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:

Vegans Should Consider Taking DHA Supplements

We are all fatheads.

Indeed, about half the dry weight of our brain is fat. Lower levels of the long-chain omega-3 fat DHA in some areas of Alzheimer’s brains got people thinking that perhaps DHA is protective. Since the level of DHA in the brain tends to correlate with the level of DHA in the blood, cross-sectional studies of dementia and pre-dementia patients have been done. The result? The dementia and pre-dementia subjects do tend to have lower levels of both long-chain omega-3s, EPA and DHA, circulating in their bloodstream. This doesn’t necessarily mean that lower omega-3 levels cause cognitive impairment, however. It was just a snapshot in time, so we don’t know which came first. As I discuss in my video Should Vegans Take DHA to Preserve Brain Function?, maybe the dementia led to a dietary deficiency, rather than a dietary deficiency leading to dementia.

What we need is to measure long-chain omega-3 levels at the beginning and then follow people over time, and, indeed, there may be a slower rate of cognitive decline in those who start out with higher levels. We can actually see the difference on MRI. Thousands of older men and women had their levels checked and were scanned and then re-scanned. The brains of those with higher levels looked noticeably healthier five years later.

The size of our brain actually shrinks as we get older, starting around age 20. Between ages 16 and 80, our brain loses about 1 percent of its volume every two to three years, such that by the time we’re in our 70s, our brain has lost 26 percent of its size and ends up smaller than that of 2- to 3-year-old children.

As we age, our ability to make long-chain omega-3s like DHA from short-chain omega-3s in plant foods, such as flaxseeds, chia seeds, walnuts, and greens, may decline. Researchers compared DHA levels to brain volumes in the famed Framingham Study and found that lower DHA levels were associated with smaller brain volumes, but this was just from a snapshot in time, so more information was needed. A subsequent study was published that found that higher EPA and DHA levels correlated with larger brain volume eight years later. While normal aging results in overall brain shrinkage, having lower levels of long-chain omega-3s may signal increased risk. The only thing we’d now need to prove cause and effect is a randomized controlled trial showing we can actually slow brain loss by giving people extra long-chain omega-3s, but the trials to date showed no cognitive benefits from supplementation…until now.

A “double-blind randomized interventional study provide[d] first-time evidence that [extra long-chain omega-3s] exert positive effects on brain functions in healthy older adults,” a significant improvement in executive function after six and a half months of supplementation, and significantly less brain shrinkage compared to placebo. This kind of gray matter shrinkage in the placebo might be considered just normal brain aging, but it was significantly slowed in the supplementation group. The researchers also described changes in the white matter of the brain, increased fractional anisotropy, and decreases in mean and radial diffusivity—terms I’ve never heard before but evidently imply greater structural integrity.

So, we know that having sufficient long-chain omega-3s EPA and DHA may be important for preserving brain function and structure, but what’s “sufficient” and how do we get there? The Framingham Study found what appears to be a threshold value around an omega-3 index of 4.4, which is a measure of our EPA and DHA levels. Having more or much more than 4.4 didn’t seem to matter, but having less was associated with accelerated brain loss equivalent to about an extra two years of brain aging, which comes out to about a teaspoon less of brain matter, so it’s probably good to have an omega-3 index over 4.4.

The problem is that people who don’t eat fish may be under 4.4. Nearly two-thirds of vegans may fall below 4.0, suggesting a substantial number of vegans have an omega-3 status associated with accelerated brain aging. The average American just exceeds the threshold at about 4.5, though if we age- and gender-match with the vegans, ironically, the omnivores do just as bad. There aren’t a lot of long-chain omega-3s in Big Macs either, but having a nutrient status no worse than those eating the Standard American Diet is not saying much.

What we need is a study that gives those with such low levels some pollutant-free EPA and DHA, and then sees how much it takes to push people past the threshold…and here we go: Phase 2 of the study gave algae-derived EPA and DHA to those eating vegan diets with levels under 4.0. About 250mg a day took them from an average of 3.1 over the threshold to 4.8 within four months. This is why I recommend everyone consider eating a plant-based diet along with contaminant-free EPA and DHA to get the best of both worlds—omega-3 levels associated with brain preservation while minimizing exposure to toxic pollutants.


A list of my recommendations can be found here: Optimum Nutrition Recommendations.

Why not just eat fish or take fish oil? I explain why in these videos:

How else can we protect our brains? See, for example:

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: