Almost every book written on wild foods mentions the substances oxalates and nitrates. Often in the context of giving you a word of caution: “Don’t eat too much because this plant contains oxalates,” or nitrates. These warnings are not generally understood by wild food authors and therefore are never explained. Some of the plants covered in this book contain either one or both of these substances. So it is only fair that I explain to you in detail why you should NOT generally be worried about them being in your diet. People ordinarily do not talk about these substances when eating conventional foods, even though they are present. They are mentioned with wild foods mostly because authors feel responsible to mention things they’ve heard about that might be a problem, but they cannot explain why.
Most substances like oxalates and nitrates only become a concern in certain unusual circumstances and not in the context of a normal healthy and diverse diet in normal healthy people. In fact, in certain amounts, these substances may have some beneficial roles in the same way that other phytochemicals may be beneficial.
The purpose of this section is to clarify what oxalates do and why this author believes that they are mostly a non-issue—just one more thing you shouldn’t have to worry about when you are trying to enjoy your wild food meal.
Warnings about oxalates are typically nonspecific, giving the impression that they are in some way poisonous. One warning is specific: oxalates bind calcium in the digestive tract. The recommendations are typically “Don’t eat too much” or “Don’t eat more than one bowl.” The consequence of these statements is to give novices one more reason to needlessly be intimidated by wild foods.
Let me first say that soluble oxalates are the topic of this section, not calcium oxalate crystals. Calcium oxalate crystals (Kingsbury, 1964; Kallas, 1997) are found in skunk cabbage (Symplocarpus foetidus [eastern] / Lysichitum americanum [western]), jack-in-the-pulpit (Arisaema triphyllum), and dumb cane (Dieffenbachia seguine); these present a real problem that is not discussed here.
Oxalates, also known as oxalic acids, are naturally occurring substances found in almost every living thing. They are soluble in water as sodium oxalate or potassium oxalate salts, and are typically found in greater quantities in members of the wood sorrel family (Oxalidaceae), the buckwheat family (Polygonaceae), the purslane family (Portulacaceae), and the goosefoot family (Chenopodiaceae).
Plants and foods known to have high concentrations of oxalates include, but are not limited to, the following:
| Domesticated Wild | Wild |
|---|---|
| Spinach | Wild spinach |
| French sorrel | Sheep sorrel |
| Rhubarb | Wood sorrel |
| Swiss chard | Purslane |
| Beet leaves | Docks |
| Black tea | Japanese knotweed |
| Cocoa | Pokeweed |
In green plants, higher concentrations of oxalates are often accompanied by higher concentrations of calcium.
Oxalates are a normal part of the human diet and are a normal part of human amino acid and ascorbic acid metabolism. You know a food like spinach is high in oxalates because your teeth get this funny sandpapery feel when you eat it. When this happens, the oxalates in the food are temporarily binding to the calcium of your teeth. This quickly resolves itself within a few minutes but is fun while it lasts.
One of the big problems in the field of wild foods is that misconceptions and misattributions are made regularly and then cited repeatedly in ensuing literature. They eventually become “truisms” that everybody believes, including professionals who cite these same misconceptions.
The misconception that soluble oxalates are a great concern to humans essentially began with John Kingsbury’s classic 1964 book, Poisonous Plants of the United States and Canada. While his book was primarily a review of animal research combined with smatterings of human data, many writers interpreted the information as applicable to humans—falsely raising fears. Kingsbury himself warned readers that “Oxalate poisoning (even in animals) is fundamentally complex and poorly understood.” Since Kingsbury’s book, retrospective and targeted studies have been done to look directly at the oxalate issue—dismissing many of the fears.
There were claims during World War II that the cause of poisonings from people eating rhubarb leaves was the oxalates contained there. Unfortunately, the proponents of this logic did not know at the time that the stalks, which we do eat, have almost as much oxalates as the leaves. In fact, spinach leaves have about 30 percent more oxalates than rhubarb leaves. I do not see people in North America dropping like flies as they enjoy their spinach salad. Rhubarb leaves are poisonous for reasons that have nothing to do with oxalates.
In 1989, the first and only report of a human poisoning from oxalates was titled Fatal Oxalic Acid Poisoning from Sorrel Soup (Farre, 1989). The tabloid title really makes one think “Wow, am I lucky I haven’t died from all those times I ate gobs of sorrel soup, spinach, and other oxalate-containing greens. How did I survive, as did millions of other people around the planet who eat oxalate-containing plants on a regular basis. We should all be dead—but wait! We aren’t!”
Here’s the problem: From what I’ve read, that report could have been more accurately titled “Fifty-three-year-old man dies of poor health, failing blood chemistry, liver, and kidneys due to a life of excessive drinking, smoking, and poorly managed insulin-dependent diabetes after enjoying several bowls of sorrel soup.” It is not unreasonable to assume that this fellow’s body was ready for catastrophic failure, and he only needed a catalyst to set death in motion. Calcium oxalate crystals were found in his kidneys because his abnormal blood chemistry did not prevent the crystals from forming. My normal digestive tract absorbs only a small fraction of dietary oxalates, and my normal blood pH does not allow oxalates to bind with calcium. Those crystals in his kidney were probably building over a long time from bad blood chemistry, not just from one meal as was the impression left by the report. So this fellow had lots of problems independent from sorrel soup.
To this day, I still hear from people afraid to eat oxalates for fear that they will be poisoned. This bad information gets repeated again and again, from book to book, and now it is all over the Web.
As early as 1973, the National Research Council of the National Academy of Sciences came up with some conclusions (Fassett, 1973) about oxalates in human metabolism, as stated in their report “Toxicants Occurring Naturally in Foods.” What follows is my perspective on the oxalate issue based on information from that report and my general knowledge of human physiology.
Humans are not cattle or sheep in their dietary habits, their physiology, or even their number of stomachs. While I love rhubarb, I would not enjoy eating five pounds of it per day for a month at the exclusion of other foods. Like most humans, I enjoy a diverse diet; cattle and sheep do not have a diet that diverse. This focus on cattle and sheep data greatly affects the exaggerations about dietary calcium deficiencies and the idea of toxic intakes in humans. As far as I know, only the one case I just mentioned, concerning toxic intake of naturally occurring soluble oxalates, has ever been reported, and that case has nothing to do with normal humans.
Oxalates can bind with calcium and other minerals in the digestive tract, making both the calcium and the oxalates unavailable for absorption. This may be a natural protective effect that calcium provides to further decrease the amount of oxalates absorbed. In a normal healthy diet that has foods eaten by a normal healthy human, almost all dietary oxalates are excreted with the feces, with little being absorbed through the intestinal membranes. It is interesting to note that plants with high oxalate content are often high in calcium. So, dietarily, there would be no net loss of calcium; the plant supplies the calcium so that is not depleted in your diet.
Food and intestinal secretions in a typical digestive tract create a complex chemical environment in which calcium complexes and oxalate salts are in relatively small and dispersed amounts. So many other things can happen to calcium and so many other things can happen to oxalates within the total of stomach contents that it is difficult to justify the often-repeated and somewhat-absolute statement that oxalates “block” the absorption of calcium.
Since oxalates bond to calcium in the digestive tract, they may also bond to toxic metals like mercury, lead, and cadmium, helping to eliminate them from the body before they can be absorbed. In fact, the calcium oxalate compound itself may bond to toxic metals, so do not rule out a positive role for oxalates. The point I am making is that some things we think are bad turn out to have a more nuanced and potentially positive story in the context of a healthy diet.
There is little scientific evidence that dietary oxalates promote the development of kidney stones or gallstones in healthy people. Oxalates have to transport from the gut into the bloodstream for that to happen. Since most is excreted in the feces, little dietary oxalate gets to the kidneys or the liver. People who develop kidney stones have a physiological abnormality that promotes excessive “creation” and deposition of oxalates within the body. Even so, many physicians think it is “prudent” to limit dietary oxalates for these people, “just in case.”
If you are really heart-set on pumping your blood full of oxalates, take megadoses of vitamin C. Ascorbic acid is oxalate’s “Trojan horse.” Vitamin C is easily absorbed from the digestive tract into the bloodstream. In normal metabolism, humans convert excess ascorbic acid (vitamin C) into oxalates and other breakdown products that get filtered through the kidneys and end up in the urine. High intake of vitamin C results in much greater metabolic oxalate production than any healthy consumption of high oxalate vegetables. Those oxalates have to be excreted through the kidneys where the stones can form. Even oxalates that are in the blood do not bind with calcium in healthy individuals because our blood chemistry/pH will not allow it.
In summary, my understanding and opinion is that in the context of a normal, healthy, diverse diet, dietary oxalates are a nonissue for healthy people. Unfortunately, they still cause a lot of unnecessary fear in the wild food community. Consume sorrel, dock, purslane, and wild spinach without fear unless you are chronically malnourished, have complicated or unusual blood chemistry, or are counseled by your doctor not to.
If you have an abnormal physiological propensity for kidney stones or digestive issues, observe how your body reacts when you do eat high oxalate foods. If you have a sensitivity, then by all means heed those feelings and react accordingly. And always follow the directions of your physician.
As you read through wild food literature, you often hear a warning that some plants are nitrate accumulators. You do not hear much beyond that—just a warning. So what does that mean from a practical standpoint? What should you do with that information? The following is my understanding of nitrate accumulators and nitrite physiology.
Nitrates are a class of substances containing nitrogen and other molecules.
In caring for a yard, a garden, or a farm, you should know that nitrogen is an important part of fertilizer. Plants use nitrogen for growth. Nitrates are building blocks for DNA, amino acids, and proteins. Without nitrates, growth comes to a halt in plants and humans.
Since the primary concern in the scientific literature of nitrate accumulation and toxicity is in the poisoning of livestock, this is where most of the research has been conducted. Humans and livestock are different physiologically and dietarily. Direct comparisons are difficult, so I will try to give you a more human point of view. Just looking at this from a consumption perspective, livestock often eat large amounts of the same food from the same land for days and weeks at a time. Humans have a more diverse diet, so any one substance found in a particular food gets diluted. Diversity in the diet is the best defense against small amounts of potentially toxic constituents in what we consider to be normal foods. Diversity includes both the types of foods you eat and the different lands from which they are harvested.
Overall, there appears to be no actual risk of nitrate toxicity to healthy human adults or even children over three months of age. I could find no incidence of recorded poisonings over three months of age. As far as I can tell, humans four months old and older have nothing to fear and can ignore warnings about nitrates.
There have been rare instances, only a handful in the last 100 years, of recorded poisonings of infants due to ingestion of high nitrate spinach that was puréed into baby food. I could find no instances of other plants being a problem, even though other plants accumulate nitrates. The rarity makes one think that the high concentrations of nitrates were an unlucky and rare combination of circumstances, that the infants were not given a diverse enough diet, and/or the infants already had compromised health. The point is that it is so rare that we should not worry about it. Being informed is better than worrying.
In humans, nitrates are not toxic. Nitrates play a variety of roles in human physiology. It is the nitrites that are of concern, and that concern only applies to infants under four months of age. If infants are breast-fed, that would solve any nitrate accumulation problem and make this whole section a moot point.
But, if a parent were to make a purée of a nitrate-accumulating plant and feed it in enough quantity to an infant (this would be difficult to do), here is what would happen:
Once the infant had eaten the food, natural digestive bacteria would begin converting nitrates (useful) to nitrites (the bad guys). This does not happen in older humans (four months old and older) because their digestive tracts are more mature and their stomachs are more acidic, preventing the conversion. Nitrites in the infant stomach are absorbed and pass into the bloodstream.
Once in the blood, adult physiology converts nitrites back to nitrates. Infant physiology is not mature enough to do that yet, so nitrites stay nitrites. Since these kids are very young, about 80 percent of their hemoglobin is leftover fetal hemoglobin; that is, made by the fetus for fetal physiology. Only about 20 percent is new adult-style hemoglobin. Fetal hemoglobin has an affinity for nitrites that is much stronger than adult hemoglobin. So hemoglobin gets covered with nitrite molecules in infants. These nitrites block oxygen from attaching to the hemoglobin. Since oxygen has trouble attaching to hemoglobin, breathing brings in less oxygen, and the infant starts showing signs of oxygen deficiency. If enough nitrites are in the body, the infant eventually turns blue and can suffocate if not treated quickly. This condition of nitrite-surrounded hemoglobin is called methemoglobinemia. In contrast, adult hemoglobin can fend off whatever nitrites have survived in the blood up to that point.
The first symptoms in low levels of methemoglobinemia in infants are a flushing of the face and extremities, headache, and stomach discomfort. This will pass shortly if the offending plant matter is no longer eaten. Higher, more dangerous levels can produce increasing levels of abdominal pain, nausea, vomiting, a bluish coloration of the skin, and eventual collapse.
Again, keep in mind that while methemoglobinemia is theoretically possible, dangerous levels have only been documented a few times in the last hundred years. It’s so rare that I will not mention it in my plant chapters.
Here are a few plants considered to be nitrate accumulators; there are many more nitrate accumulators than those listed here. I just wanted to point out a few representative ones.
| Domesticated Wild | Wild |
|---|---|
| Turnip greens | Purslane |
| Spinach | Wild spinach |
| Celery | Curly dock |
| Corn | Miner’s lettuce |
For healthy humans over three months of age, there is no evidence that I can find to suggest any harm from eating plants high in nitrates in the context of a normal and diverse diet. Nitrates are a normal part of eating, and our bodies have the means for processing them.
I do not recommend feeding plants growing in uncontrolled conditions, nitrate accumulators or not, to infants. Even though the risk is probably very low, making baby food out of any plants, wild or cultivated, is unnecessary.
If you chose to feed puréed vegetables of any kind to infants under four months of age, keep these things in mind: This is a complex decision of which you can not have all the facts, particularly with wild plants growing in uncontrolled conditions. Without laboratory testing of the soil and of the plants growing in them, you cannot know the nitrate content of the parts you are feeding your infant. The risk outweighs the benefit, even though that risk is low. Diversity in a baby’s diet is a good hedge against any one food causing a problem. So, as long as you don’t feed homemade puréed vegetables to infants, nitrate accumulation is another non-issue that you do not have to worry about.