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:

How to Increase Gut Bacterial Richness

We live in an “obesogenic environment,” with cheap junk food everywhere, thanks in part to subsidies going to the “‘food industrial complex,’ which manufactures obesogenic foods that foster addiction…The root causes…[may] make obesity difficult to escape,” but a lot of people do. If it were simply the external environment, why isn’t everyone obese?

“Some individuals seem to be more susceptible to the obesogenic environment…than others,” which suggests a genetic component, supported by studies of twins and adopted kids, but the genes that have been identified so far account for only 6 to 11 percent of the genetic variation in body mass index between individuals. Perhaps variation in our “other genome”—that is, all the different microbes that inhabit our body, known as the microbiome—may be playing a role. We have a hundred times more bacterial genes inside us than human genes.

As I discuss in my video Gut Microbiome: Strike It Rich with Whole Grains, a study found that people tend to fall into one of two groups: those who have lots of different types of bacteria in their gut (high “gut bacterial richness”) and those with relatively few types. Those with low bacterial richness had more overall body fat, insulin resistance, which is the cause of type 2 diabetes, high triglycerides, and higher levels of inflammatory markers, like C-reactive protein, compared to those with high bacterial richness. Not only did people with lower bacterial richness start out heavier, but the obese individuals with lower bacterial richness also gained more weight over time.

The question then becomes: Can a dietary intervention have any impact “A number of studies have associated increased microbial richness…with diets higher in fruits, vegetables, and fiber.”

Just giving fiber-type supplements doesn’t seem to boost richness, however, but the “compositional complexity” of a whole food, like whole grains, “could potentially support a wider scope of bacterial taxa,” types of bacteria, “thereby leading to an increase in diversity.” Human studies to investigate the effects of whole grains had been neglected, though…until now.

Subjects were given whole-grain barley, brown rice, or a mixture of both for a month, and all three caused an increase in bacterial community diversity. Therefore, it may take a broad range of substrates to increase bacterial diversity, and this can be achieved by eating whole plant foods.

Moreover, the alterations of gut bacteria in the study coincided with a drop in systemic inflammation in the body. We used to think that the way fiber in whole grains helped us was by gelling in our small intestine right off of our stomach, slowing the rate at which sugars were absorbed and blunting the spike in blood sugars one might get from refined carbs. We now know, however, that fiber is broken down in our colon by our friendly flora, which release all sorts of beneficial substances into our bloodstream that can have anti-inflammatory effects, as well. So, perhaps what’s happening in our large intestine helps explain the protective effects of whole grain foods against type 2 diabetes.

Interestingly, the combination of both barley and brown rice worked better than either grain alone, suggesting a synergistic effect. This may help explain “the discrepancy of the health effects of whole grains obtained in epidemiological [population-based] and interventional studies.”

Observational studies “strongly suggest” that those who consume three or more servings of whole grains a day tend to have a lower body mass index, less belly fat, and less tendency to gain weight, but recent clinical trials, where researchers randomized subjects to eat white bread rolls versus whole-wheat rolls, failed to provide evidence of a beneficial effect on body weight. Of course, whole grains are so superior nutritionally that they should continue to be encouraged. However, the “[i]nterventional trials might have failed to show [weight] benefits because they focused on a limited selection of whole grains, while in epidemiological trials [or the population studies], subjects are likely to consume a diverse set of whole grains which might have synergistic activities.”


Until recently, we knew very little about how powerfully our gut bacteria can affect our health. Catch up on the latest science with these related videos:

When it comes to rice, even white rice can be better than many choices, but brown rice is better and pigmented rice is probably the best. See my videos Kempner Rice Diet: Whipping Us Into Shape and Is It Worth Switching from White Rice to Brown? for more.

But what about the arsenic in rice? Learn more:

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:

How Can Animal Protein Intake Increase Childhood Obesity Risk?

If pregnant crickets are exposed to a predatory wolf spider, their babies will hatch, exhibiting increased antipredator behavior and, as a consequence, improved survival from wolf spider attack. The mother cricket appears to be able to forewarn her babies about the threat when they are still inside her, so they would be pre-adapted to their external environment. This even happens in plants. If you grow two genetically identical plants—one in the sun, one in the shade—the sun-grown plant will produce seeds that grow better in the sun, and the shaded plant will produce seeds that grow better in the shade—even though they’re genetically identical.

What’s happening is called epigenetics, external factors changing gene expression.

