Mad Cow Disease and Cosmetics

As I discuss in my video Which Intestines for Food and Cosmetics?, the Food and Drug Administration (FDA) recently reopened comments about its policy of allowing some intestines, but not others, into the U.S. food supply. When the first few cases of mad cow disease started popping up, the FDA’s gut reaction was to ban all guts from food and personal care products. Then, in 2005, the U.S. Department of Agriculture and FDA amended their draft rule to “permit the use of the entire small intestine for human food” if the last 80 uncoiled inches going to the colon is removed. Since then, however, studies have shown that infectious mad cow prions can be found throughout all parts of the intestine, from the stomach down to the cow’s colon, raising the question of whether all entrails should be removed once again from the food supply.

The North American Meat Association said no, wanting to keep cattle insides inside the food supply. Similarly, the Cosmetic, Toiletry, and Fragrance Association (CTFA, now the Personal Care Products Council) protested the concern, arguing that banning downer and dead cattle, as well as their brains, skulls, eyes, spinal cords, intestines, and tonsils, could put our nation’s supply of cosmetics in jeopardy. There could be a tallow shortage for soap, for example. The FDA may not realize that cosmetics and personal care products are a quarter trillion-dollar industry worldwide.

In the end, the FDA “tentatively” concluded that intestines should continue to be allowed in the food and cosmetic supply because “[o]nly trace amounts of infectivity have been found” throughout the bowels of cattle. The agency had to come to that conclusion because, otherwise, the meat would have to be banned as well. Indeed, new research shows there’s mad cow infectivity in the animals’ muscles, too, and not just in the atypical cases of bovine spongiform encephalopathy (BSE), like the last mad cow found in California. We now know it’s in typical BSE as well: Low levels of infectious prions have also been found in the ribs, shoulders, tenderloins, sirloin tips, and round cuts of meat.

The latest estimates from Britain suggest 15,000 people are currently incubating the human form of mad cow disease, contracted through the consumption of infected meat. Fewer than 200 Brits have died so far of variant Creutzfeldt-Jakob disease, but the incubation period for this invariably fatal neurodegenerative disease—that is, the time between eating the meat and one’s brain filling up with holes—can be decades. The fact that so many people are carrying it has important implications for the safety of blood transfusions, which is why many Americans who’ve lived in England are barred by the Red Cross from donating blood. Also at risk is the safety of handling surgical instruments that may have cut into someone who’s a carrier, as it is so difficult to sterilize anything once it’s been contaminated.

Given these factors, it may be prudent to err on the side of caution when regulating which intestines are allowed on and in our mouths, but it’s a balance. As one meat company pointed out, guts are not just used for lipstick—intestines are human food, “providing us with a precious source of protein which is essential for our human population.”

Unfortunately, this is not the first time the FDA has caved to industry pressures. See, for example:

As scary as rare infections like mad cow disease are, we are much more likely to be disabled or killed by more conventional foodborne pathogens such as bacteria. Check out:

In health,
Michael Greger, M.D.

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

Alzheimer’s Disease and Dietary Copper

Though the underlying cause of Alzheimer’s disease has yet to be found, there is increasing concern about the role of metals in the development of the disease, as I discuss in my video Alzheimer’s Disease, Copper, and Saturated Fat. “Iron and copper,” for example, “are strongly concentrated within the neuritic plaques and neurofibrillary tangles that represent the hallmarks of the [Alzheimer’s] brain.”

Alzheimer’s disease victims have higher levels of copper in their blood and in the fluid that surrounds their brain, as well as inside their brain. Researchers found that in a slice of Alzheimer’s-diseased brain tissue, the amyloid plaques correspond to copper hotspots. Copper may then make these amyloid plaques more toxic, “leading to increased oxidative stress.” “Free Cu [copper] is extremely efficient in the generation of free radicals,” and when copper is removed with a chelating (metal-binding) drug, the free radical oxidation drops.

Unfortunately, when researchers gave that drug to nine Alzheimer’s patients in a pilot study, it did not seem to have any effect on slowing the clinical progression of the disease. Perhaps we need to prevent the copper buildup in the first place?

“Organ meats and shellfish are the richest food sources of copper,” but should we also consider cutting down on plant sources, such as nuts, seeds, legumes, and whole grains? Copper intake only seems to be a problem when consumed with saturated fat or trans fat. In the Chicago Health and Aging Project, thousands of elderly Chicagoans were followed for six years. Those who were getting the highest copper doses, largely from multivitamin supplements, combined with a diet high in saturated fats, lost cognition as if they had aged 19 years in a period of 6 years, tripling their rate of cognitive decline. However, copper intake “was not associated with cognitive change when the diet was not high in saturated fats.”

Diet-induced high cholesterol “has been shown to increase the formation and progression of [amyloid] plaques in the brain.” As well, “dietary copper may interfere with clearance of [amyloid] from the brain and may further promote [the plaque] accumulation that results from elevated cholesterol levels.” Copper has been shown to interact badly with amyloid, causing its clumping and the production of hydrogen peroxide, a potent pro-oxidant neurotoxin.

This may explain why the higher the levels of copper, the quicker Alzheimer’s disease may progress, particularly among people with high cholesterol levels. What do we think may be happening? As cholesterol and copper levels rise, cholesterol is incorporated into the nerve cell membrane, causing it to stiffen. The amyloid protein in the membrane detaches to form plaques, at which point iron and copper generate neurotoxic free radicals. Inside the cell, similar havoc is created. Finally, cholesterol-enriched diets can lead to nerve cell death, DNA damage, and blood-brain barrier disruption.

“In conclusion, the present systematic review suggests that a diet rich in [copper and iron] might aggravate the detrimental effects of a high intake of cholesterol and [saturated fat] on the risk of developing [Alzheimer’s disease].” So, diets rich in saturated fat and deficient in antioxidants appear to promote the onset of the disease, while more plant-based diets would likely suppress its onset. There are compounds in plant foods that not only scavenge free radicals and prevent oxidative damage, but are also known to chelate, or bind up, metals, potentially making them additionally protective against the onset of Alzheimer’s. Therefore, the practical implications could be to eat lots of fruits and vegetables, avoid copper-containing supplements, and avoid high intakes of saturated fat and excessive iron intake.

Isn’t Alzheimer’s genetic? What about the “Alzheimer’s gene”? Just because we’ve been dealt some bad genetic cards doesn’t mean we can’t reshuffle the deck with diet. See The Alzheimer’s Gene: Controlling ApoE.

If the relationship between cholesterol and dementia is new to you, see Alzheimer’s and Atherosclerosis of the Brain and Cholesterol and Alzheimer’s Disease for more.

What else can we do to protect our brain? Check out:

It’s never too early to start eating healthier, because Alzheimer’s May Start Decades Before Diagnosis.

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:


Plant vs. Animal Food Purines for Preventing Gout

More than 2,000 years ago, “Hippocrates described gout as a disease of kings primarily because it was the wealthy who could afford the ‘rich’ foods, which seemed to precipitate gouty attacks.” Today, however, we can all eat like kings and acquire some diseases of royalty ourselves. That’s why I produced my video Preventing Gout Attacks with Diet.

Gout is caused by needle-sharp crystals of uric acid in our joints. Uric acid comes from the breakdown of purines, which are the breakdown product of genetic material—DNA, the foundation of all life. So, “there is no such thing as a purine-free diet, but foods do vary in their purine content.” It was long thought that people with gout just needed to stay away from all high-purine foods, whether from animals, like organ meats, or plants, like beans, but this strategy proved ineffective. Yes, all uric acid comes from the breakdown of purines, so limiting meat makes sense, but plant sources “have largely been exonerated.”

“The association of gout with alcohol intake and increased dietary purine consumption had been known since ancient times, but there were no prospective trial data” to back it up until fairly recently. The Harvard Health Professionals Follow-Up Study, which followed about 50,000 men for a dozen years, found that alcohol intake was “strongly associated with an increased risk of gout.” In terms of food, they found “an increased risk of gout with higher meat consumption or seafood consumption,” but not with higher consumption of purine-rich plant foods. Perhaps this is because the purines in plants are less bioavailable? So, though it had been suggested that gout sufferers should moderate purine-rich animal and plant foods, their “results suggest that this type of dietary restriction may be applicable to purines of animal origin but not to purine-rich vegetables.”

Although it was not surprising that meat, including seafood, had significant associations with the incidence of gout, this lack of effect of purine-rich plant foods was new. There don’t appear to be any long-term studies showing purine-rich plant foods increase risk, though there are still some guidelines continuing to disseminate those outdated recommendations.

Not only has the intake of purine-rich plants not been associated with high uric acid levels, but the vegetables gout sufferers are specifically told to stay away from—mushrooms, peas, beans, lentils, and cauliflower—were actually found to be protective. This may be because foods rich in fiber, folate, and vitamin C appear to protect against uric acid buildup and gout. “Fiber,” for example, “has been recognized as having a potential role in binding uric acid in the gut for excretion.”

Lack of association between purine-rich vegetables and urate could be due to the co-packaging of these “beneficial plant components (such as vitamin C, dietary fiber or some phytochemicals), which may have masked an effect of purine on [uric acid]. Vegetable intake, regardless of purine content, may also be protective as it may increase [uric acid] excretion.”

By changing the pH of our urine, we can change uric acid clearance. Eating an alkaline diet, which was a vegetarian diet in the case of the study I profile in my video, was found “effective for removing uric acid from the body.” Those eating the alkaline diet excreted significantly more uric acid than those eating the acidic diet. As such, uric acid levels in the blood of those eating the acid-forming diet rose within days.

So, one would assume uric acid levels are lower in vegetarians, and, indeed, those eating vegetarian diets long-term were found to have significantly lower levels in their blood. To prove cause and effect, though, you need to do an interventional trial, where you take people, change their diets, and see what happens. Researchers took ten guys to study the build-up of uric acid in their kidneys, kept them on a standard Western diet for five days, and measured their relative supersaturation for uric acid. Then, they tried a vegetarian diet for five days. The result? Within days, the intake of the vegetarian diet led to a 93 percent decline in the risk of uric acid crystallization.

You can do it the other way, too: Take a bunch of people with gout, feed them a big meal of meat, and see if you can trigger an attack. Seven patients were put in a hospital, “stabilized on a low-purine diet and then challenged with a meat-laden dinner.” In response, their uric acid levels shot up, and they started getting gout attacks. Then they added alcohol, and their uric acid levels shot up even further. In all, the researchers were able to trigger gout attacks in six out of the seven patients with just single meals.

Now, some meats have less purines than others. For those who aren’t squeamish, inches-long superworms, for example, have particularly low purine levels.

Not all animal foods increase gout risk, though. Low-fat dairy products were found to be protective. Given that, we would predict vegans to be at a disadvantage, which is indeed what was found, though all groups tested—meat eaters, fish eaters, vegetarians, and vegans—were within the normal range of around 3.5 to 7.

Should gout patients add milk to their diets? Well, although drinking the equivalent of ten cups of skim milk at a time appears to have an acute lowering effect on uric acid levels, in the long term over months, at the equivalent of two cups a day, there was not a statistically significant lowering effect. Gout patients were given skim milk powder for three months, and it did not appear to help. Though soymilk has also been associated with a lower risk of uric acid buildup, there are no interventional trials to back that up.

The bottom line is that we now have good research on how to reduce risk of gout “without the use of drug treatments through modification of diet.” That’s important, because allopurinol is the “drug of choice.” It’s considered generally safe, but what does it mean when doctors talk about a relatively safe drug? Well, about “2% of patients develop hypersensitivity reactions, which can sometimes be severe and fatal with a mortality rate of ~20%”—and that’s the safe drug. The other leading drug, colchicine, has “no clear-cut distinction between nontoxic, toxic, and lethal doses.”

A better choice is through diet, and these videos show you how sweet that diet choice can be:

And, for alkalinizing your urine, see How to Treat Kidney Stones with Diet and Testing Your Diet with Pee and Purple Cabbage.

Uric acid is double-edged sword, as both high and low levels are associated with increased mortality. If our uric acid levels are too high, we can get gout; if they’re too low, it may increase our risk of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. This is presumed to be because uric acid acts as a powerful brain antioxidant. See my videos Miocene Meteorites and Uric Acid and Parkinson’s Disease and the Uric Acid Sweet Spot for more on this.

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: