No, not a food posting. Just an interesting metabolic backwater posting.
I had picked up some very small Fava beans (at the local “Mediterranean” grocer that is actually a Persian store) that had some interesting characteristics. Aside from being about the size and shape of a very large pea (i.e. not the usual European “horse bean” sized fava that’s like a medium large Lima bean), they had a more mild flavor. All it says about the beans in English on the bag is “Fava Beans (medium)” which implies there is a “small” and “large”; so now I’m wondering how small is small? They are packed for Kradjian Importing Company, Inc. of Glendale, California and are called “all natural”. http://www.kraimpco.com.
These guys have the nice feature that the seed coat is thin enough you don’t need to individually peel each one like the more common European bean. I cooked some and they have a nice flavor. I’m also seeing if any of them will sprout, but so far “no joy”, so they may have been heat processed or irradiated to kill bugs (or are just slow to germinate). While they say “All Natural, No Additives, No-Preservatives” there is still “dried in a gas drier” as a possible. But there is still time for these to sprout as the soil is cool and they may be waiting for warmth. I’m hoping they do sprout as the bunnies would like winter bean greens next winter ;-)
OK, the brand name on the front is “Mid East”. This got me thinking:
Isn’t Favism a disease where folks have a significant (sometimes life threatening) reaction to Fava beans, and isn’t it most common among folks from “The Middle East”? Seemed just a bit odd for folks with that kind of “issue” to be having a lot of Fava Beans; so I went off to learn a bit more about Favas and Favism.
It was more interesting than I’d expected.
For a food to become a national dish of a country, it has to represent that country in a way to make that food unique, usually by being popular or native to the country. Quite possibly, in the case of Egypt, a food may be a national dish simply because of its taste!
Okay, so that may not be the only reason, but the national dish of Egypt, Ful Medames, easily lives up to its reputation. What is it that makes this dish so special? The fava bean! While it may not be the most popular pea in the pod, what it lacks in appearance it definitely makes up in taste. After all, Ful Medames wouldn’t be Ful Medames without them! You may be surprised to know that the fava bean dates back to around 6500 BCE where they are believed to have originated in the Eastern Mediterranean. They resemble lima beans except they are larger and, when dried, are brown or tan in color.
Many people of Middle Eastern descent eat Ful Medames during Ramadan as an early breakfast meal before fasting. Fava beans may also be used in falafel, but they are not quite as popular in that dish as its cousin, the chickpea. Fava beans are also used in some stews and can be made into a fava bean sauce that goes perfect over pasta. Another great reason to enjoy fava beans are for their nutritional content! They are low in fat and calories and high in protein and fiber. Unfortunately, they are not so easy to find as more popular beans are. There are some retailers online that will sell them, and you can find them fresh, frozen, canned or dried. By all means though, check your local supermarket or Middle Eastern store. They are worth the search!
With a history like that, clearly these guys are widely eaten and in quantity. In the Mediterranean.
One important tidbit about fava beans is that they can be harmful to some people. A condition known as favism has been recognized in some people in the Middle East who develop adverse reactions to eating the beans or inhaling their pollen. Anemia can develop as the main reaction to eating fava beans by those who have enzyme deficiencies of the blood. Favism, though, is a rare disorder, affecting an estimated 1 out of 2000 people. It is thought that some people of the Middle East lack a specific enzyme in the blood that would prevent them from developing favism.
OK, having an attack of anemia from inhaling the pollen of a widely grown food crop sounds like it’s all bad all the time. This is looking kind of grim. How could such a thing arise and be at 1:2000 levels?
The wiki on these is pretty good, but only shows pictures of the more common bigger “broad bean”.
Vicia faba, the Broad Bean, Fava Bean, Field Bean, Bell Bean or Tic Bean, is a species of bean (Fabaceae) native to north Africa and southwest Asia, and extensively cultivated elsewhere. A variety is provisionally recognized:
Vicia faba var. equina Pers. – Horse Bean
Although usually classified in the same genus Vicia as the vetches, some botanists treat it in a separate monotypic genus Faba.
I’d grown out some of the common larger Favas (from the grocer here). It was a few years back, but they grew easily in our mild California Winter and would be a great “off season” food here. They have a beautiful flower that is a joy in the cold rainy season.
As there are several sizes I’ve seen in the stores, before finding these smaller ones, I think there must be more varieties than the Wiki is stating.
At any rate, they grew well, and were OK in the pot, but with a thick “skin” over each seed and I’m just not going to stand there peeling individual beans. The big beans have a skin that, IMHO, is just too thick to leave on them as it’s a bit tough. Maybe I just don’t know the “magic” to cooking them so it’s not an issue…
It is a rigid, erect plant 0.5-1.8 m tall, with stout stems with a square cross-section. The leaves are 10–25 cm long, pinnate with 2-7 leaflets, and of a distinct glaucous grey-green color; unlike most other vetches, the leaves do not have tendrils for climbing over other vegetation. The flowers are 1-2.5 cm long, with five petals, the standard petal white, the wing petals white with a black spot (true black, not deep purple or blue as is the case in many “black” colorings, and the keel petals white. Crimson flowered broad beans also exist, which were recently saved from extinction. The fruit is a broad leathery pod, green maturing to blackish-brown, with a densely downy surface; in the wild species, the pods are 5–10 cm long and 1 cm diameter, but many modern cultivars developed for food use have pods 15–25 cm long and 2–3 cm thick. Each pod contains 3-8 seeds; round to oval and 5–10 mm diameter in the wild plant, usually flattened and up to 20–25 mm long, 15 mm broad and 5–10 mm thick in food cultivars.
OK, so there are a whole lot of varieties, including one near extinction with a very special flower color. Extinction of particular colored types is not unusual in food crops. The “pink” flower salsify was at one time the most common, it is now extinct and only blue flowered types are found. This is an area of seed saving that could really use some more hands (and freezers!) working on it.
At any rate, I note the “round to oval” seed shape in “the wild plant”. That implies the seeds I have are closer to the wild sort. There is also considerable variation in plant sizes and pod sizes. So this plant has a very long history, but little formal development into the myriad named varieties of most food crops, per the wiki description of it.
Broad beans have a long tradition of cultivation in Old World agriculture, being among the most ancient plants in cultivation and also among the easiest to grow. It is believed that along with lentils, peas, and chickpeas, they became part of the eastern Mediterranean diet in around 6000 BC or earlier. They are still often grown as a cover crop to prevent erosion, because they can over-winter and because as a legume, they fix nitrogen in the soil. These commonly cultivated plants can be attacked by fungal diseases, such as rust (Uromyces viciae-fabae) and chocolate spot (Botrytis fabae). It is also attacked by the black bean aphid (Aphis fabae).
The broad bean has high hardiness cvs. This means it can withstand rough climates, and in this case, cold ones. Unlike most legumes, the broad bean can be grown in soils with high salinity. However, it does prefer to grow in rich loams.
In much of the Anglophone world, the name broad bean is used for the large-seeded cultivars grown for human food, while horse bean and field bean refer to cultivars with smaller, harder seeds (more like the wild species) used for animal feed, though their stronger flavour is preferred in some human food recipes, such as falafel. The term fava bean (from the Italian fava, meaning “broad bean”) is sometimes used in English speaking countries, however the term broad bean is the most common name in the UK.
OK, now here they are asserting that the smaller one has the stronger flavor and harder coat, but to my taste, the ones I’ve got are thinner skinned and more mild on the tongue. OK, maybe it’s a carefully selected food type that is NOT from the “field bean” group. But it is just a bit of a mystery now…
Then there are some cooking tips, and a short tour of some places that eat a lot of Favas. Being of English extraction, I was more familiar with the English use. But here the “top 3” are all Mediterranean. So now I’m thinking “Hang on a moment… why is something that causes Mediterranean people to get ill a common food for them?” Something is missing here…
Broad beans are primarily cultivated in the central part of Iran. The city of Kashan has the highest production of broad beans with high quality in terms of the taste, cooking periods and color. However, broad beans have a very short season (roughly two weeks.) The season is usually in the middle of spring. When people have access to fresh beans in season, they cook them in brine and then add vinegar and Heracleum persicum depending on taste. They also make an extra amount to dry to be used year round. The dried beans can be cooked with rice, which forms one of the most famous dishes in Iran called baghalee polo (Persian : باقالی پلو) which means rice with broad bean. In Iran broad beans are cooked, served with pepper and salt and sold on streets in the winter. This food is also available preserved in metal cans.
I can attest to Fava Beans being fast growers (though mine were more like a month instead of 2 weeks!) I have to think there is just a bit of “poetic licence” in that length of time…
Fava beans (Arabic: فول) are a common staple food in the Egyptian diet, eaten by rich and poor alike. Egyptians eat fava beans in various ways: they may be shelled and then dried, bought dried and then cooked by adding water in very low heat for several hours, etc. They are the primary ingredient in Ta`meyyah (Arabic: طعميه) (Egyptian Arabic for falafel), and Egyptians have made deriding Levantine felafel (made from chickpeas) as inferior something of a national sport. However, the most popular way of preparing fava beans in Egypt is by taking the mashed, cooked beans and adding oil, garlic, lemon, salt and cumin to it. It is then eaten with bread. The dish, known as ful medames, is traditionally eaten with onions (generally at breakfast) and is considered the Egyptian national dish.
Now that’s nice to know, as I’m not able to eat chickpeas. So I could eat felafel from Egypt. Nice. Just need to make sure I take one each (chick pea and fava) with me for “show and tell” with the waiter ;-)
Broad beans (Greek: κουκιά, koukiá) are eaten in a stew combined with artichokes, while they are still fresh in their pod. Dried broad beans are eaten boiled, sometimes combined with garlic sauce (skordalia). In Crete fresh broad beans are shelled and eaten as companion to tsikoudia, the local alcoholic drink. Favism is quite common in Greece because of malaria endemicity in previous centuries, and people afflicted by it do not eat broadbeans.
The Greek word fáva (φάβα) does not refer to broadbeans, but to the yellow split pea and also to the legume Lathyrus sativus, either of which are boiled with salt to the local variety of pease pudding, also called fáva. This creamy fáva is then served hot or cold, sprinkled with olive oil and garnished with a variety of condiments and seasonings such as diced onion, capers, parsley, pepper, lemon juice, etc.
OK the wiki goes on to talk about Ethiopia and how much they love Fava Beans there… but there was one line in that description that caught my attention. Malaria? What in the heck does Favism have to do with Malaria?
Broad beans are rich in tyramine, and thus should be avoided by those taking monoamine oxidase (MAO) inhibitors.
Raw broad beans contain the alkaloids vicine, isouramil and convicine, which can induce hemolytic anemia in patients with the hereditary condition glucose-6-phosphate dehydrogenase deficiency (G6PD). This potentially fatal condition is called “favism” after the fava bean.
Broad beans are rich in L-dopa, a substance used medically in the treatment of Parkinson’s disease. L-dopa is also a natriuretic agent, which might help in controlling hypertension.
Broad beans are widely cultivated in the Kech and Panjgur districts of Balochistan Province in Pakistan, and in the eastern province of Iran. In the Balochi language, they are called bakalaink, and baghalee in Persian.
Areas of origin of the bean correspond to malarial areas. There are epidemiological and in vitro studies which suggest that the hemolysis resulting from favism acts as protection from malaria, because certain species of malarial protozoa such as Plasmodium falcipacrum are very sensitive to oxidative damage due to deficiency of the glucose 6-phosphate dehydrogenase enzyme, which would otherwise protect from oxidative damage via production of glutathione reductase.
The seed testas contain condensed tannins of the proanthocyanidins type that could have an inhibitory activity on enzymes.
OK, a lot going on with these guys. Potential benefits for Parkinson’s. Need to be avoided by folks on MAO inhibitors (a widely used class of drugs for depression… so invite your celebrity over for favas and find out who is taking meds ;-) But at least it will help keep your blood pressure down.
Oh, and we find out the proper name of the thing that makes Favas a “No No” for some folks… and it has to do with a particular oxidative stress enzyme. Hmmm… that has implications. But these beans can cause “oxidative stress” to some forms of Malaria. Nice.
But now we know where to go to learn more…
OK, big long words to say some folks are missing an enzyme that breaks down a substance. What does that do?
Glucose-6-phosphate dehydrogenase deficiency is an X-linked recessive hereditary disease characterised by abnormally low levels of glucose-6-phosphate dehydrogenase (abbreviated G6PD or G6PDH), a metabolic enzyme involved in the pentose phosphate pathway, especially important in red blood cell metabolism. G6PD deficiency is the most common human enzyme defect. Individuals with the disease may exhibit nonimmune hemolytic anemia in response to a number of causes, most commonly infection or exposure to certain medications or chemicals. G6PD deficiency is closely linked to favism, a disorder characterized by a hemolytic reaction to consumption of broad beans, with a name derived from the Italian name of the broad bean (fava). The name favism is sometimes used to refer to the enzyme deficiency as a whole, although this is misleading as not all people with G6PD deficiency will manifest a physically observable reaction to consumption of broad beans.
Well, part of the answer is in the “sex linked”. So you can have women carriers that do not have the disease or have it in a weaker form. We also see that it’s not just Broad Beans, but many things that can be an issue; and that there are variations in the genetic variation such that some folks don’t have a reaction to Favas… Another example of how humans can be highly variable even inside a very small class of folks with a specific gene defect. This, BTW, is why statements like “Vaccines are safe” are simply broken. Safe for WHOM? Not safe for WHOM? Very few things are 100% safe for everyone. Take Tylenol, or even aspirin for example. (I’ve got family who can not take aspirin due to bleeding issues). So as soon as you have a blanket “X is safe” from anyone about a drug or a food for ALL people, you know they are wrong.
So what’s up with this particular variation on human types? Are they just “broken” and ought to be weeded out?
Favism may be formally defined as a haemolytic response to the consumption of broad beans. All individuals with favism show G6PD deficiency. However, not all individuals with G6PD deficiency show favism. For example, in a small study of 757 Saudi men, more than 42% showed a variant of G6PD deficiency, but none displayed symptoms of favism. Favism is known to be more prevalent in infants and children, and G6PD genetic variant can influence chemical sensitivity. Other than this, the specifics of the chemical relationship between favism and G6PD are not well understood.
OK… so we’ve got one sample of Greeks who are very prone to Favism, while Saudis are showing another version of the trait, but not so much reaction to beans…
Many substances are potentially harmful to people with G6PD deficiency, variation in response to these substance makes individual predictions difficult. Antimalarial drugs that can cause acute haemolysis in people with G6PD deficiency include primaquine, pamaquine and chloroquine. There is evidence that other antimalarials may also exacerbate G6PD deficiency, but only at higher doses. Sulfonamides (such as sulfanilamide, sulfamethoxazole and mafenide), thiazolesulfone, methylene blue and naphthalene should also be avoided by people with G6PD deficiency, as should certain analgesics (such as aspirin, phenazopyridine and acetanilide) and a few non-sulfa antibiotics (nalidixic acid, nitrofurantoin, isoniazid and furazolidone). Henna has been known to cause haemolytic crisis in G6PD-deficient infants.
Well, that’s quite a list! So if we mandate, for example, that everyone in the military or in the Peace Corps or even just all “students on a field trip” must take their anti-malarials, we could kill them… Maybe “one size fits all” doesn’t.
Heck, even aspirin! And hair coloring!
Why in the world would folks with that genetic “burden” still be “in the gene pool”? And in many variations? (The wiki at that point has a chart of at least 9 major genetic variations).
How it works
The G6PD / NADPH pathway is the only source of reduced glutathione in red blood cells (erythrocytes). The role of red cells as oxygen carriers puts them at substantial risk of damage from oxidizing free radicals except for the protective effect of G6PD/NADPH/glutathione.
People with G6PD deficiency are therefore at risk of hemolytic anemia in states of oxidative stress. Oxidative stress can result from infection and from chemical exposure to medication and certain foods. Broad beans, e.g., fava beans, contain high levels of vicine, divicine, convicine and isouramil, all of which are oxidants.
So ANY product that causes oxidative stress can nuke your red blood cells.
Lots of things cause oxidative stress…
When all remaining reduced glutathione is consumed, enzymes and other proteins (including hemoglobin) are subsequently damaged by the oxidants, leading to electrolyte imbalance, cross-bonding and protein deposition in the red cell membranes. Damaged red cells are phagocytosed and sequestered (taken out of circulation) in the spleen. The hemoglobin is metabolized to bilirubin (causing jaundice at high concentrations). The red cells rarely disintegrate in the circulation, so hemoglobin is rarely excreted directly by the kidney, but this can occur in severe cases, causing acute renal failure .
Deficiency of G6PD in the alternative pathway causes the build up of glucose and thus there is an increase of advanced glycation endproducts (AGE). The deficiency also causes a reduction of NADPH which is necessary for the formation of Nitric Oxide (NO). The high prevalence of diabetes mellitus type 2 and hypertension in Afro-Caribbeans in the West could be directly related to the incidence of G6PD deficiency in those populations.
So once it busts up the red blood cells, you get collateral damage all over the place.
Sounds just horrible. Such a defective group of genetics. Perhaps we ought to cull them?
But Wait, There’s More
Think back to those Greeks with Favism…
G6PDH is the most common human enzyme defect, being present in more than 400 million people worldwide. African, Middle Eastern and South Asian people are affected the most along with those who are mixed with any of the above. A side effect of this disease is that it confers protection against malaria, in particular the form of malaria caused by Plasmodium falciparum, the most deadly form of malaria. A similar relationship exists between malaria and sickle-cell disease. One theory to explain this, is that cells infected with the Plasmodium parasite are cleared more rapidly by the spleen. This phenomenon might give G6PDH deficiency carriers an evolutionary advantage by increasing their fitness in malarial endemic environments.
Oh. So maybe it’s a “Feature” instead of a “defect”, eh?
Don’t need to take antimalarial drugs because they have built in antimalarial metabolism. Don’t need to eat Fava Beans for their added oxidative stress on the malarial parasites, but do need to avoid them…
IMHO, this is just a stellar case for why the mass medicine one size fits all approach to things is horribly broken. You simply can NOT say “This pill is safe” or “this vaccine is safe” or “this food is safe” for everyone. We are all unique genetic collections. And with unique exposure histories.
I’ve now got 3 major foods I can’t eat without significant reactions (one could be life threatening). Another person I know is so allergic to horses that just being down wind of one can cause hives. imagine what a “horse serum” based inoculation would do to them?
Tylenol causes some folks liver to die if they have had even a modest couple of drinks (yet folks regularly take it for hangovers when they still have high blood alcohol levels… it is one of the highest causes of liver damage around). Other folks bleed out on modest doses of aspirin. Yet I can eat aspirin like candy (and also get very little benefit from it).
We are all unique.
And some of us benefit greatly from being more immune to malaria. For them, it’s not a ‘defective gene’, it kept their ancestors alive and well through generations of malaria. And as malaria becomes resurgent (as we’ve squandered pesticides and stopped eradication just short of completion…) they will live; as we who can eat Fava Beans die off from our “defect”… unless we manage to eat enough Fava Beans for IT to protect us via MORE oxidative stress…
Alcohol consumption can also cause oxidative stress. I wonder to what extent the Islamic prohibition of alcohol stems from their high levels of a genetic type that is made ill by such oxidative stress? And if so, would they ever realise that “one size fits all” doesn’t work for those of us who have no such issue? The whole “One Mandate For All” behaviour is just so broken. In religion, in medicine, in social order. Yet it is the dominant theme of so much of the world. And so doomed to failure.
I also note this line in the wiki:
Although female carriers can have a mild form of G6PD deficiency (dependent on the degree of inactivation of the unaffected X chromosome—see lyonization), homozygous females have been described; in these females there is co-incidence of a rare immune disorder termed chronic granulomatous disease (CGD).
It is structurally almost identical to the one about autism rates in girls vs boys and to me strongly implies a similar X-linked genetic variation that manifests in a different response to some environmental insult (be it vaccination, metals loading, “oxidative stress”, Vitamin-A metabolism, or whatever). And I wonder what that “defect” might provide in the way of a “feature” in its normal state? And what we are removing from our gene pool in our ignorance and stupidity. Perhaps even the particular mix of genes that grants extra immunity and no need for vaccination. Much as those of us with allergies have an added immunoglobulin (IG-E) that grants extra resistance to parasites.
We have a load of internal organs that do a vast number of intricate metabolic things. Chemistry of all sorts, and with all kinds of specialized environmental adaptations. It is wrong to assume that any one of those differences is just “bad” until we know what it is, and what it does. It is just as wrong to assume that any given substance can be given to all people with impunity. We already know people are different in many critical ways. Yet the present trend in “Public Health” is ever more toward government mandated Thou Shalt.
And it will kill some people.
The only person who can be responsible for your life is you. Petty tyrants can never make the right decision for each individual. The only system that can ever work well is distributed decision making at the lowest possible level and with individual control of individual decisions and individual destiny.