By Michael Astera
“When we think of metal poisoning; lead, mercury and aluminium intoxication invariably springs to mind. But the insidious toxic properties of the metal manganese have almost been completely overlooked. Modern health authorities could learn a lesson from the alchemists of the Byzantine era who regarded manganese as the black magic metal; whereby the quantum capacity of manganese to absorb light and sound, can induce a lethal ‘Jekyll and Hyde’ style conversion of this metal from innocuous to toxic form.
"Manganese exposure has been associated with the original cause of many neuro-degenerative diseases.”
Mark Purdey “To the Ends of the Earth” http://www.markpurdey.com/articles_endearth.htm
My first exposure to the idea of Manganese as a potential toxin came when I read an interview with Mark Purdey in the December 2001 issue of Acres USA magazine. Mark was a dairy farmer whose farm and herd had been at the center of the “Mad Cow Disease” outbreak in England. Despite being surrounded by farms who lost their herds to BSE (Bovine Spongiform Encephalopathy), with his cattle even rubbing noses across the fence with infected animals, Purdey’s organic herd was unaffected by the outbreak. At first, the only reason he could see why his cows escaped the disease was that he had refused to treat them with an organophosphate insecticide that had been mandated by the government in a bid to eradicate warble flies. As an intelligent and curious self-taught scientist he was intrigued enough to begin researching BSE and trying to find a link between this systemic insecticide and susceptibility to Mad Cow disease.
From the Acres interview:
ACRES U.S.A. They call it transmissible, but is it really transmissible?
PURDEY. It is, in a sense. I do support the prion hypothesis of Stanley Prusiner. But what I am saying that is different is that it is the chemical cocktail that produces the abnormal prion protein, and organophosphates are well known to deform the molecular shape of proteins in the nerves — this is how they produce their well-known toxic effect, the acute effect. They deform a protein called cholinesterase at high doses, and that damages the balance of the nerves because cholinesterase is involved in counterbalance of the nervous impulse. So, if you remove the cholinesterase, then you get an overdrive of nervous impulses and at the very worst you get a paralysis, which would mean death when you paralyze the nerves that control the lungs or the heartbeat.
ACRES U.S.A. The prion doesn’t have a nucleus, does it?
PURDEY. It is like any other protein — it is produced by genetic material in the cell — but basically, the [TSE] prion is a malformed prion protein.
ACRES U.S.A. Is it infectious in the same way that a virus is?
PURDEY. No, it is totally different. There is no evidence for such a conclusion, and I believe it certainly does not act as an infectious virus does. It doesn’t infect people or animals horizontally. A good example of this lack of infectious action is that there hasn’t been a single case of BSE in a home-reared cow on a fully converted, organic farm in Britain. Yet when you buy cows for breeding purposes, as I do, and those cows then get BSE, it never spreads across to your home-reared cows. This, in a sense, shows that it is not horizontally transmitted.
ACRES U.S.A. So the term “transmissible” is really conjectural?
PURDEY. That’s right. It is just an interpretation of what is going on. If you inject it into an animal’s brain, then you will pass the disease on.
ACRES U.S.A. This is what Prusiner did, isn’t it?
PURDEY. Yes, but that is not saying that it is the virus. I believe, maybe this is jumping the gun a little bit, but the prion in its active form will generate a free-radical chain reaction, and this is due to the presence of an abnormal metal that has bonded onto the prion protein in place of copper. It is basically the metal manganese that replaces copper on the prion protein. [emphasis added]
Purdey’s researches on BSE and the role of manganese in its development led him on a fifteen year journey to the ends of the earth. He found that high levels of manganese in the soil, combined with a deficiency of copper and zinc, were associated with degenerative nervous system diseases as diverse as scrapie in sheep in Iceland and the “laughing disease” kuru in New Guinea.
More from the Acres interview:
PURDEY. I went back to square one and designed this world tour where I would go around the world on my own to pockets where this disease had clustered — these were tiny little pockets of the world. My first port-of-call was in Colorado in a tiny area of the Rocky Mountains where chronic wasting disease was a hot spot in deer and elk. Then I went to Iceland to certain valleys where sheep scrapie is very intense, and to adjoining valleys where there is no scrapie at all in the sheep. I went to Slovakia, where CJD [Creutzfeld-Jakob disease, one of the human forms of BSE] is present in three villages. I went to Calabria, where one hamlet has experienced 20 cases of CJD since 1995.
