Is Milk Lowering Uric Acid a Good Thing or a Bad Thing?

Parkinson’s disease, the second most common neurodegenerative disorder after Alzheimer’s, is characterized by a slowness of movement, rigidity, tremor, and stooping posture, all of which worsen over time. Non-movement symptoms such as cognitive impairment and sleep, smell, and mood disturbances occur as the disease spreads to other areas of the brain. The cause of Parkinson’s is perhaps “one of the important questions posed by the neurobiology [science] of aging.” For example, why is the consumption of dairy products associated with increased risk of Parkinson’s? Perhaps because they contribute to our exposure to pesticides and other neurotoxins like dieldrin, which continues to be found in the autopsied brains of Parkinson’s victims. Even though dieldrin was banned decades ago, it lingers in the environment and we “continue to be exposed to the pesticide through contaminated dairy and meats…”

The cause of Parkinson’s “is unlikely to be due to milk compounds such as calcium, vitamin D, total fat, or total protein as these compounds are not associated with [the disease] when derived from other sources.” However, it could be lactose, the milk sugar, perhaps accounting for the increased associated risk of death and bone fractures, as well as Parkinson’s. Earlier onset of Huntington’s disease has also been identified. There is, however, a third possibility.

As I discuss in my video Parkinson’s Disease and the Uric Acid Sweet Spot, milk lowers uric acid levels, and uric acid may be protective against Huntington’s and also slow the decline caused by Parkinson’s. More importantly, it may lower the risk of getting Parkinson’s in the first place. Why? Perhaps because uric acid is an important antioxidant in the brain, something we’ve known for more than 30 years. We can demonstrate uric acid’s importance directly on human nerve cells in a petri dish. When the pesticide rotenone is added, oxidative stress goes up. Add the pro-oxidant homocysteine, and it goes up even more. But, when uric acid is added, it completely suppresses the oxidative stress caused by the pesticide.

Drinking milk, however, has a uric acid-lowering effect. In the paper making this assertion, a study they cited was “A cute effect of milk on serum urate concentrations,” but that was just a cute typothey meant Acute effect. Indeed, drink cow’s milk, and, within hours, uric acid levels drop 10 percent. Drink soymilk, and, within hours, they go up 10 percent. Now, for gout, a painful arthritic disease caused by too much uric acid, the uric acid-lowering effect of dairy is a good thing—but uric acid is “a double-edged sword.”

If our uric acid levels are too high, we can get gout, but, if they’re too low, it may increase our risk of neurodegenerative diseases, such as Alzheimer’s, Huntington’s, Parkinson’s, and multiple sclerosis.

Incidence rates of gouty arthritis over five years indicate that if our uric acid is over 10.0 mg/dl, we have a 30 percent chance of suffering an attack of gout within the next 5 years. However, at levels under 7.0 mg/dl, our risk is less than 1 percent, so it might make sense to have levels as high as possible without going over 7.0 to protect the brain without risking our joints. But having excessive uric acid in the blood puts more than just our joints in jeopardy. Yes, having levels that are too low may increase our risk of MS, Parkinson’s, Alzheimer’s, and even cancer, but having levels that are too high may increase our risk of gout, kidney disease, and heart disease.

In fact, having a uric acid level over 7.0 mg/dl isn’t only associated with an increased risk of gout, but also an increased risk of dying from all causes. However, having a low uric acid level may also shorten our lifespan by increasing mortality. High uric acid levels are associated with increased risk of death from heart disease, but low uric acid levels are associated with increased risk of fatal stroke. So, keeping uric acid at optimum levels, the sweet spot between 5.0 and 7.0 mg/dl, may protect the brain in more ways than one.

If we measure the uric acid levels in patients with Parkinson’s, they come in around 4.6 mg/dl, which may help explain why dairy consumption may increase risk for Parkinson’s since milk pushes down uric acid levels. Dairy intake may also explain the differences in uric acid levels among meat-eaters, vegetarians, and vegans. In the graph in my video, you can see that vegan men have significantly higher uric acid levels at 5.7 mg/dl than vegetarians, presumably because vegans don’t drink milk, and those who both eat meat and consume milk fall between the vegans and vegetarians.


For more on Parkinson’s see:

Uric acid as an antioxidant? I’ve touched on that before in Miocene Meteorites and Uric Acid.

If uric acid levels are too high consider cutting down on Flesh and Fructose and eating cherries. (See Gout Treatment with a Cherry on Top and Treating Gout with Cherry Juice for more information.) Also, check out Preventing Gout Attacks with Diet.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

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

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 Diet and 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 Answers and Diet and Amyotrophic Lateral Sclerosis (ALS).

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

The Role of Pesticides in Parkinson’s Disease

In the original description of Parkinson’s disease by none other than Dr. James Parkinson himself, he described a characteristic feature of the disease: constipation, which may precede the diagnosis by many years. In fact, bowel movement frequency may be predictive. Men with less than one bowel movement a day were four times more like likely to develop Parkinson’s an average of 12 years later. This could be simply a really early symptom of the disease tied to decreased water intake, however. Many Parkinson’s patients report never really feeling very thirsty, and perhaps that led to the constipation. “Alternately, one may speculate that constipation also increases the risk of Parkinson’s disease as constipation results in a longer stay of the feces in the bowel and thus more absorption of neurotoxicants,” neurotoxins from the diet.

Two studies suggest an association between constipation and Parkinson’s, but, at the same time, 38 studies link the disease to pesticide exposure and by now more than 100 studies link pesticides to an increased risk of up to 80 percent.

Many of these studies are on occupational exposure, like that experienced by farmworkers, who may reduce their risk of Parkinson’s by wearing gloves and washing their clothes, but Parkinson’s has also been linked to ambient exposure. In the United States where approximately a billion pounds of pesticides are applied annually, just living or working in high-spray areas may increase Parkinson’s risk. It’s the same with using pesticides in the home. I didn’t realize how common household pesticide use was, and a study out of UCLA suggests it might not be such a good idea. 

Pesticides may cause DNA mutations that increase susceptibility for Parkinson’s or play a more direct role. Many neurodegenerative diseases appear to be caused by the buildup of misfolded proteins. In Alzheimer’s, it’s the protein amyloid beta; in Creutzfeldt-Jakob and mad cow disease, it’s prions; in Huntington’s, it’s a different protein; and in Parkinson’s disease, it’s a protein called alpha synuclein. A variety of pesticides—8 out of the 12 tested by researchers—were able to trigger synuclein accumulation in human nerve cells, at least in a petri dish, though the study has since been retracted so it’s unclear what the data actually showed.

The buildup of synuclein may play a role in killing off specialized nerve cells in the brain, 70 percent of which may be gone by the time the first symptoms arise. Pesticides are so good at killing these neurons that researchers use them to try to recreate Parkinson’s disease in animals. Is there any way to stop the process? As of this writing, there aren’t yet any drugs that can prevent this protein aggregation. What about flavonoid phytonutrients, natural compounds found in certain fruits and vegetables? Flavonoids can cross the blood-brain barrier and may have neuroprotective effects, so researchers tested 48 different plant compounds to see if any could stop the clumping of synuclein proteins into the little fibers that clog up the cell. And, indeed, they found a variety of flavonoids that can not only inhibit the spider web-like formation of synuclein fibers, but some could even break them up. It turns out flavonoids may actually bind to synuclein proteins and stabilize them.

In my video Berries vs. Pesticides in Parkinson’s Disease, you can see healthy nerve cells and the neurites, the arms they use to communicate to one another. After exposure to a pesticide, however, you can see how the cell is damaged and the arms are retracted. But, if you first incubate the nerve cells with a blueberry extract, the nerve cell appears better able to withstand the pesticide effects. So, this implies that flavonoids in our diet may be combating Parkinson’s disease as we speak, and healthy diets may be effective in preventing and even treating the disorder. However, these were all petri dish experiments in a laboratory. Is there any evidence that people eating berries are protected from Parkinson’s?

A study published quite a long time ago suggested the consumption of blueberries and strawberries was protective, but it was a tiny study and its results were not statistically significant. Nevertheless, that was the best we had…until now. In a more recent study, those eating a variety of phytonutrients were less likely to develop Parkinson’s disease. Specifically, higher intake of berries was associated with significantly lower risk. The accompanying editorial, “An Apple a Day to Prevent Parkinson Disease,” concluded that more research is necessary, but, until then, “an apple a day might be a good idea.” Of course, that’s coming from a man. Apples appeared protective against Parkinson’s for men, but not women. However, everyone appeared to benefit from the berries.

We may not want to have our berries with cream, though, as milk may be contaminated with the same kind of neurotoxic pesticide residues found in the brains of Parkinson’s disease victims.


I’ve produced other videos on Parkinson’s disease, including: 

Learn about other neurological muscular disorders, including essential tremor and ALS:

The same reason Parkinson’s may be related to constipation may also explain the breast cancer connection. For more on this, see my video Breast Cancer and Constipation.

What else can berries do?

But what about all the sugar in fruit? See my videos If Fructose Is Bad, What About Fruit? and How Much Fruit Is Too Much?.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: