Potatoes and Human Health, Part II

Glycoalkaloids in Commonly Eaten Potatoes

Like many edible plants, potatoes contain substances designed to protect them from marauding creatures. The main two substances we're concerned with are alpha-solanine and alpha-chaconine, because they are the most toxic and abundant. Here is a graph of the combined concentration of these two glycoalkaloids in common potato varieties (1):

We can immediately determine three things from this graph:

• Different varieties contain different amounts of glycoalkaloids.
• Common commercial varieties such as russet and white potatoes are low in glycoalkaloids. This is no accident. The glycoalkaloid content of potatoes is monitored in the US.
  
• Most of the glycoalkaloid content is in the skin (within 1 mm of the surface). That way, predators have to eat through poison to get to the flesh. Fortunately, humans have peelers.

I'll jump the gun and tell you that the generally accepted safe level of potato glycoalkaloids is 200 mcg/g fresh weight (1). You can see that all but one variety are well below this level when peeled. Personally, I've never seen the Snowden variety in the store or at the farmer's market. It appears to be used mostly for potato chips.

Glycoalkaloid Toxicity in Animals

Potato glycoalkaloids are undoubtedly toxic at high doses. They have caused many harmful effects in animals and humans, including (1, 2):

• Death (humans and animals)
  
• Weight loss, diarrhea (humans and animals)
  
• Anemia (rabbits)
• Liver damage (rats)
  
• Lower birth weight (mice)
  
• Birth defects (in animals injected with glycoalkaloids)
  
• Increased intestinal permeability (mice)

However, it's important to remember the old saying "the dose makes the poison". The human body is designed to handle a certain amount of plant toxins with no ill effects. Virtually every plant food, and a few animal foods, contains some kind of toxic substance. We're constantly bombarded by gamma rays, ultra violet rays, bacterial toxins, free radicals, and many other potentially harmful substances. In excess, they can be deadly, but we are adapted to dealing with small amounts of them, and the right dose can even be beneficial in some cases.

All of the studies I mentioned above, except one, involved doses of glycoalkaloids that exceed what one could get from eating typical potatoes. They used green or blemished potatoes, isolated potato skins, potato sprouts or isolated glycoalkaloids (more on this later). The single exception is the last study, showing that normal doses of glycoalkaloids can aggravate inflammatory bowel disease in transgenic mice that are genetically predisposed to it (3)*.

What happens when you feed normal animals normal potatoes? Not much. Many studies have shown that they suffer no ill effects whatsoever, even at high intakes (1, 2). This has been shown in primates as well (4, 5, 6). In fact, potato-based diets appear to be generally superior to grain-based diets in animal feed. As early as 1938, Dr. Edward Mellanby showed that grains, but not potatoes, aggravate vitamin A deficiency in rats and dogs (7). This followed his research showing that whole grains, but not potatoes, aggravate vitamin D deficiency due to their high phytic acid content (Mellanby. Nutrition and Disease. 1934). Potatoes were also a prominent part of Mellanby's highly effective tooth decay reversal studies in humans, published in the British Medical Journal in 1932 (8, 9).

Potatoes partially protect rats against the harmful effects of excessive cholesterol feeding, when compared to wheat starch-based feed (10). Potato feeding leads to a better lipid profile and intestinal short-chain fatty acid production than wheat starch or sugar in rats (11). I wasn't able to find a single study showing any adverse effect of normal potato feeding in any normal animal. That's despite reading two long review articles on potato glycoalkaloids and specifically searching PubMed for studies showing a harmful effect. If you know of one, please post it in the comments section.

In the next post, I'll write about the effects of potatoes in the human diet, including data on the health of traditional potato-eating cultures... and a curious experiment by the Washington State Potato Commission that will begin on October 1.


*Interleukin-10 knockout mice. IL-10 is a cytokine involved in the resolution of inflammation and these mice develop inflammatory bowel disease (regardless of diet) due to a reduced capacity to resolve inflammation.

Potatoes and Human Health, Part I

Potatoes: an Introduction

Over 10,000 years ago, on the shores of lake Titicaca in what is now Peru, a culture began to cultivate a species of wild potato, Solanum tuberosum. They gradually transformed it into a plant that efficiently produces roundish starchy tubers, in a variety of strains that suited the climactic and gastronomic needs of various populations. These early farmers could not have understood at the time that the plant they were selecting would become the most productive crop in the world*, and eventually feed billions of people around the globe.

Wild potatoes, which were likely consumed by hunter-gatherers before domestication, are higher in toxic glycoalkaloids. These are defensive compounds that protect against insects, infections and... hungry animals. Early farmers selected varieties that are low in bitter glycoalkaloids, which are the ancestors of most modern potatoes, however they didn't abandon the high-glycoalkaloid varieties. These were hardier and more tolerant of high altitudes, cold temperatures and pests. Cultures living high in the Andes developed a method to take advantage of these hardy but toxic potatoes, as well as their own harsh climate: they invented chuños. These are made by leaving potatoes out in the open, where they are frozen at night, stomped underfoot and dried in the sun for many days**. What results is a dried potato with a low glycoalkaloid content that can be stored for a year or more.

Nutritional Qualities

From a nutritional standpoint, potatoes are a mixed bag. On one hand, if I had to pick a single food to eat exclusively for a while, potatoes would be high on the list. One reason is that they contain an adequate amount of complete protein, meaning they don't have to be mixed with another protein source as with grains and legumes. Another reason is that a number of cultures throughout history have successfully relied on the potato as their principal source of calories, and several continue to do so. A third reason is that they're eaten in an unrefined, fresh state.

Potatoes contain an adequate amount of many essential minerals, and due to their low phytic acid content (1), the minerals they contain are well absorbed. They're rich in magnesium and copper, two minerals that are important for insulin sensitivity and cardiovascular health (2, 3). They're also high in potassium and vitamin C. Overall, they have a micronutrient content that compares favorably with other starchy root vegetables such as taro and cassava (4, 5, 6). Due to their very low fat content, potatoes contain virtually no omega-6, and thus do not contribute to an excess of these essential fatty acids.

On the other hand, I don't have to eat potatoes exclusively, so what do they have to offer a mixed diet? They have a high glycemic index, which means they raise blood sugar more than an equivalent serving of most carbohydrate foods, although I'm not convinced that's a problem in people with good blood sugar control (7, 8). They're low-ish in fiber, which could hypothetically lead to a reduction in the number and diversity of gut bacteria in the absence of other fiber sources. Sweet potatoes, an unrelated species, contain more micronutrients and fiber, and have been a central food source for healthy cultures (9). However, the main reasons temperate-climate cultures throughout the world eat potatoes is they yield well, they're easily digested, they fill you up and they taste good.

In the next post, I'll delve into the biology and toxicology of potato glycoalkaloids, and review some animal data. In further posts, I'll address the most important question of all: what happens when a person eats mostly potatoes... for months, years, and generations?


* In terms of calories produced per acre.

** A simplified description. The process can actually be rather involved, with several different drying, stomping and leaching steps.

Speaking at Wise Traditions 2010

I'm happy to announce that I'll be presenting at the Weston A. Price foundation's 2010 Wise Traditions conference. The conference will be held in King of Prussia, Pennsylvania, Nov 12-14. The theme is the politics of food.

Sally Fallon Morell has invited me to give a talk on the diet and health of Pacific islanders. The talk will be titled "Kakana Dina: Diet and Health in the Pacific Islands", and it will take place on Sunday, November 14th from 4:00 to 5:20 pm. In preparation for the talk, I've read eight books and countless journal articles. Although some of the material will be familiar to people who follow the blog, I will not be rehashing what I've already published. I have nearly an hour and a half to talk, so I'll be going into some depth on the natural history and traditional food habits of Pacific island populations. Not just macronutrient breakdowns... specific foods and traditional preparation methods.

Learn about the health of traditional Pacific island populations, and what has changed since Western contact. Learn about traditional cooking and fermentation techniques. See unpublished photos from the Kitava study, courtesy of Dr. Staffan Lindeberg. Learn about the nutritional and ceremonial role of mammals including pork... and the most gruesome food of all.

I hope to see you there!


Kitava photo courtesy of Dr. Staffan Lindeberg

Dogen Zenji on Nutritionism

Dogen Zenji was the man who brought the Soto lineage of Zen Buddhism to Japan. He was a prolific writer, and many of his texts are respected both inside and outside the Soto Zen community. Last week, my Zen group was discussing the Genjo Koan, one of his works that is frequently used as a chant. Here's an excerpt. It may seem cryptic but bear with me:

...when you sail out in a boat to the middle of an ocean where no land is in sight, and view the four directions, the ocean looks circular, and does not look any other way. But the ocean is neither round or square; its features are infinite in variety... It only look circular as far as you can see at that time. All things are like this.

Though there are many features in the dusty world and the world beyond conditions, you see and understand only what your eye of practice can reach. In order to learn the nature of the myriad things, you must know that although they may look round or square, the other features of oceans and mountains are infinite in variety; whole worlds are there. It is so not only around you, but also directly beneath your feet, or in a drop of water.

What Dogen meant, among other things, is that the world is much more complex than what our conscious minds can perceive or understand. It was true in the 13th century, and it's still true today, despite our greatly expanded understanding of the natural world.

We can apply this principle to nutrition. For example, what is red palm oil? Two hundred years ago, perhaps we only knew a few basic facts about it. It's a fat, it's red, it comes from an African palm fruit and it has a particular melting point and flavor. Then we learned about vitamins, so we knew it contained vitamin E, carotenes (provitamin A), and vitamin K. Then fatty acid composition, so we found out it's mostly palmitic and oleic acids. Now we know red palm oil contains an array of polyphenols, sterols, coenzyme Q10 and many other non-essential constituents. We don't know much about the biological effects of most of these substances, particularly in combination with one another.

Add to that the fact that every batch of red palm oil is different, due to strain, terroir, processing, storage, et cetera. We know what the concept "red palm oil" means, roughly, but the details are infinitely complex. Now feed it to a human, who is not only incredibly complex himself, but genetically and epigenetically unique. How can we possibly guess the outcome of this encounter based on the chemical composition of red palm oil? That's essentially what nutritionism attempts to do.

To be fair, nutritionism does work sometimes. For example, we can pretty well guess that a handful of wild almonds containing a lot of cyanide won't be healthy to eat, due at least in part to the cyanide. But outside extreme examples like this, we're in a gray zone that needs to be informed by empirical observation. In other words, what happens when the person in question actually eats the red palm oil? What happened when a large group of people in West Africa ate red palm oil for thousands of years? Those questions are the reason why I'm so interested in understanding the lives of healthy non-industrial cultures.

I'm not criticizing reductionist science or controlled experiments (which I perform myself); I just think they need to be kept in context. I believe they should be interpreted within the framework of more basic empirical observations*.

One of the most important aspects of scientific maturity is learning to accept and manage uncertainty and your own ignorance. Some things are more certain than others, but most aren't set in stone. I think Dogen would tell us to be wary of nutritionism, and other forms of overconfidence.

* Wikipedia's definition of empirical: "information gained by means of observation, experience, or experiment." As opposed to inferences made from experiments not directly related to the question at hand.

The China Study on Wheat

Denise Minger has just put up another great China Study post that's worth reading if you haven't already. Denise has been busy applying her statistics skills to the mountain of data the study collected. She noted in a previous post that wheat intake was strongly associated with coronary heart disease (CHD), the quintessential modern cardiovascular disease. I, and several other people, requested that she work her mathmagic to see if the association could be due to some other factor. For example, wheat is eaten mostly in the Northern regions of China, and CHD rates are generally higher at higher latitudes (vitamin D insufficiency?). This is true in Europe as well, and may be partly responsible for the purported benefits of the Mediterranean diet. You can mathematically determine if the association between wheat and CHD is simply due to the fact that wheat eaters live further North.

To make a long story short, nothing could explain the association except wheat itself, even latitude. Furthermore, she found a strong association between wheat intake and body mass index, typically a predictor of fat mass although we can't say that for sure. That finding echos a previous study in China where wheat eaters were more likely to be overweight than rice eaters (1, 2). Head over to Denise's post for the full story.

The China Study has major limitations built into its basic design, due to the fact that it was observational and pooled the blood samples of many individuals. Therefore, its findings can never prove anything, they can only suggest or be consistent with hypotheses. However, the study also has some unique advantages, such as a diversity of diets and regions, and the fact that people had presumably been eating a similar diet for a long time. I feel that Denise's efforts are really teasing out some useful information from the study that have been de-emphasized by other investigators.

There has been so little serious investigation into the health effects of wheat in the general population that I have to rely mostly on indirect evidence, such as the observation that the diseases of civilization tend to closely follow the introduction of white flour around the globe. Researchers studying celiac disease and other forms of gluten allergy, and the efforts of the paleolithic diet community in spreading that information (for example, Loren Cordain and Pedro Bastos), have been major contributors to understanding the health effects of wheat. Denise's analysis is one of the strongest pieces of evidence I've come by so far. One of these days, I'll post all of my references incriminating wheat. There are quite a few, although none of them is the smoking gun. I think there's enough indirect evidence that investigators should begin taking the idea seriously that wheat, particularly in the form of industrial flour products, may contribute to chronic disease in more than just a small subset of the population.

Saturated Fat, Glycemic Index and Insulin Sensitivity: Another Nail in the Coffin

Insulin is a hormone that drives glucose and other nutrients from the bloodstream into cells, among other things. A loss of sensitivity to the insulin signal, called insulin resistance, is a core feature of modern metabolic dysfunction and can lead to type II diabetes and other health problems. Insulin resistance affects a large percentage of people in affluent nations, in fact the majority of people in some places. What causes insulin resistance? Researchers have been trying to figure this out for decades.*

Since saturated fat is blamed for everything from cardiovascular disease to diabetes, it's no surprise that a number of controlled trials have asked if saturated fat feeding causes insulin resistance when compared to other fats. From the way the evidence is sometimes portrayed, you might think it does. However, a careful review of the literature reveals that this position is exaggerated, to put it mildly (1).

The glycemic index, a measure of how much a specific carbohydrate food raises blood sugar, is another darling of the diet-health literature. On the surface, it makes sense: if excess blood sugar is harmful, then foods that increase blood sugar should be harmful. Despite evidence from observational studies, controlled trials as long as 1.5 years have shown that the glycemic index does not influence insulin sensitivity or body fat gain (2, 3, 4). The observational studies may be confounded by the fact that white flour and sugar are the two main high-glycemic foods in most Western diets. Most industrially processed carbohydrate foods also have a high glycemic index, but that doesn't imply that their high glycemic index is the reason they're harmful.

All of this is easy for me to accept, because I'm familiar with examples of traditional cultures eating absurd amounts of saturated fat and/or high-glycemic carbohydrate, and not developing metabolic disease (5, 6, 7). I believe the key is that their food is not industrially processed (along with exercise, sunlight exposure, and probably other factors).

A large new study just published in the American Journal of Clinical nutrition has placed the final nail in the coffin: neither saturated fat nor high glycemic carbohydrate influence insulin sensitivity in humans, at least on the timescale of most controlled trials (8). At 6 months and 720 participants, it was both the largest and one of the longest studies to address the question. Participants were assigned to one of the following diets:

1. High saturated fat, high glycemic index
2. High monounsaturated fat, high glycemic index
3. High monounsaturated fat, low glycemic index
4. Low fat, high glycemic index
5. Low fat, low glycemic index

Compliance to the diets was pretty good. From the nature of the study design, I suspect the authors were expecting participants on diet #1 to fare the worst. They were eating a deadly combination of saturated fat and high glycemic carbohydrate! Well to everyone's dismay except cranks like me, there were no differences in insulin sensitivity between groups at 6 months. Blood pressure also didn't differ between groups, although the low-fat groups lost more weight than the monounsaturated fat groups. The investigators didn't attempt to determine whether the weight loss was fat, lean mass or both. The low-fat groups also saw an increase in the microalbumin:creatinine ratio compared to other groups, indicating a possible deterioration of kidney function.

In my opinion, the literature as a whole consistently shows that if saturated fat or high glycemic carbohydrate influence insulin sensitivity, they do so on a very long timescale, as no effect is detectable in controlled trails of fairly long duration. While it is possible that the controlled trials just didn't last long enough to detect an effect, I think it's more likely that both factors are irrelevant.

Fats were provided by the industrial manufacturer Unilever, and were incorporated into margarines, which I'm sure were just lovely to eat. Carbohydrate was also provided, including "bread, pasta, rice, and cereals." In other words, all participants were eating industrial food. I think these types of investigations often run into problems due to reductionist thinking. I prefer studies like Dr. Staffan Lindeberg's paleolithic diet trials (9, 10, 11). The key difference? They focus mostly on diet quality, not calories or specific nutrients. And they have shown that quality is king!


* Excess body fat is almost certainly a major cause. When fat mass increases beyond a certain point, particularly abdominal fat, the fat tissue typically becomes inflamed. Inflamed fat tissue secretes factors which reduce whole-body insulin sensitivity (12, 13). The big question is: what caused the fat gain?

Tropical Plant Fats: Coconut Oil, Part II

Heart Disease: Animal Studies

Although humans aren't rats, animal studies are useful because they can be tightly controlled and experiments can last for a significant portion of an animal's lifespan. It's essentially impossible to do a tightly controlled 20-year feeding study in humans.

The first paper I'd like to discuss come from the lab of Dr. Thankappan Rajamohan at the university of Kerala (1). Investigators fed three groups of rats different diets:

1. Sunflower oil plus added cholesterol
2. Copra oil, a coconut oil pressed from dried coconuts, plus added cholesterol
3. Freshly pressed virgin coconut oil, plus added cholesterol

Diets 1 and 2 resulted in similar lipids, while diet 3 resulted in lower LDL and higher HDL. A second study also showed that diet 3 resulted in lower oxidized LDL, a dominant heart disease risk factor (2). Overall, these papers showed that freshly pressed virgin coconut oil, with its full complement of "minor constituents"*, partially protects rats against the harmful effects of cholesterol overfeeding. These are the only papers I could find on the cardiovascular effects of unrefined coconut oil in animals!

Although unrefined coconut oil appears to be superior, even refined coconut oil isn't as bad as it's made out to be. For example, compared to refined olive oil, refined coconut oil protects against atherosclerosis (hardening and thickening of the arteries) in a mouse model of coronary heart disease (LDL receptor knockout). In the same paper, coconut oil caused more atherosclerosis in a different mouse model (ApoE knockout) (3). So the vascular effects of coconut oil depend in part on the animals' genetic background.

In general, I've found that the data are extremely variable from one study to the next, with no consistent trend showing refined coconut oil to be protective or harmful relative to refined monounsaturated fats (like olive oil) (4). In some cases, polyunsaturated oils cause less atherosclerosis than coconut oil in the context of an extreme high-cholesterol diet because they sometimes lead to blood lipid levels that are up to 50% lower. However, even this isn't consistent across experiments. Keep in mind that atherosclerosis is only one factor in heart attack risk.

What happens if you feed coconut oil to animals without adding cholesterol, and without giving them genetic mutations that promote atherosclerosis? Again, the data are contradictory. In rabbits, one investigator showed that serum cholesterol increases transiently, returning to baseline after about 6 months, and atherosclerosis does not ensue (5). A different investigator showed that coconut oil feeding results in lower blood lipid oxidation than sunflower oil (6). Yet a study from the 1980s showed that in the context of a terrible diet composition (40% sugar, isolated casein, fat, vitamins and minerals), refined coconut oil causes elevated blood lipids and atherosclerosis (7). This is almost certainly because overall diet quality influences the response to dietary fats in rabbits, as it does in other mammals.

Heart Disease: Human Studies

It's one of the great tragedies of modern biomedical research that most studies focus on nutrients rather than foods. This phenomenon is called "nutritionism". Consequently, most of the studies on coconut oil used a refined version, because the investigators were most interested in the effect of specific fatty acids. The vitamins, polyphenols and other minor constituents of unrefined oils are eliminated because they are known to alter the biological effects of the fats themselves. Unfortunately, any findings that result from these experiments apply only to refined fats. This is the fallacy of the "X fatty acid does this and that" type statements-- they ignore the biological complexity of whole foods. They would probably be correct if you were drinking purified fatty acids from a beaker.

Generally, the short-term feeding studies using refined coconut oil show that it increases both LDL ("bad cholesterol") and HDL ("good cholesterol"), although there is so much variability between studies that it makes firm conclusions difficult to draw (8, 9). As I've written in the past, the ability of saturated fats to elevate LDL appears to be temporary; both human and certain animal studies show that it disappears on timescales of one year or longer (10, 11). That hasn't been shown specifically for coconut oil that I'm aware of, but it could be one of the reasons why traditional cultures eating high-coconut diets don't have elevated serum cholesterol.

Another marker of cardiovascular disease risk is lipoprotein (a), abbreviated Lp(a). This lipoprotein is a carrier for oxidized lipids in the blood, and it correlates with a higher risk of heart attack. Refined coconut oil appears to lower Lp(a), while refined sunflower oil increases it (12).

Unfortunately, I haven't been able to find any particularly informative studies on unrefined coconut oil in humans. The closest I found was a study from Brazil showing that coconut oil reduced abdominal obesity better than soybean oil in conjunction with a low-calorie diet, without increasing LDL (13). It would be nice to have more evidence in humans confirming what has been shown in rats that there's a big difference between unrefined and refined coconut oil.

Coconut Oil and Body Fat

In addition to the study mentioned above, a number of experiments in animals have shown that "medium-chain triglycerides", the predominant type of fat in coconut oil, lead to a lower body fat percentage than most other fats (14). These findings have been replicated numerous times in humans, although the results have not always been consistent (15). It's interesting to me that these very same medium-chain saturated fats that are being researched as a fat loss tool are also considered by mainstream diet-heart researchers to be among the most deadly fatty acids.

Coconut Oil and Cancer

Refined coconut oil produces less cancer than seed oils in experimental animals, probably because it's much lower in omega-6 polyunsaturated fat (16, 17). I haven't seen any data in humans.

The Bottom Line

There's very little known about the effect of unrefined coconut oil on animal and human health, however what is published appears to be positive, and is broadly consistent with the health of traditional cultures eating unrefined coconut foods. The data on refined coconut oil are conflicting and frustrating to sort through. The effects of refined coconut oil seem to depend highly on dietary context and genetic background. In my opinion, virgin coconut oil can be part of a healthy diet, and may even have health benefits in some contexts.


* Substances other than the fat itself, e.g. vitamin E and polyphenols. These are removed during oil refining.