Vole pups born in the winter come out growing thicker coats. Vole mothers are able to communicate the season to their babies in utero and tell them to put a coat on even before they’re born. We’re no different. You know how some people have different temperature tolerances, resulting in “battles of the bedroom”? Do you turn the AC on or off? Open the windows? It’s not just genetics. Whether we’re born in the tropics or in a cold environment determines how many active sweat glands we have in our skin.

What does this have to do with diet? As I discuss in my video Animal Protein, Pregnancy, and Childhood Obesity, can what a pregnant woman eats—or doesn’t eat—permanently alter the biology of her children in terms of what genes are turned on or off throughout life?

What happened to the children born during the 1944 – 1945 Dutch famine imposed by the Nazis? They had higher rates of obesity 50 years later. The baby’s DNA gene expression was reprogrammed before birth to expect to be born into a world of famine and conserve calories at all cost. But when the war ended, this propensity to store fat became a disadvantage. What pregnant women eat and don’t eat doesn’t just help determine the birth weight of the child, but the future adult weight of the child.

For example, maternal protein intake during pregnancy may play a role in the obesity epidemic—but not just protein in general. “Protein from animal sources, primarily meat products, consumed during pregnancy may increase risk of overweight in offspring…” Originally, researchers thought it might be the IGF-1, a growth hormone boosted by animal product consumption, that may increase the production of fatty tissue, but weight gain was tied more to meat intake than dairy. Every daily portion of meat intake during the third trimester of pregnancy resulted in about an extra 1 percent of body fat mass in their children by their 16th birthday, potentially increasing their risk of becoming obese later in life, independent of how many calories they ate or how much they exercised.  But no such link was found with cow’s milk intake, which would presumably boost IGF-1 levels just as high.

Given that, perhaps instead of IGF-1, it’s the obesogens in meat, chemicals that stimulate the growth of fatty tissue. “[E]merging evidence demonstrates that environmental factors can predispose exposed individuals to gain weight, irrespective of diet and exercise.” After all, even our infants are fatter, and we can’t blame that on diet and exercise. Animals are fatter, too, and not just our pampered pets—even rats in laboratories and subways are bigger. “The likelihood of 24 animal populations from eight different species all showing a positive trend in weight over the past few decades by chance was estimated at about 1 in 10 million” so it appears something else is going on—something like obesogenic chemicals.

One such candidate is polycyclic aromatic hydrocarbons (PAHs), which are found in cigarette smoke, vehicle exhaust, and grilled meat. A nationwide study of thousands found that the more children were exposed to PAHs, the fatter they tended to be. The researchers could measure the level of these chemicals right out of their urine. Exposure can start in the womb. Indeed, prenatal exposure to these chemicals may cause increased fat mass gained during childhood and a higher risk of childhood obesity.

If these pollutants sound familiar, I’ve covered them before in relation to increasing breast cancer risk in the Long Island Breast Cancer Study Project. So, perhaps they aren’t just obesogens, but carcinogens, as well, which may help explain the 47 percent increase in breast cancer risk among older women in relation to a lifetime average of grilled and smoked foods.

If we look at one of the most common of these toxins, smokers get about half from food and half from cigarettes. For nonsmokers, however, 99 percent comes from diet. The highest levels of PAHs are found in meat, with pork apparently worse than beef. Even dark green leafies like kale can get contaminated by pollutants in the air, though, so don’t forage for dandelion greens next to the highway and make sure to wash your greens under running water.

These are fat-soluble pollutants, so they need lots of fat to be absorbed. It’s possible that even heavily contaminated plant-based sources may be safer, unless you pour lots of oil on your food, in which case the toxins would presumably become as readily absorbed as the toxins in meat.

The good news is they don’t build up in our body. As I show in my video, if we expose people to barbecued chicken, they get a big spike in these chemicals—up to a hundred-fold increase—but our body can get rid of them within about 20 hours. The problem, of course, is that people who eat these kinds of foods every day could be constantly exposing themselves, which may not only affect their health and their children’s health, but maybe even their grandchildren’s health.

Being pregnant during the Dutch famine of the mid-1940s didn’t just lead to an increase in diseases among their kids, but even apparently their grandkids. What a pregnant woman eats now may affect future generations. “The issue of generation-spanning effects of poor conditions during [pregnancy]…may shed light on the epidemic of diabetes, obesity and cardiovascular disease,” which is associated with the transition towards Western lifestyles.


Epigenetics is the science of altering the expression of our genes. No matter our family history, some genes can be effectively turned on and off by the lifestyle choices we make. See, for example:

For more on “obesogenic” chemicals, see:

I previously touched on PAHs in Meat Fumes: Dietary Secondhand Smoke.

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: