Cold Rice and Bean Salad

I arrived back to San Jose yesterday afternoon, after a week away giving Beatrice time off from attending to two very spoiled and ornery rat terriers (she spoiled them; see how charitable I am IRL?).

Checked email when I got back and a blog reader, Brian, had a link for me: Rice and Bean Resistant Starch Salad; a post at Food Renegade by  Shannon Stonger (wouldn’t it be cool if she was ‘Shannon Stronger’ or, ‘Shannon Stoner’?).

I looked around. Bea had a pot of pinto beans in the fridge, and the rice cooker was on the countertop, with a full load from the night before. Hmmm, beans & rice dish? I’m in. After a quick surveillance of what else there was on hand, I set off to the market.

All I needed was two large heirloom tomatoes (I got a big red and a big yellow) a big [h]ass avocado, and a block of cheddar cheese. It calls for Mexican oregano, but I had Greek, which is the closest. Substitute a little lime juice for some of the vinegar and you’ll approximate that lemon verbena thingy (I googled it on my iPhone 6, in the store).

See her full recipe here.

My variations:

  1. the rice was Ben’s Parboiled. Doubt it makes any difference. It’s just starch.
  2. went with 2 tsp of sea salt instead of 1 1/4.
  3. 1/2 tsp cayenne instead of 1/4.
  4. for the vinegar, used juice of a whole lime, 1 TBS coconut vinegar, and 2 TBS ACV.
  5. recipe calls for black beans or whatever your preference. I had pintos, but bought a can of black at the market which when drained, was 1 1/2 cup of the 3 cups called for. So, half pinto, half black.

The recipe doesn’t specify, but you want to drain the beans of their liquid. Ought be obvious, but you never know. Some people do beans more like soup, so you want to start off the same.

My only thing I’d do different next time is to go with less onion. Recipe calls for a medium, the two I had were large and I picked the smallest one. Bit more chunky raw onion than I’d have preferred. Beatrice, on the other hand, loved it more than I. Definitely go with doubling the cayenne if you at all like a little kick. Even still, it’s a small kick.

IMG 2682
Yea, it’s a lot

So, there you have a week’s worth of starchy, side-dish substrate for your proteins for lunch and dinner, for two people; and it’s as cheap as sewer water.

IMG 2684
Yin Yang. Grace and Evil.

…I really loved the idea of a whole avocado for the dressing substrate (as opposed to mayonnaise, which I hate to make). Word of caution: if you go with the 2 tsp salt as I did, the dressing will be very salty. Remember, it’s to dress a lot of stuff. You’ll not need to add any more salt.

Potential future variations: Olives? How about fresh cilantro, either as garnish or in the dish itself?

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  1. Jane Karlsson on October 1, 2014 at 03:06

    Still white rice, not brown rice. Why? I think you need to explain exactly what it is about brown rice that’s so awful. Is it the phytic acid? No? What is it then?

    • Richard Nikoley on October 1, 2014 at 06:48

      I don’t know that it makes a difference, anymore, especially if it causes no problems for you.

    • Jane Karlsson on October 3, 2014 at 04:25

      But how do you know whether it’s causing problems? In the short term, it probably won’t. For some people, it might never do. But if the rest of their diet isn’t perfect, or they are stressed, or their environment is polluted, or their gut bacteria aren’t as healthy as they might be, eating refined carbs of any sort makes no sense. Detoxification depends on micronutrients, stress resistance depends on micronutrients, and gut bacteria depend on minerals as well as fibre. I do not believe that gut bacteria like to get their minerals from a pill.

      People think it’s OK to eat white rice as long as you eat lots of veggies, but the evidence suggests otherwise. This study for instance shows a ‘strong linear association’ between white rice consumption and diabetes risk in China, and veggie intake was positively, not negatively, associated with white rice intake. In fact one interpretetation might be that veggies cause diabetes. Clearly that’s not the case, so it must have been the white rice, meaning white rice is bad however many veggies you eat.

    • Duck Dodgers on October 3, 2014 at 08:54

      “This study for instance shows a ‘strong linear association’ between white rice consumption and diabetes risk in China, and veggie intake was positively, not negatively, associated with white rice intake. In fact one interpretetation might be that veggies cause diabetes. Clearly that’s not the case, so it must have been the white rice, meaning white rice is bad however many veggies you eat.”

      I’m afraid you can’t draw that conclusion either. The study simply tells us that people who are diabetic are more likely to be observed as being diabetic (i.e. more likely to be diagnosed) by increasing their carb intake. Not exactly surprising. There is nothing telling us that white rice causes diabetes. And I know that you know this because you also say:

      “But if the rest of their diet isn’t perfect, or they are stressed, or their environment is polluted, or their gut bacteria aren’t as healthy as they might be, eating refined carbs of any sort makes no sense.”

      Ding, ding, ding! One of the big problems with the carbophobia crowd is that they make the assumption that the data is saying ‘x causes y’ when the more likely culprit may in fact be other underlying issues that need to be dealt with. Avoiding white rice, or carbophobia in general, does not cure diabetes—it does not change the underlying issue that actually needs fixing.

      The more white rice populations eat, the lower their incidence of diabetes is. You’ve claimed in the past that this is because these populations consume less wheat, and wheat is worse. Well, either way, we just don’t know. You can certainly hypothesize that, but we just don’t know. We don’t know enough about diabetes to be sure.

      “People think it’s OK to eat white rice as long as you eat lots of veggies, but the evidence suggests otherwise.”

      About 4 billion people on the planet eat bowls of white rice every day. And for far longer than industrially-produced foods have been around, they’ve preferred white rice. There is no pandemic of diabetes in that enormous white rice eating population.

      “Is it the phytic acid? No? What is it then?”

      I think the phytic acid is no big deal (thanks to your previous comments!). One drawback with brown rice may be the higher toxin load in the bran (you did mentioned pollution after all) and the fact that the oils in brown rice do not store well and will go rancid. I’m sure that freshly milled brown rice grown in a pristine organic field is perfectly fine. But, it’s virtually impossible for most people to get fresh brown rice grown in such conditions. The biggest problem I have with brown rice is that it tends to taste like crap compared to white rice. Perhaps this has to do with the rancid oils? Either way, people prefer white rice and the populations that use it as a staple seem to do fine.

      I don’t think brown rice is some kind of superfood. And really, I doubt any of this discussion really matters since few, if any, Westerners ever rely on rice as a staple. If people want to eat rice a few times a week, it’s probably not going to make much of a difference. To say otherwise is perhaps a little bit ortharexic. I think people should be able to enjoy their meals after all.

  2. Jane Karlsson on October 4, 2014 at 03:09

    Hi Duck
    I should have said hyperglycemia, not diabetes risk, sorry. The ‘strong linear association’ was between white rice intake and hyperglycemia. If you read the paper you will see that it’s difficult to avoid the conclusion that white rice is somehow causing the hyperglycemia.

    The point here is that carbohydrate metabolism is completely dependent on the minerals which get removed from white rice. If you look up ‘diabetes magnesium’ or ‘diabetes manganese’ you will find what I am talking about. White rice has had nearly all of its Mg and Mn removed.

    “The more white rice populations eat, the lower their incidence of diabetes is. You’ve claimed in the past that this is because these populations consume less wheat, and wheat is worse.” Yes, WHITE wheat flour is probably worse than WHITE rice. Neither is good. Have you read any of McCarrison’s work?

    • Duck Dodgers on October 5, 2014 at 09:54


      The studies you reference (Shi, et al; and McCarrison) are studying diets of people who use rice as a staple. For instance, McCarrison’s work shows that a population with a limited diet which does not supplement the white rice, brown rice helps to prevent the disease beriberi.

      [Yawn.] Big deal. Nobody here tries to get their nutrition/minerals from rice. It’s a freakin recipe that happens to taste better with white rice. I hardly think it makes a difference for Westerners who certainly do not eat +400g of rice per day.

    • Jane+Karlsson on October 6, 2014 at 05:18

      You are forgetting something. The people who eat rice as a staple eat very little meat, or at least they used to. Nowadays they eat much more, and they have much more diabetes. Look up ‘heme iron diabetes’. If you eat a lot of meat you need more of the minerals which prevent iron-dependent damage.

      Nowadays our food is seriously depleted of minerals even before it gets into the factories. You do not know whether eating white rice 3 times a week is harmful, and you cannot know this.

    • Duck Dodgers on October 6, 2014 at 09:22

      “If you eat a lot of meat you need more of the minerals which prevent iron-dependent damage.”

      Sorry, not buying it…

      See: Chris Kresser: Does Eating Red Meat Increase the Risk of Diabetes?

      “Nowadays they eat much more, and they have much more diabetes”

      You know that there are many other variables, right? (sugar, antibiotics, wheat, etc.)

      “You do not know whether eating white rice 3 times a week is harmful, and you cannot know this.”

      4 billion Asians have been eating buckets of polished rice, every week, since about the beginning of the 18th century. By your logic they should have all turned diabetic by the mid 1700s. But, we know that’s not the case. They have some of the lowest incidences of diabetes in the world. You’re simply choosing to ignore that.

      Why not try to simply emulate healthy populations? I’m not aware of any healthy populations that go out of their way to consume brown rice. They overwhelmingly prefer white rice.

    • Duck Dodgers on October 6, 2014 at 11:01

      I would also point out that your timeline does not match up with your own hypothesis. Rice polishing became advanced enough by the late 1800’s that it caused rampant Beriberi to be observed in the Japanese navy:

      From: Wikipedia: Beriberi

      “In the late 1800s, beriberi was studied by Takaki Kanehiro, a British-trained Japanese medical doctor of the Japanese Navy. Beriberi was a serious problem in the Japanese navy: sailors fell ill an average of four times a year in the period 1878 to 1881, and 35% were cases of beriberi. In 1883, Kanehiro learned of a very high incidence of beriberi among cadets on a training mission from Japan to Hawaii, via New Zealand and South America. The voyage lasted more than 9 months and resulted in 169 cases of sickness and 25 deaths on a ship of 376 men. With the support of the Japanese Navy, he conducted an experiment in which another ship was deployed on the same route, except that its crew was fed a diet of meat, fish, barley, rice, and beans. At the end of the voyage, this crew had suffered only 14 cases of beriberi and no deaths. This convinced Kanehiro and the Japanese Navy that diet was the cause. In 1884, Kanehiro observed that beriberi was endemic among low-ranking crew who often were provided nothing but rice, but not among crews of Western navies and nor among Japanese officers who consumed a more varied diet.”

      Yet, the rise in diabetes is a very new and rapidly growing phenomenon in Asian countries:

      From: Trends in prevalence of diabetes in Asian countries

      “In the past two decades, the prevalence [of diabetes] in urban areas has increased re-markably in most countries, the increase being phenomenal in Nepal and China. The national prevalence has increased by two fold or more within a decade in many countries. Rural prevalence has increased considerably in India, Nepal and China…In 1980, less than 1% of Chinese adults had diabetes and in 2008, the prevalence had increased to nearly 10%.

      You would have us believe that this extremely recent rise in diabetes is all due to modern milling practices, but your timeline does not match up with the Asian diabetes explosion. You claim it’s related to meat intake, but the data suggests that diabetes and obesity are rising, simultaneously, together—and that suggests something more than overlysimplistic macro/micronutrient intakes.

      Maybe you can think of a few other modern inventions that may have contributed to diabetes and obesity over the past two decades?

    • Jane Karlsson on October 7, 2014 at 02:42

      Wheat? Wheat causes diabetes? You have not read your McCarrison. WHITE wheat flour almost certainly does, just like WHITE rice. Yes there are other variables, like WHITE sugar and antibiotics. And meat.

      If you don’t agree that eating a lot of meat increases the need for minerals which prevent iron-dependent damage, have a look at this paper. Until it was published last year, it was not known how excess iron causes diabetes. It turns out that iron stops manganese from getting into mitochondria, so the enzyme MnSOD, which protects them, does not work. Please note that the animals had been made diabetic by means of a high fat diet. Fat is yet another variable, and its effects can be prevented by manganese.

      “Why not try to simply emulate healthy populations?” Good idea. I’ve been doing exactly that for 30 years. Once again, you have not read your McCarrison. No population in Asia today is nearly as healthy as the Asians he studied, who ate whole wheat, vegetables and milk, just like I do.

    • Duck Dodgers on October 7, 2014 at 07:38


      Your study specifically says, “shown in a mouse model of hereditary iron overload that cytosolic iron levels affected mitochondrial manganese availability.” Wonderful. Nobody here advocates eating tons of meat and tons of rice, every day.

      You seem to be obsessed with the extremes. You cite studies of people consistently eating enormous quantities of rice every day, for eternity, then you back it up with iron overload studies to simulate, as you put it, “eating a lot of meat.”

      Well, nobody here eats like that. Nobody here advocates eating rice as a staple. Nobody here advocates “eating a lot of meat.”

      It’s a freaking recipe that would fit right into any Blue Zone diet. Even if you’re right, there’s no need to be ortharexic about it.

    • JaneKarlsson on October 7, 2014 at 08:46

      It was first shown in a mouse with hereditary iron overload, and then in wild type mice on a high fat diet. Please read the paper again.

    • Jane Karlsson on October 8, 2014 at 02:42

      Duck, I think you have misinterpreted the study. The mice did not have hereditary iron overload, or even dietary iron overload. Their diabetes was caused by a high fat diet, but still the problem was too little manganese. Here is a paper showing that saturated fat can inhibit manganese absorption. It also increases iron absorption.

      “There is evidence that manganese (Mn) metabolism may be altered by the form and amount of dietary fat. Also, iron (Fe) absorption is greater with saturated fats, as compared to polyunsaturated fatty acids (PUFAs). The absorption of Fe and Mn are interrelated in many aspects; therefore, the form of dietary fat may indirectly alter Mn absorption. …Manganese absorption was significantly (p < 0.05) lower in the stearic acid group (0.9-4.8%) than in the safflower oil group (20-33.8%)…"

      The people reading this blog eat meat, saturated fat, and white rice. All three are implicated in causing diabetes, and all by increasing the iron-manganese ratio. Richard needs to think about this. Either he recommends less meat, or less saturated fat, or brown rice instead of white rice. I think the brown rice option is the easiest.

    • Duck Dodgers on October 8, 2014 at 09:02

      “Their diabetes was caused by a high fat diet, but still the problem was too little manganese”

      Well, maybe I missed it but I don’t think the mice technically got “diabetes” from the experiment. There glucose was worse, but with a high fat diet, but wouldn’t we expect blood glucose to be worse with higher fat intake and therefore lower fiber intake? That doesn’t exactly seem surprising to me. And my uneducated guess is that it’s the decrease in fiber that might be the problem in those studies.

      If Richard’s readers, who make an effort to eat high-RS foods are noticing the lowest blood glucose readings of their life, don’t you think they might be on to something?

    • Richard Nikoley on October 8, 2014 at 10:19


      In the interest of full disclosure, honesty and all that stupid shit, mind telling us why you just popped up here in full force?

      Anything to do with being banned elsewhere?

    • Duck Dodgers on October 9, 2014 at 08:06

      C’mon Jane. The prebiotic fiber intake may very well playing a greater role than you initially thought. Once again, gut bugs are where it’s at…

      From: Prebiotics, Probiotics, and Synbiotics Affect
      Mineral Absorption, Bone Mineral Content,
      and Bone Structure

      Several studies in animals and humans have shown positive effects of nondigestible oligosaccharides (NDO) on mineral absorption and metabolism and bone composition and architecture. These include inulin, oligofructose, fructooligosac- charides, galactooligosaccharides, soybean oligosaccharide, and also resistant starches, sugar alcohols, and difructose anhydride. A positive outcome of dietary prebiotics is promoted by a high dietary calcium content up to a threshold level and an optimum amount and composition of supplemented prebiotics. There might be an optimum composition of fructooligosaccharides with different chain lengths (synergy products). The efficacy of dietary prebiotics depends on chronological age, physiological age, menopausal status, and calcium absorption capacity. There is evidence for an independent probiotic effect on facilitating mineral absorption. Synbiotics, i.e., a combination of probiotics and prebiotics, can induce additional effects. Whether a low content of habitual NDO would augment the effect of dietary prebiotics or synbiotics remains to be studied. The underlying mechanisms are manifold: increased solubility of minerals because of increased bacterial production of short-chain fatty acids, which is promoted by the greater supply of substrate; an enlargement of the absorption surface by promoting proliferation of enterocytes mediated by bacterial fermentation products, predominantly lactate and butyrate; increased expression of calcium-binding proteins; improvement of gut health; degradation of mineral complexing phytic acid; release of bone-modulating factors such as phytoestrogens from foods; stabilization of the intestinal flora and ecology, also in the presence of antibiotics; stabilization of the intestinal mucus; and impact of modulating growth factors such as polyamines. In conclusion, prebiotics are the most promising but also best investigated substances with respect to a bone-health-promoting potential, compared with probiotics and synbiotics. The results are more prominent in animal models, where more studies have been performed, than in human studies, where experimental conditions are more difficult to control.

      As one might expect, mineral absorption is more complex than just boiling it down to overly-simplistic fat and meat intake. Don’t forget the fiber…

    • Jane Karlsson on October 9, 2014 at 03:21

      Don’t worry Richard, I know exactly what your problem is. You can never accept what I say about manganese, because Wooo will crucify you.

      I need to tell you one last thing about it. The enzyme MnSOD doesn’t just prevent diabetes, it does a lot more than that. The hydrogen peroxide it produces goes to the nucleus and activates an anti aging programme.

      “The data suggest that MnSOD up-regulation and a retrograde signal of reactive oxygen species from the mitochondria normally function as an intermediate step in the extension of lifespan caused by reduced insulin-like signaling in various species. The results implicate a species-conserved net of coordinated genes that affect the rate of senescence by modulating energetic efficiency, purine biosynthesis, apoptotic pathways, endocrine signals, and the detoxification and excretion of metabolites.”

    • Richard Nikoley on October 9, 2014 at 07:17

      That’s odd, since I can’t ever recall stating any opinion about it one way or the other.

      You can believe what you want but Woo ( with OCD that causes her to put up 4 posts about others with OCD) just doesn’t seem to worry me at all.

    • Jane Karlsson on October 9, 2014 at 08:11

      Good for you. Glad to hear it. She scares the sh*t out of me. Well actually … perhaps she doesn’t. When she banned me I felt nothing, to my great surprise. Except mild irritation that she claimed I was sending her nasty emails when I didn’t even have her email address.

    • Duck Dodgers on October 9, 2014 at 08:19

      And, you can apparently find heat-stable MnSOD in mushrooms. Yum!

      From: Activity, thermostability and isozymes of superoxide dismutase in 17 edible mushrooms

      Activity, thermostability and isozymes of superoxide dismutase (SOD) of 17 edible mushrooms from China were investigated in this study. The results indicated that most of these mushrooms have high SOD activities, especially Pleurotus citrinopileatus [golden oyster mushroom], Agaricus bisporus [common/button mushroom] , Pleurotus ostreatus [oyster mushroom], Volvariella volvacea [straw mushroom] and Agrocybe aegerita [poplar mushroom], which contained SOD activities of higher than 1000 units per gram fresh weight (U/g FW). The cap of Coprinus comatus [shaggy mane] and P. citrinopileatus [golden oyster mushroom] contain the highest SOD specific activities. Usually the SOD activity of the cap was higher than in the stipe. SODs of edible mushrooms show high thermal stability, with 40–95% activity still present after treatment at 90 °C for 10 min. Both manganese superoxide dismutase (MnSOD) and iron superoxide dismutase (FeSOD) were identified. The main isozymes were MnSODs and ranged from 0.8 to >10 μg/g FW in whole mushrooms, from 0.1 to 6.2 μg/g FW in cap, and from 0.06 to 3.5 μg/g FW in stipe. This was much higher than the concentration of FeSODs at 31–489 ng/g FW. MnSOD content of the cap was higher than that of the stipe and the highest level of MnSODs occurring in A. bosporus [common/button mushroom] and the cap and stipe of A. aegerita [poplar mushroom].

      Mushroom pizza anyone?

    • Duck Dodgers on October 9, 2014 at 08:32

      And… whaddayaknow… Our gut bugs play a role in MnSOD.

      From: Anti-inflammatory properties of Lactobacillus gasseri expressing manganese superoxide dismutase using the interleukin 10-deficient mouse model of colitis

      Emerging evidence has implicated reactive oxygen species (ROS) in the pathogenesis of inflammatory bowel disease (IBD). Although intestinal epithelial cells produce the ROS-neutralizing enzyme superoxide dismutase (SOD), the protein and activity levels of copper/zinc (Cu/Zn) and manganese (Mn) SOD are perturbed in inflamed tissues of IBD patients. Thus we investigated the ability of MnSOD from Streptococcus thermophilus to reduce colitis symptoms in interleukin (IL) 10-deficient mice using Lactobacillus gasseri as a delivery vehicle. Cohorts of 13–15 IL-10-deficient mice were left untreated or supplemented with native L. gasseri or L. gasseri expressing MnSOD for 4 wk. Colonic tissue was collected and inflammation was histologically scored. The presence of innate immune cells was investigated by immunohistochemistry and the host antioxidant response was determined by quantitative PCR. It was demonstrated that L. gasseri was stably maintained in mice for at least 3 days. L. gasseri producing MnSOD significantly reduced inflammation in IL-10-deficient mice compared with untreated controls (P < 0.05), whereas the anti-inflammatory effects of both native and MnSOD producing L. gasseri were more pronounced in males. The anti-inflammatory effects of L. gasseri were associated with a reduction in the infiltration of neutrophils and macrophages. Transcripts of antioxidant genes were equivalent in colonic tissues obtained from control and probiotic-treated IL-10-deficient mice. This study demonstrates that L. gasseri producing MnSOD has significant anti-inflammatory activity that reduces the severity of colitis in the IL-10-deficient mouse.

      For those wondering, Lactobacillus gasseri is part of the vaginal flora.

      From: MicrobeWiki: Lactobacillus gasseri

      Even though this bacterium is most commonly found in the gastrointestinal tract, it can also be found in various other places.

      One very important location is in the vaginal tract of reproductive, normal women. Its role is to protect the vagina from infections.

    • Richard Nikoley on October 9, 2014 at 09:17

      She lies all the time, including about stuff I’ve blogged or tweeted (what exactly was written, context, etc.). Narcissistic sociopath.

    • Jane Karlsson on October 10, 2014 at 02:24

      Yes, gut bugs are where it’s at. According to the paper on fibre and magnesium absorption, it’s the SCFA made by gut bugs which carry minerals into the cell. The SCFA go in together with protons, which come out again in exchange for metal ions.

      Protons mean acid of course, so acid not only encourages the right gut bugs, it also helps mineral absorption. According to Dr Jarvis the apple cider vinegar man, this is now vinegar works. People think it works by killing off the gut bugs, but I think it’s much more likely to work by providing minerals to the gut immune system, which can then kill only the bugs you don’t want.

    • Jane Karlsson on October 10, 2014 at 03:16

      Yes, quite a lot of what she says is untrue. Including what she has said about Stephan Guyenet’s work. I think she banned me for saying that.

      There is no evidence on her blog that she was once massively obese. The photos are either so dark you can’t see who it is, or so confused you can’t see whether she was fat. Her followers believe it because she says it.

    • Jane Karlsson on October 10, 2014 at 04:02

      Duck, you really have been doing your homework. I’ve been wondering about Lactobacillus bugs because they all like Mn and some of them like it a lot. They break down lactose, don’t they. I’ve heard people say the gene for lactase persistence isn’t necessary if you have the right gut bugs. What do you think about that?

  3. Jane+Karlsson on October 4, 2014 at 03:45

    “The biggest problem I have with brown rice is that it tends to taste like crap compared to white rice. ”

    Tastes like crap? Well I think white rice tastes of nothing. I don’t like long grain brown rice because it goes to mush, but short grain is chewy and nutty and absolutely delicious. I suspect people who prefer white rice haven’t tried it.

    • Richard Nikoley on October 4, 2014 at 08:10

      To me, brown rice tastes like musty bed sheets locked up all summer in a travel trailer smell.

    • Jane Karlsson on October 5, 2014 at 03:58

      Go on Richard, you’ve never actually tried musty bed sheets. A controlled experiment is in order here.

      How can it be that I used to eat brown rice every day and never noticed a bad taste? A good taste, yes, I certainly noticed that.

    • Duck Dodgers on October 5, 2014 at 08:01

      No idea. Nevertheless, the rancidity issues are well known.

      From: Method of stabilizing rice products, US Patent 2585978 A

      A problem that has plagued the rice industry for many years is the instability of the oil in the bran coating on rice, particularly after the hull has been removed. This oil develops fatty acids at a rapid rate and also rapidly becomes rancid in taste and odor. For this reason, brown rice (which is hulled rice consisting of the endosperm, the germ, and the bran layers) develops an unpleasant, rancid odor in a very short time, in a matter of weeks in the warmer climates. The instability of brown rice has therefore prevented the wide-spread use of this foodstuff despite the fact that it is more nutritious than white (polished) rice.

    • Jane Karlsson on October 6, 2014 at 02:05

      Yes the rancidity issues are well known. People used to pound their rice before machines were introduced. Home pounded rice is much better than machine polished rice because there is some bran (and germ?) left. When the machines were introduced there were epidemics of micronutrient deficiency disease.

      What’s the problem with eating your brown rice shortly after you buy it? Or keeping it in the fridge? If this really were a problem manufacturers would pack in in nitrogen.

    • Duck Dodgers on October 6, 2014 at 09:42

      “Home pounded rice is much better than machine polished rice because there is some bran (and germ?) left. When the machines were introduced there were epidemics of micronutrient deficiency disease.”

      Again, you are talking about people who use rice as a staple and are on a limited diet. It does not apply to people who occasionally have rice and make an effort to get even more nutrition from a wide range of sources.

      “What’s the problem with eating your brown rice shortly after you buy it?”

      Because it still tastes like crap, even when it’s right out of the bag. Don’t you think more Asians would have figured this out if it were that easy? I mean, most Asians go through rice very quickly. And yet, they still avoid brown rice. From the same study you linked to:

      From: Rice intake, weight change and risk of the metabolic syndrome development among Chinese adults: the Jiangsu Nutrition Study (JIN)

      “In the region, more than 99% of the rice consumed is white rice.”

      It’s like you think 99% of Asians are idiots. If brown rice is so essential, you would think you might see a little more excitement for the product if it’s as tasty and great as you claim it is.

    • Richard Nikoley on October 6, 2014 at 10:04


      I respect you on some levels. Really do, but you strike me as OCD, like a terrier that will not let go of a toy.

      It’s a fucking recipe, girl. Seriously? Use fucking brown rice if you like, let us know how it goes.

      I’m happy to give it a try. No big. Rice is not a staple for me, never has been. If it was, then I might try and understand better the pros and cons. And I understand that just because tons of people do one thing, doesn’t mean it’s best. On the other hand, if the whole rice-eating world goes with white polished, then I’m more inclined to go with “the wisdom of crowds” (especially since it’s ancient and not tainted by govco) and just do the white, which i prefer.

      So Sowwy.

    • Jane+Karlsson on October 7, 2014 at 03:09

      Well you obviously think most of your countrymen are idiots. They eat white flour, don’t they. They LIKE it. Perhaps they like being sick too. Nowadays we are so stressed illness is a welcome relief. Just wait until good healthcare is no longer available and see how much people still like eating this crap.

    • Jane+Karlsson on October 7, 2014 at 03:27

      Richard, if you are ‘so sowwy’ for your insults, your apology is accepted.

      “Use fucking brown rice if you like, let us know how it goes” …. I have already told you that I used to eat brown rice every day. You do not read what I write. This is your problem, not mine.

  4. Duck Dodgers on October 7, 2014 at 08:03

    Jane, we prefer to discuss bacteria here these days. So, if I can take this opportunity to redirect your talents—instead of obsessing about a salad ingredient, what do you make of this study?

    From: New insights into the protective effect of manganese against oxidative stress

    What other roles could manganese play to facilitate cell growth under conditions of oxidative stress? Anjem et al. (2009) remind us that, in addition to activation by OxyR, expression of mntH is repressed by iron-containing Fur, leading to the conclusion that E. coli switches on manganese uptake via MntH when iron levels are low. This observation leads to the authors to hypothesize that the role of manganese is to compensate for low availability of iron in the cell. Although manganese cannot be used in haem- and iron–sulphur-containing prosthetic groups, it could take the place of ferrous iron in some mononuclear metalloenzymes. Hence, manganese might serve to metallate certain key enzymes under conditions of iron limitation or peroxide stress. There is an additional complication in this scenario, namely the interaction between ferrous iron and hydrogen peroxide (the Fenton reaction), which generates the hydroxyl radical. Anjem et al. (2009) show that manganese can rescue an Hpx Δdps mutant. The Hpx mutant was previously shown to contain more iron in its ‘low molecular weight pool’ that the wild-type strains as a consequence of the oxidative degradation of iron–sulphur clusters, while Dps is an iron-binding protein that can protect DNA from oxidative damage (Park et al., 2005). Thus, it appears that manganese can also protect the bacteria from iron overload, consistent with the observation that an iron chelator can rescue an Hpx δmntH mutant…

    …It seems likely that the results from this study in E. coli will be applicable across a range of bacteria, even those where manganese plays a more prominent role. Many bacteria possess a high-affinity ABC cassette transporter for manganese and, at least in Gram-positive bacteria, production of this transporter is under the control of the manganese-dependent repressor MntR (reviewed by Kehres and Maguire (2003). The ability to accumulate manganese and the low requirement for iron in streptococci means that manganese might take on a more central role in cell metabolism as a prosthetic group in enzymes in such bacteria. Further investigation of the interplay between iron and manganese across a range of bacteria will be of great interest. The study by Anjem et al. (2009) helps rationalize the protective effects of manganese on cells and it should have an impact beyond the microbial world.

    I don’t pretend to know what any of that fully means, so would love to hear your thoughts.

    • Jane Karlsson on October 8, 2014 at 03:34

      Yes I think the interaction of bacteria with manganese could turn out to be very interesting indeed. The Lyme bacterium likes manganese, and lots of people think the symptoms of Lyme disease are due to manganese depletion.

      I have been wondering for a long time whether the benefits of resistant starch might be due in part to improvement of manganese absorption. We know that fermentable fibre improves magnesium absorption.

      I don’t think anyone has looked at its effects on manganese aborption, but Mn and Mg are chemically similar, and channels which transport Mg often transport Mn too. So it’s likely.

      One more thing about bacteria and manganese. Mn undergoes ‘enterohepatic circulation’, meaning it’s excreted in the bile and re-absorbed further down the gut. In the colon? Where all the friendly bacteria are? Might it be excreted in the bile for the express purpose of encouraging them?

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