ACRES U.S.A. What were you able to find out?
PURDEY. What I did in each area was test the environment for all of the different trace elements in metals, because I was interested in the possibility that there might be something abnormal in the particular environment. I was asking the question: why is the disease present in these environments and not spreading to disease-free areas adjoining where the same animals and humans are living but not getting the disease? That in itself shows that it doesn’t spread horizontally, otherwise it would have spread like wildfire, for instance, right across the Rocky Mountains, because, as you know, there are deer all over the Rockies. So why is it just staying in one tiny area?
ACRES U.S.A. What did you find in the case of chronic wasting disease?
PURDEY. I found in every single area really high levels of the metal manganese and rock-bottom levels of copper.
ACRES U.S.A. And manganese inhibits the uptake of copper.
PURDEY. Well, that is true, but I found very low levels of copper in the soil anyway, which could have been due to the high levels of manganese or even molybdenum. I also found low selenium and low zinc. All of the trace metals that are involved in antioxidant enzymes in the body, the activators, were at a low level, but manganese was high. I then got interested in people who had died from manganese intoxication, for instance, miners who were working in manganese mines. It seemed that their death was caused by the manganese getting out of control and setting off these free-radical chain reactions. That really interested me, because I thought: if manganese is setting off these chain reactions in deer and sheep and humans in these pockets all over the world, and there are no antioxidants there to mop up and scavenge these free-radical chain reactions because of the low selenium, zinc and copper also found in all of these areas, then spongiform disease could be a free-radical disease that is caused by oxidizing agents in the environment.
ACRES U.S.A. Your organophosphates are the oxidizing agents?
PURDEY. Yes. So, it was beginning to become very clear to me what was happening with the disease. The source of manganese was also quite interesting to me. In Colorado it seemed to be coming from the pine needles that the deer were wolfing down in this one area where the disease was really intense. Ranchers in that area told me that the deer were very overpopulated in this region. There was a shortage of pasture and food. They somehow thought this had something to do with the cause of chronic wasting disease. I think they were right. Other ranchers said that the animals were eating pine needles to make up for their lack of food. So, I took home pine needles from the area, and I got extractable manganese at 2,000 parts per million, which is very high.
“In Iceland it was coming from volcanoes that were spewing out manganese in certain valleys. In Slovakia it was coming specifically from the steel factories that the communists had erected, but they hadn’t filtered the chimneys. Immediately downwind of those factories were the cases of CJD in the villages that were in the rain-belt region of these factories. All the manganese was being rained down on these villages to the extent that the pine trees were actually dying in the villages where there was CJD. Furthermore, the local people in this area of Slovakia are so poor that they actually used pine needles for tea and for syrup. So you have this intriguing link up with pine needles, which bio-concentrate manganese anyway, and Creutzfeldt-Jakob disease. In Italy, where I went in Calabria, where the scrapie and CJD cases have been breaking out since 1995, these cluster regions were immediately downwind of the petrol refineries. I found that in 1990 they switched from using lead to manganese in the refining process. I think these clusters initially — this started quite recently, in 1995 — were all linked to the fallout of manganese from the petrol refining process.”
[end Acres interview excerpt]
I you read the Acres interview and other parts of Purdey’s investigations into prion diseases you will find that he emphasizes a “triggering mechanism” that causes a cascade of malformed proto-proteins. The potential triggers he suspected and documented as being present in the areas where these diseases were occurring ranged from the organophosphates mentioned above to subsonic vibrations from earthquakes, volcanic activity, low overflights of certain aircraft such as the SST, and military bombing and other explosive weapons testing.
Purdey kept on with his research around the world, paid for by his own funds and a few charitable donations. He met with MPs (Ministers of Parlaiment) in the UK and shared his findings; they promised funding but of course it never materialized; or rather, what funding materialized went to established academics who literally stole the work Purdey had done and then proceeded to capitalize on it where they could. Not surprisingly, the role of organophosphates was downplayed but the connection between manganese and malformed prions was unavoidable.
From a study (supposedly*) published in 2006:
Subject: FATEPriDE Environmental Factors that Affect the Development of Prion Diseases Date: February 18, 2006
Project funded by the European Commission under the Quality of Life Programme.
Introduction
The work proposed here brings together top EU geo and biochemists focusing on determining the environmental factors that affect the development of prion diseases such as scrapie, bovine spongiform enchpalitis (BSE), chronic wasting disease (CWD) and Creutzfeld-Jacobs disease (CJD). First the geographical distribution of manganese and copper in soils will be investigated as risk factors. This will be undertaken due to the fact that prion diseases often are found in clusters. It now has been established that the normal metal for prion protein is copper but if that metal is replaced with manganese, the structure of the prion protein is altered. The role of organophosphate pesticides will also be investigated because it has been suggested that copper is complexed with organophosphate, preventing copper absorption.
Objectives
There is clear evidence that the occurrence of prion diseases often has a non-random distribution, suggesting a link to some environmental factors. The work proposed here will investigate risk factors, including the role of trace elements and organophosphates. Analysis of regional variation in local manganese/copper levels will be determined and compared to the incidence of the diseases. The ability of manganese and/or organophosphates in influencing conversion of the prion protein to an abnormal and/or infectious protein will be determined. In combination with geographical occurrence and geo-chemical considerations this program will identify whether these environmental considerations should be acted upon to bring about effective prevention or at least risk minimalisation of prion diseases in the EU and further afield.
Description of the Work
Recently it has been suggested that disbalance in dietary trace-elements and/or exposure to organophosphates might either cause or be a risk factor for prion disease development. In particular, high incidence of scrapie (e.g. in Iceland), chronic wasting disease, and in Slovakia and Italy CJD are associated with regions where soil and foliage are reported to be low in copper and high in manganese. This proposal will address whether exposure to a diet that has a high manganese/copper ratio can influence prion disease will also be addressed. In particular, we shall investigate this theory at the level of protein, cells, animals as well as geographical and geo-chemical associations with prion diseases. Animal models of prion disease and sheep from farms in regions of high scrapie will be investigated for a possible influence of level of manganese and copper on incidence or onset of these diseases. Bio-chemical and biophysical techniques will be used to investigate interaction of the prion protein with copper and manganese to determine the mechanism by which Mn substitution for Cu influences conversion to the abnormal isoform of the protein and whether such conversion results in protein that is infectious in mouse bioassay for infectivity. Additionally, a cell culture model will be used to generate abnormal prion protein by exposure to manganese. Cell culture model of infection will be used to assay whether prion disease alters manganese metabolism and transport of manganese into cells. The level of expression of the prion protein is in itself a risk factor for prion disease as it shortens the incubation time for the disease. This research will result in understanding of the role of disbalance in the trace elements Cu and Mn on the onset and mechanisms behind the occurrence of prion diseases and will for the first time define whether there are environmental risk factors for prion diseases.
Milestones and Expected Results
The study proposed here will produce a geo-chemical map of Europe for manganese and copper. These maps will be used to target field areas where prion diseases have occurred as clusters. The bio-chemical studies will establish whether the replacement of manganese for copper in prion protein is a risk factor for the disease _development_. Organophosphate will also be investigated as a risk factor. The study aims at minimising the risk of prion diseases for humans and animals in the EU.
(*I have written "supposedly" because although the text above and quoted directly below can be found at a number of web sites, the link to the study and its conclusions has seemingly been scrubbed from the web. This link no longer works: http://www.arp-manchester.org.uk/FatePride.htm )
ITEM 6 FATEPRIDE (SEAC 97/4) 35.
The Chair explained that FATEPriDE is a multi-centre European Union funded project that examined the possible influence of environmental trace elements on the occurrence of TSEs. 36. Professor David Brown (University of Bath) explained that the project had principally studied potential interactions between prion disease and copper and manganese, although interactions with other environmental factors such as organophosphates had also been assessed. No link, other than with manganese, between many environmental factors studied, including organophosphates, and TSEs was found. The key experiments and findings had been summarised in SEAC paper 97/4. The main conclusions were that manganese binds to PrP with similar affinity to known manganese binding proteins, induces conformational change in PrP, catalyses PrP aggregation, induces protease resistance in PrP, increases PrP expression levels and increases cellular susceptibility to prion infection. Manganese had also been found at high levels on farms with a high classical scrapie incidence and manganese was found to increase the stability of PrP in soil. Although it had been the intention to create maps of bioavailable manganese and compare those to similar maps of TSE hotspots, this had not been possible as no data of sufficient precision relating the location of BSE or scrapie cases was made available. Further studies were required to investigate the interactions of manganese and prions.
37. Members noted that the study suggested an association between high levels of bioavailable manganese, low levels of bioavailable copper and classical scrapie in field studies. (Source: Another link that doesn’t work: http://www.arpmanchester.org.uk/documents/FINALDetailedProgrammeandAbstracts.pdf
But as of April 2011 you can find a more complete version of the extracts above at: http://chronic-wasting-disease.blogspot.com/2010_08_01_archive.html
Here is the abstract of a more recent study from 2009:
“Manganese Enhances Prion Protein Survival in Model Soils and Increases Prion Infectivity to Cells
Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom
Prion diseases are considered to be transmissible. The existence of sporadic forms of prion diseases such as scrapie implies an environmental source for the infectious agent. This would suggest that under certain conditions the prion protein, the accepted agent of transmission, can survive in the environment. We have developed a novel technique to extract the prion protein from soil matrices. Previous studies have suggested that environmental manganese is a possible risk factor for prion diseases. We have shown that exposure to manganese in a soil matrix causes a dramatic increase in prion protein survival (~10 fold) over a two year period. We have also shown that manganese increases infectivity of mouse passaged scrapie to culture cells by 2 logs. These results clearly verify that manganese is a risk factor for both the survival of the infectious agent in the environment and its transmissibility. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0007518”
[Note that there is no mention of Mark Purdey, the person whose selfless, unpaid work led to the very idea of investigating these co-factors in prion diseases. For shame.]
At the time I read the Acres interview I was only a couple of years into my own investigation of the role of soil minerals in health and nutrition. I had sent soil samples from my property to a lab for testing and they came back at 39ppm (parts per million) manganese with almost no detectable copper. Was this bad? I didn’t know so I emailed Mark Purdey and asked him. He wasn’t sure either, but we both knew that almost no copper was not a good thing. Back in the 1920s the French Scientist Andre Voisson had shown a number of links between low copper in the soil and degenerative diseases in people and animals. Voisson’s book “Soil, Grass, and Cancer” was one both Mark and I had read and valued.
As it turned out, 39ppm manganese in my soil was not anything to worry about. I found out later that some areas near where I lived at the time had levels much higher than that when I met a fellow who had had to put a special water filter on his well to take out manganese. Interestingly enough, the active elements in his special manganese-removing water filter were zinc and copper. These things all tie together, the chemistry, the electrical charges, the oxidants and antioxidants.
By this point I was both curious and concerned about the potential toxicity of manganese so I kept on looking. My next finding was the association between the symptoms of manganese poisoning and Parkinson’s disease (the following are from more recent publications, not 2002):
“Manganism, or manganese poisoning, is prevalent in such occupations as mining, welding, and steel manufacturing. It is caused by exposure to excessive levels of the metal manganese, which attacks the central nervous system, producing motor and dementia symptoms that resemble Parkinson’s disease.” http://www.uphs.upenn.edu/news/News_Releases/2009/02/parkinsons-manganese-print.html
“Manganese poisoning is referred to as manganism, the result of excessive or prolonged exposure to manganese. When the human body absorbs a large amount of manganese there is a toxic effect, resulting in serious health conditions and diseases. Sometimes people use manganism and Parkinson’s disease to describe the same adverse manganese effect due to the similarity of the conditions. Manganese has a very long elimination from the central nervous system so the effects of manganism are not always immediately evident.
“Miners are considered to be at the highest risk for developing manganism. There are three different stages that are differentiated in manganism, including behavioral changes, parkinsonian features, and dystonia and gait disturbances. The onset of manganism can be observed through symptoms of fatigue, headache, muscle cramps, loss of appetite, apathy, insomnia, and a diminished libido.
“Other symptoms of manganism can include:
- muscle stiffness
- weakness
- tremors
- breathing and swallowing problems
Welders, factory workers, and communities in areas of high manganese industry are also at an increased risk for developing manganism. Workplace hazards are considered the highest risk for developing manganism so understanding how to follow workplace standards to reduce risk is especially important to ensuring the well being of individuals that work closely with the dangerous element. Communities that exist in areas where manganese is released into the air will have a higher risk for manganism.” http://www.manganese-wilsons-parkinsons-disease.com/manganese/manganism_information.html
“Manganese miners or steel workers exposed to high levels of manganese dust in air may have mental and emotional disturbances, and their body movements may become slow and clumsy. This combination of symptoms is a disease called manganism. Workers usually do not develop symptoms of manganism unless they have been exposed for many months or years. Manganism occurs because too much manganese injures a part of the brain that helps control body movements. Some of the symptoms of manganism can be reduced by medical treatment, but the brain injury is permanent.
“A common effect in men who are exposed to high levels of manganese dust in air is impotence. As a result, men exposed to high levels may not be able to father children. Studies in animals show that too much manganese may also injure the testes.” http://www.eco-usa.net/toxics/chemicals/manganese.shtml
This wasn’t sounding good to me: Malformed prions, TSE, manganism, impotence, brain damage. At the same time I knew that Mn was an essential mineral nutrient:
“Eating a small amount of manganese each day is important in maintaining your health. The amount of manganese in a normal diet (about 2,000-9,000 ug/day) [2-9mg] seems to be enough to meet your daily need, and no cases of illness from eating too little manganese have been reported in humans.” http://www.eco-usa.net/toxics/chemicals/manganese.shtml
“Manganese is a trace mineral that is present in tiny amounts in the body. It is found mostly in bones, the liver, kidneys, and pancreas. Manganese helps the body form connective tissue, bones, blood-clotting factors, and sex hormones. It also plays a role in fat and carbohydrate metabolism, calcium absorption, and blood sugar regulation. Manganese is also necessary for normal brain and nerve function.
“Manganese is a component of the antioxidant enzyme superoxide dismutase (SOD), which helps fight free radicals. [ed note: it seems likely that the powerful oxidizers known as organophosphates would put an end to this role for manganese in the body. Organophosphates are well-known oxidizing agents. The active ingredient in the herbicide Roundup, glyphosate, is an organophosphate and its main method of action is to oxidize manganese in plant tissue.]
“Free radicals occur naturally in the body but can damage cell membranes and DNA. They may play a role in aging as well as the development of a number of health conditions including heart disease and cancer. Antioxidants, such as SOD, can help neutralize free radicals and reduce or even help prevent some of the damage they cause.
“Low levels of manganese in the body can contribute to infertility, bone malformation, weakness, and seizures.” http://www.umm.edu/altmed/articles/manganese-000314.htm
So how much manganese is in a normal human body? Around 12 to 20 milligrams, not much. The chart of the human body’s mineral content at bloodindex.com reports that a normal person weighing 70kg (154lbs) should have 13mg of manganese and 90mg of copper. There’s copper showing up again, and it appears that the correct copper to manganese ratio in the body should be around six or seven parts copper to one part manganese. It starts to make sense that animals and people would develop problems if their food and environment was high in Mn and seriously deficient in Cu.
A couple of other important elements come into play here as well. That 70 kg body should also have 4,200mg of iron and 2,400mg of zinc. In the soil and in the body, zinc and copper are complementary and antagonistic, as are iron and manganese. High levels of manganese in the diet strongly suppress iron absorption http://www.ajcn.org/content/54/1/152.abstract and high levels of zinc interfere with copper absorption http://lpi.oregonstate.edu/infocenter/minerals/zinc/. It all ties together.
My goal, my challenge back in the early 2000s, was to figure out what levels of iron, manganese, copper and zinc in the soil would result in healthy soil and crops as well as optimum health in the people and animals relying on the crops for their food. The ratio of copper to zinc in the body is around 27 to 1, that of iron to manganese closer to 300 to 1. A little studying of soil test results and various soil fertility books showed the ratios in the soil were not nearly that wide. Some soils had more manganese than iron, most soils seemed to have a little more zinc than copper. I was mostly concerned with making sure the food crops didn’t have an excess of manganese and that they had a sufficient amount of copper.
At the time, I found little in the agricultural literature regarding an optimum level of copper in the soil. The best source of information was a book I already owned, Soil Fertility by Foth and Ellis (Wiley 1988). Soil Fertility told me that the earth’s crust contained on average 55ppm copper and 70ppm zinc. It also told me that most of the copper in the topsoil was attached to organic matter, as was the majority of the zinc. Recommendations for adding copper were for 3ppm per year until 10 to 20 ppm had been applied. Recommendations for zinc were similar, with the note that 25 lbs of zinc per acre (12ppm in the top 6” to 7” of soil) should be sufficient for many years.
I was looking for more than that. Soils vary a lot in their texture and ability to hold onto nutrients and release them to crops and soil organisms when needed. Most heavy clay soils can hold on to many times the amount of nutrients that a coarse sandy soil can; the level of organic matter in a soil also affects its ability to hold nutrients. The ability of a soil to hold on to nutrients, either adsorbed onto exchange sites or as part of organic complexes, also affects the availability of the minerals. In a loose, sandy soil with low organic matter 2 or 3 ppm of copper might be readily available; in a tight clay soil with a good humus level the plants might starve for copper at levels higher than that. I was looking for a way to tie in the optimum amount of minerals to the ability of the soil to hold on to them, known as “exchange capacity”. [see “Cation Exchange Simplified”]
I found some clues in Soil Fertility where the relationship between zinc and phosphorus were discussed. High levels of phosphorus, it seemed, could make zinc unavailable especially in calcareous (high calcium) soils; there were also hints that iron had a role.
The next important clue came from reading a comment made by Graeme Sait in his 2003 collection of interviews called Nutrition Rules (2003 http://nutri-tech.com.au). In an offhand way he mentioned a phosphorus to zinc ratio of 10:1. When I read that something “clicked” in my thoughts. I knew that was “it”: one part zinc to ten parts phosphorus in the soil, and the results so far have given me no reason to change that. The next question was “then how much phosphorus?”
That one wasn’t as hard to answer. From what I had read, starting with the work of Justus von Liebig in the mid-1800s and going up to at least 1930, phosphorus and potassium had been used in equal amounts in most fertilizer blends. The commonly measured form of phosphorus is phosphate, which is 44% actual P. Potash in fertilizers is 83% actual K. The old formulations had twice as much phosphate as potash, which works out to just about equal amounts of elemental P and K. Carey Reams recommended the same ratio, and somewhere in my reading of William Albrecht I recall him saying the same thing, equal amounts of P and K. As the human body contains more P than K this made sense as well, even if it didn’t “jibe” with the ratios of most modern fertility recommendations which often call for more potash than phosphate.
The next step was simple: Albrecht, Firman Bear, and several others had done a lot of investigation of the optimum ratios of the basic cation nutrients calcium, magnesium, and potassium from the 1920s on; by around 1950 the consensus was that the soil’s CEC (cation exchange capacity) should be saturated with 60-80% calcium, 10 to 20% magnesium, and 2 to 5% potassium. If I knew the CEC of the soil, and how many parts per million of potassium it was going to have for a given crop, that told me how much phosphorus I would want, e.g. equal to potassium, and how much zinc: 1/10th of actual P. Entirely on a hunch I decided to set the optimum copper level at ½ of zinc; it worked.
What I had so far was K, potassium, at 3-5% of CEC; P, phosphorus equal to K; zinc 1/10th of P, and copper ½ of zinc. What about manganese?
Manganese is closely tied to iron, just as copper is to zinc. I found different opinions on what the ideal ratio of Mn to Fe should be, and a lot of variation based on soil pH. I knew that highly acid soils could easily develop toxic levels of manganese and iron, and that in high-calcium high-pH soils crops were often deficient in Mn, Fe, or both. As well, some soils are very high in manganese and/or iron; iron is one of the more abundant elements in the earth’s crust. It seemed more important to decide on a minimum level of iron, so based on a number of soil tests and crop tissue tests and a little bit of intuition I set the minimum iron level at 1/3 to ½ of phosphorus, and the optimum manganese at 1/3 to ½ of iron. Soils that naturally have a high manganese content are amended to bring the iron level up to equal manganese or a bit more.
So far the ratios are working fine. The crops grown in soils balanced this way have good levels of all of the mineral nutrients, at or above USDA averages for food crops (often considerably higher) with zinc consistently higher than copper and iron consistently higher than manganese. I don’t foresee any problems due to excess manganese or deficient copper with this method of balancing soil minerals.
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Michael Astera is the author of The Ideal Soil: A Handbook for The New Agriculture. His web site, which is all about growing more nutritious food, is at http://soilminerals.com
