Why Some Dairy Products are More Closely Linked to Parkinson’s Disease

Image Credit: Wikimedia Commons

Parkinson’s is the second most common neurodegenerative disease after Alzheimer’s. Each year in the United States, approximately 60,000 new cases are diagnosed, bringing the total number of current cases up to about a million, with tens of thousands of people dying from the disease every year. The dietary component most often implicated is milk, as I discuss in my video Could Lactose Explain the Milk and Parkinson’s Disease Link?, and contamination of milk by neurotoxins has been considered the “only possible explanation.” High levels of organochlorine pesticide residues have been found in milk, as well as in the most affected areas in the brains of Parkinson’s victims on autopsy. Pesticides in milk have been found around the world, so perhaps the dairy industry should require toxin screenings of milk. In fact, inexpensive, sensitive, portable tests are now available with no false positives and no false negatives, providing rapid detection of highly toxic pesticides in milk. Now, we just have to convince the dairy industry to actually do it.

Others are not as convinced of the pesticide link. “Despite clear-cut associations between milk intake and PD [Parkinson’s disease] incidence, there is no rational explanation for milk being a risk factor for PD.” If it were the pesticides present in milk that could accumulate in the brain, we would assume that the pesticides would build up in the fat. However, the link between skimmed milk and Parkinson’s is just as strong. So, researchers have suggested reverse causation: The milk didn’t cause Parkinson’s; the Parkinson’s caused the milk. Parkinson’s makes some people depressed, they reasoned, and depressed people may drink more milk. As such, they suggested we shouldn’t limit dairy intake for people with Parkinson’s, especially because they are so susceptible to hip fractures. But we now know that milk doesn’t appear to protect against hip fractures after all and may actually increase the risk of both bone fractures and death. (For more on this, see my video Is Milk Good for Our Bones?.) Ironically, this may offer a clue as to what’s going on in Parkinson’s, but first, let’s look at this reverse causation argument: Did milk lead to Parkinson’s, or did Parkinson’s lead to milk?

What are needed are prospective cohort studies in which milk consumption is measured first and people are followed over time, and such studies still found a significant increase in risk associated with dairy intake. The risk increased by 17 percent for every small glass of milk a day and 13 percent for every daily half slice of cheese. Again, the standard explanation is that the risk is from all the pesticides and other neurotoxins in dairy, but that doesn’t explain why there’s more risk attached to some dairy products than others. Pesticide residues are found in all dairy products, so why should milk be associated with Parkinson’s more than cheese is? Besides the pesticides themselves, there are other neurotoxic contaminants in milk, like tetrahydroisoquinolines, found in the brains of people with Parkinson’s disease, but there are higher levels of these in cheese than in milk, though people may drink more milk than eat cheese.

The relationship between dairy and Huntington’s disease appears similar. Huntington’s is a horrible degenerative brain disease that runs in families and whose early onset may be doubled by dairy consumption, but again, this may be more milk consumption than cheese consumption, which brings us back to the clue in the more-milk-more-mortality study.

Anytime we hear disease risks associated with more milk than cheese—more oxidative stress and inflammation—we should think galactose, the milk sugar rather than the milk fat, protein, or pesticides. That’s why we think milk drinkers specifically appeared to have a higher risk of bone fractures and death, which may explain the neurodegeneration findings, too. Not only do rare individuals with an inability to detoxify the galactose found in milk suffer damage to their bones, but they also exhibit damage to their brains.


Other than avoiding dairy products, what can we do to reduce our risk of Parkinson’s? See Is Something in Tobacco Protective Against Parkinson’s Disease?and Peppers and Parkinson’s: The Benefits of Smoking Without the Risks?.

You may also be interested in my videos Treating Parkinson’s Disease with Dietand Parkinson’s Disease and the Uric Acid Sweet Spot.

For the effect of foods on another neurodegenerative disease that affects our ability to move normally, see ALS (Lou Gehrig’s Disease): Fishing for Answersand Diet and Amyotrophic Lateral Sclerosis (ALS).

Written By 

In health,
Michael Greger, M.D.

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Commonly prescribed drugs are tied to nearly 50% higher dementia risk in older adults

(CNN) – Scientists have long found a possible link between anticholinergic drugs and an increased risk of dementia.

A study published in the journal JAMA Internal Medicine on Monday suggests that the link is strongest for certain classes of anticholinergic drugs — particularly antidepressants such as paroxetine or amitriptyline, bladder antimuscarinics such as oxybutynin or tolterodine, antipsychotics such as chlorpromazine or olanzapine and antiepileptic drugs such as oxcarbazepine or carbamazepine.

Researchers wrote in the study that “there was nearly a 50% increased odds of dementia” associated with a total anticholinergic exposure of more than 1,095 daily doses within a 10-year period, which is equivalent to an older adult taking a strong anticholinergic medication daily for at least three years, compared with no exposure.

“The study is important because it strengthens a growing body of evidence showing that strong anticholinergic drugs have long term associations with dementia risk,” said Carol Coupland, professor of medical statistics in primary care at the University of Nottingham in the United Kingdom and first author of the study.

“It also highlights which types of anticholinergic drugs have the strongest associations. This is important information for physicians to know when considering whether to prescribe these drugs,” she said, adding “this is an observational study so no firm conclusions can be drawn about whether these anticholinergic drugs cause dementia.”

She said that people taking these medications are advised not to stop them without consulting with their doctor first, as that could be harmful. The study involved analyzing data on 284,343 adults in the United Kingdom, aged 55 and older, between 2004 and 2016. The data came from QResearch, a large database of anonymized health records.

The researchers identified each adult’s anticholinergic exposure based on details of their prescriptions. The researchers found the most frequently prescribed anticholinergic drugs were antidepressants, drugs to treat vertigo, motion sickness or vomiting and bladder antimuscarinic drugs, such as to treat overactive bladder. The researchers also took a close look at who was diagnosed with dementia and found that 58,769 of the patients had a dementia diagnosis.

The researchers found no significant increases in dementia risk associated with antihistamines, skeletal muscle relaxants, gastrointestinal antispasmodics, antiarrhythmics, or antimuscarinic bronchodilators, according to the data, but associations were found among other classes of anticholinergic drugs. The researchers found that the odds of dementia increased from 1.06 among those with the lowest anticholinergic exposure to 1.49 among those with the highest exposure, compared with having no prescriptions for anticholinergic drugs.

The study had some limitations, including that some patients may not have taken their prescribed medication as directed, so anticholinergic exposure levels could have been misclassified. The researchers found only an association between anticholinergic drugs and dementia risk, not a causal relationship.

“However, if this association is causal, the population-attributable fractions indicate that around 10% of dementia diagnoses are attributable to anticholinergic drug exposure, which would equate, for example, to around 20,000 of the 209,600 new cases of dementia per year in the United Kingdom,” the researchers wrote in the study.Since the study shows only an association, more research is needed to “clarify whether anticholinergic medications truly represent a reversible risk factor” for dementia, wrote experts Noll Campbell, Richard Holden and Dr. Malaz Boustani in an editorial that published alongside the new study in JAMA Internal Medicine.

“Additionally, deprescribing trials can evaluate potential harms of stopping anticholinergic medications, such as worsening symptoms of depression, incontinence, or pain, as well as the potential unintended increase in acute health care utilization,” Campbell, Holden and Boustani wrote in the editorial.”With little evidence of causation, the next steps for research on anticholinergic medications in older adults must improve knowledge of the effect of deprescribing interventions on cognitive outcomes and important safety outcomes such as symptom control, quality of life, and health care utilization,” they wrote. “We propose deprescribing research as a high priority.”

It has been well known that anticholinergic agents and confusion or memory issues are linked, but the new study investigated this association over a long period of time, said Dr. Douglas Scharre, director of the division of cognitive neurology at the Ohio State University Wexner Medical Center in Columbus, who was not involved in the study.

He encouraged any patients who might have questions about this association to talk to their physicians. “I spend a lot of my time in the memory disorder clinic seeing geriatric patients and taking people off medications, mostly ones that have anticholinergic properties, and many times there can be another drug out there that has less anticholinergic impact or is non-anticholinergic that may work,” Scharre said.

“Some of the medications that they list in the study may be quite critical and important and are well worth the person taking for their seizures or their psychosis, and so it’s a risk-benefit discussion,” he added. “So have a conversation with your doctor.”