Parkinson’s, they have fewer nicotinic acetylcholine receptors.
Epidemiological studies showed that cigarette smoking protects against PD. […] Finally, most postmortem studies showed widespread decrease of nAChRs both in striatum and cerebral cortices of PD patients.
So Parkinson’s is characterized by a decrease in nicotinic choline receptors.
But smoking increases the production of these receptors.
Analysis of the binding data suggested that the increased binding reflected an increase in the density of the receptors rather than a change in their affinity for nicotine.
For people who don’t want to smoke, coffee also appears to reduce Parkinson’s risk as well.
But the main thing is to avoid organophosphates.
These phosphates are so deadly militaries make weapons out of them!
The nerve gas sarin is an organophosphate.
Worse, we use them on our foods as insecticides and weed killers.
We find residue sticking around on fruits, vegetables, and even on the golf course.
And the EPA keeps approving new ones — the most recent one is chlorpyrifos.
They are here to stay, but you can limit your exposure.
And you can feel better about your coffee and cigarettes — particularly if you smoke organic tobacco.
Neuroprotection by Nicotine in Mouse Primary Cortical Cultures Involves Activation of Calcineurin and L-Type Calcium Channel Inactivation
Environmental antecedents of young‐onset Parkinson's disease
Lifestyle-related risk factors for Parkinson's disease: a population-based study.