How Not to Die from Kidney Disease

Kidney failure may be both prevented and treated with a plant-based diet, and it’s no wonder: Kidneys are highly vascular organs, packed with blood vessels. Harvard researchers found three significant dietary risk factors for declining kidney function: “animal protein, animal fat, and cholesterol.” Animal fat can alter the actual structure of our kidneys. In my video How Not to Die from Kidney Disease, you can see plugs of fat literally clogging up the works in autopsied human kidneys from a study published in The American Journal of Pathology.

Animal protein can have a “profound effect” on normal kidney function, inducing “hyperfiltration,” increasing the workload of the kidney. Not plant protein, though. After eating a meal of tuna fish, the increased pressure on the kidneys goes up within only a few hours. We aren’t talking about adverse effects decades down the road, but literally within hours of it going into our mouths. What happens if, instead of having a tuna salad sandwich, you had a tofu salad sandwich with the exact same amount of protein? No effect on your kidneys. Our kidneys have no problem dealing with plant protein is no problem.

Why does animal protein cause the overload reaction, but plant protein doesn’t? It appears to be due to the inflammation triggered by the consumption of animal products. Indeed, taking a powerful, anti-inflammatory drug along with that tuna fish sandwich can abolish the hyperfiltration, protein-leakage response to meat ingestion.

There’s also the acid load. Animal foods, such as meat, eggs, and dairy, induce the formation of acid within the kidneys, which may lead to “tubular toxicity,” damage to the tiny, delicate, urine-making tubes in the kidney. Animal foods tend to be acid-forming—especially fish, which is the worst, followed by pork and poultry—whereas plant foods tend to be relatively neutral, or actually alkaline or base-forming to counteract the acid, especialy green leafy vegetables. So, “[t]he key to halting progression of CKD [chronic kidney disease] might be in the produce market, not in the pharmacy.”

It’s no wonder plant-based diets have been used to treat kidney disease for decades. In my video, you can see a remarkable graph that follows the protein leakage of subjects first on a conventional, low-sodium diet, which is what physicians would typically put someone with declining kidney function on, then switched to a supplemented vegan diet, back to the conventional diet, once more on the plant-based diet, and back and forth again. The chart is filled with zig-zags, showing kidney dysfunction was effectively turned on and off like a light switch, based on what was going into their mouths.


The first time someone visits NutritionFacts.org can be overwhelming. With videos on more than 2,000 health topics, where do you even begin? Imagine stumbling onto the site not knowing what to expect and the new video-of-the-day is about how a particular spice can be effective in treating a particular form of arthritis. It would be easy to miss the forest for the trees, which is precisely why I created a series of overview videos that are essentially taken straight from my live, hour-long 2016 presentation How Not to Die: Preventing, Arresting, and Reversing Our Top 15 Killers.

For the other videos in this overview series, see:

Inspired to learn more about the role diet may play in preventing and treating kidney disease? Check out these other popular videos on the topic:

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:

The Answer to a Colon Cancer Mystery

Colorectal cancer is the third most common cause of cancer death in the world. Thankfully, the good bacteria in our gut take the fiber we eat and make short-chain fatty acids, like butyrate, that protect us from cancer. We take care of them, and they take care of us. If we do nothing to colon cancer cells, they grow. That’s what cancer does. But if we expose the colon cancer cells to the concentration of butyrate our good bacteria make in our gut when we eat fiber, the growth is stopped in its tracks. If, however, the butyrate stops, if we eat healthy for only one day and then turn off the fiber the next, the cancer can resume its growth. So, ideally, we have to eat a lot of fiber-rich foods—meaning whole plant foods—every day.

What about the populations, like those in modern sub-Saharan Africa, where they don’t eat a lot of fiber yet still rarely get colon cancer? Traditionallly. they used to eat a lot of fiber, but now their diet is centered around highly refined corn meal, which is low in fiber—yet they still have low colon cancer rates. Why? This was explained by the fact that while they may be lacking protective factors like fiber, they are also lacking cancer-promoting factors like animal protein and fat. But are they really lacking protective factors?

If you measure the pH of their stools, the black populations in South Africa have lower pH, which means more acidic stools, despite comparable fiber intakes. That’s a good thing and may account for the lower cancer rates. But, wait a second. Low colon pH is caused by short-chain fatty acids, which are produced by our good bacteria when they eat fiber, but they weren’t eating any more fiber, suggesting there was something else in addition to fiber in their diets that was feeding their flora. And, indeed, despite low fiber intake, the bacteria in their colon were still churning out short-chain fatty acids like crazy. But if their bacteria weren’t eating fiber, what were they eating? Resistant starch. “[T]he method of cooking and eating the maize [corn] meal as a porridge results in an increase in resistant starch, which acts in the same way as fiber in the colon,” as a prebiotic, a food for our good bacteria to produce the same cancer-preventing, short-chain fatty acids.

As I discuss in my video Resistant Starch and Colon Cancer, “[r]esistant starch is any starch…that is not digested and absorbed in the upper digestive tract [our small intestine] and, so, passes into the large bowel,” our colon, to feed our good bacteria. When you boil starches and then let them cool, some of the starch can recrystallize into a form resistant to our digestive enzymes. So, we can get resistant starch eating cooled starches, such as pasta salad, potato salad, or cold cornmeal porridge. “This may explain the striking differences in colon cancer rates.” Thus, they were feeding their good bacteria after all, but just with lots of starch rather than fiber. “Consequently, a high carbohydrate diet may act in the same way as a high fiber diet.” Because a small fraction of the carbs make it down to our colon, the more carbs we eat, the more butyrate our gut bacteria can produce.

Indeed, countries where people eat the most starch have some of the lowest colon cancer rates, so fiber may not be the only protective factor. Only about 5 percent of starch may reach the colon, compared to 100 percent of the fiber, but we eat up to ten times more starch than fiber, so it can potentially play a significant role feeding our flora.

So, the protection Africans enjoy from cancer may be two-fold: a diet high in resistant starch and low in animal products. Just eating more resistant starch isn’t enough. Meat contains or contributes to the production of presumed carcinogens, such as N-nitroso compounds. A study divided people into three groups: one was on a low-meat diet, the second was on a high-meat diet including beef, pork, and poultry, and the third group was on the same high-meat diet but with the addition of lots of resistant starch. The high-meat groups had three times more of these presumptive carcinogens and twice the ammonia in their stool than the low-meat group, and the addition of the resistant starch didn’t seem to help. This confirms that “exposure to these compounds is increased with meat intake,” and 90 percent are created in our bowel. So, it doesn’t matter if we get nitrite-free, uncured fresh meat; these nitrosamines are created from the meat as it sits in our colon. This “may help explain the higher incidence of large bowel cancer in meat-eating populations,” along with the increase in ammonia—neither of which could be helped by just adding resistant starch on top of the meat.

“[T]he deleterious effects of animal products on colonic metabolism override the potentially beneficial effects of other protective nutrients.” So, we should do a combination of less meat and more whole plant foods, along with exercise, not only for our colon, but also for general health.


This is a follow-up to my video Is the Fiber Theory Wrong?.

What exactly is butyrate? See:

For videos on optimizing your gut flora, see:

Interested in more on preventing colon cancer? See:

If you’re eating healthfully, do you need a colonoscopy? Find out in Should We All Get Colonoscopies Starting at Age 50?.

When regular starches are cooked and then cooled, some of the starch recrystallizes into resistant starch. For this reason, pasta salad can be healthier than hot pasta, and potato salad can be healthier than a baked potato. Find out more in my video Getting Starch to Take the Path of Most Resistance.

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: